Wednesday, January 14, 2009

The Tokelau Island Migrant Study: Cholesterol and Cardiovascular Health

Let's get right to the meat of this study. It's relevant to the hypothesis that saturated fat is a cause of cardiovascular disease.  Tokelauans traditionally obtained 40-50% of their calories from saturated fat, in the form of coconut meat. That's more than any other group I'm aware of.

So are the Tokelauans dropping like flies of cardiovascular disease?  I don't have access to the best data of all: actual heart attack incidence data. But we do have some telltale markers. In 1971-1982, researchers collected data from Tokelau and Tokelauan migrants to New Zealand on cholesterol levels, blood pressure and electrocardiogram (ECG) readings.

The Tokelauan diet, as I've described in detail in previous posts, is traditionally based on coconut, fish, starchy tubers and fruit. By 1982, their diet also contained a significant amount of imported flour and sugar. Migrants to New Zealand had a much more varied diet that was also more typically Western: more carbohydrate, coming chiefly from wheat, sugar and potatoes; more processed sweet foods and drinks; more red meat; more vegetables; more dairy and eggs. Sugar intake was 13 percent of calories, compared to 8 percent on Tokelau. Saturated fat intake in NZ was half of what it was on Tokelau, while total fat intake was similar. Polyunsaturated fat intake was higher in NZ, 4% as opposed to 2% in Tokelau. I don't have data to back this up, but I think it's likely that the n-6:n-3 ratio increased upon migration.

Blood pressure did not change significantly over time in Tokelau from 1971 to 1982, if anything it actually declined slightly. It was consistently higher in NZ than in Tokelau at all timepoints. Men were roughly three times more likely to be hypertensive in NZ than on Tokelau at all timepoints (4.0% vs. 12.0% in the early 1970s). Women were about twice as likely to be hypertensive (8.1% vs. 15.0%).

On to cholesterol. Total cholesterol in male Tokelauans was a bit lower on average than in New Zealand, but neither was particularly elevated (182 vs. 199 mg/dL). LDL was also a bit higher in NZ males (119 vs. 132 mg/dL). Triglycerides were lower in Tokelauan men than in NZ (80 vs. 114 mg/dL). There were no differences in total cholesterol, LDL cholesterol or triglycerides between Tokelauan and NZ women.  It's interesting that serum lipids don't correspond at all to saturated fat intake.

But does it cause heart attacks? The best data I have from this study are ECG readings. These use electrodes to monitor the electrical activity of the heart. There are certain ECG patterns that suggest that a person has had a heart attack (Minnesota codes 1-1 and 1-2). The data I am going to present here are all age-standardized, meaning they are comparing between groups of the same age. On Tokelau in 1982, 0.0% of men 40-69 years old showed ECG readings that indicated a probable past heart attack. In NZ in 1980-81, 1.0% of men 40-69 years old showed the same ECG readings. In Tecumseh U.S.A. in 1965, 3.5% of men 40-69 years old showed the same ECG pattern. I don't have data for women.

These data don't prove that no one ever has a heart attack on Tokelau. Tokelauans do have heart attacks sometimes, and they also have strokes (at least in modern times). But they do allow us to compare in quantitative terms between genetically similar people living in two different environments.

This is consistent with what has been observed on Kitava and other traditional Pacific island cultures: a vanishingly small incidence of cardiovascular disease while they retain their traditional diet and lifestyle (and sometimes even when some processed Western food has been introduced). When diets and lifestyles become modern, there is invariably a rise in the incidence of chronic disease.

These data raise serious questions about the role of saturated fat in cardiovascular disease. Tokelau underlines the fact that a non-industrial diet and lifestyle may be a more significant protective factor than the quality of ingested fat.

Unless otherwise noted, the data in this post are from the book Migration and Health in a Small Society: the Case of Tokelau.


Matt Stone said...

Great post Stephen. I agree that type of fat and quantity of fat in the diet don't appear to follow any kind of reliable trend. Just like the exceedingly low cholesterol levels found amongst the Masai (something like 125 mg/dl was the median serum cholesterol level).

It's virtually impossible to strongly link saturated fat, or any kind of fat (even polyunsaturates despite the theories against it), with heart disease. Plain and simple, fat, especially saturated fat, appears to be unrelated to heart disease.

Fitnatic said...

I have recently stumbled onto this realm of blogs (started with heartscan blog) as I am trying to figure out a diet for me! I have family history of heart disease at a very young age. I also have PCOS I was on metformin for a couple of years.
The diet has to be so that it will not cause bloating. The metformin really messed up my system and I am always highly bloated no matter what I eat! I have started majorly reducing wheat from my diet- a very very difficult thing for me since I grew up vegetarian eating bread and vegetables.

so I was very happy to have stumbled upon blog like yours and others that discuss diet based on how our body chemistry responds to it.
Any suggestions for a diet for me? One that will NOT cause gas and bloating? I also need to loose a lot of weight on this diet, but do not want to crash diet.

Nancy said...


I suggest looking into the Paleo diet. Loren Cordain wrote a book about it, which I like except for the nonsense about saturated fat. There's also Neanderthin but I think that is out-of-print. Like this blog's author, I think a there's a lot of nonsense about saturated fat that has ingrained itself as truth, simply because it was repeated very often. An information cascade... but a wrong one.

Grains are pretty awful. They do terrible things to me. I wish it hadn't taken me 47 years to figure that out!

Fitnatic said...


Yes, I am trying to find out more about the Paleo diet! The problem is, I cannot stand meat! I eat chicken and fish and occasionally goat meat, but cannot consume any other kind of meat!

Stephan Guyenet said...


