Linoleic Acid: Is This The Key That Unlocks The Quantum Brain?

Amazoniac

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@Travis do you think that thiamine and riboflavin induce deficiencies in each other if not given together?
I get something like that from this study: http://www.jbc.org/content/154/1/69.full.pdf

Also here's a neat little diagram.
It is missing some stuff (like b2 not showing in pyruvate -> AcetylCoA) but I find it useful.

NB5Moad.jpg
https://raypeatforum.com/community/...nsive-megaloblastic-anemia.16022/#post-218040
 

Amazoniac

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Travisord, you're a beast.

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"total collagen content of the dermis of pellagrins is lower than that found in normal subjects. Copper appears to be necessary for the maturation of collagen (2-4). Therefore, a study was undertaken to determine whether copper metabolism was in any way altered in pellagra. As it has been clearly demonstrated that excess dietary leucine is etiologically related to endemic pellagra in this part of the world (5, 6), the effect of leucine on copper metabolism in normal human subjects was also investigated."

"More than 90% of serum copper in man circulates as ceruloplasmin and the rest is in loose combination with albumin. A small amount of copper is also present in combination with amino acids (10).
It is generally believed that although the non-ceruloplasmin copper is freely exchangeable and is in equilibrium with tissue copper, copper in ceruloplasmin is not available to the tissues. High serum total copper levels with normal ceruloplasmin activity observed in pellagrins indicate that the non-ceruloplasmin fraction of serum copper is raised in this disease. An increase in the non-ceruloplasmin fraction of serum copper alone is rare, but it has been recently reported to occur in psoriasis (11). It may be significant that in psoriasis, as in pellagra, dermatitis is a characteristic feature.
The high amounts of urinary copper in pellagrins may be due to an increase in the non-ceruloplasmin moiety of serum copper. The increases in urinary and serum total copper brought about in normal subjects by the administration of leucine appears to be a specific reaction to excess leucine, and not a result of any amino acid excess, as shown by the fact that valine, another branched-chain amino acid, failed to induce these alterations."

"The observations made in this study indicate that the changes in copper metabolism observed in pellagra may also be due to an excessive intake of this amino acid. Studies both in experimental animals (12) and in human subjects (13) have shown that metabolic changes induced by excess dietary leucine could be reversed by the administration of isoleucine."
 
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Travis

Travis

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Do you think water in the microtubules will be an issue with PUFA,
I don't think so, unless there are areas on the outside they could interfere with. Tubulin, and hence microtubules, are probably too dense-walled to admit a fatty acid. Microtubules are constructed fromm identical monomers of α- and β-tubulin, although they can exist in different diameters. Below is an electron density map of tubulin:

tubulin.png


By valine³⁵¹ you can see a 14-atom peptide chain, which consists of ⅔ carbon–carbon single or double bonds. The carbon–nitrogen bonds are only slightly shorter. Imagine linoleic acid as about 25- or 30% longer, kinked back onto itself, and potentially even 3× bulkier if pack into a triglyceride or phospholipid.

But . . . perhaps the interstices between the tubulin monomers could admit one:

microtubule.png


I think general anesthetics diffuse into these and interfere with nervous transmission. General anesthetics are small and lipid-soluble, and some—like the noble gasses—are entirely unreactive. I think that if fatty acids routinely entered we would never be able to think straight, and the ones that matter most are covered in myelin. Fatty acids also have polar heads. If fatty acids were a hazard for nervous transmission, I would then think the short-chained fatty acids would be most dangerous.

Here is a cool electron micrograph of a few microtubules:

electron.png


Amos, Linda A. "Microtubule structure and its stabilisation." Organic & biomolecular chemistry 2.15 (2004): 2153-2160.
Nogales, Eva, Sharon G. Wolf, and Kenneth H. Downing. "Correction: Structure of the α–β tubulin dimer by electron crystallography." Nature 393.6681 (1998): 191.
Li, Huilin, et al. "Microtubule structure at 8 Å resolution." Structure 10.10 (2002): 1317-1328.
 
