HDAC 4 Is most likely the cause of our suffering

[RagnarLothbrok]

Then why the lack of media converge and insane excitement. I mean finasteride worked on the monkeys and humans. So if it worked on monkeys it must work on humans. I mean obviously not a guarantee but it’s looking likely. But if it likely then it’s a hollygrail. Unless their is something they aren’t telling us.

The media is now spamming news about a "balding cure" because some JAK inhibitor got approved for areata in USA... I don't think they give a sh*t, the before / after picture of Areata recovery is flashy enough to publish it and get their clicks. Most Androgenetic Alopecia treatments are less flashy in result photos.

About excitement, for people who follow hair loss research i'd say HMI is the most over-hyped treatment by far (which sounds scary given past history)

 

[RagnarLothbrok]

Also GNC product has B-12
Magnesium has a calming effect on the body. Helps some to sleep better. Less stress hormones are therefore produced.
Perhaps less sebum.

I have never supplemented Magnesium in my life.

I live in one of the sunniest EU countries and I was shocked when I came out severely Vitamin D defficient so wouldn't surprise me if im also Magnesium defficient. I'm gonna start supplementing and see if it helps. Recovering from Vitamin D deficiency definetely helped with my hair.

Whats the standard dose? And why do you choose bisglicenate over malate/citrate?

 

[Jakejr]

Great question. When I was choosing among the 10 types.. I found some positive reviews.

What Is Magnesium Glycinate?
Magnesium is an essential nutrient found in many foods. Magnesium Glycinate is a magnesium salt that consists of Magnesium and Glycine and is commonly taken as a Magnesium supplement. Magnesium Glycinate has a higher bioavailability than many other forms Magnesium.
That’s not best review/description because doctors usually prescribe other forms, but I read it raises magnesium levels faster than other forms, but can’t find it at the moment.
250/500 mg a day. Taking more usually isn’t harmful..

 

[EndlessPossibilities]

No, it doesn't make sense. TPRS is the loss of all TRPS1 function. Ambras syndrome is the loss of most TRPS1 function, 97-98% of it. Inhibiting TPRS1 by 98% causes massive hair growth, but inhibiting it 100% causes hair loss. That's not an expected result.

I went and reviewed this.

here is what I learned.

Zero tprs1 elevates hdac4. Hairloss.
Very little tprs1 ( very little hdac4) sh*t load of hair.
Normal Tprs1 ( theory medium levels of hdac4). Normal hair progression. And possible Androgenetic Alopecia.
elevated tprs1 ( theory zero hdac4) zero hairloss.
It could be some sort of biphasic effect.

hdac4 I learned regulates angiogenesis and hif1a highly implicated in our case for hairloss.

in other words. I am super confident it all has to do mainly with this gene.


it seems to me the solution is inhibiting hdac4 but does it have to be targeted or can it be systemic. Not entirely inhibiting.

there is a drug that inhibits hdac4 and it used and tested for guess what prostate cancer. It can’t be a Coincidence

but I am not entirely sure if we need to inhibit it or lower it . Osteocalcin is super related.

I feel like the answer Is right there i front of us.

 

[EndlessPossibilities]

Molecular Biology of the Cell (MBoC)

News | Harvard T.H. Chan School of Public Health

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www.hsph.harvard.edu

hdac4 also increases osteocalcin. I bet if they ran A study today and compared osteocalcin level of Androgenetic Alopecia be healthy controls. Osteocalcin would be higher. And apparently after 50 it increases in women and men. This is he marked right here. This doesn’t mean we lower osteocalcin and solve the problem. hdac4 does a lot of things. And one of them is increasing osteocalcin. It’s just a marker.

at this point i think it’s fair to we need to lower our hdac4 expression mainly in bome and thus we slow or even possible stop Androgenetic Alopecia completely


more and more supporting evidence. https://www.hindawi.com/journals/omcl/2022/3087916/


also read that stress increases hdac4 explaining so much. It’s all coming together. E need a damn specific hdac4 inhibitor. But not too strong.

 

[Hairful]

Calcification means nothing man. It’s a result not the cause.

 

[today]

Curcumin​

The polyphenol curcumin (2), as mentioned earlier, was isolated from the rhizome Curcuma longa (Soleimani et al., 2018). Curcumin (2) is known to possess HDAC inhibitory activity in different cancer cell lines (Soflaei et al., 2018). Indeed, induction by curcumin of cell cycle arrest at G2/M phase, apoptosis, and increase in tubulin acetylation in medulloblastoma cells, through the inhibition of HDAC, in particular HDAC4 was reported (Lee et al., 2011). It has been reported that 2 may be of considerable value in synergistic therapy of cancer in a manner that the drug dose level could be strongly minimized to reduce the associated toxicity (Roy et al., 2011). Indeed, 2 combined with other HDAC inhibitors such as vorinostat resulted in a marked enhancement of the antiproliferative activity of the associated drug, and sensitization to apoptosis (Giommarelli et al., 2010). A similar observation was made when 2 was combined with cyclophosphamide and paclitaxel (Roy et al., 2011). Nevertheless, curcumin is known to show pan-activities, which is why any reported specificity needs to be seen with caution.

 

[pegasus2]

Zero tprs1 elevates hdac4. Hairloss.
Very little tprs1 ( very little hdac4) sh*t load of hair.

Do you have a source for this?

 

[Mr. Slap Head]

It’s your sh*t genes

 

[EndlessPossibilities]

Do you have a source for this?

