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

hans

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JWM said:
Is it possible that some people just are more prone to lose hair from testosterone rather than DHT? I have an inkling that this is possible because there are people that report negative results from taking propecia, which is known to increase your testosterone levels.

I am starting to think this is a possiblity. I have NONE of the typical signs a young man struggling with male pattern baldness has. I have ZERO body hair (people think I shave my legs and arms and my face only needs to be shaved once every few days) and I have never had an oily or problem scalp.

I have always had very thick, dark straight hair. Around 20 years of age I started getting obsessed with bodybuilding. I overtrained and was in the gym 6-7 days a week. After a year or so, my hair began to thin, BUT not in the typical male pattern baldness style. I had no bald spot and no receeding hairline, but I did have a part down the middle of my head get wider and wider.

I decided to try Propecia and after 6 months I noticed the part was even wider! My g/f at the time even joked with me about it. I have since been on finasteride for 8 years now and my loss has continued at a slow pace in the same pattern. I am wondering if simply wouldn't have responded better if I never took finasteride at all and instead tried a topical approach with spironolactone or soemthing.

And BTW, no, I never did roids.

I also never had the classic signs such as excess body hair (i basically have none). However since taking propecia ive noticed few body hairs here and there pop out on my legs and arms which i never had before. Ive also develop scalp pimples and back pimples which i never had before. The worst thing is i started propecia in order to curb a receding hairline, but instead ive notice thinning from all over my head which i never had before. I can even see the hair thin as it goes down to the root since i have longer hair (ive kept my hair long since starting propecia). Whether all these negative things are caused by the extra T produced by propecia, i just dont know...
 

HARM1

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I DO NOT THINK T CAN CAUSE MUCH DAMAGE: The guys with bo DHT and with T never grow bald!!
 

wookster

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DHT causes beard hair and body hair to grow but causes hippocratic wreath hair to also become thinned out?

DHT is an amplified form of T and the sensitivity to DHT and then even T, appears like an allergic reaction, it seems.

There also appear to be androgen independent mechanisms for hair growth that supercede the androgen factors. Copper peptides, superoxide dismutase, minoxidil, cyclosporine, etc. causes scalp hair growth.

And stump tailed macaques can halt baldness 100% of the time with just 5AR inhibitors? Do copper peptides regrow hair on balding stump tailed macaques?

It seems that Foote's hypothesis still cannot be ruled out yet :freaked:
 

Bryan

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wookiewannabe said:
It seems that Foote's hypothesis still cannot be ruled out yet :freaked:

Why do you say that?

Bryan
 

S Foote.

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Bryan said:
michael barry said:
This slams the door on any who say androgens dont cause baldness on the males head.

LOL!! That's certainly true, but there are certain individuals (cough::cough) who, no matter HOW many times they get the door slammed in their face, will continue to deny that that damned door really DID get slammed right on their schnoz! :wink:

Bryan

So yet another "mechanism of the day" to explain the direct theory then Bryan? :roll:

When are people going to realise that these in-vitro tests mean "nothing" at all in the genuine scientific context!

These cultured cells are completely different to the in-vivo cells we need to understand. The cell culturing "itself" creates major genetic changes in these cells, reducing both androgen receptor expression and the expression of 5AR type 2.

Just one example of the blatent contradictions these in-vitro studies throw up, is clear when you compare this study with the others.

The claim in this one is that the growth effect of androgens is "significant" upon cultured DP cells. But other in-vitro tests, androgens have ZERO effect on the growth of DP cells!

It is only when DP cells are co-cultured with outer root sheath cells that growth is effected (according to other in-vitro studies!).

http://endo.endojournals.org/cgi/content/full/138/1/356

So which of these "artificial" studies do we believe?

Non of them is the scientific answer, because we know the cells are changed by culturing so any results cannot be trusted, simple!

Tomato ketchup could cause growth restrictions in such "altered" cells. Do we then say tomato ketchup causes male pattern baldness?

Again, consider this study posted by Michael?

The claim is that even in the Hippocratic wreath, high levels of androgens cause significant hair loss.

Don't you think the body builders etc that shoot themselves up with androgens, would have noticed this in the "real" world?

