The Travis Corner

[Tenacity]

I think it tells us that it's a complete food, yet has a relatively high tryptophan ratio:

'This man ate 25 eggs per day apparently due to an obsession tied to mental problems. Repeated attempts at changing his behavior were unsuccessful. He said: “Eating these eggs ruins my life, but I can't help it.”' ―Ned Kock​

'He was an articulate, well-educated elderly man, healthy except for an extremely poor memory without other specific neurologic deficits...' ―Ned Kock​

You think the tryptophan might have exacerbated his mental problems?

 

[Koveras]

From your list: I had counted eight instances of egg yolk eating, one of egg white eating (inapplicable: no linoleic acid), and one of 'fondness for custard' (inapplicable: proclivity for dessert ≠ dietary staple). Confirmed cases of daily, or near daily, egg‐eating represents the following centenarians:

Besse Cooper - 116 years, 100 days
Charlotte Hughes - 115 years, 228 days
Edna Parker - 115 years, 220 days
Gertrude Baines - 115 years, 158 days
Walter Breuning - 114 years, 205 days
Florrie Baldwin - 114 years, 38 days
Emma Morano - 113 years, 231 days
George Francis - 112 years, 204 days​

I had also found three so‐called vegetarians, those who ostensibly avoid eggs entirely.

Marie-Louise Meilleur - 117 years, 230 days
Christian Mortensen - 115 years, 252 days
Reg Dean - 110 years, 62 days​

Eggs do not appear to be required to live 117 years.

The NIH reports the prevalence of 'vegetarianism' to be quite low really. Even among people claiming only 4–6 days of vegetarianism per week, the prevalence was only 3.5–4.2% (depending on year; Table 1). Naturally, the prevalence of strict vegetarians are even lower.

'A 1980 study of 605 Massachusetts physicians and lawyers, however, found that 1.5% called themselves vegetarian (although this population is also atypical).' ―White​

Are these people deluded? Well, here are some characteristics of of those who claim to be vegetarians:

'We found that vegetarians were rare in the population, and there was no change in prevalence during the 1980s (P > .25 for a logistic regression with a y variable of >0 vegetarian days per week) (Table 1). Those with more vegetarian days in the previous week were significantly (P < .05) more likely to be younger, female, more educated, and of higher household income. Those with more vegetarian days had lower weight, plasma cholesterol levels, systolic and diastolic blood pressures, and lower (better) Framingham risk scores. Regarding their health and dietary habits, they had higher health knowledge scores, exercised more, and consumed fewer calories and less fatty food.' ―White​

No mention of choline deficiency was made among this cohort.

Since linoleic acid becomes prostaglandin E₂, and prostaglandin E₂ upregualtes ornithine decarboxylase, you might expect higher cancer rates among egg eaters. This has in fact been found by some researchers.

Among inhabitants of Uraguay, a dose‐dependent effect had been found in a case–control study:

'A high intake of eggs has been associated with increased risk of colorectal cancer in several previous studies (Steinmetz and Potter, 1994).' ―Aune​

View attachment 7817 ​

'Conclusions: We found an association between higher intake of eggs and increased risk of several cancers. Further prospective studies of these associations are warranted.' ―Aune
​

I think you'd have to expect this based on the proliferative effects of prostaglandin E₂. I have yet to see any indication that linoleic acid found in eggs is less carcinogenic than the linoleic acid found in corn oil.

But, of course, linoleic acid alone is not sufficient for particularly high prostaglandin E₂ levels. The expression of induced phospholipase A and cyclo‐oxygenase play a considerable role, and this is powerfully effected by cytokine levels. Other fatty acids will compete for this pathway, and the higher incidence of chocolate eating—a low ω−6 vegan food mentioned by ten centenarians—could have relevance. Stearic acid is the fatty acid historically found most protective, likely on account of its persistence. The short chained fatty acids are metabolized quickly, and only palmitic and stearic acids are long enough to be incorporated into membrane phospholipids:

View attachment 7820 ​

This means that caproic, caprilic, and myristic acids wouldn be expected to prevent cancer since the neither displace linoleic acid from the cell membrane or significantly compete with cyclooxygenase. These short‐chained fatty acids undergo β-oxidation quickly and represent a great source of energy. Coconuts and goat cheese appear to be more Peat-friendly than eggs, both due to the lower Fernstrom ratios and their ω−6 contents.

