Folinic Acid Stops My Hair Loss

[ddjd]

For years now I have tried to identify the root of my constant hair shedding. It seems to be a mixture of high serotonin, histamine, and adrenaline.

Before peating, I went down the methylation route and experimented with Methyl Folate, and found out that regular Folic Acid is to be avoided completely. I noticed the methylfolate gave my hair a bushier and thicker appearance but didnt stop the shedding.

Recently I came across Folinic Acid which is completely different to regular Folic Acid. Folinic is already metabolically active meaning it doesn’t need any enzymatic conversion to be used. Methylfolate is also metabolically active but in the process of breakdown it adds a methyl before taking away methyl making it harder on the overmethylated people than folinic since it doesn’t need that conversion. Apparantly, Folinic Acid is used primarily by the body for tissue / DNA repair.

Within a day I noticed my hair shedding had stopped. Its been a week now of 800mcg per day, and I've had no hair loss. Even more interesting is that Folinic Acid causes my skin to become extremely soft, has smoothed out my Keratosis Pilaris, and significantly reduced my addictive behaivours.

Id be very interested to hear if anyone else benefits from this supplement.

 

[rawmeat]

interesting. following

 

[Spondive]

For years now I have tried to identify the root of my constant hair shedding. It seems to be a mixture of high serotonin, histamine, and adrenaline.

Before peating, I went down the methylation route and experimented with Methyl Folate, and found out that regular Folic Acid is to be avoided completely. I noticed the methylfolate gave my hair a bushier and thicker appearance but didnt stop the shedding.

Recently I came across Folinic Acid which is completely different to regular Folic Acid. Folinic is already metabolically active meaning it doesn’t need any enzymatic conversion to be used. Methylfolate is also metabolically active but in the process of breakdown it adds a methyl before taking away methyl making it harder on the overmethylated people than folinic since it doesn’t need that conversion. Apparantly, Folinic Acid is used primarily by the body for tissue / DNA repair.

Within a day I noticed my hair shedding had stopped. Its been a week now of 800mcg per day, and I've had no hair loss. Even more interesting is that Folinic Acid causes my skin to become extremely soft, has smoothed out my Keratosis Pilaris, and significantly reduced my addictive behaivours.

Id be very interested to hear if anyone else benefits from this supplement.

Where did you get it?

 

[anyfit]

sounds like you might have a MTHFR gene mutatuion which impaires your folic acid to folate covertion.

might be a good idea for you to stay away from folic acid fortified food entirely and stick to natural folate and folinic acid.

 

[Ras]

Where did you get it?

You didn't ask me, but I've been using Kirkman Labs for several months now. I believe it stopped my shedding, too.

 

[brix]

What’s your hair loss like? Thinning or mpb?

 

[Mary Lyn]

@Joeyd

I have been back on the folinic acid the last 6 weeks or so, and am MTHFR, doing badly on methyl doners, and my shedding has eased off. I thought it was the biotin so thanks for that.

 

[LCohen]

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.

 

[Terma]

This is a popular supplement and I've used it on and off for 5 years. It has a longer half-life than methylfolate (in that form) and unlike it doesn't modulate liver GNMT directly while in the folinic(-derived) form, and is used in mainstream as Leucovorin. [Edited: I confused Deplin (methylfolate) for Leucovorin here - they can both be used for antidepressant treatment, but in the mainstream I believe it's mainly Deplin that's used for that purpose... stupid brand names]

With sufficient Serine, high added folate acts as a NADPH recycler through methylation (this was pointed out several years ago by a very educated member of another forum - almost their own travis), independent of the pentose phosphate pathway (PPP) which is the largest producer in normal circumstances. So it tends to worsen cancers (in fact you could possibly help define cancer as a state of abnormally high NADPH production through the methylation pathway) - but thus may help cell survival, which you could also exploit to help a different condition.

So it's quite circumstantial and there's a huge difference between its physiological roles and pharmacological dosing, but on the whole, what is sure is for most people without cancer, you never want to be folate-deficient, because it's one of the ways the body prevents formaldehyde formation in a few pathways and in cell nucleus (which is actually suggestive of a protective effect against cancer... there's nothing simple about it, and my guess is the body can deal with a certain folate overload naturally - the problem might be when you introduce too much serine on top, but I digress).

