The Case of the Missing Extinctions

Or, The Pleistocene Extinctions Pattern Implications For Understanding Human Evolutionary Nutrition

Prior to fifty thousand years ago, before the Pleistocene extinctions, ancestors of modern humans lived in Africa.   Modern man, Homo sapiens sapiens, emerged in Africa, before these extinctions. 

As explained by geneticist Spencer Wells in the documentary film Journey of Man, by tracking the Y chromosome, we now know that all modern humans are descendants of a few men among the ancestors of the !Kung people currently living in the Khalahari desert. 

But in ancestral times, the Khalahari was not a desert. During the Pleistocene ice ages, “the great deserts of North Africa and Western North America today were mostly vast grasslands with large permanent lakes and abundant game animals.” [1]  

Many believe that humans evolved primarily by hunting those land animals, and take the Pleistocene extinctions as evidence that humans evolved as top predators of grassland animals in Africa.

In "Of mice, mastodons and men: human-mediated extinctions on four continents" [2], Lyons et al provide several convincing lines of evidence and reasoning that indicate that humans must have caused the Pleistocene extinctions.  To simplify, no other known natural phenomenon (such as climate change) could account for the sudden selective extinctions of the megafauna, without simultaneous extinctions of smaller species. 

But there is something very interesting about the pattern of the Pleistocene extinctions.

The following graph from Lyons et al [2] shows the pattern.  The hatched bars show the species exterminated in the late Pleistocene.  As you move from left to right, the bars represent increasingly larger species.   Notice anything unique about Africa?

On every continent where humans were an invasive species, the largest animals went extinct.  

Source:  Networkroundtable.org

But not in Africa.

There, most of the large body species survived.   

Source:  Vivagoal.com

It appears that as humans invaded Australia and the Americas they succeeded in exterminating the fat megafauna, but humans who remained in Africa did not, and many, including giraffes, elephants, and rhinos,  have remained to this day.  Why?

Lyons et al have a suggestion:

“The lack of extinctions in Africa (Fig. 1) is especially notable given the long history of humans on this continent. The co-evolution of man with the African megafauna may have resulted in the evolution of effective anti-predator behaviours (Diamond, 1984; Martin, 1984).”[Italics added]

In other words, upper Paleolithic humans did not exterminate the megafauna of Africa because the African megafauna had plenty of experience with and knew how to avoid human predation.  Just the smell of humans probably sent them running.

Source: bioweb.uwlax.edu

  

In contrast, animals in Europe, Asia, Australia, and the Americas most likely evolved independent of human predation.  This meant that they were, for humans, relative to African fauna, ‘sitting ducks.’ 

Thus, considering the co-evolution of humans with African fauna, the fact that the extinctions did not occur in Africa supports the hypothesis that humans, as an invasive species, caused those extinctions on other continents.

It also suggests that the invasion of other continents allowed humans to pursue a subsistence strategy––hunting large, fat anmals––that would not have been as successful in Africa.

Moreover, we could reasonably take the statement by Lyons et al and modify it slightly:

The co-evolution of man with African fauna (mega or not) most likely resulted in those fauna evolving behaviors effective for avoiding human predation.

This further suggests that the human exodus out of Africa into other continents may have resulted in a significant change in human diet composition, after H. sapiens sapiens had already emerged.  In other words, it suggests that the later Paleolithic diet of humans outside of Africa may have contained much larger amounts of land animal meat and fat than would have been possible in the early Paleolithic among the far more wary wildlife of the homeland.

Let me put it this way.   An animal adapted to a diet obtained in the Africa invades a new ecosystem.  In this new ecosystem, this invasive species finds that hunting is a lot easier than it was in the homeland, because the animals are relatively oblivious to the danger presented by humans.  Consequently, in accord with optimal foraging theory, this animal goes for the easiest calories possible:  large animals that don’t know that they should run away from anything that smells, sounds, or looks like a human.

If this new diet supports health adequately to allow reproduction for a majority of individuals, but disrupts homeostasis just enough that it gradually induces metabolic disorders that emerge over time, past the time of reproduction,  or shortens the average individual’s lifespan by inducing chronic diseases, the new diet will not select against those not adapted to the new diet, nor produce a population better adaptated to the diet.

I might even call it the upper Paleolithic dietary revolution. 

Now, let’s consider Africa again.  As noted above, the great deserts of Africa were grasslands with large “permanent” lakes (well, permanent during those ages).  If hunting land animals was not as easy in Africa as in Eurasia and the Americas, what about hunting animals living in those lakes?  Would they all catch the smell of humans or run away easily?

Lacustrine, riverine, and wetland environments are very rich in food resources, both plant and animal, including animals that don't move very fast (shellfish).  Foraging in such environments might just provide greater return on investment than possible on a grassland.

Some people studying human evolutionary nutrition believe that the archaeological, cultural, nutritional, biochemical, and medical evidence points in the direction of humans evolving in those econiches, where shellfish, fish, and amphibious animals could have been the primary sources of animal foods.  These animals have nutritional properties significantly different from  those of savannah animals—the protein, fats, and mineral contents of water animals all differ significantly from land-based animals, in very interesting ways relative to specifically human nutritional requirements, particularly for the nervous and cardiovascular systems.

