Age, DHT levels, prevalence of balding and oxidative stress

[Bryan]

Hi Bryan;

thank you for your suggestion
You used sebutape test-strip in fronhead but, are they useful to test sebum in hairy zones?

They may not be terribly appropriate for use on VERY hairy areas of the scalp, because the hair could be a physical impediment when you try to press the test-strip against the scalp skin. You'd probably have to shave a small portion of the scalp for that test. There are various versions of those Sebutape strips that are available, and the ones I'd recommend are quite small, with an "active" area (the portion of the strip that actually reacts to sebum) of only about 1 square centimeter. Shaving that small amount of a child's scalp for the purpose of testing your theory shouldn't be that much of a problem!

I really do wish you'd do that, Armando. It could finally settle this issue once and for all. Do YOU happen to have any children of that age (pre-pubertal)?

 

[docj077]

I really do wish you'd do that, Armando. It could finally settle this issue once and for all. Do YOU happen to have any children of that age (pre-pubertal)?

I can see the headline on CNN now.

 

[powersam]

This deliverances from greece or egypt,whatever....are scientific non valid,because informations like for example,what will happen when a castrated subject will get thyroid disease,or has low Iron are missing.Noone investigated that....the only thing they saw is,that there was a difference to their genetic kinsman,when castrated.What makes you so sure that they keeped their hair full and healthy until they died?Again,Castration does maybe stopp further progression of androgen induced Apoptotic influence,but it can do nothing for other influences.The complete inhibition of a important hormone,is no adhesive tape for hair and skin aging.

I've watched this back-and-forth discussion with some amusement, and I agree with Michael Barry that the genetic factor having to do with the response to androgens is BY FAR the most important component of androgenetic alopecia. Having said that, I don't doubt that some of these other peripheral issues (like having to do with antioxidants and various nutritional factors) have _some_ relevance for balding, but I think they are minor issues. If I were forced to put a number to it, I'd make a wild guess and say that maybe they are only 5% or so of the problem.

Your statements above about thyroid disease and "low iron" problems are themselves pretty irrelevant, because the issue here is true androgenetic alopecia, not other forms of hairloss.

citation:Your statements above about thyroid disease and "low iron" problems are themselves pretty irrelevant, because the issue here is true androgenetic alopecia, not other forms of hairloss.

Oh bryan,im very surprised

If there is a praedispostion to male pattern baldness.....(i would like to call it genetic patttern baldness here,because i dont belive that every so called male pattern baldness is strong androgen dependet),than the androgenic influence,for example in cases of rather long CAG Repeats,must not be so strong,that it reduces other known APOPTOSIS inducing influences to a minimum.Week genetic meets one strong trigger like for example iron deficiney,or bad adjusted thyroid disease,or week genetic meets more week trigger together,like for example zinc deficiency,latent malnutrition,smoking,Stress.

For example.....


http://www.nature.com/jid/journal/v121/ ... 2007a.html


what is to fault whith that?

I think you know the works about stress and apoptosis of HF.....and i think you also saw the study about Caspase-3 and Zink i have posted.

Men do not develop hair loss due Iron deficiency,thyorid diseases,or whatever?Ok you can argument that the hairloss in such cases will be diffuse.But think about the lack of resistance,once attacked/insufficient hair follicles have against all the winds.The hair follicle is a little hormonal factory,which has the capacity to protect himself,when he is young.Old hair follicles fall quicker,like old men,when they develop pneumonia.Its absoloutly logical,that aged follickles will fall as first,under bad influences from every direction.

Ok,we can get agreed,when we talk about cases,which show extreme strong progression in their mid twenties,signed due quick temple receeding,and Tonsur.In such cases,i think that genetic can override triggers.And maybe then,in Fact androgenes have the strongest influence.


But what about temple receeding guys like Johnny deep,Tom Selleck,or unknown people,who develop a slow patternd thinning in their 30 for the first time?Is that really classic male pattern baldness,basically induced due the prooven Androgenetic pathogenesis?Sure...normal non scientific working doctors would say yes....under appointment of JB Hamilton

i post this as i also believe environmental factors can seriously affect the outcome of ones male pattern baldness.

