The Truth Behind Cholesterol
Guest blog by Robert C. Jacobs
What You’ve Been Told About Cholesterol Is Wrong
For the last half a century, the general wisdom regarding dietary recommendations for the treatment and prevention of cardiovascular disease in the United Stated has been the reduction of saturated fat and cholesterol in the diet.
This reduction in saturated fat is aimed at decreasing concentrations of Low-Density Lipoproteins (LDL’s). The Framingham Heart Study, in 1957, established the first link to LDL’s and incidence of coronary heart disease. What we have with Framingham is a case of causation confused with correlation. Future studies like the Lyon Diet Heart Study and The Minnesota Coronary Study would show that even when or if LDL’s are decreased through dietary changes, there are no significant changes in incidence of myocardial infarction, sudden death or all-cause mortality. It is believed that particle size, organ damage, specifically arterial stiffness and inflammation, are better predictors of heart disease. The use of nuclear magnetic resonance (NMR) has made possible the study of lipoprotein particle size and volume. LDL particle size has become one of the leading points of concern to accurately assess cardiovascular risk.
The cholesterol myth began many years ago with a man named Ancel Keys and his Diet-Heart Hypothesis. In the early 1950’s studies done in Russia on atherosclerosis and rabbits demonstrated that when rabbits were fed diets high in saturated fat, they developed arteriosclerosis. This is the genesis of the flawed cholesterol hypothesis; indicating the link between saturated fat and heart disease. In his 2012 book with Dr. Steven Sinatra, Dr. Jonny Bowden, a clinical nutritionist, points out that when you feed a baboon, an omnivore whose natural diet is high in saturated fat, the same diet, similar incidence of atherosclerosis is not observed. Ancel Keys then found data to further support his hypothesis, in what was called the Seven Countries Study. This study showed a direct correlation between diets high in saturated fats and incidence of heart disease. What didn’t become public until years later was that there were actually twenty-two countries studied. When the data from all twenty-two countries are placed on a graph the data does not support the same decisive conclusions reached by Ancel Keys.
As this hypothesis spread, the demonization of saturated fat in the diet increased exponentially with time. Within two decades the official dietary policy of the United States government now advocated a low fat, high carbohydrate diet. Food companies began removing the natural dietary fat from their products. The dairy industry, who’s products contain higher amounts of saturated, were among the first to offer low fat versions of their products. Cheeses and yogurts and many other foods containing natural saturated fats were being processed to have the fat removed and, in most cases, replaced by sugary substitutes. Margarine was developed to replace natural butter. Crisco, developed from cotton seeds, replaced natural cooking lard, and vegetables grew in popularity. As these new low fat products and guidelines took hold in the US, the stead rise of obesity and diabetes began.
From a practical application stand-point, an eradication of saturated fat in the diet must be accompanied by an increase in another macronutrient. Carbohydrates were the weapon of choice. In their analysis of the data, Siri-Tarino et al. state “For a large proportion of the population, however, the effect of higher-carbohydrate diets, particularly those enriched in refined carbohydrates, coupled with the rising incidence of overweight and obesity, creates a metabolic state that can favor a worsening of atherogenic dyslipidemia that is characterized by elevated triglycerides, reduced HDL cholesterol, and increased concentration of small, dense LDL particles (Siri-Tarino et al 2010).” Recent studies are showing strong evidence to suggest that the reduction in carbohydrates, not saturated fat, benefit these dyslipodemic conditions.
We know the effect saturated fats have on lipids and lipoproteins can be easily modulated based on the available amounts of polyunsaturated fats in the diets. Amongst the studies analyzed by Siri-Tarino et al. were the Lyon Diet Heart Study and the Women’s Health Initiative. The Women’s Health Initiative is the largest controlled dietary intervention study to date, using forty-eight thousand subjects. These two studies in particular, are quite significant. The Women’s Health Initiative randomly assigned each of it’s forty-eight thousand subjects to either a low-fat intervention or a “free-living” setting. “After six years of follow up, there were no differences between the groups in incidence of fatal and non-fatal coronary heart disease and total cardiovascular disease, and stroke (Siri-Tarino et al. 2010).”
The Lyon Diet Heart Study looked at a standard western style diet higher in carbohydrates compared to a “Mediterranean” style diet. The “Mediterranean” style diet included significantly higher amounts of omega 3 fatty acids, specifically alpha linoleic acid. This type of diet resulted in a seventy-two percent reduction in coronary heart disease (CHD) events in patients with previous myocardial infarctions. Further analysis of the data showed no significant differences in cholesterol levels between the two groups. However, the biggest difference amongst the two groups was the seventy-two percent reduction in CHD events in the “Mediterranean” style group.
The Women’s Health Initiative and The Lyon Diet Heart Study both clearly demonstrate that a change in saturated fat intake not only causes no significant changes in cholesterol levels, but also that incidence of cardiovascular disease can change dramatically with no change in the levels of cholesterol. “A landmark systemic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischemic stroke or (5) Type 2 Diabetes in healthy adults (Molhotra et al 2017).” Not only does the data show no association of the previously stated issues, it also indicates that there is no benefit from reduced fat intake on cardiovascular and all-cause mortality and myocardial infarctions. Greater intakes of carbohydrates and polyunsaturated fats have been associated with increased progression of atherosclerosis, whereas increased saturated fat intake is associated with less progression of these problems.