In fact, the earliest human fossils are consistently found associated with lacustrine or marine fossils indicating humans inhabiting niches incorporating a land-water interface:  wet woodlands, flood plains, wetlands, rivers, lakes, and coastlines.  In these two segments of the Journey of Man, we learn about archaeological evidence of humans living along the African coastline and consuming large amounts of seafoods, leaving large heaps of seashells as evidence (segment starts about 5:00 of first video):

 Also, and again, as explained in the  Journey of Man, the first exodus of humans from Africa appears to have followed a path along the marine coastline to Australia; it does not track through a grassland.   And, in this segment, we learn that some of the first humans in Australia lived in a lacustrine environment (now a desert), described as "quite a rich environment," eating fish (leaving hearths and fish bones as evidence):

Indeed, in the two segments below, Wells point out that, at the end of this journey, to get from Indonesia to Australia, it appears that people had to find a way across 150 miles of open ocean (segment starts at about 3:20 of the first video).  

The animal capable of this seafaring--150 miles of open ocean with only the most primitive of boats--would have had to have been very familiar with and physically very well adapted to a marine environment.  Not a likely accomplishment for a mammal specialized in exploiting the dry savannah environment. 

Which leads me again back to Michael Crawford and David Marsh, co-authors of Nutrition and Evolution.   Crawford, a biochemist, has devoted his life work to study of the effects of fats on human physiology, and has a bit to say on the subject and its relation to human evolution.  Some others have something to say about the differences between land and animal foods with regard to human brain nutrition.

But for now I have run out of time.  To be continued.

Melting Temperatures of Dietary Fats

Click on image for larger version.  Source:  Bettelhiem, Brown, and March:  Introduction to General, Organic, & Biochemistry, Sixth Edition.  Page 472.

The human body operates at about 95-100 degrees F. Notice that the saturated fats don't melt--i.e. become liquid--until you reach more than 110 degrees.

 The unsaturated fats all remain liquid at temperatures well below human body temperature.

Fats travel in the body packed in triglycerides:  three fatty acids bound to a glycerol backbone.  The following depicts a triglyceride composed of three saturated fatty acids:

Source:  Reducetriglycerides.com

In this picture, the little grey dots represent hydrogen atoms.  Notice that in such a triglyceride, the little grey dots lie close to each other, stacking cleanly like Lego blocks.   When triglycerides containing a high proportion of long-chain saturated fatty acids are packed close to one another, the hydrogen atoms of fatty acids on one will bond to those on another by London dispersion forces, which makes the fat firm at low temperatures; to melt it, you have to add heat to break the bonds between the hydrogen molecules.  In contrast, the following shows a triglyceride containing one unsaturated fatty acid (the one with the bend):

Source:  biology.clc.uc.edu

 In this type of triglyceride, the top two fats form bonds between 9 hydrogens, but because the bottom, monounsaturated fat has a bend in it, the middle and lower fats bond only at 6 hydrogens.  Because of this, a mix of triglycerides containing unsaturated fats have weaker bonds to one another and this makes the fat less firm; it will melt at a lower temperature.

If you substitute a polyunsaturated fatty acid for one or more of those fats, the triglyceride will form weaker bonds to others.  Also, if you use shorter chain saturated fats (e.g. coconut oil), there are fewer hydrogens available for binding, lowering the melting point of the fat.

Most dietary and endogenously produced triglycerides are like the second example, a mix of fatty acids, some saturated and some unsaturated.  Nevertheless, the higher the number of saturated fatty acids in a mix of  triglycerides, the higher its melting point.  Thus, beef tallow, a mix primarily of long-chain saturated and monounsaturated fats, has a higher melting point than coconut fat, a mix of primarily medium and short chain fats, and both of these have a higher melting point than flax oil, in which the triglycerides consist primarily of polyunsaturated fats.

This is really obvious in our experience.  Beef triglycerides are solid at room temp, and start to melt around 100 degrees.  Coconut triglycerides melt at about 75 degrees, and fish and flax triglycerides stay fluid even at temperatures below freezing. This means beef triglycerides are more viscous/less fluid at body temperature than flax triglycerides.

Similarly, compare the texture of cold raw beef to cold raw salmon.  The former is stiffer, in part because the fats in beef are more solid at refrigerator temperature than are the fats in salmon.

Nature also distributes the fats differently. Warm blooded animals and plants living in warm enviroments tend to have higher proportions of the saturated fats with higher melting points, e.g. beef and palm oils.  Cold blooded animals and plants and animals originating in cold environments tend to have higher proportions of unsaturated fats with low melting points, e.g. reptiles, salmon, and flax.  If salmon had a high proportion of saturated fats in their tissues, their bodies (muscles) would not be fluid enough to swim in Arctic oceans.  If flax plants produced saturated fats, they would not be fluid enough to transport about the flax plant in the native environment. 

The body uses different types of fatty acids specifically implementing their abilities to form more or less solid structures.  For instance, the fat pads of the palms and feet have a high proportion of saturated fats, because this makes a more firm, noncompliant structure for padding.  On the other hand, nerve membranes have a high proportion of highly unsaturated fats (specifically, arachidonic acid and DHA), presumably because these membranes must have a less firm structure in order to serve their purposes, which involve rapid fluctuations in sodium and potassium flow across the membranes.