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Drareg

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I don't think so, unless there are areas on the outside they could interfere with. Tubulin, and hence microtubules, are probably too dense-walled to admit a fatty acid. Microtubules are constructed fromm identical monomers of α- and β-tubulin, although they can exist in different diameters. Below is an electron density map of tubulin:

View attachment 6892

By valine³⁵¹ you can see a 14-atom peptide chain, which consists of ⅔ carbon–carbon single or double bonds. The carbon–nitrogen bonds are only slightly shorter. Imagine linoleic acid as about 25- or 30% longer, kinked back onto itself, and potentially even 3× bulkier if pack into a triglyceride or phospholipid.

But . . . perhaps the interstices between the tubulin monomers could admit one:

View attachment 6893

I think general anesthetics diffuse into these and interfere with nervous transmission. General anesthetics are small and lipid-soluble, and some—like the noble gasses—are entirely unreactive. I think that if fatty acids routinely entered we would never be able to think straight, and the ones that matter most are covered in myelin. Fatty acids also have polar heads. If fatty acids were a hazard for nervous transmission, I would then think the short-chained fatty acids would be most dangerous.

Here is a cool electron micrograph of a few microtubules:

View attachment 6894

Peat mentions the anesthetic forms a cage creating water structure,admantane does something similar.
So this is fascinating if no fats can get inside,they are outside assisting the structure of the tube?

If consciousness resides in here yet no fat involvement it would be facinating.
 
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Travis

Travis

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Interesting study:

In young rats depletion in thiamine was found to increase the concentration of riboflavin in the liver above that of control animals. In riboflavin deficiency, the thiamine concentration of the liver was higher than in control animals. The concentrations of thiamine and riboflavin in the liver of rats deficient in pyridoxine, in pantothenic acid, in biotin, or in vitamin A were not significantly different from those of litter mate*controls maintained on adequate amounts of these vitamins. The results are interpreted as evidence of an interdependence of thiamine and riboflavin.

I think the authors came to the only logical conclusion, unless there is something that I'm missing—some unusual interaction between thiamine and riboflavin.
On the contrary, our thiamine-deficient rats had more riboflavin available than controls, and the feeding with thiamine resulted in a dispersal of the excess riboflavin from the liver.

Along with niacin, these are both Krebs Cycle vitamins. A deficiency in one apparently leads to an excess in the other since they both can only be utilized at a constant ratio, and excess is noticed in the liver. It might appear as though the liver stores excess thiamine and riboflavin—whatever cannot fit in the enzymes. Niacin can be made from tryptophan.

I'm still not sure why niacin, biotin, and pyroxidal are the ones which cause skin issues. I mean, why not riboflavin and biotin as well?
 
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Travis

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Peat mentions the anesthetic forms a cage creating water structure,
This was what Linus Pauling proposed:

  • Pauling, Linus. "A Molecular Theory of General Arlesthesia." (1961).
It's very interesting. Linus Pauling figured out the molecular model for sickle-cell anemia and cardiovascular disease, but his theory for anesthesia only presents half the story—perhaps just a side-effect.

pauling.png


Anesthetic action correlates very well with the gas' ability to form cage-like clathrates, but so do their solubilities in lecithin.

lecethin.png


Notice the highest correlation was found in lecithin!

But these two effects generally are one, and the same. The less a small molecule can interact with water, the more ordered the water cage around it will be; also, it will be more soluble in lecithin—a a phosphilipid which makes up lipid bilayers. The clathrate could be just a side-effect, although it could have relevance. Imagine xenon entering a microtubule based on it's lecithin-solubility and small size: it would still form a clathrate, although it might actually be more stable sticking to the nonpolar amino acids and aromatic rings.

A more ordered water structure would resemble water of a lower temperature. This might be expected to actually increase electrical transmission, as it does in physical systems.

But I suppose these clathrates could structure water to the extent that diffusion is limited and metabolism slowed—I'm not sure. I like to think of it as gasses entering the microtubules and physically-interposing themselves in the path of nervous transmission.

Taheri, Shahram, et al. "What Solvent Best Represents the Site of Action of Inhaled Anesthetics in Humans, Rats, and Dogs?." Anesthesia & Analgesia 72.5 (1991): 627-634.
 
