Age, DHT levels, prevalence of balding and oxidative stress

[docj077]

i do not controvert that there is a DHT mediated event before ROS are generated.Cellulaer Stress,mitochondrial stress for example.But i think this would be rather "dispensable",if it would not induce a ROS imbalance. in my opinion,the complete apoptotic causale,which leads to balding over time starts when ROS,and the following apoptotic switches will be induced.I also think that you can interrupt the TGF-beta mediated apoptosis,by applying a liposomal(follicle targeting liposomes) SOD-Catalase mimetic,together whith a a glutathione distributor,....for example.For me,ROS are the most important target,last but not least,cause there are more factors and genes than DHT and or the AR,which will lead to this fatal ROS induced causal.And non mechanic vessel obliteration is also possible due ROS.ROS have indeed biphasic effects on Vessels/angiogenesis,but the wrong outwight,will disrupt angiogenesis,probable due TGF-b oversecretion.


I think you know that ROS inhibitors are often prooven to interact whith negativ factors behind the ROS-for example Procyanidines which can inhibit PKC and TGF-beta.When only one antioxidant like procyanidine is powerfoul enough to induce regrowth and or hairshaft thickening,than this is proove enough for the importance Role of ROS.For me they are no worthless endproduct,respectively no product of important prior apoptotic occurences.

It is quite foolish and quite worthless to target the end result of a molecular pathway long term. Especially, when one can target the original molecular activators of said pathway.

Inhibition of ROS is nice in theory, but in practice it simply does nothing to help hair loss. They slow ROS damage to surrounding tissue, but the damage to the follicles is internal and not mediated by ROS whatsoever. TGF-beta is the factor that initiates the Smad pathway and it's the same molecule that will eventually begin the apoptotic pathway by causing the release of cytochrome C from the mitochondria and activation of the caspase network leading to cellular death. Free radical release is a process that is completely seperate and after the fact. It doesn't matter if you inhibit free radicals if every single follicle in a particular region is being inundated by androgens causing keratinocyte demise through TGF-beta action. Inhibition of ROS won't matter if all the follicles are already in the process of undergoing apoptosis secondary to the action of initiator molecules in the first place.

If you inhibit ROS and that's all you do, then you still leave the cells open to the effects of TGF-beta and TGF-beta will still induce apoptosis and cause perifollicular fibrosis. ROS are not required for TGF-beta release. Only androgens are required. In vitro evidence demonstrates that fact.

 

[tino]

i do not controvert that there is a DHT mediated event before ROS are generated.Cellulaer Stress,mitochondrial stress for example.But i think this would be rather "dispensable",if it would not induce a ROS imbalance. in my opinion,the complete apoptotic causale,which leads to balding over time starts when ROS,and the following apoptotic switches will be induced.I also think that you can interrupt the TGF-beta mediated apoptosis,by applying a liposomal(follicle targeting liposomes) SOD-Catalase mimetic,together whith a a glutathione distributor,....for example.For me,ROS are the most important target,last but not least,cause there are more factors and genes than DHT and or the AR,which will lead to this fatal ROS induced causal.And non mechanic vessel obliteration is also possible due ROS.ROS have indeed biphasic effects on Vessels/angiogenesis,but the wrong outwight,will disrupt angiogenesis,probable due TGF-b oversecretion.


I think you know that ROS inhibitors are often prooven to interact whith negativ factors behind the ROS-for example Procyanidines which can inhibit PKC and TGF-beta.When only one antioxidant like procyanidine is powerfoul enough to induce regrowth and or hairshaft thickening,than this is proove enough for the importance Role of ROS.For me they are no worthless endproduct,respectively no product of important prior apoptotic occurences.

It is quite foolish and quite worthless to target the end result of a molecular pathway long term. Especially, when one can target the original molecular activators of said pathway.

Inhibition of ROS is nice in theory, but in practice it simply does nothing to help hair loss. They slow ROS damage to surrounding tissue, but the damage to the follicles is internal and not mediated by ROS whatsoever. TGF-beta is the factor that initiates the Smad pathway and it's the same molecule that will eventually begin the apoptotic pathway by causing the release of cytochrome C from the mitochondria and activation of the caspase network leading to cellular death. Free radical release is a process that is completely seperate and after the fact. It doesn't matter if you inhibit free radicals if every single follicle in a particular region is being inundated by androgens causing keratinocyte demise through TGF-beta action. Inhibition of ROS won't matter if all the follicles are already in the process of undergoing apoptosis secondary to the action of initiator molecules in the first place.

If you inhibit ROS and that's all you do, then you still leave the cells open to the effects of TGF-beta and TGF-beta will still induce apoptosis and cause perifollicular fibrosis. ROS are not required for TGF-beta release. Only androgens are required. In vitro evidence demonstrates that fact.

citation: Only androgens are required. In vitro evidence demonstrates that fact.
Role of reactive oxygen species (ros) on androgen-inducible tgf-beta1 regulation of dermal papilla cells.
Hyeon Gyeong Yoo, Yong Jung Kang, Se Rah Lee, Hyun Keol Pyo, Oh Sang Kwon, Kyu Han Kim, Hee Chul Eun, Kwang Hyun Cho, Department of Dermatology, Seoul National University, College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital and Institute of Dermatological Science, Seoul National University, Seoul, Korea
Little is known about the roles of androgen on the regulation of redox state in the dermal papilla cells, a cellular process known to profoundly increase with aging. The androgen receptor (AR) has been reported to modulate tgf-beta1/Smad signaling and to be overexpressed in androgen-dependent scalp area of the patients with androgenetic alopecia. The rat vibrissae dermal papilla cell line (DP-6) overexpressed with AR was investigated to evaluate the role of ros on androgen-induced increase of tgf-beta1 secretion. The AR stably-transfected DP-6 cells were incubated with R1881 or dihydrotestosterone (DHT). Flow cytometry and laser scanning confocal microscopy were undergone to measure ros production and ELISA assay to evaluate tgf-beta1 secretion after androgen treatment. tgf-beta1 promoter activity assay was also performed whether to be influenced by pretreatment of ros scavengers. Androgen markedly increased ros generation and the androgen-inducible ros augmented tgf-beta1 secretion from dermal papilla cells. Treatment with ros scavenger or several species of inhibitors decreased ros production and tgf-beta1 expression. Luciferase reporter assays showed suppression of tgf-beta1 promoter signaling by ros scavengers. In conclusion, our study shows for the first time that androgen-induced tgf-beta1 accumulation in dermal papilla cells would be mediated by ros production and prevented by antioxidants or ros inhibitors.





I mean.....i could start to split around whith Studys which comes to the same results...studys in vivo and in vitro,studys on patients whith kidney and heart diseases about fibrotic and apoptotic influences mediated by ros and tgf-beta....but that would cost me much time.The findings of this investigators,were aware to me almost four years ago.I wrote exactly all this on my homepage,long before this investigators found it out.Fred knew it long before too.And dr proctor is a veteran in concerns of male pattern baldness and ROS.



citation:Inhibition of ROS is nice in theory, but in practice it simply does nothing to help hair loss.


And then....why does Procyanidin and Roxythromicin help hair regrowth in the line of male pattern baldness?



Citation: TGF-beta is the factor that initiates the Smad pathway and it's the same molecule that will eventually begin the apoptotic pathway by causing the release of cytochrome C from the mitochondria and activation of the caspase network leading to cellular death.

