Dietary Sugar, Salt and Fat in Human Health

Poland

Preface

Harry G. Preuss, Departments of Biochemistry, Physiology, Medicine and Pathology, Georgetown University Medical Center, Washington, DC, United States

Debasis Bagchi, Department of Pharmacological and Pharmaceutical Sciences, University of Houston College of Pharmacy, Houston, TX, United States, VNI Life, Lederach, PA, United States

Approximately 415 million adults worldwide are suffering from the dreadful consequences of the metabolic syndrome, an entity that includes among many common chronic malfunctions diabetes mellitus, obesity, and a variety of cardiovascular maladies to name but a few. The number of unfortunate individuals involved in these chronic perturbations is estimated to soar as high as 642 million by 2040 [1]. According to the National Diabetes Statistics Report of 2014, nearly 30.3 million people in the United States, representing about 9.4% of the US population suffer from diabetes [1–3]. To compound the difficulties, persistent hyperglycemia in Type 2 Diabetes Mellitus cases can cause development of serious secondary complications including diabetic neuropathy, nephropathy, retinopathy, peripheral vascular diseases, and numerous cerebrovascular afflictions [1–3]. All the above individual health difficulties can be intricately correlated with poor choices in diet—particularly overindulgence of dietary fat, sugar, and salt often in a setting of a sedentary lifestyle. To give substance to the last statements, information concerning the previously described practices have been detailed in this book Influence of Dietary Sugar, Salt and Fat on Human Health.

This collection of chapters is divided into seven major sections in addition to a commentary from the editors’ desk. The initial general background section, that is, the first section, provides a broad overview concerning epidemiological perspectives relative to dietary sugars, salt, and fats. In brief this section is a compilation of chapters reviewing the influence of dietary sugars, salt, and fats on chronic degenerative diseases as well as many different elements included in the metabolic syndrome. The social misfortune that occurs following overindulgence of dietary sugars, salt, and fats has been emphasized in this opening chapter. The remaining four chapters in the first section highlight the influences of food ingredients on enterohepatic circulation of bile acids and the influence that overindulgence of dietary sugars, salt, and fats has on hemoglobin, which subsequently can lead to anemia.

The second section discusses in depth the unfortunate consequences of food behavior, food addiction, and the metabolic syndrome in four individual chapters. The first chapter points out the drivers of food behavior, while the second one elaborates on the battle against processed food addiction. The third chapter emphasizes the dietary influences on pediatric aspects of obesity and the metabolic syndrome, and the fourth chapter focuses on an overview of sugar addiction.

The third section emphasizes the effects of dietary sugars on human health in eight individual chapters. The writers of the first chapter emphasize vital aspects of the historical, epidemiological, and laboratory considerations concerning the role of dietary sugars on blood pressure regulation. The second chapter details the cellular toxicity wrought by glycation-induced protein aggregation, while the third chapter brings forth various pro and con health aspects of the glucose–insulin system in nondiabetics with a special focus on insulin resistance and dietary implications. The fourth chapter explains various aspects of insulin resistance in nondiabetics with a special emphasis on triglyceride/high-density lipoprotein (HDL)-cholesterol ratio versus fasting blood glucose in estimating insulin resistance. The fifth chapter portrays the association of high blood sugar with oxidative stress and inflammation in patients suffering from type 2 diabetes. The sixth chapter discusses the triglyceride/HDL-cholesterol ratio as a surrogate for insulin resistance and its link to the consequences of the metabolic syndrome in Hispanics and African-Americans. Finally, the seventh chapter brings forth the benefits of Indian Jaggery over sugar in human health. The last chapter links fasting blood glucose quartiles in nondiabetic volunteers aged 21–84 years with the components of metabolic syndrome. The importance of the role of fasting blood sugar values in nondiabetics to estimate the intensity of a variety of risk factors for the components of the metabolic syndrome is unique and vitally important in the realm of preventive medicine. A pathway to a longer healthier lifespan is proposed using the enclosed information.

The fourth section, comprised of three chapters, emphasizes the harmful effects of overindulgence of dietary salt. The first chapter highlights the influence of salt-induced inappropriate augmentation of intrarenal renin-angiotensin-aldosterone-system (RAAS) system in chronic renal diseases. The second chapter discusses the vital aspects of table salt (sodium chloride) on metabolism and blood pressure regulation, and the third chapter discusses the important role of nutraceuticals and functional foods as a remedy for excessive intake of dietary salt in hypertension. The author demonstrates the basic science behind hypertension including pathophysiology and related complications and the link between dietary salt and hypertension as well as the possible current treatment regimen-like standard antihypertensive drugs and functional foods/nutraceuticals for the prevention, management, or delaying of hypertension and its associated conditions.