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Travis

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Interesting article. The last time I heard about cerruloplasmin was in Hoffer and Osmond's Book:
Ceruloplasmin, a copper protein enzyme, normally present in serum oxidizes catechol, adrenaline, serotonin, and other amines. Leach et al. (1956) believed it was the catalyst in the oxidation of adrenaline to adrenochrome.
Melander (1957) found that ceruloplasmin absorbs adrenolutin. Adrenolutin readily dialyzes through a semipermeable membrane. When ceruloplasmin is added, no further dialysis occurs. Other globulins do not bind adrenolutin.
Payza and Zaleschuk (1959) showed that adrenolutin strongly inhibits ceruloplasmin activity on p-phenylenediamine. Adrenochrome does not. Ceruloplasmin also protects animals against catatonic dosages of adrenolutin. Perhaps it is the rule of ceruloplasmin to bind adrenolutin and thus protect against excessive quantities.
2. Deficiency in ceruloplasmin will be harmful and may be responsible for some toxemias of pregnancy and for puerperal psychosis. 3. Ceruloplasmin will be therapeutic. If not available, transfusions from pregnant women in third trimester may be therapeutic. 4. Schizophrenics, lacking ceruloplasmin, will not bind adrenolutin and thus by some chemical mass action may decrease oxidation of hypodermically administered adrenaline. Administration of ceruloplasmin will thus allow more rapid metabolism of adrenaline.
Porter et al. (1957) suggested that ceruloplasmin catalyzed the conversion of serotonin to paraquinone amines which on further oxidation would be converted into aminochromes.
G. Martin et al. (1958) also found that serum oxidized serotonin to colored compounds. They believed the enzyme was ceruloplasmin. It was inhibited 80% by 0.003 M iproniazid.
Leach and Heath's (1956) observation that adrenaline was oxidized more rapidly in schizophrenics' plasma to adrenochrome and eventually into adrenolutin gave some urgency to these problems for it was then believed that ceruloplasmin was the oxidase which oxidized both adrenaline and DPP.
Pig plasma was fractionated for ceruloplasmin. Adrenaline oxidase activity was decreased in these fractions.
Ceruloplasmin irreversibly binds adrenolutin (Melander, 1957) and histamine (Martens et al., 1959). When animals were pretreated with ceruloplasmin, they were protected against the psychotomimetic properties of LSD alone or LSD followed by other compounds listed by these authors above. It also decreased the toxicity of histamine. Further support for the protective role of ceruloplasmin were the interesting therapeutic responses of schizophrenic patients to ceruloplasmin, reported by Martens et al. (1959).
(a ) Ceruloplasmin is a powerful binder of adrenolutin but not of adrenochrome, (b ) Walaas and Walaas (1965) have shown in vitro that ceruloplasmin oxidizes noradrenaline and adrenaline to their chrome derivatives.
Recently Tsaune (1963) and Tsaune and Upenietse (1962) reported that toxicity in the proteinfree fractions prepared from schizophrenic blood was inversely proportional to ceruloplasmin levels, as would be Psychological Properties 551 expected. He used Macht's phytotoxic test.
 

Regina

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Interesting article. The last time I heard about cerruloplasmin was in Hoffer and Osmond's Book:
Phew Travis. That's a hefty book. Did the writers say how one could increase ceruloplasmin levels?

From a lighter source, "Similarly, individuals lacking ceruloplasmin display iron overload in selected tissues, including liver, brain, and retina This supports the idea that the ferroxidase activity of ceruloplasmin is essential to the flux of iron in the body."
Copper
It makes me think that eye floaters are made of iron.
 
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Travis

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They did experiment with giving people cerruloplasmin. I think it was probably fractionated from blood donors back then, but today they could probably just genetically-engineer it.

I don't recall them talking about the biosynthetic pathway. I'm not sure they even knew back then.
 

schultz

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I had no idea that root beer was actually fermented. I suppose this was one of the few ways of creating carbonation back in the day . .

I was thinking about looking into the yeast, but had—and I ran out of coffee—decided that the controls got the exact same yeast. I think if I go down this rabbit hole some more, I will look into what high-sucrose diets do to B-vitamin levels. I know that B-vitamins are water-soluble, and that the metabolism of glucose creates more water than the metabolism of an isocaloric amount of fat. Perhaps it can be partially explained in this way? But probably only slightly . . .

