I'm fairly new to the Forums and have been researching primarily to plan my future protocol in hormone therapy. Previously I have used direct DHT treatment by way of Proviron (mesterolone) which I had prescribed in the UK, my home country, and is available to me o.t.c. where I live now.
My own long held belief, from personal experience, is that for sexual function (libido & EQ) mood and drive the most important factors, from a hormonal perspective are an adequate level of T and the balance of DHT and E2. T, in this context, is merely the prohormone.
There is a lot of discussion, and use in studies, of T:E2 ratios. My own preoccupation is with the DHT:E2 ratio in the presence of adequate T - in the absence of adequate T the ratio of the 2 metabolites is moot.
The main advantage to me of supplementing DHT (the strongest of the androgens) separately is the flexibility to allow it's levels to fluctuate, along with the associated levels of Dopamine, whilst maintaining T and E2 relatively stable. To put some numbers to the theory my TT is normally around 800 and my E2 ~30. SHBG averages around 40. To feel at my best I need my DHT to be between 80 and 110 (ie around the top end, or just over, of most ranges). I know from experience that at those sort of levels my 5a-r conversion is around 8 or 9% of TT. So I need to supplement DHT and I titrate the amount up and down according to occasion.
Therefore the ratio of DHT:E2 (ng/dl to pg/ml) fluctuates around 3or4:1
It's my subjective belief that DHT, like Dopamine, works best when it is in flux and at adequate levels. Having that hormone and the associated neurotransmitter, together with E2, working in synergy is particularly beneficial for sexual function, mood and drive.
Most TRT protocols involve a regimen of injectable T plus an AI "if needed" (leaving aside hCG for now). I would postulate that many patients would have a better outcome, and avoid the need for an AI entirely, by injecting a lesser amount of T with the addition of direct DHT supplementation.
The "need" for an AI is created by sending E2 too high in the first place (by the use of too much aromatisable T). How much better, where efficacious, to use less T plus DHT thereby lessening the potential for high hematocrit, raised blood pressure and (worse still) raised prolactin.
It is encouraging to me to see the success that numerous guys are reporting in using T Cream direct to the scrotum to elevate DHT levels. Looking from across the pond it appeared, at first sight, that the FDA's prohibition of DHT products (no Proviron or Andractim) would disadvantage patients in hormone therapy. However it now seems that this "workaround" method of raising DHT is particularly effective and has a beneficial systemic effect.
The question that interests me here is whether, in addition to the systemic effect, the T Cream applied to the scrotum is having a local effect in the testes ie is it possible that there is an effect on intratesticular aromatase? If it is possible that this strong androgen can somehow dissipate the localised aromatase then could this have potential as an adjunctive therapy for patients using hCG? (DHT cream does have a local effect in treating gynaecomastea).
My own long held belief, from personal experience, is that for sexual function (libido & EQ) mood and drive the most important factors, from a hormonal perspective are an adequate level of T and the balance of DHT and E2. T, in this context, is merely the prohormone.
There is a lot of discussion, and use in studies, of T:E2 ratios. My own preoccupation is with the DHT:E2 ratio in the presence of adequate T - in the absence of adequate T the ratio of the 2 metabolites is moot.
The main advantage to me of supplementing DHT (the strongest of the androgens) separately is the flexibility to allow it's levels to fluctuate, along with the associated levels of Dopamine, whilst maintaining T and E2 relatively stable. To put some numbers to the theory my TT is normally around 800 and my E2 ~30. SHBG averages around 40. To feel at my best I need my DHT to be between 80 and 110 (ie around the top end, or just over, of most ranges). I know from experience that at those sort of levels my 5a-r conversion is around 8 or 9% of TT. So I need to supplement DHT and I titrate the amount up and down according to occasion.
Therefore the ratio of DHT:E2 (ng/dl to pg/ml) fluctuates around 3or4:1
It's my subjective belief that DHT, like Dopamine, works best when it is in flux and at adequate levels. Having that hormone and the associated neurotransmitter, together with E2, working in synergy is particularly beneficial for sexual function, mood and drive.
Most TRT protocols involve a regimen of injectable T plus an AI "if needed" (leaving aside hCG for now). I would postulate that many patients would have a better outcome, and avoid the need for an AI entirely, by injecting a lesser amount of T with the addition of direct DHT supplementation.
The "need" for an AI is created by sending E2 too high in the first place (by the use of too much aromatisable T). How much better, where efficacious, to use less T plus DHT thereby lessening the potential for high hematocrit, raised blood pressure and (worse still) raised prolactin.
It is encouraging to me to see the success that numerous guys are reporting in using T Cream direct to the scrotum to elevate DHT levels. Looking from across the pond it appeared, at first sight, that the FDA's prohibition of DHT products (no Proviron or Andractim) would disadvantage patients in hormone therapy. However it now seems that this "workaround" method of raising DHT is particularly effective and has a beneficial systemic effect.
The question that interests me here is whether, in addition to the systemic effect, the T Cream applied to the scrotum is having a local effect in the testes ie is it possible that there is an effect on intratesticular aromatase? If it is possible that this strong androgen can somehow dissipate the localised aromatase then could this have potential as an adjunctive therapy for patients using hCG? (DHT cream does have a local effect in treating gynaecomastea).
