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Cannabis use and incidence of testicular cancer: a 42-year follow-up of Swedish men between 1970 and 2011

Given current drug-policy reforms to decriminalize or legalize cannabis in numerous countries worldwide, it is critically important to understand the potential impacts of cannabis use on the development of cancer. The current study aims to assess the relation between cannabis use and the development of testicular cancer.


The current study relied on a population-based sample (n = 49 343) of young men aged 18–21 years who underwent conscription assessment for Swedish military service in 1969–1970. The conscription process included a non-anonymous questionnaire eliciting information about drug use. Individual-level conscription information was linked to Swedish health and social registry data. Testicular cancers diagnosed between 1970 and 2011 were identified by ICD-7/8/9/10 testicular cancer codes in the Swedish National Patient Register, the Cancer Register, or the Cause of Death Register. Cox regression modeling was used to estimate the hazards associated with cannabis use and time to diagnosis of testicular cancer.


No evidence was found of a significant relation between lifetime “ever” cannabis use and the subsequent development of testicular cancer [n = 45 250; 119 testicular cancer cases; adjusted hazard ratio (AHR) 1.42, 95% CI, 0.83, 2.45]. “Heavy” cannabis use (defined as usage of more than 50 times in lifetime, as measured at conscription) was associated with the incidence of testicular cancer (n = 45 250; 119 testicular cancer cases; AHR 2.57, 95% CI, 1.02, 6.50).


The current study provides additional evidence to the limited prior literature suggesting cannabis use may contribute to the development of testicular cancer.

Cannabis is the most widely used illicit drug worldwide (1). According to 2015 World Drug Report (1) approximately 180 million people (3.9% of the global population) consumed cannabis in the past year, and it is likely that these numbers are due, in part, to the common perception that its use confers minimal health risks (2).

Globally, a range of nations, including countries of the European Union, Australia, and the Americas have recently implemented or proposed reforms to the ways in which they control cannabis use (3–6), thereby departing from traditional approaches of criminal prohibition dominant throughout most of the 20 th century (7). In light of the current international debates and policy changes regarding cannabis decriminalization/legalization in many regions (8–10), as well as its widespread global use, it is critically important to assess the impact of cannabis smoking on human health, especially on the development of cancers (11–13). Almost all research on the potential cannabis-cancer connection has focused on those cancers causally related to tobacco smoking (e.g., lung cancer, head and neck cancers) (11, 12), but a small group of recent studies (14–16) also has found a suggestive link between cannabis use and the development of testicular cancers, which are traditionally unassociated with tobacco use (17).

Testicular cancer is the most common type of cancer among young men, with a peak incidence occurring between the ages 15–40 years (18) – an age range in which cannabis use most frequently occurs (1). Rates of testicular cancer appear to be increasing rapidly over time in the United States and Europe (16, 19, 20), but the etiology remains unclear. Three US-based case-control studies (14–16) have found that cannabis use appears to confer an increased risk of developing testicular cancer. A meta-analytic summary of these three studies has shown that current, chronic (defined as cannabis use ≥ 10 years), and frequent (defined as at least once per week) cannabis use were all significantly associated with testicular cancer incidence (21). While a recent review on this topic (11) has called for longitudinal studies to address the potential weaknesses of recall and selection biases in the available case-control studies, it is important to note that the relatively low incidence of testicular cancer creates nearly insurmountable cohort-design challenges, such as enrollment of sufficiently large samples and follow-up over long time periods.

Drawing upon a uniquely large, population-based sample (n = 49 343) of Swedish young men aged 18–21 years undergoing extensive medical and psychiatric assessments required during the process of compulsory conscription into military service in Sweden in 1969–1970, the current retrospective cohort study aimed to assess the possible link between self-reported cannabis use, measured at conscription, and the subsequent development of testicular cancer over a 42-year follow-up period.


Study cohort

The study cohort included 49 343 Swedish males born between 1949–1951 who underwent extensive medical and psychological assessment for the nationwide conscription for compulsory Swedish military service occurring in 1969–1970 (see Table 1 for initial sample details). Cohort members’ ages (at conscription assessment) ranged from 18–21 years. Only 2–3% of all young men were exempted from the conscription process due to severe mental or physical conditions.

Table 1

Baseline characteristics of the study sample of 49 343 conscripts born in 1949–1951 and aged 18–21 at conscription by exposure status

