Back to the roots: Causes and effects of elevated DHT
- Thread starter benjt
- Start date
I dont agree on the AR sensitivity part (nor do I disagree - I simply don't know). The thing about diffuse thinning is that DHT only exceeds the threshold level for follicles in the area slightly, while in recession it goes way above threshold level. In diffuse thinning, for some the DHT level already exceeds threshold, for others it doesn't. But I don't know if its because of sensitivity or amount produced.
By the way, after xRedStaRx's explanation I don't know if the avalanche property really exists. Likely not, though.
By the way, after xRedStaRx's explanation I don't know if the avalanche property really exists. Likely not, though.
Likely amount produced first and foremost.
AR transcripts are only inherited from the mother, and we know male pattern baldness comes equally from both sides of the family. Some statistics even show the paternal side has a bigger influence. Not only that, but AR sensitivities should not matter much, seeing as DHT is produced inside the hair follicle so that would be the primary factor.
Hey guys,
I have been reading this thread for several days and I am now so excited how many subjects you have touched there and what can eventually come out of that. Just registered to tell you I will be connecting some dots in about 8 hours from now because now it's too late and I don't have much time to write anymore.
(first post, sorry for "spam-like" enthusiasm)
I have been reading this thread for several days and I am now so excited how many subjects you have touched there and what can eventually come out of that. Just registered to tell you I will be connecting some dots in about 8 hours from now because now it's too late and I don't have much time to write anymore.
(first post, sorry for "spam-like" enthusiasm)
helpmyhairplease
Member
- Reaction score
- 4
my Doctor says hormonal changes always stop at late 16 years old and all other extra substances wash off.
but for some of us our hormones remain haywire for extra or even longer time than others. some of this is activated by hormones simulation which is caused by dozens of reasons, even put blame on preserv chemicals found in food.
but for some of us our hormones remain haywire for extra or even longer time than others. some of this is activated by hormones simulation which is caused by dozens of reasons, even put blame on preserv chemicals found in food.
Gene which encodes AR has been found only on X chromosome so far, but probably there are other genes which also contribute to androgen receptor transcription and so determine sensitivity. Who knows.... So it doesn't mean there aren't other genes, located on autosomal chromosomes and inherited from father side, which can control AR.
Since this research http://www.karger.com/Article/FullText/78584 has yielded that men whose fathers had experienced hair loss were 2.5 times more likely to experience hair loss themselves, regardless of the mother's side of the family., it means there is more then one factor men inherits from his fathers side.
5-ard biolocations in scalp and hormonal profile are inherited from father's side rather then maternal, but I think the level of fibrosis/inflammation trigger, and auto-immune response is also what you inherit from you father and these factors also play huge role in male pattern baldness.
Everyone here agrees that balding resistant hair (donor hair) has less AR sensitivity and less DHT follicular production ? And what happens to hair extracted from back of the head but outside 'safe zone' and transplanted to front. Why this hair follicles thin out in some cases, and why they haven't thinned at their original place ?
http://press.endocrine.org/doi/abs/10.1210/endo.133.2.8344190
"IGF-I may be an important regulator of skin 5 alpha R activity and, thus, may influence DHT formation."
IGF-1 increases 5ar/DHT directly?
Made me think of this dude, although he was thinking along the lines how IGF-1 suppresses SHBG, which in turn increases free T:
http://www.hairlosstalk.com/interact/showthread.php/43442-A-Closer-Look-At-Insulin-amp-IGF-1
"IGF-I may be an important regulator of skin 5 alpha R activity and, thus, may influence DHT formation."
IGF-1 increases 5ar/DHT directly?
Made me think of this dude, although he was thinking along the lines how IGF-1 suppresses SHBG, which in turn increases free T:
http://www.hairlosstalk.com/interact/showthread.php/43442-A-Closer-Look-At-Insulin-amp-IGF-1
In this post I'd like to sum up on what I have been reading here and expand on what I have studied along with it. Here is my theory on what might or might not going on in the process of Androgenetic Alopecia and during the treatments people/scientists have tried.