These examples show that the melting points of fats (triglycerides) are very important in biological functions, and that nature naturally favors the use of unsaturated fats to keep things fluid and flexible, and the saturated fats to make things more stiff and noncompliant.  

Taking a look at how nature uses these fats for differential effects, we might predict that these fats will have different effects on blood flow.  increasing the amount of saturated fats in the triglycerides in mammalian blood stream will increase blood viscosity, which would impede flow of blood through the tiniest capillaries, impair delivery of oxygen and nutrients to and removal of wastes from the tissues (thus promoting ischemia and toxicity), and increase blood pressure.  Since oils in general are viscous compared to water, it also predicts that reducing total fat, or replacing high-melting-point fats with low-melting-point fats, would have the opposite effects.

Tai et al fed rats diets supplying either 10% of energy as soyabean oil (control group) or 40 % energy from soyabean oil (USFA), palm oil (SFA) and vegetable shortening (TFA) for 8 weeks.  They found:  "rats fed high-fat diets exhibited significant increases in serum TAG levels (P < 0.01), plasma viscosity (P < 0.01), whole blood viscosity (P < 0.01) and internal viscosity (P < 0.01) compared to the controls."

Hall reviewed the available data and reported that although good-quality intervention data on dietary fatty acid composition and vascular function are scarce, so far what we have indicates the following:


1) A single high-fat meal can impair endothelial function compared to a low-fat meal, apparently due to increased circulating lipoproteins and nonesterified fatty acids which may induce pro-inflammatory pathways and increase oxidative stress.

2) Cross-sectional data suggest that saturated fat adversely affects vascular function whereas polyunsaturated fat (mainly linoleic acid (18 : 2n-6) and n-3 PUFA) are beneficial.  

3) The superunsaturated, very low-melting-point fats EPA (20 : 5n-3) and DHA (22 : 6n-3) can reduce blood pressure, improve arterial compliance in type 2 diabetics and dyslipidaemics, and augment endothelium-dependent vasodilation.

Steer et al performed another human study.  Saturated fatty acids impaired endothelial function, and alpha-linolenic acid (omega-3) improved endothelial function. 

These findings alone might help explain why the Masai have atherosclerosis.  The dairy-based Masai diet would increase blood viscosity, impair blood circulation, and induce vascular tissue ischemia, oxidative stress, and inflammation, compared to a lower fat diet.

As noted by Stephan, Mann et al tried to blame the atherosclerosis of the Masai on foods other than dairy fats, based on the fact that the disease appeared prevalent only in Masai after the age of 40 years, after the Muran period during which they lived almost exclusively on dairy products.   Mann et al believed that some noxious agent introduced after the Muran period had to account for the atherosclerosis:

"We believe... that the Muran escapes some noxious dietary agent for a time. Obviously, this is neither animal fat nor cholesterol. The old and the young Masai do have access to such processed staples as flour, sugar, confections and shortenings through the Indian dukas scattered about Masailand. These foods could carry the hypothetical agent."

This line of reasoning has a major flaw: Simply, if flour, sugar, etc are the cause of the atherosclerosis, and both young and old Masai eat these things, then it should appear in both the young and the old Masai...both before and after the dairy period. But in fact, their own data, in the chart below, shows it substantially increasing in frequency only after their long period of a high fat dairy based diet.

If those non-dairy foods were the cause of Masai aortic fibrosis, and those foods were eaten by both young and old, but not those in the 20-40 age group, then the frequency of fibrosis should be high both before the Muran period (ages 10-20) and after (ages 40+).  But in fact the frequency is substantially elevated only after the Muran period.

The data actually suggests four possibilities that occur to me: Either 1) aortic fibrosis is simply a fact of life for Masai after the age of 40, due to some aging factor, or 2)  it is the 20 years of eating a high dairy fat diet that eventually causes the atherosclerosis to develop, or 3) the late life combination of dairy fats and flour etc. promotes atherosclerosis, or 4) there is some dietary factor other than the flour, etc. that promotes atherosclerosis in the aging Masai.

Given what we know about the effect of saturated fats on the viscosity of blood and endothelial function, I feel inclined to consider their high dairy fat diet a contributor to their atherosclerosis.  The fact that the frequency of fibrosis in the young Masai (under 20 years of age) is practically the same as that of the Masai during the late Muran period (30-40 years of age) argues against non-dairy foods contributing to the process.  I feel, at this time, more inclined to view their atherosclerosis as the result of 20 years of their vascular systems having to respond to high fat meals.

Song et al found that "rats on a diet rich in either saturated or unsaturated fat had higher blood pressure compared with chow-fed rats (approximately 130 vs 100 mmHg, respectively), along with hyperlipidaemia and insulin resistance."  Repeat:  High fat diets induced high blood pressure in rats, regardless of whether the diet was high saturated or high unsaturated fat.

Only a rat study?

Let's compare two human primitive populations, one with a long history of a high unsaturated fat diet--Eskimos--and one with a low fat, high carbohydrate diet--Yanomamo.
 
