MENT solo in lieu of TRT

Why dut without testoserone?

Interesting, I didn't know it was possible for one of the liver function tests to be about 30 times above normal and the other one to be normal.
Apologies, 1200 was something else. AST 656, ALT 146. Bilirubin was fine (compared to these values and reference numbers).

DUT is simply not enough to stop my hair loss. I will try oral DUT with topical FIN (maybe, but most likely will just get a HT).

1700104597608.png

Did they put you on dialysis; you mentioned a rhabdo diagnosis? Did you leave against medical advice?
Again apologies, actual values were actually 656/146. No they didn't mention it. They mostly were concerned about my kidneys, bc of CK. Or maybe they thought it wasn't necessary since bilirubin was fine. Doctors were quite on point, immediately asked if I taken any testosterone analogues.
 
Last edited:
DUT is simply not enough to stop my hair loss. I will try oral DUT with topical FIN (maybe, but most likely will just get a HT).
I completely dont understand your approach to the problem of hair loss, finasteride does not do anything better than dutasteride in this aspect, especially since without taking testosterone your DHT values would already be very low even without 5 alpha reductase inhibitors

I have met people who did everything to preserve their hair and took exogenous estrogen, dutasteride and anti-androgens such as cyproterone acetate at the same time
 
I have met people who did everything to preserve their hair and took exogenous estrogen, dutasteride and anti-androgens such as cyproterone acetate at the same time
Yeah no, I probably tried every protocol there is, save for estrogens and anti-androgens (not counting topical spiro). Not my cup of coffee.
 
Yeah no, I probably tried every protocol there is, save for estrogens and anti-androgens (not counting topical spiro). Not my cup of coffee.
The problem of androgenetic alopecia probably lies in the activity of the prolactin receptor in the scalp, current very promising researches in China gives hope that in the next few years the problem will be solved
 
The problem of androgenetic alopecia probably lies in the activity of the prolactin receptor in the scalp, current very promising researches in China gives hope that in the next few years the problem will be solved
Hmmm. Did you mean prolactin, or prostaglandin

1700106435939.png
 
prolactin, just read about 'HMI-115' on hairlosstalk or reddit

It has always been nonsense to me that DHT, which is responsible for fertility, causes baldness in young men. This is not typical of nature
It might not make a lot of sense, yet it most likely is the case, specifically, it's sensitivity of hair root apparatus (DP etc AFAIK) to DHT and testosterone. For me, that makes a lot of sense.
 
It might not make a lot of sense, yet it most likely is the case, specifically, it's sensitivity of hair root apparatus (DP etc AFAIK) to DHT and testosterone. For me, that makes a lot of sense.
I am not saying that dht or androgens in general are not necessary to trigger the mechanism of hair loss, but that the individual expression of the prolactin receptor in the scalp is responsible for the susceptibility to this disease.

All other DHT effects on men are attractive to women, balding just must have another mechanism
 
prolactin, just read about 'HMI-115' on hairlosstalk or reddit

It has always been nonsense to me that DHT, which is responsible for fertility, causes baldness in young men. This is not typical of nature
I'm not an expert on this drug or the full spectrum of androgenic alopecia etiology. But, clearly androgens that increase ROS thereby increase TGF-β1 secretion (thereby stimulating procollagenous activity, but perversely by this same mechanism, inducing androgenic alopecia in scalp), no?

Androgenic alopecia may be treated better than 5AR inhibitors by other drug classes; but DHT does cause baldness in men that are prone to it according to my cursory understanding. Do you have any scholarly material that totally shifts this paradigm of understanding, and not Reddit posts?

Also, from a teleological perspective, humans have virtually adapted out of the need for body hair due to our ability to lodge in domiciles, no?
 
I am not saying that dht or androgens in general are not necessary to trigger the mechanism of hair loss, but that the individual expression of the prolactin receptor in the scalp is responsible for the susceptibility to this disease.

All other DHT effects on men are attractive to women, balding just must have another mechanism
Ah, there we go, more in line with what I understand. I do not think evolutionary pressures from mating confer protection against androgenic alopecia that generally occurs after historical (think eons, rather than the last half-century blip) fertility, given that not 100 years ago, men would have multiple children by the time they were 25 in most of the world.
 
I'm not an expert on this drug or the full spectrum of androgenic alopecia etiology. But, clearly androgens that increase ROS thereby increase TGF-β1 secretion (thereby stimulating procollagenous activity, but perversely by this same mechanism, inducing androgenic alopecia in scalp), no?
I understand your arguments, but I still believe that the key to androgenetic alopecia is other than the traditional mechanism of "higher dht = more hair lose" in prone guys

But maybe I just cope because I have MPB too

Research on the influence of the prolactin receptor on hair loss has been conducted for several years, also by Bayer.

HMI-115 has proven to be very effective in the treatment of alopecia in macaques, phase II trials are currently underway and will end next year
 
Do you have any scholarly material that totally shifts this paradigm of understanding, and not Reddit posts?
many studies have been cited in this thread

 
many studies have been cited in this thread

Good, thank you. You're pegasus2, right? Don't take this the wrong way, but this seems like it's a pet issue of yours; a particular interest. This makes me think you are very knowledgeable about this, but perhaps myopically focused and putting great stock in the promises of this drug. This is an impersonal observation; but one to consider.
 