Certain aspects of dietary fat and cholesterol are discussed in the fifth section comprised three chapters. The first chapter explains the physiological role of cholesterol in human body, the second chapter discusses the interplay between dietary sugars/fats with insulin resistance, and the third chapter details the erythrocyte membranes in metabolic and neurological diseases and the effect of supplementation of fatty acids on membrane remodeling.

In the sixth section comprised of two chapters, the first one reviews dietary fibers extensively, while the next emphasizes ketogenic and low-carbohydrate diets in the realm of health and disease.

The seventh section stresses the viewpoint of a successful super high school student contemplating the health effects following overindulgence of dietary sugars, salt, and fats in humans. Hopefully this will create an early understanding of the importance of good nutrition in the younger generation.

Finally the commentary section written by the editors’ points out the changes in nutritional risk factors based on nutritional status over recent times. How well is the up-to-date nutritional advice working in the general population to lower risk factors?

In summary, this book covers a broad range of topics related to the good but primarily the bad effects of dietary sugars, table salt, and fats on human health that can subsequently cause the development of an array of degenerative diseases, disorders, and complications.

Our sincere thanks to all our eminent contributors, as well as helpful Elsevier team members including Megan Ball, Lindsay Lawrance, Nancy Maragioglio, and Indhumathi Mani for their continued support, cooperation, and assistance.

References

1. National Institute of Diabetes and Digestive and Kidney Diseases. Diabetes facts and statistics. <https://www.niddk.nih.gov/health-information/health-statistics/diabetes-statistics> [accessed 31.07.19].

2. Fat, Salt and Sugar: Not All Bad. <https://www.healthychildren.org/English/healthy-living/nutrition/Pages/Fat-Salt-and-Sugar-Not-All-Bad.aspx> [accessed 31.07.19].

3. Health impact of high fat, sugar and salt (HFSS) foods. <https://www2.gov.scot/resource/0043/00438754.pdf> [accessed 31.07.19].

General background

Outline

Chapter 1 Epidemiological perspectives of dietary sugars, salts and fats

Chapter 2 Advancing age, influence of dietary sugars, salts, and fats on chronic diseases and metabolic disorders

Chapter 3 Dietary fat, salt, and sugar: a clinical perspective of the social catastrophe

Chapter 4 Influences of food ingredients on enterohepatic circulation of bile acids

Chapter 5 Anemia: influence of dietary fat, sugar, and salt on hemoglobin and blood health

Chapter 1

Epidemiological perspectives of dietary sugars, salts and fats

Rokeya Pervin¹, Md Akil Hossain¹, Dipti Debnath² and Biddut Deb Nath³,    ¹Animal and Plant Quarantine Agency, Gimcheon-si, Republic of Korea,    ²Department of Pharmacy, Atish Dipankar University of Science and Technology, Dhaka, Bangladesh,    ³Department of Physiotherapy, Centre for the Rehabilitation of the Paralysed (CRP), Dhaka, Bangladesh

Abstract

People from different regions of the world are currently experiencing an epidemic of noncommunicable diseases such as metabolic diseases, hypertension, cardiovascular diseases, kidney diseases, and cancers. Intake of excessive amount of calories and lack of physical activity are probable vital factors leading to the epidemic of various diseases. A healthy diet is generally known as an essential approach to promote health and a major part of nonpharmacological therapy for a number of health conditions. Several noncommunicable diseases are believed to be linked with the intake of some dietary nutrients such as sugar, salt, and fat. Conversely the associations of dietary sugar, salt, and fat with various diseases have been debated for many years. It is very crucial to confirm whether the hypotheses of the associations of dietary sugar, salt, and fat with various diseases are true or false. This paper summarizes current epidemiological evidences on these hypotheses.

