Author Topic: Gyno from Marijuana  (Read 11927 times)

Offline Zippy211

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lol @ notanymore...

fu** all yall who say i shouldnt say anything... if someone posts a stupid question or comment that i dont agree with ill speak my mind... bit*hes

Offline Allan7865

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I 100% agree with Zippy211.

Ive never smoked a day in my life and I still had Gyne, but some potheads still get a perfectly flat chest?

If I had the choice to chosse if I got puffy nipples or not.... same goes for people who get lung cancer without smoking a ciggerate in there life, Id imagine they would feel much the same way I do.

Yes, that people can fucking smoke 10 packs a day and not get cancer, while someone who hasent smoked a day in there life is diagnosed. Same thing, people abuse without getting Gyne.. and when they do get it, its as simple as stopping the Marijuana use.

Offline rhinopothole

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i developed gyne inmy laer years of puberty and i started smoking when i was 15 unfortunately...  i dont feel that someone shuld be putdown for smoking buti do believe that is can affect some poeple.  i dont think is made a difference in my case becuase is started before i smoked and continued during the times of my life wheni had stopped.

Offline moobius

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marijuana does not cause gyno... there were some studys WAY back that suggested this but have since been dissproved by more recent research. why dont' you guys look into any of this on your own?

heres one study i found on pubmed in like 5 seconds:





Am J Surg. 1977 Nov;134(5):613-5. Related Articles, Links  


Gynecomastia and cannabis smoking. A nonassociation among US Army soldiers.

Cates W Jr, Pope JN.

Eleven patients diagnosed with idiopathic gynecomastia requiring mammoplasty were compared with matched controls to determine if there was an association between cannabis use and gynecomastia. Patients with gynecomastia were not significantly different from controls regarding their history of cannabis use. For those who admitted using cannabis, patients had a higher frequency but a shorter median duration of use than controls; differences were not statistically significant. Our epidemiologic evidence does not support the previously reported relationship between chronic cannabis use and gynecomastia.

PMID: 920892 [PubMed - indexed for MEDLINE]
« Last Edit: May 03, 2006, 08:37:11 PM by moobius »

Offline bogieman

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saw that- again- show me one person on this board that got this from pot- just one-
ie someone later in life getting this
most got this when they were in their early teens

Offline Paa_Paw

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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.
Grandpa Dan

Offline moobius

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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]

« Last Edit: May 06, 2006, 07:20:28 AM by moobius »

Offline markashleigh1979

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Chronic users get gyne

Offline moobius

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Quote
Chronic users get gyne


this was posted above but you must not have read it as it is information that goes against your preconceived notion that MJ causes gyne:

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]  

Offline Hypo-is-here

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Moobius,

None of your studies tested SHBG.

Do you know what that means?  


Offline moobius

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Moobius,

None of your studies tested SHBG.

Do you know what that means?  



yes, i know what it is. i'll leave it to you to show me a study where MJ effects SHBG.

Offline Hypo-is-here

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The onus is not on me to provide you with studies.

My point was simply that the studies you have provided are flawed.  The fact that they do not include SHBG testing adequately shows that.

I could write a thesis on how flawed they are (they are laughably bad), but I am not wasting my time.






Offline markashleigh1979

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HAHAH John Smith says " Ave it!!" ;D

Offline Hypo-is-here

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If you want to look at another flawed but more comprehensive tombstone have a look at this;

http://www.nida.nih.gov/pdf/monographs/44.pdf

pages 55-68 might interest ;) ;)

So far the vast majority of the medical community believe marijuana to be a causative factor in gynecomastia development.

They believe it has a weak but certain association.

I am sat right at this very minute looking at the white paper written by Glenn D Braunstein M.D that states it as a causative factor.

If the medical community change there mind then presumably so should we.

Until such time...if indeed there is such a time however we should accept that the medical fraternity believe it to be a causative factor.

I have no view one way or the other as to smoking marijuana.

I drink alcohol and that is more toxic to the testes and therefore androgen status.

In other words my drug of choice is more harmful than marijuana.

My drug of choice also does more long term damage, as quitting smoking often leads to a cessation of problems, whereas drinking can cause long term damage to the testes.

So I am not doing a holy joe routine...I’m just stating the facts.



Offline moobius

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i'll read the full report when i have some time, but to say that the "vast majority of the medical community believe marijuana to be a causative factor in gynecomastia development" is false.

i don't doubt that you are looking at the white paper by Glenn D Braunstein M.D, but i wouldn't take one doctor's beliefe as the final say in the matter...  besides, all but 2 of the studies he referenced were from before 1980. ie OLD RESEARCH. this is exactly what i was referring to when i said that the OLD RESEARCH backs up your claim. however, more modern studies have shown the results of those OLD RESEARCH studies to be flawed and not reproducable.

i'd be really interested to find out who funded those studies and that report... government perhaps?
« Last Edit: May 06, 2006, 12:12:03 PM by moobius »


 

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