Month: March 2018

The Diet-Heart Hypothesis

The diet-heart hypothesis is the belief that eating foods high in saturated fat contributed to heart disease was first proposed in the 1950s by a scientist named Ancel Keys who believed that by replacing saturated fat from meat, butter and eggs with newly-created industrial polyunsaturated vegetable oil (such as soybean oil) that heart disease and the deaths allegedly associated with it would be reduced by lowering blood cholesterol levels.

In 1952, Keys suggested that Americans should reduce their fat consumption by 1/3 – while at the same time acknowledged that he had no idea whether he was right;

“Direct evidence on the effect of the diet on human arteriosclerosis is very little and likely to remain so for some time” [1].

In 1953, Ancel Keys published the results of his ”Six Countries Study” [1], where he said that he had demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease.

Four years later, in 1957, Yerushalamy published a paper with data from 22 countries [2], which showed a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s Six Countries Study data.

 

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Nevertheless, in 1970, Keys went on to publish his Seven Countries Study in which maintained there was an associative relationship between increased dietary saturated fat and Coronary Heart Disease -basically ignoring the data presented in Yerushalamy’s 1957 study and failing to study countries where Yerushalamy found no relationship, such as France. In a paper published in 1989 based on food consumption patterns in the 1960s in the seven countries [3], Keys said that the average consumption of animal foods (with the exception of fish) was positively associated with 25 year CHD mortality (death) rates and the average intake of saturated fat was strongly related to 10 and 25 year CHD mortality rates. Keys knew of Yerushalamy’s data from 1957 and ignored it.

Keys methodology has been widely criticized for selecting data only from the 7 countries that best fit his hypothesis.

The Sugar Industry Funding of Research Vilifying Fat

In August of 1967, just as Ancel Keys had published his Seven Country Study, Stare, Hegsted and McGandy – the 3 Harvard researchers paid by the sugar industry published their review in the New England Journal of Medicine, titled ”Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (see previous article on that topic).

Stare, Hegsted and McGandy concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis) and resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids;

”Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol…the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.” [4]

These researchers concluded that there was major evidence available at the time which suggested that there was only ONE avenue for diet to contribute to hardening of the arteries and the development of heart disease – yet a year later in 1968 the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done [5];

”the committee strongly recommended to the National Heart Institute that a major definitive study of the effect of diet on the primary prevention of myocardial infarction be planned and put into operation as soon as possible. “

This is an important point; prior to a major study having ever been conducted to determine whether changes in dietary cholesterol impacts heart disease, 3 Harvard researchers paid by the sugar industry concluded that there was “only one avenue” by which diet contributed to the development and progression of atherosclerosis (i.e. “hardening of the arteries”) and heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids.

Researcher Paid by the Sugar Industry Helps Develop the 1977 US Dietary Guidelines

Only ten years after the sugar industry paid Stare, Hegsted and McGandy to write their reviews, the same Dr. Hegsted was directly involved with  developing and editing the 1977 US Dietary Guidelines [6] which recommended an increase in dietary  carbohydrate and a decrease in saturated fat and cholesterol in the diet.

Historic changes in the Dietary Recommendation in Canada have largely been based on changes to the Dietary Recommendations in the US, and as a result both stemmed from a belief that eating saturated fat increases total cholesterol and therefore increases the risk of heart disease.

The problem is this belief is just that, a belief.

There have been many studies that have disproved this including a  randomized, controlled dietary intervention trial from 2008 which compared a low calorie, low in fat with a low carbohydrate, high fat diet of the same number of calories. This study found that overall heart health is significantly improved when carbohydrate is restricted, rather than fat [7,8].

Not all LDL cholesterol is “bad” cholesterol.

Small, dense LDL (“Pattern B”)  causes more “hardening of the arteries” than the large, fluffy LDL particles (“Pattern A”)[9].

