3alpha-hydroxysteroid reductase and hair loss - a theory from Tressless

Jakejr

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As I remember Rob has a full head of hair. So he is astute, but he’s like the Bob Lazar of male pattern baldness. He has his carbon dioxide theory, his mitochondrial energy theory & this whole scalp massage business. I’ve tried all of them & concluded as far as scalp massage.. I’ve seen the videos, I bought a growband, I’ve has several electric models, I’ve done it by hand.. After few months I sold them all. For scalp massage I just use a scalp brush I got from Virtue shampoo & it works better than the rest. Microneedling makes more sense & you can do it yourself. It’s no panacea however, but I do it several times a week. I wouldn’t pay much attention to people with full heads of hair trying to lecture on male pattern baldness.
 

JaneyElizabeth

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As I remember Rob has a full head of hair. So he is astute, but he’s like the Bob Lazar of male pattern baldness. He has his carbon dioxide theory, his mitochondrial energy theory & this whole scalp massage business. I’ve tried all of them & concluded as far as scalp massage.. I’ve seen the videos, I bought a growband, I’ve has several electric models, I’ve done it by hand.. After few months I sold them all. For scalp massage I just use a scalp brush I got from Virtue shampoo & it works better than the rest. Microneedling makes more sense & you can do it yourself. It’s no panacea however, but I do it several times a week. I wouldn’t pay much attention to people with full heads of hair trying to lecture on male pattern baldness.
Lol. I only read his articles and his published studies and I rarely if ever disagree but he is a salesman. The only thing that semi offends me is that he clearly tries often to act like he is one of our bald fellow homies with male pattern baldness to .sort of ingratiate himself into the baldness club which I care zero about with a lot of chatter about his 25 cent piece size baldness which could be covered by about $200 of grafts in about ten minutes, lol. But I think his analytical skills apart from that are top level. Hopefully mine are similar but I read for the data points and science and not for encouragement or discouragement either way. I probably started both HRT and microneedling based upon his articles and I still often refer back to them. I use higher doses than he recommends but I went through both articles on oral min for men and women and everything he says is correct and if he doesn't know how high is safe, he is virtually always giving risk adverse advice such as not going higher than 5mg of oral min for men.
 

Armando Jose

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fugged

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re: massages and scalp tension/fibrosis/calcification.. I really don't know. Rob clearly doesn't have bad hair loss but maybe on the vertex he caught it early. It is so polygenetic everyone is different. I did major massage after becoming interested about 2 years ago and it blew out most of my weak hair.. felt really good though and also led to the exfoliation a weird hard skin layer for lack of better description.. The hair is slowly recovering, but I had sort of stopped massage for a long time in exchange for needling. I will say, on the exact areas I have the most struggling/minaturtized follicles, my scalp is very, VERY tight and difficult to push together with two hands and "pinch", whereas it is very easy elsewhere.. So it does resonate personally that that skin/scalp difference and its thickness/tightness is related. I'm back to trying pinch type massage and seems somewhat positive, in my case anyway.
 

Finasteridegyno

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Alopecia is caused by inflammation, not DHT.

All androgens cause inflammation.

Inflammation reduces bloodflow and nutrients to the follicle. A hair follicle or graft is an organ that dies without proper oxygen and blood.

If you block DHT you reduce inflammation, if you block T you reduce inflammation. If you use minoxidil you increase blood flow despite having inflammation and the same with laser level therapy. The more things you do the better.

The big 4. Dutasteride Mesotherapy, finasteride/dutasteride, minoxidil and laser level light. You can expect the same results as these 2 guys posted above. It will halt and reverse hair loss on 90% of guys. The rest will need CB or RU being sensitive to T.

There is not one cure to reduce inflammation. Everything helps.
Basically every cortison reduce inflammation but they don’t work against AA....
 

