Liver

The liver is a vital organ of vertebrates and some other animals. In the
human it is located in the upper right quadrant of the abdomen, below
thediaphragm. The liver has a wide range of functions,
including detoxification of various metabolites, protein synthesis, and the
production of biochemicals necessary for digestion. The liver is a gland and
plays a major role in metabolism with numerous functions in the human
body, including regulation of glycogen storage, decomposition of red blood
cells, plasma protein synthesis, hormone production, and detoxification.[3] It
is an accessory digestive gland and produces bile, an alkaline compound
which aids in digestion via theemulsification of lipids. The gallbladder, a
small pouch that sits just under the liver, stores bile produced by the liver.
The liver's highly specialized tissue consisting of
mostly hepatocytes regulates a wide variety of high-volume biochemical
reactions, including the synthesis and breakdown of small and complex
molecules, many of which are necessary for normal vital functions.
Estimates ).There is currently no way to compensate for the absence of
regarding the organ's total number of functions vary, but textbooks
generally cite it being around 500. Terminology related to the liver often
starts in hepar- or hepat- from the Greekword for liver, hpar (, root
hepat-, - liver function in the long term, although liver
dialysis techniques can be used in the short term.]Liver transplantation is
the only option for complete liver failure.

Hepatitis

Hepatitis

Alcoholic hepatitis evident by fatty

change, cellnecrosis, Mallory bodies
Classification and external resources
Specialty

Infectious
disease,gastroenterolog
y

ICD-10

K75.9

ICD-9-CM

573.3

DiseasesD
B

20061

MedlinePlu 001154
s
MeSH

D006505

Hepatitis (plural: hepatitides) is a medical condition defined by the

inflammation of the liver and characterized by the presence
of inflammatorycells in the tissue of the organ. Hepatitis may occur with
limited or no symptoms, but often leads to jaundice (a yellow discoloration
of the skin,mucous membrane, and conjunctiva), poor appetite,
and malaise. Hepatitis is acute when it lasts less than six months and
chronic when it persists longer.
Acute hepatitis can be self-limiting (healing on its own), can progress to
chronic hepatitis, or, rarely, can cause acute liver failure.[1] Chronic hepatitis

may have no symptoms, or may progress over time to fibrosis (scarring of

the liver) andcirrhosis (chronic liver failure).[2] Cirrhosis of the liver increases
the risk of developing hepatocellular carcinoma (a form of liver cancer).[3]
Worldwide, viral hepatitis is the most common cause of liver inflammation.
[4]
Other causes include autoimmune diseases and ingestion of toxic
substances (notably alcohol), certain medications (such as paracetamol),
some industrial organic solvents, and plants.
The term is derived from the Greek hpar (), meaning "liver", and the
suffix -itis (-), meaning "inflammation"
Contents
1 Signs and symptoms
1.1 Acute
1.2 Chronic
2 Causes
2.1 Viral hepatitis
2.2 Alcoholic hepatitis
2.3 Toxic and drug-induced hepatitis
2.4 Autoimmune
2.5 Non-alcoholic fatty liver disease
2.6 Ischemic hepatitis
2.7 Giant cell hepatitis
3 Mechanism
4 Diagnosis
4.1 Viral hepatitis
4.2 Differential diagnosis

4.3 Pathology
5 Prognosis
6 Prevention
6.1 Vaccines
7 See also
Signs and symptoms

A person with jaundice

Acute
Initial symptoms are non-specific and flu-like, common to almost all
acute viral infections, and may include malaise, muscle and joint
aches, fever, nausea orvomiting, diarrhea, and headache. More specific
symptoms, which can be present in acute hepatitis from any cause, are
profound loss of appetite, aversion
to smokingamong smokers, choluria (dark urine), jaundice (yellowing of the
eyes and skin), and abdominal discomfort. Before patients develop
jaundice, physical findings are uncommon. However, 5-10% of people with
hepatitis develop tender enlargement of the liver, enlarged lymph nodes,
and enlargement of the spleen.[6] Acute viral hepatitis is more likely to
be asymptomatic in children. General symptoms may last for 12 weeks
before jaundice develops, with the total illness lasting weeks. [7]
A small proportion of people with acute hepatitis progress to acute liver
failure, in which the liver is unable to remove harmful substances from the
blood (leading to confusion and coma due to hepatic encephalopathy) and
produce blood proteins (leading to peripheral edema and bleeding).[6]
Chronic
Chronic hepatitis may cause nonspecific symptoms such as malaise,
tiredness, and weakness, and often leads to no symptoms at all. It is

commonly identified on blood tests performed either for screening or to

evaluate nonspecific symptoms. The presence of jaundice indicates
advanced liver damage. On physical examination there may be
enlargement of the liver.[8]
Extensive damage to and scarring of liver (i.e., cirrhosis) leads to weight
loss, easy bruising and bleeding, peripheral edema(swelling of the legs),
and accumulation of ascites (fluid in the abdomen). Eventually, cirrhosis
may lead to various complications: esophageal varices (enlarged veins in
the wall of the esophagus that can cause life-threatening bleeding),hepatic
encephalopathy (confusion and coma), and hepatorenal syndrome (kidney
dysfunction).
Acne, abnormal menstruation, lung scarring, and inflammation of
the thyroid gland and kidneys may be present in womenwith autoimmune
hepatitis.[8] Hepatitis associated aplastic anemia may occur 2-3 months
after an acute attack of hepatitis.[9][10]
Causes

Viral hepatitis is the most common cause of hepatitis worldwide. [11] Other
common causes of non-viral hepatitis include toxic and druginduced, alcoholic, autoimmune, fatty liver, and metabolic disorders.[12] Less
commonly some bacterial, parasitic, fungal, mycobacterial and protozoal
infections can cause hepatitis.[13][14] Additionally, certain complications of
pregnancyand decreased blood flow to the liver can induce hepatitis.[13]
[15]
Cholestasis (obstruction of bile flow) due
to hepatocellulardysfunction, biliary tract obstruction, or biliary atresia can
result in liver damage and hepatitis.[16][17]
Viral hepatitis
The most common causes of viral hepatitis are the five unrelated
hepatotropic viruses hepatitis A, hepatitis B, hepatitis C,hepatitis D (which
requires hepatitis B to cause disease), and hepatitis E.
Hepatitis B is the most common viral hepatitis worldwide, affecting as much
as 10% of the adult population in endemic areas [18] and causing

approximately 780,000 deaths per year worldwide. It is most

often transmitted vertically in areas of high incidence (perinatally) from
mother to baby during birth) or horizontally by being exposed to infected
blood or blood products. While less common, Hepatitis B can also be
spread through exposure to mucous membranes. A vaccine is routinely
given in the developed world.[19]
In the United States, Hepatitis C has become the most common viral
hepatitis since widespread vaccination of Hepatitis B in the mid-1980's. It
affects an estimated 3.2 million adults living in the United States. Roughly
60-70% of HCV-infected adults living in the United States are unaware of
their infection. Even following decades without symptoms, HCV-infected
persons remain a source of transmission to others and they are also at
elevated risk for developing chronic liver disease and/or other chronic HCVrelated diseases.[20]

Alcoholic hepatitis
Excessive alcohol consumption is a significant cause of hepatitis and liver
damage (cirrhosis). Alcoholic hepatitis usually develops over years-long
exposure to alcohol. Alcohol intake in excess of 80 grams of alcohol a day
in men and 40 grams a day in women is associated with development of
alcoholic hepatitis. Alcoholic hepatitis can vary from mild asymptomatic
disease to severe liver inflammation and liver failure. Symptoms and
physical exam findings are similar to other causes of hepatitis. Laboratory
findings are significant for elevated transaminases, usually with elevation
of aspartate transaminase(AST) in a 2:1 ratio to alanine
transaminase (ALT).
Alcoholic hepatitis may lead to cirrhosis and is more common in patients
with long-term alcohol consumption and those infected with hepatitis C.
[23]
Patients who drink alcohol to excess are also more often than others
found to have hepatitis C.[24] The combination of hepatitis C and alcohol
consumption accelerates the development of cirrhosis. [25]
Toxic and drug-induced hepatitis

A large number of medications and other chemical agents can cause

hepatitis. In the United States acetaminophen,antibiotics, and central
nervous system medications are among the most common causes of druginduced hepatitis. Acetaminophen, also known as paracetamol, is the
leading cause of acute liver failure in the United States. Herbal remedies
and dietary supplements may also cause hepatitis; these are the most
common causes of drug-induced hepatitis in Korea. Risk factors for druginduced hepatitis include increasing age, female sex, and previous druginduced hepatitis. Genetic variability is increasingly understood as a key
predisposing risk factor to drug-induced hepatitis. Toxins and medications
can cause liver injury through a variety of mechanisms, including direct cell
damage, disrupting cell metabolism, and inducing structural changes.
Some medications, like acetaminophen, cause predictable doserelatedliver damage, whereas others cause idiosyncratic reactions that vary
among individuals. Exposure to other hepatotoxins can occur accidentally
or intentionally through ingestion, inhalation, and skin
absorption.Occupational exposure may occur in many work fields and can
present acutely or insidiously.[31] Mushroom poisoning is a common toxic
exposure that may result in hepatitis.

Autoimmune

Autoimmune hepatitis is a chronic disease caused by an abnormal immune

response against liver cells.[33] The disease is thought to have a genetic
predisposition as it is associated with certain human leukocyte antigens.
[34]
The symptoms of autoimmune hepatitis are similar to other hepatitides
and may have a fluctuating course from mild to very severe. Women with
the disease may have abnormal menstruation or become amenorrheic. The
disease occurs in people of all ages but most commonly in young women.
Many people with autoimmune hepatitis have other autoimmune diseases.
[35]

Non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is the occurrence of fatty liver in

people who have little or no history of alcohol use. In the early stage there
are usually no symptoms, as the disease progresses symptoms typical of
chronic hepatitis may develop.[36] NAFLD is associated with metabolic
syndrome, obesity, diabetes, and hyperlipidemia.[37] Severe NAFLD leads to
inflammation, fibrosis, and cirrhosis, a state referred to as non-alcoholic
steatohepatitis (NASH). Diagnosis requires excluding other causes of
hepatitis, including excessive alcohol intake. [38] While imaging can show
fatty liver, only liver biopsy can demonstrate inflammation and fibrosis
characteristic of NASH.[39] NASH is recognized as the third most common
cause of liver disease in the United States.[36]

Ischemic hepatitis

Injury to liver cells due to insufficient blood or oxygen results in ischemic

hepatitis (or shock liver).[40] The condition is most often associated
with heart failure but can also be caused by shock or sepsis. Blood
testing of a person with ischemic hepatitis will show very high levels
of transaminase enzymes (AST and ALT). The condition usually resolves if
the underlying cause is treated successfully. Ischemic hepatitis rarely
causes permanent liver damage.[41]

Giant cell hepatitis

Giant cell hepatitis is a rare form of hepatitis that predominantly occurs
in newborns and children. Diagnosis is made on the basis of the presence
of multinucleated hepatocyte giant cells on liver biopsy.[42] The cause of
giant cell hepatitis is unknown but the condition is associated with viral
infection, autoimmune disorders, and drug toxicity.

Mechanism
The specific mechanism varies and depends on the underlying cause for
the condition. In viral hepatitis, the presence of the virus in the liver cells
causes the immune system to attack the liver, resulting in inflammation and

impaired function. In autoimmune hepatitis, the immune system attacks the

liver due to the autoimmune disease.[46] In some hepatitis, often including
hepatitis caused by alcoholism, fat deposits accumulate in the liver,
resulting in fatty liver disease, also calledsteatohepatitis.

Diagnosis
Diagnosis is made by assessing an individual's symptoms, physical exam,
and medical history, in conjunction with blood tests, liver biopsy,
and imaging. Blood testing includes blood chemistry, liver
enzymes, serology and nucleic acid testing. Abnormalities in blood
chemistry and enzyme results may be indicative of certain causes or
stages of hepatitis. Imaging can identify steatosis of the liver but liver
biopsy is required to demonstrate fibrosis and cirrhosis. A biopsy is
unnecessary if the clinical, laboratory, and radiologic data suggests
cirrhosis. Furthermore, there is a small but significant risk to liver biopsy,
and cirrhosis itself predisposes for complications caused by liver biopsy.
Viral hepatitis

Viral hepatitis is mostly diagnosed through clinical laboratory testing. Some

of these tests react with the virus or parts of the virus, such as the Hepatitis
B surface antigen test or nucleic acid tests.[51][52] Many of the tests
are serological tests that react to the antibodies formed by the immune
system. For some major causes of viral hepatitis, such as Hepatitis B, there
are multiple serological tests used that provide additional information for
diagnosis.

Differential diagnosis
Several diseases can present with signs, symptoms, and/or liver function
test abnormalities similar to hepatitis. In severe cases of alpha 1-antitrypsin
deficiency (A1AD), excess protein in liver cells causes inflammation and
cirrhosis.[ Somemetabolic disorders cause damage to the liver through a
variety of mechanisms. In hemochromatosis and Wilson's diseasetoxic
accumulation of dietary minerals results in inflammation and cirrhosis.]

Pathology
The liver, like all organs, responds to injury in a limited number of ways and
a number of patterns have been identified. Liver biopsies are rarely
performed for acute hepatitis and because of this the histology of chronic
hepatitis is better known than that of acute hepatitis.
Acute
In acute hepatitis the lesions (areas of abnormal tissue) predominantly
contain diffuse sinusoidal and portal mononuclear infiltrates
(lymphocytes, plasma cells, Kupffer cells) and
swollen hepatocytes. Eosinophilic cells (Councilman bodies) are common.
Hepatocyte regeneration and cholestasis (canalicular bile plugs) typically
are present. Bridging hepatic necrosis(areas of necrosis connecting two or
more portal tracts) may also occur. There may be some lobular disarray.
Although aggregates of lymphocytes in portal zones may occur these are
usually neither common nor prominent. The normal architecture is
preserved. There is no evidence of fibrosis or cirrhosis (fibrosis plus
regenerative nodules). In severe cases prominent hepatocellular necrosis
around the central vein.
In submassive necrosis a rare presentation of acute hepatitis there is
widespread hepatocellular necrosis beginning in the centrizonal
distribution and progressing towards portal tracts. The degree
of parenchymal inflammation is variable and is proportional to duration
of disease. Two distinct patterns of necrosis have been recognised: (1)
zonal coagulative necrosis or (2) panlobular (nonzonal) necrosis.
Numerous macrophages and lymphocytes are present. Necrosis and
inflammation of the biliary tree occurs. Hyperplasia of the surviving biliary
tract cells may be present. Stromal haemorrhage is common.
The histology may show some correlation with the cause:
Zone 1 (periportal) occurs in phosphorus poisoning or eclampsia.
Zone 2 (midzonal) rare is seen in yellow fever.

Zone 3 (centrilobular) occurs with ischemic injury, toxic effects, carbon

tetrachloride exposure or chloroform ingestion. Drugs such as
acetaminophen may be metabolized in zone 1 to toxic compounds that
cause necrosis in zone 3.
Where patients have recovered from this condition, biopsies commonly
show multiacinar regenerative nodules (previously known as adenomatous
hyperplasia). Massive hepatic necrosis is also known and is usually rapidly
fatal. The pathology resembles that of submassive necrosis but is more
marked in both degree and extent.

Chronic
Chronic hepatitis has been better studied and several conditions have been
described.
Chronic hepatitis with piecemeal (periportal) necrosis (or interface hepatitis)
with or without fibrosis. (formerly chronic active hepatitis) is any case of
hepatitis occurring for more than 6 months with portal based inflammation,
fibrosis, disruption of the terminal plate, and piecemeal necrosis. This term
has now been replaced by the diagnosis of 'chronic hepatitis'.
Chronic hepatitis without piecemeal necrosis (formerly called chronic
persistent hepatitis) has no significant periportal necrosis or regeneration
with a fairly dense mononuclear portal infiltrate. Councilman bodies are
frequently seen within the lobule. Instead it includes persistent
parenchymal focal hepatocyte necrosis (apoptosis) with mononuclear
sinusoidal infiltrates.
The older terms have been deprecated because the conditions are now
understood as being able to alter over time so that what might have been
regarded as a relatively benign lesion could still progress to cirrhosis. The
simpler term chronic hepatitis is now preferred in association with the
causative agent (when known) and a grade based on the degree of
inflammation, piecemeal or bridging necrosis (interface hepatitis) and the
stage of fibrosis. Several grading systems have been proposed but none
have been adopted universally.

Cirrhosis is a diffuse process characterized by regenerative nodules that

are separated from one another by bands of fibrosis. It is the end stage for
many chronic liver diseases. The pathophysiological process that results in
cirrhosis is as follows: hepatocytes are lost through a gradual process of
hepatocellular injury and inflammation. This injury stimulates a regenerative
response in the remaining hepatocytes. The fibrotic scars limit the extent to
which the normal architecture can be reestablished as the scars isolate
groups of hepatocytes. This results in nodule formation. Angiogenisis (new
vessel formation) accompanies scar production which results in the
formation of abnormal channels between the central hepatic veins and the
portal vessels. This in turn causes shunting of blood around the
regenerating parenchyma. Normal vascular structures including the
sinusoidal channels may be obliterated by fibrotic tissue leading to portal
hypertension. The overall reduction in hepatocyte mass, in conjunction with
the portal blood shunting, prevents the liver from accomplishing its usual
functions the filtering of blood from the gastrointestinal tract and serum
protein production. These changes give rise to the clinical manifestations of
cirrhosis.
Specific causes

Most of the causes of hepatitis cannot be distinguished on the basis of the

pathology but some do have particular features that are suggestive of a
particular diagnosis. The presence of micronodular cirrhosis, Mallory
bodies and fatty change within a single biopsy are highly suggestive of
alcoholic injury. Perivenular, pericellular fibrosis (known as 'chicken wire
fibrosis' because of its appearance on trichrome or Van Gieson's stains)
with partial or complete obliteration of the central vein is also very
suggestive of alcohol abuse.
Cardiac, ischemic and venous outflow obstruction all cause similar
patterns. The sinusoids are often dilated and filled with erythrocytes. The
liver cell plates may be compressed. Coagulative necrosis of the
hepatocytes can occur around the central vein. Hemosiderin and
lipochrome laden macrophages and inflammatory cells may be found. At

the edge of the fibrotic zone cholestasis may be present. The portal tracts
are rarely significantly involved until late in the course.
Biliary tract disease including primary biliary cirrhosis, sclerosing
cholangitis, inflammatory changes associated with idiopathic inflammatory
bowel disease and duct obstruction have similar histology in their early
stages. Although these diseases tend to primarily involve the biliary tract
they may also be associated with chronic inflammation within the liver and
difficult to distinguish on histological grounds alone. The fibrotic changes
associated with these diseases principally involve the portal tracts with
cholangiole proliferation, portal tract inflammation
with neutrophils surrounding the cholangioles, disruption of the terminal
plate by mononuclear inflammatory cells and occasional hepatocyte
necrosis. The central veins are either not involved in the fibrotic process or
become involved only late in the course of the disease. Consequently the
centralportal relationships are minimally distorted. Where cirrhosis is
present it tends to be in the form of a portalportal bridging fibrosis.
Hepatitis E causes different histological patterns that depend on the host's
background. In immunocompetent patients the typical pattern is of severe
intralobular necrosis and acute cholangitis in the portal tract with numerous
neutrophils. This normally resolves without sequelae. Disease is more
severe in those with preexisting liver disease such as cirrhosis. In the
immunocompromised patients chronic infection may result with rapid
progression to cirrhosis. The histology is similar to that found in hepatitis C
virus with dense lymphocytic portal infiltrate, constant piecemeal necrosis
and fibrosis.

Prognosis
The outcome of hepatitis depends heavily on the disease or condition that
is causing the symptoms. For some causes, such as subclinical Hepatitis A
infection, the person may not experience any symptoms and will recover
without any long-term effects. For other causes hepatitis can result in
irreparable damage to the liver and require a liver transplant. A subset

referred to in a 1993 classification as "hyperacute" liver failure can happen

in less than a week.
The liver can regenerate damaged cells. Chronic damage to the liver can
result in the formation of scar tissue calledfibrosis and can result
in nodules that block the liver from functioning properly; this condition is
called cirrhosis and is not reversible. Cirrhosis may indicate a liver
transplant is necessary. Another complication of chronic hepatitis is liver
cancer, specifically hepatocellular carcinoma.
In March 2015 the World Health Organisation issued its first guidelines for
the treatment of chronic hepatitis B. This condition is affecting some 240
million people worldwide. These guidelines are for the prevention, care and
treatment of persons living with chronic hepatitis B.
Prevention

Vaccines
Vaccines are available to prevent hepatitis A and B. Hepatitis A immunity is
achieved in 99-100% of persons receiving the two-dose inactivated virus
vaccine. The hepatitis A vaccine is not approved for children under one
year of age. Vaccines to prevent hepatitis B have been available since
1986 and have been incorporated into at least 177 national immunization
programs for children. Immunity is achieved in greater than 95% of children
and young adults receiving the three-dose recombinant virus vaccine.
Vaccination within 24 hours of birth can prevent transmission from an
infected mother. Adults over 40 years of age have decreased immune
response to the vaccine. TheWorld Health Organization recommends
vaccination of all children, particularly newborns in countries where
hepatitis B is common to prevent transmission from the mother to child.
Alcoholic liver disease

Alcoholic liver disease

Microscopy of liver showing fatty change,

cell necrosis, Mallory bodies
Classification and external resources
Specialty

Gastroenterology

ICD-10

K70

ICD-9-CM

571.1

MedlinePlus

000281

MeSH

D008108

Alcoholic liver disease is a term that encompasses the liver manifestations

of alcohol overconsumption, including fatty liver, alcoholic hepatitis, and
chronic hepatitis with liver fibrosis or cirrhosis.
It is the major cause of liver disease in Western countries.
Although steatosis(fatty liver) will develop in any individual who consumes
a large quantity of alcoholic beverages over a long period of time, this
process is transient and reversible. Of all chronic heavy drinkers, only 15
20% develop hepatitis or cirrhosis, which can occur concomitantly or in
succession.
How alcohol damages the liver is not completely understood. 80% of
alcohol passes through the liver to be detoxified. Chronic consumption of
alcohol results in the secretion of pro-inflammatory cytokines (TNFalpha, Interleukin 6[IL6] and Interleukin 8 [IL8]), oxidative stress, lipid
peroxidation, andacetaldehyde toxicity. These factors cause

inflammation, apoptosis and eventually fibrosis of liver cells. Why this

occurs in only a few individuals is still unclear. Additionally, the liver has
tremendous capacity to regenerate and even when 75% of hepatocytes are
dead, it continues to function as normal.[3]
Contents

1 Risk factors
2 Pathophysiology
2.1 Fatty change
2.2 Alcoholic hepatitis
2.3 Cirrhosis
3 Diagnosis
3.1 Laboratory findings
4 Treatment
4.1 Medications
4.2 Transplantation
4.3 Antioxidants
5 Prognosis

Risk factors

The risk factors presently known are:

Quantity of alcohol taken: Consumption of 6080g per day (about 75100
ml/day) for 20 years or more in men, or 20g/day (about 25 ml/day) for
women significantly increases the risk of hepatitis and fibrosis by 7 to 47%,

Pattern of drinking: Drinking outside of meal times increases up to 3 times

the risk of alcoholic liver disease.
Gender: Women are twice as susceptible to alcohol-related liver disease,
and may develop alcoholic liver disease with shorter durations and doses
of chronic consumption. The lesser amount of alcohol dehydrogenase
secreted in the gut, higher proportion of body fat in women, and changes in
fat absorption due to the menstrual cycle may explain this phenomenon.
Hepatitis C infection: A concomitant hepatitis C infection significantly
accelerates the process of liver injury.
Genetic factors: Genetic factors predispose both to alcoholism and to
alcoholic liver disease. Both monozygotic twins are more likely to be
alcoholics and to develop liver cirrhosis than both dizygotic twins.
Polymorphisms in the enzymes involved in the metabolism of alcohol, such
as ADH, ALDH, CYP4502E1, mitochondrial dysfunction, and cytokine
polymorphism may partly explain this genetic component. However, no
specific polymorphisms have currently been firmly linked to alcoholic liver
disease.
Iron overload (Hemochromatosis)

Diet: Malnutrition, particularly vitamin A and E deficiencies, can worsen

alcohol-induced liver damage by preventing regeneration of hepatocytes.
This is particularly a concern as alcoholics are usually malnourished
because of a poor diet, anorexia, and encephalopathy.

Pathophysiology

Pathogenesis of alcohol induced liver injury

Fatty change
Fatty change, or steatosis is the accumulation of fatty acids in liver cells.
These can be seen as fatty globules under the microscope. Alcoholism

causes development of large fatty globules (macro vesicular steatosis)

throughout the liver and can begin to occur after a few days of heavy
drinking.Alcohol is metabolized by alcohol dehydrogenase (ADH)
into acetaldehyde, then further metabolized by aldehyde
dehydrogenase (ALDH) into acetic acid, which is finally oxidized
into carbon dioxide(CO2) and water (H2O).This process generates NADH,
and increases the NADH/NAD+ ratio. A higher NADH concentration
induces fatty acid synthesis while a decreased NAD level results in
decreased fatty acid oxidation. Subsequently, the higher levels of fatty
acids signal the liver cells to compound it to glycerol to formtriglycerides.
These triglycerides accumulate, resulting in fatty liver.

Alcoholic hepatitis

Causes
Alcoholic liver disease occurs after years of heavy drinking.
Alcohol can cause inflammation in the liver. Over time, scarring
and cirrhosis can occur. Cirrhosis is the final phase of alcoholic
liver disease.
Alcoholic liver disease does not occur in all heavy drinkers. The
chances of getting liver disease go up the longer you have been
drinking and more alcohol you consume. You do not have to get
drunk for the disease to happen.
The disease seems to be more common in some families. Women
may be more likely to have this problem than men.

Symptoms

Symptoms vary, based on how bad the disease is. You may not
have symptoms in the early stages. Symptoms tend to be worse
after a period of heavy drinking.
Digestive symptoms include:
Pain and swelling in the abdomen
Decreased appetite and weight loss
Nausea and vomiting
Fatigue
Dry mouth and increased thirst
Bleeding from enlarged veins in the walls of the lower part of the
esophagus (tube that connects your throat to your stomach)
Skin problems such as:
Yellow color in the skin, mucus membranes, or eyes (jaundice)
Small, red spider-like veins on the skin
Very dark or pale skin
Redness on the feet or hands
Itching
Brain and nervous system symptoms include:
Problems with thinking, memory, and mood
Fainting and lightheadedness
Numbness in legs and feet
Exams and Tests
Complete blood count (CBC)
Liver biopsy

Liver function tests

Tests to rule out other diseases include:
Abdominal CT scan
Blood tests for other causes of liver disease
Ultrasound of the abdomen
Treatment
The most important part of treatment is to stop using alcohol
completely. If liver cirrhosis has not yet occurred, the liver can
heal if you stop drinking alcohol.
An alcohol rehabilitation program or counseling may be necessary
to break the alcohol addiction. Vitamins, especially B-complex and
folic acid, can help reverse malnutrition.
If cirrhosis develops, you may need to manage the complications
of cirrhosis. You may need a liver transplant if there has been a lot
of liver damage.

Support Groups
Many people benefit from joining support groups
for alcoholism or liver disease.
Outlook (Prognosis)
Continued excessive drinking can shorten your lifespan. Your risk
for complications such as bleeding, brain changes, and severe
liver damage go up. The outcome will likely be poor if you keep
drinking.
When to Contact a Medical Professional
Call your health care provider if:
You develop symptoms of alcoholic liver disease.

You develop symptoms after a long period of heavy drinking.

You are worried that drinking may be harming your health.

Prevention
Talk to your doctor about your alcohol intake. The doctor can
counsel you about how much alcohol is safe for you.

Alcoholic hepatitis is characterized by the inflammation of hepatocytes.

Between 10% and 35% of heavy drinkers develop alcoholic hepatitis
(NIAAA, 1993). While development of hepatitis is not directly related to the
dose of alcohol, some people seem more prone to this reaction than
others. This is called alcoholic steato necrosis and the inflammation
appears to predispose to liver fibrosis. Inflammatory cytokines (TNF-alpha,
IL6 and IL8) are thought to be essential in the initiation and perpetuation of
liver injury by inducing apoptosis and necrosis. One possible mechanism
for the increased activity of TNF- is the increased intestinal permeability
due to liver disease. This facilitates the absorption of the gut-produced
endotoxin into the portal circulation. The Kupffer cells of the liver then
phagocytose endotoxin, stimulating the release of TNF-. TNF- then
triggers apoptotic pathways through the activation of caspases, resulting in
cell death.
Cirrhosis

Cirrhosis is a late stage of serious liver disease marked

by inflammation (swelling), fibrosis (cellular hardening) and damaged
membranes preventing detoxification of chemicals in the body, ending in
scarring and necrosis (cell death). Between 10% to 20% of heavy drinkers
will develop cirrhosis of the liver (NIAAA, 1993). Acetaldehyde may be
responsible for alcohol-induced fibrosis by stimulating collagen deposition
by hepatic stellate cells.[2] The production of oxidants derived from NADPH
oxi- dase and/or cytochrome P-450 2E1 and the formation of acetaldehyde-

protein adducts damage the cell membrane.

[2]
Symptoms include jaundice (yellowing), liver enlargement, and pain and
tenderness from the structural changes in damaged liver architecture.
Without total abstinence from alcohol use, will eventually lead to liver
failure. Late complications of cirrhosis or liver failure include portal
hypertension (high blood pressure in the portal vein due to the increased
flow resistance through the damaged liver), coagulation disorders (due to
impaired production of coagulation factors), ascites (heavy abdominal
swelling due to buildup of fluids in the tissues) and other complications,
including hepatic encephalopathy and the hepatorenal syndrome. Cirrhosis
can also result from other causes than alcohol abuse, such asviral
hepatitis and heavy exposure to toxins other than alcohol. The late stages
of cirrhosis may look similar medically, regardless of cause. This
phenomenon is termed the "final common pathway" for the disease. Fatty
change and alcoholic hepatitis with abstinence can be reversible. The later
stages of fibrosis and cirrhosis tend to be irreversible, but can usually be
contained with abstinence for long periods of time.
Diagnosis

In the early stages, patients with ALD exhibits subtle and often no abnormal
physical findings. It is usually not until development of advanced liver
disease that stigmata of chronic liver disease become apparent. Early ALD
is usually discovered during routine health examinations when liver enzyme
levels are found to be elevated. These usually reflect alcoholic hepatic
steatosis. Microvesicular and macrovesicular steatosis with inflammation
are seen in liver biopsy specimens. These histologic features of ALD are
indistinguishable from those of nonalcoholic fatty liver disease. Steatosis
usually resolves after discontinuation of alcohol use.Continuation of alcohol
use will result in a higher risk of progression of liver disease and cirrhosis.
In patients with acute alcoholic hepatitis,clinical manifestations include
fever, jaundice, hepatomegaly, and possible hepatic decompensation with
hepatic encephalopathy,variceal bleeding,and ascites accumulation.Tender
hepatomegaly may be present, but abdominal pain is unusual.
Occasionally, the patient may be asymptomatic.

Laboratory findings
In people with alcoholic hepatitis, the serum aspartate aminotransferase
(AST) to alanine aminotransferase (ALT) ratio is greater than 2:1.AST and
ALT levels are almost always less than 500. The elevated AST to ALT ratio
is due to deficiency of pyridoxal-6-phosphate, which is required in the ALT
enzyme synthetic pathway. Furthermore, alcohol metaboliteinduced injury
of hepatic mitochondria results in AST isoenzyme release. Other laboratory
findings include red blood cell macrocytosis (mean corpuscular volume >
100) and elevations of serum -glutamyl transferase, alkaline phosphatase,
and bilirubin levels. Folate level is reduced in alcoholic patients due to
decreased intestinal absorption, increased bone marrow requirement for
folate in the presence of alcohol,and increased urinary loss.The magnitude
of leukocytosis reflects severity of liver injury. Histologic features include
Mallory bodies, giant mitochondria, hepatocyte necrosis, and neutrophil
infiltration at the perivenular area. Mallory bodies, which are also present in
other liver diseases,are condensations of cytokeratin components in the
hepatocyte cytoplasm and do not contribute to liver injury.Up to 70% of
patients with moderate to severe alcoholic hepatitis already have cirrhosis
identifiable on biopsy examination at the time of diagnosis. Treatment
Not drinking further alcohol is the most important part of treatment. People
with chronic HCV infection should abstain from any alcohol intake, due to
the risk for rapid acceleration of liver disease.
Medications

A 2006 Cochrane review did not find evidence sufficient for the use
of corticosteroids.[10] They are sometimes; however, recommended when
severe liver inflammation is present.
The effects of antitumor necrosis factor medication such
as infliximab and etanercept are unclear and possibly harmful.
Evidence is unclear for pentoxifylline.
Propylthiouracil may result in harm.
Evidence does not support supplemental nutrition in liver disease. [14]

Transplantation
Although in rare cases liver cirrhosis is reversible,the disease process
remains mostly irreversible. Liver transplantation remains the only definitive
therapy.Today,survival after liver transplantation is similar for people with
ALD and nonALD. The requirements for transplant listing are the same as
those for other types of liver disease, except for a 6-month sobriety
prerequisite along with psychiatric evaluation and rehabilitation assistance
(i.e., Alcoholics Anonymous). Specific requirements vary among the
transplant centers. Relapse to alcohol use after transplant listing results in
delisting. Re-listing is possible in many institutions, but only after 36
months of sobriety. There are limited data on transplant survival in patients
transplanted for acute alcoholic hepatitis,but it is believed to be similar to
that in nonacute ALD, non-ALD, and alcoholic hepatitis with MDF less than
32.
Antioxidants

Alcohol-induced liver damage occurs via generation of oxidants.

Thus alternative health care practitioners often recommend
natural antioxidant supplements like milk thistle. Currently, there exists no
substantive clinical evidence to suggest that milk thistle or
other antioxidant supplements are efficacious beyond placebo in treating
liver disease caused by chronic alcohol consumption.
One review claimed benefit for S-adenosyl methionine in disease models.
There however is insufficient human evidence.
Prognosis

The prognosis for people with ALD depends on the liver histology as well
as cofactors, such as concomitant chronic viral hepatitis.Among patients
with alcoholic hepatitis, progression to liver cirrhosis occurs at 1020% per
year, and 70% will eventually develop cirrhosis. Despite cessation of
alcohol use, only 10% will have normalization of histology and serum liver
enzyme levels. As previously noted, the MDF has been used to predict
short-term mortality (i.e., MDF 32 associated with spontaneous survival of
5065% without corticosteroid therapy, and MDF < 32 associated with

spontaneous survival of 90%).The Model for End-Stage Liver Disease

(MELD) score has also been found to have similar predictive accuracy in
30day (MELD > 11) and 90-day (MELD > 21) mortality. Liver cirrhosis
develops in 614% of those who consume more than 6080 g of alcohol
daily for men and more than 20 g daily for women. Even in those who drink
more than 120 g daily, only 13.5% will suffer serious alcohol-related liver
injury. Nevertheless, alcohol-related mortality was the third leading cause of
death in 2003 in the United States. Worldwide mortality is estimated to be
150,000 per year.[22]
Symptoms of alcohol-related liver disease

In many cases, people with alcohol-related liver disease (ARLD) do

not have any noticeable symptoms until their liver is badly damaged.
Early symptoms
If you do experience early symptoms of ARLD, these are often quite vague,
such as:
tummy (abdominal) pain
loss of appetite
fatigue
feeling sick (nausea)
diarrhoea
feeling generally unwell
Advanced symptoms
As your liver becomes more severely damaged, you will usually develop
more obvious and serious symptoms, such as:
yellowing of the skin and whites of the eyes (jaundice)
swelling in the legs, ankles and feet due to a build-up of fluid (oedema)
swelling in your abdomen due to a build-up of fluid known as ascites

a high temperature (fever) and shivering attacks

very itchy skin
hair loss
unusually curved fingertips and nails (clubbed fingers)
blotchy red palms
significant weight loss
weakness and muscle wasting
confusion and memory problems, problems sleeping (insomnia) and
changes in your personality due to a build-up of toxins in the brain
vomiting blood and black, tarry stools due to internal bleeding
a tendency to bleed and bruise more easily, such as
frequent nosebleeds and bleeding gums
increased sensitivity to alcohol and drugs (because the liver cannot
process them)

These recommendations provide a data-supported approach.

They are based on the following: (i) a formal review and analysis
of the recently published world literature on the topic (Medline
search); (ii) American College of Physicians Manual for Assessing
Health Practices and Designing Practice Guidelines (1); (iii)
guideline policies, including the American Association for the
Study of Liver Diseases (AASLD) Policy on the development and
use of practice guidelines and the AGA Policy Statement on
Guidelines (2); and (iv) the experience of the authors in the
specified topic. Intended for use by physicians, these
recommendations suggest preferred approaches to the
diagnostic, therapeutic, and preventive aspects of care. They are

intended to be flexible, in contrast to the standards of care, which

are inflexible policies to be followed in every case. Specific
recommendations are based on relevant published information. To
more fully characterize the quality of evidence supporting the
recommendations, the Practice Guideline Committee of the
AASLD requires a Class (reflecting the benefit vs. risk) and Level
(assessing the strength or certainty) of Evidence to be assigned
and reported with each recommendation (Table 1, adapted from
the American College of Cardiology and the American Heart
Association Practice Guidelines) .
T
Alcohol consumption is a major risk factor for chronic disease
worldwide; it accounted for 3.8% of all deaths in 2004. 1 It is also a
major cause of chronic liver disease in Western countries. Alcoholrelated liver deaths account for up to 48% of cirrhosis-associated
deaths in the United States2 and are also major contributors to
liver disease-related mortality in other countries. 1 Research on
alcoholic liver disease (ALD) has been rapidly growing since the
early 1960s; at that time, Lieber et al used experimental models
to show that alcohol is a true hepatotoxin, which causes
hepatocellular damage, and that ALD is not simply caused by
malnutrition.3 Early studies indicated that ethanol metabolismassociated oxidative stress, glutathione depletion, abnormal
methionine metabolism, malnutrition, ethanol-mediated induction
of leakage of gut endotoxins, and subsequent activation of Kupffer
cells have important roles in the pathogenesis of ALD. 4-9 We
review advances made in the past 10 years in our understanding
of the roles of lipopolysaccharide (LPS) signaling, innate
immunity, and transcription factors in the pathogenesis of ALD.
We also review recent studies showing that alcohol mediates
changes in epigenetic features, microRNAs (miRNAs), and stem
cells, which could also contribute to ALD.
Despite the profound economic and health impact of ALD, little
progress has been made in the management of patients with this

severe clinical condition. There are no modern diagnostic tools to

assess individual susceptibility to the development of ALD, and
the pathogenesis of ALD in humans is incompletely understood.
As a consequence, no new drugs for ALD have been successfully
developed since the early 1970s, at which time the use of
corticosteroids was proposed for the treatment of severe alcoholic
hepatitis.10 The poor therapeutic progress in the field of ALD has,
in part, resulted from the lack of experimental models of
advanced ALD and from difficulties in performing clinical trials in
patients with an active addiction. We review several potential
targets that could generate therapeutic interventions for ALD.
Spectrum, Risk Factors, and Comorbidities
ALD presents as a broad spectrum of disorders, ranging from
simple fatty liver to more severe forms of liver injury, including
alcoholic hepatitis (AH), cirrhosis, and superimposed
hepatocellular carcinoma (HCC) Fatty liver, an early response to
alcohol consumption, develops in most (more than 90%) heavy
drinkers, with early-mild steatosis in zone 3 (perivenular)
hepatocytes; it can also affect zone 2 and even zone 1 (periportal)
hepatocytes when liver injury is more severe. Interestingly, only
about 30% of heavy drinkers develop more severe forms of ALD,
such as advanced fibrosis and cirrhosis. In patients with
underlying ALD and heavy alcohol intake, episodes of
superimposed AH may occur. In severe cases and in patients with
liver cirrhosis, AH leads to severe complications related to liver
failure and portal hypertension and has high short-term mortality.

Spectrum of ALD, risk factors, and comorbidity. More than 95% of

heavy drinkers develop fatty liver, but only up to 35% of this
population develops more severe forms of ALD, including fibrosis,
alcoholic hepatitis, cirrhosis, and HCC. Many risk factors ...

The fact that only about 35% of heavy drinkers develop advanced
ALD indicates that other factors are involved. Several risk factors
for ALD have been identified (These include sex, obesity, drinking
patterns, dietary factors, non-sex-linked genetic factors, and
cigarette smoking Female sex is a well-documented risk factor for
susceptibility to ALD; the increased risk among women likely
results from lower levels of gastric alcohol dehydrogenase, a
higher proportion of body fat, and the presence of estrogens.
Obesity represents another important risk factor that accelerates
fibrosis progression and the development of cirrhosis in
ALD.14,15 Experimental studies indicate that the synergistic effects
of obesity and alcohol abuse involve the endoplasmic reticulum
response to cell stress, type I macrophage activation, and
adiponectin resistance.16 Daily or near-daily heavy drinking, begun
at an early age, increases the risk of the development of severe
forms of ALD compared with episodic or binge drinking. 17 Genetic
factors might also influence susceptibility to advanced ALD, but
little data are available. Variations in genes that encode
antioxidant enzymes, cytokines and other inflammatory
mediators, and alcohol-metabolizing enzymes could have a
role.13 Also, recent studies indicate that variations in patatin-like
phospholipase domain-containing protein 3 ( PNPLA3) affect
development of alcoholic cirrhosis in white alcoholic subjects. 1820
Despite the strong link between the PNPLA3 polymorphisms and
fatty liver diseases, deletion of this gene did not affect obesityassociated fatty liver or levels of liver enzymes in mice fed a highfat diet.21 Further studies are required to clarify the role
ofPNPLA3 variants in the pathogenesis of ALD.
Finally, long-term alcohol drinking has synergistic effects with
hepatitis virus B or C and/or human immunodeficiency virus
infection, nonalcoholic fatty liver disease, and disorders such as
hemochromatosis to accelerate progression of liver diseases. For
example, many patients with viral hepatitis consume alcohol,
which accelerates progression of liver fibrosis, cirrhosis, and HCC,

likely via multiple mechanisms.22,23 A greater understanding of the

interaction between alcohol and these comorbid factors could
help us design better therapies for the treatment of chronic liver
disease.
Pathogenesis
Alcoholic Fatty Liver (Steatosis)
Steatosis, the earliest response of the liver to alcohol abuse, is
characterized by the accumulation of fat (mainly triglycerides,
phospholipids, and cholesterol esters) in hepatocytes. Early
studies indicated that alcohol consumption increases the ratio of
reduced nicotinamide adenine dinucleotide/oxidized nicotinamide
adenine di-nucleotide in hepatocytes, which disrupts
mitochondrial -oxidation of fatty acids and results in steatosis.
Alcohol intake has also been shown to augment the supply of
lipids to the liver from the small intestine, increasing mobilization
of fatty acids from adipose tissue and uptake of fatty acids by the
liver. However, the contribution of these mechanisms to the
development of steatosis after long-term alcohol consumption is
not clear and requires further investigation.
Recent studies indicate that alcohol exposure, directly or
indirectly, regulates lipid metabolism-associated transcription
factors; this stimulates lipogenesis and inhibits fatty acid
oxidation. Ethanol increases fatty acid synthesis in hepatocytes
via up-regulation of sterol regulatory element-binding protein 1c
(SREBP-1c), a transcription factor that promotes fatty acid
synthesis via up-regulation of lipogenic genes. Alcohol
consumption could directly increase transcription of SREBP-1c
gene via its metabolite acetaldehyde or indirectly up-regulate
SREBP-1c expression by activating processes and factors that
stimulate SREBP-1c expression, such as the endoplas mic
reticulum response to cell stress, adenosine, endocannabinoids,
LPS signaling via Toll-like receptor (TLR) 4, and its downstream

proteins, including IRF-3, Egr-1, or tumor necrosis factor (TNF)- .

Alcohol also down-regulates factors that reduce SREBP-1c
expression, such as AMP-activated protein kinase (AMPK),
Sirtuin1, adiponectin, and signal transducer and activator of
transcription 3 (STAT3). Disruption of SREBP-1c in mice reduced
ethanol-induced fatty liver, indicating its role in ALD.

Mechanisms of alcoholic fatty liver. (1) Alcohol consumption can

directly (via acetaldehyde) or indirectly (via regulation of multiple
factors) up-regulate the expression of SREBP-1c and downregulate the expression of PPAR-, leading to the induction ...
Alcohol consumption inhibits fatty acid oxidation in hepatocytes
mainly via inactivation of the peroxisome proliferator-activated
receptor (PPAR)-, a nuclear hormone receptor that controls
transcription of a range of genes involved in free fatty acid
transport and oxidation. The ethanol metabolite acetaldehyde,
but not ethanol itself, directly inhibits the transcriptional
activation activity and DNA-binding ability of PPAR- in
hepatocytes. Ethanol consumption can also indirectly inhibit PPAR via up-regulation of cytochrome P450 2E1-derived oxidative
stressand adenosine, both of which inhibit PPAR- , or via downregulation of adiponectin and zinc, which each activate PPAR-.
In addition to regulating fat metabolism-associated transcription
factors, ethanol can also affect the activities of enzymes involved
in fat metabolism by inhibiting AMPK, which reduces fat
metabolism and fatty liver. AMPK is a serine-threonine kinase that
can phosphorylate and subsequently inactivate acetyl-CoA
carboxylase (ACC), a rate-limiting enzyme for fatty acid synthesis.
Inactivation of ACC also reduces levels of malonyl-CoA, a
precursor in fatty acid synthesis and an inhibitor of carnitine
palmitoyltransferase 1, a rate-limiting enzyme for fatty acid
oxidation. In addition, AMPK directly phosphorylates and inhibits

SREBP activity in hepatocytes, thereby attenuating steatosis. In

this man ner, AMPK inhibits fatty acid synthesis but promotes
fatty acid oxidation via the inactivation of ACC enzyme activity.
Alcohol consumption inhibits AMPK activity in the liver, leading to
decreased phosphorylation and increased activity of ACC and
decreased activity of carnitine palmitoyltransferase 1; each has
an important role in the development of alcoholic fatty liver.
Ethanol-induced steatosis is markedly reduced in many strains of
mice, including HIF-1/,C3/,C1qa/,PKC/, and iNOS,/
indicating that regulation of these genes also contributes to the
pathogenesis of alcoholic fatty liver. However, the underlying
mechanisms remain to be determined.
Finally, autophagy has an important role in removing lipid droplets
in hepatocytes. Long-term alcohol consumption inhibits
autophagy. However, a recent study showed that short-term
ethanol exposure activates autophagy by generating reactive
oxygen species and inhibiting the mammalian target of
rapamycin, indicating that acute ethanol activation of autophagy
could have a compensatory role that prevents development of
steatosis during the early stages of alcoholic liver injury. The
inhibitory and stimulatory effects of ethanol on autophagy require
further studies to clarify.
AH
AH is a syndrome characterized by infiltration of the liver by
inflammatory cells and hepatocellular injury. AH develops in
patients with steatosis and is usually associated with progressive
fibrosis. The prevalence of AH has not been accurately
determined; it is believed to occur in 10% to 35% of heavy
drinkers. AH includes a spectrum of diseases that range from mild
injury to severe, life-threatening injury. The histologic
characteristics of AH include centrilobular ballooning of
hepatocytes, neutrophilic infiltration, MalloryDenk hyaline

inclusions, steatosis, and a chicken wirelike pattern of fibrosis.

In many cases, there is underlying cirrhosis. A large body of
evidence indicates that many factors contribute to alcoholinduced inflammation.

Mechanisms underlying inflammation in ALD. (1) Activation of

innate immunity. Parenchymal infiltration of neutrophils and
macrophages is a prominent feature of ALD and is likely due to
ethanol-mediated activation of innate immunity and subsequent
induction ...

Hepatotoxicity of ethanol
In hepatocytes, ethanol is primarily metabolized into
acetaldehyde by alcohol de hydrogenase in the cytosol,
cytochrome P450 in micro-somes, and catalase in peroxisomes.
Ethanol metabolism generates reactive oxygen species and
causes lipid peroxidation, mitochondrial glutathione depletion,
and S-adenosylmethionine depletion; all of these products
subsequently prime and sensitize hepatocytes to injury.
Acetaldehyde is rapidly metabolized into acetate by alde-hyde
dehydrogenase in mitochondria. Acetaldehyde is a reactive
compound; it is highly toxic to hepatocytes because it forms a
variety of protein and DNA adducts that promote glutathione
depletion, lipid peroxidation, and mitochondrial damage. The
acetate that results from acetaldehyde breakdown is rapidly
released from the liver into the circulation and is then
metabolized into CO2 via the TCA cycle in heart, skeletal muscle,
and brain. Although acetate has no direct hepatotoxicity, it is
believed to regulate the inflammatory response in patients with
AH via the up-regulation of proinflammatory cytokines in
macrophages.
Hepatocyte apoptosis

Hepatocyte apoptosis is an important pathologic feature of human

ALD. Apoptosis results from multiple mechanisms, including
ethanol-mediated hepatotoxicity, induction of oxidative stress,
inhibition of survival genes (c-Met), and induction of proapoptotic
signaling molecules (TNF- and Fas ligand).
Activation of innate immunity
Alcohol consumption not only causes enteric dysbiosis and
bacterial over-growth but also increases gut permeability and the
translocation of bacteria-derived LPS from the gut to the liver.
These changes affect each other and ultimately contribute to the
increased levels of LPS observed in patients with ALD. In Kupffer
cells, LPS interacts with TLR4 to activate the MyD88-independent
(TRIF/IRF-3) signaling pathway, leading to production of oxidative
stress and proinflammatory cytokines, including TNF- , that cause
hepatocellular damage. Alcohol consumption also activates
complement C3 and C5, which subsequently activate Kupffer cells
via binding to their receptors on these cells; complement
activation is followed by production of TNF- and induction of
hepatocyte injury. Interestingly, activation of TLR4 and
complement factors also cause Kupffer cells to produce
hepatoprotective cytokines such as interleukin (IL)-6 and antiinflammatory cytokines such as IL-10. These cytokines activate
STAT3 in hepatocytes and macrophages/ Kupffer cells,
respectively, to prevent alcohol-induced liver injury and
inflammation. Collectively, the activation of innate immunity
components not only initiates alcoholic liver injury but also
triggers hepatoprotective, regenerative, and anti-inflammatory
responses that reduce alcohol-induced hepatocellular damage.
Infiltration by neutrophils
Infiltration of liver by parenchymal neutrophils is a prominent
feature of AH. Up-regulation of IL-8, CXCL1 (Gro- ), and IL-17 in
liver contributes to this infiltration and the severity of AH. Multiple

factors stimulate parenchymal and nonparenchymal cells to

produce these chemokines and cytokines in patients with AH.
These include acetaldehyde, LPS, TNF-, palmitic acid, and downregulation of proteasome functions. IL-17, which is increased in
patients with AH, not only directly induces neutrophil recruitment
but also stimulates hepatic stellate cells (HSCs) to produce IL-8
and CXCL1; this is followed by induction of neutro-phil infiltration.
In addition, IL-8 and CXCL1 are secreted by activated HSCs and
Kupffer cells, which might promote recruitment of neutrophils.
Furthermore, many other chemokines (eg, CXCL5, CXCL6, CXCL4)
and cytokines (eg, TNF-, IL-1, osteopontin) are markedly upregulated and could promote infiltration of neutrophils during
progression of AH. Although neutrophil infiltration correlates with
the severity of AH, because there is no rodent model of this
disease, no direct experimental evidence supports the role of
neutrophils in pathogenesis. Studies from other liver injury
models in rodents indicate that, after systemic activation,
neutrophils migrate into the liver parenchyma and subsequently
kill sensitized hepatocytes by releasing reactive oxygen species
and proteases, likely contributing to alcoholic liver injury.
Activation of adaptive immunity
Patients with AH have increased levels of circulating antibodies
against lipid peroxidation adducts and increased numbers of T
cells in the liver, indicating that activation of adaptive immunity is
involved in the pathogenesis of ALD, including AH. Long-term
alcohol consumption increases oxidative stress, which generates
lipid peroxidation products such as malondialdehyde and 4hydroxynonenal; these compounds can modify many proteins,
inducing the formation of protein adducts that can serve as
antigens to activate the adaptive immune response. However, the
precise mechanisms by which adaptive immune responses induce
hepatocellular damage and inflammation in patients with AH are
not known.

Inhibition of liver regeneration

The liver can regenerate after injury or loss of tissue; recovery of
liver mass occurs mainly via proliferation of remaining adult
hepatocytes, biliary epithelial cells, and endothelial cells. Under
pathogenic conditions in which proliferation of hepatocytes is
inhibited, liver progenitor cells (oval cells or ductular hepatocytes)
proliferate and differentiate into hepatocytes or biliary epithelial
cells. Although long-term alcohol consumption inhibits hepatocyte
proliferation after partial hepatectomy in a rodent model, the
effect of alcohol on hepatocyte proliferation in patients has not
been explored. It is probable that long-term alcohol consumption
not only causes hepatocyte death but also inhibits hepatocyte
proliferation in patients, thereby contributing to the pathogenesis
of ALD.
Alcoholic Fibrosis
Liver fibrosis is a wound-healing response to virtually all forms of
chronic liver injury; it is characterizedby excessive accumulation
of collagen and other extracellular matrix proteins. Activated
HSCs are the major source of the increased production of
extracellular matrix proteins, along with portal fibroblasts and
bone marrowderived myofibroblasts. Hepatocellular damage
increases levels of and activates many cytokines, chemokines,
neuroendocrine factors, angiogenic factors, and components of
the innate immune system that subsequently induce HSC
activation and fibrogenesis. Most of these fibro genic mechanisms
occur during alcoholic liver fibrogenesis, whereas some unique
mechanisms also contribute to alcoholic liver fibrosis .

