Lets set the facts straight! I have this post broken down into 2 sections, Alcohol and marijuana with alcohol being comprised of many subsections. I won't personally dispute some of the posts on this thread, you can read it for yourself...
ALCOHOL
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Growth Hormone </DIV>The deleterious effects of ethanol on humans and animals is consistent and well-established in both adults and adolescents, with decreases in GH levels, GH mRNA (24), as well as GH releasing factor mRNA levels (25). In adolescent rats, administration of 3g/kg of ethanol, which, due to the faster metabolism of rats produced blood alcohol levels equivalent to only about 4-6 drinks for humans, caused a massive drop in GH levels to just 4-7% of control by the 1.5 hour mark (26) -- Levels were still down 66-86% after 24 hours. In adult rats, the same 3g/kg caused total suppression of GH release, with 2g/kg causing significant but not total suppression (27).
In young adult male humans, 1.5mg/kg disrupted the nocturnal rhythm of GH secretion in all subjects, as well as decreasing overall release by 30% (28). 1g/kg almost completely inhibited the nocturnal rise in growth hormone levels, while a mere .5mg/kg resulted in levels 1/3 that of control (29). Inhibition of hepatic IGF-1 synthesis (30, 31), and the IGF-1/IGFBP-1 ratio (31, 32), a marker of IGF-1 bioavailability, have also been shown to be negatively effected by ethanol.
CORTISOL
<DIV class=sectionText>Ethanol has been found to both directly, and indirectly -- via increases in ACTH (33), increase cortisol production. 1.75g/kg increased levels by 152% at 4 hours and was still significantly higher than control at 24 hours in adult males (34). In addition, consumption of ethanol along with exercise resulted in a 61% increase in cortisol over alcohol alone (35) . A study of adolescents admitted to the hospital with acute alcohol intoxication showed ACTH and cortisol levels 10 and 1.6 times that of controls in females, and 5.9 and 1.4 times as high in males -- however, a general stress response much be considered as a possibility in these circumstances (36).
Other studies, however, have not found such effects (28, 37, 38). Thus, some researchers have concluded that any increases in cortisol are due to a stress response from nausea rather than a direct effect of ethanol (38, 39). And, indded, in one study, a subjects that vomited displayed cortisol levels 5 times as high as his baseline value (28).
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Testosterone
Finally, we get to the good part -- or bad, if you like to hit the sauce with regularity. Acute ingestion of ethanol has been fairly consistently shown to significantly suppress testosterone production in both animals and humans, adults and adolescents. We will first look at the mechanisms involved, then turn to studies looking at actual testosterone levels.
Ethanol exerts its hypogonadic effects through several direct and indirect mechanisms. The primary mechanism is through direct suppression of leydig cell functions, either through a direct toxic effect (including reduction of LH receptors) (47,48), free radical activity -- selenium was found to ameliorate ethanol induced testosterone suppression (49), through reductions of 3beta-HSD (this is the enzyme that converts androstenediol to testosterone as well as DHEA to androstenedione) (50), 17beta-HSD (converts androstenedione to testosterone) (51), and 17,20 lysase (converts progesterone to androstenedione) (50), and through depletion of NADPH generating enzymes -- NADPH is a cofactor utilized in many steps of steroidogenesis (52), and ethanol administration has been shown to result in a decrease in the enzymes responsible for the generation of NADPH (53, 54).
Ethanol has also been shown to decrease LH releasing hormone at the hypothalamus (55), to decrease LH release at the pituitary (56), as well as to inhibit betaLH mRNA in vitro (57). This could be mediated by endogenous opiates as they are known to be increased by ethanol, and opiate antagonists have been shown to increase LH release as well as to block ethanol induced testosterone suppression at the testicular level (58).
Nitric oxide (NO) has also been implicated in this suppression (remember that next time you pop some Viagra or a tribulus product). While NO stimulates LH releasing hormone in the hypothalamus (59) and LH release in the pituitary (60), its overall effect on testosterone is negative due to its effects at the gonadal level (61). Substances that increase NO levels have been shown to inhibit testosterone secretion (61), as well as possibly inhibiting steroidogenic enzymes (62). Concomitant use of L-NAME, L-NA, or 7Ni (nitric oxide synthase inhibitors) with ethanol completely prevented the fall in testosterone seen with 3g/kg ethanol (63,64).
