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

[Travis]

Cocchi, Massimo, et al. "Linoleic acid: Is this the key that unlocks the quantum brain? Insights linking broken symmetries in molecular biology, mood disorders and personalistic emergentism." BMC neuroscience 18.1 (2017): 38.

A study was published early this year entitled, "Linoleic acid: Is this the key that unlocks the quantum brain? Insights linking broken symmetries in molecular biology, mood disorders and personalistic emergentism [sic]." This is not a joke. This was published in BioMed Central Neuroscience in April, and he cites the Peat-debunked Burr and Burr study:

Cocchi: Since 1929 when Burr and Burr demonstrated the characteristics of essentiality of linoleic acid for animal organisms...

Ray Peat: In 1929 George and Mildred Burr published a paper claiming that unsaturated fats, and specifically linoleic acid, were essential to prevent a particular disease involving dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration.

In 1929, most of the B vitamins and essential trace minerals were unknown to nutritionists. The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn't know about.

What really happens to animals when the "essential fatty acids" are lacking, in an otherwise adequate diet?

Their metabolic rate is very high.

Their nutritional needs are increased.

They are very resistant to many of the common causes of sickness and death.

They are resistant to the biochemical and cellular changes seen in aging, dementia, autoimmunity, and the main types of inflammation.

The amount of polyunsaturated fatty acids often said to be essential (Holman, 1981) is approximately the amount required to significantly increase the incidence of cancer, and very careful food selection is needed for a diet that provides a lower amount.*

​

Cocchi: A classic example involves a magnetic system composed of tiny magnets represented by spins arranged geometrically in a regular array. In principle they can be oriented in arbitrary directions but they also interact with each other via nearest-neighbor coupling which is called a spin–spin interaction. For this system, there is a competition between entropy that favors disorder in the spin orientations and spin alignment along one direction due to their spin–spin coupling energy, which is minimized for parallel alignment. At high temperatures, entropy “wins” and the system is disordered. At low temperatures, the opposite happens and the spins orient themselves along the same axis. The boundary between two ranges of temperature is called the critical point...

It looks like he's trying to model membrane fluidity as a function of temperature and electron spin orientation, and using a magnetic analogy to explain the parallel double-bond alignment. But unsaturated fatty acid bonds are only slightly polar, so he had better so this is probably better explained by anomeric effects.

Cocchi: By analogy with the above example, we propose that linoleic acid’s concentration in the membrane of neurons or glia acts as a control parameter (corresponding to temperature for magnetic systems), effectively behaving like a switch in a system close to criticality, i.e. resulting in a phase transition between a normal brain and a pathological brain when the linoleic acid concentration falls below its set value.

But it turns-out to be a put-on. The analogy was only intended to explain how a critical concentration of linoleic acid could act like an on/off switch, by using temperature and magnets (of all things.)

So why linoleic acid? He never says. The brain has many different types of lipids. I don't think the physical properties of linoleic acid are particularly unusual considering the brain has fatty acids which have less, and have more, double-bonds. These are what create fluidity; double-bonds create kinks in the acyl chains.

Cocchi: Recent observations, conducted on the characterization of the platelet fatty acids in mood disorders and ischemic heart disease have consistently shown that a very low concentration of linoleic acid is correlated with these diseases. This observation was found to be particularly interesting in brains of depressed subjects who had completed suicide.

Oh! So this is why he automatically just assumes that linoleic acid would "unlock the quantum brain?" and not, say . . . palmitic acid which would be better-expected to lower membrane fluidity.

There's actually a very good explanation for this: Both tryptophan — the serotonin precursor —and fatty acids compete for the same binding sites on serum albumin. There are five high-affinity tryptophan binding sites on serum albumin. Linoleic acid is the fatty acid which binds albumin, on average, most strongly.†

...and displaces tryptophan from serum albumin raising brain serotonin synthesis (Fernstrom).

Cocchi: For the benefit of the reader, we explain the key features of the model in order to better understand how it can be made useful in applications to brain dynamics. The total energy of this type of magnetic system is calculated using the so-called Hamiltonian function, namely:

where J is the interaction constant, sᵢ is the spin, whose value can be either −1/2 or 1/2, for the i-th magnetic particle in the spin lattice [...] Cocchi: How can this be translated into the dynamics of membrane’s phospholipids?

