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Paleo Diet Q & A - Saturated Fat

Dear Readers,

This question has come up several times in recent weeks. Maelán's response warrants breaking this out from among the other questions answered in the original post. Included in this post is a link to Dr. Cordain's paper on the subject.

Q: I wanted to ask you why it is that you discourage saturated fats in the paleo diet? From what I have read their are healthy saturated fats from coconuts that are used for around 17% of the Kitavan diet. Also, what about tubers such as sweet potato and yam, do you think that consuming these in moderate portions (small enough to keep a low glycemic load) could be detrimental?

A: Regarding saturated fats:

Saturated fatty acids intake and the risk of developing cardiovascular disease (CVD) is a topic with a lot of controversy. In recent years a wide body of research has suggested that increased consumption of certain saturated fatty acids (Lauric acid, myristic acid and palmitic acid)
down-regulate LDL receptor and thereby increase LDL plasma levels, and this has been associated to increased risk of CVD. On the other hand, stearic acid (a 18 carbon saturated fatty acid) has been shown to decrease LDL plasma levels. However, this view is too simplistic as they are several other factors contributing to CVD, such as smoking, exercise, trans-fatty acids, increased omega-6/omega-3 ratio, free-radicals, nutrient deficiency, homocysteine, alcohol intake and low-grade chronic inflammation among others.

Moreover, some studies have suggested that there’s not enough scientific data to support the view that increased total or LDL cholesterol is an independent risk factor for CVD, but rather oxidized LDL. Plaque production is mediated by oxidized LDL but not LDL. Oxidized LDL can produce shedding of the inner layer of the artery namely glycocalix. Then oxidized LDL infiltrates in the intima of the artery. Oxidized LDL is eaten by macrophagues, a process known as phagocytosis, and therefore macrophagues are transformed into foam cells which produce the fibrous cap.

Once the fibrous cap has been produced we need to break it down in order to produce an ischemic event. Lectins and low-grade chronic inflammation are involved in the activation of matrix metalloproteinases which break down the fibrous cap.

In summary, high total cholesterol or LDL levels do not increase CVD risk but rather oxidized LDL. To produce oxidized LDL we need the factors mentioned above. Hence, consumption of saturated fatty acids is not an issue if we control several other factors such as those mentioned before.

Dr. Cordain wrote a book chapter where he shows that saturated fat consumption in ancient hunter-gatherer populations were usually above recommended 10% (American Heart Association) of energy from saturated fats yet non atherogenic.

The bottom line is that we do not recommend cutting down saturated fatty acid intake but rather decrease high-glycemic load foods, vegetable oils, refined sugars, grains, legumes and dairy.

I hope this helps.
Maelán

Link to supporting paper.

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