I agree with Nancy that a paleo-type diet is a good way to go (although not necessarily Cordain's version of it). You might also try keeping carbs and fiber low. I would treat gluten and dairy protein with a high degree of suspicion at this point. Butter and ghee are your friends though. Also, make sure to find a good source of vitamin D, whether it's sunlight, high-vitamin cod liver oil or supplementation (make sure it's D3).

If you would like some data/encouragement on helping blood glucose problems and overweight with a paleo-type diet, please see my posts "paleolithic diet clinical trials".

Robert Andrew Brown said...


Saturated fats.

The problem is we are not just looking at saturated fats.

What we call saturated fats are a mix of mono poly and saturated.

We hydrogenate animal fats to make lard.

We remove the nutrients in animal fats to make lard.

We distort the Omega 36 content of animal fats.

We pre oxidise fats before we eat them.

Higher omega 6 lower omega 3 trans fats, lack of minerals and fat soluble mineral all contribute to vascular disease.


A paleo diet with fish / shellfish would be fine.

High Omega 6 vegetable fat and low long chain Omega 3 combined with a lack of fat soluble vitamins, and minerals, arguable promotes inflammation and oxidation.

Inflammation and oxidation are factors in PCOS, and poor digestion, cardiovascular disease and diabetes.

Inflammation lead to mucus. Mucus stops the digestion working properly leading to poor digestion. Poor digestion leads to bad bacteria . . . Refined carbohydrates particularly sugar and fructose feed bad bacteria.

Excess Omega 6 and lack of 3 also contribute to PCOS by causing imbalances in the hormone cycle and arguably lead to a failure of the cycle to close down properly.

Inflammation and oxidative stress are increased by Omega 6 and factors in cardiovascular disease.

I have written a book that looks at the impact of excess Omega 6 and lack of 3 on a wide range of health factors including PCOS, the menstrual cycle, diabetes and digestion. It is not the easiest of reads but may help you understand why the Omega 3 : 6 balance is so important. There is an update coming which is a big improvement but it may be a while (-:

Stephan's blogs deal with the needs for vitamin D and K and other fascinating subjects and are excellent.

Minerals and iodine are important as levels in the soil have fallen significantly over the last 50 years but shellfish and fish are good sources.

Robert Brown

Author Omega Six The Devils Fat

StephenB said...

Nice entry, as usual. As I'm trying to improve my understanding of diet and longevity, I have some thoughts and questions.

Can it be possible that saturated fats might be less healthy in some conditions and not others? For example, are they an issue when carbohydrate intake passes a certain amount?

Another concern I have is that discussion about ratios and subtypes of fats, carbohydrates, and proteins most often does not take into account how the food is prepared. How the food is prepared will impact its dietary advanced glycation endproduct (AGE) content, which is particularly important because it may be that the mechanism why caloric restriction leads to longer lives is that less food eaten translates into less dietary AGEs (PMID 18599606).

On the endogenous AGE side, cutting out high glycemic carbs is a no-brainer.


Anonymous said...


Thanks for another great post. I wanted to bring up a confounding factor in the study that may be present to some extent in various other studies of traditional societies - the negative effects of stress caused by exposure to modern western culture. Robert Sapolsky has written extensively on the negative effects of stress in his book Why Zebras Don't Get Ulcers. He presents evidence that stress has a horrible effect on health, and that one of the most stressful things is loss of community and downward social mobility. It occurs to me that these are two stressful events that traditional cultures would be experiencing in abundance upon exposure to modern culture. Although I have no doubt that modern foods are a big part of the degeneration observed upon such exposure, I wonder to what extent these stresses also play a role. Has anyone read Sapolsky? Highly recommended and very thought provoking.

Fitnatic said...

Yes, I am trying hard to stick to fish and vegetables plan. What is really difficult for me is the grain prohibition. We are so used to eating bread or other grain concoction as a vehicle for food consumption, eating veggies just by themselves is hard. Also the nagging feeling of incomplete lunch or dinner does not go away due to lack of bread! Sigh. I guess that I will have to do that because of the whole litany of inflammation and autoimmune conditions that I have.
We have already stopped vegetable oil- replaced with peanut oil/olive oil/ coconut oil. I try and stick to brown rice and quinoa. But just found out that quinoa though low carb, is high in Omega-6. So that basically leaves occasional indulgence in brown rice till I get the weight off I guess.
Any good brands for it D3 gelcaps?

Aaron said...

I hope we all remember that this is coconut oil we are talking about-- the 16:0, 18:0 saturated fats may have very different effects on the body. We need more studies before we totally validate saturated fats of the 16:0, 18:0 at 40-50% of diet.

Robert Andrew Brown said...

Peanut is high 6 and very little 3.

Macademia and some others are lower 6

Virgin olive is about 10% 6 very little 3.

You need to balance the plant based omega 3 and 6, which means maybe a little flax oil.

You may also want to look at up to 1.5grams EPA and 1.5 DHA but if on blood thinners please talk to your doctor first. DHA is a NSAID

Fitnatic said...
This comment has been removed by the author.
Fitnatic said...

Ah, I thought that olive oil contained high Omega-3? which other oils besides macademia are low O-6? I take fish oil capsules with about 1400mg of EPA DHA total. Maybe I should increase that? No, I am not on any blood thinners right now but maybe next month as part of IVF protocol - baby aspirin to be precise. Will remember to go down on EDP-DHA when doing that.

Thanks all for your suggestions! Stephan I might try the diet outlined in the trials. Maybe once or twice a week I can eat wheat?

Stephan Guyenet said...


I have no reason to believe saturated fat is a problem at any level of intake, with or without carbohydrate.