It can't

Cocchi: This mechanism could bring a completely new perspective on the interpretation of quantum effects in the brain, which have been debated ever since the work of Penrose was published [16, 17].

He's inspired by Penrose's microtubule quantum paper and proposes another, but goes for the Rube Goldberg approach.

Cocchi: This could affect the decoherence times of quantum excitations in the collective states of ions traversing the ion channels and in turn affect mental processes. Decoherence times define the duration of a quantum state before it manifests itself by a so-called wave function collapse meaning its actual value can be measured or observed. [...] Microtubule depolymerizing agents (e.g., colchicine) eliminate peripheral cytoskeleton and action potential together [31, 32] and modify G protein signaling in mammalian cerebral cortex [33]. Microtubule stabilizing agents restore cytoskeleton and action potential together [31, 32]. Divalent ions such as magnesium and zinc restore cytoskeleton and action potential, according to Tasaki et al. [34]. On the other hand, calcium ions destabilize microtubules and actin filaments directly or indirectly by interactions with the various associated proteins.

So the concentration of linoleic acid is imagined to strongly control the permeability of ion channels, controlling the quantity and quality of ions which stabilize – during assembly – the microtubules necessary for consciousness: yet no other fatty acid can do this.

Cocchi: This can be metaphorically illustrated by having simultaneous thoughts of ordering sushi and pasta before making a decision. Once we order sushi, this is akin to the wave function collapse and making an actual choice. Decoherence time is the time it takes to collapse a quantum state.

He didn't seem to properly think this through. He is using quantum woospeak, but he should probably confound the reader further by bringing a high-linoleic acid food into the analogy—like walnuts. You cannot unlock the quantum brain with these foods.

Cocchi: Cell membrane and fatty acids, in particular linoleic acid is the “key that opens to the quantum brain” through the dynamics of the cytoskeleton.

No it's not. Linoleic acid raises serotonin in the brain by displacing tryptophan from serum albumin. It also is the only precursor for arachidonic acid, which is the only precursor of eicosanoids. These act on nuclear PPAR receptors to upregulate a suite of genes that shift the cell towards an fat-synthesizing, fat-storing, and subsequent insulin-resistant state. High amounts found in tissue are associated with cancer.§

Cocchi: In a nutshell...

No.

​

*Unsaturated fatty acids: Nutritionally essential, or toxic?
†Spector, Arthur A. "Fatty acid binding to plasma albumin." Journal of lipid research 16.3 (1975): 165-179.
‡Curzon, G., June Friedel, and P. J. Knott. "The effect of fatty acids on the binding of tryptophan to plasma protein." Nature 242 (1973): 198-200.
§Godley, Paul A., et al. "Biomarkers of essential fatty acid consumption and risk of prostatic carcinoma." Cancer Epidemiology and Prevention Biomarkers 5.11 (1996): 889-895.

 

[Such_Saturation]

Poor Sir Penrose

 

[Tarmander]

Marvelous

 

[schultz]

Linoleic acid, the key to lipofuscin filled lysosomes inhibiting the proteasome and causing cellular senescence.

 

[FredSonoma]

anyone care to translate this to english

 

[Travis]

Reading that Cocchi article↑ will send anyone here into rant mode . . . after the mind-stunning shock wears-off.

(You can't say that I didn't warn you.)

 

[Hugh Johnson]

This is not a joke. This was published in BioMed Central Neuroscience in April
​

April 1st?

 

[burtlancast]

Well, he's only riding the same wagon Chris Masterjohn does.
Chris seems well liked on this forum, of all places.

 

[Such_Saturation]

Chris is driven by curiosity, unlike that other brain surgeon...

 

[Travis]

Chris Masterjohn seems to have omnivore bias. I read something, somewhere, that he had been sponsored at one time by the WAPF.* When I had first become aware of him. I didn't like him. I didn't like his attitude and demeanor shown in this video, and had questioned his motives.

But he does seem a bit different now; he seems more independent, and the articles I saw seem logically-sound — but that's probably because I hadn't read them all.

Even though he seems entirely independent, he might be hesitant to backtrack on his prior claims of when he was working for the WAPF* or whatever. People who make a name for themselves don't usually seem to like contradicting prior work. People who are ambivalent don't generally have much of a following; and since having a following appears to be his source of income at the moment, being ambivalent means not having much of a job.

