Type-IIx
Well-known Member
The scientific:
One must read the article series by Peter Bond on this matter:
I. Anabolic Steroids and Hair Loss (Androgenic Alopecia) [Article] for an overview
II. Treatment and Prevention of AAS-Induced Hair Loss, Part 1 [Article] for an introduction to treatment modalities
III. Treatment and Prevention of AAS-Induced Hair Loss, Part 2 [Article] for a discussion of (including experimental) treatment modalities
This all boils down to providing an essential basic (as in fundamental) understanding of AAS & androgenic alopecia.
To this, I will just add, that for those of you interested in the mechanism at play:
synthetic AAS (but not T) ⇒ ↑ROS ⇒ ↑TGF-β1 secretion (thereby stimulating procollagenous activity, but perversely by this same mechanism, inducing androgenic alopecia in scalp)
(AAS, e.g., R1881 & DHT, serve to ↑TGF-β1 by regulating cellular redox state, particularly with respect to ROS homeostasis [epithelial cells, dermal papilla cells, human dermal fibroblasts])
For the parent AAS. Of course, human metabolism & its products (metabolites) have an influence here also.
My motivation for writing this post is that I continually receive correspondence pertaining to the task of ascertaining or evaluating comparative AAS potencies to induce hair loss.
To this comparative task, we do not have enough particularized data on AAS writ large to deduce a continuum from least to most potent. At best we can make comparisons between (usually 2) AAS, so long as they have been compared in an ecologically valid manner (e.g., we can say that Methyltestosterone has greater potency to induce hair loss than Masteron at doses likely to have some efficacy in treatment-resistance [e.g., ER-negative] breast cancer) or so long as there are similar assay conditions used to measure, e.g., ROS induction of TGF-β1 (e.g., we can likely say that DHT > R1881 (methyltrienolone) > stanozolol, with some simplifying assumptions) in potency to induce hair loss.
Using the deductive approach to ascertain an answer (to the question of rank ordering AAS & hair loss potencies) is limited here by the absence of any study seeking to rank order the AAS & hair loss effects.
The bro-scientific:
At its heart, the bro-scientific method is one of inductive reasoning. Unfortunately, too often (near universally), the assumptions used are erroneous and the inferences drawn based on invalid measurements; profound deficits exist in understanding research and statistical methods so as to be unable to evaluate the weaknesses in drawing conclusions from anecdotes, etc. These profound deficits and erroneous assumptions often originate from reliance on gurus (so-called authorities in the community). Though perhaps that reliance arises for reasons that are difficult to address.
Rather than attempt to dissuade from the use of inductive reasoning, promote the superiority of published data and deductive logic, etc. I would prefer to just give you what in my estimation is a just plain decent bro-scientific quasi-article.
This quasi-article was written by a pseudonymous Dr. Noe. This bro-scientific writing at least passes the more rudimentary weaknesses and typical pitfalls of other bro-science. So here, I provide it to you, as a sort of approximation/guess of where synthetic AAS may at least likely rank on a putative continuum in potency to induce hair loss:
I am not here to defend any of the claims therein on Dr. Noe's behalf (e.g., his understanding of DHEA sulfate action in men; promotion of spironolactone; belief that nandrolone is more HPG axis suppressive than testosterone; etc.); it was just a mostly accurate contribution made by a good bro in my opinion some time ago that holds up to some scrutiny, and seems to use a decent inductive reasoning approach.
Consider this as an illustration of Good Bro-Science (opinion).
One must read the article series by Peter Bond on this matter:
I. Anabolic Steroids and Hair Loss (Androgenic Alopecia) [Article] for an overview
II. Treatment and Prevention of AAS-Induced Hair Loss, Part 1 [Article] for an introduction to treatment modalities
III. Treatment and Prevention of AAS-Induced Hair Loss, Part 2 [Article] for a discussion of (including experimental) treatment modalities
This all boils down to providing an essential basic (as in fundamental) understanding of AAS & androgenic alopecia.
To this, I will just add, that for those of you interested in the mechanism at play:
synthetic AAS (but not T) ⇒ ↑ROS ⇒ ↑TGF-β1 secretion (thereby stimulating procollagenous activity, but perversely by this same mechanism, inducing androgenic alopecia in scalp)
(AAS, e.g., R1881 & DHT, serve to ↑TGF-β1 by regulating cellular redox state, particularly with respect to ROS homeostasis [epithelial cells, dermal papilla cells, human dermal fibroblasts])
For the parent AAS. Of course, human metabolism & its products (metabolites) have an influence here also.
My motivation for writing this post is that I continually receive correspondence pertaining to the task of ascertaining or evaluating comparative AAS potencies to induce hair loss.
To this comparative task, we do not have enough particularized data on AAS writ large to deduce a continuum from least to most potent. At best we can make comparisons between (usually 2) AAS, so long as they have been compared in an ecologically valid manner (e.g., we can say that Methyltestosterone has greater potency to induce hair loss than Masteron at doses likely to have some efficacy in treatment-resistance [e.g., ER-negative] breast cancer) or so long as there are similar assay conditions used to measure, e.g., ROS induction of TGF-β1 (e.g., we can likely say that DHT > R1881 (methyltrienolone) > stanozolol, with some simplifying assumptions) in potency to induce hair loss.
Using the deductive approach to ascertain an answer (to the question of rank ordering AAS & hair loss potencies) is limited here by the absence of any study seeking to rank order the AAS & hair loss effects.
The bro-scientific:
At its heart, the bro-scientific method is one of inductive reasoning. Unfortunately, too often (near universally), the assumptions used are erroneous and the inferences drawn based on invalid measurements; profound deficits exist in understanding research and statistical methods so as to be unable to evaluate the weaknesses in drawing conclusions from anecdotes, etc. These profound deficits and erroneous assumptions often originate from reliance on gurus (so-called authorities in the community). Though perhaps that reliance arises for reasons that are difficult to address.
Rather than attempt to dissuade from the use of inductive reasoning, promote the superiority of published data and deductive logic, etc. I would prefer to just give you what in my estimation is a just plain decent bro-scientific quasi-article.
This quasi-article was written by a pseudonymous Dr. Noe. This bro-scientific writing at least passes the more rudimentary weaknesses and typical pitfalls of other bro-science. So here, I provide it to you, as a sort of approximation/guess of where synthetic AAS may at least likely rank on a putative continuum in potency to induce hair loss:
I am not here to defend any of the claims therein on Dr. Noe's behalf (e.g., his understanding of DHEA sulfate action in men; promotion of spironolactone; belief that nandrolone is more HPG axis suppressive than testosterone; etc.); it was just a mostly accurate contribution made by a good bro in my opinion some time ago that holds up to some scrutiny, and seems to use a decent inductive reasoning approach.
Consider this as an illustration of Good Bro-Science (opinion).