There are several factors in how hair can be negatively affected in Androgenetic Alopecia
1. Natural process of follicular aging, can be sped up by food, bad habits, environment, etc. You can see this in older men with pretty much no Androgenetic Alopecia (androgenic alopecia), their hair not being quite as when they were young. Diet especially [western, think insulin spikes and insulin restistance, caffeine overdosing etc.] have been anecdotally connected with Androgenetic Alopecia.
2. Androgenic hormones (T, DHT but also perhaps others like androstenedione) accelerate the aging process above in genetically susceptible individuals and may have direct additional miniaturizing influence on the follicles. Blocking them have definitely given good results but not full regrowth of lost hair. The good news is that androgens are not at it alone, i.e. they start a follicular destruction cascade. Without specifying it, this cascade affects not only follicles that are directly affected but also their neighboring follicles, possibly even triggering more of the androgen-related changes in them.
What could do we do with Androgenetic Alopecia now:
1. one pathway how to address the aging process would be to make a complete change of lifestyle to minimize insulin spikes, T spikes, oxidating processes in body etc.. This would mean no western lifestyle, no sports (T spikes), hardcore caloric restriction (I spikes), various herbal teas to increase antioxidating processes. Also no-fap and no pr0n (minimizing T levels), no sex and no hard physical work. Also rather not looking at human females [or any females of any kind] nor speaking to them, all of that would increase a healthy man's T. Yep, it's generally out of question for most of us living modern man's life but still, perhaps it's possible. Any volunteers?
2. another way shown to fix Androgenetic Alopecia at least temporarily would be using a nitric oxide (NO) donor such as nitrovasodilators (minoxidil). I'd call this "raping follicles from behind" because we're circumventing the androgens problem and treating the follicles from different angle. Vasodilation enhances follicular nutrition and spurs regrowth, i.e. minoxidil is believed to act by increasing vascular circulation to the hair follicle. It is certainly a radical nitric oxide (NO) donor which releases NO that activates the enzyme guanylate cyclase (sGC) which then causes the synthesis of the smooth muscle relaxant guanosine 3′,5′-monophosphate (cGMP), thereby promoting systemic vascular relaxation and dilation in order to increase vascular circulation and blood flow to hair follicles and hair bulbs. However, as soon as cGMP is produced another enzyme called phosphodiesterase 5 (PDE5) tends to degrade it and eliminate it. That is one of the reasons why topical Minoxidil is known to have certain shortcomings. It is effective in only about eight percent of adult male users. It produces “lanugo,†or baby-type, hair, which is relatively thin. Further, and perhaps most significantly, after approximately 30 months of continuous use, minoxidil shows a sharp drop in effectiveness probably due to local abundance of PDE5 which tends to fight the synthesis of cGMP which is needed as a vasodilator to enhance blood flow and vascular circulation to hair follicles and hair bulbs. This can be prevented by PDE5 inhibitor such as sildenafil (well know as male potency ehancer) which can be applied topically, as described in this patent.
HOWEVER nitric oxide (NO) is also a free radical. Its oxidative degradation and products can most probably degrade the cells and speed up their aging. Human body produces its own antioxidant which is quite potent and has a powerful effect on NO: melatonin. But the effect of melatonin was abolished in the presence of the PDE5 inhibitors zaprinast and sildenafil (described in this study). The direct toxicity of nitric oxide is modest but is greatly enhanced by reacting with superoxide to form peroxynitrite (ONOO-). Additionally, nitric oxide is the only biological molecule produced in high enough concentrations to out-compete superoxide dismutase for superoxide [which would otherwise degrade superoxide to less damaging products].
Interestingly and probably most unfortunaly, this would give mixed results to a human guinea pig such as me regarding hair growth. I suspect the regrowth would be fast and notable but in time the faster degradation of follicular cells would result in apoptosis and enhanced hairloss (I am going to try anyway, this is just a theory after all).
3. Blocking androgens is yet another way to rape the follicles, this time directly from the front. This has been done to very good extent with eunuchs. A much more modern way would be to prevent T from reaching the follicles and/or prevent T from converting to DHT, possibly also block other androgens. I am surprised that after 10+ years of research there is no topical androgen blocker which would block these hormones from acting in the skin and follicles. The only one I can mention here is ketaconazole which should act as antiandrogen both preventing DHT synthesis even in skin (needs to be confirmed) and as a weak androgen receptor antagonist. What we really have are those 5-alpha-reductase (5AR) blockers which are not topical as far as I know and could have systemic effects throughout the body.