That's an interesting AGE paper you cited, I'll have to read the full text. I've had a tendency not to take AGEs seriously because of the fact that we've been eating roasted meat for probably 1.5 million years or so without major ill effect. But I will check that paper out.


I agree, that is a confound. A large part of the TIMS was actually dedicated to understanding the social and psychological determinants of health upon migration. I haven't paid much attention to it because it's not my specialty, but it could very well be a factor. You could say I'm a guy with a hammer and everything looks like a nail.

But I think it's important to keep in mind that Tokelauan culture has been crushed and altered repeatedly over the course of the past few hundred years. This isn't a case of an idyllic Pacific island culture moving to the fast-paced modern world. It's more like a crushed, exploited and evolving culture moving to the fast-paced modern world. So the argument based on stress and social change is not straightforward.


I wouldn't worry too much about quinoa. If you are going to eat whole grains, remember to soak them for 12+ hours before cooking. Better yet, replace the whole grains with starchy tubers (or nothing at all).

If you have autoimmune problems, I would avoid wheat strictly. It might be worth getting the stool gluten sensitivity test from EnteroLab. Most people with autoimmune disease have gluten sensitivity, and I suspect gluten is often behind it.


Saturated fat (including 16:0 and 18:0) is one of the things the human body has been dealing with since the beginning of time. Around 20% of historical humter-gatherers were completely or nearly carnivorous, meaning they ate 65% or more of their calories as fat, nearly all from animals. Some groups got it from sources low in sat fat (coastal Inuit), while others got it from sources very high in sat fat (inland Inuit).

Palmitic acid (16:0) is what the liver makes when there is too much carbohydrate to store. In that context, I would argue animal fat is innocent until proven guilty. And it certainly has not been proven guilty up to now.

Robert M. said...


A lot of things can cause bloating: legumes, wheat, milk, soy, etc. Unfortunately, pretty much every staple of the vegetarian diet except maybe squash causes adverse reactions in large segments of the population.
You basically have to eliminate them for about four to six months and then come back and reintroduce them one at a time and see if your symptoms return.

On quinoa: I eat it perhaps once a week. I find it takes a couple of days of soaking for it to sprout. I typically soak 1/3 cup of quinoa with 2/3rds cup of water and a dash of baking soda and sea salt. I leave it in a sealed container for a day and then put it in the fridge until I want to cook it with a dollop of coconut oil. I usually add a handful of frozen berries towards the end to make compote. I avoid the red quinoa; it seems to have more indigestible fibre content.

Unknown said...


Re: good Vit D3 capsules try these:

Robert Andrew Brown said...


Clearly you must talk to your doctor but long chain Omega 3s are essential to baby formation from the earliest stages and are themselves COX blockers.

I have heard of those with PCOS / related issues who have altered their diets and got pregnant.

You probably need to read round the subject.

JMC said...

Interesting Post as usual Stephan.

Nevertheless, although this study proves that once traditional people abandon their traditional lifestyle (exercise, diet,sun exposure, stress, polution, etc. AND NOT JUST DIET) they develop a suboptimal phenotype or even diseases, it can't really be used to prove that saturated fat has no relation to atherosclerosis.

As you briefly point out certain saturated fatty acids (12:0, 14:0 and 16:0) downregulate te LDL receptors and hence LDL increases (that doesn't happen with 18:0,which, if I'm not mistaken, represents a significant percentage of the saturated fat content of wild game as opos to grain fed beef).

The problem here is that many people who defend saturated fat say that LDL has no effect on atherosclerosis and that it is inflammation and oxidation of LDL that matters.

As some of you may know (from previous comments), I follow Cordain' plan and feel great (I have RA) and I don't think he's som misguided or miinformed guy. In fact, judging fom his papers, articles and posts on the web he has done 10 years ago on I have to accept that he has a very good brain and an enciclopedic knowledge, but Ialso recognize that he hasn't been able to properly explai his position. So instead of focusing on a popular book wrote 7 years ago for lay persons (which is not his best work) and using it to criticize him, we should read his work more carefully and try to understand why he thinks saturated is a player (albeit not a major one) on atherosclerosis.

Here's something from his website:

Coronary heart disease (CHD) consists of myocardial infarctions (heart attacks) and angina pectoris and accounts for 54% of the deaths from a larger category of heart and blood vessel illnesses called cardiovascular disease (CVD) which accounts for 40.6% of all deaths in the U.S. CVD not only includes CHD, but also stroke, congestive heart failure, hypertension, rheumatic heart disease, congenital cardiovascular defects, artery diseases and others. The physiological mechanism underlying CHD is atherosclerosis, a complex process involving interactions among environmental factors (both nutritional and non-nutritional) and the genome. Environmental factors such as exercise, smoking, and inflammation clearly influence the development and progression of atherosclerosis. Numerous nutritional factors can serve to either (1) promote or (2) inhibit atherosclerosis via modulation of one or more of the steps involved in the atherosclerotic process.

