Inuit did have atherosclerosis, agreed, and Dr. Cordain stated that they probably weren’t having MIs– also agreed, since they currently still have a very low rate of MI despite eating a partially Westernized diet. Could have to do with the omega-3s. However, to attribute the atherosclerosis on their high-fat diet is premature. They ate a diet that was all-around extreme and could have been atherogenic in many ways, for example due to magnesium deficiency. I do agree with Dr. Cordain that the Inuit diet– and any all-meat diet– is probably not optimal for humans.

The idea that saturated fat raises cholesterol and leads to CHD is poorly supported by the scientific literature as a whole. If this mechanism of LDL receptor downregulation was happening in the long term, why is it that there’s typically no correlation between SFA intake and serum cholesterol in observational studies (particularly when PUFA intake is similar across SFA groups)? For example, the physician’s health study (free full text, see table 1):

http://www.bmj.com/cgi/content/full/313/7049/84?view=long&pmid=8688759

The Masai and the Samburu have low to normal cholesterol on a diet that provides 2/3 of calories as animal fat rich in palmitic acid. The vast majority of observational studies to date have found no association between saturated fat intake and heart attack risk. If SFA elevate LDL, and high LDL increases the risk of heart attacks, what gives? The explanation is that the studies Keys, Hegsted, Krauss etc. used to determine the effects of SFA on cholesterol in humans were all short term. SFA elevates cholesterol and LDL in the short term, and it seems to revert in the long term (>1 yr). This has been seen in highly controlled animal studies as well, so it’s probably not just a problem with measurement accuracy or diet adherence in the human studies. For example:

http://circres.ahajournals.org/cgi/content/abstract/20/6/658

The study in monkeys Dr. Cordain referenced used megadoses of added cholesterol to produce atherosclerosis. This gave the monkeys cholesterol levels of 800-900 mg/dL. That’s higher than you see in most familial hypercholesterolemia patients, and it can not be produced in animals or humans by saturated fat feeding. Peanut oil was also apparently more effective at producing heart attacks than lard in that study (perhaps due to the peanut lectin, which Dr. Cordain has written about before).

When you try to give animals atherosclerosis using saturated fat without megadosing them with purified cholesterol, it doesn’t work (which is why cholesterol is generally added in these studies). In most studies and most species including several primates, it doesn’t elevate their LDL relative to monounsaturated fat (like olive oil) and it doesn’t give them atherosclerosis. For example:

http://www.ncbi.nlm.nih.gov/pubmed/20032571
http://www.ncbi.nlm.nih.gov/pubmed/12492629
http://www.ncbi.nlm.nih.gov/pubmed/1728820

In the second study, palm oil was used, which is extremely rich in palmitic acid. The palm oil group showed less lesion development than the MUFA group and had similar LDL.

Does eating a high proportion of saturated fat have some kind of negative effect on the human body? I don’t know. I can’t say for sure that it doesn’t. I just haven’t seen any convincing data that it does yet.

Thanks to Dr. Cordain for his work on health, nutrition and the Paleolithic diet which I admire.

Stephan Guyenet, Ph.D.
University of Washington

Cordially,

Loren

Loren Cordain, Ph.D., Professor
Department of Health and Exercise Science
Colorado State University
Fort Collins, CO 80523
Tel: (970) 491-7436
Fax: (970) 491-0445
mailto:lcordain@cahs.colostate.edu
http://www.thepaleodiet.com

Steve Phinney replies to Loren Cordain’s discussion of Saturated Fats. Here are a few comments/responses I might make to Loren.

On the topic of saturated fat, I might respond to Professor Cordain’s concerns by pointing out that keto-adapted individuals fed a high fat diet actually experience a reduction in the proportion of palmitate (16:0) in their serum triglycerides. Jeff Volek has done two human studies (one published, one submitted) that demonstrate this, and Craig Warden (PhD, UC Davis) has done two mouse studies that confirm this observation in tissue triglycerides as well. These studies indicate that the body’s adaptation to a low carb diet (let’s say less than 10% of energy) includes a shift in metabolism that preferentially oxidizes 16:0. So then the question is, if it’s been made into CO2 and water, how can it harm you?

And as for pemmican, my point (see Steve Phinney’s discussion of Pemmican) is that it was a reserve food, and only used in intervals when fresh meat was unavailable. But the fact that it could sustain people for months at a time is often ignored or denigrated. Clearly the many hunting cultures of North America had complex and varying dietary practices, involving which parts of which animals were consumed, and by whom. Among the hunters of caribou, moose, elk and bison, it was common to break open the long bones to eat the marrow – a source of minerals from the trabecular bone as well as fat. And the Inuit were reported by Stefansson to enjoy gnawing seal ribs back from their cartilagenous insertion at the sternum towards the dorsal end where they were heavily calcified -again a source of marrow fat and bone mineral.

And finally, I think the topic of low carb diets and vitamin C is pretty much academic – literally. In ‘The New Atkins’, we advise people to eat 3-5 servings of vegetables and/or berry fruit daily, and for the sake of “insurance’, a daily multivitamin as well. The academic question is, before they had year-round access to fruits and vegetables, how could hunting cultures maintain health and function? And this is where our emerging understanding of the role of oxidative stress and inflammation stemming from dietary carbohydrate intake offers a fascinating hypothesis, if not valuable insight.

Best,
Steve