Submitted to the Dietary Guidelines Advisory Committee on April 30, 2015.
In 1980, the first report by the Dietary Guidelines (DG) Advisory Committee was authored by two friends of mine, the late Harvard School of Public Health Professor Mark Hegsted PhD (representing the McGovern Committee and the USDA) and Allan Forbes MD, formerly FDA Chief of Nutrition. I have remained keenly interested in the 5-year reports ever since.
Unfortunately, I have gradually lost much of my early enthusiasm for this advisory committee. During the past 35 years, I have seen little if any progress toward a better understanding of diet, nutrition and health. This is regrettable because these reports serve as guidelines for health education, government school lunch, WIC (women, infants and children), and other important public programs. I do not see how this report is any more progressive or insightful than its predecessors. Previous reports have included new words and phrases which unfortunately did not lead to any real change. These modifications seem more intended for media attention, and I have found them to be cosmetic. Over the decades, we have witnessed the recommendations take the form of a square (“Basic Four”) turned into a pyramid, into a dinner plate, and (almost) into a circle—all with similar content. Marketing yes, but science no.
Failing to be more critical of the relationship between food and health favors the status quo, which already promotes the consumption of food that promotes costly diseases. A more impactful message is needed if the health of the nation is to be advanced.
Some people are pleased that the 2015 DG report mentions an association between livestock-based food and climate change. But USDA Secretary of Agriculture Vilsack has already stated that the environment-food association is unlikely to be taken seriously. This coincides with food industry leaders’ contention that this committee has no expertise in this area. Others are impressed with the phrase “plant-based food” as evidence that there might be enlightenment in the air. Sadly, I believe that merely using this language without being more specific is relatively superficial. The urgency for real dietary changes should be taken seriously.
The DG committee likes to develop its advice especially from the more in-depth content and findings of the Food and Nutrition Board (FNB) of the Institute of Medicine (IOM). Thus my comments—mostly concerning the scientific evidence—probably should be directed to the FNB/IOM. The executive summary of the 2002 FNB report made the extraordinary statement that up to 35% protein is associated with “minimizing risk for chronic disease” when 10% protein (the RDA) is enough. The 35% protein recommendation was accepted and is still promoted by the DG committee. Promoting 35% protein as an acceptable level for the school lunch and WIC programs, for example, is a disaster. In fact a whole food plant based (WFPB) diet, with no added oil, can easily provide 10-12% total protein, which meets the long established recommended daily allowance (RDA) of 9-10% protein. The continued use of an upper ‘safe’ level of 35% protein of total, daily dietary calories in my view is grossly unscientific and completely irresponsible.
Whether overtly stated or not, this ‘safe’ level of protein has major implications for virtually everything that is said about the effects of food and nutrients on human health. Another advisory with a much longer history, recommends abolishing the 300 mg/day limit on cholesterol consumption “because available evidence shows no appreciable relationship between … dietary cholesterol and serum cholesterol”. I agree with the proposal that the association of dietary cholesterol with serum cholesterol is very weak, if not non-existent. It should also be added that the ability of serum cholesterol to predict heart disease for individual people is not especially impressive, even though serum cholesterol is useful 1) for monitoring time-dependent change in disease risk for individuals upon dietary intervention (i.e, inter-individual variance is eliminated) and 2) for comparing health status of large populations. Dietary cholesterol is not a good predictor of heart disease or other degenerative diseases if this is based on the assumption that cholesterol specifically causes heart disease. But removing this dietary limit should not be interpreted as welcome news for carnivores, an implication that is left unexplained by the committee.
