Category Archives: Paleolithic Diet

Paleolithic Cuisine: How Gourmet Was It?

The Perfect Health Diet is based on biological evidence for what it is healthiest for humans to eat, not on mimickry of Paleolithic diets. Nevertheless, we believe our diet is a pretty good representation of what Paleolithic hunter-gatherers ate – in fact, a better representation than conventional “Paleo.”

We also frequently note that our diet resembles gourmet cuisines. Julia Child would have loved PHD food!

(Hat tip: Cheeseslave)

So does this mean Paleolithic humans were eating gourmet food?

It sounds unlikely. Modern hunter-gatherers tend to eat similar foods day after day, often prepared simply. Lacking supermarkets, it is difficult for them to gather ingredients; lacking refrigeration, they often have to eat food soon after it is obtained; lacking kitchens and equipment, many cooking techniques were not available to them.

But in many ways Paleolithic food may have been quite a bit more Julia Child-like than anthropologists suppose.

Delicious Macronutrient Ratios

In the book, we argue that:

  • The most healthful macronutrient mix is about 30% carb 15% protein 55% fat, with over 90% of the fats saturated or monounsaturated.
  • This healthful mix of macronutrients is also the most delicious, because the reward system of the brain evolved to encourage us to eat healthful food.
  • Paleolithic humans usually succeeded in approaching this optimal macronutrient mix. The Paleolithic diet was typically minority-carb – 15-20% carb much of the time with excursions toward 50% during periods of carb availability – and minority protein – generally 15-30% – and therefore roughly half fat by calories.

Paleolithic food may have been simple, but it had the most delicious mix of macronutrients.

That Paleolithic diets were rich in fat is supported by the observation that hunter-gatherers have always striven for a high fat-to-protein ratio in their diet. Here is anthropologist John Speth:

Inuit diet was actually composed primarily of fat, not lean meat, with the protein contribution seldom surpassing about 35 per cent of their calories, and usually lower, closer to 25 per cent. Pemmican, the traditional mainstay of Native Americans and First Nation peoples (‘Indians’) inhabiting the Great Plains of mid-continental North America, was a mixture of rendered fat and dried, pulverized lean meat, the mix carefully prepared so that the protein component did not exceed 25–30 per cent of total energy (eg, Stefansson 1956; Speth 2010). [1]

Classic gourmet cuisines also generally have this fat-rich macronutrient mix. Classic French cuisine, for instance, is notably rich in saturated fat. This has influenced everyday French eating in a healthful direction, as Wikipedia notes in its discussion of the “French paradox”:

In 2002, the average French person consumed 108 grams per day of fat from animal sources, while the average American consumed only 72 grams. The French eat four times as much butter, 60 percent more cheese and nearly three times as much pork. Although the French consume only slightly more total fat (171 g/d vs 157 g/d), they consume much more saturated fat because Americans consume a much larger proportion of fat in the form of vegetable oil, with most of that being soybean oil. However, according to data from the British Heart Foundation, in 1999, rates of death from coronary heart disease among males aged 35–74 years were 115 per 100,000 people in the U.S. but only 83 per 100,000 in France.

French cuisine is famously delicious. The resemblance of the macronutrient proportions in French cuisine and Paleolithic food suggest that the Paleolithic wasn’t a time of dreary food.

Delicious Plant, Herb, and Spice Combinations

Paleolithic hunter-gatherers ate a much wider variety of plant foods than we do. Gordon Hillman found archaeological residues from 157 plant species at the village of the Paleolithic hunter-gatherers at Abu Hureyra, Syria, and believed that at least another hundred species must have been eaten that left no residues. (Source: note 15 of chapter 24 of our book.) Modern Americans, in contrast, typically confine themselves to about 30 plant species.

So it’s fair to say that Paleolithic cuisine had a much richer variety of plant foods, herbs, and spices than modern cuisines. Paleolithic humans were intimately familiar with their natural environment, and made full use of the diverse foods available to them.

Likewise, hunter-gatherers ate a much wider range of animal organs and tissues than modern Americans, and probably a wider range of fish and animals too. They must have been familiar with a great diversity of ingredients.

What about flavor combinations? Evidence is sparse on this point, but as far back as we have archaeological evidence, we find that foods were combined in tasty ways.

Via John Hawks, I learned of a story in Slate (The Mystery of Curry) that reported the discovery of residues of a ginger, garlic, and turmeric curry from an ancient cooking pot of the Indus civilization. The sub-head of the story: “It turns out we’ve been eating the spiced dish [curry] for a lot longer than anyone ever imagined.”

Paleolithic Cooking Techniques

If Paleolithic humans had access to a great variety of foods and combined them in delicious proportions and flavor combinations, the last obstacle to the Paleolithic Julia Child would have been cooking methods. What cooking technologies did she have?

Fire has been under human control for a long time – the first known use of fire was a million years ago, and fire for heating and cooking was in routine use by 300,000 to 400,000 years ago; heat treatment of tools is known to have been practiced 164,000 years ago (for sources see the discussion in Chapter 2 of the book).

Roasting and broiling on hot coals or stones heated in a fire was undoubtedly the first Paleolithic cooking technology. Cooking in earthen ovens was routine among Native Americans [3] and probably was a Paleolithic technology.

But boiling is more controversial. Ceramic pots were invented only fairly recently, about 20,000 years ago in China and were not used in western Eurasia until the Neolithic. Steam-cracked rocks, a sign that fire-heated rocks were being used to boil water, were not common in Europe until about 25,000 years ago.

Yet archaic humans seem to have been boiling foods long before 25,000 years ago. Neanderthals were boiling their starches at least 46,000 years ago [2], and Speth has argued that to survive at northern latitudes, they must have been obtaining fat from boiled animal bones 200,000 years ago.