Study covariates Total Never drug use “Ever” use of cannabis p-value a Among “ever” cannabis users b Unclear/missing/use of other drugs c
Use more than 50 times p-value a Cannabis as “most frequently used drug” p-value a
Total, n (%) d 49 343 (100) 40 271 (81.6) 5 326 (10.8) 879 (1.8) 4 323 (8.8) 3 746 (7.6)
Birth year <0.001 <0.001 <0.001
1949 2 833 (100) 2 122 (74.9) 336 (11.9) 73 (2.6) 265 (9.4) 375 (13.2)
1950 8 826 (100) 6 741 (76.4) 1 161 (13.1) 194 (2.2) 952 (10.7) 924 (10.5)
1951 37 684 (100) 31 408 (83.3) 3 829 (10.2) 612 (1.6) 3 106 (8.2) 2 447 (6.5)
Cryptorchidism 0.864 0.528 0.805
No 49 085 (100) 40 059 (81.6) 5 297 (10.8) 873 (1.8) 4 299 (8.8) 3 729 (7.6)
Yes 258 (100) 212 (82.2) 29 (11.2) 6 (2.3) 24 (9.3) 17 (6.6)
Paternal testicular cancer 0.139 0.001 0.476
No 49 267 (100) 40 214 (81.6) 5 314 (10.8) 874 (1.8) 4 315 (8.8) 3 739 (7.6)
Yes 76 (100) 57 (75.0) 12 (15.8) 5 (6.6) 8 (10.5) 7 (9.2)
Tobacco smoking <0.001 e <0.001 e <0.001 e
Never 20 906 (100) 18 273 (87.4) 790 (3.8) 75 (0.4) 628 (3.0) 1 843 (8.8)
1–5 cig/day 5 428 (100) 4 557 (83.9) 477 (8.8) 57 (1.1) 396 (7.3) 394 (7.3)
6–10 cig/day 10 058 (100) 8 114 (80.7) 1 294 (12.9) 194 (1.9) 1 059 (10.5) 650 (6.4)
11–20 cig/day 11 198 (100) 8 229 (73.5) 2 268 (20.2) 405 (3.6) 1 861 (16.6) 701 (6.3)
More than 20 cig/day 1 747 (100) 1 098 (62.8) 497 (28.5) 148 (8.5) 379 (21.7) 152 (8.7)
Missing 6 (100) 0 0 0 0 6 (100)
Alcohol consumption (g of 100% alc/week) <0.001 e <0.001 e <0.001 e
Abstainers (0 g) 2 957 (100) 2 738 (92.6) 44 (1.5) 20 (0.7) 35 (1.2) 175 (5.9)
Light (1–100 g) 36 253 (100) 31 134 (85.9) 2 761 (7.6) 395 (1.1) 2 217 (6.1) 2 358 (6.5)
Moderate (101–250 g) 7 904 (100) 5 475 (69.3) 1 883 (23.8) 277 (3.5) 1 564 (19.8) 546 (6.9)
Heavy (> 250 g) 1 454 (100) 730 (50.2) 594 (40.8) 176 (12.1) 470 (32.32) 130 (8.9)
Missing 775 (100) 194 (25.0) 44 (5.7) 11 (1.4) 37 (4.8) 537 (69.3)

Data collection: process, sources, and linkage

Conscription assessment

The Swedish conscription process included a large battery of evaluations, including physical and psychological assessments, as well as non-anonymous self-report questionnaires on familial, social, and behavioral items (22). The 1969–1970 conscription also collected additional self-reported information about use of alcohol, drugs, tobacco, as well as questions on familial, social and behavioral items. All men underwent a medical examination, and diagnoses were recorded according to ICD-8. Persons who reported or showed signs of mental disorder were referred to a psychiatrist, who recorded a diagnosis, if a disorder was identified (23).

Linkage of conscription-assessment data with other Swedish health and social registries

All individuals living in Sweden are assigned a unique personal number in national Swedish registers, enabling linkage of data across registries (24). The Stockholm Regional Ethical Review Board provided permission for data linkage (Dnr 2016/3:7).

Our cohort study relied on the linkage of 6 data sources: 1) information from Swedish young men undergoing conscription assessment in 1969–1970; 2) the Swedish Patient Register, 1964–2011; 3) the National Cancer Register, 1958–2010; 4) the National Cause of Death Register, 1952–2011; 5) the Swedish Total Population Register, 1968–2011 (which captures date of emigration out of and immigration into Sweden); and 6) the Swedish Multigenerational Register, 1973–2011.

Study outcome: Testicular cancer

Diagnoses of testicular cancer were identified by use of the Swedish version of ICD-7/8/9/10 codes appearing in the National Patient Register, the Cancer Register, or the Cause of Death Register (see Supplemental Table 1). Incident cases of testicular cancer were identified in the main and supplemental diagnoses in the National Patient Register and the primary diagnoses in the Cancer Register, as well as in the underlying and contributory causes of death diagnoses in the Cause of Death Register. Additionally, in the initial sample, no cases of testicular cancer were identified during the period before conscription or at the conscription assessment. The current study was not able to access histological subtype information on testicular cancer and, as a result, assessment of the potential association between cannabis use and specific subtypes was not possible.

Measurement of cannabis use

Lifetime, ever cannabis use

The variable instantiating lifetime, “ever” use of cannabis was created from the following 3 questions in the self-reported, non-anonymous conscription-assessment questionnaire: 1) Have you ever tried the following substances? (Give an answer yes or no about every drug); 2) What substance did you take first?; and 3) What substance have you taken most frequently? If the participant indicated cannabis use in response to any of these three questions, the variable of lifetime, ever cannabis use was coded as “yes”.

Lifetime frequency of cannabis use

The variable capturing lifetime frequency of cannabis use was constructed from the following conscription survey question: “How many times have you used drugs?” (response options: 1, 2–4, 5–10, 11–50, more than 50 times). For those conscripts indicating “ever” cannabis use, it was assumed that the lifetime drug-use frequency question applied to their cannabis use, especially as cannabis use was, by far, the most frequently used drug in the sample. Of the 5326 persons who indicated ever using cannabis (with or without use of other drugs), 4323 (81.2%) indicated cannabis as the drug most frequently used. Among the 879 young men who reported use of cannabis more than 50 times (with or without use of other drugs), 743 (84.5% out of 879) individuals indicated cannabis as the drug most frequently used.

Other covariates included in statistical modeling

The selection of covariates for the statistical analyses in the current study included, where possible, the variables selected for the statistical modeling in the three prior case-control studies (14–16), as well as the modeling covariates recommended in a recent systematic review of the cannabis-testicular cancer area (11): age, cryptorchidism, family history of testicular cancer, tobacco use, and alcohol use.


Cryptorchidism was identified by retrieving individual-level information from the National Patient Register [using Swedish ICD-7/8/9/10 codes (see Supplemental Table 1)] and from the results of medical examination performed at the conscription evaluation.

Paternal history of testicular cancer

Using the Swedish Multigenerational Register, the conscripts were linked to their biological fathers. Paternal diagnoses of testicular cancer were identified from the National Patient Register, the Cancer Register and the Cause of Death Register using the same ICD-7/8/9/10 codes defining the testicular cancer outcome (see Supplemental Table 1).

Tobacco smoking

Data on frequency of tobacco smoking reported at the conscription assessment were retrieved from individuals’ survey responses and categorized as: never smoking tobacco (reference group); 1–5 cig/day; 6–10 cig/day; 11–20 cig/day; more than 20 cig/day.

