Reviewing Our Approach to the Obesity Crisis

(originally published Feb 1st 2011)

The traditional approach to the management of obesity has been the recommendation to “diet and exercise”, and to elicit the support of family doctors with aims to modify unhealthy lifestyle habits.

The limited success of such conventional strategies is clearly apparent in the unabated escalation of global obesity and its wide range of adverse consequences for human health.

It is appropriate, therefore, to review current paradigms in respect of nutritional policy, and to evaluate the content of public health messages according to the principles of emerging evidence.

A review of the relevant literature suggests that conventional dietary theories do not reflect the consensus findings of critical science regarding nutritional requirements for optimal health.

Within this context there is an opportunity for national health bodies to revise the content of public health messages, and to facilitate a paradigm shift in perceptions of “healthy” and “unhealthy” foods, not only for health professionals, but also for the public who are heavily influenced by dietary guidelines and nutritional propaganda.

THE MESSENGERS:

While the co-ordinated efforts of national bodies are to be welcomed and supported, their failure to escape the influence of American dietary policy has long been apparent. There exists now an opportunity to establish national dietary guidelines which are divorced from the political and economic persuasions which gave content to the policies of the American Heart Association (AHA) four decades ago, and which still influence bio-medical models on a global scale. ( 1 )

Ireland has an opportunity to establish independent dietary policies based on emerging nutritional data and local health requirements, and to take a lead in the “war” against unhealthy eating habits, as it did in the war against the unhealthy smoking habits of the past.

The understandable reservations of many GPs to address lifestyle issues with their patients can be circumvented by a renewed confidence rooted in credible research, and the provision of updated resource material for patients which is innovative, science based and user friendly.

THE MESSAGE:

Public health messages should reflect current evidence in respect of dietary impact on health outcomes. Outdated and politically driven information from American sources should be critically evaluated and discarded. (2)

The current “war on obesity” is essentially a “war on fats”, as portrayed ad nauseum in the public media and sections of the medical literature which constantly echo the outdated dogma of the AHA.

Current health messages consistently and incorrectly portray saturated fats as harmful, and fail to distinguish between these healthy fats, and the potentially unhealthy dietary fats, such as transfats, interesterified fats and industrially produced polyunsaturated fats, which predominate in commercially prepared foods and are widely portrayed as “healthy”.

They also fail to distinguish the nutritional differences between simple and complex carbohydrate groups and their variable impact on health within different sub – groups, such as those who are carb-sensitive or have grain allergies.

Similarly, distinctions have not been made between “complete proteins” as found in animal and dairy products, and the “incomplete proteins” derived from nuts, seeds and legumes, and the deficiencies of vegetable proteins.

National Health policies reflect dietary guidelines that have been historically portrayed by the United States Dept. of Agriculture (USDA) and its past Food Pyramids. ( 3)

A review of the critical evidence will show that these guidelines are more likely to contribute to, rather than prevent, the current escalation of obesity and diabetes and their related consequences.

Such diets can hardly be called “prudent”, as defined by the AHA.

PART II

THE PYRAMIDS:

The USDA Food Pyramid was introduced in 1992 and updated in 1995, and its continued incompatibility with clinical evidence prompted a further review and revision in April 2005, and was named “MyPyramid” (4)

MyPyramid, despite its marked improvement over previous pyramids, continues to ignore emerging clinical evidence in respect of healthy dietary requirements for fats, proteins and carbohydrates, and harbours deficiencies which renders it an incomplete, and somewhat limited, food guide for health professionals and the public alike.

The acknowledged distinctions in MyPyramid between simple and complex carbohydrates are to be welcomed, but the distinctive differences between healthy and unhealthy fats are blurred, while all proteins are treated alike, without recognition being given to the nutritional differences between “complete” animal proteins and “incomplete” vegetable proteins.

The anti-fat and anti-cholesterol policies of the AHA continue to dominate the current dietary guidelines, and continue to be embodied within the Pyramid, rendering it an inadequate testimony to the recognised health benefits of saturated fats, which contrast sharply with the ill effects of unsaturated fatty acids.

According to its website, the MyPyramid Education Framework “provides specific recommendations for making food choices that will improve the quality of an average American diet”.

In reality, the poor quality of the American diet and its adverse health outcomes are universally recognised, prompting pertinent questions about the content and quality of the dietary guidelines that are endorsed by all major health bodies in the USA.

Since Irish dietary guidelines are heavily influenced by the USDA model, it is appropriate to evaluate current national guidelines against the backdrop of escalating obesity and diabetes, given the limited success of current interventive strategies.

It is disconcerting to note the repeated mantra of the USDA in its recommendations for “lowered intakes of saturated fats, transfats, and cholesterol, and increased intake of fruits and vegetables, and whole grains to decrease risk for several chronic diseases”.

By their inclusion of saturated fats with unhealthy transfats in their dietary warnings the authors ignore the findings of critical science that have established saturated fats as healthy and capable of conferring multiple health benefits that are clearly absent from all other types of fat.