Mustang

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" Evidence and implications of inflammation as a characteristic feature of MPHL and FPHL are highlighted through evaluation of clinical and quantitative data. Comparable results suggest the presence of significant perifollicular inflammatory infiltrates, such as lymphocytes and histiocytes, as well as the involvement of inflammatory genes, such as CASP7 and TNF, in the presentation of MPHL and FPHL. Resurfacing of the inflammatory aspect in MPHL and FPHL pathogenesis will advance future developments in MPHL and FPHL therapeutic options."

" In a related study, biopsy specimens obtained from over 400 patients with MPHL and FPHL were used to evaluate the presence of perifollicular inflammation with results indicating that approximately 71% of the MPHL and FPHL specimen samples exhibited inflammation"

"Inflammatory infiltrates have been characterized and suggested in the pathogenesis of MPHL and FPHL as observed by an increase in lymphocytes.17 Immunohistochemical analysis of biopsies obtained from 3 males and 1 female with progressive alopecia revealed follicular infiltration of CD4+ T-cells at the bulge of the hair follicle while control specimen showed a sparse number of T cells.17 This study concluded that infiltration of inflammatory T-cells at the follicular bulge may be the culprit of the impaired hair cycle and successive hair loss in MPHL and FPHL. Similar evaluation of the role of the inflammatory process in the onset of MPHL was conducted using biopsy specimens from 19 MPHL patients and compared to 6 control subjects.18 Histopathology of the specimens revealed significant lymphocytic infiltrates in the MPHL patients in comparison to the control subjects. More recently, the role of inflammation in FPHL was studied using scalp biopsies from 52 women with female pattern hair loss.19 Lymphocytic folliculitis was observed in the obtained biopsies, indicating the presence of inflammation and suggesting lymphocytic infiltrations as a histological feature of MPHL and FPHL"

"The inflammatory role in the pathogenesis of MPHL and FPHL is supported by clinical, histological, and sequencing findings. Perifollicular infiltration of inflammatory cells such as lymphocytes, histocytes, and mast cells is exhibited in biopsy samples of MPHL and FPHL patients. Significant follicular infiltration of CD4+ T-cells has also been observed as a source for impairment of the hair cycle and the consequential hair loss in MPHL and FPHL. RNA sequencing data signifies differential expression of inflammatory genes in MPHL pathogenesis. Conclusively, these findings suggest inflammation is elemental to MPHL and FPHL pathology and reinforce the need to address inflammation in prospective therapeutic developments. "

"We review evidence supporting and challenging dihydrotestosterone’s causal relationship with androgenic alopecia, then propose an evidence-based pathogenesis model that attempts to answer the above questions, account for additionally-suspected androgenic alopecia mediators, identify rate-limiting recovery factors, and elucidate better treatment targets. The hypothesis argues that: (1) chronic scalp tension transmitted from the galea aponeurotica induces an inflammatory response in androgenic alopecia-prone tissues; (2) dihydrotestosterone increases in androgenic alopecia-prone tissues as part of this inflammatory response; and (3) dihydrotestosterone does not directly miniaturize hair follicles. Rather, dihydrotestosterone is a co-mediator of tissue dermal sheath thickening, perifollicular fibrosis, and calcification – three chronic, progressive conditions concomitant with androgenic alopecia progression. These conditions remodel androgenic alopecia-prone tissues – restricting follicle growth space, oxygen, and nutrient supply – leading to the slow, persistent hair follicle miniaturization characterized in androgenic alopecia."

"Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group.

Conclusion: A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia"

The studies go on and on and on and on ............

But let's listen to a 25 year old forum kid who knows more than all hair transplant surgeons in the world.

Quite a bold statement. I wonder what powers he has to know exactly what every single doctor has studied and their knowledge about the mechanisms of hair loss.
 
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BetaBoy

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" Evidence and implications of inflammation as a characteristic feature of MPHL and FPHL are highlighted through evaluation of clinical and quantitative data. Comparable results suggest the presence of significant perifollicular inflammatory infiltrates, such as lymphocytes and histiocytes, as well as the involvement of inflammatory genes, such as CASP7 and TNF, in the presentation of MPHL and FPHL. Resurfacing of the inflammatory aspect in MPHL and FPHL pathogenesis will advance future developments in MPHL and FPHL therapeutic options."

