The Travis Corner

Travis

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@Travis, a few quick questions for you:
1. I would presume sheep yogurt is less immunogenic than cow yogurt but it’s also more expensive. What’s your opinion on yogurts, standard, Greek or sheep?
2. Does the lactic acid in yogurt need to be avoided?
3. Although not great, is skinless chicken breast is an acceptable protein? More acceptable than low fat fish?
Thanks and I look forward to your opinions

I. I had always like Greek the best, and had preferred to eat it on top of a pile of red grapes. But the lactic acid bacteria do have enzymes, and their proteolytic activity is catalyzed by the low pH environment consequent of their lactic acid. For instance: it only takes twenty-four hours for Lactobacillus sanfransiscensis to sufficiently hydrolzye wheat gluten to the point of non-immunogenicity, making a sourdough bread innocuous enough for celiac's to eat (but it's actually more likely that wheat lectins cause the physical damage, and not the immunogenic gliadins as commonly supposed). The effects of the fermentation cannot be disregarded, and I would say that the opiate effect of yogurt cannot be reliably inferred simply on account of its original casein content. So on account of Lactobacilli having a theoretical ability to degrade β-casomorphin, further investigation is required:
This study indicates that the initial casomorphin concentrations of yogurt are insignificant compared to the amounts you'd expect after digestion. For that, there is another study:

De Noni, I. "Occurrence of β-casomorphins 5 and 7 in commercial dairy products and in their digests following in vitro simulated gastro-intestinal digestion." Food chemistry (2010)

'Use of probiotic strains in fermented milk production may modify the peptide pattern in the final product and the potential release of β-casomorphins during stimulated gastric digestion could be affected as well. Nevertheless, a ultra-high temperature pasteurized milk fermented by the probiotic Lactobacillus GG strain and subsequently digested by pepsin and trypsin was not found to contain β-casomorphin-7 whilst only peptide sequences such as β-casomorphin-11 and β-casomorphin-4 were revealed.' ―de Noni

So exactly how the casein is degraded is somewhat stochastic, and only brie cheese had significant levels of pre-made β-casomorphin-7. Some bacterial strains do act on casein, yet no evidence I've seen as of yet indicates that the casomorphins are inactivated by them (that is, cleaved somewhere in the central region of Tyr–Pro–Phe–Pro–Gly (or YPFPG)—the core peptide region corresponding to amino acids № 75–82 of bovine β-casein as sequenced here).

And further complexifying the quality and quantity of peptide fragmentation, this initial peptide confetti—often created by multiple strains in just one cheese type—is further hydrolyzed by gastric trypsin and pepsin. Below is the result of thirty-one dairy products after simulated gastric digestion:

cheese.png

The cheeeses make everything else look insignificant, and even approach the values 'milk protein concentrate.' But they had only analyzed analyzed the dairy products for β-casomorphin-7 and β-casomorphin-5 (not present), and the longer β-casomorphin-11 is considered a proto-opiate.

'In the present work, pepsin and Corolase™ were used for SGID at the end of which none of the analysed dairy samples released BCM5.' ―de Noni
But β-casomorphin-4 certainly bioactive, and could potentially be present in yogurt. This species isn't always looked for, but perhaps it should be:

Matar, C. "β-casomorphin 4 from milk fermented by a mutant of Lactobacillus helveticus." International Dairy Journal (1996)

'Casomorphins are physiologically important peptides, that can be isolated from enzymatic digests of caseins (Brantl et al., 1979). Morphiceptin, which is an amide derivative of β-casomorphin-4 (Tyr-Pro-Phe-Pro), is a highly selective opioid agonist for both μ receptors in guinea pig ileum and morphine binding sites in rat brain (Chang et al., 1985); it is as potent as morphine (Ramabadran & Basinath, 1989).' Matar

'In order to grow in milk, lactic acid bacteria must have the ability to attack milk proteins by proteases and peptidases leading to limited proteolysis during the fermentation and to the release of peptides (Thomas & Pritchard, 1987). The breakdown of proline-rich proteins such as caseins often involves proline-specific peptidases; many lactobacilli possess this type of exopeptidase (Barnett, 1977).' Matar

