Has Anyone Questioned Androgenetic Factors

[Bryan]

Yes but even if you believe that scalp follicles are being subject to "unnaturally harsh" conditions - a controversial contention - the fact is that some people go bald, and others don't, when exposed to those same conditions.

No, I believe that in susceptible men, follicles are exposed to harsh environments. I believe that even in non-bald men, the same exposure will damage the follicles.

Really? Then why don't beards ever go bald? :wink:

A recent experiment that involved male and female mice may indicate that male hormones play a less-than significant role in pattern hair loss.
In this experiment, immunodeficient male and female mice were grafted with scalp tissue that contained vellus looking hairs from human male and female donors affected by pattern hair loss 8.
In 15 to 20 weeks after the transplant, the vellus looking hair grew into terminal (normal) hair. The then vellus looking hair even surpassed the terminal hairs in diameter. The fact that the results were equally the same with male and female mice 8 is an indication that there is something else in humans besides androgenetic factors.
8. Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice Rozlyn A. Krajcik, PhD, Joseph H. Vogelman, DEE, Virginia L. Malloy, MS, and Norman Orentreich, MD Cold Spring-on-Hudson, New York

CAN SOMEONE TELL ME WHERE THE SUPPOSED 'ANDROGEN DEPENDENT OR SENSITIVE FOLLICLES ARE???

Did you ever consider that maybe, just maybe, there wasn't a high enough level of androgens in those mice to suppress the growth of the transplanted hair follicles?

Bryan

 

[bobmer]

No. The level of androgens is immaterial. The sensitivity or the number of androgen receptors is what seem to be the problem.

The experiment involved only two subjects. We can assume that they are right but only with those two subjects. We can also assume that the others are right too. But if they are both right, it can only mean that hair loss is multifactorial.

The very reason I refrain from contesting many claims. I don't have the silver-bullet mentality of most people. But I strongly disagree that 'defective' genes are involved.

Really? Then why don't beards ever go bald?

If you went through my previews posts, you would have known why.

 

[So]

Bomberman,

I am interested for several reasons.

If you want a database of 10,000+ interested buyers then there is a specific way in which you should go about achieving this.

Frankly, these forums are not going to yield you too much interest, also for several reasons. You may be lucky to garnish a few souls! I am one of those for pure curiosities sake, but I doubt I am prepared to wait for a hard back or paper back to go to press.

People selling products on forums like this and other hair loss sites do not fair well in general. There is a stigma associated with people like you, that of a snake oil merchant, even if you're only selling "text" as such.

What you need is a bona fide Internet marketer to help you build your double opt in list of genuinely interested buyers.

... and guess who is a bona fide Internet marketer, search engine optimizer, extraordinaire? :wink:

 

[bobmer]

I guess we be on to a totally different topic. You know the site i put up? Contact me through the email address I have there.

I say again . . . . KUDOS TO THIS SITE FOR BEING FAIR.

 

[Armando Jose]

Bobmer;

Do you ask yourself the possibility of existence of androgens in hair follicle environment before puberty in both sexes?
I think that it is vital a certain level of androgens in healthy hairs, in other things to have a functional sebaceosu gland. Then, androgens are neccesary years before puberty. What do you think?

BTW, I am with you, genetics are only a factor in common baldness.

Armando Jose wrote:
Androgens inside the hair follicle are the important ones in common baldness. Do you agreed?


The important ones are testosterone from outside the hair follicle, and DHT from inside the hair follicle.

Bryan, thank you for your reply but then, are a great difference in men and women respect DHT?

Armando

 

[Pondle]

Bryan, thank you for your reply but then, are a great difference in men and women respect DHT?

From a study in the Journal of Investigative Dermatology, (1997) 109, 296–300

Different Levels of 5-Reductase Type I and II, Aromatase, and Androgen Receptor in Hair Follicles of Women and Men with Androgenetic Alopecia
Marty E Sawaya and Vera H Price

There are marked quantitative differences in levels of androgen receptors and the three enzymes, which we find to be primarily in the outer root sheath of the hair follicles in the two genders. Androgen receptor content in female frontal hair follicles was approximately 40% lower than in male frontal hair follicle. Cytochrome P-450-aromatase content in women's frontal hair follicles was six times greater than in frontal hair follicles in men. Frontal hair follicles in women had 3 and 3.5 times less 5- reductase type I and II, respectively, than frontal hair follicles in men. These differences in levels of androgen receptor and steroid-converting enzymes may account for the different clinical presentations of androgenetic alopecia in women and men.