Dietary saturated fats are nutritional elements that may promote atherosclerosis. As consumption of certain saturated fatty acids (12:0, 14:0, 16:0, but not 18:0) increases, the number of hepatic (liver) and peripheral low-density lipoprotein (LDL) receptors decreases which in turn causes serum concentrations of LDL cholesterol to rise (a process called down regulation). Down regulation occurs because internalization of 12:0, 14:0 and 16:0 within cells reduces the expression of genes which code for the LDL receptor protein. At low blood LDL cholesterol concentrations (20-50 mg/dl), LDL cholesterol molecules move freely in and out of the arterial intima (the portion of the artery where atherosclerosis arises). When blood levels of LDL cholesterol molecules rise, LDL molecules tend to become "stuck" in the intima where they undergo oxidation and glycation to become "modified LDL." Modified LDL stimulates arterial endothelial cells to display adhesion molecules which latch onto circulating monocytes and T cells. The endothelial cells then secrete chemokines which bring the monocytes and T cells into the intima where they mature into macrophages. T cells release cytokines causing inflammation and cell division within the artery. The macrophages are different from all other cells in the body in that they display a scavenger receptor which is not down regulated by LDL cholesterol molecules. The macrophages "feast" upon modified LDL cholesterol in the intima and become filled with these fatty droplets and become foam cells. Cytokines cause smooth muscle cells to grow over the lipid core of multiple foam cells forming a tough fibrous cap which becomes the characteristic plaque which defines atherosclerosis. Finally, inflammatory cytokines secreted by foam cells weaken the fibrous cap by digesting the collagen matrix. If the weakened cap ruptures, a substance secreted by the foam cells called "tissue factor" interacts with clot promoting elements in the blood causing a thrombus (clot) to form. If the clot is large enough to halt blood flow, it causes a myocardial infarction (heart attack).

Dietary saturated fats do not always elevate blood LDL concentrations. When consumed under hypocaloric (reduced energy) conditions they may improve most blood lipid parameters including total and LDL cholesterol, HDL cholesterol, and total triacylglycerol (TG). This phenomenon typically explains why Atkins-like diets (such as recently reported this spring in the New England Journal of Medicine) may be as or more effective than hypocaloric, low-fat, high-carbohydrate diets. However, under isocaloric (normal energy) conditions, studies of healthy normal subjects show increased consumption of saturated fats significantly raises blood LDL concentrations.

A further confounding factor in this scenario is the presence of a specific type of LDL cholesterol molecule in the blood called "small dense LDL." The rate of influx of LDL into the intima is not only related to the blood concentration of LDL cholesterol, but also to the size of the LDL molecule. Small dense LDL have a greater flux into the intima than normal LDL and they are more likely to get "stuck" in the intima because of increase binding to proteoglycans. The primary metabolic source of small dense LDL is very low density lipoprotein molecules (VLDL) whose blood concentration is greatly influenced by dietary carbohydrate, particularly high-glycemic-load carbohydrates. Hence foods with high glycemic loads such as those made with refined sugars and grains may also operate synergistically with high dietary saturated fats to promote atherosclerosis. Additionally, high-glycemic-load carbohydrates are positively correlated with plasma concentrations of C reactive protein, an important marker for systemic inflammation, a key element of the atherosclerotic process, as I previously noted.

The gold standard procedure for demonstrating cause and effect between diet and disease is called a dietary intervention. Subjects are either fed or not fed a certain food or nutrient and then either presence or absence of a disease or disease symptom is monitored over time. With CHD, the results of dietary interventions in which saturated fats have been lowered, frequently have been unable to demonstrate a reduced mortality from CHD. The problem with the majority of these studies is that they were conducted prior to the knowledge that high-glycemic-load carbohydrates were an important promoting factor in CHD etiology. Further, most of these studies did not control for inhibitory dietary factors such as omega-3 fatty acids, fiber, phytochemicals, antioxidants etc. Hence, the interpretation of whether or not dietary saturated fats cause CHD in these interventions is confounded by a number of crucial variables. In animal studies, including primates, these confounding dietary factors can be completely controlled and atherosclerosis is routinely induced by solely feeding high amounts of saturated fats.

To what extent do you think the level of small-dense LDL cholesterol explains the "badness" of LDL? This is relevant to The Paleo Diet because small-dense LDL is strongly correlated with triglycerides. On some conceptions of The Paleo Diet, a more Atkins-like approach is taken: liberal saturated fat, very low carb. The result is often somewhat elevated LDL, but very low triglycerides. The low triglycerides probably indicate low levels of small-dense particles in the LDL fraction. This is why the Eades are not concerned about increases in LDL on their plan (for example). What is your take on this?

Excellent point. We need more information to determine if very-low-carbohydrate, high-fat diets reduce small-dense LDL in all people or only in certain genetically predisposed people ala the multiple studies done by Dreon et al. Further it will be necessary to determine whether or not the total increase in LDL (even with a concomitant decrease in small-dense LDL) still accelerates the atherosclerotic process. It seems most likely that small-dense LDL is derived from triacylglycerols carried in the VLDL fraction, hence the possibility looms that a major determinant of atherosclerosis is the ratio of total LDL/small-dense LDL.

LATTER ON, he recognizes that lectins and Omega 3 faty acids are bigger players in the atherosclerosis process and in his newsletter, they already talk about Vitamin K2.

This explain why the Masai and the Inuit had atherosclerotic plaques (a friend of mine who works with Cordain sent me 3 papers showing this and the Inuit data comes from mummies datting back 500 years) ,but didn't die from it. hey had:

- Low Carb diet (see Forsythe CE, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids. 2008 Jan;43(1):65-77)
- No wheat, other gluten cereals and other potential sources of dangerous lectins
- Sufficient Vitamin D
- I believe that Vitamin K2 intake would be enough
- Low Omega 6/Omega ratio
- Low trans
- Low sugar intake (including low Fructose)
- I believe that they didn't suffer fom micronutrient deficiency as modern people do.
- Regular Exercise
- Acute as opposed to chronic stress
- Regular sleep
- Etc (I can't remember other variables)

This is what's so great about the Paleo template: you know that unless you emulate the environment (not just K2, D, types of fat and absence of wheat, but a lot of variables) our ancestors live in, it wil be very hard to decrease the risk for various diseases.

