Free DHT levels peak and decline at the same time as free testosterone:
The Free DHT / Free testosterone levels are stable it seems with age.
Does that still mean there’s a difference in 5ar activity?
10.1016@j.jsbmb.2009.05.008.pdf (290.5 KB)
Does the free DHT/Testosterone graph imply higher 5ar activity in young age (low testosterone but higher DHT)?
I once got a finasteride Rx for gender dysphoria, I should try that again (idk if new people are less liberal than old people on this)
What about dutasteride?
A new dissertation on this topic:
TYSM for this. can someone summarize the main findings?
FYI chatgpt thinks “spiro bodies” aren’t a concern (and don’t last long-term).
I have serious trauma over this but I cannot give details yet. It would do so much good for the world to resolve this, but I don’t know how yet (TMS, tFUS could help).
I don’t know what to do over this. I don’t know about transgender culture - I have some similarities, but believe more in gender-neutering than transitioning
Generally, shifting resources from reproduction to life preservation/extension seems to be a theme. Look at one of the side effects of very high dose rapamycin, testicular shrinkage and sperm production suppression. Severe CR results in the suppression of reproductive behavior, loss of menstruation etc.
Evolutionarily it makes sense. If an organism is in an environment of scarcity, it would be suboptimal to spawn the young into this circumstance.
There’s probably many clinical trials on different aspects of this, I don’t know enough about it
If the goddamn organ can be shrunk by >50%, that would do a lot alone…
OK, I missed the exact definition, I had to look it up to be sure. I also understand the neutrality = asexuality status you would like to achieve.
But I wonder, that’s a niche for endocrinologists, is it wise to mess with these subtle mechanisms on one’s own? Are you unsatisfied with the solutions proposed by specialists?
Perhaps you might develop some degree of acceptance about the physical garb you’ve been assigned at birth. Sometimes it’s better to embrace the suck, as they say in the military jargon, rather than fight it in a war of attrition that you will probably lose.
I wonder if psychopharmacological treatment would help, modulating neural networks and the flow of neurotransmitters can often achieve some results, like in depression states, stressful conditions and so on.
Also, pure mental desire or libido can be often abated by epigenetic signalings, like CR+exercise, or low-carb diet which increases SHBG.
does this mean that 17-alpha estradiol could be used in place of fin?
If you use the oral food concentrations used in the ITP, most likely yes. The topical formula sold otc in some European countries definitely won’t be enough.
Supposedly inhibits type 1 and 2
Not sure if you’ve seen this?
“Long-term treatment with dutasteride therapy is associated with significant improvements in LUTS, as assessed by reduction in prostate volume, IPSS and prostate specific antigen (PSA). Long-term dutasteride therapy, however, resulted in increased blood glucose, HbA1c, TC and LDL levels, ALT and AST activities, AMS Score and reduced T levels and worsened ED as assessed by the IIEF-EF scores. No worsening of ED, glucose, HbA1c, ALT, AST, AMS were observed in men treated with tamsulosin. Most importantly, long-term dutasteride therapy resulted in reduction in total T levels, contributing to a state of hypogonadism.”
As posted elsewhere in this thread, there is evidence that dutasteride but not finasteride may increase HbA1c. As for testosterone, the rcts do point to a slight increase of testosterone. I wonder if this association accounts for normalizing testosterone levels over the long term.
The reason it increases testosterone is because it stops 5AR turning testosterone into dihydrotestosterone. I’m unsure why higher doses or dutasteride would lower testosterone.
Me being on TRT, I wouldn’t need to worry about levels normalizing or lowering as I have complete control on those numbers.
My only concern when it comes to hormones here are either:
a. Losing 5AR would increase amount of testosterone aromatizing to estrogen to a negative degree.
b. Losing 5AR causes PFS style symptoms.
The latter is most concerning to me, because aromatization can be easily controlled in many ways including just lowering body fat which is very prominent with aromatase.
If I were to use any 5ARi I would consider low dose finasteride topically, probably in a 5% minoxidil liquid base.
a. Losing 5AR would increase amount of testosterone aromatizing to estrogen to a negative degree.
Isn’t that already an issue with TRT? I’m guessing you will have to play around with the dose, frequency and aromatase inhibitors.
5ar inhibitors are not CRISPR. Your body will continue producing 5ar enzymes indefinitely even while you are on 5ari but they will be bound to by finasteride/dutasteride while they are in your system. If you go off them, your DHT levels will go back to previous levels after the drug has cleared from your system.
If I were to use any 5ARi I would consider low dose finasteride topically, probably in a 5% minoxidil liquid base.
If you’re planning on using topical minoxidil anyway, mixing it with finasteride is reasonable.
“honokiol was identified as an inhibitor of aromatase, with a half-maximal inhibitory concentration (IC(50)) of about 50 μM. In addition, honokiol was shown to be an inhibitor of 5-alpha-reductase type 1, with an IC(50) of about 75 μM. Taken together, these data indicate that honokiol modulates testosterone levels, and its structure has the potential to serve as a lead for future designs of highly selective inhibitors of 5-alpha-reductase type 1.” https://www.researchgate.net/publication/232226355_Modulating_testosterone_pathway_A_new_strategy_to_tackle_male_skin_aging
I sponsored an Ora Biomedical lifespan test of honokiol a few days ago. Just discovered this. Very interesting.
