Back to the roots: Causes and effects of elevated DHT

[Ventures]

I'd say a mixture of both.

http://www.ncbi.nlm.nih.gov/pubmed/9284093

Balding follicles had around 80% more DHT than non-balding follicles.

So even though they are transplanted to the vertex or frontal part, they continue to produce less DHT than native follicles ? On the other hand, hair from balding scalp regions also continue to produce same level of DHT inside DP after transplantation to arm, or back of the head. In other words hair characteristics(both the level of follicular DHT produced inside it and sensitivity ) remain the same, they are invariant of recipient location. This is why Orentreich’s experiments showed when balding hair transplanted to the arm continued to bald , because hair characteristics inside follicles haven't changed, and these hair continue to produce same level of DHT inside it.


Would donor hair gradually start to thin out if exposed to extra follicular DHT ? Do you think that young bald guys with aggressive male pattern baldness might have more sensitive donor hair than non-balding guys ?

 

[benjt]

In other words hair characteristics(both the level of follicular DHT produced inside it and sensitivity ) remain the same, they are invariant of recipient location. This is why Orentreich’s experiments showed when balding hair transplanted to the arm continued to bald , because hair characteristics inside follicles haven't changed, and these hair continue to produce same level of DHT inside it.

For the most part, yes.

In that context I want to talk about the "avalanche property" of Androgenetic Alopecia/male pattern baldness and its feed-forward-mechanism. The "avalanche property" is not an established term. The problem is that there is no scientific literature about it so no numenclature has been agreed on. What I mean with it is the feed-forward mechanism which both localizes and advances the balding effect, at least in non-diffuce thinners (though I suspect that this effect also exists to some degree in people thinning instead of receding).
Observation: If you have hairloss only at the hairline which just recedes further and further to the back, you can halt or slow down your hairloss with minoxidil applied only at your hairline (if you are a responder). Assuming that the balding process is scalp-global and all hair suffers from it, even though at different speed, this shouldn't be possible. If it was a global process advancing on the whole scalp, applying minoxidil only at the hairline should only save hair at the hairline. The expected outcome, if we assumed a global process, would be balding behind the hairline and hair remaining only where minoxidil is applied. However, even the hair behind the hairline is saved by applying minoxidil only at the hairline. This means: local application at a site of early hairloss prevents hairloss from happening at sites that would be affected later in the recession. This shouldn't happen if balding was a consistent process all over the scalp (!).

The conclusion is that balding seems to have an "avalanche" or "infection" (this is only a metaphor, nothing to do with any bacteria or viruses!) property. Balding follicles seem to push their neighbors into balding too in the long run. This makes balding seem like a "catch-on feed-forward mechanism". Once a critical level of whatever substance it is the causes the miniaturization at its root has built up, it leads to a self-sustained process of production in the next follicle and so forth. This substance is likely DHT or PGD2. In histograms it has been shown that both DHT and PGD2 actually spill over from the follicle to the surrounding tissue. My theory here is that this spill over triggers processes in neighboring follicles, making them start production of DHT (maybe because of increases AR activity as a consequence to DHT overspill form the first follicle) or PGD2 too.

This, of course, is only a theory with no confirmation in studies whatsoever - the reason could be completely different. Nonetheless, the avalanche or infection or chain reaction or whatchamacallit property does exist. It is useful because it localizes the effect of balding and renders us capable of slowing down the whole balding process with only local application.
Either way, I find this "infection"-like property, where apparently follicles kickstart the balding of their neighbors in a very slow chain reaction quite interesting.

 

[xRedStaRx]

So even though they are transplanted to the vertex or frontal part, they continue to produce less DHT than native follicles ? On the other hand, hair from balding scalp regions also continue to produce same level of DHT inside DP after transplantation to arm, or back of the head. In other words hair characteristics(both the level of follicular DHT produced inside it and sensitivity ) remain the same, they are invariant of recipient location. This is why Orentreich’s experiments showed when balding hair transplanted to the arm continued to bald , because hair characteristics inside follicles haven't changed, and these hair continue to produce same level of DHT inside it.


Would donor hair gradually start to thin out if exposed to extra follicular DHT ? Do you think that young bald guys with aggressive male pattern baldness might have more sensitive donor hair than non-balding guys ?