I kind of doubt that last part has much to do with hair loss, though. There could always be purine and thymidylate synthesis affecting hair loss somehow, but as a very best guess (not a hair loss expert here) it could be either a DNA transcription effect (LSD1/other), or methylation- or NADPH-related.

To test if it were NADPH-related you might try a NAC/glycine combo to see if you benefit, otherwise you probably wouldn't (NAC is a gold standard for increasing NADPH in things like Lupus trials). Of course it could be totally unrelated, e.g. some indirect effect on hormones or on some other growth factor such as TGF (which is a huge factor in several disease). You could even suggest that NADPH should modulate TGF-β activation, which iirc was thought to be involved in hair loss.

On top of that, as I mentioned, NADPH/NAC can modulate immune diseases (in case that has anything to do with your problems, including possibly hair loss - who knows? Not me) - in particular through the Kynurenine Pathway. The KP appears to be "wired" as an NADPH sensor and when NADPH gets compromised, Kynurenine (Kyn) accumulates (in Lupus).

Now here's where it gets interesting: Tryptophan->Kyn is performed by TDO or IDO. Well, first off, the biggest TDO inducer is Cortisol. So what happens if you have high cortisol and low NADPH? -> Kynurenine accumulation.

One interesting property of Kyn itself (not so much its metabolites, so it has to accumulate) is that it can substitute for Trp in tissues to an extent - however, Kyn is unable to promote normal tissue or cellular growth the way Trp does, so you get a growth-inhibiting effect from high Kyn and low Trp:Kyn ratio. You can see how this could possibly relate. Even more interesting from an immune disease standpoint, if you refer to the Lupus article, in immune cells it appears to have the opposite effect and stimulates T-cell proliferation through mTorC1, whereas Trp does not do this. (Meanwhile, most of the Kynurenine Pathway metabolites produced from Kyn with sufficient NADPH are immunosuppressive.)

So, somewhere between NADPH, TGF, Cortisol, Trp:Kyn, and finally the complex influence of prostaglandins (on virtually all of these) there's a potential explanation and it's all connected in a kind of beautiful way.

It's interesting you think it helps your hair loss, and I'm not even that big into the topic, honestly. Keep in mind I've read barely any posts about hair loss on this forum - I just barely noticed Travis's posts on prostaglandins and some stuff about TGF - otherwise this is disjointed from all past conversations.

[I've omitted a related discussion about the KAT enzyme that normally can divert Kyn toward Kynurenic Acid (KYNA) and away from Niacin - if you throw that in you get an extra layer of energy/immune modulation and possibly an indication that yet something else could be wrong - but at that point it becomes too hard to communicate this picture]

[Edited: Sorry it's Leucovorin, not Deplin]

 

[Pointless]

I'm gonna try this out, because I react very very badly to methylfolate and methyl-B12. Incredibly strong depression. But I've never tried folinic acid.

 

[xetawaves]

Gonna give this a go. I wonder how well it would work topically..

 

[Mito]

I'm gonna try this out, because I react very very badly to methylfolate and methyl-B12. Incredibly strong depression. But I've never tried folinic acid.

 

[Pointless]

Before finding Peat, I tried many "methylation" protocols and found that they were not helpful for me. I also found a lot of people in my research that were struggling with perpetual "die-off" and incremental microdoses that never resolved anything. It's also outrageously complicated and very cloudy scientifically.

 

[ddjd]

This is a popular supplement and I've used it on and off for 5 years. It has a longer half-life than methylfolate (in that form) and unlike it doesn't modulate liver GNMT directly while in the folinic(-derived) form, and is used in mainstream as Leucovorin. [Edited: I confused Deplin (methylfolate) for Leucovorin here - they can both be used for antidepressant treatment, but in the mainstream I believe it's mainly Deplin that's used for that purpose... stupid brand names]

With sufficient Serine, high added folate acts as a NADPH recycler through methylation (this was pointed out several years ago by a very educated member of another forum - almost their own travis), independent of the pentose phosphate pathway (PPP) which is the largest producer in normal circumstances. So it tends to worsen cancers (in fact you could possibly help define cancer as a state of abnormally high NADPH production through the methylation pathway) - but thus may help cell survival, which you could also exploit to help a different condition.

