Exploring The Hormonal Route. Hair=life.

Experimentality

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I read about this today. There is a form of Dexamethasone that can be injected into the muscle. Could this be helpful?
Perhaps. I have to admit I am not very knowledgeable on the subject. You would have to inject it precisely at the right location though (if you go subQ it will have greater/full prospensity to go systemic, and if you inject too shallow it would still cause skin atrophy just like topical applications). Not worth it, I would say.
 

Experimentality

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General comment: some people on this thread have been acting like E2 is some kind of fountain of youth. In reality, it is the only human hormone that is classified as carcinogen. I am not here to bash E2 because it has many useful effects (in particular for hair, which we are here for of course), but I want to break the tendency of literally worshipping a single hormone. It is dangerous when abused and should be handled with respect, just like and probably even more than other hormones because of its carcinogenicity. There is a reason why women have very similar E2 levels to men for a big chunk of the month (hint: because E2 is dangerous in much higher concentrations for longer periods of time).

Back on-topic: @didone_glyph thanks for posting your results with topical Bicalutamide. Again amazing proof that topical regimens can definitely work to improve things. I ran topical Bica for a short while before my stint on topical Apalutamide (now on topical Darolutamide as AA). Question: how did you manage to make a 5% solution with Bica? DMSO solubility is only 14 mg/mL (see here) and in my experience this value is pretty accurate. Main reason I switched was because I did not want to use DMSO (higher prospensity to go systemic) and because I could not get it dissolved in anything else (the long half-life was not very appealing as well).
 
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Almas_NW0

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General comment: some people on this thread have been acting like E2 is some kind of fountain of youth. In reality, it is the only human hormone that is classified as carcinogen. I am not here to bash E2 because it has many useful effects (in particular for hair, which we are here for of course), but I want to break the tendency of literally worshipping a single hormone. It is dangerous when abused and should be handled with respect, just like and probably even more than other hormones because of its carcinogenicity. There is a reason why women have very similar E2 levels to men for a big chunk of the month (hint: because E2 is dangerous in much higher concentrations for longer periods of time).
My E level never drops below 200 pg / ml. Is it unhealthy? Please tell us more about this if you have time. On the other hand, without the use of CPA, this is the only way to suppress T to the female level, so I would not say that we have a choice.
 

Experimentality

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My E level never drops below 200 pg / ml. Is it unhealthy? Please tell us more about this if you have time. On the other hand, without the use of CPA, this is the only way to suppress T to the female level, so I would not say that we have a choice.
I am not a doctor, so I cannot give you advise about anything health related. I do know that E2 is dose-dependently carcinogenic, which would suggest we try to minimize systemic concentrations. However, E2 also has many good functions: for example, it increases HDL and lowers LDL; it is neuroprotective; it stimulates collagen production in the skin; good for hair etc. Hence, the healthiest option would be to stay within the reference range. If you are female (or want to mimic the hormonal profile of a young female) this reference range fluctuates over the course of a month as we all know. During ovulation, E2 levels peak (median) at around 200 pg/mL. During follicular phase, E2 levels very much resemble that of males: constant concentrations of around 50 pg/mL. Even if we would integrate the curve over the whole month (the so-called area under the curve, AUC), it would be well shy of 100 pg/mL. That should give you some background information, but I encourage you to do your own research.

Regarding CPA: I would imagine that running a very low dose of CPA in conjunction with physiological E2 levels would be "healthier" than running supraphysiological doses of E2. Even "healthier" would be castration, which would completely eliminate the need for hardcore drugs and allow one to just run physiological doses of E2. Again, do your own research. Maybe find a progessively-orientated doctor (if there are any, haha). Monitoring of blood parameters is extremely important to warrant your health.
 

franzliszt

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It amazes me that Derek (MPMD) has been able to hold on to his own hair. He has put his endocrine system through the ringer over the years. I believe his current regiment is simple. Minoxidil and Finasteride and occasionally micro neddling . He is also on TRT.

