DHT and Testosterone kills hair DIRECTLY........study

[docj077]

It's okay, Foote. I understand you're scared of defending your theory.

You still haven't proven anything to me. I undertand, you don't have any scientific studies to back up your claims. Merely a beginning and an end with no middle. Like a sloppy sh*t sandwich minus the sh*t.

As for that website, find a study that proves what it says. My pathology book says differently.

Clinical course:

Varicose dilation of veins renders the valves incompetent and leads to venous stasis, congestion, edema, pain, and thrombosis. The most disabling sequelae include persistant edema in the extremity and trophic changes in the skin that lead to dermatitis, ulcerations, vulnerability to injury, and poorly healing wounds and infections that become chronic varicose ulcers.

Morphology:

Veins with varicosities are dilated, tortuous, elongated, and scarred, with thinning at the ponits of maximal dilation. Intraluminal thrombosis and valvular defomities are frequently discovered when these vessels are opened. Microscopically, the changes consist of variations in the thickness of the wein wall cfaused by dilation in some areas and by compensatory hypertrophy of the smooth muscle and subintimal fibrosis in others. Frequently there is elastic tissue degeneration and spotty calcifications within the meda.

Notice the lack of any mention of an inflammatory response in the vein. There can be associated responses around the vein at the sites of ulceration and inflammation, but the vein is not invovled. No neutrophils, no macrophages, and no lymphocytes.

Robbins and Cotran. Pathologic Basis of Disease. 7th edition. copyright 2005.

Seriously, you still haven't proven anything to me.

It's okay. I understand you don't want to defend yourself or your theory. Both positions mean that your argument and your position can not be proven.

 

[docj077]

Also, Foote, I'm waiting on your molecular mechanisms.

Don't disappoint me.

 

[Widows_Peak]

Hello all,

I saw this study on another site and wanted to comment on it.
I haven't read through all 22 pages of this thread, so forgive me if someone has said some of this before.

One of the first responders, Bryan, essentially said what I was thinking.
"Well, it doesn't conclusively PROVE that testosterone can do that, since it obviously could have been metabolized into DHT after it entered the hair follicle cells."

Here's the thing.....

If high levels of testosterone killed your hair, you would go bald when you hit puberty.
For most men, baldness starts around 30, which is when testosterone levels start to seriously decline.

Eunuchs don't go bald, because there isn't enough T to convert to DHT.
But they also don't regrow their hair, due to the lack of testosterone.

I have been taking beta-sitosterol for over 2 1/2 years and it has regrown a good deal of my hair, as you can see from these photos.

http://hairregrowth.blogspot.com

Beta-sitosterol works by blocking the binding of 5ar to T to make DHT.
Propecia works by "destroying" 5ar, so that T is not converted to DHT.

In both cases, you end up with higher testosterone levels, which leads to hair regrowing.

Here's how testosterone grows hair, according to my research...

http://www.medscape.com/medline/abstrac ... ext=orgasm

Endocrine response to masturbation-induced orgasm in healthy
men following a 3-week sexual abstinence.
Medscape Newsletters

This current study examined the effect of a 3-week period of
sexual abstinence on the neuroendocrine response to
masturbation-induced orgasm. Hormonal and cardiovascular
parameters were examined in ten healthy adult men during
sexual arousal and masturbation-induced orgasm. Blood was
drawn continuously and cardiovascular parameters were
constantly monitored. This procedure was conducted for each
participant twice, both before and after a 3-week period of
sexual abstinence. Plasma was subsequently analysed for
concentrations of adrenaline, noradrenaline, cortisol,
prolactin, luteinizing hormone and testosterone
concentrations. Orgasm increased blood pressure, heart rate,
plasma catecholamines and prolactin. These effects were
observed both before and after sexual abstinence. In contrast,
although plasma testosterone was unaltered by orgasm, higher
testosterone concentrations were observed following the period
of abstinence. These data demonstrate that acute abstinence
does not change the neuroendocrine response to orgasm but does
produce elevated levels of testosterone in males.