Yes i know.But why do more that 100 ore more experiments from different cell types show,that such a causale is ROS mediated,and can be blocked by antioxidants?You forgot nf-kb.Why does the antioxidant N-acetylcysteine,help people whith idiopatic pulmonary fibrosis,which is probable mainly tgf-beta induced?


citation: Inhibition of ROS won't matter if all the follicles are already in the process of undergoing apoptosis

Sure it will help-just one more example for their acting.Antioxidants do free the insulin receptor,which has crosstall whith igf-1.Androgenic action induces insulinresistance over ROS .Free this receptors,helps to regenerate shrinked follicles.Insulin and igf-1,makes follikels(miniatur-organes) bigger.The bigger the hair factory follicle,the more vindicative potential he has.

citation:Only androgens are required. In vitro evidence demonstrates that fact.[/quote]


If you mean this relative old japanese studys about androgenes and tgf-beta,then most of this investigators did not investigated a possible ROS influence.Other facts are there up.....the standart of knowledge is changing year for year.And the knowledge of the daily dermatological practice.......is terrible backward-still in j.b hamiltons age.

 

[michael barry]

Tino,

Im one of those old "Hamilton-age" adherents that believes what happens in baldness is utterly and completely based on what happens inside the dermal papilla of individual hairs. Keep in mind, in modern transplants, single hairs are often transplanted to hairlines with mere "slivers" of skin around them---just enough to encompass the sebaceous gland and dermal papilla almost like a "sleeve to an arm". Thats all, no "extraneous skin" is accompanying these grafts--and yet they grow just fine in the new frontal scalp which may have been bald for decades.

Consider pictures of these bald men who now have hair due to transplantation. The new hair will grow for the rest of their lives, or as long as the hair in the wreath does anyway (extreme old age usually),
Note this guy in particular, http://www.bernsteinmedical.com/patient ... s/1061.php
He had obviously been bald a long, long time..........................scalp skin was "old" bald scalp, yet he now has hair growing from it. Here is another man in a similar circumstance, http://www.bernsteinmedical.com/patient ... s/1005.php



Here is a whole page of men, many of whom are in similar circumstances, http://www.bernsteinmedical.com/patient ... /index.php



Although I dont look anything like this man pictured, http://www.bernsteinmedical.com/patient ... s/1051.php, my own hair isn't much better than his. He and I are in a similar circumstance. Ive had success with thickness and darkness with prox-n and finasteride (for the most part, I also use nizoral and a peppermint oil/water mixture), in keeping what Ive had, but havent regrown frontal hair. Thats the boat Im in personally.



Myself aside, you can see why some of us think its what is happening in the papilla---irregardless of the unfortunate oxidative stress to the scalp, that really is making baldness happen. I think the simpleist solution personally is going to be to find something that just blocks or downregulates the androgen receptor. I know that Doctor would like to see countermeasures to the individual dermal papilla negative growth factors like TGF-beta, thrombosponidin, TNF-alpha, FGF-5, DKK-1, be utilized, but they have to be found first. That may take some doing by science though through alot of research. In the near term, I think alpha five inhibition and receptor-inhibition might be the easiest thing we can do until more is known--as clumsy as that may seem to someone who wants it "solved" at the problem level. Counteracting the genes acting in the papilla also seem a ways off to me personally. Im also "scared" of system-wide inhibition of particular pathways like TGF-beta as that might help fight things in the rest of our bodies that might be bad for us in the long term (I wouldn't want some necessary cellular function *stopped cold* in the rest of me just to inhibit it in my hair follicles on the top of my head). You bring up some interesting stuff though..................

BTW---proanthocyandins from apples and barley inhibit TGF-beta topically.

 

[tino]

Tino,

Im one of those old "Hamilton-age" adherents that believes what happens in baldness is utterly and completely based on what happens inside the dermal papilla of individual hairs. Keep in mind, in modern transplants, single hairs are often transplanted to hairlines with mere "slivers" of skin around them---just enough to encompass the sebaceous gland and dermal papilla almost like a "sleeve to an arm". Thats all, no "extraneous skin" is accompanying these grafts--and yet they grow just fine in the new frontal scalp which may have been bald for decades.

Consider pictures of these bald men who now have hair due to transplantation. The new hair will grow for the rest of their lives, or as long as the hair in the wreath does anyway (extreme old age usually),
Note this guy in particular, http://www.bernsteinmedical.com/patient ... s/1061.php
He had obviously been bald a long, long time..........................scalp skin was "old" bald scalp, yet he now has hair growing from it. Here is another man in a similar circumstance, http://www.bernsteinmedical.com/patient ... s/1005.php



Here is a whole page of men, many of whom are in similar circumstances, http://www.bernsteinmedical.com/patient ... /index.php



Although I dont look anything like this man pictured, http://www.bernsteinmedical.com/patient ... s/1051.php, my own hair isn't much better than his. He and I are in a similar circumstance. Ive had success with thickness and darkness with prox-n and finasteride (for the most part, I also use nizoral and a peppermint oil/water mixture), in keeping what Ive had, but havent regrown frontal hair. Thats the boat Im in personally.



Myself aside, you can see why some of us think its what is happening in the papilla---irregardless of the unfortunate oxidative stress to the scalp, that really is making baldness happen. I think the simpleist solution personally is going to be to find something that just blocks or downregulates the androgen receptor. I know that Doctor would like to see countermeasures to the individual dermal papilla negative growth factors like TGF-beta, thrombosponidin, TNF-alpha, FGF-5, DKK-1, be utilized, but they have to be found first. That may take some doing by science though through alot of research. In the near term, I think alpha five inhibition and receptor-inhibition might be the easiest thing we can do until more is known--as clumsy as that may seem to someone who wants it "solved" at the problem level. Counteracting the genes acting in the papilla also seem a ways off to me personally. Im also "scared" of system-wide inhibition of particular pathways like TGF-beta as that might help fight things in the rest of our bodies that might be bad for us in the long term (I wouldn't want some necessary cellular function *stopped cold* in the rest of me just to inhibit it in my hair follicles on the top of my head). You bring up some interesting stuff though..................

BTW---proanthocyandins from apples and barley inhibit TGF-beta topically.

Citation;Im one of those old "Hamilton-age" adherents that believes what happens in baldness is utterly and completely based on what happens inside the dermal papilla of individual hairs. Keep in mind, in modern transplants, single hairs are often transplanted to hairlines with mere "slivers" of skin around them---just enough to encompass the sebaceous gland and dermal papilla almost like a "sleeve to an arm". Thats all, no "extraneous skin" is accompanying these grafts--and yet they grow just fine in the new frontal scalp which may have been bald for decades.

If i understand you right,you will say that the fact that the difference between transplanted grafts from the donor aerea,and dht sensitive frontal parts,speaks for androgenes as mean factor,and that this fact excludes other influences?If you really mean it so,than i say,that the fact,that different parts of the scalp,whith different genetic,do not exclude other influences.To my knowledge,people whith AR CAG-Repeat-Polymorphisms,have carry this defect also in occiptal aereas.Let us assume,that the male pattern baldness,which experts constitute as polygenic,depends on more than one systemic genetical defect.Let us speculate,and take the mineralocorticoid receptor. In fact,there must be some defect locally,concerning parts of the hair follicle,and or the tissue around.It could be an encym which neutralizes in non bald individuals,which are also carrier of systemic unfavourable genetic ,the destructive influences of thir genetics.It could be a defect in the superoxide dismutase releated gen,or something what induces glutathione expression,or something what induces propper expression of catalase.

