Investigating An "immuno-androgenic" Model Of male pattern baldness

That Guy

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Inaccurate. It has only been proven that DHT is necessary for progression and never been proven to be the primary factor. You don't even need to try too hard to disprove that, just consider the fact that lots of high DHT generating individuals don't go bald ever.

And also consider then that the 286 genes identified with male pattern balding still don't garrauntee male pattern balding...

And you didn't even address the point that even when DHT is removed from system that the stem cells do not receive the signal to initiate the hair cycle as occurs in non balding individuals...
Nor did you address the immunodeficient mouse experiment which DID regenerate vellus male pattern baldness transplanted hairs in the presence of DHT....
In fact you didn't even read my opening post, you just weighed in by parroting off the brain dead mantra that you've been fed, and then stated "fact" afterwards....

Some of you guys are absolute f*****g wankers.

Androgenetic Alopecia is named so because a doctor in 50s carried out experiments on Eunuchs, who he noticed did not go bald, and injected them with testosterone; those with a genetic history of balding...wait for it...started balding.

Keep coping, a**h** — male sex hormones and heredity are at the heart of the problem.
 

Afro_Vacancy

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Androgenetic Alopecia is named so because a doctor in 50s carried out experiments on Eunuchs, who he noticed did not go bald, and injected them with testosterone; those with a genetic history of balding...wait for it...started balding.

Keep coping, a**h** — male sex hormones and heredity are at the heart of the problem.

Eunuchs have any number of hormonal differences with respect to the general population, and it's known that intravenous testosterone does not necessarily work the same as intrinsic testosterone. Moreover many people in the general population have very high testosterone and DHT levels and don't go bald.

A good analogy is that of peanut butter allergies. You're arguing that it's caused by peanut butter, but others are saying that there's nothing wrong with peanut butter, but sometimes people are sensitive to peanut butter due to other issues.

If a single teaspoon of peanut butter will kill you, you shouldn't blame the peanut butter imo. But by all means cut it out of your life until a better scientific theory is made available.
 

baldboys

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Eunuchs have any number of hormonal differences with respect to the general population, and it's known that intravenous testosterone does not necessarily work the same as intrinsic testosterone. Moreover many people in the general population have very high testosterone and DHT levels and don't go bald.

A good analogy is that of peanut butter allergies. You're arguing that it's caused by peanut butter, but others are saying that there's nothing wrong with peanut butter, but sometimes people are sensitive to peanut butter due to other issues.

If a single teaspoon of peanut butter will kill you, you shouldn't blame the peanut butter imo. But by all means cut it out of your life until a better scientific theory is made available.

Of course you wont blame the f*****g peanut butter, you will blame your f*****g immune system that overreacted to that sh*t and killed you. Same way you dont blame the f*****g dht, you blame your f*****g sensitive folicles. But if your f*****g folicles are sensitive, the only known way to stop the danm process is by stoping the dht. Same way if your stupid imune system overreacts to peanut butter you wont eat f*****g peanut butter

Jesus christ, whats going on with you dumb fucks. What kind of f*****g stupid post is that
 

That Guy

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Eunuchs have any number of hormonal differences with respect to the general population, and it's known that intravenous testosterone does not necessarily work the same as intrinsic testosterone. Moreover many people in the general population have very high testosterone and DHT levels and don't go bald.

A good analogy is that of peanut butter allergies. You're arguing that it's caused by peanut butter, but others are saying that there's nothing wrong with peanut butter, but sometimes people are sensitive to peanut butter due to other issues.

If a single teaspoon of peanut butter will kill you, you shouldn't blame the peanut butter imo. But by all means cut it out of your life until a better scientific theory is made available.

The experiment is still valid in its conclusion that without the requisite hormone, the hereditary sensitivity isn't a problem.

My point is that you require the hereditary sensitivity to the DHT in order to go bald.

We can eliminate the DHT aspect fairly easily; who knows if we'll ever truly identify, let alone eliminate the hereditary aspects.

Curing immune reactions involved are not going to resurrect the lost hair. Significant progress is being made in creating brand-spankin' new hair or stopping the loss entirely via cells, so people who are like 'We need to think of it as an immune problem!' are both high and losing the battle against hairloss anyway.
 

That Guy

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You my good sir, are patently wrong on this line of thinking. This has been proven many times in Alopecia Areata and Alopecia Totalis cases, and yes Androgenic Alopecia follows a similar mechanism.

1 - DHT is produced in AR located in scalp
2 - Immune system, dysfunctionally sensitive to DHT, releases an attack on the scalp
3 - Mast cells, activated in response to the DHT "threat", release large amounts of PGD2
4 - PGD2 causes slow but certain death of hair follicles

It is not the DHT that is causing the hairloss - it is the dysfunctionally sensitive immune system that is reacting to it, and triggering PGD2 production from mast cells that kills HFs.

