Back to the roots: Causes and effects of elevated DHT
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Free T is "simply floating around". It is neither bound to SHBG nor to an androgen receptor. It is bioavailable. If I remember correctly, free T is less than 2% of all T in a body.
Free T = bioavailable T by definition ("bioavailable" = unbound). However, the definition has a pitfall: SHBG does not degrade T and will sooner than later release T, which will then - with a higher affinity - bind to androgen receptors or 5ar. Nonetheless, as this is a stochastical process, the more SHBG, the less T will bind to 5ar or androgen receptors.
So we have two opposing forces here: SHBG, on the one hand, transports T to DHT production sites for example in the scalp, which is bad for us. On the other hand, SHBG reduces T's bioavailability, which is good for us.
The question is: Which effect is bigger?
I read up a bit on this matter since my last post, and while I disagreed with odalbak before, I now agree with him. Not because of my own deeper understanding, but because most studies support the notion that SHBG's effect of binding is stronger (for matters of Androgenetic Alopecia/male pattern baldness) than its effect of transport.
As you can see, the matter is complex and it would need confirmation in its very own study. Until then, we can only try to reason which of the two effects is bigger. High SHBG being beneficial for us is the more supported notion by studies in that field. Unless we have substantial reason to doubt previous studies (e.g. by completely new findings), it makes more sense to assume that this notion is right, i.e. high SHBG is better to counter hairloss.
Then again: How big exactly would the effect of increased SHBG be? Big enough to make a difference?
Edit: The effect might be quite high, actually. Just reading up on this and it turns out that SHBG is often substantially lower in people with Androgenetic Alopecia/male pattern baldness. This also supports that high SHBG is beneficial to counter hair loss. Please consider my post #36 in this thread wrong.
Free T = bioavailable T by definition ("bioavailable" = unbound). However, the definition has a pitfall: SHBG does not degrade T and will sooner than later release T, which will then - with a higher affinity - bind to androgen receptors or 5ar. Nonetheless, as this is a stochastical process, the more SHBG, the less T will bind to 5ar or androgen receptors.
So we have two opposing forces here: SHBG, on the one hand, transports T to DHT production sites for example in the scalp, which is bad for us. On the other hand, SHBG reduces T's bioavailability, which is good for us.
The question is: Which effect is bigger?
I read up a bit on this matter since my last post, and while I disagreed with odalbak before, I now agree with him. Not because of my own deeper understanding, but because most studies support the notion that SHBG's effect of binding is stronger (for matters of Androgenetic Alopecia/male pattern baldness) than its effect of transport.
As you can see, the matter is complex and it would need confirmation in its very own study. Until then, we can only try to reason which of the two effects is bigger. High SHBG being beneficial for us is the more supported notion by studies in that field. Unless we have substantial reason to doubt previous studies (e.g. by completely new findings), it makes more sense to assume that this notion is right, i.e. high SHBG is better to counter hairloss.
Then again: How big exactly would the effect of increased SHBG be? Big enough to make a difference?
Edit: The effect might be quite high, actually. Just reading up on this and it turns out that SHBG is often substantially lower in people with Androgenetic Alopecia/male pattern baldness. This also supports that high SHBG is beneficial to counter hair loss. Please consider my post #36 in this thread wrong.
So, Total T is sum of free T(or un-bound) and bound T(bound both to SHBG and albumin). Is that correct ?
Article in this site http://www.lifelabs.com/Lifelabs_ON/Patients/TestInfo/Special/Malemenopause.asp states that: Free fraction of testosterone could be taken up by tissues and the protein-bound testosterone complex was inactive. It has now been demonstrated that the albumin bound fraction of testosterone readily dissociates and is absorbed up by the tissues along with the 'free' fraction. Together, these two fractions are referred to as the bioavailable testosterone (Bio-T) fraction.
So, T bound to albumin (which is 50% of all T) can also be taken up by tissue. I other words, that T can be converted to DHT inside hair folicles or sab. glands.
Article in this site http://www.lifelabs.com/Lifelabs_ON/Patients/TestInfo/Special/Malemenopause.asp states that: Free fraction of testosterone could be taken up by tissues and the protein-bound testosterone complex was inactive. It has now been demonstrated that the albumin bound fraction of testosterone readily dissociates and is absorbed up by the tissues along with the 'free' fraction. Together, these two fractions are referred to as the bioavailable testosterone (Bio-T) fraction.
So, T bound to albumin (which is 50% of all T) can also be taken up by tissue. I other words, that T can be converted to DHT inside hair folicles or sab. glands.
