Young men who smoke marijuana are more likely to develop testicular cancer than those who have never tried it, The Guardian reports. It says that a study has found that smoking the drug at least once a week, or using it regularly from adolescence, doubled the risk of a fast-growing form of the disease.
This study compared marijuana use in men with testicular cancer with use in men without the disease. It found that previous use of the drug was slightly more common in men with cancer compared with the controls. This worked out to be a borderline significant increased risk of testicular cancer for men who had ever used marijuana. The risk was greatest for those who currently used marijuana once or more per week. Further analysis showed that the risk only increased significantly for the nonseminoma type of cancer and not for seminomas.
As the study researchers acknowledge, there are some limitations to the findings and further research is needed to investigate this link.
Where did the story come from?
Dr Janet Daling and colleagues from the Fred Hutchinson Cancer Research Centre, the University of Washington and the Vanderbilt University Medical Center in the US carried out this research. The work was funded by the National Institutes of Health, the National Institute on Drug Abuse and the Fred Hutchinson Cancer Research Centre. The study was published in the (peer-reviewed) medical journal Cancer .
What kind of scientific study was this?
This case-control study investigated cannabis use as a possible cause for the increase in testicular tumours in recent decades. Testicular tumours typically affect men in their 20s, 30s and 40s. There are two main types of testicular cancer: seminomas and nonseminomas. They are both types of germ (seed) cell tumours. The peak age for developing these types of tumour is between 20 and 35 years for nonseminomas and between 30 and 45 years for seminomas. The aim of this study was to compare previous cannabis use in men who had developed testicular cancer with a group of matched controls who had not.
The ATLAS study recruited men between 18 and 44 years living in three counties of Washington State who had been diagnosed with invasive testicular cancer between January 1999 and January 2006. Of the possible 550 cancer cases, the researchers interviewed and enrolled 369 men in their study.
Men who did not have testicular cancer were identified for the control group by a technique called random digit dialling. This involves calling random phone numbers and establishing if there is somebody matching certain criteria living at that address. In this case, the controls were male, matched to the cases by age and had to have been living in the same area during the diagnosis period. The researchers interviewed 979 of 1,875 eligible controls.
All cases and controls were interviewed using a questionnaire asking about demographics, cigarette smoking, alcohol use, recreational drug use, family history and other known risk factors for testicular cancer. The cases were asked to give their exposure to these risks for the time before they were diagnosed with cancer. The controls were then asked about their behaviour from that same date. Each man who reported marijuana use was asked to recall the times in his life when he used marijuana or hashish (or both), the age at which he first and last used it, and the frequency (times per day, week, month or year).
The researchers carried out statistical analyses for all testicular cancers combined, and then separately for type of cancer: seminomas, nonseminomas and each particular subtype of nonseminomas. They looked at risk of cancer according to marijuana use, while adjusting for (taking into account) confounders such as smoking and alcohol use.
What were the results of the study?
Compared with controls, cases were more likely to be from a lower socioeconomic background and to have less than college education. There were also no men of African-American origin in the cases. Cases were also more likely to have a first-degree relative with testicular cancer and to have a history of cryptorchidism (undescended testis/testes).
A slightly higher proportion of men with testicular cancer had ever smoked marijuana (72.6%) compared to the controls (68.0%). However, from this, the calculated risk of testicular cancer with ever having used marijuana was only borderline significant (OR, 1.3; 95% CI, 1.0-1.8). A higher proportion of cases reported being current marijuana users (26% versus 20%), and to have started using marijuana below the age of 18 years (21% versus 15%). How many years the men had used marijuana did not significantly affect the risk of testicular cancer.
Men with testicular cancer more commonly used marijuana once or more times per week (15% versus 10% of the control group). Using marijuana once or more times per week doubled the risk of testicular cancer (OR, 2.0; 95% CI, 1.3-3.2) compared with never using it. Using marijuana less than once a week was not associated with a significantly increased risk.
When the researchers carried out subgroup analyses by type of testicular cancer they found that the increased risk of seminoma from current marijuana use was non-significant, but the increased risk for nonseminoma was significant (OR, 2.3; 95% CI, 1.3-4.0).
What interpretations did the researchers draw from these results?
The researchers conclude that they found a link between marijuana use and the occurrence of nonseminomas. They say that additional studies are needed to test further the theory of a link between marijuana use and testicular cancer, and to explore the possible biological reasons for this.
What does the NHS Knowledge Service make of this study?
This study found previous use of marijuana to be slightly more common in men with testicular cancer compared with controls. This equated to a borderline significant increased risk of testicular cancer for men who had ever used marijuana. The risk was greatest for those who were currently using marijuana one or more times per week, and on subgroup analysis risk was found to be significantly increased only for nonseminomas and not for seminomas.
- Marijuana use prior to diagnosis with cancer may be investigated to find out whether it is linked with cancer risk. However, current use of marijuana when cancer is already diagnosed cannot prove that one caused the other. The study reportedly questioned use prior to diagnosis. However, current use referred to the “reference date” when cancer was diagnosed. It is therefore difficult to establish causation.
- Case control studies often suffer from their reliance on the participants remembering their exposure to things often many years in the past. Asking people to recall marijuana use in previous years is likely to involve some inaccuracy, particularly relating to how frequently they used it. Additionally, men who already had cancer may have recalled using it more frequently if they considered it to be a possible cause of their cancer. It should also be noted that as marijuana is an illegal substance, some men might not have reported their use truthfully.
- When carrying out subgroup analyses for type of testicular cancer, the numbers of men that were included in each analysis were relatively small. This decreases the accuracy of the risk estimates (139 men had nonseminomas and 230 had seminomas).
- As the researchers acknowledge, they were only able to interview 67.5% of eligible cases and 52.2% of controls. If the men who were not interviewed were different enough from those that took part, the results could be biased.
- Although several newspapers mention links with the “most aggressive” types of testicular cancer, the researchers did not look at what stage the cancer was at or prognosis for the disease.
As the researchers say, further research is needed to investigate the link between cannabis use and risk of testicular cancer.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
BBC News, 10 February 2009
The Guardian, 10 February 2009
The Independent, 10 February 2009
Daily Mail, 10 February 2009
The Daily Telegraph, 10 February 2009
Links to the science
Cancer 2009; Published Online: February 9 2009
Cochrane Database of Systematic Reviews 2008, Issue 3