I dont now exactly what you will say,but the differences of frontal and occiptal scalp parts,do not exclude other non androgenic genes,other triggers,and the influence of ROS.Sure it is absoloutly important to find out the local genetic defects.Maybe they are in the local scalp antioxidative network.Or it is tgf-beta himself.Bcl-2,BAX,and many more.


Hamilton and the difference of different scalp parts,are two differnt shoes.

I never saw a documentation about hamiltons castrated males over years.I even dont saw pictures of them.This story is 50 or 60 years old.When you castrate horses,some of them will get a very poor coat quality.So as if the coat has aged.How quick does castrated male hair age?Castration drops down testosterone,and testosterone keeps the igf-1 high, aromatase converts it to estrogen.,and possibly it supplyes importand anabolic factors to the cells.To be in no accordance to my ROS thinking, i do belive that androgenes induce the strongest influence on hair growth inhibtion,as systemic modulators,in genetic praedisposed individuals.50 or 60 years ago,that is a long time.Epigenetic and environmental influences may made other factors dangerous for our generation.It is hard for me to accept this almost one century old castration studys.They are not scientific valid.I do not belive that a strong liposomal androgen receptor blocker,regenerates shrinked hair follicles more than for example dutasteride or spironolactone.I take both medications,and my hair quality,i mean thickness and darking of lighter hair from insufficient frontal follicles,improved as first due supplementation of different antioxidants.Yes,even there is a still unknown locally defect,you can improve the state of the follicle,over oral regenerating substances.


You are right a little.....supressing a tumor supressor like tgf-beta in the hall system,is maybe dangerous in the long term.But i do not think that we have to do that for such a long time,because i think that a good local solution will be found in the next 7 years.And i dont think,that TGF-beta supression over antioxidants,surpresses this growth factor in a dangerous amount,and maybe it surpresses him just there where he is overexpressed.

 

[tino]

Re: addition

Procyanidines supress tgf-beta and PKC over ROS interception.I dont know if they wold do it oral also propper.I f i remember right,i know a study which schows that the have helped orally in psoriasis

 

[michael barry]

Tino,

Here is a photo of two TWIN SISTERS. One takes testosterone to be like a man, the other doesn't. One is going bald, the other has a full head of hair. They are both female, as the sex change is incomplete at this stage. Look at the picture:
http://www.oprah.com/tows/slide/200509/ ... _106.jhtml



Here is a photo of 2 more female TWINS. One takes testosterone to be like a man, the other is happy as a woman. Look at the picture of the twins, http://www.oprah.com/tows/slide/200509/ ... _102.jhtml



Tino, now look at her UP CLOSE, http://www.oprah.com/tows/slide/200509/ ... _103.jhtml
She is genetically a twin of her sister, yet her face has aged a great deal as well as her hair. Even though she has not lost her hair, its aged and greyed.




I read a study a while back that followed something like 20 women who wanted to be men and took testosterone (hormone therapy). At 13 years, half were going bald in various states of norwood progression from NW3 to NW7. One went horseshoe bald in less than two years.




Tino,
Bear in mind that Norman Orentreich transplanted scalp hair from balding areas, bald areas, and donor areas to other parts of the body many years ago to find out if androgen-related balding truly was all "in the follicle". He found the hair from balding areas continued to go bald, the bald hair did not grow back, and hair from the "donor" area kept on growing.




Tino,
Its ALL in the hair.




Tino,
I have one more question. Did you NOT EVEN LOOK AT THE PICTURES THAT I PROVIDED OF THE MEN WHO HAD TRANSPLANTS that were completely bald beforehand? It completely showed you that the differences are in the hairs themselves, not the skin around them. There is no room for argument at all-none whatsoever. Hair grows fine, even in frontal scalp that has been bald for 30 years, when transplanted from the back.


Did you know that some men actually have their body hair transplanted to the scalp. It grows, but it looks lousy like body hair does---yet sometimes it does grow a little longer. It retains its characteristics however. If it was curly on the body, it will be curly on the scalp. If it was black on the body, it will be black on the scalp. If it was grey on the body, it will be grey on the scalp. If it was kinky on the body, it will be kinky on the scalp. If it was straight on the body, it will be straight on the scalp. The thickness of the hairs remains the same. It does not gain circumference at all. They have actually moved pubic hair to the scalp which looked like.........................drum roll please..............................pubic hair on the scalp.



The genes responsible for baldness are contained in the hairs themselves---period. If you transplant a grey ageing hair from your head to your arm.......................you will have a grey ageing hair on your arm despite the rest of the hair on your arm being brown. Dr. Colin Jahoda moved hair cells of HIS OWN to his then blonde wife's (Amanda Reynolds) arm years ago, resulting in dark hair on her arm. If she had any hair on her arm, it would have been blonde as she was a blonde woman. The surrounding skin and genes therein had nothing to do with it whatsoever.




I hope you noted the ageing that the testosterone brings in the dermis of the picture of the woman in the Oprah Link. Ive posted other pictures of females on testostere before (one of a p**rn star named Buck Angel) who is still a woman in genitalia, but has the aged face of a man now despite the fact that she was a pretty woman just a few years ago with a pretty feminine face. She looks like a truck driver with a big moustache on steroids now and an aged face only a few years later. Androgens age the dermis, badly.

I had a link with many female-to-male transexuals with their pictures but lost it. In that link you could see the quick ageing of skin. The women got to look just like men, even though they still made estrogen in many cases because they had'nt removed ovaries. Many also were going bald in various states of baldness. They all had beard hair that they either shaved or let grow as beards and moustaches. Many had chest hair and arm hair and otherwise looked just like men in their thirties and forties. I knew right then hormones literally determine what we look like sexually. There is no "change" in hair at puberty that damns it forever. If you remove androgens from male hair, they will keep it just like their sisters do. If you add male hormone to the sister, and she has baldness genetics, she will lose her hair just as her brother or father did, usually in the exact same way. Transplant her hair from the sides to the front, and it will grow with the same color and texture as it did up front. Period. End of discussion.

 

[michael barry]

http://www.bernsteinmedical.com/patient ... s/1018.php

http://www.bernsteinmedical.com/patient ... s/1005.php


Again Tino, LOOK AT THE PHOTOS Scalp has been bald for years, yet hair grows just fine there with donor characteristics in color, thickness, wave, etc. when transplanted from the back. All in the hair. End of discussion. Period.

 

[tino]

Tino,

Here is a photo of two TWIN SISTERS. One takes testosterone to be like a man, the other doesn't. One is going bald, the other has a full head of hair. They are both female, as the sex change is incomplete at this stage. Look at the picture:
http://www.oprah.com/tows/slide/200509/ ... _106.jhtml



Here is a photo of 2 more female TWINS. One takes testosterone to be like a man, the other is happy as a woman. Look at the picture of the twins, http://www.oprah.com/tows/slide/200509/ ... _102.jhtml



Tino, now look at her UP CLOSE, http://www.oprah.com/tows/slide/200509/ ... _103.jhtml
She is genetically a twin of her sister, yet her face has aged a great deal as well as her hair. Even though she has not lost her hair, its aged and greyed.




I read a study a while back that followed something like 20 women who wanted to be men and took testosterone (hormone therapy). At 13 years, half were going bald in various states of norwood progression from NW3 to NW7. One went horseshoe bald in less than two years.