Andersen et al found elevated blood pressure but without modernized risk of ischemic heart disease in non-Westernized Inuit past the age of 40:

"Among the 812 Inuit aged 18 years or above blood pressure was unaltered until the age of 39 years (systolic, p=76; diastolic, p=0.36) and increased subsequently (both, p=0.001). Systolic blood pressure ≥140mmHg was more frequent when aged >40years (p=0.001) and diastolic blood pressure ≥90mmHg was more common in men (p=0.001) and in men and women aged ≥40years (p=0.001)."

"Blood pressure rose only after the age of 40 years in pre-western Inuit. Left ventricular hypertrophy peaked among 30-year olds and was independent of elevated blood pressure. It may be speculated that the common left ventricular hypertrophy was due to marked physical activity that contributed to the low occurrence of ischemic heart disease among pre-western Inuit."

In contrast, Yanamamo natives of Brazil demonstrated no age-related increase in blood pressure.  Yanomamo live largely on plantains, sweet potatoes, manioc, and various fruits, supplemented by insects, grubs, and hunted meat.  The Inuit have a much higher intake of omega-3 fats, and a much higher total fat intake.  These findings support the idea that chronic high fat intake promotes age-related elevations in blood pressure, even if a large portion of the fat consists of omega-3 fatty acids, even absent Western foods, and even if your ancestors have been eating an Inuit diet for more than ten thousand years.  

As I have said before, we have no reason to believe that all primitive diets had the same health effects.  The differences in blood pressure between Yanamamo and Inuit clearly provide evidence that different primitive diets have different health effects.  By the way, the study of the Yanomamo was conducted in 1989 as part of the Intersalt project, while the study of the Inuit was conducted in 1962-1964.  Both of these populations had exposure to Western civilization, the Yanomamos for 25 more years than the Inuit.  The investigators of the Inuit blood pressure were satisfied that the Inuit they studied were not Westernized.  Yanomamo in fact have the high carbohydrate diet that introduction of sugar, flour, etc would induce.  I would find any attempt to blame the elevated blood pressure of Inuit on carbohydrates in the diet unconvincing. 

 Kjaergarrd et al also report that found electrocardiograms indicating coronary ischemia in 5.5% of non-westernized Inuit.  It is a low rate compared to modern populations, but indicates that isolated Inuit were not totally immune to ischemic coronary disease.

By the way, Masai appear to have a special adaptation to dietary cholesterol not present in Caucasians. According to Taylor and Ho, controlled studies on the Masai show that they "have a much larger capacity for intestinal cholesterol absorption than whites and a greater ability to suppress endogenous cholesterol synthesis, averaging 50.5%, for compensation of their intestinal absorption of dietary cholesterol. This efficient feedback control is the only homeostatic mechanism that protects the Masai from developing hypercholesteremia."  In other words, if you aren't of Masai descent, your high-dairy diet mileage may vary.

Who Said Paleo Diet Had High Fat Percentages? Part 1

In 1988, physicians S. Boyd Eaton and Melvin Konner, and Emory University anthropologist Marjorie Shostak published “Stone Agersin the Fast Lane:  ChronicDegenerative Diseases in Evolutionary Perspective” in the American Journal of Medicine.  They expanded this paper to produce the book, The Paleolithic Prescription.  

By the way, Shostak lived among African hunter-gatherers for two years, and wrote the book Nisa: The Life and Words of a !Kung Woman.

 In these works, Eaton et al provided their estimates of the fat contents and composition of stone age diets.  They based their estimates on known nutritional values of 43 different wild game animals and over one hundred species of plants consumed by modern day hunter gatherers. 

The data on nutritional value of wild game came largely from Ledger, who dissected 220 different animals of 16 species. [1]  Ledger worked in the field of zoology, and published this data in a zoological journal, for the purpose of comparative studies of African mammals, so we have no reason to suspect that he had any interest in advancing any nutritional dogma. 

We have a very important reason to focus on the nutritional value of African mammals.  The human genome evolved to the present species, H. sapiens sapiens, in Africa, as an adaptation to the African environment, over the course of 6 million years (from the divergence from the common ancestor of great apes and humans).  Of 6 million total years of hominin evolution, the 50K years that have passed since humans left Africa constitutes only eight-tenths of one percent. Virtually all of human evolution took place in Africa, so we can expect our baseline physiology to be more adapted to the diet available to our African ancestors, than to any human diet that emerged after the African exodus in northern environments. 

The animals included goat, Cape buffalo, warthog, horse, wild boar, antelope, beaver, muskrate, caribou, moose, kangaroo, turtle, opossum, wildebeest, Thomson’s gazelle, kob (waterbuck), pheasant, rabbit, impala, topi, deer, and bison.  The fat content of meat from these animals ranged from a low of 1.2 g% in kangaroo, to a high of 5.4 g% in wildebeest. 

In 1964, Ledger and Smith reported the results of their dissection of 40 Uganda kob, 10 mature and 10 immature of either sex.  They found that “all kob had a low level of carcass fatness (maximum 6.2 percent), associated with high carcass yields”  and when compared to steers, the “ratio of fat to lean showed a higher proportion of lean in kob carcasses. The food value of kob per pound liveweight is superior in terms of animal protein and inferior in terms of calorific value to that of steers.”[2]  Indeed, a modern grain-fed steer has around 25% of the carcass as fat, making it 4 times fatter than the kob.

