Kurt G. Harris MD

The PāNu approach to nutrition is grounded on clinical medicine and basic sciences disciplined by knowledge of evolutionary biology and paleoanthropology. The best evidence from multiple disciplines supports eating an animal-based diet high in fat, low in cereal grains and relatively low in carbohydrate.

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« Calorie Restriction: partial restoration, not enhancement | Main | Calorie Restricted Monkeys Part I »

Calorie Restricted Monkeys Part II


In part one, I described the results of a recent study of calorie restriction in rhesus monkeys. Best read that post first.

In my correspondence with Dr. Coleman, I asked her if any of these monkeys had what would be considered the kind of heart disease that kills 500,000 Americans annually, that is, evidence of coronary artery stenosis, thrombosis, or evidence of myocardial infarction (MI). She said the autopsies were performed by a pathologist and were quite thorough, including the brain and heart. One long-term diabetic C monkey had an ischemic stroke, but there were no MIs or coronary occlusions identified. She also said, “In general we don't see much if any coronary artery disease likely due to the low fat diet the animals receive. In other monkey studies diets had to be increased to >30-35% fat for disease development. We have not, to date, seen any MIs.”

Now I was originally going to post this review on Saturday, but I had not counted on having to slay the diet-heart hypothesis in writing about this monkey study. I was on my way to seeing validation of low carb nutrition > low insulin and glycated hemoglobin > worm-like longevity effects, but was now slightly derailed. So now I had to do some research, as firstly, half the C monkeys had diabetes or metsyn but there were no human style heart attacks, and now Dr. Coleman was telling me 30% fats in a monkey diet gives them coronary disease. 

Here is what I found out. There are different primates used as models for CAD (that is the MD acronym for coronary artery disease) but references I read indicated that in addition to feeding 30-35% or more of calories as fat, almost all of these primates require huge supplemental amounts of cholesterol be given at the same time as the fat. These amounts ranged from the human equivalent of 8 eggs a day for macaca mulata to 16 eggs a day for baboons. Suffice to say these amounts would never be eaten by wild monkeys and these are therefore highly artificial laboratory efforts to get a model to study CAD and not realistic studies of monkey diets or disease. (I also found out some primate trials use hydrogenated soybean oil and call that “saturated fat” but that’s another story altogether)

I think this also points up the danger of using any non-human animal to draw conclusions about human diseases. 30% of total calories from fat is not only not atherogenic in humans, it is lower than the current already low total fat consumption in the US, to say nothing of the fat levels eaten by Inuit, Masai, Plains Indians or the French. There is also zero evidence of atherogenesis due to dietary cholesterol in humans. Leaving aside the cholesterol-as-a-supplement issue, non-human primates may be as ill-adapted to carnivory and the accompanying levels of dietary fat consumption as we are to getting only 10% of calories from dietary fat and eating 75% carbs.

Indeed, Let’s see what the monkeys were eating. The feed components are not published in the article. However, Dr. Coleman has kindly provided me with the formula.






93131 (Exp.)

Diet Composition















Corn Starch










Corn Oil















Vitamin Mix










Calcium Phosphate, dibasic





Calcium Carbonate





Potassium Citrate,monohydrate





Sodium Chloride





Magnesium Oxide





Ferric Citrate





Manganese Carbonate





Zinc Carbonate





Cupric Carbonate





Chromium Potassium Sulfate





Potassium Iodate





Sodium Selenite











According to the published study methods, this was a diet that was 15% protein and 10% fat by weight, or 64% carbs, 14% protein and 22% fat by calories. Note that carb calories were just under half sucrose and just over half cornstarch + dextrin. Rhesus monkeys are colon fermenters, and I could not get a precise figure, but they probably get some additional fatty acids via fermentation of the minimal cellulose they were given. Unlike humans, rhesus monkeys do some foregut fermentation as well. When laboratory diets contain too many simple sugars that can be fermented rapidly in the stomach, the animals are susceptible to gastric bloat from too-rapid fermentation. The sugars are feeding bacteria in the stomach faster than they can be absorbed. This can be fatal and at least one of the non-age related deaths in CW09 was due to gastric bloat. Interestingly, one reference on nutrition in laboratory animals I found warned against providing too much succulent domestic fruit like bananas, etc., as the monkeys could eat so much it would contribute to gastric bloat. What does that tell you about how healthy our domestic frankenfruit is for us? It is so full of highly bioavailable sugar it is even dangerous for known frugivores!