'Numerous reports suggest that the biological activity of casomorphins is principally analgesic (Brantl et al., 1979), affecting the gastrointestinal tract and the central respiratory control mechanism (Ramabadran & Bansinath, 1989).' Matar

'This study demonstrated the presence of β-casomorphin l-4 in milk fermented by an X-PDAP-deficient mutant of Lactobacillus helveticus, suggesting a hitherto unexplored use of fermented milk as a potential source of bioactive peptides.'

But entire study was somewhat artificial, as he had mutated a strain of bacteria using ethyl methyl sulfonate from Sigma–Aldrich. The result was a mutant strain having protelytic enzymes of a different specificity as compared to the wild type, and this had shifted its hydrolytic propensity for specific peptide bonds:

peptide.png

II. Someone sent me a private message about lactic acid a few months ago and I did some calculations. Let me see if I can find it.. .

I had read a few studies about lactic acid, did some math, and had concluded this (here is the link to the entire thread):

'I think it will cause about as much of a lactic acid spike as a mild jog. Our livers turn lactic acid back into glucose constantly, and physical exertion increases this. It's certainly not a stranger to normal metabolism. Ray Peat has a point in that it would theoretically occupy the liver with more work, but this does result in glucose so it's not a total loss.

My calculation indicates that a person at rest metabolizes 4× more lactic acid through their liver than what is found in 500 grams of generic commercial yogurt, per day.' ―Travis

III. The fish topic is somewhat controversial it seems because aquatic species have essentially no ω−6 fatty acids. These are certainly the worst ones and the sole precursor to the 1- and 2-series prostaglandins (via arachidonic acid). A person eating fish while also avoiding ω−6 fatty acids will have quite a bit more eicosapentaenoic acid at the sn-2 position of cell membrane phospholipids. This lipid will form the 3-series prostaglandins when released by trauma or phospholipase A₂, but these (as PGE) have only has about ¹⁄₄ of the carcinogenic activity as the 2-series prostaglandins (derived via ω−6); some researchers even characterized the 3-series as 'anti-inflammatory' or 'protective.' Eicosapentaenoic acid actually does appear beneficial in many studies, but perhaps this is only due to it's ability to displace the more dangerous arachidonic acid. Eicosapentaenoic acid could only be good to the extent that it's not arachidonic acid.

ω−6 dihomo-γ-linolenic acid (20∶3) + ONOO⁻ ⟶ cyclooxygenase ⟶ 1-series prostaglandins + ṄO

ω−6 arachidonic acid (20∶4) + ONOO⁻ ⟶ cyclooxygenase ⟶ 2-series prostaglandins + ṄO

ω−3 eicosapentaenoic acid (20∶5) + ONOO⁻ ⟶ cyclooxygenase ⟶ 3-series prostaglandins + ṄO

But ω−9 Mead acid is also a 20-carbon membrane lipid (20∶3), and this can displace both of them. And unlike arachidonic and eicosapentaenoic acid, this one is not a legitimate substrate for cyclooxygenase. While true that it forms a peroxide under the agency of that enzyme, this is not a endoperoxide ring which eponymously defines that enzyme (also called a cycloperoxide). This endoperoxide ring is also the defining feature of prostaglandin H, cyclooxygenase's main product and precursor to all others. Hence, it forms a leukotriene-type eicosanoid that is in no way similar to the prostaglandins. So even though eating fish would probably lead to improvements in a person replacing dark chicken or pork, for example, you cannot say that it would be better a better substitute for beef (unless acne should be the primary focus, in which case the increased sebum fluidity consequent of replacing beef with fish could help).

