A Fallacious, Faulty and Foolish Discussion About Saturated Fat
The New York Times has done it again, reporting on a summary of studies on the associations of various dietary and clinical risk factors with heart disease in a way that creates, in my opinion, more confusion than clarity. According to journalist Anahad O’Connor, the researchers claimed that saturated fat, “the type found in meat, butter and cheese”, does not cause heart disease, suggesting that it is not as bad as we have been led to believe. Both the researchers’ report and the journalist’s commentary illustrate the huge costs of scientific reductionism.
We have long been advised to limit our consumption of saturated fat, as well as total fat and cholesterol. This concern about fat sprang to life several decades ago when population studies across countries were showing that dietary fat was impressively correlated with heart disease and some cancers. Animal based products like saturated fat-laden butter and lard were out; plant-based cooking oils, dessert toppings and salad dressings rich in unsaturated oils were in. These findings prompted several national food and health policy reports to recommend lower fat intakes, down to 30% or less of total diet calories. The public generally responded by opting for low fat foods, especially dairy and meats, but not without rancorous debate.
Vegans and vegetarians were somewhat encouraged by these recommendations because this meant cutting back on animal-based foods. The question concerning the amount of saturated fat in our diets often became the focal point of discussions between the ‘V’ people and the omnivores. Now that butter, bacon and cream are back on the plate with this new report, the score has tilted in favor of the eaters of animals. In contrast, the wailing of vegetarians and vegans can be heard far and wide. At least, so it seems.
I propose that this argument for or against saturated fat should have been moot from the very beginning of this research. Here’s why. The original hypothesis that dietary fat, especially saturated fat, is chiefly responsible for heart disease began with laboratory studies over a century ago and the findings ere, at best, uncertain. Much more impressive evidence also was published to show that the early stages of heart disease, atherosclerosis, and its predictive serum cholesterol marker, were increased much more by dietary protein than by dietary fat, especially the protein in animal-based foods. Later, around 1940, more of the same evidence favoring protein was published. The animal protein, casein, was shown to be five times more effective in raising cholesterol in experimental rabbits than the plant protein, soy. In a human study, replacing dietary protein (mostly animal based) with soy protein lowered serum cholesterol much more effectively than lowering dietary fat.
In brief, the more impressive evidence showing animal-based protein to increase serum cholesterol and atherosclerosis was ignored.
A few decades later—during the 1940s to 1990s—this protein effect continued to be ignored in favor of a fat effect, both for heart disease and certain cancers, based both on experimental animal evidence and human population (correlation) studies. But, once again, the human correlation studies claiming a fat effect could just as easily have been due to animal-based protein because of the very close correlation between these two nutrients (r=0.94). But, still again, the evidence favoring animal-based protein as the causal factor mysteriously was not told, even though the evidence in the population studies clearly showed that it was animal-based protein instead of plant-based protein that accounted for these increasing rates of disease.
Saturated fat, mostly found in animal-based foods, is not and should never have been considered the chief cause of heart disease and certain cancers (the same is true for the dietary lipid, cholesterol). I suggest that it would have been more productive to ask not which nutrient acts through which mechanism to produce which outcome but whether there might be multiple factors acting through multiple mechanisms to produce multiple outcomes having shared etiologies.
The concept of wholistic nutrition—readily observed at the intracellular level, now gives us a new lens to see whether there might be more to this story than first meets the eye. For example, we can ask about mechanisms accounting for the disease modifying effects of nutrients and nutrient-like factors in foods containing animal-based protein and/or saturated fat. We also know that as more and more animal-based foods become part or our diets, they displace plant-based foods, thus adding to our list of mechanisms that might be considered. Combining the disease causal mechanisms of animal-based foods with the absence of disease preventive mechanisms provided by plant-based foods is additive. This will undoubtedly lead to and account for effects that are much larger than those resulting from a single nutrient, whether it is protein or fat or any other nutrient.
Because the early research on the causes of atherosclerosis clearly showed a much more pronounced effect from animal-based protein and not saturated fat, let’s then explore some candidate mechanisms that might help to explain the effects of a diet of foods high in animal-based protein. These mechanisms will include those that account for the effects 1) of protein itself, 2) of non-protein factors that are part of animal-based foods and 3) of plant-based factors that are displaced from the diet by animal-based foods.