Here's how it works:

As we saw from the aforementioned study, abstinence increases
testosterone.
Increased testosterone increases acetylcholine.

http://www3.interscience.wiley.com/cgi- ... 1&SRETRY=0

Testosterone increases acetylcholine receptor number in
the levator ani muscle of the rat.
William V. Bleisch, Allan L. Harrelson, Victoria N. Luine
Rockefeller University, New York, New York 10021

The levator ani muscle of male rats provides a
neuromuscular system in which both the muscle and its
motoneurons have high levels of androgen receptors. Two
weeks of castration caused a 48% loss of acetylcholine
receptors in this muscle. One week of testosterone propionate
injections initiated one week after castration increased
receptor number by 27% over untreated castrate levels.
These changes paralleled changes in muscle protein content. In
contrast, castration and testosterone treatments of castrates
had no effect on total, Triton X-100-extractable
acetylcholinesterase activity. This system may provide a
useful model of synaptic plasticity.

Increased acetylcholine raises Nitric Oxide levels.

http://www.raysahelian.com/nitricoxide.html

Acetylcholine -induced vasodilation is mediated by nitric
oxide and prostaglandins in human skin.
J Appl Physiol. 2005 Feb;98(2):629-32.

Acetylcholine can effect vasodilation by several
mechanisms, including activation of endothelial nitric oxide
synthase and prostaglandin (PG) production. In human skin,
exogenous acetylcholine increases both skin blood flow (SkBF)
and bioavailable nitric oxide levels, but the relative
increase is much greater in SkBF than nitric oxide. This
led us to speculate acetylcholine may dilate cutaneous blood
vessels through PGs, as well as nitric oxide. To test this
hypothesis, we performed a study in 11 healthy people. We
measured SkBF by laser-Doppler flowmetry (LDF) at four skin
sites instrumented for intradermal microdialysis. We conclude
that a portion of the vasodilation effected by exogenous
acetylcholine in skin is due to nitric oxide; however, a
significant portion is also mediated by PGs.

Nitric Oxide initiates and maintains hair growth.

http://www.####.com/newsletter/modules.php?op=modload&name=News&file=article&sid=190

The reason NO is of interest where hair loss and growth are
concerned is that those vasodilators in which NO plays a role
stimulate hair growth.

 

[S Foote.]

It's okay, Foote. I understand you're scared of defending your theory.

You still haven't proven anything to me. I undertand, you don't have any scientific studies to back up your claims. Merely a beginning and an end with no middle. Like a sloppy $#iT sandwich minus the $#iT.

As for that website, find a study that proves what it says. My pathology book says differently.

OH i see "you" have a book!

Well good for you :wink:

I have defended my theory with proper references. I cannot help the fact that you are obviously on another planet!

I am just too busy talking to real scientists at the moment, to be bothered with responding anymore to this BS! :roll:

This is my last post in this thread.

S Foote.

 

[amibald]

Hello all,

I saw this study on another site and wanted to comment on it.
I haven't read through all 22 pages of this thread, so forgive me if someone has said some of this before.

One of the first responders, Bryan, essentially said what I was thinking.
"Well, it doesn't conclusively PROVE that testosterone can do that, since it obviously could have been metabolized into DHT after it entered the hair follicle cells."

Here's the thing.....

If high levels of testosterone killed your hair, you would go bald when you hit puberty.
For most men, baldness starts around 30, which is when testosterone levels start to seriously decline.

Eunuchs don't go bald, because there isn't enough T to convert to DHT.
But they also don't regrow their hair, due to the lack of testosterone.

I have been taking beta-sitosterol for over 2 1/2 years and it has regrown a good deal of my hair, as you can see from these photos.

http://hairregrowth.blogspot.com

Beta-sitosterol works by blocking the binding of 5ar to T to make DHT.
Propecia works by "destroying" 5ar, so that T is not converted to DHT.

In both cases, you end up with higher testosterone levels, which leads to hair regrowing.