But since very few people avoid both fish and linleic acid, the presence of lipid profiles dominated by Mead acid is quite rare. Many coconut- and fish-eating islanders avoid ω−6 nearly entirely, which is easy for them since those temperate fatty acids hardly exist anywhere on their island. Vegetarians and vegans avoid fish, by definition, yet most of them consume substantial amounts of arachidonic acid precursors. The only mead acid dominated people would have to be those living near exclusively off coconut, fruit, and leaves. Beef and dairy are quite low, but they still could have the small amount necessary to prevent the synthesis of Mead acid. But as stated before, there isn't too much research on this; finding Mead acid in a person is a rare even these days. But if I were to guess, I'd say there are enough earlier studies to get a good idea of the extent you have to avoid ω−6 to fully deplete the cell membranes of arachidonic acid.
 

Wagner83

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In the last few posts you mentioned lectins as being harmful, the greatly missed tyw was an other member who acknowledged these concerns, he went as far as saying the lectins in potatoes could be an issue for some (a leaky intestinal barrier from eating potatoes being a possibility).
Do you have any information on lectins in potatoes and their potential harmful effects?
 

Fractality

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I've heard that rumor as well but not sure it applies to snus (in a pouch). Here are the ingredients of the snus I recently picked up at a local store. I figured I could try a brand like this to get a feel for it before delving into other brands with perhaps less additives. The humectant below is propylene glycol since that is listed on my can. The sweetener is artificial. Any glaring issues here?

General White Wintergreen Portion Snus

Ingredients: Water, Tobacco, Salt, Flavors incl. Smoke Flavor, Humectant (E 1520), pH Adjuster (E 500), Sweetener (E 950)

Just in case you didn't see my last reply, I have quoted my post.

Also, what are your thoughts on non-psychedelic mushrooms as a (vegan) protein source? Do you eat them?
 

Wagner83

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Also, what are your thoughts on non-psychedelic mushrooms as a (vegan) protein source? Do you eat them?
Why would anyone do that? That's like drinking beer without alcohol, eating eggs without the yolks, loving battlefields but being in the Swiss army.
 

sladerunner69

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Why would anyone do that? That's like drinking beer without alcohol, eating eggs without the yolks, loving battlefields but being in the Swiss army.

Have you heard of the "Swiss Guard"? These are troops trained by the state for national defense but also function as for-hire mercenaries. They have been involved in most European wars going back to the middle ages.
 

Broken man

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Well, the easiest and safest way to get that much protein is likely beef or lamb. I don't think high protein is especially troublesome in many cases, but the ratios certainly need to be considered in times of cancer (i.e. methionine, selenomethionine, leucine) and infection (i.e. glutamine, arginine). Glutamate and aspartate are safe, and they will readily enter the citric acid cycle after losing ammonia (NH₃). I think there are ways of eating that much protein while also dodging ω−6 fatty acids, lectins, glutamine, immunogenic proteins, etc. Even though the entire chicken is high in linoleic acid, due to what they're fed, certain parts of this animal are very low; these parts are low in essentially all fatty acids.

As a food having exorphins: wheat, soy, and dairy are probably the most addictive. To give you an idea of the difficulty experienced in the process of quitting, perhaps you can read the comment section of this article.
Thank you. But how will I be getting calcium? Vitamin D, A? Without milk...
 

Mito

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A person eating fish while also avoiding ω−6 fatty acids will have quite a bit more eicosapentaenoic acid at the sn-2 position of cell membrane phospholipids.
What other types of fatty acids (besides the ω−3, ω−6, and ω−9 fatty acids) can occupy the sn-2 of the cell membrane phospholipids? Are they all equally likely to occupy the sn-2 position depending on the quantity of each fatty acid in the body?
 

Travis

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In the last few posts you mentioned lectins as being harmful, the greatly missed tyw was an other member who acknowledged these concerns, he went as far as saying the lectins in potatoes could be an issue for some (a leaky intestinal barrier from eating potatoes being a possibility).
Do you have any information on lectins in potatoes and their potential harmful effects?