" In a related study, biopsy specimens obtained from over 400 patients with MPHL and FPHL were used to evaluate the presence of perifollicular inflammation with results indicating that approximately 71% of the MPHL and FPHL specimen samples exhibited inflammation"

"Inflammatory infiltrates have been characterized and suggested in the pathogenesis of MPHL and FPHL as observed by an increase in lymphocytes.17 Immunohistochemical analysis of biopsies obtained from 3 males and 1 female with progressive alopecia revealed follicular infiltration of CD4+ T-cells at the bulge of the hair follicle while control specimen showed a sparse number of T cells.17 This study concluded that infiltration of inflammatory T-cells at the follicular bulge may be the culprit of the impaired hair cycle and successive hair loss in MPHL and FPHL. Similar evaluation of the role of the inflammatory process in the onset of MPHL was conducted using biopsy specimens from 19 MPHL patients and compared to 6 control subjects.18 Histopathology of the specimens revealed significant lymphocytic infiltrates in the MPHL patients in comparison to the control subjects. More recently, the role of inflammation in FPHL was studied using scalp biopsies from 52 women with female pattern hair loss.19 Lymphocytic folliculitis was observed in the obtained biopsies, indicating the presence of inflammation and suggesting lymphocytic infiltrations as a histological feature of MPHL and FPHL"

"The inflammatory role in the pathogenesis of MPHL and FPHL is supported by clinical, histological, and sequencing findings. Perifollicular infiltration of inflammatory cells such as lymphocytes, histocytes, and mast cells is exhibited in biopsy samples of MPHL and FPHL patients. Significant follicular infiltration of CD4+ T-cells has also been observed as a source for impairment of the hair cycle and the consequential hair loss in MPHL and FPHL. RNA sequencing data signifies differential expression of inflammatory genes in MPHL pathogenesis. Conclusively, these findings suggest inflammation is elemental to MPHL and FPHL pathology and reinforce the need to address inflammation in prospective therapeutic developments. "

"We review evidence supporting and challenging dihydrotestosterone’s causal relationship with androgenic alopecia, then propose an evidence-based pathogenesis model that attempts to answer the above questions, account for additionally-suspected androgenic alopecia mediators, identify rate-limiting recovery factors, and elucidate better treatment targets. The hypothesis argues that: (1) chronic scalp tension transmitted from the galea aponeurotica induces an inflammatory response in androgenic alopecia-prone tissues; (2) dihydrotestosterone increases in androgenic alopecia-prone tissues as part of this inflammatory response; and (3) dihydrotestosterone does not directly miniaturize hair follicles. Rather, dihydrotestosterone is a co-mediator of tissue dermal sheath thickening, perifollicular fibrosis, and calcification – three chronic, progressive conditions concomitant with androgenic alopecia progression. These conditions remodel androgenic alopecia-prone tissues – restricting follicle growth space, oxygen, and nutrient supply – leading to the slow, persistent hair follicle miniaturization characterized in androgenic alopecia."

"Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group.

Conclusion: A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia"

The studies go on and on and on and on ............

But let's listen to a 25 year old forum kid who knows more than all hair transplant surgeons in the world.

Quite a bold statement. I wonder what powers he has to know exactly what every doctor has studies and knows about the mechanisms of hair loss.
What use is targeting different inflammatory proteins when they are all downstream of AR signalling?
 

joaopassos4444

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The difference between bald scalp and non-bald scalp isn't the level of 3a HSD it's the number of androgen receptors. This angle is covered by anti-androgens thus this conversation gets us nowhere.
Do you have a source for that, if you mind?
 

whatevr

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Androgen receptors aren't the only thing that's different. Large differences in hormonal levels have been found as well, which immediately implies differences in hormone-producing/converting enzymes, therefore 3a-HSD is potentially affected as well, although to my knowledge, there is no direct evidence.
 