As we know the androgen glands produce daily a specific amount of androgen Testosterone (T), let’s say 600 units.From this amount, a specific quantity is used for the bodily functions, such as muscle metabolism, and another quantity is left free, and it is unbound (unused), called free testosterone Free T. So, in the process of the formation of DHT, T is not “consumed” in any way. It is not destroyed, it is simply transformed. The molecule of T receives 2 atoms of Hydrogen and it is converted to DHT.
The amount of T required to form DHT is about 1/100 to 1/200 of the total T produced in the body, meaning you need 1 molecule of T from 100 to obtain the amount of DHT present in the body. So, the amount of T needed to form DHT is so small that in the endocrinology filed, this amount of T which is used in the conversion process, is considered not to be a of major significance.
DHT is in blood serum measured in pg / ml, and T in ng / ml. So the amount of DHT is hundreds of time less then the amount of T.
As such, there from mathematical point of view there is no biological great increase or decrease in T. Mathematically speaking we can can see that from the 600 units of T produced only about 3 to 6 units were converted to DHT.
However, the remaining 594 units left, have a just an equal effect on the body, as 600 units.
The body naturally does not compensate such small reduction of T.
As result, there is no increase of T in the body, but merely a very small, really small reduction of T.
Also as result, the glands will not necessarily compensate for the use of T in the DHT formation, because T was already produced.
I know if you reduce conversion of T to DHT (T - > DHT) Then if I understand simply math there is more amount of T which is not converted to DHT, so as result we have increased level of Testosterone in blood, scalp and etc, but my question is why Propecia raises Testosterone (and therefore because of aromatization Estrogen level) by 10-15 %, if as I just described 1% or even less of T is converted to DHT?
I suppose finasteride. inhibits production of 5ard enzymes or interferes in production of other substances which causes other imbalances with hormonal and enzyme levels.I have question regarding changes in hormonal levels while using DHT inhibitors like finasteride (etc. Propecia).
Is this because DHT is 2- 6 times more powerful than T. I believe the body is trying to compensate by increasing T for the lack of DHT being created. Estrogen increases as T increases to maintain homeostasis.
If that is true why body bothers with DHT production if it can produce sufficient quantities of T when there is lack of DHT ?
The amount of T required to form DHT is about 1/100 to 1/200 of the total T produced in the body, meaning you need 1 molecule of T from 100 to obtain the amount of DHT present in the body. So, the amount of T needed to form DHT is so small that in the endocrinology filed, this amount of T which is used in the conversion process, is considered not to be a of major significance.
DHT is in blood serum measured in pg / ml, and T in ng / ml. So the amount of DHT is hundreds of time less then the amount of T.
As such, there from mathematical point of view there is no biological great increase or decrease in T. Mathematically speaking we can can see that from the 600 units of T produced only about 3 to 6 units were converted to DHT.
However, the remaining 594 units left, have a just an equal effect on the body, as 600 units.
The body naturally does not compensate such small reduction of T.
As result, there is no increase of T in the body, but merely a very small, really small reduction of T.
Also as result, the glands will not necessarily compensate for the use of T in the DHT formation, because T was already produced.
I know if you reduce conversion of T to DHT (T - > DHT) Then if I understand simply math there is more amount of T which is not converted to DHT, so as result we have increased level of Testosterone in blood, scalp and etc, but my question is why Propecia raises Testosterone (and therefore because of aromatization Estrogen level) by 10-15 %, if as I just described 1% or even less of T is converted to DHT?
I suppose finasteride. inhibits production of 5ard enzymes or interferes in production of other substances which causes other imbalances with hormonal and enzyme levels.I have question regarding changes in hormonal levels while using DHT inhibitors like finasteride (etc. Propecia).
Is this because DHT is 2- 6 times more powerful than T. I believe the body is trying to compensate by increasing T for the lack of DHT being created. Estrogen increases as T increases to maintain homeostasis.
If that is true why body bothers with DHT production if it can produce sufficient quantities of T when there is lack of DHT ?
I wouldn't agree on that. The way you formulated it right now ("required"), with a total amount of 600 units of T in a body, you would "require" 1/100 to 1/200 of that to produce "normal" amounts of DHT. In concrete numbers that's 3 to 6 units of T required for x units of DHT.