Extra follicular DHT is meaningless if it cannot make it inside the follicle. But since donor hair don't have much ARs to begin with, then they don't accumulate high levels of androgens.

No, donor hairs do not miniaturize. Irregardless who it's from. There may be slight differences between individuals, but the idea is the same.

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For the most part, yes.

In that context I want to talk about the "avalanche property" of Androgenetic Alopecia/male pattern baldness and its feed-forward-mechanism. The "avalanche property" is not an established term. The problem is that there is no scientific literature about it so no numenclature has been agreed on. What I mean with it is the feed-forward mechanism which both localizes and advances the balding effect, at least in non-diffuce thinners (though I suspect that this effect also exists to some degree in people thinning instead of receding).
Observation: If you have hairloss only at the hairline which just recedes further and further to the back, you can halt or slow down your hairloss with minoxidil applied only at your hairline (if you are a responder). Assuming that the balding process is scalp-global and all hair suffers from it, even though at different speed, this shouldn't be possible. If it was a global process advancing on the whole scalp, applying minoxidil only at the hairline should only save hair at the hairline. The expected outcome, if we assumed a global process, would be balding behind the hairline and hair remaining only where minoxidil is applied. However, even the hair behind the hairline is saved by applying minoxidil only at the hairline. This means: local application at a site of early hairloss prevents hairloss from happening at sites that would be affected later in the recession. This shouldn't happen if balding was a consistent process all over the scalp (!).

The conclusion is that balding seems to have an "avalanche" or "infection" (this is only a metaphor, nothing to do with any bacteria or viruses!) property. Balding follicles seem to push their neighbors into balding too in the long run. This makes balding seem like a "catch-on feed-forward mechanism". Once a critical level of whatever substance it is the causes the miniaturization at its root has built up, it leads to a self-sustained process of production in the next follicle and so forth. This substance is likely DHT or PGD2. In histograms it has been shown that both DHT and PGD2 actually spill over from the follicle to the surrounding tissue. My theory here is that this spill over triggers processes in neighboring follicles, making them start production of DHT (maybe because of increases AR activity as a consequence to DHT overspill form the first follicle) or PGD2 too.

This, of course, is only a theory with no confirmation in studies whatsoever - the reason could be completely different. Nonetheless, the avalanche or infection or chain reaction or whatchamacallit property does exist. It is useful because it localizes the effect of balding and renders us capable of slowing down the whole balding process with only local application.
Either way, I find this "infection"-like property, where apparently follicles kickstart the balding of their neighbors in a very slow chain reaction quite interesting.

This theory sounds interesting and would explain the pattern involved in balding. But it still has a few holes. We have to strike it out unfortunately.

 

[Armando Jose]

The conclusion is that balding seems to have an "avalanche" or "infection" (this is only a metaphor, nothing to do with any bacteria or viruses!) property.


In my theory is very similar,
more isolated is the hair shaft more prone to develop problems....
My theory can explain it easily: the forehead and crown swirls act as focus initiator bald area, because these hairs are the most likely to have problems in the renovation of sebum
I like your ideas.
The specific situation in the scalp hair has advantages and disadvantages. The more solitary hair, more chance of losing are. The hairs located on the front are more susceptible and can progress baldness back from outside to inside. The lost hair transferred their problems to the next line.In the swirl is different, from the inside out, due its spiral shape.


Mi teorí*a lo puede explicar de forma fácil: la frente y los remolinos de la coronilla actúan como foco iniciador de la zona calva, debido a que estos cabellos son los más susceptibles de tener problemas en la renovación de sebum
Here is a spanish forum in 2005
http://www.ganarpelo.biz/viewtopic.php?f=2&t=8737&hilit=modelo&start=0

 

[benjt]

This theory sounds interesting and would explain the pattern involved in balding. But it still has a few holes. We have to strike it out unfortunately.

I dont think it even explains the pattern in balding. Why would balding start at the middle of the crown and the temples and not in some other spots? Either way, even though my theory for explanation might not be the correct one - it was only a first guess anyway - the avalanche or infection property for receders (not for diffuse thinners) seems to hold. That is how many people who apply minoxidil at their hairline successfully keep their hair for a while. Why else would the hairs behind not miniaturize?

