Ecdysterones could possibly help with muscular symptoms. What sounds promising is that ecdysterones do not act via the androgen receptor but via the beta estrogen receptor. This sounds unfavorable at first, but the common estrogen-related side effects are caused by the alpha receptor, so this should not be a problem. The exact mechanism of action is not yet clear, but the drug seems to increase protein synthesis and interact in a certain way with the beta receptor. Previous studies have not found any inhibition of endogenous hormone production or other hormonal changes. I believe that ecdysterone is not a cure in any way, but rather may alleviate certain symptoms like muscle atrophie or muscle weakness.
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very positive experience for me
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Can you elaborate what symptoms it helped you with and to which extent
It has definitely helped my muscular problems, my muscles have become a little harder again. But especially it has improved my fatigue, a difference like day and night. My anxiety and sleep have also gotten much much better, probably due to ecdysteroneâs positive modeling of the GABA A receptor. I have been taking turkesterone, by the way.
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Did it help with sexual sides ?
I donât really have sexual sides
Finasteride inhibits epinephrine synthesis in humans: implication for sexual dysfunction
Finasteride is a 5alpha-reductase (5Îą-R) inhibitor used in clinics to treat androgen-dependent conditions, such as benign prostate hyperplasia and androgenetic alopecia (AGA). Its use has been associated with several adverse effects, including sexual complaints. However, to date, no hypothesis to explain such adverse effects has been proposed. This is a consequence of the still incomplete knowledge of the intricate network of motivational, psychological, and molecular inputs that are involved in sexual behavior. In this work, a multidisciplinary approach has been used to evaluate whether finasteride may interact with targets different from 5Îą-R (i.e., off-target proteins â OTPs). In silico analysis (SPILLO-PBBS software and docking/molecular dynamics) indicated that the enzyme phenylethanolamine N-methyltransferase (PNMT), the limiting enzyme in epinephrine production, might be a finasteride OTP. This is interesting, since epinephrine and norepinephrine are involved in erection (Becker et al ., 2000, J Urol), and alterations in their levels has been observed in patient with erectile dysfunction (Becker et al ., 2002, Urology). An inhibitory assay developed in vitro confirmed that finasteride blocks the human PNMT. Finally, to verify the in vivo interaction, adult male rats were treated with finasteride (1 mg/rat/day s.c. daily for 20 days). Ex vivo analysis indicated that epinephrine levels were decreased by finasteride treatment in adrenal glands, while those of norepinephrine were increased. This, together with no variation in PNMT protein levels, confirmed the hypothesis of a block in epinephrine synthesis. Therefore, we explored if corpora cavernosa (CC) of finasteride-treated rats presented molecular alterations. A decreased protein level of estrogen receptor beta was observed in CC of finasteride-treated rats, in line with evidence in aging and diabetic rats with erectile dysfunction (Shirai et al ., 2004, Urology). Moreover, the levels of dopamine, which improve the penis relaxation, were significant decreased in CC tissue after finasteride administration. Overall, the data here presented indicate that finasteride affects epinephrine synthesis by blocking PNMT enzymatic activity in humans. This block can have an impact in sexual behavior, as suggested in an animal model treated with finasteride. In addition, the alterations observed in CC indicate possible impairment of erectile function. Our results suggest possible mechanisms for the sexual dysfunction observed after finasteride treatment in humans and add a piece of knowledge on the mechanisms controlling sexual function in mammals.
But possibly it could help, since ecdysterones act, among other things, via the estrogen receptor beta
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I can confirm Ecdystrone works. Ive been on it for 1 month
In terms of physical changes , not too much noticeable difference to be completely honest. Muscles are denser forsure tho!
Strength however⌠MAJOR GAINS. My lifts have been going through the roof ever since starting.
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The only times I have had short term recoveries (full on recoveries) was from a supplement that had tribulus, mucuna pruriens, ecdysterone, and zinc in it.
I never considered ecdysterone as what was helping, but it now makes me wonder.
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This Ecdysterone is pretty interesting stuff. My main remaining PFS symptoms are very stubborn muscle atrophy, intermittent fatigue, and brain fog. Ecdysterone seems harmless enough to try out between my DHT cyclesâŚalthough a bit pricey for a supplement and there arenât too many reliable looking brands out there.
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There are also some studies on the relationship between Estrogen Receptor Beta and the Androgen Receptor.
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I use turkesterone from vemoherb. The price is okay and the brand is reliable
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Update: The estrogen receptor Beta is also involved in reversing DNA hypermethylation, according to the study.
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ecdysterones have been of interest to me for awhile. How long did you use turkesterone until you noticed positive benefits? Do you take the recommend dose on the bottle?
My coworker randomly handed me a bottle of Ecky. Itâs been sitting at my desk, may need to try itâŚ
Anyone know if there are any risks?