He's better than David Aprey, whose writings are nearly 70% total woo.

He seems to create or explain molecular mechanisms within an omnivorous framework. I think Ray Peat's articles are better. It the area where their spheres of explanation may overlap [imagine 3-dimensional Venn diagram], Peat's understanding is likely more fundamentally-sound. Chris Masterjohn went to school at Champaign-Urbana. This is American's Heartland; an agricultural area. All you see around there are cornfields, and cows.

*Impossible to track down the source for this. Consider it a rumor.

 

[burtlancast]

Lying through his teeth with a straight face.
Should have been a politician.

https://www.westonaprice.org/health-topics/know-your-fats/precious-yet-perilous/

 

[johnwester130]

.................so I should start taking fish oil again ?

 

[Travis]

Masterjohn: The Burrs purified casein through repeated rounds of precipitation and purified sugar [interesting] through repeated rounds of crystallization. They used yeast to supply B vitamins...[*whoa*]

Didn't Ray Peat say that Burrs' rats suffered a B-vitamin deficiency? Ray knew very well about yeast as a source of these, and I don't see how he could have overlooked this:

Peat: Although “Burr's disease” clearly turned out to be a B-vitamin deficiency, probably combined with a mineral deficiency, it continues to be cited as the basis justifying the multibillion dollar industry that has grown up around the “essential” oils.†

Peat: Burr's experimental diet consisted of purified casein (milk protein) and purified sucrose, supplemented with a vitamin concentrate and some minerals. Several of the B vitamins weren't known at the time, and the mineral mixture lacked zinc, copper, manganese, molybdenum, and selenium.

Peat: The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn't know about.§

The same study is cited by both Ray Peat and Chris Masterjohn in the footnotes or their articles:‡

Burr GO, Burr MM. A New Deficiency Disease Produced by the Rigid Exclusion of Fat from the Diet. J Biol Chem. 1929;82(2):345-367.​

This must be it ― the study which has "serendipitously" led to unknown cases of diabetes, prostate cancer, and and gunky cooking utensils. It has been cited 1318 times and was even reprinted in 1973, in the journal Nutrition Reviews.

A Ctrl+F search gives 14 results for the term "yeast." This, or an extract, was obviously-used.

The vitamin B (complex) is furnished by Northwestern pure dehydrated yeast which has been extracted for 48 hours with ether in a Soxhlet apparatus. [...] ...this extraction, and the product is designated as Yeast 5. [...] The dose is evaporated on the yeast,which is then mixed with distilled water and fed at once. [...] When the rat (either the Wistar or Long-Evans strain) is reared on Diet 550 (Diets 550 A and 550 B) supplemented by 0.65 gm. of ether-extracted yeast and the non-saponifiable matter...[et cetera]

But yeast contains (in one cup):

(click to embiggen)​

The Cronometer makes no mention of biotin (which was discovered by our friend Dean Burk) which, based on preliminary investigation, appears to be a vitamin for yeast.

Biotin is necessary growth factor for baker's yeast and when the amount in the growth medium is limited the effect can be observed on all cellular functions.

​

Which leads me to assume that yeast cannot synthesize it's own biotin. But since yeast cannot grow without it, dried yeast must contain some of it.

(click to embiggen)​

This is five times lower that a standard Harlan–Tekand (formerly Harlan–Sprague-Dawley) rodent chow indicates, so even an all-yeast diet would be five times lower. There is no official human RDA. An informative online chat-box dialogue with a rodent nutritionist (ENVIGO + Helping customers secure the potential of life enhancing research and products | Envigo) is given below, verbatim:

Ask a Nutritionist: Hello, welcome to Envigo Teklad. May I answer any Teklad diet questions?

TRAVIS: How much biotin to rats need per day?

Ask a Nutritionist: Hi Travis. Could you share which research institute you are associated with?

TRAVIS: [lies] University of Cork, Ireland.

Ask a Nutritionist: The NRC estimates the biotin require for rats to be 0.2 mg/kg of diet. Nutrient requirements for rodents are on a unit per diet basis rather than unit per day.

Are you looking to induce a biotin deficiency or some other manipulation of the dietary biotin level?

