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(Looking at the Science on Raw vs. Cooked Foods--continued, Part 1G)

Natural toxic constituents in food, and effect
(or absence of effect) of cooking

Here, we will only investigate a few examples, since the list of all natural toxic constituents would be extremely long [Ames 1983], besides which not all have been studied yet.

It will appear that heating does not destroy all of these constituents, and that some (but not all) of the toxins listed below are found in foods that are commonly eaten cooked, but that are inedible raw, except perhaps in small quantities (like potatoes). Thus a good argument in favor of eating raw is that you reduce your exposure to many natural toxins.

"Avoiding toxins" does not solve the nutritional cost/benefit trade-off. On the other hand, as we shall see in Part 3, there is a trade-off between toxicity and deficiencies, in that if one tries to avoid as many toxins as absolutely possible, they would have to avoid so many foods that deficiencies would likely ensue from the severe dietary restriction. Also, from the examples that will be presented below, trying to eliminate toxins completely is a hopeless task in any event (for raw as well as cooked-food eaters).

"Alien" proteins vs. cooked forms of proteins. Finally, we notice that with the Paleolithic diet, which is not an all-raw diet, foods that are not edible raw are avoided but for different reasons than toxicity per se. From the Paleolithic diet point of view, it is more important to avoid "alien" proteins that cause problems via molecular mimicry (i.e., autoimmune reactions) than to avoid cooked forms of proteins we are adapted to. In this view, it is more a consideration that foods requiring processing were ones that were introduced relatively late in human history, so that genetic adaptation to them is not yet complete, irrespective of any cooking/toxicity concerns, which are seen as more minor issues.

Considering the practicalities. Remark: We do not recommend worrying excessively about completely avoiding (all of) the foods listed below, first of all because the list is not exhaustive and toxins are quite widespread in nature. And secondly because our body has many detoxification mechanisms which are specifically designed to allow it to handle moderate, relatively normal amounts of toxins without deleterious consequences. Our goal, rather, is to show that one needn't be excessively concerned about potential harmful effects of the chemical constituents created by cooking, since all living animals are naturally exposed to quite a variety of toxins in the foods they eat anyway.


From Marth [1990], mycotoxins (toxins produced by molds) are completely destroyed at their melting point, which is generally at high temperatures: 164°C (327°F) for Zearalenone, 170°C (338°F) for Rubratoxia. When roasting peanuts, the toxicity of aflatoxin B1 is reduced by 70%, and that of aflatoxin B2 by 45%. Thus, heat treatment cannot be considered as a satisfactory means to eliminate mycotoxins.


Raw kidney beans at a level as low as 1% of diet can cause death in rats in two weeks. Beans cooked at 100°C (212°F) for 30 minutes, and incorporated at a level as high as 20% of diet, do not retard growth when tested against casein. (Feeding rats with casein instead of beans doesn't affect their growth rate, and can therefore be used as a baseline for comparison.) However, when beans which have been cooked at the lesser temperature of 70°C (158°F) for 30 minutes are incorporated, growth retardation is almost as great as that which occurs when raw beans are fed. The small amount of lectin present in beans cooked at 70°C might be responsible for this effect [McPherson 1990]. However, cooking kidney beans doesn't destroy all antinutrients [Grant et al. 1982].

Fava beans. The well-known disease "favism" is caused by consumption of fava beans in genetically susceptible individuals. Such individuals carry a polymorphism of a gene (present in some regions where malaria is prevalent) that is thought to protect against malaria but also results in severe deficiency of glucose-6-phosphate dehydrogenase (G6PD) [Golenser 1983].

Soybeans. From Liener [1994], soybeans contain some heat-labile protease inhibitors and hemagglutinins. ("Heat-labile" means those susceptible to changes by heat; a hemagglutinin is something that causes red blood cells to clump together.) Soy also contains factors that are relatively heat-stable, though of lesser significance, such as:

From Faldet [1992], heat treatment of soybeans destroys or reduces heat-labile antinutritional factors, improves digestibility and availability of sulfur amino acids, and increases fat digestibility by non-ruminants, but excessive cooking will reduce protein availability. (Note: Ruminants are hoofed, cud-chewing animals such as cattle, sheep, goats, deer, and giraffes, having multiple stomach chambers that are specially adapted for digesting tough cellulose raw.) Thus, there is an optimal heat treatment, which was found to be 120 minutes at 140°C (284°F), or 30 minutes at 160°C (320°F).


The antinutrients here (anti-amylases, phytates) are affected by heating, but phytates require other processing (such as fermentation) for further neutralization, which is still only partial. Also, soaking/germination (sprouting) reduces phytates [Hurrell 1997]. Soaking under optimal conditions (55°C, pH 4.5-5.0) can eliminate phytates [Sandberg and Svanberg 1991].

