Age, DHT levels, prevalence of balding and oxidative stress

[CCS]

Topical application of vitamin C would likely be incredibly detrimental to hair loss long term. It would simply lead to more fibrosis as increased vitamin C locally will lead to increased collagen production.
...
DHT causes TGF-beta production, which leads to increased collagen production by dermal fibroblasts and perifollicular fibrosis. The fibrosis causes vessel obliteration reducing nutrient supply to the dermal papillae which will lead to hypoxic follicles.

Doctor, I'm thinking of putting alpha lipoic acid and ascorbyl palmitate in my body wash. Do you think that would age my body skin faster?

 

[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.

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.

citation;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.


Sure,i cant puzzle the hall truth together.I still haven t all the puzzle pieces.But i puzzled so far that i knew hair biologic processes long before other investigators deduced them from other systemic events to the hair follicle.What i told people years ago,its now proven and under investigation under condition of the same thoughts like mine.A good,...and ONLY good researchers deduces hair follicle releated events,from other events releated to other organs.Only over this way you will learn the secrets of the hair follicle and metabolism.Hair biologie is a very young science-other organes and appendant metabolisms are much better explored.I think i have puzzled so far,that it i can help much more than a dermatologist,who is dependet on his pharmareferends arguments,and conservative further educations,which tell him,that the stand of knowledge is that dihydrotestosterone shrinks the follicle,over unknown mechanisms,or that zinc or iron deficiencies additional to male pattern baldness,induce only diffuse hair loss.


citation;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.

lol.....you,me and all others here are completly bald if we would wait for Studys you want.There are enough ideas,but the industrie thinks,that for example procianydine thicks hair a little,why should we bring such a product on the market,where still there is minoxidil,which works stronger.They do not think about additional effects,respectivley synergetic interplay whit products of other pharmaconcerns.I talked whith many of them......i dont want to sound arrogant,but they are no discussion partner for me.

We people here have no other choice than using our knowledge to help ourselfs.And we have to go on a mission whith that attitude.We ourselfs must test arguable substances,topically or oral.Waiting like sheeps for something that may come,is the death for our follicles.And the more vital a follicle is,the better he is regenerable.....if there really will be something in 5 or 6 years.


citation;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.

As first.....substances which worked in animals,and failed in humans,can only called failures,when the investigators, used a DNA-Flowcytometrie,to mess a changed proliferationsactivity during the treatment phase.Further and additive useful messmethodes are messing of hair shaft diameter by trichoscan.A trichogramm says nothing,a trichoscan without messing the hair shaft diameter says also nothing.Same for hair count.Changed hair shaft diameter which showes changed size of the follicle,and or proliferative s-phase activity,says that there goes something on,what shows that the substance can work.at least additive to other.Many studys in humans which so called failure may not failed,because the messmethodes were unusable.

i also think that japanese move i a very right direction.Very good resaerchers.


citation;If ROS are to blame for hair loss, then why aren't all potentially androgen affected tissues involved?

who says that it isnt so?Isn t it possible,that other androgen affected tissues have better defense mechanisms against upregulated ROS,or that ROS do upregulate the strong expressed antioxidative encymes there-sperm production for example?Or DHT induces ROS there were they are needed for other duties?Myogenesys for example needs Inflammation and growth factors together to work.Tumor supression needs ROS.DHT starts when the childhood ends,it takes things the adult men dont need anymore(like strong IGF-1 expression for growth lenght),and assitst functions important for adult people,for example spermatogenesis for reproduction.Ros,and ROS induced inflammation do not always do bad things.It is all tissue specific.Why should the system be so silly and fibrose everything?In the line of some diseases,it does that.Also in partial androgen mediated/gender specific diseaes,like heart disease(myocard fibrosis),or some kidney diseases.But its not only Androgenes who do fibrosis-the next male pattern baldness gen candidat the mineralocorticoid receptor,and his friend Aldosterone,do the same i a double edged way.



citation;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.

