12/3/2015 Underactive Thyroid - a nutritional approach | Institute for Optimum Nutrition

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By:
ION ARCHIVES
Issue: Summer
Year of publication: 2002
Underactive thyroid or hypothyroidism is a complicated condition associated with a
shortage of thyroid hormone. Karen Goodfellow, BSc, BEd (Hons) DPSN pinpoints
the causes of the disorder and provides sound nutritional advice for its management
The thyroid gland is a tiny slither of tissue in the neck that weighs less than 30
grams yet the hormones it produces are essential to life. When thyroid hormone is
in short supply, symptoms soon develop. Thyroid hormone has two roles:

It accelerates metabolism so that sufficient energy is available to drive the functions

that keep us alive and healthy.
It increases protein synthesis to enable maintenance and repair of the body, as well
as growth and development, which is especially important in children.
Shortage of thyroid hormone is called hypothyroidism. It affects more women than
men in a ratio of approximately 3:1. It has several causes, which can be summarised
into three main categories:
Failure of the thyroid gland.
Failure of the feedback mechanisms which tell the thyroid gland to secrete its
hormone.
Failure to use thyroid hormone in the tissues.
Hypothyroidism affects people in all age ranges and there are several predisposing
factors that increase the risk of it developing:(1) (see figure 1.)
PROBLEMS WHICH CAN LEAD TO UNDERACTIVE THYROID:
A SEVERE INFECTION
TONSILLECTOMY
MAJOR BLOOD LOSS OR TRAUMA
THYROID SURGERY
GENETIC PREDISPOSITION
GLANDULAR FEVER
POST PREGNANCY
PITUITARY INSUFFICIENCY
ENVIRONMENTAL TOXINS
DRUGS
Figure 1
WHAT HAPPENS WHEN THYROID HORMONE IS IN SHORT SUPPLY?
When there is a shortage of thyroid hormone, the cells of the body immediately feel
the loss. The cells suffer an energy crisis. Without thyroid hormone the cells cannot
produce the energy they need to carry out the thousands of day-to-day functions
that keep us alive and healthy. The sufferer feels exhausted and drained of energy
– even after a full night’s sleep. Then, they begin to notice other symptoms…

Figure 2
THE PROBLEM OF UNDERDIAGNOSIS

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Figure 2 identifies some of the many symptoms that can develop as a result of a
lack of thyroid hormone. However, standard medical text tends to identify only six
main symptoms: Feeling cold, dry skin, dry hair, depression, constipation and
fatigue.
A doctor may suspect a thyroid problem only if the patient presents with these
symptoms, but as can be seen from figure 2, there are dozens of signs and
symptoms of hypothyroidism and they range from the mildly irritating to the
devastating and distressing. Hypothyroidism does not only affect physical health,
the symptoms can be mental as well, with depression being relatively common. (2)
Because the presenting signs and symptoms can vary from person to person,
hypothyroidism is an illness that is woefully under-diagnosed. (1,3)
There is also a substantial amount of evidence that the condition known as
fibromyalgia is hypothyroidism by another name. (4)
WHY SO MANY SYMPTOMS?
Hypothyroidism produces such a wide range of symptoms because every cell in the
body needs thyroid hormone. As the energy supply decreases along with the
amount of thyroid hormone, economies have to be made. Each individual has their
own physical strengths and weaknesses derived from a variety of causes, for
example environment, lifestyle, diet and genetic inheritance.
In a state of deficiency, the most vulnerable systems of the individual will succumb to
the effects of the energy gap first, and so the presenting symptoms will be different
from one person to another.
As the deficiency becomes more pronounced, the number of symptoms increase, so
that by the time the patient approaches a doctor for help, they have a variety of
complaints each varying in their degree of severity. To a doctor with a limited
understanding of hypothyroidism, these symptoms may appear to be the disparate,
unconnected niggles of the neurotic, depressed, patient. This response by doctors
is all too common, and is a significant cause of distress to undiagnosed hypothyroid
patients. Even when the doctor suspects a thyroid disorder, there is a heavy
reliance on blood tests, at the expense of clinical judgement, for the diagnosis of the
disorder (3,4). Such is the faith in blood tests, a physician will disregard the
diagnosis if the blood tests are normal even if the clinical evidence would strongly
suggest otherwise. The sufferer is condemned to years of misery as the symptoms
become progressively worse. They are passed from doctor to doctor and sometimes
acquire judgemental labels such as “hypochondriac” or “neurotic”.
A CHANGE IS UNDERWAY
Fortunately for sufferers of hypothyroidism, there is a growing number of experts
who now believe that although blood tests can be useful in identifying many cases of
hypothyroidism, they do not pick up a substantial number of others.4,5,6 Scientific
evidence in favour of this view is accumulating, and it is becoming apparent that this
is a complex disorder, which requires a holistic approach to treatment, not simply a
blood test and an unvarying daily dose of levothyroxine.
NUTRITIONAL SUPPORT: HOW CAN NUTRITIONAL THERAPY HELP?
Although there is no substitute in nutritional terms for thyroid hormone, there are
several nutritional approaches that can be used to help improve and / or preserve
the patient’s remaining thyroid function and enhance any thyroid hormone
replacement therapy they may be receiving.
Nutritional support can maximise metabolic function by:
Ensuring that all the steps of the metabolic pathway are intact.
Ensuring that thyroid hormone is active.
Advising on nutrients that act as hormone disruptors.
ENSURING THAT THE METABOLIC PATHWAYS ARE INTACT
Inside the mitochondria of cells, (7) the process of energy production follows a chain
of well-trodden steps. Under the influence of dozens of enzymes and co-factors,