Mechanisms of liver fibrosis in patients with ALD. (1) Alcohol

consumption causes hepatocyte damage, which leads to the
release of a variety of mediators and the subsequent induction of

stellate cell activation. (2) Acetaldehyde directly targets

stellate ...
LPS activates TLR4
Increased serum levels of LPS are commonly found in patients
with ALD. LPS not only stimulates Kupffer cells to produce reactive
oxygen species and cytokines that subsequently promote
activation of HSCsbut also directly activates HSCs via TLR4. LPS
can also activate TLR4 signaling in liver sinusoidal endothelial
cells, resulting in the regulation of angiogenesis and subsequent
promotion of fibrogenesis. Collectively, TLR4 signaling in immune
cells (Kupffer cells) and liver nonparenchymal cells (HSCs and
endothelial cells) therefore contribute to the pathogenesis of
fibrosis, which is further supported by a recent report using
chimeric mice in which wild-type mice underwent transplant with
bone marrow cells from TLR4 knockout mice and vice versa.
Activation of HSCs by acetaldehyde
Acetalde-hyde is produced mainly by hepatocytes and acts on
HSCs in a paracrine manner; it directly increases expression of
collagen I in HSCs via activation of multiple signaling pathways
and transcription factors. Acetaldehyde reacts rapidly with cellular
components, producing adducts such as malondialdehyde, 4hydroxynonenal, and malondialdehyde-acetaldehyde, which help
maintain HSC activation.
Ethanol suppresses antifibrotic effects
Activated natural killer cells inhibit liver fibrosis by destroying
activated HSCs or producing interferon (IFN)-, which directly
induces HSC cell cycle arrest and apoptosis. These could play an
important role in preventing progression of liver fibrosis in
humans but are blocked by long-term alcohol
consumption. Disrupted activity of natural killer cells and IFN-
could be important factors in the pathogenesis of alcoholic liver

fibrosis and alcohol-mediated acceleration of liver fibrosis in

patients with viral hepatitis.
HCC
Like cirrhosis of any other etiology, alcoholic cirrhosis is a major
risk factor for HCC. The mechanisms that contribute to
development of HCC in patients with cirrhosis, including alcoholic
cirrhosis, are complex and include telomere shortening (which
induces chromosomal instability), alterations of the
microenvironment and macroenvironment that promote tumor
cell survival and proliferation, impairment of hepatocyte
proliferation, loss of cell cycle checkpoints, and activation of
oncogenic pathways.
There are some unique mechanisms that contribute to the
development of HCC specifically in patients with ALD. These
include the formation of acetaldehyde, which is a carcinogen with
mutagenic properties, ethanol-stimulated induction of CYP2E1,
which metabolizes many of the procarcinogenic compounds in
alcoholic beverages, and the immunosuppressive effect of
alcohol. Increased levels of LPS in patients with ALD might
synergize with HCV infection to promote liver tumorigenesis via
up-regulation of cancer stem cells, indicated by analysis of stem
cell markers.
Epigenetics is the study of heritable changes in phenotype
(appearance) or gene expression that are caused by mechanisms
other than alterations in DNA coding sequences. Epigenetic
modifications include DNA methylation, histone modifications, and
RNA-based mechanisms. Ethanol consumption causes epigenetic
changes that contribute to alcohol-induced organ damage,
including ALD. In an extensive study, ethanol affected metabolism
of methionine and thereby DNA methylation. Methionine
metabolism occurs primarily in the liver, where homocysteine is
methylated to methio-nine and then S-adenosylmethionine

(SAMe) in a transmethylation reaction catalyzed by methionine

adenosyltransferase. SAMe is a principal methyl donor in
methylation and has an important role in inducing DNA and
histone methylation. Long-term ethanol consumption reduces
hepatic levels of SAMe and DNA and histone methylation,
increasing expression of genes that regulate the endoplasmic
reticulum stress response and alcoholic liver injury. Alcohol
feeding has been shown to modulate histone methylation and
acetylation in livers of mice, although the mechanism by which
ethanol induces these modifications and their roles in the
pathogenesis of ALD are not known. Exposure to ethanol or its
metabolite acetate up-regulates histone acetylation in
macrophages, contributing to the up-regulation of several
proinflamma-tory cytokines that could promote AH.
miRNAs are short, noncoding RNAs that are an average of only 22
nucleotides long; they control expression of genes involved in cell
growth, differentiation, and apoptosis and are believed to be
involved in the pathogenesis of liver disease, especially
cancer. Several studies have examined the role of miRNAs in liver
disorders such as ALD. Ethanol exposure up-regulates miRNA-155
in macrophages, which increases TNF- production (via increased
mRNA stability); short-term ethanol exposure up-regulates
miRNA-212 in intestinal epithelial cells, which down-regulates
zonula occludens-1 protein, a factor that maintains intestinal
permeability. Expression of liver miRNAs has also been shown to
be significantly altered in ethanol-fed mice, but the functions of
these miRNAs in the pathogenesis of ALD are not clear.
The number of oval cells (liver progenitor cells) is significantly
increased in patients with ALD; it correlates with disease severity
and might increase the risk of alcoholic liver cancer. There is also
evidence that bone marrow-derived stem cells contribute to the
pathogenesis of ALD. However, in early-stage clinical studies,
infusion of autologous, expanded, mobilized, adult bone marrow-

derived CD34+ stem cells (or in vivo mobilization of these cells by

injections of granulocyte colony-stimulating factor) 112 did benefit
patients with ALD. It is therefore important to clarify the
pathogenic and therapeutic roles of CD34 + bone-derived stem
cells in patients with ALD.
Current Therapies and Future Approaches
Patients with ALD are most commonly treated with approaches to
eliminate alcohol intake; continued alcohol ingestion is the single
most important risk factor for progression of the disease.
Abstinence is also critical for patients with advanced disease who
could eventually require liver transplantation, because patients
who actively engage in alcohol consumption are not eligible for
most transplantation programs. Referral to rehabilitation
programs, in combination with family support, is usually
necessary. Some patients also require specific pharmacologic
treatment. Disulfiram, an irreversible inhibitor of alcohol
dehydrogenase, is frequently prescribed to treat alcoholism but is
not recommended for patients with advanced ALD because of
potential severe hepatotoxicity. Anticraving drugs (eg,
acamprosate) are effective at preventing relapses, but special
care must be taken because of the potential hepatotoxicity of
some of these drugs. An agonist of the -aminobutyric acid B
receptor, baclofen, has been found to be effective in maintaining
abstinence and is safe even for cirrhotic patients. The opioid
antagonist naltrexone has been shown to reduce relapse,
although its efficacy is modest.
There are no approved antifibrotic drugs to prevent disease
progression in patients with moderate ALD. The extent of liver
fibrosis can be estimated by liver biopsy analysis or with
noninvasive tools such as elastography or measurements of
serum markers. Clinical trials are hampered by the poor
compliance of patients with alcohol abuse and by the fact that

patients enrolled in therapeutic studies often modify their drinking

behavior, which can have a positive influence on disease severity.
Once cirrhosis is established, abstinent patients usually have
slower disease progression than those consuming alcohol.
Moreover, patients with persisting alcohol intakecan develop
some degree of alcoholic steatohepatitis, which increases the risk
of decompensation (conditions such as ascites, hepatic
encephalopathy, variceal bleeding, or renal dysfunction) and HCC.
There is no evidence that different management strategies
prevent clinical decompensation in patients with alcoholic
cirrhosis compared with other causes of cirrhosis, other than
encouragement of alcohol intake cessation.
AH is a severe form of ALD; its treatment has been summarized in
many excellent reviews. We briefly summarize the treatment of
AH, focusing mainly on recently identified potential therapeutic
targets .
Algorithms for treatment of compensated ALD and
decompensated ALD with superimposed AH. DF, discriminant
function; MELD, Model for End-Stage Liver Disease; ABIC,
age/bilirubin/international normalized ratio/creatinine scoring
system; OLT, orthotopic liver ...
Treatment of AH
Supportive treatment
Patients with severe AH could require admission to an intensive
care unit. The airway should be protected in patients with acute
alcoholic intoxication or an advanced degree of hepatic
encephalopathy. The use of benzodiazepines is contraindicated in
these patients. Given the potential risk of Wernicke
encephalopathy among alcoholic and malnourished patients, the
administration of B-complex vitamins is often required. A daily
protein intake of 1.5 g/kg body wt has been proposed. Patients

with AH are predisposed to develop severe infections, so early

diagnosis and empiric antibiotic treatment are advised.
Corticosteroids
The efficacy of corticosteroids in treating patients with AH is
controversial, with different findings from individual studies and
meta-analyses. Several meta-analyses reported that
corticosteroids increased patient survival times, and one did not
support use of corticosteroids because of the heterogeneity of the
clinical trials and the high risk of bias. Nevertheless, the current
American Association for the Study of Liver Diseases practice
guidelines recommend the use of corticosteroids for patients with
severe AH, defined by Maddreys discriminant function 32 or
hepatic encephalopathy. Patients must also be intensively
monitored for evidence of infections, which occur in almost 25%
of patients during corticosteroid treatment and are associated
with a poor prognosis. The decision to stop corticosteroids can be
based on calculation of the Lille Model after 7 days of treatment; a
Lille Model score greater than 0.45 indicates failure to respond to
corticosteroid treatment and predicts a 6-month survival rate of
less than 25%. Severe acute AH is associated with significant
lymphocyte corticosteroid insensitivity, which can be reduced ex
vivo by theophylline administration or reagents that block the IL-2
receptor. These drugs might therefore improve the efficacy of
corticosteroids in treating AH.
Pentoxifylline
Pentoxifylline is a phosphodiesterase inhibitor that blocks
transcription of TNF- to decrease serum levels of the gene
product. Pentoxifylline can be used to treat patients with severe
AH who cannot be given corticosteroids. It was shown to reduce
the mortality of patients with severe AH, which was related to
decreased development of hepatorenal syndrome. However, this
effect was not appreciable after adjustment for multiple testing.

Importantly, pentoxifylline was not effective as rescue therapy for

patients who did not respond to corticosteroids.
Anti-TNF- agents
TNF- has an important role in the pathogenesis of ALD in animal
models, so there have been several clinical studies of the effects
of infliximab or etanercept (reagents that block this cytokine) in
patients with AH. Early-stage studies showed positive results in
terms of survival and safety,132 but later-stage clinical trials
showed that these drugs actually increased mortality and risk of
infection among patients with AH. These reagents are therefore
not recommended for the treatment of AH.
Nutrition therapy
Alcoholic patients often experience protein calorie malnutrition,
which can promote bacterial infections. Nutritional support is
recommended in patients with AH; it improves liver function and
results from histologic analyses and might increase survival times
based on results of short-term follow-up studies.
SAMe
SAMe is a methyl donor that has been shown to protect against
alcoholic liver injury via multiple mechanisms, including
antioxidant functions, maintenance of mitochondrial function, and
down-regulation of TNF-. An early-stage trial showed that
administration of SAMe as a supplemental agent significantly
decreased mortality and need for liver transplantation among
patients with ALD; it had a favorable safety profile. However, in a
Cochrane report, there was no evidence to support the use of
SAMe in treatment of patients with ALD. Long-term, high-quality,
randomized trials are required to establish its therapeutic effects.
Liver transplantation

Liver transplantation has been used to treat patients with

decompensated ALD. Outcomes are equal to or better than those
obtained when it is used to treat end-stage liver disease from
other causes. Several liver transplantation centers have therefore
proposed that this be a rescue option for patients with severe AH
who do not respond to medical therapy and are unlikely to survive
the mandatory, 6-month abstinence period but who fulfill all other
standard criteria for transplantation, including a thorough
psychosocial evaluation.
Other therapies
Androgen corticosteroids have been used in attempts to improve
the nutritional status of patients with AH. Although initial trials
with oxandrolone had positive results, they were not confirmed in
further studies; no benefit was shown in a meta-analysis. Pro
pylthiouracil, an antithyroid drug, has also been evaluated for the
treatment of acute AH. A meta-analysis of 6 clinical trials showed
that propylthiouracil did not affect survival times and was
associated with adverse effects. Because ALD is associated with
increased levels of oxidative stress, a number of studies have
investigated the benefits of antioxidants (eg, vitamin E and
silymarin). Unfortunately, in early-stage studies, survival times of
patients with AH did not increase. However, a study that
evaluated the potential benefit of combining N-acetylcysteine
with corticosteroids showed an increased number of patients
survived a short follow-up period compared with controls.
New Targets
The identification of therapeutic targets for ALD has been
hampered by the fact that in most animal models, the extent of
liver injury is mild; animals do not develop liver failure or severe
portal hypertension. Animal models are urgently needed that
have the features of liver injury in patients with severe forms of
ALD so we can test the effects of targeting factors found to be

involved in pathogenesis. Liver samples from patients with ALD

are probably most suited to identify therapeutic targets because
serum levels of cytokines such as TNF- may correlate with
disease severity but are likely to have less pathophysiological
significance due to confounding factors such as impaired liver
clearance or bacterial infections. A straightforward approach
would be to investigate the expression and/or activation of
different mediators in liver tissues from patients and correlate
these with disease severity and patient outcomes and then test
the biological significance of these factors in animal models. The
following are examples of therapeutic targets that fulfill several of
these criteria.
CXC chemokines
The CXC family of chemokines includes IL-8 and Gro- ; these
usually attract neutrophils, which infiltrate livers of patients with
ALD. In patients with AH, hepatic expression of CXC chemokines is
increased and correlates with survival time and the degree of
portal hypertension. Reagents that target CXC chemokines might
be developed as therapeutics for AH.
IL-22
IL-22 is a member of the IL-10 family of cytokines, which control
bacterial infection, homeostasis, and tissue repair. IL-22 might be
used to treat patients with ALD because of its antioxidant,
antiapoptotic, anti-steatotic, proliferative, and antimicrobial
effects. In addition, the side effects of IL-22 could be minimal,
because the IL-22 receptor is only expressed on epithelial cells
such as hepatocytes. Corticosteroids, which are widely used to
treat AH, have well-documented side effects that include
increased risk of infection. Corticosteroids and IL-22 could
therefore be a good combination treatment for AH, because IL-22
might overcome the corticosteroid-mediated promotion of
infection.

Complement
Activation of complement is an important step in the development
of ethanol-induced liver injury in mice. Therapeutic interventions
to either block complement activation or increase the activity of
negative regulators of complement might be used to treat
patients with ALD. Several compounds that inhibit complement
activation are in phase 1 or 2 trials for the treatment of agerelated macular degeneration. These drugs may be developed to
treat patients with ALD.
Gut microbiota and LPS pathway
Modulation of the gut microbiota and LPS pathways might also be
used to treat patients with ALD. The gut microbiota and
LPSsignaling can be modified by probiotics and TLR4 antagonists,
respectively, with the latter being proposed as therapeutic agents
for the treatment of chronic liver diseases, including ALD. Results
from a placebo-controlled trial recently showed that the
nonabsorbable antibiotic rifaximin, which modifies the gut
microbiota, protected patients from hepatic
encephalopathy. Reagents that alter the gut microbiota might also
prevent ALD, so further studies are required.
Inhibition of apoptosis
Apoptosis is a prominent feature of chronic liver disease, so
apoptosis inhibitors have been investigated in animal models of
liver injury and patients with chronic liver diseases. Multiple
clinical trials have shown that various caspase inhibitors reduced
liver injury and fibrosis in patients with chronic HCV infectionor
nonalcoholic steatohepatitis. ALD is also associated with
significant levels of hepatocyte apoptosis, so inhibitors might be a
treatment option for ALD.
Osteopontin

Osteopontin is an extracellular matrix protein that is markedly upregulated in patients with ALD. The basal expression levels of
osteopontin correlate with disease severity (R. Bataller et al,
unpublished data, September 2011), indicating that osteopontin
contributes to the pathogenesis of ALD. Blockade of osteopontin
might be effective for amelioration of ALD.
Endocannabinoids
Endocannabinoids have been shown to be involved in the
pathogenesis of ALD, signaling through cannabinoid receptor (CB)
1 and CB2. CB1-deficient mice are resistant whereas CB2deficient mice are more susceptible to ethanol-induced fatty liver
and hepatocellular damage. These findings indicate that CB1
antagonists and CB2 agonists could be therapeutic agents for the
management of ALD. Because the neuropsychiatric side effects of
CB1 antagonists limit their therapeutic potential for the treatment
of liver disease, the peripherally restricted CB1 antagonists have
been actively explored and might offer therapeutic benefits for
patients with ALD.
NOSTRIN
NOSTRIN regulates synthesis of nitric oxide, an effector of chronic
liver diseases. Patients with ALD have increased hepatic levels of
NOSTRIN protein and messenger RNA; this might contribute to the
decreased enzymatic activity of endothelial nitric oxide synthase
and was associated with more severe portal hypertension. Further studies are needed to determine whether
NOSTRIN mediates the hemodynamic derangements observed in
patients with AH. It could be a therapeutic target for reducing the
increased hepatic resistance observed in patients with AH.
Conclusions
ALD is a major cause of advanced liver disease worldwide. Major
advances in understanding its mechanisms of pathogenesis have

been made at the experimental level using animal models.

Translational studies, using human liver samples, have identified
new therapeutic tar gets. However, translation of basic and
translational research findings into new therapies has been
modest. Future efforts should be directed toward identifying the
main factors that promote disease in patients with moderate and
severe ALD to develop new therapies
f page
Alcoholic liver disease (ALD) encompasses a spectrum of injury,
ranging from simple steatosis to frank cirrhosis. It may well
represent the oldest form of liver injury known to mankind.
Evidence suggests that fermented beverages existed at least as
early as the Neolithic period (cir. 10,000 BC) .Alcohol remains a
major cause of liver disease worldwide. It is common for patients
with ALD to share the risk factors for simultaneous injury from
other liver insults (e.g., co-existing non-alcoholic fatty liver
disease, or chronic viral hepatitis). Many of the natural history
studies of ALD and even treatment trials were performed before
these other liver diseases were recognized, or specific testing was
possible. Thus, the individual effect of alcohol in some of these
studies may have been confounded by the presence of these
additional injuries. Despite this limitation, the data regarding ALD
are robust enough to draw conclusions about the pathophysiology
of this disease. The possible factors that can affect the
development of liver injury include the dose, duration, and type
of alcohol consumption, drinking patterns, gender, ethnicity, and
associated risk factors, including obesity, iron overload,
concomitant infection with viral hepatitis, and genetic factors.
Geographic variability exists in the patterns of alcohol intake
throughout the world . Approximately two-thirds of the adult
Americans drink alcohol . The majority drink small or moderate

amounts and do so without evidence of clinical disease . A

subgroup of drinkers, however, drink excessively, develop
physical tolerance and withdrawal, and are diagnosed with alcohol
dependence . A second subset, alcohol abusers and problem
drinkers, are those who engage in harmful use of alcohol, which
is defined by the development of negative social and health
consequences of drinking (e.g., unemployment, loss of family,
organ damage, accidental injury, or death) .Failure to recognize
alcoholism remains a significant problem and impairs efforts at
both the prevention and the management of patients with ALD .
Although the exact prevalence is unknown, approximately
7.4% of adult Americans were estimated to meet the Diagnostic
and Statistical Manual of Mental Disorders, 4th edition, criteria for
the diagnosis of alcohol abuse and/or alcohol dependence in 1994
; more recent data suggest 4.65% meet the criteria for alcohol
abuse and 3.81% for alcohol dependence . In 2003, 44% of all
deaths from liver disease were attributed to alcohol .
The population-level mortality from ALD is related to the per
capita alcohol consumption obtained from national alcoholic
beverage sales data. There are conflicting data regarding a
possible lower risk of liver injury in wine drinkers . One
epidemiological study has estimated that for every 1 l increase in
per capita alcohol consumption (independent of the type of
beverage), there was a 14% increase in cirrhosis in men and
8% increase in women .These data must be considered in the
context of the limitations of measuring alcohol use and defining
ALD. The scientific literature has also used a variety of definitions
of what constitutes a standard drink Most studies depend on
interviews with patients or their families to quantify drinking
patterns, a method that is subject to a number of biases, which
may lead to invalid estimates of alcohol consumption .

Although there are limitations of the available data, the World

Health Organization's Global Alcohol database, which has been in
existence since 1996, has been used to estimate the worldwide
patterns of alcohol consumption and allow comparisons of
alcohol-related morbidity and mortality .The burden of alcoholrelated disease is the highest in the developed world, where it
may account for as much as 9.2% of all disability-adjusted life
years. However, even in the developing regions of the world,
alcohol accounts for a major portion of the global disease burden,
and is projected to take on increasing importance in those regions
over time .
Topof page
The spectrum of alcohol-related liver injury varies from simple
steatosis to cirrhosis. These are not necessarily distinct stages of
evolution of the disease, but rather, multiple stages that may be
present simultaneously in a given individual .These are often
grouped into three histological stages of ALD, including fatty liver
or simple steatosis, alcoholic hepatitis (AH), and chronic hepatitis
with hepatic fibrosis or cirrhosis .The latter stages may also be
associated with a number of histological changes (which have
varying degrees of specificity for ALD), including the presence of
Mallory's hyaline, megamitochondria, or perivenular and
perisinusoidal fibrosis Fatty liver develops in about 90% of
individuals who drink more than 60g/day of alcohol but may also
occur in individuals who drink less .Simple, uncomplicated fatty
liver is usually asymptomatic and self-limited, and may be
completely reversible with abstinence after about 46 weeks
However, several studies have suggested that progression to
fibrosis and cirrhosis occurs in 515% of the patients despite
abstinence .In one study, continued alcohol use (>40g/day)
increased the risk of progression to cirrhosis to 30%, and fibrosis
or cirrhosis to 37% .

Fibrosis is believed to start in the perivenular area and is

influenced by the amount of alcohol ingested .Perivenular fibrosis
and deposition of fibronectin occur in 4060% of the patients who
ingest more than 4080g/day for an average of 25 years.
Perivenular sclerosis has been identified as a significant and
independent risk factor for the progression of alcoholic liver injury
to fibrosis or cirrhosis .Progression of ALD culminates in the
development of cirrhosis, which is usually micronodular, but may
occasionally be mixed micro- and macronodular .A subset of
patients with ALD will develop severe AH, which has a
substantially worse short-term prognosis .AH also represents a
spectrum of disease, ranging from mild injury to severe, lifethreatening injury, and often presents acutely against a
background of chronic liver disease .The true prevalence is
unknown, but histological studies of patients with ALD suggest
that AH may be present in as many as 1035% of hospitalized
alcoholic patients . Typically, symptomatic patients present with
advanced liver disease, with concomitant cirrhosis in more than
50% of the patients, and superimposed acute decompensation.
However, even patients with a relatively mild presentation are at
high risk of progressive liver injury, with cirrhosis developing in
up to 50% of the patients,. The likelihood that AH will progress to
permanent damage is increased among those who continue to
abuse alcohol. Abstinence from alcohol in one small series did not
guarantee complete recovery. Only 27% of the abstaining
patients had histological normalization, whereas 18% progressed
to cirrhosis, and the remaining patients had persistent AH when
followed for up to 18 months .
Topof page
RISK FACTORS

Unlike many other hepatotoxins, the likelihood of developing

progressive alcohol-induced liver disease or cirrhosis is not
completely dose-dependent, as it occurs in only a subset of
patients. A number of risk factors that influence the risk of
development and progression of liver disease have been
identified.
The amount of alcohol ingested (independent of the form in which
it is ingested) is the most important risk factor for the
development of ALD .The relationship between the quantity of
alcohol ingested and the development of liver disease is not
clearly linear .However, a significant correlation exists between
per capita consumption and the prevalence of cirrhosis .The risk
of developing cirrhosis increases with the ingestion of >6080
g/day of alcohol for 10 years in men, and >20g/day in
women .Yet, despite drinking at these levels, only 641% of the
individuals develop cirrhosis .In a population-based cohort study
of almost 7,000 subjects in two northern Italian communities,
even among patients with very high daily alcohol intake (>120
g/day), only 13.5% developed ALD .The risk of cirrhosis or noncirrhotic chronic liver disease increased with a total lifetime
alcohol intake of >100kg, or a daily intake of >30g/day .The
odds of developing cirrhosis or lesser degrees of liver disease with
a daily alcohol intake of >30g/day were 13.7 and 23.6,
respectively, when compared with non-drinkers .The type of
alcohol consumed may influence the risk of developing liver
disease. In a survey of over 30,000 persons in Denmark, drinking
beer or spirits was more likely to be associated with liver disease
than drinking wine .
Another factor that has been identified is the pattern of drinking.
Drinking outside of meal times has been reported to increase the
risk of ALD by 2.7-fold compared with those who consumed
alcohol only at mealtimes .Binge drinking, defined by some

researchers as five drinks for men and four drinks for women in
one sitting, has also been shown to increase the risk of ALD and
all-cause mortality .
Women have been found to be twice as sensitive to alcoholmediated hepatotoxicity and may develop more severe ALD at
lower doses and with shorter duration of alcohol consumption
than men .Several studies have shown differing blood alcohol
levels in women vs. men after consumption of equal amounts of
alcohol .This might be explained by differences in the relative
amounts of gastric alcohol dehydrogenase, a higher proportion of
body fat in women, or changes in alcohol absorption with the
menstrual cycle .Based on epidemiological evidence of a threshold
effect of alcohol, a suggested safe limit of alcohol intake had
been 21 units per week in men and 14 units per week in women
who have no other chronic liver disease .(wherein a unit is
defined as the equivalent of 8g of ethanol). However, other data
suggest that a lower quantity may be toxic in women, implying a
lower threshold of perhaps no more than 7 units per week .A
higher risk of liver injury may be associated with an individual's
racial and ethnic heritage .The rates of alcoholic cirrhosis are
higher in African-American and Hispanic males compared with
Caucasian males and the mortality rates are the highest in
Hispanic males .These differences do not seem to be related to
differences in the amounts of alcohol consumed .The presence
and extent of protein calorie malnutrition have an important role
in determining the outcome of patients with ALD. Mortality
increases in direct proportion to the extent of malnutrition,
approaching 80% in patients with severe malnutrition (i.e.,
<50% of the normal) .Micronutrient abnormalities, such as
hepatic vitamin A depletion or depressed vitamin E levels, may
also potentially aggravate the liver disease .Diets rich in
polyunsaturated fats promote alcohol-induced liver disease in

animals .whereas diets high in saturated fats may be protective.

Obesity and excess body weight have been associated with an
increased risk of ALD .
In addition to environmental factors, genetic factors predispose to
both alcoholism and ALD.. Children of alcoholics raised in adopted
families had a significantly higher rate of alcohol dependence than
adopted children of non-alcoholics, who served as controls
(18% vs. 5%) . In population-based studies, monozygotic twins
were approximately twice as likely to drink as dizygotic twins;
among those who drank, monozygotic twins were more likely to
have a similar frequency and quantity of alcohol consumption
.Moreover, monozyotic twins had a significantly higher prevalence
of alcoholic cirrhosis than dizygotic twins .Finally, polymorphisms
of genes involved in the metabolism of alcohol (including alcohol
dehydrogenase, acetaldehyde dehydrogenase, and the
cytochrome P450 system) and in those that regulate endotoxinmediated release of cytokines have been associated with ALD
.However, specific genetic abnormalities for susceptibility to
alcohol abuse and the development of ALD have not yet been
firmly established.
There is a clear synergistic relationship between chronic viral
hepatitis and alcohol, resulting in more advanced liver disease
jointly than separately. The combination of HCV and alcohol
predisposes to more advanced liver injury than alcohol alone .
with disease at a younger age, more severe histological features,
and a decreased survival .In a large-cohort study of the effect of
heavy alcohol abuse in patients with post-transfusion hepatitis C,
the risk of cirrhosis was elevated 30-fold . Although the precise
toxic threshold for alcohol is not known, and may be lower and
non-uniform among patients at risk, it seems prudent in light of
these data to advise patients with hepatitis C to abstain from
consuming even moderate quantities of alcohol.

Topof page
DIAGNOSIS
The diagnosis of ALD is based on a combination of features,
including a history of significant alcohol intake, clinical evidence
of liver disease, and supporting laboratory abnormalities .
Unfortunately, the ability to detect these is constrained by patient
and physician factors, as well as diagnostic laboratory
shortcomings. Denial of alcohol abuse and underreporting of
alcohol intake are common in these patients . Physicians
underestimate alcohol-related problems and make specific
recommendations even less frequently . Both the physical
findings and laboratory evidence for ALD may be non-diagnostic,
especially in patients with mild ALD or early cirrhosis . Therefore,
the clinician must have a low threshold to raise the issue of
possible ALD, and has to rely on indirect evidence of alcohol
abuse, such as questionnaires, information from family members,
or laboratory tests to strengthen or confirm a clinical suspicion .
Screening for alcohol abuse
Clinicians commonly fail to screen patients, and thus fail to
recognize or treat alcoholism appropriately . Clinical history that
may suggest alcohol abuse or alcohol dependence includes the
pattern, type, and amount of alcohol ingested, as well as
evidence of social or psychological consequences of alcohol
abuse. These may be suggested by other injuries or past trauma,
such as frequent falls, lacerations, burns, fractures, or emergency
department visits . Biochemical tests have been considered to be
less sensitive than questionnaires in screening for alcohol abuse ,
but may be useful in identifying relapse . Various questionnaires
have been used to detect alcohol dependence or abuse, and
include the CAGE, the Michigan Alcoholism Screening Test, and
the Alcohol Use Disorders Identification Test . A structured

interview, using instruments such as the Lifetime Drinking

History, is often used as a gold standard for quantifying lifetime
alchohol consumption .
The CAGE questionnaire was originally developed to identify
hospitalized inpatients with alcohol problems, and remains among
the most widely used screening instruments. It has been faulted,
however, on several measuresit focuses on the consequences of
alcohol consumption rather than on the amount of actual
drinking, and it refers to lifetime patterns of behavior, rather than
short-term or recent changes. Its virtues, however, include its
ease of implementationit is short (four questions), simple
(yes/no answers), and can be incorporated into the clinical
history or self-administered as a written document. As a result of
its longevity, it has been tested in a wide range of populations.
One meta-analysis of its characteristics, using a cutoff of more
than two positive responses, found an overall pooled sensitivity
and specificity of 0.71 and 0.90, respectively . The CAGE
questionnaire is familiar to most physicians, and has been
suggested for use in general screening . The Alcohol Use
Disorders Identification Test is a 10-item questionnaire developed
by the World Health Organization to avoid ethnic and cultural bias
and focus on the identification of heavy drinkers. It has a higher
sensitivity and specificity than shorter screening instruments
(with sensitivity ranging from 51 to 97%, and specificity from 78
to 96% in primary care) . It has been suggested that it has three
advantages over other screening tests: it may identify drinkers at
risk who are not yet alcohol-dependent; it includes a measure of
consumption; and lastly, it includes both current and lifetime
drinking time spans. It is more likely to detect problem drinking
before overt alcohol dependence or abuse might be diagnosed,
and thus may be more robust and effective across a variety of
populations . One possible algorithm for clinicians suggests asking

about the quantity of alcohol consumed, and the number of heavy

drinking days in the preceding year (i.e., 5 drinks/day for men
or 4 drinks/day for women), as well as administering a version
of the Alcohol Use Disorders Identification Test questionnaire . An
Alcohol Use Disorders Identification Test score of 8, or having
had 1 heavy drinking days constitutes a positive screening test,
and should prompt further evaluation to rule out an alcohol use
disorder .

Regardless of which screening instrument is selected, however, it

is important for clinicians to incorporate screening into their
general practice . This may be especially important, as some data
suggest that these screening instruments may improve the ability
of physicians to predict long-term clinical outcomes, including
hospitalization for alcohol-related diagnoses .
One particular biomarker in longstanding use, gamma glutamyl
transpeptidase (GGT), has been evaluated in a number of
settings, including large population surveys . Unfortunately, its
low sensitivity and specificity limit the usefulness of elevated GGT
to diagnose alcohol abuse , the levels of which may fluctuate with
extensive liver injury . Lower levels of GGT (<100) or a total
bilirubin/GGT ratio >1 has been described as a predictor of 1-year
mortality in patients with alcoholic cirrhosis , although this has
not consistently added the prognostic ability to other lab tests .
However, in combination with other biomarkers, GGT may help
add independent information in diagnosing alcohol abuse or
problem drinking . Macrocytosis is seen in individuals abusing
alcohol but lacks sensitivity. A combination of raised GGT and
mean corpuscular volume or changes in these values over time in
hospitalized patients may improve the sensitivity for diagnosing

alcohol abuse. Multiple other candidate biomarkers that may

detect alcohol use or abuse objectively have been studied .
Carbohydrate-deficient transferrin has been the biomarker best
studied, but has limited sensitivity and specificity . Its test
characteristics are also influenced by a number of other factors,
including age, gender, BMI, and other chronic liver diseases .
Despite the enthusiasm about a possible quantitative, reliable
assay of alcohol consumption or abuse, the lack of sensitivity and
specificity prevent reliance on any single biomarker .
Diagnosis of ALD
The diagnosis of ALD is made by documentation of alcohol excess
and evidence of liver disease . No single laboratory marker
definitively establishes alcohol to be the etiology of liver disease.
Furthermore, alcohol may be one of a number of factors causing
liver injury, and the specific contributory role of alcohol alone may
be difficult to assess in a patient with multifactorial liver disease.
A number of laboratory abnormalities, including elevated serum
aminotransferases, have been reported in patients with alcoholic
liver injury, and used to diagnose ALD . Serum AST is typically
elevated to a level of 26 times the upper limits of the normal in
severe AH. Levels of AST >500IU/l or ALT >200IU/l are rarely
seen with AH (other than alcoholic foamy degeneration or
concomitant acetaminophen overdose) , and should suggest
another etiology. In about 70% of patients the AST/ALT ratio is
>2, but this may be of greater value in patients without
cirrhosis . Ratios >3 are highly suggestive of ALD .
Physical examination
Physical examination findings in patients with ALD may range
from normal to those suggestive of advanced cirrhosis. As in
other forms of chronic liver disease, physical examination
features generally have low sensitivity, even for the detection of

advanced disease or cirrhosis, although they may have higher

specificity . Therefore, it has been suggested that the presence of
these features may have some benefit in ruling in the presence
of advanced disease . Features specific for ALD are perhaps even
more difficult to identify. Palpation of the liver may be normal in
the presence of ALD, and does not provide accurate information
regarding liver volume .Certain physical examination findings
have been associated with a higher likelihood of cirrhosis among
alcoholics . Although some of the physical findings are more
commonly observed in ALD (parotid enlargement, Dupuytren's
contracture, and especially those signs associated with
feminization) than in non-ALD, no single physical finding or
constellation of findings is 100% specific or sensitive for ALD
.Some of the physical examination features may also carry some
independent prognostic information, with the presence of specific
features associated with an increased risk of mortality over 1
year. These include (with their associated relative risks) hepatic
encephalopathy (4.0), presence of visible veins across the
anterior abdominal wall (2.2), edema (2.9), ascites (4.0), spider
nevi (3.3), and weakness (2.1) . Although this is somewhat
helpful clinically, findings from the physical examination must be
interpreted with caution, as there is considerable heterogeneity in
the assessment of each of these features when different
examiners are involved . Several authors have reported the
detection of a hepatic bruit in the setting of AH . This has been
used in some centers as a diagnostic criterion for AH . However,
the sensitivity, as well as the specificity of this finding is uncertain
. In one series of 280 consecutive hospitalized patients, only 4 of
240 (or 1.7%) with AH and cirrhosis had an audible bruit .
Caution about adopting this as a diagnostic criterion has therefore
been advised .

It is important for physicians caring for these patients to

recognize that ALD does not exist in isolation, and that other
organ dysfunctions related to alcohol abuse may coexist with
ALD, including cardiomyopathy , skeletal muscle wasting ,
pancreatic dysfunction, and alcoholic neurotoxicity . Evidence of
these must be sought during the clinical examination, so that
appropriate treatment may be provided .
Hepatic imaging
Imaging studies have been used to diagnose the presence of liver
disease but do not have a role in establishing alcohol as the
specific etiology of liver disease. However, the diagnosis of fatty
change, established cirrhosis, and hepatocellular carcinoma may
be suggested by ultrasound, CT scan, or magnetic resonance
imaging and confirmed by other laboratory investigations . The
major aim of imaging studies is to exclude other causes of
abnormal liver tests in a patient who abuses alcohol, such as
obstructive biliary pathology, or infiltrative and neoplastic
diseases of the liver . Magnetic resonance imaging has been used
as an adjunct to diagnose cirrhosis, and to distinguish end-stage
liver disease related to viral hepatitis infection from ALD. Specific
features that may be suggestive of alcoholic cirrhosis include a
higher volume index of the caudate lobe, more frequent
visualization of the right posterior hepatic notch, and smaller size
of regenerative nodules of the liver in patients with cirrhosis on
the basis of a comparison of ALD with chronic viral hepatitis .
Although changes were identified on ultrasound and magnetic
resonance imaging, it is unclear whether these results are
generalizable .
Liver biopsy in ALD

Although not essential in the management of ALD, a liver biopsy

is useful in establishing the diagnosis . As many as 20% of the
patients with a history of alcohol abuse have a secondary or
coexisting etiology for liver disease . In the absence of
decompensated disease, clinical and biochemical indicators are
poor markers of the severity of the liver disease and a biopsy is
useful in establishing the stage and severity of the liver disease .
The histological features of alcohol-induced hepatic injury vary,
depending on the extent and stage of injury. These may include
steatosis (fatty change), lobular inflammation, periportal fibrosis,
Mallory bodies, nuclear vacuolation, bile ductal proliferation, and
fibrosis or cirrhosis . However, these may co-exist in the same
biopsy, and are not individually pathognomonic of ALD. The
clinical diagnosis of AH is made based on a typical presentation,
with severe liver dysfunction in the context of excessive alcohol
consumption, and the exclusion of other causes of acute and
chronic liver disease. In a subset of patients with AH, a liver
biopsy may show specific histological features, including confluent
parenchymal necrosis, steatosis, deposition of intrasinusoidal and
pericentral collagen, ballooning degeneration, and lobular
inflammation affecting the perivenular regions in the earliest
stages . The liver may be infiltrated with polymorphonuclear cells,
typically clustered around cytoplasmic structures known as
Mallory bodies , which represent aggregated cytokeratin
intermediate filaments and other proteins. In addition to
confirming the diagnosis and staging the extent of the disease,
specific features on liver biopsy also convey prognostic
importance. The severity of inflammation (i.e., degree of
polymorphonuclear leukocyte infiltration) and cholestatic changes
correlate with increasingly poor prognosis, and may also predict
response to corticosteroid treatment in severe AH .
Megamitochondria in AH may be associated with a milder form of

AH, a lower incidence of cirrhosis, and fewer complications, with a

good long-term survival . AH is associated with perivenular and
pericellular fibrosis, which may be a harbinger of future cirrhosis,
especially in patients who continue to abuse alcohol or those who
are co-infected with hepatitis C virus . Mallory bodies, giant
mitochondria, neutrophilic infiltration, and fibrosis may be seen in
conditions other than ALD .
Although a liver biopsy may not be practical in the management
of all patients, it has been shown that physicians clinical
impression may correlate only moderately well with the
histological findings on liver biopsy. Studies that have included a
liver biopsy in all patients with presumed AH have shown
histological confirmation in only 7080% of the patients .
However, the incentive to make a definitive histological diagnosis
is partly dependent on the possible risks of a biopsy, as well as on
the risks involved with particular treatments. If no treatment for
ALD or AH is contemplated, based on noninvasive estimates of an
individual patient's prognosis, it is usually not necessary to make
a histological diagnosis. Alternatively, if an investigational
treatment or a therapy with associated risk is contemplated, the
riskbenefit ratio involved in pursuing a liver biopsy may change.
Recommendations:
1. Clinicians should discuss alcohol use with patients, and any
suspicion of possible abuse or excess should prompt use of a
structured questionnaire and further evaluation (Class I, level C).
2. For patients with a history of alcohol abuse or excess and
evidence of liver disease, further laboratory tests should be done
to exclude other etiologies and to confirm the diagnosis (Class I,
level C).

3. Patients with ALD and suggestive symptoms should be

screened for evidence of other end-organ damage, as appropriate
(Class I, level C).
4. For patients with a clinical diagnosis of severe AH for whom
medical treatment is contemplated, or for those in whom
reasonable uncertainty exists regarding the underlying diagnosis,
a liver biopsy should be considered. This decision will depend on
local expertise and ability in performing a liver biopsy in patients
with coagulopathy, the patient's severity of illness, and the type
of therapy under consideration (Class I, level C).
Topof page
PROGNOSTIC FACTORS
Prognosis in AH
Decisions regarding treatment are critically dependent on the
ability to estimate a given patient's prognosis. Many individual
clinical and laboratory features, along with specific histological
features have also been tested as measures of disease prognosis.
In AH, the Maddrey discriminant function, a disease-specific
prognostic score, has been used to stratify a patient's severity of
illness . The initial formula was derived in the context of clinical
trials of AH, and later modified to Maddrey discriminant function
(MDF)=4.6 (patient's PTcontrol PT)+total bilirubin (mg/dl) .
Patients with a score of 32 were at the highest risk of dying,
with a 1-month mortality as high as 3050% . In particular, those
with evidence of both hepatic encephalopathy and an elevated
discriminant function were at highest risk. Although relatively
easy to use, and based on standard laboratory tests, several
drawbacks to the use of the MDF have been noted. Although it is
a continuous measure, its interpretation (using a threshold of 32)
has converted it into an essentially categorical method of

classification. Once patients have exceeded that threshold, their

risk for dying is higher, but not specified. Dynamic models, which
incorporate the changes in laboratory studies over time, have also
been used to estimate the outcome in patients, including the
change in bilirubin in the first week of hospitalization, which is
significantly associated with the outcome of patients with AH
treated with prednisolone .
Other scoring systems have also been proposed to stratify
patients, including the combined clinical and laboratory index of
the University of Toronto , the Beclere model , the model for endstage liver disease (MELD) score , and the Glasgow AH Score .
The diagnostic abilities of the latter two models have been tested
against the MDF and other scoring systems for cirrhosis (such as
the ChildTurcottePugh score) in terms of specific test
characteristics, including sensitivity and specificity, at least in
some populations . Owing to the inherent trade-offs involved in
setting test thresholds, optimal cut points are not clearly
established for each of these indices. Some investigators have
suggested specific cutoffs for these indices, including an MDF 32
or a MELD score >11, that seem to be roughly equivalent in their
ability to detect patients with a poor prognosis, with similar
sensitivity and specificity .
Several studies have also shown the utility of repeat testing and
calculation of these indices during the course of hospitalization,
including MELD or MDF score at 1 week, and degree of change. A
change of 2 points in the MELD score in the first week has been
shown to independently predict in-hospital mortality . The
Glasgow AH Score was recently derived, and its test
characteristics compared with the MDF and the MELD scores.
Although it had an overall higher accuracy, it was substantially
less sensitive for predicting the 1-month and 3-month mortality
compared with either the MDF or the MELD . The degree of portal

hypertension may be a sensitive marker for the severity of liver

injury . A recently proposed scoring system combines
measurements of a marker of portal hypertension, asymmetric
dimethylarginine, and of its stereoisomer to predict the
outcomes . This combined score has been compared with the
ChildTurcottePugh score, MELD, and MDF, and shown to have
an overall sensitivity of 73% and a specificity of 83%, which were
at least as good as those of other scoring systems .These results,
however, require further validation.
As the aim of early detection of patients at highest risk of poor
outcome requires maximization of the sensitivity of the test
score, it would seem reasonable to use the MDF (with a cutoff of
32, and/or the presence of encephalopathy) to select patients for
therapy.
Recommendation:
5. Patients presenting with a high clinical suspicion of AH should
have their risk for poor outcome stratified using the Maddrey
discriminant function, as well as other available clinical data.
Evaluating a patient's condition over time with serial calculation of
the MELD score is also justified (Class I, level B).
Topof page
THERAPY
Therapy of ALD is based on the stage of the disease and the
specific aims of treatment . Complications of cirrhosis, including
evidence of hepatic failure (encephalopathy) as well as portal
hypertension (ascites, variceal bleeding), are treated as in
patients with non-ALD, with additional attention given to other
organ dysfunctions associated specifically with alcohol .
Abstinence

Abstinence is the most important therapeutic intervention for

patients with ALD . Abstinence has been shown to improve the
outcome and histological features of hepatic injury, to reduce
portal pressure and decrease progression to cirrhosis, and to
improve survival at all stages in patients with ALD . However, this
may be less likely to occur in female patients. This improvement
can be relatively rapid, and in 66% of the patients abstaining
from alcohol, significant improvement was observed in 3 months .
Continued alcohol ingestion results in an increased risk of portal
hypertensive bleeding, especially in patients who have previously
bled, and worsens both short- and long-term survival .
Recidivism is a major risk in all patients at any time after
abstinence . Estimates vary, depending on the time course of
follow-up and the definition of recidivism (e.g., any alcohol
consumption, vs. moderate-to-harmful drinking), but over the
course of 1 year, relapse rates range from 67% to
81% .Therefore, several medications have been tried to help
sustain abstinence. One of the first agents to be used, disulfiram,
was approved by the Food and Drug Administration in 1983.
However, a review of the published literature concluded that there
was little evidence that disulfiram enhances abstinence , and
based on its poor tolerability, its use has been largely supplanted
by newer agents. Naltrexone, which was approved in 1995 for the
treatment of alcoholism, is a pure opioid antagonist and controls
the craving for alcohol. However, it has also been shown to cause
hepatocellular injury. A Cochrane systematic review of the use of
naltrexone and nalmefene (another opioid antagonist) in 29 RCTs
concluded that short-term treatment with naltrexone lowers the
risk of relapse . Acamprosate (acetylhomotaurine) is a novel drug
with structural similarities to the inhibitory neurotransmitter
gamma aminobutyric acid, and is associated with a reduction in
withdrawal symptoms . In 15 controlled trials, acamprosate has

been shown to reduce withdrawal symptoms, including alcohol

craving, but its effects on survival are not yet known . Its effect is
more pronounced in maintaining rather than inducing remission
when used in combination with counseling and support. In
detoxified alcoholics, it has been shown to decrease the rate of
relapse, maintain abstinence, and decrease the severity of
relapse when it occurs. It has not been shown to have a
significant impact on alcoholics who have not been detoxified or
become abstinent. Whether it has any additional effect in
combination with naltrexone is controversial. A recent large
randomized controlled clinical trial did not suggest substantial
benefit of acamprosate compared with naltrexone or with
intensive counseling in maintaining abstinence . There is a
paucity of data about the use of these interventions in patients
with advanced liver disease. One randomized clinical trial in
patients with cirrhosis suggested benefit in achieving and
maintaining abstinence with the use of baclofen, a gamma
aminobutyric acid B receptor agonist .
Recommendations:
6. In patients with evidence of alcohol-induced liver disease, strict
abstinence must be recommended, because continued alcohol use
is associated with disease progression (Class I, level B).
7. Naltrexone or acamprosate may be considered in combination
with counseling to decrease the likelihood of relapse in patients
with alcohol abuse/dependence in those who achieve abstinence
(Class I, level A).
Therapy for AH
The cornerstone of the therapy for AH is abstinence, although
even patients who become abstinent have an increased risk of
developing cirrhosis. However, the risk of cirrhosis is clearly

higher in those who continue to drink . particularly among women

. Although there are no clear doseeffect data, a threshold exists
for the development of AH, with the risk increasing with
consumption beyond 40g of alcohol per day . Furthermore, after
an episode of AH, there is no safe amount of alcohol consumption
that can be recommended, as AH can persist or re-develop. There
is a significant risk of recidivism in patients who attempt to cut
back but not stop drinking altogether . Complete abstinence is
therefore a reasonable lifetime recommendation.
The need to consider therapy is less urgent in patients with AH
who have a low risk of complications as defined by an MDF score
of <32, without hepatic encephalopathy, or a low MELD score
(e.g., MELD<18), or a Glasgow AH Score of <8. This is
particularly true in those whose liver score improves during
hospitalization, with a decrease in total bilirubin, as they will
likely improve spontaneously with abstinence and supportive care
alone. For those with more severe disease and therefore a more
dismal prognosis, however, medical treatment should be
considered.
Nutrition therapy

The presence of significant protein calorie malnutrition is a

common finding in alcoholics, as are deficiencies in a number of
vitamins and trace minerals, including vitamins A, D, thiamine,
folate, pyridoxine, and zinc . In a VA Cooperative study of 363
patients with AH, 100% of patients were found to have protein
and/or combined protein calorie malnutrition, based on
anthropometric and laboratory testing . Moreover, the severity of
malnutrition correlated with the disease severity and outcomes .

This early finding was the motivation for a number of clinical trials
of anabolic steroids, nutritional supplementation, or aggressive
enteral feeding. Several of these studies showed an improvement
in the biochemical markers of liver function or nutritional
parameters, but were unable to show an improvement in shortterm survival . However, at least in some trials subgroups of
patients who achieved nutritional goals and positive nitrogen
balance had improved survival compared with those who did not .
As an example, in one study, the mortality rate was 3.3% in the
30 patients in whom positive nitrogen balance was achieved, but
58% in patients who remained in negative nitrogen balance .
The most recent study of nutritional therapy compared the
outcomes of 35 patients who were randomized to 1 month of
enteral tube feeding of 2,000kcal/day with 40mg of
prednisone/day . No difference in mortality was noted, but the
time course of deaths was different, with the patients randomized
to enteral feeding dying at a median of 7 days, vs. 23 days in the
steroid-treated group. Patients treated with nutritional support
who survived past the first month seemed to have a decreased
mortality compared with the steroid-treated patients (8% vs.
37%) . Although technically a negative study, the similar overall
mortality rates in the treatment groups suggests a role for
nutritional intervention , particularly in light of the relatively
benign risk:benefit ratio. Based on these data, other societies
have recommended oral or parenteral supplements for patients
with AH at risk of undernutrition .

Steroids

The most extensively studied intervention in AH is the use of

steroids, based on 13 clinical trials that date back almost 40
years .
Most of these trials were small, and therefore had only limited
statistical power to detect even moderate treatment effects; five
suggested an improvement in outcome, with decreased shortterm mortality in steroid-treated patients compared with placebotreated patients, whereas eight showed no effect. It is important
to note, however, that these trials used varying inclusion and
exclusion criteria, dosing, and were conducted in a variety of
patient populations. Three meta-analyses have analyzed data
from these trials, and showed an improvement in survival in the
treated patients ; one meta-regression, however, using a different
statistical weighting of the varying trials, was unable to show any
difference . The most recent meta-analysis of these data did not
show a statistically significant effect of steroids on mortality
among all patients treated, although it did show an effect of
steroids in the subgroup of patients with hepatic encephalopathy
and/or an MDF score 32 . The presence of substantial statistical
heterogeneity in this subgroup of studies prevented the authors
from reporting an overall beneficial effect. The implication of this
finding is unclear, as statistical heterogeneity among subgroups is
a function of both clinical differences and/or methodological
differences among studies, and these analyses may be reflect
bias or confounding . One potential approach to resolve this is the
use of individual patient data across clinical trials, which
represents the gold standard approach to meta-analysis .
Although it is impractical to retrieve and combine primary data
from all the clinical trials in this field, in which large variation in
studies over time exists, this approach was pursued using a
combined dataset, using pooled primary data from three placebocontrolled trials in patients with comparable measures of disease

severity (i.e., an MDF 32). The results showed a significant

increase in short-term survival among the treated patients
compared with the control patients: 84.6% vs. 65% . This
represents a modest absolute reduction in risk, but a
30% reduction in the relative risk, and translates into a number
needed to treat of 5i.e., five patients need to be treated to
avert one death. This last meta-analysis also excluded a recent
trial comparing steroids with a combination of anti-oxidants,
which showed a similar protective effect of corticosteroids among
treated patients . Although it is possible that anti-oxidants
themselves may be detrimental , the doses used seem unlikely to
account for the differences in survival, and the consistency of the
data suggests a protective effect of steroids.
Although the doses and durations of steroid treatment used in the
clinical trials were variable, the best available evidence suggests a
dose of prednisolone (40mg/day for 4 weeks, then tapered over
24 weeks, or stopped, depending on the clinical situation)
should be used in favor of prednisone .
An important issue in all studies of medical therapy, and one that
has been recognized for some time in this literature, is the
possibility that these therapies may not be effective at an
advanced stage of disease. Just as there is a threshold for the use
of steroids (i.e., identifying patients at high risk of mortality
defined by an MDF score 32), there may also be a ceiling
beyond which medical therapies aimed at decreasing the
inflammatory cascade may cause more harm than benefit. One
study examined this issue, and suggested that patients with a
MDF >54 were at a higher mortality risk from use of steroids than
from not being treated . This cutoff, however, needs to be
confirmed.

