[quote]katzenjammer wrote:
DrSkeptix wrote:
what, in your view, are the practical implications of this way of thinking about all this?
Cheers, ~katz
[/quote]
Great question.
My prior response was a comment on the study.
What we do is to question further and I will try not to be pedantic.
Practical application of isolated studies is just a step above anecdote.
In your case, transdermal DHEA “caused” desirable effects. Or was it something else that you were doing? I can’t know.
In the more general case, the study which you cited, contrary results were obtained. So i guess, practically speaking, I would not recommend DHEA based on your experience alone; and I might recommend against young men using it based on the cited study.
These threads are full of inconsistencies, and misapplications of physiology. But they have been adopted–wholesale–as dogma. For example:
- HCG is recommended to prevent testicle shrinkage while on exogenous T.
But if the testicle is capable of responding to low-doses of T, why is the T needed at all? Why not use HCG only? (I suspect that many men here have arrived at T supplementation through a circuitous route, and have had temporary screw-ups interpreted as a permanent disability.)
- If HCG works in such men, why wasn’t LH sufficient to increase T production? I posit: E2 and DHT suppress LH better than T. Those men with low LH and low T (and whatever measured E2) may respond to aromatase inhibition alone. (My friend Chushin may have heard my rants before.) Perhaps effected men would respond to AIs alone. I have done this, and it works, but it isn’t part of “standard medical practice.”
So, practically speaking, where does that leave our neglected OP?
I guess he took DHEA unnecessarily, elevated his estrone and E2 (see your cited article, KJ), further depressing T production. (Now all sorts of blood tests will be subject to question.)
Here is my heretical dogma.
The only surrogate measurement of “total body aromatase activity” that we have is the measurement of E2 (or estrogen, or estrone). But the tissue effects of E (on and by fat, on bone, muscle, brain) may not always be reflected by high serum E2. So many posters have a obsessive respect for small changes in T or E. It really doesn’t matter whether blood or urine is measured–we all rely on the test numbers to the exclusion of the effect on the “end-organ.”
For purposes of the foregoing discussion, the “end-organ” is the pituitary.
Practical lesson:
–The Pituitary: figure out why it is unhappy, then fix it. (If the LH is low or normal, and E is “normal,” that does not exclude the utility of an AI.)
–The Balls: if the Pituitary is happy, figure out what ails the Balls. Use what makes sense, allow for errors of judgment, use supplements only very carefully.