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energy is produced at each step.
The raw materials essential for the manufacture of these enzymes are dependent
upon adequate nutrition, since the enzymes and co-factors are derived from the
diet. If the patient is deficient in just one enzyme or co-factor, the continuity of the
chain is broken and energy production is impaired beyond that point.
Unless the person is receiving adequate amounts of these essential nutrients, (see
figure 3) energy production will be impaired, even if they have sufficient amounts of
thyroid hormone.
ENSURING THAT THYROID HORMONE IS ACTIVE
Ensuring that thyroid hormone is working correctly is as important as having a
sufficient quantity of it.
Thyroid hormone contains five compounds: Iodine is required for its manufacture as
is the amino acid tyrosine, which is derived from phenylalanine. The two main
compounds are T4 or tetra iodothyronine which contains four iodine molecules and
T3 or tri iodothyronine which contains three iodine molecules.
THE GOAL OF NUTRITIONAL THERAPY IS TO ENSURE THAT THERE ARE NO
GAPS IN THE METABOLICPATHWAY CAUSED BY THE ABSENCE OF A NUTRIENT
NUTRIENTS WHICH PLAY A PART IN THE METABOLIC PATHWAY
NUTRIENT SUGGESTED DAILY INTAKE USE IN THE PRODUCTION OF ENERGY
Magnesium 270 – 400 mg Needed to ensure the release of energy from ATP. ATP
is an immediate energy supply inside the cell. (7)
Vitamin B1 (Thiamine) 50 mg Needed to form ATP, the cell’s energy store.
Vitamin B5 (Pantothenic acid) 50 mg Needed to release energy from glucose in
Krebs’ cycle. Also needed to release energy from fats.
Vitamin B2 (Riboflavin) 50 mg Needed to produce the hydrogen acceptor which
allows energy to be released.
Vitamin B3 (Niacin) 50 mg Needed to produce the hydrogen acceptor, which allows
energy to be released from glucose.
Vitamin B6 (Pyridoxine) 1.5 – 2.1 mg Allows energy to be stored as ATP.
Co-enzyme Q10 (Ubiquinone) 50 – 100 mg Up to 300 mg has been used. Perhaps
most accurate dose is 2mg per kg of body weight. Part of the carrier system which
causes the release of energy from glucose.
Chromium 50 – 200 µg Is a hydrogen acceptor on the electron transport chain,
which allows energy to be released from glucose.