Eaton et al assumed a diet providing 35% of weight from animals, and 65% from plant, and a total food consumption of 2250 g (nearly 5 pounds) daily to provide around 3000 kcal daily.   I consider this a very reasonable amount of food.  I have measured my own food intake many times and when eating 65% plants and 35% meat, it consistently has ranged between 4 and 5 pounds.  The following provides an example day on which I ate 4.7 pounds of food, which I published in The Garden of Eating:

Click for larger version

Ledger’s analysis of wild game meat showed that on average a 100 g portion provides 133 kcal, 22 g protein, and 4.3 g fat, 32% of which, on average (based on 17 species evaluated), occurred as polyunsaturated fats (ranging from 20-60%, largely as linoleic acid, omega-6), and well under 40% saturated fats.  For comparison, four types of untrimmed domestic meats (beef, pork, lamb, ham) can supply an average of as much as 386 kcal and 29 g fat per 100 g, and average 45% saturated fat, and only 7 percent as polyunsaturates.

To estimate the contribution of wild plants to fat intake, they used an analysis of 36 wild foods eaten by the Hadza, the San (Bushmen), and other African tribal groups, which indicated generally a very low fat content, of which 39 percent, on average, occurred as polyunsaturated fat.

Isolated fats in Paleolithic diets

Hunter-gatherers do not have any fluid seed, nut, or fruit (olive, avocado) oils.  I don’t think we can consider olive oil, avocado oil, or coconut oil paleo foods, since production of these fats requires technology not available in the stone age.

Like modern !Kung, Paleolithic hunter-gatherers living fifty thousand years ago also did not have pots necessary for rendering, i.e. refining and isolating, animal fat. Nor did they have cream or butter.  Based on this, I have come to realize that I can’t consider isolated lard or tallow or similar refined, animal-derived fats “Paleolithic” foods. We really can’t consider any isolated oil, whether animal or vegetable, a paleo food.  

Actually,  after thinking about this for some time, I have come to realize that all isolated fats belong to the class of refined foods; fragments of the whole from which they came.  I have also realized that adding these to the diet constitutes a significant deviation from ancestral nutrition.  Using the paleo paradigm, because these foods deviate significantly from anything had by humans 100 thousand years ago, we have to consider them suspect from the get go, guilty until proven innocent.  

Effects of Paleolithic cooking techniques on dietary fat

If you have television and want to see how hunter-gatherers cooked meat, watch the Bizarre Foods episode titled “Adventures in the Khalahari,” in which Andrew Zimmern visits the Ju (!Kung, San) people.  They either throw the meat directly into the fire, or bury it in the ashes.  Similarly,  as reported in the following passage, Australian Aborigines cooked meat by burying it in a pit. 

“A large fire was made in a depression in the sand, and stones and shells were heated. Small green branches were placed on top of the stones and the wallaby was flung on these. After 5-10 minutes it was taken off the fire, placed on a layer of green leaves, and the singed fur was removed with a tomahawk. The first cut was made horizontally on the ventral surface at the level of the anus, and the next on the dorsal surface along both sides to sever the leg muscles.  Another cut was then made from the anus to the neck.  The viscera were pulled out; and the kidneys, liver, heart and lungs, and the omental and mesenteric fat were separated from the rest, and cooked [directly] on the hot stones and coals for 5 minutes [Editorial note: allowing the fat to seep into the fire].   The cooked lungs were used to soak up the blood inside the carcass and then eaten.  The offal was regarded as a delicacy by everybody and a certain amount of squabbling always followed its distribution. The tail was cut off, and during the cooking was put on or alongside the body.  The carcass was laid flat, dorsal side downwards, on the hot stones and ashes and the body cavity was filled with hot stones.  Sheets of paperbark formed a cover over the animal, and sand was scooped out to make an oven. Wallabies weighing 15-20 pounds were cooked for 25-35 minutes.  Everything edible was eaten except the stomach and intestines.  The skull was cracked open to get the brain, and the bones were broken to extract the marrow.”  [Source: Anthropology and Nutrition, vol. 2 of Records of the American-Australian Scientific Expedition to Arnheim Land, ed. C.P. Mountford (Melbourne: Melbourne University Press, 1960).]

In any of these methods, hunter-gatherers lost significant amounts of animal fat into the fire, stones, coals, ashes, or soil.  Indeed, since paleo people didn’t have neolithic pots we really can’t consider cooking in such pots a Paleolithic technique, and I believe it important to notice that cooking meat in neolithic pots results in capturing more of the fat of foods than a hunter-gatherer could capture.  We especially can’t consider frying in fat a Paleolithic diet method. 

Regarding pemmican, consider that one hundred thousand years ago, no human had the technology required to render fat to produce pemmican, even if we assume available African game could have provided the required amounts of fat (it didn't). The invention of suitable pots occurred about the time of the agricultural revolution.  This means that the human genome has probably not adapted to the level of dietary fat that is possible through the use of this technology any more than it has adapted to the use of cereal grains.