Here's how testosterone grows hair, according to my research...

http://www.medscape.com/medline/abstrac ... ext=orgasm

Endocrine response to masturbation-induced orgasm in healthy
men following a 3-week sexual abstinence.
Medscape Newsletters

This current study examined the effect of a 3-week period of
sexual abstinence on the neuroendocrine response to
masturbation-induced orgasm. Hormonal and cardiovascular
parameters were examined in ten healthy adult men during
sexual arousal and masturbation-induced orgasm. Blood was
drawn continuously and cardiovascular parameters were
constantly monitored. This procedure was conducted for each
participant twice, both before and after a 3-week period of
sexual abstinence. Plasma was subsequently analysed for
concentrations of adrenaline, noradrenaline, cortisol,
prolactin, luteinizing hormone and testosterone
concentrations. Orgasm increased blood pressure, heart rate,
plasma catecholamines and prolactin. These effects were
observed both before and after sexual abstinence. In contrast,
although plasma testosterone was unaltered by orgasm, higher
testosterone concentrations were observed following the period
of abstinence. These data demonstrate that acute abstinence
does not change the neuroendocrine response to orgasm but does
produce elevated levels of testosterone in males.

Here's how it works:

As we saw from the aforementioned study, abstinence increases
testosterone.
Increased testosterone increases acetylcholine.

http://www3.interscience.wiley.com/cgi- ... 1&SRETRY=0

Testosterone increases acetylcholine receptor number in
the levator ani muscle of the rat.
William V. Bleisch, Allan L. Harrelson, Victoria N. Luine
Rockefeller University, New York, New York 10021

The levator ani muscle of male rats provides a
neuromuscular system in which both the muscle and its
motoneurons have high levels of androgen receptors. Two
weeks of castration caused a 48% loss of acetylcholine
receptors in this muscle. One week of testosterone propionate
injections initiated one week after castration increased
receptor number by 27% over untreated castrate levels.
These changes paralleled changes in muscle protein content. In
contrast, castration and testosterone treatments of castrates
had no effect on total, Triton X-100-extractable
acetylcholinesterase activity. This system may provide a
useful model of synaptic plasticity.

Increased acetylcholine raises Nitric Oxide levels.

http://www.raysahelian.com/nitricoxide.html

Acetylcholine -induced vasodilation is mediated by nitric
oxide and prostaglandins in human skin.
J Appl Physiol. 2005 Feb;98(2):629-32.

Acetylcholine can effect vasodilation by several
mechanisms, including activation of endothelial nitric oxide
synthase and prostaglandin (PG) production. In human skin,
exogenous acetylcholine increases both skin blood flow (SkBF)
and bioavailable nitric oxide levels, but the relative
increase is much greater in SkBF than nitric oxide. This
led us to speculate acetylcholine may dilate cutaneous blood
vessels through PGs, as well as nitric oxide. To test this
hypothesis, we performed a study in 11 healthy people. We
measured SkBF by laser-Doppler flowmetry (LDF) at four skin
sites instrumented for intradermal microdialysis. We conclude
that a portion of the vasodilation effected by exogenous
acetylcholine in skin is due to nitric oxide; however, a
significant portion is also mediated by PGs.

Nitric Oxide initiates and maintains hair growth.

http://www.####.com/newsletter/modules.php?op=modload&name=News&file=article&sid=190

The reason NO is of interest where hair loss and growth are
concerned is that those vasodilators in which NO plays a role
stimulate hair growth.

i just read that last bit, vasodilation if i remember clearly is the enlarging of the blood vessels which increases blood flow, im pretty sure in certain individuals where hair loss is caused by non genetic factors, and problems to the scalp, increased bloodflow allows more oxygen and other nutrients to be carried to the follicle, thus a possibility of stimulating hair growth.

Cheers

 

[docj077]

It's okay, Foote. I understand you're scared of defending your theory.