Alcohol consumption

Alcohol consumption was calculated by combining data on self-reported quantity and frequency of consumption of beer, wine, and spirits and expressed as grams of 100% alcohol (ethanol) per week: light drinkers [(0–100 g 100% alc/week); reference group]; abstainers (0 g 100% alc/week); moderate drinkers (101–250 g 100% alc/week); heavy drinkers (more than 250 g 100% alc/week). The Swedish alcohol retail monopoly provided information about the alcohol content (ethanol) for all alcohol beverages available in Sweden in 1969–1970 (25).

Statistical analyses

We evaluated whether lifetime cannabis use and lifetime frequency of cannabis use were related to incidence of testicular cancer. We applied Cox proportional hazards modelling to estimate the hazard ratio (HR) and 95% confidence intervals (CI) associated with cannabis use and time to diagnosis of testicular cancer. In multivariate analyses, we applied a stepwise adjustment strategy, based on the stepwise modeling recommendations of a recent systematic review of the cannabis-testicular cancer area (11). In Model 1 we adjusted for the conscripts’ birth year and for established risk factors for testicular cancer (i.e., conscripts’ cryptorchidism and paternal testicular cancer); in Model 2, we adjusted for the conscripts’ birth year and factors associated with cannabis use (i.e., frequency of tobacco smoking and alcohol consumption volume); and finally, Model 3 was a fully-adjusted model where all abovementioned risk factors were included. The presentation of model results in each stepwise strategy gives the reader an important description of the stability of the estimates across covariate combinations in each model.

All analyses relied on list-wise deletion of individuals missing data on any variables included in the analyses. A flowchart ( Figure 1 ) describes the initial sample and final cohort based on list-wise deletion, along with the linkage of the conscription-assessment information with other population-based health registries used in the study. Person-time was counted from January 1, 1970 until the date of diagnosis, date of death due to other reasons, date of emigration or until end of follow-up on December 31, 2011, whichever occurred first. Person-time comprised 1 803 490.9 person-years for the analyses associated with lifetime “ever” use of cannabis and 1 799 273.2 person-years for those analyses associated with lifetime frequency of cannabis use. The proportional hazard assumption was checked by the log-rank test for equality of survival function and the log-survival plots and was met in all models. All reported p-values were two-sided, with p < 0.05 considered as statistically significant. Statistical analyses were performed using STATA version 13.1.

Cohort profile and flow-chart for final analytic sample and 42-year follow-up

a Exposure variables: “ever” use of cannabis before conscription and lifetime frequency of cannabis use; b Covariates: conscript’s birth year, history of cryptorchidism, parental testicular cancer, frequency of tobacco smoking and volume of alcohol drinking


Testicular cancer cases

Figure 2 depicts the 135 testicular cancer cases identified in the initial sample (n = 49 343) during the follow-up between 1970 and 2011. Over 50% of the cases occurred among men aged 25–40 years.

Number of incident cases (n = 135) of testicular cancer diagnosed during follow-up time (1970–2011) among original sample of conscripts born in 1949–1951 (n = 49 343) by age at diagnosis across levels of cannabis use.

* Information on drug use is unclear, missing or use of other drugs, but not cannabis indicated

** Defined as use of cannabis (with or without use of any other illicit drugs) ever before conscription more than 50+ times.

Cohort description

Table 1 provides a description of the baseline characteristics of cohort members in the initial study sample. More than half of the cohort members indicated that they were current smokers, and approximately 20% reported moderate-to-heavy alcohol consumption. Approximately 11% of the baseline sample reported lifetime “ever” cannabis, and among these “ever” cannabis users, approximately 16.5% (n = 879) indicated cannabis usage of more than 50 times in lifetime.

Cox modeling results

In Table 2 , the fully adjusted model (Model 3) demonstrated no evidence of a significant relation between “ever” cannabis use and development of testicular cancer [Adjusted hazard ratio (AHR) 1.42, 95% CI, 0.83, 2.45]. In the fully adjusted model, cryptorchidism was the only variable significantly associated with development of testicular cancer (AHR 6.26, 95% CI, 2.30, 17.01).

Table 2

Incidence rates (IR), hazard ratios (HR) and 95% confidence intervals (CI) for testicular cancer (n = 119 cases) by exposure to “ever” cannabis use in 45 250 conscripts with data available on all study covariates