 

[Ventures]

@benjt Your explanation is very interesting and it certainly makes sense. This process would explain full blown receding mechanism in males, which often also happens in postmenopausal women, who also have NW1 and sometimes very thin NW2 hairline. The point is that various growth inhibitors (apparently PGD2 or other we haven't discovered yet) can spill over the follicle to surrounding tissue and reach neighboring follicles. In that way 'helathy' hair follicles which haven't generate DHT inside it, and thus haven't experienced miniaturisation and production of substances which cause downstream effects as inflammation and fibrosis, can slowly become more vulnerable and thin out.

And this is actually what happens in early stages of hair loss, which in majority of men occurs as receding process. Follicles in frontal part, especially near hairline, since 5ard level is abundant in forehead and frontal part of scalp , start to miniaturise first, and then this effect by avalanche mechanism, spreads over follicles behind the hairline, and actually whole region between NW1-hairline and NW4-hairline start to miniaturise. Looking at average male we can notice that this region of scalp hair is usually thin and have less density than vertex and parietal region; it's possible to detect this shape region above forehead when hair is buzzed short; just look at some photos guys posted here:

 

[Armando Jose]

Maybe the process of PGD2 is the witness in this kind relay race

Ithink that the oxidatión/acumulation/degeneration of sebum take time to work

 

[Ventures]

I dont think it even explains the pattern in balding. Why would balding start at the middle of the crown and the temples and not in some other spots? Either way, even though my theory for explanation might not be the correct one - it was only a first guess anyway - the avalanche or infection property for receders (not for diffuse thinners) seems to hold. That is how many people who apply minoxidil at their hairline successfully keep their hair for a while. Why else would the hairs behind not miniaturize?

I think avalanche property can explain pattern of Androgenetic Alopecia. There are many variations of balding patterns. See my post above. Some people start to first lose their vertex, and their hairline is intact, even though 5ard-I and maybe II, is higher in frontal part in majority of men. Maybe men who only have thinning and hair loss on crown, could have increased sensitivity and/or biolocations of 5ard enzymes in those regions compared to the rest of the hair. I actually noticed that gypsies and native people from India, Afghanistan, who tend to have NW0 hairline and very thick hair usually have thinning at vertex - it could be their follicles there are more sensitive.

But full blown recession of hairline might have some connections with avalanche effect. Of course in case of moderate aggressive Androgenetic Alopecia, miniaturisation subsequently affects all NW6 or NW7 region. Because, as you mentioned baldness is result of accumulative process, and after years of exposure to androgens all genetically susceptible follicles (In caucasians these follicles are located in whole NW6-7 region (top of the head)) become affected. This results as diffuse pattern of thinning/miniaturised hair. my father first had receded NW2 hairline, and in his 40s he start do diffusely loose his hair and now he is NW6 in his 60s.

 

[I.D WALKER]

If anyone is able to tell me off the top of their heads to what extent does minoxidil locally effects T and/or 5alpha any? I'm looking for identifiable minoxidil.-induced reduction levels , disbursement, and/ or displacement, etc.,.

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For users addressing frontal hair loss in particular.

 

[xRedStaRx]

I dont think it even explains the pattern in balding. Why would balding start at the middle of the crown and the temples and not in some other spots? Either way, even though my theory for explanation might not be the correct one - it was only a first guess anyway - the avalanche or infection property for receders (not for diffuse thinners) seems to hold. That is how many people who apply minoxidil at their hairline successfully keep their hair for a while. Why else would the hairs behind not miniaturize?

This is is the first time I've heard of such a thing.

The avalanche theory is most likely not true. As mentioned before, susceptible follicles to miniaturizing do that anyway, it's part of the genetic coding. Some go faster than others, the pattern shape could be explained through either higher androgen exposure, or the skull remodeling theory from sexual dimorphism.

If anyone is able to tell me off the top of their heads to what extent does minoxidil locally effects T and/or 5alpha any? I'm looking for identifiable minoxidil.-induced reduction levels , disbursement, and/ or displacement, etc.,.

It only has a small nullifying effect on androgen receptors, it mainly works through other mechanisms however.

 

[I.D WALKER]

I brought this on as a result of a admitted half-baked premise that was founded on the shaky grounds of this"what if "hypothesis : Minoxs' working ability as a growth stimulant for genetic hair loss might be partly explained/attributed to it's observed cleansing capacity. In other words, how well it washes off or dilutes concentrated or accumulated levels of suspected androgens in and around neighboring areas of treatment. Xxtra thanx XRed.

