Why Your Doctor Recommends a Low-Fat Diet and What It Has to Do with a Rabbit and a Little Lie.


Caveman Doctor recently received an email from a subscriber asking why his doctor seems to be against fat in the diet. This made Caveman Doctor very confused because his diet has a decent amount of fat in it. In fact, Caveman Doctor is eating a juicy grass-fed and grass-finished steak right now and washing it down with this delicious purple liquid called wine. Caveman Doctor decided to figure out what was going on here, just as soon as he finished his delicious feast…

To Russia with Love

This story begins in a most unexpected way: with a Russian scientist and a rabbit in the early 1900s. The scientist, Anichkov, found that rabbits might develop atherosclerosis after eating heavy amounts of cholesterol in a non-vegetarian diet of meat and eggs.1 This little experiment put the target on cholesterol as the cause of all clogged arteries. However, there was one main and consequential issue with this study rarely discussed: rabbits are vegetarians and high fat foods are not part of their natural diet.2-4 The other obvious issue is the fact that the experiment is studying rabbits and not humans.
In fact, rabbits are near incapable of processing heavy fats in their diet, as their livers are inept at processing excess cholesterol (unlike human livers which do it without an issue). Rabbits digest food within their hindgut. The large intestine of rabbits is very big in proportion to the stomach, and it makes up 40% of the digestive tract. Here, digestible elements of the diet is separated from the fibrous and undigested parts. Later studies confirmed this with diets where cholesterol was replaced with fat, causing similar clogged arteries in rabbits.5
As a side note, cows, different from rabbits in that they are ruminants, have bodies that are made to eat grass. While we can’t even digest most of the cellulose-containing food that cows and rabbits eat, cows have a rumen where grass sits and ferments and bacteria ends up eating the fermenting grass. The cows then end up, for simplicity sake, eating the bacteria and getting nourishment. We do not process grass and cellulose in this way and it simply passes through us undigested. This is not the case with fat and cholesterol, as our digestion tract is made to digest and process them.  So, as you see, we are not like rabbits, and they are not like us.

What If It’s More than Cholesterol?

Interestingly, decades later, further experiments were done on rabbits that were fed high lipid (fat) diets. However, in these studies half of the rabbits fed this diet had damage inflicted to their arteries by the injection of a foreign protein and half did not.6 While both groups of rabbits were fed a high-fat diet, only the group whose arteries were damaged developed clogging of their arteries during the study similar to that in humans. The other group did not develop atherosclerosis. This study points to arterial damage as the culprit of clogged arteries, not the fat. Arterial damage can happen from several mechanisms, including trauma, inflammation, smoking, stress, infection, etc. A different study even pointed to the oxidized (damaged, free radical producing) cholesterol as the culprit.7 This presents the question: Is cholesterol the issue, or is it the Band-Aid that is patching up the real damage that has already occurred to the walls of our arteries?

What Questions Remain After the Rabbit Studies?

So the first and obvious question is can these studies translate to humans? We cavepeople have eaten large amounts of fat and animal meat over the last two million years or so. Also, even if you ignore the inter-species leap of faith, is cholesterol or fat, or neither the enemy? The rabbit studies even show it may not be cholesterol or fat alone, but damage to the arteries that causes them to clog and perhaps the cholesterol is just the Band-Aid for the damaged arteries. What if we never damage our arteries? Will they even clog?
Anichkov’s initial studies are very interesting (at least to me). However, does this mean we should base anything on his experiments, let alone our entire dietary recommendations? We run human clinical trials as animal trial results often (and usually) don’t show the same results in humans.

Present Day Implications from the Rabbit Studies

We took an animal that was given a foreign diet that its body was incapable of handling and watched as it resulted in changes to its arteries. We then extrapolated these results to humans, whose dietary patterns are completely different, as we are very capable of handling fat and cholesterol (after eating it for millions of years), and based our entire dietary recommendations on this data for decades. In fact, fat and cholesterol in our diet is what separates us from the monkey in both brain size (larger), height (taller), and gut size (smaller – well at least for most of our history…).8,9
P.S. After the new recommendations came out promoting low-fat diets, obesity10 (heavily related to cardiovascular disease)11 hypertension, diabetes (also heavily related to cardiovascular disease,12) and cancer13 all rose in prevalence. Though it proves nothing, it is rather interesting.