There are lectins in potatoes but these appear to lose their carbohydrate-binding affinity after cooking. Not all lectins are considered equal, and they all bind with varying affinities to various polysaccharides. The most well-known mammalian lectin is one in our liver, and this binds and removes from the circulation certain polysaccharides. The lectins most dangerous to humans would be the ones which bind strongly to the intestinal polysaccharides which form the slippery barrier between the enteral cells and the foods. Wheat lectins are capable of doing this, and there's very good indication that the physical damage seen in celiac disease is lectin-mediated. I suppose the 'conventional' view is that the immune system causes the damage somehow after being sensitized against a gluten peptide—perhaps using an autoantibody—but I think there's more evidence pointing towards wheat lectins being the cause. This is not to say that wheat peptides do not create autoantibodies, they most certainly do, but the location and character of the damage appears more consistent with the lectin explanation; there are many good studies on this. An autoantibody-mediated condition would likely be damaging more indiscriminately and not strictly localized to the duodenum-jejunum; the structural bodily proteins expressed in that location are expressed throughout the entire length.

Many foods have lectins, and I don't think they are all necessarily there for defense. I think its easy to imagine that some proteins would need to bind carbohydrates for a seed to develop properly and/or germinate. But that's not to say that evolution couldn't have favored a few mammalian-damaging lectins for defense, tending towards increased survival (a Darwinian outlook); I certainly think this would be expected to occur (i.e. ricin), but domestic crops are under anthropogenic selection—not natural selection. This would tend towards the decrease in damaging lectins unless those who are selecting should be doing so in a manner which opposes to the welfare of those who eat them. Most lectins appear to lose their high-affinity carbodyhydrate-binding ability the moment they are cooked while others don't even bind to intestinal polysaccharides at all (although the must bind to some other polysaccharides, by definition). Plant lectins—which are all proteins—are often added to the litany of 'plant toxins' by those who argue against their consumption, serving as an embarrassing form of contradiction in those who also claim plants aren't supposed to have any. I don't think lectins should be considered harmful as a class because most of them lose their polysaccharide-binding affinity the moment they're cooked, after which they are no longer even considered lectins (by definition).
 

Travis

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Just in case you didn't see my last reply, I have quoted my post.

Also, what are your thoughts on non-psychedelic mushrooms as a (vegan) protein source? Do you eat them?
I think mushrooms might be good—I know they can taste good—but I don't eat them. But perhaps we should; maybe it's good to have other spores to compete with the dangerous Candida albicans? I do think I've read something about this once. Perhaps I will read more into eating mushrooms soon here as I always like eating portobellos and they do have trace minerals (I think they do have Cu²⁺ and Zn²⁺, right?).
 
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Travis

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Thank you. But how will I be getting calcium? Vitamin D, A? Without milk...
I've said before and I'll say it again: The RDA is such that a person would practically have to eat either leaves or dairy products. There are other ways besides, but far less Peat-friendly ways. Certain legumes, seeds, and nuts could realistically provide enough (or very close to enough) but also would deliver prohibitive levels of linoleic acid. Things like chickpeas, sunflower seeds, and almonds are ruined by their ω−6 fatty acids; this is as unfortunate as it is undeniable. Leaves also have high levels of K⁺ and Mg²⁺ along with the calcium, and appear to provide a balanced mineral ratio (or so claims the giraffes). Raw milk must provide a very good mineral balance as this is naturally the exclusive infant food for months-to-years—a person can hardly argue against the minerals, or the fatty acids, in that. Cheese is fractionated milk and could thus would have a more unbalanced mineral ratio (assuming that found in milk is 'balanced').