It has been reported that when dietary fat is replaced by carbohydrate, the percentage of the small, dense LDL particles  (the ones that cause hardening of the arteries) is increased, increasing risk for heart disease.  Furthermore,  the low carb diet increased HDL (so-called “good” cholesterol), which are protective against heart disease and HDL and small, dense LDL were made worse on the low fat diet. Quite opposite to the “Diet-Heart Hypothesis, this study demonstrated improvements in the risk of heart disease for those eating a low carbohydrate, high fat diet compared to those eating a low fat, low calorie diet – which is not all that surprising given that it had been reported previously that a diet high in saturated fat actually lowers small, dense LDL (the type of LDL that causes hardening of the arteries) and raises the large fluffy LDL; actually improving risk factors for heart disease [15].

There are also other randomized controlled trials from 2004-2008 which demonstrate that a low carb diet improves blood cholesterol test results more than a low fat diet [10,11,12,13,14] – yet despite this, the belief that eating saturated fat increases blood cholesterol, persists.

Both the American and Canadian governments are in the process of revising their Dietary Guidelines and what is clear is that what is needed is an external, independent scientific review of the current evidence-base for the enduring false belief that dietary fat, especially saturated fat contributes to heart disease.

What are the findings of current scientific literature?

Eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials (RCT) that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease [16-21].

Furthermore, recently published results of the largest and most global epidemiological study published in December 2017 in The Lancet [23] found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality and that low consumption (6-7% of calories) of saturated fat was associated with increased risk of stroke.

Here is a synopsis of the findings of the eight meta-analysis and systemic reviews;

”Intake of saturated fatty acids was not significantly associated with coronary heart disease mortality” and “saturated fatty acid intake was not significantly associated coronary heart disease events”

Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled

“There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality”.

Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

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. 2014 Mar 18;160(6):398-406

“The present systematic review provides no moderate quality evidence for the beneficial effects of reduced/modified fat diets in the secondary prevention of coronary heart disease. Recommending higher intakes of polyunsaturated fatty acids in replacement of saturated fatty acids was not associated with risk reduction.”

Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4

“The study found no statistically significant effects of reducing saturated fat on the following outcomes: all-cause mortality, cardiovascular mortality, fatal MIs (myocardial infarctions), non-fatal MIs, stroke, coronary heart disease mortality, coronary heart disease events.”

Note: The one significant finding was an effect for saturated fats on cardiovascular events however this finding lost significance when subjected to a sensitivity analysis (Table 8, page 137).

Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)

“Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalizability for population-wide guidelines.”

Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749

“Available evidence from randomized controlled trials (1968-1973) provides no indication of benefit on coronary heart disease or all-cause mortality from replacing saturated fat with linoleic acid rich vegetable oils (such as corn oil, sunflower oil, safflower oil, cottonseed oil, or soybean oil).”

Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353

“Available evidence from adequately controlled randomised controlled trials suggest replacing saturated fatty acids with mostly n-6 PUFA is unlikely to reduce coronary heart disease events, coronary heart disease  mortality or total mortality. These findings have implications for current dietary recommendations.”

Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30

Only one recent meta analysis conducted by the American Heart Association (by the authors of the Diet-Heart Policy for Americans, mentioned above) found a relationship between saturated fat intake and coronary heart disease, yet failed to examine cardiovascular mortality (death) or total mortality [24].

NOTE: In 1961, the American Heart Association was the author of the original policy paper recommending to limit saturated fats to protect against heart disease and therefore has a significant interest in defending its longtime institutional position.

With the exception of the American Heart Association review, the conclusion of 9 different meta-analysis and review papers of randomized control trials conducted by independent teams of scientists worldwide do not support the belief that dietary intake of saturated fat causes heart disease.

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The PURE (Prospective Urban Rural Epidemiology) was the largest-ever epidemiological study and was published in The Lancet in December 2017 [25]. It recorded dietary intake in 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations.  It found;

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062

Those critical of the study say that it has methodological problems, including problems related to the authors dividing consumption of macronutrients (protein, fat and carbohydrate) into 4 groups (quintiles).  Some say that this is reason the data showed an inverse relationship between saturated fat and cardiovascular disease [26]. Criticisms also include that one cannot compare data between countries of substantially different level of income because “low fat consumption is very uncommon in high income countries” and that ‘the ability to afford certain foods may change the dietary pattern (e.g. high-carbohydrate and low-fat diets may be associated with poverty) [26].