TRAVIS: I am interested in knowing the precise level in which mortality is induced, in rats.

Ask a Nutritionist: From a deficiency or toxicity?

TRAVIS: From deficiency.

Ask a Nutritionist: A diet without supplemented biotin would likely not cause a deficiency unless some other ingredient is added that would bind biotin - such as sprayed dried egg white solids which are a natural source of avidin.

TRAVIS: Even a refined, and highly heated, diet?

Ask a Nutritionist: My understanding is the biotin requirement can be meet the intestinal microflora and coprophagy. What prompts your question?

TRAVIS: A re-appraisal of a former experiment; that is all. ―Thank you.

Ask a Nutritionist: There is possibility that a deficiency could occur with a purified diet if you were feeding on a wire grid (preventing coprophagy), the animals were germ-free or maybe if a sulfa-drug was added to the diet.

Do you have the formula for the diet you fed?

TRAVIS: It had a yeast-extract, extracted at 100°C.

Ask a Nutritionist: Was there a fiber source? What vitamin mix was added to the diet?

At 100C even if the yeast had avidin present I would think it would be denatured at that temperature.

TRAVIS: No fibre. I need to look into the heat-lability of such vitamins. Thiamine and pantothenic acid appear similarly affected.

Ask a Nutritionist: What were the signs of morbidity? Did you see a significant weight loss after feeding the diet for a few weeks?

TRAVIS: Weight loss and mortality.

Ask a Nutritionist: I would check thiamin especially if the diet contained a high level of carbohydrate that are more refined like cornstarch, sucrose or maltodextrin.

My experience with thiamin deficiency is that animals will grow or not loss weight for a couple of weeks until stores are depeleted and then experience significant weight loss followed by mortality fairly quickly.

Thiamin is heat liable as well.

TRAVIS: Thank you.

Ask a Nutritionist: You're welcome. I am going to leave for the day now so I have to exit our chat feature.

Thanks for chatting with me today. If you need to get in touch with me in the future you can contact me directly at [email protected] or 800-483-5523 ext. 30297

[I forgot to ask about skin conditions.]

I think she's right about the biotin. I just found a study where they used both a suspension cage and egg-white to induce deficiency.​

Heat damage could have been a factor. The B-vitamin complex used by Burrs' extract was heated, by definition, as a Soxhlet extractor cannot work without. Some B-vitamins are sensitive to heat.

(click to embiggen)

...namely, pantothenic acid and thiamine. But pyroxidine and niacin are sensitive to such things as, light, reducing agents, and pH. There are no details of the yeast vitamin-B extraction; and since they weren't even all known back then, they could have perhaps been a bit reckless with the procedure.​

Quotes from Burr:

A basal diet of the greatest simplicity was desired and everything was left out which was not definitely known to be necessary for the production of healthy, vigorous animals. Vitamin E was therefore omitted from the diet (which, accordingly, always produces sterile animals, readily curable).

...an abnormal, scaly condition of the skin is observed between the 70th and the 90th day of life. Later the tip of the tail may become inflamed and swollen, and the whole tail soon is heavily scaled and ridged. Hemorrhagic spots through the entire length of the tail. The swelling of the tip may gradually be replaced by a true necrosis, resulting in the loss of 1 to 3 cm. of the tail. The hind feet become red and somewhat swollen at times, in some cases with large scales over the dorsal surfaces. The hair on the back of the body becomes filled with dandruff. There is a tendency to lose the hair, especially about the face, back, and throat. Sores often appear on the skin.

The loss of hair and the skin lesions remind us of the pellagra symptoms in the rat described by Goldberger and Lillie (6). The following description of the development of the pellagra-like condition in the rat is given by these authors (p. 1028) :

Pellagra was my first thought too. He speaks about the lower-in-protein diets 550 A and 550 B as the higher "550", so just glancing at Table 1 appears to give the wrong impression. Perhaps he chose only to graph the lower-protein diets because the higher protein diets provided enough niacin derived from tryptophan?

But besides niacin, both pyrixodine and biotin can produce similar skin manifestations. A deficiency in thiamine does not, this produces the more the neurological beriberi.

Barthelemy, H., B. Chouvet, and F. Cambazard. "Skin and mucosal manifestations in vitamin deficiency." Journal of the American Academy of Dermatology 15.6 (1986): 1263-1274.

