Age, DHT levels, prevalence of balding and oxidative stress

[harold]

Not so much research but a bit of speculation question:
we know that the incidence of male pattern baldness increases with age.
We also know that testosterone levels fall with age as do DHT levels to a somewhat lesser extent.
We know from finasteride and other drugs that it doesnt take that long for the damaging effects of DHT to make themselves known. On thee order of months to years but not decades.
Given this it would seem that we should be seeing much more balding occuring earlier in life and less later.
It also seems that DHT causes an upregulation if oxidative stress in general in the dermal paillae and this may trigger the secondary messengers that lead to apoptosis.
Oxidative stress is hypothesised to be one of if not the major cause of aging. At the same time the ability to deal with it decreases as a person ages.
Could it be that the reason more people are balding later in life is just that those cells already undergoing increasing levels of oxidative stress are more likely to bow out altogether amongst more oxidative damge all round.
Thoughts? any supporting or opposing pieces of evidence?
hh

 

[sphlanx2006]

I think the real problem is that your hair as time passes become more and more sensitive to DHT. So even if there is less DHT when your are older there is enough off it to take effect and on the same time its effect is much worse on hair than it was when you were younger.

 

[docj077]

If oxidative stress was the only thing causing hair loss, then all the people on this forum that basically O.D. on anti-oxidants everyday along with their anti-oxidant shampoos would have full heads of hair that was all the way down to their knees.

Plus, the body generates a lot of free radicals. There is no reason for all of them to localize to the scalp and there is also no reason for this process to only occur in the scalp if this is the case. Many other hair follicles have androgen receptors and demonstrate a clear response to androgens/estrogens, as well.

 

[tino]

Not so much research but a bit of speculation question:
we know that the incidence of male pattern baldness increases with age.
We also know that testosterone levels fall with age as do DHT levels to a somewhat lesser extent.
We know from finasteride and other drugs that it doesnt take that long for the damaging effects of DHT to make themselves known. On thee order of months to years but not decades.
Given this it would seem that we should be seeing much more balding occuring earlier in life and less later.
It also seems that DHT causes an upregulation if oxidative stress in general in the dermal paillae and this may trigger the secondary messengers that lead to apoptosis.
Oxidative stress is hypothesised to be one of if not the major cause of aging. At the same time the ability to deal with it decreases as a person ages.
Could it be that the reason more people are balding later in life is just that those cells already undergoing increasing levels of oxidative stress are more likely to bow out altogether amongst more oxidative damge all round.
Thoughts? any supporting or opposing pieces of evidence?
hh

this is partially absolout correct.DHT,respectively the genetic modulated much to strong absorption of the Androgenreceptor,and other genetic and extrinsic factors in men with Androgenetic Alopecia,causes as first oxidative stress.This leads to tgf-beta overexpression,and this causes igf-1 deprevation over upregulation of igfbp.Its almost the same like a tumor supression.Aging of hair,the so called natural aging,is caused by the same intracellulaer causal,just much slower.Premature Androgenetic Alopecia is basically not more than genetic forced hair aging.When balding...slow balding starts with over 35,40 or later,DHT ist not the basic cause anymore.In my opinion,it is a natural and or genetic decline in estrogen,estrogen modulated igf-1 receptors,and serum igf-1.Estrogen and igf-1 are potent antioxidants and tgf-beta antagonists.Sure.....DHT in age classes until 50,ist still a secondary trigger for once attaced hair follicles.But it does not play the chief part anymore.Individuals who start to get bald after the age of 35,are no carrier of very short cag repeats in the Androgenreceptor gen.Senile involutionsalopecia at the age of 60,goes on with very little DHT and very little testosterone in the scalp skin.At this age,other factors decline to a minimum,for example igf-1.And certanly the oxidative stress in the hall system rises high.

 

[tino]

If oxidative stress was the only thing causing hair loss, then all the people on this forum that basically O.D. on anti-oxidants everyday along with their anti-oxidant shampoos would have full heads of hair that was all the way down to their knees.

