The study involved 369 men with testicular cancer, and 979 cancer free individuals.
All participants filled out a questionnaire. Of those, only 250 of the cancer patients could be interviewed, and just over half the cancer free subjects.
The conclusions of the study itself say this:
An association was observed between marijuana use and the occurrence of nonseminoma TGCTs. Additional studies of TGCTs will be needed to test this hypothesis, including molecular analyses of cannabinoid receptors and endocannabinoid signaling, which may provide clues regarding the biologic mechanisms of TGCTs.The study led to a hypothesis, not a concrete (nor even a silly putty) result. The study results translate into plain english thus:
After the resulting surveys and interviews, we came to the conclusion that we think there might be a possible link between testicular cancers and smoking cannabis. However, we need to do a lot more study to be able to draw any firm conclusions. After all, this is just a hypothesis.
Now, add to this the fact that the incidence of testicular cancer amongst men in general is (for the United States) about 1% of all cancers diagnosed in the male population. That is, about 8000 cases. Of those 8000, about 400 people die from the disease. Of those 8000, only 3200 of them will have the specific cancer that this study leans toward; the nonseminoma variety. Even if there were a proven link, it would be on par with eating margarine on burnt toast as a risk factor for cancer. Or, in a statistical sense, IF a valid association between cannabis smoking and nonseminoma testicular cancer is found, heavy pot smoking males will have around a 0.8% chance of developing this form of the disease, compared to a 0.5% chance for the rest of the population.
Smoking cannabis and tobacco will give you a threefold increased risk of developing COPD.
Once again, rather than throw up a bunch of media links, I'll cut to some pages that deal directly with the study that drew the above conclusion. Suffice to say, cannabis is not the cause of the problem:
These studies, involving mainly younger individuals, have provided inconsistent but suggestive evidence that smoking marijuana only may lead to modest airflow obstruction and hyperinflation that could predispose the individual to COPD later in life. The findings of Tan and colleagues9 add to the limited evidence of an association between use of marijuana and COPD because their study focuses on an older population ( aged 40 or older ) that is at greater risk of COPD. Their finding that concurrent smoking of marijuana and tobacco is associated with a greater likelihood of COPD than smoking only tobacco implies a possible additive effect of the 2 substances on lung health. An additive effect was also suggested by Taylor and colleagues, whose study involved a younger population. By contrast, Aldington and colleagues concluded that concurrent smoking of marijuana and tobacco attenuated the association between smoking tobacco and a reduced ratio of FEV1 to FVC and respiratory symptoms.
Firm conclusions cannot be drawn about the association between use of marijuana and COPD based on the limited and inconsistent data available. The studies that address this topic are limited by their small numbers of participants and by the uncertain accuracy of self-reported use of marijuana, particularly in view of its illegality and the difficulty of accurately recalling amounts previously used. Some of these studies are also limited by their cross-sectional design, and most are limited by the young age ( 40 years or younger ) of participants. Nevertheless, the consistency of some aspects of the available data allows us to more firmly conclude that smoking marijuana by itself can lead to respiratory symptoms because of injurious effects of the smoke on larger airways. Given the consistently reported absence of an association between use of marijuana and abnormal diffusing capacity or signs of macroscopic emphysema, we can be close to concluding that smoking marijuana by itself does not lead to COPD.
To further ease your mind on this issue, check out the American Journal of Respiratory and Critical care Medicine:
We conclude that regular tobacco, but not marijuana, smoking is associated with greater annual rates of decline in lung function than is nonsmoking. These findings do not support an association between regular marijuana smoking and chronic COPD but do not exclude the possibility of other adverse respiratory effects.
Smoking cannabis will lead to a psychotic episode or schizophrenia
This statement has been discredited a number of times. However, for the point of argument, check out the transcript of this documentary episode from the Australian ABC TV 'Catalyst' program:
Narration: But if that’s true, how come so few cannabis users become psychotic? One third of Australians have tried marijuana, yet only 1% of the population have schizophrenia. Who are the people at risk? The answer, perhaps surprisingly, was discovered in a picturesque corner of South Island, New Zealand. Dunedin is home to one of the world’s best longitudinal studies. Since 1972, they’ve been subjecting a group of 1000 people to a barrage of tests and questions. In 2005, they announced an astonishing discovery – a gene for vulnerability to cannabis.
Professor Richie Poulton: The gene we looked at is called the catechol-O-methyltransferase – or COMT for short. And we looked at it because it’s a gene that stands out in families that have schizophrenia.
Narration: And what does this COMT gene do? Well, as it happens, it regulates our old friend, dopamine.
Jonica: Let’s say these are the COMT genes – this is the good gene – this is the bad gene. Now, everyone gets two of them, so you can get two good genes or one each. But, if you get two of the bad genes, well it seems your ability to regulate dopamine is impaired.
Narration: Which might not matter, unless you smoke cannabis.
Professor Poulton: We found that among adolescents who had used cannabis on a monthly basis or more, who had the bad version of the gene, their chances of developing psychosis by their mid 20’s were increased 11 fold.
Jonica: 11 fold. That’s extraordinary.
Professor Poulton: It is. So this explains why the use of cannabis among a small group of people has a devastating effect in terms of the likelihood of developing psychosis, but most people remain unharmed and unscathed.
So, if I understand correctly, the crux of this is that a defective gene and not cannabis is the reason for some people becoming psychotic when smoking pot?
Another ABC program, 'Quantum', has this on its 'What's Your Poison?' page:
Does cannabis cause psychosis?
It is believed that cannabis use may cause a condition known as a drug-induced psychosis which can last for up to a few days and is often characterised by hallucinations, delusions, memory loss and confusion. However, in some cases, cannabis use may contribute to the development of a serious mental illness, such as schizophrenia. Cannabis use can prolong the duration of symptoms of mental illness and can lower a person's chances of recovering from a psychotic episode.
People most at risk are those with a family history of psychotic illness or those who have already experienced a psychotic episode. Other legal and illicit drugs should also not be ignored. For example, some evidence suggests that substances such as alcohol and amphetamines have a greater effect than cannabis in the development of psychosis. So, people with a family or a personal history of psychotic illness should avoid drugs like cannabis completely and try other healthier ways of relaxing
I was going to list more of these mistruths. But I'm over it for now...