I dont think DHT is the cause of hairloss

I agree with most of what you said, however I must disagree with the statement that says DHT is the root cause of MPB...

If DHT is the root cause, why dont we lose hair on te sides of our head? What makes this hairs immune?

Some say these hairs have less androgen receptors... Why is it then that hair replacement surgeons recommend finasteride after a surgery? They are supposed to be immune to DHT...

The only major difference between the two areas of the scalp, that I can find, is the amount of blood flow...

SlowMoe wrote:I agree with most of what you said, however I must disagree with the statement that says DHT is the root cause of MPB...

If DHT is the root cause, why dont we lose hair on te sides of our head? What makes this hairs immune?

Some say these hairs have less androgen receptors... Why is it then that hair replacement surgeons recommend finasteride after a surgery? They are supposed to be immune to DHT...

The only major difference between the two areas of the scalp, that I can find, is the amount of blood flow...

Every area of hair expresses different genetics. Look at your stomach. You have peach fuzz, long hairs near the naval, a triangular distribution towards the groin area, fine (and colored) hair leading towards the naval, etc. Some of these hairs are affected by DHT while others are not (the peach fuzz, for example.) The skin on your nose is different from the skin on your cheek which is different from the skin under your eye which is different than the skin on the palm of your hand, etc. The same goes for hair follicles, no matter that they may appear externally identical.

Likewise, the male pattern of balding relates to the distribution of active androgen receptors being expressed in different ways in different areas of the scalp.

This has been proven for two reasons:

First, you can transplant a hair follicle to almost any area of skin. If you want to transplant a hair to the tip of your nose, it can actually grow there.

Second, studies have already proven that if you transplant a hair from the scalp to a location such as the forearm, the hair follicle will "go bald" at the same time as the hairs that would have been surrounding it in the same area of the scalp. This shows us that there is an exposure/timing element that is different in each band of hair when that hair has a sensitivity to androgens and moreover that culprit is not something unique to the scalp itself.

So, with today's hair transplant therapy, our only option is to take hairs that we know are not susceptible to androgenic hair loss from the sides and rear of the head, and place them on the areas that have lost hair. These hair follicles are immune (or /more/ immune) to androgenic hair loss.

Females have a different distribution of androgen receptors. They don't typically have the "banding" that is seen in males, and therefore experience androgenic hair loss in a diffuse way. Hair follicles atrophy uniformly along the vertex of the scalp because the follicles have equal sensitivity in this area, and little to no sensitivity towards the hairline (unlike males, who are have little to no sensitivity along the back and sides.)

Finasteride is recommended when the area of the transplant butts against an area that is not bald, but that is still likely to go bald because it is near the top of the scalp.

Concisely, the hair follicles on the lower area of the male scalp do not have the same sensitivity to androgens as the hair on the top of the head. You can transplant those follicles anywhere on the body and have them grow indefinitely, short of actual physical reasons relating to a bad transplantation.

Different estrogens and androgens have very different effects on inflammation, blood flow, pressure, and circulation, androgens generally being accepted as having a negative impact on cardiovascular illness. I was going to post some studies but the amount of extrapolation and medical dictionary time it would take to get any sense out of must of them would be absurd.

When CS says that most of these conditions are more of a downstream problem of Estrogen he's right too, the estrogen is taking up far too much room in SHBG and thats when you get excess T, aka more estrogen or DHT.

Also ViolatedBird, you're making a lot of statements and not backing it up, care to do so?

a
Also ViolatedBird, you're making a lot of statements and not backing it up, care to do so?

If you point out something that you disagree with, I will locate the study.

In short: We know DHT is the root cause because a particular SNP on the X-linked AR is required for male pattern baldness. This information is everywhere from Wikipedia to SNPedia to scholarly journals. We know that transplanting hair from the back and sides of the scalp results in a very high liklihood of the hair being immune to male pattern baldness. This proves that PATTERN LOSS has nothing to do with the blood flow of a particular area of scalp, the bacteria in a particular area of scalp, or anything else scalp related.

