A series of new studies and re-evaluation of old studies published over the past few months [1-6] have very clearly dispelled the myth that high levels of serum cholesterol or high intake of saturated fats are the causative factors for heart attacks or for increased mortality. It is about time for the world to accept that cholesterol or saturated fats are not our enemies, but sugars are.
Blaming and shaming of cholesterol and saturated fats started in the early 30s of the last century, got louder by the mid and late seventies, got stamped authoritatively by eighties. But the Diet- Heart hypothesis is being quietly shoved off almost half a century after its first proposal, and after tripling of metabolic diseases and after the deaths of millions due to coronary artery disease, stroke, hypertension and diabetes.
In the early years of 19th century, sugars, fats and proteins were all blamed for atherosclerosis., diabetes and other modern diseases, with works of Warburg and Price pointing at sugars.[7-14] By 1955, Ancel Keys of Minnesota University fixed the blame on cholesterol and advised restriction of saturated fats to contain coronary artery disease.[15-17]
But this was countered by Yudkin J and others, who attributed the rising incidence of modern diseases on rising consumption of sugars, rather than fats. According to Yudkin, the hypothesis of Ancel Keys and his collaborators that a high intake of fat, especially of saturated fat, was a potent cause of the disease was a false conclusion; and, in general, as populations become wealthier, their consumption of fat increases, and so does their consumption of sugar.[18-22] Campbell GD of The Diabetes Clinic, Durban also observed that the diabetes-prone have a diet consisting totally of refined carbohydrate; in almost every instance in tropical countries, as soon as per capita annual sugar intake passes 70 lb. per annum then diabetes becomes “common,“ and he proposed a “Rule of Twenty Years”, wherein he found strikingly constant period of exposure to ingestion of the Westernized diet before diabetes emerged and also “The Rule of the Ten Per Cent“, finding diabetes to be particularly common when the caloric intake of refined sugar exceeded 10 per cent of the total per capita caloric intake.
But the debate turned nasty. Keys described Yudkin’s evidence as “flimsy indeed”. The British Sugar Bureau dismissed Yudkin’s claims as “emotional assertions“. Yudkin was “uninvited” to international conferences and his papers that attacked sugar were omitted from publications. And when Yudkin, in 1972, published his assertions as book titled ‘Pure, White and Deadly’, the World Sugar Research Organisation described his book as “science fiction“.[24,25]
The Diet Heart Hypothesis became a juggernaut. The recommendations to reduce cholesterol in the diet, to reduce calories, to reduce fat, particularly saturated fats like whole milk, cheese, cream, butter, coconut oi, meat, to increase polyunsaturated fats like corn, cotton, soya oil etc., became mainstream and the American Heart Association, along with Keys, published and publicised these recommendations. Even though the suggestions were emphatic, and later became worldwide dietary policy, the publication chose the words carefully: a reduction in blood cholesterol MAY lessen the development or extension of atherosclerosis and hence the risk of heart attacks or strokes, it said, and then went on to add a disclaimer that ‘it must be emphasised there is as yet no final proof that heart attacks of strokes will be prevented by such measures. There was no proof against cholesterol or fats, yet, it was suggested by AHA that reduction of cholesterol and fats may reduce heart attacks and strokes!
Such wordplay did not weaken the Diet Heart Hypothesis, but strengthened it and Ancel Keys found a place on the cover of Time Magazine in 1963. In early 1977, the US Senate Select Committee on Nutrition and Human Needs recommended Dietary Goals for the American people and in February 1980, the Dietary Guidelines for Americans brochure was issued. It recommended to decrease dietary fat intake to no more than 30 percent of calories, with a reduction in intake of saturated fat, to decrease cholesterol intake to 300 mg per day, to increase carbohydrate intake to 55 to 60 percent of calories, to decrease sugar intake to 15 percent of calories and to decrease salt intake to 3 g per day.