So where are these reports of "total" scalp hair loss?

These out of context and contradictory studies are just "journal fodder". The motive for such studies is often just to add to a professional scientists CV of "publications".

Bryan now desperate to grasp any straw that could add some spin to his rapidly sinking pet theory, will try to attach some significance to these red herring studies.

But then Bryans regular contradictions in these debates are a simple matter of record, as i have demonstrated time and time again.

At the end of the day, that one "in-vivo" mouse study with "real" male pattern baldness follicles, blows all this in-vitro speculation out of the water!! :wink:

http://www.hairlosshelp.com/forums/mess ... &forumid=1

So where's this immunology "in-vitro"??? :roll: :roll: :roll:

S Foote.
 

michael barry

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Im going to post from the 2006 EHRS society absracts and from other sources concerning tests on WHOLE HAIR FOLLICLES in test tubes and sustances that DIRECTLY AFFECT THEM>

Roxythromicin.
Caffeine.
RU58841

I'll also touch on Latanaprost and Minoxidil and Proanthocyandin B-3 and abscorbic acid (in Prox-N) and Jack Daniels whiskey (dont laugh....you'll see).

Roxythromycin is now in Clinical trials (I have a link) for Androgenetic Alopecia. It was tested in Human hair follicles, obtained from plastic surgery with informed consent, cultured for 6 days. Hair elongation was 1.96 mm's on average in the control group...........................................compared to 3.4 mm's in the Roxythromicyn group (it was only 3.32 mm's in the highest dosage Roxythromicyn group). This is all in vitro. ENTIRE HAIR FOLLICLES IN TEST TUBES.

11 men with Androgenetic Alopecia were given topical roxythromicyn (which is a topical immunosuppressant, anti-microbial, anti-fungal) and 4 showed great improvement, 4 slight improvement, 3 no change in 6 months time. Its now, again, in clinical trials. Its an attempt to interefere with T-cells in the immune response most likely, but it obviously positively effected hairs in test tubes. Source EHRS. http://content.karger.com/ProdukteDB/pr ... =92842.pdf



Now, Caffeine...................some of this will come from Alpecin's site also as well as the EHRS. "Hair follicles from 14 biopsies, taken from vertex areas of male Androgenetic Alopecia patients, were cultivated fro 120-192 hours in the presence of normal William's E medium (control) or William's E medium containing different concentarions of testosterone and/or caffeine. Testosterone alone with the follicles suppressed growth . The WHOLE HAIR FOLLICLES have, of course, alpha five reductase enzymes in the outer root sheath.................so there was DHT made in those test tubes. Over a six to ten day period the Department of Dermatology and Allergology at the Fredrich-Shiller University in Jena, Germany and the University Hospital Schelswig-Holstein, University of Lubeck, Germany found that Testosterone alone inhibited growth, Caffeine alone stimulated growth, and that testosterone and caffeine together produced normal growth and EVEN SLIGHTLY above normal growth. All entire hairs in test tubes.

Tested in vivo over four months, the caffeine complex seen hair counts increase in Androgenetic Alopecia men, but I have not committed the specifics to memory.



RU58841. We all know this. Receptor blocker, Bryan posted on it. Whole follicles for two weeks. Beard hair denied testosterone slows growth, head hair denied testosterone grew much better. Head hair with just testosterone had growth slowed 23% in regards to keratinocyte activity and 12% polymerase DNA/RNA activity. WHOLE FOLLICLES


Copper peptides in South Korea................this was written:
Here is one study:
P38 THE EFFECTS ON HAIR GROWTH OF TRIPEPTIDE-COPPER COMPLEX L-ALANINE-L-HISTIDINE-L-LYSINE-CU2+(AHK-CU) IN CULTURED HUMAN OCCIPITAL DERMAL PAPILLA CELLS
Pyo HK, Yoo HG, Choi SJ, Won CH, Chung JH, Cho KH, Eun HC, Kim KH
Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging & Hair Biology Research, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea

INTRODUCTION: Tripeptide copper complex L-Alanyl-L-histidyl-L-lysine Cu2+ (AHK-Cu) is a growth factor for many kinds of cells. AHK-Cu is also known to increase growth factors such as VEGF and FGF, and to promote wound healing. OBJECTIVE: To evaluate the effect of tripeptide copper complex L-Alanyl-L-histidyl-L-lysine Cu2+ (AHK-Cu) on hair growth. METHODS: Cultured human dermal papilla cells (DPCs) were exposed to AHK-Cu (1 x 10-9 mol/L). The cytotoxicity and proliferation of cultured human DPCs were evaluated by MTT assay (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide). Annexin V-FITC staining was used for identifying apoptotic cells. We measured the expression of caspase-3, PARP (poly ADP-ribose polymerase), Bcl-2, and Bax by Western blot. We measured the length of the hair follicle in vitro organ culture. RESULTS: AHK-cu stimulated growth of DPCs. Apoptotic cells were decreased compared with control. The level of caspase-3 and PARP was decreased in AHK-cu treated group than serum-free control. In human hair follicle organ culture, the elongation of hair was increased over 155% in AHK-cu treated group. CONCLUSION: AHK-Cu seems to promote the survival of human DPCs by anti-apoptotic effects. Those results were confirmed by the decrease of the expression of caspase-3 and PARP, and by the increase of the ratio of Bcl-2/Bax. AHK-cu promotes the growth of human hair follicle and also has anti-apoptotic effects on the DPCs, which may play an important role in hair growth.


The study above didn't use whole follicles. HOWEVER, the peptides protected the hair cells from apoptosis, excited their growth RIGHT ALONG with what we would expect given to how well they did in phase 2 trials, where they achieved improved hair counts slightly better than minoxidil. The peptides tested were the alanine/histidine/lysine amino complex that is available in Tricomin and American Crew Revitalize.

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract. The scientists studying it in Japan attribute its growth induction in hair to it being an analogue of prostaglandin F2alpha. They used another analogue of prostaglandin F2alpha, isorophyl unoprostone, and got stimulatory effects in the mice hair they tested it on in vivo. They ended in saying that the "stimulatory effects of PGF2 and PGE2 on hair growth have been discussed with regard to the role of protien kinase C and mast cells. This is what the scientists think about how this drug effects hair growth. It improved hair growth on macaques.

Minoxidil. Opens potassium channels, ups prostaglandin release, fights hardening of the connective tissue sheath that restricts dermal papilla enlargement that we see in male pattern baldness, ups VEGF.................very explainable.


Jack Daniels for hair?

quote:
Separation and identification of phytoestrogenic compounds isolated from bourbon.
Alcohol Alcohol Suppl. 1987; 1:551-5 (ISSN: 1358-6173)Rosenblum ER ; Van Thiel DH ; Campbell IM ; Eagon PK ; Gavaler JS
University of Pittsburgh School of Medicine, PA.

There is considerable evidence that several plant metabolites have estrogenic properties. Given that many alcoholic beverages are made from plants which have been shown to possess estrogenic activity, we considered the possibility that alcoholic beverages may contain estrogenically active substances. To evaluate this hypothesis we first extracted and then used gas chromatography/mass spectrometry to identify two phytoestrogens, biochanin A and beta-sitosterol in the bourbon extracts. Based on these findings we suggest that the feminization observed in chronic male alcoholics with liver disease may reflect, at least in part, the presence of biologically active phytoestrogens in the alcoholic beverages they consume.

PreMedline Identifier: 3426733


That was posted by Wookie on hair loss-R. Tom Hagerty mentioned a man that was admitted to a clinic in his hometown who drank a PINT of JD a day. He had very little body hair growth, b**ch-tits, 3+edema of his legs, testicular atropy, a phucked up liver.........................and probably a pretty damn good head of hair. Ive been interested in beta sis for a while because I think it mimics estrogen. Recently its been found out that stone/bronze/iron age Celts in Ireland used Pine oil as a hair gel. Pine oil has (BY VERY FAR) the highest amount of beta-sis of any known substance (about 18%). Avacoda oil only has .5% but is accredited with Mexicans having such a low incidence of prostate problems because they eat tons of the stuff. Rice bran oil (in American Crew Revitalize) has .75%. Its in sugar cane pulp (Garnier Fructis shampoo) and Soy also (.5%). I think it inhibits receptors or mimics estrogen in some fashion and yes, Im going to test it on my body hair to see what it does (currently a bit of avocado oil thats in garnier fructis hair gel, but going to buy some pine oil to really test it.................will let folks know in about six months. Its on the back of one hand---Im a fairly hairy guy).