One recently derived model used six variables to predict the sixmonth mortality in patients who were universally treated with
steroids (including age, renal insufficiency (serum creatinine >1.3
or creatinine clearance <40), albumin, prothrombin time,
bilirubin, and change in bilirubin over 1 week), and showed an
improved prognostic ability compared with MDF or GAH scores .
This model, may allow identification of patients who are at high
risk to be treated with other interventions.
Anti-cytokine therapy

A wealth of evidence suggests that dysregulated cytokines,

including tumor necrosis factor alpha (TNF-) and a host of
downstream cytokines have a pivotal role in the pathophysiology
of AH. Thus, several agents have been studied that affect the
immunologic milieu, targeting specific cytokines, and TNF- in
particular.
Among the first agents to be studied was pentoxifylline, an oral
phosphodiesterase inhibitor that also inhibits the production of
TNF-, among other cytokines. A randomized placebo-controlled
clinical trial tested pentoxifylline in 101 patients with clinical
evidence of severe AH . The in-hospital mortality in the treated
patients was 40% lower than in the placebo arm, with the bulk of
the reduction related to a substantially lower likelihood of
developing hepatorenal syndrome. The hepatorenal syndrome
was responsible for 50% of the 12 deaths in the treatment arm,
compared with 91.7% of the 24 deaths in the placebo group.
Other specific inhibitors of TNF that have been studied include
infliximab, a monoclonal chimeric anti-TNF antibody, and
etanercept, a fusion protein containing the ligand-binding portion
of the human TNF receptor fused to the Fc portion of human IgG1

. In the first clinical trial of infliximab, 20 patients with biopsyproven AH and an MDF score between 32 and 55 (based on the
original Maddrey score, which showed an increased mortality at a
score >93) were randomized to either 5mg/kg of infliximab plus
40mg/day of prednisone (n=11) or prednisone alone . No
substantial difference in overall mortality was found, but
substantial decreases in other prognostic markers, including
cytokine levels and MDF scores, were seen in patients treated
with the combination therapy. Another trial, which was performed
at 19 centers in France, randomized 36 patients with biopsyproven AH and an MDF 32 to prednisolone (40mg/day for 4
weeks), vs. prednisolone along with infliximab (10mg/kg, given
at study entry, and again at 2 and 4 weeks after entry) . The trial
was stopped prematurely after seven deaths had occurred in the
infliximab group, compared with three in the prednisolone arm.
Four of the seven deaths in the infliximab arm were related to
infectious etiologies, compared with one in the prednisolone
group. The design, and, in particular, the dose of infliximab
chosen in the study, has been criticized as predisposing to these
infections . The utility of etanercept (given six times over three
weeks) was tested in 48 patients with moderate-to-severe AH
(MELD score >15); unfortunately, no significant difference in 1month mortality was seen in the treated patients compared with
patients given placebo, and an increased mortality was seen at 6
months .
Although a strong rationale remains for the use of anti-TNF
therapy in AH, there is also a theoretical basis for minimizing TNF
inhibition, as it has a role in liver regeneration as well as
apoptosis .Thus, in light of the poor clinical outcomes observed in
the largest of the infliximab trials and the etanercept study, the
use of these parenteral TNF inhibitors should be confined to
clinical trials, and recommendations regarding specific therapy

will need to await the results of these trials. There are no

substantive clinical data comparing the use of steroids or nutrition
with specific anti-TNF therapies.
Combination therapy

Although it is assumed that each of these different treatments

may operate through independent mechanisms, there are only
minimal data regarding the comparative benefit of sequential
therapies or combined approaches. One study tested the use of
pentoxifylline in 29 patients with severe AH (MDF 32) who did
not respond to steroids based on a drop in bilirubin level after 1
week of prednisolone treatment. Compared with previously
treated patients (who were continued on steroids despite lack of
bilirubin response), there was no improvement in 2-month
survivalarguing against a two-step strategy with an early switch
to pentoxifylline . Several older studies had examined the role of
anabolic steroids with nutritional interventions (based on the
presumption that both interventions acted through a similar
mechanism, i.e., by correction of protein calorie malnutrition) .
One pilot study evaluated the role of steroids in combination with
enteral nutrition in 13 patients with severe AH, and found an
overall mortality of 15%possibly an improvement from that
expected . With the advent of new therapies, it is necessary to
reconsider the riskbenefit ratio of medical treatment. It has been
suggested that it may be possible to use less toxic therapies at a
lower threshold of disease severity . However, the exact role of
these new therapiesand the threshold for their useis still
undefined.
Other treatments

Many other therapeutic interventions have been studied in AH,

but have not been able to show convincing benefit, including
trials of anti-oxidants (vitamin E, silymarin, combination antioxidants), anti-fibrotics (colchicine), anti-thyroid drugs (PTU),
promoters of hepatic regeneration (insulin and glucagons),
anabolic steroids (oxandrolone and testosterone), as well as
calcium channel blockers (amlodipine), polyunsaturated lecithin,
and a number of complementary and alternative medicines
(reviewed in OShea and McCullough). In addition to medical
treatment directed at the underlying pathophysiological
abnormalities, several studies have tested other aggressive
interventions in patients with AH, such as a molecular adsorbent
recirculating system . Although the results of early studies were
optimistic, with better than predicted outcomes in treated
patients, a further case series was less promising . Case reports
have also described the outcome of patients with severe AH
treated with leukocytapharesis after failing to improve
substantially on steroids .These reports are promising, but
recommendations regarding their appropriate use must await
results of comparative studies of outcomes in these patients.

Recommendations:
8. All patients with AH should be counseled to completely abstain
from alcohol (Class I, level B).
9. All patients with AH or advanced ALD should be assessed for
nutritional deficiencies (protein-calorie malnutrition), as well as
vitamin and mineral deficiencies. Those with severe disease

should be treated aggressively with enteral nutritional therapy

(Class I, level B).
10. Patients with mild-to-moderate AHdefined as a Maddrey
score of <32, without hepatic encephalopathy, and with
improvement in serum bilirubin or decline in the MDF during the
first week of hospitalizationshould be monitored closely, but will
likely not require nor benefit from specific medical interventions
other than nutritional support and abstinence (Class III, level A).
11. Patients with severe disease (MDF score of 32, with or
without hepatic encephalopathy) and lacking contraindications to
steroid use should be considered for a 4-week course of
prednisolone (40mg/day for 28 days, typically followed by
discontinuation or a 2-week taper) (Class I, level A).
12. Patients with severe disease (i.e., a MDF 32) could be
considered for pentoxifylline therapy (400mg orally 3 times daily
for 4 weeks), especially if there are contra-indications to steroid
therapy (Class I, level B).
Long-term management of ALD
Nutritional therapy

Protein calorie malnutrition is common in ALD, is associated with

an increased rate of major complications of cirrhosis (infection,
encephalopathy, and ascites), and indicates a poor prognosis .
A total of 13 studies (7 randomized and 6 open-label studies)
have examined the effect of oral or enteral nutritional
supplementation in patients with alcoholic cirrhosis, with
interventions that ranged from 3 days to 12 months (reviewed in
Stickel et al. Most of these studies are limited by small sample
sizes and short durations of therapy. In one study, enteral feeding

for 34 weeks in 35 hospitalized, severely malnourished, or

decompensated patients with alcoholic cirrhosis seemed to
improve the survival (P<0.065), hepatic encephalopathy, liver
tests, and ChildPugh score, as compared with controls who
received a standard oral diet . In longer-term studies,
equinitrogenous amounts of dietary branched chain amino acids
(BCAA) were compared with casein supplements for 36 months
in patients with chronic hepatic encephalopathy , and shown to
improve encephalopathy, nitrogen balance, and serum bilirubin
compared with casein. Intake of supplemental protein and of
1,000 kilocalories in decompensated patients with alcoholic
cirrhosis has also been shown to reduce hospitalizations for
infections over a 1-year period ,
Long-term aggressive nutritional therapy by the enteral or oral
route in patients with alcoholic cirrhosis is supported by studies
that have shown improved nutritional status . Although
controversial, this may possibly prevent the complications of
cirrhosis . Multiple feedings, emphasizing breakfast and a
nighttime snack, with a regular oral diet at higher-than-usual
dietary intakes (1.21.5g/kg for protein and 3540kcal/kg for
energy) seem beneficial . Finally, during intermittent acute illness
or exacerbations of the underlying chronic liver disease, an
above-normal protein intake (1.5g per kg body weight) and
kilocalorie intake (40kilocalories per kg) improves the protein
calorie malnutrition , and should be considered in the treatment
of these patients.
Recommendation:
13. Patients with alcoholic cirrhosis should receive frequent
interval feedings, emphasizing a nighttime snack and morning
feeding, to improve the nitrogen balance (Class I, level A).
Medical therapies

A number of other agents have been tested in patients with ALD,

including propylthiouracil, which was thought to decrease the
hypermetabolic state induced by alcohol . A Cochrane review of
six randomized controlled trials of PTU in ALD, with a total of 710
patients administered either PTU or placebo, did not show any
benefit of PTU over placebo on the total or liver-related mortality,
complications of liver disease, or liver histology in patients with
ALD . A possible benefit of supplementation with S-adenosyl Lmethionine, a precursor to glutathione, has also been studied
extensively . One trial showed a statistically significant
improvement in survival in patients with Childs A and B cirrhosis
randomized to S-adenosyl L-methionine compared with placebo .
Despite a strong theoretical rationale, and a number of supportive
clinical trials , a Cochrane review of published data, based on nine
randomized controlled trials with 434 patients in different stages
of ALD, did not show any significant benefit of S-adenosyl Lmethionine on total mortality, liver-related mortality,
complications, or liver transplantation (LT) in patients with ALD .
Colchicine, which has both anti-inflammatory and antifibrotic
properties, has also been tested in alcoholic cirrhosis after several
small clinical trials, and has suggested improvement in fibrosis on
serial liver biopsies in treated patients . However, a systematic
meta-analysis of 15 randomized trials with 1,714 patients
(including patients with alcoholic fibrosis, AH, and/or alcoholic
cirrhosis, as well as patients with viral induced or cryptogenic
fibrosis and/or cirrhosis) by the Cochrane group showed no
benefit of treatment on overall mortality, liver-related mortality,
liver tests, or histology. In addition, there was an increased risk
of adverse effects related to colchicine therapy.

Emerging data suggest a role for TNF--mediated apoptosis in

AH, and therapy targeting this cytokine to inhibit apoptosis may
be effective . Thalidomide, misoprostol, adiponectin, and
probiotics have been shown to have anti-cytokine properties in
preliminary reports . Although promising, these treatments
cannot be considered as standard treatment for ALD and AH until
further evidence of efficacy has been obtained.
Complementary and alternative medicine treatment options

Various alternative treatment options have been tested in the

therapy of ALD.
Silymarin, the presumed active ingredient in milk thistle, is
postulated to protect patients from ALD on the basis of its
antioxidant properties. Six published trials of the use of silymarin
in patients with ALD have tested its effects on normalizing liver
tests and on improving liver histology. One study suggested a
possible survival benefit compared with placebo . However, a
Cochrane systematic review and a meta-analysis of the 13
published studies of silymarin in ALD and other liver diseases
found that the overall methodological quality of the studies was
low. Based on the few high-quality trials, it was concluded that
milk thistle does not significantly influence the course of patients
with ALD .
Recommendations:
14. PTU and colchicine should not be used in the treatment of
patients with ALD;S-adenosyl L-methionine should be used only in
clinical trials (Class III, level A).
15. The use of complementary or alternative medicines in the
treatment of either acute or chronic alcohol-related liver disease

has shown no convincing benefit and should not be used out of

the context of a clinical trial (Class III, level A).
LT for ALD
ALD is the second most common indication for LT for chronic liver
disease in the Western world . Despite this, it is estimated that as
many as 95% of patients with end stage liver disease related to
alcohol are never formally evaluated for their candidacy for LT .
This is attributed to perceptions that ALD is self-induced, the
possibility of recidivism or non-compliance, and the shortage of
organs .
A 6-month period of abstinence has been recommended as a
minimal listing criterion .This time period allows chemical
dependency issues to be addressed; in patients with recent
alcohol consumption, it may also allow sufficient clinical
improvement to make LT unnecessary. This requirement for a
fixed abstinence period has not been shown to accurately predict
future drinking by alcoholic candidates for LT . Despite some data
suggesting that patients with ALD were more ill at the time of LT,
and were likely to have prolonged intensive care unit stays and
increased blood product requirements , the overall survival rates
are generally similar between alcohol-related and non-alcoholrelated LTX recipients .
Patients transplanted for ALD are highly likely to drink after
transplantation . It has been suggested that the consequences of
alcohol use are minimal for many recipients, because the
amounts consumed are small and infrequent, but there are little
reliable data to support this contention. Rates of recidivism
between 1149%(defined as any alcohol consumption after
transplantation) at 35 years after LT have been reported . In
general, however, only a small fraction of those who undergo LT
for ALD revert to heavy alcohol use or abuse . Poor follow-up and

non-compliance with therapy are observed in only a minority of

patients, and graft rejection rates are similar for patients with
ALD compared with non-ALD patients .
An important issue that is still unresolved is the role of LT in
patients with AH, who are generally excluded from transplant . In
one study using retrospective histological analysis of the
explanted liver, superimposed AH did not worsen the outcome
after LT .The availability of living donor transplantation and
extended criteria donor LT are likely to heighten the debate on
this issue.
Recommendation:
16. The appropriate patients with end-stage liver disease
secondary to alcoholic cirrhosis should be considered for LT just
as other patients with decompensated liver disease, after a
careful evaluation of their medical and psychosocial candidacy. In
addition, this evaluation should include a formal assessment of
the likelihood of long-term abstinence (Class I, level B).

Fatty liver
Fatty liver

Micrograph showing a fatty

liver(macrovesicular steatosis), as
seen in non-alcoholic fatty liver
disease. Trichrome stain.
Classification and external resources
Specialty

Gastroenterology

ICD-10

K70, K76.0

ICD-9-CM

571.0, 571.8

DiseasesDB 18844
eMedicine

med/775 article/17040
9

MeSH

C06.552.241

Fatty liver, also known as fatty liver disease (FLD), is a reversible condition
wherein large vacuoles of triglyceride fat accumulate in liver cells via the
process of steatosis (i.e., abnormal retention of lipids within a cell). Despite
having multiple causes, fatty liver can be considered a single disease that
occurs worldwide in those with excessive alcohol intake and the obese
(with or without effects of insulin resistance). The condition is also
associated with other diseases that influence fat metabolism.[1] When this
process of fat metabolism is disrupted, the fat can accumulate in the liver in
excessive amounts, thus resulting in a fatty liver.[2] It is difficult to distinguish

alcoholic FLD from nonalcoholic FLD, and both show microvesicular and
macrovesicular fatty changes at different stages.
Accumulation of fat may also be accompanied by a progressive
inflammation of the liver (hepatitis), called steatohepatitis. By considering
the contribution by alcohol, fatty liver may be termed alcoholic steatosis
or nonalcoholic fatty liver disease (NAFLD), and the more severe forms as
alcoholic steatohepatitis (part of alcoholic liver disease) and Non-alcoholic
steatohepatitis (NASH).
Contents
1 Causes
2 Pathology
3 Diagnosis
4 Treatment
5 Complication
6 Epidemiology

Causes

Different stages of liver damage

Fatty liver (FL) is commonly associated with alcohol or metabolic
syndrome(diabetes, hypertension, obesity, and dyslipidemia), but can also
be due to any one of many causes:
Metabolic
Abetalipoproteinemia, glycogen storage diseases, Weber-Christian
disease,acute fatty liver of pregnancy, lipodystrophy
Nutritional

Malnutrition, total parenteral nutrition, severe weight loss, refeeding

syndrome,jejunoileal bypass, gastric bypass,
jejunal diverticulosis with bacterial overgrowth
Drugs and toxins
Amiodarone, methotrexate, diltiazem, expired tetracycline, highly active
antiretroviral therapy, glucocorticoids, tamoxifen,
environmental hepatotoxins (e.g., phosphorus, mushroom poisoning)
Alcoholic
Alcoholism is one of the major cause of fatty liver due to production of toxic
metabolites like aldehydes during metabolism of alcohol in the liver. This
phenomenon most commonly occurs with chronic alcoholism.
Other
Inflammatory bowel disease, HIV, hepatitis C (especially genotype 3), and
alpha 1-antitrypsin deficiency [5]
Pathology

Micrograph of periportal hepaticsteatosis, as may be seen due

tosteroid use, trichrome stain
Fatty change represents the intracytoplasmatic accumulation of
triglycerides (neutral fats). At the beginning, the hepatocytes present small
fat vacuoles (liposomes) around the nucleus (microvesicular fatty change).
In this stage, liver cells are filled with multiple fat droplets that do not
displace the centrally located nucleus. In the late stages, the size of the
vacuoles increases, pushing the nucleus to the periphery of the cell, giving
characteristic signet ring appearance (macrovesicular fatty change). These
vesicles are well-delineated and optically "empty" because fats dissolve

during tissue processing. Large vacuoles may coalesce and produce

fattycysts, which are irreversible lesions. Macrovesicular steatosis is the
most common form and is typically associated
with alcohol, diabetes, obesity, and corticosteroids.Acute fatty liver of
pregnancy and Reye's syndrome are examples of severe liver disease
caused by microvesicular fatty change. The diagnosis of steatosis is made
when fat in the liver exceeds 510% by weight.

Mechanism leading to hepatic steatosis

Defects in fatty acid metabolism are responsible for pathogenesis of FLD,
which may be due to imbalance in energy consumption and its combustion,
resulting in lipid storage, or can be a consequence of peripheral resistance
to insulin, whereby the transport of fatty acids from adipose tissue to the
liver is increased. Impairment or inhibition of receptor molecules (PPAR, PPAR- and SREBP1) that control the enzymes responsible for the
oxidation and synthesis of fatty acids appears to contribute to fat
accumulation. In addition, alcoholism is known to damage mitochondria
and other cellular structures, further impairing cellular energy mechanism.
On the other hand, nonalcoholic FLD may begin as excess of
unmetabolised energy in liver cells. Hepatic steatosis is considered
reversible and to some extent nonprogressive if the underlying cause is
reduced or removed.

Micrograph of inflamed fatty liver (steatohepatitis)

Severe fatty liver is sometimes accompanied by inflammation, a situation
referred to assteatohepatitis. Progression to alcoholic steatohepatitis (ASH)

or Non-alcoholic steatohepatitis (NASH) depends on the persistence or

severity of the inciting cause.Pathological lesions in both conditions are
similar. However, the extent of inflammatory response varies widely and
does not always correlate with degree of fat accumulation. Steatosis
(retention of lipid) and onset of steatohepatitis may represent successive
stages in FLD progression.
Liver disease with extensive inflammation and a high degree of steatosis
often progresses to more severe forms of the disease.
Hepatocyte ballooning and necrosis of varying degrees are often present at
this stage. Liver cell death and inflammatory responses lead to the
activation of stellate cells, which play a pivotal role in hepatic fibrosis. The
extent of fibrosis varies widely. Perisinusoidal fibrosis is most common,
especially in adults, and predominates in zone 3 around the
terminal hepatic veins.
The progression to cirrhosis may be influenced by the amount of fat and
degree of steatohepatitis and by a variety of other sensitizing factors. In
alcoholic FLD, the transition to cirrhosis related to continued alcohol
consumption is well-documented, but the process involved in nonalcoholic
FLD is less clear.
Diagnosis

.
Flow chart for diagnosis, modified from [4]

Elevated liver enzyme

Serology to exclude viral hepatitis

Imaging study showing

fatty infiltrate

Excess alcohol intake

Less than two drinks per

day

More than two drinks

per day

Nonalcoholic fatty liver

disease likely

Alcoholic liver
disease likely

Criteria for nonalcoholic fatty liver disease:

consumption of ethanol less than 20 g/day for women and

30 g/day for men[13]
Most individuals are asymptomatic and are usually discovered incidentally
because of abnormal liver function tests or hepatomegaly noted in
unrelated medical conditions. Elevated liver biochemistry is found in 50% of
patients with simple steatosis. The serum alanine transaminaselevel
usually is greater than the aspartate transaminase level in the nonalcoholic
variant and the opposite in alcoholic FLD (AST:ALT more than 2:1).
Imaging studies are often obtained during the evaluation
process. Ultrasonography reveals a "bright" liver with
increasedechogenicity. Medical imaging can aid in diagnosis of fatty liver;
fatty livers have lower density than spleens on computed tomography (CT),
and fat appears bright in T1-weighted magnetic resonance images (MRIs).
No medical imagery, however, is able to distinguish simple steatosis from
advanced NASH. Histological diagnosis by liver biopsy is sought when
assessment of severity is indicated.
Treatment

The treatment of fatty liver depends on its cause, and, in general, treating
the underlying cause will reverse the process of steatosis if implemented at
an early stage. Two known causes of fatty liver disease are an excess
consumption of alcohol and a prolonged diet containing foods with a high
proportion of calories coming from lipids. For the patients with non-alcoholic
fatty liver disease with pure steatosis and no evidence of inflammation, a
gradual weight loss is often the only recommendation. In more serious
cases, medications that decrease insulin resistance, hyperlipidemia, and
those that induce weight loss have been shown to improve liver function. [4]
For advanced patients with non-alcoholic steatohepatitis (NASH), there are
no currently available therapies.
Complication

Up to 10% of cirrhotic alcoholic FLD patients will develop hepatocellular

carcinoma. The overall incidence of liver cancer in nonalcoholic FLD has
not yet been quantified, but the association is well-established.
Epidemiology
The prevalence of FLD in the general population ranges from 10% to 24%
in various countries. However, the condition is observed in up to 75% of
obese people, 35% of whom progressing to NAFLD, despite no evidence of
excessive alcohol consumption. FLD is the most common cause of
abnormal liver function tests in the United States.[3] "Fatty livers occur in
33% of European-Americans, 45% of Hispanic-Americans, and 24% of
African-Americans."
Fatty Liver

Overview
Symptoms and Causes
Types
Risk Factors
Diagnosis
Treatment and Prevention

Overview

Fatty liver, or steatosis, is a broad term that describes the buildup

of fats in the liver. Having fat in your liver is normal, but if more
than 5 to 10 percent is fat, then its called fatty liver disease.
Fatty liver is a reversible condition that can be resolved with:
diet

exercise
alcohol avoidance
other lifestyle changes
Fatty liver often has no symptoms and typically does not cause
any permanent damage.
The liver is the second largest organ in the body. The livers
function is to process everything we eat or drink and filter any
harmful substances from the blood. This process is interfered with
if too much fat has accumulated in the liver. The liver commonly
repairs itself by rebuilding new liver cells when the old ones are
damaged. When there is repeated damage to the liver,
permanent scarring takes place. This is called cirrhosis.
Fatty liver is quite common. Around 10 to 20 percent of Americans
have too much fat in their liver, but no inflammation or damage is
present. Most cases of fatty liver are detected between ages 50
and 60. When fatty liver is caused by an underlying condition, it
can become harmful to the liver if the cause is not recognized and
treated.
Part 2 of 7: Symptoms and Causes
What Are Symptoms and Causes of Fatty Liver?
There are typically no symptoms of fatty liver. Some people experience
fatigue or vague abdominal discomfort. The liver may become slightly
enlarged which your doctor will notice with a thorough physical exam.
If the liver has become inflamed, there may be other symptoms, such as
poor appetite, weight loss, and feeling extremely weak, sick, or tired.
The most common cause is alcoholism. Almost all heavy drinkers have
fatty liver disease. Other causes are toxins, certain drugs, and inherited
metabolic disorders. In many cases, doctors are not exactly sure what

causes fatty liver in people who arent alcoholics, but it has been
associated with high blood cholesterol, obesity, and type 2 diabetes.
Fatty liver develops when the body creates too much fat or cannot
metabolize fat fast enough. As a result, the leftover is stored in
liver cells where it accumulates to become fatty liver disease.
Eating a high-fat diet does not directly result in fatty liver.
Besides alcoholism, other common causes of fatty liver include:
obesity
hyperlipidemia (high levels of fats in the blood)
diabetes
genetic inheritance
rapid weight loss
side effect of certain medications, including aspirin, steroids,
tamoxifen, and tetracycline
What Are the Types of Fatty Liver?
There are four types of fatty liver.
Nonalcoholic Fatty Liver
Nonalcoholic fatty liver (NAFL) develops when the liver has
difficulty breaking down fats, which causes a buildup in the liver
tissue. The cause is not related to alcohol. NAFL is diagnosed
when more than 10 percent of the liver is fat.
Alcoholic Fatty Liver

Alcoholic fatty liver is the earliest stage of alcohol-related liver

disease. The liver is damaged by heavy drinking and unable to
break down fats. If the patient abstains from alcohol, the fatty
liver will go away. Within six weeks of being alcohol-free, the fat

will disappear. However, if excessive alcohol use continues,

cirrhosis may develop.
Nonalcoholic Steatohepatitis (NASH)
When the fat builds up enough, it will cause the liver to swell. If
the original cause is not from alcohol, its called NASH. This
disease can impair liver function. Symptoms can be seen with this
disease, such as loss of appetite, nausea, vomiting, abdominal
pain, and yellowing of the skin. If left untreated, NASH can
progress to permanent scarring of the liver and eventual liver
failure.
Acute Fatty Liver of Pregnancy
This is a rare complication of pregnancy that can be life
threatening. Symptoms begin in the third trimester and include
persistent nausea and vomiting, pain in the upper-right abdomen,
jaundice, and general malaise. Women who are pregnant will be
screened for this condition. Most women improve after delivery
and have no lasting effects.
Part 4 of 7: Risk Factors
Who's at Risk for Fatty Liver?
Since fatty liver is the buildup of extra fats in the liver, its more
likely to develop if youre overweight or obese.
Other factors that may increase your risk for fatty liver are:
excessive alcohol use (drinking large amounts of alcohol can
damage your liver)
excessive use of over-the-counter medication (taking more than
the recommended doses of certain medications, such as
acetaminophen, can increase your risk of fatty liver)

type 2 diabetes (fat accumulation in the liver has been linked to

insulin resistance, the most common cause of type 2 diabetes)
pregnancy
high cholesterol
high triglyceride levels
malnutrition
metabolic syndrome
Part 5 of 7: Diagnosis
How Is Fatty Liver Diagnosed?
Physical Exam
If the liver has become inflamed, your doctor can detect it by
examining the abdomen. An extensive history may reveal fatigue
or loss of appetite as well. A thorough history will include alcohol,
medication, and supplement use.
Blood Tests
Higher than normal liver enzymes may be found on a routine
blood test. This does not confirm a diagnosis of fatty liver. Further
analysis will look for the cause of inflammation.
Ultrasound
The fat on your liver will show up as a white area on the image.
Other imaging studies may be done as well such as a CT scan or
MRI. Imaging studies can detect fat in the liver, but will not be
able to confirm any further damage.
Liver Biopsy
A needle is inserted into the liver to remove a piece of tissue for
examination (after giving a local anesthetic to lessen the pain).

This is the only way to know for certain if you have fatty liver. The
biopsy will also help your doctor determine the exact cause.
Part 6 of 7: Treatment and Prevention
How Is Fatty Liver Treated and Prevented?
Treatment focuses on the factors that may cause the disease.
Common interventions center around:
treatment of alcoholism
cholesterol management
weight loss
blood sugar control
To reduce your risk of fatty liver, make healthy lifestyle choices,
such as:
limiting or avoiding alcohol consumption
eating a healthy diet
maintaining a healthy weight
Most cases of fatty liver will not lead to progressive liver disease. If the
cause is related to high cholesterol, diabetes, or obesity, then treating the
cause will reverse the fatty liver process.
If the cause is alcoholism, cessation of drinking may allow the liver to heal
completely. A biopsy can determine if there is permanent damage, how bad
the damage is, and how it needs to be treated.
Non-alcoholic fatty liver disease
Overview
Community
Non-alcoholic fatty liver disease

Introduction
Non-alcoholic fatty liver disease (NAFLD) is the term for a wide range of
conditions caused by a build-up of fat within the liver cells. It is usually seen
in people who are overweight or obese.
A healthy liver should contain little or no fat. Most people with NAFLD only
carry small amounts of fat in their liver, which doesn't usually cause any
symptoms. This early form of the disease is known as simple fatty liver, or
steatosis.
Simple fatty liver is very common in the UK, reflecting the number of people
who are obese or overweight. It is one of the most common forms of liver
disease, with an estimated 25-30% people in the UK having early forms of
NAFLD.
In most people, simple fatty liver is unlikely to cause harm, but that doesn't
mean it's not a serious condition. This is because:
in some people, if the fat builds up and gets worse, it can eventually lead to
inflammation (non-alcoholic steatohepatitis, or NASH) and scarring of the
liver
as the disease is linked to being overweight or obese, people with any
stage of the disease are more at risk of developing a stroke or heart
attack this risk appears to be higher in those who have NASH
NAFLD is often diagnosed after liver function tests (a type of blood test)
produce an abnormal result and other liver conditions, such as hepatitis,
are ruled out. However, NAFLD can be present even when routine liver
blood tests are normal.
This page explains:
the four stages of NAFLD and the symptoms at each stage
who is affected, and the causes of NAFLD
living with NAFLD

Four stages of NAFLD

NAFLD is very similar to alcoholic liver disease, but is caused by factors
other than drinking too much alcohol. The four stages are described below.
Stage 1: simple fatty liver (steatosis)
Hepatic steatosis is stage 1 of the condition. This is where excess fat builds
up in the liver cells, but is considered harmless. There are usually no
symptoms, and you may not even realise you have it until you receive an
abnormal blood test result.
Stage 2: non-alcoholic steatohepatitis (NASH)
Only a few people with simple fatty liver go on to develop stage 2 of the
condition, called non-alcoholic steatohepatitis (NASH). It is estimated that
around 2-5% of the UK population has NASH.
NASH is a more aggressive form of the condition, when the liver has
become inflamed. Inflammation is part of the body's response to injury,
which suggests that cells in the liver are being damaged and that some
liver cells are dying.
A person with NASH may have a dull or aching pain in the top right of their
abdomen (over the lower right side of their ribs), although there may be no
symptoms at all.
Unfortunately, routine blood tests alone do not help doctors work out if
someone has simple steatosis or NASH, meaning that other specialist tests
are needed.
Stage 3: fibrosis
Some people with NASH go on to develop fibrosis, which is
where persistent inflammation in the liver results in the generation of
fibrous scar tissue around the liver cells and blood vessels.
This fibrous tissue replaces some of the healthy liver tissue, but there is still
enough healthy tissue for the liver to function normally.

Stage 4: cirrhosis
This is the most severe stage, where bands of scar tissue and clumps of
liver cells develop. The liver shrinks and becomes lumpy (known as
cirrhosis).
Cirrhosis tends to occur after the age of 50-60, following many years of
liver inflammation associated with the early stages of the disease.
However, this can happen much earlier in some people.
People who have type 2 diabetes are at the greatest risk of developing
cirrhosis of the liver caused by NAFLD.
The damage caused by cirrhosis is permanent and can't be reversed.
Cirrhosis progresses slowly, over many years, gradually causing your liver
to stop functioning. NAFLD can also lead to primary liver
cancer(hepatocellular carcinoma). This is what is known as liver failure.
Learn more about cirrhosis of the liver, including the warning signs.
Who is affected?
You are more likely to develop NAFLD and more severe forms of the
disease, such as NASH, fibrosis or cirrhosis if you:
are obese or overweight
have type 2 diabetes (this causes an increased uptake of fat into the liver
cells)
have high blood pressure
have high cholesterol
are over the age of 50
smoke
Living with NAFLD
Most people with NAFLD do not develop serious liver problems and just
have stage 1 of the disease (simple fatty liver).

Simple fatty liver may go away if the underlying cause is tackled. For
example, losing excess weight or controlling diabetes better can make fatty
liver disappear.
Many people do not have symptoms, although it's common to feel tired and
some people have a persistent pain in the upper right part of their abdomen
(where their liver is).
It can take years for symptoms of fibrosis or cirrhosis to appear. It is
important to make lifestyle changes to prevent the disease progressing to a
more serious stage and to lower your risk of having a heart attack or stroke.
Losing weight and exercising
The most important thing that people with NAFLD can do is to go on a
gradual weight loss programme and exercise regularly. This helps in by:
reducing the amount of fat in your liver cells this helps to heal
inflammation
lowering your risk of stroke and heart attack
Losing weight is particularly important if you have type 2 diabetes, but is
important for everyone with NAFLD.
Read more on how to start losing weight.
Stopping smoking
If you smoke, it's really important to give up, as this will also help to reduce
your risk of heart attack and stroke. Take steps now to stop smoking.
Medication
If you have high blood pressure or cholesterol, you may need medical
treatment for these. Read about the treatment of high blood
pressure andtreatment of high cholesterol.
If you have type 2 diabetes, you may need medicines that reduce high
blood sugar levels. At first, this will usually be in the form of tablets, and
sometimes a combination of more than one type of tablet. It may also

include injections of insulin. Learn more about the medical treatment of

type 2 diabetes.
There are currently no specific medicines for NAFLD, but certain medicines
used to treat high blood pressure and diabetes also have a beneficial effect
on the liver. Your doctor may prescribe a particular medicine to help reduce
the chance of NAFLD causing cirrhosis or liver cancer.
Alcohol
NAFLD is not caused by alcohol, but it may make the condition worse. It's
therefore advisable to stop drinking alcohol. Read our tips on cutting down
alcohol consumption.

Role of the liver

The liver has many important functions, which keep the body working
normally. These include:
storing glycogen, which is broken down in to glucose (sugar) and released
into the bloodstream when the body needs energy
helping to process fats and proteins
making proteins that enable the blood to clot
helping to remove or process alcohol, drugs and toxins
making bile, which is a fluid that passes through the bile duct to the gut.
This is needed to break down digested food into fatsLiver disorder forum

cirrhosis is a slowly progressing disease in which healthy liver tissue is

replaced with scar tissue, eventually preventing the liver from functioning
properly. The scar tissue blocks the flow of blood through the liver and

slows the processing of nutrients, hormones, drugs, and naturally produced

toxins.

Cirrhosis
From Wikipedia, the free encyclopedia
Cirrhosis

The abdomen of a person with cirrhosis

showing massive fluid buildup and very
visible veins
Classification and external resources
Specialty

Gastroenterology

ICD-10

K70.3, K71.7, K74

ICD-9-CM

571

DiseasesDB

2729

MedlinePlus

000255

eMedicine

med/3183 radio/175

Patient UK

Cirrhosis

MeSH

D008103

Cirrhosis /sross/ is a condition in which the liver does not function

properly due to long-term damage. Typically, the disease comes on slowly
over years. Early on, there are often no symptoms. As the disease
worsens, a person may become tired, weak, itchy, have swelling in the
lower legs, developyellow skin, bruise easily, have fluid build up in the

abdomen, or developspider-like blood vessels on the skin. The fluid buildup in the abdomen may become spontaneously infected. Other
complications include hepatic encephalopathy, bleeding from dilated veins
in the esophagus or dilated stomach veins, and liver cancer. Hepatic
encephalopathy results in confusion and possibly unconsciousness.[1]
Cirrhosis is most commonly caused by alcohol, hepatitis B, hepatitis C,
andnon-alcoholic fatty liver disease.[1][2] Typically, more than two or three
drinks per day over a number of years is required for cirrhosis to occur.
Non-alcoholic fatty liver disease is due to a number of reasons, including
being overweight,diabetes, high blood fats, and high blood pressure. A
number of less common causes include autoimmune hepatitis, primary
biliary cirrhosis,hemochromatosis, certain medications, and gallstones.
Cirrhosis is characterized by the replacement of normal liver tissue by scar
tissue. These changes lead to loss of liver function. Diagnosis is based on
blood testing,medical imaging, and liver biopsy.[1]
Some causes of cirrhosis, such as hepatitis B, can be prevented
byvaccination. Treatment partly depends on the underlying cause. The goal
is often to prevent worsening and complications. Avoiding alcohol is
recommended. Hepatitis B and C may be treatable with antiviral
medications. Autoimmune hepatitis may be treated with steroid
medications. Ursodiol may be useful if the disease is due to blockage of
the bile ducts. Other medications may be useful for complications such as
swelling, hepatic encephalopathy, and dilated esophageal veins. In severe
cirrhosis, a liver transplant may be an option.
Cirrhosis resulted in 1.2 million deaths in 2013, up from 0.8 million deaths
in 1990.[2] Of these, alcohol caused 384,000, hepatitis C caused 358,000,
and hepatitis B caused 317,000.[2] In the United States, more men die of
cirrhosis than women.[1] The first known description of the condition is
by Hippocrates in the 5th century BCE.[3] The word cirrhosis is
fromGreek: ; neologism from kirrhos "yellowish" and the
suffix -osis (-) meaning "condition".
Contents

1 Signs and symptoms

1.1 Liver dysfunction
1.2 Portal hypertension
1.3 Unestablished cause
1.4 Advanced disease
2 Causes
3 Pathophysiology
4 Diagnosis
4.1 Lab findings
4.2 Imaging
4.3 Endoscopy
4.4 Pathology
4.5 Grading
5 Prevention
6 Management
6.1 Preventing further liver damage
6.2 Transplantation
6.3 Decompensated cirrhosis
6.4 Palliative care
7 Complications
7.1 Ascites
7.2 Esophageal variceal bleeding
7.3 Hepatic encephalopathy

7.4 Hepatorenal syndrome

7.5 Spontaneous bacterial peritonitis
7.6 Portal hypertensive gastropathy
7.7 Infection
7.8 Hepatocellular carcinoma
8 Epidemiology
9 Etymology

Signs and symptoms

Cirrhosis has many possible manifestations. These signs and symptoms
may be either as a direct result of the failure of liver cells or secondary to
the resultant portal hypertension. There are also some manifestations
whose causes are nonspecific, but may occur in cirrhosis. Likewise, the
absence of any does not rule out the possibility of cirrhosis. Cirrhosis of
the liver is slow and gradual in its development. It is usually well advanced
before its symptoms are noticeable enough to cause alarm. Weakness and
loss of weight may be early symptoms.
Liver dysfunction
The following features are as a direct consequence of liver cells not
functioning.
Spider angiomata or spider nevi are vascular lesions consisting of a central
arteriole surrounded by many smaller vessels (hence the name "spider")
and occur due to an increase in estradiol. One study found that spider
angiomata occur in about 1/3 of cases.
Palmar erythema is a reddening of palms at the thenar and hypothenar
eminences also as a result of increased estrogen. Gynecomastia, or
increase in breast gland size in men that is not cancerous, is caused by

increased estradiol and can occur in up to 2/3 of patients. This is different

from increase in breast fat in overweight people.
Hypogonadism, a decrease in sex hormones manifest as impotence,
infertility, loss of sexual drive, and testicular atrophy, can result from
primary gonadal injury or suppression of hypothalamic/pituitary function.
Hypogonadism is associated with cirrhosis due to alcoholism and
hemochromatosis.[12]
Liver size can be enlarged, normal, or shrunken in people with cirrhosis.
Ascites, accumulation of fluid in the peritoneal cavity (space in the
abdomen), gives rise to flank dullness (needs about 1500 ml to detect flank
dullness). This may be visible as increase in abdominal girth.
Fetor hepaticus is a musty breath odor resulting from increased dimethyl
sulfide.
Jaundice is yellow discoloration of the skin and mucous membranes (with
the eye being especially noticeable) due to increased bilirubin (at least 2
3 mg/dL or 30 mol/L). Urine may also appear dark.
Portal hypertension
Liver cirrhosis increases resistance to blood flow and higher pressure in the
portal venous system, resulting in portal hypertension. Effects of portal
hypertension include:
Splenomegaly (increase in size of the spleen) is found in 35% to 50% of
patients.
Esophageal varices result from collateral portal blood flow through vessels
in the stomach and esophagus (a process called Portacaval anastomosis).
When these blood vessels become enlarged, they are called varices and
are more likely to burst.
Caput medusa are dilated periumbilical collateral veins due to portal
hypertension. Blood from the portal venous system may be shunted

through the periumbilical veins and ultimately to the abdominal wall veins,
manifesting as a pattern that may resemble the head of Medusa.
Cruveilhier-Baumgarten murmur is a venous hum heard in the epigastric
region (on examination by stethoscope) due to collateral connections
forming between portal system and the periumbilical veins as a result of
portal hypertension.
Unestablished cause
There are some changes seen in cirrhosis whose causes are not clearly
known. They may also be a sign of other non-liver related causes.
Nail changes.
Muehrcke's lines - paired horizontal bands separated by normal color
resulting from hypoalbuminemia (inadequate production of albumin). It is
not specific for cirrhosis.
Terry's nails (double nails) - proximal two-thirds of the nail plate appears
white with distal one-third red, also due to hypoalbuminemia
Clubbing - angle between the nail plate and proximal nail fold > 180
degrees. It is not specific for cirrhosis and can therefore happen in a
number of conditions
Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long
bones that can cause considerable pain. It is not specific for cirrhosis.
Dupuytren's contracture. Thickening and shortening of palmar fascia
(tissue on the palm of the hands) that leads to flexion deformities of the
fingers. Caused by fibroblastic proliferation (increased growth) and
disorderly collagen deposition. It is relatively common (33% of patients).
Other. Weakness, fatigue, anorexia, weight loss.[13]
Advanced disease
As the disease progresses, complications may develop. In some people,
these may be the first signs of the disease.

Bruising and bleeding resulting from decreased production

of coagulation factors.
Hepatic encephalopathy - the liver does not clear ammonia and related
nitrogenous substances from the blood, which are carried to the brain,
affecting cerebral functioning: neglect of personal appearance,
unresponsiveness, forgetfulness, trouble concentrating, or changes in
sleep habits. This can be seen on exam by asterixis which is bilateral
asynchronous flapping of outstretched, dorsiflexed hands seen in patients
with hepatic encephalopathy.
Sensitivity to medication caused by decreased metabolism of the active
compounds.
Acute kidney injury (particularly hepatorenal syndrome)
Causes
It has many possible causes; sometimes more than one cause is present in
the same person. Globally, 57% of cirrhosis is attributable to either hepatitis
B (30%) or hepatitis C (27%).Alcohol consumption is another important
cause, accounting for about 20% of the cases. [18]
Alcoholic liver disease (ALD). Alcoholic cirrhosis develops for 1020% of
individuals who drink heavily for a decade or more. Alcohol seems to injure
the liver by blocking the normal metabolism of protein, fats, and
carbohydrates. This injury happens through the formation of acetaldehyde
from alcohol which itself is reactive, but also leads to the accumulation of
products in the liver. Patients may also have concurrent alcoholic
hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT
are both elevated but less than 300 IU/litre with an AST:ALT ratio > 2.0, a
value rarely seen in other liver diseases. In the United States, 2/5 of
cirrhosis related deaths are due to alcohol.
Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver
and eventually causes scar tissue. This type of hepatitis appears to be
associated with obesity (40% of NASH patients) diabetes, protein
malnutrition, coronary artery disease, and treatment with corticosteroid

medications. This disorder is similar to that of alcoholic liver disease but

patient does not have an alcohol history. Biopsy is needed for diagnosis.
Chronic hepatitis C. Infection with the hepatitis C virus causes
inflammation of the liver and a variable grade of damage to the organ. Over
several decades this inflammation and grade change can lead to cirrhosis.
Among patients with chronic hepatitis C 20-30% will develop cirrhosis. Host
risk factors include human promoter polymorphisms such as TGF-1 and
angiotensin as well as host immune phenotype variations, such as
immunosuppressed patients . Cirrhosis caused by hepatitis C and alcoholic
liver disease are the most common reasons for liver transplant. Can be
diagnosed with serologic assays that detect hepatitis C antibody or viral
RNA. The enzyme immunoassay, EIA-2, is the most commonly used
screening test in the US.
Chronic hepatitis B. The hepatitis B virus causes liver inflammation and
injury that over several decades can lead to cirrhosis. Hepatitis D is
dependent on the presence of hepatitis B and accelerates cirrhosis in coinfection. Chronic hepatitis B can be diagnosed with detection of HBsAG >
6 months after initial infection. HBeAG and HBV DNA are determined to
assess whether patient needs antiviral therapy.
Primary biliary cirrhosis. Damage of the bile ducts leading to secondary
liver damage. May be asymptomatic or complain of fatigue, pruritus, and
non-jaundice skin hyperpigmentation with hepatomegaly. There is
prominent alkaline phosphatase elevation as well as elevations in
cholesterol and bilirubin. Gold standard diagnosis is antimitochondrial
antibodies (positive in 90% of PBC patients). Liver biopsy if done shows
bile duct lesions. It is more common in women.
Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder
presenting with pruritus, steatorrhea, fat-soluble vitamin deficiencies, and
metabolic bone disease. There is a strong association with inflammatory
bowel disease (IBD), especially ulcerative colitis. Diagnosis is best with
contrast cholangiography showing diffuse, multifocal strictures and focal

dilation of bile ducts, leading to a beaded appearance. Non-specific serum

immunoglobulins may also be elevated.
Autoimmune hepatitis. This disease is caused by the immunologic damage
to the liver causing inflammation and eventually scarring and cirrhosis.
Findings include elevations in serum globulins, especially gamma globulins.
Therapy with prednisone and/or azathioprine is beneficial. Cirrhosis due to
autoimmune hepatitis still has 10-year survival of 80+ %.
Hereditary hemochromatosis. Usually presents with family history of
cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or
cardiomyopathy, all due to signs of iron overload. Labs show fasting
transferrin saturation of > 60% and ferritin > 300 ng/ml. Genetic testing may
be used to identify HFE mutations. If these mutations are present, biopsy
may not need to be performed. Treatment is with phlebotomy to lower total
body iron levels.
Wilson's disease. Autosomal recessive disorder characterized by low
serum ceruloplasmin and increased hepatic copper content on liver biopsy,
and elevated 24-hour urine copper. May also have Kayser-Fleischer
rings in the cornea and altered mental status. This condition affects 1 in
30,000 people.
Indian childhood cirrhosis is a form of neonatal cholestasis characterised
by deposition of copper in the liver.
Alpha 1-antitrypsin deficiency (A1AD). Autosomal recessive disorder of
decreased levels of the enzyme alpha 1--antitrypsin. Patients may also
have COPD, especially if they have a history of tobacco smoking. Serum
AAT levels are low and liver biopsy is positive for Periodic acidSchiff Recombinant AAT is used to prevent lung disease due to AAT
deficiency.
Cardiac cirrhosis. Due to chronic right sided heart failure which leads to
liver congestion.
Galactosemia

Glycogen storage disease type IV

Cystic fibrosis
Hepatotoxic drugs or toxins
Pathophysiology

The liver plays a vital role in synthesis of proteins (for

example, albumin, clotting factors and complement), detoxification, and
storage (for example, vitamin A). In addition, it participates in the
metabolism of lipids and carbohydrates.
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis),
independent of the cause. If the cause is removed at this stage, the
changes are still fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that
replaces normal parenchyma. This scar tissue blocks the portal flow of
blood through the organ therefore disturbing normal function. Recent
research shows the pivotal role of the stellate cell, a cell type that normally
stores vitamin A, in the development of cirrhosis. Damage to the hepatic
parenchyma (due to inflammation) leads to activation of the stellate cell,
which increases fibrosis (through production ofmyofibroblasts) and
obstructs blood flow in the circulation.[24] In addition, it secretes TGF-1,
which leads to a fibrotic response and proliferation of connective tissue.
Furthermore, it secretes TIMP 1 and 2, naturally occurring inhibitors
ofmatrix metalloproteinases, which prevents them from breaking down
fibrotic material in the extracellular matrix.
The fibrous tissue bands (septa) separate hepatocyte nodules, which
eventually replace the entire liver architecture, leading to decreased blood
flow throughout. The spleen becomes congested, which leads
to hypersplenism and increased sequestration of platelets. Portal
hypertension is responsible for most severe complications of cirrhosis.
Diagnosis

Micrograph showing cirrhosis.Trichrome stain.

The gold standard for diagnosis of cirrhosis is a liver biopsy, through
apercutaneous, transjugular, laparoscopic, or fine-needle approach. A
biopsy is not necessary if the clinical, laboratory, and radiologic data
suggests cirrhosis. Furthermore, there is a small but significant risk to liver
biopsy, and cirrhosis itself predisposes for complications caused by liver
biopsy. The best predictors of cirrhosis are ascites, platelet count
<160,000/mm3, spider angiomata and Bonacini cirrhosis discriminant score
greater than 7.
Lab findings
The following findings are typical in cirrhosis:
Thrombocytopenia - typically multifactorial. Due to alcoholic marrow
suppression, sepsis, lack of folate, sequestering in the spleen as well as
decreased thrombopoietin. However, this rarely results in platelet count <
50 000/mL.[29]
Aminotransferases - AST and ALT are moderately elevated, with AST >
ALT. However, normal aminotransferases do not preclude cirrhosis.
Alkaline phosphatase - slightly elevated but less than 2-3 times the upper
limit of normal.
Gamma-glutamyl transferase correlates with AP levels. Typically much
higher in chronic liver disease from alcohol.
Bilirubin - Levels normal when compensated but may elevate as cirrhosis
progresses.

Albumin - levels fall as the synthetic function of the liver declines with
worsening cirrhosis since albumin is exclusively synthesized in the liver
Prothrombin time - increases since the liver synthesizes clotting factors.
Globulins - increased due to shunting of bacterial antigens away from the
liver to lymphoid tissue.
Serum sodium - hyponatremia due to inability to excrete free water
resulting from high levels of ADH and aldosterone.
Leukopenia and neutropenia - due to splenomegaly with splenic
margination.
Coagulation defects - the liver produces most of the coagulation factors
and thus coagulopathy correlates with worsening liver disease.
There is now a validated and patented combination of 6 of these markers
as non-invasive biomarker of fibrosis (and so of cirrhosis): FibroTest.
Other laboratory studies performed in newly diagnosed cirrhosis may
include:
Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth
muscle, anti-mitochondria, anti-LKM)
Ferritin and transferrin saturation: markers of iron overload as in
hemochromatosis, copper and ceruloplasmin: markers of copper overload
as in Wilson's disease
Immunoglobulin levels (IgG, IgM, IgA) - these immunoglobins are nonspecific but may help in distinguishing various causes
Cholesterol and glucose
Alpha 1-antitrypsin
Imaging

Liver cirrhosis as seen on a CT of the abdomen in transverse orientation.

Ultrasound is routinely used in the evaluation of cirrhosis. It may show a

small and nodular liver in advanced cirrhosis along with increased
echogenicity with irregular appearing areas. Other findings suggestive of
cirrhosis in imaging are an enlargedcaudate lobe, widening of the liver
fissures and enlargement of the spleen. An enlarged spleen
(splenomegaly), which normally measures less than 1112 cm in adults, is
suggestive of cirrhosis with portal hypertension in the right clinical setting.
Ultrasound may also screen for hepatocellular carcinoma, portal
hypertension, andBudd-Chiari syndrome (by assessing flow in the hepatic
vein).
Cirrhosis is diagnosed with a variety of elastography techniques. Because
a cirrhotic liver is generally stiffer than a healthy one, imaging the liver's
stiffness can give diagnostic information about the location and severity of
cirrhosis. Techniques used include transient elastography, acoustic
radiation force impulse imaging, supersonic shear imaging and magnetic
resonance elastography. Compared to a biopsy, elastography can sample
a much larger area and is painless. It shows reasonable correlation with the
severity of cirrhosis.[31]
Other tests performed in particular circumstances include
abdominal CT and liver/bile duct MRI (MRCP).
Endoscopy
Gastroscopy (endoscopic examination of the esophagus, stomach,
and duodenum) is performed in patients with established cirrhosis to
exclude the possibility of esophageal varices. If these are found,
prophylactic local therapy may be applied (sclerotherapy or banding)
and beta blocker treatment may be commenced.
Rarely are diseases of the bile ducts, such as primary sclerosing
cholangitis, causes of cirrhosis. Imaging of the bile ducts, such
as ERCP or MRCP (MRI of biliary tract and pancreas) may aid in the
diagnosis.
Pathology

Cirrhosis leading to hepatocellular carcinoma (autopsy specimen).

Macroscopically, the liver is initially enlarged, but with progression of the
disease, it becomes smaller. Its surface is irregular, the consistency is firm,
and the color is often yellow (if associated steatosis). Depending on the
size of the nodules there are three macroscopic types: micronodular,
macronodular, and mixed cirrhosis. In micronodular form (Laennec's
cirrhosis or portal cirrhosis) regenerating nodules are under 3 mm. In
macronodular cirrhosis (post-necrotic cirrhosis), the nodules are larger than
3 mm. The mixed cirrhosis consists of nodules with different sizes.
However, cirrhosis is defined by its pathological features on microscopy: (1)
the presence of regenerating nodules of hepatocytes and (2) the presence
of fibrosis, or the deposition of connective tissue between these nodules.
The pattern of fibrosis seen can depend upon the underlying insult that led
to cirrhosis. Fibrosis can also proliferate even if the underlying process that
caused it has resolved or ceased. The fibrosis in cirrhosis can lead to
destruction of other normal tissues in the liver: including the sinusoids,
the space of Disse, and other vascular structures, which leads to altered
resistance to blood flow in the liver and portal hypertension.[32]
As cirrhosis can be caused by many different entities which injure the liver
in different ways, cause specific abnormalities may be seen. For example,
in chronic hepatitis B, there is infiltration of the liver parenchyma
with lymphocytes.[32] In cardiac cirrhosis there are erythrocytes and a
greater amount of fibrosis in the tissue surrounding the hepatic veins.
[33]
In primary biliary cirrhosis, there is fibrosis around the bile duct, the
presence of granulomas and pooling of bile.[34] Lastly in alcoholic cirrhosis,
there is infiltration of the liver with neutrophils.[32]
Grading
The severity of cirrhosis is commonly classified with the Child-Pugh score.
This score uses bilirubin, albumin, INR, presence and severity of ascites,
and encephalopathy to classify patients in class A, B, or C. Class A has a

favourable prognosis, while class C is at high risk of death. It was devised

in 1964 by Child and Turcotte and modified in 1973 by Pugh and others. [35]
More modern scores, used in the allocation of liver transplants but also in
other contexts, are the Model for End-Stage Liver Disease (MELD) score
and its pediatric counterpart, the Pediatric End-Stage Liver Disease (PELD)
score.
The hepatic venous pressure gradient, (difference in venous
pressure between afferent and efferent blood to the liver) also determines
severity of cirrhosis, although hard to measure. A value of 16 mm or more
means a greatly increased risk of dying. [36]
Prevention
Key prevention strategies for cirrhosis and its compensation are populationwide interventions to reduce alcohol intake (through pricing strategies,
public health campaigns and personal counseling), programs to reduce the
transmission of viral hepatitis, and screening of relatives of people with
hereditary liver diseases.Little is known on modulators of cirrhosis risk and
progression. Coffee consumption appears to help protect against cirrhosis.
Management
Generally, liver damage from cirrhosis cannot be reversed, but treatment
could stop or delay further progression and reduce complications. A healthy
diet is encouraged, as cirrhosis may be an energy-consuming process.
Close follow-up is often necessary. Antibiotics are prescribed for infections,
and various medications can help with itching. Laxatives, such aslactulose,
decrease risk of constipation; their role in preventing encephalopathy is
limited.
Alcoholic cirrhosis caused by alcohol abuse is treated by abstaining from
alcohol. Treatment for hepatitis-related cirrhosis involves medications used
to treat the different types of hepatitis, such as interferon for viral hepatitis
and corticosteroids for autoimmune hepatitis. Cirrhosis caused by Wilson's
disease, in which copper builds up in organs, is treated with chelation
therapy (for example, penicillamine) to remove the copper.

