CottonNathaniel
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- Dec 15, 2019
- Messages
- 5
Could you use andosterone at high doses. I just have no idea where to get Dht gel.
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How bad is finasteride?
- Thread starter Lee Simeon
- Start date
Seems scrotal application is best.
Also what alphagels recommends and he also recovered from PFS:
View: https://www.reddit.com/r/FinasterideSyndrome/comments/u1svwo/comment/i4eg1it/?context=3
Do people trust the alphagels DHT gel? I vaguely remember a few people saying it wasn’t very good?
Yup, was sceptical for a very long time. But a couple of guys on the whatsapp group ordered from him and both got their products, they even showed pictures of the product. One of them who ordered was Pete (if you're in the whatsapp group you will know him) and at first he thought he was scammed because it took so long for alphagels to answer his mails and took 5 weeks if I recall correctly for it to get delivered too, seems alphagels is very busy and gets many orders. So yeah that's good news, lol I thought he scammed Pete too since it took a week for alphagels to reply to his mail but all good in the end.
@Jremy25 also ordered with alphagels and is happy with his results.
But remember you can also make your own dht gel but I have no idea how to do this properly.
The half life of proviron is like 10-15 times longer than DHT, which is why it tends to still work ok, despite having low bioavailability. Any steroid taken transdermally is likely to have better uptake than oral administration unless it's something like Anavar or a few other oral steroids with decent bioavailability.
I applied 4-6 x per day on scrotal and penile tissue, abdomen and hips, and even on the thin skin under the eyes. The half life of DHT is under an hour so it's best to apply every 2-4 hours.
No, it really needs to be a strong, 5a-reduced androgen. I'd suggest DHT as the best choice since it's native and it's the most potent androgen in existence outside maybe one other synthetic steroid. After DHT, I would either suggest proviron or masteron as they are both 5a-reduced androgens. They're not as potent as DHT, but they do have much longer half lives.
I believe it's also important that you don't take anything to increase gonadal steroidogenesis or use testosterone along side the DHT. Because your androgen metabolism favors the aromatase pathway when you have PFS, it's best if you just deal with having low T and low E2 for 4-6 weeks, as this is the inverse of the state that finasteride induces. Having high DHT and low T and E2 is what you want to lower AR expression to restore proper androgen signaling in the hypothalamus and pituitary, as well as restore dopaminergic signaling and keep prolactin subdued.
Where do you get DHT from? I’ve tried 11 KETO DHT, quite androgenic.
Your masteron/proviron comment makes sense to an extent. Masteron as compound was actually modified to be less androgenic than DHT itself since it was used for breast cancer and they wanted to avoid virilization for the women. So you would probably have to take a much higher dosage and/or for longer period of time compared to DHT itself.
Injectable DHT attached to a long ester would be the perfect candidate for your protocol. Since you will have constantly circulating DHT and the bioavailability would be high as well.
You might be able to stack eucommia with DHT or a potent androgen to enhance the effect on the AR gene expression side. It seems it boosted the potency of DHT to almost 100%.
Novel phytoandrogens and lipidic augmenters from Eucommia ulmoides
Plants containing compounds such as the isoflavonoids, with female hormone-like effects that bind to human estrogen receptors, are known. But none has been previously shown to have corresponding male hormone-like effects that interact with the human androgen ...
www.ncbi.nlm.nih.gov
Remarkably, combination of DHT and the E. ulmoides extract in the presence of the AR led to increases in AR-mediated reporter gene expression ranging from 112% to 204%, even at saturating levels of DHT (figure (figure8).8). This potentiating effect was a tripartite synergism between the AR protein, its cognate steroidal ligand and E. ulmoides's extract. This is highly unusual as normally, androgen-mediated AR transcriptional capacity, akin to all ligand-dependent steroid receptors, plateaus at saturating doses of its cognate ligand. A similar synergistic effect was observed when E. ulmoides extract was tested in combination with estradiol in the presence of the estrogen receptor (ER) α (figure (figure99).
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Check bodybuilding forums for reputable sources or maybe buy from purple panda labs like some people on here have done.
I so hope you're right.
Let's try to get some people to reproduce your assumed strategy.