How do you come to such an idea??I never heard something like that,and a quick research,did not told me that catalase or SOD releated polymorphisms are releated to such events.Maybe there is a little case report.......but this is no proove for the commones of such events.Melatonin deficiencies make decreased skin antioxidant activity,and many deficiencies too.Also there is no such a relationship.But the theory is interesting.me,for instance do think that itching and seborrheic dermatitis in the line of male pattern baldness and pco-s are possible mediated by inflammation induced by a redox imbalance.Did you know that sebum is rich in antioxidative Vitamines like Vitamin E?It delivers it.The antioxidative network of the system and skin is big.When one policeman will get attacked,others do help to fight the enemy.Sometimes not even all together can fight the enemy,and sometimes ROS themself are killing life-threatening factors.Wasnt it so that somewhere there is a theory which says,that balding is a evolutionaery relict,which had his roots in keeping bacteria away from the scalp skin?Maybe thats why ROS are stronger expressed there

 

[docj077]

Re: to Doctor and michael

citation;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.

How do you come to such an idea??I never heard something like that,and a quick research,did not told me that catalase or SOD releated polymorphisms are releated to such events.Maybe there is a little case report.......but this is no proove for the commones of such events.Melatonin deficiencies make decreased skin antioxidant activity,and many deficiencies too.Also there is no such a relationship.But the theory is interesting.me,for instance do think that itching and seborrheic dermatitis in the line of male pattern baldness and pco-s are possible mediated by inflammation induced by a redox imbalance.Did you know that sebum is rich in antioxidative Vitamines like Vitamin E?It delivers it.The antioxidative network of the system and skin is big.When one policeman will get attacked,others do help to fight the enemy.Sometimes not even all together can fight the enemy,and sometimes ROS themself are killing life-threatening factors.Wasnt it so that somewhere there is a theory which says,that balding is a evolutionaery relict,which had his roots in keeping bacteria away from the scalp skin?Maybe thats why ROS are stronger expressed there

Well, everything you posted before this was rather arrogant and believing that you're the only one that is capable of putting hair loss puzzle pieces together makes you not only arrogant, but lacking in humility, as well.

You have two diseases that you need to read up on. One is Chronic granulomatous disease. The other is Myeloperoxidase deficiency.

You also need to do some research regarding cytokine activity (TGF-beta in particular) in the presence of inflammation.

 

[michael barry]

Tino wrote:

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.

Im out and out laughing at this response Tino. Of COURSE ONLY FIFTY PERCENT OF WOMEN BALD WHEN GIVEN ANDROGENS, THEY ARE JUST LIKE THEIR BROTHERS. NOT ALL MEN BALD. ONLY ABOUT HALF DO IN MIDDLE AGE EXHIBIT HAIR LOSS. Ive seen MANY pictures of women who took testsoterone, but unfortunately lost the link that had them. About thirty percent or a little more than that were balding. Nobody was over about fifty. Just think, they have estrogens still in many cases because they all didn't get their ovaries removed. Even though they had some estrogen binding with androgen receptors, they were still balding. Most all had "aged" and "unfeminine" skin. They had beards or had to shave and you could see the "shadow" where they had to shave




You (Tino) mentioned Fluridil. Ive seen a study (no Im not going to look it up for you) that had pictures of a woman who used fluridil on her unfortunate moustache. It pretty much got rid of the moustache. The fluridil was judged by the team of investigators conducting the study as a worthy treatment for hirsutism in females.



My "problem" with fluridil is that its encased in Grapeseed oil. Reservatrol is an angiogenesis inhibitor as is green tea, licorice, and CURCUMIN too (for Doctor). I dont know if one can REGROW much hair while using something that inhibits new blood vessel and capillary formation in the area. Revivogen and Crinagen also use grape seed proanthocyandins...............................this might be a weakness as far as a long term regrowth stimulant.