When most people think of calcium they thing of things such as osteoporosis and bone mineral density, but this is largely under hormonal control. The highest levels of osteoporosis are found in Scandanavia, the same region having the highest dairy consumption. Some have argued that 'milk causes osteoporosis' but this is of course absurd; what seems to be the issue is a combination of low vitamin D (high latitude) exacerbated by their exceeding-high retinol intakes. In Scandanavia in the '90s, the milk had been sold fortified with vitamin A, as a Government mandate, and the great majority of Scandanavians had also been taking cod liver oil. This shows that bone density is under hormonal control of the two aforementioned vitamin–hormones, and even twice the RDA of calcium cannot prevent this. Besides effecting the osteblast∶osteoclast ratio, vitamin D also transcribes for transforming growth factor β and bone morphogenic protein. The protein matix of bone also needs to be modified post-tranlationally to chelate calcium properly: The glutamate side-chains must be converted into γ-carboxylglutamate side-chains, forming a Ca²⁺-chelating dicarboxylate. This is done enzymatically using vitamin K as a cofactor, another fat-soluble vitamin the Scandanavians were probably deficient in.
 

ivy

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@Travis, exactly how dangerous do you reckon Candida Albicans to be? How does your diet tackle its potential overgrowth?
 

Travis

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What other types of fatty acids (besides the ω−3, ω−6, and ω−9 fatty acids) can occupy the sn-2 of the cell membrane phospholipids? Are they all equally likely to occupy the sn-2 position depending on the quantity of each fatty acid in the body?
I'm fairly certain that Mead acid (ω−9) can, and of course DHA and DPA (in the brain). There seems to be a very strong trend towards the longer 20- or 22-carbon lipids being found at the sn-2 position, with only shorter ones occupying the sn-1. Besides palmitic (16∶0) and myristic acids (14∶0) found there, there's also the less-talked-about palmitoleic (16∶1); this is actually an ω−7 fatty acid, but this would appear safe from a spontaneous oxidation perspective as it has only one double bond. When two double bonds are found close together—not conjugated but separated by a space—the bis-allylic hydrogen found in between the two bonds is the one most-easily extracted, by far. This initial hydrogen extraction must occur before spontaneous peroxidation can occur, in water, and is the rate-limiting step. For this reason—also because stearate is routinely converted to oleate in the body—I don't consider monounsaturated fatty acids particularly damaging. I don't really even try to avoid them, and would consider macadamia nuts a Peat-acceptable food (although you'd have to ask him to be sure, but I think he'd agree).
 

Travis

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@Travis, exactly how dangerous do you reckon Candida Albicans to be? How does your diet tackle its potential overgrowth?
I think it's damaging. I took antibiotics in the past which is a predisposing factor, along with glucocorticoids, so I'm always on the look-out. Biochemistry indicates that high-starch and high-glutamine foods, such as grains, are the very worst. This is because Candida albicans, which exists safely in everyone, becomes pathological when allowed to transform into its invasive hyphal state. This is accomplished most powerfully by N-acetylglutamine, and the reason for this is that chitin is composed exclusively of this monosaccharide. Chitin is not made by vertebrates; only yeast, fungi, insects, and crustaceans synthesize this polymer. In Candida albicans, chitin forms an obligatory structural component of the cell wall. They hypae are particularly enriched, especially the septum which is dissolved in the round yeast state after mitosis—separating mother and daughter cells. In a highchitin condition, this septum is never dissolved and is technically considered a mycelial filament (or hypha). The yeast form is roughly 1% chitin by mass and the mycelial form contains ~5%. It should then be no wonder why N-acetylglutamine has been found to be the most powerful inducer of the yeast ⟶ hyphal transition in C. albicans.

But no common foods, besides shellfish and mushrooms, contain N-acetylglutamine to any significant extent. Nonetheless, Candida grows regardless and person might wonder why. The reason it can do this is through its enzyme called glucosamine-6-phosphate synthase, which creates the obligatory N-acetylglutamine from glucose and glutamine:

glucose + x·glutamine ⟶ x·(N-acetylglutamine) ⟶ (N-acetylglutamine)ₓ = chitin polymer