You still haven't proven anything to me. I undertand, you don't have any scientific studies to back up your claims. Merely a beginning and an end with no middle. Like a sloppy $#iT sandwich minus the $#iT.

As for that website, find a study that proves what it says. My pathology book says differently.

OH i see "you" have a book!

Well good for you :wink:

I have defended my theory with proper references. I cannot help the fact that you are obviously on another planet!

I am just too busy talking to real scientists at the moment, to be bothered with responding anymore to this BS! :roll:

This is my last post in this thread.

S Foote.

Like I said, you can't defend your theory on the molecular level. Thus, it fails.

 

[htownballa]

All of your theories are WRONG

 

[wookster]

:freaked: :freaked: :freaked:

http://veille-srv.inist.fr/bin/dilib/Ap ... wsh+040938

From a population survey of 828 healthy families comprising 3000 individuals, we identified 58 young bald men (aged 18-30 y) and 114 older nonbald men (aged 50-70 y) for a case control comparison. No significant differences were found between cases and controls in allele, genotype, or haplotype frequencies for restriction fragment length polymorphisms of either gene. These findings suggest that the genes encoding the two 5alpha-reductase isoenzymes are not associated with male pattern baldness. Finally, no clear inheritance pattern of male pattern baldness was observed. The relatively strong concordance for baldness between fathers and sons in this study was not consistent with a simple Mendelian autosomal dominant inheritance. A polygenic etiology should be considered. ;

 

[michael barry]

Wookie,

I see what you posted about no difference in the genetic inheritence of male pattern baldness males and non-male pattern baldness males. However, isn't it your hair's dermal papilla's instructions once DHT is transcripted that is the "difference" between men who go bald and men who dont?

Byran has posted in the past studies where male hormone is added to hairs from the back and sides of the head, and nothing happens. Testosterone added to hair from a male pattern baldness-area, sees slowing of the growth of the hair. Its "sensitive" to it. Alpecin.com has PDF downloads of the experiments conducted by a German University (Jena) that adds testosterone to male pattern baldness hairs and a control group that added nothing to other male pattern baldness hairs. The testosterone groups hair grew much slower for the ten day cultivation period. Groups that had caffeine added overcame testosterone's effect and grew just as well as the control group with nothing added. The group that had no testosterone AND caffeine grew fastest of all. This was conducted at a German University. Its described in the 2006 European Hair Research Society abstracts. I have the links if you'd like.

Ive seen Ken Washenik describe the process whereby skin grows upwards from the brow in embryological development. He thinks something happens within this time that makes hair more susceptible to androgens later in life. If you seen the way he described it, the skin follows the male pattern baldness pattern as it develops over the fetal cranium. Temples first over the top, meeting in the back (vertex bald spot). I thought that was interesting.


I work with a balding man who has a buzzcut. That decisive LINE that demarcates his increasing bald spot. Hair is heavy and thick below it (the horseshoe), but above it quite thin. He has a buzzed tuft surrounded by skin, and thin hair like in the vertex over the top. Deepest temporal recession points are peach fuzz. SIdes are recessed, not back to the ears, but are getting there.

It seems as if there is a LINE of seperation where the skin developed differently. Perhaps the skin grew upwards from the neck in fetal development in the wreath area or a mixture of growth from the front and back?

Tom Hagerty has mentioned that the galea in puberty with boys who have high testosterone gets thicker. Ive considered the possibility that this might impede drainage and give DHT made in the root sheath a few more oppurtunities to bind before it gets drained downward or the impeded circulation provides a stagnant environment for androgens to to "stay" in for a bit longer, thus giving them extra chances of hooking up with a dermal papilla receptor during this time. Ive seen scientist speculate that high androgens during puberty might cause baldness before.

You know though man, for us.........................really doesnt matter as we are past puberty and cant go back and do anything about it.


By the way Wookie, what is your regimine these days?

 

[amibald]

i get the feeling that some of you are doctors here... seriously. or advanced minds.