DOCJO77, on vitamin C----------------------Dr. Peter Proctor puts that in prox-n in the form of abscorbyl palmitate. If he includes it, I wouldn't worry about it. He knows more about the pathiogeneis of baldness than just about anyone





Keep in mind gents, taht Intercytex has just finished an initial phase two trial in England where HAIR CELLS were placed in bald scalp, and they grew some hair there. The fibrosis didn't stop the cells. The trialees were NOT allowed to be on any hair medication or therapy. No finasteride, etc. The best responder grew 103-percent more hair in the treated area. They are now working on creating new hairs to grow on a matrix OUTSIDE THE BODY until fully differentiated, and then reinplanted as whole hairs ensuring proper density and direction. They have filed a patend based on getting dp cells to multiply and make many new hairs to grow on "mediums" for re-implantaion as full hairs (not mere hair-inductive cells). Its the practical "cure" for baldness.





Tino,

You still haven't answered how many men who get transplants on long-bald scalp see them grow just fine despite the collagen-depostion, fibrosis, years of oxidative stress. I linked a ton of photos of this, and you just ignored them. Whats you excuse for that? Gotta be something.






All the docs and trichologists, and surgeons, and derms will tell you "donor dominance" when you ask them about hair. I used to think there was something more to it, but I was wrong. They aren't lying. The accepted theory of baldness is right in androgenic alopecia.

 

[harold]

Let me put it to you this way. If you don't have scurvy, you're making collagen, you don't have diarrhea/dermatitis/dementia/ and your skin isn't desquamating, then you have absolutely no problem whatsoever getting nutrients to both the dermis and the epidermis and that includes ALL antioxidants.

Irrelevant. You seem to be implying that I am suggesting male pattern baldness is a form of nutritional deficiency. I am not.

With the bolded and underlined above, you're actually implying that balding as a process is strictly due to oxidative stress,

I really fail to see how you conclude that. The bold text has me questioning why you think I am suggesting that all the free radicals produced in the body "localize to the scalp".

which it isn't as it has been proven time and again that the only molecule that is necessary is TGF-beta combined with the presence of the dermal papillae cells and dermal fibroblasts.

That has not been proven to be the case time and time again. Research has shown other factors such as IGF-1 and Dickkopf are important. Nobody has tried to say which is more important and there are only a handful of studiwes even looking at TGF-Beta and male pattern baldness.

There is no reason for male pattern baldness to be limited to the scalp if oxidative stress is indeed the reason for the problem.

How could male pattern baldness spread beyond the scalp?

The scalp has an incredibly rich blood supply and is typically well supplied with nutrients.

This nutrient argument is somebody elses.

Lastly, do you understand why beards keratincytes and dermal papillae respond differently to androgens when compared to scalp cells of the same type?

Yeah Ive read the study you are alluding to thanks.

They are of the same embryonal origin and yet they demonstrate a different response to the same molecular mediators.

They respond differently to the same hormonal signals by releasing different paracrine/autocrine messengers which then inhibit or encourage the proliferation of dermal papillae. The difference in response is at the androgen level - tgf-beta would almost vcertainly do to beard hairs what it does to scalp hairs much as IGf-1 does.
And all cells in our body are of "the same embryonal origin".

Such a system is far more complicated than anything as simple as ROS. Topical application of vitamin C would likely be incredibly detrimental to hair loss long term. It would simply lead to more fibrosis as increased vitamin C locally will lead to increased collagen production.

I doubt it would.

Sung YK, Hwang SY, Cha SY, Kim SR, Park SY, Kim MK, Kim JC.
The hair growth promoting effect of ascorbic acid 2-phosphate, a long-acting Vitamin C derivative.
J Dermatol Sci. 2006 Feb;41(2):150-2. Epub 2006 Jan 9.

By the way, it is quite likely that it isn't the ROS that are produced first.

Actually the only research that I have seen on the matter suggests that it is.
"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. "

DHT causes TGF-beta production, which leads to increased collagen production by dermal fibroblasts and perifollicular fibrosis. The fibrosis causes vessel obliteration reducing nutrient supply to the dermal papillae which will lead to hypoxic follicles.