Jakejr

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If we could find a way to shut down androgen receptors in the hair follicles
 

joaopassos4444

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" Evidence and implications of inflammation as a characteristic feature of MPHL and FPHL are highlighted through evaluation of clinical and quantitative data. Comparable results suggest the presence of significant perifollicular inflammatory infiltrates, such as lymphocytes and histiocytes, as well as the involvement of inflammatory genes, such as CASP7 and TNF, in the presentation of MPHL and FPHL. Resurfacing of the inflammatory aspect in MPHL and FPHL pathogenesis will advance future developments in MPHL and FPHL therapeutic options."

" In a related study, biopsy specimens obtained from over 400 patients with MPHL and FPHL were used to evaluate the presence of perifollicular inflammation with results indicating that approximately 71% of the MPHL and FPHL specimen samples exhibited inflammation"

"Inflammatory infiltrates have been characterized and suggested in the pathogenesis of MPHL and FPHL as observed by an increase in lymphocytes.17 Immunohistochemical analysis of biopsies obtained from 3 males and 1 female with progressive alopecia revealed follicular infiltration of CD4+ T-cells at the bulge of the hair follicle while control specimen showed a sparse number of T cells.17 This study concluded that infiltration of inflammatory T-cells at the follicular bulge may be the culprit of the impaired hair cycle and successive hair loss in MPHL and FPHL. Similar evaluation of the role of the inflammatory process in the onset of MPHL was conducted using biopsy specimens from 19 MPHL patients and compared to 6 control subjects.18 Histopathology of the specimens revealed significant lymphocytic infiltrates in the MPHL patients in comparison to the control subjects. More recently, the role of inflammation in FPHL was studied using scalp biopsies from 52 women with female pattern hair loss.19 Lymphocytic folliculitis was observed in the obtained biopsies, indicating the presence of inflammation and suggesting lymphocytic infiltrations as a histological feature of MPHL and FPHL"

"The inflammatory role in the pathogenesis of MPHL and FPHL is supported by clinical, histological, and sequencing findings. Perifollicular infiltration of inflammatory cells such as lymphocytes, histocytes, and mast cells is exhibited in biopsy samples of MPHL and FPHL patients. Significant follicular infiltration of CD4+ T-cells has also been observed as a source for impairment of the hair cycle and the consequential hair loss in MPHL and FPHL. RNA sequencing data signifies differential expression of inflammatory genes in MPHL pathogenesis. Conclusively, these findings suggest inflammation is elemental to MPHL and FPHL pathology and reinforce the need to address inflammation in prospective therapeutic developments. "

"We review evidence supporting and challenging dihydrotestosterone’s causal relationship with androgenic alopecia, then propose an evidence-based pathogenesis model that attempts to answer the above questions, account for additionally-suspected androgenic alopecia mediators, identify rate-limiting recovery factors, and elucidate better treatment targets. The hypothesis argues that: (1) chronic scalp tension transmitted from the galea aponeurotica induces an inflammatory response in androgenic alopecia-prone tissues; (2) dihydrotestosterone increases in androgenic alopecia-prone tissues as part of this inflammatory response; and (3) dihydrotestosterone does not directly miniaturize hair follicles. Rather, dihydrotestosterone is a co-mediator of tissue dermal sheath thickening, perifollicular fibrosis, and calcification – three chronic, progressive conditions concomitant with androgenic alopecia progression. These conditions remodel androgenic alopecia-prone tissues – restricting follicle growth space, oxygen, and nutrient supply – leading to the slow, persistent hair follicle miniaturization characterized in androgenic alopecia."

"Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group.

Conclusion: A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia"

The studies go on and on and on and on ............

But let's listen to a 25 year old forum kid who knows more than all hair transplant surgeons in the world.

Quite a bold statement. I wonder what powers he has to know exactly what every single doctor has studied and their knowledge about the mechanisms of hair loss.
Do all hair surgeons know this?
 
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