The guidelines repeatedly recommend “fat free” or “low fat” milk, “low fat” meat, and the use of “vegetable oils rather than tropical oils” because vegetable oils “do not raise LDL (“bad”) cholesterol”.

This misleading statement ignores the fact that saturated fatty acids (SFA), more than any other fats, raise beneficial HDL levels and have greater cardio-protective properties.

Monounsaturated (MUFAS) and polyunsaturated fats (PUFAS) are recommended in place of saturated fats (SFA) while no reference is made to the potential harm arising from excess PUFAS.

The reference to “limited evidence” for the cardiovascular benefits of omega 3 ignores the wealth of evidence that attests their uniquely protective properties at several levels of disease.

AMERICAN HEART ASSOCIATION (AHA) GUIDELINES:

The AHA continues to promote the perception that dietary fat intake, obesity and heart disease are causally linked, and that “low fat” and “fat free” are synonymous with “heart health”. Their policy statements are clearly presented on their official website and uncompromisingly warn of the “dangers” to health presented by dietary saturated fats. ( 5 )

It states, “ eating food that contains saturated fats raises the level of cholesterol in your blood. High levels of blood cholesterol increase your risk of heart disease or stroke. Be aware too, that many foods high in saturated fat are high in cholesterol which raises your blood cholesterol even higher”.

The website then recommends preferable substitutes for saturated fat, such as vegetable oils and vegetable replacements for traditional meat and dairy products. It also recommends the avoidance of tropical oils in favour of vegetable oils.

Numerous lines of critical evidence have not only challenged the substance of these recommendations, but have repeatedly demonstrated their failure to support optimum health.

National dietary guidelines which echo these principles are similarly culpable, and not only distort, or ignore, the findings of science, but instil in the public mind unwarranted fears, and a conscious preference for foods that are labelled “low fat”, yet lack nutritional value, and carry the potential for health impairment.
Such foods invariably contain high levels of polyunsaturated fats, trans fats or vegetable oils, and carry risks for health that are absent from saturated fat consumption. (6)

Tropical oils at worst are atherogenically neutral, and at best can significantly raise HDL levels, lower cholesterol in hypercholesterolaemic people, and confer anti-carcinogenic and anti-microbial benefits, and their exclusion from a diet, partly due to the soybean lobby, is the loss of a highly beneficial functional food.

The continued vilification of these important dietary fats undermines the opportunity for consumers to make, and enjoy, healthy food choices, and their avoidance, as a result of widespread scare-mongering, must be viewed as a contributory factor in the current epidemic of chronic ill health.

The AHA Guidelines derive from the USDA recommended daily allowance (RDA) of carbohydrates (60%), fats (30%) and protein (10%) with recommendations to limit saturated fats to 7% of daily energy requirements.

Clinical outcomes from research trials which have tested these traditional proportions against variable alternatives have demonstrated greater health benefits from those with reduced carbohydrate proportions and increased fat or protein proportions.

These findings must serve to question the wisdom of conventional guidelines, and prompt a willingness to reshape dietary recommendations in accordance with emerging evidence. (7)

Within the current context of contradictory science and failed popular hypotheses, the prevailing dogma that high carbohydrate / low fat diets represent the “prudent diet” is no longer tenable. (8)

PART III

DIETARY POLICY REVISIONS:

The Harvard School of Public Health produced an alternative food guide to the USDA Food Pyramid, and called it “Healthy Eating Pyramid” in an attempt to improve the perceived weaknesses of MyPyramid. (9)

However, this pyramid continues to promote an unwarranted fear of fats, and calls for a preference of lean meat over animal fats, even though acknowledging that “healthy fats” exist, which it places alongside “healthy carbohydrates”.

The Harvard Pyramid does have the merit of recognising that it is the type of fat, rather than the total content of fat, that is important for health, but relegates red meat and butter to its top shelf, recommending them to be used sparingly in the diet, on the grounds that “red meat is high in saturated fat, and is related to increased risks of colon and prostate cancer, as well as diabetes”. (9)

These fears have repeatedly been shown to be unfounded, with experimental evidence showing that it is dietary carbohydrates, rather than fats, which adversely affect insulin resistance and increase the risk of developing diabetes and weight gain and associated disorders. (10)( 11 ) (12 )
( 13) ( 14)

Dr. Walter Willett, of the Harvard School, gives recognition to these findings and acknowledges that high-fat/ low-carbohydrate diets are good for weight loss, and correctly states that “carbohydrates are not an essential part of the human diet”, and that fuel for the brain can be generated through ketones, from proteins and fats, as an alternative to glucose.

While the Harvard School of Public Health perpetuates the dietary dogma of the American Heart Association (AHA), that saturated fats are harmful because “they raise blood cholesterol”, it nevertheless fails to reflect in its literature, the growing awareness that saturated fats improve the anti-atherogenic lipid profile, and enjoys numerous metabolic advantages over carbohydrates and unsaturated fats.

REVIEWING THE EVIDENCE:

The Food and Agriculture Organization of the U.N. (FAO), in conjunction with the World Health Organization (WHO), produced an Expert Consultation Report in 1994 which reflected the policy statements of the AHA that dietary fat consumption was causally linked to obesity, coronary heart disease (CHD) and some cancers.