Keywords

Nutrients; nonpharmacological therapy; noncommunicable diseases; healthy diet; metabolic diseases; cardiovascular diseases; hypertension

1.1 Introduction

Humans have had a long and beneficial relationship with salt, sugar, and fat that dates back to the origin of the species. Sugar provides energy for physical and mental activities, salt is necessary for fluid balance, while various types of fats make up most of the mass of the brain. The seemingly magical properties of these three constituents for transforming stale, smelly, and near tasteless foods into savory, sweet, and pleasantly tasty nutrition were discovered over time. Due to their ability to flavorize a wide variety of foods, these three nutrients became a culinary treasure and are used globally to make those wonderful foods we have come to associate with indispensable elements in religious rituals, feasts, important historical events, festivals as well as those sweet memories from our youth. The consumption of this trio to have satiety and pleasure has increased globally a lot[1].

It is claimed by many nutritionists, researchers, epidemiologists, different regulatory agencies, and health practitioners that this increased consumption of salt, sugar, and fat is inducing the epidemic of noncommunicable diseases such as obesity, hypertension, diabetes, cardiovascular diseases, and certain cancers. It was concluded in an article published in The Lancet that one-fifth of deaths around the world were related with the consumption of poor diets. Diets those contain noticeably higher amount of salt, sugar, and trans fats but less amount of fresh vegetables, nuts, and seeds are defined as poor diets. It is reported that 11 million people died in 2017 due to poor diet, and about 10 million among those deaths were caused by cardiovascular diseases. The second biggest cause of poor diet-related death was cancer which accounted for the death of 913,000 people, and lastly the type 2 diabetes which accounted for the death of 339,000 people [2]. Many researchers have reported that the deaths of this large number of people could have been avoided. These numbers are really striking, and consequently the treasured trios of sugar, salt, and fat have turned into a matter of much criticism by the public and different national and international agencies [1]. However, most of the hypothesis regarding the associations of disease burdens with the increased consumptions of dietary salt, sugar, and fat have not yet been well established due to inconsistencies found in different studies [2].

Everybody, including consumers, nutritionists, national and international regulatory agencies, and policy makers should have well understanding on these correlations. By knowing the associations of each nutrient with specific disease, policy makers can make dietary recommendations and consumers can choose their required food. This paper summarizes the current evidence on the associations of dietary nutrient (sugars, salts, and fats) consumption with increased incidence and risk of certain diseases such as type 2 diabetes, cardiovascular diseases, and certain cancers.

1.2 Dietary sugars

There is indeed compelling evidence that consumption of sugars has increased continuously over the past 50 years, contributing to 15%–20% of total energy intake in several North American and European countries and is rising toward this level in many developing countries [3]. Over the same period, the prevalence of obesity and its associated metabolic diseases has increased dramatically [4]. Now sugar consumption is suspected to play an important role in the pathogenesis of not only obesity but also of noncommunicable disorders including diabetes, fatty liver disease, cardiovascular diseases, and certain types of cancers as well as oral health problems. The hypothesis that dietary sugars play a vital role in linking diet, obesity, and metabolic disease outcomes has gained substantial consideration over the past decades. A wide range of research approaches including epidemiological studies, ecological studies, human clinical study, and animal models utilizing sucrose- or fructose-rich diets are currently being used to study the links among sugar, obesity, and risks of other diseases [3].

1.2.1 Effects of dietary sugars on body weight and obesity

Based on seven cohort studies in adults, with 174,252 participants, an increase of one serving of sugar-sweetened beverages per day was correlated with an extra weight gain of 0.22 kg in random-effect models and 0.12 kg in fixed-effect models over 1 year. In an earlier study [5] conducted on 50,000 participants in the Nurses’ Health Study II (NHS II), women who increased the consumption of sugar-sweetened beverages and continued to intake high amount gained on an average 8.0 kg of body weight over 8 years, whereas women who reduced the consumption of sugar-sweetened beverages and continued to intake low amount gained on an average 2.8 kg in the same period. Similar results have been observed in other populations including over 40,000 women in the Black Women’s Health Study [6] and over 43,000 Chinese men and women in Singapore in a cohort study [7]. Among studies that were excluded from the metaanalysis and reviewed qualitatively, the majority [7–10] found positive correlations between the intake of sugar-sweetened beverages and weight gain in either primary analysis or subgroup findings, while two studies [11,12] could not find significant associations.