However, if there's more than 600 units of T you would need less than 1/100 to 1/200 of total T to produce the same amount of DHT. So the "requirement" should not be expressed in relative terms in my opinion. This would also mean that somebody with higher serum T would need more T to produce the same amount of DHT as someone else - this is definitely not the case. Only if you consider the relation between T and DHT, then your equation holds.
Please remember that serum DHT is a) not the problem and b) a very bad indicator for relevant (i.e. scalp) DHT levels. DHT is produced locally in the skin and scalp, and consumed locally in the skin and scalp again. It will not show up in the serum, or only small parts of the local production of the scalp will spill to the serum.
On this I agree.
Because, as pointed out above, I think your model for the conversion of T is wrong.
My theory is that the body uses DHT and 5ar to modulate the effects of T selectively. Where the body needs stronger T effects, it produces DHT - but only locally. T is supplied in the serum in an even ditribution, but if the body wants higher effects of T (e.g. for body hair) in one place, what can it do? It can use a metabolite of DHT which is only produced locally and which has 4 to 7 times stronger effect. This way, the body can develop local sexual features even though the base level of the respective hormones is systemically even - the effects only show due to local modulation by 5ar and DHT production. It is local on-demand modulation/amplification of effects, so to say.
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Those numbers I wrote were rough. But can you be more explicit and explain why using finasteride increases systematic T and E level by 15% (According to MERCK those increased values still remain in permitted ranges). We agree that in the endocrinology filed, this amount of T which is used in the conversion process to DHT, is considered not to be a of major significance, and in in majority of individuals it definitely isn't 15%, but maybe 2-8%. Is it because as mentioned in my previous post DHT is 4-7 times more powerful than T (in certain tissues even more). So the body is trying to compensate lack of DHT being created by increasing T. On the other hand, E increases as T increases to maintain homeostasis ? What is your opinion about that clue ?
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Yes, I am perfectly aware that probably scalp DHT is what we have to be concerned about, but not serum DHT. With regards to your explanation and theory of role of DHT in local modulation of androgen effects in target tissues it perfectly makes sense. From this it follows scalp and systemic (serum) DHT levels can vary significantly? Individuals with lots of body hair should have higher levels of DHT in their skin, even though their serum DHT is in normal ranges. Of course their androgen receptor sensitivity should not be excluded. In opposite case there are individuals with high levels of serum DHT but low levels of scalp and skin DHT, those individuals generally don't have problems with hair loss or excessive body hair.
I think you wrote great explanation of role of DHT. So in your opinion DHT is autocrine hormone, but not endocrine hormone like T ? http://en.wikipedia.org/wiki/Autocrine_signalling
Other members here also proposed theory that DHT has effects only in tissues where it is generated. Still there are other gaps in this theory. It is still fact that people experience sides when using oral DHT inhibitors, like loss of libido, ED, fatigue, even though as you described DHT has effects only in target tissues (scalp, skin, prostate...).
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Not everyone can. Testosterone affects metabolism, and is taxing on the immune system -- it is immunosuppresive. Only men with good health can afford to have high levels of testosterone, in fact high testosterone is a display of good health, which is probably more true for animals with greater sexual dimorphism.
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DHT is a cheaper way of maintaining certain bodily functions related to procreation
That makes sense, especially thinking of DHT as a hormone which has role of local modulation of androgen effects in target tissues. But what control or feedback mechanism decides how many 5ard will be produced in some tissues ? Let me ask you this. Can body produce more 5ard when it notice DHT suppression which is result of using finasteride ? In that case we have some kind of endless loop, finasteride inhibits DHT, and body in response produces more of it. Since finasteride and dutasteride in majority of people gives results obviously this is not correct.
That is is why I ask you to explain, why body and its endocrine system simply don't generate more 5ard when using oral or topical finasteride, but rises systemic T by 15%? Wouldn't it be more convenient for body to upregulate production of DHT in tissues where it notice DHT supresion, in our case in scalp when using oral or topical DHT inhibitors ?
That is is why I ask you to explain, why body and its endocrine system simply don't generate more 5ard when using oral or topical finasteride, but rises systemic T by 15%? Wouldn't it be more convenient for body to upregulate production of DHT in tissues where it notice DHT supresion, in our case in scalp when using oral or topical DHT inhibitors ?
Your absolute numbers were not the problem, but your theory that the body needs a relative amount of its T (no matter how high the specific T value is!) to produce the DHT it requires is the problem.