Additionally, one could try to apply alfatradiol (or estradiol hormone/steroid) topically to modify aromatase activity to convert T in skin to estrogens. From trans-gender treatments we know that estrogens are considered to be beneficial for ARA suffering people.
Next we could do something about blocking the androgen-induced cascade downstream. This can be probably accomplished at least partially with antihistamine cetirizine which partially blocks prostaglandin D2(PGD2) production [which was shown to minimize follicles in at least one study]. Interestingly enough PGD2 also has vasodilatory effect.
4. Another way to go would be preservation: to use topical melatonin, a potent anti-oxidant hormone, to prevent oxidative damage to the follicles, as has been done in at least one study before. From the little web research I've done it's obvious it can easily cross the skin and brain barrier and has accumulatory effect in the stratum corneum (dead skin cells on top of living skin). HOWEVER this readily available therapeutic agent most probably cannot be used with minoxidil as it counteracts the NO releasing effects of minoxidil and other vasodilators based on NO release. Too bad, but perhaps minoxidil has also a de-scarring and skin-thinning effect (it reportedly depletes skin of keratin) which would warrant use of both agents together. Other cheap antioxidants like ascorbic acid (vit C) could be used systemically.
This preservative way could perhaps have nice results if combined with the anti-androgen way described above. One of the substances to avoid would be caffeine though, as it seems to increase androgen activity all over body (there are several studies confirming it). Interestingly enough there was one study which confirmed topical efficacy of caffeine in counteracting hairloss. That's how we got the Alpecin(R) product. However anecdotal evidence related to hair and stress points otherwise. Caffeine may actually raise the flee-or-fight body response: it stimulates a release of adrenalin which becomes a part of stress response in our organism. And body/hair doesn't react nicely to stress, regardless if it is just induced by a foreign substance several times a day. There might be a caffeine/stress threshold different for each individual because after I stopped with caffeinated coffees, I noticed my shedding has altogether stopped. While I still get a daily coke, it has most probably no negative effect on my hair.
5. Yet another way is hypoxia, as mentioned by one poster before, which perhaps disallows access of androgens and other substances to follicles. I have also read somewhere that there is a layer of stem cells which need a hypoxic environment to stimulate their division to begin new hair follicles or whatever they do. Not sure if this is related, this needs to be researched more.
In any case, from the above we can see how difficult this Androgenetic Alopecia problem is... if we block androgens, we get systemic problems and the effect is still not enough to get all of our hair back. If we introduce vasodilators to increase NO, the increased blood flow probably brings some more androgens along with melatonin every night which counters the NO and its activity. Even if we reduce scarring, we might get more androgens due to increased blood flow. If you go hypoxic on the little bastards, you risk their premature death. Just like you risk it when you go fully nitrous on them. And probably not one of these ways fcuks the follicles hard enough to make a complete overgrowth like we see at trans-gender people who go fully woman with their hormones.
These are exciting times though. I feel like we're finally cracking this thing. These are the times of real discoveries being made, really perhaps Flemming-like or Marshall-like (the guy who ingested the helicobacter to prove it creates peptic ulcers).
There are several factors in how hair can be negatively affected in Androgenetic Alopecia
1. Natural process of follicular aging, can be sped up by food, bad habits, environment, etc. You can see this in older men with pretty much no Androgenetic Alopecia (androgenic alopecia), their hair not being quite as when they were young. Diet especially [western, think insulin spikes and insulin restistance, caffeine overdosing etc.] have been anecdotally connected with Androgenetic Alopecia.
2. Androgenic hormones (T, DHT but also perhaps others like androstenedione) accelerate the aging process above in genetically susceptible individuals and may have direct additional miniaturizing influence on the follicles. Blocking them have definitely given good results but not full regrowth of lost hair. The good news is that androgens are not at it alone, i.e. they start a follicular destruction cascade. Without specifying it, this cascade affects not only follicles that are directly affected but also their neighboring follicles, possibly even triggering more of the androgen-related changes in them.
