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winny vs masteron for hairloss?

cal

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Experienced user have used most of the common PEDS, never any hair loss or receding hair etc.

Interested in trying masteron, I have used winstrol and experienced no hair loss but seemed to get some pretty acne which I normally don't get.

Reading about masteron and hair loss made me wonder if someone is prone to hair loss is masteron worse than winstrol ? Or any other drug for that matter. Have been using for 20 years and no hair loss, but have no idea what my genetics are being adopted as a small child. Thanks for any insight or experience.
 
Interested in this too. Perhaps member Type-IIx can chime in and comment , that would be appreciated. Thank you.
 
Experienced user have used most of the common PEDS, never any hair loss or receding hair etc.

Interested in trying masteron, I have used winstrol and experienced no hair loss but seemed to get some pretty acne which I normally don't get.

Reading about masteron and hair loss made me wonder if someone is prone to hair loss is masteron worse than winstrol ? Or any other drug for that matter. Have been using for 20 years and no hair loss, but have no idea what my genetics are being adopted as a small child. Thanks for any insight or experience.

Winstrol is worse and the reason is that it increase TGF-Beta, this is directly linked to androgenetic alopecia and hairloss.

(Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells)


(The anabolic steroid stanozolol upregulates collagen synthesis through the action of transforming growth factor–β1)
 
Winstrol is worse and the reason is that it increase TGF-Beta, this is directly linked to androgenetic alopecia and hairloss.

(Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells)


(The anabolic steroid stanozolol upregulates collagen synthesis through the action of transforming growth factor–β1)
Black Beard, this is a great contribution with respect to the primary mechanism by which stanozolol causes hair loss.

But I don't think we have the data to say whether drostanolone (Masteron) has weaker potency to cause hair loss than stanozolol (Winny).

Now check my math, Black Beard:

From Falanga [1], we can say that 5 μg/ml stanozolol ⇒ 140 mg/ml TGF-β; and from Shin [2], we can say that 10 μg/ml R1881 ⇒ 180 pg/mL. Shin's luciferase assay (Fig. 4) showed DHT > R1881 in luciferase activity (TGF-β1 promoter levels)... So DHT > R1881 (methyltrienolone) > stanozolol? I could make that argument (it's not exactly clear without knowing the precise dose-response of an equimolar concentration of R1881 vs. TGF-β, but it's if anything very close. I (or you) certainly CANNOT make the argument that stanozolol has any particular potency to cause hair loss by this data, right?

What do we know about Masteron?
- Well it differs from DHT by the placement of a 2α-methyl group
- Its main metabolite is the 17-keto-oxidized 3α-hydroxy-reduced product, 3α-hydroxy-2α-methyl-5α-androstan-17-on ,which in comparison with T metabolism, is the 2α-methyl androsterone analog... we don't know its effect in scalp nor its nuclear receptor potencies (not in Houtman's supplementary data)
- Whereas stanozolol is an attenuated androgen, Masteron is quite androgenic, but certainly less virilizing in women than testosterone propionate... what about the data on hair loss in man? Unknown, to me at least. Have you seen this data?
... These facts all seem to point in different directions, i.e., it's certainly still unclear to me at least, where Masteron fits. Maybe I'm not as smart as you.

Can you explain why, aside from there being this sort of mechanistic data (dermal papilla cells, human dermal fibroblasts, etc.) on stanozolol, it ostensibly has particular potency to cause hair loss versus drostanolone in your estimation?

To my eyes, and I've looked, I'm not seeing any data on Masteron's net potency to cause hair loss by androgen (we should include its metabolites and their potencies as well to be relevant to man) effects on the cellular redox state with respect to ROS homeostasis. So, again, to me at least, it's unclear whether it acts like DHT in this regard, or whether the 2α-methyl group dramatically attenuates the increase to TGF-β1. It's unclear whether its metabolites are more or less potent in their effects on ROS.

It just seems to me that, despite the very clear temptation to give a confident definitive answer here, there is a dearth of any particularized data on Masteron with respect to these mechanisms involved in hair loss...

References:
[1] Falanga, V., Greenberg, A. S., Zhou, L., Ochoa, S. M., Roberts, A. B., Falabella, A., & Yamaguchi, Y. (1998). Stimulation of Collagen Synthesis by the Anabolic Steroid Stanozolol. Journal of Investigative Dermatology, 111(6), 1193–1197. doi:10.1046/j.1523-1747.1998.00431.x
[2] Shin, H., Yoo, H. G., Inui, S., Itami, S., Kim, I. G., Cho, A.-R., … Won, C. H. (2013). Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells. BMB Reports, 46(9), 460–464. doi:10.5483/bmbrep.2013.46.9.228
 
Anabolic on top of test seems to bring out the side effects of TEST. Hypothetically, doing fine with zero sides on 500 test. Then add 300 mast and hairloss becomes an issue. Must be the masteron, right? I guess not.

@Type-IIx am I way off base to hypothesize that the anabolic isn't necessarily responsible for the side effect appearing at the same as the introduction of the anabolic? I realize this is sort of a elementary question but curious what you think.
 
for sure i cant say better or worse but if one is prone to hair loss or its thinning things like mast, mast, wini, primo maybe even drol may speed that up.

age can also be a factor.
alcahol and stimulants also seem to push things along too.
 
Anabolic on top of test seems to bring out the side effects of TEST. Hypothetically, doing fine with zero sides on 500 test. Then add 300 mast and hairloss becomes an issue. Must be the masteron, right? I guess not.

@Type-IIx am I way off base to hypothesize that the anabolic isn't necessarily responsible for the side effect appearing at the same as the introduction of the anabolic? I realize this is sort of a elementary question but curious what you think.