Note that lactalbumin as a protein source is from milk and is amino acid complete, so these are not vegan monkeys: ) There is a lot of sucrose, I am not sure how different from a wild diet in total amount, but I would bet it is much more bioavailable without the several hours a day a wild monkey spends chewing on wild fruit. Note that the fat all comes from industrial corn oil! The vitamins and minerals were adjusted to be at higher concentration in the CR feed, to avoid confounding by deficiencies.

What are the implications of this experimental diet in the context of the study findings and the fact that macaca mulata certainly has a different food niche (and evolutionary metabolic milieu) than Homo Sapiens?

Here are some conclusions and speculations:

In the study, every marker for metabolic syndrome and reduced protein glycation that was assessed showed the same direction of improvement humans can achieve with a very low carbohydrate (VLC) diet.

Basal insulin levels in particular showed sustained and significant decreases, suggesting that high insulin levels are very likely a mediator, if not the mediator, of the diseases of civilization we are all familiar with, like diabetes, metabolic syndrome and cancer.

Here is a good review of calorie restriction. Sirtuin and MTOR pathways are two of the specific biochemical pathways being investigated. You may have heard of Sirtuin indirectly via hype about resveratrol if you have encountered Oprah or her pal Mehmet Oz (what's up with scrubs outside the OR, anyway?). Resveratrol is a compound found in red wine alleged to have anti-aging properties. I believe resveratrol has so far failed to be significant in mammals, whereas, some recent work on MTOR in mice is quite promising

Regardless of which pathway mediates increased longevity at the molecular level, we already have evidence that reduced caloric intake is the trigger, and the hormone insulin seems like the most likely nexus for the effects. The intense research interest in the molecular biology of CR is so that an expensive drug can be marketed to mimic the effects we already know we can get for free with CR itself. I predict these drug efforts will have the same crude consequences as attempt to lower “bad” cholesterol with molds (statins) or attempts to lower blood sugar by helping it into cells Over and over the mainstream media claim we must find a synthetic pill, as practicing CR itself is just plain impossible and too uncomfortable for humans

Anyone one on an ad-lib VLC diet is already practicing CR right now.

How is it that an ad libitum VLC diet can have the same effect as calorie restriction? Let me count the ways.

The most obvious way is that when VLC is followed, there is a spontaneous decrease in caloric intake. Interestingly, the decline in intake is often on the order of 30% or more of calories. I believe there is a metabolic advantage due to differences in caloric utilization or “wastage” with VLC, but the main effect is due to spontaneous reduction in intake.

Why does this happen? Stimulation of the appetite with excess fructose and glucose consumption mediated via hormones is reduced with VLC, and if fat consumption is increased, the hormonal satiety provided by fat (cholecystokinin, ghrelin etc.) will decrease appetite as well. More importantly, on VLC, if approaching ketosis, the whole body shifts its bias towards fatty acids and ketone bodies as fuels, and away from glucose metabolism. There is reduction in the rate of glycolysis, and therefore a likely reduction in glycosylation, which mediates many of the putative aging related effects. See this, this and this.

The reduction in glycosylation and increase in lipolysis, with accompanying changes at the mitochondrial level, themselves decrease appetite, as avoiding burning glycogen for your fuel needs and favoring your vastly greater reserves of fats decreases the constant hormonal call to hunger required by the glucose dependent energy metabolism. Good review here. Calorie restricted monkeys also show increasing levels of ketone bodies with age, and ketone bodies are a sign of the shift away from glucose and towards fat metabolism in humans, further supporting the idea that CR and VLC are metabolically the same phenomenon.

PaNu dogma is that the EM2 (evolutionary metallic milieu) for humans is to use fatty acids and ketones for fuel. Our glucose dependent metabolism is therefore a deviation from the EM2 that contributes to the diseases of civilization. Whether what is abnormal is the relative abundance of all food or the increased fraction and bioavailability of carbohydrate food sources or just fructose is irrelevant to how to return to the EM2.

All the evidence so far is that we are healthier if we are mostly in the fat-burning state. We know that if you are human a VLC, high fat diet will get you there without counting measuring, weighing or living in a cage.

How else could both CR and VLC work? Lets look at the three Neolithic Agents (hat tip to Stephan) that may contribute to our deviation from the EM2. These Neolithic Agents are all foods that were not part of the EM2 prior to agriculture, and each has a wealth of evidence that they are related to poor health in humans. They are: Wheat, fructose and linoleic acid.