The Champion of Low Fat

Then came Ancel Keys. He saw fat as the enemy and set out to relay the message to the world.14,15 Notably, even he thought that Anichkov’s experiments proved nothing, and he thought cholesterol caused more of an inflammatory reaction in the arteries of the rabbits instead of merely clogging them.
Keys then performed a big “study” where he looked at the fat intake and death from heart disease in seven countries (Japan, Italy, England, Wales, Australia, Canada, and the USA), appropriately calling it the 7 Countries Study.16 He found that the more fat citizens in these countries ate, the more they got heart disease and died. In 1956 the American Heart Association used this data to inform the public that consuming animal fat causes heart disease. Here are his graphs (thanks to Petro Dobromylskyj):

However, there is one little issue with Keys’ experiment – he actually looked at 22 countries and then picked seven that showed an association between heart disease and fat intake. He apparently selectively ignored the rest and pretended he never saw them. Ok, fair enough, it’s a big issue. This was pointed out by Yerushalmy and Hilleboe who showed the graphs he used before he cherry-picked his countries17:

It’s pretty obvious from this graph that if you pick only certain countries, your data can show anything. This kind of dishonesty in science is what normally ends your career and makes you an outcast in the research community. In his case, his punishment was a shot on the cover of Time magazine and we based our dietary recommendations on his work.
These results created some confusion in the field, and it has even led to the French Paradox, which is basically the fact that the French eat tons of saturated fat but don’t get much heart disease. But what if the paradox isn’t a paradox? What if eating fats, like cheese and whole milk lowered our risk of heart attack like in this study?18 The cholesterol/fat hypothesis is still highly questioned in the field.19

Some of These Questions Are:

1. Can data from animals, that consume markedly different diets, be translated to humans?
2. Why do only arteries get clogged?
3. What if clogged arteries have nothing to do with cholesterol?
4. Can carbohydrates clog arteries as well?
5. What if there is never an insult to the wall of the arteries via stress, inflammation, oxidation, etc?
6. What if it is all based on obesity?

Similar Animal Studies

A similar study of feeding animals very large amounts of food they have not evolved to process has also taken place. However, you don’t hear about this one often and no food recommendations from our government are based on its results. This experiment is the one in which grains are fed to cows and other animals, instead of their typical grass diet. Remember how cows derive nutrition from eating grass and letting it ferment in their rumen? Feeding beef and chicken grains is markedly different than the grass they are made to process, and it significantly affects their fatty acid profile. The saturated fat and total fat in the meat increases markedly, replacing the healthy benefits that naturally come with these fats in free-range and wild animals20, such as the content of healthy omega-3 fatty acids and cancer-fighting conjugated linoleum acid.21 The result of this is a change from once healthy fat to one with the antioxidant and anti-inflammatory benefits removed and replaced with saturated, oxidized fat.22 Interestingly, if you take rabbits again and stuff them with cholesterol, but this time along with antioxidants, the arterial changes are prevented.23 Once again, this points to inflammatory damage (via free radical damage, oxidation, etc.) as the culprit and not necessarily cholesterol, the same changes that happens in cows fed grains.24
However, the main point is the fact that a simple switch from grass to grains causes immense weight gain and fatty stranding in the muscles of these animals as well as an increase in cholesterol. Just as stuffing rabbits with cholesterol raised their cholesterol, so does feeding animals grains. We are not stuffing them with food full of cholesterol or fat, but rather corn and other grains. Yet, the fat and cholesterol profiles of these animals still changes remarkably.  However, one food source is demonized in our society and the other is promoted as the basis of our government dietary recommendations. How did that happen?
So while we all know that grain-fed beef is fatter and to most, tastier, we somehow pretend that the same doesn’t happen to us when we eat grains. Yet, when rabbits are stuffed with cholesterol, and their arteries get clogged, we pay attention. Similar to the rabbits fed high amounts of foods they never consumed, humans are on the losing end of this experiment.
As a side-note, here are where modern hunter gatherers stand, including the Inuit (Eskimos), Rendille, Masai, and Todelau, when added to Keys data (thanks again to Petro Dobromylskyj and Donald Miller, M.D.)
Similar to the rabbits fed high amounts of foods they never consumed, humans are on the losing end of this experiment.
Then came the late 1970’s.
The Pittsburgh Steelers owned the NFL with their “Steel Curtain” defense. Apple Computers was incorporated in 1977, and in the same year, George McGovern decided the dietary habits of the citizens of the United States of America had to change. Under his guidance, the food pyramid was formed.