Plus, the body generates a lot of free radicals. There is no reason for all of them to localize to the scalp and there is also no reason for this process to only occur in the scalp if this is the case. Many other hair follicles have androgen receptors and demonstrate a clear response to androgens/estrogens, as well.

Antioxidant shampoo is worthless!

It is not so easy to heal a once attacked follicle.If the genetic cause in a Androgenetic Alopecia individual is the short AR Cag repeat,he should treat it with a 5-a-r blocker,AND Antioxidants in high doses.For example N-Acetylcysteine.It is a dose dependent potent tgf-beta antagonist.It does not occur only in the scalp.But the system knows that scalp hairs are not indispensable of life,and so it protecs other organs as first and much stronger.First in much later years,when other protecting factors collapse because of aging,a further symptom of the unfavourable genetic will be coronaery heart disease in some individuals with very early premature balding.

 

[mumuka]

Tino you mean that i`m balding now and later i get another good one :coronary disease? .Thats great.I could not asked for more :sobbing:

By the way welcome to the forum. Could you please post your regimen. Thanks.

 

[tino]

Tino you mean that i`m balding now and later i get another good one :coronary disease? .Thats great.I could not asked for more :sobbing:

By the way welcome to the forum. Could you please post your regimen. Thanks.

There are many studys which will have found a correlation between balding and coronary heart disease.Another study which summarises all the studys,says that only men with agressive premature balding have a higher risk to get coronaery heart disease in later life.No people with only fronto temporal problems,or hair aging.Many of my bald friends have bald fathers who have heart problems.


Im taking 200 mg spironolactone oral,0,5 mg Avodart,2000 mg NAC,1 gramm Vitamin c,5 mg Folic Acid,1 time day one vitamin b komplex,500 IE Vitamin E ,20 mg Zinc,sometimes iron,2 gramm acetyl-l-carnitine,100 mg selenium,one ampulle amino acid complex day,5 mg biotin,one pill crateagutt,sometimes creatine monohydrate,one multimineral complex,one ampulle orthomol immun-a multivitamin dring high dosed.

 

[mumuka]

There are many studys which will have found a correlation between balding and coronary heart disease.Another study which summarises all the studys,says that only men with agressive premature balding have a higher risk to get coronaery heart disease in later life.No people with only fronto temporal problems,or hair aging.Many of my bald friends have bald fathers who have heart problems.

My mothers father went Norwood 7 in his 40`s and than he died in his 60`s.Guess what finished him? Yup you have guessed it: coronary heart disease.

By the way thats an impressive regimen you have there.No topicals?

 

[tino]

There are many studys which will have found a correlation between balding and coronary heart disease.Another study which summarises all the studys,says that only men with agressive premature balding have a higher risk to get coronaery heart disease in later life.No people with only fronto temporal problems,or hair aging.Many of my bald friends have bald fathers who have heart problems.

My mothers father went Norwood 7 in his 40`s and than he died in his 60`s.Guess what finished him? Yup you have guessed it: coronary heart disease.

By the way thats an impressive regimen you have there.No topicals?

i uesd minoxidil some years ago,but i stoppt it quick,because i was afraid to set my follicles in an addition to it.There is a study which shows that after stopping minoixdil,a great shed will set in,and finasteride could not stopp it.It s not worth,...my regiemen without minoxidil works well for me.Genetics and intrinsic factors come from the system,and in my opinion,its the best way to cure over this way.

I do not think that minoxidil ist bad,...but i think the best results come when you use it together with zinc and antioxidants orraly.A study by upjohn says that minoxidil may works better in the presence of insulin and igf-1.Vitamin C for example,works against hair diseases over increasing igf-1.

 

[CCS]

There are many studys which will have found a correlation between balding and coronary heart disease.Another study which summarises all the studys,says that only men with agressive premature balding have a higher risk to get coronaery heart disease in later life.No people with only fronto temporal problems,or hair aging.Many of my bald friends have bald fathers who have heart problems.