The summation of these mechanistic effects is not easily measured but I believe that they are far more than adequate to explain profound and broad-acting disease-producing effects of animal protein rich diets. Animal-based protein itself, when fed at dietary levels above the total protein recommendation (an amount readily provided by whole plant-based foods), may 1) increase normal cell growth, as evidenced by increased levels of insulin-like growth factor thus also accelerate cancer growth, 2) increase enzymatic activation of chemical carcinogens to cause mutations and initiate carcinogenesis, 3) dispose of energy in a manner that favors cancer promotion, 4) increase production of reactive oxygen metabolites that encourage cancer growth, cell aging and atherogenesis and 5) depress immune system cells that kill cancer cells.
Animal protein rich diets also include non-protein factors that exhibit mechanisms thought to lead to disease. One recent well-researched hypothesis concerns a group of lipid-like small molecules mostly found in meat and dairy products called phosphatidylcholine (PC) and its metabolite, choline (CH). Upon ingestion, PC and CH travel to our gut where they are metabolized by gut microorganisms to give trimethylamine (TMA). TMA is absorbed and enzymatically oxidized in the liver to trimethylamine oxide (TMAO), a product that promotes atherosclerosis.
I cite these research findings as an example of ‘non protein’ based mechanisms intrinsic to a high protein diet that causes heart disease. Although the researchers ignored a major role for protein (what’s new?), I am confident that protein is the main behind-the-scene factor causing this cascade of events. First, people justify eating meat and dairy for its protein content. Second, they therefore consume lots of PC and CH, the substrates that initiate this scheme. Third, this diet changes the gut microflora to organisms more likely to convert PC and CH to TMA (changing gut microflora populations was a major theme of my Masters thesis in 1957 and my PhD dissertation in 1962, a half century before the references on this topic cited by the authors). Fourth, the oxidase enzyme converting the TMA to TMAO is substantially increased by dietary animal protein. Each of these steps in the cascade of events and reactions are dependent on the consumption of animal-based protein in this diet. Thus, instead of speculating on “probiotic intervention” or development of a “non-systemically absorbed inhibitor” as a “therapeutic strategy for cardiovascular disease”, why not eliminate consumption of animal-based protein? Many more scenarios involving non-protein dependent mechanisms of disease formation resulting from animal-based food consumption could also be cited. Together, whether these mechanisms are directly focused on protein or result from our preference to consume diets high in animal-based protein, the result is the same. It is a dynamic and highly integrated disease-producing event that could easily be like an animal-based protein effect.
Can you now see the folly of the NY Times article and the research report being discussed? The researchers published their findings by focusing their attention on single dietary (i.e., saturated fat and cholesterol) and clinical factors (i.e., serum total, HDL and LDL cholesterol) as causes of heart disease. This is reductionist experimentation that encourages the development of out-of-context remedies targeted to one risk factor or one causal event at a time, a recipe for failure. Reductionist experimentation is valuable for understanding nutrient structure and function, but it too often encourages endless speculation and confusion caused by highly subjective, personal preferences as to which factor to favor in research and to offer to the market.
Very simply, I am not aware of any serious evidence on function, which suggests that dietary saturated fat or cholesterol are causes of heart disease or cancer. Associations of these dietary factors with these diseases are nothing more than reflections of the consumption of animal-based foods and, by inference, inverse associations with whole plant-based foods (i.e., remember that animal-based foods tend to displace plant-based foods).
In the research report reviewed here, I see no evidence that any of the 660,000 subjects in these compiled studies were using a WFPB diet that, unlike the standard American diet (SAD), which is relatively high in fat, protein and animal-based foods. As a consequence, disease rates already are mostly maximized, leaving little or no room for further diet responsiveness. In such a setting, trying to tease out a specific saturated fat or dietary cholesterol effect is foolhardy.
Consider how this interpretation can explain present diet and health practices in the U.S. and other Western countries. As a society, we have become accustomed to diets relatively rich in animal-based foods. In the average American diet, for example, 70-75% of total dietary protein is contributed by animal-based protein, evidence of an insatiable desire for animal-based food that leads to decreased consumption of whole plant-based foods. This results in 1) decreased consumption of really important nutrient groups like antioxidants and complex carbohydrates and 2) less healthy combinations of omega 6:omega 3 fats, micronutrients (e.g., Ca:P, Ca:Mg, Fe:vit C, polyunsaturated fats:vit E), among other dietary distortions. As such, the standard American diet is substantially different from the WFPB diet, which is the only dietary practice that is able to reverse heart disease, type 2 diabetes and, very likely (but yet to be formally confirmed) certain cancers, among other ailments.
This history illustrates two main concerns. First, diet-based-hypotheses on human health should not solely rely on evaluation of one nutrient at a time (saturated fat, total fat, protein, vitamins or any other factor presumed to be important). Such focus permits too much personal subjectivity and encouragement to make ineffective pills to prevent disease and side-effect laden drugs to treat unnecessary disease. Second, it makes no sense to shape our food choices by our voracious appetite for eating animals, generally expressed by consuming so-called ‘high quality’ animal-based protein. Both of these ill-considered perceptions have done incalculable harm to our understanding of diet and health.