Mean Joe Green says ignore the food pyramid… Actually, I have no idea what Mean Joe actually thinks of the food pyramid, but Troy Polamalu definitely doesn’t like it.

Actually, I have no idea what Troy Polamalu thinks of it either, but he definitely sports the caveman hairdo.

There was only one problem…
George McGovern, from his grain-producing bastion of South Dakota, knew nothing about nutrition. He was a politician that set up the guidelines with his cronies, set to make millions off of the changes. Under his guidance the Dietary Goals of the United States were released, forever changing the face of American dieting and the rates of obesity.25 As a result, we took studies giving rabbits drastically altered diets that they were unable to handle, and started a new study: giving humans drastically altered diets that they were unable to handle. Many who spoke at these committee meetings ferociously questioned McGovern, some actually blaming carbohydrates for obesity. In the words of Phil Handler, the president of the National Academy of Scientists;

“What right has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?”

As a result, we took studies giving rabbits drastically altered diets that they were unable to handle, and started a new study: giving humans drastically altered diets that they were unable to handle.

The Goals Were Stated As:

1. Increase carbohydrate consumption to account for approximately 55 to 60% of energy intake.
2. Reduce overall fat consumption from 40 to 30% of energy intake.
3. Reduce saturated fat consumption to account for about 10% of total energy intake; and balance that with polyunsaturated and monounsaturated fat, which should account for 10% of energy intake each.
4. Reduce cholesterol consumption to about 300 mg/day.
5. Reduce sugar consumption by about 40% to account for about 15% of total energy intake.
6. Reduce salt consumption by about 50 to 85% to about 3 g/day.
The first one, of course, is my least favorite. That puts the recommendation at around 300 grams of carbohydrates a day, which alone is enough to cause the rates of obesity to skyrocket over the next 30 years.10

The Food Pyramid: An Easy Path to Obesity

Even more interesting, the Nutritional Committee of the American Heart Association (AHA) issued guidelines in 1982 aimed at reducing fat to less than 10% of calories, citing epidemiologic studies for support that actually showed no significant correlations with fat, cholesterol, and heart disease.25 As Kritchevsky astutely points out in his thorough review, this included two large studies:
1. The famous Framingham Study, which showed no relationship between diet and cholesterol26.
2. The Tecumseh Study, which showed that serum cholesterol was not related to our diet, but rather how much adipose tissue (fat) someone has on their body27 (once again pointing to obesity as the main underlying issue with health status).
Basically, we were basing our nutritional guidelines on data that didn’t exist. Interestingly, while we know that stuffing rabbits with cholesterol also fills their arteries, what about in humans? Looking past Keys’ disregard for the scientific method and several rabbit studies, what happens when we take a look in the arteries of humans? Secondly, does cholesterol value even matter?
Way back in 1936, research done at NYU reviewed autopsies of healthy subjects who died suddenly, and showed no correlation between blood cholesterol levels and atherosclerosis, but rather only between atherosclerosis and age.28 These results were confirmed several times over in hundreds of autopsied patients.29-32 These data are largely ignored in medicine today. Newer studies have associated low HDL, and high VLDL and LDL (along with smoking) with atherosclerosis.33 The only issues here are

1. They are correlated with clogged arteries (association not causation).
2. HDL is raised more often than not while VLDL is lowered in higher-fat, low-carb diets.34-40

Interestingly, one study even looked at electron beam tomography to assess calcified plaques in patients. This is basically fancy imaging that can show calcium in your arterial plaques, which is often what causes the clogged arteries. They then put the patients on statins to aggressively lower their LDL. After a year, lipids were lowered over 80mg/dl in some patients.  However, repeat imaging showed no change in calcified plaques.41

As a Result:


1.We still don’t know much in regards to cholesterol’s relationship with heart disease and how much of this is dependent on diet and other factors.
2. We also don’t know if aggressively lowering cholesterol lowers atherosclerosis, and if anything, we may know that aggressively lowering it doesn’t decrease plaques from the study above.
3. The data may actually point to a low-carb diet as being more heart healthy than low-fat diets from randomized trial data.34-40,42-44

Also, low cholesterol has been associated with increased cancer risk25 and studies looking at cholesterol levels and death show that people with very high and very low cholesterol have higher death rates than those that hover in the middle. Therefore, severely lowering cholesterol may be just as harmful as severely raising it based on this data, though much data shows dietary fat intake to have no affect on clogged arteries.45 In fact, recent data has showed low cholesterol levels to be correlated with increased mortality.46 Critics to the low cholesterol theory state that the low cholesterol is likely the result of underlying disease – putting the low cholesterol as the result, not cause of disease. While this justification is certainly agreeable, then why can’t high cholesterol be the result, and not cause, of underlying artery disease? This is what happens when we base things on associations, but I digress.
Data for the lipid hypothesis – that fats and cholesterol causes heart disease – is full or holes. Yet, somehow, the fats-cause-heart-disease theory has expanded to the fats cause heart disease and obesity. No good data supports this. In fact, I have quoted most randomized studies several times in this article and the data overwhelmingly points to carbohydrates as the enemy to weight loss, not fats.34-40,43,47
Perhaps, cholesterol levels aren’t the cause of the disease, but rather the result of it and all this fuss is over nothing. Maybe it is the cause and there just isn’t good data. Maybe (and likely) it’s just all related to obesity. We can run around in circles for days trying to figure out what causes what, and what leads to what. However, I am pointing my money on one message:

When it comes to causing disease, obesity is king.
And when it comes to obesity, insulin and excess carbohydrates are king.

The main cause of obesity is drastically increased levels of carbohydrates, especially sugars, grains, wheat, and cereal in our diets, which our bodies are unable to handle. To add insult to injury, these same carbohydrates were recommended to us by our governing bodies and health practitioners. And then when we gain weight, it’s our fault because we’re lazy and eat too much.
Don’t take my word for it, take the word of Galen, the famous Roman physician of Marcus Aurelius, stated:

“Chinese slaves, sometimes acquire an enormous size during the sugar season, by drinking the cane-juice; and it was remarked by Galen, the keepers of vineyards, who live on nothing but figs and grapes, become fat. The ladies of Tunis and Tripoli are fattened, to please the tastes of their lords, with farinaceous [starch] foods.”48

Or let’s listen to Count Leo Tolstoy, who wrote War and Peace and Anna Karenina, both considered two of the greatest novels of all time:

“He had no need to be in strict training, as he had very quickly been brought down to the required weight of one hundred and sixty pounds, but still he had to avoid gaining weight, and he avoided starchy foods and desserts.”49

Or Sir William Osler, considered one of the greatest physicians in the history of the world and a founding physician of Johns Hopkins Hospital:

“In the case of women who tend to grow stout after child-bearing or at the climacteric, in addition to systematic exercise, they should be told to avoid taking too much food, and particularly to reduce starches and sugars.”50


In Summary

When cholesterol and fat causes clogged arteries in rabbits, we pay attention and blame everything on it under the sun. Even though rabbits are different creatures than us and have totally different diets. When other foods (grains) cause detrimental changes and obesity in cows, however, we ignore it. And that is basically why your doctor tells you to eat a low-fat diet.. Makes sense? Nope, not to me either, and that’s why you’ll never hear me suggest it to a patient.



1. Konstantinov IE, Mejevoi N, Anichkov NM. Nikolai N. Anichkov and his theory of atherosclerosis. Tex Heart Inst J 2006;33:417-423.

2. Matrai K. AV, Hahn I. Seasonal diet of rabbits and their browsing effect on juniper in Bugac Juniper Forest (Hungary). Acta Theriologica 1998;43:107-112.

3. Martins H, Milne JA, Rego F. Seasonal and spatial variation in the diet of the wild rabbit (Oryctolagus cuniculus L.) in Portugal. Journal of Zoology 2002;258:395-404.