Another interesting possibility is a mechanism involving a neural connection between the brain and the gonads via adrenergic receptors. It has been shown that direct injection of adrenergic agonists into the hypothalamus decreased testosterone production at the testes, without a change in LH levels (65). As we saw in part 1, ethanol is known to increase catecholamine levels in the CNS. And, indeed injection of both phentolamine (alpha adrenergic antagonist) and propranolol (beta antagonist) were found to partially overcome ethanol's suppressive effect on HCG stimulated testosterone production (66).
Before you go out and get these drugs, remember that adrenergic stimulation, PERIPHERALLY, has a positive effect on testosterone levels. However, if anyone knows of adrenergic antagonists that only act centrally, not peripherally, feel free to let us know.
Let's now turn to some studies that looked directly at testosterone levels following acute alcohol administration. In adult males, 1.3g/kg of ethanol (about 10 drinks for a 200 lb person), caused a significant decrease vs. basal levels at the 60 minute mark. Differences for the next two hours were not significant, though the researches did not utilize a control group, so the natural morning rise in testosterone could have masked any effects (38). 1.5g/kg lowered levels by an average of 23% over a 24 hour period (28). 1.75g/kg lowered levels by 27% and 16% at 12 and 24 hours, respectively (34). Adolescent males admitted to the hospital for alcohol intoxication were found to have 21% lower testosterone levels than controls (36).
A couple of studies have looked at alcohol and exercise. 1.5g/kg depressed testosterone by more than 20% by 1 hour and was still depressed by the same margin at hour 10 (37). Interestingly, when the same ethanol dose was preceded by an exercise session, the suppressive effect continued for 22 hours -- and when exercise was performed during a hangover, significant suppression (21-32%) vs. ethanol alone continued for 26 hours. Compared to control, both ethanol groups had significantly lower testosterone levels for 42 hours - this is almost 2 full days. A much smaller intake (.83g/kg) did not result in a significant decrease (35).
All of this is at what are fairly moderate doses. Let's take a look at binge drinking doses.
Probably for ethical reasons, doses equating to 20+ drinks have not been studied in humans, so we must settle for rat data, but considering the effects at lower doses seem quite similar, these studies are likely quite relevant -- and could actually underestimate the effect, since, as we mentioned, these doses resulted in much lower blood alcohol levels in rats than humans.
3g/kg caused massive suppression of testosterone (67). Between hours 1.5 and 96 (yes, 4 days later), testosterone was reduced between 50-75% and, even a full week later, it was still down 40%. By week two, it was finally back to control level. 3g/kg also reduced HCG stimulated testosterone secretion by 75% (66). In male macaque monkeys, 2.5 and 3.5g/kg reduced testosterone levels by 63 and 70%, respectively (68)
One study in adolescent rats found that testosterone levels doubled for the first 3 of weeks of ethanol ingestion (69) -- however, this was with an intake equal to 90 drinks per day for a 200 lb person. If anyone tries this, please report back with your results.
On the other hand, levels below 1g/kg seem to have no deleritous effects (35, 70).
Another interesting tidbit -- increased testosterone levels were found to correlate with decreased symptoms of withdrawal in alcoholics -- and the authors recommended supplemental testosterone as a possible treatment strategy (71). Wonder if a doctor would buy this?? </DIV>
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Alcohol and Estrogen</DIV>
<DIV class=sectionText>Chronic alcoholics, in addition to being hypogonadal, exhibit sign of overt feminization (72). There is some evidence to suggest that ethanol might also increase the aromatization of testosterone to estradiol. Consumption of .9 - 2.1g/kg of beer or wine significantly (P <0.05 to P< 0.001) increased estradiol levels in healthy adult humans (73). A study in rats found levels of estradiol increased by 60% (to go along with 55% lower test levels) - however, this was with the equivalent of about 13 drinks/day for 1-2 months (74).
In addition, alcohol administration has been shown to increase estrogen receptor density (75, 76) and to decrease levels of a estradiol binding protein (77, 78) -- as well as to lower androgen receptor numbers (76). However, this has primarily been found in conjunction with alcoholic liver disease, so its relevance to acute consumption in questionable.
Another possibility is the existence of phytoestrogens in alcoholic beverages. Hops, used as a flavoring agent and preservative in beer, contains several powerful phytoestrogens, including 8-prenylnaringenin, genistein, and daidzein (79, 80). And, congeners, which are found primarily in dark liquors such as bourbon and wines have been found to contain biochanin A, beta-sitosterol (72, 80)
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Protein Synthesis </DIV>
<DIV class=sectionText>Both ethanol and its metabolic byproduct, aldehyde, have been shown to reduce protein synthesis in skeletal muscle (85, 86, 87, 88). To make matters worse, it is predominately Type II, fast-twitch fibers that are affected, with type IIB being hit the hardest (85, 86, 87). This is not a good thing for bodybuilders, and it is a very bad thing for athletes.