Bigger would probably be the higher activity of B-vitamin-dependent glycolytic enzymes which would necessarily create more free-radicals in close proximity to their co-factors—the B-vitamin coenzymes—causing superoxide adducts, ring scission, and divers other examples of oxidative damage.

I'm sure this has been studied before. Sometimes it's just a matter of finding the right keywords . . .

I was looking through my notes on chickens and EFAD (yes I have these types of notes.... and no, I do not have any friends :( ) and I found an interesting quote I saved.

"Although Reiser in 1950 claimed that chickens needed a source of essential fatty acids during growth, the same author later concluded that mature hens, maintained for a full year on a fat-free diet, did not require essential fatty acids for egg production or hatchability. More recently Bieri et al. showed that chicks could be grown to maturity on an essentially fat-free ration without marked deficiency symptoms and suggested that Reiser's purified chick ration may have been deficient in thiamine and vitamin A."

I think the source for the quote is: EGG QUALITY: A STUDY OF THE HEN'S EGG By T. C. CARTER

I didn't check the paper by Bieri et al. yet to see what they say.

I also found this quote from a 30's paper that is amusing to me...

"No effect on the flavour of the egg was observed during the feeding of experimental rations, except in the case of linseed oil, which produced an unpleasant taste in the soft-boiled egg." Cruikshank, 1934

haha, it does indeed make eggs taste awful, like those omega-3 eggs. They figured this out in the 30's already :lol:
 

schultz

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Sorry if I am going off topic again, but I glanced over the Bieri paper and he says this...

"It would appear that the diet used by Reiser was probably deficient in nutrients other than fat. The difficulty in insuring a sufficient intake of vit. A in a fat-free diet has already been discussed above. In addition to a possible vit. A deficiency, the diet of Reiser may also have been low in thiamine since the soybean protein, used in his diets, contains sulfite which has been shown to destroy thiamine (10)."

Here is where he talks about the vitamin A:

"In initial experiments it was found that 3 mg of vit. A acetate/kg, mixed into the diet in ethanol, was so rapidly destroyed (as found by analysis) that vit. A deficiency frequently developed in the chicks in 3-4 weeks. This could be prevented by increasing the level to 30 mg/kg. However, occasional appearance of vit. A deficiency symptoms even under these conditions prompted a study of parenteral and oral administration of this vitamin."

They specifically use the word "destroyed". I wonder if some was just not being absorbed? It could be that, combined with the animals having an increased need for vitamin A. In any event, this kind of thing shows that we are not completely clear what levels of nutrients EFA deficient animals need, and mistakes with the amounts assumed can easily be made, leading to false conclusions and/or assumptions. The EFAD chicks needed 10x more vitamin A and yet still occasionally became vitamin A deficient. This seems to jive with what Ray talks about in regards to vitamin A.
 
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Travis

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No effect on the flavour of the egg was observed during the feeding of experimental rations, except in the case of linseed oil, which produced an unpleasant taste in the soft-boiled egg." Cruikshank, 193
Nice. The fact that linseed oil made its appearance in the yolk does not surprise me, I've seen a chart on the incorporation of dietary fatty acids in egg yolk before . . . and linseed oil really is bad-tasting.

Someone needs to tell the chickens this. They could use their linseed oil rations instead for oil painting—perhaps mix it with dried clays to produce ochre with their scratchy claws. I particularly like Windsor & Newton's #745. I think we owe Ray Peat a debt of gratitude for being the first popular figure to call attention to the fact that linseed oil and flax seed oil are synonymous, and have gained popularity in paint formulations as one of the fastest drying and most readily oxidizable oils available—even faster than walnut oil and poppyseed oil (used for it's stunning clarity.) 'Drying' velocity is proportional to the oxidation potential, and oxidation is inversely proportional to longevity.