So foods high in both glucose and glutamine would necessarily be the most potent inducers of the yeast ⟶ hyphal transition. These are found as grains, which has glucose in the form of amylopectin polymers and a very high density of glutamine in their seed-storage proteins. Plants store extra nitrogen either as glutamine or asparagine for easy access during germination, released as ammonia, and most plants use predominately one or the other. Legumes, tree nuts, and corn are mostly asparagine-storing; wheat, rye, and oats are glutamine-storing. Tomatoes are particularly rich in glutamine, perhaps explaining why these are often included on the 'not to eat' list of many people's anti-Candida recommendations (though they appear to be oblivious of how glutamine plays a role). Culture media sold for yeast and mycelial growth most often have L-glutamine added, and this is important enough that many researchers modify stock solutions to increase it (see the Materials & Methods section). It's not simply carbohydrates, which are unavoidable anyways, Candida albicans also has a specific requirement for L-glutamine.
 

Wagner83

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[...] lectins [...]
Thanks a lot, very clear writing.
I've said before and I'll say it again: The RDA is such that a person would practically have to eat either leaves or dairy products. There are other ways besides, but far less Peat-friendly ways.

According to nutritiondata 1 kg of sweet potatoes provides with close to 27% of calcium (as well as vitamin A, C, K and E, and a ratio with phosphate much closer to Ray's ideal than potatoes), I have access to a mineral water that provides 50% of calcium per liter of water. So one could eat two kg of sweet potatoes and when the individual eats rice he/she could cook it with the mineral water until complete absorption, or he could simply drink the water but I don't know how it would be absorbed in such form. If herbs (so..leaves) like coriander are added to the broth they should contribute some more. Besides a lot of copper, dried oriental radishes are a source of a lot of nutrients, calcium included.
 
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Obi-wan

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Most grains are stored and if left in a moist environment will grow fungi
 

Travis

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Just in case you didn't see my last reply, I have quoted my post.
Also, what are your thoughts on non-psychedelic mushrooms as a (vegan) protein source? Do you eat them?
On second though, the N-acetylglucosamine in mushrooms might preclude rational consumption for people who've taken a lot antibiotics and/or glucocorticoids. Prostaglandin E₂ and N-acetylglucosamine are the two things which most powerfully stimulate the yeast ⟶ hyphal transition of C. albicans, by far, so mushrooms and ω−6 fatty acids could logically be avoided for these reasons. Mycelial masses can actually form tumors which are often mistaken for cancer, as can be read about here:

Nemenqani, Dalal. "Gastrointestinal basidiobolomycosis: an unusual fungal infection mimicking colon cancer." Archives of pathology & laboratory medicine (2009)

The general recommendation is to 'avoid refined carbohydrates,' but this is just too simplistic on account of it ignoring glutamine and glucosamine (and prostaglandin E₂). Another one is to 'avoid sugar and fat together,' but this can just be frankly wrong: Short chained fatty acids (i.e. lauric) are very powerful antifungal agents and so are the chitinases in pineapple, making the piña colada fat & sugar combination acceptable (that is, keeping Bacardi™ between about 3–5 ounces).
Most grains are stored and if left in a moist environment will grow fungi
I think this yeast must have co-evolved with grains to feed on them. Although some species can do this: Candida albicans does not appear capable of synthesizing N-acetylglucosamine (for chitin) without glutamine. This makes nuts and legumes a relatively poor food for it, of which a different species would be more suitable to degrade, as well as fruit and leaves (and of course things like beef and eggs would be even more unsuitable).
Thanks a lot, very clear writing.

According to nutritiondata 1 kg of sweet potatoes provides with close to 27% of calcium (as well as vitamin A, C, K and E, and a ratio with phosphate much closer to Ray's ideal than potatoes), I have access to a mineral water that provides 50% of calcium per liter of water. So one could eat two kg of sweet potatoes and when the individual eats rice he/she could cook it with the mineral water until complete absorption, or he could simply drink the water but I don't know how it would be absorbed in such form. If herbs (so..leaves) like coriander are added to the broth they should contribute some more. Besides a lot of copper, dried oriental radishes are a source of a lot of nutrients, calcium included.
I guess that depends on how many potatoes you can eat. I have little experience buying potatoes so I don't even know what a kilo of them would look like. I do know I can eat a kilogram of apples per day without much effort, in addition to other things, and for all I know potatoes would have more-or-less the same caloric density.
 