Experimental evidence from many lines of study now serve to refute the policy statements of the FAO, and call for a review of the claims regarding saturated fat intake. (15)

The outcomes from several prospective and observational studies conclude that there “is no, or small, association between total daily fat intake and obesity, weight gain, CHD and cancer. (16) (17)

Many of these studies show that low-fat / high carbohydrate diets did not favourably affect serum lipids, fasting serum glucose, fasting serum insulin, or blood pressure, compared with high fat intake diets. (18) (19)

Current recommendations to reduce total fat intake to <30% of daily energy were tested against low carbohydrate (<60%), non-energy restricted diets and resulted in LDL-C reductions, but did not improve weight loss after 12 months, and furthermore, caused an increase in triglycerides and reductions in HDL-C. (20)

The conventional view which favours dietary fat restriction has become increasingly untenable in the wake of research outcomes which expose the lack of scientific credibility for such recommendations.

Reductions of total fat to 30% of daily energy appear to compromise the optimal intake of beneficial fatty acids, particularly when substituted with carbohydrates, according to Hu et al (21) and Mozaffarian et al (22)

In 2002 Willett and Leibell reported the lack of evidence for correlations between obesity and fat intake, and stated that “fat consumption within the range of 18% to 40% of energy appears to have little, if any, effect on body fatness. (23)

Their conclusions were, “ in the USA a substantial decline in the percentage of energy from fat during the last 2 decades has corresponded with a massive increase in the prevalence of obesity. Diets high in fat do not appear to be the primary cause of the high prevalence of excess body fat in our society and reductions in fat will not be a solution”

DENYING THE EVIDENCE:

The UK Food Standards Agency (FSA) has launched a “Saturation Fat & Energy Intake Programme” in an attempt to lower consumer fat intake to below 11%, and have called on businesses to set interval targets for developing and promoting reduced fat, milk cheddar cheese and yogurt products. (24)
By so doing they have failed to acknowledge the real culprits and will thus restrict the healthy food sources while promoting those that endanger health.
The European Dairy Association (EDA) hosted an international Conference in Copenhagen on 25 Sept. 2009 at which a consensus report from experts found no health concerns for dairy consumption, and that fears about saturated fat intake were unfounded and not supported by recent scientific studies. (25)

Fact sheets from the Irish Nutrition & Dietetic Industry (INDI) also convey concerns about “elevated cholesterol”, without making reference to the health benefits of raised HDL which can arise from saturated fat intake. They do correctly advise that “not all types of fats raise blood cholesterol” but do not clarify the distinction. (26)

The documented recommendations to limit fats to 33% of intake and saturated fat to one third of these are linked to statements that “saturated fats increase blood cholesterol and should be limited” and that dietary “hydrogenated vegetable oil” indicates the presence of saturated fats in a product. Clearly, this is not factual. Furthermore, polyunsaturated (pufas) and monounsaturated fats (mufas) are recommended as preferences to saturated fats.

The conventional recommendations to choose polyunsaturated fats and monounsaturated fats on the basis that they are “less harmful to our bodies than saturated fats, and are found in most vegetable oils, for example sunflower oil, olive oils and rapeseed oils” do not reflect the evidence from 27 controlled studies showing that unsaturated fats are in fact more detrimental to health than saturated fats, and that increasing levels of unsaturation diminish the beneficial effects of HDL. (27)

In other words, dietary saturated fats yield greater health benefits than do either the MUFAS or the PUFAS, and these findings are supported in a growing number of comparative studies.

PART IV

THE HISTORICAL EVIDENCE:

Historically, the health benefits in respect of obesity and diabetes, for fat consumption compared to carbohydrate consumption, was evident in a comparison of the Kikuyu and Maasai tribes in Africa. (28)

The Kikuyu lived mainly on cereals and had a mortality rate from respiratory disorders 10 times greater than the Masaai whose staple diet was animal meat and blood. The Maasai were found to have normal blood cholesterol levels and did not suffer with obesity or diabetes.

In a Brazilian study the adverse effects of public health recommendations to reduce fat intake resulted in an increase in the prevalence of obesity, from 17% to 24%, in at risk groups who reduced their intake of fat and increased their intake of carbohydrates. (29)

North American Indians consumed high levels of saturated fat for centuries and only experienced an epidemic of obesity, diabetes, heart disease and cancer when they abandoned their pemmican diet, consisting of 50% protein (lean meat) and 50% fat.

The Eskimos, likewise, enjoyed excellent health while consuming seal meat and seal fat in a proportion of 80% fat and 20% protein.

Observations from the Framingham Study show that those who ate the most saturated fat and the most calories, and ate the most cholesterol, were the most physically active. They also weighed the least, and had the lowest levels of serum cholesterol, were the most healthy, and had the lowest risk of heart disease. (30)

Obesity is not caused by saturated fat ingestion, since dietary fat is a source of energy and does not stimulate insulin secretion, which is a natural response to a high carbohydrate intake.

