Has there been any history of Vitamin A supplementation from Fin or SSRI users on here?

General Discussion
#1

Im not recommending this, but I was just curious as I know alot of supplements have been looked at or experimented with.
Vitamin D and even k2 has gotten alot of attention, what about vitamin a?
Im looking at mostly Fin users right now, as we all know of the potential interactions of vitamin a with accutane.
I suppose I’ll tag you @Dubya_B you’ve been around for awhile.

I found this kind of randomly, obviously butyrate has gotten alot of attention for some reason, I imagine it has something to do with the AR gene?

Butyrate can improve gut epithelial barrier integrity, increasing mucus layer thickness (enhancing mucin genes’ expression, in particular Muc2) ( 1 ) and tight junction expression ( 2 ). Among immune mechanisms, butyrate acts on intestinal epithelial cells (IECs) through two different pathways: (a) the inhibition of histone deacetylases (HDAC) 1 and 3 with subsequent increases in retinaldehyde dehydrogenases (RALDH) 1 activity and retinoic acid (RA) levels ( 3 ); (b) the interaction with G-protein-coupled receptor (GPR) 43, with subsequent increases in Vitamin A metabolism and epithelial barrier integrity. The effect of butyrate on dendritic cells (DCs) results in increasing RALDH2 activity and RA levels through direct (interaction with GPR109A expressed by DCs) and indirect (RA produced by IECs) mechanisms ( 4 ). Butyrate is also able to induce retinoic acid-related orphan receptor γt (RORγt)+ Forkhead box P3 (FoxP3)+ T regulatory (Treg) cells thanks to the inhibition of HDAC6 and 9, which leads to increase of FoxP3 gene expression, as well as the production and suppressive function of Treg cells ( 5 ). The induction of RORγt+ FoxP3+ Treg cells is also mediated by DCs interaction ( 6 ).

I guess another way to put this would be you got threads on here saying vitamin d, k2, milk thistle, b-vitamins, tribulus made me worse.
Are there any posts like this on vitamin A coming from Fin users?

#2

It has been discussed, but I don’t remember many members taking very high doses or that it had much of an effect, either positive or negative.

Here is one anecdote about a crash on vit-A, but the guy was banned for still being on finasteride:

1 Like
#3

A little footnote here. I think it might open up some possibilities knowing Accutane does not bind to Retinoid receptors and might even interfere with them.

Two isomers of retinoic acid (RA) may be necessary as ligands for retinoid signaling: all-trans -RA for RA receptors (RARs) and 9- cis -RA for retinoid X receptors (RXRs). This was explored by using retinaldehyde dehydrogenase ( Raldh)2 -/- mouse embryos lacking mesodermal RA synthesis that display early growth arrest unless rescued by all-trans -RA administration. Because isomerization of all-trans -RA to 9- cis -RA can occur, it is unclear whether both ligands are needed for rescue. We show here that an RAR-specific ligand can rescue Raldh2 -/- embryos as efficiently as all-trans -RA, whereas an RXR-specific ligand has no effect. Further, whereas all-trans -RA was detected in embryos, 9- cis -RA was undetectable unless a supraphysiological dose of all-trans -RA was administered, revealing that 9- cis -RA is of pharmacological but not physiological significance. Because 9- cis -RA is undetectable and unnecessary for Raldh2 -/- rescue, and others have shown that 4-oxo-RA is unnecessary for mouse development, all-trans -RA emerges as the only ligand clearly necessary for retinoid receptor signaling.

#4

It’s a difficult drug to try to make sense of. I’m not surprised the MOA in treating acne is still not clear after 40 years.

Isotretinoin/13-cis has been shown to interfere with steroidogenic enzymes and binding of 11-cis-retinal to rhodpsin.

But I’m not aware of any studies differentiating between hypothetical direct genomic effects of 13-cis-RA and indirect genomic effects via 11-trans isomerization.

#5

You could start to wonder about the birth defects as well with Accutane and any type of endogenous interference of vitamin a metabolism.
RALDH2 seems to be the most important enzyme and all-trans retinoic acid the most important metabolite of vitamin A for its biological effects and activation of retinoid receptors.

Metabolism of vitamin A and the production of all- trans retinoic acid

RALDH2 was identified as a crucial enzyme for atRA synthesis in different organisms. Knockout of RALDH2 was embryonic lethal during the post-implantation period in mice [40], suggesting that atRA is essential for normal embryonic development.

Another example looking at the skin, I think ive posted this before.

Oral isotretinoin (13-cis-retinoic acid) therapy in severe acne: drug and vitamin A concentrations in serum and skin

the retinol level in the epidermis increased by an average of 53% (p less than 0.01) and the dehydroretinol level decreased by 79% (p less than 0.001) as a result of 3 months of treatment. Both changes were reversible. The results suggest that isotretinoin therapy interferes with the endogenous vitamin A metabolism in the skin.

So basically Accutane could cause an interference with vitamin a metabolism and turnover, so you could both have an excess of vitamin a, but lack of its most important end product (retinoic acid) that could also act as a clearance pathway for retinol/retinal.
There’s a chance some of this could be mediated by bacteria. Some bacteria can respond to outside sources of nutrients and shutdown their own production.
Possibly.

#6

So this is what im currently looking at right here, something ive mentioned before.
Once again its from a patent.

In one embodiment the Bifidobacterium comprises Bifidobacterium infantis 35624 In one case the formulation comprises Bifidobacterium infantis 35624 with vitamin A. The formulation induces optimal retinoic acid production in vivo, thereby promoting immune regulatory functions and inhibiting inflammatory diseases.

I also got a response from an Assistant Professor of Molecular Microbiology and Immunology on Vitamin A metabolism. Its something she has an interest in.
A couple lines from her reply,

  1. Our main claim is that gut commensals regulate RA production by modulating levels of vitamin A metabolism in the gut that then has an effect on antimicrobial production.
  2. RA regulates antimicrobial response by upregulating IL-22
  3. when there is an infection or dysbiosis in the gut microbiome more RA is produced that results in a higher antimicrobial activity that can kill gut bacteria.
  4. This antimicrobial activity is indiscriminate in that it kills both good and bad bacteria in the gut.