Recently a metaanalysis and systematic review were commissioned by the World Health Organization to determine the effects of dietary sugar on body weight and to reveal whether the existing evidences support the current recommendations of dietary sugar intake [13]. It was concluded in those studies that consumption of sugar-sweetened beverages or free sugars is a determinant of body weight among free-living people involving ad libitum diets. Authors also mentioned, When considering the rapid weight gain that occurs after an increased intake of sugars, it seems reasonable to conclude that recommendation relating to sugar consumption is a pertinent factor of an approach to reduce the increased risk of overweight and obesity in most countries. At present, it is generally accepted that dietary sugars lead to expand adverse metabolic effects by gaining weight via their role in energy intake. It is also evident that dietary sugars are related with the increase of serum lipids and blood pressure independent of body fat [14]. Consequently it is suggested that dietary sugars may also be correlated with increased metabolic risk, independent of body weight and energy intake.

1.2.2 Effects of dietary sugars on diabetes

Evidences from different studies indicate that the consumption of sugar-sweetened beverages is correlated with increased risk of diabetes through its effects on adiposity and through other metabolic outcomes. Even though experimental evidence from randomized controlled trials is insufficient because of high expense and other feasibility factors, findings from prospective cohort studies have revealed a relatively consistent and strong correlation in well-powered studies. A metaanalysis of eight prospective cohort studies investigating the intake of sugar-sweetened beverages and risk of diabetes has been carried out [15]. Based on 310,819 participants and 15,043 cases, individuals in the highest category of sugar-sweetened beverage intake (usually 1–2 servings per day) had a 26% greater risk of developing diabetes compared to those in the lowest category (none or less than one per month). An increase of one serving per day of sugar-sweetened beverage was correlated with approximately 15% increased risk of diabetes. This correlation is consistent across ethnic groups (Asians, African-Americans, and Caucasians), gender, and age groups. A similar correlation was recently observed in a subcohort of 15,374 participants and 11,684 incident cases from eight cohorts participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study [16]. In adjusted models, a one serving per day increase in sugar-sweetened beverages was associated with a 22% increased risk of diabetes. As expected, the association was attenuated after further adjustment of total energy intake and body mass index. In a separate study, the French component of EPIC, which included 66,118 women and 1369 incident cases, found that women in the highest quartile of sugar-sweetened beverage intake had a 34% increase of diabetes compared to nonconsumers [17]. In sensitivity analyses, correlations were arbitrated in part by body mass index, although there was still a strong significant independent effect.

1.2.3 Effects of dietary sugars on cardiovascular diseases

There is increasing evidence that the increased consumption of sugar-sweetened beverages increases cardiovascular risk by contributing to the progression of hypertension, stroke, coronary heart disease, inflammation, and dyslipidemia. Intake of sugar-sweetened beverages and risk of metabolic syndrome, which is a clustering of metabolic risk factors including central obesity, elevated triglycerides, reduced high-density lipoprotein (HDL) cholesterol, elevated fasting plasma glucose, and elevated blood pressure, were evaluated from three prospective cohort studies [15]. Based on 19,431 participants and 5803 cases, it observed a 20% increased risk of metabolic syndrome comparing highest to lowest categories of intake. In the Coronary Artery Risk Development in Young Adults (CARDIA) study, higher consumption of sugar-sweetened beverages was correlated with a number of cardiometabolic effects, high low-density lipoprotein (LDL) cholesterol, high triglycerides, hypertension, and high waist circumference [18].

Findings for hypertension are supported by considerable correlations in the Nurses’ Health Study (NHS) and NHS II. Women who consumed ≥4 servings per day of sugar-sweetened beverages had a 44% greater risk of developing hypertension, whereas 28% greater risk was accounted for those who consumed infrequently [19]. In a post hoc analysis of an 18-month behavioral intervention trial, a reduction of sugar-sweetened beverage consumption was notably correlated with the reduction of blood pressure, even after adjusting the weight change [20]. Dhingra et al. [21] found that daily soft drink consumers had a 22% greater risk of developing hypertriglyceridemia and low HDL cholesterol compared to nonconsumers. Similarly among participants in the Multi-Ethnic Study of Atherosclerosis, daily consumers of sugar-sweetened beverage had a 28% greater risk of developing hypertriglyceridemia and low HDL cholesterol than nonconsumers [22]. Data from short-term trials also provide important evidence linking the intake of sugar-sweetened beverages with the elevated risk of cardiovascular diseases [23–25].