Final thoughts…

Both the American and Canadian governments are currently in the process of revising their Dietary Guidelines and I feel that what is needed now is an external, independent scientific review of the current evidence-base for the belief that saturated fat contributes to heart disease.

Have questions about which types of fats are best to include in your diet and which are best to limit? Please send me a note using the “Contact Me” tab above and I will reply shortly.

References

1. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118—139 (1953).
2. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343—54
3. Kromhout D, Keys A, Aravanis C, Buzina R et al, Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May; 49(5):889-94.
4. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242—47
5. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
6. Introduction to the Dietary Goals for the United States — by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
7. Volek JS, Fernandez ML, Feinman RD, et al. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008;47:307—18
8. Forsythe CE, Phinney SD, Fernandez ML, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids 2008;43:65—77
9. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189—99
10. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082—90.
11. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778—85
12. Gardner C, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women. JAMA 2007;297:969—77
13. Yancy WS Jr., Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769—77
14. Shai I, Schwarzfuchs D, Henkin Y, et al. Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;359:229—41
15. Dreon DM, Fernstrom HA, Campos H, et al. Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am J Clin Nutr 1998;67:828—36
16. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
17. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
18. 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. 2014 Mar 18;160(6):398-406
19. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
20. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
21. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
22. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
23. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
24. Sachs FM, Lichtenstein AH, Wu JHW et al, Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association,  Circulation. 2017 Jul 18;136(3)
25. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
26. Sigurdsson, AF, The Fate of the PURE Study — Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/

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Copyright ©2018 BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Yesterday, in preparing to begin a new series of articles on the relationship between polyunsaturated vegetable fats to obesity, I came across an old, yellowed sheet titled “Comparison of Dietary Fats” that I was given as an undergrad Dietetic student at McGill, in 1989.

It was designed to help us teach consumers how to choose the “healthiest” dietary fats.

As indicated at the bottom of both sides of the handout (see full size photos, below), it was “provided as a Professional Service by Proctor and Gamble“.

Why would Proctor and Gamble, a soap company provide future Dietitians with a teaching handout on choosing healthy oils for cooking? A bit of understanding about how soap is made, will help.

At the time, the making of soap required a mixture of animal fats and lye, however William Procter and James Gamble (brothers-in-law living in Cincinnati in the late 1800s and who formed Proctor and Gamble) needed to find an inexpensive replacement for animal fat for the creation of individually wrapped bars of soap.

The source of soap fat they turned to was a waste-product of the cotton industry – cottonseed oil. It was literally the garbage leftover when cotton was produced and is cloudy, red and bitter to the taste, and toxic to most animals.

They needed to make cottonseed oil solid in order to make bar soap and utilized a newly patented technology to produce a creamy, pearly white substance out of cottonseed oil. This fat resembled lard (the most popular natural animal fat baking and frying fat at the time), so with a little more tweaking, this hydrogenated cottonseed oil was then sold in 1911 by Procter & Gamble to home cooks as Crisco® shortening.

All that was needed now was for Proctor and Gamble to market this industrially-produced seed oil fat, and market it they did. They hired America’s first full-service advertising agency, the J. Walter Thompson Agency that employed graphic artists and professional writers.

“Samples of Crisco were mailed to grocers, restaurants, nutritionists, and home economists. Eight alternative marketing strategies were tested in different cities and their impacts calculated and compared.

Doughnuts were fried in Crisco and handed out in the streets.

Women who purchased the new industrial fat got a free cookbook of Crisco recipes. It opened with the line, “The culinary world is revising its entire cookbook on account of the advent of Crisco, a new and altogether different cooking fat.” [1]

From the very beginning, Proctor and Gamble marketed their industrially-created solid fat (Crisco®) to “nutritionists” and “home economists” – the forerunners to Dietitians.