However, precise isoniazid effects are not clear, since pyridoxine [B₆] deficiency can induce nicotinic acid deficiency and pellagra-like cutaneous manifestations. These skin alterations decrease rapidly with topical niacinamide applications

Biotin: [...] Skin lesions resemble ichthyosis or generalized seborrheic dermatitis. The later infantile form resembles acrodermatitis enteropathica. Skin lesions are diffuse, and the face is brilliant red and resembles a mask. Scaly dermatitis and alopecia are associated. These skin signs are similar to those in deficiencies of zinc and essential fatty acid.

So we have niacin, biotin, and pyroxidine as potential suspects based-on syptoms, but biotin-deficiency is unheard-of without egg albumin or antibiotics. It might seem as thought the very high-sugar and low-protein diet used (Table 1) could have accelerated the depletion – and increased the need – of niacin and/or pyroxidine. These deficiencies are commonly found associated with high-sucrose diets, but this is usually just explained by the fact that sucrose has no B-vitamins and eaten at the expense of that which does.

I think Ray Peat was right about this. I have heard of similarly-induced B-vitamin deficiencies on high-sucrose diets. Such things appear in the writings of Shelton, Tilden, and other classic nutritionists.

Although pellagra was well-known in 1929, it hadn't yet been proven to be caused by a vitamin deficiency. Many—and perhaps even most—people thought it was infectious; a microbial theory of pellagra was commonly presumed.

*A Keanu Reeves "whoa." Not ― definitely not ― a Joey Lawrence "whoa."
‡Masterjohn's Article
†Fats and degeneration
§Unsaturated fatty acids: Nutritionally essential, or toxic?
¶Copping, Alice Mary, and Margaret Honora Roscoe. "The water-soluble B-vitamins in yeast, flour and bread." Biochemical Journal 31.10 (1937): 1879.
¶Oura, Erkki, and Heikki Suomalainen. "Biotin and the metabolism of baker's yeast." Journal of the Institute of Brewing 84.5 (1978): 283-287.

Approximate years of discovery:
B₁=1897 —— B₄≠exist —— B₇=1930s –– B₁₀≠exist
B₂=1920 —— B₅=1933 —— B₈≠exist —— B₁₁≠exist
B₃=1937 —— B₆=1934 —— B₉=1931 —— B₁₂=1920s

(Ray Peat's point stands about most B-vitamins not being known before 1929. I just glanced at a study on B-vitamins in yeast from 1937, and only thaimine and flavin were even mentioned.)

 

[schultz]

​

Didn't Ray Peat say that Burrs' rats suffered a B-vitamin deficiency? Ray knew very well about yeast as a source of these, and I don't see how he could have overlooked this:

​

The same study is cited by both Ray Peat and Chris Masterjohn in the footnotes or their articles:‡

Burr GO, Burr MM. A New Deficiency Disease Produced by the Rigid Exclusion of Fat from the Diet. J Biol Chem. 1929;82(2):345-367.​

This must be it ― the study which has "serendipitously" led to unknown cases of diabetes, prostate cancer, and and gunky cooking utensils. It has been cited 1318 times and was even reprinted in 1973, in the journal Nutrition Reviews.

A Ctrl+F search gives 14 results for the term "yeast." This, or an extract, was obviously-used.

​

But yeast contains (in one cup):

View attachment 6832 (click to embiggen)​

The Cronometer makes no mention of biotin (which was discovered by our friend Dean Burk) which, based on preliminary investigation, appears to be a vitamin for yeast.

​

Which leads me to assume that yeast cannot synthesize it's own biotin. But since yeast cannot grow without it, dried yeast must contain some of it.

View attachment 6834 (click to embiggen)​

This is five times lower that a standard Harlan–Tekand (formerly Harlan–Sprague-Dawley) rodent chow indicates, so even an all-yeast diet would be five times lower. There is no official human RDA. An informative online chat-box dialogue with a rodent nutritionist (ENVIGO + Helping customers secure the potential of life enhancing research and products | Envigo) is given below, verbatim:

I think she's right about the biotin. I just found a study where they used both a suspension cage and egg-white to induce deficiency.​

Heat damage could have been a factor. The B-vitamin complex used by Burrs' extract was heated, by definition, as a Soxhlet extractor cannot work without. Some vitamins are sensitive to heat.