Preventing further liver damage

Regardless of underlying cause of cirrhosis, alcohol and paracetamol, as
well as other potentially damaging substances, are discouraged.
Vaccination of susceptible patients should be considered for Hepatitis
A and Hepatitis B.
Transplantation

If complications cannot be controlled or when the liver ceases

functioning, liver transplantation is necessary. Survival from liver
transplantation has been improving over the 1990s, and the five-year
survival rate is now around 80%. The survival rate depends largely on the
severity of disease and other medical problems in the recipient. [39] In the
United States, theMELD score is used to prioritize patients for
transplantation.[40] Transplantation necessitates the use of immune
suppressants (ciclosporin or tacrolimus).
Decompensated cirrhosis
In patients with previously stable cirrhosis, decompensation may occur due
to various causes, such as constipation, infection(of any source), increased
alcohol intake, medication, bleeding from esophageal varices or
dehydration. It may take the form of any of the complications of cirrhosis
listed below.
Patients with decompensated cirrhosis generally require admission
to hospital, with close monitoring of the fluid balance, mental status, and
emphasis on adequate nutrition and medical treatment - often
with diuretics, antibiotics, laxatives and/orenemas, thiamine and
occasionally steroids, acetylcysteine and pentoxifylline. Administration
of saline is avoided as it would add to the already high total body sodium
content that typically occurs in cirrhosis.
Palliative care

Palliative care is specialized medical care that focuses on providing

patients with relief from the symptoms, pain, and stress of a serious illness,
such as cirrhosis. The goal of palliative care is to improve quality of life for
both the patient and the patient's family and it is appropriate at any stage
and for any type of cirrhosis.[41]
Especially in the later stages, people with cirrhosis experience significant
symptoms such as abdominal swelling, itching, leg edema, and chronic
abdominal pain which would be amenable for treatment through palliative
care.[42] Because the disease is not curable without a transplant, palliative
care can also help with discussions regarding the person's wishes
concerning health care power of attorney, Do Not Resuscitate decisions
and life support, and potentially hospice.[42] People with cirrhosis are rarely
referred to palliative care.[43]
Complications
Ascites
Salt restriction is often necessary, as cirrhosis leads to accumulation of salt
(sodium retention). Diuretics may be necessary to suppress ascites.
Diuretic options for inpatient treatment include aldosterone
antagonists (spironolactone) and loop diuretics. Aldosterone antagonists
are preferred for people who can take oral medications and are not in need
of an urgent volume reduction. Loop diuretics can be added as additional
therapy.[44]
If a rapid reduction of volume is required, paracentesis is the preferred
option. This procedure requires the insertion of a plastic tube into the
peritoneal cavity. Human albumin solution is usually given to prevent
complications from the rapid reduction. In addition to being more rapid than
diuretics, 45 liters of paracentesis is more successful in comparison to
diuretic therapy.[44]
Esophageal variceal bleeding
For portal hypertension, propranolol is a commonly used agent to lower
blood pressure over the portal system. In severe complications from portal

hypertension, transjugular intrahepatic portosystemic shunting is

occasionally indicated to relieve pressure on the portal vein. As this
shunting can worsen encephalopathy, it is reserved for those patients at
low risk of encephalopathy. TIPS is generally regarded only as a bridge to
liver transplantation or as a palliative measure.
Hepatic encephalopathy
High-protein food increases the nitrogen balance, and would theoretically
increase encephalopathy; in the past, this was therefore eliminated as
much as possible from the diet. Recent studies show that this assumption
was incorrect, and high-protein foods are even encouraged to maintain
adequate nutrition.[45]
Hepatorenal syndrome
The hepatorenal syndrome is defined as a urine sodium less than
10 mmol/L and a serum creatinine > 1.5 mg/dl (or 24 hourcreatinine
clearance less than 40 ml/min) after a trial of volume expansion without
diuretics.[46]
Spontaneous bacterial peritonitis
People with ascites due to cirrhosis are at risk of spontaneous bacterial
peritonitis.
Portal hypertensive gastropathy
Which refers to changes in the mucosa of the stomach in people with portal
hypertension, and is associated with cirrhosis severity.[47]
Infection
Cirrhosis can cause immune system dysfunction, leading to infection. Signs
and symptoms of infection may be aspecific and are more difficult to
recognize (for example, worsening encephalopathy but no fever).
Hepatocellular carcinoma[edit]

Hepatocellular carcinoma is a primary liver cancer that is more common in

people with cirrhosis. People with known cirrhosis are often screened
intermittently for early signs of this tumor, and screening has been shown to
improve outcomes.[48]
Epidemiology

Cirrhosis and chronic liver disease were the tenth leading cause of death
for men and the twelfth for women in the United States in 2001, killing
about 27,000 people each year.[50] Also, the cost of cirrhosis in terms of
human suffering, hospital costs, and lost productivity is high.
Established cirrhosis has a 10-year mortality of 3466%, largely dependent
on the cause of the cirrhosis; alcoholic cirrhosis has a worse prognosis
than primary biliary cirrhosis and cirrhosis due to hepatitis. The risk of
death due to all causes is increased twelvefold; if one excludes the direct
consequences of the liver disease, there is still a fivefold increased risk of
death in all disease categories.[51]
Etymology
The word "cirrhosis" is a neologism derived from Greek kirrhs meaning
"yellowish, tawny" (the orange-yellow colour of the diseased liver) and the
suffix -osis, i.e. "condition" in medical terminology. While the clinical entity
was known before, it wasRen Laennec who gave it this name (in the same
1819 work in which he also described the stethoscope).[52]

Cirrhosis of the Liver: Causes, Symptoms and Treatments

Cirrhosis is an abnormal liver condition in which there is irreversible

scarring of the liver. The main causes are sustained excessive alcohol
consumption, viralhepatitis B and C, and fatty liver disease - however, there
are many possible causes.

People with cirrhosis may develop jaundice(yellowing of the skin, eyes and
tongue), itching and extreme tiredness.
For cirrhosis to develop long-term, continuous damage to the liver needs to
occur. When healthy liver tissue is destroyed and replaced by scar tissue
the condition becomes serious, as it can start blocking the flow of blood
through the liver.
Cirrhosis is a progressive disease, developing slowly over many years, until
eventually it can stop liver function (liver failure).
The liver carries out several essential functions, including the detoxification
of harmful substances in the body. It also purifies the blood and
manufactures vital nutrients.
If cirrhosis is mild the liver can make repairs and continue functioning
properly. If the cirrhosis is advanced and more and more scar tissue forms
in the liver, the damage is irreparable. The liver tissue is replaced by fibrous
scar tissue as well as regenerative nodules (lumps that appear as a
consequence of a process in which damaged tissue is regenerated).

Causes of cirrhosis
Common causes of cirrhosis are long-term alcohol abuse, hepatitis B and
C infection, and fatty liver disease. Of those, hepatitis B and C together are
said to be the leading cause of cirrhosis (WHO). We will take a look at each
of these causes in detail below.
Overconsumption of alcohol
According to the NHS (National Health Service), UK, excessive alcohol
consumption is when a man drinks more than 21 units and a woman drinks
more than 14 units per week.
Alcohol is one of the leading causes of liver cirrhosis.

Toxins, including alcohol, are broken down by the liver. However, if the
amount of alcohol is too high the liver will be overworked and liver cells can
eventually become damaged.
Heavy, regular, long-term drinkers are much more likely to develop
cirrhosis, compared to other healthy people. It is a myth that only alcoholics
are at risk - regular and heavy social drinking is also linked to a higher
probability of developing cirrhosis.
Typically, heavy drinking needs to be sustained for at least ten years for
cirrhosis to develop. The period varies according to each individual.
Regular heavy female drinkers are more likely to develop symptoms
compared to men who consume the same amount.
Heavy drinkers will eventually develop fatty liver. The liver breaks down
alcohol into carbon dioxide and water, causing fatty liver. As soon as
excessive drinking stops the symptoms of fatty liver go away. However,
20% to 30% of those who continue drinking heavily will develop alcoholic
hepatitis, the next stage. Approximately 10% of heavy drinkers will
subsequently develop cirrhosis - the third stage of alcoholic liver disease.
Health authorities in the UK urge males not to exceed three to four units of
alcohol consumption per day, and women should not have more than two
to three units daily - to reduce the risk of developing alcohol hepatitis and
cirrhosis.
Hepatitis
Hepatitis C, a bloodborne infection, can damage the liver and eventually
lead to cirrhosis. Hepatitis C is a common cause of cirrhosis in Western
Europe, North America, and many other parts of the world. Cirrhosis can
also be caused by hepatitis B and D.
Non-alcoholic steatohepatitis (NASH)
NASH is more likely to occur with people who are obese, diabetes patients,
those with high blood lipid (fat) levels, as well as individuals with
hypertension (high blood pressure). NASH, in its early stages, begins with

the accumulation of too much fat in the liver. The fat

causesinflammation and scarring, resulting in possible cirrhosis later on.
Autoimmune hepatitis
The person's own immune system attacks healthy organs in the body as
though they were foreign substances. Sometimes the liver is attacked.
Eventually the patient can develop cirrhosis.
Some genetic conditions
Hemochromatosis - iron accumulates in the liver and other parts of the
body.
Wilson's disease - copper accumulates in the liver and other parts of the
body.
Blockage of bile ducts
Some conditions and diseases, such as cancer of the bile ducts, or cancer
of the pancreas can block the bile ducts, increasing the risk of cirrhosis.
Budd-Chiari syndrome
There is thrombosis (blood clots) in the hepatic vein, the blood vessel that
carries blood from the liver, leading to liver enlargement and the
development of collateral vessels.
Other diseases and conditions
Some of the other diseases and conditions that can contribute to cirrhosis
are:
Cystic fibrosis
Primary sclerosing cholangitis - hardening and scarring of the bile ducts
Galactosemia - inability to process sugars in milk
Schistosomiasis - a parasite commonly found in some developing countries
Biliary atresia - badly formed bile ducts in babies

Glycogen storage disease - problems in the storage and energy release

vital for cell function.
Symptoms of cirrhosis
Cirrhosis Overview
Cirrhosis is a chronic (ongoing, long-term) disease of the liver. It means
damage to the normal liver tissue that keeps this important organ from
working as it should. If the damage is not stopped, the liver gradually loses
its ability to carry out its normal functions. This is called liver failure,
sometimes referred to as end-stage liver disease.
The liver is the largest organ in the body and one of the most essential.
It is about the size a football and is located on the right side in front, just
below the lower rib cage.
It produces substances that help fight infections and clot blood, filters toxins
and infectious agents out of the blood, helps in the absorption of certain
nutrients from foods, and stores energy for later use.
These are just some of its many functions in the body.
The liver may be injured by a single event, as in acute (new, short-term)
hepatitis; by regular injury over months or years, as in biliary tract blockage
or chronic hepatitis; or by continuous injury, as in daily alcohol abuse.
The liver responds to cell damage by producing strands of scar tissue that
surround islands (nodules) of healing cells, making the liver knobby.
At first, the inflammation in the liver causes it to swell. As the disease
progresses and the amount of scar tissue in the liver increases, the liver
will actually shrink.
The scar tissue presses on the many blood vessels in the liver. This
interrupts flow of blood to liver cells, which then die.
Loss of liver cells hinders the liver's ability to perform its normal functions.

Loss of liver function affects the body in many ways. Cirrhosis, if severe
enough, can cause many different complications. These can be severe, as
follows:
Portal hypertension: The nodules and scar tissue can compress veins
within the liver. This causes the blood pressure within the liver to be high, a
condition known as portal hypertension.
High pressures within blood vessels of the liver occur in a majority of
people who have cirrhosis.
Cirrhosis is the most common cause of portal hypertension in the United
States.
Portal hypertension may cause bleeding into the intestines and fluid
accumulation throughout the body.
Hepatic encephalopathy: In this condition, toxins build up in the
bloodstream because the scarred liver is unable to rid them from the body.
The toxins can cause you to behave bizarrely, to become confused, and to
lose your ability to take care of yourself or others.
Some people become very sleepy and cannot waken easily.
Gastrointestinal bleeding: Portal hypertension causes backing up of blood
flow in the veins of the stomach and esophagus.
This causes the veins to enlarge, forming "varices" (varicose veins).
These varices can tear and bleed, and this bleeding can be life threatening.
This usually shows up as vomiting bright red blood.
Infection: If you have cirrhosis, you are at risk for many infections because
your liver cannot form the proteins needed to fight off infection.
Fluid retention (ascites): High pressures (portal hypertension) force fluid out
of blood vessels in your liver, pooling it in your abdomen.

Several liters of this fluid can pool in your abdomen, causing pain,
swelling, difficulty breathing, and dehydration.
As fluid pools in your abdomen, your kidneys will try to hold onto
more water, because they think your body is dehydrated. The
excess fluid collects in your lungs, legs, and abdomen.

Hepatorenal syndrome: For unknown reasons, liver failure leads to kidney

failure in some people.
Often the progress toward liver failure is slow and gradual.
Although cirrhosis has traditionally been linked with alcoholism, it
has many causes. The most common causes in the United States
are chronic alcoholism and hepatitis C.
There is no cure for cirrhosis, but removing the cause can slow the
disease. If the damage is not too severe, the liver can heal itself
over time.
cirrhosis

A symptom is something the patient feels and reports, while a sign is

something other people, including a doctor or a nurse may detect. For
example, pain may be a symptom while a rash may be a sign.
Symptoms are not common during the early stages of cirrhosis. However,
as scar tissue accumulates the liver's ability to function properly is
undermined. The following signs and symptoms may occur:
Blood capillaries become visible on the skin on the upper abdomen
Fatigue
Insomnia
Itchy skin
Loss of appetite

Loss of bodyweight
Nausea
Pain or tenderness in the area where the liver is located
Red or blotchy palms
Weakness.
The following signs and symptoms may appear as liver cirrhosis
progresses:
Abdomen fills up with fluid, giving the patient a large tummy (ascites)
Accelerated heartbeat
Altered personality (as blood toxins build up and affect the brain)
Bleeding gums
Body and upper arms lose mass
Body finds it harder to process alcohol
Body finds it harder to process drugs
Confusion
Dizziness
Fluid buildup on ankles, feet and legs (edema)
Hair loss
Higher susceptibility to bruising
Jaundice (yellowing of the skin, whites of the eyes, and tongue)
Loss of libido (sex drive)
Memory problems
More frequent fevers (susceptibility to infections)

Muscle cramps
Nosebleeds
Pain on the right shoulder
Panting (breathlessness)
Stools become black and tarry, or very pale
Urine becomes darker
Vomiting blood
Walking problems (staggering).

Diagnosis of cirrhosis
Cirrhosis in its early stages is often diagnosed when the patient is being
tested for some other condition or disease because symptoms are not
present.
Anybody who has the following symptoms should see their doctor
immediately:
Fever with shivering
Panting (shortness of breath)
Vomiting blood
Dark stools, or tarry stools (as if covered with tar)
Episodes of drowsiness or confusion.
The liver is located in the upper-right section of the abdominal cavity,
underneath the diaphragm.

A GP (general practitioner, primary care physician) will examine the patient

and feel around the liver area to determine whether it is enlarged. The
patient will be asked about his/her medical history and lifestyle (drinking,
etc).
The following tests may also be ordered:
A blood test - to measure how well the liver is functioning and determine
whether there is any damage. If levels of ALT (alanine transaminase) are
high the patient may have hepatitis.
Imaging tests - this may involve an ultrasound, CT (computerized
tomography), or MRI(magnetic resonance imaging) scan of the liver. Apart
from seeing whether the liver is enlarged, the doctor will also be able to
detect any scarring.
A biopsy - a small sample of liver cells are extracted and examined under a
microscope. The doctor inserts a fine needle in between the ribs and into
the liver. The patient will receive a local anesthetic. The biopsy not only
confirms or rules out cirrhosis, but may also reveal its cause (if it is
cirrhosis).
Endoscopy - an endoscope, a long, thin tube with a light and video camera
at the end goes down the patient's windpipe (esophagus) and into their
stomach. The doctor sees the inside of the stomach on a screen, and looks
out for swollen blood vessels (varices); a hallmark sign of cirrhosis.
Child-Pugh Score
Also known as the Child-Turcotte-Pugh score, assesses the prognosis
(outlook) of chronic liver disease, mainly cirrhosis. Originally, it was used to
predict mortality during surgery, but is now used to determine prognosis, as
well as the required treatment strength, and whether or not the patient
needs a liver transplant. It is a combination of numbered points and the
letters A, B, C (see below):
Class

Points

5-6

7-9

10-15

Recent developments on diagnosing cirrhosis from MNT news

Breath test for early-stage liver disease steps closer
Scientists have identified a biomarker that could form the basis of a breath
test for the detection of early-stage liver disease. The study suggests that
high levels of a natural compound called limonene in the breath could be a
sign of early-stage cirrhosis of the liver.
Treatments for cirrhosis
If the cirrhosis is diagnosed early enough, damage may be minimized by
treating its underlying cause.
Alcohol dependency (alcoholism) treatment - it is important for the patient
to stop drinking if their cirrhosis was caused by long-term, regular heavy
alcohol consumption. In many cases the doctor will recommend a treatment
program for alcoholism.
Medications - the patient may be prescribed drugs to control liver cell
damage caused by hepatitis B or C.
Treating cirrhosis complications
Ascites or edema - ascites (accumulation of fluid in the abdomen) or
edema (fluid retentionin the legs) can be treated with a low-sodium (salt)
diet and water pills. In severe cases the fluid may have to be drained.
Sometimes surgery is required.
Pressure in the portal vein and collateral smaller veins - hypertension (high
blood pressure) drugs are usually prescribed to control the increasing
pressure in the blood vessels around the liver; the aim is to prevent severe

bleeding. In some cases a stent may be surgically placed in the portal vein
to hold it open. Signs of bleeding can be detected via an endoscopy.
Treatment of swollen varices - if the patient vomits blood or passes bloody
stools they probably have esophageal varices (in the food pipe). Urgent
medical attention is required. The following procedures may help:
Banding - a small band is placed around the base of the varices to control
bleeding. An endoscope goes down the patient's throat and esophagus
during the procedure.
Injection sclerotherapy - after an endoscopy a substance is injected into the
varices which triggers a blood clot and scar tissue to form; this helps stem
the bleeding.
A Sengstaken tube with a balloon - the balloon is at the end of the tube. If
endoscopy does not stop the bleeding a tube goes down the patient's
throat and into their stomach. The balloon is inflated; this places pressure
on the varices and stops the bleeding.
TIPSS (transjugular intrahepatic portosystemic stent shunt) - if the abovementioned therapies do not stem the bleeding, a stent (metal tube) is
passed across the liver to join the portal and hepatic veins, creating a new
route for the blood to flow through. This reduces pressure - pressure which
was causing the varices.
Infections - the patient will be given antibiotics, and some other treatments.
Screening for liver cancer - patients with cirrhosis have a much higher risk
of developingliver cancer. The doctor may recommend regular blood tests
and imaging scans.
Hepatic encephalopathy (high blood toxin levels) - drugs can help treat
excessive blood toxin levels. The signs and symptoms need to be
explained to the patient so that they know what to look out for.
Liver transplant - if the cirrhosis is advanced and there is liver failure (liver
does not function) the patient may need a liver transplant.

Prevention of cirrhosis
Alcohol - do not exceed the recommended daily/weekly alcohol limit.
Men: maximum of 21 units per week, or three/four units per day
Women: maximum of 14 units per week, or two/three units per day
Individuals who have cirrhosis should abstain from alcohol completely.
Alcohol accelerates the progression of the disease.
Hepatitis B and C
Use a condom when having sex
Do not share needles when injecting drugs
People at risk of becoming infected with hepatitis B, such as health care
workers, social care workers, and police personnel can be vaccinated
(there is currently no vaccine forhepatitis C

HEP1 {bunch of organics}

1 chicorium intibus
2

punica granatum

Mentha Arvensis,

bamboo silica

Acorus calamus

daucus carota

Nardostachys jatamansi

2. HEP 2 Hepato protective,hepatic regenerative and metabolic regulators

1

Valeriana officinalis

Pistacia lentiscus

bamboo silica

Andropogon schoenanthus

chicorum intybus

Apium graveolens

Calotropis procera

commiphora opobalsamum

Foeniculum vulgare

10 Syzygium aromaticum.

3 HEP 3 (BUNCH OF ORGANIC)

1 Artemisia absinthium
2 solanum nigrum

Cichorium intubus

Botanical Source : Whole plant of Cichorium intubus and C. endive.

Family : Asteraceae
Common Names :
English Name : Endive/ Chicory
Sanskrit Name : Kasni
Arabic Name : Hinduba
Botanical Description :

Habitat : In India plant is found in the northwestern regions like Kashmir

and Punjab and in area of south India. In western countries is now a days
cultivated with the name endive. It is cultivated in completely black outed
area to make leaf soft and pale in appearance. This plant has it origin in
Europe and now has spread all over world.
Morphology : It is a bushy perennial plant that attains a height of 1 to 3
feet. The stem has edges having hard branches. Leaves are sphere
shaped having a bitter taste. Flowers are of blue of lavender color having a
diameter of 1 to 1 inch, which is bit thicker at the center. Fruit is angular,
having light color. Root is like a tail of a cow and is fleshy having brownish
color from outside and white color from inside. It has a length of 2 feet
and has a bitter taste. The other related species that is cultivates
is Cichorium endivia. It is generally found in cultivated lands and gardens.

Chemical Constituents : Their seed contains oil. Roots has sticky

substance which is about 7.5 %, glucose 1.1 %, bitter substance 4 %, fat
0.6 %, cellulose, insulin and resins etc. ash contains more of potassium. It
also contains colorless potassium glycosides, cichorin and lactucina and
intybin. There is very peculiar smell when the root is roasted and is very
often used as coffee.
Properties :
properties - light and dry
taste - bitter
potency - hot
Actions :
Indication : Head ache, Indigestion, Hypertension, Urticaria, Gouty arthritis,
Burning sensation, Insomnia, Jaundice, Dehydration, Liver related
disorders, Dysurea, Blood impurity, Menstrual disturbances, Chronic fever,
General body weakness.

Pharmacology : It is kapha and pitta suppressant. It is relaxant and induces

sleep. It acts as pain reliever and anti inflammatory agent. It works as
appetizer, liver stimulant and increases digestive powers. It acts as blood
purifier and provides strength to heart. It is a diuretic. Its roots reduce
menstrual disturbances. It has good effect in lowering down the burning
sensations in the body. It also helps in lowering the blood pressure. It
decreases the raised body temperature in fevers.

Part Used : Roots, leaves and seeds.

.
Common Chicory

1885 illustration[1]

Scientific
classification
Kingdom: Plantae
(unranke Angiosper
d):
ms
(unranke Eudicots
d):

(unranke Asterids
d):
Order:

Asterales

Family:

Asteracea
e

Tribe:

Cichoriea
e

Genus:

Cichorium

Species: C. intybus
Binomial name
Cichorium intybus
L.

Common chicory, Cichorium intybus, is a somewhat

woody, perennialherbaceous plant usually with bright blue flowers, rarely
white or pink. Many varieties are cultivated for salad leaves, chicons
(blanched buds), or for roots (var. sativum), which are baked, ground, and
used as a coffee substitute and additive. It is also grown as a forage crop
for livestock. It lives as a wild plant on roadsides in its native Europe, and
now common in North America, China, and Australia where it has become
widely naturalized.
"Chicory" is also the common name in the United States for
curly endive(Cichorium endivia); these two closely related species are often
confused.
Contents

1 Names
2 Description
3 Leaf chicory
3.1 Wild
3.2 Cultivated
4 Root chicory
5 Agents responsible for bitterness
6 Medicinal use
6.1 Alternative medicine
7 Forage
7.1 Forage chicory varieties
8 History

Names
Common chicory is also known as blue daisy, blue dandelion, blue
sailors,blue
weed, bunk, coffeeweed, cornflower, hendibeh, horseweed,ragged
sailors, succory, wild bachelor's buttons, and wild endive. (Note:
"Cornflower" is commonly applied to Centaurea cyanus.) Common names
for varieties of var. foliosum include endive, radicchio, Belgian endive,
French endive, red endive, sugarloaf and witloof (or witlof).
Description
When flowering, chicory has a tough, grooved, and more or less hairy
stem, from 30 to 100 centimetres (10 to 40 in) tall.

The leaves are stalked, lanceolate and unlobed.

The flower heads are 2 to 4 centimetres (0.79 to 1.6 in) wide, and usually
bright blue, rarely white or pink. There are two rows of involucral bracts; the
inner are longer and erect, the outer are shorter and spreading. It flowers
from July until October.
The achenes have no pappus (feathery hairs), but do have toothed scales
on top.
Leaf chicory
Wild
Wild chicory leaves usually have a bitter taste. Their bitterness is
appreciated in certain cuisines, such as in the Ligurianand Apulian regions
of Italy and also in Catalonia (Spain), in Greece and in Turkey. In Ligurian
cuisine the wild chicory leaves are an ingredient of preboggion and in
Greek cuisine of horta; in the Apulian region wild chicory leaves are
combined with fava bean puree in the traditional local dish Fave e Cicorie
Selvatiche.;
in Albania the leaves are used as a spinach substitute, mainly served
simmered and marinated in olive oil, or as ingredient for fillings of byrek.
By cooking and discarding the water the bitterness is reduced, after which
the chicory leaves may be sauted with garlic,anchovies and other
ingredients. In this form the resulting greens might be combined
with pasta or accompany meat dishes.
Cultivated
Chicory may be cultivated for its leaves, usually eaten raw as salad leaves.
Cultivated chicory is generally divided into three types, of which there are
many varieties:
Radicchio usually has variegated red or red and green leaves. Some only
refer to the white-veined red leaved type as radicchio. Also known as red
endive and red chicory. It has a bitter and spicy taste, which mellows when

it is grilled or roasted. It can also be used to add color and zest to salads. It
is largely used in Italy in different varieties, the most famous being the ones
from Treviso (known as Radicchio Rosso di Treviso),
from Verona (Radicchio di Verona), and Chioggia (Radicchio di Chioggia),
which are classified as an IGP It's also common in Greece.
Sugarloaf looks rather like cos lettuce, with tightly packed leaves.
Witloof, Belgian endive
Belgian endive, known in Dutch as witloof or witlof ("white leaf"), endive or
(very rarely) witloof in the United States, indivia in Italy, endivias in Spain,
chicory in the UK, as witlof in Australia, endive in France, and chicon in
parts of northern France and in Wallonia. It has a small head of creamcoloured, bitter leaves. It is grown completely underground or indoors in the
absence of sunlight in order to prevent the leaves from turning green and
opening up (etiolation). The plant has to be kept just below the soil surface
as it grows, only showing the very tip of the leaves. It is often sold wrapped
in blue paper to protect it from light and so preserve its pale colour and
delicate flavour. The smooth, creamy white leaves may be served stuffed,
baked, boiled, cut and cooked in a milk sauce, or simply cut raw. The
tender leaves are slightly bitter; the whiter the leaf, the less bitter the taste.
The harder inner part of the stem at the bottom of the head should be cut
out before cooking to prevent bitterness. Belgium exports chicon/witloof to
over 40 different countries. The technique for growing blanched endives
was accidentally discovered in the 1850s at the Botanical Garden of
Brussels in Saint-Josse-ten-Noode, Belgium. Today France is the largest
producer of endive.

leaves unlobed and pointed

Inflorescences of a blue-flowered form. Note the two rows of bracts

The Catalogna chicory (also known as puntarelle) includes a whole

subfamily (some varieties from Belgian endive and some from radicchio) of
chicory and used throughout Italy.
Although leaf chicory is often called "endive", true endive (Cichorium
endivia) is a different species in the genus and shouldn't be confused
with Belgian endive.
Root chicory

Root chicory (Cichorium intybus var. sativum) has been cultivated in

Europe as acoffee substitute. The roots are baked, ground, and used as a
coffee substitute and additive, especially in the Mediterranean region
(where the plant is native). As a coffee additive, it is also mixed in Indian
filter coffee, and in parts of Southeast Asia, South Africa and southern
United States, particularly in New Orleans. It has been more widely used
during economic crises such as the Great Depression in the 1930s and
during World War II in Continental Europe. Chicory, with sugar beet andrye,
was used as an ingredient of the East German Mischkaffee (mixed coffee),
introduced during the "East German coffee crisis" of 1976-79.
Some beer brewers use roasted chicory to add flavor to stouts (commonly
expected to have a coffee-like flavour). Others have added it to strong
blond Belgian-style ales, to augment the hops, making a "witlofbier", from
the Dutch name for the plant.
Around 1970 it was found that the root contains up to 20% inulin,
a polysaccharidesimilar to starch. Inulin is mainly found in the plant
family Asteraceae as a storage carbohydrate (for example Jerusalem
artichoke, dahlia, yacon etc.). It is used as a sweetener in the food industry
with a sweetening power 110 that of sucrose and is sometimes added to
yogurts as a prebiotic. Inulin is also gaining popularity as a source of
soluble dietary fiber and functional food.
Chicory root extract is a dietary supplement or food additive produced by
mixing dried, ground chicory root with water, and removing
the insoluble fraction by filtrationand centrifugation. Other methods may be
used to remove pigments and sugars. It is used as a source of soluble

fiber. Fresh chicory root typically contains, by dry weight, 68% inulin,
14% sucrose, 5% cellulose, 6% protein, 4% ash, and 3% other compounds.
Dried chicory root extract contains, by weight, approximately 98% inulin
and 2% other compounds. Fresh chicory root may contain between 13 and
23% inulin, by total weight.
Agents responsible for bitterness

The bitter substances are primarily the

two sesquiterpene lactones lactucin and lactucopicrin. Other ingredients
areaesculetin, aesculin, cichoriin, umbelliferone, scopoletin, 6,7dihydrocoumarin, and further sesquiterpene lactones and theirglycosides.[29]
Medicinal use

Root chicory contains volatile oils similar to those found in plants in the
related genus Tanacetum which includes Tansy, and is similarly effective at
eliminating intestinal worms. All parts of the plant contain these volatile oils,
with the majority of the toxic components concentrated in the plant's root.
Chicory is well known for its toxicity to internal parasites. Studies indicate
that ingestion of chicory by farm animals results in reduction of worm
burdens, which has prompted its widespread use as a forage supplement.
Only a few major companies are active in research, development, and
production of chicory varieties and selections, most in New Zealand.
Chicory (especially the flower), used as a folk medicine in Germany, is
recorded in many books as an ancient German treatment for everyday
ailments. It is variously used as a tonic and as a treatment
for gallstones,gastro-enteritis, sinus problems and cuts and bruises.
(Howard M. 1987). Chicory contains inulin, which may help humans with
weight loss, constipation, improving bowel function, and general health. In
rats, it may increase calcium absorption and bone mineral density.
Chicory has demonstrated antihepatotoxic potential in animal studies.
Alternative medicine

Chicory has been listed as one of the 38 plants that are used to
prepare Bach flower remedies,[41] a kind of alternative medicine. However
according toCancer Research UK, "there is no scientific evidence to prove
that flower remedies can control, cure or prevent any type of disease,
including cancer".
Forage

Chicory is highly digestible for ruminants and has a low fiber concentration.
Chicory roots are an "excellent substitute for oats" for horses due to their
protein and fat content. Chicory contains a low quantity of reduced tannins
that may increase protein utilization efficiency in ruminants. Some tannins
reduce intestinal parasites. Large quantities of tannins bind with and
precipitate proteins, resulting in low digestibility and nutrient reduction.
Although chicory might have originated in France, Italy, and India, much
development of chicory for use with livestock has taken place in New
Zealand.
Forage chicory varieties
Puna (Grasslands Puna)
Developed in New Zealand, Grasslands Puna is well adapted to different
climates, being grown from Alberta, Canada, to New Mexico and Florida. It
is resistant to bolting, which leads to high nutrient levels in the leaves in
spring. It also has high resistance to grazing.
Forage Feast
A variety from France used for human consumption and also for wildlife
plots. It is very cold-hardy and, being lower in tannins than other forage
varieties, is suitable for human consumption.
Choice
Choice has been bred for high winter and early-spring growth activity, and
lower amounts of lactucin and lactone, which are believed to taint milk. It is
also use for seeding deer wildlife plots.

Oasis
Bred for increased lactone rates for the forage industry, and for higher
resistance to fungal diseases like Sclerotinia.
Puna II
More winter-active than most other varieties, which leads to greater
persistence and longevity.
Grouse
A New Zealand variety used as a planting companion for forage brassicas.
More prone to early flowering than other varieties, with higher crowns more
susceptible to overbrowsing.
Six Point
History
The chicory plant is one of the earliest cited in recorded
literature. Horace mentions it in reference to his own diet, which he
describes as very simple: "Me pascunt olivae, me cichorea, me malvae"
("As for me, olives, endives, and mallows provide sustenance").In
1766, Frederick the Great banned the importation of coffee
into Prussia leading to the development of a coffee-substitute
by Brunswick innkeeper Christian Gottlieb Frster (died 1801), who gained
a concession in 1769/70 to manufacture it in Brunswick and Berlin. By 1795
there were 22 to 24 factories of this type in Brunswick. Lord
Monboddo describes the plant in 1779 as the "chicoree", which the French
cultivated as a pot herb. In Napoleonic EraFrance, chicory frequently
appeared as either an adulterant in coffee, or as a coffee substitute.
Chicory was also adopted as a coffee substitute by Confederate soldiers
during the American Civil War, and has become common in the United
States. It was also used in the United Kingdom during the Second World
War, where Camp Coffee, a coffee and chicory essence, has been on sale
since 1885.

The cultivated chicory plant has a history reaching back to ancient Egyptian
time. Medieval monks raised the plants and when coffee was introduced to
Europe, the Dutch thought that chicory made a lively addition to the bean
drink.
In the United States chicory root has long been used as a substitute for
coffee in prisons. By the 1840s, the port of New Orleans was the second
largest importer of coffee (after New York). Louisianans began to add
chicory root to their coffee when Union naval blockades during the
American Civil War cut off the port of New Orleans, thereby creating a longstanding tradition.
A common meal in Rome, puntarelle, is made with chicory sprouts. The
United Nations Food and Agriculture Organization (FAO) reports that
Chicory is a native plant of western Asia, North Africa, and Europe.
Chicory is also mentioned in certain sericulture (silk-growing) texts. It is
said that the primary caretaker of the silkworms, the "silkworm mother",
should not eat or even touch it.
The chicory flower is often seen as inspiration for the Romantic concept of
the Blue Flower (e. g. in German language 'Blauwarte' 'blue lookout by
the wayside'). It could open locked doors, according to European folklore.
Chicory Root
Uses
Benefits
Cautions
Other Names
References
Chicory Root

Chicory is a plant. Its roots and dried, above-ground parts are used to make
medicine.
Uses
Chicory is used for loss of appetite, upset stomach, constipation, liver and
gallbladder disorders, cancer, and rapid heartbeat.
It is also used as a tonic, to increase urine production, to protect the liver,
and to balance the stimulant effect of coffee.
Some people apply a paste of chicory leaves directly to the skin for swelling
and inflammation.
In foods, chicory leaves are often eaten like celery, and the roots and leaf
buds are boiled and eaten. Chicory is also used as a cooking spice and to
flavor foods and beverages. Coffee mixes often include ground chicory to
enhance the richness of the coffee.
Benefits
Chicory root has a mild laxative effect, increases bile from the gallbladder,
and decreases swelling. Chicory is a rich source of beta-carotene.
Cautions
Chicory allergy: If you are allergic to chicory, dont take it by mouth or
handle it.
Allergy to ragweed and related plants: Chicory may cause an allergic
reaction in people who are sensitive to the Asteraceae/Compositae family.
Members of this family include ragweed, chrysanthemums, marigolds,

daisies, and many others. If you have allergies, be sure to check with your
healthcare provider before taking chicory.
Gallstones: Chicory can stimulate the production of bile. This could be a
problem for people with gallstones. Dont use chicory without medical
supervision if you have gallstones.
Other Names
Achicoria, Barbe de Capucin, Blue Sailors, Cheveux de Paysans, Chicore,
Chicore Amre, Chicore Sauvage, Cichorii Herba, Cichorium intybus,
Cichorii Radix, Common Chicory Root, coubette, Hendibeh, Herbe
Caf, Hinduba, Kasani, Kasni, Racine de Chicore Commune, Succory,
Wild Chicory, Wild Endive, Yeux de Chat.

PUNICA GRANATUM

Fruit of Punica
granatum split open
to reveal the
clusters of juicy,
gem-like seeds on
the inside.
Scientific
classification
Kingdom: Plantae
(unranke Angiosper
d):
ms

(unranke Eudicots
d):
(unranke Rosids
d):
Order:

Myrtales

Family:

Lythracea
e

Genus:

Punica

Species: P.
granatum
Binomial name
Punica granatum
L.
Synonyms
Punica
florida Salisb.
Punica
grandiflora hort. ex
Steud.
Punica nana L.
Punica spinosa Lam.
[1]

Young trees

The pomegranate (/pmrnt/), botanical name Punica granatum, is

a fruit-bearing deciduous shrub or small tree growing between 5 and 8 m
(16 and 26 ft) tall.
In the Northern Hemisphere, the fruit is typically in season from September
to February, and in the Southern Hemisphere from March to May. As
intact arils or juice, pomegranates are used in cooking, baking,
meal garnishes, juice blends,smoothies, and alcoholic beverages, such
as cocktails and wine.
The pomegranate originated in the region of modern day Iran, and has
been cultivated since ancient times throughout the Mediterranean region
and northernIndia. It was introduced into America (Spanish America) in late
1500s andCalifornia by Spanish settlers in 1769.
Today, it is widely cultivated throughout the Middle
East and Caucasus region, north Africa and tropical Africa, the Indian
subcontinent, Central Asia, and the drier parts of southeast Asia.[3] It is also
cultivated in parts of California and Arizona. In recent years, it has become
more common in the commercial markets of Europe and theWestern
Hemisphere.
Contents

1 Etymology
2 Description
3 Cultivation
3.1 Varieties
3.2 Cultivars
4 Cultural history
4.1 Culinary use
4.2 In traditional medicine

5 Research
5.1 Nutrients and phytochemicals
5.1.1 Polyphenols
5.1.1.1 Juice
5.1.1.2 Peel
5.2 Potential health benefits
5.2.1 Clinical trial disease targets
6 Symbolism
6.1 Ancient Egypt
6.2 Ancient Greece
6.3 Ancient Israel and Judaism
6.4 In European Christian Motifs
6.5 In the Qur'an
6.6 Afghanistan
6.7 Armenia
6.8 Azerbaijan
6.9 Iran and ancient Persia
6.10 Pakistan
6.11 India
6.12 China

Etymology

The name pomegranate derives from medieval Latin pmum "apple"

and grntum"seeded.
Perhaps stemming from the old French word for the fruit, pomme-grenade,
the pomegranate was known in early English as "apple of Grenada"a
term which today survives only in heraldic blazons. This is a folk etymology,
confusing Latin granatuswith the name of the Spanish city of Granada,
which derives from Arabic.
Garnet derives from Old French grenat by metathesis, from Medieval
Latin granatumas used in a different meaning "of a dark red color". This
derivation may have originated from pomum granatum describing the color
of pomegranate pulp or fromgranum referring to "red dye, cochineal".
The French term grenade for pomegranate has given its name to the
militarygrenade.
Description
A shrub or small tree growing 6 to 10 m high, the pomegranate has multiple
spiny branches, and is extremely long-lived, with some specimens in
France surviving for 200 years. P. granatum leaves are opposite or
subopposite, glossy, narrow oblong, entire, 37 cm long and 2 cm broad.
The flowers are bright red and 3 cm in diameter, with three to seven petals.
Some fruitless varieties are grown for the flowers alone.

Pomegranate blossom before petal fall

Pomegranate sepals and dryingstamens after fertilization and petal fall

Unripened pomegranate fruit on a small tree in India

A pomegranate fruit
The edible fruit is a berry, intermediate in size between a lemon and
a grapefruit, 512 cm in diameter with a rounded shape and thick, reddish
skin. The number of seeds in a pomegranate can vary from 200 to about
1400. Each seed has a surrounding water-laden pulp the
edible sarcotesta that forms from the seed coat ranging in color from
white to deep red or purple. The seeds are "exarillate", i.e., unlike some
other species in the order, Myrtales, no aril is present. The sarcotesta of
pomegranate seeds consists of epidermis cells derived from
the integument. The seeds are embedded in a white,
spongy, astringent membrane.
Cultivation

Illustration by Otto Wilhelm Thom, 1885

P. granatum is grown for its fruit crop, and as ornamental trees and shrubs
in parks andgardens. Mature specimens can develop sculptural twistedbark multiple trunks and a distinctive overall form. Pomegranates
are drought-tolerant, and can be grown in dry areas with either a
Mediterranean winter rainfall climate or in summer rainfall climates. In
wetter areas, they can be prone to root decay from fungal diseases. They
can be tolerant of moderate frost, down to about 12 C (10 F).
Insect pests of the pomegranate can include the pomegranate
butterfly Virachola isocratesand the leaf-footed bug Leptoglossus zonatus,
and fruit flies and ants are attracted to unharvested ripe fruit.
[12]
Pomegranate grows easily from seed, but is commonly propagated from
25 to 50-cm hardwood cuttings to avoid the genetic variation of
seedlings. Air layeringis also an option for propagation, but grafting fails.
Varieties

P. granatum var. nana is a dwarf variety of P. granatum popularly planted as

an ornamental plant in gardens and larger containers, and used as
a bonsai specimen tree. It could well be a wild form with a distinct origin. It
has gained the Royal Horticultural Society's Award of Garden Merit. The
only other species in the genus Punica is the Socotran pomegranate (P.
protopunica), which isendemic to the island of Socotra. It differs in having
pink (not red) flowers and smaller, less sweet fruit.
Cultivars
P. granatum has more than 500 named cultivars, but evidently has
considerable synonymy in which the same genotype is named differently
across regions of the world.
Several characteristics between pomegranate genotypes vary for
identification, consumer preference, preferred use, and marketing, the most
important of which are fruit size, exocarp color (ranging from yellow to
purple, with pink and red most common), seed-coat color (ranging from
white to red), hardness of seed, maturity, juice content and its acidity,
sweetness, and astringency. Scientists at Indian Institute of Horticulture
Research are developing varieties tolerant to bacterial blight disease using
sub-Himalayan accessions.
Cultural history

Pomegranate, late Southern Song dynasty or early Yuan

dynasty circa12001340 (Los Angeles County Museum of Art)
Pomegranate is native to Iran and northeast Turkey.[3] Pomegranates have
been cultivated throughout the Middle East, South Asia, and Mediterranean
region for several millennia, and also thrive in the drier climates of
California and Arizona.
Carbonized exocarp of the fruit has been identified in early Bronze
Age levels ofJericho in the West Bank, as well as late Bronze Age levels
of Hala Sultan Tekke onCyprus and Tiryns. A large, dry pomegranate was

found in the tomb ofDjehuty, the butler of

Queen Hatshepsut in Egypt; Mesopotamian cuneiform records mention
pomegranates from the mid-third millennium BC onwards. [18]
It is also extensively grown in South China and in Southeast Asia, whether
originally spread along the route of the Silk Road or brought by sea
traders. Kandahar is famous in Afghanistan for its high-quality
pomegranates.
Although not native to Korea or Japan, the pomegranate is widely grown
there and many cultivars have been developed. It is widely used
for bonsai because of its flowers and for the unusual twisted bark the older
specimens can attain.[19] The term "balaustine" (Latin: balaustinus) is also
used for a pomegranate-red color.
Coat of arms of Granada
The ancient city of Granada in Spain was renamed after the fruit during
the Moorish period and today the province of Granada uses pomegranate
as a charge in heraldry for its canting arms.[citation needed]
Spanish colonists later introduced the fruit to the Caribbean and America
(Spanish America), but in the English colonies, it was less at home: "Don't
use the pomegranate inhospitably, a stranger that has come so far to pay
his respects to thee," the English Quaker Peter Collinson wrote to the
botanizing John Bartram in Philadelphia, 1762. "Plant it against the side of
thy house, nail it close to the wall. In this manner it thrives wonderfully with
us, and flowers beautifully, and bears fruit this hot year. I have twenty-four
on one tree... Doctor Fothergill says, of all trees this is most salutiferous to
mankind."
The pomegranate had been introduced as an exotic to England the
previous century, byJohn Tradescant the elder, but the disappointment that
it did not set fruit there led to its repeated introduction to the American
colonies, even New England. It succeeded in the South: Bartram received
a barrel of pomegranates and oranges from a correspondent in Charleston,
South Carolina, 1764. John Bartram partook of "delitious" pomegranates

with Noble Jones at Wormsloe Plantation, near Savannah, Georgia, in

September 1765. Thomas Jeffersonplanted pomegranates at Monticello in
1771: he had them from George Wythe of Williamsburg.[22]
Culinary use

After the pomegranate is opened by scoring it with a knife and breaking it

open, the seeds are separated from the peel and internal white pulp
membranes. Separating the seeds is easier in a bowl of water because the
seeds sink and the inedible pulp floats. Freezing the entire fruit also makes
it easier to separate. Another effective way of quickly harvesting the seeds
is to cut the pomegranate in half, score each half of the exterior rind four to
six times, hold the pomegranate half over a bowl and smack the rind with a
large spoon. The seeds should eject from the pomegranate directly into the
bowl, leaving only a dozen or more deeply embedded seeds to remove.
The entire seed is consumed raw, though the watery, tasty sarcotesta is the
desired part. The taste differs depending on the variety or cultivar of
pomegranate and its ripeness.

Pomegranate juice can be sweet or sour, but most fruits are moderate in
taste, with sour notes from the acidic tannins contained in the juice.
Pomegranate juice has long been a popular drink in Armenia, greater Iran,
Israel and India, and now is widely distributed in the United States and
Canada.
Grenadine syrup long ago consisted of thickened and sweetened
pomegranate juice, now is usually a sales name for a syrup based on
various berries, citric acid, and food coloring, mainly used
in cocktail mixing. In Europe, Bols still manufactures grenadine syrup with
pomegranate. Before tomatoes, a New World fruit, arrived in the Middle
East, pomegranate juice, molasses, and vinegar were widely used in many
Iranian foods, and are still found in traditional recipes such as fesenjn, a

thick sauce made from pomegranate juice and ground walnuts, usually
spooned overduck or other poultry and rice, and in ash-e
anar (pomegranate soup).

An Indian pomegranate
Pomegranate seeds are used as a spice known
as anardana (from Persian: anar + dana, pomegranate + seed), most
notably in Indian and Pakistani cuisine. Dried whole seeds can often be
obtained in ethnic Indian subcontinent markets. These seeds are separated
from the flesh, dried for 1015 days, and used as an acidic agent
for chutney and curry preparation. Ground anardana is also used, which
results in a deeper flavoring in dishes and prevents the seeds from getting
stuck in teeth. Seeds of the wild pomegranate variety known as daru from
the Himalayas are regarded as quality sources for this spice.
Dried pomegranate seeds, found in some natural specialty food markets,
still contain some residual water, maintaining a natural sweet and tart
flavor. Dried seeds can be used in several culinary applications, such
as trail mix, granola bars, or as a topping for salad, yogurt, or ice cream.
Chocolate-covered seeds may be added to desserts and baked items.
In the Caucasus, pomegranate is used mainly for juice. In Azerbaijan, a
sauce from pomegranate juice narsharab, (from Persian: (a)nar + sharab,
lit. "pomegranate wine") is usually served with fish or tika kabab. In Turkey,
pomegranate sauce (Turkish: nar ekisi) is used as a salad dressing, to
marinate meat, or simply to drink straight. Pomegranate seeds are also
used in salads and sometimes as garnish for desserts such
as glla. Pomegranate syrup or molasses is used in muhammara, a
roasted red pepper, walnut, and garlic spread popular in Syria and Turkey.
In Israel, pomegranate is used for Tabbouleh salad during Rosh HaShana.
In Greece, pomegranate (Greek: , rodi) is used in many recipes,
includingkollivozoumi, a creamy broth made from boiled wheat,

In traditional medicine
In the Indian subcontinent's ancient system of traditional medicine, the
pomegranate has been used extensively as a source of traditional
remedies.
The rind of the fruit and the bark of the pomegranate tree are used as a
traditional remedy against diarrhea, dysentery, and intestinal parasites. The
seeds and juice are considered a tonic for the heart and throat, and
classified as having bitter-astringent taste plus a range of taste from sweet
to sour, depending on ripeness. Thus, pomegranate is considered a
healthful counterbalance to a diet high in sweet-fatty (kapha or earth)
components.
Especially when sweet, pomegranate fruit is nourishing for pitta or fire
systems and is considered a blood builder. The astringent qualities of the
flower juice, rind, and tree bark are considered valuable for a variety of
purposes, such as stopping nose bleeds and gum bleeds, toning skin,
(after blending with mustard oil) firming-up sagging breasts, and treating
hemorrhoids. Pomegranate juice (of specific fruit strains) is also used as an
eyedrop, as it is believed to slow the development of cataracts.
Unani differentiates between pomegranate varieties and employs them for
different remedies.
Pomegranate has been used as a contraceptive and abortifacient by
means of consuming the seeds, or rind, as well as by using the rind as a
vaginal suppository. This practice is recorded in ancient Indian literature, in
medieval sources, and in modern folk medicine.
Pomegranate extracts (alkaloids) are used to treat intestinal parasite
infestations in some nations.

Making pomegranate juice at a stall in Turkey

Research

Nutrients and phytochemicals

{{nutritional value

| kJ=346 | protein=1.67 g | fat=1.17 g | carbs=18.7 g | fiber=4 g |

sugars=13.67 g | calcium_mg=10 | iron_mg=0.3 | magnesium_mg=12 |
phosphorus_mg=36 | potassium_mg=236 | sodium_mg=3 | zinc_mg=0.35 |
manganese_mg=0.119 | vitC_mg=10.2 | thiamin_mg=0.067 |
riboflavin_mg=0.053 | niacin_mg=0.293 | pantothenic_mg=0.377 |
vitB6_mg=0.075 | folate_ug=38 | choline_mg=7.6 | vitE_mg=0.6 |
vitK_ug=16.4 | source_usda = 1 | note=Link to USDA Database entry }} A
100-g serving of pomegranate seeds provides 12% of the Daily Value (DV)
for vitamin C, 16% DV for vitamin K and 10% DV for folate (table).
Pomegranate seeds are an excellent source of dietary fiber (20% DV)
which is entirely contained in the edible seeds. People who choose to
discard the seeds forfeit nutritional benefits conveyed by the seed fiber
and micronutrients.
Pomegranate seed oil contains punicic acid (65.3%), palmitic
acid (4.8%), stearic acid (2.3%), oleic acid (6.3%), and linoleic acid (6.6%).
[40]

Polyphenols
Juice
The most abundant phytochemicals in pomegranate juice are polyphenols,
including the hydrolyzable tannins calledellagitannins formed when ellagic
acid and/or gallic acid binds with a carbohydrate to form pomegranate
ellagitannins, also known as punicalagins.
The red color of juice can be attributed to anthocyanins, such
as delphinidin, cyanidin, and pelargonidin glycosides. Generally, an
increase in juice pigmentation occurs during fruit ripening.

The phenolic content of pomegranate juice is adversely affected by

processing and pasteurization techniques.
Peel
Compared to the pulp, the inedible pomegranate peel contains as much as
three times the total amount of polyphenols,
Including
condensedtannins, catechins, gallocatechins and prodelphinidins.
The higher phenolic content of the peel yields extracts for use in dietary
supplements and food preservatives.
Potential health benefits
Pomegranate ellagitannins, also called punicalagins, have shown freeradical scavenging properties in laboratory experiments and are being
studied for their potential biological activity in humans.
Pomegranate juice is under research for affecting heart disease risk
factors, including LDL oxidation, macrophage oxidative status, and foam
cell formation.
In a limited study of hypertensive patients, consumption of pomegranate
juice for two weeks was shown to reduce systolic blood pressure by
inhibiting serum angiotensin-converting enzyme.
Despite limited research data, manufacturers and marketers of
pomegranate juice have liberally used evolving research results for product
promotion. In February 2010, the FDA issued a Warning Letter to one such
manufacturer, POM Wonderful, for using published literature to make illegal
claims of unproven anti-disease benefits.
Many food and dietary supplement makers use pomegranate phenolic
extracts as ingredients in their products instead of juice, such as ellagic
acid which may be bioavailable only after punicalagins are metabolized.
However, ingested ellagic acid is rapidly and nearly completely excreted,
indicating it likely does not have significant biological roles in humans.