What's good for a painter, is bad for cellular membranes. This also applies to mercury-, lead-, and arsenic-containing pigments such as vermillion, lead white, and Paris green. This should perhaps be called "Peat's Law."
...did not require essential fatty acids for egg production or hatchability.
This is the first time that I've seen—or've even heard of—the word "hatchability." I am rather fond of that word. Although somewhat whimsical-sounding, it has actually a strict mathematical definition: the ratio of hatched eggs over all eggs.
The data for the hatchability of fertile eggs for Trials 1 and 2 were pooled because there were no significant differences between the trials (P = 0.419). Egg storage for 14 versus 4 d significantly depressed the hatchability of fertile eggs by 6.49% (Table 3)

[1] Hatchability is usually around 70% for chickens.
[2] Fasenko, G. M., et al. "Examining the effects of prestorage incubation of turkey breeder eggs on embryonic development and hatchability of eggs stored for four or fourteen days." Poultry Science 80.2 (2001): 132-138.
 
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Travis

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  • SMITH, DAVID T., and JULIAN M. RUFFIN. "Effect of sunlight on the clinical manifestations of pellagra." Archives of Internal Medicine 59.4 (1937): 631-645.
The influence of the sun's rays on the lesions of pellagra has been a subject of debate for nearly two hundred years. Casal noted a seasonal variation in the incidence of pellagra, with a peak which corresponded to the spring equinox. In Italy one of the common names applied to this disease by the peasants is mal del sole (disease of the sun), while certain Italian physicians have described the lesions as due to "sunstroke of the skin." Many modern clinicians have stated their conviction that there is a close relationship between exposure to sunlight and the development of cutaneous lesions in a pellagra. Various observers have produced typical cutaneous lesions in pellagrins by exposing normal or recently healed areas of skin to direct sunlight. Gherardini demonstrated the effect of the sun by systematically uncovering various parts of the body of each patient.
I did some looking into pellagra and found some interesting things. Apparently, niacin is thought necessary to absorb some amino acids. Other conditions, such as Hartnup disease, where the same amino acid malabsorption is seen (but for apparently different reasons) produces an almost identical condition. Also, all patients diagnosed as having xeroderma pigmentosum have markedly high renal losses of a few amino acids (Cys, His, Arg, Lys).* This also produces a pellagra-like condition, where sunlight is contraindicated. A common explanation is a lack of cysteine leads to low glutathione levels which then cannot provide UV protection leading to increased DNA damage, mutation, and the consequent skin disorders.

But copper is also brought into the discussion by noting that glutathione has an affinity for such, and so does the Cu²⁺-dependent tyrosinase—which produces UV-protective melanin from catecholamines (see Osmond). Low melatonin means less sun protection, and this causes increased sensitivity and with more damage if exposed—hence the associations with the sun exposure and pellagra.

In essence, three diseases: pellagra, Hartnup disease, and xeroderma pigmentosum, all produce nearly-identical skin manifestations. They all also share one common root: the malabsorption of a few select amino acids, with special emphasis on cysteine. The ability of glutathione to protect against sun damage is striking.†
We identified a single disease locus that harbors a novel mutation in ERCC5 , thus confirming that the condition is in fact xeroderma pigmentosum/Cockayne syndrome (XP/CS) complex. Importantly, we also show that the previously described dermatological response to niacin is consistent with a dramatic protective effect against ultraviolet-induced DNA damage in patient fibroblasts conferred by niacin treatment.‡
Since copper deficiency only produces mainly skin-lightening with few dramatic effects, I am inclined to believe that the changes in Cu²⁺ levels seen in pellagra are secondary effects.


And interestingly, vitamin B₆ is required for the enzymatic production of cysteine from methionine within the cell, through cystathionine-β-synthase. This could be another reason why a deficiency of pyroxidal also produces similar skin disorders, besides the conversion of tryptophan to niacin. Perhaps this could eliminate some confusion, as the kynurenine pathway is generally thought to provide only a fraction of the total niacin intake.

Glutathione cannot be directly absorbed into the cell, it gets destroyed by γ-glutamyl transferase. This is why Thornally's powerful glyoxylase inhibitor wouldn't on his first try. The only way to raise intracellular glutathione appears to be with dietary cysteine/methionine and B-vitamins.

And NADH is responsible for regenerating glutathione via glutathione reductase.