1.2.4 Effects of dietary sugars on kidney diseases

At least five epidemiologic investigations have focused particularly on the consumption of sugar and kidney diseases so far. It is very difficult to determine the relationship precisely from these investigations as all of these investigated only sugary-soft drinks but not the full range of dietary sources of sugar. In the United States, a considerable percentage of added sugars come in the form of sugar-sweetened beverages, which provide almost 10% of the total intake of calorie [26]. The cross-sectional and case–control studies exploited a variety of definitions of the intake and effect. For example, Saldana [27] and his group defined intake of two or more regular size colas per day and the effect as diagnosed kidney disease in their case–control study. An odds ratio of 2.51 was reported by this study considering the response of self-respondents. Similarly Shoham [28] and his group used the consumption of two or more sugar-sweetened beverages per day and an effect of gender-specific urinary cut-points ratios of albuminuria to creatinine, which were >25 mg/g for female and >17 mg/g for male. An odds ratio of 1.40 was reported by this study after adjusting of 2 or more soda consumption per day, race ethnicity, gender, age, and living under double the poverty level. However, the results were not altered significantly after adjusting the levels of serum uric acid. Bomback [29] and his group utilized the intake of >1 sugar-sweetened soda per day and the effect of chronic kidney disease prevalence. Bomback reported an odds ratio of 1.46 after adjusting for total calorie consumption, sodium consumption, sex, age, race, body mass index, hypertension, diabetes, current alcohol and tobacco use, and education.

The prospective cohort studies that investigated the correlation of the intake of sugar-sweetened beverages with kidney diseases also used different definitions of the intake and effect. The exposure was defined as intake of >1 sugar-sweetened soda per day by Bomback [29] and his group in 2010, whereas the exposure was defined in 2009 as intake of 7 or more sugar-sweetened drinks per week by Bomback [30] and his group. However, the studies by Bomback [30] and colleagues and Lin [31] and colleagues stated that the consumption of sugar-sweetened beverages elevate the risk of chronic kidney disease. Adjustment of mediating factors including hypertension, body mass index, and diabetes usually reduces the degree of association in an attempt which can promote identifying the independent outcome of sugar-sweetened beverages on the risk of kidney diseases.

1.2.5 Effects of dietary sugars on cancer

The range of estimates for the proportion of cancers that may be attributed to diet and related lifestyle variables remains wide and varies by cancer site [32,33]. It is concluded form the largest systematic reviews of diet and cancer that the evidence of sugars and cancer risk was limited. The only potential relationship of note was that foods containing nonmilk-added sugars may increase risk of colorectal cancer [34]. Case–control studies have provided some evidence of positive relationships between intake of dietary sugars and cancer risk [35,36]. However, inherent limitations of case–control study design make the interpretation of findings difficult. Prospective cohort studies do not suffer from the same biases as case–control studies and have generally not seen positive associations between sugar intakes and cancer risks. It is particularly difficult to measure the effect of sugars on cancer risk because of inconsistency in the classification of sugars across studies.

1.3 Dietary salt

It is estimated that the elevation of blood pressure attributes to about 49% of ischemic heart disease and 62% of cerebrovascular disease globally. Considering the adverse effects of excessive salt intake on health, specifically on the level of blood pressure and cardiovascular diseases, the World Health Organization [37] has urged member nations for taking action to reduce population-wide dietary salt consumption for reducing the mortality rates from stroke, cardiovascular diseases, and hypertension. Over the past century, sodium chloride has been the matter of intense scientific research related to the elevation of blood pressure and cardiovascular disease–associated mortalities. However, recently some in the academic society and lay media dispute the benefits of salt restriction, pointing to inconsistent outcomes noted in some observational studies [38,39].

1.3.1 Effects of dietary salts on blood pressure and cardiovascular diseases

Epidemiological investigations, animal studies, and clinical trials bring remarkable evidence for an adverse effect of sodium consumption on the blood pressure of both normotensive and hypertensive individuals [40–46]. Together with its effects on blood pressure, excessive intake of dietary sodium has been directly correlated with coronary heart disease [47,48], stroke [49], and noncardiovascular diseases [50]. Nonoptimal blood pressure was considered to be the cause of ~7.1 million deaths worldwide in 2000 [51,52]. Reducing the intake of salt by individuals may alter the blood pressure toward more optimal levels in people, which prevents significant number of deaths from stroke and cardiovascular diseases. It was predicted in the United Kingdom that a reduction of 100 mmol sodium intake per day per person would lead to the fall of 2.8 mm Hg mean diastolic blood pressure and 5.0 mm Hg mean systolic blood pressure, which can prevent about 15,000 deaths from stroke and 22,000 deaths from coronary heart disease [53]. Reduction of salt intake is one of the efficient, cost-effective and easily implementable measure to minimize the global burden of cardiovascular diseases and consequently attention should be paid on this initiative [54].