I recently attended something of a family reunion for my fathers immediate family and noticed something very interesting. My father has 5 brothers 4 of whom are similar to him in that they are all fat in the midsection and have lost most of their hair. One brother however is rake thin and has all his hair still. It turns out he has coeliac disease , a condition in which wheat kills the bacteria in your stomach and prevents adequate digestion from taking place. My grandmother has type2 diabetes and its reasonably certain most of my uncles have insulin resistance. coeliac disease would be the perfect protection against insulin resistance as you could never over feed yourself. in my head this at the very least adds some weight to the argument that heightened insulin levels cause or aggravate hairloss.

 

[Armando Jose]

Hi Bryan;

thank you for your suggestion
You used sebutape test-strip in fronhead but, are they useful to test sebum in hairy zones?

They may not be terribly appropriate for use on VERY hairy areas of the scalp, because the hair could be a physical impediment when you try to press the test-strip against the scalp skin. You'd probably have to shave a small portion of the scalp for that test. There are various versions of those Sebutape strips that are available, and the ones I'd recommend are quite small, with an "active" area (the portion of the strip that actually reacts to sebum) of only about 1 square centimeter. Shaving that small amount of a child's scalp for the purpose of testing your theory shouldn't be that much of a problem!

I really do wish you'd do that, Armando. It could finally settle this issue once and for all. Do YOU happen to have any children of that age (pre-pubertal)?

Hi Bryan;

thank you for your suggestion. I have three daughters, 13,12 and 10 years old. The idea is test the hypothesys in children about four o five years old, no more. I tried to measure DHEA, DHT, even the activation of 5 alfa reductases with PCR with plucked hairs, but it is nececsary a lab. Where are good and honest scientist on earth?!!

Yo said a lot of times that the androgens important in baldness are that situated in the viccinity of pilosebaceus area.

I'll try to purchase sebum strip test in order to make any measure, shaving the area to test.

Best regards

Armando

 

[tino]

Very good example.


you wrote:some weight to the argument that heightened insulin levels cause or aggravate hairloss.



The heightened insulin essentially is not the cause.Respectively,you are not wrong,but the aggravation depends on the missing cellulaer capacity to take up insulin,which leads to heightened levels.If the hair follicle cant get enough insulin or igf-1,genetics,extrinsic factors,and maybe even normal androgen activity,without short AR CAG influence can do their destroying work much easyer when there is no sufficient growth factor presence.

 

[Bryan]

Hi Bryan;

thank you for your suggestion. I have three daughters, 13,12 and 10 years old. The idea is test the hypothesys in children about four o five years old, no more.

Why do you suggest NO MORE than four or five years old?? If you were to test the scalp sebum secretion in your 10 year-old daughter and found that it is indeed still virtually nonexistent (assuming that she's not experiencing precocious puberty), then wouldn't that ALSO spell doom for your sebum-is-required-for-hairgrowth theory?

I'll try to purchase sebum strip test in order to make any measure, shaving the area to test.

I look forward to hearing your results! I hope that you post all the details of how you did the test, and scan the actual test-strip results, so I can download them and take a look at them.

BTW, I did that exact same thing over on acne.org a couple of years ago when I ran a test on my own face to prove that washing my skin doesn't cause an increase in sebum production (see the third statement in my signature-file below). I used Sebutape test-strips, and I scanned them and posted them for everyone to see for themselves. I posted all the details of the experiment and the scans of the test-strips over there in a thread titled, "FINALLY: a more direct test of the 'feedback theory'//Using Sebutape test-strips, of course!". It's in the Acne Research forum.

 

[Bryan]

If you get the chance Bryan could you take a look at my question here
viewtopic.php?f=23&t=42194
would really love to get an answer on this - I suspect not much is known for certain though.

I answered in that thread.

 

[Armando Jose]

Hi Bryan;

thank you for your suggestion. I have three daughters, 13,12 and 10 years old. The idea is test the hypothesys in children about four o five years old, no more.

Why do you suggest NO MORE than four or five years old?? If you were to test the scalp sebum secretion in your 10 year-old daughter and found that it is indeed still virtually nonexistent (assuming that she's not experiencing precocious puberty), then wouldn't that ALSO spell doom for your sebum-is-required-for-hairgrowth theory?

[quote="Armando Jose"nq896r1]I'll try to purchase sebum strip test in order to make any measure, shaving the area to test.

