Saturated fat, cholesterol and heart disease: The myth

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How did it start?

The Seven Countries Study was an epidemiological longitudinal study directed by Ancel Keys at what is today the University of Minnesota Laboratory of Physiological Hygiene & Exercise Science (LPHES). It began in 1956 with a yearly grant of US $200,000 from the U.S. Public Health Service.The study was first published in 1970 and then followed up on its subjects every five years thereafter.

Keys wanted to prove that the intake of saturated fat is highly correlated with the risk of cardiovascular disease. Moreover, in another (Framingham) study, the assumption was that serum cholesterol was strongly related to coronary heart disease.

The fact is that he originally selected 22 countries and ended up only publishing the data from 7  of them because the other 15 didn´t fit his hypothesis.

The graph taking into account 22 countries that took part in the study

The graph that leaves 7 countries that did fit Keys´ hypothesis

 

As it can be seen, if taken into account, the original graph shows NO correlation between intake of saturated fat and heart disease. If that was not enough, during the study the researchers found out that within the same islands in which population ate the same amount of fat, people had radically different risk of heart disease.

The truth is that in the countries selected by Keys, people who ate more saturated fat also indulged more frequently in other not-so-healthy habits like smoking, eating more sugar and carbohydrates, exercising less and eating more grains. It´s like the theory about the firefighter and the fire. Just because the fireman has been found at the crime scene, does that make him the culprit?

Remember, association doesn´t mean causation.

Another hypothesis from the Framingham study was that ingestion of cholesterol would raise the serum cholesterol levels.

That´s of course another myth that has been proven wrong. In fact, dietary cholesterol has a very important function: mantaining the HDL/LDL cholesterol ratio which is one of the most important factors for coronary disease. It should be noted than more than 50% of the heart attacks occur in people with normal serum levels of cholesterol.

If it´s not cholesterol nor saturated fat, then which is the culprit of the heart disease epidemy we´re suffering?

Well, in the last twenty years we´ve had a fairly decent amount of studies comparing the effect of saturated and trans fats on heart disease.  An increase of trans fats always came with a brutal increase in heart disease.

Resultado de imagen de times eat butter

We needed 54 years to change our point of view

John Yudkin was the first to raise the alarm about sugar being guilty for the higher incidence of cardiovascular disease. Over the years, the sugar industry tried very hard to dismantle his theory to the point that some doctors still think sugar has nothing to do with heart disease.

Fortunately, nowadays a few well conducted studies have shown the clear correlation. So sugar and trans fats are supposed to be the culprits. Moreover, both are usually found together as a pack in some products.

Returning to  cholesterol, we´ve seen the “healthy” limit dropping from 250mg/dl to 200mg/dl. The fact is that cholesterol is treated with the well-known statins. Where´s the problem then?

Well, if you intentionally forget the fact that cholesterol has nothing to do with heart disease and you´re treating it, there´s a problem. Furthermore, by dropping the healthy limit of cholesterol you include more people into the treatable group, so you´re selling more statins and making more money.

The nurses´ health study conducted by  Harvard University in the 70´s didn´t show any correlation between the intake of cholesterol and mortality. Sadly, that result has been ignored for almost 30 years and doctors still treat their patients with statins, being the cholesterol the wittness of the crime and not the culprit.

Just imagine, a nice study conducted by japanese researchers showed that people with lowest serum levels of cholesterol had the highest cardiovascular mortality rate!

And yes, the statins work because of their anti-inflammatory effect (reducing C reactive protein) and not because of their ability to reduce serum cholesterol, so they shouldn´t be prescribed for people without history of cardiovascular events as Dr. Stephen Sinatra and Dr. Sherif Sultan say.

In the next chapter we´ll talk about the risk/benefit profile of statins and we´ll explain why cholesterol is so important for human life and why we shouldn´t be demonizing it.

You should look at your your trygliceride/HDL ratio, if it´s under 2 then you´ve a very low risk of having a cardiovascular event.

Mercola´s graph explaining basics about cholesterol

Summary:

-The level of cholesterol in your analysis has nothing to do with your need of statins and your risk of heart disease.

-Increasing your saturated fat intake won´t make you prone to heart disease.

-The culprits of heart disease are trans fats, sugar and of course high levels of stress.

-Statins should be recommended only to people who have had a cardiovascular event previously.

-In order to calculate your risk of developing heart disease, divide your tryglicerides between your HDL. If the result is 2 or less, don´t worry.

References:

http://ajcn.nutrition.org/content/89/4/1037.short

http://www.sciencedirect.com/science/article/pii/0002934384909525

https://www.ncbi.nlm.nih.gov/pubmed/22037012

http://www.bmj.com/content/313/7049/84.short

http://ajcn.nutrition.org/content/early/2010/01/13/ajcn.2009.27725.short

http://www.drtimdelivers.com/EEasy122605/Harvardtransfats/transfats.html

http://aje.oxfordjournals.org/content/161/7/672.short

http://www.sciencedirect.com/science/article/pii/014067369390350P

http://www.sciencedirect.com/science/article/pii/S0140673600041660

http://www.nejm.org/doi/full/10.1056/NEJM196708032770505

http://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2548255

http://www.sevencountriesstudy.com/

https://www.ncbi.nlm.nih.gov/pubmed/19696528

http://aje.oxfordjournals.org/content/161/7/672.short

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