*EL‐HEFNAWI, H., and M. F. S. EL‐HAWARY. "CHROMATOGRAPHIC STUDIES OF AMINO ACIDS TN SERA AND URINE OF PATIENTS WITH XERODERMA PIGMENTOSUM AND THEIR NORNIAL RELATIVES." British Journal of Dermatology 75.6 (1963): 235-244.
†Tyrrell, R. M., and M. Pidoux. "Correlation between endogenous glutathione content and sensitivity of cultured human skin cells to radiation at defined wavelengths in the solar ultraviolet range." Photochemistry and photobiology 47.3 (1988): 405-412.
‡Hijazi, H., et al. "Pellagra‐like condition is xeroderma pigmentosum/Cockayne syndrome complex and niacin confers clinical benefit." Clinical genetics 87.1 (2015): 56-61.
§De Vries, Nico, and Silvio De Flora. "N‐acetyl‐l‐cysteine." Journal of cellular biochemistry 53.S17F (1993): 270-277.
 
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  • SMITH, DAVID T., and JULIAN M. RUFFIN. "Effect of sunlight on the clinical manifestations of pellagra." Archives of Internal Medicine 59.4 (1937): 631-645.
I did some looking into pellagra and found some interesting things. Apparently, niacin is thought necessary to absorb some amino acids. Other conditions, such as Hartnup disease, where the same amino acid malabsorption is seen (but for apparently different reasons) produces an almost identical condition. Also, all patients diagnosed as having xeroderma pigmentosum have markedly high renal losses of a few amino acids (Cys, His, Arg, Lys).* This also produces a pellagra-like condition, where sunlight is contraindicated. A common explanation is a lack of cysteine leads to low glutathione levels which then cannot provide UV protection leading to increased DNA damage, mutation, and the consequent skin disorders.

But copper is also brought into the discussion by noting that glutathione has an affinity for such, and so does the Cu²⁺-dependent tyrosinase—which produces UV-protective melanin from catecholamines (see Osmond). Low melatonin means less sun protection, and this causes increased sensitivity and with more damage if exposed—hence the associations with the sun exposure and pellagra.

In essence, three diseases: pellagra, Hartnup disease, and xeroderma pigmentosum, all produce nearly-identical skin manifestations. They all also share one common root: the malabsorption of a few select amino acids, with special emphasis on cysteine. The ability of glutathione to protect against sun damage is striking.†

Since copper deficiency only produces mainly skin-lightening with few dramatic effects, I am inclined to believe that the changes in Cu²⁺ levels seen in pellagra are secondary effects.


*EL‐HEFNAWI, H., and M. F. S. EL‐HAWARY. "CHROMATOGRAPHIC STUDIES OF AMINO ACIDS TN SERA AND URINE OF PATIENTS WITH XERODERMA PIGMENTOSUM AND THEIR NORNIAL RELATIVES." British Journal of Dermatology 75.6 (1963): 235-244.
†Tyrrell, R. M., and M. Pidoux. "Correlation between endogenous glutathione content and sensitivity of cultured human skin cells to radiation at defined wavelengths in the solar ultraviolet range." Photochemistry and photobiology 47.3 (1988): 405-412.
‡Hijazi, H., et al. "Pellagra‐like condition is xeroderma pigmentosum/Cockayne syndrome complex and niacin confers clinical benefit." Clinical genetics 87.1 (2015): 56-61.
§De Vries, Nico, and Silvio De Flora. "N‐acetyl‐l‐cysteine." Journal of cellular biochemistry 53.S17F (1993): 270-277.
Your posts are so good travis.
 