Koveras

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I think it's damaging. I took antibiotics in the past which is a predisposing factor, along with glucocorticoids, so I'm always on the look-out. Biochemistry indicates that high-starch and high-glutamine foods, such as grains, are the very worst. This is because Candida albicans, which exists safely in everyone, becomes pathological when allowed to transform into its invasive hyphal state. This is accomplished most powerfully by N-acetylglutamine, and the reason for this is that chitin is composed exclusively of this monosaccharide. Chitin is not made by vertebrates; only yeast, fungi, insects, and crustaceans synthesize this polymer. In Candida albicans, chitin forms an obligatory structural component of the cell wall. They hypae are particularly enriched, especially the septum which is dissolved in the round yeast state after mitosis—separating mother and daughter cells. In a highchitin condition, this septum is never dissolved and is technically considered a mycelial filament (or hypha). The yeast form is roughly 1% chitin by mass and the mycelial form contains ~5%. It should then be no wonder why N-acetylglutamine has been found to be the most powerful inducer of the yeast ⟶ hyphal transition in C. albicans.

But no common foods, besides shellfish and mushrooms, contain N-acetylglutamine to any significant extent. Nonetheless, Candida grows regardless and person might wonder why. The reason it can do this is through its enzyme called glucosamine-6-phosphate synthase, which creates the obligatory N-acetylglutamine from glucose and glutamine:

glucose + x·glutamine ⟶ x·(N-acetylglutamine) ⟶ (N-acetylglutamine)ₓ = chitin polymer

So foods high in both glucose and glutamine would necessarily be the most potent inducers of the yeast ⟶ hyphal transition. These are found as grains, which has glucose in the form of amylopectin polymers and a very high density of glutamine in their seed-storage proteins. Plants store extra nitrogen either as glutamine or asparagine for easy access during germination, released as ammonia, and most plants use predominately one or the other. Legumes, tree nuts, and corn are mostly asparagine-storing; wheat, rye, and oats are glutamine-storing. Tomatoes are particularly rich in glutamine, perhaps explaining why these are often included on the 'not to eat' list of many people's anti-Candida recommendations (though they appear to be oblivious of how glutamine plays a role). Culture media sold for yeast and mycelial growth most often have L-glutamine added, and this is important enough that many researchers modify stock solutions to increase it (see the Materials & Methods section). It's not simply carbohydrates, which are unavoidable anyways, Candida albicans also has a specific requirement for L-glutamine.

N-acetylglutamine or N-acetylglucosamine?
 

Travis

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N-acetylglutamine or N-acetylglucosamine?
Gluocosamine is the monosaccharide which constitutes chitin, but C. albicans can make this de novo using both glucose and glutamine (supplies the amino group). But N-acetylglucosamine can probably be considered the only transformation factor of the two because it also—besides being a structural unit—has actually been shown to signal hormonally. Glutamine is probably best seen on a lower tier, perhaps as a growth factor, analogous to glucose but far more specific to certain foods (i.e. wheat).
 

barefooter

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Hey @Travis, how important do you think the calcium/phosphorous intake ratio is? If 1:1 or even more calcium than phosphorous is desirable, how do you achieve this without eating dairy? I've been looking at the composition of various fruits and vegetables, and it seems that most have more phosphorous than calcium, and at best they are even. I didn't see any where there was more calcium, do you have any examples? Also, any idea if there are general botanical patterns to help guide one towards plant parts that would be likely to store more calcium? For example, kale seems to have a more favorable ratio than broccoli, which leads me to believe this has to do with it being a leaf, vs. broccoli being a flower. Which makes sense, because I now remember seeing higher phosphorous fertilizers being sold specifically to enhance plant blooming.
 

Fractality

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@Travis have you ever experienced nausea from ingesting too much nicotine? Do you know what causes it? Is it related to dopamine? It feels that way.
 

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