Stephan, don't take this the wrong way, since I admire you a lot and think you're doing on hell of a job, but I want a more serious debate about this, without insulting people (which you do not do) an without putting passion into it (all I want is to be sure that what I do and recomend is a good option and not to be right).


What we need is to promote a debate between Cordain and a knowledgeable defendor of the saturated fat hpothesis, jut like the Performance Menu did between Cordain and Campbell regarding animal protein.

StephenB said...

Stephan, you can get the full text of the paper along with some discussion here:

I was flabbergasted to read a study showing two groups of rats, both receiving the same caloric portion of bread in their diet. One of the two groups received bread crusts, high in AGEs:

Bread crusts are a convenient source of high AGE content food. An experimental group of rats were fed chow with bread crusts replacing 25% of the wheat flour in the control group. Both groups were pair-fed resulting in each pair of animals having identical calorie intake. The rats fed bread crusts for six weeks weighed ~25% more and had higher internal organ weight than the control group fed regular rat chow. The rats fed bread crust also had a 3 times higher level of a tumor causing agent and had approximately 70% kidney function loss (proteinuria) (PMID 16037270, I think).


Stephan Guyenet said...


I recognize that diet is not the only factor changing here. But the message I'm trying to counter is the one we're bombarded with every day: saturated fat is a dominant factor in CHD. It's clearly not: the data are quite internally consistent between the controlled clinical trials and studies like this one.

If saturated fat causes CHD, it does it so subtly that it hasn't successfully been measured yet.

The problem with Cordain's argument is it's hypothetical. He likes to bury you with molecular arguments, but the empirical fact is, the controlled clinical trials have already been done, and reducing saturated fat has no effect on CHD.

Also, grass-fed beef has a very similar fat composition to grain-fed. The only major difference is the n-6:n-3 ratio. The saturated fraction is nearly identical. Grass-fed is leaner, but the fat it does have is not that different from grain fed in composition, and it's basically the same as the subcutaneous fat of wild ruminants (where most of the fat would be in the fall and winter).

Robert Andrew Brown said...

JMC _ thanks for posting that fascinating abstract.

"In animal studies, including primates, these confounding dietary factors can be completely controlled and atherosclerosis is routinely induced by solely feeding high amounts of saturated fats."

A big ask but do you have any links to whatever are regarded as the best of primate trials and sat fats

Questions I have are as to the type of sat fats used, were the diets restricted sufficient or in excess of need, antioxidant status, dietary basis etc.

What is Cordain's position on the impact of cholesterol v oxidised cholesterol.

JMC said...

Hi Staffan, I understand what you're saying, but if you really want to know if saturated fat doesn't have anything to do with CHD or even if it's beneficial, you have to control various variables, as Cordain said. And the studies that looked at it, didn't used a healthy diet, so the conclusion that we can extract from these studies is: in the context of the typical western lifestyle, saturated fat doesn't have any influence or better yet, the fact that it elevates LDL (because, under the typical western diet, it does elevate LDL and here you can obviously argue that LDL doesn't have anything to do with CHD, but I would really like that theory better explained) is not related to CHD in this population.

Also, how can we explain the Inuit mummies having coronary atherosclerosis 500 years ago? And the autopsies on the Masai showing the same? We know that they probably didn't die from it, because the lumen wasn't compromised (this may be due to the fact that inflammation has a much bigger impact). But the atherosclerosis existed, so it is possible that primitive people didn't have atherosclerosis, but were healthy nonetheless.

To better explain what I am saying, because clearly I wasn't able to explain my message, I give an example: As you are aware, Type 1 Diabetes may be caused (among other causes) by gluten. Nevertheless, it seems that type 1 diabetes is rare or non existent zero in regions worldwide with high UVB irradiance. There's also at least one prospective study showing 2000 UI of Vitamin D decreases the risk for the disease in high risk children.

So, what does this mean: should we discard gluten, just because in these countries it is not related to the disease?

As I said in my previous post, al the healthy populations living in there traditional manner have a very healthy lifestyle and a very healthy diet, so to dismiss saturated fat or to claim it is very healthy (it could be one way or the other - I don't know and I am very interesting in knowing it, but apparently nobody is interested in debating this further, which is frustrating: the low carb guys say that saturated fat is totally healthy and the low fat proponents sa it is evil - this is the kind of attitude that doesn't lead us to knowledge)

We need to do more studies and I would like to see better explanations and not just empirical data. The fact that Cordain has many theories and uses molecular mechanisms to formulate them doesn’t mean that he likes to throw sand on your eyes, but that he likes to understand the mechanisms, as I do (any theory presented has to talk about the fact that 12:0, 14:0 and 16:0 elevate LDL in the typical western diet), and was hopping that these blogs could be a good place to debate these questions and learn more.

As for grass fed beef, I didn't mention this in my previous post, but wild game. Also, I didn't say that it had less or more saturated fat, but that 40 to 50% of the saturated fat was stearic acid (at least it is so in dear and antelope).

Sorry for the long posts and for disagreeing with you (which I consider a very sane and knowledgeable person), but I think that debating ideas is how knowledge evolves.

Robert, regarding oxidized cholesterol, here's something from his newsletter:

"Canning also increases the level of oxidized cholesterol in fish, specifically increasing a molecule called 25 hydroxycholesterol that is extremely destructive to the linings of arterial blood vessels. This is so destructive, in fact, that oxidized cholesterol is routinely fed to laboratory animals to accelerate the artery-clogging atherosclerotic process in order to test theories of heart disease. In animal models of atherosclerosis and heart disease, only 0.3 % of the total ingested cholesterol needs to be in the form of oxidized cholesterol to cause premature damage to arterial linings."