So how did they boil without fire-safe pots? Speth again:

Boiling can in fact be done quite effectively without fireproof containers or heated stones. I first became aware of this possibility … [from] an episode of ‘Survivorman’ on the Discovery Channel (2008, Season 2, Episode 4, Part 3, Day 3, African Plains), a program in which wilderness survival expert Les Stroud had to use his wits to stay alive and functioning for several days, alone, in the bush, having with him only the cameras needed to record his daily activities and a very minimal assortment of modern items that he either brought with him or found along the way. He had to improvise almost everything. What caught my attention on that particular occasion was that Stroud had decided to boil water, but the only container he had was a plastic water bottle. To my utter astonishment, he filled it with water, suspended it over an open fire with the bottle squarely in contact with the flames, and proceeded to bring the contents to a rolling boil without destroying the container, noting in passing that so long as the portion of the bottle that came in contact with the flames was filled with liquid the bottle would not burn. [1]

Here is a re-enactment of Stroud’s demonstration on Youtube:

Speth notes that the Ojibwa commonly boiled water and cooked in birch bark baskets, and states, “Direct boiling over an open fire in perishable containers made from paunches, skins, or birch bark – without the use of heated stones – seems to have been a fairly common practice in the temperate and northern latitudes of North America, as amply documented by Driver and Massey (1957:229–231).” [1]

Herodotus, too, noted that the Scythians commonly boiled meaty stews in paunches, with fatty animal bones supplying fuel for the fire when wood was unavailable. In east and southeast Asia and Melanesia, bamboo tubes were the most popular choice for boiling water and steaming rice.

If Paleolithic chefs didn’t bother to invent pottery, perhaps it’s because it wasn’t superior to their hides, bark, and bamboo:

Experiments conducted by Margaret Holman and Kathryn Egan (1985; see also Munson 1989) … [showed that] direct heating with the tray-like bark vessels required substantially less fuel and less time than applying heat indirectly by stone-boiling … [and] also showed that producing syrup in flat-bottomed bark containers was only marginally less efficient in time and labour than using a metal kettle. [1]

From Speth’s perspective, the invention of pottery and stone heating probably signified the increased use of slow-cooking methods such as simmering, not any dramatic change in how food was prepared. [1]

What about frying? If Paleolithic chefs were using hides as pots for boiling, could they have used the same hides to hold fat for frying?

Leather ignites at 210ºC / 410ºF – a warm enough temperature to support frying. Hides can be tanned using vegetable compounds or brains, both materials available to Paleolithic man. I suspect that frying was, if not an everyday technology, certainly a technology that more sophisticated Paleolithic chefs would have experimented with.


It looks like Paleolithic chefs employed a variety of cooking methods – roasting, broiling, boiling, baking, and possibly even frying at temperatures up to 210ºC / 410ºF – and had regular access to a variety of foodstuffs which they were able to combine in the most delicious proportions and flavor combinations. They had, in other words, the ingredients, knowledge, and technology to engage in gourmet cooking.

It’s sad that writing was not invented earlier. We have forever lost the lore of the Paleolithic Julia Child who 50,000 years ago might have written Mastering the Art of Neanderthal Cooking!


[1] Speth JD. Middle Paleolithic subsistence in the Near East: zooarchaeological perspectives – past, present and future. Before Farming 2012(2): 1. Hat tip John Hawks and Melissa McEwen.

[2] Henry A, Brooks A & Piperno D. Microfossils in calculus demonstrate consumption of plants and cooked foods in Neanderthal diets (Shanidar III, Iraq; Spy I and II, Belgium) Proceedings of the National Academy of Sciences, 108 (2), 486-491. See also Henry A, Brooks A & Piperno D. (2011) Reply to Collins and Copeland: Spontaneous gelatinization not supported by evidence Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1104199108. Hat tip Julien Salvatore.

[3] Kroeber, AL 1925. Handbook of the Indians of California. Bureau of American Ethnology Bulletin 78. Washington, DC: Smithsonian Institution. Cited in [1].

Perspectives on Low-Carb, I: Dr. Kurt Harris

Last week in An Anti-Cancer Diet (Sep 28, 2011), I recommended that cancer patients eat 400 to 600 carb calories per day, but combine it with a program of daily intermittent fasting plus longer “ketogenic fasts” and periods of ketogenic dieting or low-protein dieting to promote autophagy.

The recommendation to eat some carbohydrates, plus my statement that it was possible for cancer patients to develop a “glucose deficiency” which might promote metastasis and the cancer phenotype, seems to have stirred a bit of a fuss.

In addition to making @zooko sad, it led Jimmy Moore to reach out to a number of gurus to ask their opinion. On Twitter, Jimmy says:

Working on an epic blog post today about @pauljaminet and his “safe starches” concept. Input from numerous #Paleo and #lowcarb peeps.

I’m excited to have this discussion. As Jimmy later tweeted:

Should be fun to hash all this out publicly for ALL of us to understand better about your concepts. Here’s to education.

So far, I have seen responses from Dr. Kurt Harris and Dr. Ron Rosedale. On PaleoHacks, there is an extensive discussion on a thread started by Meredith.

UPDATE: Jimmy’s post is up: Is There Any Such Thing as “Safe Starches” on a Low-Carb Diet?.

I think this discussion is wonderful. With so many people putting effort into this, I have an obligation to respond. I’ll start with Kurt’s perspective today, then Ron Rosedale’s early next week, then whoever else participates in Jimmy’s epic post.

PHD and Archevore: Similar Diets

Kurt and I have essentially identical dietary prescriptions. However, our reasoning sometimes works from different premises. Kurt observes:

My arguments are based more on ethnography and anthropology than some of Paul’s theorizing, but I arrive at pretty much the same place that he does.

An example of a point of agreement is Kurt’s endorsement of glucose-based carbs:

[I] see the human metabolism as a multi-fuel stove, equally capable of burning either glucose or fatty acids at the cellular level depending on the organ, the task and the diet, and equally capable of depending on either animal fats or starches from plants as our dietary fuel source …

We are a highly adaptable species. It is not plausible that carbohydrates as a class of macronutrient are toxic.

I think that if there is no urgency about generating ATP then fatty acid oxidation is slightly preferable to glucose burning. But essentially, I share Kurt’s point of view. Our ancestors must have been well adapted to consuming high-carb diets, and necessity surely thrust such diets upon some of our ancestors. Certainly there’s no reason why consuming starch per se should be toxic.

Kurt and I also agree on which starches are safe:

These starchy plant organs or vegetables are like night and day compared to most cereal grains, particularly wheat. One can eat more than half of calories from these safe starches without the risk of disease from phytates and mineral deficiencies one would have from relying on grains.

White rice is kind of a special case. It lacks the nutrients of root vegetables and starchy fruits like plantain and banana, but is good in reasonable quantities as it is a very benign grain that is easy to digest and gluten free.

We agree that safe starches are a more useful part of the diet than fruits and vegetables:

[E]ating starchy plants is more important for nutrition than eating colorful leafy greens …

I view most non-starchy fruit with indifference. In reasonable quantities it is fine but it won’t save your life either. I like citrus now and then myself, especially grapefruit. But better to rely on starchy vegetables for carbohydrate intake than fruit.