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Travis

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nicotine is apparently the key to the quantum brain
Someone's paying attention (†‡§¶).
Using a double-blind procedure, half the subjects chewed nicotine gum and the other half chewed placebo gum prior to performing the memory task. Results support previous research Þndings which show that nicotine signifcantly improves short-term memory. ―Phillips*

*Phillips, Sarah, and Pauline Fox. "An investigation into the effects of nicotine gum on short-term memory." Psychopharmacology140.4 (1998): 429-433.
†Lee, P. N. "Smoking and Alzheimer's disease: a review of the epidemiological evidence." Neuroepidemiology 13.4 (1994): 131-144.
‡Semenova, Svetlana, Ian P. Stolerman, and Athina Markou. "Chronic nicotine administration improves attention while nicotine withdrawal induces performance deficits in the 5-choice serial reaction time task in rats." Pharmacology Biochemistry and Behavior 87.3 (2007): 360-368.
§Guan, Zhi‐Zhong, et al. "Decreased protein levels of nicotinic receptor subunits in the hippocampus and temporal cortex of patients with Alzheimer’s disease." Journal of neurochemistry74.1 (2000): 237-243.

¶Nordberg, Agneta, and Bengt Winblad. "Reduced number of [³H] nicotine and [³H] acetylcholine binding sites in the frontal cortex of Alzheimer brains." Neuroscience letters 72.1 (1986): 115-120.
 
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Travis

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Orch OR [!]←→Ray PEAT←→CTMU
@Such_Saturation I have to admit that this Hameroff article* got me interested in microtubules. I am not sure about the explanation, because I'm skeptical of the entanglement and nonlocality aspects of quantum physics. Perhaps I'll look at the old double-slit experiments and go from there . . . Most of the weirdness of quantum mechanics seems to stem from just this one category of experiments.
"Feynman was fond of saying that all of quantum mechanics can be gleaned from carefully thinking through the implications of this single experiment."
However, microtubules are without a doubt the source of consciousness and the only structure which seems capable of transmitting signals inside of the body at high speeds. It would be nice to model it using tryptophan-to-tryptophan Förster Resonance Energy Transfer. This is not too radical of an idea, considering papers such as this:

. . . and the fact that the inside of microtubles are lined with a regular, repeating array of tryptophan side-chains.

Mircotubules lead from the retina, down the optic nerve, and then into the brain. Either light is getting there inside of microtubules, or the information is transduced in the manner of George Wald's imaginings.† His explanation depends on molecular diffusion, a low-fidelity and slow process that would be expected to distort the signal through Brownian motion—and snailish reaction times measured in centiseconds if it'd work at all. Nonetheless, he won a Nobel Prize for that particular unicorn so they have to pretend that it's accurate for at least another . . . [calculating] . . . nine years and two months.

  • Sale, Winfield S., Joseph C. Besharse, and Gianni Piperno. "Distribution of acetylated α‐tubulin in retina and in in vitro—assembled microtubules." Cytoskeleton 9.3 (1988): 243-253.
microtubule2.png click to embiggen

Not only can they function as waveguides, they can apparently produce light of their own. This was shown by Yan Sun using a photographic technique. Biophotons emanating from the nerve interact with silver nitrate to produce metallic silver deposits (C). This was inhibited by procaine (F).

The specific steps for the IBA procedures were as follows: (1) tissues immersed in 10% AgNO₃ in a container for 30 min in a dark box in a dark room; (2) rinse in 252 mM sucrose for 15 min; (3) fixation by 10% formaldehyde for 5 min; (4) rinse in de-ionized water for 5 min;... ―Sun
microtubule3.png click to embiggen
The eyes of certain animals give-off far too much light to be simply "reflected moonlight." These are probably biophotons emitting from the retina, out of microtubules. Certain molecules can turn electrons into light, and microtubles are known to travel through mitochondria. They are routinely stained with anti-tubulin antibodies conjugated with chromophores.
These experiments demonstrate that in several different types of cultured cells most, if not all, of the mitochondria are associated with cytoplasmic microtubules. This association is not adventitious because there is no indication of an association of mitochondria with cytoplasmic actin in these cells. The association of mitochondria with microtubules strongly suggests the existence of some kind of specific linkage, either direct or indirect, between them; no other reasonable explanation has occurred to us. It is hard to imagine, for example, that some nonspecific electrostatic interaction can be responsible for the association when so many other intracellular components (such as actin) are also present in the immediate vicinity of the mitochondria and microtubules. ―Heggeness
NADH doesn't really have to travel anywhere special to donate its electrons to microtubules, as they are already coupled directly to the mitrochondria. You can only imagine that the main function of the electron transport chain is not to create ATP, but to create energy for the microtubule network. Microtubules are a direct link from the mitochondria to muscle and have been shown experimentally to emit light, so there is no need to use a low-fidelity and clumsly explanation to describe this. Adenosine triphosphate can be seen as a product, but it can also be seen simply as a byproduct—a pH buffer and magnesium chelator that can also decrease entropy. A great article on the dubious nature of the role commonly attributed to ATP is given by Barbara Banks:
  • Banks, Barbara EC, and C. A. Vernon. "Reassessment of the role of ATP in vivo." Journal of theoretical biology 29.2 (1970): 301-326.
Electricity itself can cause muscle contraction, as can many charged molecules. The fact that ATP had been shown to do so in one experiment is only proof that it's a charged molecule, something that had already been know decades before that. The so-called "high-energy phosphate" bond has been experimentally-confirmed multiple times to be no more energetic that any other phosphodiester bond. Gilbert Ling talks about this as well.