When Procter & Gamble introduced Puritan Oil® in 1976, a liquid cooking oil made of sunflower oil which became 100% canola oil by 1988, it was natural for them to market their newly created oil to Dietitians.

Proctor & Gamble now had a lucrative business manufacturing industrial seed oils as dietary fats and they wanted to make sure that we, as Dietitians encouraged people to use their “healthy” fats.

I’ve scanned in both sides of the handout (it’s old and yellowed, having been kept in the back of my “new” 1988 Canada’s Food Guide book for almost 30 years). As can be seen, in first place on the front side of the handout is canola oil identified by the trade name “Puritan Oil®”, a registered trademark of Proctor and Gamble.

On the reverse side, is what consumers should know about these oils, including that canola oil is “better than all other types of vegetable oil“.

I’ve highlighted some of the wording that makes Proctor & Gamble’s bias apparent;

Some Final Thoughts…

From the very beginning, industrially-produced seed  fats and oils have been marketed to nutritionists, home economists and Dietitians by the companies that created them, in some cases as a “Professional Service”.

As will become clear in the next article we, as Dietitians were tasked by the Dietary Guidelines in both Canada and the US with promoting “polyunsaturated vegetable oils” to the public as ‘healthful alternatives’ to presumably unhealthy saturated animal fats. The manufacturers were there to ‘assist’ as a ‘Professional Service’.

Looking back on the role of fat manufacturers and the sugar industry (outlined in the preceding article) on which foods were recommended and promoted, it makes me question what I was taught and who affected what I was taught. Given that it was known at the time the sugar industry funded the researchers that implicated saturated fat as the alleged cause of heart disease, I wonder what we don’t know about which industry funded which research.  After all, the knowledge about the sugar industry having funded the researchers that implicated saturated fat only ‘came out’ in November 2016 when it had occurred decades earlier.

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NOTE: It is increasingly my conviction that the simultaneous (1) marketing of polyunsaturated vegetable oil (soybean oil, canola oil) along with (2) changes in the Dietary Recommendations for people to (a) eat no more than 20- 30% of calories from fat and to (b) limit saturated fat to no more than 10% of calories, combined with the recommendations for people to (c) eat 45-65% of calories as carbohydrate was the “perfect storm” that may well explain the current obesity crisis and associated  increase in metabolic health problems that we now see 40 years later.

In subsequent articles I’ll elaborate on why I believe this is the case.

References

1. Ramsey, D*., Graham T., The Atlantic. How Vegetable Oils Replaced Animal Fats in the American Diet, April 26 2012 (www.theatlantic.com/health/archive/2012/04/how-vegetable-oils-replaced-animal-fats-in-the-american-diet/256155/)

*Dr. Drew Ramsey, MD is an assistant clinical professor of psychiatry at Columbia University.

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Copyright ©2018 BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

A year ago, I found out from a fellow Dietitian that a recently published article in the Journal of the American Medical Association revealed that the sugar industry had secretly funded a group of renowned Harvard researchers to write an influential series of articles which downplayed, discredited or outright ignored research known at the time, and which demonstrated that sugar was a contributor to heart disease.

I read the article and was stunned at its significance.

As I am in the midst of a new series of articles on the role of saturated fat and polyunsaturated fat in health and disease, I felt it was important that people understand the sugar industry’s involvement in potentially skewing the scientific evidence at the very time that the original 1977 low-fat, high-carb Dietary Guidelines were being formulated. I researched further and wrote this article.

Two of the prominent Harvard researchers that were paid by the sugar industry and who wrote articles dismissing that sugar was a significant contributor to heart disease and implicating saturated fat as the cause were the late Dr. Fredrick Stare, chair of Harvard’s School of Public Health Nutrition Department and the late Dr. D. Mark Hegsted, a professor in the same department [2].