 

[wookster]

Wookie,

I see what you posted about no difference in the genetic inheritence of male pattern baldness males and non-male pattern baldness males. However, isn't it your hair's dermal papilla's instructions once DHT is transcripted that is the "difference" between men who go bald and men who dont?

:freaked: :freaked: :freaked:

Nitric oxide and prostaglandins modulate lymphatic vasomotion, and, compounds like minoxidil and latanoprost[a prostaglandin analog] stimulate hair growth. Obviously for Mr. Foote's contact inhibition and consequent follicular miniaturization to occur, a constant minimal pressure must be maintained in the scalp hypodermal tissues. I suppose that random fluctuations in hydrostatic pressure above that minimal ceiling pressure could occur though...

:hairy: :hairy: :hairy:

 

[docj077]

:freaked: :freaked: :freaked:

http://veille-srv.inist.fr/bin/dilib/Ap ... wsh+040938

From a population survey of 828 healthy families comprising 3000 individuals, we identified 58 young bald men (aged 18-30 y) and 114 older nonbald men (aged 50-70 y) for a case control comparison. No significant differences were found between cases and controls in allele, genotype, or haplotype frequencies for restriction fragment length polymorphisms of either gene. These findings suggest that the genes encoding the two 5alpha-reductase isoenzymes are not associated with male pattern baldness. Finally, no clear inheritance pattern of male pattern baldness was observed. The relatively strong concordance for baldness between fathers and sons in this study was not consistent with a simple Mendelian autosomal dominant inheritance. A polygenic etiology should be considered. ;

The question is, why didn't they look at the androgen receptor on the X-chromosome where known triplet repeat mutations have occurred in vivo and have been proven through gene analysis.

There will be no difference in balding vs. non-balding males with male pattern baldness if you look at the 5AR enzymes and genes. Every male has them unless you have a true gene mutation causing a deficiency. It's what gives them secondary sex characteristics.

Also, the 5AR enzyme genes are autosomal, but the androgen receptor gene is X-linked.

Their study was looking on the wrong chromosomes for genes that are known to not influence male pattern baldness whatsoever. Only their enzymatic products influence male pattern baldness and they are not overproduced in male pattern baldness.

 

[Bryan]

Wookie,

I see what you posted about no difference in the genetic inheritence of male pattern baldness males and non-male pattern baldness males. However, isn't it your hair's dermal papilla's instructions once DHT is transcripted that is the "difference" between men who go bald and men who dont?

Nitric oxide and prostaglandins modulate lymphatic vasomotion, and, compounds like minoxidil and latanoprost[a prostaglandin analog] stimulate hair growth. Obviously for Mr. Foote's contact inhibition and consequent follicular miniaturization to occur, a constant minimal pressure must be maintained in the scalp hypodermal tissues. I suppose that random fluctuations in hydrostatic pressure above that minimal ceiling pressure could occur though...

It's interesting to me that your "response" to Michael had nothing to do with what he actually said. Wookie, your posts have always struck me as being rather odd and oblique.

Bryan

 

[CCS]

Wookie,

I see what you posted about no difference in the genetic inheritence of male pattern baldness males and non-male pattern baldness males. However, isn't it your hair's dermal papilla's instructions once DHT is transcripted that is the "difference" between men who go bald and men who dont?

Nitric oxide and prostaglandins modulate lymphatic vasomotion, and, compounds like minoxidil and latanoprost[a prostaglandin analog] stimulate hair growth. Obviously for Mr. Foote's contact inhibition and consequent follicular miniaturization to occur, a constant minimal pressure must be maintained in the scalp hypodermal tissues. I suppose that random fluctuations in hydrostatic pressure above that minimal ceiling pressure could occur though...

It's interesting to me that your "response" to Michael had nothing to do with what he actually said. Wookie, your posts have always struck me as being rather odd and oblique.

Bryan

I'll answer Micheal's question somewhat. I read that balding hair has twice as much DHT as non-balding hair, as well as twice as many androgen receptors, on average. Anyone know if that is true? Then docj077 says that how the instructions are carried out is different. Maybe all of the above.

