Meat Toxins: What they are, why they exist, how to avoid them.

Evolutionary Nutriton Preface

Nothing wants to be eaten, everything wants to survive.

Because of this, everything that we see today (those that successfully survived and reproduced) has developed a capacity to defend itself against predators.

For vegetables and plants, this is the development of phytoalexins. Compounds that can cause toxicity to the predators when the predators eat a leaf or plant and deter further eating. This can be as simple as having a displeasing taste, or it can be as potent as a neurotoxin (like caffeine is to insects). Compounds that successfully do this to humans are not things we call veggies, but things we call toxins (there is a reason we don’t serve hemlock with our salads; our ancestors found that out for us).

Animals? They tend to attack you or run away; that is their defense. They don’t need any fancy chemical defenses when they can shove a hoof into your throat.

So does that mean that meat and eggs are completely harmless? Technically, meats found in their true form (raw, freshly killed) do not possess any toxins in them and are too freshly killed to have harvested much bacteria. Killing a deer and then feasting upon its limbs immediately, however gruesome, is free of almost all toxins (unless the animal rolled around in the stuff, or was infected while still alive).

Enter Cooking

Seems in our attempts to preserve or to make things palatable, humans have been screwing up since the dawn of time.

Cooking, or basically a very high temperature and volatile reaction, is able to cause structural changes to animal tissue which can result in what are known as ‘pre-carcinogens’. They are not carcinogenic per se, but can be turned into carcinogens in the body. Preserving meat with various agents (nitrites in particular) can sometimes introduce new intermediates by which cooking can form pre-carcinogens, however its very hit or miss (nitrites can create carcinogens, salt does not).

Before we begin: A primer on the P450 system

This article will rely on some knowledge of the P450 detoxification system. It is a system of non-specific enzymes expressed almost everywhere, but mostly in the liver. It is divided into classes called CYPs, and each enzyme has a certain denotation to it (CYP1A1 is in the 1st CYP family, the first of the A subset; it is also known as aromatase. It should be noted that CYP1A2 is also aromatase, but just the aromatase found in other parts of the body. Many times you see the denotation of CYP1A1/2 to refer to all aromatase enzymes)

There are two ‘Phases’, or steps, in toxin detoxification. The first step is designed to make an unreactive molecule reactive, and the second step is to grab the now reactive toxin and excrete it (phase II cannot work without phase I starting the process).

The CYP denotation applies to Phase I enzymes only. They recognize a part of a molecule (a planar surface, a ring structure, etc.), bind to it with an Iron ion which is in the center of the enzyme, and basically falcon punch it with an Oxygen molecule. This makes the normally unreactive compound a reactive one, since it now has a functional oxygen group on it.

Phase II enzymes are not CYP class, and have no real labelling system. They are a class of enzymes which recognize these functional groups and then ‘tag’ them with compounds to direct them to urinary excretion. This tagging should deactivate the compound again. Enzymes in the second phase include Glutathione transferases, Glucuronidation enzymes, Sulphation enzymes, and N-acetyl transferases (NATs). Each enzyme tags a reactive group with a different ‘tag’, and tend to favor some metabolites over others (Glutathion likes electrophilic (electron liking) intermediates, glucuronides and sulphates like nucleophilic ones)

We can see the logic behind why the body does this through looking at the ‘exceptions that define the rule’. Dioxins, Methyl-mercury, and PCBs are 3 classes of toxins that do not undergo any P450 detoxification whatsoever. All three can build up in the body over time, and all three cause neural damage when they build up in brain tissue.

The body has P450 so you don’t die from neural damage by the age of 5 by merely breathing. Despite its downsides, it saves our asses on a routine basis.

So the above, bulleted is:

  • The body has a 2-Phase enzyme defense designed to protect the body from unknown compounds
  • It either tags the compounds for excretion directly, or forces the unreactive compound into a reactive state so it can be tagged
  • If they didn’t do this, toxins would build up in our bodies and cause neural damage
  • Sometimes forcing a safe compound into a reactive state makes it carcinogenic; Shit happens yo

Heterocyclic Amines (HCAs); the dry condition concern

Heterocyclic Amines are compounds that are formed from (1) a creatine molecule (2) an amino acid and (3) some form of reducing sugar, although that is not wholly needed.