POST PUBLICATION NOTE (March 12, 2018): Dr. Hegsted, one of the 3 Harvard researchers paid by the sugar industry to write these review articles, was directly involved in developing and editing the 1977 US Dietary Guidelines [6].

A commentary in the Journal of Accountability in Research [4] summarized the significance of those articles as follows;

“Researchers were paid handsomely to critique studies that found sucrose [sugar] makes an inordinate contribution to fat metabolism and heart disease leaving only the theory that  dietary fat and cholesterol was the primary contributor.”

In the mid-1960s, the Sugar Research Foundation (which is the predecessor to the Sugar Association) wanted to counter research that had been published at the time, which suggested that sugar was a more important cause of atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Stare of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board. It then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the dangers of sucrose[2].  Letters exchanged between the parties were brought to light in the November 2016 article published by Kearns et al [1], which maintained that the Sugar Research Foundation tasked the researchers with preparing ”a review article of the several papers which find some special metabolic peril in sucrose [sugar] and, in particular, fructose [3].”

This would seem akin to the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967, the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted, and McGandy titled ”Dietary fats, carbohydrates and atherosclerotic vascular disease”[3], which stated;

”Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol”

The report concluded;

”the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.”

The Harvard researchers went on to say;

”there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet.”

The Harvard researchers concluded;

“on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.”

Stare, Hegsted, and McGandy did not disclose that the Sugar Research Foundation paid them for the two-part review [4].

In response to Kearns et al article in the Journal of the American Medical Association in November 2016 [1], the Sugar Association responded [5] by stating that it;

”should have exercised greater transparency in all of its research activities, however, when the studies in question were published funding disclosures and transparency standards were not the norm they are today.” [5]

Some final thoughts…

The reviews written by these influential Harvard School of Public Health Nutrition Department researchers and paid for by the sugar industry have the appearance of being a deliberate manipulation of the perception of the scientific evidence known at the time. 

Whether deliberate or inadvertent, the fact that such sponsorship occurred at the very period in time when the Dietary Guidelines were under revision to emphasize that saturated fat intake must be reduced and carbohydrate consumption must be increased cannot be understated — a move which certainly benefited the sugar industry.

POST PUBLICATION NOTE (March 12, 2018): Discovered after publication of this article, one of the three Harvard researchers funded by the sugar industry, Dr. D.M. Hegsted, was one of the scientists who worked on the 1977 US Dietary Guidelines[6].

How has this turned out for us?

For the last 40 years, Americans and Canadians have diligently eaten more carbohydrates (including foods containing sucrose and fructose) and more polyunsaturated fats (especially soybean and canola oil) just as the Harvard researchers paid for by the sugar industry recommended — and to what end?

Obesity rates have gone from ~10% in the 1950s and 60’s in both countries to 26.7% in Canada (2015) and ~34% in the US (2017), and diabetes and high blood pressure (hypertension) rates have risen exponentially.

Could it be that the shift to a diet abundant in omega-6 polyunsaturated fat (such as soyabean oil) and which supplies 45-65% of daily calories as carbohydrate created the ‘perfect storm‘ which inadvertently fueled the obesity and health epidemic we now see?

To our good health!

Joy

References

1. Kearns C, Schmidt LA, Glantz SA, et al. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016 Nov 01; 176(11):1680-1685.
2. Husten, L, How Sweet: Sugar Industry Made Fat the Villain, Cardio|Brief, 2016 Sept 13.
3. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242—47
4. Krimsky, S. Sugar Industry Science and Heart Disease, Accountability in Research. 2017 Oct 07; 24:2, 124-125.
5. Sugar Association, The Sugar Association Statement on Kearns JAMA Study, 2016 Sep 12
6. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF

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Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Note: This article was originally posted on March 1, 2018, and was edited on November 23, 2025

This article is based largely on a lecture given by Dr. Donald Layman, PhD – Professor Emeritus from the University of Illinois (Nutrition Forum, June 23, 2013, Vancouver, British Columbia, Canada) [1].

People understand it’s important for children to eat enough protein because they’re growing, but adults and older adults need to eat enough protein each day, as well.

