Chewing the fat....on fat - I

Being born in the late 80s, many of my readers will have first hand experience of a critical shift in how we eat (or were advised to) that I can only read about.

Luckily, being such a contentious area, there has been no shortage of writing and research in this area carried out. 

My nana tells me about the good old times in the 50s and 60s where everything was cooked in butter and lard and how she would look forward to picking up her joint of meat from the butchers (with suet!). She tells me about how people fried things more and that this was before the nationwide health campaign to shift away from traditional animal fats and move toward the more 'healthful' vegetable fats, including margarine. Oh, and also that when you looked around back then, people were not 'fat', or obese, like we might see today. A brief tour in the history of this topic is in order.

In the early 1900s, the Russian scientist Anichkov found that Rabbits who were given a non-vegetarian diet consisting of meat and eggs led to the development of atherosclerosis1 (fat clogged arteries). Findings from this landmark study were then extrapolated to humans despite the fact that A) it was not performaed on humans and B) rabbits are vegetarians, their physiology is not designed to process meat or fat!

Rabbits are notoriously associated with carrots as they are true vegetarians

Rabbits are notoriously associated with carrots as they are true vegetarians

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. (Colin Champ, MD)

Some decades later, further atherosclerosis studies in rabbits found that it was not so much an issue of dietary fat or cholesterol, but one of fat and cholesterol in the presence of but not necessarily causing arterial damage. Arterial damage can be caused by a host of mechanisms not limited to but including; smoking, stress, trauma and infection. Only those rabbits who had experimentally induced damage went on to develop 'clogged arteries' on a high fat diet, those not damaged did not 2 . Aside from the fact humans have ate fat, cholesterol and meat for as long as records can trace, it appears that damage to the arteries and not neccessarily the fat, cholesterol and meat that cause us to have clogged arteries.

These findings went a long way toward dietary recommendations to demonise fat through the 80s and 90s. Incidentally, after this advice rates of obesity 3 , hypertension, diabetes5 and cancer6 (all associated with cardiovascular disease 4 ) have all rose in prevalence. Nothing conclusive can be drawn from this, interesting none the less.


Next in the story was Ancel Keys and his landmark 'seven-countries' study7. In this study he reported fat intake and death rates in Japan, Italy, England, Wales, Australia, Canada and USA. This formed the basis of the American Heart Associations' (AHA) warning to the public of the danger of fat causing heart disease; the more fat people ate based on this data, the more they die(see figure 1); avoid fat.

Figure 1: Ancel Keys infamous seven-country study demonstrating a strong correlation between percentage of fat consumed and death rate. *Image taken from Petro Dobromylskyj

Figure 1: Ancel Keys infamous seven-country study demonstrating a strong correlation between percentage of fat consumed and death rate.

*Image taken from Petro Dobromylskyj

The fundamental fine print of Keys work however illustrated that the 'seven-countries' study wasn't infact seven countries but TWENTY-TWO where only the countries showing what the author wanted were cherry picked and published (see figure 2).

Figure 2: Keys actual raw data scattered much more randomly, any number of lines could be drawn connecting these data points which would show a very different relationship to the seven countries eventually published to demonise fat.  *Image taken from Yerushalmy and Hilleboe (1957)

Figure 2: Keys actual raw data scattered much more randomly, any number of lines could be drawn connecting these data points which would show a very different relationship to the seven countries eventually published to demonise fat. 

*Image taken from Yerushalmy and Hilleboe (1957)

We took studies that gave rabbits drastically altered diets that they were unable to handle, and started a new study: giving humans dratsically altered diets theat they were unable to handle.
— Colin Champ, MD

The unfortunate end result of this propaganda is that we have significant confusion in the field. We took studies that gave 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. We listened to the experts and we believed that fat really is bad for us. We stopped drinking whole milk, ate less red meat and fewer eggs, used less butter and other fats and oils and here emerged the French paradox; the french eat tons of animal fat and have comparatively low rates of heart disease. But what if it is not a paradox? What if eating whole milk, red meat, butter, eggs and cheese actually lowered our risk of heart disease? That is exactly what this study by Kanavos found 9 . The cholesterol-fat hypothesis is still highly questioned in the field 10 .

Fat, as it turned out was a scapegoat. It was calories all along.
— Alan Aragon

Something else happened at the same time as we reduced our animal fat intake, we ate more of everything else, a lot more. The per-capita food supply in the USA increased 15 per cent between 1970 and 1994 11 .

Fat, as it turned out was a scapegoat. It was calories all along.

If good fats and bad fats even exist they are discussed in part II of 'chewing the fat'....

 

Luke R. Davies :)


 

REFERENCES

1. Konstantinov, I. E., Mejevoi, N., Anichkov, N. M. and Nikolai, N. (2006). Anichkov and his Theory of Atherosclerosis, Tex Heart Inst Journal, 33, P.417-423.

2.Minick, C. R. and Murphy, G. E. (1973). Experimental Induction of Atherosclerosis 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, American Journal of Pathology, 73(2), P.265-300.

3. Cite Centers for Disease Control and Prevention, The Obesity Epidemic. Available at: http://www.cdc.gov/cdctv/ObesityEpidemic/>. Accessed November, 2016

4.Van Gaal, L. F., Mertens, I. L. and De Block, C. E. (2006). Mechanisms Linking Obesity with Cardiovascular Disease. Nature444(7121), P.875-80. 

5. Kannel, W. B. and McGee, D. L. (1979). Diabetes and Cardiovascular Disease. The Framingham Study, JAMA, 241(9), P.2035-8. 

6. Parkin, D M. (2000). Global Cancer Statistics in the year 2000. Lancet Oncology, 2(9), P.533-43. 

7. Keys A. (1953). Atherosclerosis: a Problem in Newer Public Health. J Mt Sinai Hosp N Y 20, P.118-139.

8. Yerushalmy, J. and Hilleboe, H. E. (1957). Fat in the Diet and Mortality from Heart Disease; a Methodologic Note, New York State Journal of Medicine, 57, P.2343-2354.

9. Kanavos, P. (2006). The Rising Burden of Cancer in the Developing World, nnals of Oncology, 17(8).

10. Kratz, M. (2005). Dietary Cholesterol, AtherosclerosiS and Coronary Heart Disease, andb Exp. Pharmacy, 170, P.195-213.

11. Aragon, A. and Schuler, L. (2014). The Lean Muscle Diet, Rodale Inc, New York, USA, P.29-33.

12. Why Your Doctor Recommends a Low-Fat Diet and What It Has to Do with a Rabbit and a Little Lie. CavemanDoctor.com accessed 20.11.16