DHT may very well indeed cause decreased immunity, increased inflammation, PGD-2 expression, etc. The point is, though, that the hair follicle's response to DHT is what causes any of the above to become active/relevant.

If diseases like hypothyroidism and insulin resistance caused identical male pattern hair loss then we could say that these sort of diseases had a direct effect. However, they do not. Gender does play a role -- males have a distinct pattern of loss while women have diffuse loss. Both hypothyroidism and insulin resistance have the highest correlation with markedly impaired SHBG expression, which is the only protein in the body that strongly binds androgens and thus mediates their activity and entrance into cells. You can simply PubMed and find that out. This is well known, not a theory. Males with low SHBG go bald earlier (pre-30) than those that do not. Thyroid and insulin issues are strongly correlated with SHBG.

They KEY is this. No matter WHAT disease you have, if you don't have the SNP on AR that allows for androgenic hair loss, you simply won't experience it. To go bald quickly, have a "bad" AR copy on your X chromosome and have high DHT either via disease, diet or genetics. How fast it occurs may or may not relate to intenstinal flora, toxins, etc, but the point is that it is the root cause.

I'm totally with everyone here on figuring how to attack the other parts of the pathway once our genetics respond negatively to DHT, but I think it would be silly to look at the evidence and blame blood flow.

There are other components. A friend and I have the same sequences on the AR receptor, but he has much, much more hair loss than I. Why? He's a diabetic and he takes steroids. Both of these directly affect free/bound androgen levels.

There is a chance that when follicle is transplanted, the wounding action stimulates angiogenisis and the follicle can then tap into an active blood network.

It is miiighty strange that my hair loss is occurring ONLY where the skin on my scalp is very tight, and how my hair is full only 1/2" over, where my skin is much much looser. Funny how those DHT sensitive follicles are only located where the blood flow is worst on my scalp.

Also funny how minoxidil works beings it works by improving circulation, and how blood flow is 2.6x lower in balding scalps than is scalps with no signs of MPB..

I'm not saying DHT doesn't play a big role, I am saying that, in my opinion, the hair papilla that have been weakened by a low oxygen, low nutrient environment become vulnerable to and react negatively to, DHT.

Wait so there is some truth to the Hair Loss coming from the Mother sides on the X chromosome? I always thought that was a myth.

There's been a recent post showing that the method of transplantation has a lot to do with whether it survives. It's well known that many surguries go very very wrong and people end up just as bald as they would have been without plugs. I'll track down that post in a bit. Hopefully this study CS recently posted will shed more light on how sex hormones and the immune system interact.

CausticSymmetry wrote:J Drugs Dermatol. 2011 Dec 1;10(12):1404-11.
The role of inflammation and immunity in the pathogenesis of androgenetic alopecia.
Magro CM, Rossi A, Poe J, Manhas-Bhutani S, Sadick N.

Background: Female pattern hair loss affects many women; its pathogenetic basis has been held to be similar to men with common baldness. Objective: The objective of this study was to determine the role of immunity and inflammation in androgenetic alopecia in women and modulate therapy according to inflammatory and immunoreactant profiles. Materials and Methods: 52 women with androgenetic alopecia (AA) underwent scalp biopsies for routine light microscopic assessment and direct immunofluroescent studies. In 18 patients, serologic assessment for antibodies to androgen receptor, estrogen receptor and cytokeratin 15 was conducted. Results: A lymphocytic folliculitis targeting the bulge epithelium was observed in many cases. Thirty-three of 52 female patients had significant deposits of IgM within the epidermal basement membrane zone typically accompanied by components of complement activation. The severity of changes light microscopically were more apparent in the positive immunoreactant group. Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group. Conclusion: A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia and could point toward an immunologically driven trigger. Cases showing a positive immunoreactant profile respond well to combined modality therapy compared to those with a negative result. J Drugs Dermatol. 2011;10(12):1404-1411.

https://immortalhair.forumotion.com/t6603-susceptibility-variants-on-chromosome-7p211-suggest-hdac9-as-a-new-candidate-gene-for-male-pattern-baldness

Threads like this are also a good read. Everytime I read about a condition being genetic, that gene is usually always an "immune" allele, whether upstream or downstream.