Heterocyclic Amines are formed at around temperatures of 100-250C, and are enhanced by dry conditions; they are found mostly in meats cooked via roasting, baking, and frying; beef jerky is the highest normal source of HCAs. The production of HCAs during cooking is very much a time X heat equation, with more heat and longer cooking equaling more HCA formation. [x]

HCAs are, like the other compounds, stable. When metabolized, it gets falcon punched by aromatase (CYP1A1/2). At this point it is reactive, but not overly carcinogenic.

Then the Phase II enzyme, N-Acetyltransferase (NAT) tags it with an acetyl group. This is a facepalm moment, because he just screwed up his job and now made it dangerous. Until glutathione rushes in and tags it again, this secondary intermediate can act as a carcinogen. [x]

Due to the above metabolism and production conditions, you can reduce the harm HCAs exert on you (potentially) by either cooking in moist conditions, not cooking above 100C (hard to do), or surprisingly by marinating meat prior to cooking. The addition of spices and oils seems to suppress HCA formation, and it seems to be through the anti-oxidant potential of the oils and spices. [x] The spices added seem to be non-specific, as inhibition has been seen with red wine marinades [x] [x] and various anti-oxidant containing spices and oils, just don’t use a sugar based marinade, as soy + sugar has been shown to increase HCA formation. [x]

It should be noted that at least one study has found no effect at higher anti-oxidant doses, and even an increase in HCA formation with a very high level of anti-oxidants. [x] It would probably be best to marinade meats anyways, but be aware that the most significant reduction in HCA intake will come from limiting meat consumption or limiting cooking time (rare steaks over well done) or from in vivo prevention of carcinogenesis, by inhibiting aromatase with veggies. [x]

Nitrosamines (NAs); the preservative concern

Nitrosamines are a class of compounds that are created when the compound ‘nitrite’ combines with amino acids. Their mechanism of carcinogenesis is through being metabolized by a P450 enzyme (CYP2E1), which forms an unstable intermediate. This unstable intermediate passively degrades into a compound known as methyl carbonium [x], which is the main carcinogen. The parent nitrosamines and the nitrates themselves are not carcinogenic per se, like the other compounds in this list. [x] [x] Heck, nitrates and nitrites may even be healthy. [x]

Nitrosamines are produced when nitrite is added to foods during processing as a preservative (usually in cured and ‘pink’ meats like ham or bacon), however they can also be formed from dietary nitrates which are high in vegetables and especially beets. However, the risk from vegetables seems to be much less than the risk from meat. [x]

This is due to nitrate being unable to form nitrosamines, but nitrite can. Nitrite is the oxidized form of nitrate, and this conversion can be prevented by consuming ‘reducing agents’, or compounds able to donate an electron. The most common is vitamin C, found almost ubiquitously in vegetables (Note: Vitamin C is the most common electron donating compound studied in regards to nitrosamines, but is not the only compound able to do this). [x] [x]

Most bioactive nitrosamines are actually formed in the stomach or the intestines, thus cooking methods are unlikely to be the best cause of prevention. Its much more plausible to focus on co-consumption of vegetables and reducing agents in vegetables, and get the two-sided benefits of less bioactive methyl carbonium (carcinogen) and more bioactive nitrates (beneficial?). Taking vitamin C capsules alongside meat consumption also works well.

Polyaromatic Hydrocarbons (PAHs); the barbeque concern

Meat has fatty acids, chains of carbon molecules. These are stable and the source of PAHs (note, even the leanest horse meat can develop PAHs during cooking).

An example my toxicology professor taught me to view PAHs is like a candle. The wax of the candle is fatty acids. As they are brought up the wick they are oxidized one carbon at a time. The flame you see (reddish yellow) is where a bunch of short -chain fatty acids are still undergoing oxidation, whereas the smoke you see above is the complete oxidation (free oxygen, hydrogen, and carbon molecules). They tend to be formed at temperatures exceeding 250C. [x] [x]

PAHs form when you oxidize fatty acids, but not completely; this occurs when smoking meat or preventing ventilation (keeping the hood on the barbeque). They break down into chains of about 2-4, and then like lego pieces they spontaneously combine with each other to form 6-carbon benzene rings. This is a process known as pyrosynthesis. PAHs are actually a class of numerous compounds that are just benzene rings structures, although the most well researched is benzo(a)pyrene.