The monkeys in this study ate no wheat (gluten grains), unless the dextrin came from wheat ( EDIT: IT APPEARS THE DEXTRIN IS FROM CORNSTARCH AND THERE WAS NO WHEAT IN THE DIET: PC -RJC), so we can’t invoke gliadin or WGA reduction with less effect on Leptin receptors, etc. In humans on VLC, I have no doubt that many of the metabolic effects may be due to reduced gluten load – I have seen this clinically in patients with autoimmune diseases. Nevertheless, reduction in O-6 PUFAs and reduced insulin levels could also mediate reductions in inflammation independent of gluten exposure. The fact that dramatic improvements in metabolism and reduced aging were seen in this study with neither set of monkeys eating wheat might indicate that wheat is not as important as the other agents, at least in monkeys. OTOH, if the dextrin were from wheat, maybe both sets of monkeys would have been healthier without it ?

How about Fructose? Improved insulin sensitivity could be gained in both the monkey study and in humans on VLC just due to fructose reductions, as 30% for a monkey may well improve their glucose control by itself. As humans are not frugivores, and monkeys are either frugivores or heavily fruit-eating omnivores, yet monkeys get diabetes on high carb diets, fructose per se may well be the major Neolithic Agent. Complete elimination of fructose containing foods alone would decrease American carb consumption from 55% to 35% of calories, and VLC diets usually cut fructose by 80-90%, so it could just be Fructose causing the metabolic disturbance.

The monkey diet, I would guess, deviates from the wild monkey EM2 in the bioavailability of carbohydrate, especially the fructose. Based on my reading, some captive monkeys will get obese or get gastric bloat from too much sugar in domestic fruit in ad lib diets. I find this very interesting. To me this indicates that we did not lose our fructose satiety signal, we likely never had one – I believe no animals rely on hormonal satiety to stop eating fructose, even the frugivores. As Wrangham has described, a diet of raw wild fruit is terribly metabolically inefficient, taking hours of chewing a day for the monkeys to get sustenance, due to the low ratio of sugars to pectins and starches and fibers in wild fruit. There is no satiety “off” switch for fructose, there is instead likely postitive feedback to keep eating in the interest of dispersing seeds for the plant. It might indeed have been adaptive (not just for the plants) to have no satiety switch for fructose, as it would signal to keep eating even though it’s a lot of work!

This all supports PaNu dogma that fructose is outside the EM2 due to its artifical bioavailability, and moves me even further in the Steffanson/Hyperlipid direction that all animal products are blessed and it’s the plants we should be wary of. 

PaNu Central Dogma II: Favor Foods that are Defenseless When Dead. ( Hint: Eat animals)

The monkeys were getting their 22% of dietary fat calories from corn oil. How does that fit with our thoughts about PUFA ratios and Linoleic acid (LA)? I have no idea what wild monkey PUFA ratios would look like. My guess is that non-human primates, most of whom are omnivores on the vegetarian end of the scale or even essentially vegan like gorillas, probably have an EM2 that has more PUFAs and fewer saturated fatty acids (SFAs) than what I argue to be the human EM2. A such, they may tolerate excess O-6 PUFAs like the 58g/100g of linoleic acid (versus 0.7 g ALA O-3) found in corn oil. (EDIT - IT WOULD BE INTERESTING TO SEE THE MONKEYS 6:3 RATIO IN TISSUES OR THEIR OMEGA 3 INDEX FROM RED BLOOD CELLS AS A PROXY)

I plan to read some more on primates and PUFAs, but I see several possibilities. 1) The excess LA may be harmless to the monkeys, as they are primarily plant eaters. 2) The excess LA and out of whack 6:3 ratio may be the major cause of disease and this was mitigated by CR – this seems unlikely as the 6:3 ratio would have been the same between the two groups or 3) The excess LA is causing disease in the monkeys, but the effects are only additive to and potentiating the pro-inflammatory effects of the excess fructose/ insulin on the C diet. If the 6:3 ratio was that of wild monkeys, C monkeys might have had less disease and CR had no effect 4) LA and fructose independently cause disease, aging, and inflammation, and if the C diet were closer to the EM2 but still had excess fructose bioavailability, there would have been less disease in the C group but the CR group would have been even healthier – i.e., there might have been less overall disease, but the effect size might have been greater. I favor #4. There is no reason to believe non-human primates have hugely different eicosanoid pathways, but I’ll keep looking on this. (EDIT - TISSUE 6:3 RATIOS ALSO DEPEND ON FATTY ACID SYNTHESIS BY THE ANIMAL - I THINK THIS IS PROBABLY MINIMAL IN NON-RUMINANTS LIKE M. MULATA)