We agree on the optimal amount of carbs to eat:

I personally eat around 30% carbohydrate now and have not gained an ounce from when I ate 10-15% (and I have eaten as high as 40% for over a year also with zero fat gain) If anything I think even wider ranges of carbohydrate intake are healthy.

One can probably eat well over 50% of calories from starchy plant organs as long as the animal foods you eat are of high quality and micronutrient content.

I think being slightly low-carb, in the sense of eating slightly below the glucose share of energy utilization which I estimate at about 30% of energy, is optimal. However, I think we are metabolically flexible enough that a very broad range of carb intake may be nearly as good. I would consider 10% a minimal but healthy intake of carbs, and 50% a higher-than-optimal, but still healthy, intake so long as the carbs are “safe” and the diet is nourishing.

Differing Origins of Our Ideas

Kurt mentions that his ideas are more derived from ethnography and anthropology than mine.

I give great weight to evolutionary selection as an indicator of the optimal diet, and am friendly to ethnographic and anthropological arguments. If I don’t give tremendous weight to such arguments, it’s because I think some other lines of argument give us finer evidence about the optimal diet.

Here, from a paper by Loren Cordain et al [1], are representations of hunter-gatherer diets:

The top graph shows plant food consumption by calories, the bottom graph animal+fish consumption by calories. The numbers are how many of 229 hunter-gatherer societies ate in that range. Typically, hunter-gatherers got 30% of calories from plant foods and 70% of calories from animal foods.

I think the Cordain et al data supports my argument that obtaining 20% to 30% of calories from carbs is probably optimal. However, it’s hardly decisive. There is considerable variability, mainly in response to food availability in the local environment. Inuits, who had few edible plants available, ate hardly any plant foods; tropical tribes with ready access to starchy plants, fruits, and fatty nuts sometimes obtained a majority of calories from plants.

Hunter-gatherer diets, therefore, are a compromise between the diet that is healthy and the diet that is easy to obtain. A skeptic could argue that hunter-gatherers routinely ate a flawed diet because some type of food was routinely easier to obtain than others, and thus systematically biased the diet.

I believe evidence from breast milk is both more precise about what diet is optimal, and much harder for skeptics to refute. Breast milk composition is nearly the same in all humans worldwide, and it has been definitely selected to provide optimal nutrition to infants.

So breast milk, I think, gives us a much clearer indication of the optimal human diet than hunter-gatherer diets. It is an evolutionary indicator of the optimal diet, but it is not ethnographic or anthropological.

There are other evolutionary indicators of the optimal diet — mammalian diets, for instance, and the evolutionary imperative to function well during a famine — which, as readers of our book, we also use to determine the Perfect Health Diet. So, while I think ethnographic and anthropological findings give us important clues to the optimal diet, I think there are plenty of other sources of evidence to which we should give weight. Fortunately, all of these sources of insight seem to be consistent in supporting low-carb animal-food-rich diets — a result which is gratifying and should give us confidence.

Food Reward and Obesity

Kurt seems to have been more persuaded than I am by Stephan Guyenet’s food reward hypothesis (which is, of course, not of Stephan’s creation – it is the dominant perspective in the community of academic obesity researchers). Kurt writes:

Low carb plans have helped people lose fat by reducing food reward from white flour and excess sugar and maybe linoleic acid. This is by accident as it happens that most of the “carbs” in our diet are coming in the form of manufactured and processed items that are simply not real food. Low carb does not work for most people via effects on blood sugar or insulin “locking away” fat. Insulin is necessary to store fat, but is not the main hormone regulating fat storage. That would be leptin.

I agree with Kurt in rejecting what he calls the carbohydrate-insulin hypothesis of obesity, but I am uneasy at the confident assertion that “reducing food reward” is the mechanism by which excluding flour, sugar, and omega-6 fats helps people lose weight.

Let me say first that there is no doubt that the brain has a food reward system that regulates food intake, and also an energy homeostasis system that regulates activity and thermogenesis, and that these systems are coupled. The brain is the coordinating organ of metabolic activity. And the brain’s food reward and energy homeostasis systems are altered in obesity.

But the direction of causality is unclear. Is “reducing food reward” the best strategy against obesity, or is “maximizing food reward with nourishing food” the best strategy?

Some data may illustrate what I mean. Here’s an investigation of how the food reward system in rats controls appetite to regulate protein and carbohydrate consumption. The data is from multiple studies and was collected by Simpson and Raubenheimer [2].

Rats were given a chow consisting of protein and carbohydrate in varying proportions. The figure below shows how much of the protein-carb chow they ate.

I’ve drawn a kinked blue line to show what a “Perfect Health Diet” analysis would consider optimal. Protein needs consist of a fixed amount of protein, around 70 kJ, to meet structural needs, plus enough protein to make up any dietary glucose deficiency via gluconeogenesis. Glucose is preferable to protein as a fuel. Glucose needs in rats are in the vicinity of 180 kJ. When dietary glucose intake falls short of 180 kJ, rats eat extra protein; they seek to make carb+protein intake equal to 250 kJ so they can meet both their protein and carb needs, with gluconeogenesis translating the dietary protein supply into the body’s glucose utilization as necessary.

As the data shows, the food reward system in rats seems to organize food intake to precisely match this:

  • When the chow is low-carb, the food reward system directs rats to eat until carb+protein intake is precisely 250 kJ – then they stop eating.
  • When the chow is high-carb, the food reward system directs rats to eat until protein intake is precisely 70 kJ – then they stop eating.

I interpret this to show that the food reward system evolved to optimize our health, and in healthy animals does an excellent job of getting us to eat in a way that achieves optimal health.

Note that if the chow is high-carb, rats eat more total calories. Is this because their diet has “high food reward”? No, it is because it is malnourishing. It is protein deficient.

Now, a diet of wheat, sugar, and omega-6 fats is malnourishing. There are any number of nutrients it is deficient in. So the food reward system ought to persuade people to eat more until they have obtained a sufficiency of all important nutrients, and rely on the energy homestasis system to dispose of the excess calories in one way or another. But if the energy homeostasis system fails to achieve this, then obesity may be the result.

If this picture is correct, then what is the solution to obesity? Is it to eat a diet that is bland and low in food reward? I don’t think so; the food reward system evolved to optimize our health. Rather the diet that defeats obesity will be one that is efficiently nourishing and maximally satisfies the food reward system at the minimum possible caloric intake.

