If you have health problems, I would have to do some research to
determine what seems best to do, but I'd need a lot more information.
Here's the "food to avoid" material.  It's from beyondveg.com's web
site.

I did not post the parts of this page that contained speculation about

the diets of prehistoric humans.  Note that lipid peroxidation is
mentioned, but they seem unaware at how dangerous the highly
unsaturated oils are (it's interesting that talk about prehistoric
peoples, yet don't realize how these new oils, which are potent
oxidizing agents, can cause so much damage to the body).

"Mycotoxins

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.

Beans

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:

Goitrogens: substances that cause goiters, i.e., an enlargement of the
thyroid gland.

Tannins: complex plant compounds that are often bitter or astringent.

Phytoestrogens: plant analogues of the hormone estrogen.

Flatus-producing oligosaccharides: carbohydrates of small molecular
weight that cause flatulence (gas).

Phytates: which bind minerals preventing absorption.

Saponins.

Antivitamins.

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).

Grains

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.

Mushrooms

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

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.

Taro

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

Parsnips

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

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:

Quercetin, a very common flavonoid in the human diet, is known to be
mutagenic [Nagao 1981]. However, it is not carcinogenic, and has been
shown to have anticarcinogenic properties in tests in vitro; see Hertog

and Katan [1998], and Chung et al. [1998].

Flavonoids can inhibit enzyme systems in mammals [Hollman 1997].

The flavonoid phloridzin (and its breakdown products) can inhibit
respiration in animal tissues [McClure 1975].

Certain flavonoids can function as antioxidants and help preserve
vitamin C [McClure 1975].

Some flavonoids protect against the mutagenic effect of other
substances. (Refer to the previous section on Mutagenicity and
Carcinogenicity, subtopic "Other Factors Influencing Carcinogenesis.")

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]."

If you have health problems, I would have to do some research to
determine what seems best to do, but I'd need a lot more information.
Here's the "food to avoid" material.  It's from beyondveg.com's web
site.

I did not post the parts of this page that contained speculation about

the diets of prehistoric humans.  Note that lipid peroxidation is
mentioned, but they seem unaware at how dangerous the highly
unsaturated oils are (it's interesting that talk about prehistoric
peoples, yet don't realize how these new oils, which are potent
oxidizing agents, can cause so much damage to the body).

"Mycotoxins

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.

Beans

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:

Goitrogens: substances that cause goiters, i.e., an enlargement of the
thyroid gland.

Tannins: complex plant compounds that are often bitter or astringent.

Phytoestrogens: plant analogues of the hormone estrogen.

Flatus-producing oligosaccharides: carbohydrates of small molecular
weight that cause flatulence (gas).

Phytates: which bind minerals preventing absorption.

Saponins.

Antivitamins.

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).

Grains

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.

Mushrooms

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

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.

Taro

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

Parsnips

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

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:

Quercetin, a very common flavonoid in the human diet, is known to be
mutagenic [Nagao 1981]. However, it is not carcinogenic, and has been
shown to have anticarcinogenic properties in tests in vitro; see Hertog

and Katan [1998], and Chung et al. [1998].

Flavonoids can inhibit enzyme systems in mammals [Hollman 1997].

The flavonoid phloridzin (and its breakdown products) can inhibit
respiration in animal tissues [McClure 1975].

Certain flavonoids can function as antioxidants and help preserve
vitamin C [McClure 1975].

Some flavonoids protect against the mutagenic effect of other
substances. (Refer to the previous section on Mutagenicity and
Carcinogenicity, subtopic "Other Factors Influencing Carcinogenesis.")

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]."