I believe the C monkeys in the study were actually eating a monkey junk-food diet. The study was therefore comparing a junk food diet with and without CR. What would results have been if the intervention diet had been simply an ad-lib intake of natural wild foods that take much more effort to chew with less carbohydrate bioavailability and had better PUFA ratios? We will never know but we could speculate that it might parallel the human observations of Greenland Inuit and there might have been no cancer at all, in addition to no diabetes.

Finally, why don’t the monkeys get CAD, despite our successful efforts to give them the metabolic syndrome that correlates so closely with CAD risk in humans?

photo of H. Habilis reconstruction courtesy Wikipedia

My shoot-from-the-hip speculation is that Homo Sapiens, during two million years of evolution since H.Habilis, lost what little tolerance for excess fructose we started with at the same time we acquired our metabolic preference for exploiting the fat stores of other mammals and became more tolerant of saturated fat than fructose.

Sugar is just more poisonous to humans, and that is why you have to try so hard to give CAD to monkeys, even if you are stimulating inflammation with gobs of linoleic acid. CAD may depend on not tolerating fructose. That would explain a lot and we should keep that in mind when reading animal studies.

So among the Neolithic agents, excess industrial oils are probably bad for most mammals, but sugar may be peculiarly bad for humans. Step one of PaNu stays step one.


Acknowledgement: Thanks again to Dr. Coleman for cooperating with my inquiries about this important study.

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Reader Comments (30)

This was an excellent post. I usually stick to a low carb diet, but I have been cheating by eating lots of berries, some nuts, etc. I will try to be more diligent.

I have to think more about resveratrol. I started taking it a few days ago. My goal from the supplement would be to have a healthier old age, rather than an old age full of decay. But you are correct in that the mice in those studies could have been on junk food diets.

July 14, 2009 | Unregistered CommenterJeremy

Hi jeremy

I think eliminating the fructose, wheat and linoleic acid will do more for you than any supplement.

I predict that any drug they do come up with (I don't think resveratrol has worked in mammals yet) will work no better than VLC eating without wheat and if the drug does work it will have nasty side effects.

July 14, 2009 | Registered CommenterKurt G. Harris MD

Looks like
14% Protein from lactalbumin (whey protein isolate)
23% Fat from corn oil (Omega 6/Omega 3 ration of 46/1)
63% Carbohydrate from corn starch (@300 g/Kg), sucrose (@285 g/Kg), and dextrin (@50 g/Kg).

Not 15/10/75. Or did I make a math error?

Be well,
Ben Fury

July 14, 2009 | Unregistered CommenterBen Fury

Ben Fury

"Animals in this study are fed a semipurified,
nutritionally fortified, low fat diet containing 15% protein and 10% fat"

100 - (15+10) = 75 for 15/10/75

This quote is directly from the supplemental methods section of the article as published on the Science website.

The composition table was emailed to me by the author. I suppose they changed the diet at some point but I don't know for sure.

I'd rather have the 20% fat.

July 15, 2009 | Registered CommenterKurt G. Harris MD


good posts, I have 2 questions:

I eat VLC, BUT I am trying to gain weight, so actively try to increase my calorie intake (maybe about 3000kcal per day on average for 6ft1 27yr old male, 71kg). Does this mean I am less healthy in some way? If I eat 'ad lib' I easily lose a few kilos.

I eat 4 eggs a day so was slightly worried about the implied link between cholesterol in eggs and diseases/ill health. Mark Sissons also recently advocated eating a dozen eggs a day to gain weight on a VLC diet. is this safe? What is the truth about the relationship between deitary cholesterol and blood cholesterol / illness? i am confused!

many thanks


July 15, 2009 | Unregistered CommenterAlex

Some considerations about trials on a sterile environments versus real world:



July 15, 2009 | Unregistered CommenterMario

I appreciate your efforts, and I am very happy that there is another blog dealing with the issues that I consider important. Sorry for jumping in the middle of it without reading both of your posts related to the study, and for being so counterproductive but what it's the point in talking about the diet of rhesus monkeys that have a different GI tract and natural diet. Poor monkeys in captivity, being given pseudo food and semi-starved.