Approximately 80% of the hormone secreted by the thyroid gland is T4 and

approximately 15% is T3. The other compounds make up the remaining 5%. The
common name for thyroid hormone is thyroxine but in fact, thyroxine is T4.
T4 (thyroxine) is a prohormone and must be converted to T3 (activated form) as
needed. T3 is the active hormone that carries out all the metabolic functions
associated with the thyroid. This conversion takes place mainly in the liver and
muscles. As can be seen in figure 4, the activation process involves an enzyme
called deiodinase which removes an iodine molecule from the T4 converting it into
T3.
Production of T3 should meet demand, so that if the individual is very active and
using more energy, the conversion rate will speed up to stimulate energy production
to meet the extra demand.
For the person with hypothyroidism it is a different story. Energy demands can
easily outstrip production. In other words, T3 production will not be able to meet
energy demands, thus not stimulating enough energy production. Even moderately
extra energy demands can leave the sufferer ill and exhausted, sometimes for many
days, as the symptoms of hypothyroidism come crashing back upon them.
HOW TO HELP: IT’S THE RATE OF CONVERSION THAT COUNTS
Taking extra thyroid hormone is not always the answer. The standard replacement

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therapy currently offered is the synthetic form of thyroxine, levothyroxine (brand
names: Eltroxin or Synthroid) which is not a total replacement for the body’s own
thyroid hormone. Levothyroxine is the prohormone T4 only, without the other
compounds.
How much energy a person has is determined by the rate of conversion of T4 to T3,
and the rate of uptake of T3 by the cells, not the amount of T4 present in the blood.
Therefore, if the person takes extra levothyroxine, and they do not have enough
deiodinase enzymes to convert it, the medication will not be effective because the
sufferer will not have the means to convert or activate it. In fact, the increase in dose
may cause unpleasant symptoms such as agitation, sweating and a rapid heart rate.
USING NUTRITIONAL THERAPY TO INCREASE CONVERSION RATES
If T4 is converted to T3 by the deiodinase enzymes, it follows that the pace of
conversion depends upon having sufficient deiodinase to meet the demand for T3.
The trace element selenium is a vital component of the deiodinase enzymes and so
selenium deficiency will exacerbate thyroid deficiency.(8) Even if an individual has
sufficient T4, they will be unable to activate it and turn it into T3 if they lack this
mineral.8 Supplementing the diet with extra selenium, has been found to improve
the symptoms of hypothyroidism because it accelerates the conversion of T4 to T3.
(9) A word of caution however, excess selenium in the diet can induce
hypothyroidism by suppressing the serum T3 levels.(8)
Zinc is needed for the manufacture and use of thyroid hormone. In one study, the
activity of liver deiodinases was reduced by 67% where zinc deficiency was present.
(10)
Iodine is needed for the manufacture of thyroid hormone. Iodine deficiency often co-
exists alongside selenium deficiency. It may be advisable for the patient to seek the
advice of a nutritional consultant and have the levels of these nutrients assessed
before commencing thyroid hormone replacement with levothyroxine or increasing
the dose of levothyroxine (see figure 5 for summary).
Some patients have lost the ability to convert T4 to T3 to such an extent that even
dietary supplements are not sufficient and they need to take ready converted T3
(brand names: Tertroxin or Cytomel).
NUTRIENTS WHICH ACTIVATE THYROID HORMONE
NUTRIENT SUGGESTED DAILY DOSE USES IN ACTIVATING THYROID HORMONE
Selenium 100 - 200 µg Necessary for the production of the deiodinase enzymes,
which convert T4 to T3.
Zinc 12 – 19 mg In animal studies, severe deficiency causes hypothyroidism. Zinc is
needed for the manufacture and use of thyroid hormone.
Iodine 150 – 200 mg Is a component of thyroid hormone. If the diet is deficient in
iodine, thyroid hormone cannot be manufactured in sufficient quantities. This often
results in a swelling of the neck called a goitre.
* iodine and selenium deficiency often occur together.
Figure 5
Fluoride displaces iodine in the thyroid gland, preventing the formation of thyroxine
AVOIDING HORMONE DISRUPTORS
The extents to which chemicals in the environment affect health are rapidly
becoming apparent. Thyroid function is not immune from the effects of hormone
disruptors. There is evidence that some widely used chemicals and pollutants can
have a detrimental effect upon thyroid function.
Fluoride
Before the invention of better methods, fluoride used to be given as a treatment for
hyperthyroidism (over-active thyroid) because of its ability to interfere with the
thyroid.(11) Fluoride displaces iodine in the thyroid gland, preventing the formation
of thyroxine (12). It is also thought to interfere with the feedback mechanism
between the hypothalamus and pituitary gland which control the manufacture and