Study covariates Cases/Non-cases Crude incidence rate per 10 000 PY Crude model Model 1 a Model 2 b Model 3 c
N IR (95% CI) HR (95% CI) HR (95% CI) HR (95% CI) HR (95% CI)
Ever use of cannabis
Never use of any drugs 102/39975 0.64 (0.53, 0.77) 1.00 1.00 1.00 1.00
Ever use of cannabis d 17/5156 0.85 (0.53, 1.37) 1.32 (0.79, 2.21) 1.32 (0.79, 2.21) 1.44 (0.83, 2.47) 1.42 (0.83, 2.45)
Birth year
 1949 10/2427 1.06 (0.57, 1.97) 1.00 1.00 1.00 1.00
 1950 16/7836 0.52 (0.32, 0.85) 0.49 (0.22, 1.08) 0.49 (0.22, 1.09) 0.49 (0.22, 1.08) 0.50 (0.22, 1.09)
 1951 93/34868 0.67 (0.54, 0.82) 0.63 (0.33, 1.22) 0.65 (0.34, 1.24) 0.64 (0.33, 1.23) 0.64 (0.34, 1.24)
 No 115/44897 0.64 (0.54, 0.77) 1.00 1.00 1.00
 Yes 4/234 4.23 (1.59, 11.27) 6.59 (2.43, 17.86) 6.42 (2.37, 17.42) 6.26 (2.30, 17.01)
Parental testicular cancer
 No 118/45063 0.66 (0.55, 0.79) 1.00 1.00 1.00
 Yes 1/68 3.58 (0.50, 25.40) 5.46 (0.76, 39.05) 4.95 (0.69, 35.57) 4.82 (0.67, 34.72)
Tobacco smoking
 Never 46/18776 0.61 (0.46, 0.82) 1.00 1.00 1.00
 1–5 cig/day 16/5004 0.80 (0.49, 1.30) 1.31 (0.74, 2.31) 1.37 (0.77, 2.44) 1.38 (0.77, 2.46)
 6–10 cig/day 18/9349 0.48 (0.30, 0.77) 0.79 (0.46, 1.36) 0.83 (0.47, 1.45) 0.83 (0.47, 1.45)
 11–20 cig/day 33/10420 0.80 (0.57, 1.13) 1.30 (0.83, 2.04) 1.41 (0.88, 2.28) 1.41 (0.88, 2.28)
 More than 20 cig/day 6/1582 0.98 (0.44, 2.18) 1.58 (0.68, 3.71) 1.95 (0.80, 4.71) 1.90 (0.79, 4.60)
Alcohol consumption (g of 100% alc/week)
 Abstainers (0 g) 10/2770 0.90 (0.48, 1.67) 1.00 1.00 1.00
 Light (1–100 g) 91/33731 0.67 (0.55, 0.83) 0.75 (0.39, 1.44) 0.67 (0.34, 1.32) 0.67 (0.34, 1.32)
 Moderate (101–250 g) 17/7311 0.59 (0.37, 0.95) 0.65 (0.30, 1.42) 0.49 (0.21, 1.14) 0.49 (0.21, 1.14)
 Heavy (more than 250 g) 1/1319 0.20 (0.03, 1.41) 0.22 (0.03, 1.70) 0.13 (0.02, 1.09) 0.14 (0.02, 1.11)

In Table 3 , “heavy” cannabis use (AHR 2.57, 95% CI, 1.02, 6.50) and cryptorchidism (AHR 6.24, 95% CI, 2.30, 16.97) were significantly related to testicular cancer, whereas tobacco use and alcohol consumption showed no evidence of significant associations with the outcome.

Table 3

Incidence rates (IR), hazard ratios (HR) and 95% confidence intervals (CI) for testicular cancer (n = 119 cases) by exposure to frequency of cannabis use in 45 250 conscripts with data available on all study covariates

Study covariates Cases/Non-cases Crude incidence rate per 10 000 PY Crude model Model 1 a Model 2 b Model 3 c
N IR (95% CI) HR (95% CI) HR (95% CI) HR (95% CI) HR (95% CI)
Frequency of ever cannabis use d
Never use of any drugs 102/39975 0.64 (0.53, 0.77) 1.00 1.00 1.00 1.00
1–4 times 6/2704 0.57 (0.25, 1.26) 0.88 (0.39, 2.01) 0.90 (0.40, 2.05) 0.94 (0.41, 2.17) 0.95 (0.41, 2.19)
5–10 times 4/861 1.20 (0.45, 3.19) 1.86 (0.68, 5.05) 1.90 (0.70, 5.15) 2.13 (0.77, 5.90) 2.15 (0.77, 5.95)
11–50 times 2/728 0.70 (0.18, 2.81) 1.09 (0.27, 4.43) 1.04 (0.26, 4.25) 1.25 (0.30, 5.15) 1.17 (0.28, 4.85)
More than 50 times 5/863 1.56 (0.65, 3.74) 2.40 (0.98, 5.88) 2.32 (0.94, 5.70) 2.68 (1.06, 6.77) 2.57 (1.02, 6.50)
Birth year
 1949 10/2427 1.06 (0.57, 1.97) 1.00 1.00 1.00 1.00
 1950 16/7836 0.52 (0.32, 0.85) 0.49 (0.22, 1.08) 0.50 (0.23, 1.10) 0.49 (0.22, 1.09) 0.50 (0.23, 1.10)
 1951 93/34868 0.67 (0.54, 0.82) 0.63 (0.33, 1.22) 0.65 (0.34, 1.25) 0.64 (0.33, 1.24) 0.65 (0.34, 1.25)
 No 115/44897 0.64 (0.54, 0.77) 1.00 1.00 1.00
 Yes 4/234 4.23 (1.59, 11.27) 6.59 (2.43, 17.86) 6.37 (2.35, 17.28) 6.24 (2.30, 16.97)
Parental testicular cancer
 No 118/45063 0.66 (0.55, 0.79) 1.00 1.00 1.00
 Yes 1/68 3.58 (0.50, 25.40) 5.46 (0.76, 39.05) 4.84 (0.67, 34.91) 4.62 (0.64, 33.60)
Tobacco smoking
 Never 46/18776 0.61 (0.46, 0.82) 1.00 1.00 1.00
 1–5 cig/day 16/5004 0.80 (0.49, 1.30) 1.31 (0.74, 2.31) 1.37 (0.77, 2.44) 1.38 (0.77, 2.46)
 6–10 cig/day 18/9349 0.48 (0.30, 0.77) 0.79 (0.46, 1.36) 0.82 (0.47, 1.44) 0.82 (0.47, 1.44)
 11–20 cig/day 33/10420 0.80 (0.57, 1.13) 1.30 (0.83, 2.04) 1.40 (0.87, 2.26) 1.40 (0.87, 2.26)
 More than 20 cig/day 6/1582 0.98 (0.44, 2.18) 1.58 (0.68, 3.71) 1.87 (0.77, 4.54) 1.84 (0.76, 4.46)
Alcohol consumption (g of 100% alc/week)
 Abstainers (0 g) 10/2770 0.90 (0.48, 1.67) 1.00 1.00 1.00
 Light (1–100 g) 91/33731 0.67 (0.55, 0.83) 0.75 (0.39, 1.44) 0.68 (0.35, 1.34) 0.68 (0.35, 1.34)
 Moderate (101–250 g) 17/7311 0.59 (0.37, 0.95) 0.65 (0.30, 1.42) 0.50 (0.22, 1.14) 0.50 (0.22, 1.15)
 Heavy (more than 250 g) 1/1319 0.20 (0.03, 1.41) 0.22 (0.03, 1.70) 0.12 (0.01, 1.01) 0.13 (0.02, 1.04)