 

[Hairbackpls]

Interesting theory.

Somehow it brings demodex mite in my mind... I know i know, everyone has demodex mites in their follicles but what IF certain amount of DHT makes our (people with balding gene) follicles vulnerable for the demodex mite infection? It kinda breaks the barrier that blocks these mites from doing any harm. Women and young boys (with MBP Gene) have less DHT on male pattern baldness area so the barrier is still standing and mites are not causing any harm. And hair of the people without male pattern baldness Gene is immune to DHT so the barrier wont break.


DHT->more sebum and broken barrier->food for demodex->increased number of demodex->spreading (avalance)->male pattern baldness pattern thinning/receding, itching etc..

Finasteride ->less DHT->less sebum -> less food for mites->decreased number of mites->temporal halt/regrowth->???

Why not donor hair then? Because of less DHT on that area or follicles are simply just immune.

This theory might be COMPLETE BULL**** tho.. im sorry

 

[Python]

Interesting theory.

Somehow it brings demodex mite in my mind... I know i know, everyone has demodex mites in their follicles but what IF certain amount of DHT makes our (people with balding gene) follicles vulnerable for the demodex mite infection? It kinda breaks the barrier that blocks these mites from doing any harm. Women and young boys (with MBP Gene) have less DHT on male pattern baldness area so the barrier is still standing and mites are not causing any harm. And hair of the people without male pattern baldness Gene is immune to DHT so the barrier wont break.


DHT->more sebum and broken barrier->food for demodex->increased number of demodex->spreading (avalance)->male pattern baldness pattern thinning/receding, itching etc..

Finasteride ->less DHT->less sebum -> less food for mites->decreased number of mites->temporal halt/regrowth->???

Why not donor hair then? Because of less DHT on that area or follicles are simply just immune.

This theory might be COMPLETE BULL**** tho.. im sorry

Wouldn't these parasites have been detected during biopsy already?

 

[Hairbackpls]

Wouldn't these parasites have been detected during biopsy already?

Umm... Maybe. Idk. I have read some studies about demodex mite hairloss stuff but it sounds pretty much BS. But that would explain the avalance kind of receding, so it just got me thinking.

Everyday i feel like something is moving in my hair and its itching.. :/

 

[xRedStaRx]

Interesting theory.

Somehow it brings demodex mite in my mind... I know i know, everyone has demodex mites in their follicles but what IF certain amount of DHT makes our (people with balding gene) follicles vulnerable for the demodex mite infection? It kinda breaks the barrier that blocks these mites from doing any harm. Women and young boys (with MBP Gene) have less DHT on male pattern baldness area so the barrier is still standing and mites are not causing any harm. And hair of the people without male pattern baldness Gene is immune to DHT so the barrier wont break.


DHT->more sebum and broken barrier->food for demodex->increased number of demodex->spreading (avalance)->male pattern baldness pattern thinning/receding, itching etc..

Finasteride ->less DHT->less sebum -> less food for mites->decreased number of mites->temporal halt/regrowth->???

Why not donor hair then? Because of less DHT on that area or follicles are simply just immune.

This theory might be COMPLETE BULL**** tho.. im sorry

That doesn't explain why 5-AR I inhibitors don't work for hair loss, even though they greatly reduce the amount of sebum.

All we know up to this point is that people susceptible to balding will experience male pattern baldness at some point in their lives. Mainly due to increased 5-AR II activity on the scalp, which both directly and indirectly inhibit hair growth and disrupt their cycles. The rate and onset on this process is genetic, and nurtured.
.

 

[benjt]

The avalanche theory is most likely not true. As mentioned before, susceptible follicles to miniaturizing do that anyway, it's part of the genetic coding. Some go faster than others, the pattern shape could be explained through either higher androgen exposure, or the skull remodeling theory from sexual dimorphism.

RedStar, are you entirely sure of that? I trust your knowledge on these matters more than my own. Many reports, though not clinically supported, can be found on the web of people applying minoxidil only at the hair line and still maintaining their hair "on this front" (crown loss may still occur later, but no hairs beyond the hair line). Indeed, the regaine/rogaine package insert states that minoxidil should only be applied in affected areas. I was pretty sure that there is an avalanche property to the whole process where balding/miniaturizing follicles induce the balding effect on each their neighbors, but if you say there is no way it happens, I'll take your word for it.