Tino,
Bear in mind that Norman Orentreich transplanted scalp hair from balding areas, bald areas, and donor areas to other parts of the body many years ago to find out if androgen-related balding truly was all "in the follicle". He found the hair from balding areas continued to go bald, the bald hair did not grow back, and hair from the "donor" area kept on growing.




Tino,
Its ALL in the hair.




Tino,
I have one more question. Did you NOT EVEN LOOK AT THE PICTURES THAT I PROVIDED OF THE MEN WHO HAD TRANSPLANTS that were completely bald beforehand? It completely showed you that the differences are in the hairs themselves, not the skin around them. There is no room for argument at all-none whatsoever. Hair grows fine, even in frontal scalp that has been bald for 30 years, when transplanted from the back.


Did you know that some men actually have their body hair transplanted to the scalp. It grows, but it looks lousy like body hair does---yet sometimes it does grow a little longer. It retains its characteristics however. If it was curly on the body, it will be curly on the scalp. If it was black on the body, it will be black on the scalp. If it was grey on the body, it will be grey on the scalp. If it was kinky on the body, it will be kinky on the scalp. If it was straight on the body, it will be straight on the scalp. The thickness of the hairs remains the same. It does not gain circumference at all. They have actually moved pubic hair to the scalp which looked like.........................drum roll please..............................pubic hair on the scalp.



The genes responsible for baldness are contained in the hairs themselves---period. If you transplant a grey ageing hair from your head to your arm.......................you will have a grey ageing hair on your arm despite the rest of the hair on your arm being brown. Dr. Colin Jahoda moved hair cells of HIS OWN to his then blonde wife's (Amanda Reynolds) arm years ago, resulting in dark hair on her arm. If she had any hair on her arm, it would have been blonde as she was a blonde woman. The surrounding skin and genes therein had nothing to do with it whatsoever.




I hope you noted the ageing that the testosterone brings in the dermis of the picture of the woman in the Oprah Link. Ive posted other pictures of females on testostere before (one of a p**rn star named Buck Angel) who is still a woman in genitalia, but has the aged face of a man now despite the fact that she was a pretty woman just a few years ago with a pretty feminine face. She looks like a truck driver with a big moustache on steroids now and an aged face only a few years later. Androgens age the dermis, badly.

I had a link with many female-to-male transexuals with their pictures but lost it. In that link you could see the quick ageing of skin. The women got to look just like men, even though they still made estrogen in many cases because they had'nt removed ovaries. Many also were going bald in various states of baldness. They all had beard hair that they either shaved or let grow as beards and moustaches. Many had chest hair and arm hair and otherwise looked just like men in their thirties and forties. I knew right then hormones literally determine what we look like sexually. There is no "change" in hair at puberty that damns it forever. If you remove androgens from male hair, they will keep it just like their sisters do. If you add male hormone to the sister, and she has baldness genetics, she will lose her hair just as her brother or father did, usually in the exact same way. Transplant her hair from the sides to the front, and it will grow with the same color and texture as it did up front. Period. End of discussion.

citation:Tino,
Its ALL in the hair.


You are interesting,....but arduous

Again,i do not negate,that there is a locally defect in the androgen sensitive parts of the scalp skin.But he will lose his scare,when we inhibit systemic or extrinsich influences.On the other hand,the locally defect,will may not do hair follicle damages,despite the existence of unfavourable systemic genetic.when we are able to fight him.

Do you know that it is absoloutly prooven that male pattern baldness candidates habe their AR polymorphysm completly systemic,and not just in the scalp skin?What i dont know is,if ALL individuals who have this systemic defect in the hall system,become male pattern baldness.Do you know some more like me about this haplotype,and his prevalence to male pattern baldness?If every men whit schort CAG-Repeats will develope male pattern baldness,than this would hang a shadow over the importance of the locally defect in the frontal and vertex aerea.

I do not belive that androgenes,especially testosterone forces skin aging in general.It is prooven that men whith higher testosterone and igf-1 levels,live longer than individuals whith lower Testosterone and IGF-1.This study says nothing about the skin,but i think,that testosterone does not influence skin aging,when the aromatase and the igf-1 expression expression runs paralel to testo in a good ratio.If the outwight is ok,testosterone wont force skin aging.Annotation:i do not talk about people whith AR overactivity here.I also dont know which kind of haplotype hamilton has castrated.If he had only twins,where one were bald,then we must assume that he has catched only AR-Polymorphysm haplotypes.So i ask myself,what would happen,when you castrate a male who has a very good outwight of T,Aromatase,IGF-1?What shuld i say to the people ophra winfrey has presented in her show.I dont know their genetics,and you dont know them too.I know that senile hair aging,also body hair goes on whith low tissue testosterone and low tissue aromatase


citation:Andropause is associated with a decrease in lean body mass due to a diminution in muscle volume that also causes a measurable reduction in muscle strength.8,9 There are changes in the skin and hair, typified by the development of hair in ears and nose, a decrease in body hair, and thinning and hyperpigmentation of the skin.10


Fulltext http://www.pubmedcentral.nih.gov/articl ... d=16985938



citation;It completely showed you that the differences are in the hairs themselves, not the skin around them.


Ok,i cant remember that i denined this.I can remember that i wrote maybe the tissue around also.



There are prooven systemic genetic which is bad for hair.Local defects are not prooven,but it is logical,that such factors must exist.I think there are many many candidates.

The problem for me is,that you apparently don know that this systemic AR Polymorphysm the complete system concerns?You said many times,that its all in the hair,although Sawaya,Nieschlag and others prooved the male pattern baldness relevant existence of a AR-Polymorphysms which are expressed in the complete system.And other genes responsible for male pattern baldness,are currently unter investigation in Germany Bonn.Investigated via haemogramm extracted from the arm.

Maybe the problem for you is that you wont understand,that i do not negate an additional local gen defect in the frontal and vertex scalp.






















;

 

[tino]

Re: adittion

many doctors traet skin problems caused by aging in the female whith a mix from testosterone end estrogen.


citationie Behandlung besteht in der Anwendung antiandrogen wirksamer Substanzen wie z. B. Cyproteronacetat, Etonogestrel, Drospirenon, Chlormadinonacetat sowie lokaler östrogenhältiger Mittel zur Unterdrückung der Testosteronwirkung. Sie sind in Form von Injektionen, Tabletten und Cremen, Gelen und Lotionen anwendbar.

Im normalen Unterhautgewebe muss dagegen genügend Testosteron vorhanden sein, damit unter seinem Einfluss die Bindegewebsfasern mit Kreuz- und Querverstrebungen ein Stützgerüst bilden, in dem das Unterhaut-Fett fest verpackt ist.

Bei einem Testosteronmangel der Frau fehlen die Kreuz- und Querverstrebungen und die Fettzellen werden zwischen den Bindegewebsfasern nur senkrecht nebeneinander gepackt und bilden dadurch die Cellulite.

Kneift man in das Gewebe, so erscheint an der Oberfläche die typische Orangenhaut der Cellulite.
Östrogen und Testosteron beeinflussen die Ausbildung jener Zellen, die die Hautoberfläche bilden und für die Hautstruktur verantwortlich sind (Keratinozyten).