Our large Swedish data-linkage project found that self-reported “heavy” cannabis use – defined as self-reported use of more than 50 times in lifetime at the conscription assessment period – was significantly associated with a 2.5-fold increased hazard of subsequent testicular cancer. The study found no evidence of a significant relation between “ever” cannabis use and the development of testicular cancer. This null finding may be due to heterogeneity of cannabis use in the “ever” group, as this category contained only a minority who reported “heavy” cannabis use and a majority of individuals indicating minimal lifetime cannabis exposure (e.g., 1–4 times in lifetime). In addition to the current study finding a significant relation between cannabis use and testicular cancer, our prior work drawing upon the same Swedish conscript cohort found that cannabis use was significantly associated with the development of lung cancer (12).

The available three prior case-control studies in the area have shown a significant pooled association between testicular cancer and current, frequent (i.e., ≥ weekly use) and lengthy cannabis use (i.e., ≥ 10 years), as well as a much stronger relation between cannabis use and the development of nonseminomatous germ cell tumors rather than seminomatous germ cell tumors (21). The Daling et al. (14) and Lacson et al. (15) case-control studies found a modest but statistically significant association between “ever” cannabis use and testicular cancer, whereas Trabert et al. (16) found no evidence of a relation between “ever” cannabis use and testicular cancer. Meta-analytic estimates have shown no evidence of a statistically significant pooled relation between “ever” use and testicular cancer, when these three case-control studies were aggregated (11, 21). While the current study and the three previous studies have shown a relation between frequency and duration of cannabis use and the development of testicular cancer, the field still lacks evidence of a clear dose-response curve – a prerequisite for establishing a persuasive argument for the causal link. The current study showed no evidence of a gradient of risk across cannabis-use frequency variables, and the three prior case-controls studies relied on dichotomized cannabis-use frequency variables, such as “≥ weekly use: yes/no”– a design structure which does not allow for the assessment of a dose-response relation.

The mechanism by which cannabis affects the development of testicular cancer is not well elucidated. It is known, however, that active compounds in phytocannabinoids, such as tetrahydrocannabinol (THC) and cannabidiol (CBD), bind to cannabinoid receptors (CB1 and CB2) in many human organs, including the testes (26, 27). Experimental animal studies have shown that by binding to CB1 and CB2 in Leydig cells and Sertoli cells of the testes, levels of testosterone, follicle-stimulating hormone and luteinizing hormone are affected, as is the survival of Sertoli cells (28–31). Aberration in both steroid hormone levels and gonadotropin levels suggests that cannabinoids may cause a general perturbation to the hypothalamic-pituitary-gonadal axis which could result in tumorigenesis (32). Much more research in this area, including timing of exposure, is required, however.

Our results should be interpreted with caution, given a number of important study limitations. The key variable instantiating conscripts’ lifetime frequency of cannabis use relied on an indirect assessment of cannabis use. It was assumed that for those conscripts indicating “ever” cannabis use, the conscription survey question eliciting information about lifetime drug-use frequency (i.e., “How many times have you used drugs?”) applied to individuals’ cannabis use. This appears to be a reasonable assumption, given that cannabis users in the sample typically indicated cannabis as their most frequently used drug. For example, approximately 81% of “ever” cannabis users and 84% of “heavy” cannabis users indicated cannabis as their most frequently used drug. In addition, the current study did not have information about cannabis use after the conscription-assessment period, but European studies have demonstrated that adolescent cannabis use, especially those patterns associated with regular use, abuse, or dependence, tend to persist and remain relatively stable throughout the developmental years of the 20s and early 30s (33, 34). Even though unmeasured post-conscription changes in cannabis use may have affected our results, such misclassification biases would tend to attenuate our hazard ratio estimates and push our findings toward the null. For example, if “heavy” cannabis users (at baseline) later became nonusers of cannabis, this pattern would lead to a diminished hazard of testicular cancer associated with the cannabis-use variable; if nonusers of cannabis (at baseline) became cannabis users during the follow-up, this pattern would lead to an underestimate of the testicular-cancer risk in the initial cannabis-exposed groups, as this pattern would create an inflated risk in the non-using reference group (defined at baseline). An additional limitation was that the study had no information on the histology of the testicular cancers. While meta-analytic pooled estimates of the three existing case control studies have shown a relation between cannabis-use frequency and testicular cancer, especially the non-seminoma subtype, the current study was not able to estimate the hazards of cannabis use and the subsequent development of seminoma or non-seminoma subtypes.

While the current study does have limitations, it is important also to acknowledge the project’s strengths. The study included a very large population-based sample of young men, who underwent an extensive conscription assessment. This individual-level conscription information was also linked to population-based health registries, including the Swedish cancer registry. This data-linking procedure allowed the study to incorporate a very lengthy 42-year follow-up for members of the initial cohort. As a result, the project is the first cohort study assessing the potential relation between cannabis use and the development of testicular cancer, and it makes an important contribution to the small literature finding a potential association between cannabis use and the incidence of testicular cancer. Given current international developments to decriminalize or legalize cannabis use in a number of countries worldwide, it is critically important for legislation initiatives to consider the possible health consequences of cannabis use in the cost-benefit analysis underpinning rational drug-policy development.

Can Medical Cannabis Treat Chronic Epididymitis

After decades of stalling, governments are now beginning to ease the unwarranted restrictions on marijuana. Scientific studies have proven time and again that medical marijuana is effective in treating a wide range of conditions. This unrefutable evidence has helped shape public opinion and forced the authorities to reconsider their policies on cannabis. One condition that marijuana is used to take care of is epididymitis.