Please explain to me how if, by your own words, follicles in Androgenetic Alopecia undergo a "slow but certain death" that a reversal of the immune component after the fact will bring those dead follicles back from the grave?

Because if it can't, then nobody cares.
 

pegasus2

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We will have a cell based cure long before we know the causes of hair loss, so stop worrying about what angles are being studied. It doesn't matter in terms of a functional cure.
 

abcdefg

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Couldnt we say that male pattern baldness is caused by prostaglandin imbalance, wnt pathway, vitamin D3 receptor defect, or any number of things? Why is the immune system piece such an important head to cut off on this many headed snake? Its not an easy beast to slay that is for sure, and treating that can cause many dangerous side effects.
Is this the best angle of attack when male pattern baldness has so many different components? At this point your better off taking your propecia because its going to be a looong wait for anything that alters any of this.
I havent seen any human evidence that jak inhibitors work for male pattern baldness as they did for AA.
 

GiveMeAccessToMyAccount

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Couldnt we say that male pattern baldness is caused by prostaglandin imbalance, wnt pathway, vitamin D3 receptor defect, or any number of things? Why is the immune system piece such an important head to cut off on this many headed snake? Its not an easy beast to slay that is for sure, and treating that can cause many dangerous side effects.
Is this the best angle of attack when male pattern baldness has so many different components? At this point your better off taking your propecia because its going to be a looong wait for anything that alters any of this.
I havent seen any human evidence that jak inhibitors work for male pattern baldness as they did for AA.

If jak inhibitors can reverse AA, AT, AU, vitiligo and greying hair I think that would be big and it would be a step in the right direction even for the research of male pattern baldness. I won't pretend to know if male pattern baldness is an issue with our immune system, but let's if it is, the reversal of the aforementioned diseases would be big then. Just because there's no evidence that jak inhibitors work for male pattern baldness, doesn't mean there will never be evidence. I mean isn't there jak inhib for male pattern baldness/aa in FDA pre clinical right now? Let's wait and see, they're supposedly aiming for both hair loss disorders aren't they?
 

That Guy

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i don't have to spend time educating you man - just read up on JAK inhibitors and what they do for AA and AT; it's self explanatory. The issue is the belief that Androgenic Alopecia is different than AA and AT, which is wrong.

You can choose to believe what you want (despite the enormous amount of evidence available in the numerous studies published) - i'm not here to argue with someone who's made up their mind already.

No, I haven't made up my mind — I'm more than open to it being changed, but you seem to refuse to do so.

It's interesting that every time I bring up this fundamental problem, the people assuring me that JAK is going to cure Androgenetic Alopecia because "it's totally an immune problem like AA" always back out of explaining this. I'm starting to get concerned that it is because they don't have an explanation.

Until such time as someone can explain to me and provide solid proof that solving the immune problems after the fact in Androgenetic Alopecia will resurrect dead organs, I'm forced to believe

pile_of_shit.gif
 

Armando Jose

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TNF promotes the inflammatory response, which, in turn, causes many of the clinical problems associated with autoimmune disorders such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis, hidradenitis suppurativa and refractory asthma


Then, inflammatory response is before autoimmune disordes?
 

That Guy

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I'm not here to educate ignorant people - I have better things to do. The funny thing is that you are always the first to jump on a research discussion acting like you have some authority on the subject, when in fact you don't seem to know anything about it - it's pretty amazing actually. I suggest you go and educate yourself, and when your caught up, come back and try to have an educated conversation on this topic.

So you have nothing then.

Okay
 

distracted

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Please see first post for the established connections between Immune system and Androgenetic Alopecia... No really, read it this time please.

I haven't seen a single scientific post by him yet, so I wouldn't expect one now.

If anything Swoop is usually the one to be all over this since he actually believes, from a scientific standpoint, that this is the wrong avenue. Haven't seen him around very much recently though.
 

baldboys

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Well the fact is nobody knows if sending the correct signal to follicle stem cells in the bald scalp will result in proliferation of hair progenitor cells...

...In fact, we don't know what exactly the signal is. There is evidence building to suggest that the signal is supposed to come from the Immune system, hence the relevance of this discussion thread.
What's even more intriguing is that the immune system also makes a good candidate for the unusual almost "allergic" response to your own androgens.

Additionally, immune dysfunction could also explain male pattern baldness's correlation with other health problems.

...so then, we should investigate this til we know either way.

