If you smoke some mary jane every now and then. You'll be fine.
THE FACTS
There is no evidence that marijuana impairs male reproductive functioning.
The Jamaican and Costa Rican field studies detected no differences in hormone levels between marijuana users and non-users.
In epidemiological surveys of marijuana users, no problems with fertility have emerged as important.
In 1974, researchers reported diminished testosterone, reduced sexual function and abnormal sperm cells in males identified as chronic marijuana users. 34 In a laboratory study, the same researchers reported an acute decrease in testosterone, but no chronic effect after nine weeks of smoking; they did not evaluate sperm volume or quality. 35 In other laboratory studies, researchers have been generally unable to replicate these findings, 36 although by administering very high THC doses - up to 20 cigarettes per day for 30 days - one study found a slight decrease in sperm concentrations. 37 In all studies, test results remained within normal ranges and probably would not have affected actual fertility.
Severe adverse consequences have also been produced in male laboratory animals, although only with extremely high daily THC doses. 38
More importantly, in both the human and animal laboratory studies, all observed changes were reversed once THC administration was halted.
Fantastic read.
Acute effects of smoking marijuana on hormones, subjective effects and performance in male human subjects.
Cone EJ, Johnson RE, Moore JD, Roache JD.
Four healthy male subjects smoked two marijuana cigarettes or one marijuana cigarette and one placebo cigarette, or two placebo cigarettes on separate days in a random order crossover design. Each marijuana cigarette contained 2.8% delta-9-tetrahydrocannabinol (THC). Plasma hormones and THC were measured before and after each smoking session. Plasma LH was significantly depressed and cortisol was significantly elevated after smoking marijuana. Nonsignificant depressions of prolactin, FSH, testosterone and free testosterone and elevation of GH also occurred. Concurrent measures of subjective effects via subscales of the Addiction Research Center Inventory, Single Dose Questionnaire and a Visual Analog Scale were generally elevated. Significant impairment on a psychomotor performance task paralleled elevations in subjective effects, hormone effects and peak THC determinations. Although all the hormone effects were within normal basal ranges, interactions between these systems, and their effects on behavior cannot be discounted.
Marijuana extracts possess the effects like the endocrine disrupting chemicals
Kazuhito Watanabea, Corresponding Author Contact Information, E-mail The Corresponding Author, Erina Motoyaa, Naoki Matsuzawaa, Tatsuya Funahashia, Toshiyuki Kimuraa, Tamihide Matsunagab, Koji Arizonoc and Ikuo Yamamotod
aDepartment of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Ho-3 Kanagawa-machi, Kanazawa 920-1181, Japan bDivision of Pharmacy, Shinshu University Hospital, 3-1-1 Asahi, Matsumoto 390-8621, Japan cLaboratory of Toxicological Science, Faculty of Environmental and Symbiotic Sciences, Prefectural University of Kumamoto, 3-1-100 Tsukide, Kumamoto 862-8502, Japan dSchool of Pharmaceutical Sciences, Kyushu University of Health and Welfare, 1714-1 Yoshino-cho, Nobeoka 882-8508, Japan
Received 21 July 2004;
revised 1 August 2004;
accepted 11 August 2004.
Available online 16 September 2004.
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Abstract
The progesterone 17α-hydroxylase activity, which is one of the steroidogenic enzymes in rat testis microsomes, was significantly inhibited by crude marijuana extracts from Δ9-tetrahydrocannabinolic acid (THCA)- and cannabidiolic acid (CBDA)-strains. Δ9-Tetrahydrocannabinol, cannabidiol and cannabinol also inhibited the enzymatic activitiy with relatively higher concentration (100–1000 μM). Testosterone 6β- and 16α-hydroxylase activities together with androstenedione formation from testosterone in rat liver microsomes were also significantly inhibited by the crude marijuana extracts and the cannabinoids. Crude marijuana extracts (1 and 10 μg/ml) of THCA strain stimulated the proliferation of MCF-7 cells, although the purified cannabinoids (THC, CBD and CBN) did not show significant effects, such as the extract at the concentration of 0.01–1000 nM. These results indicate that there are some metabolic interactions between cannabinoid and steroid metabolism and that the constituents showing estrogen-like activity exist in marijuana.
Effects of delta 9-THC and castration on behavior and plasma hormone levels in male mice.
Dalterio SL, Mayfield DL, Michael SD, Macmillan BT, Bartke A.
Gonadectomy resulted in a rapid increase in plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels, but had no consistent effects on plasma prolactin (PRL) and growth hormone (GH) levels. In castrated males, oral administration of THC (50 mg/kg) significantly increased plasma LH levels within hours following surgery and again from 3 to several weeks post-castration, while THC treatment decreased LH levels between 1 day and 2 weeks postcastration. Administration of THC to 12-hour sham castrates significantly increased plasma LH levels. Plasma FSH, PRL and GH levels were either reduced or unchanged by THC. Administration of THC significantly reduced levels of gonadotropins, PRL and GH in intact males. In additional studies, we examined the influence of THC on the negative feedback response of the anterior pituitary to gonadal steroids. In testosterone propionate (TP)-treated castrated males, concomitant administration of THC increased plasma testosterone (T) and LH at 20 min, while plasma FSH levels were elevated after 60 min. In contrast, in intact TP-treated mice, concomitant THC exposure reduced plasma T levels except at 60 min, when plasma LH levels were significantly increased. Testosterone replacement failed to restore copulatory behavior in castrated mice given a single dose (50 mg/kg) of THC. In fact, acute THC administration to these TP-treated castrates resulted in marked sedation, which was not observed in intact mice given the same dose of THC in an earlier study. The present findings indicate that the effects of acute THC treatment on pituitary gonadotropin release is dependent upon the time after castration. Furthermore, THC administration can suppress copulatory behavior even in animals whose peripheral T levels have been maintained. Effects of THC on plasma androgen levels in animals injected with TP suggest that THC can alter the metabolism or target tissue response to gonadal steroids.