So according to this study, there isn't an actual antibody for the androgen receptor in male androgenetic alopecia? Or for the estrogen receptor? Then what is the immunoreactant component? It says significant IgM deposits were found, but what is actually being signalled for attack here? And if its not the androgen receptor, what is the role of DHT?

And again, I'm not saying that DHT doesn't have anything to do with it, I'm just pointing out that it's much more complicated and less fatalistic than usually assumed to be.

Does anyone know if DHT has any role in regards to inflammation?
Because it appears I am capable of stopping my shedding just from consistent intake of supplemental omega3's, and more sunlight,
the higher the dose the better...

A < R,

My bad. I guess my question wasn't so much what cells are being attacked (the study says its the bulge epithelium, although I'm not too studied on the actual structure of the hair follicle) but what is causing the immune system to react to them. I can't wrap my head around why these cells would suddenly be recognized as harmful unless there is some type of cross-reactivity, perhaps a similar membrane protein or functional region as another protein or cell that is legitimately foreign (like gluten) and the immune system can't tell the difference.

If this is completely off track, let me know. I need to understand how after years the body could begin to turn on the hair follicle, when it seemed like their relationship was pretty stable to begin with haha. Obviously androgens are playing some type of role, but admittedly not the only and not the most important one.

FWIW,

This study:
Levy-Nissenbaum E, Bar-Natan M, Confirmation of the association between male pattern baldness and the androgen receptor gene, Danek Gartner Institute of Human Genetics, Sheba Medical Center, Tel Hashomer, Israel

... is the one that proves the androgen link to male pattern baldness. They conclude that a certain variant of the androgen receptor is needed for AGA to develop. In the same year the results of this study were confirmed by other researchers.

I think some people are confusing male PATTERN hair loss with diffuse thinning. Two entirely different things.

The only mystery now, is just why DHT inhibition sucks so much as a theraputic agent against male patter baldness

anthonyspencer54 wrote:A < R,

My bad. I guess my question wasn't so much what cells are being attacked (the study says its the bulge epithelium, although I'm not too studied on the actual structure of the hair follicle) but what is causing the immune system to react to them. I can't wrap my head around why these cells would suddenly be recognized as harmful unless there is some type of cross-reactivity, perhaps a similar membrane protein or functional region as another protein or cell that is legitimately foreign (like gluten) and the immune system can't tell the difference.

If this is completely off track, let me know. I need to understand how after years the body could begin to turn on the hair follicle, when it seemed like their relationship was pretty stable to begin with haha. Obviously androgens are playing some type of role, but admittedly not the only and not the most important one.

It's driven by adverse lipid metabolism (inflammatory prostaglandins).

aThe only mystery now, is just why DHT inhibition sucks so much as a theraputic agent against male patter baldness

It's not a mystery at all.

DHT is volatile and is therefore created from testosterone at the point of use in tissues that need it. The skin, prostate and penis have the highest concentrations of 5-AR. Serum concentrations of DHT do not accurately represent tissue concentrations of DHT.

5-ARis do not eradicate DHT. They simply inhibit production to some degree. The serum reduction by a 5-ARi is greater than than the reduction of DHT that occurs in the scalp. Off the top of my head, the reduction of DHT in scalp tissue is between 60 and 72% while systemic serum reduction is in the 90% range, depending on the individual. It would stand to reason that finasteride has the capacity to slow down baldness by 1/2 to 2/3rds of the intensity, depending on an individual's particular CAG repeat on the AR gene.

Do DHT starved receptors become increasingly sensitive to DHT over the years? Probably.