Egg Whites

Raw egg white contains a protein called "conalbumin" which binds to iron. Additionally, raw egg white contains avidin, which binds to biotin and can impair metabolism of other B-vitamins. Note however that raw egg toxicity should not be overstated: 20 raw eggs per day for several weeks would be necessary to create a biotin deficiency.


The most common commercial mushroom, Agaricus bisporus, causes cancer in mice [Toth 1986]. The dosages required were almost half of their total food intake.

Concerning poisonous mushrooms, obviously cooking amanitas (an extremely poisonous variety of mushroom) won't make them edible, but there are examples of mushrooms which become edible after cooking. Since these varieties are very special and can't be found at the grocery, we won't expand further.


Potatoes contain solanine and chaconine, which are not hazardous unless large quantities are eaten. They don't accumulate in the body, and are not destroyed by heat.

Spinach and Rhubarb

These contain oxalates, which among other effects inhibit calcium absorption. Again, they are not hazardous unless large quantities are eaten. They don't accumulate in the body, and are not destroyed by heat.

Cyanogenic Glycosides

These are found in lima beans, cassava, and many fruit pits [Beier et al. 1994]. Processing techniques partially destroy cyanogenic glycosides, but some poisonings caused by the consumption of large amounts of cassava or fruit pits have been reported, including apricot kernels. When in contact with stomach acids, the cyanogenic glycosides release cyanide, which is the active component in Zyklon B (used by the Nazis in death camps). So indeed cyanide is toxic in large amounts, but obviously a few apricot kernels will not do much harm.


Contains some trypsin inhibitors and lectins, which are destroyed by heat [Seo 1990].


These contain toxic psoralens, which are potent light-activated carcinogens and mutagens not destroyed by cooking [Ivie 1981]. Parsnips contain psoralens at a concentration of 40 ppm, and Ivie [1981, p. 910] reports:

[C]onsumption of moderate quantities of this vegetable by man can result in the intake of appreciable amounts of psoralens. Consumption of 0.1 kg of parsnip root could expose an individual to 4 to 5 mg of total psoralens, an amount that might be expected to cause some physiological effects under certain circumstances...


Flavonoids are a broad class of compounds common in plants and in the human diet. The basic characteristic of flavonoids is that their chemical structure includes what is known as the flavonoid skeleton, that is, a skeleton (core) of diphenylpyrans, i.e., C6-C3-C6, where the C stands for carbon, and C6 is a benzene ring [Hertog and Katan 1998]. Over 4,000 flavonoids are known, and new ones are being researched and described [Hollman 1997]. In plants, flavonoids serve a number of functions: as pigments (the color of fruits and flowers is due to flavonoids), antioxidants, sunscreens, etc.

Because of the large number of compounds in this class, generalizations about the function of flavonoids are difficult [McClure 1975]. However, the following can be said about certain flavonoids:

Alfalfa Sprouts

Alfalfa sprouts contain approximately 1.5% canavanine, a substance which, when fed to monkeys, causes a severe lupus erythematosus-like syndrome. (In humans, lupus is an autoimmune disease.) Canavanine is an analog for the amino acid arginine, and takes its place when incorporated into proteins. However, alfalfa that is cooked by autoclaving (i.e., subjected to pressure-cooking) doesn't induce this effect [Malinow 1982, Malinow 1984].

Note here that the monkeys were fed semi-purified diets, with a canavanine content of 1-2%, versus a typical canavanine content of 1.5% (dry weight--that is, when completely dehydrated) for alfalfa sprouts [Malinow 1982]. Thus, although it would be very difficult for a human to eat enough fresh alfalfa sprouts to ingest even 1% canavanine, individuals should be aware of the potential risks, and consume (or not consume) alfalfa sprouts accordingly. (In particular, those rawists who juice sprouts should probably strictly limit or avoid the consumption of alfalfa sprout juice, due to the concentration effect that results from juicing.)

Other Examples

Let's mention quickly a few other examples: pyrrolizidine alkaloids, present in herbal teas, are carcinogenic, mutagenic, and teratogenic (cause birth defects); gossypol in cottonseed causes abnormal sperm and male sterility, and is a carcinogen; piperine in black pepper causes tumors in mice; capsaicin in hot pepper is a mutagen; allyl iosthiocyanate, in oil of mustard and horseradish, is a carcinogen in rats; quinones and their phenol precursors (in many different plants) have mutagenic and antimutagenic properties.

Other toxic effects of cooking

Heated Milk Protein

It is possible that heated milk protein may be a factor in atherosclerosis [Annand 1971, 1972, 1986].

Heated Fats

Oxidized fats, oils, and cholesterol. Research reveals that in animal models, oxidized fats, oils, and cholesterol induce higher levels of arterial plaque (i.e., atherogenesis) than do the corresponding non-oxidized fats, oils, and cholesterol [Taylor et al. 1979, Kummerow 1993, Kubow 1993, O'Keefe et al. 1995]. The biochemical processes that make oxidized fats atherogenic are the subject of scientific controversy; however, one suggestion is that the heating of fats, oils, and cholesterol increases the levels of lipid peroxide products. The idea is that the peroxides (in combination with lipids) promote an atherogenic response [Kubow 1993].