Good, thank you. You're pegasus2, right? Don't take this the wrong way, but this seems like it's a pet issue of yours; a particular interest. This makes me think you are very knowledgeable about this, but perhaps myopically focused and putting great stock in the promises of this drug. This is an impersonal observation; but one to consider.
No, it's not me, I don't even have close knowledge to him

The fact is that I have too much hope for this drug, but the prospect of the first drug that is not an anti-androgen seems great to me.
 
No, it's not me, I don't even have close knowledge to him

The fact is that I have too much hope for this drug, but the prospect of the first drug that is not an anti-androgen seems great to me.
OK, I 25% believe that you're not fully capable of doing what pegasus2 does :).

I'm going to try to read through that data, hopefully this week. I should educate myself more about androgens & hair loss; somewhat selfishly it seems I can never seem to get too deep into the weeds with it because, honestly, I am resilient against this effect thankfully, and I regard it as a mere cosmetic effect, so it doesn't captivate me fully.

I have certainly done some study of AAS with respect to hair loss, of course.

And I pored over this great series by @PeterBond – (collated by Millard in a forum post) – who I just exchanged emails with the other day (yeah, this is a brag to me!):


His ability to assess strengths & weaknesses of study design is unparalleled, it always strikes awe in me. He has spent a great deal of time gaining experience by reviewing academic papers for peer review. I've never met anyone so talented at it.
 
New member here, first post.

About a month ago, I began using it solo in lieu of TRT. It has advantages over testosterone - basically for a dose similarly androgenic to test, it is about 3x as anabolic. It converts via multiple pathways into estrogen, via aromatase as well as through an estrone intermediary, but is not subject to 5a-reductase so cannot convert to DHT. It also does not raise hematocrit and is more selective than test, at least at lower dosages, so is less likely to cause hair loss and BPH. It's also an ideal compound to 'blast and cruise' on... cruise <5mg/day, increasing up to 50mg/day for a blast.

The 7a-methylestradiol activates ER similarly to regular estradiol, but it is eliminated from the body more slowly so can accumulate resulting in estrogenic effects. So AI and/or SERM can be useful - particularly at higher dosages, in those also using test, or those with genetically high aromatase activity. It also activates progesterone receptors and therefore should be expected to increase prolactin in a dose-dependent manner; at all but high dosages, this is probably insignificant although I am taking Inhibit-P/P5P; at very high dosages, something stronger i.e. cabergoline or praxiprexole might be needed for some.

I'm currently injecting 20mg/day subQ (completely painless) in divided doses for a mini-blast. My adjuncts are Raloxifene 30mg/day for gyno prophylaxis, since 7a-methylestradiol cannot be measured via blood, and Aromasin 12.5mg EOD. I have neither excess water retention or elevation of BP, nor have I had any low E2 symptoms. My joints feel great and libido is improving. Over the past few weeks I have noticed a significant increase in muscle mass (+1 inch on my arms) and strength, with my weight remaining stable @ 200lbs... so it is working well, as intended, for body recomposition purposes.

Btw I'm a 54 year old physician (MD/radiologist) and have done extensive research on this compound.
now this right here is anabolic. BEING NATTY
people that use steroids are SMALL LOSERS
im bigger than youll ever get you fucking steroid abuser. :P

just kidding nigga im on tren only no test
i attached a pic for you to look at and weep in sorrow.. youll always be tiny and only pull gay men for sex.
( we did cardio in the bed after this session with my trainer)
i also pinned him in the ass with tren :P
meontrenornattynigg.jpg
 
Hey folks, just FYI: had to abort the experiment. I wasn't recovering at all, and got a severe rhabdomyolysis. Stay safe. :)
Holy shit that's rough! Hope you're on the way back, brother.

I tell guys all the time, low and slow so you can bail when it's time to. I'm a fan of MENT but I know not everyone would respond or not have sides.

Get healthy, stay safe!:cool:
 
now this right here is anabolic. BEING NATTY
people that use steroids are SMALL LOSERS
im bigger than youll ever get you fucking steroid abuser. :p

just kidding nigga im on tren only no test
i attached a pic for you to look at and weep in sorrow.. youll always be tiny and only pull gay men for sex.
( we did cardio in the bed after this session with my trainer)
i also pinned him in the ass with tren :p
View attachment 270329
Huh?
 
Holy shit that's rough! Hope you're on the way back, brother.

I tell guys all the time, low and slow so you can bail when it's time to. I'm a fan of MENT but I know not everyone would respond or not have sides.

Get healthy, stay safe!:cool:
Thank you brother. My kidneys filtered all kilos of creatine kinase by now, and I even did a physiotherapy (it was interesting - probably very educated (judging by them NOT HAVING rhabdo), but also skinny as fuck. I know I know it means nothing, but feels awkward being trained by a dude 75kg lol. Thankful for everyone's wishes for speedy recovery.

Are you not the original OP? I have been wondering how he's (you's) doing.
 
Back
Top