After youth have finished growing, they are at their maximum physical capacity between the ages of 20 and 30 years old, and after the age of 30 years old, adults begin to lose muscle mass at the rate of 1% per year [2].

We’ve come to expect that as people age, they will gain more fat, lose bone mass, and that they’ll have decreased muscle strength — leading to difficulty getting around, a greater risk of falls, and eventually to physical disability. We commonly see older people with spindly legs and bony arms and think of this as ‘normal,’ but we’ve mixed up what is “common” with what is “normal.” When we look at seniors in Okinawa, Japan, for example, we don’t see this. They continue to do manual jobs and practice martial arts well into their 80s and 90s. Aborigine elders in Australia also remain lean, fit, and active as seniors. This is normal.

The physical deterioration that we associate with aging — including weak bones (osteoporosis) and the loss of skeletal muscle mass (sarcopenia) — doesn’t develop suddenly, but takes place over an extended period of time, brought on by less than optimal practices in early middle age.

How Much Protein?

The Recommended Dietary Allowance (RDA) for protein is set at 0.8 g protein/kg per day and describes the minimum quantity of protein that needs to be eaten each day to prevent deficiency. Protein researchers propose that while sufficient to prevent deficiency, this amount is insufficient to promote optimal health as people age [3].

Several recent position statements issued by experts working with older adults indicate that protein intake between 1.0 and 1.5 g protein/kg per day may provide optimal health benefits during aging [4,5]. This appears at odds with the 2010 Dietary Guidelines Advisory Committee report [6], which states that ‘protein intake in the US is more than adequate’ and that ‘inadequate protein intake is rare.’ These seemingly contradictory positions are largely due to differences in how protein adequacy is assessed.

The RDA, more specifically the Estimated Average Requirement (EAR), is the minimum amount of protein intake required to prevent deficiency and is based on nitrogen balance studies (since nitrogen is the main component of amino acids that make up proteins). The EAR evaluates overall protein intake by measuring nitrogen balance (protein synthesis vs. protein breakdown). Evaluation of optimal protein intake not only considers total daily protein but also the metabolic roles of individual amino acids. While the EAR may suffice for healthy younger adults, higher intakes of specific essential amino acids (EAAs) — ones the body cannot make, such as leucine, isoleucine, and valine — have been reported to improve body composition (muscle mass and strength) in older adults [7,8].

Another factor is that nitrogen balance studies consider total protein consumed in a day but not the amount eaten per meal [9,10] nor the role of the essential amino acid leucine, which is required for protein synthesis to begin (including synthesis of new protein for muscle and bone) [10]. Leucine is indispensable in the making of all types of protein, but has a unique role in signalling the initiation of muscle protein synthesis. Much research has been done with large doses of free leucine; however, a 2012 animal study [10] found that in small meals with limited protein intake (common in older adults), a specific minimum amount of leucine is required before protein synthesis occurs. This “leucine threshold” must be met or exceeded before the body will engage in the energy-expensive process of building new proteins.

Typically, the average American eats only 10 g of protein for breakfast, 15 g of protein for lunch, and most of their daily protein at supper (~65 g). Since the minimum leucine needed in a meal (“leucine threshold”) is not met at breakfast or lunch, protein synthesis is only triggered after the evening meal. As elaborated below, this pattern is suboptimal for maintaining muscle mass.

A 2013 study of muscle protein synthesis in adults in their late 30s found that when protein is distributed evenly throughout the day (30 g per meal at breakfast, lunch, and dinner), significantly more muscle protein is synthesized [4]. Importantly, the amount of protein needed to trigger synthesis differs with age — older adults require higher intakes of protein and leucine than younger adults [4]. This reduced muscle protein synthesis has been referred to as “anabolic resistance.” This can be overcome by eating meals with higher amounts of essential amino acids, particularly leucine [4]. These findings led to dietary recommendations for older adults emphasizing a minimum of 20 g of protein per meal containing more than 2.3 g leucine to optimize muscle protein synthesis [4,10].