Yeah, so dutasteride = first defense. Topical spironolactone = second defence (GTE can help here too) and then GTE and procyanidins B-2, B-3 and C1 as the next defense to post bonding problems, and then there is other stuff to for other angles, many of which overlap.

 

[michael barry]

Collegechemistrystudent wrote: "Yeah, so dutasteride = first defense. Topical spironolactone = second defence (GTE can help here too) and then GTE and procyanidins B-2, B-3 and C1 as the next defense to post bonding problems, and then there is other stuff to for other angles, many of which overlap"

Collegechemistrystudent, I looked up that applepoly proanthocyandin site again (I have some of that stuff) and lo and behold, just as you said, they "added C-1 {grapeseed} and B-3 {barley} proanthocyanidins. Good stuff man.


The scenario you describe above would seeminlgy be a good way to stop/slow further baldness to a great degree if the products are active for enough hours.











Wookie,
Why do you think prostaglandin analogues like GLA, latanaprost, and much more weakly, minoxidil, often see the melanocytes DARKEN existing hair?

Tom Hagerty, who has taken black currant or borage seed oil internally for years, has darker hair now at 74 than he did in his youth. He started balding at 19, but has kept his hair. Both black currant and borage seed oils have GLA, a prostaglandin E-1 precurser. I used to have (cant find it) his scalp excercise video. Dark brown hair. It used to be blonde.

I have been using a little loreal anti-frizz serum before grooming for several months and sometimes have used Nanoguard shampoo that also contains borage seed oil over the past year {out of that now}. I used to have blonde hair. Now its damn near medium brown. My uncle remarked at a wedding that "your hair gets darker and darker every time I see you" and how I used to be "towheaded (very light blonde)" when I graduated high school. It would seem prostaglandins effect melanocytes directly to me.

Bryans prox-n photos on this website in the gallery section show that Dr. Proctors very good (my opinion) prox-N apparently effect melanocytes also as his slightly greying hair definitely got darker (and more abundant) during its use in which he used no anti-androgens at all. There is abscorbyl palmitate in Prox-N and we both know that excited follicle cells directly in experiments as well as copper peptides, a particular kind of which was shown by Korean researchers to protect whole hairs from apoptosis ex vivo. Zinc, in good doses also helps protect against greying.

I'll never forget Tom Hagerty posting that melanocytes only make up about 1% of the hair follicle, but control the color of your hair. They die off somewhat...................you get grey hair. Keep em' alive, your hair will get as dark as the blotting pattern they are genetically inscribed with will allow. Red-heads for instance have a staining pattern of direct LARGE blots of melanin staining seperating from each other with lots of space between them. Blondes have lots of SMALL blots, without much space between them. Black hair has large blots relatively close together...............making all the hair dark. We can "amp" up the blotting, but cannot seem to make the genetic instructions for the blotting turn blonde hair red or black because of the "print" pattern genetically given to the melanocytes. Its FASCINATING to me that something that small can make such a huge difference in someone's appearance.

 

[michael barry]

Stephen will love this: http://ajpregu.physiology.org/cgi/conte ... 274/3/R790

and especially this : http://content.karger.com/ProdukteDB/pr ... elNr=68942


I'll say this in response to prostaglandin E-1 and lymphatic vaosomotion and Stephen's theory........................this is why I'd like to see Stephen get his theory tested finally and officially. So we could either pursue it or forget it. Lots of coincidences like I list earlier in the thread incredibly seeminlgy fit his idea. That prostaglandin analogues apparently slow the pumps indirectly buy f*****g with the capillaries beneath them, thus lowering upward pressure on the scalp................is 'convienient' to his idea.


Yet another coincidence. Stephen, I hope you can get your idea studied someday to give yourself personal satsfaction yea or nea. I have a very hard time thinking so many scientists who are balding themselves the world over could have all missed something one man could spot, but you still deserve that confirmation.

 

[CCS]

I have a very hard time thinking so many scientists who are balding themselves the world over could have all missed something one man could spot, but you still deserve that confirmation.