I have never seen reversal of hair loss by using vitamin supplements alone. Whether it be topically or internally.

And I have never suggested you would.
hh

 

[harold]

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.
........
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.

Am still working my way through this long thread but you appear to be talking at cross purposes. Nothing you are saying here about it being "in the hair" or "in the skin" has any bearing on the aargument over the influence of ROS on male pattern baldness. I, and I suspect Tino, are talking about ROS damaging the dermal papillae themselves in response to the stimulus of androgens - nothing you say here is incongruent with that.
hh

 

[harold]

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.

Obviously we are all working with what little information is at hand and making inferences in the light of information we dont yet have.

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.
[\quote]
Agreed.
[quote:26ockyeg]
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?
[quote:26ockyeg]
In the scalp the bound androgen receptor activates genes that upregulate the production of ROS. These in turn trigger the release of TGF-Beta all of which leads to inhibition/apoptosis of dermal papillae in the scalp.
In the beard bound androgen receptor activates the transcription of genes for IGF-1 and possibly other growth factors. Dermal papillae proliferate.

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.
[/quote:26ockyeg][/quote:26ockyeg]

You seem to assume that if local androgen induced oxidative stress plays a key role that the whole scalp, skin and/or body must be affected and not just keratinocytes/dp. There is no reason for this to be the case. You seem also to argue that androgen receptors respond differently in the scalp re subsequent tgf-beta production than elsewhere in the body but disallow the possibility that this could also be the case for androgen receptors in the scalp and ROS vs those in the rest of the body.
hh

 

[harold]

Tino,

You still haven't answered how many men who get transplants on long-bald scalp see them grow just fine despite the collagen-depostion, fibrosis, years of oxidative stress. I linked a ton of photos of this, and you just ignored them. Whats you excuse for that? Gotta be something.

Not Tino but what is the relevance? The dermal papillae/keratinocytes that have been transplanted in are not damaged by oxidative stress if indeed that is important. As for fibrosis and collagen-deposition why dont you take that up with Doctor - that seems to be his preferred explanation.
Honestly Tino obviously doesn't speak much english but you are just coming at him/us with more or less unrelated stuff about transplants and transexuals. We are talking downstream of androgens here.

All the docs and trichologists, and surgeons, and derms will tell you "donor dominance" when you ask them about hair. I used to think there was something more to it, but I was wrong. They aren't lying. The accepted theory of baldness is right in androgenic alopecia.

Nobody is challenging the "accepted theory" ie DHT/androgens cause male pattern baldness. At least I'm not. Just trying to expand on it. To pretend otherwise is to engage in some kind of bizarre straw man argument.
hh

 

[tino]

[ Yeah Ive read the study you are alluding to thanks.

They respond differently to the same hormonal signals by releasing different paracrine/autocrine messengers which then inhibit or encourage the proliferation of dermal papillae. The difference in response is at the androgen level - tgf-beta would almost vcertainly do to beard hairs what it does to scalp hairs much as IGf-1 does.
And all cells in our body are of "the same embryonal origin".

you talk about this study?

http://www.nature.com/jidsp/journal/v10 ... 0206a.html

 

[tino]

Re: to Doctor and michael

citation;. There is no reason for this to be the case.

I mean the point androgenes and ROS Production in the hall system,respectively especially in some target cells,include vital parts.


http://ajprenal.physiology.org/cgi/cont ... 289/5/F941


Citation;Androgens and Oxidative Stress

The role of oxidative stress in acute renal failure and ischemia-reperfusion is widely accepted. However, oxidative stress also plays a role in chronic renal disease (1, 49). Men have higher levels of oxidative stress than do age-matched women as measured by F2-isoprostanes or thiobarbituric acid-reactive substances in plasma (34), despite the reduction in androgen levels in aging men. Postmenopausal women also exhibit higher levels of oxidative stress than premenopausal women (31). Oxidative stress is increased in the kidney with normal aging (72), and we have been able to protect against age-related renal injury in Sprague-Dawley rats by treating them chronically with vitamin E (65).