4. Reddiex B. Diet selection of European rabbits (Oryctolagus cuniculus) in the semi-arid grasslands of the Mackenzie Basin, New Zealand Department of Ecology: Lincoln University, 1998.

5. Wilson R, Miller R, Middleton C, Kinden D. Atherosclerosis in rabbits fed a low cholesterol diet for five years. Arteriosclerosis, Thrombosis, and Vascular Biology 1982;2:228-241.

6. Minick CR, Murphy GE. Experimental induction of atheroarteriosclerosis by the synergy of allergic injury to arteries and lipid-rich diet. II. Effect of repeatedly injected foreign protein in rabbits fed a lipid-rich, cholesterol-poor diet. Am J Pathol 1973;73:265-300.

7. Staprans I, Pan X-M, Rapp JH, Feingold KR. Oxidized Cholesterol in the Diet Accelerates the Development of Aortic Atherosclerosis in Cholesterol-Fed Rabbits. Arteriosclerosis, Thrombosis, and Vascular Biology 1998;18:977-983.

8. Mann N. Dietary lean red meat and human evolution. European Journal of Nutrition 2000;39:71-79.

9. Larsen CS. Animal Source Foods and Human Health during Evolution. The Journal of Nutrition 2003;133:3893S-3897S.

10. Cite Centers for Disease Control and Prevention, The Obesity Epidemic. Available at: < http://www.cdc.gov/cdctv/ObesityEpidemic/>. Accessed July 27, 2011

11. Van Gaal LF, Mertens IL, De Block CE. Mechanisms linking obesity with cardiovascular disease. Nature 2006;444:875-880.

12. Kannel WB, McGee DL. Diabetes and Cardiovascular Disease. JAMA: The Journal of the American Medical                                                 Association 1979;241:2035-2038.

13. D Maxwell P. Global cancer statistics in the year 2000. The Lancet Oncology 2001;2:533-543.

14. Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease.: Harvard University Press, 1980.

15. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y 1953;20:118-139.

16. Keys A. Coronary heart disease in seven countries. 1970. Nutrition 1997;13:250-252; discussion 249, 253.

17. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease; a methodologic note. New York state journal of medicine 1957;57:2343-2354.

18. Kanavos P. The rising burden of cancer in the developing world. Ann Oncol 2006;17 Suppl 8:viii15-viii23.

19. Stehbens WE. The controversial role of dietary cholesterol and hypercholesterolemia in coronary heart disease and atherogenesis. Pathology 1989;21:213-221; discussion 222.

20. DAVIDSON B, MACIVER J, LESSARD E, CONNORS K. Meat Lipid Profiles: A Comparison of Meat from Domesticated and Wild Southern African Animals. In Vivo 2011;25:197-202.

21. Rule DC, Broughton KS, Shellito SM, Maiorano G. Comparison of muscle fatty acid profiles and cholesterol concentrations of bison, beef cattle, elk, and chicken. Journal of Animal Science 2002;80:1202-1211.

22. Realini CE, Duckett SK, Brito GW, Dalla Rizza M, De Mattos D. Effect of pasture vs. concentrate feeding with or without antioxidants on carcass characteristics, fatty acid composition, and quality of Uruguayan beef. Meat Science 2004;66:567-577.

23. Xiu RJ, Freyschuss A, Ying X, Berglund L, Henriksson P, Bjorkhem I. The antioxidant butylated hydroxytoluene prevents early cholesterol-induced microcirculatory changes in rabbits. J Clin Invest 1994;93:2732-2737.

24. Mahfouz M, Kawano H, Kummerow F. Effect of cholesterol-rich diets with and without added vitamins E and C on the severity of atherosclerosis in rabbits. Am J Clin Nutr 1997;66:1240-1249.

25. Kritchevsky D. History of Recommendations to the Public about Dietary Fat. J Nutr 1998;128:449S-452S.

26. Kannel WB GT. The Framingham Diet Study: diet and the regulations of serum cholesterol (Sect 24). Washington DC: Dept of Health, Education and Welfare, 1970.

27. Nichols AB, Ravenscroft C, Lamphiear DE, Ostrander LD. Independence of Serum Lipid Levels and Dietary Habits. JAMA: The Journal of the American Medical                                                Association 1976;236:1948-1953.