VB,
Explain why DHT doesn't attack hair in the MPB region..

This doesn't at all touch on why topical DHT inhibition on the scalp doesn't sprout new hairs. Based on your assertion, you'd really think it would.

Slowmoe, do you mean "not in the mpb region?"

i think topical inhibition can reverse miniaturization, and regrow hair to an extent. systemic definitely can. the further along one is on the norwood the harder this becomes.

SlowMoe wrote:VB,
Explain why DHT doesn't attack hair in the MPB region..

Do you mean to ask why DHT doesn't attack hair in the the "donor area" that is normally used for hair transplantation? Men have a distribution of genetically sensitive androgen receptors in hair follicles that is not even along the surface of the scalp. In most males, the hair follicles on the sides and back of the head are resistant DHT. When moved to the top and front of the head, the follicle retains this resistance, and the transplanted hair thrives where the genetically sensitive hair failed.

Again, check your stomach. The "peach fuzz" hairs are the ones that ignore DHT. The hairs you gained during puberty -- those are the genetically DHT sensitive ones. Same skin area, different reactions.

Women tend to have a different distribution of DHT sensitive hair (IF they acquire two of the hair loss prone AR genes on both X chromosomes (the one necessary for hair loss is actually recessive.)) It is focused only on the vertex of the scalp and all hairs are of seemingly random sensitivity. Hence, a diffuse thinning from androgenic alopecia, verus the progressive "M" shaped recession in a male is typical in females with too much testosterone and who have the genes for MBP (yes, this happens, but is just rarely expressed since women don't normally have enough DHT to initiate the process.)

aThis doesn't at all touch on why topical DHT inhibition on the scalp doesn't sprout new hairs. Based on your assertion, you'd really think it would.

Slowmoe, do you mean "not in the mpb region?"

As far as I know, we don't actually have any DHT inhibitors that are proven to reach the hair follicle after topical administration. In fact, I don't think we have a topical DHT inhibitor other than attempts at liquefying finasteride and trying to get it through the skin in an active form.

Spironolactone is one androgen receptor blocker that is often used, but we have no idea how well it is getting through the skin, remaining intact and staying in the hair follicle to offer protection. The fact that spironolactone is said not to enter the blood is interesting and offers us a hint, because it means that it rapidly breaks down while travelling through the skin.

So, science has never actually sucessfully blocked DHT in the scalp. However, if you look at individuals who GENETICALLY have no DHT in their scalp (or anywhere else in the body, for that matter) you will find that they never experience male pattern baldness. So, no DHT in scalp does = no hair loss.

We've never been able to create the no-DHT scenario in the scalp... only just a "1/2 to 2/3rds lower DHT" scenario... and this scenario has positive results in most males.

I've looked for sources on the whole sensetive, non-sensetive to DHT follicle distribution proclamations, and I couldn't find anything at all to support it, unless you have something. Also, many hair transplants fail miserably. It depends on how deeply the new hair is rooted and how the procedure was done.

You didnt look hard enough

http://www.nature.com/jid/journal/v109/n3/abs/5610071a.html

aI've looked for sources on the whole sensetive, non-sensetive to DHT follicle distribution proclamations, and I couldn't find anything at all to support it, unless you have something. Also, many hair transplants fail miserably. It depends on how deeply the new hair is rooted and how the procedure was done.

I'm pretty sure it is observational science. Males don't normally bald around the ring of the head, and if you transplant those hairs to the front of the head, and the hair takes root, they remain as unaffected by DHT as they did in the previous location.

Hair transplants fail because of the transplantation itself -- damage, trauma, scarring, etc.

"Hair restoration surgery works by relocating the bald resistant hair follicles from the back of the head to the balding areas on top. Because the transplanted hair follicles retain their genetic resistance to DHT and balding they continue to grow for a life time."

A Google search brings up thousands of variations of the above paragraph. I'm pretty sure it's accepted science.