I'm already on DHT cream 50mg (2 x 1G of 2.5% DHT cream) per day for 6 weeks now. I haven't noticed any improvements yet.
If this does not work in 10 weeks I'm considering doing 100mg per day for 10 weeks. I will keep everyone updated.
ChemHead, maybe you've mentioned this already: what cycle length and pause length would you suggest?
Would alpha gels DHT be good for this
I would recommend between 150-200 mg per day. You should only expect around 30-40% uptake so it sounds like a lot more than it is. I would also do this for at least 4 weeks.
The thing about DHT is that I always experience a pretty strong rebound in terms of steroidogenesis around 2-3 weeks after stopping. I actually think that this is probably due to its suppression of estrogenic activity. So, despite being mildly suppressive to the HPTA due to androgenic stimulation, it might actually kind of act in a manner similar to a SERM for a short period of time once it is discontinued.
Others on this forum would be a better judge. I've never purchased anything from them. I think I've seen some people pretty happy with it, though, I guess.
How would you make your own DHT from a powder from purple panda ?
Yup DHT acts a bit like a SERM:
A neat little study, and in-vivo at that, which demonstrates that DHT is a direct estrogen receptor (ER) antagonist. According to the study, so are testosterone, nandrolone and a few other steroids with demonstrated therapeutic effects on ER-positive breast cancer (BC). However, all of the other steroids mentioned by the study are aromatizable and as such suboptimal as anti-estrogens compared to DHT. This is probably one of the reasons that back in the 1960s when synthetic steroids for treatment of BC were first developed, only DHT derivatives such as Proviron and Masteron eventually made it to clinical trials and got approval for this condition. None of the aromatizable synthetic androgens (or testosterone for that matter) made it through the clinical trials despite being much more widely used (experimentally) for BC at the time. When we also consider the fact that DHT (and other 5-AR derives steroids) are also aromatase inhibitors, it becomes clear that DHT is right up there with progesterone in terms of importance for estrogen antagonism, and perhaps the main anti-estrogen in males. Another interesting finding of the study was that the anti-estrogenic effects of DHT were independent from its role as an androgen agonist. However, androgen agonists are well-known known to have anti-estrogenic effects of their own, so the effectiveness of DHT as an anti-estrogen is actually amplified by its role as a strong androgen. Finally, the study provide some information on what a physiological dose of DHT would be, which is subject to much debate in the literature and in the blogosphere. As the study states, healthy males produce about 45 mcg estrogen daily and DHT amounts need to be about 50 times higher in order to fully block the effects of a given amount of estrogen. This means that a daily physiological dose is about 2mg for healthy adult males, and that dose may need to be increased with increasing age or pathological conditions resulting in elevated estrogens such as liver disease, diabetes, prostate cancer, etc.
Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor - PubMed
“…Estrogen treatment to such mice stimulates breast growth and as in other species increases the amount of progesterone receptor in the breast. Both effects of estradiol can be inhibited by dihydrotestosterone. We concluded that this might be an adequate model system for investigating the mechanism of the antiestrogenic action of androgen, and we designed experiments to assess two mechanisms that have been proposed for this action, namely that androgen acts at the genomic level via its own receptor to block estrogen action or that androgen acts as a pharmacological antagonist and/or weak estrogen agonist by competing with estradiol for the estrogen receptor. The findings in these experiments favor the latter possibility. Indeed, the fact that dihydrotestosterone was equally effective in blocking estrogen effects in tfm/Y and control mice suggests that this action of androgen is not mediated by the androgen receptor. If this interpretation is correct, then this effect of androgen is different than the antiestrogenic effect of the hormone in the embryonic mouse breast (11) and in the uterus (12). Dihydrotestosterone binds weakly to the estrogen receptor in mouse breast and like some other antiestrogens appears to anchor the estrogen-receptor in the nucleus of the cell. These effects have only been studied with pharmacological amounts of hormone, but the fact that the relative binding affinities of dihydrotestosterone, 313-androstanediol, testosterone, and Sfdihydrotestosterone correlate with their capacities to inhibit induction of the progesterone receptor is in keeping with the finding in MCF7 tumor cells (10) that androgens bind to the estrogen receptor. Unlike the situation in MCF7 cells, however, we were unable to demonstrate any estrogen-like effects of dihydrotestosterone on the mouse breast.”