A good test of these two strategies is the severely calorie (and nutrient) restricted diet. It would be hard to conceive of a diet lower in food reward than one with no food at all. Yet severe calorie restriction produces temporary weight loss followed by regain – often to even higher weights. This “yo-yo dieting” cycle may be repeated many times. I think this proves that at least some methods of “reducing food reward” – the malnourishing ones – are obesity-inducing.

So I would phrase the goal of an anti-obesity diet as achieving satisfaction of the food reward system, rather than as reducing food reward; and would say that wheat, sugar, and seed oils are obesogenic because they fail to provide genuine food reward, and thus compel the acquisition of additional calories.


Jimmy Moore is friends with the smartest people in the low-carb movement, so this discussion is sure to be interesting. I’m grateful that he’s persuaded people to comment on Shou-Ching’s and my ideas, and I’m eager to hear what Jimmy’s experts have to say.

One thing I’m sure of, the discussion will help us understand the many open issues in low-carb science. It should be a lot of fun!


[1] Cordain L et al. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr 2000 Mar;71(3):682-92.

[2] Simpson SJ, Raubenheimer D. Obesity: the protein leverage hypothesis. Obes Rev. 2005 May;6(2):133-42.

Serum Cholesterol Among Hunter-Gatherers: Conclusion

So far we’ve looked at serum cholesterol among Eskimos/Inuit (Serum Cholesterol Among the Eskimos and Inuit, July 1, 2011) and !Kung San bushmen (Serum Cholesterol Among African Hunter-Gatherers, July 5, 2011). The Inuit, who live in the Arctic and eat a high-fat low-carb diet, generally had serum TC over 200 mg/dl unless parasitic diseases were common and life expectancy was short. The !Kung San, who live in sub-Saharan Africa and eat more carbs, were below 160 mg/dl and ridden with parasitic diseases and short life expectancy.

I thought I’d wrap up the hunter-gatherer cholesterol series by looking at some tropical populations outside Africa. These peoples may help us evaluate the merit of several explanations that have been put forth for variations in serum cholesterol:

  • Genetic differences. Africans tend to have lower cholesterol than non-Africans, wherever they live. Is the difference genetic? Chris Masterjohn believes genetic differences might account for up to a 30 mg/dl difference in TC. Emily Deans suggests LDL receptor variants are the most important alleles.
  • Dietary differences such as fat intake. For decades it was said that higher fat diets produce higher TC, and this was the favored explanation for variations in serum cholesterol. However, when these ideas were tested in clinical trials, diet-induced changes in TC were inconsistent.
  • Infectious disease burden. Eukaryotic pathogens such as protozoa, worms, and fungi – ie, pathogens that have mitochondria and therefore can metabolize fat and ketones – are often able to take up human lipoproteins from blood and use their fats and cholesterol for their own purposes. This tends to lead to low TC in people with a high burden of parasites. Is parasite burden the key to hunter-gatherer cholesterol levels?

We started this detour (see Did Hunter-Gatherers Have Low Serum Cholesterol?, June 28, 2011) to evaluate the claims of S. Boyd Eaton, Loren Cordain, and collaborators [1], [2], [3], [30]. Their papers tended to promote the following syllogism:

  1. Diet determines TC.
  2. Low TC is healthy.
  3. Hunter-gatherers had low TC.
  4. Therefore, hunter-gatherer diets are healthy.

So to conclude today’s post, I’ll review: Which of these four theses is supported by the data?

Australian Aborigines

There are a fairly large number of papers on cholesterol levels in Australian aborigines. Unfortunately, the vast majority are from journals, such as the Medical Journal of Australia and the Australian and New Zealand Journal of Medicine, to which I don’t have electronic access.

Therefore I’ll just cite one, a 1957 paper from Schwartz et al in the Australian Journal of Experimental Biology and Medical Science. [31]

This paper looked at aborigines from central Australia. Occupying marginal territory, they were still living a hunter-gatherer lifestyle. But there weren’t many animal foods available, nor seafoods:

The animal fat intake of the Central Australian aborigines from the Haast’s Bluff region involved in this present study is decidedly low when compared with the average intake of white Australians. This low intake of fat results both from a scarcity of fat itself, and also from demands made upon available supplies by native customs. It is likely that the males eat more animal fat than the females, because of their readier access to it after hunting, but the difference is probably small. Wichitty grubs (larvae of several species of Xyleutes moths) are an important source of fat for both women and children, however. Somewhat less than 10 p.c. of the calories in the aboriginal diet is derived from animal fat, i.e. less than one-third of the calories so derived in the white Australian diet (N. B. Tindale, personal communication). [31]

To get even 10% of calories from animal fat, they had to eat a lot of grubs.

So did this low-fat diet produce high or low cholesterol?

Serum cholesterol: … There is no significant difference between the mean values for aboriginal male (217.0 mg/dl) and aboriginal female (207.9 mg/dl). [31]

This is right in line with the levels in Eskimos and Inuit, and in the minimum mortality range of 200 to 240 mg/dl.

Australian aborigines were said to have a mean TC of 146 mg/dl (male) and 132 mg/dl (female) in Eaton et al [1]. Australian aborigines were deleted from the list of hunter-gatherers with low cholesterol in a subsequent Cordain et al paper [2]. I don’t know why this was, but I can say that at least some Australian aboriginal populations had TC over 200 mg/dl.


Kitavans preserved their hunter-gatherer lifestyle until recently, and Staffan Lindeberg and colleagues were able to assess cholesterol levels using modern procedures. They reported serum total cholesterol in men of 4.7 mmol/l (182 mg/dl) and in women of 6.1 mmol/l (236 mg/dl), for a male-female average of 5.4 mmol/l (209 mg/dl). [32]

Health in Kitava was generally good, although life expectancy was only 45 years [33]. Causes of death were infectious disease (notably malaria) and accidents such as drowning and falling from coconut trees.

So we have another tropical, high-carb population with normal (200 to 240 mg/dl) serum cholesterol.

New Zealand Maoris

New Zealand Maoris are probably genetically similar to Australian aborigines and Kitavans. I didn’t survey the literature on New Zealand Maoris. However, I did come across one paper [35] that led me to an interesting 1980 study of Maoris by Dr Robert Beaglehole [36].

The study was quite simple:

The relation between serum cholesterol concentration and mortality was studied prospectively over 11 years in 630 New Zealand Maoris aged 25-74. Serum cholesterol concentration was measured at initial examination in 1962-3 in 94% of the subjects and whether each was dead or alive was determined in 1974. The causes of death were divided into three categories: cancer, cardiovascular disease, and “other.” [36]

Mean serum cholesterol was 5.50 mmol/l (213 mg/dl) among women, 5.82 mmol/l (225 mg/dl) among men, for a population mean of 219 mg/dl.