Never think that way. My professor told me if I can research and find something better than propecia, businesses would have found it first and been marketting it, and since they have not, I should give up. Yet look at all the info we have that most balding doctors don't, that is not even sold.

Anyway, thanks for the updates. I found borageseed oil for $120 per 7 pounds. It is for making soaps. I'd like to buy it and split it 4 ways, $30 per person, so we get 1L each and can take 2-3 grams in a year if we want. It might last that long in the freezer if we mix in some anti-oxidants. If no one is interested, I'll have to buy 32oz for $50 at another site. It is organic and intended for eating. I put the stuff in my minoxidil too, though I have capsules, 60 1g caps for $22. That is about 15x the price of the gallon. Who's interested? $2.5 per month.

And what are prostaglandin analogues? Will borage oil make them or make a different kind? Just wondering if what foot said would mean my treatment is bad in anyway, just in case. What is his proposed solution, anyway?

 

[michael barry]

Collegechemistrystudent,

Just buying the latanaprost would be cheaper. And its an analouge of three or four different prostaglandins. However the E-1 prostaglandin, the one borage ups...............seems to be the primary one.


Dr. Hideo Uno, who wrote the manual on minoxidil for Upjohn pharacueticals (back when they were in business) did his last experiment before reitrement with RU58841, minoxidil 5% and latanaprost .05% in stumptailed macaques..............................he considered the results "even", so latanaprost must be pretty strong stuff. You can buy it up to 5% in concerntration and take borage seed oil internally in tablets. Getting it above and below if you know what I mean. I had found a canadian site that sold the stuff relatively cheap if you bought alot of it.......................dont have the link handy.

Heres the link about prostaglandin and latanprost http://dermatology.cdlib.org/93/comment ... /wolf.html

Interesting sh*t isnt it?

 

[abcdefg]

Hey you guys are pretty smart. What do you think of propecia and long term safety? Is lowering DHT going to cause chaos with DHT being in the brain, liver, skin.

 

[docj077]

I talked to a dermatopathologist today...

I spoke with Dr. Koch, a dermatopatholigist in Sioux Falls, South Dakota today and I wanted to demonstrate to you all a very interesting case along with the discussion we had together.

First, I spoke with Dr. Koch about the differences in the scalp in men with no androgenic alopecia and men with androgenic alopecia. As I feared, he told me that microscopic examination of men with androgenic alopecia clearly demonstrates both fibrosis and collagen deposits.

I also asked him about about a possible inflammatory component. His response was that there is rarely edema, but in people with an inflammatory component in their hair loss, immune system infiltrates are observed. He also mentioned that the edema is secondary to the immune response.

The following article is an interesting case involving a post-menopausal woman going through post-menopausal frontal fibrosing alopecia. This disorder, which is recognized in women, begins after menopause and can involve both scalp hair and eyebrows.

http://dermatology.cdlib.org/114/NYU/NYUtexts/0315059.html

Even with the inflammatory component being present, no anti-inflammatory drugs work and no cure has yet been found. Typically, there are no autoimmune signs as the antinuclear antibody and dsDNA antibody tests come back negative. Also, the erythrocyte sedimentation rate is typically normal which is sometimes elevated in people with ongoing inflammatory responses such as in Giant Cell Temporal Arteritis.

The slide of a hair follicle undergoing the fibrotic response is very similar to what Dr. Kock described to me. You can see the clear collagen deposition around the follicle and the immune response in the form of the little nuclei scattered about.

What I find interesting is that this disease typically takes place after menopause during a time when a female is very susceptible to androgens in her body. Her female sex hormones no longer protect her.

So, what I'm trying to figure out is, if this occurs in women and it turns out to be androgen related, then it must be DHT and testosterone that cause the same phenomenon in men.

I emailed NYU medical school and I have not received a reply. I will try again if they do not reply to my mail.

The article is quite fascinating and I urge the scientifically adept to read it.