I believe Derek has also mentioned in the past, what is already known, that Estrogenic therapy is the nuclear option for guys. Basically sacrificing masculinity for POSSIBLE results. He is right.
I could be wrong, but I thought RU 58841 was his main hairloss treatment (he may not be on it right now though). He even said he was a hyper responder to it, but anyway he does some great videos, he's literally a guinea pig for experimental hormonal drugs.
 

subsidence82

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RU58841 is promising. However, like with any topical anti androgen you have to be careful of it going systemic. Very promising stuff in moderation.
 

subsidence82

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How can it be promising when its been around since forever and tried countless times?
You’re right, it has been around for awhile. I guess what I meant is that more people seem to be using and the good results are getting more publicity as of late.

Id like to give it a try myself on some of my thin spots.
 

Experimentality

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Leaving aside injecting which I don't consider a problem, contrary to the approach that people are taking on this thread what I want to do is inject Testosterone. Because I am already taking a high dose of Dutasteride ( and consider to go even further with injections in the future) this would lead to more aromatization. Now this aromatization will lead to higher estrogen and ER activity.

I believe that the presence of ERa in hair follicles dermal papilla cells and the fact that they promote prolactin needs to be related to hairloss in some way. This is because after starting to take a ERa inhibitor drug that at the same time reduces basal prolactin levels I have had results with my hair in the form of even less shedding when combing hair wet (something I was not happy with even on 2.5 dutasteride) and regrowth of my temples which are basically covering my old native hairline.
After that I would be using Dexamethasone, which would lead to increased ERb expression and activity and should give me even better results with my hair. I do not really have a problem with it going systemic because I actually have reasons to use this drug besides hairloss, but I understand it can't be used permanently so injecting can be an option and anyway would have a more powerful effect locally.

PD: I'm not intending to take Test to recreate this hypothesis, I have other goals, but since I am doing it I am trying to find the way to at least no hurt my hair in the process.
I already take T, as in TRT. It is pretty good, but I would not advise it unless you are truly primary hypogonadal. DHT is not even correlated with T levels (within physiological ranges). Of course, T is mildly androgenic as well, that is why I am using a topical regimen in conjunction to oral dutasteride. I think people on 5ARI's need to make sure that their T levels are adequately high. In my opinion, you cannot crush your DHT, walk around with low T and expect to function decently. You need to have adequate androgenic activity, which must come from T if you are on dutasteride.

And yes, prolactin seems to be heavily involved in male pattern baldness, possible as much as androgens. My next experiment will be with Metergoline (taken orally). Apart from its dopaminergic effect (which is responsible for the lowering of prolactin) it is also a serotonin antagonist, which is really nice from a longevity perspective. I will keep you guys updated!

Edit: did you take Cyproheptadine? How did you like it? I think it is an extemely versatile compound, not necessarily for hairloss but moreso for correcting deep neurological pathways.
 
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keepcoolmybabies

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I already take T, as in TRT. It is pretty good, but would not advise it unless you are truly primary hypogonadal. DHT is not even correlated with T levels (within physiological ranges). Of course, T is mildly androgenic as well, that is why I am using a topical regimen in conjunction to oral dutasteride. I think people on 5ARI's need to make sure that their T levels are adequately high. In my opinion, you cannot crush your DHT, walk around with low T and expect to function decently. You need to have adequate androgenic activity, which must come from T if you are on dutasteride.