The centenarians prove that you can still live a long time eating linoleic acid, but I am willing to bet that these people didn't eat very many calories. More highly active people, both physically and intellectually, simply must eat more food—upwards of 3000–4000·Cal·d⁻¹. Although eggs are fun to eat and cook with, I think logic would tend towards more beef and less eggs for those concerned about choline. Compared with eggs, beef is both more saturated and has a lower Fernstrom ratio: W/(T+V+I+L+F).

Beef has much less linoleic acid. Even its total PUFA% is less than the total linoleic acid% found in eggs.

White, Randall. "Health effects and prevalence of vegetarianism." Western Journal of Medicine (1994)
Raes, Katleen. "Meat quality, fatty acid composition and flavour analysis in Belgian retail beef." Meat science (2003)
Aune, Dagfinn. "Egg consumption and the risk of cancer: a multisite case-control study in Uruguay." Asian Pac J Cancer Prev (2009)
Borkman, Mark. "The relation between insulin sensitivity and the fatty-acid composition of skeletal-muscle phospholipids." New England Journal of Medicine (1993)​

Any idea on the time frame from the ingestion of linoleic acid to the synthesis of prostaglandin E2?

 

[Travis]

Any idea on the time frame from the ingestion of linoleic acid to the synthesis of prostaglandin E2?

This is variable. It first needs to be elongated by elongase, desaturated further to arachidonic acid, and then incorporated into a cell membrane phospholipid (usually, arachidonic acid occupies the sn‐2 position of the glycerol backbone). Prostaglandins are synthesized at low levels all the time by phospholipase A₂ and cyclooxygenase‐1. However, cytokines can induce two enzymes with the same function: phospholipase A₂ (inducible form) and cyclooxygenase‐2. These are different enzymes than the constitutional ones—having different protein sequence—and greatly increase both the release of arachidonic acid (via phospholipase) and it's transformation to the prostaglandins (via cyclooxygenase‐2). The induction of cyclooxygenase‐2 by cytokines increases the ratio of prostaglandins over the other eicosanoids (i.e. the leukotrienes).

So it really matters: (1) How much you eat total since spare linoleic acid can be oxidized for fuel, and: (2) The amount of cytokines in the body, some of which can induce the enzymes that greatly increase the rate of prostaglandin synthesis.

The most damaging cytokines appear to be gamma-interferon, interleukin-one, tumor necrosis factor alpha, and interleukin-six.

Killer cytokines!

INF-γ
TNF-α
INF-1
INF-6
​

It's hard to keep track of them all since there are certainly over forty, but some of them are minor and some are actually safe. For instance: interleukin-4 transcribes for the interferon-1 binding protein, which actually binds this killer cytokine and prevents it from working. Besides these, there are also 'dummy receptors.' Vitamin D, for instance, upregulates a decoy receptor for interleukin-one. This allows high-affinity binding on the cell membrane, yet does nothing.

Interleukin-10 is also a friendly cytokine.

This is why some tropical parasitic infections lead to patchy hair loss in both humans and animals; the cytokines upregulate cyclooxygenase-2 and phospholipase A₂ to the point of hair loss as excessive prostaglandin D₂ is created. This happens more in male animals since they have more prostaglandin D₂ synthase, a cortisol-induced enzyme.

So I think it's mostly just enzymes and arachidonic acid (from linoleate). The prostaglandin E₂ flux can be estimated by the kinetic rates of the enzymes, amount of these enzymes, and linoleic acid concentration. In enzyme kinetics the rate is also determined by any competitors, so the ratio of arachidonic to other fatty acids in the sn-2 position of membrane phospholipids matters a great deal (i.e. eicosapentaenoic acid; Mead acid).

 

[Koveras]

This is variable. It first needs to be elongated by elongase, desaturated further to arachidonic acid, and then incorporated into a cell membrane phospholipid (usually, arachidonic acid occupies the sn‐2 position of the glycerol backbone). Prostaglandins are synthesized at low levels all the time by phospholipase A₂ and cyclooxygenase‐1. However, cytokines can induce two enzymes with the same function: phospholipase A₂ (inducible form) and cyclooxygenase‐2. These are different enzymes than the constitutional ones—having different protein sequence—and greatly increase both the release of arachidonic acid (via phospholipase) and it's transformation to the prostaglandins (via cyclooxygenase‐2). The induction of cyclooxygenase‐2 by cytokines increases the ratio of prostaglandins over the other eicosanoids (i.e. the leukotrienes).