Masteron will lower shbg and increase free test versus the same dose of test by itself. Effect is very significant so to your point of increasing test sides, that's logical as your free test is much higher.

On the hair loss there doesn't seem to be a rule and anecdotal evidence points to individual variation. Some are fine on primo but shed on mast. Some are the complete opposite. Throw winstrol in for either of those as well.
 
Winstrol is worse and the reason is that it increase TGF-Beta, this is directly linked to androgenetic alopecia and hairloss.

(Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells)


(The anabolic steroid stanozolol upregulates collagen synthesis through the action of transforming growth factor–β1)
Interesting. Here is a link to a review on TGF beta inhibitors if anyone is interested.

biomolecules article
 
Anabolic on top of test seems to bring out the side effects of TEST. Hypothetically, doing fine with zero sides on 500 test. Then add 300 mast and hairloss becomes an issue. Must be the masteron, right? I guess not.

@Type-IIx am I way off base to hypothesize that the anabolic isn't necessarily responsible for the side effect appearing at the same as the introduction of the anabolic? I realize this is sort of a elementary question but curious what you think.
I generally agree that with multiple independent variables (i.e., compounds, doses thereof) at play in our idiographic trial of 1 experiments (idiographic research refers to investigations conducted on an individual that is conducted via single-subject designs, like attempts to analyze our own bloodwork and draw conclusions from it), the dependent variables (i.e.., changes in hair thickness) are influenced in a complex way that is not well understood.

It's very difficult to falsify any of the following hypotheses, in the case presented - introducing 300 mg Masteron/w at an arbitrary time-point during a course of 500 mg testosterone/w:

a) the time-course of testosterone's amplification to DHT in "scalp tissue" simply ran its course independently of adding Mast, such that if you had not added Mast, by the same time-point, DHT's actions would have led to the same loss of hair
b) Mast & testosterone greater than additively (1 + 1 > 3), or synergistically, accelerate hair loss
c) There is some tipping point of total AAS dose, reflected by their androgenic potencies * concentration/dose and plotted as an asymptote, where hair loss proceeds rapidly (below which, some lower dose might not lead to weekly visual losses of hair).
 
@Type-IIx do we have good information on what causes temporary shedding/telogen effluvium wrt AAS?

Masteron in particular has maybe the highest amount of "Masteron wrecked my hair!" anecdotes that are based almost entirely on temporary shedding people noticed within days of hopping on Mast.

Everyone associates DHT with hair loss, combine that with the notion that Masteron "is a DHT" and it gets sort of set in stone. Whereas the deeper you dive into the science the murkier it becomes to be assured that Masteron causes androgenic alopecia.

I suspect there may be other compounds that are considered "hair safe" because anecdotally people notice little to no temporary shedding, but may increase androgenic alopecia significantly over time.

I'm mostly curious if there is some overlap between compounds being more likely to cause TE and being more likely to cause AA. It does seem that DHT-based compounds that anecdotally act the most similar to DHT in various tissues also tend to be those known for calling TE.
 
Op, if u didn't experience hair loss on winstrol I would think you would be safe with masteron. How much winny did u run
 
Just shave your head and be done with it..................
 
@Type-IIx do we have good information on what causes temporary shedding/telogen effluvium wrt AAS?

Masteron in particular has maybe the highest amount of "Masteron wrecked my hair!" anecdotes that are based almost entirely on temporary shedding people noticed within days of hopping on Mast.

Everyone associates DHT with hair loss, combine that with the notion that Masteron "is a DHT" and it gets sort of set in stone. Whereas the deeper you dive into the science the murkier it becomes to be assured that Masteron causes androgenic alopecia.

I suspect there may be other compounds that are considered "hair safe" because anecdotally people notice little to no temporary shedding, but may increase androgenic alopecia significantly over time.

I'm mostly curious if there is some overlap between compounds being more likely to cause TE and being more likely to cause AA. It does seem that DHT-based compounds that anecdotally act the most similar to DHT in various tissues also tend to be those known for calling TE.
Although acutely hair shedding on a cycle/blast might be transient, it's still classic androgenic alopecia given the etiology.

From Peter Bond Article, Oct 18 2021:
..[T]he effect of anabolic steroids... decrease the length of the anagen phase and increase the length of the telogen phase in selected hair follicles (7). With each successive hair cycle, the anagen phase continues to decrease in length and the telogen phase continues to increase in length. As a result, at any given moment in time, there will be more hair follicles in the telogen phase—with easily sheddible hairs—and less hair follicles in the anagen phase. Thus, less hair strands will reach out of the scalp in such an area. At some point, the anagen phase can become so short in duration, that a new hair strand barely reaches the surface of the skin.
Moreover, androgens induce something called miniaturization (8). The hair follicle becomes progressively smaller, and so does the hair shaft and resulting hair strand. The terminal hairs (which are the normal hairs on top of your head), turn into vellus hairs. Vellus hairs are very short hairs that are soft and lack pigment.

So on cycle/blast, AAS push hair follicles to the telogen phase & induce miniaturization.

If it were true that "DHT compounds" (5α-androstan-3-ones, like Mast, Anadrol, Superdrol) truly had a class effect of causing androgenic alopecia with particular potency, then Anavar would be included in this class. But since Anavar is perceived as "hair safe" by the bulk of the anecdotes on this effect, it just shows that people are really bad at attributing cause/effect. There's just no known structure/activity relationship for potency to cause androgenic alopecia, and no real data that exists to place any AAS on any sort of continuum. This thread is probably the first to, in any sort of evidence-based manner, show that DHT > R1881 (methyltrienolone) > stanozolol, probably, in potency to induce androgenic alopecia.
 

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