For decades, the unusual focus on cholesterol, without considering other possibilities, has been an exceptionally reductionist and misleading interpretation. Dietary cholesterol may help to clog arteries but this condition accounts for only a small fraction (~10%) of coronary heart disease events. Far too much attention has been given to cholesterol as if it is a major cause of disease. Such focus diverts attention away from the much more reliable evidence showing that a diet rich in animal protein, which represents multiple risk factors, is the main dietary cause of heart disease, cancer and related degenerative diseases. In experimental animal studies begun over a century ago, animal-based protein (casein), not cholesterol, was more responsible for increasing blood cholesterol and its association with the development of atherosclerosis. Later studies (about 75 years ago) in experimental rabbits showed that casein (an animal protein) was five times more effective than soy protein (a plant protein) in raising serum cholesterol and in generating angiogenesis (early cardiovascular disease). Animal proteins as a group are more effective in raising serum cholesterol in experimental animal studies than plant proteins, as a group. Although follow-up human studies do not appear to respond to the specific effects of casein on serum cholesterol levels in the same way as do experimental animals, a broader perspective clearly shows that high animal protein based diets increase risk. Some of this is attributed to the direct effects of animal protein (by many mechanisms) and some of this is due to the displacement of whole plant –based food containing disease protective nutrients (e.g., antioxidants, complex carbohydrates), also by countless mechanisms.
On a related topic, the long held belief that saturated fat is a major cause of heart disease and certain cancers also should be questioned. The 2015 report ignores research showing that dietary cholesterol and saturated fat are indicators of animal protein consumption, thus of animal food in general.
The long time tendency to infer disease causality to fats (e.g., saturated fats, cholesterol), intentional or unintentional, was generally accepted by the marketplace because it allowed for the removal of fat from animal based foods (lean meat, low fat and skim milk), thus maintaining continued consumption of these foods. Removing protein from these products was not an option because this would no longer even remotely be considered the same food or the same diet. This latest 2015 DG report repeatedly assumes that saturated fat is independently unhealthy, thus recommending that its intake be controlled. This interpretation is short-sighted because it tends to suggest that unsaturated fats should be preferred. In contrast, about 30-40 years ago, in experimental animal studies on mammary cancer, unsaturated fats were shown to promote cancer substantially more than saturated fats, albeit at high levels of total dietary fat. Also, the ratio of omega-3:omega-6 fats is a function of total fat intake and is distorted in the wrong direction when total dietary fat becomes high. High dietary total fat means a high ratio of pro-inflammatory omega-6:anti-inflammatory omega-3. A low fat WFPB diet shifts this ratio into a much healthier balance of about 3-4:1. Bottom line? Minimize use of added fat, regardless of fat type.
Although technically correct, abolishing the limit on dietary cholesterol is likely to encourage people to consume more animal-based foods, which conflicts with the report’s recommendation to consume more plant-based foods. Removing this upper limit corrects the highly reductionist and inappropriate interpretation for dietary cholesterol as a primary cause of disease but it is likely to lead to practices that are even less healthy, like more cardiovascular disease and more cancer. There also is substantial evidence, for example, showing that animal protein promotes cancer development in experimental animals (studied in great depth), which correlates with several human cancers in observational studies (usually expressed through its covariate, total fat) and functions through varied mechanisms to make plausible these observational studies.
Adverse effects of animal protein-rich diets were first reported over a century ago, especially concerning their effects on physical performance and heart disease, although animal protein also was suggested as a cause of cancer. But this information has been consistently ignored in every DG report since 1980. It is not only a question of the direct adverse effects of animal protein on cancer and heart disease but, even more so, on the indirect effects resulting from the dietary displacement of whole plant based foods.
Not addressing information concerning the proper amount and kind of dietary protein, an essential major nutrient, will continue to have serious consequences. For example, on the topic of the causes of cancer, it is popular to assume that this disease is mainly caused by exposure to certain chemicals in food, water and air. These ‘environmental’ chemicals are judged to be cancer-causing (carcinogenic) when they are shown to be mutagenic and when they produce tumors in a formal experimental animal bioassay program. It should be noted that exposure amounts of suspect chemical carcinogens are tested at 2-3 orders of magnitude, or higher, than levels expected during human exposure. In reality, there is precious little or no human evidence that these ‘proven’ chemical carcinogens are anything more than insignificant causes of cancer. Cancer promotion by animal protein and related nutrients is more relevant than any suspect chemical carcinogen ever identified in this program.