So it really matters: (1) How much you eat total since spare linoleic acid can be oxidized for fuel, and: (2) The amount of cytokines in the body, some of which can induce the enzymes that greatly increase the rate of prostaglandin synthesis.

The most damaging cytokines appear to be gamma-interferon, interleukin-one, tumor necrosis factor alpha, and interleukin-six.

Killer cytokines!

INF-γ
TNF-α
INF-1
INF-6
​

It's hard to keep track of them all since there are certainly over forty, but some of them are minor and some are actually safe. For instance: interleukin-4 transcribes for the interferon-1 binding protein, which actually binds this killer cytokine and prevents it from working. Besides these, there are also 'dummy receptors.' Vitamin D, for instance, upregulates a decoy receptor for interleukin-one. This allows high-affinity binding on the cell membrane, yet does nothing.

Interleukin-10 is also a friendly cytokine.

This is why some tropical parasitic infections lead to patchy hair loss in both humans and animals; the cytokines upregulate cyclooxygenase-2 and phospholipase A₂ to the point of hair loss, as excessive prostaglandin D₂ is created. This happens more in male animals since they have more prostaglandin D₂ synthase, a cortisoldependent enzyme.

So it's just enzymes. I think the prostaglandin E₂ flux can be estimated by the kinetic rates of the enzymes, amount of these enzymes, and linoleic acid concentration. In enzyme kinetics the rate is also determined by competitors, so the ratio of arachidonic to other fatty acids in the sn-2 position of membrane phospholipids matters a great deal (i.e. eicosapentaenoic acid; Mead acid).

I was just reading this study

Consumption of whole eggs promotes greater stimulation of postexercise muscle protein synthesis than consumption of isonitrogenous amounts of egg whites in young men

...and wondering if that could be one mechanism for the increased growth from whole eggs. There was some resistance exercise which could have upregulated cytokines, followed by food ingestion, and the last muscle biopsy 300 minutes later.

 

[Travis]

You think the tryptophan might have exacerbated his mental problems?

Just a though. One thing I remember from the Fernstrom studies was that egg albumin had the second highest tryptophan content for a food protein behind lactalbumin, found in whey. Since the egg white represents the great majority of egg protein, I would imagine the egg to be somewhat high in tryptophan. The lactalbumin in milk is of course balanced by just as much, and probably even more, casein protein; cheese has a lower Fernstrom ratio than milk.

The things which affect the brain the most, it appears, are neurotransmitters, aluminum, and homocysteine. Much of the damage from aluminum is a result of lipid peroxidation, as it displaces iron, but I think the inflammation from the inclusion bodies and crosslinks would also increase histamine (a neurotransmitter). Homocysteine causes lipid peroxidation by forming a stable free radical which crosses the blood–brain barrier, causing damage in that way.

So besides the frank damage caused by some things, all that is left are neurotransmitters. High levels of serotonin and histamine have both been shown detrimental in studies, and the direct precursors of these are tryptophan and histidine. Fernstrom has shown that changes in circulating amino acid ratios will reflect changes in brain neurotransmitters, and inflammatory mast cells can greatly increase brain histamine (in the rat, at least) and have been shown capable of migrating to the brain.

So the protein ratios will effect consciousness to some degree. Most people eat eggs with cheese, which lowers the tryptophan ratio. I think eating straight eggs all day would lead to a high level of serotonin in the brain, the only explanation I can think of since they are low in aluminum and hypoallergenic. But homocysteine, from methionine, could also play a role. Homocysteine is strongly correlated with dementia and they should have tested for that. Anything over 14 micromoles per liter is considered damaging, and those with Down's syndrome can have upwards of 40⋅μmol/L.

 

[Travis]

I was just reading this study

Consumption of whole eggs promotes greater stimulation of postexercise muscle protein synthesis than consumption of isonitrogenous amounts of egg whites in young men

...and wondering if that could be one mechanism for the increased growth from whole eggs. There was some resistance exercise which could have upregulated cytokines, followed by food ingestion, and the last muscle biopsy 300 minutes later.

I think so, but eggs also have androgens: another thing, besides prostaglandin E₂, which can increase growth by inducing ornithine decarboxylase (polyamines).

It certainly makes sense, and eggs do seem anabolic. Perhaps someone needs to start a business where chickens are fed coconuts to decrease the linoleic acid concentrations to around 2% (like the tropical pigs), since they seem to be a decent food besides (for some people.)