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secretion of thyroid hormone. The debate about the fluoridation of water continues
to rage.
Chlorides
Chlorides are a group of chemicals with many variations depending upon the kind of
chemicals they hook up with. Organochlorides are one example of the toxic
compounds that chlorides can make. They come from the manufacture of PVC
products and so are widespread in the environment. Chlorides are related to
fluoride and iodine. They block the uptake of iodine into the thyroid gland thereby
reducing its ability to produce thyroid hormone.
Mercury
The debate about amalgam fillings used in dentistry continues as hotly as the
fluoride debate. Large doses of mercury can induce hyperthyroidism. Smaller
amounts can induce hypothyroidism by interfering with both the production of T4
and the conversion process.
Mercury interferes with selenium and zinc metabolism both of which play a part in
the manufacture and use of thyroid hormone.(13) Selenium seems to protect the
body from mercury.(13)
PCBs (Polychlorinated Biphenyls)
PCB contamination, generated by industrial plants, is widespread. According to
Zoeller (14) there are at least three ways in which PCBs interfere with thyroid
hormone. They alter the structure of the thyroid gland, so altering its ability to
respond to the hormone signals i.e. thyroid stimulating hormone (TSH) from the
pituitary gland. They increase excretion of T4, so reducing its serum half-life. They
can bind to the thyroid carrier proteins in the blood possibly displacing T4, so
reducing the ability of the blood to carry thyroid hormone to the cells. It is also
possible that PCBs bind to thyroid hormone receptors and prevent the entry of the
hormone into the cell.
Goitrogenic Chemicals
Goitrogenic chemicals promote hypothyroidism by interfering with the thyroid gland,
causing it to enlarge and producing the swelling in the throat known as a goitre.
Goitrogenic foods include members of the cabbage family (Brussels sprouts,
turnips, cauliflower, cabbage and kale) (15) which contain glucosinolates which have
a similar effect to anti-thyroid drugs. Cooking is thought to reduce the amount of
goitrogens in these vegetables. Raw swedes, turnips and kale are sometimes fed to
cattle and goitrogenic chemicals can make their way into the diet via milk products.
Soya beans contain compounds that inhibit thyroid peroxidase (TPO), an enzyme
which catalyses reactions essential to thyroid hormone synthesis.(16) The
isoflavones, daidzein and genistein, in the presence of iodide ions, block TPO
catalysed tyrosine iodination, by acting as an alternative to iodine, yielding its own
products instead of thyroid hormone. Genistein also inhibits thyroxine synthesis by
using its proteins to bind the thyroid hormone carrier protein, thyroglobulin.(17)
Soya can also act as a phyto-oestrogen which cancels out thyroid hormone and
reduces its absorption from the bowel.(16)
Medical Drugs
Although not considered in this article, certain drugs interfere with thyroid function.
More information about the effects of drugs on thyroid function can be found at the
Thyroid UK website (address overleaf).
CONCLUSION
Hypothyroidism is far from a simple disease that requires nothing more than a blood
test and a daily pill. It is a complex disorder, which can have a number of causes
that interplay one upon another, and impact upon the success of treatment. The
sufferer must be looked at as a whole person, who may need advice about changes
to their diet and lifestyle, to ensure successful treatment.
Note: It is strongly advised you consult a nutritional therapist before embarking on a