Stephan Guyenet said...


You don't need to apologize for disagreeing with me.

I see your point about the clinical trials being a test of saturated fat in a particular context, I think it's a valid statement.

Here's where my basic argument comes from: I've come to the conclusion through my reading that saturated fat has been a substantial part of the human diet since the beginning of our species. Not all groups ate a lot of it, but many did. I believe it's clear that a high-saturated fat diet is part of our ecological niche. So I feel that saturated animal fat is innocent until proven guilty. And if the clinical trials and studies like this one (where people are eating an extreme amount of saturated fat (although not from animals)) fail to turn up anything, then I would say the presumption of innocence stands.

The whole idea doesn't make much sense to me to begin with, to be honest. The liver makes saturated fat from carbohydrate and pumps it into the bloodstream. We have the enzymes to desaturate palmitic acid, so why does the liver choose to secrete it into the blood in its saturated form? Furthermore, our own body fat is pretty saturated, roughly resembling lard.

I acknowledge that dietary saturated fat doesn't seem to be good for certain primates. But these species tend to be adapted largely to a plant-based diet in the first place, unlike humans. You can't translate diet-health studies between species that are adapted to radically different diets.

I'm really not trying to be too hard on Dr. Cordain here. I respect the research he's done and I think he's a great source of information. We do have this one point of disagreement, but I would say it's fairly minor. Cordain does acknowledge that saturated fat is not one of the dominant factors in CHD.

Stephan Guyenet said...

By the way, JMC, I'd be interested to take a look at the Inuit atherosclerosis paper if you wouldn't mind posting it. Thanks.

gunther gatherer said...

Stephen B,

That study is fascinating. Is there any other information on how endogenous AGEs affect mammals?

Just because humans have been doing something traditionally for a long time does not make it optimal for health. It may make it optimal for immediate survival, which is all any animal really cares about, but not overall health and longevity markers. That goes for foods as well as food-preparation techniques.

Also, when everyone in a hunter-gatherer tribe cooks the food together, they aren't going to notice wide health changes in their tribe. Everyone will more or less have the same lifespan and health. Maybe they just overlooked the harm done by cooking, or attributed it to something else, or just accepted quicker aging and death so that younger members of the tribe could survive?? If you think about it, it doesn't really hurt the tribe to have the elders die of earlier...

Stephan Guyenet said...


True, but we're also the only mammal that's been eating cooked food for 1.5 million years or so. That may have been enough time to adapt to dietary AGEs.

Elders are in fact very valuable to a group of humans as a source of knowledge. That may be part of the reason why we evolved to be so long-lived for our size.

Matt Stone said...

Are you guys still trying to figure out which type of fat causes heart disease? I'd suggest looking elsewhere altogether.

Robert Andrew Brown:

If polyunsatures are so vile and causal of heart disease, then why, during early heart disease trials in which polyunsatures substituted for other fats, did heart disease incidence not show significant signs of increase compared to controls? Actually, incidence tended to run slightly lower. Plus, who in the U.S. eats hydrogenated lard except a microfraction of "Enig" ma's and Latinos?

I follow your logic and am in agreement. Adulterated fats are not the smartest foods for humans to be eating. But when looking at things from the most comprehensive perspective as possible, adulterated carbohydrates, not fats appear to be far more causal of heart disease and other illnesses. Their mechanism - slowing down the metabolism (type II hypothyroidism), damaging mitochondrial DNA (WAP's 'intercepted heredity'), and leading to things like...

PCOS, which is a consequence of hypothyroidism, which also slows digestion and causes "bloating no matter what you eat," while contributing to weight gain. I guarantee you that P's basal body temperature is below normal.

The dietary remedy for that? Eat fat like it's going out of style, the only form of energy that doesn't raise insulin.

And it just so happens to be great for weight loss too, eliminating the subtle divergence between appetite and metabolism that leads to a slow, steady accumulation of excess fat. P - don't eat too much meat. Eat too much fat. Please! Coconut oil, butter, and cream - like it's going out of style!

I had 2 sticks of butter and a pint of heavy whipping cream yesterday and woke up a pound lighter than yesterday. That's what I"m talkin' about. Went great with the eggs, sausage, ribeye, and vegetables I ate along with it.

Robert M. said...

It's quite likely that the positive benefits of cooking meat (i.e. killing parasites) greatly outweighs the negatives.

StephenB said...

Hi gunther gatherer. A pub med search for "Vlassara H"[Author] will turn up a lot of good studies; she seems to be a leader in the field. See especially PMID 12429856:

We explored the effects of two equivalent diets, one regular (high AGE, H-AGE) and the other with 5-fold lower AGE (L-AGE) content on inflammatory mediators of 24 diabetic subjects [...] C-reactive protein increased by 35% on H-AGE and decreased by 20% on L-AGE (P = 0.014), and vascular adhesion molecule-1 declined by 20% on L-AGE (P < 0.01) and increased by 4% on H-AGE"

It takes a while for dietary AGEs to build up. I think I read that on average 1/3 of the body's collagen is glycated in the very elderly (sorry, no source). The process is accelerated in diabetes.

Also, some primitive cultures may have also cooked at lower temperatures, right? (I'm thinking of the underground slow cooking of meat.) As long as you cook under the boiling point of water, you should avoid most AGEs.


As for the role that AGEs play in aging, isn't

Half Navajo said...

Elders are helpful to have around to help raise your own over them when you can't, and as stephen said, a source of wisdom.

gunther gatherer said...