 

[Dan W]

Perhaps someone needs to start a business where chickens are fed coconuts to decrease the linoleic acid concentrations to around 2% (like the tropical pigs), since they seem to be a decent food besides (for some people.)

Tropical Traditions has these (very expensive) eggs from chickens fed coconuts:
Cocofeed.com: Soy-free organic chicken feed from Tropical Traditions

They mention doing a fatty acid test, but don't mention the specific results.

 

[raypeatclips]

I was just reading this study

Consumption of whole eggs promotes greater stimulation of postexercise muscle protein synthesis than consumption of isonitrogenous amounts of egg whites in young men

...and wondering if that could be one mechanism for the increased growth from whole eggs. There was some resistance exercise which could have upregulated cytokines, followed by food ingestion, and the last muscle biopsy 300 minutes later.

I would have liked a third category for that study, that was egg yolk only, and see what happens, I'm intrigued.

 

[Amazoniac]

Travisord, the concern here is that the more restriction you have, the harder it's to keep healthy. The list has a vegetarian tendency but not to the extreme, however I can't find vegans there: it's quite probable that those who drank milk also ate eggs, especially growing up in farms.

The link I posted commented on the disease association.

Don't you think that eating more foods to thrive means that eggs become almost a necessity? How else would you get enough choline without bumping on the negatives of other foods?
If you buy good eggs and discart the whites, you take care of two of the main problems and it becomes a longevity food.
There's also the fact the birds already processed the PUFA in vegetables, so you can expect them to be more suitable for humanoids than ingesting those straight from copious amounts of vegetables. With just 1-2 eggs on top of a regular diet you cover your choline needs.

Rayzord for example is so diligent with PUFA restriction yet he consumes eggs, but he objects them if the kitcheI mean, chickens are fed a poor diet.

I'm not saying this to defend my omelet, I'm not a big fan of eggs anyway.

https://chrismasterjohnphd.com/2010/12/04/meeting-choline-requirement-eggs-organs/

"folate, vitamin B12, B6, and betaine can spare choline, but only methionine can be used to make choline. The B vitamins and betaine can thus fulfill choline's role in methylation, at least in the liver and kidney, but only methionine can provide the choline needed to export liver fat, to serve as a neurotransmitter, or to make our cell membranes work properly."

"the PEMT enzyme actually creates homocysteine in the process of creating choline! So, if your PEMT engine is running nice and smoothly, you can make your own choline, but you still need more betaine and B vitamins to neutralize the homocysteine that’s generated in the process. If your PEMT engine is working like this, however…

… well, then, you’ve got another problem. If PEMT isn’t using up your methionine to make choline, the methionine is just going to go further on down that pathway shown above and make more homocysteine anyway!"​

Now if someone restricts both choline and methionine, is not very efficient in synthesizing its own (common), and ingest a lot of fructose; how is that going to end up well?
And take a case for example of someone that needs 550mg of choline a day. How to get that much without eggs and without bumping on the negatives of other foods? Not a rhetorical question.

 

[Amazoniac]

@Amazoniac Health Correlator: The man who ate 25 eggs per day: What does this case really tell us?

Thanks for the link!
I'm pretty sure eating a low-carb diet was protective in his case and adding carbs (especially if complex) would create problems for him.

 

[raypeatclips]

Thanks for the link!
I'm pretty sure eating a low-carb diet was protective in his case and adding carbs (especially if complex) would create problems for him.

Why do you think this?

 

[Amazoniac]

Why do you think this?

"The dog is essentially carnivorous with a protein digestive capacity of high caliber. They may masticate or swallow the meat chunks whole and thrive nutritionally. Yet they often die of cancer. On a pure meat diet, however, they form fewer sulfides than on a mixed diet."

When people are dealing with excess endotoxin issues, they find relief with the extremes and feel worse on the mixed diet.
With so much fat, any carbs in greater amounts can have a negative effect.

 

[raypeatclips]

When people are dealing with excess endotoxin issues, they find relief with the extremes and feel worse on the mixed diet.
With so much fat, any carbs in greater amounts can have a negative effect.

Interesting, thank you guru.

 

[noordinary]

Eggs are low in aluminum, and not especially immunogenic, so any mental problems could very well have been due to either serotonin (tryptophan) or homocysteine (methionine).