With acute administration of real-world doses (.8 - 2.0g/kg) of ethanol, reductions in protein synthesis of 20-30% have been seen within about one to two hours of administration, this is before the previously reviewed hormonal changes occur, indicating that alcohol is exerting a direct effect (85, 86, 88). Within 24 hours, decreases of as high as 63% have been shown to occur (86), which likely reflects the added contribution of negative hormonal changes.
The mechanism behind this is not fully characterized. Reduction in both mRNA (86) and translational efficiency (87) have been observed. The generation of free-radicals, which are known to be increased by ethanol (89, 90), could be involved (91). Low levels of selenium and alpha-tocopherol (vitamin E) are found in alcoholics with myopathy (muscle wasting) (92). However, there is also evidence that does not support this theory (93). Another possibility is direct ischemic damage (94).
Given alcohol's hormonal effects and its direct effects on protein synthesis, if you are going to indulge in fairly heavy alcohol consumption, it would probably be a very good idea to utilize a topical prohormone formulation (or a short-acting injectable ester of the real thing) the evening of drinking and the next day in order to minimize the damage to your hard earned muscle. </DIV>
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Indirect Effects: Immune System </DIV>
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<DIV class=sectionText>Even moderate, acute ethanol consumption can significantly influence susceptibility to infections caused by viral and bacterial pathogens -- and alcohol is usually consumed in a social setting, where exposure to pathogens will be increased. Obviously, if one is sick, workouts will suffer. -- thus, this is important.
Both in vitro and in vivo administration of ethanol blunts inflammatory cytokine response to bacterial stimulation (95, 96). Monocyte production of IL-1, IL-6, and TNF-alpha are decreased (97) - leading to defective host defense against microbial infection (98). In addition, immunomodulatory cytokines such as IL-10 and TGF-beta as well as the prostaglandin PGE2, are increased (97), leading to a downregulation of production of antigen specific T-cells - increasing susceptibility to viral infections (99).
Testosterone and Females
Ethanol's effects on the female bodybuilder, however, are not so bleak. Because female testosterone production occurs primarily outside the gonadal structures (81), ethanol's effect on LH is not as relevant -- and its effects on Leydig cells obviously are not at all relevant. In addition, ethanol is known to stimulate adrenal activity (82) -- 25% of female testosterone production is produced as an intermediate in the production of cortisol in the adrenals (81).
This results in INCREASED testosterone levels in women after ethanol consumption. As little as .4g/kg caused a significant increase in testosterone levels (83),and 1.2g/kg and 2g/kg caused increases of 25% and 54% respectively (84).
Interestingly, serum epitestosterone is not proportionally increased, nor are urinary levels, thus the testosterone to epitestosterone ratio (T:Ep) used in athletic drug screenings is skewed. The same study mentioned above resulted in a T:Ep ratio of around 4.5 compared to 1.5 before drinking. Individual increases ranged from 1.9 to 8.7 times baseline (84). Given that the testing cutoff is 6:1, it is easy to see that this could result in a false positive (or perhaps be used as a handy excuse for a true positive).</DIV>
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Marijuana!
Marijuana has long been reputed to either decrease testosterone levels, increase estrogen levels, or both. This would have negative effects on bodybuilders for many obvious reasons. In this post, I will explore this issue. A related issue I will also explore is marijuana's effects on fertility.
Laboratory Research
Animal studies have shown that THC can have an effect on sex hormones. Unfortunately, because these studies were done for primarily political reasons, extremely large doses were administered. A single large dose has a temporary effect, repeated administrations of smaller doses have little effect to no effect at all. When there is an effect, tolerance quickly develops and levels return to normal. Even when the THC administration gets to the level of severely abusing the animal, no permanent harm to hormone levels or reproductive function have been shown.
Someone who examines the laboratory research without making note of the amount of THC used in the experiments might well be convinced that THC has an appreciable effect on sex hormones. However, as with the first issue, the empirical evidence and human studies will prove much more revealing.
Empirical Research On Men
The first issue is whether or not marijuana reduces testosterone levels in men. One of the first researches to explore this issue was Robert Kolondy, a pseudoscientist who had previously "proved" that homosexuals had lower testosterone levels. In his 1974 studies, he "conclusively" showed that marijuana had a negative effect on testosterone production in men, and his studies are still frequently referenced in the anti-drug literature of today. Numerous studies since then negate his finding. They show no effects on testosterone levels, even after smoking very high doses (1, 2, 3, 4, 5). Also, studies of the general population haven't found a difference in testosterone levels of users and nonusers (6, 7, 8).
