That must have been some study, it involved eleven patients.
Give me a break!
To have a statistically significant study, you would need sampling groups in the hundreds of cases. I can prove anything if I am allowed to pick my own subjects and use such a small test group.
you must have never studied statistics... one hardly needs a sample size in the "hundreds of cases" to derive a statistically accurate sample of the target population.
show me the study that you keep referencing that supports your claim that marijuana causes gyne.
i'll admit that 11 patients is a poor sample size, but that was just one study i found in about 5 seconds on pubmed. there are plenty more out there to support my claim
heres one that shows marijuna smoke potentially has ANTIESTROGENIC effects:
Arch Pharm Res. 2005 Dec;28(12):1365-75. Related Articles, Links
Antiestrogenic effects of marijuana smoke condensate and cannabinoid compounds.
Lee SY, Oh SM, Lee SK, Chung KH.
National Institute of Scientific Investigation, Seoul, Korea.
The antiestrogenic effects of marijuana smoke condensate (MSC) and three major cannabinoids, ie., delta9-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN), were evaluated using in vitro bioassays, viz., the human breast cancer cell proliferation assay, the recombinant human estrogen receptor (ER) competitive binding assay, and the reporter gene assay. The inhibitory effects on estrogen were also examined using the ethoxyresorufin-O-deethylase (EROD) assay, the aromatase assay, and the 17beta-estradiol (E2) metabolism assay. The results showed that MSC induced the antiestrogenic effect via the ER-mediated pathway, while THC, CBD, and CBN did not have any antiestrogenic activity. This suggests that the combined effects of the marijuana smoke components are responsible for the antiestrogenicity of marijuana use. In addition, MSC induced the CYP1A activity and the E2 metabolism, but inhibited the aromatase activity, suggesting that the antiestrogenic activity of MSC is also related to the indirect ER-dependent pathway, as a result of the depletion of the in situ E2 level available to bind to the ER. In conclusion, pyrogenic products including polycyclic aromatic hydrocarbons (PAHs) in the non-polar fraction, which is the most biologically active fraction among the seven fractions of MSC, might be responsible for the
antiestrogenic effect.
PMID: 16392670 [PubMed - indexed for MEDLINE]
heres one that found that even though components of MJ outcompete estadiol for its receptor there was no demonstrated estrogenic activity.
J Pharmacol Exp Ther. 1983 Feb;224(2):404-7. Related Articles, Links
Marijuana: interaction with the estrogen receptor.
Sauer MA, Rifka SM, Hawks RL, Cutler GB Jr, Loriaux DL.
Crude marijuana extract competed with estradiol for binding to the estrogen receptor of rat uterine cytosol. Condensed marijuana smoke also competed with estradiol for its receptor. Pure delta 9-tetrahydrocannabinol, however, did not interact with the estrogen receptor. Ten delta 9-tetrahydrocannabinol metabolites also failed to compete with estradiol for its receptor. Of several other common cannabinoids tested, only cannabidiol showed any estrogen receptor binding. This was evident only at very high concentrations of cannabidiol. Apigenin, the aglycone of a flavinoid phytoestrogen found in cannabis, displayed high affinity for the estrogen receptor. To assess the biological significance of these receptor data, estrogen activity was measured in vivo with the uterine growth bioassay, using immature rats. Cannabis extract in large doses exhibited neither estrogenic nor antiestrogenic effects. Thus, although estrogen receptor binding activity was observed in crude marijuana extract, marijuana smoke condensate and several known components of cannabis, direct estrogenic activity of cannabis extract
could not be demonstrated in vivo.PMID: 6296360 [PubMed - indexed for MEDLINE]
heres one showing the effects of chronic MJ use:
Drug Alcohol Depend. 1991 Aug;28(2):121-8. Related Articles, Links
Effects of chronic marijuana use on testosterone, luteinizing hormone, follicle stimulating hormone, prolactin and cortisol in men and women.
Block RI, Farinpour R, Schlechte JA.
Department of Anesthesia, College of Medicine, University of Iowa, Iowa City 52242.
To investigate possible effects of chronic marijuana use on reproductive and stress hormones, we assayed testosterone, luteinizing hormone, follicle stimulating hormone, prolactin, and cortisol in 93 men and 56 women with a mean (+/- S.E.) age of 23.5 +/- 0.4 years. Hormone values were compared among groups of subjects stratified according to frequency of marijuana use (frequent, moderate and infrequent; N = 27, 18, and 30, respectively) and non-using controls (N = 74).
Chronic marijuana use showed no significant effect on hormone concentrations in either men or women.PMID: 1935564 [PubMed - indexed for MEDLINE]
here's one where monkeys were given MEGA doses and hormonal profiles were statistically unchanged:
J Toxicol Environ Health. 1980 Mar;6(2):297-313. Related Articles, Links
Cannabinoid-induced hormone changes in monkeys and rats.
Rosenkrantz H, Esber HJ.
Previous findings at various laboratories indicated that cannabinoids distribute to sexual behavior centers in the brain, and endocrine aberrations have consistently been observed in animals treated with cannabis constituents. Subacute and chronic studies were performed to monitor hormone changes in rats and monkeys exposed to marihuana smoke or pure cannabinoids. In oral studies, young Fischer rats of both sexes were given delta 9-tetrahydrocannabinol (delta 9-THC) doses of 2, 10, or 50 mg/kg for 14--180 d and pregnant rats received 1, 5 or 10 mg/kg during gestation and lactation. Other male rats were exposed to marihuana smoke at delta 9-THC doses of 2 or 4 mg/kg for 14 d. Rhesus monkeys of either sex were given oral cannabidiol doses of 30, 100, and 300 mg/kg for 90 d. Serum pituitary, steroid, and thyroid hormone levels were determined by radioimmunoassay. Marihuana smoke (and oral delta 9-THC) depressed testosterone 20--30% and triiodothyronine 17--29%. In pregnant rats, small doses of delta 9-THC suppressed luteinizing hormone, but larger doses elevated both follicle-stimulating hormone and estrogens (approximately 50--100%) without affecting progesterone levels. Prolonged oral administration of delta 9-THC to young rats tended to increase gonadotropins, to which tolerance developed in males. Cannabidiol-treated monkeys responded with slight elevations in luteinizing hormone and follicle-stimulating hormone in males, whereas
steroid hormones were essentially unchanged for both sexes. Hormone imbalance may explain cannabinoid-induced embryotoxicity and impaired gonadal function.
PMID: 6248648 [PubMed - indexed for MEDLINE]
another:
Am J Drug Alcohol Abuse. 1975;2(2):269-75. Related Articles, Links
Plasma testosterone levels in healthy male marijuana smokers.
Cushman P Jr.
Plasma testosterone, FSH, and LH levels were obtained from 25 healthy consecutive heterosexual male mauijuana smoking university students. All values were within the range of normal and the means did not differ significantly from those of 13 normal controls. These data suggest that the casual marijuana smoker (at least one time weekly with an average of 5.1 joints per week) may have plasma testosterone levels which are
normal for the time of day and the laboratory.
PMID: 1211384 [PubMed - indexed for MEDLINE]
Topic: Gyno from Marijuana (Read 11929 times)
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