In tests feeding high-cholesterol diets to rabbits, the consumption of scrambled or baked eggs produced increases in serum cholesterol of 6-7 times the pre-existing levels, while fried or hard-boiled eggs raised levels by 10-14 times [Pollack 1958]. Cordain [in a posting to the Paleodiet list of 10/9/1997] also reports that his research group routinely induces atherogenesis in test animals (miniature swine) by feeding oxidized fats/cholesterol.

Role of oxidized LDL cholesterol in atherogenesis. O'Keefe et al. [1995, pp. 70, 72] explain the role of oxidized cholesterol in atherogenesis as follows:

LDL cholesterol must be oxidized or glycosylated (or both) before it becomes atherogenic.(8,9) Oxidative modification of cholesterol occurs by means of oxygen free radical processes. Only after the LDL has been modified (through oxidation or glycosylation) does it activate differentiation and migration of macrophages. The scavenger receptors on the macrophages recognize oxidized LDL (but not unmodified LDL) and allow for subsequent phagocytosis. When the macrophage becomes filled with oxidized LDL cholesterol, it becomes the foam cell that is typically observed in early atherosclerotic lesions...

The oxidative modification of LDL cholesterol seems to be the final common pathway in the process of atherosclerosis.

Steinberg et al. [1989] also report that oxidized LDL cholesterol, at high levels, is atherogenic. For a good summary of the atherogenic properties of oxidized LDL cholesterol, see Table 2 in O'Keefe et al. [1995, p. 72], and Table 1 in Steinberg et al. [1989, p. 917].

Here it should be noted that some aspects of the effects of oxidized cholesterol are controversial in the sense that a scientific consensus has not yet been reached. Readers are encouraged to consult O'Keefe et al. [1995] and Steinberg et al. [1989] for a detailed overview of current knowledge in this field.

The paradox of relatively high cholesterol intake and cooked meats vs. rarity of heart disease in hunter-gatherer groups. It is also worth remarking that many other factors than lipid peroxides influence the development and/or prevention of atherogenesis, such as the amount of saturated fat, amount of mono- or polyunsaturated fat, amount of carbohydrates and insulin response, etc. Of particular note here is the example of hunter-gatherer societies, where the incidence of heart disease is extremely low (perhaps the lowest that has been seen among human groups), despite the fact that relatively large amounts of cooked meat are consumed. (See Part 3's discussion of hunter-gatherers for a look at some of their food preparation practices; as well as another site link, Hunter-Gatherers: Examples of Healthy Omnivores, for a look at disease incidence.) This is in marked contrast to the high levels of atherosclerosis in Western diets containing cooked meat.

This divergence may be due to the differences between the type of meat (wild game) in hunter-gatherer diets--which in general is quite lean--compared to modern domesticated meats (five times less fat, and one-fifth to one-sixth as saturated [Eaton 1996]), and/or the difference may be due to a range of other factors. Of specific interest regarding the subject of oxidized cholesterol is that while hunter-gatherers eat roughly the same amount of cholesterol (480 mg) as in the modern Western diet [Eaton 1992] (from meat, presumably cooked), their serum cholesterol levels, as measured in five modern hunter-gatherer groups, averaged a very low 123.2 mg/dL [Eaton 1992].

Viewing single factors out of context can be misleading. Thus if cholesterol and/or oxidized cholesterol are in fact atherosclerotic in effect, then the implication is that there must be something else in the diets/lifestyles of hunter-gatherer groups mitigating or negating this effect. (A good overview of the large divergences between hunter-gatherer diets and the modern Western diet can be found in Eaton [1996]. Major differences are to be found in consumption levels of saturated and polyunsaturated fats, preformed long-chain fatty acids, protein, carbohydrate, phytochemicals, etc., as well as in exercise levels.)

The general point here is to keep in mind that, before attempting to form conclusions that might be premature, it is important to view the role of any one factor in the equation of health in the context of the overall diet rather than in isolation. Depending on the situation, the benefits of a food or class of foods may mean more for the health of the body than whatever associated negatives there may be--or vice versa. That nutritional benefits from foods, whether raw or cooked, unavoidably come at the expense of costs and tradeoffs is a central issue that we will return to more than once, in different forms, as this paper proceeds.


(Lesson of the Pottenger's Cats Experiment: Cats Are Not Humans)

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GO TO PART 1 - Is Cooked Food "Toxic"?

GO TO PART 2 - Does Cooked Food Contain Less Nutrition?

GO TO PART 3 - Discussion: 100% Raw vs. Predominantly Raw

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