Loren Cordain – Caution: Saturated Fats – Disaster with Grains

Inuit Village around 1575

Inuit Village around 1575

CSU scientist and author of The Paleo Diet, Loren Cordain responds to U-C Davis Scientist and co-author of the New Atkins, Steve Phinney’s discussion on Pemmican.  This interview includes Loren’s opinion that saturated fats DO increase plaque in the arteries.  However, Loren says, this only becomes very hazardous when saturated fats are eaten in combination with grains, beans, dairy, high-sugar foods or other foods that tend to increase inflammation.  Cordain says the combination of saturated fats and inflammatory foods such as grains is a deadly formula for a heart attack.

Listen to Loren Cordain (15 minutes)

Here are articles Loren references in this discussion:

Artery Plaque in Pre-Westernized Inuit

Research on Heart Attacks in Monkeys

Interview with Loren Cordain about Steve Phinney’s discussion of Pemmican.

I am impressed with Steve Phinney’s earlier work, that was clinically based. I think he’s got some good ideas. But there are parts of this, particularly the scurvy situation, which I’m a little bit skeptical about.

Anything else like that? I’m curious because you’re one of the few experts in the world on Paleolithic diets. Steve Phinney’s focusing in on a particular kind . . .

I’m very familiar with pemmican. I’ve got all the pemmican stuff forever. Stefansson tried to get a grant in World War II from the U-S army to feed the troops pemmican.

I’m not saying that pemmican isn’t a healthy food. It’s probably an expedient way to provide calories over a North American winter. It’s a very great way to store these things. An all pemmican diet, I don’t think is a healthy diet for a number of reasons. If you only eat pemmican, I think you’ll become osteoporotic. You won’t get any vitamin A. If you eat only pemmican, you will promote atherosclerosis. So I just bring to you one paper that I’d like you to distribute. That paper is published in an obscure journal, the Texas Heart Institute Journal in 1993.  So nobody’s read it, because you can’t get it on Medline. What this guy did, he was a physician, an MD PhD by the name of Zimmerman. Zimmerman was a pathologist, and he was lucky enough to be in Alaska when a 400 AD, so we’re talking 1600 year old, frozen Inuit mummy was recovered. He did an autopsy on this, and he sectioned the coronary arteries. So this is 400 AD. These people had never seen white people. They had only eaten what Steve Phinney had suggested people eat–fat and protein–and significant atherosclerosis in a 53 year old Inuit woman, on pathology. That wasn’t just the only case. He then was privy to another group of frozen Eskimo bodies that were recovered in Barrow, Alaska, and these people date to about 1520 AD, so just slightly after the time Columbus had discovered America. Once again, no influence of Western civilization. So presumably, they were living at Barrow, 60 degrees north, they were eating meat and fat their entire life. They might get a little bit of berries sometime in the summer. Extensive atherosclerosis was in the older woman, who was 30. All three of them were osteoporotic. They were severely osteoporotic on that type of diet. So you can give this to people who claim that all we need to eat is meat and fat.

And then I’ll take this one step further, and here’s another obscure paper because we’re no longer allowed to perform these experiments in primates in which we feed them atherosclerotic diets and try to induce an MI.

That means a heart attack. A Myocardial Infarction.  An MI.

In 10 rhesus monkeys and two other monkeys, they were able to induce myocardial infarctions, and electrocardiographic abnormalities, unexpected and relative sudden death in these non human primates are also consistent with signs that are frequently observed in humans. This is an obscure paper that absolutely needs to be addressed by the unlimited saturated fat type groups.

Let’s see what the response of people like Steve Phinney, Eric Westman and Jeff Volek would be. They have a new book out, the Atkins diet book. There’s some difference of opinion between the three. They’re all top-notch scientists.

I agree. I respect all these people. I respect all the scientists. I’m on record stating that saturated fats are not uni-dimensionally responsible for cardiovascular disease. They represent a risk factor. And the risk factor of saturated fats can be small. In the context of a Paleolithic diet I don’t believe that high stearic acid levels which is 18-O, is atherogenic. I don’t believe high 12-O or 14-O is atherogenic because they occur in such small concentrations.

Palmitic acid is atherogenic. And there’s not an experiment in humans or animals or tissue to show that it doesn’t down regulate the LDL receptor. This is a point that is never addressed in Gary Taubes’s book or Eric Westman’s articles, or Ron Krauss. You need to address the down regulation of the LDL receptor. That controls the flux of oxidized LDL in and out of the intima.

So on a molecular basis, you can’t deny this information. Now, how relevant is that information under the umbrella of a high carbohydrate diet? A high carbohydrate diet combined with a high saturated fat diet is even worse.

And that’s something that it seems like all you researchers tend to agree on. Steve Phinney did mention that he thinks there are islands of safety in many ways of eating.

Yes. I would agree.

You would agree with that?

Yes. I think you can tend to eat a high saturated fat diet. A high animal food diet. You’re going to be at risk for osteoporosis, Vitamin A deficiency and some other factors, if you don’t eat some plants in your diet. Now if you eat liver, the Vitamin A is a non-issue.  But if you only ate muscle meat and fat, then it’s not going to work.

