Cholesterol and Fats: Back to the Good Old Days!

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.

dietheartIn 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]

dietheart3But 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.[23]

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]

dietheart2The 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.[26] 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!

dietheart6Such 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.[27]

dietheart5There 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]

dietheart7In 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.[41] 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.[50] 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.[66]

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.[67]

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.[1]

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.[2]

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.[4]

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.[58] 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.[68] 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.[72] 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.[22]

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.[34] The 2015–2020 Dietary Guidelines for Americans has indeed dropped that recommendation.[73] Is it not time to switch over to our ancestral diet?


  1. Virtanen JK, Mursu J, Virtanen HEK et al. Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary artery disease according to apolipoprotein E phenotype in men: the Kuopio Ischaemic Heart Disease Risk Factor Study. Am J Clin Nutr. February 10, 2016, doi: 10.3945/ajcn.115.122317. Available at
  2. Ramsden CE, Zamora D, Majchrzak-Hong S, Faurot KR, Broste SK, Frantz RP et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016;353 :i1246. Available at
  3. Lennert VJ. Dietary fats: a new look at old data challenges established wisdom. BMJ 2016; 353 :i1512. Available at
  4. Ravnskov U, Diamond DM, Hama R et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Ope.n 2016;6:e010401 doi:10.1136/bmjopen-2015-010401. Available at
  5. Malhotra A. Saturated fat is not the major issue. BMJ 2013;347:f6340. Available at
  6. The BMJ Press Release. Lowering cholesterol with vegetable oils may not curb heart disease risk or help you live longer. 13 April 2016. Available at
  7. Ignatowski AI. Ueber die Wirkung der tierschen Einweisse auf der Aorta. Virchow’s Arch Pathol Anat 1909;198:248.
  8. Anitschkow N, Chalatow S. Ueber experimentelle Cholester-insteatose und ihre Bedeutung fuer die Entstehung einiger pathologischer Prozesse. Zentrbl Allg Pathol Pathol Anat 1913;24:1–9.
  9. Gofman JW et al. The Role of Lipids and Lipoproteins in Atherosclerosis. Science 17 February 1950:166-186.
  10. Allen F. Studies Concerning Glycosuria and Diabetes. Cambridge MA: Harvard University Press; 1913.
  11. Allen FM, Stillman E, Fitz R. Total dietary regulation in the treatment of diabetes. Monographs of the Rockefeller Institute for Medical Research, No 11, Oct 15, 1919
  12. The Hospital 1913-35 in Corner GW. The Rockefeller Institute 1901-1953 The Origins and Growth. The Rockefeller Institute Press New York City 1964. PP 269-271
  13. Warburg O, Posener K, Negelein E. Ueber den stoffwechsel der tumoren. Biochem Z 1924;152:319-344
  14. Price WA. Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects. At
  15. Keys A, Anderson JT, Fidanza F, Keys MH, Swahnt B. Effects of Diet on Blood Lipids in Man: Particularly Cholesterol and Lipoproteins. Clinical Chemistry February 1955;1(1):34-52.
  16. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp. 1953;20(2):118-139.
  17. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. N Y State J Med 1957;57(14):2343-2354.
  18. Yudkin J Diet and coronary thrombosis hypothesis and fact. 1957;273:155-62.
  19. Yudkin J. Dietary fat and dietary sugar in relation to ischaemic heart-disease and diabetes. 1964;2:4-5.
  20. Yudkin J, Roddy J. Levels of dietary sucrose in patients with occlusive atherosclerotic disease. 1964;2:6-8.
  21. Yudkin J, Roddy J. Levels Of Dietary Sucrose In Patients With Occlusive Atherosclerotic Disease. 1964 Jul 4;2(7349):6–8.
  22. Yudkin J. Evolutionary and historical changes in dietary carbohydrates. Am J Clin Nutr. 1967 Feb;20(2):108-15. At
  23. Campbell GD, Batchelor EL, Goldberg MD. Sugar Intake and Diabetes. 1967;16(1):62-63
  24. Smith JL. John Yudkin: the man who tried to warn us about sugar. The Telegraph. Feb 17, 2014. Available at
  25. William B. Grant. Saturated fat is not the major issue. BMJ 2013;347:f6340 At
  26. Page IH, Allen EV, Chamberlain FL, Keys A at al. Dietary Fat and Its Relation to Heart Attacks and Strokes. Report by the Central Committee for Medical and Community Program of the American Heart Association. 1961;23:133-136
  27. US Gov. Nutrition and Your Health: Dietary Guidelines for Americans. Appendix G-5: History of the Dietary Guidelines for Americans. Available at http://gov/dietaryguidelines/dga2005/report/html/G5_History.htm
  28. Zoë Harcombe Z et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2: doi:10.1136/openhrt-2014-000196. At
  29. Taubes G. Nutrition. The soft science of dietary fat. 2001 Mar 30;291(5513):2536-45. At
  30. Armstrong BK, Mann JI, Adelstein AM, Eskin F. Commodity consumption and ischemic heart disease mortality, with special reference to dietary practices. J Chronic Dis. 1975;28:455-69.