I'm sure you claimed "homocysteine (methionine)" for a reason, but
It was not the case for me (and i had DNA analysis I don't have any mutations (including MTFR) that could influence what i will post below),
I pulled up my blood work notes, here are my Homocysteine levels
Aug 2014 (vegan*) 11.5
June 2015 (vegan*) 18.3
July 2015 (first month non vegan HF**) 9.4 (note the drop! in just a month)
Nov 2015 (non vegan HF**) 8.8
March 2017 (non vegan Peat***) 5.5
I had more blood work done, but those were the only times homocysteine was measured.
* vegan: I ate all organic fruits (lots of tropical and ripe, cost me a couple thousand a month, considering I lived in Seattle and tropical fruits are nowhere to be seen and had to be delivered), all organic greens (about a pound a day), all organic salads with no dressing, coconuts young (a couple a day) and matured, only used coconut oil (as a body lotion) no other fats (even in soap), ate maybe an avocado once in 2 weeks (I'm just not a fan), was raw vegan, did not eat out (so no PUFAs for me), no breads or pasta, no legumes, and I can count only few times i had rice or potatoes during 3 years being vegan, ate close to 3000 cal/day I was 5'6 and 110 lbs
**non vegan HF: basically hight (saturated fat only) diet low carb moderate protein, again only highest quality food (all grass fed, organic and what not), only A2 dairy and so on, by the end of 2015 i transitioned to ketogenic (what?!) with carbs below 20g/day from wild berries, with keto bodies measured in blood (was monitoring) sad sad sad....
***non vegan Peat: we all know what that means (protein intake much higher than on high fat diet)
Total: As my protein intake increased (more and more animal protein) -> methionine increased -> homocysteine dropped
"Thats my story and I'm sticking to it" LOL
@Travis Protein amount of the an egg is almost equal in egg white and egg yolk (close to 50/50%). It's a myth that egg white is the sole source of protein in an egg.
I do not eat whites, I don't like how they taste.

Tropical Traditions has these (very expensive) eggs from chickens fed coconuts:
Cocofeed.com: Soy-free organic chicken feed from Tropical Traditions

They mention doing a fatty acid test, but don't mention the specific results.

Thank you! I emailed them asking for FA composition analysis, hope they will get back to me.
Have you asked for it yourself and they didn't disclose it?

 

[Dan W]

Have you asked for it yourself and they didn't disclose it?

I've never asked. It'll be interesting to see the composition if they provide it, I just remembered that they've mentioned them being high omega-3 because of feeding the chickens fish and crabs.

 

[noordinary]

@Travis What if high homocysteine is not because of exogenous consumption of proteins high in methionine but
because of stress (for whatever reason including insufficient protein consumption) and cortisol dissolving muscle tissues -> endogenous methionine ?

 

[Travis]

Protein amount of the an egg is almost equal in egg white and egg yolk (close to 50/50%). It's a myth that egg white is the sole source of protein in an egg.

Well I knew there was some protein in the yolk, but the yolk contains the lipids; the white is nearly all protein (calorically). And on a per weight basis, the white constitutes a heavier fraction of the egg:

click to embiggen​

So the white both has: (1) Essentially no lipids and is nearly all protein (calorically), and: (2) Constitutes roughly 2.5× more of the egg's mass than the yolk. So what is going on? I mean . . . WTF is going on?

Water sneaks into to equation, massively diluting the egg white and lowering its protein density:

click to embiggen​

So the yolk, despite being nearly ¹⁄₃ the mass of the white, actually has ~70% more protein—by mass—simply because it has much less water. The nutritiondata.com site kills my browser, so I can't confirm, but based on these numbers it does appear that they both contribute similar amounts to the total egg protein (per mass).

And I stumbled across this:

Looks like even with tallow, the chickens either desaturate the lipids or preferentially enrich the egg with linoleic acid fourfold. Regardless, the 8.9% in the tallow‐fed chickens is better than the 26% in the safflower‐fed. Unusual is the difference between the hens fed soybean oil and those fed linseed oil: The linoleic acid in the eggs doesn't intuitively reflect the linoleic acid in the yolk. Perhaps there is some displacement going on with some other fatty acid not measured?