Clinical trial disease targets

In 2015, 60 clinical trials were registered with the National Institutes of
Health to examine effects of pomegranate extracts or juice consumption on
a variety of human disorders, including:[59]
prostate cancer
prostatic hyperplasia
diabetes
lymphoma
rhinovirus infection
common cold
oxidative stress in diabetichemodialysis
atherosclerosis
coronary artery disease
infant brain injury
hemodialysis for kidney disease
male infertility
aging
memory
pregnancy complications
osteoporosis
erectile dysfunction
Symbolism
Ancient Egypt

Ancient Egyptians regarded the pomegranate as a symbol of prosperity

and ambition. According to the Ebers Papyrus, one of the oldest medical
writings from around 1500 BC, Egyptians used the pomegranate for
treatment of tapeworm and other infections.
Ancient GreeceThe Greeks were familiar with the fruit far before it was
introduced to Rome via Carthage. In Ancient Greek mythology, the
pomegranate was known as the "fruit of the dead", and believed to have
sprung from the blood of Adonis.
The myth of Persephone, the goddess of the underworld, prominently
features the pomegranate. In one version of Greek mythology, Persephone
was kidnapped by Hades and taken off to live in the underworld as his wife.
Her mother, Demeter(goddess of the Harvest), went into mourning for her
lost daughter, thus all green things ceased to grow. Zeus, the highestranking of the Greek gods, could not allow the Earth to die, so he
commanded Hades to return Persephone. It was the rule of the Fates that
anyone who consumed food or drink in the underworld was doomed to
spend eternity there. Persephone had no food, but Hades tricked her into
eating six pomegranate seeds while she was still his prisoner, so she was
condemned to spend six months in the underworld every year. During
these six months, while Persephone sits on the throne of the underworld
beside her husband Hades, her mother Demeter mourns and no longer
gives fertility to the earth. This was an ancient Greek explanation for the
seasons. Dante Gabriel Rossetti's painting Persephona depicts
Persephone holding the fatal fruit. The number of seeds Persephone ate
varies, depending on which version of the story is told. The number ranges
from three to seven, which accounts for just one barren season if it is just
three or four seeds, or two barren seasons (half the year) if she ate six or
seven seeds.
The pomegranate also evoked the presence of the Aegean Triple
Goddess who evolved into the Olympian Hera, who is sometimes
represented offering the pomegranate, as in the Polykleitos' cult image of
the Argive Heraion (see below). According to Carl A. P. Ruck and Danny
Staples, the chambered pomegranate is also a surrogate for the

poppy's narcotic capsule, with its comparable shape and chambered

interior. On a Mycenaean seal illustrated inJoseph Campbell's Occidental
Mythology 1964, figure 19, the seated Goddess of the double-headed axe
(the labrys) offers three poppy pods in her right hand and supports her
breast with her left. She embodies both aspects of the dual goddess, lifegiving and death-dealing at once. The Titan Orion was represented as
"marrying" Side, a name that in Boeotia means "pomegranate", thus
consecrating the primal hunter to the Goddess. Other Greek dialects call
the pomegranate rhoa; its possible connection with the name of the earth
goddess Rhea, inexplicable in Greek, proved suggestive for the
mythographer Karl Kerenyi, who suggested the consonance might
ultimately derive from a deeper, pre-Indo-European language layer.
In the fifth century BC, Polycleitus took ivory and gold to sculpt the
seated Argive Hera in her temple. She held a scepter in one hand and
offered a pomegranate, like a 'royal orb', in the other.[65] "About the
pomegranate I must say nothing," whispered the traveller Pausanias in the
2nd century, "for its story is somewhat of a holy mystery." In the Orion story,
Hera cast pomegranate-Side (an ancient city in Antalya) into dim Erebus
"for daring to rival Hera's beauty", which forms the probable point of
connection with the older Osiris/Isis story. Since the ancient Egyptians
identified the Orionconstellation in the sky as Sah the "soul of Osiris", the
identification of this section of the myth seems relatively complete. Hera
wears, not a wreath nor a tiara nor a diadem, but clearly the calyx of the
pomegranate that has become her serrated crown. The pomegranate has a
calyx shaped like a crown. In Jewish tradition, it has been seen as the
original "design" for the proper crown. In some artistic depictions, the
pomegranate is found in the hand of Mary, mother of Jesus.
A pomegranate is displayed on coins from the ancient city of Side,
Pamphylia.
Within the Heraion at the mouth of the Sele, near Paestum, Magna
Graecia, is a chapel devoted to the Madonna del Granato, "Our Lady of the
Pomegranate", "who by virtue of her epithet and the attribute of a
pomegranate must be the Christian successor of the ancient Greek

goddess Hera", observes the excavator of the Heraion of Samos, Helmut

Kyrieleis.

In modern times, the pomegranate still holds strong symbolic meanings for
the Greeks. On important days in the Greek Orthodox calendar, such as
the Presentation of the Virgin Maryand on Christmas Day, it is traditional to
have at the dinner table polysporia, also known by their ancient
name panspermia, in some regions of Greece. In ancient times, they were
offered to Demeter and to the other gods for fertile land, for the spirits of the
dead and in honor of compassionate Dionysus. When one buys a new
home, it is conventional for a house guest to bring as a first gift a
pomegranate, which is placed under/near the ikonostasi (home altar) of the
house, as a symbol of abundance, fertility, and good luck. Pomegranates
are also prominent at Greek weddings and funerals.When Greeks
commemorate their dead, they make kollyva as offerings, which consist of
boiled wheat, mixed with sugar and decorated with pomegranate. It is also
traditional in Greece to break a pomegranate on the ground at weddings
and on New Years.Pomegranate decorations for the home are very
common in Greece and sold in most home goods stores.
Ancient Israel and Judaism
Pomegranates were known in Ancient Israel as the fruits which the scouts
brought to Moses to demonstrate the fertility of the "promised land".The
Book of Exodus describes the me'il ("robe of the ephod") worn by
the Hebrew high priest as having pomegranates embroidered on the hem
alternating with golden bells which could be heard as the high priest
entered and left the Holy of Holies. According to the Books of Kings, the
capitals of the two pillars (Jachin and Boaz) that stood in front of Solomon's
Temple in Jerusalem were engraved with pomegranates. Solomon is said
to have designed his coronet based on the pomegranate's "crown" (calyx).
It is traditional to consume pomegranates on Rosh Hashana because, with
its numerous seeds, it symbolizes fruitfulness.[ Also, it is said to have 613
seeds, which corresponds with the 613 mitzvot or commandments of

the Torah. This particular tradition is referred to in the opening pages

of Ursula Dubosarsky's novel Theodora's Gift.[75]
The pomegranate appeared on the ancient coins of Judea. When not in
use, the handles of Torah scrolls are sometimes covered with decorative
silver globes similar in shape to "pomegranates" (rimmonim). Some Jewish
scholars believe the pomegranate was the forbidden fruit in the Garden of
Eden. Pomegranates are one of the Seven Species (Hebrew:
, Shiv'at Ha-Minim) of fruits and grains enumerated in the Hebrew
Bible (Deuteronomy 8:8) as being special products of the Land of Israel.
The pomegranate is mentioned in the Bible many times, including this
quote from the Songs of Solomon, "Thy lips are like a thread of scarlet, and
thy speech is comely: thy temples are like a piece of a pomegranate within
thy locks." (Song of Solomon 4:3). Pomegranates also symbolize the
mystical experience in the Jewish mystical tradition, or kabbalah, with the
typical reference being to entering the "garden of pomegranates" or pardes
rimonim; this is also the title of a book by the 16th-century mystic Moses
ben Jacob Cordovero.
In European Christian Motifs
Detail from Madonna of the Pomegranate by Sandro Botticelli, ca. 1487
(Uffizi Gallery, Florence)
In the earliest incontrovertible appearance of Christ in a mosaic, a fourthcentury floor mosaic from Hinton St Mary, Dorset, now in the British
Museum, the bust of Christ and the chi rho are flanked by
pomegranates. Pomegranates continue to be a motif often found
in Christian religious decoration. They are often woven into the fabric
of vestments and liturgical hangings or wrought in metalwork.
Pomegranates figure in many religious paintings by the likes of Sandro
Botticelli andLeonardo da Vinci, often in the hands of the Virgin Mary or
the infant Jesus. The fruit, broken or bursting open, is a symbol of the
fullness of Jesus' suffering andresurrection.

In the Eastern Orthodox Church, pomegranate seeds may be used

in kolyva, a dish prepared for memorial services, as a symbol of the
sweetness of the heavenly kingdom.
In the Qur'an
According to the Qur'an, pomegranates grow in the gardens of paradise
(55:68). The Qur'an also mentions pomegranates three times (6:99, 6:141,
55:68) as examples of good things Allah creates.
Afghanistan
Pomegranate production in Afghanistan
Pomegranate, a favorite fall and winter fruit in Afghanistan, has mainly two
varieties: one that is sweet and dark red with hard seeds growing in and
around Kandhar province, and the other that has soft seeds with variable
color growing in the central/northern region. The largest market for Afghan
pomegranates is India followed by Pakistan, Dubai, Russia, United Arab
Emirates and Europe.
Armenia
The pomegranate is one of the main fruits in Armenian culture (the others
being apricot and grapes). Its juice is famous with Armenians in food and
heritage. The pomegranate is the symbol of Armenia and represents
fertility, abundance and marriage. For example, the fruit played an integral
role in a wedding custom widely practiced in ancient Armenia: a bride was
given a pomegranate fruit, which she threw against a wall, breaking it into
pieces. Scattered pomegranate seeds ensured the bride future children. In
Artsakh, it was customary to put fruits next to the bridal couple during the
first night of marriage, among them the pomegranate, which was said to
ensure happiness. It is likely that newlyweds also enjoyed pomegranate
wine. The symbolism of the pomegranate is that it protected a woman from
infertility and protected a man's virility. Currently, pomegranate juice is
popular with Armenians in food and heritage. The Color of
Pomegranates (1969) is a movie directed by Sergei Parajanov. It is a

biography of the Armenian ashug Sayat-Nova (King of Song) which

attempts to reveal the poet's life visually and poetically rather than literally.
Azerbaijan
Pomegranate Festival
Annually in October, a cultural festival is held
in Goychay, Azerbaijan known as Pomegranate Festival. The festival
featuresAzerbaijani fruit-cuisine mainly the pomegranates from Goychay. At
the festival, a parade is held with traditional Azerbaijani
dances and Azerbaijani music.[80]
Iran and ancient Persia

Black pomegranate
Pomegranate was the symbol of fertility in ancient Persian culture. In
Persianmythology, Isfandiyar eats a pomegranate and becomes invincible.
In the Greco-Persian Wars, Herodotus mentions golden pomegranates
adorning the spears of warriors in thephalanx. Even in today's Iran,
pomegranate may imply love and fertility.
Iran produces pomegranates as a common crop. Its juice and paste have a
role in some Iranian cuisines, e.g. chicken, ghormas and refreshment bars.
Pomegranate skins may be used to stain wool and silk in the carpet
industry.
Pomegranate Festival is an annual cultural and artistic festival held during
October in Tehran[ to exhibit and sell pomegranates, food products and
handicrafts.
Pakistan
The pomegranate (known as "anr" in Urdu) is a popular fruit in Pakistan. It
is grown in Pakistan and is also imported from Afghanistan.

India

The pomegranate is regarded as a symbol of fertility in China

In some Hindu traditions, the pomegranate (Hindi: anr) symbolizes
prosperity and fertility, and is associated with both Bhoomidevi (the earth
goddess) and Lord Ganesha (the one fond of the many-seeded fruit).[81]
[82]
The Tamil name maadulampazham is a metaphor for a woman's mind. It
is derived from, maadhu=woman, ullam=mind, which means as the seeds
are hidden, it is not easy to decipher a woman's mind.
China
Introduced to China during the Tang Dynasty (618-907 AD), the
pomegranate (Chinese: ; pinyin: shliu) in olden times was considered
an emblem of fertility and numerous progeny. This symbolism is a pun on
the Chinese character (z) which, as well as meaning seed, also means
"offspring" thus a fruit containing so many seeds is a sign of fecundity.
Pictures of the ripe fruit with the seeds bursting forth were often hung in
homes to bestow fertility and bless the dwelling with numerous offspring, an
important facet of traditionalChinese culture.
Description
Punica granatum, commonly known as Pomegranate, is a species of fruitbearing deciduous shrub or small tree, growing to 5-8 m height. The leaves
are opposite or sub-opposite, glossy, narrow, oblong, entire, 3-7 cm long
and 2 cm broad. The flowers are bright red, with five petals each. Native to
the southwest zones of Asia, the plant species was originally cultivated in
the Caucasus region in ancient times. Pomegranate was later introduced in
parts of Latin America and California by the early Spanish settlers, during
the year 1769. There, the plant species was mainly used for the purpose of
juice production. Today, pomegranate is widely cultivated in North India,
Pakistan, Afghanistan, Armenia, Azerbaijan and parts of the Middle East.
The cultivation of the fruit usually takes place during the months of

September to February in the Northern Hemisphere, while in the Southern

Hemisphere; it is from March to May.
Plant Chemicals
Pomegranate is a rich source of potassium and antioxidant polyphenols.
These polyphenols mainly include hydrolysable tannins called punicalagins.
Polyphenols catechins, gallocatechins, and anthocyanins such as
prodelphinidins, delphinidin, cyanidin, and pelargonidin are other
phytochemicals present in the plant species.
Uses & Benefits of Pomegranate
Pomegranate is great for curing a number of ailments and diseases. The
juice of its fruit helps to reduce the risk of strokes, heart diseases and heart
attacks. It prevents the formation of Low Density Lipoprotein (LDL) or bad
cholesterol, through its antioxidant properties and hence, helps in the
clearance of blood clots in the arteries.
Many women claim that the extracts of the fruit helps to overcome feelings
of weakness or malaise during and after menopause.
The fruit is a rich source of vitamins and is particularly high in vitamin A, C
E and folic acid.
Regular intake of pomegranate juice helps to reduce the possibility of
developing Alzheimers disease by the elderly.
It also helps to strengthen the normal human defense mechanism and
prevents the occurrence of certain types of cancer. This is mainly because
of the fact that the fruit contains high amounts of antioxidants called
flavenoids, which are believed to counteract the actions of cancer-causing
radicals and thereby promote good health.
Another major health benefit of pomegranate is that it helps to prevent and
control anemic conditions like weakness, dizziness, fatigue and hair loss,
as it provides support to the blood by supplying it with iron.

A decoction of its seeds is used to treat syphilis. The juice helps treat
jaundice and diarrhea. Even the juice of its flower is used to treat
nosebleeds.
The fruit pulp and seeds of pomegranate are stomachic.
It also helps to cure conditions like diabetes, osteoarthritis and
atherosclerosis.
The antioxidants present in pomegranate contribute to the antiviral
properties in the fruit.
Curing skin inflammation and similar type of skin conditions is yet another
beneficial effect of consuming pomegranate on a regular basis.
Caution:
Certain allergic reactions may occur due to consumption of pomegranate.
Serious reactions like difficulty in swallowing, skin rashes, wheezing and
swelling of the lips, mouth, throat or tongue may also occur at times

Mentha Arvensis,

Mentha
Mint

Mentha longifolia
Scientific classification
Kingdom:

Plantae

(unranked) Angiosperm
:
s
(unranked) Eudicots
:
(unranked) Asterids
:
Order:

Lamiales

Family:

Lamiaceae

Tribe:

Mentheae

Genus:

Mentha
L.

Type species

Mentha spicata
L.
Synonyms[1]
Pulegium Mill.
Preslia Opiz
Audibertia Benth.
Menthella Prard
Minthe St.-Lag.
Mentha (also known as mint, from Greek mntha, Linear B mi-ta) is a genus
of plants in the family Lamiaceae (mint family).
The species are not clearly distinct, and estimates of their number vary
from 13 to 18. Hybridization between some of the species occurs naturally.
Many other hybrids, as well as numerous cultivars, are known
as cultivation.
The genus has a subcosmopolitan distribution across Europe, Africa, Asia,
Australia, and North America.
Mints are aromatic, almost exclusively perennial, rarely annual, herbs. They
have wide-spreading underground and overground stolons and erect,
square, branched stems. The leaves are arranged in opposite pairs,
from oblong tolanceolate, often downy, and with a serrated margin. Leaf
colors range from dark green and gray-green to purple, blue, and
sometimes pale yellow. The flowers are white to purple and produced in
false whorls called verticillasters. The corolla is two-lipped with four
subequal lobes, the upper lobe usually the largest. The fruit is a nutlet,
containing one to four seeds.
While the species that make up the Mentha genus are widely distributed
and can be found in many environments, most grow best in wet

environments and moist soils. Mints will grow 10120 cm tall and can
spread over an indeterminate area. Due to their tendency to spread
unchecked, some mints are considered invasive.
Contents
1 Species
2 Taxonomy
3 Selected hybrids
4 Cultivation
5 Uses
5.1 Food safety
5.2 Culinary
5.3 Traditional medicine and cosmetics
5.3.1 Allergic reaction
5.4 Insecticides
5.5 Room scent and aromatherapy
6 Diseases
7 Etymology of "mint"

Species

The list below includes all of the taxa recognized as species in recent
works onMentha. No author has recognized all of them. As with
all biological classifications of plants, this list can go out of date at a
moment's notice. Common names are also given for species that have
them. Synonyms, along with cultivars and varieties, are given in articles on
the species.

Mentha aquatica water

mint, marsh mint
Mentha arvensis corn
mint, wild mint, Japanese
peppermint, field mint,
banana mint

Mentha laxiflora forest mint

Mentha longifolia (syn. Mentha
sylvestris) horse mint
Mentha piperita peppermint
Mentha pulegium pennyroyal

Mentha asiatica Asian mint Mentha requienii Corsican mint

Mentha australis
Australian mint
Mentha canadensis
American wild mint
Mentha cervina Hart's
pennyroyal
Mentha citrata bergamot
mint, orange mint

Mentha sachalinensis garden mint

Mentha satureioides native
pennyroyal
Mentha spicata (syn. M. viridis, M.
cordifolia) spearmint, curly mint (a
cultivar of spearmint)[10]
Mentha suaveolens apple mint,
pineapple mint (a variegated cultivar
of apple mint)

Mentha crispata wrinkledleaf mint

Mentha vagans gray mint
Mentha dahurica Dahurian
thyme
Mentha diemenica slender
mint
Taxonomy

Mentha is a member of the tribe Mentheae in the subfamily Nepetoideae.

The tribe contains about 65 genera, and relationships within it remain
obscure. Authors have disagreed on the circumscription of Mentha. Some
authors have excluded M. cervina from the genus. M. cunninghamii has
also been excluded by some authors, even in some recent treatments of
the genus.[11] In 2004, a molecular phylogenetic study indicated both of
these species should be included inMentha.

Selected hybrids

The mentha x piperita hybrid, known as "chocolate mint."

The mint genus has a large grouping of recognized hybrids. Synonyms,
along with cultivars and varieties where available, are included within the
specific species.

Cultivation

Mentha x gracilis and M. rotundifolia: The steel ring is to control the spread
of the plant.
All mints thrive near pools of water, lakes, rivers, and cool moist spots in
partial shade. In general, mints tolerate a wide range of conditions, and can
also be grown in full sun. Mint grows all year round.
They are fast-growing, extending their reach along surfaces through a
network ofrunners. Due to their speedy growth, one plant of each desired
mint, along with a little care, will provide more than enough mint for home
use. Some mint species are more invasive than others. Even with the less
invasive mints, care should be taken when mixing any mint with any other

plants, lest the mint take over. To control mints in an open environment,
they should be planted in deep, bottomless containers sunk in the ground,
or planted above ground in tubs and barrels.
Some mints can be propagated by seed, but growth from seed can be an
unreliable method for raising mint for two reasons: mint seeds are highly
variable one might not end up with what one supposed was planted
and some mint varieties are sterile. It is more effective to take and plant
cuttings from the runners of healthy mints.
The most common and popular mints for cultivation
are peppermint (Mentha piperita), spearmint (Mentha spicata), and (more
recently) apple mint (Mentha suaveolens).
Mints are supposed to make good companion plants, repelling pesty
insects and attracting beneficial ones. They are susceptible
to whitefly and aphids.
Harvesting of mint leaves can be done at any time. Fresh leaves should be
used immediately or stored up to a few days in plastic bags in a
refrigerator. Optionally, leaves can be frozen in ice cube trays. Dried mint
leaves should be stored in an airtight container placed in a cool, dark, dry
area.
Uses

Food safety
182.10 Spices and other natural seasonings and flavorings, including
mint, are generally regarded as safe (GRAS) for food uses in the United
States.
Peppermint Mentha piperita L.
Spearmint Mentha spicata L.
182.20 Essential oils, oleoresins (solvent-free), and natural extractives
(including distillates).
Menthol Mentha spp.

Peppermint Mentha piperita L.

Spearmint Mentha spicata L.
Culinary

A jar of mint jelly: Mint jelly is a traditional condiment served with lamb
dishes.

Limonana (mint lemonade) served in Damascus, Syria

The leaf, fresh or dried, is the culinary source of mint. Fresh mint is usually
preferred over dried mint when storage of the mint is not a problem. The
leaves have a warm, fresh, aromatic, sweet flavor with a cool aftertaste,
and are used in teas, beverages, jellies, syrups, candies, and ice creams.
In Middle Eastern cuisine, mint is used on lamb dishes, while in British
cuisine and American cuisine, mint sauce and mint jelly are used,
respectively.
Mint is a necessary ingredient in Touareg tea, a popular tea in northern
African and Arab countries. Alcoholic drinks sometimes feature mint for
flavor or garnish, such as the mint julep and the mojito. Crme de
menthe is a mint-flavored liqueur used in drinks such as thegrasshopper.
Mint essential oil and menthol are extensively used as flavorings in breath
fresheners, drinks, antiseptic mouth rinses, toothpaste, chewing
gum, desserts, and candies, such asmint (candy) and mint chocolate. The
substances that give the mints their characteristic aromas and flavors are
menthol (the main aroma of peppermint and Japanese peppermint)
and pulegone (in pennyroyal and Corsican mint). The compound primarily
responsible for the aroma and flavor of spearmint is L-carvone.
Mints are used as food plants by the larvae of some Lepidoptera species,
including buff ermine moths.
Traditional medicine and cosmetics

Mint was originally used as a medicinal herb to treat stomach

ache and chest pains. There are several uses in traditional medicine and
preliminary research for possible use in treating irritable bowel syndrome.
Menthol from mint essential oil (4090%) is an ingredient of
many cosmetics and someperfumes. Menthol and mint essential oil are
also used in aromatherapy which may have clinical use to alleviate postsurgery nausea.
Allergic reaction
Although it is used in many consumer products, mint may cause allergic
reactions in some people, inducing symptoms such as abdominal
cramps, diarrhea, headaches, heartburn, tingling or numbing around the
mouth, anaphylaxis or contact dermatitis.[17][20]
Insecticides
Mint oil is also used as an environmentally friendly insecticide for its ability
to kill some common pests such as wasps, hornets, ants, and cockroaches.
Room scent and aromatherapy
Known in Greek mythology as the herb of hospitality,, one of mint's first
known uses in Europe was as a room deodorizer. The herb was strewn
across floors to cover the smell of the hard-packed soil. Stepping on the
mint helped to spread its scent through the room. Today, it is more
commonly used for aromatherapy through the use of essential oils.
Diseases
List of mint diseases
Etymology of "mint"

An example of mint leaves

Mint descends from the Latin word mentha, which is rooted in
the Greek wordminthe, personified in Greek mythology as Minthe, a nymph
who was transformed into a mint plant. The word itself probably derives
from a now extinct pre-Greek language (see Pre-Greek substrate).
Mint leaves, without a qualifier like 'peppermint' or 'apple mint', generally
refers tospearmint leaves.
In Spain and Central and South America, mint is known as menta.
In Lusophonecountries, especially in Portugal, mint species are popularly
known as hortel. In many Indo-Aryan languages, it is called pudna,
(Sindhi: ),
The taxonomic family Lamiaceae is known as the mint family. It includes
many other aromatic herbs, including most of the more common cooking
herbs, such as basil, rosemary, sage, oregano, and catnip.
As an English colloquial term, any small mint-flavored confectionery item
can be called a mint.
In common usage, other plants with fragrant leaves may be called "mint",
although they are not in the mint family.
Vietnamese mint, commonly used in Southeast Asian cuisine is Persicaria
odorata in the family Polygonaceae, collectively known as smartweeds or
pinkweeds.
Mexican mint marigold is Tagetes lucida in the sunflower family
(Asteraceae).

Botanical Name(s): Mentha Arvensis, Pipertia

Family Name: Lamiaceae
Kingdom: Plantae
Division: Magnoliophyta
Class: Magnoliopsida
Order: Lamiales
Family: Lamiaceae
Genus: Mentha
Species: M. piperita
Popular Name(s): Field Mint, Corn Mint, Japanese Mint, Wild Mint, Pudina.
Parts Used: Whole Plant, Oil.
Habitat: Found through out India.
Description
Podina is an herbaceous perennial herb that grows to a height of 10 to 60
cm. This downy herb has running rootstocks and a rigid branching stem.
The lanceolate oblong leaves are simple and sharply toothed, paired in
opposites with minute hair. They are 2 to 6.5 cm in length and 1 to 2 cm in
width. The pale purple flowers (sometimes white or pink) are found in
clusters at the stem where each flower measures 2 to 4 mm in length. The
plant is native to the temperate regions of Europe, western and central Asia
(eastern Siberia and east of the Himalayas) and North America. It is
commonly known as pudina in Hindi.
Plant Chemicals
(+)- volatile oil, carvone, limonene, 1,8-cineole, trans-carveol, linarin,
pulegone, menthol, menthene, menthenone.
Uses & Benefits

Podina is used as a carminative and an expectorant.

The plant is highly effective in treating headaches, rhinitis, cough sore
throat, colic, prurigo and vomiting.
It serves as a good blood cleanser, since it is antiseptic and anti-bacterial.

Podina plays a significant role in alleviating swollen gums, mouth ulcers

and toothaches.
Crushed and bruised pudina leaves are used in treating insect bites.
The decoction and infusion of its leaves and stems helps in fever,
stomachaches, dysmenorrheal and diuresis.
Fresh leaves of podina are crushed and sniffed for dizziness. Crushed
leaves are also applied on the forehead and temple, to cure headaches.
For toothaches, boil 6 tablespoons of pudina leaves in 2 glasses of water,
for 15 minutes. Strain and cool the water. Divide it into two parts and take
each part after 3 to 4 hours.
Boil 6 tablespoons of chopped leaves in 2 glasses of water, for 15 minutes.
Cool and strain. Divide the decoction into 3 parts and consume three times
a day. This will help in treating coughs.
For treating arthritis, take some fresh leaves and heat on low flame. Pound
them and apply on the painful joints or muscles, when still warm.
Soak 2 tablespoons of chopped leaves in a glass of hot water for 30
minutes and strain. Use the infusion as a mouthwash.
The menthol extracted from the plant is used in preparing balms.
It is used as a flavoring agent in many culinary preparations.
Caution
Mint oil is not safe for infants and children, especially when applied around
the nose, as it can cause serious breathing problems.
The oil should not be used by pregnant and breast-feeding women and
people with liver disease or damage, asthma and gall bladder conditions,
like inflammation, gallstones or a blocked bile duct.
When applied directly on the skin, mint oil can allergic skin reactions,
flushing, headache and vocal cord spasms.

bamboo silica

Banslochan ( , ), also spelt as Tabachir or Tabashir, is a

translucent white substance, composed mainly of silica and water with
traces of lime and potash, obtained from the nodal joints of some species
of bamboo. It is part of the pharmacology of the traditional Unani systems
of medicine of the Indian subcontinent. It is also an ingredient in
many traditional Chinese medicines.
Contents
1 Purported benefits
2 Varieties
3 Extraction
4 History
5 Etymology and alternative names
Purported benefits

Tabasheer is claimed to provide a variety of health benefits. It is variously

regarded as
an antipyretic, antispasmodic,antiparalytic, restorative and aphrodisiac.
Varieties

Tabasheer that has a blueish tint (usually called neel or neelkanth) is

considered superior to tabasheer that has the "more plain" yellow or white
color.
Extraction

Not all bamboo stems contain tabasheer. Likely candidates are found by
shaking bamboo stems, which can make the mineralized tabasheer inside
produce a rattling sound. These stems are split open to extract the
tabasheer.
History
Although a part of the ancient system of medicine, it has been postulated
that the use of tabasheer originated in the Adivasi aboriginal tribes of India.
Tabasheer was extensively exported from India for thousands of years,
including through Arab traders during the medieval period. The town
of Thane, close to the west coast of India, was famous as a clearing center
for tabasheer in the twelfth century CE. It was called in the
writings of Pedanius Dioscorides, aGreek pharmacologist who practiced in
Rome in the time of Nero.
Etymology and alternative names

Tabasheer is referred to as Tvaksheera () in Sanskrit, which

means bark milk. Other Sanskrit-derived names have been applied to
tabasheer as well, including bamboo sugar (vans-sharkar), bamboo
camphor (vans karpoor) and bamboo manna. It is called Tian Zhu Huang in
Mandarin, which means "heavenly bamboo yellow."
Bamboo silica is also known as tabasheer or Tian Zhu Huang in
Chinese (literally Heavenly Bamboo Yellow). Besides, it is
commonly referred to as the calculus in the body of bamboo
plants. When used as Chinese herbal medicine, it clears heat,
sweep phlegm, cool heart, and calm the frightened. Hence,
clinically it treats fever, coma and delirium, convulsions, epilepsy,
rheumatism, limb numbness, whooping cough, excessive vaginal
discharge, stomach trouble, acne, and so on. Now modern
medicine has found that it is one of the richest natural sources of
organic silica, which is responsible for the health of nails,
tendons, skin, hair, bones, and ligaments in human body. So, is
bamboo silica safe and really good for hair growth?

What is bamboo silica?

Medicinally it refers to the dried siliceous resin found in the nodes
of some species in the family Poaceae, mainly from Bambusa
textilis McClure and Schizostachyum chinense Rendle. Other
common names of it include bamboo sap, tabashir, Siliceous
Secretions of Bamboo, banslochan, Concretio Silicea Bambusae,
Tabasheer, bamboo manna, bamboo tears, bamboo powder,
Tabashir silica, karpoor vans (bamboo camphor), Tvaksheera
(bark milk in Sanskrit), vans-sharkar (bamboo sugar), and the
like. In China it is mainly produced in provinces of Yunnan,
Guangdong, and Guangxi. It is generally harvested in autumn
and winter by cutting the stems open. Medicinally it is generally
used raw.
The naturally occurring one is quite rare since this clotted bulk is
mainly formed from the bleeding sap stored in the nodal joints of
Bambusa textilis McClure due to the parasitic wasp bites. Now
most of them are produced by setting fire to the forest in order to
let the sudden heat force and solidify the fresh sap in the notes.
Tabasheer is in the shapes of irregular polygonal blocks or flakes.
Surface is white, gray or with a bluish tint. It is light, crisp, and
easily broken. Section is bright, slightly mealy, and with slippery
feeling when touching with hands. It is strongly absorbent but
insoluble in water. When placed in water, it produces bubbles. It is
sweet, sticky, and cool when licking with tongue. And the highquality one is drier, bigger, yellowish white, bright, and highly
absorbent.
2 polysaccharides, SB-1 and SB-2, can be isolated from The
zymotic fluid of tabasheers mycelium; other ingredients isolated
from the soluble components include proteases, amylase, Dmannitol, aspartic acid, threonine, serine, glutamic acid, glycine,
alanine, cystine, valine, methionine, isoleucine, phenylalanine,

lysine, -amino butyric acid, tyrosine, and small amount of

cysteine; ingredients isolated from the stroma are hypocrellin A,
B, C, mannitol, stearic acid, and shiraiachrome A, B, C.
Bamboo silica benefits
Does bamboo silica really work? When it comes to the sources of
naturally occurring, organic silica, horsetail grass and bamboo are
the most known two. From the eyes of Chinese, bamboo shoots
are more than just a food since eating them has a long history
there. In fact they have become a delicious dish on the table
since the Shang Dynasty, about thousands of years ago. Now
modern scientific findings seem provide a proven reason the
amount of silica contained in bamboo are about 10 times of that
of horsetail herb. If you are familiar with horsetail grass, you will
know that quite well what means behind that figure. No wonder
Enerex Bamboo Silica, a pure silica supplement extracted from its
shoots, is so popular these days for hair growth, healthy joint,
and skin health.
As a matter of fact, another 2 commonly used Chinese herbs, Zhu
Ru (Bamboo Shavings) and Zhu Li (Succus Bambusae), are
associated with tabasheer. Here are their functions in common.
All of the three are of cold nature and treat phlegm-heat induced
cough and asthma by clearing heat and dissipating phlegm. In
addition, both Succus Bambusae and tabasheer can be used in
the treatment of fever or phlegm-heat induced infantile
convulsions, epilepsy, stroke, coma, gurgling with sputum in
throat since it possesses the calming properties. So, what is the
difference between them? First and foremost, tabasheer has
preferable calming power, which makes it do a better job in
treating convulsions in children and coma due to high heat;
besides, since Succus Bambusae is of cold, slippery nature and
with better ability of clearing heat and eliminating phlegm, it is

mostly used in the adults epilepsy, stroke, and lung-heat induced

stubborn sticky phlegm that is hard to cough up; last but not
least, it is good at clearing heart heat to relieve restlessness. As a
result, it is used more in the treatment of irritability and insomnia
caused by phlegm heat disturbing the heart.
Modern pharmacology
1) Hypocrellin B has significant anti-inflammatory and analgesic
effects. It is superior to indomethacin when it comes to raising
the threshold of pain;
2) Hypocrellin A has a good inhibition on Gram-positive bacteria.
And it has significant photodynamic therapy on cultured human
cancer cells and transplanted solid tumors in mice.
Sample recipes on herbal remedies
The Chinese Pharmacopoeia tends to believe that it is sweet in
flavor and cold in nature. It goes to meridians of heart and liver.
Most important functions are clearing away heat, eliminating
phlegm, expelling heart heat, and arresting convulsion.
Principal bamboo silica uses and indications include
unconsciousness due to heat illness, stroke, epilepsy, baby night
cry, convulsions, and phlegm-heat epilepsy. Recommended
bamboo silica dosage is from 3 to 9 grams in pills and powder.
Apart from that, it is also made into a great deal of bamboo silica
products, such as extract, capsules, pills, silica liquid, shampoo,
and the like.
1) Bao Long Wan from Xiao Er Yao Zheng Zhi Jue (Key to the
Therapeutics of Childrens Diseases). It is formulated with She
Xiang (Deer Musk), Dan Nan Xing (Arisaema Cum Bile), Chen Sha
(cinnabar), etc. to treat infantile convulsions due to phlegm-heat;

2) Li Jing Wan from Key to the Therapeutics of Childrens

Diseases. It is combined with Qing Dai (Indigo), Qing Fen
(Calomel), and Qian Niu Zi (Morning Glory Seed) to cure infantile
acute convulsions;
3) Tian Zhu Huang San from Sheng Ji Zong Lu (Complete Record
of Holy Benevolence). It is matched with Chuan Xiong (lovage)
and Fang Ji (Stephania Tetrandra) to heal epistaxis;
4) Qing Fei Hua Tan Tang from the prescriptions of Dr. Guo
Zhongyuan. It is joined with Ban Lan Gen (Isatis Root), Huang
Qin (Scutellaria Baicalensis), Zhe Bei Mu (Fritillaria Bulb), Yuan
Shen (radix scrophulariae), etc. to treat chronic bronchitis;
5) Feng Long Tang from the prescriptions of Dr. Ding Jinyuan. It is
coupled with Lu Feng Fang (Hornets Nest), Di Long (Earthworm),
Jie Geng (Balloon Flower Rhizome), etc. to cure children with
asthma.
Clinical bamboo silica research
a) Tabasheer-based granule has significant effect on the
treatment of psoriasis;
b) The ointment made of hypocrellin A, isolated from Hypocrella
bambusae, can be applied to female genital lesions and
hypertrophic scars. And it has definite therapeutic effect under
lights;
c) A spray made of the mixture of hypocrellin A and B can be
used in topical treatment of burns. For the early stage of the
superficial second-degree burn wounds, it has the advantages of
fast film-forming properties, good air permeability, and quick
wound healing.
Bamboo silica side effects, drug interactions and contraindications

It shouldnt be used during pregnancy and in patients with skin

diseases like onychomycosis, tinea manuum, etc. And dont eat
radishes and sour and spicy food during the medication. Besides,
beware of the adulterants, which have been found in the market
in recent years. The adulterants are often doped with minerals
that are with no genuine healing power of tabasheer. Whats
worse, it may even lead to unexpected adverse reactions.

Coriandrum Sativum

Medicinal benefits of coriander(Coriandrum Sativum L)

Medicinal plants have therapeutic potential due to the presence of natural

antioxidants functioning as reducing agents, free radical scavengers and
quenchers of singlet oxygen. Majority of their antioxidant activity is due to
bioactive compounds viz. flavones, isoflavones, flavonoids, anthocyanins,
coumarins, lignans, catechins and isocatechins. Currently there has been
an increasing interest to identify the antioxidants that are pharmacologically
potent with low or no side effects for use in preventive medicine. Spices
have been recognized to possess several medicinal properties (diuretic,
expectorant, laxative, anti-bacterial, anti-pyretic etc.) and have been
effectively used in the indigenous systems of medicine in India and other
countries. Apart from the traditional use, a no. of beneficial physiological
effects have been identified by extensive animal studies. Among these are
their beneficial effects on lipid metabolism, efficiency as antidiabetics,
ability to stimulate digestion and to inhibit platelet aggregation, antioxidant,
antilithogenic and anti-inflammatory potential. Many spices and their active
principles are reported as excellent nutraceuticals. Coriander is among
such most commonly used spices, possessing the nutritional as well as
medicinal properties, widely distributed and mainly cultivated for the seeds
which contain an essential oil and the monoterpenoid-linalool. Coriander is
used in the preparation of many household medicines to cure bed cold,

seasonal fever, nausea, vomiting, stomach disorders and also used as a

drug for indigestion, against worms, rheumatism and pain in the joints.
Many of healing properties of coriander can be attributed to its exceptional
phytonutrients and hence, it is often referred to as store house for bioactive
compounds.
Key words: Spices, coriander, phytonutrients, diuretic, expectorant,
laxative, anti-bacterial, anti-pyretic, hypoglycemic

Coriander (Coriandrum sativum L.) essential oil: Chemistry and biological

activity Abstract
Coriandrum sativum L. (C. sativum) is one of the most useful essential oil
bearing spices as well as medicinal plants, belonging to the family
Umbelliferae/Apiaceae. The leaves and seeds of the plant are widely used
in folk medicine in addition to its use as a seasoning in food preparation.
The C. sativum essential oil and extracts possess promising antibacterial,
antifungal and anti-oxidative activities as various chemical components in
different parts of the plant, which thus play a great role in maintaining the
shelf-life of foods by preventing their spoilage. This edible plant is non-toxic
to humans, and the C. sativumessential oil is thus used in different
ways, viz., in foods (like flavouring and preservatives) and in
pharmaceutical products (therapeutic action) as well as in perfumes
(fragancias and lotions). The current updates on the usefulness of the
plant C. sativum are due to scientific research published in different webbased journals.
Keywords
Coriandrum sativum essential oil;
Coriander chemistry;

Antibacterial activity;
Antifungal activity;
Antioxidant activity;
Food spoilage prevention;
Medicinal value

1. Introduction
The essential oils and extracts of aromatic plants and spices have been
used in food preservation, pharmaceuticals, alternative medicine and
natural therapies. Currently, it is necessary to investigate those plants
scientifically, for the composition of essential oil (EO) and its biological
activities, which have been used in traditional medicine to improve the
quality of healthcare. The EO contents in different species are varied
inherently, influenced greatly by culture conditions and environment, as well
as by crop and post-crop processing, and hence evaluations of the oils
from many medicinal plants are being conducted. One of the most useful
EO bearing spices as well as medicinal plants is Coriandrum sativum L.
(C. sativum) (containing EO in its leaves, stem, flowers and fruits/seeds),
and thus updates on its usefulness, based upon the scientific studies, are
required for its better maintenance and scientific use for the mankind.
Coriander (C. sativum L.) belonging to the family Umbelliferae/Apiaceae is
a glabrous aromatic, herbaceous annual plant, which has a long history as
a culinary herb being the source of aroma compounds and EOs with
biologically active components possessing antibacterial, antifungal and
antioxidant activities, and thus C. sativum is useful in food preparation (as a
flavouring agent and adjuvant) and preservation as well in preventing food
borne diseases and food spoilage.
C. sativum provides two types of herbal raw materials fruits and leaves,
the main biologically active substance of which is EO. Coriander will be
seeds and added to dishes as an aromatic spice, which at the same time

act as digestive agent accelerating the digestion process. The yield

of C. sativum EO and its chemical composition undergoes changes during
ontogenesis , which affects the aroma of the plant, and thus the coriander
fruit aroma is completely different from the aroma of the herb . Immature
fruits and leaves have an unpleasant odour called a stink bug smell which
is due to trans-tridecen contained in the oil.
Coriander is referred to as kusthumbari or dhanayaka in the Sanskrit
literature; in Hindi it is called Dhania, while Dhane in Bengali. It is a native
plant of the eastern Mediterranean from where it may have spread to India,
China and rest of the world . In the food industry, coriander is approved for
food use by the US Food and Drug Administration, the Flavor and Extract
Manufacturers Association and the Council of Europe, and the plant can be
used as spice, medicine and a raw material in food, beverage and
pharmaceutical industries.
2. Botanicals
The C. sativum L. (family Umbelliferae/Apiaceae) is an erect annual herb
with pronounced taproot, and slender branching stems up to 2070 cm in
height. There are two varieties ofC. sativum: vulgare and microcarpum; the
former has larger fruits (35 mm diameter) with EO yields of 0.1%0.35%
(v/w) while the latter has smaller fruits (1.53 mm diameter) with EO yields
of 0.8%1.8% (v/w) . However, Ravi et al. documented that the weight of
1000 fruits, with fruit diameter >3 mm, is >10 g for C. sativum L.
var. sativum, while forC. sativum L. var. microcarpum DC, the weight of
1000 fruits is <10 g, with fruit diameter 3 mm.
The leaves are lanceolate, green or dark green, glabrous on both surfaces
and are variable in shape and lobed. The flowers are borne in small
umbels, white or light pink, asymmetrical, with the petals pointing away
from the centre. The coriander seed, is almost ovate globular dry
schizocarp with two mericarps , and multiple longitudinal ridges on the
surface possessing a sweet, slightly pungent, citrus like flavor with a hint of
sage .

Figure 1.
Dry coriander, C. sativum seeds: halves and whole.
3. Usage and nutritional value
All parts of C. sativum plant are edible; however, its fresh leaves and dried
seeds are most frequently used. Its green foliage, containing proteins,
vitamins and minerals (like calcium, phosphorus, and iron), fibres and
carbohydrates, is used as vegetable, and in salads, while both the leaves
and seeds contain EO, rich in varying components, which provides typical
flavour, when added to the food products and acts as
preservative .The C. sativum seed EO (CSEO) is triglyceride oil;
petroselinic acid, a monounsaturated fatty acid, is the major fatty acid in
CSEO. Thus, the plant is a potential source of lipids (rich in petroselinic
acid) and EO (high in linalool) isolated from the seeds and the aerial parts.
Ganesan et al. reported that matured coriander leaves are rich in moisture
(87.9%), protein (3.3%), carbohydrate (total sugar 6.5%) and total ash
(1.7%). The CSEO is intended to be marketed as a food supplement for
healthy adults, at a maximum level of 600 mg per day . The seeds are rich
source of lipids, 28.4% of the total seed weight, which may be of great
importance in the food industry . The typical compositional analysis of
coriander oil

Coriander EO also has a long history of use as a traditional medicine .

Coriander was used in time-honoured Greek medicines by Hippocrates
(460-377 BC). Decoction and tincture of powdered seeds
of C. sativum alone or in combination with other herbal agents are
recommended for dyspeptic complaints, loss of appetite, convulsion,
insomnia and anxiety . This CSEO was also found to improve blood
glucose control and thus it held promise for use as an anti-hyperglycemic
agent .4. EO chemistry
The EO can be extracted from various parts of plants including the leaves,
flowers, stem, seeds, roots and bark; however, the composition of the EO
can vary among different parts of the same plant, such as, EO obtained
from the C. sativum seed has different composition from the EO
of C. sativum flower as well as cilantro (immature leaves)
.TheC. sativum oil from fully ripe and dried seeds is a colourless or pale
yellow liquid with a characteristic odour and mild, sweet, warm and
aromatic flavour, and linalool is its major constituent . While aliphatic
aldehydes (mainly C10C16 aldehydes), with their unpleasant odour, are
the main components of the volatile oil from the fresh herb , linalool and
other oxidized monoterpenes as well as monoterpene hydrocarbons
predominate in the oil distilled from the fruit .

Coriander fruit contains about 0.2%1.5% of volatile oil and 13%20% of

fat oil ; however, it has been recorded that some cultivars contain up to
2.6% of volatile oil As has been reported by Zawislak , the EO content
ranged 1.87%2.33%. The fatty oil composition of ripe fruits mainly
includes petroselinic acid (68.8%), linoleic acid (16.6%), oleic acid (7.5%)
and palmitic acid (3.8%) The hydro-distillation of C. sativum L. aerial parts
gave EOs at vegetative, full flowering, green fruit (immature) and brown
fruit (mature) with a yield of 0.14%, 0.23%, 0.37% and 0.31% (w/w), based
on dry weight, respectively
There is variation in seed yield and EO content of C. sativum cultivars
grown at different locations. The EO content in C. sativum fruits is very

different, 0.5%2.5% , and it increases as the fruit

ripens while C. sativum leaves contain less EO than the fruit.
TheC. sativum leaves from Bangladesh had 0.1% EO and the plant
harvested in Tunisia contained 0.12% EO in leaves dried in air The amount
of EO in the coriander herb was on average 0.23 mL per 100 g, and it was
higher in the generative phase (0.29 mL per 100 g) than in the vegetative
phase (0.17 mL per 100 g)
Variation is there in the EO yield of C. sativum fruits from different origins
.The hydro-distillation of C. sativum L. aerial parts gave EOs at vegetative,
full flowering, green fruit (immature) and brown fruit (mature) with a yield of
0.14%, 0.23%, 0.37% and 0.31% (w/w), based on dry weight, respectively .
The chemical class characters of C. sativumEOs from different fruit
samples have been represented by Sriti et al. monoterpene hydrocarbons
(16.2%20.7%), monoterpene alcohols (59.4%73.8%), monoterpene
esters (3.7%9.1%), aldehydes (0.3%0.9%), ketones (3%6.5%) and
phenols (0.06%); the polyphenol contents varied from 15.16 mg GAE/g to
12.10 mg GAE/g. The C. sativumseeds yielded 0.8%, by weight, yellow oil,
with a pleasant aroma, containing oxygenated monoterpenes (80.47%),
monoterpene hydrocarbon (6.45%), fatty acids (5.06%) and long chain
alcohols (3.54%), as has been reported by Pande et al.

Acorus calamus

Common Sweet Flag

Sweet flag
Conservation status

Least Concern (IUCN

3.1)[1]
Scientific classification
Kingdom:

Plantae

(unranked) Angiosperm
:
s
(unranked) Monocots
:
Order:

Acorales

Family:

Acoraceae

Genus:

Acorus

Species:

A. calamus

Binomial name
Acorus calamus
L., 1753
Acorus calamus (also called Sweet Flag or Calamus, among many
common names[) is a tall perennial wetland monocot of
the Acoraceae family, in the genusAcorus. In spite of common names that
include the words "rush" and "sedge," it is neither a rush nor sedge.[3] The
scented leaves and more strongly scented rhizomeshave traditionally been
used medicinally and to make fragrances, and the dried and powdered
rhizome has been used as a substitute for ginger, cinnamon and nutmeg.
Contents

1 Names
1.1 Etymology
2 Botanical information
3 Uses
3.1 History
3.2 Cultural uses
3.3 Herbal medicine
3.4 Hallucinogenic properties
3.5 Horticulture
3.6 Modern Research
4 Chemistry
5 Cultural symbolism

6 Safety and Regulations

Names
In addition to "sweet flag" and "calamus" other common names
include beewort,bitter pepper root, calamus root, flag root, gladdon, myrtle
flag, myrtle grass, myrtle root, myrtle sedge, pine root, rat root, sea
sedge, sweet cane,sweet cinnamon, sweet grass, sweet myrtle, sweet
root, sweet rush, andsweet sedge. Common names in Asia include:
"shoubu ," in Japanese, "vacha"; "bacch" (Unani); "bajai," "gora-bach,"
"vasa bach" (Hindi); "vekhand" (Marathi); "vasambu"/ (Tamil);
"vadaja," "vasa" (Telugu); "baje" (Kannada); "vayambu" (Malayalam);
Haimavati, "bhutanashini," "jatila" (Sanskrit). "Bojho" Nepali.
Etymology
The generic name is the Latin word acorus is derived from
the Greek (chrou) of Dioscorides (note different versions of the
text have different spellings). The word itself is thought to have
been derived from the word (kri), which means pupil (of an eye), due
to the juice from the root of the plant being used as a remedy in diseases of
the eye ('darkening of the pupil').
The specific name calamus (meaning "cane") is derived from
Greek (klamos, meaning "reed"), which is cognateto
Latin culmus (meaning "stalk") and Old English healm (meaning "straw"),
and derived from Proto-Indo European *kole-mo- (thought to mean "grass"
or "reed"). The Arabic word ( qlam, meaning "pen") and Sanskrit
(kalma, meaning "reed used as a pen", and a sort of rice) are thought to
have been borrowed from Greek.
The name sweet flag refers to its sweet scent and its similarity
to Iris species, which are commonly known as flags in English since the
late fourteenth century.
Botanical information

There are three cytotypic forms distinguished by chromosome number: a

diploid form (2n=24), an infertile triploid form (2n=36), and a tetraploid form
(see below). The triploid form is the most common and is thought to have
arisen relatively recently in the Himalayan region through hybridisation of
the diploid with the tetraploid.
Probably indigenous to most of Asia, the triploid form Acorus
calamus var. calamus (also known as var. vulgaris or var.verus) has now
been introduced across Europe, Australia, New Guinea, South Africa,
Runion and North America. The tetraploid form Acorus
calamus var. angustatus is native throughout Asia, from India to Japan and
the Philippines and from Indonesia to Siberia. The diploid form Acorus
americanus or Acorus calamus var.americanus is found in northern
subarctic North America and scattered disjunct areas throughout the
Mississippi Valley, and furthermore diploids are also found in Mongolia,
central Siberia (Buryatia), GilgitBaltistan in Pakistan (claimed by India)
and northern Himachal Pradesh in India. It is extinct in some parts of the
United States and Canada. It may not have been native to some of these
areas, Pre-Columbian populations are thought to have dispersed it across
parts of the United States.
Currently the taxonomic position of these forms is contested. The
comprehensive taxonomic analysis in the Kew World Checklist of Selected
Plant Families from 2002 considers all three forms to be distinct varieties of
a single species. Sue A. Thompson in her 1995 Phd dissertation and in her
2000 entry in the Flora of North America considers the diploid form to be a
distinct species. Note Thompson only analyses North American forms of
the diploid variety in her treatment, and does not analyse the morphology of
Asian forms of the diploid variety. Also note that in older USA literature the
name Acorus americanus may be used indiscriminately for all forms
of Acorus calamus occurring in North America, irrespective of cytological
diversity (i.e. both the diploid and triploid forms). The recent treatment in
the Flora of China from 2010, which is followed in the Tropicos database
system, considers all varieties to be synonyms of a single taxonomically
undifferentiated species, pointing to morphological overlap in the
characteristics singled out by Thompson.