Dr Beaglehole found that mortality increased as serum cholesterol decreased. Mortality was 40% to 70% higher in Maoris with TC of 160 mg/dl than in Maoris with TC of 260 mg/dl.

The association with cancer mortality was strongest: cancer mortality was 9.6% among the low-TC group (TC < 5.1 mmol/l = 197 mg/dl), 5.8% among the medium-TC group, and 3.5% among the high-TC group (TC > 5.8 mmol/l = 224 mg/dl).

West Malaysian aborigines

Just to balance the above studies I looked for a paper showing low serum cholesterol in an aboriginal population. I found a 1972 paper by Burns-Cox et al studying aborigines in West Malaysia. [37]

Like other traditional populations living active lives, these aborigines were lean and free of heart disease. They ate a high-carb diet:

Coronary heart disease has never been found in Malaysian aborigines. We report the position regarding some of the risk factors usually associated with coronary heart disease in 73 adult aborigine men.

They lived a physically active life on a diet largely of unrefined carbohydrate in the jungles of central West Malaysia. None was obese and blood pressures remained low at all ages. [37]

Their serum cholesterol levels were low – 141 to 156 mg/dl:

While the mean serum cholesterols were low, varying between 141 and 156 mg/100 ml at different ages, the mean fasting serum triglyceride levels of 135 to 164 mg/100 ml were comparable with those found in the West. This may have been due to their high carbohydrate intake. [37]

They were mostly healthy – except that they were infested with intestinal worms and malaria:

The aborigines are thin, extremely fit physically, and for many centuries have lived in the dense hilly jungles of central West Malaysia. They have a high rate of infestation with intestinal worms and malaria but appear well nourished. Their diet consists chiefly of hand-milled rice as a staple, supplemented with cassava, millet, maize, fish, and fruit, nearly all of which they grow or gather themselves. Dairy produce is taken only in very small quantities in the form of reconstituted powdered milk and it is the large volume of starchy foods which accounts for their bulky diet. [37]

Once again, we find that low serum cholesterol is associated with a high burden of eukaryotic pathogens.

Another feature that this population shares with the !Kung San is small stature. Mean averaged 5’1” (155 cm) in height and averaged 105 lb (48 kg) in weight.


Let’s look at the four parts of the syllogism I’ve attributed to Eaton and Cordain:

Diet determines TC. Wrong. It looks like burden of parasites is the major determinant of serum cholesterol in hunter-gatherers and human populations globally.

Low TC is healthy. Wrong. It is associated with high infectious burden, small stature, high mortality, and short lifespan.

Hunter-gatherers had low TC. Some did, some didn’t. So let’s look at a specific claim, this from the classic Cordain-Eaton paper from 2002, “The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic” (thanks, Rob!):

Over the past 64 y, anthropological research has consistently demonstrated relatively low serum cholesterol and triaglycerol levels among indigenous populations that derive the majority of their diet from animal products. [30]

Wrong. Anthropological research has not consistently demonstrated low serum cholesterol and triglycerol levels from hunter-gatherers, regardless of whether the primary dietary source was animals (Eskimo/Inuit) or plants (Kitavans, Central Australian aborigines). Rather, those with high parasite burdens had low cholesterol, regardless of diet, and healthy populations without parasites had serum cholesterol over 200 mg/dl regardless of diet.

Therefore, hunter-gatherer diets are healthy. True! Except insofar as dietary practices, such as the Eskimo practice of eating raw intestines from recently killed animals, predisposed them to picking up parasitic infections.

Overall I think the data should dispose us to look toward infectious burden, rather than genetics or diet, as the primary determinant of serum cholesterol among hunter-gatherers. If genetic differences influence mean TC among hunter-gatherer populations, it is probably because of evolutionary adaptations to local pathogens, such as the heavy parasite burden in sub-Saharan Africa.

Related Posts

The posts in this series are:


[1] Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49. Full text:

[2] O’Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.

[3] Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010 Dec;25(6):594-602. Full text:

[30] Cordain L et al. The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S42-52.

[31] Schwartz CJ et al. Serum cholesterol and phospholipid levels of Australian aborigines. Aust J Exp Biol Med Sci. 1957 Oct;35(5):449-56. Full text:

[32] Lindeberg S et al. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J Intern Med. 1994 Sep;236(3):331-40.

[33] Lindeberg S et al. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study. Am J Clin Nutr. 1997 Oct;66(4):845-52.

[35] Walker AR. Cholesterol and mortality rates. Br Med J. 1980 May 31;280(6227):1320.

[36] Beaglehole R et al. Cholesterol and mortality in New Zealand Maoris. Br Med J. 1980 Feb 2;280(6210):285-7. Free full text:

[37] Burns-Cox CJ et al. Risk factors and the absence of coronary heart disease in aborigines in West Malaysia. Br Heart J. 1972 Sep;34(9):953-8.

Serum Cholesterol Among African Hunter-Gatherers

We’re in the midst of a little diversion looking at the cholesterol levels of hunter-gatherers around the world. This investigation was precipitated by the surprising claim by some Paleo authorities that hunter-gatherers had much lower cholesterol levels than any modern human population (Did Hunter-Gatherers Have Low Serum Cholesterol?, Jun 28, 2011).

We started by looking at Eskimos and Inuit (Serum Cholesterol Among the Eskimos and Inuit, July 1, 2011). We found that healthy Eskimo and Inuit groups seem to consistently have mean serum cholesterol between 200 and 230 mg/dl, with lower mean serum cholesterol levels found only in short-lived populations suffering from tuberculosis and parasite infections.

Today we’ll look at the populations with the lowest reported serum cholesterol levels: African hunter-gatherers. Africans made up 3 of the 5 groups claimed to have low serum cholesterol in the original Eaton et al paper [1] and 4 of the 5 in the later Cordain et al paper [2].

Cholesterol levels in modern Africans

Before looking at African hunter-gatherers, I think it’s worthwhile to look at modern Africans and African-Americans.

African nations have the lowest serum cholesterol levels and highest mortality levels in the world:

  • The 39 sub-Saharan African countries in O Primitivo’s cholesterol database have an average serum total cholesterol (TC) of 165.7 mg/dl (4.285 mmol/l). For comparison, the other 122 nations have an average serum TC of 201.1 mg/dl (5.20 mmol/l).
  • When the 161 countries in the database are ranked by mortality, sub-Saharan African nations occupy all but three of places 123 through 161. The non-African nations with highest mortality are Laos (#130), Cambodia (#131), and Haiti (#137). Haiti’s population is 95% of African descent, by far the largest African population share in the Americas. The only sub-Saharan African nations ranking above #123 are the island nations of Cape Verde, Comoros, and Sao Tome and Principe.