There was no evidence against fats or cholesterol then, and it has not been obtained thereafter! A systematic review and meta-analysis of RCTs, published prior to 1983, which examined the relationship between dietary fat, serum cholesterol and the development of CHD, found no differences in all-cause mortality and non-significant differences in CHD mortality, resulting from the dietary interventions. The Government dietary fat recommendations were introduced in the absence of supporting evidence from RCTs and were untested in any trial, so much so, that a review had to be abandoned.[28,29]
On the other, evidence against sugar has kept mounting. In 1975, another ecological study using dietary supply data from 1963-1965 for 30 countries found sugar supply to have the highest correlation with ischemic heart disease mortality rates in 1968 or 1969 for both males and females.[29,30]
But, the low fat propaganda went on gaining momentum, and fat lowering became a $4 Trillion (Rs. 265L Crore) business, offering low fat food, fat reducing drugs, fat reducing exercises, fat reducing surgeries etc.!
Six decades after the low fat diet was first mooted and during the 3 decades from 1980s that low fat diet was drummed up, obesity and diabetes tripled and in the US, ½ of the adults developed one or more chronic diseases and ²⁄₃ of adults became obese or over weight [31-34] and many diseases like type 2 diabetes, hypertension, coronary artery disease etc., started striking the young, even children.[35-38]
In these three decades, following the dietary guidelines of different Govts., the increased calories in our diets have come from sugars and other carbohydrates. In the past 300 years too, sugar consumption has gone up by 50 times and diabetes has gone up from 3/lakh population in late 19th century to 8000/lakh by early 21st century.[39,40] Cross-sectional data on diabetes and nutritional components of food from 175 countries have shown that for every 150 kcal/person/day increase in sugar availability (about one can of soda/day) the prevalence of diabetes increased by 1.1% (p <0.001) and that the duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner. There are many other studies that have implicated sugars and carbohydrates in the pathogenesis of modern diseases.[42-49]
The report of the Joint WHO/FAO Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases , released in 2002-3, also blamed high consumption of sugars for increasing prevalence of obesity and other chronic diseases. But this report was rejected by the US govt., presumably under pressure from the sugar industry.[51,52]
The pathophysiological basis for the role of sugar in the development of modern diseases is also getting clearer. It is increasingly becoming clear that sugar, particularly fructose, plays a major role in the pathogenesis of modern diseases. Fructose increases de novo lipogenesis and induces dyslipidemia. Sugar being the source of alcohol, behaves like alcohol on the liver and on the brain, increases hunger and decreases satiety, and is more addicting than cocaine.[53-56] Sugar drives metabolic syndrome by increasing lipogenesis, increasing uric acid, reducing nitric oxide, increasing insulin resistance, increasing leptin resistance in the liver and increasing inflammation.[55,57] Carbohydrate, directly or indirectly through the effect of insulin, controls the disposition of excess dietary nutrients. Dietary carbohydrate modulates lipolysis, lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels. Glucose and insulin operate through a collection of transcription factors to partition lipids toward anabolic pathways. Abnormal fatty acid metabolism and dyslipidemia, in turn, play an intimate role in the pathogenesis of metabolic syndrome and cardiovascular diseases.[39,58]
While the evidence against sugars is mounting, study after study has failed to prove a causal role for dietary fats in chronic diseases. Framingham study, WHI and many other studies, failed to show an association between dietary lipids and risk for cardiovascular disease (CVD), and also failed to show benefits for omega 6 polyunsaturated fats.[39,59-65] A systematic review of 32 observational studies (512 420 participants) of fatty acids from dietary intake and 17 observational studies (25 721 participants) of fatty acid biomarkers and 27 randomized, controlled trials (105 085 participants) of fatty acid supplementation concluded that current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.
Studies have also absolved cholesterol from all the blame. Nord-Trøndelag Health Study (HUNT 2, 1995–1997) comprising 52 087 Norwegians, aged 20–74, who were followed-up on cause-specific mortality for 10 years (510 297 person-years in total) did not find any evidence against cholesterol and concluded that clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised, especially for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial.
