Indeed, there is substantial evidence [3, 5-8] that the combination of insulin resistance and compensatory hyperinsulinaemia predisposes individuals to develop a high plasma triglyceride (TG) and a low high-density lipoprotein (HDL) cholesterol concentration, high blood pressure, and coronary heart disease (CHD). In 1988, I suggested that this cluster of abnormalities constituted an important clinical syndrome, designated as Syndrome X [3].

Alternative vegetarian hypothesis for insulin resistance? The second reason to discuss syndrome X is that a recent hypothesis, Provonsha [1998], might possibly be promoted by raw/veg*n advocates as a vegetarian alternative to the insulin resistance hypotheses discussed above. Provonsha's hypothesis claims (in opposition to implications of the above hypotheses) that meat consumption causes insulin resistance and related syndrome X conditions.

A brief summary of the major parts of the hypothesis of Provonsha is as follows.

• Simplistic binary logic is a basic tenet of the hypothesis. Biochemical processes can be classified in a binary manner: anabolic (associated with food intake) and catabolic (associated with fasting and recovery from injury). Implicitly, Provonsha appears to indicate that anabolic = good, and catabolic = bad, in discussing processes.

• The consumption of animal tissue (protein) results in the production of the hormones glucagon and cortisol, whose action opposes that of insulin. (Provonsha classifies insulin as anabolic, and glucagon and cortisol as catabolic.)

• Meat protein = "catabolic"; allegedly causes syndrome X. Meat protein is "catabolic" and will likely activate catabolic processes in the human body, causing insulin resistance and promoting syndrome X.

Binary logic of hypothesis is an inadequate model of reality. It appears that Provonsha believes that the human body should conform to a simplistic binary model: anabolic or catabolic, where the "or" is exclusive. However, the human body is a very complex system, with anabolic and catabolic processes underway simultaneously, and in balance. Black-and-white reasoning similar to what Provonsha appears to suggest can also be found in the simplistic approaches of certain raw vegan extremists. Suffice it to say that such reasoning does not reflect well on Provonsha's hypothesis.

Second, Provonsha argues against glucagon and cortisol, yet his criticisms of them are unconvincing. He argues that both raise blood sugar, and claims that cortisol increases insulin resistance and promotes obesity (he cites three references, the titles of two of which relate to obesity). His criticism of glucagon similarly discusses its role in promoting obesity, although he provides only one citation--a study of diabetic rats--that may indirectly support this claim.

The basic problem with his arguments here is that since studies on the direct effects of cortisol and/or glucagon are not cited (with the possible exception of the rat study above), his argument is essentially a narrow "this might happen if we look at specific processes in isolation" [not a quote from Provonsha]. Such arguments are frankly not very compelling, as the human body is a complex, interrelated system, with catabolic and anabolic processes active simultaneously. Further, glucagon and cortisol, and catabolic processes in general, are necessary and are part of the balanced homeostasis required to support life.

Fallacy that meat = high-fat consumption recited. Also, Provonsha engages, on p. 122, in the common fallacy of equating meat consumption with high-fat consumption--demonstrating ignorance of paleolithic diet research that has analyzed wild animal meats, which were part of humanity's evolutionary diet, and found them to be mostly very low-fat (muscle meats) or, at the least, low in saturated fat (organ meats), and that lean meats do exist. (The character of wild game is discussed in a later section.)

Unsupported claims in hypothesis. Third, Provonsha claims (p. 124), without evidence or citations, that if one eats meat, one will absorb "untold" chemicals that are catabolic and can disrupt human body processes. Because he provides no citations in support of the preceding claims, Provonsha's claims that eating meat might disrupt body processes appear to be speculative.

Provonsha also criticizes the fact that glucagon (produced by eating animal tissue) inhibits pancreatic enzyme production. However, he fails to mention that many grains and legumes--common plant foods, and the major caloric basis for most (conventional) vegan diets--contain significant amounts of enzyme inhibitors as well. (For more on antinutritional components in grains/legumes, see The Late Role of Grains and Legumes in the Human Diet, and Biochemical Evidence of their Evolutionary Discordance.)

Real-world dietary trials directly contradict the hypothesis. Provonsha's hypothesis that meat protein causes insulin resistance ultimately fails the test of real-world dietary trials. While it is true that eating fat with carbohydrate may lead to lower glucose and higher insulin levels (see, e.g., Collier et al. [1988]), it does not follow that meat causes chronic hyperinsulinemia or syndrome X. To the contrary, two studies on this very issue provide evidence that dramatically contradicts the core of Provonsha's hypothesis.