Dietary decisions should be made within the nutrient profile framework of plant-based foods and in the context of whole, intact foods, appropriately low in fat and protein but rich in antioxidants and complex carbohydrates.
A good illustration of this problem was the finding from the Nurses’ Health Study showing that decreasing fat intake without changing the proportions of animal and plant-based foods did nothing to decrease breast cancer.
In my experience, this more wholistic (‘w’ intended) understanding of diet, health and disease is best illustrated by the remarkable demonstrations of Esselstyn and Ornish showing that advanced heart disease can be reversed by whole foods, not be changes in single nutrients like saturated fat (actually cured when the diet is maintained). Esselstyn’s findings are especially telling with his 26-year follow-up findings (reported in the film, Forks Over Knives) and his new much anticipated report involving a much larger number of subjects. These findings involve whole foods and do not depend on selective treatment of individual risk factors and events of the heart disease process.
Is saturated fat the chief cause (or even a major contributing cause) of heart disease? The answer is, “No”, not only because of the lack of published empirical evidence of adverse effects of saturated fats but also because it was mostly a moot question from the beginning. But we (professionals and public alike) preferred to debate the fat idea and, in so doing, we ignored what really mattered as a cause of heart and related diseases: the use of an animal protein rich diet. It is clear to me that referring to saturated fat as a main cause of heart disease (and cancer) has been a diversion of epic proportions. It is far more important to focus on the avoidance of animal-based foods—and concocted ‘foods’ of plant parts—in favor of whole plant-based foods naturally low in fat and protein.
N.B. I normally would have submitted this paper to a ‘proper’ peer reviewed scientific journal. But I am not willing to wait for their uncertain decision and also, I am losing confidence in the ability of my long time ‘establishment science’ community to make objective decisions. So a couple of ‘inside’ professional reviewers will have reviewed this manuscript before publication.
- O’Connor, A. Study questions fat and heart disease link. New York Times (2014). well.blogs.nytimes.com/2014/03/17/study-questions-fat-and-heart-disease-link/
- Chowdhury, R. et al. Association of dietary, circulating, and supplement fatty acids with coronary risk. Ann. Internal Med. 160, 398-406 (2014).
- Committee on Diet Nutrition and Cancer. Diet, Nutrition and Cancer. (National Academy Press, 1982).
- National Research Council & Committee on Diet and Health. Diet and health: implications for reducing chronic disease risk., (National Academy Press, 1989).
- Select Committee on Nutrition and Human Needs (U.S. Senate). Dietary goals for the United States, 2nd Edition. 83 (U.S. Government Printing Office, Washington, DC, 1977).
- Carroll, K. K., Gammal, E. B. & Plunkett, E. R. Dietary fat and mammary cancer. Can. Med. Assoc. Journ. 98, 590-594 (1968).
- Drasar, B. S. & Irving, D. Environmental factors and cancer of the colon and breast. Br. J. Cancer 27, 167-172 (1973).
- Wynder, E. L. The epidemiogy of large bowel cancer. Cancer Res. 35, 3388-3394 (1975).
- Wynder, E. L. & Shigematsu, T. Environmental factors of cancer of the colon and rectum. Cancer 20, 1520-1561 (1967).
- Kritchevsky, D. & Czarnecki, S. K. in Animal and vegetable proteins in lipid metabolism and atherosclerosis Vol. 8 Current topics in nutrition and disease (eds M.J. Gibney & D Kritchevsky) 1-7 (Alan R. Liss, Inc., 1983).
- Clarkson, S. & Newburgh, L. H. The relation between athreosclerosis and ingested cholesterol in the rabbit. J. Exp. Med. 43, 595-612 (1926).
- Newburgh, L. H. & Clarkson, S. Production of athersclerosis in rabbits by diet rich in animal protein. JAMA 79, 1106-1108 (1922).
- Newburgh, L. H. & Clarkson, S. The production of arteriosclerosis in rabbits by feeding diets rich in meat. Arch. Intern. Med. 31, 653-676 (1923).
- 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).
- Sirtori, C. R., Noseda, G. & Descovich, G. C. in Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in Lipid Metabolism and Atherosclerosis. (eds M.J. Gibney & D. Kritchevsky) 135-148 (Alan R. Liss, Inc., 1983).