And yes, prolactin seems to be heavily involved in male pattern baldness, possible as much as androgens. My next experiment will be with Metergoline (taken orally). Apart from its dopaminergic effect (which is responsible for the lowering of prolactin) it is also a serotonin antagonist, which is really nice from a longevity perspective. I will keep you guys updated!
If prolactin induces hairloss to the degree that androgens can, I wouldn't think CPA would be of the benefit it often is for hair, as it spikes prolactin pretty substantially
 

Experimentality

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If prolactin induces hairloss to the degree that androgens can, I wouldn't think CPA would be of the benefit it often is for hair, as it spikes prolactin pretty substantially
You are right, I stand corrected. I do think prolactin is heavily involved, but in deed not to the same degree as androgens.
 

subsidence82

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I already take T, as in TRT. It is pretty good, but I would not advise it unless you are truly primary hypogonadal. DHT is not even correlated with T levels (within physiological ranges). Of course, T is mildly androgenic as well, that is why I am using a topical regimen in conjunction to oral dutasteride. I think people on 5ARI's need to make sure that their T levels are adequately high. In my opinion, you cannot crush your DHT, walk around with low T and expect to function decently. You need to have adequate androgenic activity, which must come from T if you are on dutasteride.

And yes, prolactin seems to be heavily involved in male pattern baldness, possible as much as androgens. My next experiment will be with Metergoline (taken orally). Apart from its dopaminergic effect (which is responsible for the lowering of prolactin) it is also a serotonin antagonist, which is really nice from a longevity perspective. I will keep you guys updated!

Edit: did you take Cyproheptadine? How did you like it? I think it is an extemely versatile compound, not necessarily for hairloss but moreso for correcting deep neurological pathways.
This was incredibly informative for me. Ive been considering TRT. Im 39 years old and was sucked into the BS of low T by the snake oil T Clinics. My levels were normal for my age, but was told I need to have levels that I had when I was 20. The funny thing, I feel great and probably don’t need supplemental T. Im sticking to a healthy diet, working out, going to bed at a reasonable time and reading more often. Im not hypogonadal, Ill pass.
 

Get my hair back

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And yes, prolactin seems to be heavily involved in male pattern baldness, possible as much as androgens. My next experiment will be with Metergoline (taken orally). Apart from its dopaminergic effect (which is responsible for the lowering of prolactin) it is also a serotonin antagonist, which is really nice from a longevity perspective. I will keep you guys updated!
I hooked up Cabergoline (a D2-dopamine receptor stimulator) to my regimen 38 days ago and so far I am not seeing any results. I will give this remedy 3 months.
 

ReturnOfExtreme

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Hair growth is provided by a decrease in the T level to the castration level and an increase in the E level
T levels below 50 ng / dl are normal, but the ideal level is less than 20 ng / dl, this corresponds to castration levels and affects prostate cancer outcomes. Thus, we need to reduce T as much as possible. To do this, our E levels must be at least 250-300 ng / dL
It is not advisable to raise estradiol levels above 700 pg / ml, because in this case SHBG will go crazy, the level of free estradiol will decrease. This reduces the effectiveness of HRT. Therefore, "one cannot be mistaken in the big direction" is not quite a true statement. Ideal E levels are in the 300-700 pg / ml range, SHBG levels below 115. But because the main thing is to lower the T level to the castration level, then the error in the big direction is not as critical as in the lower one, and you will still get the result

If you do injections of Enanthate every 2 weeks with a minimum of 300 pg / ml on the last day, then according to my calculations, the peak level is around 1500 pg / ml, which is a lot. If injections are done once a week, then the peak level at the same minimum does not exceed 700 ng / dl. Therefore, I will consider giving injections once a week.

The Ikarus T level was above 100 ng / dl and the E level was 195 pg / ml. These are poor numbers and this could be one of the reasons why he was unable to restore the hairline.


View attachment 165180

His T levels were that level but he was on enough bica to suppress the T levels.
 

ReturnOfExtreme

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There are enough such examples on the forum. But I will be the first to use HRT as a Norwood 1 with severe hairline thinning. It would seem that the situation is simple. However, the hairline and temples are terribly amenable to therapy, and Ikarus has never been able to repair the area. There is a point of no return when the hair can no longer be restored. I hope I haven't overcome it.

I know him personally from the old discord and you’re getting your information wrong
 
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