“…If androgen prevents the development of gynecomastia in normal men by acting as a direct antiestrogen at the level of the estrogen receptor, this is the first androgen action recognized that is not mediated by the androgen receptor.”
“…Normal men produce ~45 mcg of estradiol each day, a sixth of which is secreted by the testes and the remainder of which is derived from the extraglandular aromatization of circulating androgens (1). Extraglandular estradiol formation takes place by two mechanisms, one from the direct conversion of testosterone to estradiol and the other from androgens of adrenal origin by the sequence of androstenedione – estrone – estradiol. The function of estradiol in normal men is unknown, but feminization, commonly manifested by gynecomastia, ensues under conditions of relative or absolute estrogen excess (2)….By this estimate estradiol binds to the estrogen receptor with an affinity that is approximately fifty times greater than that of dihydrotestosterone.”
Would butea superba be good, just for general 5 alpha reductase increase, or anything better than that?
What worries me is how PSSD patients report exactly the same symptoms and experiences like PFS patients (like me). So PSSD might be caused by the same mechanism while SSRI's do not have such a direct link with DHT.
@ChemHead
When exactly did you experience with the DHT so much and why?
So would you say something like cycle 5 weeks on, 5 weeks off?
@ChemHead
When exactly did you experience with the DHT so much and why?
So would you say something like cycle 5 weeks on, 5 weeks off?
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The PSSD patients likely experienced the same issue because it probably is the same issue. Dopaminergic function seems to be at the center stage of both of these conditions. It may just be that they're induced in two different ways. With PFS, you're disrupting dopaminergic signaling by disrupting the protective anti-estrogenic, anti-progestogenic, anti-prolactinogenic effects that DHT has and this likely leads to permanent changes in the regulatory areas of the brain that prevents both central signaling that leads to expression of 5AR and also signaling which is responsible for normal steroidogenesis. With PSSD, you may be reaching a similar state, but by directly interfering with dopaminergic function rather that doing it via 5AR/DHT. There seems to be an almost interdependent relationship between DHT and dopaminergic signaling, where both are required for both of their own sustained existence and, if you knock one of them out, they both go.
This is also probably why I've consistently experienced better sleep, a change in perception of time, and very clear and vivid dreams when taking DHT. When I say a change in perception of time, I mean that the day feels significantly longer. I also slept significantly less time while feeling as if I slept significantly longer. So, I would sleep maybe 6 hours, but feel like I had just slept 10-12 hours with multiple vivid dreams.
I also experienced significantly better digestion and gut motility from the DHT.
As far as dose, all I can say is that when I fully recovered from PFS 4 years ago, I used about a gram/week for around 3 weeks. Unfortunately, I never tried using that much in the past 2-3 years, but it still had the effects I mentioned above... It just likely didn't push me into recovery because I didn't use it long enough to begin reversal of the epigenetic changes that lead to PFS in the first place. I used about a gram the last time, but only used it for maybe 8 or 9 days and then ran out. That, alone, was enough to improve digestion and sleep for a short period of time and, a couple weeks after stopping, it was also enough to induce a strong rebound effect on the HPTA and I had testicular pain/soreness and higher steroidogenesis, faster/thicker facial hair growth and oily skin.
I think the key to getting out of this state is to expose yourself to enough DHT or 5a-reduced androgen for long enough to induce epigenetic changes so that when you do stop using it and when you do experience a rebound in steroidogenesis, it becomes self-sustaining rather than reverting back to the previous state where estrogenic and prolactinogenic activity dominate androgenic and dopaminergic activity, respectively. You're just using DHT like training wheels to get your body to reestablish/restore signaling and feedback mechanisms which are responsible for sustaining 5AR expression and dopaminergic signaling for regulation of estrogenic activity, as well as regulation of prolactinogenic activity.
If I had simply taken DHT for much longer at least one of the few times I've used it in the past couple years, it's very probable that I wouldn't still be in this state. So, try a 4 week cycle and then see what happens. You should get the HPTA rebound 2-3 weeks after stopping, you should experience testicular discomfort and even increase in testicular volume, and things should continue improving and maintaining thereafter. If you feel like you're slipping back into the state you were in previously, get back on it and try again until it sticks.
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