In experimental animal studies, for example, animal-based protein (casein), when fed above a total dietary protein level that supports optimum health (i.e., above 10-12% of calories)—easily provided by a diet of whole, natural plant based foods—turns on tumor development initiated by one of the most powerful mutagens and carcinogens ever discovered. When dietary casein is subsequently decreased to levels less than 10% of calories, early cancer development can be turned off. Dietary casein, in this instance, readily controls cancer development regardless of the dosage of the initiating carcinogen. According to the experimental criteria used for testing these environmental chemicals, casein, the main protein of cow’s milk, is very likely the most relevant chemical carcinogen ever identified. This conclusion is based on extensive studies produced in my publicly funded laboratory, (mostly NIH), and supported by research in other laboratories as well.
I cite these observations from the literature, my research laboratory and from an extensive body of evidence. These sources show that nutrition, when properly understood and applied within a more comprehensive, wholistic context—countless nutrients, countless disease outcomes, countless mechanistic events—has the power to prevent, sustain and/or reverse serious diseases. Nutrition can do this far more effectively and rapidly than all of the best pharmaceutical strategies combined or, I predict, more than any genes that might be discovered to be associated with cancer.
None of this type of information is being shared with the public in this 2015 DG report. This report does not even hint that information on WFPB dietary lifestyle exists. Even more striking, this report fails to even suggest research to improve or to deny this evidence. Yet, this dietary lifestyle is the most effective remedy for health restoration and maintenance and disease prevention, in terms of its breadth and rapidity of effect, than any other environmental, pharmaceutical or dietary practice, thus making it the method of choice for treating as well as for preventing disease.
I recognize that the DG committee might claim that this kind of information is not their charge and that they are merely summarizing what other groups have reported, a practice that lends itself to highly selective reference material. But, at a minimum, this DG committee bears collective responsibility with the FNB/IOM to do a more professional job. The series of DG reports (eight since 1980) is, in reality, a major source of public nutrition information that garners considerable media promotion and publicity. I submit that, while relying on unprofessional selection of scientific evidence, these reports have done far more harm than good for public welfare. I will conclude by citing three especially significant and relevant observations to illustrate my concern.
- Heart disease is the #1 cause of death in the U.S. It is mostly treated with stents and statins, conservatively estimated at $15,000-$20,000 per year per patient (multiple stent operations and sustained statin use). This treatment has multiple side effects, but no benefit of extended life. A recent study by Caldwell Esselstyn et al showed that among 198 documented heart disease patients who were advised in one 5-hour session on how to use a WFPB diet, only one individual among 177 compliant individuals suffered an additional event during the next 2-7 years (average 3.4 years) of follow-up. That is a remarkably low rate of <1%. Among the 21 cases not complying with this advice, 62% suffered an additional event (although 25% recurrence is the more traditional rate). An earlier, smaller study by Esselstyn et al showed the same remarkable result. Only 5 of the original 18 patients died over the next 26 years, but none from a cardiac event—with no significant side effects. Similar results, although of shorter duration and including more than dietary advice, were shown by Ornish et al. Beginning with a 5-hour counseling session, as in the Esselstyn et al study, the cost of a far more effective dietary treatment would be about $100-125/yr. Patients relying on pills and procedures (i.e., stents and stains) incur 150-200 times more cost yet suffer far worse outcomes—increased side effects and lower survival. How can anyone accept this report that fails to even acknowledge these findings?
- We spend about $200 million per year to learn that a few chemicals (among about 80,000 environmental chemicals yet to be tested) are capable of causing cancer (in an experimental animal bioassay program). Yet there is virtually no evidence that these “environmental carcinogens” cause cancer among humans. The DG committee seriously deflects interest away from a consideration of nutrition in cancer causation. More specifically, diets rich in animal protein products (also high in total fat and low in complex carbohydrates and antioxidants) are likely causing well over 200,000 cancer deaths each year in the U.S. What kind of evidence will it take for this observation to be taken seriously? I presented to all three of the participating organizations (FDA, NIH and WHO) over 30 years ago, and have received no argument against this evidence. The only downside that I have heard is the very large number of experimental pathologists and related professional positions that would be lost.
- Medical care costs per capita in the U.S. is the highest among similar countries, yet indices of quality of health place us last among these same countries.
