Exploring The Hormonal Route. Hair=life.
- Thread starter bridgeburn
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Barring any other issues that you may have that do not pertain to hormones such as an illness such as thyroid issues (which even then can mostly be fixed) you should have no problem.
I am now a firm believer that hormones and not some vague concept of genes or receptors changing as we get older holds the responsibility for hair loss AND growth.
There are plenty of older women, actually quite old who have a thick head of hair, and I would imagine those women do so because they are healthy and have enough estrogen to maintain growth, so I think you keep your hormones in check and you should be good.
Check out this woman at the timestamp (it didn't work in the link code but 18:14 anyhow) in this video, a very thick, full head of hair. That's reasonably good health and ESTROGEN, that has kept it up. That's my thought anyhow.
I am now a firm believer that hormones and not some vague concept of genes or receptors changing as we get older holds the responsibility for hair loss AND growth.
There are plenty of older women, actually quite old who have a thick head of hair, and I would imagine those women do so because they are healthy and have enough estrogen to maintain growth, so I think you keep your hormones in check and you should be good.
Check out this woman at the timestamp (it didn't work in the link code but 18:14 anyhow) in this video, a very thick, full head of hair. That's reasonably good health and ESTROGEN, that has kept it up. That's my thought anyhow.
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Your hair looks really healthy, are you still shedding?
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How is the crown?
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About 160~ hairs a day, not really a shed, but it could be better
Good
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Just noticed your regimen and I had to look up Legalon, do you take it to help with the liver strain of estrofem and bica?
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Yes, alcoholics use it very often.
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It's something I might consider, I've had liver pains in the past from bica and multivitamins
No offence, but you have no discernible hair loss, why are you taking 6mg of E and 25mg of Bica? Taking that amount of E is pointless unless you are transitioning. I don't understand what you are trying to achieve with such a regimen. Do you just want to maintain?
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I take it you didn't saw these ones
But if you think i don't have hair loss that's sounds good to me
Nope, didn't see those, my apologies, how long have you been on your regimen?
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I started in 2019 Dec, my current regimen started 20 days ago. To be honest there's no real reason why i'm up to 6 mg of E, other that to see what happens. I have some vellus hairs in the red area and i'm curious if it goes terminal from E
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Did you experiment with lower doses of E before or did you hop right on to 6mg? Also have you noticed the onset of any side effects in the first 20 days?
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Do you think there's any benefit to taking E orally? From what I understand oral E promotes a higher E1:E2 ratio than transdermal. I'm considering adding 1-2mg of oral E per day as there may be benefits to higher estrone levels.
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I was on 2mg for the longest time, than on 4mg for a 2~ months the only sides i have is gyno and infertility. No ED sofar, quality is on par or about 90%. I just brought up a 30kg fridge to the 4th floor of my apartment yesterday, so no signs of weakness. I gained 4 kg of fat since i started in 2019
I'm taking it sublingually, but if i had the chance i would go for injections.
Edit: Also i do not recommend what i'm doing at all, i probably would have had better results with minoxidil than anything else.
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Your skin is healthy, so it's done something at least
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I’m starting estrogen today. Applying 2-3 pumps of estrogel topically to my scalp. I don’t know how much will be absorbed there but we’ll see.
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Best of luck, some people have had good results from estrogel. I found it made me shed when applied to the scalp, maybe it was the alcohol.
Regarding CPA, the partial agonist effect to the AR, still it is "troubling" me so much.. How could you "deactivate" the Partial Agonist effect from CPA? If you use Bicalutamide together, will the fully Silent Antagonist "diminish" the Partial Agonist effect of CPA? (A key property of partial agonists is that they display both agonistic and antagonistic effects. In the presence of a full agonist , a partial agonist will act as an antagonist, competing with the full agonist for the same receptor and thereby reducing the ability of the full agonist to produce its maximum effect.). Does this means, that in a case of a full Antagonist (Bica), the partial agonist will act as full agonist ?? But still many people, are getting very good results with CPA. It is capable of upregulating the AR receptor, or just simply the partial agonist effect, means that the AR will be still "activated" and not upregulated?? Please, if you have some free time, shed some light here.. I would totally appreciate it. Thank you very much.
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Directly from Pharmacology of CPA (Wiki): But unlike silent antagonists of the AR like nonsteroidal antiandrogens such as flutamide, bicalutamide, and enzalutamide, CPA, by virtue of its slight intrinsic activity at the AR, may be unable to fully inhibit androgenic signaling in the body, which may persist to an extent in some tissues such as the prostate gland.
Source:https://en.m.wikipedia.org/wiki/Pharmacology_of_cyproterone_acetate
Now that I read again the whole thing, I believe that this partial agonist, it means that the AR signal it will still be activated. It will get some binding though, but again it won't be fully ''binded'', like NSAAs (Bica for example). So, I believe that AR upregulation it is not very possible to happen? Please correct me if I am wrong here. Thanks
(An escape or recovery phenomenon, in which testosterone levels increase over time, has been observed with long-term CPA monotherapy.In one study in aged men with prostate cancer, testosterone levels were initially suppressed by 70%, but increased to 50% of baseline levels between 6 and 12 months, remaining stable thereafter up to 24 months of therapy.).I believe that this has to do with the prostate cancer cells and the partial agonist effect, but this again is referring to cancer cells, instead of healthy cells for example.)
Forgive me If I am bothering or being annoying. I am just looking for some answers and understand some things. Thank you.
Source:https://en.m.wikipedia.org/wiki/Pharmacology_of_cyproterone_acetate
Now that I read again the whole thing, I believe that this partial agonist, it means that the AR signal it will still be activated. It will get some binding though, but again it won't be fully ''binded'', like NSAAs (Bica for example). So, I believe that AR upregulation it is not very possible to happen? Please correct me if I am wrong here. Thanks
(An escape or recovery phenomenon, in which testosterone levels increase over time, has been observed with long-term CPA monotherapy.In one study in aged men with prostate cancer, testosterone levels were initially suppressed by 70%, but increased to 50% of baseline levels between 6 and 12 months, remaining stable thereafter up to 24 months of therapy.).I believe that this has to do with the prostate cancer cells and the partial agonist effect, but this again is referring to cancer cells, instead of healthy cells for example.)
Forgive me If I am bothering or being annoying. I am just looking for some answers and understand some things. Thank you.
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