I look forward to hearing your results! I hope that you post all the details of how you did the test, and scan the actual test-strip results, so I can download them and take a look at them.

BTW, I did that exact same thing over on acne.org a couple of years ago when I ran a test on my own face to prove that washing my skin doesn't cause an increase in sebum production (see the third statement in my signature-file below). I used Sebutape test-strips, and I scanned them and posted them for everyone to see for themselves. I posted all the details of the experiment and the scans of the test-strips over there in a thread titled, "FINALLY: a more direct test of the 'feedback theory'//Using Sebutape test-strips, of course!". It's in the Acne Research forum.[/quotenq896r1]

I know your experiment and chat in acne.org.

Thank you again my friend Bryan. I have just send an e-mail to Cuderm to inform about this product, is Houston near from Dallas?
CuDerm Corporation
2929 Carlisle, Ste.380
Dallas, TX 75204
USA

My little daughter is the unique prepubertal till now. I'll see, but I don't want have problem with the age and androgens, so my proposal was in earlier years.

BTW with this experiment I gamble also my thougth about the necessity of sebum for a healthy hair growth.

Have a nice day

Armando

 

[Bryan]

Thank you again my friend Bryan. I have just send an e-mail to Cuderm to inform about this product, is Houston near from Dallas?
CuDerm Corporation
2929 Carlisle, Ste.380
Dallas, TX 75204
USA

Dallas is about 250 miles north of Houston. When I wanted to order my Sebutape test-strips, I just called them on the phone and had a nice chat with them, and ordered a roll of test-strips with my credit card. They were very friendly and pleasant.

My little daughter is the unique prepubertal till now. I'll see, but I don't want have problem with the age and androgens, so my proposal was in earlier years.

But you understand the point I'm making, right? If you find little or no sebum production in your 10 year-old daughter (which is what I expect you to find), then you CERTAINLY couldn't expect to find any in an even YOUNGER child!

 

[Armando Jose]

Thank you again my friend Bryan. I have just send an e-mail to Cuderm to inform about this product, is Houston near from Dallas?
CuDerm Corporation
2929 Carlisle, Ste.380
Dallas, TX 75204
USA

Dallas is about 250 miles north of Houston. When I wanted to order my Sebutape test-strips, I just called them on the phone and had a nice chat with them, and ordered a roll of test-strips with my credit card. They were very friendly and pleasant.

[quote="Armando Jose":1f9oo547]My little daughter is the unique prepubertal till now. I'll see, but I don't want have problem with the age and androgens, so my proposal was in earlier years.

But you understand the point I'm making, right? If you find little or no sebum production in your 10 year-old daughter (which is what I expect you to find), then you CERTAINLY couldn't expect to find any in an even YOUNGER child![/quote:1f9oo547]

Good Morning Bryan;

I sent an e-mail to Dr. Miller and I am waiting to receive some samples of sebutape patches. All is well in this isuue.

About the age of the persons to test, I only want to avoid problems with precocious puberty, but you are right when You point out that if I don't find sebum production in 10-years old daughter, I never would find it at earlier age.

Have a nice day

Armando

 

[harold]

Hey posted this in a new thread viewtopic.php?f=32&t=42412
but I think there is some very interesting stuff for this whole debate on ROS and the balding hair follicle.
Read on....

J Invest Dermatol. 2007 Nov 8; [Epub ahead of print]Click here to read
Premature Senescence of Balding Dermal Papilla Cells In Vitro Is Associated with p16(INK4a) Expression.
Bahta AW, Farjo N, Farjo B, Philpott MP.

1Centre for Cutaneous Research, Institute of Cell and Molecular Science, Barts and The London, Queen Mary's School of Medicine and Dentistry, Queen Mary College, London, UK.