The second issue is whether or not marijuana increases estrogen levels in men. As with the testosterone issue, a large amount of studies have been done, although not quite as many. All of them show that marijuana has no effect on estrogen levels in men, even in large doses (5, 7, 9).
The final issue is fertility. Numerous studies have been done on marijuana's effect on sperm quantity and quality. Marijuana does in fact reduce sperm count. Note that this is not synonymous with impotence or infertility; marijuana should not be used for birth control. The studies only show a marginal effect. Perhaps the most comprehensive study was done by Hembree, W.C. et al. In this study, men spent 30 days in a closed laboratory smoking 20 joints a day. Decreases in sperm count and motility were found, although they were still within normal ranges. After marijuana use was discontinued, the numbers quickly returned to where they were before (10).
There have also been quite a few studies concerning the effects on sex hormones and fertility in women. I will not cover those here, but if anyone wants further information just let me know.
Conclusion
As we can see, the laboratory findings often do not match up with findings in the real world. Laboratory studies can often be tampered with, misrepresented, or misinterpreted for political reasons.
The claims of effects on testosterone and estrogen levels in men are unfounded. So why do we so commonly see it in the media? There are a few reasons. First, people generally associate marijuana with an unhealthy lifestyle, so when they are confronted with conflicting evidence, they'll choose the side that is more anti-marijuana. In other words, their preconceptions guide their decision-making. Second, in mainstream media - health magazines, bodybuilding magazines, and the like - people often regurgitate what they heard somewhere else. Staff writers are not researchers; they are entertainers. It is not their job to provide people with well-researched information, rather with information that will provoke an emotional reaction. They're writing an article on "things to avoid when bodybuilding," and they need to fill in a blank, so they type in "smoking weed." Not many people are going to know whether they're actually telling the truth, because few people have researched it in depth. Third, strong claims have a much higher chance of getting around than weak ones. Take the example of Cell-Tech. They sell a lot of that stuff, and the reason is that they make strong claims. You don't know how many people in my hometown have told me, "It's 30 times better than creatine!" The phrase "marijuana doesn't affect hormone levels" doesn't mean much, but "marijuana will turn you into a woman" is something you'll remember.
References
1. Mendelson, J.H. et al., "Plasma Testosterone Levels Before, During, And After
Marijuana Smoking," New England Journal of Medicine 291, 1051-55 (1974).
2. Schaefer, C.F. et al., "Normal Plasma Testosterone Concentrations After
Marijuana Smoking," New England Journal of Medicine 292, 867-68 (1975).
3. Mendelson, J.H. et al., "Effects of Chronic
Marijuana Use on Integrated Plasma Testosterone and Luteinizing Hormone Levels," Journal of Pharmacology and Experimental Therapeutics 207, 611-17 (1978).
4. Hembree, W.C. et al., "Marihuana's Effects on Human Gonadal Function," pp.521-32 in Nahas, G.G. (ed), Marijuana: Chemistry, Biochemistry, and Cellular Effects, New York: Springer-Verlag (1976).
5. Cone, E.J. et al., "Acute Effects on
Marijuana on Hormones, Subjective Effects and Performance in Male Human Subjects," Pharmacology Biochemistry and Behavior 24, 1749-54 (1986).
6. Cushman, P., "Plasma Testosterone Levels in Healthy Male
Marijuana Smokers," American Journal of Drug and Alcohol Abuse 2, 269-75 (1975).
7. Block, R.I. et al., "Effects of Chronic
Marijuana Use on Testosterone, Luteinizing Hormone, Follicle Stimulating Hormone, Prolactin and Cortisol in Men and Women," Drug and Alcohol Dependence 28, 121-28 (1991).
8. Coggins, W.J. Et al., "Health Status of Chronic Heavy Cannabis Users," Annals of the New York Academy of Sciences 282, 148-61 (1976).
9. Abel, E.L., "
Marijuana and Sex: A Critical Survey," Drug and Alcohol Dependence 8, 1-22 (1981).
10. Hembree, W.C. et al., "Changes in Human Spermatozoa Associated with High Dose Marihuana Smoking," pp.429-39 in Nahas, G.G. and Paton, W.D.M. (eds), Marihuana: Biological Effects, Oxford: Pergamon Press (1979).[/color][/color][/color]</DIV></DIV></DIV></DIV></DIV></DIV>