In addition, consider that, prior to the 20^th century, people used animal fats for many purposes other than eating.  Before the petrochemical age, animal fats were used as lubricants (e.g. grease for axles), for tanning leather, and to make soap, salves, paints, wood finishes, and candles.  Even Inuit used seal oil and blubber to fuel fires and candles.  These uses took animal fats out of the food supply, reducing the potential fat content of the diet.  When petrochemicals or vegetable oils replaced animal fats for these purposes, this increased the animal fats available for food use. 

Discussing cooking techniques appropriate for a Paleolithic approach, Eaton et al comment:

“Roasting, baking, and steaming (water is poured over hot stones as at a Polynesian luau) are techniques used by recent hunters and gatherers and are probably ancient.  While all cooking procedures affect the nutrient content of food, these traditional techniques are relatively healthful.  Baking and roasting reduce the fat content of meat [note: so long as you don’t retain fat of juices] while steaming (in contrast to boiling) minimizes vitamin loss.  Furthermore, none of these methods add fat.  Recently studied hunters and gatherers do not fry their food, chiefly because they lack appropriate cooking vessels….

“Nonstick pans should be used to cut down on fat or oil.  Or, oil can be spread lightly with a paper towel.  Vegetable oil sprays now available achieve the same result mechanically….

“With poultry, remove skin and visible fat.  Defat gravies with a bulb syringe or skimmer.”

So, how much fat did Eaton et al estimate to occur in a Paleolithic diet?

If you take 35% of the 2250 g diet as meat, supplying 4.3 g fat per 100g, you get ~34 total grams of fat.  Eaton et al estimated an additional ~40 g of fat supplied by plant foods 3 percent fat on average), resulting in a total fat intake of about 70 g daily, or about 21 percent of the total 3000 calories consumed.  This would translate to only 42 g of fat for 2000 kcal, and only 32 g fat for 1500 kcal.

If you take 65% of the 2250 g diet as meat, supplying 4.3 g% fat, you get 63 g fat daily from animal food, and an additional 24 g from plant food, for a total of 87g fat.   That works out to just 26 percent of calories from fat, a minor difference from the opposite plant-animal ratio, still very low in fat.  

Because wild game and plants had a relatively high percentage of polyunsaturated fats (~30%) and lower percentage of saturated fats, Eaton et al also estimated a high P:S ratio in Paleolithic diet compared to modern diets, and suggested that this accounted for the uniformly low total cholesterol levels found among hunter-gatherers, ranging from 106 (Pygmies) to 141 (Canadian Eskimos).

Eaton et al concluded:

“Late paleolithic humans must have obtained, on average, between 20 and 25 percent of their calories from fat.  Of this, polyunsaturates exceeded saturates; a typical P:S ratio might have been 7:5 (which can also be expressed as P:S = 1.4:1).”

So, it appears that Eaton et al did not have evidence or belief that evolutionary diets had high fat (or low carbohydrate) contents.  Indeed, they stated:

“Between 1910 and 1976, the consumption of fats in the United States increased by about 25 percent so that, currently [1988], fat makes up about 42 percent of the calories consumed by average Americans.  Of this fat, more that twice as much is saturated as polyunsaturated.  This level of fat consumption is unprecedented in human evolutionary experience, and results in diseases that kill us, but that are uncommon in countries where fat represents a much smaller proportion of the diet.  In rural Japan, for example, only 10 to 12 percent of daily calories come from fat (with a P:S ratio of approximately 1:1) and the prevalence of coronary heart disease among the Japanese is only a small fraction of ours.” 

Taking these and other data on the health effects of dietary fat into account, Eaton et al recommended that a modern rendition of Paleolithic diet supply only about 20% of calories as fat, with about 25% of calories as protein and 55% of calories as carbohydrate.  They outline an implementation that provides 19% of calories as fat, 26% as protein, and 55% as carbohydrate.

So it appears that the notion that modern rendition of paleo diet should have a high fat and low carbohydrate content did not come from Eaton, Konner, and Shostak.  

Next in this series, we will see what Michael Crawford and David Marsh, authors of Nutrition and Evolution, had to say about fat in human evolutionary diets. 

1.  Ledger, HP.  “Body composition as a basis for a Comparative Study of Some East African Mammals.”  Symposium of the Zoological Society of London 21 (1968): 289-310.

2.  Ledger HP, Smith NS.  The carcass and body composition of the Uganda Kob.  Journal of Wildlife Management 28(4), October 1964

Out of Office

Hey folks, not going to respond to all the comments until next week.  Tracy and I are on our honeymoon.

Only a few comments I have now:

1) Some of you need to read more carefully.  I clearly stated numerous times that I was NOT claiming that ALL upper paleolithic stone age Eurpeans were obese, only SOME.

2) The literature shows that people can both lower insulin levels and lose fat on low fat high carb diets as well as on low carb diets, so long as it results in reduced caloric intake.  This along with the Japanese experience directly contradicts the claim that 'carbs drive insulin drive fat storage.'   People wedded to this hypothesis are resorting to ad hoc hypotheses--like "Japanese are a different subspecies," or "Different races require different diets," or "we are genetically different from stone age people" -- to "save" their hypothesis.  