Proanthocyanidins http://www.ncbi.nlm.nih.gov/entrez/quer ... query_hl=7 That was used to show it sped up hair cell growth 140 percent in vitro (epilitheal cells) and induced anagen in vivo.

why is that important if it only is a hair cell test? because as a stimulant the results were exactly the opposite of what DHT and T does to hair cells and whole hair follicles in tests. It grew hair where male hormone has been shown to slow its growth or even kill it (apoptosis) in in vitro tests.



Now for my own experience with revivogen. I used revivogen on one wrist for 2 and a half months. Both my arms are fairly hairy (good density). I take propecia and drink green tea (which should inhibit type one DHT a tad). Revivogen has beta sis and saw palmetto and vitamin b6 (lessens receptor expression). The hair on the treated wrist grew very weakly compared to the untreated one. I was so convinced, I stopped my little test a bit earlier than I should have because I was persuaded that revivogen was a good anti-androgen. I have come to believe that since I was inhibiting DHT already to a great extent, that the beta-sis, and the .1-.4% of beta sis in the saw palmetto extract and the lessened receptor production induced by the vitamin b6 or pyrxidine (the correct and expensive form of it) is why it worked so well. It either must have mimicked estrogen or blocked the receptors to a great degree, because the hair growth on the treated wrist (despite the grape seed proanthocyandins therein) was really shitty. It must have lost androgenic stimulation of Testosterone also. I was convinced, anyway.


A HUGE amount of researchers would have to be dead wrong for Stephen to be right. Maybe they are, as Stenn and Costarialis are working for a company called FOLLICA now on a "novel" hair growth product at the cellular level. We, over at hairsite, have not been able to find out why they are either splitting time with Aderans or have left it completely. Aderans has STILL NOT ENTERED phase one HM tests. ICX is promising it will begin phase 2 shortly, but have been delayed all year. They are only going to test one measly f*****g centimeter of scalp. This is NOT inspiring confidence in those of us who have followed cloning.

One more additive.........................body hair to the scalp for the most part has seen the circumference of the body hair being so weak be a huge issue for men whove taken the plunge. Was reading a post the other day by a Doctor who does them, saying you need 2-4 body hairs on your head for 1 scalp hair moved to get the same hair mass in his experience. Its not enlarging to head hair width. A Korean Study over six years time demonstrated that head hair moved to the body will adjust its anagen phase to fit that of whatever recipeint site its placed on, BUT its VOLUME stays the same. Like that big fat black hair Colin Jahoda moved to Amanda Reynolds arm. It indicates that there is a genetic difference in head and body hair just like every single test on the subject has shown thusfar
 

michael barry

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Forgot,

On abscorbic acid (in prox-N)


Vitamin C is also known as "ascorbic acid" but what exactly is ascorbic acid 2-phosphate?


http://www.ehrs.org/conferenceabstracts ... 37-kim.htm



--------------------------------------------------------------------------------
quote:
P37 ASCORBIC ACID 2-PHOSPHATE PROMOTES HAIR GROWTH
Kim MK, Kim JC, Sung YK
Department of Immunology, Kyungpook National University School of Medicine, Daegu, Korea