An extensive public health campaign has been conducted in Finland with the association of food industries to diminish the occurrence of cardiovascular diseases. A noticeable reduction in salt consumption was recorded for more than a period two decades, which resulted in a reduction of ~60% stroke-associated and coronary heart disease–associated deaths [55,56]. Data on the consumption of salts by young people and children are inadequate. Within the limited data it is evident that the intake of higher amount of salts in childhood is associated with higher blood pressure later in life [57,58]. Optimum amount of salt consumption in childhood could help to prevent the rise of blood pressure in adulthood and impede the cardiovascular disease events in future [46].

The publication of the famous graph of Louis Dahl [59] in 1960 on the consumption of sodium in different populations around the world gained the attention of researchers for the first time. A positive linear correlation between mean sodium consumption and the occurrence of hypertension among populations of five different regions were revealed in that graph. It was mentioned that daily consumptions of sodium significantly varied among population groups, for example, 462 mmol/day in people of Akita prefecture (northeast Japan) to 68 mmol/day in people of Alaskan Eskimos. The mean intake of sodium was 171 mmol/day in American people. He also noted a strong north–south trend in death rates from stroke in Japan, which coincided with the variation in sodium consumption ranging from 462 mmol/day in the northeast to 239 mmol/day in the south. The very high intake of sodium in the northeast demonstrated the dietary habit of rice consumption with pickles and miso soup, and the use of soy sauce as seasoning [60]. The observations of Dahl on five populations were expanded by other authors and concluded that sodium intake varied significantly in different populations [46,61–66].

1.3.2 Effects of dietary salts on other diseases

If the amount of salt consumption increases, the loss of calcium from the body also increases by urination. Calcium can be leached out from the bones if its supply in the blood is lower. Thus a high sodium-containing diet could have an additional undesirable effect of the bone-thinning disease known as osteoporosis [67]. A study in postmenopausal women demonstrated that the loss of the density of hip bone for 2 years was related to the 24-hour excretion of urinary sodium at the start of the study and that the connection with bone loss was as strong as that for calcium intake [68]. Other studies have shown that reducing salt intake causes a positive calcium balance, suggesting that reducing salt intake could slow the loss of calcium from bone that occurs with aging. Research also shows that higher intake of sodium, salt, or salty foods are associated with the increased risk of stomach cancer. The World Cancer Research Fund and American Institute for Cancer Research concluded that the intake of salt or salted and salty foods is an attributing factor of stomach cancer [34].

1.4 Dietary fats

It is unexpected that the relationship between the consumption of dietary fat and disease risks continue to exist as a topic of controversy after doing research for so many years. Researchers who agreed or not agreed with the hypothesis of the associations of dietary fat with cardiovascular disease, obesity, and specific types of cancers have left a series of repetitive expensive studies which could not bring significant conclusions [69].

1.4.1 Effects of dietary fats on cardiovascular diseases

Dietary fats, mainly triglycerides from both animal- and plant-derived foods, are traditionally considered as unhealthy components. Nonetheless, researches over the past few decades have recognized that different types of fats have divergent effects on cardiovascular health [70]. The outcomes of large prospective epidemiologic studies uphold the theory that the risk of coronary disease is dependent on the quality of dietary fat rather than its quantity [71]. From the nutritional point of view, the epidemiology of cardiovascular diseases has mainly concentrated on the type of dietary fat (such as, polyunsaturated, monounsaturated, and saturated), lipoprotein metabolism, blood cholesterol, and coronary artery disease risks [72]. The hypothesis of the association of dietary cholesterol and saturated fat with coronary artery disease and atherosclerosis risks was demonstrated long time ago. Relocation of people, typically from the area of low to high risk, gave rise to the amount of cholesterol and saturated fat in the diet, elevated levels of blood cholesterol, and led to the increased risk of coronary heart disease–associated death [73].

In some age-adjusted large longitudinal investigations, strong correlation of coronary risks with the intake of total fat was reported. However, these correlations were mostly found in the people who smoke and intake less fiber together with the intake of high fat. The theory that the risk of coronary heart disease increases by the consumption of high total fat-containing diets is strongly opposed by the findings of these large longitudinal studies. The outcome of these studies is consistent with the earlier ecological comparisons and cohort studies [74]. It is indicated by metabolic studies that the effects of dietary changes on the amount of LDL cholesterol in serum are moderate and is accountable for risk reductions. The outcomes from controlled clinical trials [75] are consistent with the theory that the replacement of saturated fat in diet by carbohydrate mostly reduces the risk of coronary heart disease moderately, as expected by its influences on LDL cholesterol.

