Author Topic: Cannabis and Gyne, studies please.  (Read 6505 times)

Offline mouse88

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Seeing as this is my first post, let me introduce myself a bit. I'm an 18 year old American and I have had gynecomastia for a very long time. I can't exactly say when I got it, but it would have had to have been in my preteens or perhaps a little bit before. I am not sure because I was very overweight during in my early childhood. Around 7th and 8th grade I started losing weight and I noticed that my "bitch breasts" never went away. It was very annoying because they were the primary motivators for my weight loss. I thought if I kept on bench pressing and losing weight they HAD to go away. As I'm sure you guys already know, these efforts were fruitless. Around 8th grade I started smoking cannabis as well, which brings me to the main topic of this thread:
what are the studies that demonstrate a correlation between cannabis use and gyne? I have scoured the internet but have not been very successful at finding any primary sources. Usually I read about some early speculation in the 1970's, and then invariably about that study of a group of soldiers which showed no correlation. I have not been able to find any good studies, and before I decide to give up my beloved herb I would like to know where the oft-stated association with gyne comes from. On this website it says that the relationship is disputed, and I am naturally skeptical about claims like these with regards to cannabis (though I understand there are legitimate concerns associated with the use of cannabis, there is also lot of junk science out there about recreational drugs, ESPECIALLY from the 70's). I've searched the forums and have found many claims both ways, but few studies.

Now, from my own experience marijuana never seemed to make the gyne worse, if anything, it has subsided ever since I started using it. Now, when I stumbled upon this website (and finally learned that there was a name for my condition), to my horror many people were discussing cannabis causing gyne. Has the cause of my torment been right under my nose all these years? I doubt it. It certainly didn't cause it, nor has it made it worse - but I am very open to the possibility that it has prevented it from subsiding. My gyne isn't SEVERE, but it's noticeable. I can wear a shirt without a problem, it just looks like I have a muscular chest (which I do), but the puffy nipples are my main problem. Anyway, any primary sources concerning my dilemma are very much appreciated.

Offline mouse88

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I should add that recently (it being the summer of my senior year) I have been indulging almost daily since the the second week of June. I am kind of a hypochondriac, and recently when I look at myself in the mirror I seem the same, I can't help but feel it HAS gotten worse, and this is driving me insane. You guys should know that I LOVE cannabis, I have enjoyed every minute of my experience with it - (except that one time...), it has brought me happiness and a new outlook on life. However, I am willing to give it up permanently, or at least, make it a special occasion type thing. I almost certainly will get surgery at some point, but right now its not possible. I'll have to wait until at least next summer. My plan is to enjoy this first year of college with the herb, I'm going to a fairly competitive school so I probably won't be able to go crazy like I am now and stick to my normal, weekend routine. I plan on working out a shit load and MAYBE getting to a point where I can be comfortable with my chest. Then, if I still feel like I want to, I will get the surgery. I am still contemplating rolling the dice and continuing to smoke cannabis fairly regularly after a surgery. Heck, even if it does cause gyne or helps exacerbate it, it is obviously very rare (most of my friends smoke and they are all flat as boards) and perhaps isn't affecting me at all (I am almost 100% positive my weight mixed with early puberty caused my gyne). Well, I await responses. I'm so glad I found this place. I'll be posting pictures at some point.

Offline Jugernaut

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I'm new to the boards as well. When I saw a surgeon he asked me have I ever smoked and when I did he asked how much. It was in my late teens and I saw the gyno getting worse then. He believed that this did make my situation worse. My advice you need to stop smoking pot.

Offline mouse88

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I mean, I'm basically I'm going to stick to the the above plan, but I would just like to see studies.
« Last Edit: July 09, 2007, 03:07:41 AM by mouse88 »

Offline Personal

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Cannabis is this reason why I have puffy nipples. Don't do it.

Offline mouse88

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Alright guys, I was hoping you would understand what I'm requesting considering the pretty good discussions I've read so far. I'm not asking for advice or anecdotal cases, I'm asking for controlled studies that demonstrate a statistical correlation between cannabis use and gynecomastia. 

Offline sickman

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  • moobs aint cool.
i have no idea bout all of the above, all i can say is ive smoked pot for about a year
and since a year my tenderness, shape has gone a tiny bit down
so i dont see how it can be that.
enjoy life :)

Offline moobius

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since no one else is offering any pertinent replys:

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]

Offline mouse88

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Thank you, moobius. These studies seem to indicate that the active chemicals in marijuana may not have a significant effect on human hormones. However, it seems that some of these studies were in vitro, so I will reserve judgment on the causal role of cannabis with respect to gyne until I see more in vivo studies such as the second one. They do indicate that if cannabis causes gyne, it may not be through a hormonal mechanism. Seeing as many gynecomastia cases are idiopathic, I think only large scale epidemiological studies will show anything of substance, and of course then we would have to be careful with many potential lurking variables, namely those pertaining to lifestyle. 

Offline mouse88

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Hypo-is-here, I just read some of your comments on another related thread. If you could produce the studies you talk about I would greatly appreciated. I have tried going through the backlog but it has been very tedious.

Offline moobius

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Hypo-is-here, I just read some of your comments on another related thread. If you could produce the studies you talk about I would greatly appreciated. I have tried going through the backlog but it has been very tedious.

hypo won't respond... he never produced studies to back his claims when i requested and he no longer frequents the board


 

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