Results of trial on nearly 100% animal food (seafood) diet. O'Dea and Spargo [1982] investigated the plasma and glucose responses in 12 full-blooded Australian Aborigines both before and after 2 weeks on a diet of nearly 100% animal flesh (seafood). Prior to the trial, the diet of the Aborigines was, on an energy (caloric) basis, high-carbohydrate (40-50%), high in fat (40-50%), and low in protein (10% or less). The seafood diet observed for 2 weeks was, on an energy basis, 70-75% protein, 20-25% fat, and less than 5% carbohydrate. If Provonsha's hypothesis regarding animal protein causing insulin resistance were true, one would expect an increase in insulin resistance from such a high protein diet. However, the opposite was observed; from O'Dea and Spargo [1982, pp. 496-497]:

Together these findings suggest an improvement in glucose utilization and insulin sensitivity after the high protein-low carbohydrate diet...

The mechanisms by which low carbohydrate diets which are high in protein preserve glucose tolerance while those high in fat do not, is probably related to the gluconeogenic potential of high protein diets. Elevated glucose levels in response to the ingestion of protein would promote hepatic gluconeogenesis from amino acids entering the liver from the splanchnic circulation. In this way a low carbohydrate diet which was high in protein could maintain the necessary glucose supply to the body whereas one high in fat could not.

During the first 1.5 weeks (travel time), the diet was 90% animal foods on an energy (caloric) basis. The coastal diet composition was nearly all animal foods, mostly seafood with some birds and kangaroo, and was approximately 80% protein, 20% fat, and less than 5% carbohydrate. The diet at the inland location was 64% animal foods (by energy) and 36% plant foods, the macronutrient content of which was 54% protein, 13% fat, and 33% carbohydrate.

Significant improvements noted in both glucose tolerance and insulin response. Once again, if Provonsha's hypothesis that animal protein causes or aggravates insulin resistance were true, one would expect the above animal-protein-based diets to greatly aggravate the condition of the diabetics in the study. However, the opposite happened: the condition of the diabetics improved. From O'Dea [1984, pp. 601, 602]:

The major finding in this study was the marked improvement in glucose tolerance in 10 diabetic Aborigines after a 7-wk reversion to traditional hunter-gatherer lifestyle. There were two components to this improvement: a striking fall in the basal (fasting) glucose concentration and a less marked, but nevertheless significant, improvement in glucose removal after oral glucose...

The three most striking metabolic changes that occurred in this study, namely the reductions in fasting glucose, insulin, and triglyceride concentrations to normal or near-normal levels, were certainly interrelated.

The above studies that contradict Provonsha's hypothesis, plus the other problems as noted previously, suggest the hypothesis has little merit, and raw/veg*n advocates should not try to use it as a vegetarian alternative explanation to the more plausible carnivore-connection hypothesis for insulin resistance or syndrome X.

The standard fruitarian "party line" explanation for such symptoms is that they are detox and will go away once you are "pure" enough. In reality, the excess urination and frequent thirst usually persist, so long as one is consuming large amounts of sweet juicy fruit. (Consider the physics involved: large amounts of water are ingested, in the form of sweet juicy fruits, and approximately the same amount of water must be excreted, as well.) A typical response in the face of this ongoing experience is to (mentally) adjust to the symptoms; that is, one may begin to consider it normal or healthy to urinate several times per hour, have frequent mood swings, experience intermittent fatigue (which may be considered as evidence of "detox"), and so on.

(Note regarding thirst symptoms: Thirst on a fruitarian diet may seem counterintuitive, since the level of fluid intake is so high via all the fruit. However, some fruits [citrus, for example] are diuretic and increase urination. When used as staples, this can lead to thirst and/or the need to drink more water, at least in my own former experience as a fruitarian. Or instead, one may become thirsty but suppress the urge to drink because they become tired of urinating every few minutes. This syndrome may be partially responsible for why some fruitarians "don't drink water," aside from just the high water content of the diet.)

The carnivore connection hypothesis may explain these symptoms as well, i.e., the individual is consuming grossly excessive carbohydrate (sugar) given his or her level of insulin resistance. Of course other factors may also be involved (e.g., insulin inhibitors in the diet, plus other nutritional factors: zinc, B-12, taurine, insufficient calories, etc.), but the hypothesis that the "ideal" fruitarian diet is beyond the range of genetic adaptation (i.e., decidedly unnatural) for many individuals is not only tantalizing, but highly plausible as well. The wide incidence of diabetes-like symptoms among fruitarians may be (additional, circumstantial) evidence that although our prehistoric ancestors certainly consumed fruit (when available), strict fruitarian diets were never an important factor in human evolution.