View attachment 6833 (click to embiggen)

Namely, pantothenic acid and thiamine.​

Quotes from Burr:

​

Pellagra was my first thought too. He speaks about the lower-in-protein diets 550 A and 550 B as the higher "550", so just glancing at Table 1 appears to give the wrong impression. Perhaps he chose only to graph the lower-protein diets because the higher protein diets provided enough niacin derived from tryptophan?

But besides niacin, both pyrixodine and biotin can produce similar skin manifestations. A deficiency in thiamine does not, this produces the more the neurological beriberi.

Barthelemy, H., B. Chouvet, and F. Cambazard. "Skin and mucosal manifestations in vitamin deficiency." Journal of the American Academy of Dermatology 15.6 (1986): 1263-1274.

​

So we have niacin, biotin, and pyroxidine as potential suspects based-on syptoms, but biotin-deficiency is unheard-of without egg albumin or antibiotics. None of these vitamins are heat-labile. It might seem as thought the very high-sugar diet (Table 1) and low-protein could have accelerated the depletion – and increased the need – of niacin or pyroxidine. These deficiencies are commonly found associated with high-sucrose diets, but this is usually just explained by the fact that sucrose has no B-vitamins and eaten at the expense of that which does.

I think Ray Peat was right about this. I have heard of similarly-induced B-vitamin deficiencies on high-sucrose diets. Such things appear in the writings of Shelton, Tilden, and other classic nutritionists.

Although pellagra was well-known in 1929, it hadn't been shown to be caused by a vitamin deficiency back then. Many—and perhaps even most—people thought it was infectious; a microbial theory of pellagra was commonly presumed.

*A Keanu Reeves "whoa." Not ― definitely not ― a Joey Lawrence "whoa."
‡Masterjohn's Article
†Fats and degeneration
§Unsaturated fatty acids: Nutritionally essential, or toxic?
¶Copping, Alice Mary, and Margaret Honora Roscoe. "The water-soluble B-vitamins in yeast, flour and bread." Biochemical Journal 31.10 (1937): 1879.
¶Oura, Erkki, and Heikki Suomalainen. "Biotin and the metabolism of baker's yeast." Journal of the Institute of Brewing 84.5 (1978): 283-287.

Approximate years of discovery:
B₁=1897 —— B₄≠exist —— B₇=1930s –– B₁₀≠exist
B₂=1920 —— B₅=1933 —— B₈≠exist —— B₁₁≠exist
B₃=1937 —— B₆=1934 —— B₉=1931 —— B₁₂=1920s

(Ray Peat's point stands about most B-vitamins not being known before 1929. I just glanced at a study on B-vitamins in yeast from 1937, and only thaimine and flavin were even mentioned.)

Great post Travis. I especially liked the chat you had with the rodent nutritionist. Very smooth!

Do you know what kind of yeast it was? I couldn't find much on the Northwestern Yeast Company, except that they sold a product called yeast foam which could be used to make rootbeer and other things. I assume it was bakers yeast?

 

[DaveFoster]

Chris is driven by curiosity, unlike that other brain surgeon...

 

[Such_Saturation]

C'mon Dave don't make it worse

 

[Travis]

@schultz: Do you know what kind of yeast it was? I couldn't find much on the Northwestern Yeast Company, except that they sold a product called yeast foam which could be used to make rootbeer and other things. I assume it was bakers yeast?

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 . . .

 

[schultz]

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 hope you do! Looking forward to it.

Sometimes it's just a matter of finding the right keywords

Yes!!! I know what you mean. Sometimes the relevant paper has a title that you would not associate with the thing you're trying to search.

 

[Drareg]

This is great read,thanks! @Travis

Do you think water in the microtubules will be an issue with PUFA,from my limited understanding doesn’t water mix more with PUFA? Less so with saturated fat,now at individual fatty acid level I don’t know but for me it implies PUFA will not benefit structure and control of water,saturate fat will support a structure of water for example,my guess is water moving and shifting is involved with consciousness via control of electromagnetism?
A crude experiment would be,mix protein,fat,water and apply heat,the ratios will create a structure of sort,differing ratios/different structures.

 

[opiath]

@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.