If you eat organ meats like traditional people consumed then you’re going to be in pretty good shape. The osteoporosis does not clear out, and you can see that in these papers here.

If we believe the results of this pathology, that we have atherosclerosis in people who never consumed carbohydrate, always ate a high fat, high protein diet, this atherosclerosis who always consumed a high fat, high protein diet. Then the question comes up, did they ever suffer a fatal MI. My opinion is that they probably didn’t.

Even though they had hardening of the arteries, plaque, they might not have had the inflammatory conditions that cause heart attacks.

Bingo, there you go!

In that way, you and Steve Phinney might agree.

I’ve always stated that, and I’ve been misquoted so often on this saturated fat issue and atherosclerosis. The devil’s in the detail. So I believe these Inuit women who had never been exposed to Western Food did indeed have atherosclerosis.

They had a lot of plaque in their arteries, they had hardening of the arteries, but did that mean they had a heart attack?

No! What kills you is not plaque in the arteries. What kills you is the rupture of the plaque. What causes the rupture of the plaque . . . because I think what happens is that atherosclerosis goes forth. Our bodies wall it over, we wall it out, and the lumen of the artery actually expands to compensate for the thickness of the intima. What kills us in the Western world, we have this atherosclerotic process going on, like we have in these Inuit. But in contrast to them, we have a pro-inflammatory diet. If you took these 1600 year old Inuit women and fed them bread along with their high fat diet, I would be almost certain that you would see myocardial infarctions.

Inuit women in the time of the transition to Western food were eating both their high animal fat foods and also Western sugars and starches, and all of a sudden, they had obesity, they had heart disease, they had diabetes.

That’s right. We are actually exploring this, and you can mention this to Eric and Steve Phinney and all these folks because I respect them all. We believe that wheat upregulates metalloproteinases. It upregulates metalloproteinase 2 and metalloproteinase 9. If you look at the final dissolution of that fibrous plaque, what causes that fibrous plaque to rupture– it’s made out of collagen and smooth muscle and cholesterol. What causes it to rupture is metalloproteinases. They up-regulate and degrade the collagen, and when the fibrous cap breaks, that is the event that kills you. We believe elements in the Western diet, including Wheat and corn and grain and legumes and high glycemic load carbohydrates, these upregulate the enzymes that directly cause the rupture of the fibrous cap.

So that spaghetti meal could be what triggers the heart attack.

Right. But to unequivocally say that saturated fats do not cause atherosclerosis, is sheer folly. We know that they do. We awarded the Nobel Prize in medicine to Brown and Goldstein for saying that Palmitic acid down regulates the LDL receptor. Unless we’re going to take that Nobel Prize back, you cannot deny that information. So, I would like to hear a response of how in the world LDL receptors are not down regulated by palmitic acid.

Let’s see if we can get a response from Steve Phinney on that because I believe he’s an expert on saturated fats.

Let’s do it!

One other thing these scientists said is that, a person should not mix and match diets, even if there are islands of safety between ways to eat, and they have health potential in that style of eating. If one day somebody eats the fruit and vegetable diet of the Hawaiians and the next day, they eat the Pemmican diet of the plains Indians, that might be a very bad idea. What do you think?

We don’t have any randomized controlled trials of that idea. We only have four randomized trials of Paleolithic diets right now. These are all very recent. When you start mixing and matching and talking about a Hawaiian diet and an Inuit diet and this and that. Long after I’m gone, we’re going to be looking to have the data speak for itself. So we need good experiments at good laboratories, based on good hypothesis.

That opinion about, ‘Don’t mix and match diets.’ That comes from the need for the cells to be adapted to either burning fat or burning sugar.  It’s hard for them to do both, and adapting to fat-burning can take a cell several days to settle into.

You’re right, metabolic issues matter, and also looking at glycation end products and factors like that.

And upregulation of a hormone such as insulin and the need for cells to be insulin sensitive.

I don’t know that you’re going to find a huge argument about glycemic index and insulin resistance and high glycemic load carbohydrates. I think there are a few stragglers hanging on to the low-fat, high-carb diet.

Such as the American Diabetes Association, the American School Nutrition Program? A few stragglers like that.

Unfortunately, those people are politically well positioned. But, we’re getting the soft drinks out of the school environment. We realize that trans fats are not good for us, and junk food potato chips are not healthy foods. That kind of collective wisdom will be for the next generation. The people that are being taught right now in their twenties. They have to read these papers. These papers are what we teach in the universities right now. The students are taught to critically think. They need both sides of the argument. It’s very easy to get caught up by your own ideas. Good scientists don’t do that. Good scientists critically evaluate both sides of the argument, and good scientists also change their belief system when the data shows otherwise.

Thanks for being an astute critic.

I talked with a couple of your students. They said your ideas are really intriguing, but could it really work as a way to feed the world?

I’ve never said it’s a way to feed all the world’s people.