According to Thompson the primary morphological distinction between the

triploid and the North American forms of the diploid is made by the number
of prominent leaf veins, the diploid having a single prominent midvein with
on both sides of this equally raised secondary veins, the triploid having a
single prominent midvein with the secondary veins barely distinct.
Thompson notes a number of other details which she claims can be used
to tell the different forms apart in North America, such as flower length,
average maximum leaf length, relative length of the sympodial leaf with
respect to the vegetative leaves, the average length of the spadix during
flowering, and tendency of the leaf margin to undulate in the triploid. She
notes that many of these characteristics overlap, but that in general the
triploid is somewhat larger and more robust on average than most North
American forms of the diploid. According to Heng Li, Guanghua Zhu and
Josef Bogner in the Flora of China there is clear overlap in these
characteristics and the different cytotypes are impossible to distinguish
morphologically.
Triploid plants are infertile and show an abortive ovary with a shrivelled
appearance. This form will never form fruit (let alone seeds) and can only
spread asexually.
The tetraploid variety is usually known as Acorus calamus var.
angustatus Besser. A number of synonyms are known, but a number are
contested as to which variety they belong. It is morphologically diverse,
with some forms having very broad and some narrow leaves. It is
furthermore also cytotypically diverse, with an array of different karyotypes.
A further hexaploid form exists in central and northwestern Yunnan and
Kashmir. This form has not been given taxonomic status. At least 3 different
karyotypes have been classified as hexaploid; 2n=66in Yunnan and 2n=54
and 2n=72 in Kashmir.
Diploid plants in North America apparently produce no or only trace
amounts of b-asarone. According to one study, triploids produce a small
amount, constituting around 0.3% of the rhizome in crude content, whereas

tetraploids may be found in at least two chemotypes, one with 2.0%, and
one with 4.0 to 8.0%.
Uses

A. calamus has been an item of trade in many cultures for thousands of

years. It has been used medicinally for a wide variety of ailments, and its
aroma makes calamus essential oil valued in the perfume industry. The
essence from the rhizome is used as a flavor for pipe tobacco. When eaten
in crystallized form, it is called "German ginger". In Europe Acorus
calamuswas often added to wine, and the root is also one of the possible
ingredients of absinthe. It is also used in bitters. In Lithuania Ajeras (Sweet
flag) is added to home baked black bread.
History
Although probably not native to Egypt, this plant was already mentioned in
the Chester Beatty papyrus VI dating to approximately 1300 BC. The
ancient Egyptians rarely mentioned the plant in medicinal contexts (the
afore-mentioned papyrus mentioned using it in conjunction with several
ingredients as a bandage used to sooth an ailment of the stomach), but it
was certainly used to make perfumes.
Initially Europeans confused the identity and medicinal uses of the Acorus
calamus of the Romans and Greeks with their native Iris pseudacorus.
Thus the Herbarius zu Teutsch, published at Mainz in 1485, describes and
includes a woodcut of this iris under the name Acorus. This German book
is one of three possible sources for the French Le Grant Herbier, written in
1486, 1488, 1498 or 1508, of which an English translation was published
as the Grete Herball by Peter Treveris in 1526, all containing the false
identification of the Herbarius zu Teutsch. William Turner, writing in 1538,
describes 'acorum' as "gladon or a flag, a yelowe floure delyce".
The plant was introduced to Britain in the late 16th century. By at least
1596 true Acorus calamus was grown in Britain, as it is listed in The
Catalogue, a list of plants John Gerard grew in his garden at Holborn.
Gerard notes "It prospereth exceeding well in my garden, but as yet bearth
neither flowers nor stalke". Gerard lists the Latin name as Acorus verus, but

it is evident there was still doubt about its veracity: in his 1597 herbal he
lists the English common name as 'bastard calamus'
Cultural uses
In Britain the plant was cut for use as a sweet smelling floor covering for
the packed earth floors of dwellings and churches, and stacks of rushes
have been used as the centrepiece of rushbearing ceremonies for many
hundreds of years. It has also been used as a thatching material for English
cottages.
In modern Egypt it is thought to have aphrodisiac properties.
For the Penobscot people this was a very important root. One story goes
that a sickness was plaguing the people. A muskrat spirit came to a man in
dream, telling him that he (the muskrat) was a root and where to find him.
The man awoke, found the root, and made a medicine which cured the
people. In Penobscot homes, pieces of the dried root were strung together
and hung up for preservation. Steaming it throughout the home was
thought to "kill" sickness. While travelling, a piece of root was kept and
chewed to ward off illness.[33]
Teton-Dakota warriors chewed the root to a paste, which they rubbed on
their faces. It was thought to prevent excitement and fear when facing an
enemy.
The Potawatomi people powdered the dried root and placed this up the
nose to cure catarrh.

Illustration from an 1885 flora

Herbal medicine

Sweet flag has a very long history of medicinal use in Chinese and Indian
herbal traditions. The leaves, stems, and roots are used in
various unani medicines. It is widely employed in modern herbal medicine
as itssedative, laxative, diuretic, and carminative properties. It is used to
counter the side effects of all hallucinogens. Sweet Flag, known as "Rat
Root" is one of the most widely and frequently used herbal medicines
amongst theChipewyan people.
Hallucinogenic properties
Chewing the rootstock of the plant can cause visual hallucinations, possibly
due to the presence of alpha-asarone or beta-asarone.
Horticulture
This plant is sometimes used as a pond plant in horticulture. There is at
least one ornamental cultivar known, it is usually called 'Variegatus', but
the RHSrecommends calling it 'Argenteostriatus'.

Modern Research
Acorus calamus shows neuroprotective effect against stroke and
chemically induced neurodegeneration in rats. Specifically, it has protective
effect against acrylamide induced neurotoxicity.
Both roots and leaves of A. calamus have shown antioxidant, antimicrobial
and insecticidal activities.[
Acorus calamus may prove to be an effective control measure against
cattle tick, Rhipicephalus (Boophilus) microplus.
A recent study showed that beta-asarone isolated from Acorus calamus oil
inhibits adipogenesis in 3T3-L1 cells and thus reduces lipid accumulation in
fat cells.
Chemistry

Both triploid and tetraploid A. calamus contain alpha-asarone. Other

phytochemicals include:
Beta-asaroneeugenol[4]
Diploids do not contain beta-asarone (-asarone).
Cultural symbolism

The calamus has long been a symbol of love. The name is associated with
a Greek myth: Kalamos, son of the river-godMaeander, who loved the
youth Karpos, of Zephyrus (the West Wind) and Chloris (Spring). When
Karpos drowned in a swimming race, Kalamos also drowned and was
transformed into a reed, whose rustling in the wind was interpreted as a
sigh of lamentation.
The plant was a favorite of Henry David Thoreau (who called it "sweet
flag"), and also of Walt Whitman, who added a section called the
"Calamus" poems, to the third edition of Leaves of Grass (1860). In the
poems the calamus is used as a symbol of love, lust, and affection.

The root of the calamus (Tamil vasambu ) is cut into disc-shaped

beads, and made into bracelets, which are typically worn by newborns for
the first few months. A vasambu bracelet is a symbol of a newborn baby in
Tamil culture.
Safety and Regulations

A. calamus and products derived from A. calamus (such as its oil) were
banned from use as human food or as a food additive in 1968 by the United
States Food and Drug Administration. The FDA ban was the result of lab
studies that involved supplementing the diets of lab animals over a
prolonged period of time with massive doses of isolated chemicals (asarone) from the Indian Jammu strain of calamus. The animals developed
tumors, and the plant was labeled procarcinogenic. Wichtl says "It is not
clear whether the observed carcinogenic effects in rats are relevant to the
human organism." However, most sources advise caution in ingesting
strains other than the diploid strain.
In reality -asarone is neither hepatotoxic nor directly hepatocarcinogenic.
It must first undergo metabolic l'-hydroxylation in the liver before achieving
toxicity. Cyrochrome P450 in the hepatocytes is responsible for secreting
the hydrolyzing enzymes that convert -asarone into genotoxic epoxide
structure.[56] Even with the activation of these metabolites, the carcinogenic
potency is very low due to the rapid breakdown of epoxide residues with
hydrolase which leaves these compounds inert Additionally, the major
metabolite of -asarone is 2,4,5-trimethoxycinnamic acid, a derivative
which is not a carcinogen.
Description
Calamus is found all over the world. It is a semi-aquatic perennial, which is
cultivated in damp marshy places in India and Burma. The plant is big in
size, with leaves in the shape of sword and yellow-green in color. Calamus
is quite common in Manipur and the Naga Hills of India and is found on the
edges of lakes and streams. The root of the plant has anodyne,
aphrodisiac, aromatic, carminative, diaphoretic, emmenagogue,

expectorant, febrifuge, hallucinogenic, hypotensive, sedative, stimulant,

stomachic, mildly tonic and vermifuge properties.
Uses & Benefits of Calamus
Calamus is a greatly valued herb in unani, as its stimulating aroma
rejuvenates the brain and the nervous system. It is also effective against
digestive disorders.
The root of the plant is internally used to treat bronchitis, sinusitis etc. It has
the wonderful power of stimulating and normalizing the appetite. In small
doses, it also serves to reduce stomach acidity. Larger doses increase
stomach secretions.
The plant is externally used to treat skin eruptions, rheumatic pains and
neuralgia.
It is also believed to remedy arthritis, cancer, convulsions, diarrhoea,
dyspepsia, epilepsy etc.
Chewing the root of calamus helps fight tobacco addiction. It kills the taste
for tobacco over time.
The root is also used to make a type of tea. Warm calamus tea works to
soothe sore throat, when drunk warm or gargled with.
A homeopathic remedy is made from the roots of the plant, which is used to
treat flatulence, dyspepsia, anorexia and disorders of the gall bladder.
It serves as a nauseant, stomachic, anthelmentic, stimulants, emetic,
expectorant, carminative, antispasmodic and nervine sedative.
Due to its aroma, calamus is also used to make essential oil. The calamus
essential oil is much valued in the perfume industry.
The herb was added to wine in Europe. The root of the plant is also one of
the possible ingredients of absinthe.

The northern Native Americans use the herb for medical purposes as well
as a stimulant. The root is believed to be used as entheogen among them.
However, higher doses can be hallucinogenic.
Steaming the root of calamus throughout the home is believed by many to
cure certain types of sickness.
Teton-Dakota warriors used to chew the roots of this herb to make a paste,
which they rubbed on their faces. They believed it would prevent
excitement and fear, while facing an enemy.
Caution
Large doses of the distilled essential oil made from calamus can cause mild
hallucinations.

Daucus carota

Scientific
classification
Kingdom: Plantae
(unranke Angiosper
d):
ms
(unranke Eudicots
d):
(unranke Asterids
d):

Order:

Apiales

Family:

Apiaceae

Genus:

Daucus

Species: D. carota
Trinomial name
Daucus
carota subsp. sativu
s
(Hoffm.) Schbl. & G
. Martens
The (Daucus carota subsp. sativus) is a root vegetable, usually orange in
colour, though purple, red, white, and yellow varieties exist.
It has a crisp texture when fresh. The most commonly eaten part of a carrot
is ataproot, although the greens are sometimes eaten as well. It is a
domesticated form of the wild carrot Daucus carota, native to Europe and
southwestern Asia. The domestic carrot has been selectively bred for its
greatly enlarged and more palatable, less woody-textured edible taproot.
The Food and Agriculture Organization of the United Nations (FAO) reports
that world production of carrots and turnips (these plants are combined by
the FAO for reporting purposes) for calendar year 2011 was almost 35.658
million tonnes. Almost half were grown in China. Carrots are widely used in
many cuisines, especially in the preparation of salads, and carrot
salads are a tradition in many regional cuisines.
Contents
1 Etymology
2 History
3 Description

4 Chemistry
5 Nutrition
6 Methods of consumption and uses
6.1 Companion plant
7 Cultivation
7.1 Cultivation problems
8 Cultivars
9 Production trends
10 Storage

Etymology

The word is first recorded in English around 1530 and was borrowed
from Middle French carotte,[1] itself from Late Latincarta,
from Greek karton, originally from the IndoEuropean root *ker- (horn), due to its horn-like shape. In Old English,
carrots (typically white at the time) were not clearly distinguished
from parsnips, the two being collectively calledmoru or more (from ProtoIndo-European *mork- "edible root", cf. German Mhre).
History
The wild ancestors of the carrot are likely to have come
from Persia (regions of which are now Iran and Afghanistan), which remain
the centre of diversity of Daucus carota, the wild carrot. A naturally
occurring subspecies of the wild carrot, Daucus carota subsp. sativus, has
been selectively bred over the centuries to reduce bitterness, increase
sweetness and minimise the woody core. This has produced the familiar
garden vegetable.

When they were first cultivated, carrots were grown for their aromatic
leaves and seeds rather than their roots. Carrot seeds have been found
in Switzerland and Southern Germany dating to 20003000 BC. Some
close relatives of the carrot are still grown for their leaves and seeds, for
example parsley, fennel, dill and cumin. The first mention of the root in
classical sources is during the 1st century. The plant appears to have been
introduced into Europe via Spain by the Moors in the 8th century. and in the
10th century, in such locations in West Asia, India and Europe, the roots
were purple. The modern carrot originated in Afghanistan at about this
time. The Jewish scholar Simeon Seth describes both red and yellow
carrots in the 11th century. The 12th-century
Arab Andalusian agriculturist, Ibn al-'Awwam, also mentions roots of these
colours; Cultivated carrots appeared in China in the 14th century, and in
Japan in the 18th century. Orange-coloured carrots appeared in
the Netherlands in the 17th century,[11] which has been related to the fact
that the Dutch flag at the time, the Prince's Flag, included orange. These,
the modern carrots, were intended by the antiquary John Aubrey (1626
1697) when he noted in his memoranda "Carrots were first sown at
Beckington in Somersetshire. Some very old Man there [in 1668] did
remember their first bringing hither."[ European settlers introduced the
carrot to Colonial America in the 17th century.
Purple carrots, still orange on the inside, were sold in British stores starting
in 2002.
Description
Daucus carota is a biennial plant that grows a rosette of leaves in the
spring and summer, while building up the stout taproot that stores large
amounts of sugars for the plant to flower in the second year.

Seedlings shortly after germination

Soon after germination, carrot seedlings show a distinct demarcation
between the taproot and the stem. The latter is thicker and lacks lateral
roots. At the upper end of the stem is the seed leaf. The first true leaf
appears about 1015 days after germination. Subsequent leaves, produced
from the stem nodes, are alternating(with a single leaf attached to a node,
and the leaves growing in alternate directions) and compound,
and arranged in a spiral. The leaf blades are pinnate. As the plant grows,
the bases of the seed leaves are pushed apart. The stem, located just
above the ground, is compressed and the internodes are not distinct. When
the seed stalk elongates, the tip of the stem narrows and becomes pointed,
extends upward, and becomes a highly branched inflorescence. The stems
grow to 60200 cm (2080 in) tall.
Most of the taproot consists of a pulpy outer cortex (phloem) and an inner
core (xylem). High-quality carrots have a large proportion of cortex
compared to core. Although a completely xylem-free carrot is not possible,
some cultivars have small and deeply pigmented cores; the taproot can
appear to lack a core when the colour of the cortex and core are similar in
intensity. Taproots typically have a long conical shape, although cylindrical
and round cultivars are available. The root diameter can range from 1 cm
(0.4 in) to as much as 10 cm (4 in) at the widest part. The root length
ranges from 5 to 50 cm (2.0 to 19.7 in), although most are between 10 and
25 cm (4 and 10 in).

Daucus carota umbel (inflorescence). Individual flowers are borne on

undivided pedicels originating from a common node.

Top view of Daucus carotainflorescence, showing umbellets

Flower development begins when the flat meristem changes from
producing leaves to an uplifted, conical meristem capable of producing
stem elongation and an cluster of flowers. The cluster is a
compound umbel, and each umbel contains several smaller umbels
(umbellets). The first (primary) umbel occurs at the end of the main floral
stem; smaller secondary umbels grow from the main branch, and these
further branch into third, fourth, and even later-flowering umbels. A large,
primary umbel can contain up to 50 umbellets, each of which may have as
many as 50 flowers; subsequent umbels have fewer flowers. Flowers are
small and white, sometimes with a light green or yellow tint. They consist of
five petals, five stamens, and an entire calyx. The stamens usually splitand
the stamens fall off before the stigma becomes receptive to receive pollen.
The stamens of the brown, male, sterile flowers degenerate and shrivel
before the flower fully opens. In the other type of male sterile flower, the
stamens are replaced by petals, and these petals do not fall off. A nectarcontaining disc is present on the upper surface of the carpels.

Flowers consist of five petals, five stamens, and an entire calyx.

Flowers change sex in their development, so the stamens release their
pollen before the stigma of the same flower is receptive. The arrangement
is centripetal, meaning the oldest flowers are near the edge and the
youngest flowers are in the center. Flowers usually first open at the outer
edge of the primary umbel, followed about a week later on the secondary
umbels, and then in subsequent weeks in higher-order umbels. The usual
flowering period of individual umbels is 7 to 10 days, so a plant can be in
the process of flowering for 3050 days. The distinctive umbels and
floral nectaries attract pollinatinginsects. After fertilization and as seeds
develop, the outer umbellets of an umbel bend inward causing the umbel
shape to change from slightly convex or fairly flat to concave, and when
cupped it resembles a bird's nest.
The fruit that develops is a schizocarp consisting of two mericarps; each
mericarp is a true seed. The paired mericarps are easily separated when
they are dry. Premature separation (shattering) before harvest is
undesirable because it can result in seed loss. Mature seeds are flattened
on the commissuralside that faced the septum of the ovary. The flattened
side has five longitudinal ribs. The bristly hairs that protrude from some ribs
are usually removed by abrasion during milling and cleaning. Seeds also
contain oil ducts and canals. Seeds vary somewhat in size, ranging from
less than 500 to more than 1000 seeds per gram.

The carrot is a diploid species, and has nine relatively short, uniformlength chromosomes (2n=9). The genome size is estimated to be 473
mega base pairs, which is four times larger than Arabidopsis thaliana, onefifth the size of the maize genome, and about the same size as the rice
genome.
Chemistry

-Carotene structure. Carotene is responsible for the orange colour of

carrots and many other fruits and vegetables.
Polyacetylenes can be found in Apiaceae vegetables like carrots where
they show cytotoxic activities.[16][17] Falcarinol and falcarindiol (cisheptadeca-1,9-diene-4,6-diyne-3,8-diol) are such compounds. This latter
compound shows antifungal activity towards Mycocentrospora
acerina and Cladosporium cladosporioides. Falcarindiol is the main
compound responsible for bitterness in carrots.
Other compounds such as pyrrolidine (present in the leaves), 6hydroxymellein, 6-methoxymellein, eugenin, 2,4,5-trimethoxybenzaldehyde
(gazarin) or (Z)-3-acetoxy-heptadeca-1,9-diene-4,6-diin-8-ol (falcarindiol 3acetate) can also be found in carrot.
Nutrition

The carrot gets its characteristic, bright orange colour from -carotene, and
lesser amounts of -carotene, -carotene, lutein and zeaxanthin. - and carotenes are partly metabolized into vitamin A, providing more than 100%
of the Daily Value (DV) per 100 g serving of carrots (right table). Carrots
are also a good source of vitamin K (13% DV) and vitamin B6 (11% DV),
but otherwise have modest content of other essential nutrients (right table).
Carrots are 88% water, 4.7% sugar, 2.6% protein, 1% ash, and 0.2% fat.
Carrot dietary fiber comprises mostly cellulose, with smaller proportions

ofhemicellulose, lignin and starch. Free sugars in carrot

include sucrose,glucose and fructose.
The lutein and zeaxanthin carotenoids characteristic of carrots are under
study for their potential roles in vision and eye health.
Methods of consumption and uses

it can be eaten in a variety of ways. Only 3 percent of the -carotene in raw

carrots is released during digestion: this can be improved to 39% by
pulping, cooking and adding cooking oil. [28] Alternatively they may be
chopped and boiled, fried or steamed, and cooked in soups and stews, as
well as baby and pet foods. A well-known dish is carrots julienne. Together
with onionand celery, carrots are one of the primary vegetables used in
a mirepoix to make various broths.
The greens are edible as a leaf vegetable, but are only occasionally eaten
by humans; some sources suggest that the greens contain toxicalkaloids.
When used for this purpose, they are harvested young in high-density
plantings, before significant root development, and typically used stir-fried,
or in salads. Some people are allergic to carrots. In a 2010 study on the
prevalence of food allergies in Europe, 3.6 percent of young adults showed
some degree of sensitivity to carrots. Because the major carrot allergen,
the protein Dauc c 1.0104, is cross-reactive with homologues
in birch pollen (Bet v 1) and mugwort pollen (Art v 1), most carrot allergy
sufferers are also allergic to pollen from these plants.
In India carrots are used in a variety of ways, as salads or as vegetables
added to spicy rice or dal dishes. A popular variation in north India is
the Gajar Ka Halwa carrot dessert, which has carrots grated and cooked in
milk until the whole mixture is solid, after which nuts and butter are added.
Carrot salads are usually made with grated carrots with a seasoning of
mustard seeds and green chillies popped in hot oil. Carrots can also be cut
in thin strips and added to rice, can form part of a dish of mixed roast
vegetables or can be blended with tamarind to make chutney.

Since the late 1980s, baby carrots or mini-carrots (carrots that have been
peeled and cut into uniform cylinders) have been a popular ready-toeat snack food available in many supermarkets. Carrots are pured and
used as baby food,dehydrated to make chips, flakes, and powder, and
thinly sliced and deep-fried, likepotato chips.
The sweetness of carrots allows the vegetable to be used in some fruit-like
roles. Grated carrots are used in carrot cakes, as well as carrot puddings,
an English dish thought to have originated in the early 19th century. Carrots
can also be used alone or with fruits in jam and preserves. Carrot juice is
also widely marketed, especially as a health drink, either stand-alone or
blended with fruits and other vegetables.
Companion plant
Carrots are useful companion plants for gardeners. The pungent odour of
onions, leeks and chives help repel the carrot root fly, and other vegetables
that team well with carrots include lettuce, tomatoes and radishes, as well
as the herbsrosemary and sage.. Carrots thrive in the presence
of caraway, coriander, chamomile, marigold and Swan River daisy. If left to
flower, the carrot, like any umbellifer, attracts predatory wasps that kill
many garden pests.
Cultivation

Workers harvesting carrots, Imperial Valley, California, 1948

Carrots are grown from seed and take around four months to mature. They
grow best in full sun but tolerate some shade. The optimum growth
temperature is between 16 and 21 C (61 and 70 F). The ideal soil is

deep, loose and well-drained, sandy or loamy and with a pH of 6.3 to

6.8. Fertiliser should be applied according to soil type and the crop requires
low levels of nitrogen, moderate phosphate and high potash. Rich soils
should be avoided, as these will cause the roots to become hairy and
misshapen. Irrigation should be applied when needed to keep the soil moist
and the crop should be thinned as necessary and kept weed free.
Cultivation problems
See also: List of carrot diseases
There are several diseases that can reduce the yield and market value of
carrots. The most devastating carrot disease isAlternaria leaf blight, which
has been known to eradicate entire crops. A bacterial leaf blight caused
by Xanthomonas campestris can also be destructive in warm, humid areas.
Root knot nematodes (Meloidogyne species) can cause stubby or forked
roots, or galls. Cavity spot, caused by the oomycetes Pythium
violae and Pythium sulcatum, results in irregularly shaped, depressed
lesions on the taproots.[
Physical damage can also reduce the value of carrot crops. The two main
forms of damage are splitting, whereby a longitudinal crack develops during
growth that can be a few centimetres to the entire length of the root, and
breaking, which occurs postharvest. These disorders can affect over 30%
of commercial crops. Factors associated with high levels of splitting include
wide plant spacing, early sowing, lengthy growth durations, and genotype.
Cultivars

Carrot seeds

Daucus carota subsp. maximus -MHNT

Carrot cultivars can be grouped into two broad classes, eastern

carrots andwestern carrots. A number of novelty cultivars have been bred
for particular characteristics.
The city of Holtville, California, promotes itself as "Carrot Capital of the
World", and holds an annual festival devoted entirely to the carrot.
"Eastern" (a European and American continent reference) carrots were
domesticated in Persia (probably in the lands of modernday Iran and Afghanistanwithin West Asia) during the 10th century, or
possibly earlier. Specimens of the "eastern" carrot that survive to the
present day are commonly purple or yellow, and often have branched roots.
The purple colour common in these carrots comes
fromanthocyanin pigments.
The western carrot emerged in the Netherlands in the 17th century, There
is a popular belief that its orange colour making it popular in those
countries as an emblem of the House of Orange and the struggle for Dutch
independence, although there is little evidence for this. The orange colour
results from abundantcarotenes in these cultivars.
Western carrot cultivars are commonly classified by their root shape. The
four general types are:
Chantenay carrots. Although the roots are shorter than other cultivars, they
have vigorous foliage and greater girth, being broad in the shoulders and
tapering towards a blunt, rounded tip. They store well, have a pale-coloured
core and are mostly used for processing. Varieties include Carson Hybrid
and Red Cored Chantenay.
Danvers carrots. These have strong foliage and the roots are longer than
Chantaney types, and they have a conical shape with a well-defined
shoulder, tapering to a point. They are somewhat shorter than Imperator
cultivars, but more tolerant of heavy soil conditions. Danvers cultivars store
well and are used both fresh and for processing. They were developed in
1871 in Danvers, Massachusetts. Varieties include Danvers Half Long and
Danvers 126.

Imperator carrots. This cultivar has vigorous foliage, is of high sugar

content, and has long and slender roots, tapering to a pointed tip. Imperator
types are the most widely cultivated by commercial growers. Varieties
include Imperator 58 and Sugarsnax Hybrid.
Nantes carrots. These have sparse foliage, are cylindrical, short with a
more blunt tip than Imperator types, and attain high yields in a range of
conditions. The skin is easily damaged and the core is deeply pigmented.
They are brittle, high in sugar and store less well than other types. Varieties
include Nelson Hybrid, Scarlet Nantes and Sweetness Hybrid.
One particular variety lacks the usual orange pigment due to carotene, and
owing its white colour to a recessive gene fortocopherol (vitamin E).
Derived from Daucus carota L. and patented at the University of
WisconsinMadison, the variety is intended to supplement the dietary
intake of Vitamin E.

Carrots come in a wide variety of shapes, colours and sizes.

Carrots with multiple taproots (forks) are not specific cultivars but are a
byproduct of damage to earlier forks often associated with rocky soil.

Carrots can beselectively bred to produce different colours.

Carrots of Kodaikanal
Production trends

Carrot and turnip output in 2005. Green: largest producer (China). Yellow:
other major producers. Red: minor producers.
Carrot is one of the ten most economically important vegetables crops in
the world. In 2012, according to the Food and Agriculture Organization of
the United Nations, 36.917 million tonnes of carrots and turnips were
produced worldwide for human consumption, grown on 1,196,000 hectares
(2,955,000 acres) of land. With a total production of 16.907 million
tonnes, China was by far the largest producer and accounted for 45.8% of
the global output, followed by Russia (1.57 million tonnes), the United
States (1.346), Uzbekistan (1.300), Ukraine (0.916), Poland (0.835), and
the United Kingdom (0.664). About 62% of world carrot production occurred
in Asia, followed by Europe (22.6%) and the Americas (North, Central, and
South America and the Caribbean) (9.4%). Less than 6% of the world's
2012 total production was grown in Africa. Global production has increased
from 21.4 million tonnes in 2000, 13.7 million tonnes in 1990, 10.4 million
tonnes in 1980, and 7.85 million tonnes in 1970. The rate of increase in the
global production of carrots has been greater than the world's population
growth rate, and greater than the overall increase in world vegetable
production. Europe was traditionally the major centre of production, but was
overtaken by Asia in 1997. The growth in global production is largely the
result of increases in production area rather than improvements in yield.
Modest increases in the latter can be attributed to optimised agricultural

practices, the development of better cultivars (including hybrids), and

increased farmmechanisation.
Storage

Carrots ready for purchase.

Carrots can be stored for several months in the refrigerator or over winter in
a moist, cool place. For long term storage, unwashed carrots can be placed
in a bucket between layers of sand, a 50/50 mix of sand and wood
shavings, or in soil. A temperature range of 32 to 40 F (0 to 5 C) is best.
Balchad or Nardostachys Jatamansir

Musk Root, Indian Spikenard, Indian Nard

Latin Name: Nardostachys jatamansi DC.

(Valerianaceae)
Sanskrit/Indian name: Jatamansi, Bhutajata,
Tapasvini, Jatamansi, Bal-chad
General information:
The therapeutic benefits of Musk Root have been documented in
various Ayurvedic texts. The herb is recommended for combating
stress and insomnia. It is also known to enhance memory and
treat mental instability. Cardiotonic properties have also been
attributed to Musk Root.
Therapeutic constituents:
The oil of Musk Root contains dnardostachone, valeranone and
jatamansone as the major ketonic sesquiterpenes. These
components give the herb its central tranquilizer and sedative

properties.
Key therapeutic benefits:
As a tranquilizer, sedative and central nervous system
depressant, Musk Root is used to treat stress and nervine
disorders.
It is also known to treat irregular heart palpitations and as a
remedy for high blood pressure.
History
It has been in use among the Indians as a perfume and medicine
from ancient times. It is mentioned by Susruta in a prescription
for epilepsy and is prescribed by Indian physicians as a nervine
tonic, carminative and aromatic adjunct in the preparation of
medicinal oils and ghees. N.jatamansi is the Nardin of
Dioscorides, which the writer tells us, was also called Gangitis
because the Ganges flowed from the foot of the mountains where
the plant grew.
Arabic and Persian physicians call this plant Sumbul-i-Hindi,
"Indian Spike", to distinguish it from their Sumbul-i-Rumi or Ikliti
(Valeriana celtica), the root of which is used in Turkey and Egypt
as a perfume.
Habitat
It grows in the alpine Himalayas from Punjab to Sikkim
and Bhutan, at altitudes of between 3,000 and 5,000
m.
Morphology Description (Habit)
N.jatamansi is an erect perennial herb, with a long, stout and
woody rootstock. Its radical leaves are elongate and spathulate,
its cauline leaves are sessile and oblong or sub-ovate; the flowers

are rosy, pale pink or blue, in dense cymes. The drug consists of
short, thick, dark grey rhizomes crowned with reddish brown
tufted fibrous remains of the petioles of the radical leaves.
Principal Constituents

Jatamansone, Jatamanshic acid, Virolin and its diastereomer.

Pharmacology
The mucilaginous seeds are emollients and demulcents. The
mucilage has shown anticomplementary activity in human serum
and hypoglycemic activity in mice.
Indications

Traditionally the drug has been used as a herbal CNS drug in

epilepsy, hysteria, and convulsions. The oil possesses
antiarrhythmic activity with possible therapeutic usefulness in
cases of auricular flutter.

Nardostachys jatamansi
Spikenard

Scientific classification
Kingdom: Plantae
(unranked Angiosperm
):
s
(unranked Eudicots
):
(unranked Asterids
):
Order:

Dipsacales

Family:

Caprifoliace
ae

Genus:

Nardostachy
s

Species:

N. jatamansi

Binomial name
Nardostachys jatamansi
(D.Don) DC.
Synonyms[1]
Fedia grandiflora Wall.
ex DC., nom. inval.
Fedia jatamansi Wall.
ex DC., nom. inval.
Nardostachys
chinensis Batalin
Nardostachys
grandiflora DC.
Patrinia
jatamansi D.Don
Valeriana
jatamansi D.Don, nom.
illeg.
Nardostachys jatamansi is a flowering plant of the Valerian family that
grows in theHimalayas. It is a source of a type of intensely aromatic ambercolored essential oil,spikenard. The oil has, since ancient times, been used
as a perfume, as a medicine and in religious contexts. It is also
called spikenard, nard, nardin, or muskroot.
Contents
1 Description
2 Phytochemistry

3 Historical use

Description

Nardostachys jatamansi is a flowering plant of the honeysuckle family that

grows in the eastern Himalayas, primarily in a belt
through Kumaon, Nepal, Sikkim andBhutan.[2] The plant grows to about 1 m
in height and has pink, bell-shaped flowers. It is found in the altitude of
about 30005000 meters. Rhizomes (underground stems) can be crushed
and distilled into an intensely aromatic amber-coloredessential oil, which is
very thick in consistency. Nard oil is used as a perfume, anincense,
a sedative, and an herbal medicine said to fight insomnia, birth difficulties,
and other minor ailments.
Phytochemistry

The chemical components of Nardostachys jatamansi have

been assayed in a number of different studies. These compounds include:
acaciin
ursolie acid
octacosanol
kanshone A
nardosinonediol
nardosinone
aristolen-9beta-ol
oleanolic acid
beta-sitosterol
Historical use[edit]
Spikenard

Nardostachys jatamansi may have been used as an ingredient in the

incense known as spikenard, although lavender has also been suggested
as a candidate for the spikenard of classical times .
pikenard, also called nard, nardin, and muskroot, is a class of aromatic
amber-colored essential oil derived fromNardostachys jatamansi,
a flowering plant of the Valerian family which grows in
the Himalayas of Nepal, China, and India. The oil has, since ancient times,
been used as a perfume, as a medicine and in religious contexts, across a
wide territory from India to Europe.
The Bible contains several references to the spikenard, in both the Old
Testament and the New Testament, and it is used inCatholic iconography to
represent Saint Joseph. With this meaning, Pope Francis has included the
spikenard in his coat of arms.
Contents
1 Plant sources
2 Historical use
3 Religious references
3.1 The Bible
3.2 Catholic Church

Plant sources

Nardostachys jatamansi is a flowering plant of the Valerian family that

grows in the Himalayas of Nepal, China, and India. The plant grows to
about 1 meter (3 ft) in height and has pink, bell-shaped flowers. It is found
in the altitude of about 3,000 to 5,000 m (9,800 to
16,400 ft). Rhizomes (underground stems) can be crushed and distilled into
an intensely aromatic amber-colored essential oil, which is very thick in
consistency. Nard oil is used as a perfume, an incense, a sedative, and

anherbal medicine said to fight insomnia, birth difficulties, and other minor
ailments.
Lavender (genus Lavandula) was also known by the ancient
Greeks as nardos, nard, after the Sanskrit "narada" or "nalada".
Historical use

The oil was known in ancient times and was part of the unani herbal
tradition of India. It was obtained as a luxury in ancient Egypt, the Near
East. In Rome, it was the main ingredient of the
perfume nardinum (O.L. nladam), derived from the Hebrew
(shebolet nerd, head of nard bunch), which was part of the Ketoret used
when referring to the consecrated incense described in the Hebrew
Bible and Talmud. It is also referred to as the HaKetoret (the incense).

Spikenard (Nardostachys jatamansi) essential oil in a clear glass vial

It was offered on the specialized incense altar in the time when
the Tabernacle was located in theFirst and Second Jerusalem Temples.
The ketoret was an important component of the Temple service
in Jerusalem. Nard is mentioned a number of times in the Tanakh, and as
part of incense in reference to hilchot shabbat in Tractate Shabbat 78b as
well as Maimonides Hilchot Shabbat 18:16. It is mentioned twice in
the Song of Solomon (1:12 and 4:13).
Nard was used to perfume the body of Patroklos by Achilles in Book 18 of
Homer's Iliad. Pliny's Natural History lists twelve species of "nard",
identifiable with varying assurance, includingLavandula stoechas and

tuberous valerian as well as true nard (in modern terms Nardostachys

jatamansi).
It was a common flavouring in Ancient Roman foods and occurs frequently
in the recipes ofApicius, though it tends to be used sparingly.
Spikenard was used to season foods in Medieval European cuisine,
especially as a part of the spice blend used to flavor Hypocras, a
sweetened and spiced wine drink. From the 17th century it was one of the
ingredients for a strong beer called Stingo.
The ancient Greeks called the lavender herb nardus, after the Syrian city of
Naarda (possibly the modern town of Dohuk, Iraq). It was also commonly
called nard. The species originally grown was L. stoechas.
Religious references

The Bible
In the New Testament John 12:110, six days before the passover Jesus
arrives in Bethany. In Bethany, Mary, sister of Lazarus uses a pint of pure
nard to anoint Jesus's feet. Judas Iscariot, the keeper of the money-bag,
asked why the ointment was not sold for three hundred denarii instead
(about a year's wages, as the average agricultural worker received one
denarius for 12 hours work: Matthew 20:2) and the money given to the
poor. Two passages in parallel (Matthew 26:613, and Mark 14:39) speak
of an occasion two days before the passover, in which an unnamed woman
anoints Jesus's head. The costly perfume she used came from
an alabaster jar, and contained nard according to the passage in Mark.

Coat of Arms of Pope Francis. According to the Vatican, the flowering plant
is a representation of the spikenard and symbolises St Joseph
In the Song of Songs (Song of Solomon) 4:13-14, the bridegroom sings of
spikenard:

Your plants are an orchard of pomegranates

With pleasant fruits,
Fragrant henna with spikenard,
spikenard and saffron,
calamus and cinnamon,
with every kind of incense tree,
with myrrh and aloes,
and all the finest spices.

Hepato protective,hepatic regenerative and metabolic regulators

Pistacia lentiscus
Pistacia lentiscus
Botanical Classification
Botanical classification
kingdom

Plantae

Division

magnoliophyta

Class

magnolipsida

Order

anacardiales

Family

anacardiaceae

Genus

Pistacia

Species

Lentiscus

Pistacia lentiscus

Family
Botanical anacardiaceae

Synonyms
English name mastic
Hindi name rumi mastagi
Sanskrit name- rumi mastagi
Gujarati name rumimastagi

Habitat

It is a native of south Europe and Northern Africa. It is found in Iran,

Afghanistan, and India.

Morphology

It is an evergreen creeper. Fruit is 4 to 5 mm, round in shape and is of

black in color. The trunk bears a gum that is known as rumi mastagi. It is
an aromatic substance that is present in the form of granules. It tastes
sweet and is slimy to touch.

Chemical Constituents

It contains volatile oil 1 to 3 %, mistkoresin, mistconic acid, misecolic acid

and a bitter substance. .

Pharmacology

It is an excellent anti inflammatory agent due to its hot potency. It helps in

regularizing the digestive tract and also maintains the normal peristaltic
movements as because of its light properties and hot potency. It also
expels out the unwanted mucus from our respiratory tract. It also acts as
a good aphrodisiac because of its sweet taste.

Toxicology

It is safe for human consumption when taken in normal dosage.

Plant part used

Extract or gum

Indication

Inflammation
Blood disorder
Hemorrhages
Wounds
Pains
Indigestion
Loss of appetite
Liver related problems
Abdominal distension
Dysurea
Impotence
Menstrual disturbances
Cough
Asthma

Uses

Oil and paste it is applied on the inflamed area. It is also applied on the
wounds for early healing. It is also effective in mouth related problems. It
also strengthens the gums and tooth. It also prevents hemorrhages.
Powder it is effective in treating digestive tract abnormalities. It also
stimulates liver for proper functioning. It is effective in respiratory
disorders. It normalizes the menses and works and an aphrodisiac agent.
It tones up the urinary tract.

Mastic gum is a resin obtained from the plant Pistacia

lentiscus Linn., an aromatic member of
the Anarcadiaceae family. It is a shrub or small tree indigenous
to Mediterranean areas specially Spain, Portugal, Morocco, Italy,
Greece, Turkey and southern France. It has been used in Unani
system of medicine since centuries for the treatment of various
ailments like gastrointestinal disturbances, hepatobiliary
disorders, gynaecological diseases etc. Pharmacological studies
reveal that it contains resins, volatile oils, bicyclic terpenoids,
fatty acids, saponins and sugars etc. Different experimental and
clinical researches evidenced its antimicrobial, antiinflammatory, antioxidant, antiatherogenic and wound healing
properties. The Present review is aimed to explore existing
Unani classical as well as modern literature available on Pistacia
lentiscus.
Key words: Antiatherogenic, Mastagi, Pistacia lentiscus, Unani

Pistacia lentiscus (also mastic; Greek: mastkha) is

a dioeciousevergreen shrub or small tree of the pistacio genus growing up

to 4 m (13 ft) tall which is cultivated for its aromatic resin, mainly on
the Greek island of Chios.[1]
Contents
1 Description
2 Distribution
3 Resin
3.1 Cultivation history
3.2 Uses
3.2.1 Culinary art
3.2.2 Medicine
3.2.3 Miscellanea
Description

Pistacia lentiscus is a shrub or dioecious tree, with separate male and

female plants, evergreen from 1 to 5 m high, with a strong smell of resin,
growing in dry and rocky areas in Mediterranean Europe. It resists heavy
frosts and grows on all types of soils, and can grow well in limestone areas
and even in salty or saline environments, making it more abundant near the
sea. It is also found in woodlands, dehesas (almost deforested pasture
areas), Kermes oak wood, oaks wood, garrigue, maquis, hills, gorges,
canyons, and rocky hillsides of the entire Mediterranean area. It is a very
typical species that grows in Mediterranean mixed communities of myrtle,
Kermes oak, Mediterranean dwarf palm, buckthorn, sarsaparilla, etc. and
serves as protection and food for birds and other fauna in this ecosystem. It
is a very hardy pioneer species dispersed by birds. When older, it develops
some large trunks and numerous thicker and longer branches. In
appropriate areas, when allowed to grow freely and age, it often becomes a

tree of up to 7 m. However, logging, grazing, and fires often prevent its

development.
The leaves are alternate, leathery, and compound paripinnate (no terminal
leaflet) with five or six pairs[2] of deep-green leaflets. It presents very small
flowers, the male with five stamens, the female trifid style. The fruit is
a drupe, first red and then black when ripe, about 4 mm in diameter.
In tourist areas, with palmitos or Mediterranean dwarf palm, and exotic
plants, it is often chosen to repopulate gardens and resorts, because of its
strength and attractive appearance. Unlike other species of Pistacia, it
retains its leaves throughout the year. It has been introduced as an
ornamental shrub in Mexico, where it has naturalized and is often seen
primarily in suburban and semiarid areas where the summer rainfall
climate, contrary to the Mediterranean, does not hurt it.
A related species, P. saportae, has been shown by DNA analysis[3] to be a
hybrid between maternal P. lentiscus and paternal P. terebinthus (terebinth
or turpentine). The hybrid has imparipinnate leaves, with leaflets
semipersistent, subsessile terminal, and sometimes reduced. Usually, P.
terebinthus and P. lentiscus occupy different biotopes and barely overlap:
Mastic appears at lower elevations and near the sea, while the P.
terebinthus most frequently inhabits inland and mountainous areas such as
the Iberian System.
Distribution
Pistacia lentiscus is native throughout the Mediterranean region,
from Morocco and Iberian peninsula in the west through
southern France and Turkey to Iraq and Iran in the east. It is also native to
the Canary Islands. The word mastic derives either from
the Greek verb mastichein ("to gnash the teeth", origin of the English
word masticate) or massein ("to chew").
Within the European Union, mastic production in Chios is granted protected
designation of origin and protected geographical indication names.
Although the tree is native to all of the Mediterranean region, only on

southern Chios is the mastic trees' bark scored to "weep" the masticha
resin. The island's mastic production is controlled by a cooperativeof medieval villages, collectively known as the 'Mastichochoria'
(), which are also located in the southern part of Chios.
Resin

Mastic (plant resin)

An old Pistacia Lentiscus tree in Fenerbahe Park, stanbul

The aromatic, ivory-coloured resin, also known as mastic, is harvested as
a spice from the cultivated mastic trees grown in the south of the Greek
island of Chios in theAegean Sea, where it is also known by the name
"Chios tears". Originally liquid, it is hardened, when the weather turns cold,
into drops or patties of hard, brittle, translucentresin. When chewed, the
resin softens and becomes a bright white and opaque gum.
Cultivation history
The resin is collected by bleeding the trees from small cuts made in
the bark of the main branches, and allowing the sap to drip onto the
specially prepared ground below. The harvesting is done during the
summer between June and September. After the mastic is collected, it is
washed manually and is set aside to dry, away from the sun, as it will start
melting again.

Mastic shrub
Mastic resin is a relatively expensive kind of spice; it has been used
principally as a chewing gum for at least 2,400 years. [8] The flavour can be
described as a strong, slightly smoky, resiny aroma and can be an acquired
taste.
Some scholars[9] identify the bakha mentioned in the Bibleas in
the Valley of Baca (Hebrew: ) of Psalm 84 - with the mastic plant.
The word bakhaappears to be derived from the Hebrew word for crying or
weeping, and is thought to refer to the "tears" of resin secreted by the
mastic plant, along with a sad weeping noise which occurs when the plant
is walked on and branches are broken. The Valley of Baca is thought to be
a valley near Jerusalem that was covered with low mastic shrubbery, much
like some hillsides in northern Israel today. In an additional biblical
reference, King David receives divine counsel to place himself opposite
thePhilistines coming up the Valley of Rephaim, southwest of Jerusalem,
such that the "sound of walking on the tops of the bakha shrubs" (
) signals the moment to attack (II Samuel V: 2224).
Mastic is known to have been popular in Roman times when children
chewed it, and in Medieval times, it was highly prized for
the Sultan's harem both as a breath freshener and for cosmetics. It was the
Sultan's privilege to chew mastic, and it was considered to have healing

properties. The spice's use was widened when Chios became part of
the Ottoman Empire, and it remains popular in North Africa and the Near
East.
The Mastichochoria (mastic-producing villages) are located in the southern
part of Chios.
Uses

Culinary art
Mastic gum is principally used either as a flavouring or for its gum
properties, as in mastic chewing gum.
As a spice, it continues to be used in Greece to flavour spirits
and liquors (such as Chios's native drinks
of Mastichato andmastica), chewing gum, and a number of cakes,
pastries, spoon sweets, and desserts. Sometimes it is even used in making
cheese.[7] Mastic resin is a key ingredient in dondurma (Turkish ice cream)
and Turkish puddings, giving those confections their unusual texture and
bright whiteness. In Lebanon and Egypt, the spice is used to flavour many
dishes, ranging from soups to meats to desserts, while in Morocco, smoke
from the resin is used to flavour water. In Turkey, mastic is used as a flavor
of Turkish delight. Recently, a mastic-flavoured fizzy drink has also been
launched, called "Mast".
Mastic resin is a key ingredient in Greek festival breads, for example, the
sweet bread tsoureki and the traditional New Year's vasilopita.
Furthermore, mastic is also essential to myron, the holy oil used
for chrismation by the Orthodox Churches.
As well as its culinary uses, mastic continues to be used for its gum and
medicinal properties. The resin is used as a primary ingredient in the
production of cosmetics such as toothpaste, lotions for the hair and skin,
and perfumes.

Mastic resin
Medicine
People in the Mediterranean region have used mastic as a medicine
forgastrointestinal ailments for several thousand years. The first-century
Greekphysician and botanist, Dioscorides, wrote about the medicinal
properties of mastic in his classic treatise De Materia Medica ("About
Medical Substances"). Some centuries later, Markellos Empeirikos and
Pavlos Eginitis also noticed the effect of mastic on the digestive system.
Regular consumption of mastic has been proven to absorb cholesterol,
thus easing high blood pressure and reducing the risk of heart
attacks. Mastic oil also has antibacterial and antifungal properties, and as
such is widely used in the preparation of ointments for skin disorders and
afflictions. It is also used in the manufacture of plasters.
In recent years, university researchers have provided the scientific
evidence for the medicinal properties of mastic. A 1985 study by
the University of Thessaloniki and by the Meikai University discovered that
mastic can reduce bacterial plaque in the mouth by 41.5%. A 1998 study by
the University of Athens found that mastic oil
has antibacterial and antifungalproperties. Another 1998 University of
Nottingham study, claims that mastic can heal peptic ulcers by
killing Helicobacter pylori, which causes peptic ulcers, gastritis,
and duodenitis. Some in vivo studies have shown that mastic gum has no
effect on H. pylori when taken for short periods of time. However, a recent
and more extensive study showed that mastic gum reduced H.
pylori populations after an insoluble and sticky polymer (poly--myrcene)

constituent of mastic gum was removed and taken for a longer period of
time. Further analysis showed the acid fraction was the most active
antibacterial extract, and the most active pure compound was
isomasticadienolic acid.[12]
A balm was created from the mastic tree resin for use by physicians
in Biblical times. American slaves took the reference inJeremiah 8:22 to
the balm of Gilead to refer to Jesus Christ in the spiritual hymn, There is a
Balm in Gilead.
Miscellaneas
Apart from its medicinal properties and cosmetic and culinary uses, mastic
gum is also used in the production of high-gradevarnish.
The mastic tree has been introduced into Mexico as an ornamental plant,
where it is very prized and fully naturalized. The trees are grown mainly
in suburban areas in semiarid zones, and remain undamaged, although the
regime of summer rainfall is contrary to its original Mediterranean climate.
Andropogon schoenanthus
Uses

Andropogon schoenanthus Linn. Gramineae. Camel's Hay.

Geranium Grass. Lemon Grass. Oil-Plant.
Asia, African tropics and subtropics. This species is commonly
cultivated for the fine fragrance of the leaves which are often
used for flavoring custard. When fresh and young, the leaves are
used in many parts of the country as a substitute for tea and the
white center of the succulent leaf-culms is used to impart a flavor
to curries. The tea made of this grass is considered a wholesome
and refreshing beverage, says Wallich, and her Royal Majesty was
supplied with the plant from the Royal Gardens, Kew, England.

It is widely used as a culinary herb in Asian cuisine and also as medicinal

herb in India. It has a subtle citrus flavor and can be dried and powdered,
or used fresh. It is commonly used in teas, soups, and curries. It is also
suitable for use with poultry, fish, beef, and seafood. It is often used as a
tea in African countries such asTogo and the Democratic Republic of the
Congo and Latin American countries such as Mexico. Lemongrass oil is
used as a pesticide and a preservative. Research shows that lemongrass
oil has antifungal properties. Despite its ability to repel insects, its oil is
commonly used as a "lure" to attract honey bees. "Lemongrass works
conveniently as well as the pheromone created by the
honeybee's Nasonovgland, also known as attractant pheromones. Because
of this, lemongrass oil can be used as a lure when trapping swarms or
attempting to draw the attention of hived bees.

C. citratus from the Philippines, where it is locally known as tanglad

Citronella grass (Cymbopogon nardus andCymbopogon winterianus) grow
to about 2 m (6.6 ft) and have magenta-colored base stems. These species
are used for the production of citronella oil, which is used in soaps, as
an insect repellent (especially mosquitoes)[11] in insect sprays and candles,
and in aromatherapy, which is famous inBintan Island, Indonesia, and
thePhilippines. Therefore, its origin is assumed to be Indonesia. The
principal chemical constituents of citronella, geranioland citronellol, are
antiseptics, hence their use in household disinfectants and soaps. Besides
oil production, citronella grass is also used for culinary purposes, as a
flavoring.
Citronella is usually planted in home gardens to ward off insects such
as whiteflyadults. Its cultivation enables growing some vegetables (e.g.

tomatoes and broccoli) without applying pesticides. Intercropping should

include physical barriers, for citronella roots can take over the field.
Lemongrass oil, used as a pesticide and preservative, is put on the
ancient palm-leaf manuscripts found in India as a preservative. It is used at
the Oriental Research Institute Mysore, the French Institute of Pondicherry,
the Association for the Preservation of the Saint Thomas Christian Heritage
in Kerala, and many other manuscript collections in India. The oil also
injects natural fluidity into the brittle palm leaves, and
the hydrophobic nature of the oil keeps the manuscripts dry so the text is
not lost to decay due to humidity.
East Indian lemon grass (Cymbopogon flexuosus), also called Cochin
grass or Malabar grass (Malayalam: (inchippullu), is native
to Cambodia, Vietnam, India, Sri Lanka, Burma, and Thailand, while West
Indian lemon grass (Cymbopogon citratus) is native to South
Asia and maritime Southeast Asia. It is known
as serai in Malaysia and Brunei, serai or sereh in Indonesia,
and salai or tanglad in the Philippines. While both can be used
interchangeably, C. citratus is more suitable for cooking. In India, C.
citratus is used both as a medical herb and in perfumes. C. citratus is
consumed as a tea for anxiety in Brazilian folk medicine, [14] but a study in
humans found no effect. The tea caused a recurrence of contact
dermatitis in one case.
Lemon grass is also known as gavati chaha ( ) in the Marathi
language (gavat = grass; chaha = tea), and is used as an addition to tea,
and in preparations such as kadha, which is a traditional herbal 'soup' used
against coughs, colds, etc. It has medicinal properties and is used
extensively in unani medicine. It is supposed to help with relieving cough
and nasal congestion.

Valeriana officinalis

Valerian (Valeriana officinalis, Caprifoliaceae) is a perennial flowering plant,

with heads of sweetly scented pink or white flowers that bloom in the
summer. Valerian flower extracts were used as a perfume in the 16th
century.
Native to Europe and parts of Asia, valerian has been introduced into North
America. The flowers are frequently visited by many fly species,
especially hoverflies of the genus Eristalis. It is consumed as food by
the larvae of some Lepidoptera (butterflyand moth) species including
the grey pug.
Other names used for this plant include garden valerian (to distinguish it
from other Valeriana species), garden heliotrope (although not related
to Heliotropium), and all-heal (which is also used for plants in the
genus Stachys). Red valerian, often grown in gardens, is also sometimes
referred to as "valerian", but is a different species (Centranthus ruber) from
the same family and not very closely related.
Crude extract of valerian root is sold as a dietary supplement in the form
of capsules. Valerian root may have sedative and anxiolytic effects.
The amino acid valine is named after this plant.
Contents
1 History
2 Etymology
3 Valerian extract
3.1 Biochemical composition
3.2 Mechanism of action
3.3 Preparation
3.4 Medicinal use

3.5 Regulation
3.6 Oral forms, usage, and adverse effects
3.6.1 Oral forms
3.6.2 Adverse effects
4 Effect on other organisms
5 Floral symmetry

History

19th-century illustration ofValeriana officinalis

Close up of valerian foliage

Valerian has been used as a medicinal herb since at least the time of
ancient Greece and Rome. Hippocrates described its properties,
and Galen later prescribed it as a remedy for insomnia. In medieval
Sweden, it was sometimes placed in the wedding clothes of the groom to
ward off the "envy" of the elves. In the 16th century,
theAnabaptist reformer Pilgram Marpeck prescribed valerian tea for a sick
woman.
Etymology

The name of the herb is derived from the personal name Valeria and the
Latin verbvalere (to be strong, healthy).[4][5]
Valerian extract

Biochemical composition
Known compounds detected in valerian that may contribute to its method of
action are:
Alkaloids:
actinidine, chatinine, shyanthine,valerianine, and valerine
Isovaleramide may be created in the extraction process.[8]
Gamma-aminobutyric acid (GABA)
Isovaleric acid
Iridoids, including valepotriates: isovaltrate and valtrate [6]
Sesquiterpenes (contained in the volatile oil):
valerenic acid, hydroxyvalerenic acid and acetoxyvalerenic acid
Flavanones: hesperidin, 6-methylapigenin, and linarin.