  31. Office of the Assistant Secretary for Planning and Evaluation. Facts and Figures on Overweight and Obesity. US Dept. of Health and Human Services.
  32. Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States Trends 1960-1962 Through 2007 – 2008
  33. Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 Through 2007-2008.
  34. USDA, USDH and HS. Scientific Report of the 2015 Dietary Guidelines Advisory Committee. Feb 2015. P 1. Available at
  35. Ten S, Maclaren N. Insulin Resistance Syndrome in Children. JCEM 2004;89(6):2526-2539 At
  36. Steinberger J et al.Obesity, Insulin Resistance, Diabetes, and Cardiovascular Risk in Children. 2003;107:1448.
  37. Childhood Obesity Increases Early Signs Of Cardiovascular Disease. Science Daily.­ /releases/2009/06/090611142526.htm
  38. Glueck CJ et al. Risk Factors for Coronary Artery Disease in Children: Recognition, Evaluation, and Therapy. Pediatrics in Review 1980;2(5):131 -138
  39. Feinman RD et al. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Jan 2015;31(1):1-13. At
  40. Johnson RJ et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007;86:899–906.
  41. Basu S, Yoffe P, Hills N, Lustig RH. The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data. PLoS One. 2013; 8(2): e57873. At
  42. Schulze MB et al. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. 2004 Aug 25;292(8):927-34. At
  43. Malik VS et al. Sugar Sweetened Beverages, Obesity, Type 2 Diabetes and Cardiovascular Disease risk. 2010 Mar 23;121(11): 1356–1364. At
  44. Imamura F et al. Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction. July 2015;351:h3576. At
  45. DiNicolantonio JJ. Added Fructose: A Principal Driver of Type 2 Diabetes Mellitus and Its Consequences. Mayo Clin Proc. 2015 Mar;90(3):372-81. At
  46. Kuhnle GGC et al. Association between sucrose intake and risk of overweight and obesity in a prospective sub-cohort of the European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk). Public Health Nutrition. CJO2015. At
  47. Ludwig DS et al. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. 2001;357(9255):505–508..
  48. Hu FB. Pro v Con Debate: Role of sugar sweetened beverages in obesity Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity-related diseases. Obesity Reviews. 2013;14:606–619. At
  49. Malik VS et al. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr August 2006;84(2):274-288 . At
  50. Joint WHO/FAO Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases (2002 : Geneva, Switzerland): Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert consultation, Geneva, 28 January — 1 February 2002. (WHO technical report series; 916. At
  51. US government rejects WHO’s attempts to improve diet. BMJ 2004;328:1
  52. Leaked letter of Steiger W at
  53. Lustig RH. Fructose: It’s “Alcohol Without the Buzz”. Adv Nutr March 2013;4:226-235. At
  54. Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. 2012 Feb 1;482(7383):27-9. At
  55. Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23-46. At
  56. Lenoir M, Serre F, Cantin L, Ahmed SH. Intense Sweetness Surpasses Cocaine Reward. PLoS ONE 20072(8): e698. At
  57. Lim JS, Mietus-Snyder M, Valente A, Schwarz JM, Lustig RH. The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome. Nature Reviews Gastroenterology & Hepatology May 2010;7:251-264.
  58. Volek JS, Fernandez ML, Feinman RD, Phinney SD. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res. 2008 Sep;47(5):307-18.
  59. Anderson, KM et al. Cholesterol and mortality. 30 y of follow-up from the Framingham study. 1987; 257:2176–2180
  60. Howard BV et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative randomized controlled dietary modification trial. 2006;295: 655–666
  61. Siri-Tarino PW et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010; 91: 535–546
  62. Siri-Tarino PW et al. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 2010; 91:502–509
  63. Puaschitz NG et al. Dietary Intake of Saturated Fat Is Not Associated with Risk of Coronary Events or Mortality in Patients with Established Coronary Artery Disease. Nutr. 2015;145(2):299-305.
  64. Ravnskov U et al. Should we lower cholesterol as much as possible? BMJ. 2006;332:1330–1332
  65. Yancy WS et al. Diets and clinical coronary events: The truth is out there. 2003; 107:10–16
  66. Chowdhury R, Warnakula S, Kunutsor S et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Intern Med. 18 March 2014;160(6):398-406. Available at http://org/article.aspx?articleid=1846638&resultClick=3
  67. Petursson H, Sigurdsson JA, Bengtsson C, Nilsen TI, Getz L. Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study. J Eval Clin Pract. 2012 Feb;18(1):159-68. Available at
  68. Westman EC. Is dietary carbohydrate essential for human nutrition? Am J Clin Nutr May 2002;75(5):951-953.
  69. Cordain L, Eaton SB , Brand Miller J , Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. European Journal of Clinical Nutrition. 2002;56(Suppl 1):S42–S52. At
  70. Lindeberg S, Eliasson M, Lindahl B, Ahrén B. Low serum insulin in traditional Pacific Islanders–the Kitava Study 1999 Oct;48(10):1216-9.
  71. Pallavi A. Against the grain. Down to Earth. Oct 31, 2008
  72. Cordain L. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr February 2005;81(2):341-354. Available at
  73. Department of Health and Human Services and U.S. Department of Agriculture. 2015–2020 Dietary Guidelines for Americans. 8th Edition. December 2015. Available at