Stephen, Stephen B, Robert M, Half Navajo,

I agree humans have been cooking long enough to have adapted to a certain amount of dietary AGEs. But they never fried or baked their food and they certainly never added sugars, honeys or glazes to their roasted meats. BBQ is definitely a neolithic trait...

Slow boiling is really the only cooking we should be adapted to then, I think. And it just so happens to create the lowest amount of AGEs.

There were other food preparation techniques (aside from fermentation) that were used too, such as having the women chew up roots and spit them into a bowl, like the Kombai. I don't think my girlfriend will go for that.

I didn't mean to say elders weren't important in a tribe. Just that perhaps a slightly shorter lifespan for them fits within an equilibrium that a tribe can work with. Therefore they would not have noticed this as a detractor to their survival strategy and corrected the problem.

Remember AGEs are very subtle and don't kill us outright, they just contribute to general degeneration and many metabolic problems which basically amount to quicker aging and death. This will take the form of seeming "natural" and normal when it happens all around us.

How many elders would a tribe need to raise kids, tell traditional stories and help out? I guess it depends on the size of the tribe and the abundance of food.

Robert Andrew Brown said...


Hydrogenated lard.

Before hydrogenated vegetable oils were used in processed foods baked goods etc hydrogenated lard was used.

I have seen processed saturated fats used in trials

Omega Intake

If you have any trial refs on falling heart disease I would be pleased to see them. The problem with many of these trials is there are lots of confounding factors.

If you take processed saturated fats out and add vegetable oils you are adding antioxidants minerals and other nutrients that are not present in process animal saturated fats. Industrial lard has zero minerals and vitamins.

Maybe the positives of better nutrients in vegetable oils out weighed the oxidative effects when compared to empty industrial animal fat.

The effect of Omega 6 is also quantity dependent, which will also depend on fat stores and dependent of other related dietary factors - antioxidant status - oxidised food intake etc.

Introducing increased Omega 6 to an adult will have a different outcome to a lifetimes consumption.

It is complex and multifactoral and through inflammation and oxidative stress runs across most western conditions, most of which continue to rise.

Both animal and vegetable fats contained trans fats.

The biology of Omega 6 is that it causes inflammation and oxidative stress when supplied in excess.

I note your list includes lots of animal fats and not bottles of vegetable oil. (-:

Robert Andrew Brown said...

Stephen b

Thanks you for the trial link above.

Oxidation seems to be an issue underlying the detrimental effect of AGEs.

The paper also mentions oxidised fats and the potential for interaction between AGEs and oxidised fats.

Thanks for flagging this up. More reading (-:

Robert Andrew Brown said...

Stephen b

This is an interesting wide view AGE paper I have just found.

Like oxidation of fat, temperature, time exposure and storage look like factors.

The possible implication for formula are thought provoking.

Sue said...

Has anyone heard of Professor Brian Peskin and his take on omega 6 and omega 3? He thinks taking fish oils is not good as we get too much of the derivatives EPA and DHA and we should be getting the parent EFAs - omega 3 and omega 6. He thinks we are now overdosing on omega 3. Any thoughts?

Stephan Guyenet said...


I find that hard to believe. If you look at what's available in nature to a species like ourselves, there's a lot more long-chain omega-3 around than there is alpha-linolenic acid. Hunter-gatherers didn't eat flax oil, but they did eat fish and brains. Some groups may have had access to seeds that contained some alpha-linolenic acid, but it was probably only certain groups and in certain seasons.

Fish oil elevates blood n-3 much more than flax oil at an equivalent dose. You could say that fish oil elevates it too much, but I think the Japanese and the modern Inuit, who eat a lot of n-3 from fish and have very little heart disease, would disagree. The Japanese also have less chronic disease in general than the average industrial country.

Sue said...

Thanks for your reply. Yeh, what he says doesn't seem right.
Here is a link about what he says about EFAs.

JMC said...

Thanks for the kind repply Stephan.

I only have the paper on the Inuit in printed form.

Right now, I'm on vacations, but could try to run it through th scanner and post it when I return.


Stephan Guyenet said...

Sue, I just wanted to add that I think any PUFA oil can be overconsumed, including fish oil. I believe cod liver oil/fish oil is best taken in small quantities, one teaspoon per day maximum. I take about a third of a teaspoon of fermented high-vitamin cod liver oil per day. The lower your n-6 intake, and the better your diet in general, the lower your need for n-3.

Stephan Guyenet said...


If you give me the reference, I can try to look it up in my University library. Thanks.

Unknown said...


I recently received some curious results on my blood panels and am curious for your feedback. I am sorry to trouble you with my personal story but am not sure where else to go for info. I appreciate any help you can provide, in addition to what you have already done with this blog, which is a terrific resource.

In May 2007 my blood panel looked like this:

Total cholesterol 155
Trigylcerides 65
HDL 50
LDL (calc) 92

In Jan 2009 I received the following:

Total cholesterol 311!
Trigylcerides 43
HDL 88
LDL (calc) 214!

I am currently 41, athletic, do high intensity short duration exercise 3-4 times/wk, low body fat, fairly good health. I changed my diet in Jan 2008 from a standard "healthy" diet to paleo style after reading Cordain's book. I followed Cordain's recommendations fairly closely for about six months, eating lots of fruits and veggies, lean meat (trimming the fat), very few starches, and nuts seeds avocados, olive oil, etc. In summer I began reading some blogs and books which recommended a diet higher in sat fats, lower in protein and lower in PUFAs, so I made some changes by severely limiting PUFAs (no more nuts, less fatty chicken and pork) and eating fattier red meat, coconut oil. I also cut down on veggies and fruits and added starches and white rice. More of a WAPF style or Optimal Diet.