The major reactive oxygen species in the kidney is thought to be superoxide, which can quench nitric oxide (NO) (67), leading to a reduction in the NO bioavailability for dilation and thereby causing renal vasoconstriction. It is possible then that a reduction in vasodilator substances could play a role in the age-related renal vasoconstriction in males. We have found previously that there are sex differences in the renal vasculature response to NO. Young male normotensive rats without deficiencies in androgen synthesis are more dependent on the NO system for maintenance of renal hemodynamics than are age-matched females (63). Males had 80% lower renal expression of endothelial NO synthase compared with females, yet when NO synthase was blocked with nitro-L-arginine methyl ester, despite similar blood pressure increases in males and females, renal plasma flow (RPF) decreased by 40% and renal vascular resistance (RVR) increased by 23% in males compared with 20% and 60% for RPF and RVR, respectively, in females. The importance of the NO system in preserving renal hemodynamics is even more striking in aging males. When treated with NO synthase inhibitors, GFR and RPF decreased to a much greater extent and glomerular capillary pressure almost doubled in aging males compared with young males (66).

Whether androgens can directly produce oxidative stress has not been fully elucidated. In preliminary studies, we have found that physiological concentrations of dihydrotestosterone are capable of increasing dihydroethidium fluorescence in cultured SHR mesangial cells (Cucchiarelli V, Iliescu R, and Reckelhoff JF, unpublished observations). We have also found that castration reduces superoxide production in the kidneys of male SHR. In addition, tempol, a superoxide scavenger, reduces blood pressure and oxidative stress in young and aging male SHR but has little or no effect in females (21, 23).

Regardless of whether androgen supplementation directly causes oxidative stress, androgens can stimulate the RAS and endothelin production, which have been shown to increase reactive oxygen species. ANG II, at both supraphysiological and physiological levels, can increase oxidative stress (61, 71), mainly via upregulation of the subunits of NADPH oxidase (50). In addition, ANG II can stimulate the production of endothelin (3), which also causes oxidative stress by upregulating NADPH oxidase (16). Furthermore, while endothelin can cause oxidative stress, oxidative stress can also upregulate endothelin synthesis (40), setting up a vicious cycle.

Therefore, because aging is associated with increased oxidative stress, men at all ages have elevated levels of oxidative stress compared with women, and after menopause oxidative stress increases in women, androgen supplements could cause a further increase in oxidative stress in both men and women, leading to reductions in renal function and renal injury. The renal changes could be caused by the direct effect of androgens on oxidative stress or indirectly via their effect on the RAS or endothelin system. Furthermore, because estradiol is a mild antioxidant and has been shown to inhibit synthesis of NADPH oxidase (84), postmenopausal women would be at increased risk for androgen supplement-induced oxidative stress.



It is still a little controversal,but there are a few studys which shows that men have in general higher oxidative stress and impaired endothel function,and that antiandrogens,or estrogen supplemetation can reserve that.



http://sageke.sciencemag.org/cgi/conten ... type=HWCIT

 

[tino]

Re: addition

http://atvb.ahajournals.org/cgi/content ... type=HWCIT


annotation:impaired endothel function is mostly a result of ROS in many degenerative processes.

 

[tino]

Tino wrote:

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.

Im out and out laughing at this response Tino. Of COURSE ONLY FIFTY PERCENT OF WOMEN BALD WHEN GIVEN ANDROGENS, THEY ARE JUST LIKE THEIR BROTHERS. NOT ALL MEN BALD. ONLY ABOUT HALF DO IN MIDDLE AGE EXHIBIT HAIR LOSS. Ive seen MANY pictures of women who took testsoterone, but unfortunately lost the link that had them. About thirty percent or a little more than that were balding. Nobody was over about fifty. Just think, they have estrogens still in many cases because they all didn't get their ovaries removed. Even though they had some estrogen binding with androgen receptors, they were still balding. Most all had "aged" and "unfeminine" skin. They had beards or had to shave and you could see the "shadow" where they had to shave




You (Tino) mentioned Fluridil. Ive seen a study (no Im not going to look it up for you) that had pictures of a woman who used fluridil on her unfortunate moustache. It pretty much got rid of the moustache. The fluridil was judged by the team of investigators conducting the study as a worthy treatment for hirsutism in females.