It’s ironic. We can no longer eat the diet to which we’re genetically adapted. Having said that, middle class people who are middle aged in the U-S. These are the ones suffering the most from these diseases of malnutrition. And these people can afford to eat whatever they want. That is the crucial caveat. For the world’s population, unfortunately, we’ve walked down a path of total reliance of cereal grains that we can’t reverse. So yeah, you can’t feed the world without cereals grains and legumes.

Perhaps we can reduce their damaging effect of how we provide them, how processed they are, what they’re served with.

I don’t know that we can. Wheat is consumed in every country, every place in the world, and wheat causes this leaky gut that leads to this inflammatory response. So every person on the planet who regularly eats wheat probably at some point in their life, particularly as they age, has chronic inflammation.

Yet another puzzle to figure out. How to feed the planet.

Genetically we can probably make wheat without gliadin. But if you take all these anti nutrients out, then the insects have a feast and they destroy the crops.

Well, one puzzle after another.


  13 comments for “Loren Cordain – Caution: Saturated Fats – Disaster with Grains

  1. Ken L
    July 18, 2014 at 4:58 pm

    A bit late to the party but something that appears to be missed. (That i just found out about. Thanks Wikipedia)


    Excess carbohydrates in the body are converted to palmitic acid. Palmitic acid is the first fatty acid produced during fatty acid synthesis and the precursor to longer fatty acids.”

    Eating an “excess” of carbs would cause an identical Palmitic acid problem.

    ” As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to comprise 21–30% (molar) of human depot fat,[12] and it is a major, but highly variable, lipid component of human breast milk.[13]
    Palmitate negatively feeds back on acetyl-CoA carboxylase (ACC), which is responsible for converting acetyl-CoA to malonyl-CoA, which in turn is used to add to the growing acyl chain, thus preventing further palmitate generation.[14] In biology, some proteins are modified by the addition of a palmitoyl group in a process known as palmitoylation. Palmitoylation is important for membrane localisation of many proteins.”

    Also from Wikipedia
    “Palmitic acid, or hexadecanoic acid in IUPAC nomenclature, is the most common fatty acid (saturated) found in animals, plants and microorganisms.[9] Its molecular formula is CH3(CH2)14COOH. ”

    It seems like there must be other mitigating factors for eating it to cause a problem.

  2. October 14, 2012 at 12:54 pm

    The question Stephan raises – whether the high omega3:6 ratio in the inuit diet is a factor – needs to be considered. Could the same blood properties that cause frequent nosebleeds on this diet also cause a form of atherosclerosis? Does eating peroxidised HUFAs in rancid blubber etc. account for it?
    Few if any people eating a paleo or VLC diet today are going to consume as much fish oil omega 3s and rancid HUFA as Inuit did by necessity, nor as few omega 6 EFAs. This would be a very hard thing to manage unless you were living in the polar regions.

  3. October 14, 2012 at 12:46 pm

    You might want to downregulate LDL receptors if you have chronic viral hepatitis, especially Hep C – but low LDL is a risk factor for liver cancer in Hep B as well. Focusing exclusively on heart health can lead to unintended consequences in areas like cancer, mental illness, and infections.
    Palmitate is the SAFA made from carbohydrate. On a VLC diet, one that’s high in saturated fats, there is less palmitate in the blood than on an isocaloric low-fat diet. So this might be another reason why combining grain carbs and dietary palmitate is bad news.

  4. May 3, 2010 at 6:15 pm

    I just found this interview via Matt Metzgar’s blog. Thanks for posting, and thanks to Dr. Cordain for doing the interview. I’d like to make a few points in response to the interview.

    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):


    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:


    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:


    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

  5. Martin Levac
    March 31, 2010 at 3:53 pm

    The Stefansson all meat trial was supposed to answer all those questions regarding vitamin C deficiency and the like. As far as I can figure, it did answer the questions with adequate satisfaction. Why then does doubt persist? Has the Stefansson all meat trial been refuted yet? Must somebody do it all over again just to keep the new guys happy?

  6. Steve Phinney
    March 24, 2010 at 2:00 pm

    Loren Cordain Replies to Steve Phinney: Steve’s comments and follow-up are logical and I have read that paper by Jeff Volek. So, I guess we are in agreement that 16:0 downregulates the LDL receptor and that low carbohydrate diets reduce circulating 16:0, which in turn would reduce the risk for CHD. However, the paleo pathology paper by Zimmerman clearly shows atherosclerosis in the coronary arteries of adult Inuit eating their tradition diet, centuries prior to westernization. My point was that these Inuit likely never suffered fatal myocardial infarcts, as the fibrous cap covering the atherosclerotic lesion likely would have never ruptured via the necessary upregulation of MMPs (metalloproteinases) from chronic low level inflammation. High 16:0 intake combined with the typical western diet (refined CHO, wheat, vegetable oils, dairy, saponins, etc) elicits chronic low level inflammation via a number of mechanisms including increased intestinal permeability which leads to endotoxemia (leakage of lipopolysachharide (LPS) from resident gram negative gut bacteria into circulation). LPS binds toll like receptor 4 on leukocytes and antigen presenting cells to upregulate numerous inflammatory cytokines.



    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

    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.


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