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Old 08-28-2008, 07:49 PM   #1
 
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HERE's an extract from a study I've just read:


Cigarette smoking has major effects on the reproductive potential of humans. It has an anti-oestrogenic effect in women (34, 74, 75). This is probably due to changes in hepatic oestrogen metabolism induced by smoking. Smoking has a powerful effect on the 2-hydroxylation pathway of oestradiol metabolism leading to increased production of 2-hydroxyestrogens (76).

I wonder if my heavy cigarettes abuse has protected me from gyno when I was younger and used to inject myself up to 1000 mg test E without any AI? Not to say smoking is a good idea at all!
Old 08-29-2008, 07:18 AM   #2
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Isn't it always a trace element thats in cigarettes?

I mean they toss everything in cigarettes, but its in tiny doses, I'd be curious as to what truly does this? the small amount of marijuana?
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Old 08-29-2008, 08:09 AM   #3
 
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Old 08-29-2008, 09:42 AM   #4
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I believe it might have been PA that made a comment about the anti-e effect of nicotine. Maybe I'll be able to find the quote later.
Old 08-29-2008, 09:56 AM   #5
 
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Nicotine is an aromatase inhibitor(at least in vitro),but the study I quoted talks about a different pathway,similar to I3C, I guess not due to nicotine.
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Old 08-29-2008, 10:25 AM   #6
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PCTs now to include a carton of newports.
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Old 08-29-2008, 10:28 AM   #7
 
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great idea man,really.
Should be included in my medical insurance.
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Last edited by THEHUGE; 08-29-2008 at 10:48 AM.
Old 08-29-2008, 12:29 PM   #8
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Quote:
Originally Posted by usf97j4x4 View Post
PCTs now to include a carton of newports.
Ha ha
Old 08-29-2008, 01:57 PM   #9
 
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Again with the nitpicking. Smoking will keep you leaner. Admittedly Ive added a welcome 1-2% bodyfat since I quit 6 months ago. As for jamming a pack a day as an AI, I see far better benefits from actual AIs than from slowly inducing cancer.

Besides, we all know this is one of those trace amount things, and that the effective AI dose is probably like 3 or 4 packs a day - if you smoke that much, you DEF. dont train very hard.
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Old 08-29-2008, 03:13 PM   #10
 
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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.


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