Saturated fatty acids sustain cellular health and are more likely to support weight loss through a thermogenic effect. Medium chain fatty acids (MCL) like lauric acid, utilise more calories than what they produce for their oxidation, resulting in higher metabolism and body weight loss. (31)

Dietary saturated fats confer additional benefits by inducing a state of satiety, thereby diminishing the need for frequent snacks, a common and inevitable consequence of consuming high carbohydrate meals.

FATS AND WEIGHT LOSS:

Saturated fats predominate in animal fat and tropical oils, and to lesser amounts in vegetable oils, and can also be synthesised from excess dietary carbohydrates. The medium chain fats (MCT) are found in coconut oil, palm kernel oil, and butter, while the longer-chain fats (LCT) occur mainly in meat and dairy products.

Studies have shown that amongst their many health benefits saturated fats can increase energy, boost immunity, and optimise healthy digestion and nutrient absorption. Their capacity for weight reduction and cardiovascular protection are becoming increasingly evident in clinical studies.

Since medium- chain fats (C6 –C 10) have a lower caloric value than longer –chain fats (C12-C18) they are readily metabolised and are an efficient source of energy for immediate use by the organs and muscles, and are thus not stored as fat. (32)

Medium – chain fats also enhance thermogenesis, thereby enabling weight loss to occur. ( 33) They have also been shown to promote ketone production, which can be a source of brain energy, in addition to the utilization of glucose. (34)

A subtle shift in the scientific consensus regarding fats and their health benefits has occurred since the earlier attacks by the AMA on Dr. Robert Atkins for his promotion of high fat / low carbohydrate diets. Despite the several criticisms levelled against the structure of the Atkins diets, current evidence favours the principle that high-fat / low-carbohydrate diets confer health benefits which are strikingly absent in high – carbohydrate / low fat diets as promoted by the AHA and AMA.

The recent acknowledgement by Dr. Walter Willett of Harvard Public School, that the “low fat” message has failed the test of time, calls for a renewed policy statement that incorporates saturated fats into current dietary guidelines, and abandons the anti-cholesterol, anti-fat rhetoric that has not only failed to produce health benefits, but may have contributed to the current epidemic of obesity and escalating rates of diabetes. (23)

Experimental evidence from many lines of study now serve to contradict the food policy statements of the AHA and the FAO, judging them to be, not only inaccurate, but unsafe. (35)

Dr. Frank Hu of Harvard recognised this fact in 2007 at which time he stated “the need for a paradigm shift “ with respect to saturated fats. (35)

PART V

GOOD FATS – BAD FATS:

Dietary saturated fats do not cause obesity, because, unlike carbohydrates, they are not stored and are readily converted into energy for bodily requirements.

The hydrogenated and partially hydrogenated oils which now predominate in processed foods are the real culprits. During the process of fabricating artificial “food” trans-fatty acids are yielded, which by contrast to saturated fatty acids, reduce beneficial HDL levels, raise LDL, increase insulin secretion, and decrease the immune potential by an adverse effect on B cell response and T cell proliferation.

The eventual recognition of trans-fats as a health hazard has prompted their mandatory inclusion on food labels as of 2006, but levels below 0.5 grams may be reported as “zero level” in any given product, thereby masking their presence in popular food choices, yet maintaining their potential for toxicity and harm to human health.

An unintended accumulation of trans-fats may thus occur in the body through the ingestion of several products which are inaccurately labelled as “zero levels”.

The many public health statements that collectively include saturated fats and trans fats in their call for restricted consumption are ill conceived and distortions of fact. These 2 fats are distinctly different from one another in their chemical and physical structure, as well as in their biochemical actions and outcomes for health.

Saturated fatty acids are natural fats while trans fats are artificially created fats. Their vast differences should not be blurred by treating them alike.
The former will support health. The latter will destroy it.

TYPES OF FATS:

Saturated fatty acids (SFA) are characterised by the absence of double bonds with all carbon bonds occupied by a hydrogen atom. This renders them stable, resistant to oxidation, and thus less likely to form free radicles when heated, as is the case with unsaturated fats.

These stable fats predominate in animal fats and tropical oils, like coconut oil, and in smaller amounts in vegetable oils. The body can synthesize saturated fatty acids from excess dietary carbohydrates, if required.

The short – chain (SCT) and medium- chain (MCT) fatty acids are rapidly absorbed after being ingested and stored as a source of quick energy. They therefore do not have the propensity for weight gain that commercial vegetable oils have. (36) (37)

They serve a multitude of vital bodily functions and their dietary absence, or restriction, can lead to dire health consequences.

The unsaturated fatty acids are those with one (monounsaturated) or more (polyunsaturated) double bonds, and become increasingly unstable with loss of saturation, and may result in abnormal and unhealthy lipid formation, which does not occur with the ingestion of fats that are fully saturated. (38)

The main monounsaturated fatty acid (MSFA) is oleic acid (C18) and is derived from olive oil, sesame oil and a variety of nuts. The body can synthesize these fats from SFA when required.