Here are the nations in O Primitivo’s database. Sub-Saharan African countries are in blue, others in red:

Sub-Saharan African TCs cluster around 165 mg/dl, while in the rest of the world varies much more widely but generally ranges between 170 and 240 mg/dl. The only countries outside sub-Saharan Africa with a mean TC below 170 mg/dl are Bangladesh and Tunisia.

Now, African-Americans. Here are mean serum cholesterol levels from the various NHANES studies:

Mean serum cholesterol levels (mg/dl) in Americans age 20-74 from NHANES

Group 1960-1962 1971-1974 1976-1980 1988-1994 1999-2000
All 222 216 215 205 204
Whites 222 216.5 214.5 205 205
Blacks 215.5 216.5 213 202.5 195.5
Hispanics 209 205 202.5

This table makes visibly clear the triumph of modern medicine: mean serum cholesterol levels have been heroically brought down from 222 mg/dl in 1960 to 204 mg/dl today.

This data is useful, because African-Americans eat a diet similar to that of other Americans. They are also, by global standards, fairly healthy. All-cause mortality in 2005-7 in Contra Costa, California (a quick search failed to bring up numbers for the US as a whole) was 683.9 per 100,000 for whites and 1002.7 for blacks (Source).

If we look above at O Primitivo’s data, a mortality of 1002.7 is lower than that of any sub-Saharan African nation and would suggest a TC around 195 mg/dl – right where African-Americans are today. White mortality of 683.9 would suggest a mean TC between 200 and 220 – right where white Americans are.

To me, this data suggests:

  • If there is a genetic difference in Africans that lowers cholesterol, it’s not large – probably less than 10 mg/dl.
  • Africans fit spot-on the cholesterol vs mortality curve established by non-African nations. So if there are genetic differences in Africans, they haven’t altered the mortality risk of low cholesterol levels.
  • In any ethnicity or race, low serum cholesterol indicates impaired health – probably due to infections – and higher mortality.

In interpreting the serum cholesterol of African hunter-gatherers, we should keep in mind this pattern. Low TC is probably only minimally a matter of genetics or diet. It’s primarily about infectious burden.

Now let’s look at African hunter-gatherer populations. Unfortunately, there is a paucity of data in Pubmed.


A search in Pubmed for “Hadza cholesterol” produces one paper [4]. Unfortunately it dates from 1972 and electronic availability for that journal begins in 2001, so I was unable to read it.

Congo Pygmies

There are no papers in Pubmed searches for “pygmy cholesterol” or “pygmies cholesterol,” nor does “Congo cholesterol” return anything resembling a hunter-gatherer cholesterol study.

According to Wikipedia (“Pygmy peoples”), “The best known pygmies are the Aka, Efé and Mbuti of central Africa.” However, “Aka cholesterol,” “Efé cholesterol,” and “Mbuti cholesterol” return no results either.

!Kung San, Khoisan, Kalahari San, Bushmen

These people may be referred to by a variety of names, as Wikipedia (“Bushmen”) notes:

The indigenous people of southern Africa … are variously referred to as Bushmen, San, Sho, Barwa, Kung, or Khwe. These people were traditionally hunter-gatherers, part of the Khoisan group …

Searching on all these terms, I was able to find only a few reports on cholesterol levels, not all of whom were eating the hunter-gatherer diet. Here’s a summary.

Cholesterol Levels of San Bushmen

Paper [ref] Mean TC Notes
Miller et al 1968 [23] 77 mg/dl Stale samples, poorly preserved samples, “difficult” technique not normally used for cholesterol measurement
Truswell & Hansen 1968 [24] 110 mg/dl Stale unfrozen samples, obsolete technique
Bersohn & Tobias 1966 123 mg/dl Unknown technique; reported by Truswell & Hansen [24]; farm bushmen were 145 mg/dl.
Tichelaar et al 1992 [26] 143 mg/dl Semi-settled
van der Westhuyzen J et al. [21] 158 mg/dl Semi-settled

Early reports showed the lowest TCs. The one from Klara Miller and colleagues in the Archives of Internal Medicine of 1968 [23], is not available to me as full text, but this is the abstract:

Samples of the plasma from nine male adult bushmen were analyzed for their lipid content. The mean results obtained (total cholesterol = 77 mg/100 ml, phospholipids = 107 mg/100 ml, and triglycerides= 49 mg/100 ml) were extremely low. The probable reasons for this finding are the very low dietary fat content and habitually high physical activity of Kalahari bushmen. [23]

These numbers are extraordinarily low for both TC and serum phospholipids.

My other early source was a 1968 letter to Lancet by Truswell and Hansen [24] commenting on the Miller et al report:

SIR,-We can add some more data to the values for serum lipids in 9 Kalahari bushmen which you reviewed in your annotation (Aug. 17, p. 395). Our findings confirm that these hunter-gatherers have among the lowest serum-cholesterol levels in the world.

In October, 1967, and again in April-May this year we joined the Harvard social anthropologists De Vore and Lee to investigate the medical and nutritional state of the !Kung bushmen they have been studying in the northern Kalahari, Botswana. We collected venous blood from some of these bushmen. Sera were allowed to separate by clot-retraction and decanted into tubes containing a little dried methiolate solution. The sealed serum-tubes were kept in a portable gas refrigerator while we were in the desert and were carried with us in a cool box, with ice-packs, when we travelled back to Cape Town by jeep and plane. Cholesterol was measured by the standard Abell method.

The results of 67 determinations in 54 bushmen are shown in the accompanying table. The mean serum-cholesterol levels were between 100 and 121 mg. per 100 ml. The extreme range in individual bushmen was from 57 to 178 mg. per 100 ml. A Bantu control serum collected in the desert on our first visit contained 166 mg. cholesterol per 100 ml. Our own serum-cholesterol levels, taken on the second visit, were 184 and 219 mg. per 100 ml….

Our values agree very well with the mean serum-cholesterol level of 121 mg. per 100 ml. reported by Bersohn and Tobias [Tobias, P. V. in The Biology of Human Adaptability (edited by P. T. Baker and J. S. Weiner); p. 190. Oxford, 1966.] in nomadic bushmen in the central Kalahari. These workers found that farm bushmen had rather high serum-cholesterol levels, averaging 145 mg. per 100 ml.