A possible explanation for these 15%, though, is not completely related to your model: Even the T bound to SHBG or albumin will sooner or later (more sooner than later) un-bind and be available. Especially in the case of albumin it has been proven that its bound T is basically completely bioavailable. Don't base your model on the small amounts of free T, but include the T that stochastically alternates between a bound and unbound state (in the case of SHBG) and the T that is available anyway although it is bound (in the case of albumin).
Also, take into account that finasteride works systemically. It decreases DHT production all over the body. Can't imagine this would only amount to 0.5 to 1% as you stated with your 1/100 to 1/200 - Wikipedia speaks of at least 5%.
Unless we have any other indicators, I'm pretty sure that the 15% increase in T and E is because this T is simply not converted to DHT due to 5ar inhibition. And while in normal production, 5% of T is converted to DHT, a lack of production may result in a buildup of T - thus, even though only 5% of T is usually is converted, the buildup (simply because there are no consumers for the T surprlusarising from not converting it to DHT) can amount to more than 5%.
Well, the T producers in our body may be endocrine glands, but the DHT production is, as far as my understanding goes, not endocrine by definition (or at least not completely), but endocrine and autocrine.
Is there even a feedback path? I don't know if the body notices a DHT shortage and can then increase T production to counteract (and/or to make sure that enough T is available for DHT production). Remember how DHT is produced in skin and scalp - the available T is taken in certain amounts and converted to DHT. If there is less T available, less DHT will be produced. If there is no feedback path - and I haven't heard of any - then that's the end of the story.
I simply don't know if such a feedback path exists.
Maybe the body can only notice a lowering of serum DHT, but not a decrease in local DHT?
I don't know this at all, so take the following hypothesis of mine with a huge grain of salt:
Citing Wikipedia:
If more testosterone is available (because less of it converted to DHT), more estrogen will be produced automatically. Those are to a big extent stochastical processes.Wikipedia said:
Yes.
Again, its not that simple
Please remember that our reproductive organs still provide a "base level" of DHT into our serum. I don't know how much of this base DHT will have an effect in our case (i.e. on the scalp) - but there must be a reason for base DHT, otherwise it would likely not be there.The question is: How much of a role plays serum DHT and how much local DHT? I am pretty sure that serum DHT only plays the minor role of those two, but it shouldnt be ignored completely.
A good indicator whether or not serum DHT plays a role is an efficacy study of local 5ar inhibition (e.g. not systemically used as a pill, but only applied to the scalp somehow). If such an efficacy study of local 5ar inhibition shows significant and substantial results, then it is almost proven that scalp DHT is the problem and serum DHT plays almost no role at all.
Partly endocrine (otherwise we wouldnt have serum DHT), partly autocrine.
Unlike the other things in this post, this is very easy to explain and 100% confirmed: The effect of DHT is exactly that. DHT acts locally - but in many places. Locally in our chest skin (-> chest hair), locally in our scalp (-> Androgenetic Alopecia/male pattern baldness), locally in our reproductive organs (-> libido and ED).
Now, finasteride is ingested and distributed through our bloodstream to all target tissues, i.e. all local sites. So while DHT is produced locally in many sites, finasteride works globally on all those local sites. This the reason for its side effects.
Fun fact: PGs are partly responsible for creating and relaxing errections. Maybe there is a connection here? T and DHT is high in our reproductive organs and PGs partially control our reproductional capabilities, i.e. errections. In the scalp, we also have high DHT and high PGD2. Please note: Only a hypothesis I just came up with, might be completely wrong.
I don't know that, unfortunately. This is one of the three big missing links in Androgenetic Alopecia/male pattern baldness as far as I know.
If we are unlucky, this is determined directly by our genes. If so, then local 5ar inhibition is probably the best available solution outside of regenerative medicine.
True observation.
As explained above, the body does not increase T production. The 15% increase in serum T levels is very likely only a result of buildup (see above in this post for explanation).
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What good will come from this thread? When all is said and done, it will all be for not.
Yeah Bryan used to say that locally produced DHT was the problem for hair yet here we are 20 years after finasteride still without any good topical AA. The problem is they all go systemic anyways or the vehicles just arent effective enough to get decent results. So uh yeah I agree we need topical AAs the problem is there arent any.
If so, then local 5ar inhibition is probably the best available solution outside of regenerative medicine.
If so, then local 5ar inhibition is probably the best available solution outside of regenerative medicine.
I don't perfectly understand what you exactly mean by T buildup. It is clear that overall increase in T and E (According to MERCK studies) is more then amount of T not converted to DHT because of 5ar inhibition.
