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.
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“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.
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