Palmitoleic acid (C16) is a MSFA found almost exclusively in animal fats and has strong anti-microbial properties.

Polyunsaturated fatty acids (PUFA) have 2 or more double bonds, are less stable than SFA, and predominate as either linoleic acid (2 double bonds) or linolenic (3 double bonds).

They are not made by the body and are dependent on food sources in equal ratios. The dietary excess of omega 6 with respect to omega 3 has been identified as a significant cause of a wide range of chronic disorders, and their ubiquitous presence in processed foods presents a health hazard for unsuspecting consumers. (39)

Industrially produced PUFAS such as corn, safflower, soy and sunflower oils are highly unstable and should be avoided because of their propensity to form harmful free radicles and endanger health. They are present in the vegetable oils which are propagated as part of the “prudent diet”. (40)

Evidence suggests that modern diets are excessively high in PUFAS (30%) and that safe levels should not exceed 4% of daily caloric intake. (41)

TRANSFATS are not natural. They are produced by bombarding PUFAS with hydrogen (partial hydrogenation) thereby giving them a longer shelf life, thus serving as a preferential source for the many commercially prepared spreads on the market.

According to several recent studies by Roos, Judd, and Mensink, whenever trans-fats replace saturated fats, beneficial HDL levels decrease, with a dose response effect. (42)
Since food labelling regulations do not require levels below 0.5g to be stipulated on any given product, an unintended accumulation of dietary trans-fats may unwittingly occur through the ingestion of several food sources containing 0.49g of “hidden” trans-fats.

Interesterified fats have been present in commercially prepared foods since the 1950s. Like transfats, they are chemically altered oils, artificially manufactured through fractionation, hydrogenation and inter-ester-ification.

While this fat may be trans free, it can contain chemical residues, hexanes and a variety of waste products that are harmful to cellular structures.

Through inter-ester-ification a vegetable oil is combined with stearic acid, and on this basis food labelling is not required to indicate “interestified”, but may in accordance with FDA licensing use the term “high stearate” on a label.

Food products which are labelled as containing a vegetable oil are likely to contain interesterified fats or transfats.

The elimination from the diet of artificially prepared foods, vegetable oils and many alternative spreads to replace butter, should be encouraged by health professionals in efforts to redirect consumers back to natural and health giving foods, such as butter, whole milk, eggs, animal protein and tropical oils.

PART VI

THE OTHER CULPRITS:

Many popular foods and beverages contain unhealthy levels of high-fructose corn syrup (HFCS), which carries serious and unsuspected health risks.

Their ubiquitous presence in a wide variety of commonly consumed processed foods and carbonated beverages represents a hidden risk for diabetes, obesity, and several chronic disorders, yet they are overlooked as a major threat to human health and receive scant attention from health authorities. (43)

Gaby et al have presented the adverse effects of dietary fructose (44) and recent studies have demonstrated the link between HFCS and the metabolic syndrome. (45)

Because fructose is cheaper than sucrose (table sugar) its ready assimilation into a wide array of popular food products has become a common practice in the food industry, and has largely been ignored by the health industry, despite growing evidence of its associations with type 2 diabetes in the USA. (46)

As far back as 1980 the warning signs were apparent that high fructose levels impaired insulin sensitivity and posed a risk for diabetes and obesity. (47)

Compared to table sugar, which comprises sucrose (50%) and fructose (50%), HFCS contains 80% fructose and 20% glucose, and despite having similar amounts of calories to table sugar, its metabolic effects are different. Fructose results in increased triglyceride synthesis and fat storage in the liver because of its rapid rate of metabolism, compared to glucose which can be stored and utilised as energy.

Fructose ingestion, even in moderate amounts (48) can give rise to non-alcoholic fatty liver disease and impair insulin resistance, leading to impaired glucose metabolism and the metabolic syndrome. (49)

In addition to the high fructose intake from several processed foods, added consumption may occur with excessive fruit and vegetable intake, and with the great emphasis placed on these food groups in the dietary guidelines, at the expense of dietary fats, an unsuspectingly high level of fructose may occur.

It is worthy of note, that no scientific evidence supports the recommendation to eat 5 portions of fruit and vegetables daily, however innocuous such recommendations may appear to be. (50)

Fructose, rather than glucose, can precipitate the formation of toxic advanced glycation end products (AGES) by reacting with lipids, and adding to the complications of diabetes by inducing neuropathy and retinopathy, neuro-degenerative disorders, and even ageing. (51)

In the light of these findings policies which promote carbohydrate intake at the expense of saturated fats should be reviewed as a matter of urgency in the interest of public health.

PART VII

CALORIE RESTRICTION – THE EVIDENCE:

Caloric restriction has repeatedly demonstrated retardation of the ageing process and a marked reduction of risk for chronic disease.

Even minimal caloric reductions may confer health benefits and prolong lifespan. These effects were demonstrated in a 20 year study of rhesus monkeys whose caloric intake was reduced by 30% resulting in a 13% mortality rate from age-related causes, compared to 37% in those whose diets were not calorie restricted. (52)

Of note is the observation that while they lost fat weight, they did not lose muscle mass and sustained brain volume and cognitive and motor function.