....and, even if it were the year 2025 right now, and you were rocking a cellular riken primordium Afro, and I had gone for full Jesus locks cellular hair transplant,
I would still be inquiring to see if the immune system is responsible for the onset of my hairloss,
and I do give a damn why exactly this happened in the first place because it is important to know why it's happening.

Why is that, Ted? Whats your end goal in inquiring the immune system role in Androgenetic Alopecia? Are you aiming for a major breakthought? Are you gonna do science from behind your computer desk with your mental gymnastic and total lack of understaning of the basics of physiology? Are you going to crack the code by googling terms you see on random articles and learning little pieces of the puzzle without having any clue about the big picture?

Are you that dumb or that narcisistic? Probally both.
 

baldboys

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My end goal is to ensure that I do everything I possibly can to optimise my health, and not ignore significant evidence that there may be an underlying dysfunction in my body that should be addressed. This is an innate drive, the fundamental purpose of the rational brain.

I am not aiming for a major "breakthought" as you suggest.

Your second assumption is closer to the truth, that is if when you say "do science from behind your computer desk" you mean 'read published studies online'... ...and by "with your mental gymnastic" you mean 'think', ...then yes, yes that's exactly what I'm gonna do.

...and if as you say I have "a total lack of understaning" of physiology, then perhaps by studying the available resources I will develop my knowledge.


and to answer your last question, I am fortunately not burdened by being dumb......... that must suck......

Well budy, than maybe you should start by building at least some basic foundation on what you are reading, in order to avoid such a superficial graps and be more capable of understanding what the works are suggesting. Id suggest you start with those, not the all book of course, but focus on the immune and inflamation related chapters.

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It is fairly easy to find pdf's of those online.
 

hairblues

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(i am so confused by this thread)
 

That Guy

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Alright there mister, since you have so much time on your hands and seem to be so we'll educated, why don't you explain, with references, how hairloss works while proving that the immune system is in no way involved in the process. Go ahead buddy, I'll be here waiting with bated breath. My time is more precious than yours, if you can sit behind a computer and demand free education and explanations on complex subjects then so can I - it goes both ways. So rather than me convincing you, then why don't you go ahead and convince me?

No, I'm asking you to tell me how solving any immune components will bring back lost hair follicles. The burden of proof lies on you, since you believe it can.

Yet, you always just dodge answering the question and try to flip it back on me somehow. You're so well-read; this should be easy for you to put it in layman's terms?

You're dodging the question because it points out a basic, but fundamental flaw in your theory and you're at a loss to explain it. Thus, your theory doesn't hold up.

Challenge accepted. :cool:

Ohhhh sh*t
 

Zoro

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IGF-1 also happens to be a crucial hair growth factor

Someone had posted this study a while ago showing finasteride upregulated IGF-1 in some patients: https://www.ncbi.nlm.nih.gov/pubmed/12894070

TL;DR the ones who had upregulated igf-1 while on finasteride regrew hair or maintained, and those who didn't have upregulated IGF-1 had their hair worsened. Small study though

IGF-1 works locally from where it's injected, i'm curious if anyone has tried scalp injections.
 

hairblues

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Now this is more like it... this is what I had in mind.

The most knowledgeable and determined of the forum go to work on the literature, to derive a better picture of how the immune system is or isn't involved in male pattern baldness....

Allow me to begin the discussion.. with a find from "smurfy" on another hairloss forum

Re: T-cells & Stem cells

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Smurfy Today at 2:41 am


I would like to call to the witness stand.... IGF-1.

Insulin-like growth factor-1 induces regulatory T cell-mediated suppression of allergic contact dermatitis in mice

Allergic contact dermatitis (ACD) is triggered by an aberrant hyperinflammatory immune response to innocuous chemical compounds and ranks as the world’s most prevalent occupational skin condition. Although a variety of immune effector cells are activated during ACD, regulatory T (Treg) cells are crucial in controlling the resulting inflammation. Insulin-like growth factor-1 (IGF-1) regulates cell proliferation and differentiation and accelerates wound healing and regeneration in several organs including the skin. Recently IGF-1 has also been implicated in protection from autoimmune inflammation by expansion of Treg cells. Here, we demonstrate that ectopic expression of IGF-1 in mouse skin suppresses ACD in a Treg cell-specific manner, increasing the number of Foxp3+ Treg cells in the affected area and stimulating lymphocyte production of the anti-inflammatory cytokine interleukin 10. Similar therapeutic effects can be achieved with systemic or topical delivery of IGF-1, implicating this growth factor as a promising new therapeutic option for the treatment of ACD.

....in the event that Treg activity is a critical factor.

Thats awesome but when you science peeps figure it all out can you simplify it for those of us who struggled in Earth Science and Chemistry :)
 
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