Looks like I got it all wrong. Damn.
according to this

A central role for TRPS1 in the control of cell cycle and cancer development | Oncotarget

https://doi.org/10.18632/oncotarget.2291 Lele Wu, Yuzhi Wang, Yan Liu, Shiyi Yu, Hao Xie, Xingjuan Shi, Sheng Qin, Fei Ma, Tuan Zea Tan, Jean Paul Thiery, Liming Chen

www.oncotarget.com

loss of trsp1 decreases hdac4 expression.

the thing is I keep finding information that says hdac4 inhibits runx2 which I thought was necessary for hair growth.

 

[EndlessPossibilities]

Okay. Here is an update that makes more sense.


No TPRS1. Lower Hdac4. (Hairloss).


Normal TPRS1. Normal HDAC4. (Normal progression).


Slightly lower tprs1. slight lower hdac4. (Hairloss immunity?)

Trps1 and Its Target Gene Sox9 Regulate Epithelial Proliferation in the Developing Hair Follicle and Are Associated with Hypertrichosis - PMC

Hereditary hypertrichoses are a group of hair overgrowth syndromes that are extremely rare in humans. We have previously demonstrated that a position effect on TRPS1 is associated with hypertrichosis in humans and mice. To gain insight into the ...

www.ncbi.nlm.nih.gov

maybe u can crack this. Ultimately. I am trying to figure out whether we need more or less expression of hdac4

but the fact that topical valproic acid increased hair after 6 months it was moderate increase. Tell me we need to inhibit hdac4. I think valproic acid only inhibits hdac4 by a very mild amount https://onlinelibrary.wiley.com/doi/full/10.1111/1346-8138.12422


i think I can explain why topical lithium never worked. Everyone thinks jak stat inhibition was why hair grew in valproic acid but its’more likely hdac inhibition

 

[Hairful]

More likely that hdac4 has no connection to hairloss.

 

[EndlessPossibilities]

More likely that hdac4 has no connection to hairloss.

Well that’s clearly not true especially When it’s one of the top gene hit markers especially for androgenic alopecia.

Judging by your last response in this thread isn’t for you man. Honestly only Pegasus probably understand anything I am saying no offense.

 

[Hairful]

Well that’s clearly not true especially When it’s one of the top gene hit markers especially for androgenic alopecia.

Judging by your last response in this thread isn’t for you man. Honestly only Pegasus probably understand anything I am saying no offense.

So what? there are several other genes for baldness. Correlation doesn’t mean causation.

You just want it to mean something to prove your bone theory with hairloss, same as that guy with his scalp tension BS.

 

[EndlessPossibilities]

So what? there are several other genes for baldness. Correlation doesn’t mean causation.

You just want it to mean something to prove your bone theory with hairloss, same as that guy with his scalp tension BS.

u Really don’t get it do you. You realize how strong the correlation is. The p values are ridiculous. And on top of that wnt being the major driving stimulator of hair growth is the same stimulator for bone growth. There are hundreds and hundreds of studies that show the genes that stimulate hair stimulate bone growth and in trps1 syndrome and ectodermsk hyperplasia bome doesn’t grow right. Neither does the hair. And a bone drug has already been shown to grow hair.

the guy with scalp tension theory uses photos to make claims. I use science.

Your acting like a flat earther. Denying all the evidence. But hey man. You do u. I am still gonna share cause there are those like me who see the connections.

 

[Hairful]

Your acting like a flat earther. Denying all the evidence.

See these absurd connections you make just shows you’re really trying hard lol like with this theory.

Human body is extremely complex and interconnected. The fact you see varying results with hdac4 amount proves there’s another missing factor and it’s not the main factor, uh duh we know there are other genetic markers and factors that cause hairloss with direct connection.

 

[InBeforeTheCure]

The causal gene is probably not HDAC4. More likely TWIST2 due to other Androgenetic Alopecia-associated variants around classic TWIST binding factors TCF4 and TCF12 and the known important role of TWIST2 in hair biology. It shuts down hair inductivity in dermal cells by recruiting HDAC2 to critical hair-inducing genes. HDAC2 deacetylates these genes -> closed chromatin -> transcription factors can't access them. (source)

 

[EndlessPossibilities]

View attachment 182354

The causal gene is probably not HDAC4. More likely TWIST2 due to other Androgenetic Alopecia-associated variants around classic TWIST binding factors TCF4 and TCF12 and the known important role of TWIST2 in hair biology. It shuts down hair inductivity in dermal cells by recruiting HDAC2 to critical hair-inducing genes. HDAC2 deacetylates these genes -> closed chromatin -> transcription factors can't access them. (source)

So then hdac9. Which isn’t a bad call. I can’t remember where I read that all balding men of all ethnicities had this gene

 

[pegasus2]

See these absurd connections you make just shows you’re really trying hard lol like with this theory.

Human body is extremely complex and interconnected. The fact you see varying results with hdac4 amount proves there’s another missing factor and it’s not the main factor, uh duh we know there are other genetic markers and factors that cause hairloss with direct connection.

To be fair it does look like HDAC/HAT imbalance is a major contributing factor.

 

[EndlessPossibilities]

To be fair it does look like HDAC/HAT imbalance is a major contributing factor.

I wouldn’t mind him. He contributes nothing. His prerogative. But we aren’t here to convince him or anybody. Just to figure this sh*t out