Rationalizations by fruitarians. No doubt the defenders of fruitarianism will claim that a high incidence of NIDDM in former (recent) hunter-gatherer populations is all the fault of the grains/legumes in their new diet, and that there would be no NIDDM if the former hunter-gatherers were to eat the "ideal" fruitarian diet. But where is the evidence (even including anecdotal evidence) for such a claim? More to the point, the extensive anecdotal evidence surrounding fruitarianism is that it is a massive failure, in the long run, and the diabetes-like symptoms (which may be due to excess sugar consumption) are common among those who try to subsist on a diet of mostly sweet fruit. Further, such evidence is found among people of European descent, i.e., those who have had a longer time to adapt to higher carbohydrate diets.

Comparative Physiology: Overall Synopsis

Some of the physiological evidence that humans are adapted to a diet that includes substantial animal products (fauna; i.e., we are faunivores) is:

• Heme iron receptor sites. Our intestines contain receptor sites specifically for the absorption of heme iron, which is found in nutritionally significant quantities only in animal foods. This is strong evidence of evolutionary physiological adaptation to animal foods in the human diet.

• B-12 considerations. Humans need vitamin B-12, but all current evidence suggests that plant foods were not a reliable, year-round source during human evolution. Geophagy and coprophagy are not plausible sources, leaving animal foods (including insects) as the sole reliable, plausible source.

• Taurine synthesis. Relative efficiency of synthesis: the synthesis of taurine is much less efficient in humans than in herbivorous animals.

• Beta-carotene to vitamin A conversion. Relative efficiency of conversion: the conversion of beta-carotene to vitamin A is much less efficient in humans than in herbivorous animals.

• Sufficiency and balance of EFAs. Common, staple plant foods generally do not contain the right "balance" of EFAs, and production of EPA, DHA from plant source fats may be inefficient. It's hard to understand why--if humans really are natural vegans--the "optimal" balance of EFAs is apparently so difficult to achieve with plant foods.

• Bioavailability issues. Relative efficiency of digestion/bioavailability: Although animal foods are generally easier for any mammal to digest than plant foods for structural reasons (e.g., cell wall considerations), the fact that many staple plant foods contain high levels of factors that inhibit the human digestive process suggests a long evolutionary dependence on animal foods as major nutrient sources. Examples of the relative bioavailability are as follows.
  • Iron in animal foods is more bioavailable than in plant foods.

  • Zinc is more bioavailable in animal foods than in plant foods.

  • Animal protein is digested more efficiently than plant protein.

• Analysis of bitter taste thresholds by Glendinning [1994] shows that the human bitter taste threshold is in the same range as faunivores.

Also, two important hypotheses relating diet and evolution were discussed here:

• The incidence of hereditary hemochromatosis, a relatively common (in certain populations) "iron overload" disease, may be an example of a partial genetic adaptation that promotes survival in the high-carbohydrate, lower-animal-food diets of agriculture, by increasing iron absorption.

• The carnivore-connection hypothesis of Miller and Colagiuri explains the high incidence of NIDDM in former (and only recently Westernized) hunter-gatherer populations as being due to insulin resistance; i.e., their insulin resistance level has not yet begun to adapt to the high-carbohydrate diets of agriculture.

• Heightened B-12 risk. Strict fruitarianism might accelerate vitamin B-12 deficiency by decreasing production of gastric acid. This may be a low-risk issue as it is very rare for anyone to strictly follow a fruitarian diet long-term; i.e., "cheating" and binge-eating are common on the diet.

• Low zinc and feelings of "euphoria." Zinc deficiency is a plausible potential explanation for the "euphoric" mental feeling reported by some fruitarians (also an explanation for the loss of libido reported by some).

• Diabetes-like symptoms. The carnivore-connection hypothesis of Miller and Colagiuri might explain the high incidence of diabetes-like symptoms among fruitarians, and the extremely high failure rate among those who try the diet. It seems plausible, given the predominant picture presented by the anecdotal record, that most people are not genetically adapted to a diet in which (approximately) 75+% of calories come from sugar, a simple carbohydrate that requires insulin for metabolism.

Return to beginning of article

SEE REFERENCE LIST

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