So it's quite circumstantial and there's a huge difference between its physiological roles and pharmacological dosing, but on the whole, what is sure is for most people without cancer, you never want to be folate-deficient, because it's one of the ways the body prevents formaldehyde formation in a few pathways and in cell nucleus (which is actually suggestive of a protective effect against cancer... there's nothing simple about it, and my guess is the body can deal with a certain folate overload naturally - the problem might be when you introduce too much serine on top, but I digress).

I kind of doubt that last part has much to do with hair loss, though. There could always be purine and thymidylate synthesis affecting hair loss somehow, but as a very best guess (not a hair loss expert here) it could be either a DNA transcription effect (LSD1/other), or methylation- or NADPH-related.

To test if it were NADPH-related you might try a NAC/glycine combo to see if you benefit, otherwise you probably wouldn't (NAC is a gold standard for increasing NADPH in things like Lupus trials). Of course it could be totally unrelated, e.g. some indirect effect on hormones or on some other growth factor such as TGF (which is a huge factor in several disease). You could even suggest that NADPH should modulate TGF-β activation, which iirc was thought to be involved in hair loss.

On top of that, as I mentioned, NADPH/NAC can modulate immune diseases (in case that has anything to do with your problems, including possibly hair loss - who knows? Not me) - in particular through the Kynurenine Pathway. The KP appears to be "wired" as an NADPH sensor and when NADPH gets compromised, Kynurenine (Kyn) accumulates (in Lupus).

Now here's where it gets interesting: Tryptophan->Kyn is performed by TDO or IDO. Well, first off, the biggest TDO inducer is Cortisol. So what happens if you have high cortisol and low NADPH? -> Kynurenine accumulation.

One interesting property of Kyn itself (not so much its metabolites, so it has to accumulate) is that it can substitute for Trp in tissues to an extent - however, Kyn is unable to promote normal tissue or cellular growth the way Trp does, so you get a growth-inhibiting effect from high Kyn and low Trp:Kyn ratio. You can see how this could possibly relate. Even more interesting from an immune disease standpoint, if you refer to the Lupus article, in immune cells it appears to have the opposite effect and stimulates T-cell proliferation through mTorC1, whereas Trp does not do this. (Meanwhile, most of the Kynurenine Pathway metabolites produced from Kyn with sufficient NADPH are immunosuppressive.)

So, somewhere between NADPH, TGF, Cortisol, Trp:Kyn, and finally the complex influence of prostaglandins (on virtually all of these) there's a potential explanation and it's all connected in a kind of beautiful way.

It's interesting you think it helps your hair loss, and I'm not even that big into the topic, honestly. Keep in mind I've read barely any posts about hair loss on this forum - I just barely noticed Travis's posts on prostaglandins and some stuff about TGF - otherwise this is disjointed from all past conversations.

[I've omitted a related discussion about the KAT enzyme that normally can divert Kyn toward Kynurenic Acid (KYNA) and away from Niacin - if you throw that in you get an extra layer of energy/immune modulation and possibly an indication that yet something else could be wrong - but at that point it becomes too hard to communicate this picture]

[Edited: Sorry it's Leucovorin, not Deplin]

many thanks for all of this interesting info. im going to have to go over it a few times to properly digest it. i have experimented with NAC before and it definitely didnt help with the hair loss issue but i feel like i benefited in other ways from the glutathione boost, however i think it is very much anti-thyroid

 

[Terma]

It's a very interesting idea, they could be tied in several important ways, and maybe even span across several types of hair loss?

I guess you're not alone, though this is a little informal:

World Hair Research» Blog Archive » Methylation and Hair Loss

A few years ago, I came across an unpublished study where a high dose of folic acid was used, (5 milligrams = 5,000 mcg) that helped restore hair. However, it should be better to use folate (not folic acid) because as many people (as much as 50%) have a defect in the conversion process to turn synthetic vitamin B9 into folate.

It's hard to tell where the line ends but it could very well be more toward methylation/homocysteine than specifically something like NADPH, since growth in general is inhibited at multiple points by methyl deficiency in a less restrictive sense than NADPH alone. Furthermore, besides affecting the KP, Cortisol also distorts methylation...