Zur Verbesserung der Hautoberfläche und Hautstruktur hat sich eine Kombinationstherapie mit Östrogen und Testosteron bewährt. Dadurch wird die Hautalterung und Faltenbildung und das Dünnerwerden sowie die Altersflecken der Haut verhindert.


http://www.mueller-tyl.at/das-hormon-Telogen Effluvium ... r-frau.htm

http://babelfish.altavista.com/



citation Auch stehen die klinischen Zei-chen der Hautalterung im Zusam-menhang mit den Androgenen.Sie unterliegen neben anderenFaktoren auch endogenen meta-bolischen Einflüssen und unter-scheiden sich von exogen beding-ten Veränderungen. So wirkt sichauf die Kollagenproduktion auchder Androgenmangel negativ aus.Das heißt, neben den Östrogenenhaben auch die Androgene aufdie Kollagenbildung und auf dieEpidermisdicke einen positivenEinfluß, sodaß die Entstehung vonFalten verlangsamt wird


http://www.kup.at/kup/pdf/696.pdf

 

[docj077]

i do not controvert that there is a DHT mediated event before ROS are generated.Cellulaer Stress,mitochondrial stress for example.But i think this would be rather "dispensable",if it would not induce a ROS imbalance. in my opinion,the complete apoptotic causale,which leads to balding over time starts when ROS,and the following apoptotic switches will be induced.I also think that you can interrupt the TGF-beta mediated apoptosis,by applying a liposomal(follicle targeting liposomes) SOD-Catalase mimetic,together whith a a glutathione distributor,....for example.For me,ROS are the most important target,last but not least,cause there are more factors and genes than DHT and or the AR,which will lead to this fatal ROS induced causal.And non mechanic vessel obliteration is also possible due ROS.ROS have indeed biphasic effects on Vessels/angiogenesis,but the wrong outwight,will disrupt angiogenesis,probable due TGF-b oversecretion.


I think you know that ROS inhibitors are often prooven to interact whith negativ factors behind the ROS-for example Procyanidines which can inhibit PKC and TGF-beta.When only one antioxidant like procyanidine is powerfoul enough to induce regrowth and or hairshaft thickening,than this is proove enough for the importance Role of ROS.For me they are no worthless endproduct,respectively no product of important prior apoptotic occurences.

citation:Inhibition of ROS is nice in theory, but in practice it simply does nothing to help hair loss.


And then....why does Procyanidin and Roxythromicin help hair regrowth in the line of male pattern baldness?



Citation: TGF-beta is the factor that initiates the Smad pathway and it's the same molecule that will eventually begin the apoptotic pathway by causing the release of cytochrome C from the mitochondria and activation of the caspase network leading to cellular death.

Yes i know.But why do more that 100 ore more experiments from different cell types show,that such a causale is ROS mediated,and can be blocked by antioxidants?You forgot nf-kb.Why does the antioxidant N-acetylcysteine,help people whith idiopatic pulmonary fibrosis,which is probable mainly tgf-beta induced?

The problem is that antioxidants used alone to reverse fibrosis have never shown a significant effect. N-acetylcysteine is an example of such a compound. It is typically combined with a regimen including prednisone and azathioprine in order for it to work to even maintain a particular level of fibrosis. I've never read literature that suggests that upregulation of glutathione reductase using antioxidants like N-acetylcysteine causes significant reversal of fibrosis in any organ system. I've only read about maintenance and reduce progression. On the other hand, inhibition of TGF-beta using antibodies against the molecule have demonstrated reversal of fibrosis in both liver and kidney, as well as, demonstrating resumed growth of hair follicles in vitro.

In order for your "cure" to work, it has to demonstrate reversal of the process and not maintenance. Maintenance doesn't cause hair growth. The only way to do that is to prevent the activities of molecules like TGF-beta and TNF-alpha as inhibition of PKC is not an incredibly good idea long term. You need a molecule that completely inhibits the downstream actions of TGF-beta in the dermal papillae, keratinocytes, and dermal fibroblasts. Anti-oxidants won't give you that effect.

 

[michael barry]

I guess this is where I (again) point out that Bryan Shelton has a study whereby a man who had been bald for something like 30 years who went on internal spironolactone therapy for cirhosis started regrowing hair all over his bald scalp after six years on the internal receptor blocker.

He no doubt would have had alot of fibrosis, but the hair minus androgen uptake apparently was able to overcome that.





Doctor, does TGF-beta cause apoptosis of any particular follicle cell population, or does it merely inhibit cell division and arrest cell cycles? Which cells does it kill if it indeed does killl cells. We know DKK-1 kills some keratinocyte cells, and that the first inflammation seen in baldness is at the infidulum which I think is interesting.




Look at this video of Buck Angel Tino and Doctor. You will see pictures of her over her shoulder in this three minute interview. She had beautiful skin and hair when she was not taking testosterone, but now has an aged face of a male, replete with a beard. She was pretty once, now she looks like a truck driver. Its a three minute video. It says it all about testosterone in my opinion. http://www.youtube.com/watch?v=bn745EQh8iU

 

[tino]

quote="docj077"]

i do not controvert that there is a DHT mediated event before ROS are generated.Cellulaer Stress,mitochondrial stress for example.But i think this would be rather "dispensable",if it would not induce a ROS imbalance. in my opinion,the complete apoptotic causale,which leads to balding over time starts when ROS,and the following apoptotic switches will be induced.I also think that you can interrupt the TGF-beta mediated apoptosis,by applying a liposomal(follicle targeting liposomes) SOD-Catalase mimetic,together whith a a glutathione distributor,....for example.For me,ROS are the most important target,last but not least,cause there are more factors and genes than DHT and or the AR,which will lead to this fatal ROS induced causal.And non mechanic vessel obliteration is also possible due ROS.ROS have indeed biphasic effects on Vessels/angiogenesis,but the wrong outwight,will disrupt angiogenesis,probable due TGF-b oversecretion.


I think you know that ROS inhibitors are often prooven to interact whith negativ factors behind the ROS-for example Procyanidines which can inhibit PKC and TGF-beta.When only one antioxidant like procyanidine is powerfoul enough to induce regrowth and or hairshaft thickening,than this is proove enough for the importance Role of ROS.For me they are no worthless endproduct,respectively no product of important prior apoptotic occurences.

citation:Inhibition of ROS is nice in theory, but in practice it simply does nothing to help hair loss.


And then....why does Procyanidin and Roxythromicin help hair regrowth in the line of male pattern baldness?



Citation: TGF-beta is the factor that initiates the Smad pathway and it's the same molecule that will eventually begin the apoptotic pathway by causing the release of cytochrome C from the mitochondria and activation of the caspase network leading to cellular death.

Yes i know.But why do more that 100 ore more experiments from different cell types show,that such a causale is ROS mediated,and can be blocked by antioxidants?You forgot nf-kb.Why does the antioxidant N-acetylcysteine,help people whith idiopatic pulmonary fibrosis,which is probable mainly tgf-beta induced?

The problem is that antioxidants used alone to reverse fibrosis have never shown a significant effect. N-acetylcysteine is an example of such a compound. It is typically combined with a regimen including prednisone and azathioprine in order for it to work to even maintain a particular level of fibrosis. I've never read literature that suggests that upregulation of glutathione reductase using antioxidants like N-acetylcysteine causes significant reversal of fibrosis in any organ system. I've only read about maintenance and reduce progression. On the other hand, inhibition of TGF-beta using antibodies against the molecule have demonstrated reversal of fibrosis in both liver and kidney, as well as, demonstrating resumed growth of hair follicles in vitro.