Androgenetic alopecia (Androgenetic Alopecia), a hereditary disorder that involves the progressive thinning of hair in a defined pattern, is driven by androgens. The hair follicle dermal papilla (DP) expresses androgen receptors (AR) and plays an important role in the control of normal hair growth. In Androgenetic Alopecia, it has been proposed that the inhibitory actions of androgens are mediated via the DP although the molecular nature of these interactions is poorly understood. To investigate mechanisms of Androgenetic Alopecia, we cultured DP cells (DPC) from balding and non-balding scalp and confirmed previous reports that balding DPC grow slower in vitro than non-balding DPC. Loss of proliferative capacity of balding DPC was associated with changes in cell morphology, expression of senescence-associated beta-galactosidase, as well as decreased expression of proliferating cell nuclear antigen and Bmi-1; upregulation of p16(INK4a)/pRb and nuclear expression of markers of oxidative stress and DNA damage including heat shock protein-27, super oxide dismutase catalase, ataxia-telangiectasia-mutated kinase (ATM), and ATM- and Rad3-related protein. Premature senescence of balding DPC in vitro in association with expression of p16(INK4a)/pRB suggests that balding DPC are sensitive to environmental stress and identifies alternative pathways that could lead to novel therapeutic strategies for treatment of Androgenetic Alopecia.Journal of Investigative Dermatology advance online publication, 8 November 2007; doi:10.1038/sj.jid.5701147.

 

[tino]

Hey posted this in a new thread viewtopic.php?f=32&t=42412
but I think there is some very interesting stuff for this whole debate on ROS and the balding hair follicle.
Read on....

J Invest Dermatol. 2007 Nov 8; [Epub ahead of print]Click here to read
Premature Senescence of Balding Dermal Papilla Cells In Vitro Is Associated with p16(INK4a) Expression.
Bahta AW, Farjo N, Farjo B, Philpott MP.

1Centre for Cutaneous Research, Institute of Cell and Molecular Science, Barts and The London, Queen Mary's School of Medicine and Dentistry, Queen Mary College, London, UK.

Androgenetic alopecia (Androgenetic Alopecia), a hereditary disorder that involves the progressive thinning of hair in a defined pattern, is driven by androgens. The hair follicle dermal papilla (DP) expresses androgen receptors (AR) and plays an important role in the control of normal hair growth. In Androgenetic Alopecia, it has been proposed that the inhibitory actions of androgens are mediated via the DP although the molecular nature of these interactions is poorly understood. To investigate mechanisms of Androgenetic Alopecia, we cultured DP cells (DPC) from balding and non-balding scalp and confirmed previous reports that balding DPC grow slower in vitro than non-balding DPC. Loss of proliferative capacity of balding DPC was associated with changes in cell morphology, expression of senescence-associated beta-galactosidase, as well as decreased expression of proliferating cell nuclear antigen and Bmi-1; upregulation of p16(INK4a)/pRb and nuclear expression of markers of oxidative stress and DNA damage including heat shock protein-27, super oxide dismutase catalase, ataxia-telangiectasia-mutated kinase (ATM), and ATM- and Rad3-related protein. Premature senescence of balding DPC in vitro in association with expression of p16(INK4a)/pRB suggests that balding DPC are sensitive to environmental stress and identifies alternative pathways that could lead to novel therapeutic strategies for treatment of Androgenetic Alopecia.Journal of Investigative Dermatology advance online publication, 8 November 2007; doi:10.1038/sj.jid.5701147.

this is interesting.I have orderd the full text.It seems that they think the same like we do.

 

[pproctor]

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.

Dr P sez: True, there is a question about whether ROS-induced cellular damage per se is directly involved in the balding process. More likely, ROS act as mediators in something called "Redox Signaling", a concept originated by yours truly several decades ago. See, e.g., http://www.redoxsignaling.com . There is even a journal named "Redox Signaling".

Interestingly, it was the chance discovery that superoxide dismutase prevents telogen effluvium in diabetic rodents that clued me that we were looking at a messenger-mediated process and not direct cellular damage per se. The hair cycle is a very complicated developmental process, with the hair follicle being a kind of miniature organ. Ergo, anything that affects it in such a specific way must be some kind of cellular messenger. Likewise, it became evident that free radicals and the like are cellular messengers in general.

Eventually, I nailed down patents on all sorts of agents which affect this fundamental process for "cellular damage to tissues"-- SOD's, spintraps, and spin labels in particular. The spin label TEMPOL is now in clinical trials for radiation alopecia.

Interestingly, TGF-beta is strongly under the control of ROS. I won't bore you with the myriads of papers. Go to http://www.pubmed.gov and do a search.

Peter H. Proctor, PhD,MD