Maybe the KP/NADPH would only be involved in the "immune" Alopecia Areata:
Evaluation of Serum Homocysteine, High-Sensitivity CRP, and RBC Folate in Patients with Alopecia Areata
However, even there they seem to focus on methylation, though it could be a consequence rather than a cause (due to Cortisol+others).

I think in a very very general sense, methylation is a very logical candidate because it is so simply required for growth of all cells at several stages.

And if that were the case, it would make sense NAC did nothing. Rather you would hypothetically benefit from L-Serine and trade your hair loss for cancer (just kidding, there's tons in food). Maybe even phosphatidylserine to lower cortisol specifically, but it can do it dramatically and I'm not sure dramatic is good...

Serine could get compromised from bad kidneys (they produce Serine from glycine cleavage and methylated folate) or otherwise underactive SHMT anywhere else.

[Gotta point out just in case I was going to waste someone's money: I don't know if oral Serine gets absorbed intact much or not, might have read but do not remember... There could be a role for Sarcosine as a replacement but I really doubt anyone will do the research for that anytime soon]

[This'll probably be the extent of my contribution - would require a lot more reading to get a better idea and I think if I go further I will just be redoing Travis's work]

-----------

Curious: Birch BioMed: Therapies for Scarring & Alopecia Areata

Birch’s lead therapy is an anti-scarring technology called FS2. Originally dubbed “Fibrostop”, FS2 is derived from a metabolite called kynurenine.

Hah, stupid brand names!: FS2 Safety and Tolerability Study in Healthy Volunteers - Full Text View - ClinicalTrials.gov

Drug: Acute Application of kynurenic acid [KYNA] cream

From the same group:
The Safety and Tolerability of Topically Delivered Kynurenic Acid in Humans: A Phase 1 Randomized Double-Blind Clinical Trial.
Intraperitoneal injection of IDO-expressing dermal fibroblasts improves the allograft survival. - PubMed - NCBI
Kynurenine Modulates MMP-1 and Type-I Collagen Expression Via Aryl Hydrocarbon Receptor Activation in Dermal Fibroblasts. - PubMed - NCBI
Effects of kynurenine on CD3+ and macrophages in wound healing. - PubMed - NCBI
IDO expressing fibroblasts promote the expansion of antigen specific regulatory T cells. - PubMed - NCBI

 

[xTaLaLx]

I heard it was used to reverse hair loss in cancer patients and repair DNA damage from chemotherapy.
Also it has been used in kids with autism.

 

[Mito]

I heard it was used to reverse hair loss in cancer patients and repair DNA damage from chemotherapy.
Also it has been used in kids with autism.

Lynch talks about this.

 

[ddjd]

And if that were the case, it would make sense NAC did nothing. Rather you would hypothetically benefit from L-Serine and trade your hair loss for cancer (just kidding, there's tons in food). Maybe even phosphatidylserine to lower cortisol specifically, but it can do it dramatically and I'm not sure dramatic is good...

Serine could get compromised from bad kidneys (they produce Serine from glycine cleavage and methylated folate) or otherwise underactive SHMT anywhere else.

I have experimented with PhosphatidylSerine actually and i find it of great benefit for sleep (probably because of the cortisol lowering).

To clarify, why would phosphatidylserine and Folinic acid complement one another?

I'm convinced now that as you say the Folinic acid is helping my Methionine cycle somehow. I must have the genetic defect which doesn't allow me to produce folate properly.

I'm just slightly worried about taking Folinic acid long term with regard to the potential cancer risk you mentioned

 

[Curiousman]

Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia

These results suggest it is possible that increased AR methylation may protect occipital hairs from miniaturization and hair loss. Thus, the potential to take advantage of the plasticity of DNA methylation, and the accessibility of scalp hair to topical application, makes this an enticing area for the development of therapeutic strategies for AGA. Certainly, further analysis of the role of DNA methylation in AGA is warranted.

My experience with vitamin B9 : hair growth , fat loss , muscle mass gain and increase of energy. I had better results with folic acid than folinic acid . I got to take 5 mg day and stopped because a weird sensation in my mind.

 

[ddjd]

@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."