While I would consider myself a cholesterol "skeptic", I am by no means an expert and was amazed by the increase in cholesterol and am very curious what this means and why. I understand that some of the numbers here (e.g. total cholesterol) don't mean much, that some of the numbers (e.g. hdl/tris ratio) are good, that LDL calc is often inaccurate, and that based on my low tris, my LDL is likely to be large and fluffy instead of small and dense. But I am still amazed by the rise and curious what it means. Should I be concerned? Why did this happen so fast? Thanks again for any guidance you can provide.

gallier2 said...

Richard has made an interesting entry about the LDL calculation. You should read it.

Stephan Guyenet said...


I'm not too well schooled on blood lipid changes on OD-style diets. My inclination would be not to worry about it. Your trigs and HDL look great. And besides, these lipid markers were validated in people eating the standard processed Western diet, so who knows what they mean in someone eating an atypical diet.

If you really want to know your risk, you might want to consider getting a CT heart scan. It's non invasive and simply looks for calcium in the arteries. It correlates with CHD risk better than any cholesterol marker. If you get one yearly, you can see if it's progressing or regressing.

Anonymous said...

The saturated fat studies Colpo cites, (while being randomized clinical dietary intervention trials,) STILL use small sample sizes and the duration is a short . They are WEAK.

Yes, weak. You can't just have persons shove various foodstuffs into their mouths and then track their mortality for several years.

What we need is a complete understanding of cellular biochemical operations before we go around proclaming what the optimal diet is or that saturated fat is not harmful.

The science just is not there yet on the optimum diet. Colpo does not admit this. Real scientosts admit uncertainty . Colpo is far too sure of himself.

Stephan Guyenet said...


What Colpo points out is that research has failed to show that saturated fat is a problem for humans, in terms of actual health outcomes like heart attacks and overall mortality. The burden of proof is on the people trying to prove saturated fat is harmful, not the other way around. That proof has not been delivered.

Daniel said...

I was talking about this study to a friend of mine in training to be a cardiologist. First, I was rather impressed he had heard about it, but am now a little confused about its importance. My friend's take was that this study simply shows the dangers of salt use and that many of the cardiovascular benefits of the original diet are attributable to low salt intake. Indeed, the data do show that blood pressure rose dramatically wafter the move to NZ. Your thoughts?

Stephan Guyenet said...

Hi Daniel,

So wait, your friend thinks increased salt intake caused the Tokelauans to become obese, get diabetes, cardiovascular disease, asthma, gout and tooth decay?

I suppose everyone is entitled to their opinion, but I find it highly unlikely. The Tokelauans developed a classic pattern of Western degenerative diseases, including cardiovascular disease, that can't be attributed simply to salt intake. Did increased salt contribute to the problem? Perhaps, I can't say for sure that it didn't. But there are other high-salt traditional cultures like the Kuna that maintain low BP throughout life and a low CHD risk so I doubt it.

Daniel said...

Yeah, I discovered your post about the kuna and salt after my last comment. I had heard about the yanomami and their low-salt intake but never about the kuna. Very interesting. Anyway, thanks for your reply. I'm always on the look out for evidence you could be wrong since I put a lot of eggs in the Staphan basket... :)

Stephan Guyenet said...


Well that's what science is all about-- trying to prove things wrong.

I don't want to imply that I know for sure that salt had nothing to do with it. I imagine there are drawbacks to eating a of salt, given our evolutionary history.

Sandy Bloomfield said...

Appreciate your comprehensive approach, Stephen. I recently came across Brian Peskin's work and I understand why some would find his conclusions difficult to accept in light of all the studies to the contrary--but I think his arguments deserve a much longer look before dismissal as they seem to connect some dots and answer some questions for me personally. As a 49-yr. old woman who has eaten "healthy" to the point of jokes among friends and family (I realize this covers a lot of ground, but I am 80% low-carb w/lots of wild salmon, greens, pure water.air, good supplements, etc. with my only real vice being chocolate and sugar in not ridiculous amounts), I found out a few months back that I have bradycardia and a heartbeat of 52 bpm. I'm not an athlete, yet the handful of times I had to go to a doctor (a hernia 2 yrs. ago, an ob-gyn appt. about a yr ago) everyone was always praising me for my low BP. Then finally, test at a health expo about a yr. ago revealed a lack of elasticity and definite hardening of arteries. Yikes! Me? Atheroslcerosis? I had always been considered much healthier than others with no flu/cold or other issues (other than candida - another story but obviously related to my sweet tooth and I had been working on that). Anyway, I recently read Peskin' stuff and decided to put it to the test. I went to a heart center and got a CT scan for a heart calcium score (still waiting on the results) and started taking the PEO's which Peskin declares are different than EFA's due to 1) high unadulterated Omega 6 - he cedes we do get too much in regular western diets, but says because they are completely corrupted in the processed form we receive them that we are actually not getting ANY of the Omega 6 we need--also that our bodies require far more Omega 6 than 3, and 2) Most Fish Oil Omega 3's are derivatives that are not bioavailable anyway, and the body uses what it wants from the PEO form. As I said, I would not claim that he has the final answer on this, but with his engineering background he appears to be much more interested in the science & real life cases rather than funded studies due to how skewed they generally are based on who is paying for them. Anyway, I will be tracking my own progress with follow-up visits to retest and track at 3 and 6 months and then a year following his protocol. I would love to see someone address his claims based on the science he presents as it seems very compelling, and there are many doctors starting to swing his way. Thanks for the ability to share on subjects that could change (and save!) lives.