If you put PAHs in a test tube with DNA, nothing will happen. The benzene rings are very stable and not carcinogenic in the least; like the above two categories of compounds as well. This is where our beloved P450 enzymes come in; and actually, aromatase (CYP1A1/2) is to blame here (again)

Aromatase attaches an oxygen molecule onto the PAH, and turns it into an epoxide (two carbons of the ring attached to one oxygen molecule). This epoxide is rapidly attacked by the enzyme epoxide hydratase to form another intermediate (which isn’t that much of a concern) but then aromatase says “Fuck you” and adds another oxygen onto it. Now you have a potent carcinogen. [x]

It can be detoxified by phase II at any stage. So because of this the best measures to take against PAH carcinogenesis are to inhibit aromatase (which acts twice) or to just not consume the PAHs in the first place.

The best way to not consume it is to not cook your meat in a place where the smoke cannot be released. By allowing full oxidation of fatty acids you prevent build-up of short-chain intermediates and thus less PAHs; its like depriving your kid of lego, it doesn’t matter how good he is at building he cannot if he doesn’t have the bricks to build with.

PAHs are highly correlated, and in part causative, of the smoky taste in meats. So yeah, if you like health then limit consumption of smoked meats (sorry, those living in Montreal).

Alternatively, you can inhibit aromatase. As laid out in my article on the matter (found here) many vegetables are able to inhibit aromatase. Again, the same toxicology professor noted that “I have no clue if we have a society of toxicologists or are just lucky, but family gatherings that tend to serve smoked, grilled, and carcinogenic meats also tend to have a veggie platter out before the meal. Load up on bioflavonoids and enjoy your meat”.  [x] [x]

Advanced Glycemic End Products (AGEs); the browning concern

Probably the least of a concern of the list actually. AGEs are directly correlated with meat ‘browning’ as they are compounds of what is known as the Maillard Browning Reaction, a process by which a sugar and an amino acid bind together to form AGEs.

We know a lot about the biological activities of AGEs since they are naturally produced in the body from when sugar attacks proteins, and higher circulating AGE levels in diabetics gives a good indicator of acute and chronic pathology of what AGEs could do to the human. [x]

That being said, it does not get bioconverted to a carcinogen. It does not significantly interact with P450 either. Lastly, since they are naturally occurring in the body we have enzymes that are able to metabolize them. [x] [x] The main reason they are of concern is their deleterious effects on lipoproteins, by glycating them and being a risk factor for artherosclerosis. Whether this pathology applies to dietary AGE intake is uncertain as dietary intake of AGEs is much, much less that what occurs in diabetics. If anything, if AGEs concern you the best thing to do is exercise and eat right to control your blood sugar.

I mention AGEs as they are a prototypical ‘meat toxin’ from cooking, but they are very different than the other three mentioned above in that they are not carcinogenic directly and that you don’t need to worry about them too much.

Can I get a ‘Too Long; Didn’t Read’ up in here?

It was a long article, and worth a read; just to summarize though:

  • Meat, unlike plants, do not contain any inherently toxic compounds in them when you eat them like ‘our ancestors’ did; stab the animal in the eye and feast upon its tissues. This isn’t how we eat meat though.
  • When you add preservatives and cooking into the mix, you can form carcinogens. These were never ‘factored out’ by evolution or ‘adapted to’ since they only adversely affect human health well past reproductive age and natural selection doesn’t apply.
  • They can all either be avoided, or minimized.
  • Heterocyclic Amines are formed from cooking, and their amounts are directly related to heat exposure and time. You can reduce the amount in meat with herbal and oil marination, but it would be best to limit cooking time in order to avoid excessive HCA formation.
  • Nitrosamines are formed when the Nitrate preservative binds with amino acids, and can best be prevented by consuming reducing agents (vitamin C, or just veggies) alongside the meat.
  • Polyaromatic Hydrocarbons are formed during smoking, from incomplete combustion of fatty acids, and can best be avoided through aromatase inhibition (veggies) or allowing all meats to fully ventilate, thus preventing the ‘incomplete combustion’ from being incomplete.
  • Advanced Glycemic End products aren’t a huge concern, but are formed when meats get a crispy browning to them. They can be avoided by not browning the meats, but if you are worried about their effects in the body just get your blood glucose and HbA1c levels under control and don’t get fat.

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