My "problem" with fluridil is that its encased in Grapeseed oil. Reservatrol is an angiogenesis inhibitor as is green tea, licorice, and CURCUMIN too (for Doctor). I dont know if one can REGROW much hair while using something that inhibits new blood vessel and capillary formation in the area. Revivogen and Crinagen also use grape seed proanthocyandins...............................this might be a weakness as far as a long term regrowth stimulant.





DOCJO77, on vitamin C----------------------Dr. Peter Proctor puts that in prox-n in the form of abscorbyl palmitate. If he includes it, I wouldn't worry about it. He knows more about the pathiogeneis of baldness than just about anyone





Keep in mind gents, taht Intercytex has just finished an initial phase two trial in England where HAIR CELLS were placed in bald scalp, and they grew some hair there. The fibrosis didn't stop the cells. The trialees were NOT allowed to be on any hair medication or therapy. No finasteride, etc. The best responder grew 103-percent more hair in the treated area. They are now working on creating new hairs to grow on a matrix OUTSIDE THE BODY until fully differentiated, and then reinplanted as whole hairs ensuring proper density and direction. They have filed a patend based on getting dp cells to multiply and make many new hairs to grow on "mediums" for re-implantaion as full hairs (not mere hair-inductive cells). Its the practical "cure" for baldness.





Tino,

You still haven't answered how many men who get transplants on long-bald scalp see them grow just fine despite the collagen-depostion, fibrosis, years of oxidative stress. I linked a ton of photos of this, and you just ignored them. Whats you excuse for that? Gotta be something.






All the docs and trichologists, and surgeons, and derms will tell you "donor dominance" when you ask them about hair. I used to think there was something more to it, but I was wrong. They aren't lying. The accepted theory of baldness is right in androgenic alopecia.

citation:Im out and out laughing at this response Tino. Of COURSE ONLY FIFTY PERCENT OF WOMEN BALD WHEN GIVEN ANDROGENS, THEY ARE JUST LIKE THEIR BROTHERS. NOT ALL MEN BALD. ONLY ABOUT HALF DO IN MIDDLE AGE EXHIBIT HAIR LOSS. Ive seen MANY pictures of women who took testsoterone, but unfortunately lost the link that had them. About thirty percent or a little more than that were balding. Nobody was over about fifty. Just think, they have estrogens still in many cases because they all didn't get their ovaries removed. Even though they had some estrogen binding with androgen receptors, they were still balding. Most all had "aged" and "unfeminine" skin. They had beards or had to shave and you could see the "shadow" where they had to shave


For example,a female which turns to medical getting male treatment in her 30 ,hat never before contact to such a big amount of testosterone,like it comes over her due tratment.Men had contact to bigger amounts of testosterone and his affinity stronger product DHT,since puberty.I think that womens system will react much more massive-dispite estrogen protection.And who says that the DHT,metabolized from the testosterone treatment,wont inhibit armatase activity in female to male individuals?Again I do not absoloutly negate that androgenes-i think especially DHT can force skin aging.But all this,especially the extent of the skin aging process depents strong on individual genetic.


citation;You still haven't answered how many men who get transplants on long-bald scalp see them grow just fine despite the collagen-depostion, fibrosis, years of oxidative stress. I linked a ton of photos of this, and you just ignored them. Whats you excuse for that? Gotta be something.