My mothers father went Norwood 7 in his 40`s and than he died in his 60`s.Guess what finished him? Yup you have guessed it: coronary heart disease.

By the way thats an impressive regimen you have there.No topicals?

My 60 year old father has a blood pressure of 154. He's getting up into the NW4 area. I suspect it might not be a biological thing though. I think bald people have a lot more depression and stress from looking older and not getting dates. People in relationships live longer than singles, I think. Loneliness kills.

 

[CCS]

Vitamin C for example,works against hair diseases over increasing igf-1.

I'll take plenty then.

 

[tino]

There are many studys which will have found a correlation between balding and coronary heart disease.Another study which summarises all the studys,says that only men with agressive premature balding have a higher risk to get coronaery heart disease in later life.No people with only fronto temporal problems,or hair aging.Many of my bald friends have bald fathers who have heart problems.

My mothers father went Norwood 7 in his 40`s and than he died in his 60`s.Guess what finished him? Yup you have guessed it: coronary heart disease.

By the way thats an impressive regimen you have there.No topicals?

My 60 year old father has a blood pressure of 154. He's getting up into the NW4 area. I suspect it might not be a biological thing though. I think bald people have a lot more depression and stress from looking older and not getting dates. People in relationships live longer than singles, I think. Loneliness kills.

Another gen candidat for male pattern baldness is the mineralocorticoid receptor.Polymorphisms of that receptor,or aldosteron,make also high blood pressure,and heart diseseases. overactivity of his receptor,makes like dht ,apoptosis and fibrosis in and around the hair follicle.It is well known that men whith male pattern baldness have often high blood pressure.

But right,...stress is also very bad.....who knows.Professor paus wrote much about the terrible burden of hair loss,and his psychological consequences.

 

[tino]

Re: biological things

There are many studys which will have found a correlation between balding and coronary heart disease.Another study which summarises all the studys,says that only men with agressive premature balding have a higher risk to get coronaery heart disease in later life.No people with only fronto temporal problems,or hair aging.Many of my bald friends have bald fathers who have heart problems.

My mothers father went Norwood 7 in his 40`s and than he died in his 60`s.Guess what finished him? Yup you have guessed it: coronary heart disease.

By the way thats an impressive regimen you have there.No topicals?

My 60 year old father has a blood pressure of 154. He's getting up into the NW4 area. I suspect it might not be a biological thing though. I think bald people have a lot more depression and stress from looking older and not getting dates. People in relationships live longer than singles, I think. Loneliness kills.

http://jcem.endojournals.org/cgi/conten ... 86/10/4867


who konows?

 

[harold]

If oxidative stress was the only thing causing hair loss, then all the people on this forum that basically O.D. on anti-oxidants everyday along with their anti-oxidant shampoos would have full heads of hair that was all the way down to their knees.

Would they? Why would antioxidants reverse the effect of years of dermal papillae being miniaturised and eventually killed off by DHT/ROS? How much of those antioxidants reach the fibroblasts and hair folicles of the scalp? How effective would they be against a local shitstorm of androgen induced ROS? How effective would a shampoo with 0.00001% of vitamin C or whatever applied for 60 seconds and then washed off be? How many people use such a shampoo?

Plus, the body generates a lot of free radicals. There is no reason for all of them to localize to the scalp and there is also no reason for this process to only occur in the scalp if this is the case.
[quote:e292f]

Eh? I'm really not sure how you got the idea that I was suggesting this happens.

Many other hair follicles have androgen receptors and demonstrate a clear response to androgens/estrogens, as well.[/quote:e292f]

Yes. They do not produce ROS in response to androgen binding and subsequently TGF-B etc. Instead they respond by secreting growth factors like IGF-1 as is documented in beard keratinocytes/papillae.
hh

 

[antonio666]

if you start to bald in your 20,s then you will be a cue ball by 40

 

[docj077]

If oxidative stress was the only thing causing hair loss, then all the people on this forum that basically O.D. on anti-oxidants everyday along with their anti-oxidant shampoos would have full heads of hair that was all the way down to their knees.