Markers of ageing were reduced during 6 years of observation in individuals who reduced their caloric intake by 20%. (53)

Caloric restriction has been shown to prolong life span also by preserving cardiac function through increased mitochondrial formation (54)

More recently, nutrients have been identified which mimic caloric restriction and modify genetic expression leading to retardation of the ageing process. Gene regulators called paroxisome proliferator-activated receptors (PPARS) are triggered by calorie restriction, resulting in healthy fat and carbohydrate metabolism and preservation of glycaemic control. (55)

CARBOHYDRATE RESTRICTION:

The assertion that high-fat diets promote weight gain and adverse health outcomes is false, and should be assessed by evidence-based principles.

Accordingly, the benefits of conventional diets, which promote high carbohydrates and restrict fats, should be tested by these same principles.

Carbohydrate restricted diets were the standard treatment for diabetes before the advent of insulin and anti-diabetic medications, and clinical studies have consistently shown that low-carbohydrate diets improve glycaemic control in diabetic patients (56) (57) (58) (59) (60) and induce weight loss for up to 24 months. (61)

The AHA officially recommends a daily intake of 55% carbohydrate energy per day, which may amount to 75% if recommendations are followed.
Such high levels of carbohydrate intake are likely to advance rather than retard the diabetic process.

In a randomised controlled trial (RCT), involving 53 healthy obese females, a low carb diet was compared with a 55% carb diet (AHA type) and produced a weight loss of 8.5 kg compared to 3.9kg, which continued while the weight loss in the high carb group levelled out. The authors described the results as “ a surprising challenge to prevailing dietary practice”. (Brehm 2003)

Carbohydrate restricted diets have been widely tested to evaluate their effects on weight loss and long term health benefits.

In a RCT by Samaha et al comparing the outcome of a low-carb diet (1630 kcal/day) to a low fat diet (1576 kcal/day) the low carb group lost 5.8 kg compared to the low fat group ( 1.6 kg ) which was sustained at 6 months, with a triglyceride reduction of 20% compared to 4% in the low fat group.
(62)

This trial showed that calorie content is not as predictive for weight loss as is carbohydrate restriction.

Compared with a conventional diet a RCT involving 63 obese men on a low-carbohydrate demonstrated greater weight loss (6.8% vs 2.7%) (63)

A low carbohydrate – ketogenic diet, without any restriction of fats, has repeatedly been shown to produce healthy outcomes with improved lipid fractions (64)

In a 12 week study of 60 participants the NCEP diet was compared to a modified low carbohydrate diet (MCL) and found to be less effective for weight loss. (65)

A low carbohydrate, ketogenic diet improved glycaemic control in obese type 2 diabetic patients allowing many to reduce or eliminate their medication.
Compared to a low glycaemic reduced calorie group these patients had greater weight reductions ( 11.1kg vs 6.9kg) and improved their HDL levels by 5.6 times. (66)

These findings correlate with those from earlier investigations into the effects of carbohydrate restricted diets on diabetes and the metabolic syndrome.
(67) (68) (69) (70) (71)

Yancy et al demonstrated that reducing carbohydrates, rather than fats, produced not only greater weight loss ( 12.9% vs 6.7% ) with improved lipid profiles, but also better participant retention, disproving the notion that low carbohydrates diets are not sustainable. (72)

In a Spanish – ketogenic Mediterranean diet, with unlimited calories, the significant reductions in body weight, blood pressure, triacylglycerols and glucose prompted the researchers to dispel notions of the “healthy diet” as embodied in the Food Pyramid, which calls for fat reduction. (73)

In a review of 6 studies involving 594 participants, over a period of 3 to 18 months, researchers found that reducing dietary fats did not confer any significant health benefits (74)

In a high protein (30%) – low carbohydrate (40%) comparative study with low protein ( 15%) – high carbohydrate (55%) 58 obese subjects with hyperinsulinaemia experienced greater benefit, again raising questions about the health benefits of the conventional 55% carbohydrate recommendations.
(75)

And again, in a review of the Cochrane Database greater weight loss was found to occur with low carbohydrate rather than with low fat diets. The authors concluded that “low fat diets do not cause weight loss.” (76)

In a carbohydrate restricted diet, with either a high fat (45%) or high protein (34%) weight loss was similar ( 10.2kg vs 9.7kg ) with slightly greater benefit for the high fat diet, and similar improvements in insulin resistance and lipid profiles. (77)

Nordman et al (2006) reviewed 5 trials involving 447 individuals and concluded that greater weight loss (-3.3 kg ) occurred with low carbohydrate diets than with low fat diets ( –1.0 kg) within 12 months. Cardiovascular risk factors were more favourable with carbohydrate restriction than with fat restriction. (78)

And again, in a recent ( 2009) RCT of 200 overweight subjects a carbohydrate restricted diet led to greater weight loss and greater cardiovascular benefit than a fat restricted diet. (79)

PART VIII

FAT STORAGE AND OBESITY:

Saturated fats do not promote weight gain or obesity as they are readily converted into energy for physiological requirements.