The lower concentrations found by Miller et al., averaging 77 mg. per 100 ml., might have resulted from the more difficult quantitative method they used, involving recovery from thin-layer chromatographic plates or, as they suggest, from harsher conditions in the southern Kalahari….

Some bushmen in the northern Kalahari obtain milk from Herero tribesmen who manage to keep cattle and have now settled between the bushmen in the same area. The 5 Dobe adults who said they got moderate amounts of milk had a mean cholesterol of 130 mg. per 100 ml., compared with 108 mg. per 100 ml. in 5 who drank little milk, and 114 mg. per 100 ml. in the 10 who were eating pure bush food. Most of the bushmen’s dietary fat probably comes from nuts, such as mongongo or mangetti (Ricinodendron rautanenii), which Lee estimates to be the largest source of calories in the Dobe region. They contain 38-58% fat.’

It looks like we have 3 reported measurements in San hunter-gatherers: 77 mg/dl by Miller et al, about 110 mg/dl from Truswell and Hansen, and 121 mg/dl from Tobias. All are remarkably low, far below the levels found in any contemporary population.

In all cases the samples were stored for weeks or months before being measured far from the place they were drawn – a thousand miles away in Cape Town in the case of Truswell & Hansen. Because the region lacked electricity, it was impossible to keep the samples frozen and difficult to keep them cool. In Miller’s case, the method is described as “difficult.”

We concluded from the study of Eskimos by Corcoran and Rabinowitch 1937 (Serum Cholesterol Among the Eskimos and Inuit, July 1) that stale samples preserved for a long journey and then measured by the method of Abell can produce false, low cholesterol readings. That may have happened also in the case of the three San investigators.

By the 1990s, sample and measurement techniques were greatly improved. Here are the methods used in a 1992 paper by Tichelaar et al [26]:

Blood samples were taken in heparinized containers, and separated plasma samples were deep-frozen until analysis could be carried out, which was always within two weeks. Total cholesterol (TC) and triacylglycerol (TAG) concentrations were determined enzymatically (Boehringer Mannheim GmbH Diagnostica, Mannheim, Germany; CHOD-PAP and GPO-PAP kits, respectively). [26]

Heparinized sample tubes, deep-frozen samples, measurement within two weeks, and enzymatic measurement in modern kits – none of these were features of the earlier lipid measurements on !Kung San hunter-gatherers.

Tichelaar et al studied young adult Bushmen, Hereros and Kavangos. The Bushmen were “in transition”:

The Bushmen studied were no longer purely nomadic; most of them live for variable times in association with Herero villages, but tend to migrate from one place to another depending upon work and food availability. They are accordingly very much “in transition.” [26]

Mean serum cholesterol was 3.71 mmol/l (143 mg/dl) in Bushmen, 4.21 mmol/l (163 mg/dl) in Hereros, and 3.61 mmol/l (140 mg/dl) in Kavangos. These numbers are low, but not as low as the numbers quoted by Eaton et al [1]. They are also not far removed from those of South African Xhosas and Vendas, who measured 4.08 and 4.23 mmol/l respectively (158 and 164 mg/dl). [26]

The Tichelaar sample of Bushmen had an average age of 29. Their plasma fatty acids were relatively good: omega-6 fatty acid levels were far below those of South African whites (9.3% vs 24.4%), and they had the highest EPA:AA ratio among the African groups. However, they drank 2 to 4 liters per day of home-brewed beer, and “vegetable and fruit consumption is little to none at all.” [26] No specific health statistics are given, but Tichelaar indicate that the infectious disease burden was high:

The change from their traditional lifestyle has resulted in a high incidence of malnutrition (9), especially reduced fat and protein stores (70% and 75%, respectively). The severe malnutrition is primarily responsible for the predominance of infectious disease in Bushmen, especially tuberculosis (9). One fact that was extremely clear was the high incidence of alcoholism.

A 1987 study by van der Westhuyzen et al from the Journal of Tropical Medicine and Hygiene [21] corroborates the picture provided by Tichelaar et al. They studied a settled population of !Kung San in Namibia. They confirm that alcohol abuse and malnutrition (including thiamin deficiency) were widespread. Mean serum cholesterol was 4.1 mmol/l (158 mg/dl) [21].

I got a little more insight into the health of settled !Kung San from another 1984 study [22]. It provides details about the timing and health effects of the transition from hunter-gatherer to settled lifestyle:

In 1969 we carried out a study of iron, folate, and vitamin B12 nutrition in a group of!Kung living a hunter-gatherer existence in the Kalahari desert in northwestern Botswana (1). We now report on a study of a comparable group of !Kung who have followed a settled way of life in Chum!kwe, Namibia, some 40 km west of the area ofthe original study (Fig 1).

This group, who are genetically and linguistically identical (2) to the subjects of the previous study (1) have resided at Chum!kwe for at least 15 yr. At Chum!kwe they underwent slow change during the 1960’s and now constitute a settled population which has ceased to hunt game or gather wild vegetation. The men undertake casual employment and food is purchased from local stores, or provided by Government agencies. The diet consists predominantly of maize, supplemented with small and irregular quantities of meat and vegetables, a diet which resembles that of the Black peoples inhabiting the rural areas ofSouthern Africa.

The subjects comprised a group of !Kung San (Bushmen) who, until relatively recently, were hunter-gatherers inhabiting the northwestern Kalahari (Fig 1). All the subjects now reside at Chum!kwe in Namibia 40 km to the west, where they have resided for at least 15 yr….

The diet of the San has changed considerably in the period since the previous study in 1969 (1). The staple food, commercial maize meal, is eaten as a porridge or fermented with cane sugar to make beer. Frequently, this porridge or beer is the only food consumed in a day. This basic diet is supplemented irregularly with canned fruit, vegetables, and meat. One family cultivated a few melons and squashes, but pastoralism is practised on such a small scale as to be negligible. There appears to be a high consumption of alcoholic beverages by the community, and beer, either homebrewed or commercial, is consumed by all members of the society, even very young children. The former is brewed in plastic containers.

Marshall and Ritchie (3) have reported on the economy of the Chum!kwe !Kung as they found it in 1981 and they have compared it with that existing in 1958 when the people still followed a hunting and gathering way of life. This latter way of life is described by Marshall (2). In 1981 the bulk of their dietary needs were met by purchases from the local store: made up of coffee, flour, sugar, maize meal, and canned foods; consisting of maize beer, and a small amount (<1%) of liquor. A smaller proportion of their diet came from Government agencies, and very little animal husbandary, gardening, and the gathering of wild fruits and vegetables. A negligible part of their diet came from hunting activities.

