HDAC 4 Is most likely the cause of our suffering

[EndlessPossibilities]

Saethra chotzen disease. Low and or dysfunctioning twist1. Results in zero recession in all including adult males at least based on all the online presentations.


we just need to figure out a few things. how do the hdacs regulate these twists and how can we regulate them ourselves. And we need to figure out what do with twist2.

 

[EndlessPossibilities]

And now I think I figured out also why so many of us have serious oily hair issues. Twist2 !

Twist2, a novel ADD1/SREBP1c interacting protein, represses the transcriptional activity of ADD1/SREBP1c

Adipocyte determination and differentiation dependent factor 1 (ADD1)/sterol regulatory element binding protein isoform (SREBP1c) is a key transcription factor in fatty acid metabolism and insulin- dependent gene expression. Although its transcriptional ...

www.ncbi.nlm.nih.gov

it seems to me we want to increase twist 2 How is the big question.



my theory is confirmed by the genetic study that looked at the differences between balding and non balding genes. You hdac4 is mainly associated with twist2 and it’s downregukated in balding genes.

hdac9 associated with twist1.


I found out that hdac9 increases twist1. So inhibition of hdac9 seems to be vital or just twist1.

this alone could solve the problem. But twist2 needs to go up.

 

[Baldingtooyoung]

But are there medicines that up or down regulate these genes?

 

[RagnarLothbrok]

@pegasus2 So I think hdac4 is associated with vertex balding. And hdac9 causes frontal balding. Together. U go fully bald. Why do I think that. Well apparently hdac4 is overexpressed in prostate cancer. and prostate cancer is only associated with vertex balding. This could really explain alot of things.


but I am not sure. I looked at diseases with lack of twist2 expression. Most of them have vertex balding.

one thing is for sure. Twist 1 and 2 control skull shape. And this explains why we see balding people it’s bad skull shapes

looking at twist1 and what it does. I am starting to understand something. We need twist1. Just not too much. Too much and we get hairloss.
too low and we get bone abnormalities growing up.

low enough to I believe is The key. So that group buy u about to do. Keep dosage low.

bone development is over for adults tho? so it shouldn't affect much

 

[EndlessPossibilities]

bone development is over for adults tho? so it shouldn't affect much

Correct messing with the twists after being fully developed is not likely to make much of a difference on ur skull. Perhaps minor minor adjustments to jaw and skull but nothing drastic. The shape of the skull is not the cause of the hairloss. But the cause of the hairloss is the same cause of the shape of the skull

 

[RagnarLothbrok]

@pegasus2 yo check this out. TWIST1 haploinsuffecieny results in craniostenosis

look at this bottom photos. https://www.drderderian.com/sagittal-craniosynostosis


Saethre-Chotzen have twist 1 dysfunction. And low hairlines. Interestingly low twist 2 function related disease also seems relate to low hairlines. But they often have sparse hair.

lmao this is probably literally the scientific reason behind "muh galea" retarded threads

 

[EndlessPossibilities]

lmao this is probably literally the scientific reason behind "muh galea" retarded threads

Ya that thread identifies a strong correlation. But the cause and effect is absolutely misplaced.
I think the most frustrating thing is no one is focused on actually curing male pattern baldness at its root all the things coming out are just stimulators or procedures.

the medical industry does not give a f*** about curing anything besides making money period.

 

[RagnarLothbrok]

the incentive is still there, any Twist1 / hdac inhibitor molecules can be converted into millionare money making drugs still

 

[EndlessPossibilities]

the incentive is still there, any Twist1 / hdac inhibitor molecules can be converted into millionare money making drugs still

Ya. Fact is if u can cure male pattern baldness with very very minimal side effects. it could equal trillions.

but you see there are likely benefits to these genes. So say you do lower hdac1. you now now may have a higher chance of developing a stroke or something. It’s just an example.

I am most curious about how the prolactin antibody works In all this. pegasus thinks they are directly related. But I couldn’t find anything in the literature relating to twist and prolactin.

 

[RagnarLothbrok]

we are all willing to inflict some self-harm in exchange for hair, just need to choose the pathway with most results / least harm ratio

its not like oral minoxidil + dutasteride don't have implications

 

[EndlessPossibilities]

we are all willing to inflict some self-harm in exchange for hair, just need to choose the pathway with most results / least harm ratio

its not like oral minoxidil + dutasteride don't have implications

Very true. Those methods have serious effects. Honestly minoxidil may be very dangerous the long term affects on the heart may not be seen until way later.

either way I think baldness will be solved effectively in the next 20 years MAX

 

[pegasus2]

Twist2 shuts down DPC inductivity so it has to be inhibited too. That can't be done, so we can inhibit HDAC2 instead with VPA, and try to upregulate p300.

Cranial malformation is due to a lack of Twist signaling, that should be protective against hair loss in adults.

Prolactin induces PKC which upregulates Twist1.

Twist1 is necessary for the formation of the skull and many tissues during embryogenesis. Mice born without Twist1 do not survive. Postnatal deletion of Twist1 does not cause any obvious problems in mice. I intend to inhibit Twist1 topically by as close to 100% as possible.

 

[losingbattle88]

Ya. Fact is if u can cure male pattern baldness with very very minimal side effects. it could equal trillions.

but you see there are likely benefits to these genes. So say you do lower hdac1. you now now may have a higher chance of developing a stroke or something. It’s just an example.

I am most curious about how the prolactin antibody works In all this. pegasus thinks they are directly related. But I couldn’t find anything in the literature relating to twist and prolactin.

Just Buzz it and forget about your hair.

 

[EndlessPossibilities]

Twist2 shuts down DPC inductivity so it has to be inhibited too. That can't be done, so we can inhibit HDAC2 instead with VPA, and try to upregulate p300.

Cranial malformation is due to a lack of Twist signaling, that should be protective against hair loss in adults.

Prolactin induces PKC which upregulates Twist1.

Twist1 is necessary for the formation of the skull and many tissues during embryogenesis. Mice born without Twist1 do not survive. Postnatal deletion of Twist1 does not cause any obvious problems in mice. I intend to inhibit Twist1 topically by as close to 100% as possible.

I agree with u on everything except twist 2. The gene study I posted says that twist2 is downregulated in balding gene

 

[EndlessPossibilities]

Just Buzz it and forget about your hair.

My hair is fantastic now. I don’t give up. Those crazy obsessed people are the people who change the world.

 

[losingbattle88]

My hair is fantastic now. I don’t give up. Those crazy obsessed people are the people who change the world.

Castor oil and peppermint btw lol. Stop this nonsense. How do you prepare your oil and how often do you apply it? And for how Long?

 

[EndlessPossibilities]

Castor oil and peppermint btw lol. Stop this nonsense. How do you prepare your pils and how often do you apply it? And for how Long?

I don’t get it ?

 

[pegasus2]

I agree with u on everything except twist 2. The gene study I posted says that twist2 is downregulated in balding gene

Read the study IBTC posted on Twist2. It recruits HDAC2 to lock down chromatin. Upregulating it would effectively eliminate Wnt signaling.

 

[losingbattle88]

I don’t get it ?

Your regimen is Castor oil and peppermint oil thats it.

 

[EndlessPossibilities]

Read the study IBTC posted on Twist2. It recruits HDAC2 to lock down chromatin. Upregulating it would effectively eliminate Wnt signaling.

okay I will. But could you explain why that study I am referring to says it’s downregulated?