Final Thoughts…

It is not only growing children who need adequate daily protein — older adults do as well. In many Indigenous cultures, elders are often served first and consume the best of the animal proteins, which may help preserve bone and muscle mass [1].

The average protein intake for men >20 years old in the US is ~98 g/day and for women ~68 g/day. Although this amount of total protein may be adequate for healthy young adults, it is often imbalanced in distribution across the day. Dr. Layman recommends that young and middle-aged adults distribute their protein intake evenly throughout the day, with ~25 g (women)– 30 g (men) of high-quality, animal-based protein per meal to stimulate muscle protein synthesis [1,10].

For older adults, a protein intake of 1.0–1.5 g/kg/day distributed across the day as three meals (i.e., ~30–40 g of animal-based protein per meal) supports optimal muscle protein synthesis and helps prevent sarcopenia [1,10].

How Much is Too Much Protein?

According to Dr. Layman, the Upper Limit of Protein, based on the Recommended Daily Allowance for Protein, is set at ~ 2.5 g protein/kg per day, which would put the maximum amount for most adult men at ~200 g protein per day.

Not Sure You are Eating Sufficient Protein?

Routine health packages, such as the Comprehensive Dietary Package, will enable me to help you achieve your nutrition goals while ensuring you are eating sufficient protein from optimal sources.

To your good health!

Joy

References

1. Layman DK. Protein quantity and quality at meals are key to healthy aging. Nutrition Forum Lecture, University of Illinois, June 23, 2013, Vancouver, BC, Canada. [https://bcdairy.ca/2021-nutrition-forum-presentations/]
2. von Haehling S, Morley JE, Anker SD. An overview of sarcopenia: facts and numbers on prevalence and clinical impact. J Cachexia Sarcopenia Muscle. 2010 Dec;1(2):129–133. doi:10.1007/s13539-010-0014-2. [https://pubmed.ncbi.nlm.nih.gov/21475695/]
3. Volpi E, Campbell WW, Dwyer JT, et al. Is the optimal level of protein intake for older adults greater than the RDA? J Gerontol A Biol Sci Med Sci. 2013;68(6):677–681. doi:10.1093/gerona/gls229. [https://pubmed.ncbi.nlm.nih.gov/23183903/]
4. Bauer J, et al. Evidence-based recommendations for optimal dietary protein intake in older people: A position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013;14:542–559. doi:10.1016/j.jamda.2013.05.021. [https://pubmed.ncbi.nlm.nih.gov/23867520/]
5. U.S. Department of Agriculture. Dietary Guidelines Advisory Committee Report, 2010. [https://www.dietaryguidelines.gov/sites/default/files/2019-05/2010DGACReport-camera-ready-Jan11-11.pdf]
6. Paddon-Jones D, et al. Role of dietary protein in the sarcopenia of aging. Am J Clin Nutr. 2008;87:1562S–1566S. doi:10.1093/ajcn/87.5.1562S. [https://pubmed.ncbi.nlm.nih.gov/18469288/]
7. Luiking Y C, Deutz N. E. P., Memelink R, et al. Postprandial muscle protein synthesis is higher after a high-whey, leucine-enriched supplement than after a dairy-like product in healthy older people. Nutr J. 2014;13:9. DOI: 10.1186/1475-2891-13-9. [https://pubmed.ncbi.nlm.nih.gov/24450500/]
8. U.S. Department of Agriculture. FoodData Central. Leucine content of common foods. https://fdc.nal.usda.gov.
9. Volpi E, et al. Leucine supplementation chronically improves muscle protein synthesis in older adults consuming the RDA for protein.
   
   Clin Nutr. 2012;31(4):512–519. DOI: 10.1016/j.clnu.2012.01.005 [https://pubmed.ncbi.nlm.nih.gov/22357161/]
10. Norton LE, Wilson GJ, Layman DK, et al. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond). 2012;9:67. DOI: 10.1186/1743-7075-9-67. [https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-9-67]

 

 

 

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