What could do we do with Androgenetic Alopecia now:
1. one pathway how to address the aging process would be to make a complete change of lifestyle to minimize insulin spikes, T spikes, oxidating processes in body etc.. This would mean no western lifestyle, no sports (T spikes), hardcore caloric restriction (I spikes), various herbal teas to increase antioxidating processes. Also no-fap and no pr0n (minimizing T levels), no sex and no hard physical work. Also rather not looking at human females [or any females of any kind] nor speaking to them, all of that would increase a healthy man's T. Yep, it's generally out of question for most of us living modern man's life but still, perhaps it's possible. Any volunteers?
2. another way shown to fix Androgenetic Alopecia at least temporarily would be using a nitric oxide (NO) donor such as nitrovasodilators (minoxidil). I'd call this "raping follicles from behind" because we're circumventing the androgens problem and treating the follicles from different angle. Vasodilation enhances follicular nutrition and spurs regrowth, i.e. minoxidil is believed to act by increasing vascular circulation to the hair follicle. It is certainly a radical nitric oxide (NO) donor which releases NO that activates the enzyme guanylate cyclase (sGC) which then causes the synthesis of the smooth muscle relaxant guanosine 3′,5′-monophosphate (cGMP), thereby promoting systemic vascular relaxation and dilation in order to increase vascular circulation and blood flow to hair follicles and hair bulbs. However, as soon as cGMP is produced another enzyme called phosphodiesterase 5 (PDE5) tends to degrade it and eliminate it. That is one of the reasons why topical Minoxidil is known to have certain shortcomings. It is effective in only about eight percent of adult male users. It produces “lanugo,†or baby-type, hair, which is relatively thin. Further, and perhaps most significantly, after approximately 30 months of continuous use, minoxidil shows a sharp drop in effectiveness probably due to local abundance of PDE5 which tends to fight the synthesis of cGMP which is needed as a vasodilator to enhance blood flow and vascular circulation to hair follicles and hair bulbs. This can be prevented by PDE5 inhibitor such as sildenafil (well know as male potency ehancer) which can be applied topically, as described in this patent.
HOWEVER nitric oxide (NO) is also a free radical. Its oxidative degradation and products can most probably degrade the cells and speed up their aging. Human body produces its own antioxidant which is quite potent and has a powerful effect on NO: melatonin. But the effect of melatonin was abolished in the presence of the PDE5 inhibitors zaprinast and sildenafil (described in this study). The direct toxicity of nitric oxide is modest but is greatly enhanced by reacting with superoxide to form peroxynitrite (ONOO-). Additionally, nitric oxide is the only biological molecule produced in high enough concentrations to out-compete superoxide dismutase for superoxide [which would otherwise degrade superoxide to less damaging products].
Interestingly and probably most unfortunaly, this would give mixed results to a human guinea pig such as me regarding hair growth. I suspect the regrowth would be fast and notable but in time the faster degradation of follicular cells would result in apoptosis and enhanced hairloss (I am going to try anyway, this is just a theory after all).
3. Blocking androgens is yet another way to rape the follicles, this time directly from the front. This has been done to very good extent with eunuchs. A much more modern way would be to prevent T from reaching the follicles and/or prevent T from converting to DHT, possibly also block other androgens. I am surprised that after 10+ years of research there is no topical androgen blocker which would block these hormones from acting in the skin and follicles. The only one I can mention here is ketaconazole which should act as antiandrogen both preventing DHT synthesis even in skin (needs to be confirmed) and as a weak androgen receptor antagonist. What we really have are those 5-alpha-reductase (5AR) blockers which are not topical as far as I know and could have systemic effects throughout the body.
Additionally, one could try to apply alfatradiol (or estradiol hormone/steroid) topically to modify aromatase activity to convert T in skin to estrogens. From trans-gender treatments we know that estrogens are considered to be beneficial for ARA suffering people.
Next we could do something about blocking the androgen-induced cascade downstream. This can be probably accomplished at least partially with antihistamine cetirizine which partially blocks prostaglandin D2(PGD2) production [which was shown to minimize follicles in at least one study]. Interestingly enough PGD2 also has vasodilatory effect.
