Endocrine Effects

The effects of cannabis upon sexual performance are not clearly understood, and the published research available often yields conflicting results. Traditionally, high doses have been claimed to reduce libido and cause impotence, whilst more moderate intake has been associated with heightened pleasure from sexual contact (Buffman, 1982; Abel, 1981). If the drug has the ability to enhance the subjective experience of sex, then this might be due to cannabis-induced relaxation or increased tactile sensitivity.

Several animal studies have shown that THC reduces the secretion of testosterone (Abel, 1981). Kolodny et al. (1974) recruited 20 young men aged between 18 and 28 years who had used cannabis on at least four days per week for a minimum of six months. The number of cannabis cigarettes smoked per week ranged from 5 to 13; the average was 9.4. The average plasma testosterone level in the men under study was 416 ng/100 ml, compared to 742 ng/100 ml in 20 matched controls who had never used cannabis. This effect of cannabis appeared to be dose-dependent in that those who consumed ten or more cigarettes per week had a lower average testosterone (309 ng/ 100ml) than those consuming nine or less (503 ng/100 ml). Human chorionic gonadotrophin was given to four of the men who continued to use cannabis. This produced an increase in plasma testosterone of between 121% and 269%. Six of the seventeen cannabis users who were tested exhibited markedly reduced sperm counts, and two were impotent. Three users discontinued cannabis for two weeks, and this resulted in a rapid rise in plasma testosterone.

Other researchers have failed to verify the findings of Kolodny's group. Seven separate studies involving over one hundred chronic cannabis smokers have individually demonstrated an absence of significant effect upon human testosterone levels (Block et al., 1991; Cushman, 1975; Erdolu et al., 1985; Hembree et al., 1976; Mendelson et al., 1974, 1978; Schaefer et al., 1975). In 1976, Kolodny and colleagues studied the effects of cannabis upon human testosterone levels for a second time. On this occasion, the investigation was more rigorous. Plasma testosterone levels were significantly reduced at 30, 120 and 180 minutes after smoking cannabis, compared to levels measured in the same individuals during a non-smoking period. However, a study by Mendelson and co-workers in 1978, using a similarly rigorous design, again failed to reproduce these results.

It is unclear why Kolodny and associates have consistently reported that cannabis can reduce testosterone levels whilst other groups have not confirmed this finding. Testosterone plasma levels do show a very wide diurnal variation in man. Perhaps particularly high doses and/or very long duration of administration of cannabis is required. Even if cannabis can reduce testosterone levels by as much as Kolodny estimated, then the functional significance of this is unclear, since the levels reported are within the normally observed human male range for this hormone.

THC is able to trigger the growth of breast tissue in rats (Harmon and Aliapoulios, 1974). In 1972 the same authors reported three cases of human gynaecomastia which they attributed to heavy cannabis use. In 1980, Olusi reported three further cases in which the plasma prolactin levels were almost doubled in each case prompting the author to suggest a mechanism for the reaction. However, no other cases of cannabis-induced human gynaecomastia have been described in the medical literature, suggesting that the reaction is probably rare and that cannabis use might even be a coincidental finding.

Kolodny et al. (1974) reported that 6 of 17 men who habitually smoked cannabis had a reduced sperm count. This was also described in five men who were chronic users (Hembree et al, 1976). These individuals were required to discontinue cannabis for 14-21 days, before resuming for 4 weeks. Sperm count did not fall during the smoking phase, but did drop by an average of 58% during a two week post-exposure recovery phase. This was attributed to a direct action on spermatogenesis since reproductive hormone levels were unaffected; the delayed response was assumed to be due to the long time required for sperm to form in man. Another study has also reported decreased spermatogenesis in cannabis smokers (Erdolu et al., 1985). In none of these small studies was sperm count reduced to the levels of male infertility. By contrast, the research of Close and co-workers failed to find a link between cannabis use and decreased sperm count or motility (Close et al., 1990).

There is even less information available concerning the effect of cannabis upon human female reproductive function. In animals, cannabis can impair ovulation. Kolodny et al. (1979) studied the adverse effects of cannabis upon the human female reproductive cycle. Cannabis users had a greater proportion of cycles in which either ovulation did not take place, or in which the luteal phase was very short (38.3%) compared to non-users (12.5%). The duration of the human menstrual cycle was also measured. Cannabis smokers had an average cycle length of 26.8 days, compared to 28.8 days in non-users. However, cannabis smokers consumed significantly greater amounts of alcohol compared to controls, which is known to have detrimental effects upon the human menstrual cycle. Cannabis users were also more sexually active. Unexpectedly, another study has suggested that regular use of cannabis can significantly shorten the time to conception amongst fertile women (Joesoef et al., 1993).

Studies suggest that cannabis does not affect plasma levels of follicle-stimulating hormone or luteinizing hormone in men or women (Block et al., 1991; Erdolu et al., 1985; Kolodny et al., 1974). Most studies have found that cannabis does not usually affect human prolactin levels, although cases of human male hyperprolactinaemia attributed to cannabis are reported (Erdolu et al., 1985; Olusi, 1980). Cannabis does not seem to affect plasma levels of thyroid hormones, or glucocorticosteroids. The effects of cannabis upon glycaemic control are discussed below under interactions with antidiabetic drugs.

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