When one considers that in 1958, much of these people’s dietary intake came from the hunting of wild animals it will be appreciated that major changes have occurred….

Until 1980 !Kung inhabitants of Chum!kwe had lived in traditional settlements, well spaced from one another. In that year the government established three housing schemes or townships, consisting of 23, 18, and 14 single roomed houses built from cinder blocks with communal pit type lavatories and bathhouse and a single water tap situated in the centre of the township.

The people spend most of their time outside the houses and, in fact, do their cooking on, and sleep around, a fire which they light in front of the house, facing the central courtyard. The lavatories are never used because the inhabitants walk off into the surrounding bush to relieve themselves. Litter and refuse accumulate in these townships. We have observed that many of the traditional settlements in Chum!kwe moved twice, some moved three times, between August 1980 and December 1981. As a result, those that do move tend to be cleaner than the Government housing projects….

The present study has shown that the change in lifestyle undergone by the San between 1969 and 1981 has been accompanied by a deterioration in their previously excellent iron and folate nutrition and in an increase in the incidence of anemia, most of which is almost certainly nutritional in origin. Alcoholism, previously unknown, has become a major problem.

It is probably not feasible for the San to return to a hunter-gatherer existence because the available land could support only a fraction of the present populations in that mode; neither do the San wish to return to the past. [22]

So the transition to settled life occurred in the 1960s. The !Kung San now depend on government support. Their diet is corn porridge, corn beer, wheat and sugar. They are malnourished and show signs of liver damage. Their settlements are filthy, so much so that they don’t use the lavatories; when a settlement becomes intolerable they create a new one; some communities moved three times in 16 months.

Let me record here two other facts about the !Kung San that may be relevant:

  • They are small — comparable in height and weight to Central African pygmies. The average height of Bushmen males is 158 cm (5 foot 1 inch), and average weight is 46 kg (101 pounds). The average height of Bushmen females is 145 cm (4 foot 9 inch), and average weight is 38 kg (83 pounds). [27]
  • They are short-lived . The life expectancy of !Kung San in the period 1963-1974, which spans the period of transition from hunter-gatherer to settled life, may have been a bit over 50 years – or, conceivably, as low as 35 years:

How shall we interpret this?

First, let’s consider the recently acquired numbers of 143 and 158 mg/dl, which used modern measurement techniques on well-preserved samples and should be trustworthy.

These numbers are precisely what we would expect from an infection-ridden African population with short (~50 year) lifespan. Most sub-Saharan African countries with high infectious disease burdens and shortened lifespan have mean population serum cholesterol close to this.

For instance, Mauritania has mean serum cholesterol of 157 mg/dl. Life expectancy in Mauritania is 61 years. Nigeria has mean serum cholesterol of 136.9 mg/dl and a life expectancy of 47.6 years. Cameroon has mean serum cholesterol of 120.9 mg/dl – the lowest in the world – and a life expectancy of 54 years. Infectious disease risk is rated high in Mauritania and very high in Nigeria and Cameroon.

If TCs among the settled !Kung San meet our expectations, where does this leave us in regard to  to the low serum cholesterol reported for the hunter-gatherer San in the 1960s? My expectations would be:

  • If San hunter-gatherers were healthier than the settled !Kung San, then their serum TC should have been higher than the settled !Kung San TC of 143 to 158 mg/dl. In this case the 1960s measurements would have to be in error.
  • On the other hand, if San hunter-gatherers were sicker than the settled San, then a TC of 120 – similar to that of modern Cameroon – or even lower becomes plausible.

I don’t think either possibility can be ruled out.

The hunter-gatherers may have had poor health. Although anthropologists consider malnutrition more prevalent in the settled !Kung San, their data is not sufficient to show that life expectancy or infectious disease burden became worse when the !Kung San gave up their hunter-gatherer life. And recall also the statement by Fernandes-Costa et al: “neither do the San wish to return to the past.” [22] The hunter-gatherer lifestyle seems to have been no idyll.

The data may have been wrong. If the early measurements performed on stale, poorly refrigerated samples with pre-modern techniques underestimated !Kung San hunter-gatherer TC by 33%, a plausible estimate for the amount by which Corcoran & Rabinowitch 1937 may have underestimated Eskimo TC, then it would bring the measurements of Truswell & Hansen [24] and Bersohn & Tobias right in line with modern-day African TCs.


The !Kung San provide some support to the claims in Eaton et al [1] that hunter-gatherers had low serum cholesterol.

However, the data offers no support to the thesis, argued vigorously in O’Keefe et al [2], that low serum cholesterol levels are healthy. Rather, the evidence from Africa is that low serum cholesterol levels reflect a high burden of infectious disease, especially parasitic disease, and are invariably associated with shortened lifespan.

African hunter-gatherer serum cholesterol levels were probably below 160 mg/dl, maybe well below, and their low cholesterol levels marked a lifespan that was little more than 50 years.

Related Posts

The posts in this series are:


[1] Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49. Full text:

[2] O’Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.

[3] Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010 Dec;25(6):594-602. Full text:

[4] Barnicot NA et al. Blood pressure and serum cholesterol in the Hadza of Tanzania. Hum Biol. 1972 Feb;44(1):87-116.

[21] van der Westhuyzen J et al. Thiamin status and biochemical indices of malnutrition and alcoholism in settled communities of !Kung San. J Trop Med Hyg. 1987 Dec;90(6):283-9.

[22] Fernandes-Costa FJ et al. Transition from a hunter-gatherer to a settled lifestyle in the !Kung San: effect on iron, folate, and vitamin B12 nutrition. Am J Clin Nutr. 1984 Dec;40(6):1295-303.

[23] Miller K et al. Lipid values in Kalahari bushmen. Arch Intern Med. 1968 May;121(5):414-7.

[24] Truswell AS, Hansen JD. Serum-lipids in bushmen. Lancet. 1968 Sep 21;2(7569):684.

[26] Tichelaar HY et al. Plasma lipids and fatty acids in urbanized Bushmen, Hereros and Kavangos of southern Africa (Namibia). Lipids. 1992 Sep;27(9):729-32.

[27] Joffe BI et al. Metabolic responses to oral glucose in the Kalahari Bushmen. Br Med J. 1971 Oct 23;4(5781):206-8.