The prospective, population-based Kuopio Ischaemic Heart Disease Risk Factor Study that included 1032 men aged 42–60 y in 1984–1989 found that egg or cholesterol intakes were not associated with the risk of CAD and also not associated with increased common carotid artery intima-media thickness.
To cap it all, recovery and analysis of previously unpublished data from the Minnesota Coronary Experiment (MCE), from the seat of origin of the traditional diet-heart hypothesis, has disapproved the hypothesis itself. The MCE (1968-73) was a double blind randomized controlled trial designed to test whether replacement of saturated fat with vegetable oil rich in linoleic acid reduced coronary heart disease and death by lowering serum cholesterol. Recovered MCE unpublished documents and raw data, comprising of 9423 women and men aged 20-97, longitudinal data on serum cholesterol for the 2355 participants exposed to the study diets for a year or more and 149 completed autopsy files, were analyzed according to hypotheses prespecified by original investigators. Further, a systematic review and meta-analyses of randomized controlled trials that lowered serum cholesterol by providing vegetable oil rich in linoleic acid in place of saturated fat without confounding by concomitant interventions was conducted. Although the intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline −13.8% v −1.0%; P<0.001), there was no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10 808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27). The authors concluded that available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes and that findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.
Another systematic review identified 19 cohort studies including 30 cohorts with a total of 68094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found. The authors concluded that high LDL-C is inversely associated with mortality in most people over 60 years, a finding inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic), questioning the validity of the cholesterol hypothesis. The authors suggested a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.
Many studies have now shown that low carb diets are better than low fat diets in preventing and managing modern diseases. Restriction of carbohydrates has been reported to reverse metabolic syndrome. A carbohydrate restricted diet corrects hyperglycemia, reduces triglycerides, LDL and increases HDL, reduces uric acid, reduces blood pressure, reduces weight and also corrects PCOS. It is interesting to note that human beings do not need any carbohydrate intake for survival! The theoretical minimal level of carbohydrate intake is zero. Protein deprivation leads to kwashiorkor, and energy deprivation leads to marasmus; however, there is no specific carbohydrate deficiency syndrome and carbs are NOT listed as ESSENTIAL nutrients and there is no Recommended Daily Requirement. Aboriginal hunting and fishing cultures, such as Inuit of the Arctic and First Nations groups in Canada, survived for millennia with little if any identifiable dietary carbohydrate intake. Hunter gatherers, who consumed 32% plant foods and 68% animal foods, were relatively free of the signs and symptoms of CVD and hunter gatherers also have low insulin levels.[58,69-71] It is to be noted that food staples and food-processing procedures introduced during the neolithic and industrial periods have fundamentally altered 7 crucial nutritional characteristics of ancestral hominin diets: 1) glycemic load, 2) fatty acid composition, 3) macronutrient composition, 4) micronutrient density, 5) acid-base balance, 6) sodium-potassium ratio, and 7) fiber content. From the time of Australopithecus africanus, through the evolution of true hominids, up to and beyond Pithecanthropus, Neanderthal, and Cro-Magnon, man and his immediate ancestors have continued to be hunters, predators, anti scavengers, seeking their favorite food of meat and offal. With science and technology, man could separate palatability and nutrition, choosing the former over the latter and as result, in England alone, the consumption of sugar rose from 10,000 tons in 1700 to 150,000 tons by 1800.
The Dietary Guidlines for Americans, which since 1980 recommended the restriction of dietary cholesterol to <300mg per day, has withdrawn such advice in 2015-16. The Scientific Report of the 2015 Dietary Guidelines Advisory Committee explicitly stated: Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day. The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum cholesterol.. Cholesterol is not a nutrient of concern for overconsumption. The 2015–2020 Dietary Guidelines for Americans has indeed dropped that recommendation. Is it not time to switch over to our ancestral diet?
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