Let's assume 5% of T is converted to DHT. You clearly explained increase of Free T by 5 % as consequence of non-conversion to DHT. But then, how you came up with 15 %. Is that result of accumulation of free T from several days ago, 15%(at the moment) = 5%(two days ago) + 5%(a day ago) + 5%(present day) ?
If I correctly understood your explanation, you pointed increase in T (and in E) is directly result of more free T not being converted to DHT. So, In your opinion, which I partially agree, variations of the most essential hormones (T, E) are pure result of more free T because of 5ard inhibition and corresponding stochastic process of fluctuations of T from bounded and unbounded state rather then some kind of feed-back mechanism(compensatory effect) of endocrine system ?
Another reason which makes difficult to comprehend all this matter are terms and values used in published studies which are not specified correctly. For example in Propecia documentation, it is unclear to me, whether or not T refers to total T or free T?
What makes free testosterone so special in this case, is that according to Merck - (total) testosterone level increases by 10-15% - fooling people to believe that it's actually a good thing. But according to study in this topic: http://www.hairlosstalk.com/interact/showthread.php/54491-Propecia-decreases-bioavailable-testosterone!?p=1032186&viewfull=1#post1032186 total testosterone level goes up, but free testosterone level goes down.
Theory behind that is SHBG has greater affinity for DHT, and second in line is testosterone prior to estrogen, and when you reduce the amount of DHT, testosterone will take the hit. Estrogen is linked to SHBG as well, and more estrogen means more SHBG (women have a lot more SHBG than men). All this makes the estrogen dominance worse. As if that wasn't enough, all these changes causes a chain reaction in the endocrine system. Prolactin is an example of another hormone that increases with estrogen, and it takes a toll on your sexual function. It reduces libido and the intensity of orgasms, and it increases the refraction period. Estrogen dominance is a well known cause for secondary hypogonadism. That said - I could have had an estrogen level that was high before I began treatment - and lowering DHT (which is the natural estrogen antagonist) by 70% would be a very bad idea, if that was the case.
Most men (according to MERCK and other studies) do fine with even decreased bioavailable testosterone. In my opinion, libido / erectile quality is not directly related to the amount of free testosterone in blood, nor is it related to the amount of DHT. The hormonal balance of many people ranges widely and of course lifestyle (diet, stress, amount and quality of sleep, supplements) is probably a big part of it as well.
So, in my opinion it isn't like if your free T drops 50%, then your libido and erectile quality will drop by 50% as well. Most men can handle these hormonal variances. I figure that the 2-5% that have side effects with finasteride or dutasteride either already have marginal hormonal levels, or for some reason can't handle ANY decrease in free T or DHT due to their individual genetic make-up.
It could be that finasteride for some direct or indirect reason increases SHBG in certain people and therefore the free testosterone is bound. It is also a higher possibility that some peoples bodies increase production of aromatase enzyme in order to compensate for the increase in free testosterone which then gets converted to estrogen shifting (FreeT/Estrogen) ratio. This last would explain increase in Estrogen. Since, as I wrote in last post, some say increase in E is result of homeostasis, and some as you believe it is simply because there is more free T, so when you have more free T and less 5ard(competitor for free T), you have more Estrogen.
Not quite. If it worked that way, you'd have additional 5% for every day you take propecia, e.g. 20% after 4 days, 25% after 5 days, etc., so buildup cannot be linear. But it works similar. A mathematical model for this could be a bounded variant of a logarithmic function, or some other bound function with increasingly small additions depending on time (something like f(x) = sum(t = 0..n, x^(-t)) ). So for each additional period of time, you will have additional buildup - but the addition will be decreasing with time.
Probably yes. We don't have any info that would indicate something different. If there was a feedback path, it will likely only exist for the endocrine production of DHT - how should the body know if there is enough DHT in local tissues?
I can't make any statements about their terminology.
The study is extremely interesting, I wouldn't've have suspected free T decreasing. The SHBG explanation makes sense, though, but I don't think that this decrease in free T can actually lead to E dominance given how small the fraction of free T in the total of (total T + total E + total DHT) is. And if that was the case, many more people should experience such effects which would easily be discovered by clinical trials.
Libido and erectile quality probably depends on a) DHT being within a certain range, i.e. above a required minimum level (if you dont have enough DHT in your body in total, then all local sites will have shortages; in extension, this also applies to T and thus would impair DHT production), and b) hormonal balance. DHT just needs to be above a certain minimum level so that enough is available for all body functions - everything else probably does not play a major role anymore, but only impacts the extent of sexual features. T, however, also needs to be above a certain value so that enough T is available to produce the required amount of DHT for all local sites running their functions.