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Let’s dive into what this condition is and how cannabis helps.

What is Epididymitis?

Epididymitis is an inflammation of the coiled tube known as epididymis. This tube is situated at the back of the testicle, and it stores and carries sperm. When the tube swells, it causes pain and swelling in the testicles. This clinical syndrome affects men of all ages, but it’s mostly found in males between 14 and 35 years.


Epididymitis can be caused by a different range of factors, most often by a bacterial infection or a sexually transmitted infection (STI). Before puberty, it’s mainly caused by intestinal bacteria, such as E. coli. In sexually active men, the most common cause is STIs, such as chlamydia or gonorrhea. It can also affect men who have:

  • A history of urinary tract infections
  • Had prostate infections
  • Experienced trauma in the groin
  • Undergone surgery that involves the bladder or urethra
  • Urine flowing back to the epididymis
  • An anatomical abnormality of the urinary tract
  • An enlarged prostate
  • Tuberculosis


Chronic epididymitis – how symptoms appear

There are two types of epididymitis: Acute and chronic. Acute epididymitis lasts six weeks or less. Here, the symptoms develop within a short period. Chronic epididymitis lasts six weeks or more, but the symptoms develop at a slow pace. Although epididymitis begins with just some mild symptoms, they get worse if left untreated. Here are some of the most common symptoms.

  • Pain, swelling and tenderness in your testes
  • Fever and chills
  • Pain during sexual intercourse and ejaculation
  • Redness and warmth in the scrotum
  • Lymph nodes in the groin enlarge
  • Inability to walk without limping because of pain
  • Burning sensation when urinating
  • A clear, white or yellow discharge from the penis
  • Blood in urine
  • Fluid accumulation in the testicle which may feel like a lump
  • Frequent urination and bowel movements


After describing your symptoms, the doctors will ask you several questions about your medical history, surgical history, and sexual activity. He/she will then perform several tests to determine whether you have epididymitis. The tests and procedures may include:

  • A rectal exam to check for an enlarged prostate
  • Urine sample to check for STIs
  • Blood tests to determine whether you have an infection


Epididymitis is treated by addressing the underlying condition that causes it. Treatment options include.

  • Antibiotics for those with STIs or intestinal infections
  • Over the counter or prescribed pain medication
  • Anti-inflammatory medication
  • Bed rest
  • Other methods include applying an ice pack to the painful area and wearing a scrotal support

How can Marijuana be used to Treat Epididymitis

Medical marijuana for epididymitis – how it helps?

While the condition typically improves after taking medication, sometimes it takes longer. Yet, epididymitis is accompanied by constant pain, making life difficult during the treatment period. This means you may need to explore additional options to ease the pain. Marijuana can be introduced to help soothe the pain and inhibit other symptoms of epididymitis.

Ease your epididymitis symptoms. Click on the button below to get your MMJ card.

For thousands of years, cannabis has long been used as a medicinal plant by different cultures across the globe. Recent scientific studies have shown this herbal plant possesses components that have healing effects. These ingredients can be extracted from the plant and used to treat a wide range of conditions, among them epididymitis.

Researchers have tested how medical marijuana can be used to relieve pain and discovered it has relieving effects. Studies on people have concluded that when taken moderately, cannabis causes a noticeable reduction in pain. However, it’s more effective in some people than others. Based on these studies, we can’t ignore the potential of marijuana to alleviate the pain of epididymitis. If you are a sufferer, your doctor can prescribe the proper dose for dealing with the pain.

Side Effects and Symptoms of Epididymitis that Medical Marijuana can Treat

Apart from alleviating scrotal and testicular pain, medical marijuana can also be used to treat other conditions that accompany epididymitis. It’s common for sufferers to get anxious, stressed, depressed, and insomnia. Medical marijuana can treat all these effects.

Marijuana has two main active cannabinoids, THC and CBD, and they possess anti-inflammatory properties. However, CBD offers stronger anti-inflammatory action, and it can successfully be used to treat inflammation caused by epididymitis.

How to Access Medical Marijuana to Treat Epididymitis

It’s never easy dealing with a condition that causes pain and suffering. Luckily medical marijuana can offer you some respite on your road to full recovery. It not only eradicates the pain but also tackles other symptoms. To get the most out of medical marijuana it’s best you partner with qualified and experienced physicians like MMJ Doctors.

These certified physicians will assess your condition and create the ideal treatment plan depending on the type of epididymitis you have and the symptoms you are experiencing. Since there are varying legalities around medical marijuana in different states, these specialists will show you how to get a card that will allow you to legally access medical cannabis, and recommend to you the best products.

Consult MMJ Doctors

At MMJ Doctors, we know every individual has unique needs, that’s why we listen to you before determining the most appropriate solution for your condition. If you are looking for effective and safe options to treat epididymitis, talk to us today!

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Sharing my story about how cannabis benefits me, that you typically don’t read or hear about.

1. I use cannabis as a topical to minimize bruising stemming from anemia.

2. I ingest and inhale it to manage autoimmune symptoms of sarcoidosis, including chronic joint pain.

3. I use it in all forms to lessen teeth grinding and the resultant TMJ pain.

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Where to start! We are learning more and more about the benefits of marijuana every day, and here are some of the more interesting facts about marijuana during the COVID pandemic.

1) Good Start-up Business: A benefit of marijuana today is that it is easy for anyone to get involved in the industry no matter where you are based. The legal cannabis industry is projected to be worth $73 billion by 2027. So it really is worth looking at starting your own blog, podcast, affiliate marketing agency, or own your e-commerce shopping portal and making some income from the online cannabis industry. The next few years will see many more regulations easing like a more realistic framework followed in States such as Colorado and California who have pioneered successful recreational and medical marijuana markets providing 250000 new jobs already.