 

[Armando Jose]

Yes, Pondle, there is a lot of studies regarding the difference in androgens receptors between sexes, but the question is refered to healthy subjets.
It is normal that genetic expresion change with the enviroment in persons afected by common baldness, but what happen in healthy people, is there a great difference?

Armando

 

[Pondle]

Increased androgen binding capacity in sebaceous glands in scalp of male-pattern baldness.Sawaya ME, Honig LS, Hsia SL.
Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Florida 33101.

Sebaceous glands were isolated by manual dissection under a microscope from surgical specimens of scalp skin with male pattern baldness and skin specimens of hairy and bald scalp obtained at autopsy. The 800 X g pellet (nuclear fraction) and the 164,000 X g supernatant fraction (cytosol) of homogenates of the sebaceous glands were used for measurements of androgen binding characteristics, using dextran-coated charcoal and sucrose gradient methods. Scatchard plots showed high affinity binding for [3H]dihydrotestosterone (DHT) and [3H]methyltrienolone (R1881). Nuclei prepared from bald scalp contained greater total androgen binding capacity than nuclei of hairy scalp, although Kd values of type I binding were similar (0.68 vs 0.56 nM, respectively). On sucrose gradient, the binding protein from cytosol was found in the 7 to 8S density range. Androgen binding by cytosol of sebaceous glands of hairy scalp had Kd of 1.89 +/- .79 and 2.05 +/- .56 nM for DHT and R1881, respectively, and Bmax of 18.7 +/- 4.4 and 20.0 +/- 4.6 fmol/mg protein for DHT and R1881, respectively. Cytosol from sebaceous glands of bald scalp had Kd values approximately half those of hairy scalp, and Bmax values 50%-100% higher. The bound 3H labeled DHT and R1881 could be partially displaced by testosterone (40-50%), moxestrol (28-32%), promegestone (19-26%), and delta 4-androstenedione (6-12%), but not by dehydroepiandrosterone. These data demonstrate the presence of specific androgen binding protein in sebaceous glands, and that sebaceous glands of bald scalp have greater binding affinity and capacity for androgens than those in hairy scalp. This difference may explain the greater androgenic response in androgenic alopecia.

 

[Bryan]

No. The level of androgens is immaterial. The sensitivity or the number of androgen receptors is what seem to be the problem.

Wow!! So even a SINGLE MOLECULE OF DHT is sufficient to cause balding in men who have that predisposition?? Bobmer, you're a funny guy!

Really? Then why don't beards ever go bald?

If you went through my previews posts, you would have known why.

I believe I went through them, or at least most of them, and I still don't know what your explanation is.

Bryan

 

[bobmer]

You're bringing it out of context. I'll pretend I don't know the reason behind that. Everyone knows that a male mouse has a few hundred times more androgens than a female mouse. That goes with humans too. Do you?

As for beards, I don't think I have to answer that. Logic will simply work in your favor if you use it.

Yes Pondle, many researchers are looking for the answers to 'what and 'how' particularly those who conduct their's under grants from pharmaceuticals. They don't bother much with 'why' because knowing why might lead to NON-pharmacological treatments - that is the last thing pharmaceuticals want. They simply want to know how to intervene in midstream without wanting to prevent it.

The 'why' is this:
You have to go back to basics in cellular biology. Follicles are made up of cells. Hormones are biochemical messengers and contain information for the cells to use. Enzymes are responsible for breaking down nutrients so cells can eat and survive. Cells are very versatile and, as I said, can survive and multiply outside the human body when place in the right environment. IF they starve, they will produce more enzymes and more receptors as a regulatory ability to compensate for lack of nutrients and to survive. The vertex scalp of balding men are not condusive for follicle survival.
Simply put, susceptible or - predisposed as geneticist prefer to call it - men have a health issue that they have to address before it gets to the follicles. That health issue could be anything but indications are strong regarding blood supply because male pattern baldness associates with many blood circulatory diseases. The shinny and smooth scalp of somebald men is a sign of ischemia. ischemis is caused by poor blood perfusion.

They say 'healthy' men go bald. Who says one is healthy... the doctor or his instruments. Who draws teh fine line between healthy and sick.. the government?

This is my last post. I say tah tah. This site is very fair, Kudos again.