- The recommended level of dietary protein, about 10% of total calories (5-6% is the minimum requirement), can easily be provided by a WFPB diet. This diet can virtually eliminate the problems cited above, as well as many more—including much of the climate change problem. Yet, the DG report, along with the FNB/IOM companion report, have agreed that diets containing up to 35% of total calories as protein can be safely used while optimizing human health. This was and still is a preposterous misrepresentation.
The 2015 report may look impressive, because it summarizes a large amount of data on food consumption and corresponding nutrient intake by varied demographic groups. In addition, the report summarizes food consumption data with a few common diseases. The food associations are largely assessed by how well these foods meet recommended nutrient intakes. However, there is more to consider. It is questionable whether recommending nutrient intake for large groups is appropriate, especially because this information is primarily intended for individuals.
Considerable variation of nutrient activities occurs at several junctions along the pathway of nutrient disposition. This begins with discrepancies in nutrient composition for different samples of the same food. This continues with variations in the proportional amounts of nutrients that are digested, absorbed, transported, distributed to different tissues and metabolized to functional products. Connecting nutrient exposures observed within population survey data to nutrient functionality for individuals requires further information on biological plausibility and rational perspectives on research study design and data interpretation.
While relying on such survey data alone is not appropriate for individuals, it is clearly being used as background information for designing large food delivery programs. These data are also being used for forecasting economic trends in food consumption. Again, advertising yes, but science no.
Is this 2015 dietary guidelines report (or its seven predecessors) actually helping to resolve human health problems in the U.S? I think not. These reports ignore or misrepresent a striking body of evidence that could dramatically improve health. As a result, these reports have been used to create more (not less) personal health problems, as well as severe environmental and economic distress problems.
I suggest that the role of this committee should be substantially restructured, better yet even abandoned. In no way should this committee’s responsibility be controlled by a government agency (USDA) beholden to an industry (livestock) that controls what the public gets to know! The resources used to support this advisory program would be far better used to support national efforts to 1) construct an efficacious nutritional science education program for all accredited medical school curricula, 2) develop reimbursement procedures for primary care physicians who apply this nutrition strategy, 3) establish a new National Institute for Nutrition (to join its 27 companion NIH institutes), 4) suspend food subsidy programs that primarily support food producers (i.e., not consumers), 5) create a food and nutrition advisory council, which truly serves the interests of the consumer and which is financed by an endowment trust fund beyond the influence of corporate financial interests and 6) which serves as a health safety net for those unable to secure adequate nutrition for people and families in need.
It is now time to act. It is now time to minimize the corporate influence that has stifled objective scientific inquiry on the matter of food and human health. Corporate institutions that have controlled this information for far too long.
- Forrester, J. S. & Shah, P. K. Lipid lowering versus revascularization: an idea whose time (for testing) has come. Circulation 96, 1360-1362 (1997).
- Clarkson, S. & Newburgh, L. H. The relation between atherosclerosis and ingested cholesterol in the rabbit. J. Exp. Med. 43, 595-612 (1926).
- Kritchevsky, D. Dietary protein, cholesterol and atherosclerosis: a review of the early history. J. Nutr. 125, 589S-593S (1995).
- Newburgh, L. H. & Clarkson, S. The production of arteriosclerosis in rabbits by feeding diets rich in meat. Arch. Intern. Med. 31, 653-676 (1923).
- Ignatowski, A. Uber die Wirbung des tierischen eiweiss auf die aorta und die parenchymatosa organe der kaninchen. Vrichows Arch Pathol Anat Physiol Klin Med 198, 248-270 (1909).
- Campbell, T. C. Untold nutrition. Nutr. Cancer 66, 1077-1082, doi:DOI: 10.1080/01635581.2014.927687 (2014).
- Meeker, D. R. & Kesten, H. D. Experimental atherosclerosis and high protein diets. Proc. Soc. Exp. Biol. Med. 45, 543-545 (1940).
- Meeker, D. R. & Kesten, H. D. Effect of high protein diets on experimental atherosclerosis of rabbits. Arch. Pathology 31, 147-162 (1941).
