Saturated Fat Does Not Cause Heart Disease

All Aboard the Fat Bandwagon!

After our last quite extensive detour into exercise and heart health, we are back to our regularly scheduled programming. Although last week’s post was long and possibly arduous, it sets us up nicely for this week we as are continuing down the rabbit hole of fats and will be tying it to heart disease. The topic of today’s post is saturated fat, why it isn’t “evil”, and why it is relatively benign in the development of heart disease.  Essentially, I am going to convince you to eat more bacon, coconut oil, and steak, all things most people would dream about being told to eat more of.

My main goal of today’s post is to convince you of the following points.

1) Saturated fat is not the artery-clogging, heart disease developing, aficionado of the fat world that we have been led to believe.

2) That dietary saturated fat should not be avoided, in fact you probably could stand to eat more of it (including cholesterol).

Before we start I must address one quick point, please do not quote the following Wikipedia statement on saturated fat as an argument against it.

“Since the 1950s, it has been commonly believed that consumption of foods containing high amounts of saturated fatty acids (including meat fats, milk fat, butter, lard, coconut oil, palm oil, and palm kernel oil) is potentially less healthy than consuming fats with a lower proportion of saturated fatty acids. Sources of lower saturated fat but higher proportions of unsaturated fatty acids include olive oil, peanut oil, canola oil, avocados, safflower, corn, sunflower, soy, and cottonseed oils”.

The opening sentence even screams postulation and inaccuracies “Since the 1950’s it has been commonly believe . . .”  The same thing applied in 1543 when Copernicus went against what everybody knew was the truth and proposed the heliocentric model of the galaxy. “Since the dawn of man we have know the sun revolves around the earth. . .”.  Now I have to say that the source is from the Mayo Clinic Staff, but sorry Mayo Clinic, you missed the boat on this one, in fact they overlook a key point which we will get to in a bit.  Ok, that now that is off my chest lets begin!

In order to properly form the argument for point number one we need to get a little nerdy again (I know, a reoccurring theme in these posts).  Let’s attack this systematically by looking at saturated fat at a molecular level then move into the epidemiological studies surrounding saturated fat and heart disease.

Saturated Fat at a Molecular Level

We won’t get too nerdy this week, but a brief review is warranted. As we mentioned in a previous post, saturated fats are fatty acids whose carbon chain is full of hydrogen atoms. In essence, their carbons are “fully saturated” they are unable to make any more bonds.  These fatty acids are extremely stable, meaning they are not as susceptible to oxidative damage as their unsaturated counter parts. When reactive oxygen species (ROS) are floating around in the blood, they look to “complete” themselves either by stealing hydrogen atoms from molecules, or giving off their oxygen atoms to molecules. In saturated fatty acids (SFA) the hydrogen atoms are held onto tightly by the carbon atoms and there is no place for ROS to easily deposit oxygen molecules. Unlike SFA unsaturated fatty acids (UFA) have places in the chain were the bonds are weaker and ROS can steal hydrogen atoms or deposit oxygen, this results in oxidative damage to the FA. This process is important to remember as it is a key step in the development of heart disease. The picture below should help explain this process
(click on the picture and it gets nice and big!)


What does this have to do with heart disease? Well, the current hypothesis on the development of heart disease is that lipids (fats) infiltrate the endothelium (vessel walls) and when oxidative damage occurs to those lipids the endothelium is damaged and the inflammatory response to that damage yields plaque.

Quick recap: SFA’s are not as prone to oxidative damage as UFA’s. Oxidative damage in the vessels and arteries is a causative factor to heart disease and plaque build-up. Therefore, at a molecular level, the mechanism for saturated fat causing heart disease doesn’t add up.

So if saturated fats are not as prone to oxidative stress, why do we condemn SFA and hail UFA’s such as olive oil? To answer that question we move onto our second step in the argument, poorly constructed epidemiological studies and logical fallacies.

Epidemiology and Logical Fallacies

It is my understanding that the “artery clogging-saturated fat hypothesis” began with an epidemiological study by a scientist named Ansel Keys. In his study, Keys reported fat consumption with heart disease in seven countries. Do you see the problem with this? There are 195 recognized countries in the world, so Keys accounted for ½ of 1% of all the countries in the world. . . it gets even worse from there.

Keys also decided he would omit some very pertinent information so his results would show evidence in favor of his “Fat Heart” hypothesis.  Keys left out data from countries with high fat intake and low heart disease as well as countries with low fat intake and high rates of heart disease.

His epidemiology was extremely flawed, and then the media does what is typically does. It committed a big logical fallacy, a “no-no” in the world of science. The study was  retrospective, indicating that we cannot link the findings to a cause; we can only imply there is a correlation.  Unfortunately mainstream media jumped on the Ansel Keys bandwagon and began proclaiming the tagline “artery-clogging saturated fat”, which led us to believe saturated fat causes heart disease.

When scientists, journalists, and health professionals were confronted with the data about the countries with “atypical” data, they responded with, “It must be a paradox”.  In science, paradox simply means your hypothesis is inaccurate, it doesn’t account for all the variables….. or you are just plain wrong.

One last issue about Keys’ work that continues to bother me is this: Keys’ received a Ph.D. in physiology from Harvard, indicating his education was obviously prestigious and had extensive knowledge in human nutrition…. so why would he jump to the conclusions he did about saturated fat, cholesterol, and heart disease when the mechanisms don’t make a whole lot of sense.

Unlike Keys’ epidemiological studies, recent cohort studies, and meta-analysis of the literature have shown that saturated fat, independent of other factors is not related to heart disease1,2.  For now, I rest my case. Saturated fat is not the artery-clogging, heart disease developing, aficionado of the fat world that we have been led to believe, and saturated fat should not be avoided, in fact you probably could stand to eat more of it.

Next week we are going to continue on the path to better understanding fats. Since I have convinced you that saturated fats aren’t the issue in regards to heart disease we will dive deeper into saturated fats and cholesterol and why they should be incorporated into your diet as well as tackling some misinformation surrounding cholesterol!

  1. Ascherio, R., Rimm, E., Giovannucci, E., Spiegelman, D., & Willet, W. (1996). Dietary fat and risk of coronary heart disease in men: Cohort follow up study in the United States. British Medical Journal, 313-384.
  2. Siri-Tarino, P. W., Sun, Q., Hu, F., & Krauss, R. (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American Journal of Clinical Nutrition.

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