- Terpstra, A. H. M., Hermus, R. J. J. & West, C. E. in Animal and Vegetable Proteins in Lipid Metabolism and Athersclerosis (eds M.J. Gibney & D. Kritchevsky) 19-49 (Alan R. Liss, Inc., 1983).
- Keys, A. Coronary heart disease–the global picture. Atherosclerosis 22, 149-192 (1975).
- Carroll, K. K. Lipids and carcinogenesis. J. Environ. Pathol. Toxicol. 3, 253-271 (1980).
- Carroll, K. K. Dietary fats and cancer. Am. J. Clin. Nutr. 53, 1064S-1067S (1991).
- 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).
- Carroll, K. K., Braden, L. M., Bell, J. A. & Kalamegham, R. Fat and cancer. Cancer 58, 1818-1825 (1986).
- Campbell, T. C. Whole. Rethinking the science of nutrition. (BenBella Books, 2013).
- Mgbodile, M. U. K. & Campbell, T. C. Effect of protein deprivation of male weanling rats on the kinetics of hepatic microsomal enzyme activity. J. Nutr. 102, 53-60 (1972).
- Hu, J. et al. Repression of hepatitis B virus (HBV) transgene and HBV-induced liver injury by low protein diet. Oncogene 15, 2795-2801 (1997).
- Hayes, J. R. & Campbell, T. C. Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. III. Effect of 3-methylcholanthrene induction on activity and binding kinetics. Biochem. Pharmacol. 23, 1721-1732 (1974).
- Hayes, J. R., Mgbodile, M. U. K. & Campbell, T. C. Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. I. Effect on substrate interaction with cytochrome P-450. Biochem. Pharmacol. 22, 1005-1014 (1973).
- Preston, R. S., Hayes, J. R. & Campbell, T. C. The effect of protein deficiency on the in vivo binding of aflatoxin B1 to rat liver macromolecules. Life Sci. 19, 1191-1198 (1976).
- Bell, R. C., Levitsky, D. A. & Campbell, T. C. Enhanced thermogenesis and reduced growth rates do not inhibit GGT+ hepatic preneoplastic foci development. FASEB J. 6, 1395 Abs (1992).
- Horio, F., Youngman, L. D., Bell, R. C. & Campbell, T. C. Thermogenesis, low-protein diets, and decreased development of AFB1-induced preneoplastic foci in rat liver. Nutr. Cancer 16, 31-41 (1991).
- Youngman, L. D., Park, J. Y. & Ames, B. N. Protein oxidation associated with aging is reduced by dietary restriction of protein or calories. Proc. National Acad. Sci 89, 9112-9116 (1992).
- Bell, R. C., Golemboski, K. A., Dietert, R. R. & Campbell, T. C. Long-term intake of a low-casein diet is associated with higher relative NK cell cytotoxic activity in F344 rats. Nutr. Cancer 22, 151-162 (1994).
- Koeth, R. et al. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nature Med 19, 576-585 (2013).
- Wang, Z. et al. Gut flora metabolism of phosphatidylcholine promotes cardiovaccular disease. Nature 472, 57-65 (2011).
- Campbell, T. C. Increasing the crude fiber digestion coefficient by the use of bacterial transfer MS thesis, Cornell University, (1957).
- Campbell, T. C. Biuret and biocarbonate in the rations of ruminants–their incluence on general nitrogen metabolism PhD thesis, Cornell University, (1962).
- Campbell, T. C. & Hayes, J. R. Role of nutrition in the drug metabolizing system. Pharmacol. Revs. 26, 171-197 (1974).
- 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).
- Ornish, D. et al. Can lifestyle changes reverse coronary heart disease? Lancet 336, 129-133 (1990).
- Barnard, N., Cohen, J. & Ferdowsian, H. A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. Am. J. Clin. Nutr. 89, 1588S-1596S (2009).
- McDougall, J. Series of 10-day trials to reduce diabetes symptoms (Santa Rosa, CA, 2005-2011).
- Hildenbrand, G. L. G., Hildenbrand, L. C., Bradford, K. & Cavin, S. W. Five-year survival rates of melanoma patients treated by diet therapy after the manner of Gerson: a retrospective review. Alternative Therapies in Health and Medicine 1, 29-37 (1995).
- 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).
- Willett, W. C. et al. Dietary fat and fiber in relation to risk of breast cancer. An 8-year follow-up. J. Am. Med. Assoc. 268, 2037-2044 (1992).
- Ornish, D. et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA 280, 2001-2007 (1998).
- Esselstyn, C. B. J., Gendy, G., Doyle, J., Golubic, M. & Roizen, M. F. Treating the cause of coronary artery disease. J Family Practice (2014).
Copyright 2018 Center for Nutrition Studies. All rights reserved.