Maybe this is why people rolleing with betadine are getting good results as betadine is anti inflammatory due to iodine in trnf2 pathway
https://www.ncbi.nlm.nih.gov/m/pubmed/28088623/
https://www.ncbi.nlm.nih.gov/m/pubmed/28088623/
Genes Regulating Inflammation, Stress, And Fibrosis Were Massively Overexpressed In All Androgenetic Alopecia Groups
- Thread starter Warmer82
- Start date
I thought seti was a receptor antagonist?
- Reaction score
- 56
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
Experienced Member
- Reaction score
- 622
FCKW36
Experienced Member
- Reaction score
- 622
If this is true and hairloss is an autoimmune disease, there will never be a cure...
jnestor481
Member
- Reaction score
- 33
It is..... but not for androgens. It deals with the inflammation response.You are right.
- Reaction score
- 211
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
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
Senior Member
- Reaction score
- 775
Good thing immunosuppressants don't grow back hair from male pattern baldness then huh
- Reaction score
- 56
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?
Last edited:
H
Senior Member
- Reaction score
- 775
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.
- Reaction score
- 1,132
^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
- Reaction score
- 211
Exactly. Androgenetic alopecia has a different mechanism for sure. I still believe it’s reversible.
- Reaction score
- 56
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.
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.