Wu, G. "Effect of dietary energy on performance and egg composition of Bovans White and Dekalb White hens during phase I." Poultry science (2005)
Carter, Christopher. "Egg quality. A study of the hen's egg." Egg quality. A study of the hen's egg. (1968).
Naber, E. C. "The Effect of Nutrition on the Composition of Eggs 1, 2." Poultry Science (1979)​

I'm sure you claimed "homocysteine (methionine)" for a reason, but
It was not the case for me (and i had DNA analysis I don't have any mutations (including MTFR) that could influence what i will post below),
I pulled up my blood work notes, here are my Homocysteine levels
Aug 2014 (vegan*) 11.5
June 2015 (vegan*) 18.3
July 2015 (first month non vegan HF**) 9.4 (note the drop! in just a month)
Nov 2015 (non vegan HF**) 8.8
March 2017 (non vegan Peat***) 5.5
I had more blood work done, but those were the only times homocysteine was measured.
* vegan: I ate all organic fruits (lots of tropical and ripe, cost me a couple thousand a month, considering I lived in Seattle and tropical fruits are nowhere to be seen and had to be delivered), all organic greens (about a pound a day), all organic salads with no dressing, coconuts young (a couple a day) and matured, only used coconut oil (as a body lotion) no other fats (even in soap), ate maybe an avocado once in 2 weeks (I'm just not a fan), was raw vegan, did not eat out at all (so no PUFAs for me), ate close to 3000 cal/day I was 5'6 and 110 lbs
**non vegan HF: basically hight (saturated fat only) diet low carb moderate protein, again only highest quality food (all grass fed, organic and what not), only A2 dairy and so on, by the end of 2015 i transitioned to ketogenic (what?!) with carbs below 20g/day from wild berries, with keto bodies measured in blood (was monitoring) sad sad sad....
***non vegan Peat: we all know what that means (protein intake much higher than on high fat diet)
Total: As my protein intake increased (more and more animal protein) -> methionine increased -> homocysteine dropped
"Thats my story and I'm sticking to it" LOL

I don't see this as a paradox. While true that homocysteine can be made only from methionine, the blood levels show only homocysteine—or demethylated methionine. Whether or not the methyl group is on homocysteine or not depends on folate, cobalamin, and niacin. The choline found in eggs—alluded to above—is considered a 'methyl donor,' perhaps helping to keep methyl groups on homocysteine.

Niacin (B₃) has been shown to remove methyl groups from the body. The major metabolite of niacin is N¹‐methylnicotinic acid, and I read a study where administrating excessive niacin even lowered the epinenephrine/norepinephrine ratio (nor simply meaning 'without methyl group').

So even though I'd expect a vegan to have a lower homocysteine + methionine level, they could very well have a higher homocysteine/methionine ratio.

And since cobalamin (B₁₂) levels are thought to be influenced by veganism, and also that cobalamin levels influence methylation, there is actually lots of data on vegans and homocysteine:

The male vegans have lower plasma homocysteine than the male omnivores, but the trend is reversed in females. Vegans have predictably higher folate levels and predictably lower cobalamin levels. There does seem to be a trend between low cobalamin and increased homocysteine.

Pyroxidal (B₆) is measured because it is the cofactor for the enzymes which convert homocysteine into the much safer cysteine. The vegans consumed more niacin (B₃) which removes methyl groups. These methylation trends appear somewhat predictable, so keeping the homocysteine/methionine ratio to a minimum is mostly a matter of consuming the proper vitamins: cobalamin (B₁₂), pyroxidal (B₆), and folate (B₉)—the ones with subscripts divisible by three. Also thought to play a role are methyl donors (i.e. betaine; choline; creatine; methylene blue).

German vegans have slightly lower levels of homocysteine than the Austrians, but also paradoxically lower cobalamin levels:

click to embiggen​

So it's doesn't appear to be a simple function on any one vitamin, but a result of a small handful of them. The Pearson correlation coefficient of cobalamin vs homocysteine in vegans was measured to be only −.42 (Krajčovičová-Kudláčková, 2000).

Waldmann, Annika. "Homocysteine and cobalamin status in German vegans." Public health nutrition (2004)
Krajčovičová-Kudláčková, M.. "Homocysteine levels in vegetarians versus omnivores." Annals of nutrition and metabolism (2000)
Majchrzak, D. "B-vitamin status and concentrations of homocysteine in Austrian omnivores, vegetarians and vegans." Annals of nutrition and metabolism (2006)
Van Guldener, C. "Effect of folic acid and betaine on fasting and postmethionine-loading plasma homocysteine and methionine levels in chronic haemodialysis patients." Journal of internal medicine (1999)
​

 

[Lee Simeon]

Ey Travis, what do you think of supplementing with Activated Charcoal?