July 15, 2009 | Unregistered Commentersimona

I was an arts student, so I cannot argue with the science and I might be biased after reading Sandy Szwarc's articles on Resveratrol and calorie restriction. It seems I do not believe in calorie restriction for long term use. My father has been a vegetarian for the last 25 years, he is 72. He had a heart attack last autumn and they put him, obviously, on the typical cocktail of medication that goes with his condition. He is against taking any medication, he wouldn't even take something for his headaches, but now he was convinced by his doctors and by his cousin, who is a cardiologist. Like all people of a certain age, he considers himself ignorant in these matters and he listens to the doctor.
Anyway, my point is that it is important when talking about CR and reduction in circulating insulin as a positive effect (I read the link that you had regarding a recent review of CR) to consider the composition of the diet. As a vegetarian, because he was working long hours and he was away from home, he ate very little during the day. He is very skinny, with almost no muscle left, I'm surprised he can lift anything. He was also fasting many times a year for weeks at a time, eating bread and water, or doing religious fasts with no animal products. So, I say, he was definitely doing CR but not eating a proper diet (in my opinion). What would he have? Fruit, salads of carrot, cabbage, onion, depending on season, garlic, rice, rarely beans, potatoes, processed soy, only sunflower oil as fat source, some walnuts, loads of bread, very rarely eggs or yoghurt.
I know this is only clinical evidence, anecdote, but it's sad to see your father succumb to the new-age hocus-pocus of positive energy in the plants and negative energy in meat, etc. His doctors haven't said anything about dietary or life-style recommendations although they should be au fait with the AHA recommendations regarding fish and exercise at least because when I dared to question the wisdom on L-arginine based on a study that showed no beneficial effects published in Jama they got very defensive and said that the FDA this and the other, they know better and we don't know anything.
I am angry and disappointed with the medical profession, sorry for the rant, my mother has diabetes and she is on a diet that contains 200 g carbs!! and is low fat and huge amounts of insulin slow acting and fast acting, suffering from hypos and hyperglycemias. I'm worried that one day she is going to be on her own and lose consciousness.
I am trying to educate myself, to be able to raise my children properly, although my husband doesn't always agree with me. I wish all this was available before I had them and knew not to wean them on rice meal.

July 15, 2009 | Unregistered Commentersimona

You say that "The fact the captive monkeys will get obese or get gastric bloat from too much sugar in domestic fruit in ad lib diets is very interesting." After listening to G. Taubes (his lecture) I understand that appetite can be influenced by the composition of the diet. You mentioned that many times in your blog, once related to fasting after eating pasta. So, getting back to our monkeys, why do you not think that the control group might have been overfed exactly because ad lib fruit might make them to eat more than they need?

July 15, 2009 | Unregistered Commentersimona


Thank you for your great blog and for this intelligent reflection on these long awaited CR-results. How exciting that even the ad lib monkeys had no signs of CHD, despite the metabolic chaos the crap diet caused. I find this a peculiar finding. It strengthens my profound bias against wheat as a virtual sine qua non for coronary atherosclerosis/CHD. A few observations. Elephants in the wild are usually free of atherosclerosis, but rapidly develop it when they are fed hay and bread. According to Staffan Lindeberg (‘Maten och Folksjukdomarna’, unfortunately only available in Swedish), Fiennes observed that several non grass seed eating species develop atherosclerosis when they are fed wheat. I believe, but I am not sure and I am not at home right now, that Lindeberg himself proved this to be the case in pigs. (How wonderful it would be if he would comment on his findings here or on Stephan’s blog. I wonder if there is a more eager and thankful audience.) The ancient Egyptians had no sugar and no vegetable oils, but they did have wheat. Your collegues recently showed that they were not only diabetic and plagued by cancer, but also had extensive coronary aherosclerosis (dr Eades blogged about this). Finally, zoo’s around the world are reporting an epidemic of sudden cardiac death in great apes, most of whom are fed wheat based, ‘fortified’ pellets to ‘complement’ their diet of fruits and vegetables.

And a speculation. The North American Pima’s are maybe the most metabolically deranged population on earth. Yet, paradoxically, they have relatively low rates of CHD. Malcolm Kendrick explains this through a (documented) relatively undisrupted HPA-axis. Prolongued HPA-axis disruption leads to all the features of metabolic syndrome and according to Kendrick also to manifest CHD. But could it possibly be that the Pima eat all the crap in the world, but relatively little wheat? Are they still predominantly corn eaters? That would be to good to be true though ;-).