4. Another way to go would be preservation: to use topical melatonin, a potent anti-oxidant hormone, to prevent oxidative damage to the follicles, as has been done in at least one study before. From the little web research I've done it's obvious it can easily cross the skin and brain barrier and has accumulatory effect in the stratum corneum (dead skin cells on top of living skin). HOWEVER this readily available therapeutic agent most probably cannot be used with minoxidil as it counteracts the NO releasing effects of minoxidil and other vasodilators based on NO release. Too bad, but perhaps minoxidil has also a de-scarring and skin-thinning effect (it reportedly depletes skin of keratin) which would warrant use of both agents together. Other cheap antioxidants like ascorbic acid (vit C) could be used systemically.
This preservative way could perhaps have nice results if combined with the anti-androgen way described above. One of the substances to avoid would be caffeine though, as it seems to increase androgen activity all over body (there are several studies confirming it). Interestingly enough there was one study which confirmed topical efficacy of caffeine in counteracting hairloss. That's how we got the Alpecin(R) product. However anecdotal evidence related to hair and stress points otherwise. Caffeine may actually raise the flee-or-fight body response: it stimulates a release of adrenalin which becomes a part of stress response in our organism. And body/hair doesn't react nicely to stress, regardless if it is just induced by a foreign substance several times a day. There might be a caffeine/stress threshold different for each individual because after I stopped with caffeinated coffees, I noticed my shedding has altogether stopped. While I still get a daily coke, it has most probably no negative effect on my hair.
5. Yet another way is hypoxia, as mentioned by one poster before, which perhaps disallows access of androgens and other substances to follicles. I have also read somewhere that there is a layer of stem cells which need a hypoxic environment to stimulate their division to begin new hair follicles or whatever they do. Not sure if this is related, this needs to be researched more.
In any case, from the above we can see how difficult this Androgenetic Alopecia problem is... if we block androgens, we get systemic problems and the effect is still not enough to get all of our hair back. If we introduce vasodilators to increase NO, the increased blood flow probably brings some more androgens along with melatonin every night which counters the NO and its activity. Even if we reduce scarring, we might get more androgens due to increased blood flow. If you go hypoxic on the little bastards, you risk their premature death. Just like you risk it when you go fully nitrous on them. And probably not one of these ways fcuks the follicles hard enough to make a complete overgrowth like we see at trans-gender people who go fully woman with their hormones.
These are exciting times though. I feel like we're finally cracking this thing. These are the times of real discoveries being made, really perhaps Flemming-like or Marshall-like (the guy who ingested the helicobacter to prove it creates peptic ulcers).
I've never heard of donor hair miniaturizing after extraction to be honest, but I could be oblivious.
Balding follicles usually undergo miniaturization almost exclusively autocrinally.
High serum levels of IGF-1 has been shown to predict your responsiveness to finasteride. It was also positively correlated with stronger frontal hair, but not at the vertex. I'm also read some steroid users experiencing hair regrowth on the front fringe when using IGF-1 and HGH hormones, so they're definitely anabolic towards all cells, including hair. DHT has the opposite effect and inhibits IGF-1/GH production. I'm not sure what to make of all this information, but I believe people with higher IGF-1 usually have stronger hair, and slower male pattern baldness.
I cannot remember where I read this, so take that for what it is. But if I remember correctly, it's not necessarily over-production of DHT that necessarily leads to hair loss, rather, the sensitivity to it.
I read in a similar study that men who can grow thick beards and men who can't grow any beards have the same levels of testosterone, but have different sensitivities to it.
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I read in a similar study that men who can grow thick beards and men who can't grow any beards have the same levels of testosterone, but have different sensitivities to it.
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this is fascinating, I noticed my hair loss began in a stage in my life where I was basically living off caffeine (upwards of 3 cups of starbucks per day). Stress was also through the roof.
Hi, it took long enough to administrator to approve of my post, it showed very late and above subsequent posts in this thread.
It's here: http://www.hairlosstalk.com/interac...elevated-DHT?p=1201941&viewfull=1#post1201941
hope you have read it guys
It's here: http://www.hairlosstalk.com/interac...elevated-DHT?p=1201941&viewfull=1#post1201941
hope you have read it guys
this is unbelievable, do all posts of everyone else get the same kind of moderating as my own?