2) Nutritious Juice: Juicing cannabis is often an overlooked option of receiving the benefits of cannabis. Most countries have at least decriminalized cannabis for cultivation. So it’s worth growing your own pot as an herb even in the smallest of spaces to get fresh leaves that you may include in a smoothie or chopped up in a salad. Cannabis leaves contain a lot of vitamins, antioxidants, fiber, and other beneficial compounds that you should already be using for better health and wellness naturally. It helps me write better!

3) Ease of Access: The fastest-growing user group is elderly and it has seen as much as a 10-fold increase in the use of cannabis in the last decade. The most probable reason is because of easier access to medical marijuana and the fact that it works.

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Here are 3 uncommon benefits worth learning about:

1. Delta8 THC – The current trend in the hemp industry. Delta8 is an isomer of THC that can be converted from CBD, making it hemp-derived and federally legal (in theory). Extremely mild intoxication, unlike Delta9 THC, the main constituent responsible for the high feeling. Hemp retailers are salivating at the business proposition a federally legal THC product presents, but more interesting is the similar therapeutic value to Delta9 without the adverse side effect of intoxication or anxiety. This could be a game-changer, but more research is needed.

2. CBN – CBN occurs when decarboxylated cannabinoids degrade over time. It has been shown to contain antibacterial, analgesic, anti-inflammatory, and potentially sedating properties. We are seeing a lot of positive feedback from patients that complain of sleep difficulties.

3. CBG – Another non-intoxicating cannabinoid with anti-inflammatory properties. It is gaining popularity with both manufacturers and consumers. More research is needed, but some evidence shows it may offer benefits by reducing intraocular pressure, irritable bowel, bladder dysfunctions, bacterial infections, certain cancers, and appetite loss.

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These are the benefits of Marijuana:

Cannabis is a natural regulator for our bodies due to the Endocannabinoid
system. So whether you have an ailment, feeling stress, inflammation,
pain, creativity block or are just having a bad day, cannabis can bring you
back to center so you can enjoy and accomplish whatever your life

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1-Cannabis makes sex better. If you smoke it, vape it, or apply it as a sexual topical, all users I know agree that in some form, CBD and THC increase sexual pleasure. First-timers, try low dose, and give yourself time to experience the full effect before taking more. Combine a THC topical with a bit of smoke for my fave combination…enjoy.

2-People who consume cannabis regularly have a lower BMI than the general population. Given the incidences of the munchies, it stands to reason that supporting the endocannabinoid system with cannabis makes the body more efficient.

3- Cannabis is a post-workout elixir. After a hard workout, I love a 1:1 vape (THC:CBD) or a joint with a high CBD flower for the quick onset of deep relaxation and the anti-inflammatory properties the flower provides. Some people mistakenly think stoners are lazy but many athletes use cannabis for this purpose.

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My name is Sheriann Baker. I was diagnosed with terminal Oligodendroglioma Brain Cancer Stage 2 in August 2017. I was told that I had 5 to 10 years to live at most even with radiation and chemo. I was 47. I was also told that if I didn’t do chemo and radiation I would most likely die 2 years!

1. Taking the First Step: I started doing my research and in August of 2017 I decided to fight brain cancer with Rick Simpson Oil/Cannabis Oil/Phoenix Tears. As I am not ready to die yet! I started taking a gram or 2 of Rick Simpson Oil a day up until my surgery on October 3rd,2017. My goal was to take 2 ounces as fast as I could.

2. Eating Clean: I also started eating clean! That is half of the battle! No sugars, carbs, fats, flours or red meats. I do three drops of Frankincense Oil every day, 10 to 15 Vitamin C’s, and I swear by the Bud-wig Diet!

3. Strong Support: I stopped taking RSO a day before surgery as your blood pressure is very low while on RSO so it’s a MUST. Also, my doctors were aware of what I was doing and worked with me right from the start. I started taking RSO 2 days after surgery.

4. Successful Tumor Removal: On October 3rd, 2017 I had brain surgery to remove most of the tumor. My neurosurgeon was able to remove 97% of my tumor. My operation was 6 hours. 22 staples. I was up and about the same day and was released from Foothills Hospital in Calgary Alberta within 26 hours after brain surgery. I was in the gym in a week! Of course, my Oncologist highly recommends chemo and radiation but I absolutely refused to do it. I told my Oncologist to book me a follow-up MRI for January 2018.

5. A Healthier Me: I felt so healthy and strong I was 100% sure that I had made the right choice and sure enough Rick Simpson Oil/ cannabis oil killed the 3% that Dr. Kelly couldn’t remove. I am still here and still tumor-free because of cannabis oil and eating clean. Now I take a gram a day and will for the rest of my life.

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Marijuana is an unknown cure for tobacco in more ways than just helping with treating cancer. It can be used as a preventive measure and a viable alternative to smoking tobacco or actually quitting from it. I personally stopped smoking cigarettes and ended a disgusting habit that had me spending all my money on killing myself. I simply rolled a joint and smoked it every time I wanted a cigarette and a week later I was done with them.

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These are the 3 benefits of Marijuana:

1. Enhanced Creativity: Cannabis helps me find unorthodox angles to invent and create art.

2. Perspective Amplification: Bob Marley, “When you smoke the herb, it reveals you to yourself.” Favorite quote. But what it really means is that you see yourself from an outside perspective that envelopes everything in the environment.

3. Injury Sourcing: Sometimes a sports injury displays itself by swelling surrounding the injury. It can be hard to pinpoint the source of the injury. Cannabis helps alleviate the outward symptoms to focus and reveal the source of bodily injury.

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These are the top benefits of Marijuana:

1. Become Active: Marijuana can get people active and moving that would typically otherwise sit around the house. Although a lot of users do just sit around the house while high, some enjoy exercising that much more while high that they do it regularly.

2. Improve Perspective: It can help you to think of things from a different perspective. I personally have a lot of business ideas while I’m high. A lot of them are ridiculous, but some are genuinely quite great.