Thanks for ‘coming out’. The more MD’s who openly challenge the current dogma, the better.


Melchior Meijer.

July 15, 2009 | Unregistered CommenterMelchior Meijer

Kurt Harris wrote
"Animals in this study are fed a semipurified,
nutritionally fortified, low fat diet containing 15% protein and 10% fat"

100 - (15+10) = 75 for 15/10/75

This quote is directly from the supplemental methods section of the article as published on the Science website.

The composition table was emailed to me by the author. I suppose they changed the diet at some point but I don't know for sure.

I think I figured it out!
I believe the difference in values is caloric value vs weight value.
Caloric value is 14/23/63 (control group - exp group is slightly different)
Content by weight value is 15/10/75

"Attenuation of Sarcopenia by Dietary Restriction in Rhesus Monkeys"
it is described as:
"(Teklad #85387 [lactalbumin based, 10% fat, 15% protein],Madison, WI)"
with no mention of calories vs weight value. I believe they are referring to weight.

In any case, I would trust the Excel sheet from the author over the study statement.

The most interesting thing is the poor quality oil combined with simple sugars. This resembles SAD, which is really quite scary. Definitely a CAD encouraging/neoplastic diet. Eating less of it is good. Eating something entirely different would be even better.

The improvements on insulin sensitivity and sarcopenia are notweorthy. VLC diet will reliably produce the same results as well as the overall reduction in calories. No one eating an ad libitum high carb diet will ever achieve that reduction in calories without an unacceptable level of long term self torture.

Be well,
Ben Fury

July 15, 2009 | Unregistered CommenterBen Fury


Why are you trying to gaiin weight? If your adiposity is low and you can perform whatever physical activities you need, why would weight gain per se be of interest? Do you mean you want to be stronger or faster?

I can't think of any advantage to adding calories if you are eatiing ad lib VLC now. Why eat more than your body is demanding?

I eat 4 eggs a day. There is no reason to worry about dietary cholesterol if you are a human.

July 15, 2009 | Registered CommenterKurt G. Harris MD


You said "what it's the point in talking about the diet of rhesus monkeys that have a different GI tract and natural diet"

Well that is why I provided such a long explication of this study. There are many things we can learn from it, I think. I am sort of disturbed at how dismissive some of the low carb community is about the study, as if we can't learn anything from it because it did not test LC or paleo or wild diets, or because we think those who believe in CR via being hungry all the time are just nuts.

Science involves careful consideration of all the evidence we find, perhaps especially when it comes from those who don't share our biases.

Isn't it interesting that the negative effects of a suboptimal lab diet can be so easily amelioratied by reducing intake of the diet without changing its' composition?

If you peruse the rest of my blog it should be obvious that I don't recommend CR on a plant based diet, for your father or anyone else. I do think that VLC ad lb works metabolically like a CR diet , but the VLC diet must be animal based to be healthy for humans.

That's why I put PaNu central dogma II in bold - eat food that is defenseless when dead means eat animals.

Humans can't be vegan, they can only pretend to be.

Good luck with your parents. I feel your pain, but some would literally rather die than give up sugar and wheat.

July 15, 2009 | Registered CommenterKurt G. Harris MD

On resveratrol, I have already eliminated most of wheat, fructose and linoleic acid. I eat almost no wheat, I only consume fructose from berries in season (although I should cut back on those as well), and I avoid omega 6 PUFAs when I eat at home. My main dietary worry is consuming omega 6's from cooking oil when I eat at restaurants, which is often. If only restaurants cooked in butter!

Resveratrol has been shown to improve aging in mammals, namely mice, without increasing lifespans. Here are two titles to search for:

"Dietary Resveratrol Partially Mimics Caloric Restriction and Retards Aging Parameters in Mice"

"Resveratrol Delays Age-Related Deterioration and Mimics Transcriptional Aspects of Dietary Restriction without Extending Life Span"

July 15, 2009 | Unregistered CommenterJeremy

Of interest:

Eating Less May Not Extend Human Life: Caloric Restriction May Benefit Only Obese Mice


July 15, 2009 | Unregistered CommenterTodd Hargrove


I did not think the control goup was "overfed". How can you overfeed with an ad lib diet? Ad lib means they eat as much as they want. You could say the C group was overfed relative to the CR group, but that is precisely the point of the whole study. I believe ad lib diets heavy in bioavailable carbs result in higher caloric intake, even for relative vegetarians.