My posts [with links] don't appear immediately, please refer above to see them.
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Yes, exactly. The DHT is causing it AND sensitivity to it is also causing it. I view "sensitivity to DHT" as to how many androgen receptors the cells in the affected area have. Still, there could be also some skin/follicle cells which make less DHT and some which make more. I think, just like previous posters noted, these may somehow make their own DHT based on the presence/expression of 5AR and free testosterone.
BTW, it's really simple to get off the caffeine. You just endure a medium 2-day headache and get some more sleep within the next few days. And then you just have to watch your caffeine threshold, as I have described earlier. This means one small coffee doesn't make your stress levels skyrocket, just make sure it's small and you don't get any more caffeine that day. It's actually more stress-related than just caffeine-related. When you have stress, don't get any caffeine. You deal with stress by sleeping it off.
My posts [with links] don't appear immediately, please refer above to see them.
- - - Updated - - -
Yes, exactly. The DHT is causing it AND sensitivity to it is also causing it. I view "sensitivity to DHT" as to how many androgen receptors the cells in the affected area have. Still, there could be also some skin/follicle cells which make less DHT and some which make more. I think, just like previous posters noted, these may somehow make their own DHT based on the presence/expression of 5AR and free testosterone.
BTW, it's really simple to get off the caffeine. You just endure a medium 2-day headache and get some more sleep within the next few days. And then you just have to watch your caffeine threshold, as I have described earlier. This means one small coffee doesn't make your stress levels skyrocket, just make sure it's small and you don't get any more caffeine that day. It's actually more stress-related than just caffeine-related. When you have stress, don't get any caffeine. You deal with stress by sleeping it off.
@corvidae: I have no caffeine intake whatsoever (no coffee, no coke, nada) and still quite aggressive hairloss.
@beholder: I am not quite sure it's actually minoxidil's vasodilatory function (and thus increased blood flow/nutrient supply) which is responsible for its effect. Some studies report it increases PGE2 and thus reduces the inflammatory effects of PGD2. Others, however, report that minoxidil actually decreases PGE2 levels. Inconclusive and downright contradictory studies suck, but an increase in PGE2 would be a good explanation.
@beholder: I am not quite sure it's actually minoxidil's vasodilatory function (and thus increased blood flow/nutrient supply) which is responsible for its effect. Some studies report it increases PGE2 and thus reduces the inflammatory effects of PGD2. Others, however, report that minoxidil actually decreases PGE2 levels. Inconclusive and downright contradictory studies suck, but an increase in PGE2 would be a good explanation.
Nice, good to know, Benjt. I will keep that somewhere in the back of my brain.
In any case I am going to make my own study with me as guinea pig: sildenafil (\/iagra) came today and I have made a 0.5% alcohol+water solution and applied it to my skull. (there was a study they used 1% solution on reproductive organs to treat erectile dysfunction so I think I am not very far from the actual correct formula).
So IF minoxidil works primarily through vasodilation, this should help it tremendously to.. well.. vasodilate. I will see if I get some good results within 2-3 months. Hope not to get too many boners. But if it doesn't work in 1 month (no visible difference on that lanugo babyhair), I will double the concentration of sildenafil to 1%. Trying to get the synergistic effect described in this patent:
http://www.google.com/patents/US20020182162
In any case I am going to make my own study with me as guinea pig: sildenafil (\/iagra) came today and I have made a 0.5% alcohol+water solution and applied it to my skull. (there was a study they used 1% solution on reproductive organs to treat erectile dysfunction so I think I am not very far from the actual correct formula).
So IF minoxidil works primarily through vasodilation, this should help it tremendously to.. well.. vasodilate. I will see if I get some good results within 2-3 months. Hope not to get too many boners. But if it doesn't work in 1 month (no visible difference on that lanugo babyhair), I will double the concentration of sildenafil to 1%. Trying to get the synergistic effect described in this patent:
http://www.google.com/patents/US20020182162
Fbalding84
Established Member
- Reaction score
- 5
Beholder;
I must say you hit some good points. I believe there is s striking similarity between all the drugs or supplements that induce hair regrowth (or maintain) for male pattern baldness.