And Harold Hillman has interesting things to say as well. I just found these two videos yesterday and quite good.

. . . and the third one I had watched a few months ago. They are all good to watch. The astroglial cell is a misnomer.

During photosynthesis, chlorophyll turns photons into electrons. These are stored as chemical covalent bonds in the glucose molecule. Animals then essentially reverse this process‡ by ingesting glucose, stripping off the electrons, and creating energy in this process. Heme is known to occupy a clutch position in this process.


Which, as you might expect from it's structure, would function in a way similar to chlorophyll. You might expect it to occupy a place as a terminal ground, where biophotons are converted into electrons and donated to O₂ (to make H₂O.) I suppose you could see the striking similarity between heme and chlorophyll as some sort of coincidence, but . . .

No membrane pumps or high-energy phosphate bonds required. The electron should probably be seen as the primary bioenegetic unit of currency, and not the intermediate-energy phosphate bonds. The K⁺/Na⁺ ratio can be suitably explained simply by noting that K⁺ has a greater electrical mobility than Na⁺, and that the mitochondrial membrane has a potential of about −150 mV.
The above considerations hold also for more extensive systems. It seems possible that they can be applied to biological processes other than photosynthesis. For example, excitation processes in the retina could be mentioned. The light wave focused on one visual rod is coherent within the area of this rod. It s:ems probable that this collective character of the excitation is important for the formation of the signal in the adjoining nervous system. It also seems possible that collective activities play a role in the function of the central nervous system and relations may be found, say, between conscience and nonlocalized electronic states, or S and storage of memory. ―Szent-Györgyi§

*Hameroff, Stuart. "Quantum computation in brain microtubules? The Penrose-Hameroff' Orch OR'model of consciousness." Philosophical Transactions-Royal Society of London Series A Mathematical Physical and Engineering Sciences (1998): 1869-1895.
†Wald, George, Paul K. Brown, and Ian R. Gibbons. "The problem of visual excitation." JOSA 53.1 (1963): 20-35.
‡Schrodinger, Erwin. What is life?. University Press: Cambridge, 1943.
§Avery, John, Zoltan Bay, and Albert Szent-Györgyi. "On the energy transfer in biological systems." Proceedings of the National Academy of Sciences 47.11 (1961): 1742-1744.
¶Wootters, William K., and Wojciech H. Zurek. "Complementarity in the double-slit experiment: Quantum nonseparability and a quantitative statement of Bohr's principle." Physical Review D19.2 (1979): 473.
 
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Wagner83

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Perhaps I'll look at the old double-slit experiments and go from there . . . Most of the weirdness of quantum mechanics seems to stem from just this one category of experiments.

I need you to give a call to my girl .
 
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Mircotubules lead from the retina, down the optic nerve, and then into the brain. Either light is getting there inside of microtubules, or the information is transduced in the manner of George Wald's imaginings.
Photons were found to collapse at retina, not all the way into brain. Hameroff had to work around this.

Not only can they function as waveguides, they can apparently produce light of their own.

The brain is not conventional.

Increased photon emission from the head while imagining light in the dark is correlated with changes in electroencephalographic power: Support for Bókkon's biophoton hypothesis - ScienceDirect

Nonlocal correlations between separated neural networks
 

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