I partially agree. The part I agree on is that the variations in T and DHT can be dealt with by most men, because they likely have more T and DHT than only the bare minimum their body needs. However, the hormonal balance might have an effect on libido and errections, and the hormonal balance would change when DHT drops - even if DHT is still above the "threshold value".
Yes, both are valid explanations. I wish I could tell which of the two explanations is correct, but both do make sense.
I've pieced together some more. There are two effects at work in our scalp that are DHT-induced, leading to (at least) three downstream outcomes:
Each of the connections I made above can be confirmed by googling the two neighboring terms around a "->". Some sources for the less obvious connections:
I think it's important to notice that there are two immediate effects from elevated DHT: Firstly, upregulation of Dkk-1 and secondly, upregulation of COX-2. Both of these immediate effects have different downstream effects on hair growth. One, Dkk-1, destroys the follicle's essential "hair production cells" by inhibiting Wnt/β-catenin signalling. The other one a) ruins the tissue around the follicles so even if the follicles could still produce new hair, they wouldnt be able to, and b) tells the follicles to not even try producing new hair.
Now the big question that remains is what elevates DHT or increases its effects in the first place. Is it elevated 5ar, too many androgen receptors, or sensitive androgen receptors?
- ? -> DHT high -> COX-2 high -> PGD-2 way too high -> inflammation -> fibrosis
- ? -> DHT high -> COX-2 high -> PGD-2 high -> no reentering of anagen phase (also leading to: -> no adipogenesis -> no angiogenesis)
- ? -> DHT high -> Dkk-1 high ->Wnt/β-catenin impaired -> Apoptosis of follicle outer root sheath cells and cup cells without renewal -> follicle cant produce new hair
Each of the connections I made above can be confirmed by googling the two neighboring terms around a "->". Some sources for the less obvious connections:
- DHT high -> COX-2 high: Source 1, Source 2
- PGD-2 -> no reentering of anagen phase: Source
- No reentering of anagen phase -> no adipogenesis: Source
- No adipogenesis -> no angiogenesis: Source 1, Source 2, Source 3
- DHT high -> Dkk high: Source
- Dkk high -> Wnt/β-catenin impaired: Source 1, Source 2, Source 3
- Apoptosis of outer root sheath cells (transitively from DHT but through Wnt hindering): Source
I think it's important to notice that there are two immediate effects from elevated DHT: Firstly, upregulation of Dkk-1 and secondly, upregulation of COX-2. Both of these immediate effects have different downstream effects on hair growth. One, Dkk-1, destroys the follicle's essential "hair production cells" by inhibiting Wnt/β-catenin signalling. The other one a) ruins the tissue around the follicles so even if the follicles could still produce new hair, they wouldnt be able to, and b) tells the follicles to not even try producing new hair.
Now the big question that remains is what elevates DHT or increases its effects in the first place. Is it elevated 5ar, too many androgen receptors, or sensitive androgen receptors?
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Benjt, do you know if the apprpopiate levelof DHT in a healthy scalp hair is constant during all the natural hair cicle? I think that change, the same with other meadiators Wnt, beta-catenin etc.
what do you think?
what do you think?
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http://www.ncbi.nlm.nih.gov/pubmed/24344810
What changed in these girls scalphair from long term T therapy? Were normally dormant genes activated in the front temporal region? Women don't bald that way, they go diffuse. interested in your opinion.
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Interestingly, this is after an average of 10 yrs of T therapy. Kind of like developing Androgenetic Alopecia 10 yrs after puberty.
What changed in these girls scalphair from long term T therapy? Were normally dormant genes activated in the front temporal region? Women don't bald that way, they go diffuse. interested in your opinion.
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Interestingly, this is after an average of 10 yrs of T therapy. Kind of like developing Androgenetic Alopecia 10 yrs after puberty.
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I don't think that this study has any relevant implications. Remember that DHT is metabolised from T; if T levels were much lower beforehand (because the subjects were biologically not really men and thus their T levels were way too low), there was simply not enough base material to generate the DHT levels that lead to Androgenetic Alopecia. The study only shows that approx. 1/3 of the subjects were prone to Androgenetic Alopecia (and were so genetically before, but T levels were not high enough to form Androgenetic Alopecia-inducing DHT levels). There is no indication that anything in their scalp hair changed. But thanks for contributing nonetheless - the more info we find, the more we can deduce.