I read Szwarc's article and I honestly don't think she understands the study methodology. The monkeys were given enough feed so that there was a 20g (not 20%) excess at the end of the day. Indeed how could you possibly know if they had their fill unless there is leftover food? These are not Coco the gorilla, signing "I am full" when finished eating!

My observation about gastric bloat was based on reading about lab animal nutrition and not based on these monkey's diet or this study protocol.

July 15, 2009 | Registered CommenterKurt G. Harris MD


Wow, the monkey diet was full of sugar and omega-6, and almost completely devoid of omega-3! I agree with your characterization of the diet as monkey junk food. This really diminishes the relevance of the study. Yes, you can avoid chronic disease by eating less of a junk food diet, but what person who would consider CR would be eating junk food in the first place??

From what I can gather, the wild rhesus diet is only partially reliant on fruit. I think the amount of (refined) sucrose they were being fed is probably in excess of what they would naturally eat.

It's interesting that the cancers were mostly in the GI tract. To me, that suggests severe intestinal dysbiosis due to an excess of sugar and refined carbohydrate. Dysbiosis increases GI cancers in animal models. You can create dysbiosis in mice simply by feeding them proton pump inhibitors!

Excellent job covering this study. I really appreciate you digging up the details of the experimental diet. Those are so often glossed over but they're critical to understanding the results.

July 15, 2009 | Unregistered CommenterStephan

This is great stuff. I like hearing about conversations with researchers; it really makes it all so much more personal and accessible.

So did you mention your paleo-centric commentary to Dr. Coleman? Or better yet, is she aware of this posting? It would be great to get reasearchers like this involved in the discussions on these paleo blogs like yours and Stephen's and Peter's.

July 15, 2009 | Unregistered CommenterWillis Morse

Thank you for replying. Unfortunately, my parents' doctors are not telling them to give up the wheat and the sugar. They won't listen to me.
I agree with your statement about science and I am very happy that I can add your blog to my list of favourites close to Stephan's and Peter's.

Well, this is from one of their reports regarding sarcopenia and cited above. 'Attenuation of Sarcopenia by Dietary Restriction in Rhesus Monkeys' http://biomed.gerontologyjournals.org/cgi/content/full/63/6/556
"C animals were fed 20% more than their average daily intake to assure ad libitum access to food for 6–8 hours per day." That's where she took it from. I tried to find other references for the exact amounts, somewhere else they say the difference between the two groups was 20%. (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2084374) Anyway, neither here nor there.

Thank you.

July 15, 2009 | Unregistered Commentersimona


In her article Swarcz makes it sound like the monkeys were persuaded to eat more - whether the excess was grams or percent makes no difference if they were ad lib, we seem to agree on that, I got 20 grams directly from the study author. You have to supply an excess or else they cannot be ad libitum. My point was that her criticism on that point reflects that she did not understand the methodology.

Thank you for your comments

July 15, 2009 | Unregistered CommenterKurt G. Harris Md


I originally read the paper and thought it must be weights, as the fat percentage looked too low. Then I somehow managed to forget about my initial impression! I agree with you that is the explanation. I have changed the text of the essay accordingly.

4 cancers is still a lot, even though it is better than 8. I think there is likely still a lot of inflammation and immune disturbance due to the corn oil even with the improvements mediated via insulin levels

Thank You

July 15, 2009 | Unregistered CommenterKurt G. Harris Md

Cool. Glad I could help.

Too bad they didn't think to do a ketogenic diet group.
Like 85% calories from extra virgin coconut oil and 15% from albumin.
Probably could have left them ad libitum and gotten all the CR benefits without the starvation.
And quite possibly avoided those four cancers in the CR group as well.

July 15, 2009 | Unregistered CommenterBen Fury

thanks for these posts, kurt. i appreciate the effort you put into pulling together the references and doing the analysis. i plan to read the am. j clin nutr article. i continue to alter my diet, moving in your direction. my wife is pciking it up a bit, but periodically voicing concern that i'm harming myself with the increase in animal fats. did some labs on myself and was disheartened to see my hba1c at 6.3 and to learn i was vit d deficient. [when are doing your promised vit d post?] anyway, thanks for your work. i appreciate it.

July 15, 2009 | Unregistered Commenterjeff klugman


Thank You. I agree with all your comments

I think the study is quite relevant but not in the way the investigators intend. It speaks more to the concept of CR and its ontology as a phenomenon.