Individuals who consume high amount of transfatty acids have the tendency to consume higher amounts of polyunsaturated fat. Thus the beneficial effects of polyunsaturated fat abolish the adverse effects of transfatty acids in those people. The risk of coronary heart disease is increased with the consumption of transfatty acids. A 30% decreased risk of coronary heart disease is accounted by consuming the monounsaturated fat instead of saturated fat, which provides three times more reduction of coronary heart disease risk than that obtained by consuming carbohydrate instead of saturated fat. Recently, two large epidemiologic investigations on diet and coronary heart disease has been conducted in the United States which are the NHS [76,77] and the Health Professional Follow-up Study (HPFS) [78]. According to the NHS, the risks of total coronary heart disease are inversely associated with the consumption of both linolenic acid and linoleic; there is great inverse association between the risks of fatal coronary heart disease and linolenic consumption. Besides that, the HPFS stated the inverse association between consumption of linoleic acid with the risks of fatal coronary heart diseases and consumption of linolenic acid with the risks of total coronary heart diseases.

1.4.2 Effects of dietary fats on cancer

Population comparison studies and some other natural studies have displayed that breast, prostate, ovarian, and colon cancers in a population is directly associated with the intake of total fat [79,80]. Likewise, some migrant studies reported that people who migrate from lower to higher risk areas of specific cancers have increased risk of that cancer [80] which is associated with dietary changes [81].

1.4.2.1 Breast cancer

A number of reviews have been published on breast cancer and the intake of fat [82–84]. These reviews consistently reported that epidemiologic studies proved the correlations among countries of per capita fat intake with the incidence of breast cancer and the rates of mortality. It has also been proposed that most of the global variations in the risks of breast cancer may be described by some nondietary risk factors [83]. Several case–control studies demonstrated that the intake of dietary fat may be correlated with increased risk of breast cancer [5]. A pooled study of original data from eight such case–control studies was carried out by Howe et al. [85] that incorporated 4312 cases and 5798 control subjects. A substantial positive correlation of increased risk of breast cancer with the increased amount of saturated and total fats was found in this study. However, no correlation of fat consumption with the increased risk of breast cancer was observed in other case–control studies [86,87]. Considering the findings of these case–control studies, the evidence of the correlation of dietary fat with breast cancer risk is not so strong.

Even though the consumption of total dietary fat in adulthood is unlikely to have effect on breast cancer risk as seen in North American or Western European countries, some cohort and case–control studies have reported that there is correlation between the consumption of red meat with the increased risk of breast cancer [88,89]. However, this kind of correlation have not obtained in other studies [90,91], and consequently the evidence on this correlation is inconsistent and weak. A cohort study reported the positive correlation of egg consumption with the risk of breast cancer [92]. Conversely, other studies reported the correlation of vegetable consumption with lower risk of breast cancer [93]. Different case–control studies carried out in Italy, Spain, Sweden, and Greece have suggested that high content of dietary monounsaturated fatty acid, especially from olive oil, possibly correlated with decreased risk of breast cancer [94,95]. It is reported in several epidemiologic studies that there is no correlation between the consumption of polyunsaturated fats with the increased risk of breast cancer [94,96,97].

1.4.2.2 Colorectal cancer

A substantial positive correlation between the intake of dietary fat and the increased risk of colorectal cancer is indicated by international comparisons and animal studies [98]. However, numerous recent case–control studies could not find correlation between the intake of dietary fat and elevated risk of colorectal cancer [99,100]. Likewise a relatively little evidence of correlation of fat consumption and colorectal cancer risks is found in prospective cohort studies. Among such studies that evaluated the association of colon cancer with the consumption of dietary fat [101–105], only one study found an increased risk of colon cancer with the consumption of fat intake. It was reported in the study of nurses in the United States that the colon cancer risk was increased about twofold in women who consumed the highest quintile of total fat compared with women who intake lowest quintile. This increased risk of colon cancer was attributed from the intake of animal fat and not from the intake of vegetable fat [105]. Several studies stated that the intake of red meat was correlated with increased risk of colon cancer as red meat is the vital source of animal fat [104,106,107]. Numerous case–control studies have been carried out in Australia [108], Argentina [109], Belgium [110], Switzerland [111], Spain [112], Italy [113,114], the Netherlands [115], the United States [116,117] (including Hawaii [118]), Sweden [119], and Greece [120], and reported the correlations of red meat intake with the increased risks of colorectal cancer. However, no correlation between the intake of total meat and the risk of colorectal cancer were reported in six other studies [121]. Considering the findings of these studies that the intake of fat are not correlated with colon cancer indicates that the results related to the intake of meat are not ascribable to the dietary fat content per se [122–125].