Would they? Why would antioxidants reverse the effect of years of dermal papillae being miniaturised and eventually killed off by DHT/ROS? How much of those antioxidants reach the fibroblasts and hair folicles of the scalp? How effective would they be against a local shitstorm of androgen induced ROS? How effective would a shampoo with 0.00001% of vitamin C or whatever applied for 60 seconds and then washed off be? How many people use such a shampoo?

Plus, the body generates a lot of free radicals. There is no reason for all of them to localize to the scalp and there is also no reason for this process to only occur in the scalp if this is the case.
[quote:80ead]

Eh? I'm really not sure how you got the idea that I was suggesting this happens.

Many other hair follicles have androgen receptors and demonstrate a clear response to androgens/estrogens, as well.

Yes. They do not produce ROS in response to androgen binding and subsequently TGF-B etc. Instead they respond by secreting growth factors like IGF-1 as is documented in beard keratinocytes/papillae.
hh[/quote:80ead]


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.


With the bolded and underlined above, you're actually implying that balding as a process is strictly due to oxidative stress, 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. There is no reason for male pattern baldness to be limited to the scalp if oxidative stress is indeed the reason for the problem. The scalp has an incredibly rich blood supply and is typically well supplied with nutrients.

Lastly, do you understand why beards keratincytes and dermal papillae respond differently to androgens when compared to scalp cells of the same type? They are of the same embryonal origin and yet they demonstrate a different response to the same molecular mediators. 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.

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

 

[michael barry]

Doctor,

Has TGF beta been shown to cause keratinocyte apoptosis, or mere slowing or halting of cell division of the keratinocytes?


I say this because DKK-1 has been shown to cause keratincoyte apoptosis. Im interested in this because the first inflammation in Androgenetic Alopecia is near the infidulum, or the opening in the dermis where the hair exits the body. It would seem that dead keratinocyte cells would be "in the area" clinging to live hair shafts and it would also stand to reason that the immune cells would recognize and attack them at about this time, just before they left the body. If you think about it, the extra collagen formation around the follice could be some sort of protective response attempting to either expell the follicle from the body through microvascular extermination or even a wierd attempt to stop the immuno damage by shielding the follicle from the oxides and inflammatory cytokines or something.



The first inflammation being around the infidulum has got to be a "key" to something. I wonder what is going on there that gets the whole thing started?

 

[tino]

quote="docj077"]

If oxidative stress was the only thing causing hair loss, then all the people on this forum that basically O.D. on anti-oxidants everyday along with their anti-oxidant shampoos would have full heads of hair that was all the way down to their knees.

Would they? Why would antioxidants reverse the effect of years of dermal papillae being miniaturised and eventually killed off by DHT/ROS? How much of those antioxidants reach the fibroblasts and hair folicles of the scalp? How effective would they be against a local shitstorm of androgen induced ROS? How effective would a shampoo with 0.00001% of vitamin C or whatever applied for 60 seconds and then washed off be? How many people use such a shampoo?

Plus, the body generates a lot of free radicals. There is no reason for all of them to localize to the scalp and there is also no reason for this process to only occur in the scalp if this is the case.
[quote:223ef]

Eh? I'm really not sure how you got the idea that I was suggesting this happens.

Many other hair follicles have androgen receptors and demonstrate a clear response to androgens/estrogens, as well.

Yes. They do not produce ROS in response to androgen binding and subsequently TGF-B etc. Instead they respond by secreting growth factors like IGF-1 as is documented in beard keratinocytes/papillae.
hh[/quote:223ef]


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.


With the bolded and underlined above, you're actually implying that balding as a process is strictly due to oxidative stress, 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. There is no reason for male pattern baldness to be limited to the scalp if oxidative stress is indeed the reason for the problem. The scalp has an incredibly rich blood supply and is typically well supplied with nutrients.