- Carroll, K. K. in Animal and Vegetable Proteins in Lipid Metabolism and Atherosclerosis (eds M.J. Gibney & D. Kritchevsky) 9-17 (Alan R. Liss, Inc., 1983).
- Chowdhury, R. et al. Association of dietary, circulating, and supplement fatty acids with coronary risk. Ann. Internal Med. 160, 398-406 (2014).
- Armstrong, D. & Doll, R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int. J. Cancer 15, 617-631 (1975).
- Gammal, E. B., Carroll, K. K. & Plunkett, E. R. Effects of dietary fat on mammary carcinogenesis by 7,12-dimethylbenz(a)anthracene in rats. Cancer Res. 27, 1737-1742 (1067).
- Carroll, K. K. & Hopkins, G. J. Dietary polyunsaturated fat versus saturated fat in relation to mammary carcinogenesis. Lipids 14, 155-158 (1979).
- Hopkins, G. J., Kennedy, T. G. & Carroll, K. K. Polyunsaturated fatty acids as promoters of mammary carcinogenesis induced in Sprague-Dawley rats by 7,12-dimethylbenz[a]anthracene. Journ. Natl. Cancer Inst. 66, 517-522 (1981).
- Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. (American Institute for Cancer Research/World Cancer Research Fund, 1997).
- Joint FAO/WHO Expert Consultation on Diet Nutrition and the Prevention of Chronic Diseases. Diet, nutrition and the prevention of chronic diseases: report of a point WHO/FAO expert consultation. WHO technical report series, 916. (World Health Organization, Geneva, 2003).
- World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and Prevention of Cancer: A Global Perspective. (American Institute for Cancer Research, Washington, D.C>, 2007).
- Chittenden, R. H. Physiological economy in nutrition. (F.A. Stokes, 1904).
- Chittenden, R. H. The nutrition of man. (F. A. Stokes & Co., 1907).
- Newburgh, L. H. & Clarkson, S. The relation between atherosclerosis and ingested cholesterol in the rabbit. J. Exp. Med. 43, 595-612 (1926).
- Williams, W. R. The natural history of cancer, with special references to its causation and prevention. (William Heinemann, 1908).
- National Toxicology Program. Report on carcinogens. 499 (Research Triangle Park, NC, 2011).
- Dunaif, G. E. & Campbell, T. C. Relative contribution of dietary protein level and Aflatoxin B1 dose in generation of presumptive preneoplastic foci in rat liver. J. Natl. Cancer Inst. 78, 365-369 (1987).
- Dunaif, G. E. & Campbell, T. C. Dietary protein level and aflatoxin B1-induced preneoplastic hepatic lesions in the rat. J. Nutr. 117, 1298-1302 (1987).
- Appleton, B. S. & Campbell, T. C. Dietary protein intervention during the post-dosing phase of aflatoxin B1-induced hepatic preneoplastic lesion development. J. Natl. Cancer Inst. 70, 547-549 (1983).
- Youngman, L. D. & Campbell, T. C. Inhibition of aflatoxin B1-induced gamma-glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential. Carcinogenesis 13, 1607-1613 (1992).
- Campbell, T. C. Whole. Rethinking the science of nutrition (with H. Jacobson). (BenBella Books, 2013).
- Esselstyn, C. & Golubic, M. The nutritional reversal of cardiovascular disease, Fact or Fiction? Three case reports. Exper. Clin. Cardiol. 20, 1901-1908 (2014).
- Esselstyn, C. B., Jr. Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). Am. J. Cardiol. 84, 339-341 (1999).
- Fulkerson, L. 92 min (Monica Beach Productions, Santa Monica, CA, 2011).
- Ornish, D. et al. Can lifestyle changes reverse coronary heart disease? Lancet 336, 129-133 (1990).
- Esselstyn, C. B. J., Gendy, G., Doyle, J., Golubic, M. & Roizen, M. F. A way to reverse CAD? J Fam. Pract. 63, 356-364b (2014).
- OECD Health Data 2011. Why is health spending n the United States so high? OECD 50. <http://www.oecd.org/unitedstates/49084355.pdf%3E.