Some of you seem not to notice that I am including references to studies on present day Caucasians, that show fat loss on low fat diets, which contradict the hypothesis that high carb diets drive weight gain.  Moreover, I started from citing a direct experience I had with present-day Caucasian subjects gaining fat on low carb, high fat diets.   The Paleo paradigm is just a guide.  Since we don't know exactly what people ate in the stone age, nor how it affected their health or longevity, we have to rely more on studies of present day people. 

3) Studies following people prescribed low carb diets then allowed to range freely (not controlled metabolic ward studies) consistently show that people eat more carbs than prescribed (e.g. by Atkins guidelines). Why don't people comply?  If you say weak character, you are falling into the same trap of people who claim people are overweight because they are gluttons and sloths. 

I suggest that they don't comply because they have a drive to eat carbohydrate that is not satisfied by the low carb diet.  We also have a drive for essential amino acids, and for essential fatty acids.  These basic drives influence total food intake.

Please keep in mind that modern humans have 6 times more salivary amylase production than chimpanzees.  This is a clear adaptation to starch consumption.  I don't see any surprise in finding a drive to eat carbohydrate in an animal that has clear biochemical adaptation to starch digestion.  

4) I cited both rat and human studies in the one post...so you can't dismiss the human studies (or Japanese experience) by saying that rats are different from humans.

5) STudies of weight loss using low carb diets show a range of  responses....some subjects lose, some don't, some even gain.  Only the average is reported, not the individual responses...if there is loss on average, this obscures individual variations.  When I return, I will be presenting my hypothesis which I think covers all the bases and allows for individual variation...which is totally ignored in conventional science.

6) I never said that we should be eating only unsaturated fats.  If you eat beef only, as your only fat source, you will get more unsaturated than saturated fats.  Same with lard.  So, I am only saying that most of the fat we eat should be unsaturated (mono and poly, just enough of the latter).

7)  Protein-rich foods stimulate insulin release.  Using Taubesian reasoning: If insulin drives fat gain, and protein causes insulin release, then a high protein diet could drive fat gain in SOME people.  

That's enough.  More when I get back, rejuvenated.

Venus Revisited, 2

Chew on this excerpt from [full text available] "Isocaloric diets: effects of dietary changes" by Leveille and Cloutier:

"Forbes and colleagues (8, 9) published several papers in 1946 on the relationship between the level of fat in the diet of adult rats and the efficiency of use of dietary energy. In those studies dietary fat varied from 2% to 30%, while intake of gross energy, protein, and essential nutrients remained constant. Researchers
observed that as the dietary fat content increased, relative heat production decreased. Thus, with increasing fat intake the apparent efficiency of food use increased, allowing for more energy to be stored in the animal carcass (see Fig 2). In essence, more energy is stored as fat in the body as the proportion of fat to carbohydrate increases in the diet.

"Increasing the protein level of the diet at the expense of carbohydrate also results in changes in apparent energy efficiency. Donald et al (10) observed that adult rats fed a high-protein diet gained more weight than a similar group fed low-protein diet when the content of dietary  fat was maintained at a constant level and levels of protein varied from 5% to 25%. The animals had free access to food and water. Absolute food consumption, ie, g/rat, was not significantly different between the 5% and 25% groups. Yet total body weight gain and body fat were higher in the 25% group (Table 2).
 
"Humans appear to respond in much the same way as rats to changes in dietary composition. Danforth (11) noted that lean subjects gained weight relatively easily when overfed fat but not when fed a mixed diet of carbohydrate and fat. In an earlier study by Miller and Mumford (12), researchers observed that students overfed a high-protein diet gained more weight than a group of students fed a low-protein diet with a similar number of calories. The weight gain for both diets was less than the predicted value."

These studies showed that when we hold the caloric content of a  human or rat diet constant,  but vary the macronutrient composition, increasing either fat or protein at the expense of carbohydrate leads to greater gain of fat.


Here's table 2 from the paper:

 Although fed the same number of calories, the rats fed a high (25%) protein diet weighed 23% more than those fed the low (5%) protein diet, and had 50% greater body fat percentage.  


The European upper paleolithic diet was high in protein and fat and low in carbohydrate, which according to this type of research, has the highest food efficiency and promotes the highest body fat percentage.


Maybe that's why Venus was obese, maybe that's why people eating 'primal' and supposedly 'paleo' diets have trouble losing fat, maybe that's why only 3% of  Japanese are obese.

Just maybe.

Venus Revisited

Some people still think it is impossible to get as fat as Venus of Willendorf eating only meat and fat. 

Supposedly it is just too difficult to eat excessive calories when eating only meat and fat.

OK, a thought experiment.

Let's say that Venus is 100 pounds overweight.  That translates to 350, 000 stored calories.

Let's say she ate only 100 excess fat calories every day...about two teaspoons of pure fat. 

No one can tell me that it is too difficult, too painful, impossible to eat two teaspoons more fat than you need every day.

There were plenty enough calories available in ice age Europe for any one to have 100 extra calories per day on average.  They were hunting critters like mammoths:

Source:  Prehistory.com

These animals had 20-30% body fat, and weighed on average 6-8 tons, i.e. 1200 to 1600 pounds.  One animal would provide at least 240 pounds or more of adipose tissue:  840, 000 calories of pure fat.  Twenty people (the estimated typical size of a paleo tribe) would have had 420, 000 calories each just from the fat of one animal, and upper Paleolithic people were killing these animals en mass. 