I think i made a statement to that point more than one time.My last statement was,that the exact pathogenetic role of fibrosis,is still not cleared.But......transplantation storys,have not the wight to bring evidence for a assume that fibrosis in the line of male pattern baldness,is not relevant for regrowth due tratments.Because follicles there are like you know well,other follicles than follicles from the donor aerea.Have you got pictures from the regrowth of the stemm cell patients?


citation:All the docs and trichologists, and surgeons, and derms will tell you "donor dominance" when you ask them about hair. I used to think there was something more to it, but I was wrong. They aren't lying. The accepted theory of baldness is right in androgenic alopecia.[/quote]


me myself,would only accept comments about the pathogenesis of male pattern baldness from sugerons,if i can reconstruct this in a biochemic way,or if they advise me to published investigations-for example that follicles from the donor aerea secrete encymes which makes space for anagen enlargement.

 

[Bryan]

Tino, LEARN HOW TO QUOTE PROPERLY. It's often difficult as hell trying to read your posts, and figure out who said what.

 

[harold]

[ Yeah Ive read the study you are alluding to thanks.

They respond differently to the same hormonal signals by releasing different paracrine/autocrine messengers which then inhibit or encourage the proliferation of dermal papillae. The difference in response is at the androgen level - tgf-beta would almost vcertainly do to beard hairs what it does to scalp hairs much as IGf-1 does.
And all cells in our body are of "the same embryonal origin".

you talk about this study?

http://www.nature.com/jidsp/journal/v10 ... 0206a.html

Yep.
hh

 

[tino]

citation from the study

We were unable to identify androgen-responsive elements in the TGF-1 promoter. TGF-1 promoter activation by androgen is bald frontal DPC specific and is not observed in non-bald frontal DPC, suggesting that some intrinsic factor(s) in bald frontal DPC are required (data not shown). Factor(s) that are genetically involved in Androgenetic Alopecia would be the true target of the pathomechanism of the disease. Our modified co-culture system will provide clues to further explore the role of androgens in the regulation of hair growth.





Do they mean factors before tgf-beta induces his destroying work?

 

[tino]

My "problem" with fluridil is that its encased in Grapeseed oil. Reservatrol is an angiogenesis inhibitor as is green tea, licorice, and CURCUMIN too (for Doctor). I dont know if one can REGROW much hair while using something that inhibits new blood vessel and capillary formation in the area. Revivogen and Crinagen also use grape seed proanthocyandins...............................this might be a weakness as far as a long term regrowth stimulant.





there are more than a million vitro and mice or worm studys about every antioxidant,which will have found angiogenesis inhibition.I wouldn t belive them.Sometimes unknown resaerchers do everyting to proove something what isnt.

 

[michael barry]

Tino,

Here are pictures of a guy going bald from ages 15-18.

I doubt he has had time for oxidants to play a signifigant role anywhere in his dermis, but he's frontally now. Take a look,

viewtopic.php?f=11&t=41898

 

[Bryan]

citation from the study

"We were unable to identify androgen-responsive elements in the TGF-1 promoter. TGF-1 promoter activation by androgen is bald frontal DPC specific and is not observed in non-bald frontal DPC, suggesting that some intrinsic factor(s) in bald frontal DPC are required (data not shown). Factor(s) that are genetically involved in Androgenetic Alopecia would be the true target of the pathomechanism of the disease. Our modified co-culture system will provide clues to further explore the role of androgens in the regulation of hair growth."

Do they mean factors before tgf-beta induces his destroying work?

They are referring to the factor or factors which cause a difference in the RESPONSE of a given hair follicle to androgens (specifically in this case, whether or not TGF-1 is released in response to androgens).

 

[Bryan]

My "problem" with fluridil is that its encased in Grapeseed oil.

Where did you get the idea that fluridil is encased in grapeseed oil?

 

[michael barry]

"One ampule contains 2ml of 2% fluridil solution in isorophyl alcohol encased in 50mg of grapeseed oil"
http://www.menspharma.com/index.php?id=apply

Right off their webpage Bryan. Ive used fluridil before for a month to check it out also. I wish it came in a sprayer personally.