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nutritional programme to help manage
hypothyroidism.
REFERENCES
Durrant – Peatfield B. J. Aspects of a common missed diagnosis. Journal of Nutrition
and Environmental Medicine. 1996;6:28-32.
Hickie I. et al. Clinical and subclinical hypothyroidism in patients with chronic and
treatment resistant depression. Australian and New Zealand Journal of Psychiatry
1996;30:246-252.
Barnes B.O. Galton L. Hypothyroidism the unsuspected illness. Crowell 1976 p 6-7.
Lowe J.C. www.drlowe.com (http://w w w .drlow e.com)
Schachter M. The diagnosis and treatment of hypothyroidism. Available at
http://www.dcnutrition.com/problems/Detail (http://w w w .dcnutrition.com/problems/Detail) .
Langer S E Sheer J F. Solved : The Riddle of Illness, Keats Pub Inc. 2000 p3-7.
Ash M. Energy: The Currency of Life. Optimum Nutrition Vol 14 No 1 Spring 2001 p
26.
Foster H.D. Correspondance. Journal of Orthomolecular Medicine Vol 10 No 2 1995.
Olivieri O et al. Low selenium status in the elderly influences thyroid hormones.
Clinical Science 1995;89(6)637-42.
Kralik A, et al. Influence of zinc and selenium deficiency on parameters relating to
thyroid hormone metabolism. Hormone Metabolism Res 1996;28( 5)223-6.
Galetti PM, Joyet G. Effect of fluorine on thyroidal iodine metabolism in
hyperthyroidism. J Clin Endocrinol 1958;18:1102-1110.
Jones D. Fluoride: Damning New Evidence, What The Doctors Don’t Tell You,
Volume 9 No 12 1999 p 1-4.
Hansen J.C. Mercury/selenium interaction: A comparative study on pigs. Nord Vet
Med 33(2) 57-64 Feb. 1981.
ZoellerT.R. Polychlorinated biphenyls as disruptors of thyroid hormone action.
Department of Biology and Molecular Cellular Biology Program, University of
Massachusetts, Amherst, Massachusetts. Available at
www.bio.umass.edu/biology (http://w w w .bio.umass.edu/biology) . zoeller/pcbreview/htm.
Section 11 Endocrine Anon. available at
http://www.pathlights.com/nr_encyclopedia/11endo03.htm
(http://w w w .pathlights.com/nr_encyclopedia/11endo03.htm)
Soya a mostly sceptical miscellany http://www.oxford.net/~tishy/soy.html
(http://w w w .oxford.net/~tishy/soy.html)
Divi RL et al. Anti-thyroid isoflavines from soyabean: isolation characterisation and
mechanisms of action. Biochem Pharmacol 1997;54(10):1087-1096.
BIBLIOGRAPHY
Devlin T.M. (Ed.) Textbook of Biochemistry with Clinical Correlations
4th Edition, Wiley – Liss Inc. 1997.
Neil K and Holford P, Balancing Hormones Naturally, Piatkus 1998.
Murray M.T, Encyclopaedia of Nutritional Supplements, Prima Health 1996.
Lowe J.C, The Metabolic Treatment of Fibromyalgia, McDowell Publishing Company
L.C. 2000.
Kumar P and Clark M, Clinical Medicine, W.B. Saunders Co Ltd 3rd edition 1996.
If you want to know more about hypothyroidism you can visit the Thyroid UK website
at www.thyroiduk.org (http://w w w .thyroiduk.org) . or email at:
enquires@thyroiduk.org (mailto:enquires@thyroiduk.org)
Or write to Thyroid UK, 32 Darcy Road, St. Osyth, Clacton on Sea, Essex CO16
8QF.
Karen Goodfellow is Research Officer for Thyroid UK and a Senior Lecturer at the
University of Northumbria in Newcastle. She is also a Registered Nurse.

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