• Populations that have a relatively "long" history of agriculture, e.g., those of European descent, have a relatively low incidence of NIDDM, that is, non-insulin-dependent diabetes mellitus, also known as adult-onset diabetes.

• Populations that adopted agriculture more recently or, in other words, discontinued the evolutionary hunter-gatherer diet more recently, have relatively higher incidence rates of NIDDM. In some former hunter-gatherer populations, incidence levels of NIDDM range from epidemic levels (Nauruans; the Pima tribe of the U.S.), to rates that are "only" several times that of Europeans.

Our primate ancestors ate a high-carbohydrate diet and the brain and reproductive tissues evolved a specific requirement for glucose as a source of fuel...

[T]he Ice ages which dominated the last two million years of human evolution brought a low-carbohydrate, high-protein diet. Certain metabolic adaptations were therefore necessary to accommodate the low glucose intake.

Studies in both humans and experimental animals indicate the adaptive (phenotypic) response to low-carbohydrate intake is insulin resistance...

We propose that the low-carbohydrate carnivorous diet would have disadvantaged reproduction in insulin-sensitive individuals and positively selected for individuals with insulin resistance. Natural selection would therefore result in a high proportion of people with genetically-determined insulin resistance.

The hypothesis is illustrated in the following figure.

Our hypothesis hinges on four lines of evidence.

1. that during the last two million years of evolution, humans were primarily carnivorous, i.e., flesh-eating hunters consuming a low-carbohydrate, high-protein diet

2. that a low-carbohydrate, high-protein diet requires profound insulin resistance to maintain glucose homeostasis, particularly during reproduction

3. that genetic differences in insulin resistance and predisposition to NIDDM can be explained by differences in exposure to carbohydrate during the past 10,000 years

4. that changes in the quality of carbohydrate can explain the recent epidemic of NIDDM in susceptible populations.

Neel [1982] revisits the 1962 research, and notes that subsequent research invalidated several details of his 1962 paper. Neel's later paper provides three different approaches which might explain or support the original hypothesis of the "thrifty genotype" (as Neel's hypothesis is widely known). Two of the approaches revolve around having non-functional or insensitive insulin receptors, and the third approach suggests differences in insulin sensitivity between glucose and lipid pathways in each individual.

The "not-so-thrifty genotype" hypothesis of Reaven [1998a]. Reaven [1998a] hypothesizes that the underlying function of insulin resistance is not to increase fat storage as Neel suggests, but to spare muscle tissue from proteolysis, i.e., to preserve muscle tissue in periods of famine. Reaven [1998a] claims (and provides one citation in support) that there is evidence that insulin-controlled glucose disposal is genetically determined. Reaven's hypothesis is called the "not-so-thrifty genotype."

Ozanne and Hales [1998] challenge Reaven [1998a], and note that the evidence is weak in support of claims that NIDDM has a genetic basis. They also note that Reaven's approach suggests that individuals with NIDDM are sensitive to the anti-proteolytic action of insulin, while simultaneously being resistant to the glucose-disposal effects of insulin (analogous to the third approach of Neel [1982]).

Both hypotheses (Neel, Reaven) are based on a dubious assumption. Cordain et al. [1998] criticize the approaches of both Neel and Reaven, as both are based on the assumption that famine was common in evolutionary times. However, Cordain et al. cite extensive evidence that starvation was/is less common in prehistoric peoples and among modern hunter-gatherers when compared to subsistence agriculturalists. Instead of assuming periodic famine, Cordain et al. [1998] argue for insulin resistance on the basis described in Miller and Colagiuri [1994] (as outlined above on this page). (Also see Reaven [1998b] for additional comments.)

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SEE TABLE OF CONTENTS FOR:
PART 1 PART 2 PART 3 PART 4 PART 5 PART 6 PART 7 PART 8 PART 9

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GO TO PART 1 - Brief Overview: What is the Relevance of Comparative Anatomical and Physiological "Proofs"?

GO TO PART 2 - Looking at Ape Diets: Myths, Realities, and Rationalizations

GO TO PART 3 - The Fossil-Record Evidence about Human Diet

GO TO PART 4 - Intelligence, Evolution of the Human Brain, and Diet

GO TO PART 5 - Limitations on Comparative Dietary Proofs

GO TO PART 6 - What Comparative Anatomy Does and Doesn't Tell Us about Human Diet

GO TO PART 7 - Insights about Human Nutrition & Digestion from Comparative Physiology

GO TO PART 8 - Further Issues in the Debate over Omnivorous vs. Vegetarian Diets

GO TO PART 9 - Conclusions: The End, or The Beginning of a New Approach to Your Diet?

Back to Research-Based Appraisals of Alternative Diet Lore