1.4.2.3 Prostate cancer

Several case–control and epidemiologic studies on dietary fat and the risk of prostate cancer have been reviewed recently [126,127]. In general the earlier investigations indicated positive correlations with the intake of saturated fat or total fat, though current investigations have suggested that there is no correlation. It is mentioned by Kolonel [127] that the inconsistencies among the findings of these studies might be because of the adjustment of prostate cancer’s associations with dietary fat consumption for total energy consumption by latter studies. A number of cohort studies have been conducted to particularly evaluate the correlation of fat consumption with the increased risk of prostate cancer [128–131], and those studies found no considerable correlations of increased risk of prostate cancer with total fat intake or specific fatty acids intake. No correlation of prostate cancer risk with meat consumption were found in three cohort studies [132,133], whereas considerable increased risk of prostate cancer with high intake of red meat were observed in four other studies [134–137]. Eight studies stated insignificant correlation [138–145] and four suggested remarkable increased risk of prostate cancer with increased consumption of dietary fats [146–149] among twelve studies. Overall, the outcomes of case–control studies which have evaluated the correlation of prostate cancer risk with the intake of saturated fat, total fat, or red meat seem alike [127,128,137,145,150].

1.4.3 Effects of dietary fats on obesity

Dietary fat has been among the lifestyle issues which frequently demanded to be accountable for high adiposity rates [151]. A weighted regression analysis demonstrated a considerable positive correlation between fat intake and the proportion of the population who are overweight [152]. Reanalysis of the Ni-Hon-San migration study [153], where 2183 Japanese men living in Hiroshima and Nagasaki were compared with 8006 Japanese men living in Honolulu, shows that the total energy intake was only slightly lower in Hiroshima and Nagasaki than Honolulu. It was found in this study that the percentage of energy from fat was two times less in Hiroshima and Nagasaki. The Leeds Fat Study [154] shows that the proportion of obese persons was about 19 times lower among those who consumed low-fat diets than those who consumed high-fat diets. However, there were also many persons whose body mass index was normal despite their high-fat diet consumption, indicating that other attributing factors, including genetic susceptibility, play vital role for this effect.

Another ecologic investigation used the time-trend analysis for examining obese persons and their previous dietary history [155]. A remarkable proportional relationship between the percentage of fat-derived energy and the successive progression of obesity was found among 377,200 Danish military personnel. Similar outcomes were obtained in another study which was conducted on the Pima Indians in the United States [156]. Obviously the correlation of high-fat consumption with the subsequent development of obesity is compounded by other factors, such as the declining trend of physical activities. It is also suggested in a longitudinal survey in China that the increased consumption of fat led to the gain of body weight [157,158]. It was concluded from that study that the increased fat consumption may put a large number of people at the risk of obesity, especially those who are genetically predisposed to the condition [155,159–162]. From these studies we conclude that the dietary fat is one of the elements which is involved in the current epidemic of obesity.

1.5 Conclusions

A number of epidemiological and case–control studies reported the associations of dietary sugars, salts, and fats with increased risk of diseases. Several investigations concluded that increased risks of obesity, overweight, diabetes, cardiovascular diseases, kidney diseases, and some form of cancers are associated with the increased consumption of dietary sugars. Dietary salts are claimed to be an attributing factor of hypertension, cardiovascular diseases, osteoporosis, and certain type of cancers in different studies. Positive association of dietary fat consumption with increased risk of cardiovascular diseases, breast cancer, colorectal cancer, prostate cancer, and obesity are accounted in many different studies conducted in different populations. However, some of these hypotheses are nullified in different studies leading to create confusions. The fact that epidemiological evidence alone rarely establishes causal relationships; rather, evidence from many sources should be considered, including biologically plausible pathways and experimental evidences. Thus it is recommended to conduct more clinical, experimental, and epidemiological studies in different population groups and resolve these issues which are very crucial for public health.

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