Dietary carbohydrates, however, are transferred into triglycerides and stored in adipocytes as fat under the enzymatic actions of glycerol-3-phosphate dehydrogenase. These adipocytes (fat cells) regulate their size and number by secreting command signals such as leptin, adinopectin and glycerol-3-phosphate dehydrogenase.

Recent advances in the study of adipocytes have identified them as important mediators in many physiological processes that regulate energy metabolism, or cause obesity. Their capacity to differentiate in response to several transcription factors is currently the focus of enquiry into underlying genetic disorders associated with obesity. (80)

No longer are adipocytes considered to be a passive energy storage organ, but an active endocrine organ which secretes bioactive peptides, called adipocytokines, which act through autocrine, panacrine and endocrine systems. (81)

Adipocytes communicate with their environment through sending and receiving signals which determine their biological functions. (82)

Brown fat cells, by contrast to the white fat apidocytes, regulate the physiological requirements of energy by burning calories, and may thus reduce the amount of white fat in the body.

The white fat cells serve as storage cells and may increase in size to accommodate excess dietary triglyceride, but may also increase in number, through the mutation of reserve preadipocytes, under the stimulation of insulin.

It is important, therefore, to restrict the potential for white fat cells to increase in number during childhood, since they will remain present for life.

WEIGHT MANAGEMENT:

Unwanted weight gain may occur through an increase in calorie consumption, or through a decrease in the command signal network, which is a likely cause for age related weight gain.

If the major share of calories derive from an abundance of carbohydrate ingestion, as recommended in conventional food plans, a greater liklihood exists for weight gain and its related problems.

Novel ways of interrupting the command signal network, or of reducing calories, may include any of the following .

a) Caloric Restriction to under 15001800 calories per day significantly improves insulin sensitivity (83) and extends longevity. (84)

b) Carbohydrate Restriction as shown from numerous trials is safe, effective and sustainable, and offers greater health benefits than conventional high carbohydrate diets. (85)

c) Restoring Insulin sensitivity through nutrient intervention, such as chromium, (86) magnesium (87) cocoa polyphenols (88) omega 3 (89)

d) Alpha – glucosidase inhibition with Acarbose.

e) Alpha – amylase inhibitors, such as Phaseolus vulgaris, an extract from the white kidney bean, appears to have the potential to significantly inhibit the absorption of complex carbohydrates (90) and also boosts cholecystokinin (CCK) which improves satiety with a reduced urge to eat. (91)

f) Amylase inhibition with the African mango Irvingia gabonensis, not only reduces body weight, but improves lipid profiles in obese patients. (92) (93)

g) Dietary fibre has been shown to minimise the post-prandial insulin surge and improve weight loss through decreased carbohydrate absorption. (94)

h) Restoring hormonal balance by regulating oestrogen and testosterone levels, thyroid stimulating hormones, and circulating brain
serotonin with L-tryptophan. ( 95)

i) Increased physical activity to improve insulin activity. (96)

j) Boosting resting energy expenditure by enhanced thermogenesis with medium-chain saturated fatty acids. (97)

CONCLUSION:

Conventional dietary recommendations have failed to halt or reverse a trend that continues to impact negatively on human health, while simultaneously stretching health and financial resources beyond redemption.

It is timely to review the content of traditional food guidelines and to align them with the conclusive evidence of critical science, and to offer dietary information that serves, not political agendas, but the best health interests of the nation.

It is fitting that Dr. Sylvan Lee Weinberg, a former President of the American College of Chest Physicians and editor of The American Heart Hospital Journal indicted current dietary policies of low fat/high carbohydrate for their “unintended role in the current epidemics of obesity, lipid abnormalities, type II diabetes, and metabolic syndrome”, and that “this diet can no longer be defended by appeal to the authority of prestigious medical organizations, or by rejecting clinical experience and a growing medical literature suggesting that the much maligned low-carbohydrate, high protein diet may have a salutary effect on the epidemics in question”. (98)

REFERENCES:

