1. The study group was way, way too small. How can you have a control group of less 150 men
for a study like this, when the incidence of Testicular Cancer is 0.4% or 1 in 280! In my opinion, this
alone makes the report useless.
2. In the report, it is reported that the higher dose users of cannabis did NOT have an increased
incidence of Testicular Cancer. This just makes no sense at all.
3. The lead scientist of the study openly states that their selection bias might have been a
problem. This will turn out to be the real problem with this study.
4. This study was a simple retrospective or “survey” study. This type of study CANNOT EVER BE
USED TO TRY PROVE CAUSE AND EFFECT. Ultimately, the only studies that can show cause and
effect are prospective controlled studies. There are potentially 10 other differences in the
two cohort groups they studied. With a study in young males there are many issues that must
be controlled for.
5. “The people who had been diagnosed with Testicular Cancer were less likely than controls to
report religious affiliation.” This is a direct quote, so maybe the church activities are
to blame for the presumed Cancer increase.
6. Another downplayed but intriguing finding was that cocaine “protected” against Testicular
cancer. This seems as unlikely as Cannabis Causing this cancer.
7. Heavy users actually had a reduced likelihood of developing testicular cancer.
8. Thousands of good scientific articles are now flooding the world with good evidence that both
CBD and THC kill cancer cells.
There are "acid" and "neutral" forms of every cannabinoid molecule. Early man knew the difference and would either just eat the cannabis raw, or heat it to convert to the neutral or "active" forms of the cannabinoids.
Cookie Bekkar is a cancer survivor and patient of Dr Frankel's. She has created a website to share her story, what worked well for her and as a resource help inspire/educate other patients.
I am going to need SOME study that shows that cannabis causes Testicular Cancer. The study will have to be much better than poorly controlled survey type retrospective studies.
With COVID, we have never been more aware of critical shortages of masks, ventilators, hospital beds, etc., all leading to rationing. In this BLOG, Dr Frankel, examines how rationing in our medical care is a much bigger problem than just face masks.
In future studies the researchers plan to measure the expression of cannabinoid receptors in both seminomatous and nonseminomatous tumor tissue from the cases in the study, and to see whether variation in the genes for the receptors and other molecules involved in cannabinoid signaling influences the risk of testicular cancer.
The results also suggested that the association with marijuana use might be limited to nonseminoma, a fast-growing testicular malignancy that tends to strike early, between ages 20 and 35, and accounts for about 40 percent of all testicular-cancer cases.
Study participants were also asked about other habits that may be correlated with marijuana use, including smoking and alcohol consumption. Even after statistically controlling for these lifestyle factors, as well as other risk factors, such as first-degree family history of testicular cancer and a history of undescended testes, marijuana use emerged as a significant, independent risk factor for testicular cancer.
In the meantime, Schwartz said, "What young men should know is that first, we know very little about the long-term health consequences of marijuana smoking, especially heavy marijuana smoking; and second, our study provides some evidence that testicular cancer could be one adverse consequence," he said. "So, in the absence of more certain information, a decision to smoke marijuana recreationally means that one is taking a chance on one’s future health."
The male reproductive system also naturally produces a cannabinoid-like chemical that is thought to have a protective effect against cancer. The authors speculate that marijuana use may disrupt this anti-tumor effect, which could be another explanation for the possible link between marijuana and increased risk of testicular cancer.
Chronic marijuana exposure has multiple adverse effects on the endocrine and reproductive systems, primarily decreased sperm quality. Other possible effects include decreased testosterone and male impotency. Because male infertility and poor semen quality also have been linked to an increased risk of testicular cancer, this further reinforced the researchers’ hypothesis that marijuana use may be a risk factor for the disease.
"Our study is not the first to suggest that some aspect of a man’s lifestyle or environment is a risk factor for testicular cancer, but it is the first that has looked at marijuana use," said author Stephen M. Schwartz, M.P.H., Ph.D., an epidemiologist and member of the Public Health Sciences Division at the Hutchinson Center.
Forest plots – with odds ratios and heterogeneity statistics – for a ever-use, b current use, c > = weekly use, and d > =10 years of use. (Total = all histological types)
The cannabis plant has been ingested or inhaled by humans for more than 4000 years . In the 2014 United Nations World Drug Report, it was estimated that some 178 million 15–64 year-olds worldwide use cannabis at least once per year – making it the most consumed illicit drug by a factor of five . Substantial variability in the consumption of cannabis has been observed between (and within) populations – with prevalence considerably higher in the Americas, Europe and Oceania compared to Asia and Africa .
In recent years, at least three case–control studies reported associations between cannabis exposure and testicular germ cell tumour (TGCT) development [7–9]. A recent meta-analysis of these studies showed that those who used cannabis for longer than 10 years were 50 % more likely to develop testicular cancer than those who never used cannabis (summary odds ratio [OR]: 1.50, 95 % CI 1.08–2.09) . However, this review was limited in two ways: firstly, it did not assess the quality of the case–control studies – an important step toward understanding potential sources of bias introduced by the authors; and secondly, it did not differentiate between seminoma and non-seminoma tumour types  – which is also important, since a) non-seminoma tumours are typically diagnosed seven  to ten  years earlier than seminoma tumours, and may differ in terms of risk factors; and b) each of the studies showed a stronger association for non-seminoma tumours than for seminoma tumours. This review aims to address these issues.
b Adjustment for confounding achieved via inclusion as covariates in regression models
The results of this review show that current use of cannabis (pooled summary OR: 1.62, 95 % CI 1.13–2.31), using cannabis on at least a weekly basis (OR: 1.92, 95 % CI 1.35–2.72) and long duration (>10 years) of cannabis use (OR: 1.50, 95 % CI 1.08–2.09) are all associated with an increased risk of development of TGCT overall, and even more strongly with non-seminoma tumours specifically. There was insufficient evidence to conclude that there is a relationship between seminoma tumours and cannabis use.
Controls were either randomly derived from the community [8, 9] or the friend of cases . All three studies matched on age, while two of the three studies matched on region of residence [8, 9]. Two of the three studies also matched cases and controls on race and/or ethnicity [7, 8]. Two of the three studies [7, 9] frequency-matched controls to cases, while one study individually-matched controls to cases .
Meta-data for each of the included studies are presented in Table 2 . Each of the included studies were conducted in the United States, with the earliest recruitment occurring in 1986  and the most recent occurring in 2006 . A total of 719 cases with testicular germ cell tumours (TGCT) participated across the three studies, along with a total of 1419 controls. In all studies, cases were identified from local cancer registries and confirmed via review of pathology reports. In terms of histological type, two of the three studies separated the cohort into seminoma and non-seminoma sub-groups [8, 9], while the other study additionally separated non-seminoma tumours into non-seminoma and mixed-type sub-groups .