 

[michael barry]

Bobmer,

The mice in those studies were immuno-deficient mice. These animals are pretty sick for most of their lives unless they are kept in super-clean environments. Thats a fascinating study, and Stephen Foote was kind enough to share it with us. However, I'd go out on a limb and state the the androgen-levels in the little critters probably was much lower than your average healthy male mouse.

That experiment has not been duplicated that we know of, and the follicles were tested after just 22 weeks or so. They didn't wait a good year or more and check them.


Note: I dont know if Stephen minds me posting this, but he had some very interesting information he posted on another website about some drop-assay type tests with dermal papilla cells and oxides. A small, not lethal amount of a synthetic oxide was added to male pattern baldness-dermal papilla cells, and some to regular head hair cells.

The SMALL, not lethal amount of the oxide damaged and slowed the male pattern baldness-dermal papilla cells enough to impress the researchers. Perhaps androgens somehow "sensitize" hair follciles over time to relatively small amounts of oxides in the body that dont harm other follicles. Its food for thought. Ive seen on Dr. Proctor's site that he suggested that androgens "do something" to follicles that are male pattern baldness follicles, and this gets the attention of the immune system that keeps attacking them everafter.

However, RU58841's success made me think that if we could just block receptor sites, we could keep the attack from occuring. Thats why I'd like to see a great receptor-blocking topical formulated or discovered. ......if you could "stop" the immune attack, then skin-remodellers like prox-n might REALLY have a chance of growing back a suprising amount of hair.....

 

[Bryan]

You're bringing it out of context. I'll pretend I don't know the reason behind that. Everyone knows that a male mouse has a few hundred times more androgens than a female mouse. That goes with humans too. Do you?

No, I do NOT know any such thing, and neither do you! :wink:

The level of androgens in the mice in that study was not measured and not reported, so it's pure speculation on your part what relevance (if any) that has for anything. You have to keep in mind those mice are GENETIC MUTATIONS, and you have no business making speculative claims about the level of androgens in them, or making assumptions about it.

As for beards, I don't think I have to answer that. Logic will simply work in your favor if you use it.

In other words, you have no answer to that! :wink:

Bryan

 

[Bryan]

The mice in those studies were immuno-deficient mice. These animals are pretty sick for most of their lives unless they are kept in super-clean environments. Thats a fascinating study, and Stephen Foote was kind enough to share it with us.

Actually, Michael, _I_ was the first one to post about that study, and Stephen Foote almost wet his pants in excitement, thinking that it somehow supported his own eccentric theory!

Bryan

 

[abcdefg]

The sensitivity or the number of androgen receptors is what seem to be the problem.
I think that is the answer to preventing male pattern baldness. Its stopping the sensitivity to DHT or destroying the receptors where dht binds without altering DHT systemically that we all want. What has taken so long since propecia to do that and give us a safer alternative?

 

[bobmer]

Be careful guys. Bryan is a snake oil merchant.

 

[So]

Are you being sarcastic?

Out of all the content he has wrote, that I have read, I have never been influenced to buy and or try any product.

As such, he does state some high quality information along with a handful of others on this board.

 

[michael barry]

Bobmer,
YOU are the one selling an E-book. Bryan doesn't sell anything.


Im pretty sure I can answer your position on male pattern baldness increasing as industrialization does and it is one word, diet.

Pre-WW2 Japanese ate alot of soy (isoflaovnes, equol, genistien, daidzien)---lower DHT levels, inhibition of PKC, "bound" DHT , drank green tea (ECGC) Inhibits type one alpha five strongly, type two weakly, mild receptor blockage, inhibits TNF-alpha and TGF beta 1 and 2, rice (more sterols in rice bran oil than any other substance, hence some anti-androgenic activity), ate ALOT of fish (fish oil inbibits TNF-alpha, an inflammatory cytokine asssoicated with immune response, at alot of veggies rich in vitamins, silica, various plant sterols................

vs.
Eating alot of insulin-resistance building high glycemic index processed foods and sugars which get the adrenals to pump out more testosterone and DHT (the alpha five reductase type one enzyme is in the adrenal gland also), high glycemic index diets are pro-inflammatory also and will see more inflammatory cytokine production as well as more androgens in the skin.


In conclusion, its not only what they are NOW eating, but what they dont eat anymore so much (especially soy products and green tea) is why more younger men in the far East are seeing their hair thin at earlier ages.