Lastly, do you understand why beards keratincytes and dermal papillae respond differently to androgens when compared to scalp cells of the same type? They are of the same embryonal origin and yet they demonstrate a different response to the same molecular mediators. 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.

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



in principle it is strictly due to oxidative stress.All the genetic factors,and also many extrinsic trigger of male pattern baldness,do operate over a redox imbalance before they drop down the igf-1 over tgf-beta.Every in vitro experiment,and also many studys on humans,show that tgf-beta is a product of ROS in apoptotic,and or fibrotic disorders.TGF-beta is typically ROS mediated,when his expression turns over the normal limit respectively to a inflammatory level.


The scalp has an incredibly rich blood supply ....yes,but that dosn t matter.The inflammation causes also a disturbed angiogenesis.Many antioxidants workt pro angiogenThe Redox imbalance caused by DHT and other factors,brings down every activity wich leads to growth-disturbed VEGF mediated angiogenesis,apoptosis,IGF-1 and Insulin deprivation.


People who eat every day citrus fruits,or vitamin c,have higher igf-1 levels than people who do not.Vitamin c topically applied increases the igf-1 in the hair follicle.Increases igf-1,inhibits tgf-beta,and works generally antiapoptotic.Estrogen,E2 induces collagen over tgf-beta in the skin outlying the scalp skin.In scalp skin,it downregulates tgf-beta in men and women whith estrogen deficiency.I just want to clarify,that vitamin c for example works not the same way in cell type a,than it works in cell tybe b.


i also do not understand why androgenes work so paradox in different hair follicles.There must be a difference of a enzym activity.Maybe scalp skin has a stronger genetic expression of tgf-beta in some individuals,because the scalp ist more sensitive to skin cancer.Pheomelanin guys are more sensitiv to male pattern baldness,africans have the lowest rate of male pattern baldness cases.


Sure,you cant treat genetic male pattern baldness only whith antioxidants.You cant,because there is still a fire modulated due hormonal authority.As first,or paralel to antioxidant supplementation you have to block the strongest fire,then it makes sense to build regenerativ potential and additional protection over antioxidants.

 

[docj077]

in principle it is strictly due to oxidative stress.All the genetic factors,and also many extrinsic trigger of male pattern baldness,do operate over a redox imbalance before they drop down the igf-1 over tgf-beta.Every in vitro experiment,and also many studys on humans,show that tgf-beta is a product of ROS in apoptotic,and or fibrotic disorders.TGF-beta is typically ROS mediated,when his expression turns over the normal limit respectively to a inflammatory level.


The scalp has an incredibly rich blood supply ....yes,but that dosn t matter.The inflammation causes also a disturbed angiogenesis.Many antioxidants workt pro angiogenThe Redox imbalance caused by DHT and other factors,brings down every activity wich leads to growth-disturbed VEGF mediated angiogenesis,apoptosis,IGF-1 and Insulin deprivation.


People who eat every day citrus fruits,or vitamin c,have higher igf-1 levels than people who do not.Vitamin c topically applied increases the igf-1 in the hair follicle.Increases igf-1,inhibits tgf-beta,and works generally antiapoptotic.Estrogen,E2 induces collagen over tgf-beta in the skin outlying the scalp skin.In scalp skin,it downregulates tgf-beta in men and women whith estrogen deficiency.I just want to clarify,that vitamin c for example works not the same way in cell type a,than it works in cell tybe b.


i also do not understand why androgenes work so paradox in different hair follicles.There must be a difference of a enzym activity.Maybe scalp skin has a stronger genetic expression of tgf-beta in some individuals,because the scalp ist more sensitive to skin cancer.Pheomelanin guys are more sensitiv to male pattern baldness,africans have the lowest rate of male pattern baldness cases.