3. Enhance Creativity: It can bring out your creative side. While a lot of people might think of drawing or painting, there’s plenty of other creative avenues that marijuana can help in. From writing or making music, to writing articles or even putting together business plans. Of course, dosage is very important for some of these activities.

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Here is my response based on my own experiences, knowledge, understanding, and how cannabis has helped me.

1. Creativity, cannabis allows me to focus. When I put myself in a creative space after intaking THC I always have my best ideas.

2. I get relaxed. Cannabis helps me destress.

3. Scientific backed research that shows THC and CBD help reduce inflammation and treat certain diseases.

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Here are the top benefits of Marijuana:

1. Marijuana Makes You Work Out Harder: Marijuana is a great way to help you forget about your stress so you can enjoy more recreational activities including exercise. Studies have found that exercise actually activates the endocannabinoid system in the same way that the cannabis plant does.

The Sadhu’s of India is an ancient Hindu Sect that is known for getting high and doing Yoga long before marijuana-friendly yoga classes ever became a “thing” in cosmopolitan cities like L.A. and NYC. So many modern runners, tri-athletes, mixed martial artists, professional football and basketball players, and wrestlers in addition to the world’s most decorated Olympian Michael Phelps have publicly come out as marijuana users.

The health benefits of marijuana usage on athletic performance are so surprising that marijuana is actually considered a performance-enhancing drug by the World Anti-Doping Association!

2. Marijuana is Preventative, Restorative Medicine: More surprising for many people still is that taking supplemental cannabinoids by using marijuana may actually prove to be the best preventative medicine for many of the conditions it helps alleviate. In the August 2009 issue of Cancer Prevention Research, medical researchers reported that “ten to twenty years of marijuana use was associated with a significantly reduced risk of head and neck squamous cell cancer.”

In 2013 The International Journal of Neuropsychopharmacology published a study that found that CBD can actually help grow brain cells, completely contradicting the decades-old stereotype that marijuana kills brain cells and makes users stupid, and proving marijuana to be an effective treatment for depression and other mental health disorders.

Marijuana makes you feel good, or “high” because cannabinoids help you control the number one cause of all lethal afflictions – stress. Our endocannabinoid systems moderate and regulate stress hormones with naturally occurring endocannabinoids from our own bodies which belong to the same class of cannabinoids like THC and CBD. This is why supplemental cannabinoids are an ideal way to regulate dangerous levels of unhealthy stress hormones in our bodies.

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Here are my top three powerful marijuana benefits:

1. PROMOTES DIGESTIVE HEALTH: I suffer from a few digestive disorders which can be frustrating at best and debilitating at worst. It can be both physically and emotionally draining. Marijuana is a uniquely beneficial solution to promoting gut health! When you have digestive issues like IBS, indigestion, and heartburn, you may notice sleep problems as well, which leads to my next benefit!

2. HELPS WITH INSOMNIA/SLEEP ISSUES: I have had problems sleeping my entire life. The first benefit I learned from marijuana is that it helps me fall asleep. If I’m up in the middle of the night, I just have a puff or two and I’m back to sleep…and, it’s all natural!

3. PROMOTES MENTAL HEALTH: I suffer from mental health issues and I can say from experience that marijuana has helped me with social anxiety, depression, and ADD. It helps me start my day off in a good mood, checks my anxiety, and helps me concentrate on my work. This is far more useful than all of those useless medications I’ve been prescribed!

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There are so many health benefits to marijuana that the subject could fill a pretty thick book. Trying to narrow down over 100+ cannabinoids, terpenes and other plant components to the most beneficial will take years of study once research can be freely done on marijuana and ALL of its many compounds. However, there is new data coming out on a few of the most promising compounds of the cannabis plant and that is where I’ll break down the various beneficial parts as we know them now.

Everyone knows about THC, the part of the marijuana plant that gets you “high”. But many of the health benefits of using marijuana come from other compounds found in the plant.

1. Benefits of CBD: CBD (Cannabidiol) is becoming more popular and most people have heard of the health benefits of using CBD products: pain relief, or anxiety relief. But there are also several CBD products being investigated that have been shown to reduce seizures in patients with epilepsy. CBD has also been proven to counteract some of the side effects of THC (anxiety/paranoia) if given in the right ratios.

2. Benefits of CBG: CBG (Cannabigerol) is a very interesting compound that has been getting attention lately. It’s the natural precursor molecule to both THC and CBD so it’s effects on the body are somewhere between the 2 compounds except CBG does not cause a “high”. The many health benefits CBG has been proven to help with will astound you: antibacterial properties, anti-inflammatory effects similar to steroids, inhibits cell growth in tumors (that’s right, it may help cure or treat cancers!), and it also promotes bone growth and healing. CBG also counteracts THC’s paranoia effects and can reduce blood pressure. Once dosages and delivery forms can be researched the possible treatment options with this compound are endless including treatment potential for IBS, Crohn’s Disease, Huntington’s Disease, glaucoma, and any inflammatory condition as well.

3. Benefits of CBN: CBN (Cannabinol) is a compound that is formed by the degradation of THC. It can only be formed by time naturally. It’s rare and hard to isolate but maybe the sleeping aid of the future. (Non-addicting, non-narcotic, no side effects, similar potency to Valium, all-natural). It causes heavy sedation, as well as pain relief, stress relief, and anti-seizure properties as well.

The biggest thing to know/learn about using cannabis is that high THC levels have absolutely no bearing on how you will actually feel from using a strain. When you combine THC with all the other mentioned cannabinoids and also all the Terpenes (which are the smell and flavor of weed and also have medicinal benefits themselves) you get what’s called the “Entourage Effect”. The combination of THC with the exact cannabinoids (CBD, CBG) and terpenes (Linalool, Limonene, Myrcene) found in the strain you use is what will determine how your body reacts and what your overall experience will be.

I think we have an exciting future ahead of us in the cannabis research sector. There is the potential for marijuana to treat, in a natural way, many of the diseases we use damaging chemicals to treat today.