Folinic Acid Stops My Hair Loss

Curiousman

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@Curiousman thanks for that quote

@Terma just found this study which I thought you might find interesting. I noticed the chronic shedding started soon after I started drinking alcohol, but even when I stopped drinking alcohol for several years the shedding didn't stop. Suggesting maybe that alcohol has a lasting effect on DNA and methylation, but in my case clearly can be rectified with Folate in the correct form

https://www.sciencedirect.com/science/article/pii/S0741832905000996

"ethanol impedes the bioavailability of dietary folate and is known to inhibit select folate-dependent biochemical reactions. For example, alcohol ingestion in animals is known to inhibit folate-mediated methionine synthesis and thereby may interrupt critical methylation processes that are mediated by the activated form of methionine that provides substrate for biologic methylation, S-adenosylmethionine. Consistent with this observed inhibition of methionine synthesis is the observation that chronic alcohol ingestion in laboratory animals is known to produce hypomethylation of DNA in the colonic mucosa, a constant feature of early colorectal neoplasia. Inhibition of methionine synthase also creates a “methylfolate trap,” analogous to what occurs in vitamin B12 deficiency. In addition, some evidence indicates that alcohol may redirect the utilization of folate toward serine synthesis and thereby may interfere with a critical function of methylenetetrahydrofolate, thymidine synthesis."
Coffee too !!
 

Terma

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^ That is a very good lead/idea, if true.

@Joeyd Thanks, I'll have to read that one though it skirts the familiar. DNA methylation is plausible but these sorts of issues might or might not relate more to histone methylation (or both). LSD1 (FAD/B2 and folate-binding) is getting more and more research (it is used by the androgen receptor as well): Histone demethylase LSD1 is a folate-binding protein

Don't have the time but I think what would be helpful would be for someone to post a study on the quantification of the fate of folate in healthy humans (if there were one on alopecia of course that would be incredible) in all its pathways. I don't know if that was ever done.

Just have to point out in relation to my very first link, it was written speaking generally about folate. But depending on the uptake and conversion, folinic would probably be largely converting to methylene-folate (it's either that or purine synthesis, unless there's some other unmentioned pathway) which actually does the exact opposite and requires NAD(P)H to produce NAD(P). It's hard to say the impact on hair because 1) I'm not fully researched on the condition and 2) from what I know, there may be a phase where TGF-beta (due to high oxidative stress, notably from NOX with NADPH) is quite damaging, but there's also a phase in the growth that requires ROS to produce growth (anagen phase or just before, I'm not sure). The "oxidative stress" through superoxide is used by cells to manipulate K+ and Ca+ flow across the membranes, and to my knowledge hydrogen pexoride is usually growth-promoting and might be even more critical. Meaning, theoretically you could impede growth with way too much superoxide and ROS scavenging (e.g. super high NAC, glycine, maybe SOD promoters), even though that would prevent against damage by TGF-beta. So there is quite a balance of ROS production needed, one way or another. This is why I gravitated toward the NOX/NADPH idea, and because you were talking more about "stopping hair loss" than increasing growth, but I really have no tangible idea of what state you'd reflect best at the moment.

Maybe we could infer more from the fact you say it helped your keratosis pilaris, but I couldn't tell if it helped mine or not, because I took too many things.
 
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ddjd

ddjd

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Is calcium folinate same thing with folinic acid? Folinic acid is not available as
active ingredient in my country. But Google says they're same.
yes they are the same thing. i use a product called MegaFolinic from source naturals
 

Terma

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@Joeyd I liked that article quite a lot:

low dietary folate intake as risk factors for several cancers

I think what happens is folate has a protective role against cancer, but once cancer develops, it can help fuel it. Or it might depend on its usage by all the pathways. I mean, as if you'd get cancer from a bunch of vegetables grown in your own garden.

alcohol may redirect the utilization of folate toward serine synthesis and thereby may interfere with
a critical function of methylenetetrahydrofolate, thymidine synthesis

This part supports the Ben Lynch video taken verbatim - however, most likely a significant part of this happens in the kidneys, so I'm not sure to what extent it's a dominant issue in the rest of the body - hence the need for some kind of quantification of folate pathways study.

A rather interesting means by which alcohol might also reduce the bioavailability of folate is by chemically destroying the molecule. To date, the only direct evidence to support this concept has been through in vitro experi- ments. Shaw et al. (1989) observed that when the major metabolite of ethanol, acetaldehyde, was catalytically oxidized by the ubiquitous enzyme xanthine oxidase the resulting production of superoxide radicals efficiently cleaved folate into biochemically inactive metabolites.

Hmmm, perhaps you don't want to be taking high doses of methylene blue.

[Regarding DNA methylation specifically:] Although hyper- methylation would seem to be a paradoxic effect of factors that diminish the capacity for biologic methylation, there is evidence that folate inadequacy may have such an effect and that it may act in concert with excess alcohol ingestion. In mammalian cells, folate depletion has been shown to produce hypermethylation of the promoter region of the H-cadherin gene in conjunction with transcriptional silencing of the gene (Jhaveri et al., 2001).