In the wake of this paradigm shifting data, we are now faced with the question; if what we once thought was true regarding the connection of saturated fat in the diet to an increase in LDL concentrations, and the connection of this increase in LDL concentrations to heart disease are not true, what then is the root cause? Since the Framingham Study in 1957, significant improvements in measurements of lipids have been developed. Through these improvements, measures of lipid numbers and particle size can now be taken. Urbina et al. stress the importance of the improvements in measurement techniques because traditional cholesterol and triglyceride numbers provide the total amount of cholesterol in a variety of lipoprotein sizes. In 2017, authors Urbina et al. examine the hypothesis that lipid particle size is a greater predictor of heart disease than lipid concentrations alone. “The use of nuclear magnetic resonance (NMR) allows for measurement of number and size of LDL particles which may be a better predictor of cardiovascular (CV) events and early non-invasive atherosclerotic target organ damage in adults than traditional cholesterol concentration (Urbina et al. 2017).”
There are two distinctions among the LDL particle sizes, commonly referred to as Large LDL’s (pattern A), and Small LDL’s (pattern B). These distinctions reflect both particle size and concentrations. Pattern A are larger sized molecules, while pattern B are smaller sized more dense molecules. These sizes also shed light on the volume of the particles as well. In such that with larger molecules there will be an overall smaller volume of particles present due to their size and these are also viewed as more protective particles. If pattern A occupy more space, there can be less pattern B particles along for the ride. Whereas with smaller molecules, a higher volume can be present. Pattern A molecules are more analogous to cotton balls, and pattern B particles are more likened with bee-bee pellets.
The particle size now plays an important role in heart disease in a manner of concentrations and their role in repair and inflammation. Pattern B particles are believed to be more dangerous because they can more easily slide through the walls of the cells in the endothelium, making it easier to reach the arterial walls and begin to from plaque. The endothelium is a thin cellular layer protecting the arterial walls. On these endothelial walls are small gaps called tight junctions. The role of these tight junctions is to prevent leakage transported water solutes and seals the transcellular pathways. Urbina et al. reach the conclusion that LDL particle size have a “higher hazard ratio for predicting incident CV events than LDL concentrations (Urbina et al 2017).” Particle size has also been superior to concentration in predicting the degree of atherosclerosis. The main conclusion drawn by the authors from looking at this data is that managing particle size and concentration is far more effective than looking at concentrations alone.
Molhotra et al. will show that yes, “preventing the development of atherosclerosis is important, but it is atherothrombosis that is the real killer (Molhotra et al. 2017).” The authors explain that the formation and deposits of plaque on artery walls resembles a “pimple” much more than the plumbing analogy most commonly used today. Most cardiac events occur at a location of less than seventy percent obstruction of the coronary artery. The rupturing of plaques, like that of popping a pimple, myocardial infarction and coronary thrombosis can occur within minutes.
The authors go on to say that the analogy of “unclogging a pipe” comes with limitations, in that studies show that “stenting significantly obstructive stabile lesions fail to prevent myocardial infarction or to reduce mortality (Molhotra et al. 2017).” More collected data further shows that diets as high as forty-one percent saturated fat achieved a thirty percent reduction in the number need to treat (NNT of sixty-one) of seven-thousand and five hundred patients identified at high risk of cardiovascular events. NNT is a measure used in the medical field. Statin drugs, for example, have an NNT of two-hundred and fifty to three-hundred. What this means is that for every three-hundred people that take statins, one is helped by the drug.
The main conclusions now being reached by Molhotra et al. and many others in the scientific community is that it is now clear that there is no connection to saturated fat intake and heart disease. In fact, it is the replacement of fat with carbohydrates that increases not only heart disease, but obesity, and diabetes in adults. Arterial plasticity, inflammation, and insulin resistance should now be the primary matters of concern; as data now clearly indicates “coronary artery disease is a chronic inflammatory disease” that can be best treated by a reduction in refined carbohydrates, sugar, and insulin resistance (Molhotra et al 2017).
“Earn your carbs.” Charles R. Poliquin
Malhotra, A. Redberg, R.F., Meier, P. (2017). Saturated fat does not clog the arteries: coronary artery disease is chronic inflammatory condition, the risk of which can effectively reduced from healthy lifestyle interventions. British Journal of Sports Medicine, 51(15), 1111-1112.
Siri-Tarinp, P.W., Sun, Q., Hu, F.B., Krauss, R.M. (2010). Saturated Fat, Carbohydrate, and cardiovascular Disease. American Journal of Clinical Nutrition, 91, 502-509.
Urbina, E.M., McCoy, C.E., Gao, Z., Khoury, P.R., Shah, A.S., Dolan, L.M., Kimball, T.R. (2017). Lipoprotein Particle Number & Size Predict Vascular Structure & Function Better Than Traditional Lipids in Adolescents & Young Adults. Journal of Clinical Lipidol, 11(4), 1023- 1031.