 

[Amazoniac]

I was going to pull a de Fabo at this point but decided not to because it wouldn't make sense. Check this out instead:

East West: Inflammation

Q: how about the bitter chocolate to prevent the cortisol secretion before workout?

Dr. Ray Peat: Yes, chocolate has – it's probably mostly the leucine content of the chocolate, it's very high protein content, but leucine acts like insulin and helps to prevent tissue breakdown. So chocolate is an anabolic protein more than many other proteins.

 

[Travis]

I was going to pull a de Fabo at this point but decided not to because it wouldn't make sense. Check this out instead:

East West: Inflammation

Ray Peat knows about the mTOR pathway! a very good sign.. . .

Perhaps he should have mentioned these effects from high leucine before betting all his chips on calcium:

'When I lived in Mexico in the 1960s, good milk was hard to find in the cities and towns, and most women had fat hips and short legs. Twenty years later, when good milk was available in all the cites, there were many more slender women, and the young people on average had much longer legs. The changes I noticed there reminded me of the differences I had seen between Moscow and Helsinki, and I suspect that the differences in calcium intake were partly responsible for the changes of physique.' ―Peat​

It's well‐known among pellaga researchers that corn is particularly high in leucine, which can potentiate the niacin loss on a low tryptophan diet. This could be hard to imagine if it weren't for the leucine sensor, named sestrin2, and the mTOR pathway.

And it's well‐known, even among schoolchildren, that Mexico is particularly high in corn.

The decarboxylated carbon skeleton of leucine is reminiscent of isoprene—the cholesterol building block monomer—and studies using ¹⁴C‐leucine have shown it to be incorporated directly into the steroid ring. The body can apparently bypass many steps of cholesterol biosynthesis by using spare leucine directly.

Peat, Ray. "Milk in context: allergies, ecology, and some myths." www.raypeat.com (2011)​

Ey Travis, what do you think of supplementing with Activated Charcoal?

This could adsorb endotoxin, but it could be persorbed to a degree. But this is just carbon, and I don't think there would be too much harm.

I am sure there are dozens of studies on charcoal that we could read to help ascertain its long‐term safety, such as this:

Pegues, A. S. "The removal of ¹⁴C labeled endotoxin by activated charcoal." The International journal of artificial organs (1979)​

I think it could be helpful looking at what connectivity the carbons are; some cyclic carbon rings—like dimethylbenzanthracene—are carcinogenic, yet many connectivities are quite safe (i.e. squalene). When things are burned many different carbon skeletons are formed as the oxygen and nitrogen atoms leave. For instance: burning tobacco can convert the six‐carboned glucose into benzene, but anyone who eats grilled food ingests a similar mix. Although much attention is given to polycylcic aromatic hydrocarbons, it has been found in many studies that boiled meat is a greater risk factor for colon cancer than grilled. [?] This is certainly puzzling, and could have something to do with either polyamines or lipids; fatty acids can change upon high‐temperature heating, and Ray Peat does talk about the formation of conjugated linolenic acid from linoleic.

'When meat is grilled at a high temperature, the normally spaced double bonds in PUFA migrate towards each other, becoming more stable, so that linoleic acid is turned into “conjugated linoleic acid.' ―Peat
​

This is actually more stable since it doesn't have a bis‐allylic hydrogen like linoleic acid does. Also, I don't even think it can become prostaglandins.

'We, therefore, grew Salmonella typhimurium in ¹⁴C-labeled glucose to obtain ¹⁴C-labeled endotoxin. Radiolabeled endotoxin was used to measure the rate of adsorption on activated charcoal. The rates of removal of endotoxin from normal saline, plasma, and whole blood will be presented in graphical form for use in design calculations.' ―Pegues​

The whole‐text article is unfindable, but I did request it on researchgate.net so it could perhaps be coming shortly. The last two articles I had requested were given to me, so I think I could have a chance of getting this one. (Although I don't see how, since it was written in 1979 and the authors are probably in their '80s—perhaps not even having email addresses.)

But could it be worse than endotoxin? Probably not. Even if it were slightly harmful, in a way, the fact that it adsorbs much more harmful things means that it would have a net benefit for some people―if not all people.

Peat, Ray. "Fats and degeneration." www.raypeat.com (2009)
Talhout, Reinskje. "Sugars as tobacco ingredient: Effects on mainstream smoke composition." Food and Chemical Toxicology (2006)

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