All of this together is more powerful than we probably give it credit to be. Ive seen a few young hispanics and one Asian in particular with thinning hair and acne (the Asian was overweight) and it struck me that this was rare amongst those subsets in the past. Diets are a big thing. These were young people who didnt work in factories and the area Im in doesnt have many industrial enterprises anyway, so there is no way pollution from chimneys is screwing with their hormones here.



All this stuff is moot up to a point Bobmer. I just read about a company called Anaderm that is about to test a topical that will degrade androgen receptors in targeted tissue areas. Thus a real preventive cure to baldness might be available in just a few years because your hair will not have androgen receptors and will be like a woman's hair. Hair Cloning is getting closer to reality as ICX is in phase two trials right now and (somewhat overenthusiatically in my opinion) plans to have a Hair Multiplication protocol from cultured dermal papillas (the person's own) on the market by 2010 (but probably a couple of years later than that in my opinion). So one day, if your hairline is a tad high for your liking, you will be able to "make" more hair to lower it.


Every once in a while a "hippie" type comes into the hairloss forums and declares baldness is just "big pillows, TV sets, electromagnetic waves, poor circulation, modern stress, shampoo (get that one alot), hot shower water, chlorinated shower water, etc.". You have added industrial society, chairs, and a few other vague things.


But you added all of them based on a false premise that is disprovable. Lack of androgens. ...You contended based on a false premise that removal of androgens didn't stop further baldness. This is incorrect. Removal of androgens does indeed stop further baldness and will regrow a little of what is lost, especially if one is young. That increase in haircounts with finasteride in the first two years would be permanent if all androgens were removed. At any rate, the loss of hair thereafter is very slow and nothing like the loss of hair with a placebo.


I hope you make an attempt to quantitatively test your theory however with photographic documentation.



I resent you calling Bryan a snake oil merchant. Ive never seen him try and sell anything, but he's given a favorable opinion of tricomin, fatty acids, sprio, finasteride, dutasteride, ketoconazale, NANO, prox-n, RU58841, minoxidil, the possibliltiy that the various peptides in folligen might help, and retin-A. Ive never heard him claim anything unproven might help. Ive never seen him try and sell anything. Bryan has a high opinion of Proctor's products, but Bryan has proof they work (his two year photo of prox-n success is in the photo gallery of this website in which he got successful results with no anti-androgens at all in his forties, which is impressive). Bryan is a mathematician by trade and has no affiliation with anyone in the hairbiz. Ive disagreed with Bryan before, and have different political convictions than he does, but he's not tried to "snake oil" anyone on HairLossTalk.com in the years Ive read it.

 

[Guest]

Be careful guys. Bryan is a snake oil merchant.

bobmer, you're working on a ban.

 

[Old Baldy]

Be careful guys. Bryan is a snake oil merchant.

What's he sellin'??!! I'll buy it! :wink:

 

[Bryan]

The sensitivity or the number of androgen receptors is what seem to be the problem.

I want to point out here that there are at least a couple of different ways that the term "sensitivity" can be used in this context. What most people mean when they use that word (and what YOU probably mean) is the overall magnitude of the androgenic stimulus and the associated response. Obvious ways to fight that would be to lower androgens somehow, or lower the number of androgen receptors somehow, or inhibit certain important steroidogenic enzymes like 5a-reductase.

What _I_ usually mean when I use the term "sensitivity", though, is entirely different: it's the qualitative response to androgens, as opposed to the quantitative level of response. For example, the fact that beard follicles are actually stimulated by androgens is a qualitative difference in response to androgens, compared to scalp follicles. It has nothing to do with levels of androgens or androgen receptors. I think part of the reason that some people don't go bald is a qualitative difference in their response to androgens. Their scalp follicles have somewhat more of a beard-like quality than the rest of us who are balding.

I think that is the answer to preventing male pattern baldness. Its stopping the sensitivity to DHT or destroying the receptors where dht binds without altering DHT systemically that we all want. What has taken so long since propecia to do that and give us a safer alternative?

Either approach would work: either reducing androgens, or reducing androgen receptors, or both. However, I find it amusing that you think that altering or destroying androgen receptors would be somehow "safer" than merely reducing DHT with finasteride or dutasteride. It would not. For your information, genetic males with Complete Androgen Insensitivity Syndrome (they have non-functional androgen receptors) are more affected by their mutation than the pseudohermaphrodites who are 5a-reductase deficient.

Bryan