I found an interesting abstract at www.endocrine-abstracts.org /ea/0002/ea0002SP7.htm that seems to suggest that obesity actually increases testosterone production? Huh? Am I reading it correctly? It seems to be saying that the 17HSD enzyme converts androstenedione to T at a higher rate than aromatase converts T to E. Specifically…
"... A quantitative multiplex competitive RT-PCR assay was developed which allowed simultaneous assay of both 17HSD-3 and aromatase mRNA and A-T and A-E1 conversion was compared in cultured preadipocytes. These studies indicated that 17HSD-3 mRNA levels and A-T conversion was substantially greater than aromatase mRNA and A-E 1 conversion. Moreover, the level of 17HSD-3 mRNA was greater in intra-abdominal than in subcutaneous fat. Increasing central obesity increased the ratio of 17HSD:aromatase in intra-abdominal fat, suggesting that obesity accentuates intra-abdominal testosterone production."(emphasis mine)
This paper was presented just last December (2001). According to what I read in T-Mag, aromatase in fat cells converting T to E was supposed to be the problem. In fact, a different study from 1997 suggests that excess aromatase can create a hypogonadal (very low T) obesity cycle. (a reference under The War On Estrogen) This study suggests otherwise. What does this mean? How does a guy figure out who's right?
The only thing I can add is anecdotal evidence. When I am very lean, my sex drive plummets. I am very happy at my current 12-14%. I feel much stronger and more “frisky.”
I agree with Hyok on that. I have spring break in about 2 weeks and have been going something like keto/T’dawg variation in diet. My bf is close to 8 now and my sex drive has gone down. My girlfriend gets extremely pissed because shes knows exactly why I’m getting lean but what good is this body if I dont wana bone all the chicks on break. I’m sure it’ll all come back to me though when I see the hundred thongs on the beach.
My question probably needs an expert like Bill Roberts or Cy Wilson to answer it, but these two responses made something click in my head.
Suppose the aromatase and 17HSD effects are NOT linear, which is a damn good assumption. At very low body fat percentages, the effects of A-T conversion might be most important, hence low body fat means low T levels as you guys have observed. But as the percentage of body fat increases beyond a certain point, the effects of aromatization might take over. In other words, very low fat = low testosterone and very high fat = low testosterone also. There must be an optimal midpoint.
So if this assumption is correct (and that's a big "if") what is the point at which the effects of fat mediated A-T conversion stop and T-E aromatization takes over? Any endocrine specialists want to take a shot at this?
Testosterone and androstenedione simply
interconvert, and testosterone is what is
principally delivered by the testes.
The conclusions that you’re coming to here
would be valid if there were all sorts of
androstenedione being supplied, in which case,
the more enzyme you had to convert it to testosterone, the better. But that’s not
the case.
The study could equally well be interpreted
in the reverse direction (since the enzyme in fact works both ways), namely, that androstenedione production (from testosterone) is relatively high in adipose tissue. This would completely reverse the conclusion you’re coming to… though more properly, since it’s an equilibrium situation (both sides of the equation, testosterone and androstenedione, are in a balance) the real situation is that there’s relatively high futile cycling, changing back and forth from one to the other, in adipose tissue, to little net consequence
so far as systemic levels are concerned. If there is any net consequence in men, it’s probably increase of blood androstenedione levels! (Since it is testosterone that is principally being delivered.)
Bill, thanks for clearing this up. I’ve got a big T problem I’m working with an endocrinologist to remedy and I’m trying to get all the info I can so I can talk intelligently with him. Your info cleared a lot up.
Being an engineer, I tried to build a system diagram of all the inter-relating factors and the drawing got pretty complex pretty fast. The most obvious part of the diagram (to an engineer) was that aromatase conversion seems to participate in (at least) two different negative feedback loops to reduce T levels, so it must be a pretty significant factor. Thanks again.