1. The Oiling of America – Gary Taubes.
2. J Am Coll Cardiol, 2004, March 4.
3. www.health.gov/dietaryguidelines/dga 2005
4. www.mypyramid.gov/pyramid 2005
5. www.americanheartassociation
6. Experimental Biol & Medicine 233:674688 (2008)
7. Archives of Internal Med vol 165, no 9, May 9, 2005
8. Arch Intern Med 2006, April 24: 166(80:932)
9. www.discovery magazine.com/2003/mar/breakdialogue/article
10. Diabetes Care 2003, 26: 22612267
11. Diabetes Care 2004, 53:23752382
12. JAMA 1994, 271 : 14211428
13. NEJM 1988, 319: 829834
14. Diabetes Care 1989, 12: 94101
15. Annals Nutr Metab 2009; 55:4455
16. Am J Clinic Nutr, 2003: 78: 719727
17. Obesity-Silver Spring 2007; 15: 967976
18. Curr Atherosc Rep 2005; 7:427
19. JAMA 2007, 297: 969977
20. Arch Intern Med 2006: 166: 285293
21. J Am Coll Nutr 2001; 20:5.19
22. Eur J Clin Nutr 2009; 63: 522533
23. Am J Med 2002, Dec 30, 113 – Suppl 9b:475495
24. www.food.gov.uk/multimedia/page/satfatprog.pdg
25. www.euromilk.org
26. www.indi.ie
27. Arterio Thromb 1992 Aug, 12(8): 9119
28. Am J Epid 1972, 95: 2637
29. J Epid Community Health doi:10.1136/2008
30. Lancet 1983; 1:10621068
31. J of Nutr Sc. Vitaminology 2002
32. J Nutr 1995 Mar; 125(3): 5319
33. J Am Soc Clin Nutr, 1981, 34624
34. Am J Clin Nutr. 1982, 36: 950962
35. J Am. Coll. Cardiol. 2007: 50:2224
36. Int J Obes Relat Metab Disorders, Oct 1998, 22 (10); 9479
37. Metab Feb 1995, 44 (2) : 2739
38. Arterio Thromb 1992 Aug 12(8) 91
39. Biomed Pharmacother 2002 Oct, 56 (8)
40. Eat Fat Lose Fat, Mary Enig PhD, P 810
41. Lipids, 198520:4227
42. www.health.gov/dietaryguidelines/dga2005/report/HTML/D4
43. Am J Clin Nutr 2004, April;79(4):53743
44. Altern Med Review 2005,Dec 10(4) 294306
45. Curr Opin Gastroenterol 2008, Mar 24(2): 2049
46. Am J Clin Nutr 2004, May;79(5):7749
47. Am J Clin Nutr 1980 Feb; 33(2):2738
48. J Nutr 1983 Sept:113(9);181926
49. Nutr Metab (Lond) 2005 Feb 21:2(1):5
50. Nutr J 2003:2:2
51. Amino Acids 2008 June:35 (1):2936
52. Science 2009 June 10; 325(5937) 2014
53. Annal NY Acad Sc 2007 Oct, 1114; 42833
54. Am J Physiol Endocrinol Metab 2005 April 28(4): E 81825
55. Arch Cardiol Mex 2007 Oct – Dec: 77 Suppl 4:546676
56. NEJM 1988, 319:829834
57. Diabetes Care 1989, 12:94101
58. JAMA, 271: 14211428
59. Diabetes Care 2003, 26:22612267
60. Diabetes 2004, 53:23752382
61. NEJM 2008, 359. 229241
62. NEJM May 22, 2003 (vol 348, 20742081)
63. NEJM May 22, 2003 (vol 348, 20822092)
64. Arch Med vol 165 no.92005 May 9
65. Arch Intern Med 2004: 164: 21412146
66. Nutr & Metab 2008, 2008, 5:36
67. Metab Syndrome & Related Disorders 2003, 1:227232
68. Metab Syndrome & Related Disorders 2003, 1:239243
69. Am J Clin Nutr 2007, 86; 27684
70. Metab Syndrome & Related Diseases 2003, 1: 233237
71. Metab Syndrome & Related Diseases 2003, 1 : 291298
72. Annals Int Med 2004, May 18: 140(10) 76977
73. Nutr J. 2008: 7:30
74. Obes Review. 2003 Aug:4(3): 185
75. Int J Obes. Rehab Metab Disorders 2004 Sept: 28 (9):1187
76. Cochrane Database Sys Rev. 2002: (2) CDOO 3640
77. Am J Clin Nutr. 2005 Nov: 82(5):4401
78. Arch Intern Med 2006; April 24, 166:285293
79. Cardiovasc Diabetol 2009 July 18:8:36
80. J Nutr 130:3; 1653121S, 2000
81. Clin Endocrinology 2006; 64(4):355365
82. J of Cellular Physiol, vol 216, issue 1, p3132008
83. Diabetes Care 2006, June:29(6)
84. Annals NY Acad Sc 2007 Oct; 1114:42833
85. Science 2009 July 10325(5937) 2014
86. Diabetes, 1992, Nov; 40(2), 398405
87. Diabetes Care 2003, April 26(4);114752
88. Hypt 2005 Aug; 46(2); 398405
89. Int J Circumpolar Health. 2005 Sept; 64(4):396408
90. Int J Med Sci 2007:4(4);196202
91. J Agric Food Chem 2009 Oct 14:57(19):931623
92. Lipids Health Dis 2005;4:2
93. Lipids Health Dis 2008; 7:12
94. Med Hyposth 2002 June; 58(6):48790
95. Int J Eating Disorders 1985:4(3):28192
96. Acta Physiol (Oxf), 2008 Jan:192(1):12735
97. Mol Nutr Food Res 2008; 52:631645
98. J. Am Coll of Cardiology, 2004 March 4.

Dr Neville Wilson is a Doctor in Maynooth

http://www.leinsterclinic.ie

Leave a Reply

Your email address will not be published. Required fields are marked *