The Story of Cholesterol
In 1913, Russian pathologist Nikolai Anichkov fed rabbits a diet of high cholesterol and showed that cholesterol caused a build-up of debris with cholesterol in the artery walls1 together with greatly elevated blood cholesterol2.
Since rabbits are herbivores, they don’t naturally eat foods containing cholesterol, so maybe we shouldn’t translate this experiment to humans. However, the experiment became famous and the prominent researcher Ancel Keys, PhD., would have known about it.
In 1950, Dr Ancel Keys published his research findings on the Minnesota Starvation Experiment3 in The Biology of Human Starvation4. According to obesity researcher Dr Zoë Harcombe, this may quite possibly have been the most important obesity experiment ever conducted5.
Having already made a name for himself by developing the K-ration, used by the US military to feed thousands of soldiers during World War II6, it meant Keys became a prominent and influential figure in his day.
Also by the1950s, heart disease had become the leading cause of death in the USA from a mere handful in 19007. And the fear of heart attacks became very public when, in 1955, the US president, Eisenhower, suffered the first of several heart attacks7.
Keys developed his diet-heart hypothesis, which states that a diet high in saturated fat and cholesterol leads to high blood lipids, which in turn lead to atherosclerosis8.
Perhaps unsurprisingly, this first effort of its kind was not without its issues.
Take for example the choice of countries. It is now well-recognised that Keys cherry-picked his data to support his diet-heart hypothesis. Astonishingly one country he didn’t pick, France, whose population had a high animal fat diet (therefore rich in cholesterol) but didn’t often die of heart disease (think “French Paradox”), was not chosen simply because, as close colleague Henry Blackburn put it, “Keys just had a personal aversion to being in France”7. Objective? Hardly.
Another important confounder in the Seven Countries study, was that saturated fats and trans fats were lumped together. To be fair, it probably wasn’t known back then, that there was a difference in their effects on the body. We know today that dietary trans fats, produced by hydrogenating seed oils, are atherogenic10 (i.e. fur up your arteries).
Saturated fats and trans fats are not comparable. As NHS cardiologist Dr Aseem Malhotra points out, scientists universally accept that trans fats (found in many fast foods, bakery products, and margarines) increase the risk of cardiovascular disease11,12. Instead, saturated fat has been found to be protective of developing heart disease11.
Well, saturated fat does raise your LDL (so-called “bad”) cholesterol but it raises the large, fluffy, buoyant particle size13, which is not so “bad” after all.
In fact, it’s carbohydrate consumption that raises your dangerous, small dense LDL particles14, which are implicated in cardiovascular disease15. Worse is that those small dense LDL particles hang around in the bloodstream for longer and are more susceptible to getting oxidised and triggering the processes that fur up your arteries14.
That’s the bad cholesterol you don’t want circulating in your bloodstream.
As for fat…
The perception that fat is the villain is finally being laid to rest… ever so slowly. The latest report of the US Dietary Guidelines in 2015, has revised its stance on cholesterol [in the diet] by saying it is no longer a “nutrient of concern”16. There is also now an absence of an upper limit of total fat consumption, since this is also no longer listed as a nutrient of concern16. In other words, we don’t need to restrict our fat consumption any longer. Actually it will restrict itself naturally by keeping us satiated.
And now for the final twist in the tale...
In September 2016, a shocking revelation came to light about hitherto undisclosed industry funding by the Sugar Research Foundation in 1965, to downplay early warning signals that sugar consumption was a risk factor in coronary heart disease17. They “identified a strategic opportunity for the sugar industry: [namely to] increase sugar’s market share by getting Americans to eat a lower-fat diet”17,18.
The moral of the tale? Cut out sugar and refined carbohydrate (like anything made from white flour) from your diet, not the healthy fats (found in meat, poultry, oily fish, seafood, avocados, fresh nuts and seeds, coconut oil and olive oil).
To your health and bon appétit!
- 1. Konstantinov, I.E., Mejevoi, N., Anichkov, N.M., (2006). Nikolai N. Anichkov and His Theory of Atherosclerosis. Texas Heart Institute Journal. 33 (4), 417-423.
- 2. Buja, L.M., (2014). Nikolai N. Anitschkow and the lipid hypothesis of atherosclerosis. [abstract] Cardiovascular Pathology. 23 (3), 183-184.
- 3. Kalm, L.M. & Semba, R.D., (2005). They Starved So That Others Be Better Fed: Remembering Ancel Keys and the Minnesota Experiment. Journal of Nutrition. 135 (6), 1347-1352.
- 4. Keys, A., Brozek, J., Henschel, A., Mickelsen, O. & Taylor, H. L. (1950) The Biology of Human Starvation I–II University of Minnesota Press Minneapolis, MN.
- 5. Harcombe, Z., (2012). The Obesity Epidemic – Public Lecture at Cardiff Metropolitan University. [online] Zoe Harcombe. Available from: https://www.youtube.com/watch?v=ysoScJ2Q5RQ [Accessed 24 October 2016].
- 6. Oransky, I., (2004). Ancel Keys. Lancet. 364 (9452), 2174.
- 7. a. b. c. d. Teicholz, N., (2015a). The Big Fat Surprise. Scribe: London.
- 8. Sherwin, R., (1978). Controlled trials of the diet-heart hypothesis: some comments on the experimental unit. American Journal of Epidemiology. 108 (2), 92-99.
- 9. Keys, A., (1970). Coronary heart disease in seven countries. Circulation. 41 (4S1), 1-198.
- 10. Chen, C.L., Tetri, K.H., Neuschwander-Tetri, B.A., Huang, S.S. Huang, J.S., (2011). A mechanism by which dietary trans fats cause atherosclerosis. The Journal of Nutritional Biochemistry. 22 (7), 649-55.
- 11. a. b. c. Malhotra, A., (2013). Saturated fat is not the major issue. British Medical Journal. 347, f6340.
- 12. Wallace, S. & Mozaffarian, D., (2009). Trans-fatty acids and nonlipid risk factors. Current Atherosclerosis Reports. 11 (6), 423-33.
- 13. Dreon, D.M., Fernstrom, H.A., Campos, H., Blanche, P., Williams, P.T., Krauss, R.M., (1998). Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. American Journal of Clinical Nutrition. 67, 828–36.
- 14. a. b. Siri-Tarino, P.W., Chiu, S., Bergeron, N., Krauss, R.M., (2015). Saturated Fats Versus Polyunsaturated Fats Versus Carbohydrates for Cardiovascular Disease Prevention and Treatment. Annual Review of Nutrition. 35, 517–543.
- 15. Musunuru, K., (2010). Atherogenic Dyslipidemia: Cardiovascular Risk and Dietary Intervention. Lipids. 45, 907–914.
- 16. a. b. Teicholz, N., (2015b). The 2015 US Dietary Guidelines. Lifting the Ban on Total Dietary Fats. Journal of the American Medical Association (JAMA). 313 (24), 2431-2422.
- 17. a. b. c. Kearns, C.E., Schmidt, L.A., Glantz, S.A., (2016). Sugar Industry and Coronary Heart Disease Research. A Historical Analysis of Internal Industry Documents. JAMA Internal Medicine. doi:10.1001/jamainternmed.2016.5394.
- 18. Hass, H.B. (1954). What's new in sugar research. Proceedings of the American Society of Sugar Beet Technologists. [online] http://digitalcollections.qut.edu.au/1407/5/American_Society_of_Sugar_Beet_Technologists_1954_Part_1.pdf [Accessed 17 October 2016]