28. Landé K. E. SWM. Human atherosclerosis in relation to the cholesterol content of the blood. Arch Pathol 1936;22:201-312.

29. MATHUR KS, PATNEY NL, KUMAR V, SHARMA RD. Serum Cholesterol and Atherosclerosis in Man. Circulation 1961;23:847-852.

30. Paterson JC, Dyer L, Armstrong EC. Serum cholesterol levels in human atherosclerosis. Can Med Assoc J 1960;82:6-11.

31. Marek Z, Jaegermann K, Ciba T. Atherosclerosis and levels of serum cholesterol in postmortem investigations. Am Heart J 1962;63:768-774.

32. Cabin HS, Roberts WC. Relation of serum total cholesterol and triglyceride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease. Quantitative analysis of 2,037 five mm segments of 160 major epicardial coronary arteries in 40 necropsy patients. Am J Med 1982;73:227-234.

33. Relationship of Atherosclerosis in Young Men to Serum Lipoprotein Cholesterol Concentrations and Smoking. JAMA: The Journal of the American Medical Association 1990;264:3018-3024.

34. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab 2003;88:1617-1623.

35. Gardner CD, 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: the A TO Z Weight Loss Study: a randomized trial. Jama 2007;297:969-977.

36. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003;348:2074-2081.

37. Seshadri P, Iqbal N, Stern L, et al. A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Am J Med 2004;117:398-405.

38. Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;359:229-241.

39. 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;140:778-785.

40. Yancy WS, Jr., Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769-777.

41. Hecht HS, Harman SM. Relation of aggressiveness of lipid-lowering treatment to changes in calcified plaque burden by electron beam tomography. Am J Cardiol 2003;92:334-336.

42. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. Jama 2005;293:43-53.

43. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082-2090.

44. Hite AH, Berkowitz VG, Berkowitz K. Low-carbohydrate diet review: shifting the paradigm. Nutr Clin Pract 2011;26:300-308.

45. Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM 2002;95:397-403.

46. Akerblom JL, Costa R, Luchsinger JA, et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age and Ageing 2008;37:207-213.

47. Hite AH, Berkowitz VG, Berkowitz K. Low-carbohydrate diet review: shifting the paradigm. Nutr Clin Pract 2011;26:300-308.

48. Wakley T. The Lancet: A Journal of British and Foreign Medical and Chemical Science, Criticism, Literature and News London: John Churchill, 1845.

49. Tolstoy L, FitzLyon K. Anna Karenina. Oxford: Oneworld Classics, 2008:xviii, 884 p.

50. Osler W. The Principles and Practive of Medicine. New York: D. Appleton and Company, 1901.

© 2015 CDR Health and Nutrition, LLC. All Rights Reserved.


  1. xinglei

    Caveman doctor, you are my hero.

    1. CavemanDoctor (Post author)

      Thanks Xing. I’ll see you at work tomorrow…

  2. Pingback: What is My Optimal Cholesterol Level? « Caveman Doctor

  3. Pingback: Can Eating Fat Stop Cancer in Its Tracks: What is CLA and Why Do We Care? « Caveman Doctor

  4. Pingback: Stress: The Basics « Caveman Doctor

  5. Pingback: Can Eating Fat Stop Cancer in Its Tracks: What is CLA and Why Do We Care? : Caveman Doctor

  6. Pingback: What is My Optimal Cholesterol Level? : Caveman Doctor

  7. Pingback: Stress: The Basics - Caveman Doctor : Caveman Doctor

  8. silver panda coins

    Cool work. Keep it flowing! 🙂

  9. Pingback: Vegetables Oils: The “Refining” of Our Health - Caveman Doctor : Caveman Doctor

  10. Pingback: Crisco, Trans-Fats, and Revisiting Vegetable Oils - Caveman Doctor : Caveman Doctor

  11. Pingback: Checking Your Oil: The Definitive Guide to Cooking with Fat - Caveman Doctor : Caveman Doctor

  12. Elliot

    Great article! I was familar with rabbit experiment and Ancel Keyes missing data, but didn’t know the story behind G. McGovern’s dietary recommendations. Should have realized he was from a grain producing state!


Leave a Comment

Your email address will not be published. Required fields are marked *