Mechanism of action

Because of valerian's historical use as a sedative, antiseptic,

anticonvulsant, migraine treatment, and pain reliever, most basic science
research has been directed at the interaction of valerian constituents with
the GABA receptor. Many studies remain inconclusive and all require
clinical validation. The mechanism of action of valerian in general, and as a
mild sedative in particular, has not been fully elucidated. However, some of
the GABA-analogs, particularly valerenic acids as components of the
essential oil along with other semivolatile sesquiterpenoids, generally are
believed to have some affinity for the GABA A receptor, a class of receptors
on which benzodiazepines are known to act. Valeric acid, which is
responsible for the typical odor of mostly older valerian roots, does not
have any sedative properties. Valeric acid is related to valproic acid, a
widely-prescribed anticonvulsant; valproic acid is a derivative of valeric
acid.
Valerian also contains isovaltrate, which has been shown to be an inverse
agonist for adenosine A1 receptor sites. This action likely does not
contribute to the herb's possible sedative effects, which would be expected
from an agonist, rather than an inverse agonist, at this particular binding
site. Hydrophilic extractions of the herb commonly sold over the counter,
however, probably do not contain significant amounts of isovaltrate.
Valerenic acid in valerian stimulates serotonin receptors as a partial
agonist.
Preparation.

V. officinalis

The chief constituent of valerian is a yellowish-green to brownish-yellow oil

which is present in the dried root, varying from 0.5 to 2.0%, though an
average yield rarely exceeds 0.8%. This variation in quantity is partly
explained by location; a dry, stony soil yields a root richer in oil than one
that is moist and fertile. The volatile oils that form the active ingredient are
extremely pungent, somewhat reminiscent of well-matured cheese. Though
some people remain partial to the earthy scent, some may find it to be
unpleasant, comparing the odor to that of unwashed feet. Valerian tea
should not be prepared with boiling water, as this may drive off the lighter
oils.
Medicinal use

Valerian (V. officinalis) essential oil

Valerian is most often used as an alternative medicine for insomnia in place

ofhypnotic drugs. It is also sometimes used as an alternative for sedatives,
such asbenzodiazepines, in the treatment of certain anxiety disorders.

Whether or not valerian is an efficacious treatment for insomnia is still a

very open question. Multiple recent systematic reviews of the medical
research literature andmeta-analyses have produced conflicting
conclusions regarding its efficacy. One systematic review and metaanalysis published in 2006 concluded, "The available evidence suggests
that valerian might improve sleep quality without producing side effects." An
article in the Medical Science Monitor states that, "...based on cellular and
animal studies as well as human clinical trials the literature supports a role
for these preparations [including valerian root] as useful alternatives in the
management of the stress and anxiety of everyday life." However, another
systematic review, published in 2007 in the journal Sleep Medicine
Reviews, concluded valerian was safe but not clinically efficacious for
insomnia.
Regulation
In the United States, valerian extracts are sold as a nutritional
supplement under theDietary Supplement Health and Education Act of
1994.
Oral forms, usage, and adverse effects
Oral forms
Oral forms are available in both standardized and unstandardized forms.
Standardized products may be preferable considering the wide variation of
the chemicals in the dried root, as noted above. When standardized, it is
done so as a percentage of valerenic acid or valeric acid.
Adverse effects
Few adverse events attributable to valerian have been reported. Large
doses may result in stomachache, apathy, and a feeling of mental dullness
or mild depression. Because of the herb's tranquilizer properties, it may
cause dizziness or drowsiness, effects that should be considered before
driving or operating heavy or hazardous equipment.

In rare cases, valerian may cause an allergic reaction, typically as a skin

rash, hives, or difficulty breathing. This should be treated as a medical
emergency.
Because the compounds in valerian produce central nervous system
depression, they should not be used with other depressants, such
as ethanol, benzodiazepines, barbiturates, opiates, kava, or antihistamine
drugs. Moreover, non-pregnant adult human hepatotoxicity has been
associated with short-term use (i.e., a few days to several months) of
herbal preparations containing valerian and Scutellaria (commonly called
skullcap). Withdrawal after long-term use in a male has also been
associated with benzodiazepine-like withdrawal symptoms, resulting in
cardiac complications and delirium.
The very limited animal and human data do not allow a conclusion as to the
safety of valerian during pregnancy. Moreover, as a natural, unregulated
product, the concentration, contents, and presence of contaminants in
valerian preparations cannot be easily determined. Because of this
uncertainty and the potential for cytotoxicity in the fetus and hepatotoxicity
in the mother, the product should be avoided during pregnancy.
Effect on other organisms

An unusual feature of valerian is that valerian root and leaves are a cat
attractant similar to, and as safe as, catnip. Valerian contains the cat
attractant actinidine. Cat attractants might mimic the odor of cat
urine, which is caused by 3-mercapto-3-methylbutan-1-ol. Anecdotal
reports claim that valerian is also attractive to ratsso much so that it had
been used to bait traps. Stories describe the Pied Piper of Hamelin using
both his pipes and valerian to attract rats. Research also shows that
valerian root is the strongest chemoattractant of slime molds such
as Physarum polycephalum.

Valerian is well known for its sedative qualities and its ability to relax the
central nervous system and the smooth muscle groups. It has been used

as a sleeping aid for hundreds of years especially when there is excitation

or difficulty in falling to sleep due to nervousness. Over 120 chemical
components are found in valerian and although a very complex herb, it has
not been found to have any negative side effects with moderate use.
It is calming without exerting too sedative an effect and is practically nonaddictive. It is a valuable treatment for insomnia, the sedative effect due to
the valepotriates and the isovaleric acid.
At least two double-blind studies have demonstrated that valerian extract
can significantly reduce the amount of time it takes people to fall asleep
without changing the normal stages of sleep.
Documented research has noted a mild hypnotic action in both normal
sleepers and insomniacs, indicated by a beneficial effect on sleep latency,
wake-time after sleep, frequency of waking, nocturnal motor activity, inner
restlessness and tension and quality of sleep. Sleepiness and dream recall
the morning after were unaffected. The valepotriates have a regulatory
effect on the autonomic nervous system; research suggests that they have
a calming effect on agitated people but are also a stimulant in cases of
fatigue.
Valerian is used in Europe as an antispasmodic, particularly for abdominal
cramps due to nervousness and for uterine cramps and menstrual
agitation. It helps relieve dysmenorrhoea and it can be of benefit in
migraine and rheumatic pain. It may also be applied locally as a treatment
for cramps and other muscle tensions.
Valerian is also used as a mild tranquilizer for people experiencing
emotional stress, much as anti-anxiety drugs are prescribed and has been
prescribed for exhaustion. Valerian has occasionally been tried as part of a

program to take a patient off antidepressants or benzodiazepines, and is

sometimes used as a muscle relaxant to treat pain.
Valerian does not impair driving ability and produces no morning hangover
effect. It is a gentle relaxant and an effective sleep aid.
Millions of people have difficulty sleeping and the pharmaceutical industry
has cashed in on the problem to the tune of billions of dollars. But herbal
sleep aids can be as effective as the powerful prescription sedatives such
as valium and other narcotic type drugs.

bamboo silica

(Hindustani: or )or Banslochan ( , ), also spelt

as Tabachir , is a translucent white substance, composed mainly
of silica and water with traces of lime and potash, obtained from the nodal
joints of some species of bamboo. It is part of the pharmacology of the
traditional Ayurvedic and Unani systems of medicine of the Indian
subcontinent. It is also an ingredient in many traditional Chinese medicines.
Contents

1 Purported benefits
2 Varieties
3 Extraction
4 History
5 Etymology and alternative names

Purported benefits

Tabasheer is claimed to provide a variety of health benefits. It is variously

regarded as
an antipyretic, antispasmodic,antiparalytic, restorative and aphrodisiac.
Varieties

that has a blueish tint (usually called neel or neelkanth) is considered

superior to tabasheer that has the "more plain" yellow or white color.
Extraction

Not all bamboo stems contain tabasheer. Likely candidates are found by
shaking bamboo stems, which can make the mineralized tabasheer inside
produce a rattling sound. These stems are split open to extract the
tabasheer.
History

Although a part of the ancient unani system of medicine, it has been

postulated that the use of tabasheer originated in the Adivasi aboriginal
tribes of India. Tabasheer was extensively exported from India for
thousands of years, including through Arab traders during the medieval
period. The town of Thane, close to the west coast of India, was famous as
a clearing center for tabasheer in the twelfth century CE. It was called
in the writings of Pedanius Dioscorides, aGreek pharmacologist
who practiced in Rome in the time of Nero.
Etymology and alternative names

Tabasheer is referred to as Tvaksheera () in Sanskrit, which

means bark milk. Other Sanskrit-derived names have been applied to
tabasheer as well, including bamboo sugar (vans-sharkar), bamboo
camphor (vans karpoor) and bamboo manna. It is called Tian Zhu Huang in
Mandarin, which means "heavenly bamboo yellow."
Bamboo silica is also known as tabasheer or Tian Zhu Huang in
Chinese (literally Heavenly Bamboo Yellow). Besides, it is
commonly referred to as the calculus in the body of bamboo

plants. When used as Chinese herbal medicine, it clears heat,

sweep phlegm, cool heart, and calm the frightened. Hence,
clinically it treats fever, coma and delirium, convulsions, epilepsy,
rheumatism, limb numbness, whooping cough, excessive vaginal
discharge, stomach trouble, acne, and so on. Now modern
medicine has found that it is one of the richest natural sources of
organic silica, which is responsible for the health of nails,
tendons, skin, hair, bones, and ligaments in human body. So, is
bamboo silica safe and really good for hair growth?
What is bamboo silica?
Medicinally it refers to the dried siliceous resin found in the nodes
of some species in the family Poaceae, mainly from Bambusa
textilis McClure and Schizostachyum chinense Rendle. Other
common names of it include bamboo sap, tabashir, Siliceous
Secretions of Bamboo, banslochan, Concretio Silicea Bambusae,
Tabasheer, bamboo manna, bamboo tears, bamboo powder,
Tabashir silica, karpoor vans (bamboo camphor), Tvaksheera
(bark milk in Sanskrit), vans-sharkar (bamboo sugar), and the
like. In China it is mainly produced in provinces of Yunnan,
Guangdong, and Guangxi. It is generally harvested in autumn
and winter by cutting the stems open. Medicinally it is generally
used raw.
The naturally occurring one is quite rare since this clotted bulk is
mainly formed from the bleeding sap stored in the nodal joints of
Bambusa textilis McClure due to the parasitic wasp bites. Now
most of them are produced by setting fire to the forest in order to
let the sudden heat force and solidify the fresh sap in the notes.
Tabasheer is in the shapes of irregular polygonal blocks or flakes.
Surface is white, gray or with a bluish tint. It is light, crisp, and
easily broken. Section is bright, slightly mealy, and with slippery
feeling when touching with hands. It is strongly absorbent but

insoluble in water. When placed in water, it produces bubbles. It is

sweet, sticky, and cool when licking with tongue. And the highquality one is drier, bigger, yellowish white, bright, and highly
absorbent.
2 polysaccharides, SB-1 and SB-2, can be isolated from The
zymotic fluid of tabasheers mycelium; other ingredients isolated
from the soluble components include proteases, amylase, Dmannitol, aspartic acid, threonine, serine, glutamic acid, glycine,
alanine, cystine, valine, methionine, isoleucine, phenylalanine,
lysine, -amino butyric acid, tyrosine, and small amount of
cysteine; ingredients isolated from the stroma are hypocrellin A,
B, C, mannitol, stearic acid, and shiraiachrome A, B, C.

Bamboo silica benefits

Does bamboo silica really work? When it comes to the sources of
naturally occurring, organic silica, horsetail grass and bamboo are
the most known two. From the eyes of Chinese, bamboo shoots
are more than just a food since eating them has a long history
there. In fact they have become a delicious dish on the table
since the Shang Dynasty, about thousands of years ago. Now
modern scientific findings seem provide a proven reason the
amount of silica contained in bamboo are about 10 times of that
of horsetail herb. If you are familiar with horsetail grass, you will
know that quite well what means behind that figure. No wonder
Enerex Bamboo Silica, a pure silica supplement extracted from its
shoots, is so popular these days for hair growth, healthy joint,
and skin health.
As a matter of fact, another 2 commonly used Chinese herbs, Zhu
Ru (Bamboo Shavings) and Zhu Li (Succus Bambusae), are
associated with tabasheer. Here are their functions in common.
All of the three are of cold nature and treat phlegm-heat induced

cough and asthma by clearing heat and dissipating phlegm. In

addition, both Succus Bambusae and tabasheer can be used in
the treatment of fever or phlegm-heat induced infantile
convulsions, epilepsy, stroke, coma, gurgling with sputum in
throat since it possesses the calming properties. So, what is the
difference between them? First and foremost, tabasheer has
preferable calming power, which makes it do a better job in
treating convulsions in children and coma due to high heat;
besides, since Succus Bambusae is of cold, slippery nature and
with better ability of clearing heat and eliminating phlegm, it is
mostly used in the adults epilepsy, stroke, and lung-heat induced
stubborn sticky phlegm that is hard to cough up; last but not
least, it is good at clearing heart heat to relieve restlessness. As a
result, it is used more in the treatment of irritability and insomnia
caused by phlegm heat disturbing the heart.
Modern pharmacology
1) Hypocrellin B has significant anti-inflammatory and analgesic
effects. It is superior to indomethacin when it comes to raising
the threshold of pain;
2) Hypocrellin A has a good inhibition on Gram-positive bacteria.
And it has significant photodynamic therapy on cultured human
cancer cells and transplanted solid tumors in mice.

Sample recipes on herbal remedies

The Chinese Pharmacopoeia tends to believe that it is sweet in

flavor and cold in nature. It goes to meridians of heart and liver.
Most important functions are clearing away heat, eliminating
phlegm, expelling heart heat, and arresting convulsion. Principal
bamboo silica uses and indications include unconsciousness due

to heat illness, stroke, epilepsy, baby night cry, convulsions, and

phlegm-heat epilepsy. Recommended bamboo silica dosage is
from 3 to 9 grams in pills and powder. Apart from that, it is also
made into a great deal of bamboo silica products, such as extract,
capsules, pills, silica liquid, shampoo, and the like.
1) Bao Long Wan from Xiao Er Yao Zheng Zhi Jue (Key to the
Therapeutics of Childrens Diseases). It is formulated with She
Xiang (Deer Musk), Dan Nan Xing (Arisaema Cum Bile), Chen Sha
(cinnabar), etc. to treat infantile convulsions due to phlegm-heat;
2) Li Jing Wan from Key to the Therapeutics of Childrens
Diseases. It is combined with Qing Dai (Indigo), Qing Fen
(Calomel), and Qian Niu Zi (Morning Glory Seed) to cure infantile
acute convulsions;
3) Tian Zhu Huang San from Sheng Ji Zong Lu (Complete Record
of Holy Benevolence). It is matched with Chuan Xiong (lovage)
and Fang Ji (Stephania Tetrandra) to heal epistaxis;
4) Qing Fei Hua Tan Tang from the prescriptions of Dr. Guo
Zhongyuan. It is joined with Ban Lan Gen (Isatis Root), Huang
Qin (Scutellaria Baicalensis), Zhe Bei Mu (Fritillaria Bulb), Yuan
Shen (radix scrophulariae), etc. to treat chronic bronchitis;
5) Feng Long Tang from the prescriptions of Dr. Ding Jinyuan. It is
coupled with Lu Feng Fang (Hornets Nest), Di Long (Earthworm),
Jie Geng (Balloon Flower Rhizome), etc. to cure children with
asthma.
Clinical bamboo silica research
a) Tabasheer-based granule has significant effect on the
treatment of psoriasis;
b) The ointment made of hypocrellin A, isolated from Hypocrella
bambusae, can be applied to female genital lesions and

hypertrophic scars. And it has definite therapeutic effect under

lights;
c) A spray made of the mixture of hypocrellin A and B can be
used in topical treatment of burns. For the early stage of the
superficial second-degree burn wounds, it has the advantages of
fast film-forming properties, good air permeability, and quick
wound healing.
Bamboo silica side effects, drug interactions and contraindications
It shouldnt be used during pregnancy and in patients with skin
diseases like onychomycosis, tinea manuum, etc. And dont eat
radishes and sour and spicy food during the medication. Besides,
beware of the adulterants, which have been found in the market
in recent years. The adulterants are often doped with minerals
that are with no genuine healing power of tabasheer. Whats
worse, it may even lead to unexpected adverse reactions.

chicorum intybus

Cichorium Intybus
Botanical Classification | Family | Other
Names | Habitat | Morphology
Chemical Constituents | Pharmacology | Toxicology

Plant part used | Indication | Uses

Botanical Classification
Botanical classification
Kingdom

Plantae

Division

Magnoliophyta

class

Magnoliopsida

Order

Asteales

Genus

Cichorium

Species

Intybus

Cichorium intybus

Family
Botanical- asteraceae

Other Names

English name- endive / chicory

Sanskrit name- kasni
Arabic name - hinduba

Habitat

In India plant is found in the northwestern regions like Kashmir

and Punjab and in area of south India. In western countries is now
a days cultivated with the name endive. It is cultivated in
completely black outed area to make leaf soft and pale in
appearance. This plant has it origin in Europe and now has spread
all over world.

Morphology

It is a bushy perennial plant that attains a height of 1 to 3 feet.

The stem has edges having hard branches. Leaves are sphere
shaped having a bitter taste. Flowers are of blue of lavender color
having a diameter of 1 to 1 inch, which is bit thicker at the
center. Fruit is angular, having light color. Root is like a tail of a
cow and is fleshy having brownish color from outside and white
color from inside. It has a length of 2 feet and has a bitter
taste. The other related species that is cultivates is Cichorium
endivia. It is generally found in cultivated lands and gardens.

Chemical Constituents

Their seed contains oil. Roots has sticky substance which is about
7.5 %, glucose 1.1 %, bitter substance 4 %, fat 0.6 %, cellulose,
insulin and resins etc. ash contains more of potassium. It also
contains colorless potassium glycosides, cichorin and lactucina

and intybin. There is very peculiar smell when the root is roasted
and is very often used as coffee.

Pharmacology

It is relaxant and induces sleep. It acts as pain reliever and anti

inflammatory agent. It works as appetizer, liver stimulant and
increases digestive powers. It acts as blood purifier and provides
strength to heart. It is a diuretic. Its roots reduce menstrual
disturbances. It has good effect in lowering down the burning
sensations in the body. It also helps in lowering the blood
pressure. It decreases the raised body temperature in fevers.
it is

(properties) - (light) and (dry)

(taste) - (bitter)
(potency) - (hot)

Toxicology

No toxic effect was seen on human body with Cichorium intybus

consumption

Plant part used

Roots, leaves and seeds.

Indication

Head ache
Indigestion
Hypertension
Urticaria
Gouty arthritis
Burning sensation
Insomnia
Jaundice
Dehydration
Liver related disorders
Dysurea
Blood impurity
Menstrual disturbances
Chronic fever
General body weakness

Uses

Paste - paste made out of it leaves and a root is very effective in reducing
the burning sensations in the particular area and in fever of high grade. It is
also applied on the forehead as it induces sleep.
Powder- the powder made out of the leaves and roots is very effective in
treating indigestion, liver disorders and dehydration. Powder made out of
seeds also helps in relaxation of the mind thus effective in decreasing
anxiety and also it induces sleep. It also improves general health condition
of the body. It is also helpful in conditions of arthritis and especially like
gouty arthritis. It also reduces pains and is very often taken in headaches
Decoction - it is very effective in treating the blood related problems and
heart aliments. It improves blood circulation in the body and also
strengthens heart muscles. It also improves the menstrual related problems
of females and initiates easy flow.
Juice juice prepared from leaves is very helpful in urinary tract related
problems
Unani classical composition
Ark kasni

Common chicory, Cichorium intybus, is a somewhat

woody, perennialherbaceous plant usually with bright blue flowers, rarely

white or pink. Many varieties are cultivated for salad leaves, chicons
(blanched buds), or for roots (var. sativum), which are baked, ground, and
used as a coffee substitute and additive. It is also grown as a forage crop
for livestock. It lives as a wild plant on roadsides in its native Europe, and
now common in North America, China, and Australia where it has become
widely naturalized.
"Chicory" is also the common name in the United States for
curly endive(Cichorium endivia); these two closely related species are often
confused.
Contents

1 Names
2 Description
3 Leaf chicory
3.1 Wild
3.2 Cultivated
4 Root chicory
5 Agents responsible for bitterness
6 Medicinal use
6.1 Alternative medicine
7 Forage
7.1 Forage chicory varieties
8 History

Names

Common chicory is also known as blue daisy, blue dandelion, blue

sailors,blue
weed, bunk, coffeeweed, cornflower, hendibeh, horseweed,ragged
sailors, succory, wild bachelor's buttons, and wild endive.[10](Note:
"Cornflower" is commonly applied to Centaurea cyanus.) Common names
for varieties of var. foliosum include endive, radicchio, Belgian endive,
French endive, red endive, sugarloaf and witloof (or witlof).
Description

When flowering, chicory has a tough, grooved, and more or less hairy
stem, from 30 to 100 centimetres (10 to 40 in) tall.
The leaves are stalked, lanceolate and unlobed.
The flower heads are 2 to 4 centimetres (0.79 to 1.6 in) wide, and usually
bright blue, rarely white or pink. There are two rows of involucral bracts; the
inner are longer and erect, the outer are shorter and spreading. It flowers
from July until October.
The achenes have no pappus (feathery hairs), but do have toothed scales
on top.
Leaf chicory
Wild
Wild chicory leaves usually have a bitter taste. Their bitterness is
appreciated in certain cuisines, such as in the Ligurianand Apulian regions
of Italy and also in Catalonia (Spain), in Greece and in Turkey.[12] In
Ligurian cuisine the wild chicory leaves are an ingredient of preboggion and
in Greek cuisine of horta; in the Apulian region wild chicory leaves are
combined with fava bean puree in the traditional local dish Fave e Cicorie
Selvatiche. in Albania the leaves are used as a spinach substitute, mainly
served simmered and marinated in olive oil, or as ingredient for fillings

of byrek.
By cooking and discarding the water the bitterness is reduced, after which
the chicory leaves may be sauted with garlic,anchovies and other
ingredients. In this form the resulting greens might be combined with pasta
or accompany meat dishes.
Cultivated
Chicory may be cultivated for its leaves, usually eaten raw as salad leaves.
Cultivated chicory is generally divided into three types, of which there are
many varieties:
Radicchio usually has variegated red or red and green leaves. Some only
refer to the white-veined red leaved type as radicchio. Also known as red
endive and red chicory. It has a bitter and spicy taste, which mellows when
it is grilled or roasted. It can also be used to add color and zest to salads. It
is largely used in Italy in different varieties, the most famous being the ones
from Treviso (known as Radicchio Rosso di
Treviso), from Verona (Radicchio di Verona), and Chioggia (Radicchio di
Chioggia), which are classified as an IGP It's also common in Greece.
Sugarloaf looks rather like cos lettuce, with tightly packed leaves.

Witloof, Belgian endive

Belgian endive, known in Dutch as witloof or witlof ("white leaf"), endive or
(very rarely) witloof in the United States,[21] indivia in Italy, endivias in Spain,
chicory in the UK, as witlof in Australia, endive in France, and chicon in
parts of northern France and in Wallonia. It has a small head of creamcoloured, bitter leaves. It is grown completely underground or indoors in the
absence of sunlight in order to prevent the leaves from turning green and
opening up (etiolation). The plant has to be kept just below the soil surface
as it grows, only showing the very tip of the leaves. It is often sold wrapped
in blue paper to protect it from light and so preserve its pale colour and
delicate flavour. The smooth, creamy white leaves may be served stuffed,
baked, boiled, cut and cooked in a milk sauce, or simply cut raw. The
tender leaves are slightly bitter; the whiter the leaf, the less bitter the taste.
The harder inner part of the stem at the bottom of the head should be cut
out before cooking to prevent bitterness. Belgium exports chicon/witloof to
over 40 different countries. The technique for growing blanched endives
was accidentally discovered in the 1850s at the Botanical Garden of
Brussels in Saint-Josse-ten-Noode, Belgium. Today France is the largest
producer of endive.

leaves unlobed and pointed

Inflorescences of a blue-flowered form. Note the two rows of bracts

The Catalogna chicory (also known as puntarelle) includes a whole
subfamily (some varieties from Belgian endive and some from radicchio) of
chicory and used throughout Italy.
Although leaf chicory is often called "endive", true endive (Cichorium
endivia) is a different species in the genus and shouldn't be confused
with Belgian endive.
Root chicory

Root chicory (Cichorium intybus var. sativum) has been cultivated in

Europe as acoffee substitute. The roots are baked, ground, and used as a
coffee substitute and additive, especially in the Mediterranean region
(where the plant is native). As a coffee additive, it is also mixed in Indian
filter coffee, and in parts of Southeast Asia, South Africa and southern
United States, particularly in New Orleans. It has been more widely used
during economic crises such as the Great Depression in the 1930s and
during World War II in Continental Europe. Chicory, with sugar beet andrye,
was used as an ingredient of the East German Mischkaffee (mixed coffee),
introduced during the "East German coffee crisis" of 1976-79.
Some beer brewers use roasted chicory to add flavor to stouts (commonly
expected to have a coffee-like flavour). Others have added it to strong
blond Belgian-style ales, to augment the hops, making a "witlofbier", from
the Dutch name for the plant.
Around 1970 it was found that the root contains up to 20% inulin,
a polysaccharidesimilar to starch. Inulin is mainly found in the plant
family Asteraceae as a storage carbohydrate (for example Jerusalem
artichoke, dahlia, yacon etc.). It is used as a sweetener in the food industry
with a sweetening power 110 that of sucrose[25] and is sometimes added to
yogurts as a prebiotic. Inulin is also gaining popularity as a source of
soluble dietary fiber and functional food.[26]
Chicory root extract is a dietary supplement or food additive produced by
mixing dried, ground chicory root with water, and removing
the insoluble fraction by filtrationand centrifugation. Other methods may be
used to remove pigments and sugars. It is used as a source of soluble
fiber. Fresh chicory root typically contains, by dry weight, 68% inulin,
14% sucrose, 5% cellulose, 6% protein, 4% ash, and 3% other compounds.
Dried chicory root extract contains, by weight, approximately 98% inulin
and 2% other compounds.[27] Fresh chicory root may contain between 13
and 23% inulin, by total weight.[28]
Agents responsible for bitterness

The bitter substances are primarily the

two sesquiterpene lactones lactucin and lactucopicrin. Other ingredients

areaesculetin, aesculin, cichoriin, umbelliferone, scopoletin, 6,7dihydrocoumarin, and further sesquiterpene lactones and theirglycosides.[29]
Medicinal use

Chicory greens, raw

Nutritional value per 100 g (3.5 oz)
Energy

96 kJ
(23 kcal)

Carbohydrates

4.7 g

Sugars

0.7 g

Dietary fiber

4g

Fat

0.3 g

Protein

1.7 g

Vitamins
Vitamin A equiv.

(36%)

beta-carotene

286 g

lutein zeaxanthin

(32%)
3430 g
10300 g

Thiamine (B1)

(5%)
0.06 mg

Riboflavin (B2)

(8%)
0.1 mg

Niacin (B3)

(3%)
0.5 mg

Pantothenic acid (B5)

(23%)
1.159 mg

Vitamin B6

(8%)
0.105 mg

Folate (B9)

(28%)
110 g

Vitamin C

(29%)
24 mg

Vitamin E

(15%)
2.26 mg

Vitamin K

(283%)
297.6 g

Trace minerals
Calcium

(10%)

100 mg
Iron

(7%)
0.9 mg

Magnesium

(8%)
30 mg

Manganese

(20%)
0.429 mg

Phosphorus

(7%)
47 mg

Potassium

(9%)
420 mg

Sodium

(3%)
45 mg

Zinc

(4%)
0.42 mg

Link to USDA Database entry

Units
g = micrograms mg = milligrams
IU = International units
Percentages are roughly approximated
usingUS recommendations for adults.

Source: USDA Nutrient Database

Belgian endive (witloof), raw
Nutritional value per 100 g (3.5 oz)
Energy

71 kJ (17 kcal)

Carbohydrates

4g

Dietary fiber

3.1 g

Fat

0.1 g

Protein

0.9 g

Vitamins
Thiamine (B1)

(5%)
0.062 mg

Root chicory contains volatile oils similar to those found in plants in the
related genus Tanacetum which includes Tansy, and is similarly effective at
eliminating intestinal worms. All parts of the plant contain these volatile oils,
with the majority of the toxic components concentrated in the plant's root.
Chicory is well known for its toxicity to internal parasites. Studies indicate
that ingestion of chicory by farm animals results in reduction of worm
burdens, which has prompted its widespread use as a forage supplement.
Only a few major companies are active in research, development, and
production of chicory varieties and selections, most in New Zealand.
Chicory (especially the flower), used as a folk medicine in Germany, is

recorded in many books as an ancient German treatment for everyday

ailments. It is variously used as a tonic and as a treatment
for gallstones,gastro-enteritis, sinus problems and cuts and bruises.
(Howard M. 1987). Chicory contains inulin, which may help humans with
weight loss, constipation, improving bowel function, and general health. In
rats, it may increase calcium absorption and bone mineral density.
Chicory has demonstrated antihepatotoxic potential in animal studies.
Alternative medicine
Chicory has been listed as one of the 38 plants that are used to
prepare Bach flower remedies, a kind of alternative medicine. However
according toCancer Research UK, "there is no scientific evidence to prove
that flower remedies can control, cure or prevent any type of disease,
including cancer".
Forage

Chicory is highly digestible for ruminants and has a low fiber

concentration.]Chicory roots are an "excellent substitute for oats" for horses
due to their protein and fat content. Chicory contains a low quantity of
reduced tannins[ that may increase protein utilization efficiency in
ruminants. Some tannins reduce intestinal parasites. Large quantities of
tannins bind with and precipitate proteins, resulting in low digestibility and
nutrient reduction.
Although chicory might have originated in France, Italy, and India, much
development of chicory for use with livestock has taken place in New
Zealand.
Forage chicory varieties
Puna (Grasslands Puna)
Developed in New Zealand, Grasslands Puna is well adapted to different
climates, being grown from Alberta, Canada, to New Mexico and Florida. It
is resistant to bolting, which leads to high nutrient levels in the leaves in

spring. It also has high resistance to grazing.

Forage Feast
A variety from France used for human consumption and also for wildlife
plots. It is very cold-hardy and, being lower in tannins than other forage
varieties, is suitable for human consumption.
Choice
Choice has been bred for high winter and early-spring growth activity, and
lower amounts of lactucin and lactone, which are believed to taint milk. It is
also use for seeding deer wildlife plots.
Oasis
Bred for increased lactone rates for the forage industry, and for higher
resistance to fungal diseases like Sclerotinia.
Puna II
More winter-active than most other varieties, which leads to greater
persistence and longevity.
Grouse
A New Zealand variety used as a planting companion for forage brassicas.
More prone to early flowering than other varieties, with higher crowns more
susceptible to overbrowsing.
Six Point
A United States variety, very similar to Puna.
History

The chicory plant is one of the earliest cited in recorded

literature. Horace mentions it in reference to his own diet, which he
describes as very simple: "Me pascunt olivae, me cichorea, me malvae"
("As for me, olives, endives, and mallows provide sustenance").In
1766, Frederick the Great banned the importation of coffee

into Prussia leading to the development of a coffee-substitute

by Brunswick innkeeper Christian Gottlieb Frster (died 1801), who gained
a concession in 1769/70 to manufacture it in Brunswick and Berlin. By 1795
there were 22 to 24 factories of this type in Brunswick. Lord
Monboddo describes the plant in 1779 as the "chicoree", which the French
cultivated as a pot herb. In Napoleonic EraFrance, chicory frequently
appeared as either an adulterant in coffee, or as a coffee substitute.
Chicory was also adopted as a coffee substitute by Confederate soldiers
during the American Civil War, and has become common in the United
States. It was also used in the United Kingdom during the Second World
War, where Camp Coffee, a coffee and chicory essence, has been on sale
since 1885.
The cultivated chicory plant has a history reaching back to ancient Egyptian
time. Medieval monks raised the plants and when coffee was introduced to
Europe, the Dutch thought that chicory made a lively addition to the bean
drink.
In the United States chicory root has long been used as a substitute for
coffee in prisons. By the 1840s, the port of New Orleans was the second
largest importer of coffee (after New York). Louisianans began to add
chicory root to their coffee when Union naval blockades during the
American Civil War cut off the port of New Orleans, thereby creating a longstanding tradition.
A common meal in Rome, puntarelle, is made with chicory sprouts. The
United Nations Food and Agriculture Organization (FAO) reports that
Chicory is a native plant of western Asia, North Africa, and Europe. [4]
Chicory is also mentioned in certain sericulture (silk-growing) texts. It is
said that the primary caretaker of the silkworms, the "silkworm mother",
should not eat or even touch it.
The chicory flower is often seen as inspiration for the Romantic concept of
the Blue Flower (e. g. in German language 'Blauwarte' 'blue lookout by
the wayside'). It could open locked doors, according to European folklore.

Apium graveolens
Introduction
Celery) is the seed of Apium graveolens Linn commonly known as
salad. Karafs is a well known drug used in the Unani system of
medicine for a number of diseases and is one of the constituent of
many pharmacopoeal preparations. Though the entire plant
contains medicinal value however, its seeds and root are more
commonly used therapeutically for diverse pathological
conditions.
It belongs to the family Apiaceae earlier known as Umbellifereae,
over 20 species of biennial and perennial plants make up this
genus.
Taxonomical classification
Kingdom Plantae;
Sub kingdom Tracheobionta;
Superdivision Spermatophyta;
Division Magonliopisida;
Subclass Rosidae;
Order Apiales;
Family Apiaceae;
Genus Apium;

Species A graveolens Linn1 .

Nomenclature: Tukhme Karafs (seeds of Apium graveolens Linn) is
known by different names worldwide. Language/Region
Nomenclature: Arabic- Bazrul Karafs; Bengali- Chanu, Randhuni;
Bombay-Ajmud, Budiajamoda; Chinese- Qin cai; KannadaSelerina; English- Celery; GreekEleioselinon, Udasaliyun; HindiAjmud, Boriajmud; PakistanKarafs ajowan; Persian- Karasb, Karafs;
Roman- Baatrakhiyun; Sanskrit- Ajmoda
Andhapatrika,Brahmakoshi; Tamil- Asham tagam; Telugu- Ashu
magada voman, Ajmudah; Urdu- Ajmod2
Description of Karafs as described in Unani literature:
In Unani system of medicine the names of drugs are adopted from
Persian or Arabic nomenclature. In Persian Apium graveolens Linn
is known as Karafs. Hence the drug Karafs means the same as
Apium graveolens Linn and the seeds are called as Tukhme
Karafs. Hussain writes that Karafs is the Celery of Europeans and
the Udasaliyon of Greeks. He mentions five varieties of Karafs
namely Bustani, Jabli, Nabti, Sakhuri, Maiee (Tari). Bustani is
cultivated variety while Jabli grows in hills, Sakhuri on stony
surface, Nabti in shady places and Maiee or Tari near water or
ponds. According to Hussain, Sakhuri, Nabti and Maiee varieties of
Karafs are called in Greek, as Fiturasaliyun, Akusaliyun and
Samarniyun respectively3 . Al Biruni writes that the people of
Tirmidh, Khatl and Bukharistan called Karafs as Sumbul4 .
Avicenna and Baitar have also mentioned five types of Karafs i.e.
Jabli, Sakhuri, Bustani, Mashriqi and Qabrisi5,6 . The
Nomenclature of the five different varieties of Karafs as described
in the literature related to Unani system of medicine is below
(table-1). This classification of Karafs appears to be based on its
origin3-6. The Arabs probably obtained their knowledge of
Tukhme Karafs from the Greeks. Dioscorides describes five kinds
of Karafs, the Selnion of Theophrastus was probably Celery.

Celery

Scientific classification
Kingdom:

Plantae

(unranked): Angiosperm
s
(unranked): Eudicots
(unranked): Asterids
Order:

Apiales

Family:

Apiaceae

Genus:

Apium

Species:

A.
graveolens

Variety:

dulce
(Mill.) Pers.

Synonyms[1]
Apium dulce Mill
Apium
graveolens subsp. dulce(
Mill.) Schbl. & G.
Martens
Celery (Apium graveolens) is a cultivated plant, variety in the
family Apiaceae, commonly used as a vegetable. Depending on location,
either its stalks, or its hypocotyl, are eaten and used in cooking.
In North America the dominant variety most commonly available in trade is
"celery",Apium graveolens var. dulce, whose stalks are eaten raw, or as an
ingredient in salads, or as a flavoring in soups, stews, and pot roasts.
In Europe the dominant variety most commonly available in trade
is celeriac (Apium graveolens var. rapaceum) whose hypocotyl forms a
large bulb which is eaten cooked, or as a the major ingredient in a soup. It
is commonly, but incorrectly, called "celery root". The leaves
of rapaceum are used as seasoning, but the stalks find only marginal use.
Celery seed is also used as a spice. The plant grows to 1 m (3.3 ft) tall.
Contents
1 Description
2 Etymology
3 Taxonomy
4 Cultivation
4.1 North America
4.2 Europe

4.3 Wild
5 Harvesting and storage
5.1 Sulfites
6 Uses
6.1 Seeds
6.2 Celery salt
6.3 Louisiana Creole
6.4 Medicine
6.5 Nutrition
7 Allergies
8 Chemistry
9 History
9.1 Cultural depictions

Description

Leaf celery

Celery leaves are pinnate to bipinnate with rhombic leaflets 36 cm (1.2

2.4 in) long and 24 cm broad. The flowers are creamy-white, 23 mm in
diameter, and are produced in dense compound umbels. The seeds are
broad ovoid to globose, 1.52 mm long and wide. Modern cultivars have
been selected for solid petioles, leaf stalks. A celery stalk readily separates
into "strings" which are bundles of angular collenchyma cells exterior to
the vascular bundles.
Etymology

First attested in English in 1664, the word "celery" derives from

the French cleri, in turn from Italian seleri, the plural of selero, which
comes from Late Latin selinon, the latinisationof the Greek
(selinon), "parsley".The earliest attested form of the word is theMycenaean
Greek se-ri-no, written in Linear B syllabic script.
Taxonomy

Cross-section of a 'Pascal' celery rib, the petiole

Cultivation

Head of celery, sold as a vegetable. Usually only the leaf stalks are eaten

The plants are raised from seed, sown either in a hot bed or in the open
garden according to the season of the year, and, after one or two thinnings
and transplantings, they are, on attaining a height of 1520 cm (5.97.9 in),
planted out in deep trenches for convenience of blanching, which is
effected by earthing up to exclude light from the stems.
In the past, celery was grown as a vegetable for winter and early spring; it
was perceived as a cleansing tonic, welcomed to counter the salt-sickness
of a winter diet. By the 19th century, the season for celery had been
extended, to last from the beginning of September to late in April.
North America
In North America, commercial production of celery is dominated by the
cultivar called 'Pascal' celery. Gardeners can grow a range of cultivars,
many of which differ from the wild species, mainly in having stouter leaf
stems. They are ranged under two classes, white and red. The stalks grow
in tight, straight, parallel bunches, and are typically marketed fresh that
way, without roots and just a little green leaf remaining.
Europe
In Europe the dominant variety of celery most commonly grown is Apium
graveolens var. rapaceum grown because itshypocotyl forms a large bulb,
correctly called celeriac, but often incorrectly called celery root. The leaves
are used as seasoning, and the stalks find only marginal use.
Wild
The wild form of celery is known as "smallage". It has a furrowed stalk with
wedge-shaped leaves, the whole plant having a coarse, earthy taste, and a
distinctive smell. The stalks are not usually eaten (except in soups or stews
in French cuisine), but the leaves may be used in salads, and its seeds are
those sold as a spice.[13] With cultivation and blanching, the stalks lose their
acidic qualities and assume the mild, sweetish, aromatic taste particular to
celery as a salad plant.
Harvesting and storage

Harvesting occurs when the average size of celery in a field is marketable;

due to extremely uniform crop growth, fields are harvested only once.
The petioles and leaves are removed and harvested; celery is packed by
size and quality (determined by colour, shape, straightness and thickness
of petiole, stalk and midrib length and absence of disease, cracks, splits,
insect damage and rot). Under optimal conditions, celery can be stored for
up to seven weeks between 0 to 2 C (32 to 36 F). Inner stalks may
continue growing if kept at temperatures above 0 C (32 F). Freshly cut
petioles of celery are prone to decay, which can be prevented or reduced
through the use of sharp blades during processing, gentle handling, and
proper sanitation.
Sulfites
In the past, restaurants used to store celery in a container of water with
powdered vegetable preservative, but it was found that the sulfites in the
preservative caused allergic reactions in some people. In 1986, the
U.S. Food and Drug Administration banned the use of sulfites on fruits and
vegetables intended to be eaten raw.
Uses

Celery seed (Apium graveolens) essential oil

Celery is used around the world as a vegetable. In North America for the
crisp petiole (leaf stalk). In Europe the hypocotyl is used as a root
vegetable. The leaves are strongly flavoured and are used less often, either
as a flavouring in soups and stews or as a dried herb.
Seeds
In temperate countries, celery is also grown for its seeds. Actually very
small fruit, these "seeds" yield a valuable volatile oil used in the perfume
and pharmaceutical industries. They also contain an organic
compound called apiol. Celery seeds can be used as flavouring or spice,
either as whole seeds or ground.
Celery salt

The seeds can be ground and mixed with salt, to produce celery salt.
Celery salt can also be made from an extract of the roots, or using dried
leaves. Celery salt is used as a seasoning, in cocktails (notably to enhance
the flavour of Bloody Mary cocktails), on the Chicago-style hot dog, and
in Old Bay Seasoning.
Louisiana Creole
Celery, onions, and bell peppers are the "holy trinity" of Louisiana
Creole and Cajun cuisine. Celery, onions, and carrots make up the
French mirepoix, often used as a base for sauces and soups. Celery is a
staple in many soups, such as chicken noodle soup.
Medicine

Celery seeds
The use of celery seed in pills for relieving pain was described by Aulus
Cornelius Celsus around AD 30. Celery seeds contain a compound, 3-nbutylphthalide, that has been demonstrated to lower blood pressure in rats.
Celery juice significantly reduced hypertension in 87.5% of patients (14 of
16) tested. Another study showed the same effect on hypertension
associated with pregnancy.
Bergapten in the seeds can increase photosensitivity, so the use
of essential oilexternally in bright sunshine should be avoided. The oil and
large doses of seeds should be avoided during pregnancy, as they can act
as a uterine stimulant. Seeds intended for cultivation are not suitable for
eating as they are often treated with fungicides.

Celery is used in weight-loss diets, where it provides low-calorie dietary

fibrebulk. Celery is often incorrectly thought to be a "negative-calorie food,"
the digestion of which burns more calories than the body can obtain. In
fact, eating celery provides positive net calories, with digestion only
consuming a small proportion of the calories taken in.
Allergies

Celery is among a small group of foods (headed by peanuts) that appear to

provoke the most severe allergic reactions; for people with celery allergy,
exposure can cause potentially fatal anaphylactic shock. The allergen does
not appear to be destroyed at cooking temperatures. Celery root
commonly eaten as celeriac, or put into drinksis known to contain more
allergen than the stalk. Seeds contain the highest levels of allergen
content. Exercise-induced anaphylaxis may be exacerbated. An allergic
reaction also may be triggered by eating foods that have been processed
with machines that have previously processed celery, making avoiding
such foods difficult. In contrast with peanut allergy being most prevalent in
the US, celery allergy is most prevalent in Central Europe. In the European

Union, foods that contain or may contain celery, even in trace amounts,
must be clearly marked as such.[24]
Chemistry

Polyynes can be found in Apiaceae vegetables like celery, and their

extracts show cytotoxic activities.
Apiin and apigenin can be extracted from celery and parsley.
Some aromatic compounds of celery leaves and stalks are reported
asbutylphthalide and Sedanolide.
History

Selinunte didrachm coin bearing aselinon (celery) leaf, circa 515-470 BC.
Daniel Zohary and Maria Hopf note that celery leaves
and inflorescences were part of the garlands found in the tomb of
pharaoh Tutankhamun (died 1323 BC), and celery mericarps dated to the
seventh century BC were recovered in the Heraion of Samos. However,
they note "since A. graveolens grows wild in these areas, it is hard to
decide whether these remains represent wild or cultivated forms." Only by
classical times is it certain that celery was cultivated.
M. Fragiska mentions an archeological find of celery dating to the 9th
century BC, atKastanas; however, the literary evidence for ancient
Greece is far more abundant. In Homer's Iliad, the horses of
theMyrmidons graze on wild celery that grows in the marshes of Troy, and
in Odyssey, there is mention of the meadows of violet and wild celery
surrounding the cave of Calypso.
Cultural depictions

A chthonian symbol among the ancient Greeks, celery was said to have
sprouted from the blood of Kadmilos, father of the Cabeiri, chthonian
divinities celebrated inSamothrace, Lemnos, and Thebes. The spicy odour
and dark leaf colour encouraged this association with the cult of death. In
classical Greece, celery leaves were used as garlands for the dead, and
the wreaths of the winners at the Isthmian Games were first made of celery
before being replaced by crowns made of pine. According to Pliny the Elder
in Achaea, the garland worn . The Ancient Greek colony of
Selinous (Greek: , Selinous), on Sicily, was named after wild
parsley that grew abundantly there; Selinountian coins depicted a parsley
leaf as the symbol of the city.
The name "celery" retraces the plant's route of successive adoption in
European cooking, as the English "celery" (1664) is derived from the
French cleri coming from the Lombard term, seleri, from the Latin selinon,
borrowed from Greek.
Celery's late arrival in the English kitchen is an end-product of the long
tradition of seed selection needed to reduce the sap's bitterness and
increase its sugars. By 1699, John Evelyn could recommend it in
his Acetaria. A Discourse of Sallets: "Sellery, apium Italicum, (and of the
Petroseline Family) was formerly a stranger with us (nor very long since in
Italy) is an hot and more generous sort of Macedonian Persley or
Smallage...and for its high and grateful Taste is ever plac'd in the middle of
the Grand Sallet, at our Great Men's tables, and Praetors feasts, as the
Grace of the whole Board".[31]
Celery has made a surprising appearance in football folklore. Supporters of
English Premier League team Chelsea and Football League
team Gillingham regularly sing songs about the vegetable and are famed
for throwing celery during matches. This has also given rise to the "Chelsea
Cocktail", a pint of Guinness garnished with a stick of celery.
In the television program Doctor Who, the Fifth incarnation of The
Doctor (played by Peter Davison), was noted[32] for wearing a stalk of celery
on his lapel, claiming it at one point to be an excellent restorative.

Pharmacological Actions:

The primary pharmacological actions of Kasni are summarized as under:

Digestive System:
i. Cichorium intybus leaf extract holds hepatoprotective activity against
acetaminophen induced liver damage.3
ii. The red part of the leaf of Treviso red chicory with a high content of
antioxidant anthocyanins could be interesting for development of new
food supplements to improve intestinal health. 4
Endocrinal System:
i. Natural chicoric acid extract (NCRAE) presents an antihyperglycemic
effect essentially due to a peripheral effect on muscle glucose uptake.5
ii. Chicory appeared to have short-term (about 2 hours, as far as GTT is
concerned) and long-term (28 days, in this study) effects on diabetes.
Chicory may be useful as a natural dietary supplement for slowing down
the pace of diabetes progress, and delaying the development of its
complications. 6
iii. The activities possessed by C. intybus are highly desirable for the
treatment of NIDDM because it reduces blood glucose levels without
inducing adipogenesis in 3T3-L1 adipocytes. 7
Cardiovascular System:
i. The water extract of Cichorium intybus has been observed to exhibit a
remarkable antioxidative effect on LDL, and inhibitory effects on the
production of thiobarbituric acid reactive substance and the Degradation
of fatty acids in LDL. 8
Others:
i. Exhibits antibacterial and antifungal activities.
Indications:

 Liver dysfunction
Type 2 Diabetes mellitus

Calotropis procera

Calotropis procera is a species of flowering plant in

the dogbane family,Apocynaceae, that is native to North Africa, Tropical
Africa, Western Asia, South Asia, and Indochina. The green globes are
hollow but the flesh contains a toxic milky sap that is extremely bitter and
turns into a gluey coating resistant to soap.
Common names for the plant include apple of Sodom, Sodom
apple,stabragh, kapok tree, king's crown,[2] rubber bush, or rubber tree. The
name apple of Sodom derives from the Hebrew Tapuah Sdom.
Contents
1 History
2 Chemical properties
3 Literary and musical references

History

The fruit is described by the Roman Jewish historian Josephus, who saw it
growing near Sodom: "...as well as the ashes growing in their fruits; which
fruits have a color as if they were fit to be eaten, but if you pluck them with
your hands, they dissolve into smoke and ashes." (Whiston 1737: Book IV
chapter 8 section 4)
In his Biblical Researches in Palestine, Edward Robinson describes it as
the fruit of the Asclepias gigantea vel procera, a tree 1015 feet high, with
a grayish cork-like bark called osher by the Arabs. He says the fruit

resembled a large, smooth apple or orange, hanging in clusters of three or

four. When pressed or struck, it exploded with a puff, like a bladder or puffball, leaving in the hand only the shreds of the thin rind and a few fibers. It
is filled chiefly with air, which gives it the round form. In the center a small
slender pod runs through it which contains a small quantity of fine silk,
which the Arabs collect and twist into matches for their guns. The plant,
however, is not native solely to Palestine. It is known to occur throughout
the tropical belt and is also common in the West Indies (e.g. Jamaica),
where the locals know it as "pillow cotton". When the ripe "apples" burst,
the fibrous contents are ejected along with the seeds. The former are
collected by the Jamaicans and used for filling pillows.
Sodom apple is listed in the Mishnah and Talmud. The fibers attached to
the seeds may have been used as wicks. However the Mishnah forbids this
for the Sabbath.: "It may not be lighted with cedar-bast, nor with uncombed
flax, nor with floss-silk, nor with willow fiber, nor with nettle fiber.- Sabbath
Chapter 2"
Some biblical commentators believe that the Sodom Apple may have been
the poisonous gourd (or poison-tasting gourd) that led to "death in the pot"
in 2 Kings4:3841. In this story, a well-meaning servant of the prophet
Elisha gathers herbs and a large quantity of the unknown gourds, and casts
them into the pot. After the outcry from the band of prophets, Elisha,
instructs them to cast flour into the stew pot, and they are saved. The fibre
of the Sodom Apple may have been used for the linen of the high priests.
In 1938, botanists Hannah and Ephraim HaReuveni, authors of the "The
Squill and the Asphodal," speculated that Jeremiahs arar was the Sodom
apple.
Chemical properties

The milky sap contains a complex mix of chemicals, some of which are
steroidal heart poisons known as "cardiac aglycones". These belong to the
same chemical family as similar chemicals found in foxgloves (Digitalis
purpurea). The steroidal component includes an hydroxyl group in the C3
position, a second attached to the C14 carbon, a C/D-cis ring junction and

an ,-unsaturated--lactone in the C17 position. In the plants, the steroidal

component is commonly attached via a glycosidic link to a 2-desoxy or a
2,6-didesoxy sugar molecule. The features described are those required for
toxicity but in addition there can be other substitutions into the steroid
nucleus. These can be a C19-aldehyde in place of the more usual methyl
group in this position as well as additional hydroxyl functions and
sometimes epoxide structures.
In the case of the Calotropis glycosides, their names
are calotropin, calotoxin, calactin, uscharidin and voruscharin (the latter two
involve rare sugars with nitrogen and sulphur in the structures). The
steroidal moiety (known as "calotropagenin", formula C23H32O6) has one of
the more unusual structures. The C-19 formyl (CHO) group is present and
there is an additional secondary alcohol as well as the common C3 and
C14 hydroxyl functions. The position of this third hydroxyl function remains
in some doubt. It was apparently established by the Swiss group under
Thadeus Reichstein as being in the C2 position with an equatorial
configuration. However, this assignment does not explain some of the
known features and behaviours of this molecule, in particular the absence
of spin-spin coupling of the two axial protons associated with their geminal
hydroxyl groups and the failure to react with iodate in a cleavage reaction
which the presence of such a viscinal 1,2-diol would require.

commiphora opobalsamum
Commiphora
Commiphora

Commiphora caudata
Scientific classification
Kingdom:

Plantae

(unranked) Angiosperm
:
s
(unranked) Eudicots
:
(unranked) Rosids
:
Order:

Sapindales

Family:

Burseracea
e

Genus:

Commiphor
a
Jacq.

Species

Synonyms
Balsamea
Balsamodendron L.

