The word “saturated” when it comes to fat, means a fat with no double bonds in its fatty acid chain. The chain is fully saturated with hydrogen atoms. Whereas unsaturated fats like olive oil, have one or more double bonds, releasing hydrogen atoms.
The most common argument against the paleo diet (besides “You don’t eat grains? Where do you get your fiber?”) is that it contains too much fat, specifically saturated fat. Sources of saturated fat in the paleo diet are most any animal products, as well as coconuts. Why do people think we’re crazy for eating so much saturated fat? It’s because it’s ingrained in us from birth that saturated fat is going to kill you.
Let’s go over where the saturated fat=death idea came from. In the mid 1950s, an American scientist named Ancel Keys conducted the “Seven Countries” study. It was a longitudinal study that examined multiple international populations over 50 years to determine the relationship between diet, lifestyle, and health, particularly vascular diseases like heart disease and stroke. Included in the study were seven cohorts of men, over 12,000 in individuals in seven countries. It was found that serum cholesterol, cigarette smoking, overweight/obesity, and lack of physical activity were all predictors of future vascular problems. Saturated fat was predicted to increase blood cholesterol levels, which, in turn, creates heart attacks, strokes, etc.
On the outside, this study looks quite fool-proof. Watching how these cohorts eat and go about their day, and then observing their health outcomes seems reliable. But there are at least two major problems with this study.
1. It is observational. Observational data are great for determining the direction of further research. They are not sufficient research. Observational studies may display correlation, but they do not confirm causation. Don’t get me wrong, observational studies are useful, but there are too many variables. Observation is not the last step. To really define how something you works, you have to be able to control it. For example, saturated fat intake may have been high in one individual, but he may have had an extremely stressful job/relationship/anything personal. This, we now know, increases the risk for vascular events. You have to be able to control all of the variables to determine causation.
2. Keys’ original paper is not widely available (1), and the criticism of it published four years later is not either (2). Because of the lack of primary sources, I am going to use a secondary one provided by the blog “Hyperlipid,” which has access to these works. In the criticism, the authors pointed out that Keys had selected countries which he already knew would fit his hypothesis. In reality, the study was conducted in numerous cohorts in 22 countries. The only cohorts included in the published study were the seven that fit his hypothesis. The rest of the data showed quite a lack of relationship between saturated fat and blood cholesterol levels, and further, a lack of association with vascular events (3). If Keys had published all of his data, modern science would not still be referring to his work when discussing dietary fat in modern scientific literature.
I have tracked down the following graph from http://www.marksdailyapple.com/saturated-fat-healthy/#axzz2htmtSzvD of Keys original data with all 22 countries included. The red dots signify cohorts that consume huge amounts of saturated fat in comparison with standard Western diets. As you can see, there is the faintest of faint correlations here. This data would never be publishable today. No one would believe there was a relationship.
During all of this, British scientist John Yudkin was discovering REAL connections between dietary sugar and heart disease, but Keys’ hypothesis had already taken off, and Keys even appeared on the cover of Time Magazine. Ever since science has accepted this vision of saturated fat, they have had trouble letting it go. Controlled studies have since been assumed to be flukes. If they agree with the current scientific dogma, they are included in peer reviewed journals regardless of the quality of study design.
Here is an example of a study that demonstrates the ability of dietary vitamin K2 to protect against heart disease (4). Where can we get K2? Meats, and fermented cheese products. Saturated fat-laden foods. They can be protective against heart disease.
Another study confirmed that high-carbohydrate diets actually increase the development of stored body fat and plasma triglyceride levels. All subjects measured had significant up-regulation of fatty acid synthesis (5). The take-home point from this study was to monitor the quality of carbohydrates in the diet as they seemed to have a much more significant effect on plasma triglyceride levels than did fats themselves.
As a final point, let me appeal to your logic. Consider someone who wants to lose a significant amount of weight. As the study I just mentioned states, excess dietary carbohydrates that cannot be used by the body are converted to stored body fat. This body fat consists mainly of saturated fats, with some monounsaturated fats. It has roughly the same composition as lard. Our bodies have to break down that fat in order to lose weight. There is a mechanism within us that can handle breaking down our own body fat. If not, no one would ever lose any weight without developing serious heart problems. Usually, the process is the opposite. People get healthier as they lose weight. Their bodies have been breaking down huge amounts of saturated fat, so why isn’t it clogging their arteries? The simple answer: because saturated fat doesn’t clog arteries.
5. Lisa C. Hudgins. Effect of High-Carbohydrate Feeding on Triglyceride and Saturated Fatty Acid Synthesis. Exp Biol Med (Maywood) December 2000 vol. 225 no. 3 178-183.