In order for your "cure" to work, it has to demonstrate reversal of the process and not maintenance. Maintenance doesn't cause hair growth. The only way to do that is to prevent the activities of molecules like TGF-beta and TNF-alpha as inhibition of PKC is not an incredibly good idea long term. You need a molecule that completely inhibits the downstream actions of TGF-beta in the dermal papillae, keratinocytes, and dermal fibroblasts. Anti-oxidants won't give you that effect.[/quote]



Citation;The problem is that antioxidants used alone to reverse fibrosis have never shown a significant effect. N-acetylcysteine is an example of such a compound. It is typically combined with a regimen including prednisone and azathioprine in order for it to work to even maintain a particular level of fibrosis

Right.

I also dont belive that NAC alone,works wonder for Tgf-beta inhibition and Fibrosis.But unfortunately we have no TGF-beta antibodys,and no other tgf-beta inhibitor which works significant satisfactorily.So NAC and other antioxidants,are momentary the best solution to fight additional against the multifactorial induced bad tgf-beta influence.My thoughts why the combination Cortisone,Azathiprine and NAC,worked better than Cortisone and Azathiorine alone.Loung fibrosis,a autoimmune disorder,is partially TGF-beta dependet.NAC alone faild to slow the progression of this disease.When somone is very sick,and he has to go to the intensive care,his cells cant always absorb micronutrients,because of serve cellulaer inflammation.The system has something more important to do,than absorb foreign substances.Cortisol and Azathiorine,workd against the immunologig inflammatory systemic inducers of the fibrosing tgf-beta in idiopathic loung fibrosis.So the target cells,could absorb NAC,and build up a tgf-beta arrestive glutathione depot whitout beeing under fire.I Think that this event is assignable to male pattern baldness.As first you have to free the cells from DHT Attack fire.Than the cells can restore glutathione,which will help antagonize TGF-beta signals.Just one of the working pricipals of this thiol-antioxidant.Here in Germany we have a product named Priorin.It is prooven to help a little in relative big studys whith fpb and CTE Women.His mean substance of content is Cystine.Cystine makes the same like NAC,but it is much weaker.

citation: Anti-oxidants won't give you that effect

How can you be so sure?

Reserve fibrosis is very very hard,but prevent further fibrosis,is possible

by the way
http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum



http://www.blackwell-synergy.com/doi/pd ... .tb00297.x


http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum


What do you mean whit downstraem pathways?SMAD Pathways,and Caspases? To my knowledge it does interact whith the downstream signal pathways.Somewhere there is a study which prooves that NAC also inhibits the serum TNF-alpha in older individuals.But i think tnf-alpha inhibition in the long term and generally is not goot,because it is a double edged sword.Tnf-alpha inhibitors can dysregulate the hair cycle,and this can cause hair loss.I discused that whith Prof Paus from Hamburg,and he said that Tnf-alpha inhibition is not one of his favourite goals.To my knowledge,is only non selective PKC inhibition wrong in the line of curing hair diseases.

But people must be carefoul....its better to stabilize the complete antioxidative network,because working only on one construction side,can disrupt the antioxidant outwight.


If maintenance helps regrowth or not....neither you,and neither me can say that for sure.Look around you,almost noone here and on german boards is pleased whith his regimen.Most of them were glad when they coult prevent further hair loss.Maintenance is realistic,and mantenance must be practiced propper and the appendages must be multiple.

 

[tino]

I guess this is where I (again) point out that Bryan Shelton has a study whereby a man who had been bald for something like 30 years who went on internal spironolactone therapy for cirhosis started regrowing hair all over his bald scalp after six years on the internal receptor blocker.

He no doubt would have had alot of fibrosis, but the hair minus androgen uptake apparently was able to overcome that.





Doctor, does TGF-beta cause apoptosis of any particular follicle cell population, or does it merely inhibit cell division and arrest cell cycles? Which cells does it kill if it indeed does killl cells. We know DKK-1 kills some keratinocyte cells, and that the first inflammation seen in baldness is at the infidulum which I think is interesting.




Look at this video of Buck Angel Tino and Doctor. You will see pictures of her over her shoulder in this three minute interview. She had beautiful skin and hair when she was not taking testosterone, but now has an aged face of a male, replete with a beard. She was pretty once, now she looks like a truck driver. Its a three minute video. It says it all about testosterone in my opinion. http://www.youtube.com/watch?v=bn745EQh8iU

citation: guess this is where I (again) point out that Bryan Shelton has a study whereby a man who had been bald for something like 30 years who went on internal spironolactone therapy for cirhosis started regrowing hair all over his bald scalp after six years on the internal receptor blocker.

He no doubt would have had alot of fibrosis, but the hair minus androgen uptake apparently was able to overcome that.


This study is very interesting.One of the reasons why i choose spironolactone.But there is a catch.People whith liver cirrhosis have a disturbed estrogen degradation.So we must assume,that spironolactone induced this very phaenomenal regrowth process synergetic whith estrogen,which is well known als antifibrotic agent.For example it prevents kidney fibrosis in women-men tend more to kidney fibrosis in the line of some kidney diseases.


http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum


And professor paus prooved that estrogen inhibits tgf-beta in male frontal scalp skin.


I dont have the full text,can someone send it to me if he has it?Are there pictures of the regrowth hairs?




How can you say that everything depends on Androgenes...tsssssss?What about the finasteride non responders which have almost normal lenght cag repeats? i ll wagger when you castate him,his male pattern baldness will go on.Maybe a little slower,but the process will go on.There are more genes than the androgen receptor,or the 5-a-r gen.Not every female to male patient develops male pattern baldness-i have some acquaintance who made this change,and have hair more than horses.It all depends on genetic,the same for testosterone mediated skin aging.And still....the question is if testosterone himself,and not just dht can cause skin aging.Testosterone,a very important steroid makes good things,it changes to skin protecting estrogen via aromatase,and it keeps the skin protecting igf-1 high.

 

[docj077]

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum


And professor paus prooved that estrogen inhibits tgf-beta in male frontal scalp skin.


I dont have the full text,can someone send it to me if he has it?Are there pictures of the regrowth hairs?




How can you say that everything depends on Androgenes...tsssssss?What about the finasteride non responders which have almost normal lenght cag repeats? i ll wagger when you castate him,his male pattern baldness will go on.Maybe a little slower,but the process will go on.There are more genes than the androgen receptor,or the 5-a-r gen.Not every female to male patient develops male pattern baldness-i have some acquaintance who made this change,and have hair more than horses.It all depends on genetic,the same for testosterone mediated skin aging.And still....the question is if testosterone himself,and not just dht can cause skin aging.Testosterone,a very important steroid makes good things,it changes to skin protecting estrogen via aromatase,and it keeps the skin protecting igf-1 high.

This is exactly why I'm questioning your scientific principles. You say that spironolactone worked in a patient (which by the way it has worked for numerous people here internally without any cirrhosis whatsoever) with liver cirrhosis only because of its ability to inhibit androgen action while working synergistically with estrogen to overcome the actions of TGF-beta. Understandably, it is quite likely that were synergistic in action, but we don't know the degree of cirrhosis or how much estrogen metablism was truly inhibited. Making such conclusions without a full case report is, in my opinion, futile. With complete inhibition of androgen receptor action using spironolactone, there is no reason for any process to occur and no need for the effects of estrogen when it comes to maintainence of hair growth and density. However, the effects of estrogen are obviously beneficial, which is something that all the people using aromatase inhibitors on this site still haven't figured out even though we've had discussion after discussion about it.