Sure,you cant treat genetic male pattern baldness only whith antioxidants.You cant,because there is still a fire modulated due hormonal authority.As first,or paralel to antioxidant supplementation you have to block the strongest fire,then it makes sense to build regenerativ potential and additional protection over antioxidants.

In principle, it's not due to ROS at all. When you mention that TGF-beta is produced due to ROS, you're mentioning a process that requires previous cellular injury in the form of ischemia or cellular death. That very process is required in the follicles, as well. ROS are not going to be produced only in the scalp unless there is previous cellular damage. There are very few ways that you can get such damage. Thickening of the epidermal layer is one such way as it prevents gas diffusion. Vessel obliteration is another as it prevent micronutrient entry into the dermal layer. Both of these processes occur before ROS are present in the scalp and both of those processes are mediated by androgen mediated action through other pathways including the TGF-beta pathway. Fibrosis and vessel obliteration happen, because TGF-beta causes decreased production of collagenase and increased production of collagen from dermal fibroblasts.

You are oversimplifying incredibly complex cellular pathways by simply saying that ROS cause the process. They are the end result of the human body basically destroying the dermal layer that surrounds hair follicles while also inhibiting keratinocyte division and differentiation.

 

[tino]

in principle it is strictly due to oxidative stress.All the genetic factors,and also many extrinsic trigger of male pattern baldness,do operate over a redox imbalance before they drop down the igf-1 over tgf-beta.Every in vitro experiment,and also many studys on humans,show that tgf-beta is a product of ROS in apoptotic,and or fibrotic disorders.TGF-beta is typically ROS mediated,when his expression turns over the normal limit respectively to a inflammatory level.


The scalp has an incredibly rich blood supply ....yes,but that dosn t matter.The inflammation causes also a disturbed angiogenesis.Many antioxidants workt pro angiogenThe Redox imbalance caused by DHT and other factors,brings down every activity wich leads to growth-disturbed VEGF mediated angiogenesis,apoptosis,IGF-1 and Insulin deprivation.


People who eat every day citrus fruits,or vitamin c,have higher igf-1 levels than people who do not.Vitamin c topically applied increases the igf-1 in the hair follicle.Increases igf-1,inhibits tgf-beta,and works generally antiapoptotic.Estrogen,E2 induces collagen over tgf-beta in the skin outlying the scalp skin.In scalp skin,it downregulates tgf-beta in men and women whith estrogen deficiency.I just want to clarify,that vitamin c for example works not the same way in cell type a,than it works in cell tybe b.


i also do not understand why androgenes work so paradox in different hair follicles.There must be a difference of a enzym activity.Maybe scalp skin has a stronger genetic expression of tgf-beta in some individuals,because the scalp ist more sensitive to skin cancer.Pheomelanin guys are more sensitiv to male pattern baldness,africans have the lowest rate of male pattern baldness cases.


Sure,you cant treat genetic male pattern baldness only whith antioxidants.You cant,because there is still a fire modulated due hormonal authority.As first,or paralel to antioxidant supplementation you have to block the strongest fire,then it makes sense to build regenerativ potential and additional protection over antioxidants.

In principle, it's not due to ROS at all. When you mention that TGF-beta is produced due to ROS, you're mentioning a process that requires previous cellular injury in the form of ischemia or cellular death. That very process is required in the follicles, as well. ROS are not going to be produced only in the scalp unless there is previous cellular damage. There are very few ways that you can get such damage. Thickening of the epidermal layer is one such way as it prevents gas diffusion. Vessel obliteration is another as it prevent micronutrient entry into the dermal layer. Both of these processes occur before ROS are present in the scalp and both of those processes are mediated by androgen mediated action through other pathways including the TGF-beta pathway. Fibrosis and vessel obliteration happen, because TGF-beta causes decreased production of collagenase and increased production of collagen from dermal fibroblasts.

You are oversimplifying incredibly complex cellular pathways by simply saying that ROS cause the process. They are the end result of the human body basically destroying the dermal layer that surrounds hair follicles while also inhibiting keratinocyte division and differentiation.

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.