Commiphora saxicola - MHNT

The genus of the myrrhs, Commiphora, is the most speciesrich genus of flowering plants in
the frankincense and myrrh family, Burseraceae. The genus contains
approximately 190 species of shrubs and trees, which are distributed
throughout the (sub-) tropical regions of Africa, the western Indian Ocean
islands, the Arabian Peninsula, India, and Vietnam.[1][2] The genus is
drought-tolerant and common throughout the xerophytic scrub, seasonally
dry tropical forests, and woodlands of these regions.
The common name myrrh refers to several species of the genus, from
which aromatic resins are derived for various fragrance and medicinal uses
by humans.
Contents
1 Description
2 Ecology and Biogeography
3 Use by humans

4 Systematics and Taxonomy

4.1 Species

Description
Leaves in Commiphora are pinnately compound (or very rarely unifoliolate).
Many species are armed with spines. Bark is often exfoliating, peeling in
thin sheets to reveal colorful, sometimes photosynthetic bark,
below. Stems are frequentlysucculent, especially in species native to drier
environments. Flowers aresubdioecious and fruits are drupes, usually with
a 2-locular ovary (one is abortive). In response to wounding, the stems of
many species will exude aromatic resins.
Ecology and Biogeography

Commiphora can serve as a model genus for understanding plant evolution

in the drier regions of the Old World tropics, particularly in eastern
continental Africa andMadagascar, where diversity in the genus is
concentrated. The closely related sister genus to Commiphora, Bursera,
has been used as a model genus to study patterns of evolution in the New
World seasonally dry tropical forests.
Use by humans

Products from many species of Commiphora have been used for various
purposes, sometimes as timber, building material, and natural fencing, but
more often valued for the aromatic resins produced by several members of
the genus. "Myrrh", the common name for these dried resins, is fragrant
and has been used both as fragrance and for medicinal purposes
(e.g., Balsam of Mecca, C. gileadensis).[5] Use of myrrh resin is frequent
and pronounced throughout historical texts of cultural significance,
including the Bible.
Systematics and Taxonomy

Recent studies using DNA sequence data have confirmed

the monophyly of Commiphora; however, this data suggests that previous

classification of the genus into sections does not reflect monophyletic

interspecific relationships.
Medicinal use

Different parts of the plant are used as traditional remedies for disease and
skin afflictions. Juice from the leaves is used to treat warts and snakebite,
and the flower is applied to burns.[3] This species has been used as
indigenous traditional medicine in Asia for rheumatism, fractures, and other
ailments.[4] In Korean folk medicine, this impatiens species is used as a
medicine called bongseonhwa dae () for the treatment
of constipation and gastritis. Chinese used the plant to treat those bitten by
snakes or who ingested poisonous fish. Juice from the stalk, pulverised
dried stalks, and pastes from the flowers were also used to treat a variety
of ailments. Vietnamese wash their hair with an extract of the plant to
stimulate hair growth. One in vitro study found extracts of this impatiens
species, especially of the seed pod, to be active against antibiotic-resistant
strains of Helicobacter pylori. It is also an inhibitor of 5-reductases,
enzymes that reduce testosterone levels.
Chemistry

The naphthoquinones lawsone, or hennotannic acid, and lawsone methyl

ether andmethylene-3,3'-bilawsone are some of the active compounds in I.
balsaminaleaves. It also contains kaempferol and several derivatives.
Baccharaneglycosides have been found in Chinese herbal remedies made
from the seeds.
Ecology

It is widely cultivated as an ornamental plant, and has

become naturalised and invasive on several Pacific Ocean islands.
Names and etymology

Common names in other languages include mrame

lindo in Spanish, fngxinhu () in Mandarin Chinese, bng

ncor phng tin hoa () in Vietnamese, bongseonhwa (;

) in Korean, hsenka () in Japanese, elepein Hawaiian,
and kamantigi in Chamorro.
The Okinawan folk song "Tinsagu nu Hana" and the 1956 Korean
film Touch-Me-Not (Bongseonhwa in Korean) are both named for the
flower.

Foeniculum vulgare
(Foeniculum vulgare) is a flowering plant species in the carrot family. [2] It is
a hardy, perennial herb with yellow flowers and feathery leaves. It is
indigenous to the shores of the Mediterranean but has become widely
naturalized in many parts of the world, especially on dry soils near the seacoast and on riverbanks.
It is a highly aromatic and flavorful herb with culinary and medicinal uses
and, along with the similar-tasting anise, is one of the primary ingredients
of absinthe.Florence fennel or finocchio is a selection with a swollen, bulblike stem base that is used as a vegetable.
Fennel is used as a food plant by the larvae of some Lepidoptera species
including the mouse moth and the anise swallowtail.
Contents
1 Etymology and names
2 Cultural references
3 Appearance

4 Cultivation and uses

4.1 Culinary uses
4.2 Other uses
5 Chemistry
6 Production
7 Similar species

Etymology and names

The word "fennel" developed from the Middle English fenel or fenyl. This
came from the Old English fenol or finol, which in turn came from
the Latin feniculum orfoeniculum, the diminutive of fenum or faenum,
meaning "hay". The Latin word for the plant was ferula, which is now used
as the genus name of a related plant.
Cultural references

from Koehler's Medicinal-plants (1887)

As Old English finule, fennel is one of the nine plants invoked in the pagan
Anglo-Saxon Nine Herbs Charm, recorded in the 10th century.

The Greek name for fennel is marathon ()

or marathos (),and the place of the famous battle of
Marathon (whence Marathon, the subsequent sports event), literally means
a plain with fennels.The word is first attested in Mycenaean Linear B form
as ma-ra-tu-wo.
The name Funchal was given to their new town by the first settlers on
Madeira due to the abundance of wild fennel, from
the Portuguese word "funcho" (fennel) and the suffix "-al".
Appearance

Fennel, Foeniculum vulgare, is a perennial herb. It is erect, glaucous green,

and grows to heights of up to 2.5 m, with hollow stems. The leaves grow up
to 40 cm long; they are finely dissected, with the ultimate segments filiform
(threadlike), about 0.5 mm wide. (Its leaves are similar to those of dill, but
thinner.) The flowers are produced in terminal compound umbels 515 cm
wide, each umbel section having 2050 tiny yellow flowers on short
pedicels. The fruit is a dry seed from 410 mm long, half as wide or less,
and grooved.

Fennel flowerheads

Fennel seeds
Cultivation and uses
Fennel, bulb, raw
Nutritional value per 100 g (3.5 oz)
Energy

130 kJ
(31 kcal)

Carbohydrates

7.29 g

Dietary fiber

3.1 g

Fat

0.20 g

Protein

1.24 g

Vitamins
Thiamine (B1)

(1%)
0.01 mg

Riboflavin (B2)

(3%)
0.032 mg

Niacin (B3)

(4%)
0.64 mg

Pantothenic acid (B5)

(5%)

0.232 mg
Vitamin B6

(4%)
0.047 mg

Folate (B9)

(7%)
27 g

Vitamin C

(14%)
12 mg

Trace minerals
Calcium

(5%)
49 mg

Iron

(6%)
0.73 mg

Magnesium

(5%)
17 mg

Manganese

(9%)
0.191 mg

Phosphorus

(7%)
50 mg

Potassium

(9%)

414 mg
Zinc

(2%)
0.20 mg

Units
g = micrograms mg = milligrams
IU = International units
Percentages are roughly approximated
usingUS recommendations for adults.
Source: USDA Nutrient Database
Fennel is widely cultivated, both in its native range and elsewhere, for its
edible, strongly flavored leaves and fruits. Its aniseed flavor comes
from anethole, an aromatic compound also found in anise and star anise,
and its taste and aroma are similar to theirs, though usually not as strong.
Florence fennel (Foeniculum vulgare Azoricum Group; syn. F.
vulgare var.azoricum) is a cultivar group with inflated leaf bases which form
a bulb-like structure. It is of cultivated origin, and has a mild anise-like
flavor, but is sweeter and more aromatic. Florence fennel plants are smaller
than the wild type. Their inflated leaf bases are eaten as a vegetable, both
raw and cooked. There are several cultivarsof Florence fennel, which is
also known by several other names, notably the Italianname finocchio. In
North American supermarkets, it is often mislabeled as "anise".
Foeniculum vulgare 'Purpureum' or 'Nigra', "bronze-leaved" fennel, is
widely available as a decorative garden plant.
Fennel has become naturalized along roadsides, in pastures, and in other
open sites in many regions, including northern Europe, the United States,
southernCanada, and much of Asia and Australia. It propagates well by
seed, and is considered an invasive species and a weed in Australia and
the United States. In western North America, fennel can be found from the

coastal and inland wildland-urban interface east into hill and mountain
areas, excluding desert habitats.

Florence fennel bulbs

Florence fennel is one of the three main herbs used in the preparation
ofabsinthe, an alcoholic mixture which originated as a medicinal elixir
inSwitzerland and became, by the late 19th century, a popular alcoholic
drink in France and other countries.

Culinary uses

Sugar-coated and uncoated fennel seeds are used in India and

Pakistan in mukhwas, an after-meal snack and breath freshener.
The bulb, foliage, and seeds of the fennel plant are widely used in many of
the culinary traditions of the world. The small flowers of wild fennel (known
as fennel "pollen" [) are the most potent form of fennel, but also the most
expensive. Dried fennel seed is an aromatic, anise-flavored spice, brown or
green in color when fresh, slowly turning a dull grey as the seed ages. For

cooking, green seeds are optimal. The leaves are delicately flavored and
similar in shape to those of dill. The bulb is a crisp vegetable that can be
sauted, stewed, braised, grilled, or eaten raw. Young tender leaves are
used for garnishes, as a salad, to add flavor to salads, to flavor sauces to
be served with puddings, and also in soups and fish sauce.
Fennel seeds are sometimes confused with those of anise, which are
similar in taste and appearance, though smaller. Fennel is also used as a
flavoring in some natural toothpastes. The seeds are used in cookery and
sweet desserts.
Many cultures in India and Pakistan (where it is known
as saunf in Hindi),Afghanistan, Iran, and the Middle East use fennel seed in
their cookery. It is one of the most important spices in Kashmiri
Pandit and Gujarati cooking.[21] It is an essential ingredient of
the Assamese/Bengali/Oriya spice mixture panch phoron and in
Chinese five-spice powders. In many parts of India and Pakistan, roasted
fennel seeds are consumed as mukhwas, an after-meal digestive and
breath freshener.
Fennel leaves are used in some parts of India as leafy green vegetables
either by themselves or mixed with other vegetables, cooked to be served
and consumed as part of a meal. In Syria and Lebanon, the young leaves
are used to make a special kind of egg omelette (along with onions and
flour) called ijjeh.
Many egg, fish, and other dishes employ fresh or dried fennel leaves.
Florence fennel is a key ingredient in some Italian andGerman salads,
often tossed with chicory and avocado, or it can be braised and served as a
warm side dish. It may beblanched or marinated, or cooked in risotto.
Fennel seeds are the primary flavor component in Italian sausage.
In Spain, the stems of the fennel plant are used in the preparation of
pickled eggplants, berenjenas de Almagro.
An herbal tea or tisane can be made from fennel.[23]

Fennel (Foeniculum vulgare) essential oil in clear glass vial

On account of its aromatic properties, fennel fruit forms one of the
ingredients of the well-known compound liquorice powder.
In the Indian subcontinent, fennel seeds are also eaten raw, sometimes
with a sweetener.
Other uses
Fennel is one of the plants which is said to be disliked by fleas, and
powdered fennel has the effect of driving away fleas from kennels and
stables.
Chemistry

Foeniculoside I is a stilbenoid. It is a glucoside of the stilbene trimer cismiyabenol C. It can be found in Foeniculi fructus (fruit of F. vulgare).
Production
India is the leader in production of anise, badian (star anise), fennel
and coriander.
Top ten anise, badian, fennel & coriander producers

Production
(Tonnesper year)

Footnote

India

110,000

Mexico

49,688

China

40,000

Iran

30,000

Bulgaria

28,100

Syria

27,700

Morocco

23,000

Egypt

22,000

Canada

11,000

Afghanistan

10,000

415,027

Country

World

No symbol = official figure, P = official figure, F = FAO estimate, * =

Unofficial/Semi-official/mirror data, C = Calculated figure A =
Aggregate (may include official, semi-official or estimates);
Source: Food And Agricultural Organization of United Nations:
Economic And Social Department: The Statistical Division
Similar species

Many species in the family Apiaceae or Umbelliferae are superficially

similar to fennel, and some, such as poison hemlock, are toxic. It is
therefore unwise, and potentially extremely dangerous, to use any part of
any of these plants as an herb or vegetable unless it can be positively
identified as being edible.

Dill, coriander and caraway are similar-looking herbs but shorter-growing

than fennel, reaching only 4060 cm (1624 in). Dill has thread-like,
feathery leaves and yellow flowers; coriander and caraway have white
flowers and finely divided leaves (though not as fine as dill or fennel) and
are also shorter-lived (being annual or biennial plants). The superficial
similarity in appearance between these may have led to a sharing of names
and etymology, as in the case of meridian fennel, a term for caraway.
Cicely, or sweet cicely, is sometimes grown as an herb; like fennel, it
contains anethole and therefore has a similar aroma but is lower-growing
(up to 2 m (6.6 ft)) and has large umbels of white flowers and leaves that
are fern-like rather than threadlike.
Giant fennel (Ferula communis) is a large, coarse plant, with a pungent
aroma, which grows wild in the Mediterranean region and is only
occasionally grown in gardens elsewhere. Other species of the
genus Ferula are also commonly called giant fennel, but they are not
culinary herbs.
In North America, fennel may be found growing in the same habitat and
alongside natives osha (Ligusticum porteri) andLomatium species, useful
medicinal relatives in the parsley family.
Most Lomatium species have yellow flowers like fennel, but some are white
flowered and resemble poison hemlock.Lomatium is an important historical
food plant of Native Americans known as 'biscuit root'. Most Lomatium spp.
have finely divided, hairlike leaves; their roots have a delicate rice-like odor,
unlike the musty odor of hemlock. Lomatium species tend to prefer dry
rocky soils devoid of organic material.
FENNEL OVERVIEW INFORMATION
Fennel is a perennial, pleasant-smelling herb with yellow flowers. It is
native to the Mediterranean, but is now found throughout the world. Dried
fennel seeds are often used in cooking as an anise-flavored spice. But
dont confuse fennel with anise; though they look and taste similar, they are
not the same. Fennels dried ripe seeds and oil are used to make medicine.

Fennel is used for various digestive problems including heartburn, intestinal

gas,bloating, loss of appetite, and colic in infants. It is also used for upper
respiratory tract infections, coughs, bronchitis, cholera,
backache, bedwetting, and visual problems.
Some women use fennel for increasing the flow of breast milk,
promotingmenstruation, easing the birthing process, and
increasing sex drive.
Fennel powder is used as a poultice for snakebites.
In foods and beverages, fennel oil is used as a flavoring agent.
In other manufacturing processes, fennel oil is used as a flavoring agent in
certainlaxatives, and as a fragrance component in soaps and cosmetics.
How does it work?
Fennel might relax the colon and decrease respiratory tract secretions.
ENNEL USES & EFFECTIVENESS
Possibly Effective for:
Colic in breast-fed infants. Research suggests that giving fennel seed oil
can relieve colic in infants 2-12 weeks old. Also, breast-fed infants with
colic who are given a specific multi-ingredient product containing fennel,
lemon balm, and German chamomile (ColiMil) cry for a shorter period of
time than other infants with colic. In addition, giving a specific tea
containing fennel, chamomile, vervain, licorice, and balm-mint (Calma-Bebi,
Bonomelli) can reduce colic severity in infants.

Insufficient Evidence for:

Swelling of the colon (colitis). Early research suggests that taking an herbal
combination of fennel, dandelion, St. Johns wort, lemon balm, and
calendula can reduce pain along the large intestine in people with swelling
of the colon.
Constipation. Early research suggests that drinking an herbal tea
containing a combination of fennel, anise, elderberry, and senna daily for 5
days can reduceconstipation. Also, drinking a tea containing fennel, senna,
licorice, orange peel, cassia cinnamon, coriander, and ginger (Smooth
Move) for one month can reduce constipation in older people.
Painful menstruation. Some research suggests that taking fennel extract
four times daily starting at the beginning of a period can reduce pain in girls
and young women with painful menstruation called dysmenorrhea.
However, other research shows conflicting results.
Excess hair on women (hirsutism). Early research suggests that using
fennel cream for 12 weeks can reduce hair on women with male pattern
body hair.
Sunburn. Early research suggests that applying fennel to the skin before
ultraviolet (UV) exposure can reduce sunburn.
Stomach upset and indigestion.
Airway swelling.
Bronchitis.
Cough.
Mild spasms of the stomach and intestines.
Intestinal gas (flatulence).
Bloating.
Upper respiratory tract infection.
FENNEL SIDE EFFECTS & SAFETY

Fennel is LIKELY SAFE when taken by mouth in the amounts commonly

found in food. For the most part, there is not enough evidence to know
whether it is safe for adults when used in medicinal amounts.
Some people can have allergic skin reactions to fennel. People who are
allergic to plants such as celery, carrot, and mugwort are more likely to also
be allergic to fennel. Fennel can also make skin extra sensitive to sunlight
and make it easier to get a sunburn. Wear sunblock if you are light-skinned.
Special Precautions & Warnings:
Pregnancy and breast-feeding: Not enough is known about the safety of
using fennel during pregnancy. Its best to avoid use.
During breast-feeding, fennel is POSSIBLY UNSAFE. Its been reported
that two breast-feeding infants experienced damage to their nervous
systems after their mothers drank an herbal tea that contained fennel.
Children: For the most part, there is not enough evidence to know whether
it is safe for children when used in medicinal amounts. However,
researchers have studied a combination product (ColiMil) for colic that
contains fennel, lemon balm, and German chamomile. This product seems
to be safe in infants when used for up to one week.
Allergy to celery, carrot or mugwort: Fennel might cause an allergic reaction
in people who are sensitive to these plants.
Bleeding disorders: Fennel might slow blood clotting. Taking fennel might
increase the risk of bleeding or bruising in people with bleeding disorders.
Hormone-sensitive condition such as breast cancer, uterine cancer, ovarian
cancer, endometriosis, or uterine fibroids: Fennel might act like estrogen. If
you have any condition that might be made worse by exposure to estrogen,
do not use fennel.
ENNEL DOSING

The following doses have been studied in scientific research:

BY MOUTH:
For colic in breast-fed infants: a specific multi-ingredient product containing
164 mg of fennel, 97 mg of lemon balm, and 178 mg of German chamomile
(Colimil) twice daily for a week.

Syzygium aromaticum.

Scientific
classification
Kingdom Plantae
:

(unranke Angiosper
d):
ms
(unranke Eudicots
d):
(unranke Rosids
d):
Order:

Myrtales

Family:

Myrtacea
e

Genus:

Syzygium

Species: S.
aromaticu
m
Binomial name
Syzygium
aromaticum
(L.) Merrill & Perry
Synonyms[1]
Caryophyllus
aromaticus L.
Eugenia
aromatica (L.) Baill.
Eugenia
caryophyllata Thunb
.

Eugenia
caryophyllus (Spren
g.) Bullock & S. G.
Harrison
Cloves are the aromatic flower buds of a tree in the
family Myrtaceae, Syzygium aromaticum. They are native to the Maluku
Islands in Indonesia, and are commonly used as a spice. Cloves are
commercially harvested primarily in
Indonesia, India,Madagascar, Zanzibar, Pakistan, Sri Lanka and Tanzania.
The clove tree is an evergreen tree that grows up to 812 m tall, with
large leavesand sanguine flowers grouped in terminal clusters. The flower
buds initially have a pale hue, gradually turn green, then transition to a
bright red when ready for harvest. Cloves are harvested at 1.52.0 cm
long, and consist of a long calyx that terminates in four spreading sepals,
and four unopened petals that form a small central ball.
Contents
1 Uses
1.1 Non-culinary uses
1.2 Traditional medicinal uses
1.3 Potential medicinal uses
2 Adulteration
3 History
4 Active compounds

Uses

Dried cloves

Clove output in 2005

Cloves are used in the cuisine of Asian, African, and the Near and Middle
East, lending flavor to meats, curries, andmarinades, as well as fruit such
as apples, pears or rhubarb. Cloves may be used to give aromatic and
flavor qualities to hot beverages, often combined with other ingredients
such as lemon and sugar. They are a common element in spice blends
such as pumpkin pie spice and speculoos spices.
In Mexican cuisine, cloves are best known as clavos de olor, and often
accompanycumin and cinnamon.
A major component of clove taste is imparted by the
chemical eugenol, and the quantity of the spice required is typically small. It
pairs well with cinnamon, allspice,vanilla, red wine and basil, as well
as onion, citrus peel, star anise, or peppercorns.
Non-culinary uses
The spice is used in a type of cigarette called kretek in Indonesia. They
have been smoked throughout Europe, Asia, and the United States. In
2009, clove cigarettes (as well as fruit- and candy-flavored cigarettes) were

outlawed in the US. Cigarettes containing clove are now classified as

cigars when sold in the US.
Due to the bioactive chemicals of clove, the spice may be used as an ant
repellent.
They can be used to make a fragrance pomander when combined with an
orange. When given as a gift in Victorian England, such a pomander
indicated "warmth of feeling."
Traditional medicinal uses

Cloves are used in Indian unani medicine, Chinese medicine, and

western herbalism and dentistry where the essential oil is used as
an anodyne (painkiller) for dental emergencies. Cloves are used as
a carminative, to increase hydrochloric acid in the stomach and to
improve peristalsis. Cloves are also said to be a natural anthelmintic. The
essential oil is used in aromatherapy when stimulation and warming are
needed, especially for digestive problems. Topical application over the
stomach or abdomen are said to warm the digestive tract. Applied to a
cavity in a decayed tooth, it also relieves toothache.
In Chinese medicine, cloves or ding xiang are considered acrid, warm, and
aromatic, entering the kidney, spleen andstomach meridians, and are
notable in their ability to warm the middle, direct stomach qi downward, to
treat hiccough and to fortify the kidney yang. Because the herb is so
warming, it is contraindicated in any persons with fire symptoms and
according to classical sources should not be used for anything except cold
from yang deficiency. As such, it is used in formulas for impotence or clear
vaginal discharge from yang deficiency, for morning sickness together
with ginseng andpatchouli, or for vomiting and diarrhea due to spleen and
stomach coldness.
Cloves may be used internally as a tea and topically as an oil for hypotonic
muscles, including for multiple sclerosis. This is also found in Tibetan
medicine.[9] Some recommend avoiding more than occasional use of cloves
internally in the presence of pitta inflammation such as is found in acute
flares of autoimmune diseases.

Potential medicinal uses

The U.S. Food and Drug Administration (FDA) has reclassified eugenol
(one of the chemicals contained in clove oil), downgrading its effectiveness
rating. The FDA now believes not enough evidence indicates clove oil or
eugenol is effective for toothache pain or a variety of other types of pain.
Studies to determine its effectiveness for fever reduction, as
a mosquito repellent, and to prevent premature ejaculationhave been
inconclusive. It remains unproven whether clove may reduce blood sugar
levels.
In addition, clove oil is used in preparation of some toothpastes and
Clovacaine solution, which is a local anesthetic used in oral ulceration and
inflammation. Eugenol (or clove oil generally) is mixed with zinc oxide to
form a temporary tooth cavity filling.
Clove oil can be used to anesthetize fish, and prolonged exposure to higher
doses (the recommended dose is 400 mg/l) is considered a humane means
of euthanasia.
Adulteration
Clove stalks are slender stems of the inflorescence axis that show
opposite decussate branching. Externally, they are brownish, rough, and
irregularly wrinkled longitudinally with short fracture and dry, woody texture.
Mother cloves (anthophylli) are the ripe fruits of cloves that are ovoid,
brown berries, unilocular and one-seeded. This can be detected by the
presence of much starch in the seeds.
Brown cloves are expanded flowers from which
both corollae and stamens have been detached.
Exhausted cloves have most or all the oil removed by distillation. They yield
no oil and are darker in color.

History

Archeologists have found cloves in a ceramic vessel in Syria, with evidence

that dates the find to within a few years of 1721 BCE. In the third century
BCE, a Chinese leader in the Han Dynasty required those who addressed
him to chew cloves to freshen their breath. Cloves were traded
by Muslim sailors and merchants during the Middle Ages in the
profitable Indian Ocean trade, the clove trade is also mentioned by Ibn
Battuta and even famous Arabian Nights characters such as Sinbad the
Sailor are known to have bought and sold cloves from India.
Until modern times, cloves grew only on a few islands in the Maluku
Islands (historically called the Spice Islands),
includingBacan, Makian, Moti, Ternate, and Tidore. In fact, the clove tree
that experts believe is the oldest in the world, namedAfo, is on Ternate. The
tree is between 350 and 400 years old. Tourists are told that seedlings from
this very tree were stolen by a Frenchman named Poivre in 1770,
transferred to France, and then later to Zanzibar, which was once the
world's largest producer of cloves.
Until cloves were grown outside of the Maluku Islands, they were traded
like oil, with an enforced limit on exportation. As the Dutch East India
Company consolidated its control of the spice trade in the 17th century,
they sought to gain a monopolyin cloves as they had in nutmeg. However,
"unlike nutmeg and mace, which were limited to the minute Bandas, clove
trees grew all over the Moluccas, and the trade in cloves was way beyond
the limited policing powers of the corporation."
Active compounds

The compound eugenol is responsible for most of the characteristic aroma

of cloves.

Eugenol comprises 72-90% of the essential oil extracted from cloves, and
is the compound most responsible for clove aroma. Other important
essential oil constituents of clove oil include acetyl eugenol, betacaryophyllene and vanillin,crategolic acid, tannins such as bicornin,
gallotannic acid, methyl salicylate(painkiller),
the flavonoids eugenin, kaempferol, rhamnetin, and eugenitin,
triterpenoids such as oleanolic acid, stigmasterol, and campesterol, and
severalsesquiterpenes.
Eugenol is toxic in relatively small quantities; with a dose of 5 - 10 ml
severely affecting a 2 year old child.
Cloves nutrition facts
Cloves are one of the highly prized spices, widely recognized all over the
world for their medicinal and culinary qualities. The spices actually are the
"flower buds" from evergreen rain-forest tree native to Indonesia.
Botanically, clove-spice belongs to the family of Myrtaceae in the
genus; Sygyzium, and scientifically named as Sygizium aromaticum.
At their initial stages of development, flower buds are pale in color which
gradually turn to green, and, finally develop into bright-red clove buds by
the time of harvesting. The buds are generally picked up when they reach
1.5-2 cm in length.

Clove buds

Structurally, each bud consists of a long calyx; terminating in four spreading

sepals and four unopened petals. These closed petals form into a small ball
(dome) at the top. The sweet aroma of cloves is due to eugenol, an
essential oil in them.

Medicinal properties and health benefits of cloves

The active principles in the clove are known to have antioxidant, anti-septic,
local anesthetic, anti-inflammatory, rubefacient (warming and soothing),
carminative and anti-flatulent properties.
The spice contains health benefiting essential oils such as eugenol. It is a
phenyl-propanoids class of chemical compound which gives pleasant,
sweet aromatic fragrances to the clove-bud. Eugenol has local anesthetic
and antiseptic properties, hence; useful in dental care essentials as well as
in treatment procedures.
The other important constituents in this spice include:
essential oils: acetyl eugenol, beta-caryophyllene and vanillin, crategolic
acid;
tannins: gallotannic acid, methyl salicylate (painkiller);
the flavonoids: eugenin, kaempferol, rhamnetin, and eugenitin;

triterpenoids: such as oleanolic acid, stigmasterol and campesterol

and several sesquiterpenes.
The active principles in the clove may increase gut motility as well as
improve the digestion power through increasing gastro-intestinal enzyme
secretions. Thus, helps relieve indigestion and constipation problems.
The spice also contains a good amount of minerals like potassium,
manganese, iron, selenium and magnesium. Potassium is an important
electrolyte of cell and body fluids that helps control heart rate and blood
pressure. Manganese is used by the body as a co-factor for the antioxidant
enzyme, superoxide dismutase.
Further, the spice buds contain very good amounts of vitamin A and betacarotene levels. These compounds are known to have antioxidant
properties. Vitamin A is also required by the body for maintaining healthy
mucus membranes and skin in addition to essential for vision. Consumption
of natural foods rich in flavonoids helps to protect the body from lung and
oral cavity cancers.
Additionally, this spice is a good source of vitamin-K, vitamin-B6
(pyridoxine), thiamin (vitamin B-1), vitamin-C and riboflavin. Consumption
of foods rich in vitamin C helps the body develop resistance against
infectious agents and scavenge harmful oxygen-free radicals.

Clove buds can be readily available year around in the spice markets. Good
quality buds should release sweet fragrance when squeezed between the
thumb and index fingers. In the store, buy whole buds instead of powder
since oftentimes it may contain adulterated spicy powders. The buds
should be wholesome with stem and sepals, and compact.
Whole cloves should be stored in cool dark place in close containers for
many months and can be milled using "hand mill" as and when required.
Ground/powder clove should be stored inside the refrigerator in airtight
containers and should be used as early as possible since it loses its flavor
quickly.

Medicinal uses

The essential oil, eugenol in this spice has been in therapeutic use in
dentistry as a local-anesthetic and antiseptic for teeth and gum.
Eugenol also has been found to reduce blood sugar levels in diabetics, but
further detailed studies required to establish its benefits.
Its decoction is sometimes used in treating flatulence and indigestion in
traditional medicine preparations.
It is also thought to have natural anti-parasite (kills intestinal worms)
function.
The essential volatile oils functions as a rubefacient, meaning that it irritates
the skin and expands the blood vessels, increasing the flow of blood to
make the skin feel warmer, making it a popular home remedy
for arthritis and sore muscles, used either as a poultice or in hot baths.

Clove oil is also used in aromatherapy.

Culinary uses
In order to keep the fragrance and flavor intact, clove is generally grounded
just before preparing dishes and added at the last moment in the cooking
recipes. This is because prolonged cooking results in evaporation of its
essential oils.
This popular spice has been used in preparation of many regular dishes in
Asian and Chinese cuisine since ancient times. Along with other spices
like pepper, turmeric, gingeretc. is being used in marinating chicken, fish,
and meat.
Some of Indian vegetarian, chicken and rice dishes (biriyani) contain cloves
and in the Middle East, it is used in meat and rice dishes.
The spice also features in the preparation of soups, barbecue sauces,
pickling and as one of the ingredients in curry powders.

Safety profile
Consumption of dishes prepared with large quantity of clove can cause
gastrointestinal irritation, central nervous system disorders. Recipes
prepared with this spice should be avoided in individuals with stomach
ulcers, ulcerative colitis, and diverticulitis conditions. Eating cloves is also
avoided during pregnancy. (Medical disclaimer)

Artemisia absinthium

Artemisia absinthium, Linn. (Afsanteen) of the family Compositae; Astraceae

is an aromatic, bitter and perennial shrubby plant. This grows from 60 to 120
cm in height with a woody, hardy rosette and high branch bearing stem. The
leaves of the plant, probably the best known species, have been used in
medicines and such beverages as absinthe. The whole plant is an aromatic
tonic and formerly enjoyed a high reputation in debility of the digestive
organs. It was also regarded as an anthelmintic. Before the discovery of
cinchona, it was largely used in intermittent. Keeping in view the medicinal
importance of the plant in Unani Medicine, an attempt has been made to
review the available literature on its ethnobotany, medicinal uses, chemistry
and scientific studies.
Scientific Name(s): Artemisia absinthium L. Family: Asteraceae (daisies)
Common Name(s): Wormwood , absinthium , armoise , wermut , absinthe ,
absinthites , ajenjo , pelin otu , aci pelin , ak pelin , buyuk pelin , vilayati
afsanteen 1 , 2 , 3 , 4
Uses
Wormwood was traditionally used to treat worm infestations, although there
is no clinical data supporting this use. Anti-inflammatory, antipyretic, and
chemotherapeutic activity is documented in nonhuman studies. Information
regarding the plant's use in Crohn disease is limited. Wormwood is also used
as a flavoring agent.
Dosing
Wormwood is commercially available as an essential oil, as well as in
capsule, tablet, tincture, and aqueous extract dosage forms. However, there
is no recent clinical evidence to support dose recommendations for
wormwood. Traditional use for treating dyspepsia was dosed at 3 to 5 g daily
as an infusion or 2 to 3 g daily as the herb.
Contraindications
Avoid use with hypersensitivity to any of the components of wormwood,
particularly the essential oil. It may be contraindicated in patients with an
underlying defect with hepatic heme synthesis (thujone is a porphyrogenic
terpenoid).
Pregnancy/Lactation

abortifacient and emmenagogue effects. Avoid use.

Interactions
None well documented.
Adverse Reactions
Thujone produces a state of excitement and is a powerful convulsant.
Ingestion of wormwood may result in absinthism, a syndrome characterized
by digestive disorders, thirst, restlessness, vertigo, trembling of the limbs,
numbness of the extremities, loss of intellect, delirium, paralysis, and death.
Toxicology
Wormwood is classified as an unsafe herb by the Food and Drug
Administration (FDA) because of the neurotoxic potential of thujone and its
derivatives. The safety of wormwood is poorly documented despite its long
history as a food additive. Convulsions, dermatitis, and renal failure have
been documented.
Botany
Wormwood is an odorous, perennial shrub native to Europe and naturalized in
the northeastern, central, and northwestern United States. Its aromatic
leaves have a strong sage odor and bitter taste, and its multibranched stems
are covered with fine, silky hairs. The plant has a fibrous root system and
grows to about 1.2 m in height. Its small flowers, which bloom July through
August, are green to yellow and arranged in large, spike-like panicles. The
deeply lobed leaves are grayish-green in color. Leaves and stems no thicker
than 4 mm are used medicinally.
History
The name wormwood is derived from ancient use of the plant and its
extracts as an intestinal anthelmintic. In Pakistan's indigenous medicinal
systems, the leaves and flowering tops are used as an anthelmintic,
antiseptic, febrifuge, and stomachic, and to alleviate chronic fever,
dyspepsia, and hepatobiliary ailments. An ethobotanical study in Turkey
documents the plant's use as an abortifacient, as a blood depurative, and in
treating stomach aches. It has also been used as an appetizer. Caribbean
folk medicine documents the use of wormwood for menstrual pain, vaginitis,
and other unspecified female complaints. Extracts of the plant are used as a
bitter seasoning for food and added to drinks such as beer, tea, or coffee. In
western European traditional herbal medicine, wormwood was recommended
for gastric pain, cardiac stimulation, and to restore declining mental
function. French and Spanish New Mexicans used the plant species along
with other plants as an emmenagogue. In traditional Chinese medicine,
practitioners treated acute bacillary dysentery by applying fresh and dried

absinthium. A poultice of the plant has been used medicinally for tendon
inflammation, and wormwood tea was used traditionally as a diaphoretic.
Wormwood extract is the main ingredient in absinthe, a toxic liquor that
induces absinthism, a syndrome characterized by addiction, GI problems,
auditory and visual hallucinations, epilepsy, brain damage, and increased
risk of psychiatric illness and suicide. The drink has been banned in several
countries, but in the 19th century, absinthe-based liquor was known for its
aphrodisiac and healing properties and also was reputed to stimulate
creativity. The emerald-green color of absinthe liquor came from chlorophyll;
however, copper and antimony salts were reportedly added as colorants to
inferior batches, with toxic consequences. Thujone-free wormwood extract is
currently used as a flavoring, primarily in alcoholic beverages such as
vermouth.
Chemistry
The medicinal or active components in wormwood are the essential oils,
anabsinthin, absinthin, resins, and organic acids. The bitter taste of
wormwood is caused by the glucosides absinthin and anabsinthin, and
several related compounds. Lactones include arabsin, artabin,
ketopelenolide, and others related to santonin. An important isolated
flavonoid is 5,6,3,5-tetramethoxy 7,4-hydroxyflavone (p7F).
Essential oils
Many Artemisia species contain monoterpenoid thujone derivatives with
toxic CNS effects. Wormwood typically contains small amounts of thujone
derivatives, including 0.2% ( Z )-thujone and 0.5% ( E )-thujone ; however, the
thujone content varies widely.
The major components of wormwood oil include chamazulene (18%),
nuciferol butanoate (8%), nuciferol propionate (5%), and caryophyllene oxide
(4%). The essential oils also contain a large amount of aromatic compounds
(41%) and a low level of oxygenated monoterpenes (24%). The plant contains
a pleasant-smelling volatile oil (about 1% to 2% by weight), as well as
phellandrene, pinene, azulene, and more than 6 other minor components.
Flowers may contain oil composed of up to 35% thujones. Cis - andtrans epoxycymenes account for up to 57% of the volatile oil derived from Italian
absinthium. The herb is standardized based on absinthin.
Wormwood contains trace amounts of thymol and carvacrol, as well as other
phenolic compounds with potent antioxidant and free radical-scavenging
activity.
Uses and Pharmacology

Scientific literature contains mostly phytochemical, ethnopharmacological,

and ethnobotanical investigations, with little clinical investigation of
wormwood.
Anthelmintic activity
The anthelmintic activity of the plant is thought to be caused by lactones
related to santonin, which is found in wormseed and other species of
Artemisia . In addition, thujone can stun roundworms, which can then be
expelled by normal intestinal peristalsis.
Animal data
A similar study of plants in central Italy reported some veterinary use of the
plant as an anthelmintic for cows.
Clinical data
An ethnobotanical and ethnopharmacological study documented the use of
wormwood for treating intestinal worms in Dominica, West Indies.
Antifungal activity
In vitro data
The essential oils distilled from the aerial parts of A. absinthium inhibited the
growth of Candida albicans and Saccharomyces cerevisiae var. chevalieri .
Antimicrobial activity
Thujone oils are recognized as the active constituents affecting microbial
growth.
In vitro data
The essential oils of wormwood have antimicrobial activity against
Escherichia coli , Salmonella enteritidis , Pseudomonas aeruginosa ,
Klebsiella pneumoniae , Staphylococcus aureus , C. albicans , and
Aspergillus niger . The activity was considered comparable with that of
erythromycin.
Animal data
Hexane-, chloroform-, and water-soluble extracts of A. absinthium exhibited
antipyretic activity against subcutaneous yeast injections in rabbits. No
toxic effects were documented for the plant extract at doses up to 1.6 g/kg.
Crohn disease
Clinical data

In Germany, a double-blind, placebo-controlled trial examined the efficacy of

administering an herbal blend (3 500 mg per day) containing wormwood
versus placebo over 10 weeks in 40 patients suffering from Crohn disease.
Twenty patients received the treatment, while the remaining patients
received placebo. All patients achieved good control of their symptoms
through use of steroids and other medications. Outcome measures included
the effect of wormwood on steroid dependence and psychological measures,
such as decline in symptoms of depression often associated with Crohn
disease. Physical and psychological symptoms worsened for patients taking
placebo. However, those receiving wormwood showed gradual improvement
of symptoms, with 13 patients nearly free of physical and psychological
symptoms and less dependent on steroids. Patients suffered no serious
adverse reactions.
Inflammation
In vitro

pF7, a flavonoid isolated from A. absinthium , has antioxidant activity and has
inhibited nuclear factor-kappa B (NF-kappa B activation). The regulatory
functions of pF7 were examined on the production of nitric oxide (NO),
prostaglandin (E2 and PGE2), tumor necrosis factor (TNF-alpha), and
expression of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and
collagen-induced arthritis. The production of COX-2, PGE2, iNOS, and NO in
lipopolysaccharide-stimulated RAW 264.7 cells was inhibited by pF7. pF7 also
suppressed TNF-alpha activity and inhibited NF-kappa B.
Other pharmacological activity
Antihemolytic effect
In vitro, the plant species protected human erythrocytes against hypotonic
shock.
GI ulcer
In rats, extracts of the plant species reduced the volume of gastric juice,
acid output, and peptic activity in ulcerated rats.
CNS
A. absinthium has been studied for cognitive enhancement because of its
nicotinic and muscarinic cholinergic receptor activity (concentration that
inhibits 50% [IC

50

] of less than 1 mg/mL) in homogenates of human cerebral

cortical membranes. The intoxicating effects of thujone were believed to

activate receptors responsible for marijuana intoxication; however, thujone

exhibited low affinity for rat cannabinoid receptors. Methanol extracts of A.

absinthium enhanced neurite outgrowth induced by nerve growth factor and
PC12D cells.
Dosage
Wormwood is commercially available as an essential oil, as well as in
capsule, tablet, tincture, and aqueous extract dosage forms. However, there
is no recent clinical evidence to support dose recommendations for
wormwood. Its classical use for treating dyspepsia was at a dose of 3 to 5 g
daily as an infusion or 2 to 3 g daily as the herb.
Pregnancy/Lactation
Avoid use because of documented abortifacient and emmenagogue effects.
Interactions
Acetaminophen
Wormwood has a hepatoprotective action against acetaminophen and carbon
tetrachloride-induced liver toxicity in rats and mice. The mechanism of
action may be associated with inhibition of hepatic microsomal drug
metabolizing enzymes, antioxidant activity, and/or blocking calcium
channels.
GI medications
Theoretically, the plant may affect the efficacy of antacids, histaminereceptor antagonists, proton pump inhibitors, and sucralfate.
Phenobarbital
The thujones in wormwood may reduce the clinical efficacy of phenobarbital
by lowering the seizure threshold.
Adverse Reactions
Thujone produces a state of excitement and is a powerful convulsant.
Ingestion of wormwood may lead to absinthism, a syndrome characterized by
digestive disorders, thirst, restlessness, vertigo, trembling of the limbs,
numbness of the extremities, loss of intellect, delirium, paralysis, and death.
Toxicology
Avoid use with hypersensitivity to any of the components of wormwood,
particularly the essential oil composition. Theoretically, wormwood may be
contraindicated in patients with an underlying defect with hepatic heme
synthesis because thujone is a porphyrogenic terpenoid.
Wormwood is classified as an unsafe herb by the FDA because of the
neurotoxic potential of thujone and its derivatives. Few studies document the
safety of wormwood despite its long history of use as a food additive.

Thujone bears a superficial structural resemblance to camphor, pinene,

anethole, and citral.
Convulsions
In a 13-week dose-toxicity study, convulsions were observed in rats given
thujone in concentrations as low as 25 mg/kg/day. An increase in mortality
was shown in rats given 50 mg/kg/day. Other studies document a dose of
120 mg/kg as fatal, including a subcutaneous median lethal dose of thujone
in mice as 134 mg/kg.
Dermatitis
Wormwood oil is used as an ingredient in rubefacient preparations; the
flowers may induce topical eruptions in sensitized persons.
Renal failure
A 31-year-old man suffered convulsions after drinking 10 mL of essential oil
from wormwood or A. absinthium . The patient mistakenly assumed the
essential oil was actually absinthe liquor and consumed the 10 mL full
strength. The seizure was believed to be caused by the essential oil of
wormwood, which also led to rhabdomyolysis, renal failure, and congestive
heart failure. The patient recovered and laboratory parameters returned to
normal after 17 days.
Solanum nigrum

Plant species
Botanical Name

Solanum nigrum L.

Family

SOLANACEAE

Used In

Unani and Sidha

Distribution
This species is globally distributed in
the tropics. Within India, it is said to
be found throughout as a weed in
disturbed habitats, roadsides and
gardens.

Common Uses
The whole plant of Kakamachi is used in the form of juice to treat eyediseases, rat poisoning, skin diseases, oedema, cough, urticarial patches,
for achieving conception and to relieve from difficult labour. As rejuvinative /
Rasayana Kakamaci promotes strength if used as decoction with jaggery,
pippali (piper longum) or marica (piper nigrum). Ghee cooked with kakamaci
juice acts similarly (VD.4.3) Skin diseases ( Kustha) In skin diseases kustha
leaves of kakamachi is used as a vegetable. (CS.Ci.7.96; SU.3.17) Cough
Vastuka (Amaranthus ), kakamaci are useful as vegetable in cough caused
by vata (dry cough) (CS.Ci.18.81-82)

Arabic (7)

anab-ul-thalab, anab-us-salab, anb-us-salap,

anbulzahalab, enab-ul-thalab, enabus salab,
makoh

English (1)

black nightshade

Hindi (13)

chirpoti, gurkamai, gurkkamai, kabaiya, kalamako, kali-papotan, kamuni, mako, makoi, makoy,
mukko, palpotan, uda-mako

Kannada (11)

ganike, kakamachi gida, kakarundi, kakmunchi,

kanchi, kare-ganike, kare-kanchi, karee kaachi,
karikaachi gida, kempu kaachi, sunde kaachi

Malayalam (7)

karimtakkali, karintakali, karuppu-manattakali,

manattakali, manattakkali, manattan-kanni,
tudavalam

Marathi (7)

ghati, kamchi, kamoni, kangani, laghukavali,

meko, nakmachi

Persian (2)

angoor-e-shifa, robah turbuk

Solanum nigrum
Solanum nigrum

Scientific
classification
Kingdom:

Plantae

(unranked)
:

Angiosperm
s

(unranked)
:

Eudicots

(unranked)
:

Asterids

Order:

Solanales

Family:

Solanaceae

Genus:

Solanum

Species:

S. nigrum

Binomial name

Solanum nigrum
L.
Subspecies

S. nigrum subsp. nigrum

S. nigrum subsp. schultesii
European black nightshade (Solanum nigrum) or locally just

nightshade ,duscle,

black

garden nightshade, garden huckleberry, hound's

berry, petty morel,wonder berry, small-fruited black nightshade,

or popolo) is a species in theSolanum genus, native to

Eurasia and
introduced in the Americas, Australasia, andSouth Africa. Parts of
this plant can be toxic to livestock and humans, and it is considered
a weed. Nonetheless, ripe berries and cooked leaves of edible strains are
used as food in some locales, and plant parts are used as a

traditional medicine. A tendency exists in literature to incorrectly refer to

many of the other "black nightshade" species as "Solanum nigrum".

Solanum nigrum has been recorded from deposits of

Mesolithicera of ancient Britain and it is

suggested by the botanist and ecologist, Edward Salisbury , that it was
part of the native flora there before Neolithic agricultureemerged. The
species was mentioned by Pliny the Elder in the first century AD and by
the great herbalists, including Dioscorides. In 1753, Carl
Linnaeus described six varieties of Solanum nigrum in Species
Plantarum.
the

Paleolithic

and

Contents

1 Description
2 Taxonomy
3 Toxicity
4 Uses
4.1 Culinary usage
4.2 Medicinal usage
5 Cultivation
6 Weed
7 References
8 External links
Description

Black nightshade is a common herb or short-lived perennial shrub, found in

many wooded areas, as well as disturbed habitats. It reaches a height of 30
to 120 cm (12 to 48 in), leaves 4.0 to 7.5 cm (1.5 to 3.0 in) long and 2 to 5 cm
(1.0 to 2.5 in) wide; ovate to heart-shaped, with wavy or large-toothed edges;
both surfaces hairy or hairless; petiole 1 to 3 cm (0.5 to 1.0 in) long with a
winged upper portion. The flowers have petals greenish to whitish, recurved
when aged and surround prominent bright yellow anthers. The berry is
mostly 6 to 8 mm (0.3 to 0.8 in) in diam., dull black or purple-black.
another strain is found with berries that turn red when ripe.

[5]

In India,

[6]

deadly
Solanaceae

Sometimes S. nigrum is confused for the more toxic

nightshade, Atropa belladonna, in a different

genus
altogether. A comparison of the fruit shows that the black nightshade berries
grow in bunches, the deadly nightshade berries grow individually.

Taxonomy
The S. nigrum species is a highly variable taxon with many varieties and
forms described. The recognized subspecies are:
1. S. nigrum L. subsp. nigrum glabrous to slightly hairy with appressed
non-glandular hairs
2. S. nigrum L. subsp. schultesii (Opiz) Wessley densely hairy with patent,
glandular hairs
The Solanum nigrum complex also known as Solanum L.
section Solanum is the group of black nightshade species characterized
by their lack of prickles and stellate hairs, their white flowers, and their
green or black fruits arranged in an umbelliform
fashion. The Solanum species in this group can be taxonomically confused,
.

more so by intermediate forms and hybridization between the species. Some

of the major species within the S. nigrum complex are: S. nigrum,

S.

americanum, S. douglasii, S. opacum, S.

ptychanthum, S.retroflexum, S. sarrachoides, S. scabrum,
and S. villosum.
Toxicity

Leaves, flowers and fruit of S. nigrum

Solanine

levels in S. nigrum can be

poisoning after eating unripe berries.

toxic. Children have died from

[8]

However, the plant is rarely

fatal, with ripe berries causing symptoms of mild abdominal pains, vomiting,
and diarrhea.
Poisoning symptoms are typically delayed for 6 to 12 hours after

fever, sweating, vomiting,

abdominal pain, diarrhea, confusion, and drowsiness Death from
ingesting large amounts of the plant results from cardiac
arrhythmias and respiratory failure. Livestock have also been
ingestion. Initial symptoms of toxicity include

poisoned from nitrate toxicity by grazing the leaves of S. nigrum. All kinds of
animals can be poisoned after ingesting nightshade, including cattle, sheep,
.

poultry, and swine.

Black nightshade is highly variable and poisonous plant experts advise to
avoid eating the berries unless they are a known edible strain The toxin
levels may also be affected by the plant's growing conditions
The

toxins

in S. nigrum are most concentrated in the unripe green berries,

and immature fruit should be treated as toxic. Most cases of suspected

poisoning are due to consumption of leaves or unripe fruit.
There are ethnobotanical accounts of S. nigrum leaves and shoots being
boiled as a vegetable with the cooking water being discarded and replaced
several times to remove toxins.

Uses
Some of the uses ascribed to S. nigrum in literature may actually apply to
other black nightshade species within the same species complex, and proper
species identification is essential for food and medicinal uses
(See Taxonomy section).

Ripe berries of the "Red Makoi" variety of S. nigrum are edible

Culinary usage
S. nigrum has been widely used as a food since early times, and the fruit was
recorded as a famine food in 15th-century China. Despite toxicity
issues with some forms, the ripe berries and boiled leaves of edible strains
are eaten. The thoroughly boiled leaves although strong and slightly bitter
flavoured are used like spinach as horta and in fataya pies and quiches.
The ripe black berries are described as sweet and salty, with hints

liquorice and melon.

In India, the berries are casually grown and eaten, but not cultivated for

of

commercial use. In South India, the leaves and berries are routinely

consumed as food after cooking with tamarind, onion, and cumin seeds.
The berries are referred to as "fragrant tomato". Although not very popular
across much of its growing region, the fruit and dish are common in Tamil
Nadu ( in Tamil), Kerala, southern Andhra Pradesh, and southern
Karnataka.

Ripe and unripe Solanum Nigrum berries on the same stalk

In Ethiopia, the ripe berries are picked and eaten by children in normal
times, while during famines, all affected people would eat berries. In
addition, the leaves are collected by women and children, who cook the
leaves in salty water and consumed like any other vegetable. Farmers in
the

Konso Special Woreda

report that becauseS. nigrum matures

before the maize is ready for harvesting, it is used as a food source until their
crops are ready. The

Welayta people

in the nearby

Wolayita Zone

do

not weed out S. nigrum that appears in their gardens since they likewise
cook and eat the leaves.
In

Ghana, the unripe green berries are called kwaansusuaa

or abedru, and

are used in preparing various soups and stews, including the popular

palm

nut soupcommonly eaten with banku or fufu'.

In South Africa, the very ripe and hand-selected fruit
(nastergal in Afrikaans and umsobo in Zulu) is cooked into a beautiful
but quite runny purple jam.

Turkey, the leaves are called istifno, and in Crete known

as stifno. They are one of the ingredients included in the salad of boiled
greens known as horta.
In Indonesia, the young fruits and leaves of cultivated forms are used and
In

Greece

and

are known as ranti (Javanese) or leunca(Sundanese). The fruit and leaves

are eaten raw as part of a traditional salad
(fried) withoncom.
It was imported into

Australia

from

lalapan, or the fruit is cooked

Mauritius

in the 1850s as a

vegetable during the gold rush,[ but S. nigrum is now prohibited for trade as
a food by the Australia New Zealand Food Standards Code.

[25]

Medicinal usage

The plant has a long history of medicinal usage, dating back to

ancient Greece. "... In the fourteenth century, we hear of the plant under
the name of Petty Morel being used for canker and with Horehound and wine

dropsy.. It was a traditional European medicine used as a

strong sudorific, analgesic and sedative with
powerful narcotic properties, but was considered a "somewhat dangerous
remedy".Internal use has fallen out of favor in Western herbalism due to
its variable chemistry and toxicity, but it is used topically as a treatment
for herpes zoster.
taken for

S. nigrum is an important ingredient in traditional Indian medicines.

dysentery , stomach complaints, and fever. The

the plant is used on ulcers and other skin diseases. The fruits are

Infusions are used in

juice of

tonic, laxative,appetite stimulant, and for

treating asthma and "excessive thirst".Traditionally the plant was used to
treat tuberculosis. It is known as peddakasha pandla koora in
the Telangana region. This plant's leaves are used to treat mouth ulcers
that happen during winter periods of Tamil Nadu, India. It is known
used as a

as manathakkali keerai in Tamil Nadu and kaage soppu in Karnataka, and

apart from its use as a home remedy for mouth ulcers, is used in cooking like
spinach. In North India, the boiled extracts of leaves and berries are also
used to alleviate liver-related ailments, including jaundice. In Assam, the
juice from its roots is used against asthma and whooping cough.

S. nigrum is a widely used plant in oriental medicine where it is considered

antioxidant, anti.
inammatory, hepatoprotective, diuretic, and antipyretic.
Chinese experiments confirm that the plant inhibits growth of cervical
carcinoma in mice
to be antitumorigenic,

Black nightshade flowers

Cultivation
Black nightshade is cultivated as a food crop on several continents, including
Africa and North America. The leaves of cultivated strains are eaten after
cooking. A garden form with fruit 1.27 cm (0.5 in) diam. is occasionally
cultivated.

Weed
Black nightshade can be a serious agricultural

as

when it competes

crops. It has been reported as a weed in 61 countries and 37 crops.

Herbicides are used extensively to control it in field crops such
cotton.

with
[40]

weed