As for finasteride non-responders, I think that you need to get caught up when it comes to the receptor defects that cause hair loss. Previous studies have demonstrated that a triplet repeat mutation was to blame, but more recent studies have eliminated that as a possibility. Single nucleotide mutations are far more likely. The likely key to those that use finasteride and don't respond can probably be found within their estrogen metablism systems within the skin, as well as, the feedback mechanisms that control testosterone production. Estrogen is obviously required for healthy skin and the maintainence of healthy hair, but now you're shifting your argument. Which is it? Inhibition of ROS, inhibition of androgen action, or an increased estrogen response that you believe to be the most beneficial. Targeting the last two make the first one a null point. Targeting the first one will have no significant effect on hair regrowth and maintainence. The studies using only n-acetylcysteine clearly demonstrate that ROS inhibitors must be used with other products in order for there to be a beneficial outcome with fibrosis.

 

[tino]

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum


And professor paus prooved that estrogen inhibits tgf-beta in male frontal scalp skin.


I dont have the full text,can someone send it to me if he has it?Are there pictures of the regrowth hairs?




How can you say that everything depends on Androgenes...tsssssss?What about the finasteride non responders which have almost normal lenght cag repeats? i ll wagger when you castate him,his male pattern baldness will go on.Maybe a little slower,but the process will go on.There are more genes than the androgen receptor,or the 5-a-r gen.Not every female to male patient develops male pattern baldness-i have some acquaintance who made this change,and have hair more than horses.It all depends on genetic,the same for testosterone mediated skin aging.And still....the question is if testosterone himself,and not just dht can cause skin aging.Testosterone,a very important steroid makes good things,it changes to skin protecting estrogen via aromatase,and it keeps the skin protecting igf-1 high.

This is exactly why I'm questioning your scientific principles. You say that spironolactone worked in a patient (which by the way it has worked for numerous people here internally without any cirrhosis whatsoever) with liver cirrhosis only because of its ability to inhibit androgen action while working synergistically with estrogen to overcome the actions of TGF-beta. Understandably, it is quite likely that were synergistic in action, but we don't know the degree of cirrhosis or how much estrogen metablism was truly inhibited. Making such conclusions without a full case report is, in my opinion, futile. With complete inhibition of androgen receptor action using spironolactone, there is no reason for any process to occur and no need for the effects of estrogen when it comes to maintainence of hair growth and density. However, the effects of estrogen are obviously beneficial, which is something that all the people using aromatase inhibitors on this site still haven't figured out even though we've had discussion after discussion about it.

As for finasteride non-responders, I think that you need to get caught up when it comes to the receptor defects that cause hair loss. Previous studies have demonstrated that a triplet repeat mutation was to blame, but more recent studies have eliminated that as a possibility. Single nucleotide mutations are far more likely. The likely key to those that use finasteride and don't respond can probably be found within their estrogen metablism systems within the skin, as well as, the feedback mechanisms that control testosterone production. Estrogen is obviously required for healthy skin and the maintainence of healthy hair, but now you're shifting your argument. Which is it? Inhibition of ROS, inhibition of androgen action, or an increased estrogen response that you believe to be the most beneficial. Targeting the last two make the first one a null point. Targeting the first one will have no significant effect on hair regrowth and maintainence. The studies using only n-acetylcysteine clearly demonstrate that ROS inhibitors must be used with other products in order for there to be a beneficial outcome with fibrosis.

citation:This is exactly why I'm questioning your scientific principles. You say that spironolactone worked in a patient (which by the way it has worked for numerous people here internally without any cirrhosis whatsoever) with liver cirrhosis only because of its ability to inhibit androgen action while working synergistically with estrogen to overcome the actions of TGF-beta. Understandably, it is quite likely that were synergistic in action, but we don't know the degree of cirrhosis or how much estrogen metablism was truly inhibited. Making such conclusions without a full case report is, in my opinion, futile. With complete inhibition of androgen receptor action using spironolactone, there is no reason for any process to occur and no need for the effects of estrogen when it comes to maintainence of hair growth and density. However, the effects of estrogen are obviously beneficial, which is something that all the people using aromatase inhibitors on this site still haven't figured out even though we've had discussion after discussion about it.


Why should i belive credent that only spironolactone brings hair back to a men who were bald since 30 years?The first point is,that i know,that men whith liver cirrhosis,grow back frontal hairline,and decrease belly hair in many cases.The cause is the disturbed estrogen degradation.The second point is,that i never read such a story on any board,and i never read it in big studys about PCO-S women whith androgenic hair loss,respectively,it didn t worked fore those women.Even flutamide was not the heavenly solution for them.Even castration cant do such an effect.But this is another story,....castrated men have not so much Estrogen too.I think that i can draw such a conclusion cautious without reading the full report.I did not said that im absoloutly sure,but it suggest sn the other hand....i hope i be mistaken,because me myself uses spironolactone AND Dutasteride for more than four years.Maybe i chance to a young monkey in some years;-)I know endocrinolists who take estrogen orally for health and anti aging.They reported increased body hair too.Thats possibly due igf-1 and insulin receptor multiplication.One part of the multiple working principle.Do you think that men whith genetic modulated week aromatase activity,respond so well to spironolactone like a men with good genetic modulated aromatase?This spironolactone responder was 60 years old,or not?Its very hard to regrowth scalp hair in this age class-and he was actually very bald.Male in that age class,a age where the senile involutionsalopecia starts too, have demonstrable a very week aromatase activity in the scalp skin,and mostly week Serum IGF-1.Estrogen or good aromatase activity additional to antiandrogen treatment makes regrowth in such men more realistic.Unless im mistaken,he regrowth the hair first after 6 years of Spironolactone. I dont know exactly how old the oldest finasteride responder were.Bit if i remember right,the regrew hair after one or two years.So it could be so,that his existing liver cirhosis,arised in the progression over the 6 or more years of disease,and that the regrowth set first in at a point,where the disturbed estrogen degradation was in a very high stage.even the autors callenged that this was a spironolactone effect.



citation: Previous studies have demonstrated that a triplet repeat mutation was to blame, but more recent studies have eliminated that as a possibility.

considering the excellent evidence,i think we can not negate that many men whith male pattern baldness have a cag repeat mutation.More study ore one or two studys have tryed to eliminate that possibillity?



citation;The likely key to those that use finasteride and don't respond can probably be found within their estrogen metablism systems within the skin,

but couriously....the non responders had longer repeats.If you mean that the non responders did not respond because of weeker estrogen metabolism in the skin.....maybe.Hmmm...men whith shorter repeats have as a rule,fewer serum estrogen.Men whith longer repeats,have as a rule,a good aromatase activity.But that concerns the serum,and not the tissue metabolism.


citation:Which is it? Inhibition of ROS, inhibition of androgen action, or an increased estrogen response that you believe to be the most beneficial.


as a matter of course,...all together.I do it this way to.Reasonably is the way over genetic analysis for both sexual hormone genes....but hmmmmmm i dont know .Antioxidants are never bad for men,because men have a weeker antioxidant capacity than women.

 

[docj077]

Too many hypotheticals and not enough pure science.

 

[michael barry]

No. 1--

If this

And professor paus prooved that estrogen inhibits tgf-beta in male frontal scalp skin.

, is true, then something that mimics estrogen locally (lavendar, etc.) might be very very good for baldness.



