08-29-2008, 03:13 PM
|
#10
|
|
Status: IFFI Control Tower
Join Date: Jun 2007
Location: Rochester, NY / Baltimore, Md / Others
Posts: 2,184
|
While cigarette smoking is maintained as the number 1 cause of preventable morbidity and mortality worldwide (second is obesity btw), there is certainly no way I could support its use - even with positive offering in a couple of categories like Ulcerative Colitis and Weight Gain.
Bodybuilders are overtly a strange bunch in that they try and get me to thumb's up their alternate addictions in many instances and this is probably the second most common. Well, I won't codemn use per se, but I won't support it either.
The papers that suggest hormonal support offering are restricted to certain groups and even the 2-hydroxylation offering above is probably only seen in females as has tended to be the overt suggestion in the literature at large, but the steroidogenic pathways are extremely different in that regard when compared to males.
Also beneficial might be the observation that in dogs, nicotine inhibits 3 alpha-hydroxysteroid dehydrogenase, preventing metabolism of DHT to a less potent androgen. While theoretically, this would allow one to gain increased benefits from DHT, it might also potentiate DHT's negative effects on the prostate and hairline.
Unfortunately, beyond individual inhibition of enzymes, nicotine and its metabolite cotinine appear to have a largely negative effect on steroidogenesis. Both nicotine and cotinine have been implicated in decreasing testosterone synthesis in rodent leydig cells. This decrease might be due to nicotine's effect on increased ACTH release, leading to increased circulating coritcosteroids (i.e. - cortisol), which have been known to alter sex hormone synthesis (as I have pointed out countless times in my protocols for post-cycle cortisol control). While the in vivo action of nicotine on sex steroids might be less pronounced, those using nicotine with the purpose of aromatase inhibition should be aware of its other effects on steroidogenesis and because we oftentimes look to support our habits, this is unfortunately not done.
As Voo points out above, the lowering of bodyfat certainly can lower conversion to estrone through lowering the overall concentration of aromatic conversion by default, but this is pure pontification and that alone at present time. The problem that will continually plague this theory is that no systematic trials will ever be entertained because of the aforementioned problems to generalized health status.
D_
__________________
Dana Houser, MD, MHSA, CISSN
askdinoiii@hotmail.com
The Clinical Underground Official Newsletter (Volume I, Issues I & II now available) ... send "subscribe" email to the address above.
Disclaimer: Despite my being a physician, the information provided in my posts is intended for INFORMATIONAL PURPOSES ONLY and to stimulate increased rapport between physician and patient. It is asked that you embark on advice provided solely by your EXAMINING physician.
Please do NOT email, PM for scripts or referral.
|
|
|
|