Cultured dermal papilla cells exhibit normal fibroblast-like morphology at early passage. In contrast to the dermal fibroblast, cultured dermal papilla cells can induce hair follicle growth in vivo, although their inductivity is gradually lost during subculture. It is known that ascorbic acid 2-phosphate (Asc 2-P) stimulates growth of dermal fibroblasts by enhanced production of collagen synthesis. However, it is not known whether Asc 2-P stimulates growth of dermal papilla cells and promotes hair follicle growth. In this study, Asc 2-P stimulated growth of dermal papilla cells and promoted hair follicle growth in organ culture model. On the other hand, Asc 2-P did not significantly promoted the growth of outer root sheath keratinocytes. The mRNA level of IGF-1 was increased 3.8-folds with Asc 2-P treatment while that of HGF, VEGF and KGF were not affected in dermal papilla cells. Versican expression in dermal papilla was also increased by Asc 2-P. However, the mRNA level of collagen types I and III was not affected by Asc 2-P in dermal papilla cells. These data, first time to our knowledge, demonstrate that Asc 2-P stimulates growth of dermal papilla cells and promote hair follicle growth in vitro. The growth stimulation of dermal papilla cells and induction of hair follicle growth seems to be, at least in part, mediated by IGF-1 over-expression from dermal papilla cells by Asc 2-P. In addition, these data suggests that signalling pathway that leads to versican expression is activated by Asc 2-P and Asc 2-P may keep dermal papilla cells to maintain hair-inducing activity by regulating versican.





Also, things that inhibit androgen receptor expression......................................Retin-A, vitamin b6 in its pryixidine form, gensitien soy isoflavone.

Things that have proanthocyaindins,,,,,,,,,pine bark, grape seeds, green apple peels, cherry bark, barley, hops...................see all this in old remedies for baldness. The ancients werent so stupid were they? Thousands of years of trial and error.
 

Bryan

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S Foote. said:
So yet another "mechanism of the day" to explain the direct theory then Bryan? :roll:

When are people going to realise that these in-vitro tests mean "nothing" at all in the genuine scientific context!

These cultured cells are completely different to the in-vivo cells we need to understand. The cell culturing "itself" creates major genetic changes in these cells, reducing both androgen receptor expression and the expression of 5AR type 2.

Just one example of the blatent contradictions these in-vitro studies throw up, is clear when you compare this study with the others.

Oh, I don't know that it's a "blatant" contradiction, Stephen; at the most, I'd call it a relatively mild one. After all, large doses of androgens were required in this most recent study, as opposed to the (presumably) more moderate doses used in the stumptailed macaque study.

It's hilarious that the best you can do to challenge the accepted theory of balding is point out some minor inconsistency in a couple of studies. Man, you are REALLY scraping the bottom of the barrel in your desperate effort to keep your theory afloat. Sorry, but it's taking on water fast! ABANDON SHIP!! :wink: :D

Bryan
 

Old Baldy

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You know Stephen, when someone shows me a study that indicates my opinion on something is wrong I admit it and move on. I like that about myself. Call it bragging because that's what it is. :lol:

Bryan and Michael have provided you with a plethora of studies showing why they feel the way they do relative to androgens and male pattern baldness, yet you continue to defend your incorrect theory. I'm mystified.

Androgens are the driving force behind male pattern baldness, whether our scalps are "tight" or not. It's just that simple IMHO.

The studies just keep piling up indicating androgens are the DRIVING FORCE behind male pattern baldness. It is becoming so obvious that I can't believe you really disagree with that fact.

On the other hand, you have always said the scalp health side of the equation is important. Studies show you are correct on that one.

Bryan wrote:

Man, you are REALLY scraping the bottom of the barrel in your desperate effort to keep your theory afloat. Sorry, but it's taking on water fast! ABANDON SHIP!!

No, it's sunk.

The reason I'm posting this Stephen is I want newbies to realize androgens are the driving force behind male pattern baldness. Not to insult you.

Bryan and Dr. Proctor might disagree with me on this one but you MUST treat the androgen side of the male pattern baldness equation agressively or you're, most likely, "doomed" IMHO.
 

Felk

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Just out of curiousity, what is Foote's theory? I've seen allusions to it before by Bryan, michael and others many times but never knew what it was.

Is it something about the relative "tightness" of our scalps determining hair loss or something?
 

Bryan

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That's basically it. He believes that androgens don't really have any direct effect on hair follicles (either body hair or scalp hair), and balding is caused by "edema" (fluid build-up) in the scalp. He thinks that the resulting "contact inhibition" from squeezed hair follicles is what stunts their growth and makes them miniaturize.

Seriously, that's what he believes.