Let's sum them up and see if at least 50% is accurate for each of your favorite "cure".
1. Blood pressure decrease (by Cardiovascular dilation or other means)
2. Anti inflammatory properties
3. Prostaglandins analog
4. Increased insulin/carb/sugar metabolism
4. ability to reduce adipose/fat/lipid tissue
5. Activates fight or run mechanism
6. most importantly it has the ability to affect SMOOTH MUSCLE TISSUE by relaxing or contradiction
I don't believe that more DHT is found on scalp that caused male pattern baldness but instead because we are balding more DHT is deposited on our scalp vs attaching to our hairshafts.
Topical solutions of our common drugs should work but since it's not systemic we have to apply it more often, I believe.
I must say you hit some good points. I believe there is s striking similarity between all the drugs or supplements that induce hair regrowth (or maintain) for male pattern baldness.
Let's sum them up and see if at least 50% is accurate for each of your favorite "cure".
1. Blood pressure decrease (by Cardiovascular dilation or other means)
2. Anti inflammatory properties
3. Prostaglandins analog
4. Increased insulin/carb/sugar metabolism
4. ability to reduce adipose/fat/lipid tissue
5. Activates fight or run mechanism
6. most importantly it has the ability to affect SMOOTH MUSCLE TISSUE by relaxing or contradiction
I don't believe that more DHT is found on scalp that caused male pattern baldness but instead because we are balding more DHT is deposited on our scalp vs attaching to our hairshafts.
Topical solutions of our common drugs should work but since it's not systemic we have to apply it more often, I believe.
If there ever should be a connection between hair loss and the sexual function (nofap threads...), my theory is:
The body can in theory perform sexually almost entirely on testosterone alone and minimal DHT -- more or less, if you only have sex once a month
Testosterone is immunosuppresive, and it is an "expensive" way of being sexually active. One of T's primary functions is display of good health and only really virile men can afford to have high levels of T
Once your sexual performance is compromised because of poor health/age or you for some periods need to perform above you "ability", the body starts pumping DHT
From evolutionary standpoint, sex is always in high priority and the body will always find resources. DHT is just a cheaper way of doing it
Some alpha males can have unlimited sex and still have low DHT, but we -- the deadly ones -- are sufferers of the handicap principle, and have to display our bald head as a sign of bad health/poor sexual provvess, and it is exactly what I see when look at bald people: exhaustion
The body can in theory perform sexually almost entirely on testosterone alone and minimal DHT -- more or less, if you only have sex once a month
Testosterone is immunosuppresive, and it is an "expensive" way of being sexually active. One of T's primary functions is display of good health and only really virile men can afford to have high levels of T
Once your sexual performance is compromised because of poor health/age or you for some periods need to perform above you "ability", the body starts pumping DHT
From evolutionary standpoint, sex is always in high priority and the body will always find resources. DHT is just a cheaper way of doing it
Some alpha males can have unlimited sex and still have low DHT, but we -- the deadly ones -- are sufferers of the handicap principle, and have to display our bald head as a sign of bad health/poor sexual provvess, and it is exactly what I see when look at bald people: exhaustion
massa
Banned
- Reaction score
- 28
This is correct, it would be very strange for a man in his twenties to get sexual sides from finasteride. Test is at its peak but then gradually lowers as you reach your thirties and beyond.
bushbush
Established Member
- Reaction score
- 85
Based on what, your personal experience?
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This is a misunderstanding on the handicap principle (which btw. I have not read applied to male pattern baldness in any credible peer-reviewed publication). The theory is individuals can demonstrate that despite having an apparent handicap (such as a bird investing energy in the growth and maintenance of an exceptionally long tail that might hinder flight) it can still survive which therefore acts as an indicator of good genes which is attractive to the opposite sex and under subsequent sexual selection.
- Reaction score
- 1,332
Interesting discussion guys. This study goes well with this all too;
"Genetic Variation in the Human Androgen Receptor Gene Is the Major Determinant of Common Early-Onset Androgenetic Alopecia" - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1226186/?report=reader#RF15
"Genetic Variation in the Human Androgen Receptor Gene Is the Major Determinant of Common Early-Onset Androgenetic Alopecia" - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1226186/?report=reader#RF15