If we define CR as the phenomenon of enhanced lifespan or slower degeneration as a result of lower caloric intake, we can conceive of CR in one of two ways:

1) We have discovered a phenomenon that takes our natural aging phenotype and attenuates the aging process.

2) CR is a phenomenon that represents one of several ways that the damaging effects of our neolithic diets can be mitigated, and is likely mediated through lowering basal insulin levels. The CR effect is one among many changes to the neolithic diet that could be made, and which if they work, are not enhancing our natural aging phenotype, but rather restoring it. Any such maneuvers will work only to the degree we were deviating from the EM2 for our species in the first place.

Gaunt folks with no energy on plant based diets, and those searching for profitable chemicals to sell us are promoting idea #1.

I favor #2. To the degree that CR or any dietary maneuver works, it is just getting us fractionally closer to the EM2 for our species. I believe the EM2 can be achieved or closely simulated with an ad lib low carbohydrate diet relying on animal sources that minimizes excess fructose, gluten grains and excess linoleic acid. Accordingly, it is unlikely that any drug, intervention, or supplement can ever improve on what can be achieved with diet alone.

From what I know so far, I believe the laboratory experiments with mammalian species to date can be interpreted this way. If the model animal lives longer, you are just mitigating the effects of an artificially unhealthy diet.

CR is therefore partial restoration, not enhancement.

July 16, 2009 | Registered CommenterKurt G. Harris MD


I am not sure how monkeys do on Optimal Diet levels of fat. Their EM2 may have different dietary inputs than ours. Native wild fruits with less available sucrose and woody plants that take effort to eat and some invertebrates and no corn oil -all ad lib - that would be a start.

The effect sizes that medical scientists are satisfied with for cancer and heart attacks make me laugh.
Let's look for Japan vs US in coronary disease, and 19th century greenland Inuit vs US for cancer.

Hi Jeff

Thanks for your support. I'll need to make some reassuring saturated fat posts soon, I suppose.

Your HBA1c, if you go to very low carbs and eliminate wheat and sugar, will almost certainly improve with time. That kind of level is not uncommon in thin people previously on plant and grain based Ornish or Fuhrman like diets. If you were lowfat and high carb, you needed glucose as you were not burning fat.
Give it at least several more months before you test again. Have you managed to get ketones in you urine yet? Ketotis is the surefire way to shut down glycolysis. Less glycolysis, less glycosylation, fewer AGEs, lower HBA1c. I am sure it will come down with time.

If your VIt D serum level is below 60, I would start with at least 8,000 iu/ day in gel form (Carlsons) right now. Then look for my upcoming post on D. In the meantime, Free the animal and wholehealthsouurce (Stephan's blog) have good info on D

July 16, 2009 | Registered CommenterKurt G. Harris MD

Hey Jeff!

Want an HbA1c of 5.0?
Get Dr. Bernsteins book Diabetes Solution and DO THE PROGRAM TO THE LETTER.

You CAN do it!

Be well,
Ben Fury

July 16, 2009 | Unregistered CommenterBen Fury


I agree it was an informative experiment in the academic sense.

Another factor is that the monkeys' diet was highly purified. This was the opposite of a whole foods diet. In my opinion, we don't yet know enough about nutrition to create a healthy purified diet, due to the complex interplay of essential and non-essential nutrients, food and intestinal flora, etc.

July 16, 2009 | Unregistered CommenterStephan


I agree. In addition to the guesswork that is involved in micronutrient content, the costs of eating and digestion are quite significantly affected by the easy to chew biscuits form factor.

I suppose this is a bit of Heisenberg's principle at work. To control the food variables in an animal model to the point you know exactly what they are eating may inevitably perturb the the very thing you are trying to observe.

July 16, 2009 | Registered CommenterKurt G. Harris MD

"The most obvious way is that when VLC is followed, there is a spontaneous decrease in caloric intake. Interestingly, the decline in intake is often on the order of 30% or more of calories. I believe there is a metabolic advantage due to differences in caloric utilization or “wastage” with VLC, but the main effect is due to spontaneous reduction in intake."

To put this in perspective you could state that anyone eating a normal evolutionary paleolithic diet that converts to a neolithic diet will inncur a SPONTANEOUS INCREASE IN CALORIC INTAKE of nearly 43% of calories.


July 16, 2009 | Unregistered CommenterJT


Can you say "obesity epidemic"?

July 16, 2009 | Registered CommenterKurt G. Harris MD
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