No. 2--

I feel like Im on Mars on discussion boards sometimes. I show two pictures (and ONE VIDEO) of formerly feminine women who took testosterone and now look like older, wrinkling men just a few years later. One has a TWIN sister to compare herself to so the difference is huge. Same human being, wrinkles, grey hair, thinning hair, baldness. Whats different? Testosterone injections. I suppose by that logic when topical fluridil is used to get rid of moustaches, Tino would argue that it might be the alcohol actually getting rid of the moustache hair and not the receptor blocker. Its amazing how far people will go to find an alternative baldness theory, just ignoring the work of giants like Stenn and Uno. FACT--WE know that if you deprive body hair of androgen, it will eventually become vellus hair. It needs androgen to grow. Therefore why in the hell would scalp hair be any different as the opposite?



If I didnt know better, Id' swear "Tino" was Armando. The way he just ignores the evidene put before him, doesn't answer anything directly, "throws away" the work of Hamilton because it invalidates his theory. Its amazing. "They" think alike.




Did either of you two even look at "Buck Angel" back when she was a pretty female by the way? It really is amazing to see what androgens can do.




And again, before I forget, men who get transplants right up front in the middle of firbosis city, see the donor hair retain its color and characteristics for the rest of their lives. The collagen does not effect it. As Kevin McElwee, cloning researcher and hair expert has stated, for healthy hairs, collagen is no problem. They simply secrete substances (enzymes) that eat though it to make space for anagen enlargement. And he is right of course.

 

[tino]

Re: to Doctor and michael

Too many hypotheticals and not enough pure science.

i have evidences for everything i say,respectivley i can confirm everything i write here.The art is to put the puzzle reasonable together.

When i write that men with longer CAG Repeats have higher estrogen,than it is not so that a sparrow whispered them in my ears.

The androgen receptor gene CAG polymorphism is associated with the severity of coronary artery disease in men.
Clin Endocrinol (Oxf). 2003 Dec;59(6):749-55.


And Michael,Stenn is one of my favourite author.He works often together whith ralf paus,my absoloute favourite investigator.The most things i have learned,i learned from him.If you really know stenn and also paus works,than you must know how multifactorial and multiple treatable they see hair diseases inclusive male pattern baldness.Both are less than androgene and antiandrogene fixed.Both talk about differnt possibilitis to prolong the anagen phase in the line of all hair diseases,because the fact that apoptosis occurs in premature catagen,speaks strongly for great benifits when anagen phase will be prolonged. Another big international working giant is ralph trueb from switzerland.Especially he writes much about other influences than androgenes,and the role of oxidative stress.

And where is the gigantism in Uno?A giant because he investigated RU in some stump tailed macacques,some years ago?


citation:I feel like Im on Mars on discussion boards sometimes. I show two pictures (and ONE VIDEO) of formerly feminine women who took testosterone and now look like older, wrinkling men just a few years later. One has a TWIN sister to compare herself to so the difference is huge. Same human being, wrinkles, grey hair, thinning hair, baldness. Whats different? Testosterone injections. I suppose by that logic when topical fluridil is used to get rid of moustaches, Tino would argue that it might be the alcohol actually getting rid of the moustache hair and not the receptor blocker. Its amazing how far people will go to find an alternative baldness theory, just ignoring the work of giants like Stenn and Uno. FACT--WE know that if you deprive body hair of androgen, it will eventually become vellus hair. It needs androgen to grow. Therefore why in the hell would scalp hair be any different as the opposite?


I Think Not every female to male will get an significant aged skin due androgen injection.Females to male i know,have absoulutly no male pattern baldness.And if i not mistake,only 50 percent of female to male transsexuals developed fpb in studys.And if it should be so....think about the Fact,that a female organism-including the skin as biggest organ,is possibly not appointed for so much testosterone.

What about using fluridil to get rid of moustaches?Sorry...english is not my first language,and it is sometimes hard for me to differ ironie from seriousness.Or do i have a gap in education here,and there are really investigations about such a procedure?Do people here on this board really respond well to fluridil?


citation: FACT--WE know that if you deprive body hair of androgen, it will eventually become vellus hair. It needs androgen to grow. Therefore why in the hell would scalp hair be any different as the opposite?


I can just theorize about factors responsible for that difference.It could be so,that beard hair has enough antioxidative capacity to dispose the testosterone to induce growth factors.Or they dont have a genetic so strong expression of antiapoptotic,or apoptotic proteines from the bcl-2 or BAX Family for example.Possibly,if nature would not be afraid that the scalp skin,the protecting scarf of the brain,is season dependet under uv influence,she would had it arranged so that the growth factor and tumor supressor tgf-beta(a growth factor which helps also to generate the hair follicle anlage in the embryonal phase),helps keep hair in the growth phase.Remember that skin cancer fragile pheomelanin individuals,tend more to male pattern baldness.I think there was some investigations about that some time ago.I remember that there was a little difference in antiapoptotic proteines between frontal and occiptal parts of the scalp skin.But noone knows naturs thoughts about that.


Im no expert for hair transplants.I only remember a study,which schows that male pattern baldness whith fibrosis is harder to traet than male pattern baldness whithout fibrosis.The exact role,respectively the pathogen role of fibrosis,is still not exactly cleared.Latest investigations showed that also finasteride works antifibrotic over tgf-beta inhibition.


citation;They simply secrete substances (enzymes) that eat though it to make space for anagen enlargement.

yes,in the line of transplantation....follicles from non androgen sensitive parts secrete that encymes.The donor aera includes the back of the scalp.....and this parts do age too in some individuals.Some older men,have only a few hairs on the lower end of the backside.

 

[tino]

Re: Adittion

citation; Its amazing how far people will go to find an alternative baldness theory


alternative baldness theory is the wrong defination for my work.I just show hair aging as integrated process,which includes extrinsic genetic triggers,so called male pattern baldness and hair graying.

 

[docj077]

Re: to Doctor and michael

Too many hypotheticals and not enough pure science.

i have evidences for everything i say,respectivley i can confirm everything i write here.The art is to put the puzzle reasonable together.

This is something that neither you or I are qualified to do. You can't put a puzzle together if you don't have all the pieces. Besides, pretty much every single study that we have for male pattern baldness is involves a small sample that is rarely representative of the entire population of balding men. Large, double blind studies are needed combined with large retrospective studies analyzing the laboratory work of those with hair loss.

When it comes to research in male pattern baldness, it seems as though the Japanese are moving in the right direction. Unfortunately, any studies that look at animals instead of humans during the experimentation phase are pretty much worthless to us (the recent study looking at different types of tea is an excellent example). Numerous drugs including herbal compounds demonstrate a profound effect on hair growth in murine and other models. In humans, this is not always the case.


If you truly believe what you say, then you'll be able to answer these two questions:

1. If ROS are to blame for hair loss, then why aren't all potentially androgen affected tissues involved? If it's not purely in the genes, then the glutathione reductase and SOD systems should be essentially shut down in numerous tissues including the rest of the skin of the body, the muscles, the lymphatics, blood vessels, genitals, etc., etc. All of those tissues should be fibrosed, as well, as they have androgen receptors and respond to androgens.

2. If the glutathione reductase and SOD systems are affected, then why aren't every single male or female with male pattern baldness suffering from severe folliculitis and contant catalase positive organism infection of the scalp? Those systems are required for the respiratory burst and the death of staph. bacteria. More and more balding men would end up staph infections that turn out systemic. That is not the case. The elevation in sebum production that often accompanies male pattern baldness would be the perfect breeding ground for these organisms, so tell me why are they not more prevalent? They have perfect conditions if your theory is true.

I await your answers.