Genes Regulating Inflammation, Stress, And Fibrosis Were Massively Overexpressed In All Androgenetic Alopecia Groups

HairSuit

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You would think that Seti would be more beneficial, if inflammation were a key factor..... but I found it to be pretty much useless, as did many others. There’s a ton of factors as to why that might be, but.....
 

Warmer82

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Trinov has anti inflammatory properties with Linoleic acid is an essential precursor of prostaglandin E1 (PGE 1) – a very crucial component in improving the microcirculation in the body and a potent inhibitor of inflammation.
 

Warmer82

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You would think that Seti would be more beneficial, if inflammation were a key factor..... but I found it to be pretty much useless, as did many others. There’s a ton of factors as to why that might be, but.....

I thought seti was a receptor antagonist?
 

jjamerson

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Guess we will never know unless we try it.
Finisteride and minoxidil were accidental hair loss drugs. still we dont know exactly how they work. Know one has developed a cure yet, it still may be found by trialling new things

We do know how they work. We know that inflammation is one of the main causes of hair loss, because inflammation causes stiffness in arteries, restricting bloodflow (hence heart disease). minoxidil is a vasodilator which opens up blood vessels allowing more blood to flow freely, sending more oxygen and nutrients to our follicles. This will give the side effect of slowing hair loss, and in some cases, allow hair to grow.

We also know that DHT binds to the receptors in our hair follicles, causing them to shrink, weaken, and eventually die. The reason finasteride works to some degree is simply because it reduces the formation of DHT in our body.

What we don’t know is why some people have inflammation in that area of the scalp (or follicle). It’s very similar to our lack of understanding on what causes arthritis. Our body’s immune system is attacking its own tissue thinking that something is wrong (autoimmune disorder). I believe that hair loss and arthritis are very similar problems. And of course, neither have a cure.

So in the end, reducing DHT and opening blood vessels in our scalp is just a temporary solution to slow the inevitable. The problem isn’t DHT or bloodflow, the problem is our immune system is attacking healthy cells and we don’t know why.
 

FCKW36

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The problem isn’t DHT or bloodflow, the problem is our immune system is attacking healthy cells and we don’t know why.

If this is true and hairloss is an autoimmune disease, there will never be a cure...
 

Rock12

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This is consistent with my theory that balding is cause by inflammation. Dht is just part of the inflammation response.

Dht -> pdg2 -> inflammation -> fibrosis and calcification -> less blood and nutrients to hair -> hair miniaturization.
 

EndlessPossibilities

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If dht isn’t the cause then why don’t women experience androgenic alopecia often like men. Surely they have anti inflammatory regulatories just like men. I mean if dht is anti inflammation then women would have lots too.

In studies dht applies to the hair follicle in vitro damaged the hair. So idk so much about it being anti inflammatory and not the cause. Men who have high dht and don’t lose their hair probably just have follicles that react differently to dht or not at all.

The human body is not logical. The paradoxes are abundant. Everyone is trying to figure this out from a logical point. In practice that just doesn’t work
 

H

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If this is true and hairloss is an autoimmune disease, there will never be a cure...
Good thing immunosuppressants don't grow back hair from male pattern baldness then huh
 

jjamerson

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Good thing immunosuppressants don't grow back hair from male pattern baldness then huh

Good point, which actually backs up the theory. There’s a study where patients with alopecia areata were given Ruxolitinib (jak inhibitor) and within 3 months, they experienced total regrowth.

“The idea of using JAK inhibitors to treat alopecia stems from a genome analysis that determined that hair follicles in alopecia areata patients emit a signal that draws immune cells to attack. Her team identified specific cells involved and found genetic similarities to unrelated autoimmune diseases.”

https://www.mdedge.com/dermatology/...nd-alopecia-after-positive-early-data-various

Who’s to say that the same thing isn’t happening to people with androgenic alopecia?
 
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H

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Good point, which actually backs up the theory. There’s a study where patients with alopecia areata were given Ruxolitinib (jak inhibitor) and within 3 months, they experienced total regrowth.