 

[xRedStaRx]

RedStar, are you entirely sure of that? I trust your knowledge on these matters more than my own. Many reports, though not clinically supported, can be found on the web of people applying minoxidil only at the hair line and still maintaining their hair "on this front" (crown loss may still occur later, but no hairs beyond the hair line). Indeed, the regaine/rogaine package insert states that minoxidil should only be applied in affected areas. I was pretty sure that there is an avalanche property to the whole process where balding/miniaturizing follicles induce the balding effect on each their neighbors, but if you say there is no way it happens, I'll take your word for it.

I'm not saying no way it happens. I've never heard of applying minoxidil on the hair line stops the balding cascade either. If this were true, then applying minoxidil on the right temple of a balding person should stop the balding process until the left region diffuses it's avalanche cascade on the right side. I can't see that happening to be honest. Don't forget that minoxidil has a spill over effect as well, so it doesn't just treat exactly the follicles it were applied to.

The avalanche theory does not also explain why follicles susceptible to balding miniaturize when isolated elsewhere, nor why the temples recede leaving the mid anterior part of the hair intact in most males before advanced stages kick in. If this were also true, then removing the 'source' follicles, which should be a small region on both temples and the vertex should stop the contamination process before it occurs, and essentially cures baldness.

Doesn't sound right to me.

 

[I.D WALKER]

Essentially nipping hair loss in the bud. I am aware no one here is hypothesizing this concept, as even at best a marginally viable preventative for treating frontal recession. All the same, it's inspiring to hear civil exchange between knowledgeable members who are still formulating scientifically meritorious opinions and creative style to advance our mutual objective.

 

[benjt]

RedStar: The question about miniaturization of extracted follicles in different environments would be whether they miniaturize under all circumstances, or only if they were already exposed to high androgen levels in the first place, "kickstarting" their susceptability. But probably you're right, given the close-to-immunity state of donor area follicles. Most of them survive the environment in the Norwood area either way, so there is no determining factor in the interaction with their environment.

 

[Ventures]

Is it common effect that long term finasteride users get diffuse hair loss ?

My explanation is over time the most sensitive hair follicles (which are distributed in diffuse/random pattern all over top of the head) miniaturise rather then recede. This is why woman get diffuse hair loss rather then recession because recession is consequence of constantly high DHT levels, and woman of course have low DHT and T, and higher levels of E compared to male scalp. When there is high activity of DHT and T in scalp, miniaturisation of all follicles happen but if threshold level for each follicle is not too low (meaning follicles aren't so sensitive to androgens which is case in majority of men who develop baldness later in life), then only most vulnerable follicles located at the hairline will experience gradual miniaturisation due to hypoxia in surrounding tissue and this resembles as recession.

Don't get me wrong many young guys here with aggressive male pattern baldness also have diffuse hair loss in all NW6 area, a don't say high androgen levels and/or high sensitivity can't cause diffuse pattern. I only want to point out that people who've experienced recession and got on finasteride therapy may hold recession but can start to diffusely lose hair due to gradual miniaturisation of the most sensitive follicles in affected area.




To sum up:

In balding affected regions follicles have different sensitivity and follicular DHT production; this depend on genetics.

• If all follicles have the same level of internal DHT production and same AR sensitivity, then all start miniaturise at the same time, and same speed --> Diffuse hair loss
• If there is a greater DHT activity in frontal part, as in case with receders, then recession might occur. Of course avalanche effect plays certain role which means DHT and PGD2 overproduction spills over and spreads in entire hairline zone (and 1 inch below) and this amplifies inflammation and miniaturization process in those areas--> recession

So to get diffuse pattern of hair loss on of this two conditions must take its part

• DHT production must exceed threshold level of follicles diffusely distributed all over the head (remember that in case of recession, all follicles in NW6/NW7 also miniaturise, but at much slower rate than follicles near receding hairline)
• All follicles must have same AR sensitivity, apparently most caucasians probably have more receptive hair in frontal scalp, this is why almost all caucasians have recession of hairline when they reach old age, even women.