[...]

The underlying mechanism for hypermethylation in this setting seems to be a compensatory up-regulation of DNA methyltransferase activity in response to a milieu that promotes hypomethylation

Hmmm...

Further examination of Fig. 1B reveals that the in- hibition of MS by ethanol would also be expected to result in an accumulation of folate in the form of 5-methylte- trahydrofolate at the expense of the other co-enzymatic forms of folate. Experimental evidence supports this contention. The reaction by which 5,10-methylenetetrahydrofolate (5,10-methyleneTHF) is reduced to 5-methylTHF is catal- yzed by methylenetetrahydrofolate reductase (MTHFR), and it is an essentially irreversible reaction. This is important because the only means by which 5-methylTHF can be used metabolically and subsequently recycled into other co-enzymatic forms of folate is through the MS reaction. If the MS reaction is blocked, as it is in B 12 deficiency or with chronic alcohol ingestion, the conversion of 5,10-methyleneTHF to 5-methylTHF continues and causes an ever-increasing proportion of cellular folate to be locked in a metabolically unavailable form. This is the basis of the methylfolate trap that occurs in B 12 deficiency, producing a functional folate deficiency.

Methyl trap is extensively detailed by some guy named Freddd (see ME/CFS forums), so I won't bother. The only novelty is the realization that heavy alcohol abuse may cause it. That's a pretty damn good reason to avoid binging alcohol.

here exists another pathway by which alcohol might impair folate-dependent metabolism, although the evidence is indirect at present. By increasing intracellular homo- cysteine and diminishing methionine availability (see above), alcohol might stimulate serine synthesis by up-regulating the expression of the serine hydroxymethyltransferase (SHMT) enzyme (Fig. 1B). This would cause a relative depletion of 5,10-methyleneTHF and thereby diminish availability of the co-enzyme for thymidine synthesis. Although alcohol has not been shown to do this directly, the addition of 0.7 mmol homocysteine to mammalian cells has been shown to enhance serine synthesis significantly and diminish de novo thymidine synthesis by nearly 20% (Fell & Selhub, 1990). The mechanism by which this occurs is not definitively understood, but it may be due to the induction of SHMT synthesis by high levels of homocys- teine in a methionine-deplete environment (Dev & Harvey, 1984).

So, first off, you'd have to figure out if it's especially the kidneys compensating or not, but regardless, the bolded part makes a huge amount of sense - because this means - lowering methylation too much for too long could backfire spectacularly!

[Could be notably hard on the kidneys, because they sacrifice methylfolate and glycine to produce serine and produce ammonia and garbage]

So, thanks, really good information from this.
 
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anyfit

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Are there any natural sources of folinic acid? Like food sources?
foods that are high in natural folate ( not fortified) also have folinic acid in them from what i could find online.
so probably dark leafy greens , celery and some legumes should be good sources...
 

Terma

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Iirc food form is mainly THF or DHF. Folinic is formylTHF (buffers formaldehyde). P.S. Don't become low in B3/NAD when you take this.
 

GorillaHead

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What's gla and ala? What food sources?

Just so you know I am on fin. But the whole time I’ve been on fin. My shed never stopped ever in fact It has been insanely horrible gotten worse.

2 days after adding black currant oil and boom it stopped. I added it because my theory is the pufa in it will increase dlga which increases pge1 which is excellent for hair and better than pge2 which is inflammatory
 

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Repas du soir

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Just so you know I am on fin. But the whole time I’ve been on fin. My shed never stopped ever in fact It has been insanely horrible gotten worse.

2 days after adding black currant oil and boom it stopped. I added it because my theory is the pufa in it will increase dlga which increases pge1 which is excellent for hair and better than pge2 which is inflammatory
Well, that's certainly interesting. Do you think there are other ways of increasing pge1 without using gla/ala?
 

GorillaHead

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Well, that's certainly interesting. Do you think there are other ways of increasing pge1 without using gla/ala?
Not sure.

All I know is when the body has abundant alpha lineolic acid. It converts gamma loneolic acid into DGLA which then unregulated Pge1.

Tons of reviews on amazon on the product from women saying black currant oil helped their hair. But it’s amazon reviews so trust that ***t with a pinch of salt
 

Jijita

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Just so you know I am on fin. But the whole time I’ve been on fin. My shed never stopped ever in fact It has been insanely horrible gotten worse.

2 days after adding black currant oil and boom it stopped. I added it because my theory is the pufa in it will increase dlga which increases pge1 which is excellent for hair and better than pge2 which is inflammatory
Hello
So how did you aplied the oil ? And if we eat the black Currant will that make the same results?
 

Jijita

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@GorillaHead @Repas du soir @Jijita can you create a separate thread for the black currant oil. I'd prefer to stay on Folinic acid related stuff thanks
Let me be helpful
After what you said I search about B9 sources and I found that dark green leafy vegetables are great as sources for it that make sense for me how my grand ma (76 years old) made let's say 1/2 of her hair back because this years she eat darck leafy vegetable like an herbivors
 

Amazoniac

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EMF Mitigation - Flush Niacin - Big 5 Minerals

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