“The idea of using JAK inhibitors to treat alopecia stems from a genome analysis that determined that hair follicles in alopecia areata patients emit a signal that draws immune cells to attack. Her team identified specific cells involved and found genetic similarities to unrelated autoimmune diseases.”

https://www.mdedge.com/dermatology/...nd-alopecia-after-positive-early-data-various

Who’s to say that the same thing isn’t happening to people with androgenic alopecia?
They've also used them on a man who grew back a horseshoe does anyone remember whose study that was? If jaks did work for male pattern baldness you'd see more photos of horseshoes actually filling in since that would generate more hype for the scientists and companies than areata the slice of pie is way bigger for male pattern baldness.
 

BalderBaldyBald

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They've also used them on a man who grew back a horseshoe does anyone remember whose study that was? If jaks did work for male pattern baldness you'd see more photos of horseshoes actually filling in since that would generate more hype for the scientists and companies than areata the slice of pie is way bigger for male pattern baldness.

^This

They also used JAK (hard JAK, not the 'soft' they are developing for Androgenetic Alopecia) on some Aerata patients who shown a beautiful horseshoe upon Aerata recovery

Means Androgenetic Alopecia damages kept going even if he had no hair on scalp
So much for calcification bullshits
 

EndlessPossibilities

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^This

They also used JAK (hard JAK, not the 'soft' they are developing for Androgenetic Alopecia) on some Aerata patients who shown a beautiful horseshoe upon Aerata recovery

Means Androgenetic Alopecia damages kept going even if he had no hair on scalp
So much for calcification bullshits


Exactly. Androgenetic alopecia has a different mechanism for sure. I still believe it’s reversible.
 

jjamerson

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^This

They also used JAK (hard JAK, not the 'soft' they are developing for Androgenetic Alopecia) on some Aerata patients who shown a beautiful horseshoe upon Aerata recovery

Means Androgenetic Alopecia damages kept going even if he had no hair on scalp
So much for calcification bullshits

That’s intersting. I’ve never seen/heard of that study. Keep in mind that there are over 100 different types of arthritis, so just because one form of jak didn’t work doesn’t mean that it’s not an autoimmune response. Remember that there’s no cure for athritis either.
 

Rock12

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^This

They also used JAK (hard JAK, not the 'soft' they are developing for Androgenetic Alopecia) on some Aerata patients who shown a beautiful horseshoe upon Aerata recovery

Means Androgenetic Alopecia damages kept going even if he had no hair on scalp
So much for calcification bullshits

Very interesting but that still does not negate a possible roll for calcification in the Hairloss process. What this further proves is that the hair follicles themselves has nothing do with balding. It’s the sorrounding tissue that the hair follicles sits in is the issue. For some reason, dht triggers inflammation in the sorrounding tissue that damages it and leads to permanent changes of the tissue. Part of these permanent changes are via fibrosis and possible calcification.

The Hairloss process can be broken down into 2 stages.

Stage 1 is when the sorrounding tissue is inflamed (the itch) and the hair growth process is being affected due to the on going inflammation .

Stage 2 is where the inflammation has permanently damaged the surrounding tissues. This permanent change to the sorrounding tissue is no longer suitable for the hair follicles. No different than when you have a wound that heals.

Therefore, any Hairloss treatment must be targeted to the specific stage that your Hairloss is in. Blocking dht which is the first trigger in all of this will only help the areas on your scalp that is in stage 1. So even if you eliminate every last dht in your body, you will still not get regrowth in the areas that are in stage 2. But areas that are still in stage 1 will experience full regrowth because the tissue has not yet been permanently damaged.

This is why individuals that are castrated before puberty will not have male pattern baldness but being castrated after male pattern baldness will not result in full hair growth. That is because in the first case dht had no chance to damage the sorrouding tissue and in the seconds case dht had already damaged the sorrounding tissue.

This might also be the reason why Minoxidil does not work in the long run. Minoxidil works by forcing blood and nutrients to the hair follicles but it does not stop the ongoing damage being made to the sorrounding tissue, so eventually, fibrosis get stronger and the hair follicles die.

Of course this is just my theory but it seems solid base on the information that I have. But I am still interesting to hear some challenges to this theory.
 
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