Bryan
 

Felk

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Thanks for enlightening me Bryan :)

Strange sounding idea, even when ignoring all the evidence of the effect of androgens on hair follicles, the fact that minoxidil regrows hair yet sometimes causes edema would be a bit of a spoke in the theory's wheel...
 

powersam

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however to dismiss his theory straight off will probably mean something important gets overlooked. of course androgens are directly involved in the balding process, but its also true that there must be other mechanisms involved otherwise a drug like dutasteride would cure baldness completely. instead of only looking at the evidence which proves it wrong, why not look at the evidence which supports this theory and see what else you turn up?
 

Bryan

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Felk said:
Strange sounding idea, even when ignoring all the evidence of the effect of androgens on hair follicles, the fact that minoxidil regrows hair yet sometimes causes edema would be a bit of a spoke in the theory's wheel...

Oh, not to worry. He has a theory to explain that, too. He thinks that what minoxidil does is shift fluid AWAY from the hair follicles, toward the "inner volume" or whatever. He has an ad hoc explanation for most anything you can think of. He spends his time trying to think of ways to keep his theory consistent with the observed facts. Sometimes his attempts to do that go way off the deep end.

Bryan
 

Bryan

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powersam said:
however to dismiss his theory straight off will probably mean something important gets overlooked. of course androgens are directly involved in the balding process, but its also true that there must be other mechanisms involved otherwise a drug like dutasteride would cure baldness completely. instead of only looking at the evidence which proves it wrong, why not look at the evidence which supports this theory and see what else you turn up?

We ALREADY look at the other evidence, and we've done that for years and years. We freely admit that there is evidently an immune component to balding, in addition to the androgenic component, and we always have.

It is Stephen, on the other hand, who stubbornly and embarrasingly continues to deny the OVERWHELMING evidence for a direct effect of androgens on hair follicles. Instead, he makes a childish attempt to explain EVERYTHING, the whole enchilada, with one little hypothetical issue; namely, contact inhibition. However, that idea is completely incapable of explaining such things as the all-important and much-discussed Nordstrom study. Stephen's theory meets Nordstrom, and collapses like a house of cards.

In my view, Stephen's theory is not so much a serious alternative scientific theory to explain balding, it's more a psychological manifestation of someone obsessed with his own pet theory. It's Stephen's own Moby Dick.

Bryan
 

Old Baldy

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powersam said:
however to dismiss his theory straight off will probably mean something important gets overlooked. of course androgens are directly involved in the balding process, but its also true that there must be other mechanisms involved otherwise a drug like dutasteride would cure baldness completely. instead of only looking at the evidence which proves it wrong, why not look at the evidence which supports this theory and see what else you turn up?

Power: I asked Stephen once what his suggested regimen is for male pattern baldness and it was surprisingly mainstream.

He said treat for inflammation, scalp health and blood vessel health, etc.

IIRC, he even indicated androgens played a role in triggering male pattern baldness but were not directly effecting the follicles. It was edema, tissue swelling, etc.

So, his suggested treatments were basically what you would probably think we should use. I remember having no problem with his suggestions. His suggestions kind of "bolstered" my opinion of what I was using, and why I was using them!

It's just his theory of the cause and/or driving force behind male pattern baldness that causes all the controversy IMHO.

I mean, his suggested treatments followed what both of us would probably use. Looking at your regimen, I'd bet Stephen would suggest you add minoxidil. and SODases to your arsenal. :!:

I would recommend adding those two things, so I really can't argue with the most important aspect of Stephen's advice, (i.e., suggested treatments).
 
G

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Old Baldy said:
The reason I'm posting this Stephen is I want newbies to realize androgens are the driving force behind male pattern baldness. Not to insult you.

Bryan and Dr. Proctor might disagree with me on this one but you MUST treat the androgen side of the male pattern baldness equation agressively or you're, most likely, "doomed" IMHO.

Hey Old Baldy,

Can you elaborate on this quoted part of your post?

Is dutasteride 0.5 mg/day enough to treat the androgen side or do you mean applying stuff like spironolactone too?

And what do you mean by Bryan and Proctor disagreeing?
 
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