She starts at age 20.  How long will it take her to store up that excess 100 pounds?

One hundred excess calories per day for 3500 days, about 10 years, will result in 100 pounds of excess adipose weight.

She is obese by age of 30.  From a measly two teaspoons daily of excess animal fat.  

People don't grow obese in a year or two.  It takes time.

As Stephan pointed out recently, the reward value of food plays a dominant role in the genesis of obesity.  Stephan wrote:

"Experiments in rats and humans have outlined some of the qualities of food that are inherently rewarding:

• Fat
• Starch
• Sugar
• Salt
• Meatiness (glutamate)
• The absence of bitterness
• Certain textures (e.g., soft or liquid calories, crunchy foods)
• Certain aromas (e.g., esters found in many fruits)
• Calorie density ("heavy" food)

We are generally born liking the qualities listed above. In addition, aromas and flavors that are associated with these qualities can become rewarding over time."

Upper paleolithic diets of Europe had fat, meatiness, and caloric density;  all inherently rewarding.  Its easy to eat those extra two teaspoons of fat, your brain rewards you for it and you certainly do not get a stomach ache from it.  

Compare, in your own experience, the pleasure you get from eating fat, to the pleasure you get from eating boiled potatoes, sweet potatoes, or rice served without any fat.  Which do you enjoy more, one 4-ounce boiled potato (about 100 kcal), or two tablespoons of cream (also about 100 kcal).

Its obvious which has the higher caloric density.  Your brain gets more reward from the cream than the potato.  Which reminds me, I've never met a person who binges on boiled potatoes.

Moreover, when we eat extra carbohydrate, it increases metabolic rate by about 10% of the calories consumed, and converting carbohydrate to fat consumes at least 10% of the calories in the carbohydrate.  But eating extra fat has no thermogenic effect, and since it is already fat, ready to store, essentially none is lost in the process of storage.

This means most people find it a little more difficult to consume excess energy in the form of whole food starch (e.g. potatoes) compared to consuming excess energy in the form of fat.

If carbohydrates make people fat, then why does Japan have an obesity rate of only 3.2%, in comparison to the Grecian 22%?  Seven times more obesity in Greece, than in Japan.

Grecian diet:  About 40% energy from fat, 45% from carbohydrate
Japanese diet:  About 60% energy from carbohydrate (mostly white rice), 25% from fat

A beautiful theory slain by ugly facts?  Make your own conclusions.

By the way, you don't need "high" insulin to store fat.  You just need 1) normal insulin (not type 1 diabetic), 2) acylation stimulating protein, a potent regulator of fat synthesis, and 3) an excess of dietary fat.

I can easily imagine Venus eating just a little too much meat and fat often enough to average an extra 100 calories daily, for 10 or more years, gradually growing obese.  Her intake just exceeds her output by a small amount.  The same way that people grow obese today...over a long period of time, with no obvious overeating. 

 I simply do not find compelling any attempt to explain Venus by force-feeding rituals, potato or honey binges, or similar scenarios.  People do not get obese like this in a month, and ice age Europe most likely did not supply any carbohydrate-rich foods in quantities necessary to make them responsible for this level of obesity.

Making Herbal Meads: St. John's Wort and Cherry Mead

This post is part of a Wild Things Round Up. Interested in homemade elixirs, beers and other wild and crazy alcohol treats? Check out the entire listing here. 

Yesterday my husband and I bottled up the last of our wines. All of the batches turned out pretty well, but it was the St. John's Wort and Cherry mead that was the most spectacular. Light and floral and the color of a beautiful rosé. 


So, of course, I had to brag about this on my Facebook page and in response I had numerous requests for the recipe. So here you are!


For now, bookmark this page to make your own St. John's Wort and Cherry mead this summer. 

If you’ve never made mead or wine before look for my how-to video on making dandelion wine on YouTube.com. 



To make this recipe I used St. John's Wort Flowers that had been frozen for about a month. I've never used dried St. John's Wort Flowers so I can't comment on whether or not that would work. 


Thanks to Portland herbalist Missy Rohs for giving me the idea! 

St. John’s Wort and Cherry Mead

Ingredients

One gallon of water

3 pounds of honey

1/4 teaspoon of yeast nutrient

One gallon of fresh St. John’s Wort Flowers

One pound of cherries (de-stoned and crushed)

1/4 cup of lemon juice

Wine yeast

1. Place the honey and water in a pan and bring to a boil.
2. In a food-grade bucket add the St. John’s Wort Flowers, cherries, lemon juice, and yeast nutrient. 
3. Pour the just boiled honey water into the bucket and stir well. 
4. Once the mixture in the bucket has cooled to about 85 degrees F, add the wine yeast (follow the directions on the wine yeast packet). Stir well. Cover with a cloth.
5. This will stay in the primary fermenter for 3-5 days. Each day stir the mixture well. 
6. After 3-5 days in the primary fermenter, strain off the liquid and place it in a carboy with an airlock. It will be ready in a year.
   
   
   Update: This is one of my favorite meads ever! I highly recommend the recipe. This year we made another batch and this time we simmered the cherries along with the St. John's Wort. We'll have to wait another year to find out how it compares. 

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