Cannabis and Male Fertility: What the Science Actually Shows

A new narrative review maps the endocannabinoid system’s complex role in sperm production, erectile function, and prostate health, but the evidence base is predominantly preclinical and the causal conclusions remain premature for clinical translation.

Why This Matters

Cannabis use among men of reproductive age is rising sharply alongside global legalization trends, and clinicians are increasingly fielding questions about whether cannabis affects fertility, sexual function, or prostate health. The endocannabinoid system is expressed throughout the male reproductive tract, making the biological plausibility of reproductive effects genuine and worth understanding. At the same time, the gap between mechanistic science and reliable clinical guidance remains wide, making the timing of this review both useful and potentially misleading if read without appropriate caution.

Clinical Summary

The endocannabinoid system, comprising CB1 and CB2 receptors, the endogenous ligands anandamide (AEA) and 2-arachidonoylglycerol (2-AG), and their degradative enzymes FAAH and MAGL, is functionally present across the male reproductive tract. A 2025 narrative review published in Maturitas by researchers drawing on literature from PubMed, Scopus, Web of Science, and Google Scholar synthesizes evidence spanning approximately two decades to argue that this signaling system modulates spermatogenesis, erectile physiology, and prostatic inflammation. The mechanistic rationale is grounded in CB1-mediated smooth muscle relaxation and nitric oxide-dependent vasodilation in the corpus cavernosum, and CB2-mediated anti-inflammatory activity in prostate tissue, both supported primarily by animal and in vitro models.

The review reports that chronic exogenous THC exposure is associated with impaired sperm production and motility, disrupted hormonal balance including altered testosterone and luteinizing hormone levels, and uncertain effects on prostate cancer cell proliferation. However, the human evidence underpinning these associations is observational, subject to significant confounding from polydrug use and lifestyle factors, and heterogeneous in design. The review employs no systematic search protocol, PRISMA framework, or formal risk-of-bias assessment, and the total number of included studies and their individual quality are not reported. The authors themselves acknowledge that controlled research on dose, duration, and mechanism is needed before these findings can inform clinical practice or policy.

Dr. Caplan’s Take

This review is a reasonable mapping exercise for a complex and increasingly relevant topic. The endocannabinoid system clearly participates in male reproductive physiology, and the mechanistic work is interesting. But the distance between showing that CB1 receptors are present in the corpus cavernosum and being able to tell a patient that cannabis will affect their fertility in a specific, predictable way is enormous. When patients ask me whether cannabis use is hurting their chances of conceiving, the honest answer is that we have signals of concern but not enough well-controlled human data to quantify the risk.

In practice, for men actively trying to conceive who are using cannabis regularly, I discuss the animal and observational data suggesting potential effects on sperm parameters and hormonal balance, and I frame cessation or reduction as a reasonable precautionary step rather than an evidence-based mandate. For patients using cannabinoids for other indications, I weigh the reproductive concern against the treatment benefit and document the conversation. I do not cite this type of review as proof of harm, because it is not designed to provide that.

Clinical Perspective

This review sits early in the research arc for cannabinoids and male reproductive health. It confirms that the endocannabinoid system is biologically relevant to spermatogenesis, erectile physiology, and prostatic function, and it organizes a diffuse literature into a useful framework. However, it does not resolve the central clinical question of whether, and at what dose and duration, exogenous cannabinoid use causes clinically meaningful reproductive harm in humans. The preclinical evidence is suggestive but not directly translatable, and the observational human studies cited are vulnerable to confounding that the review does not formally assess. Clinicians should treat the reproductive concern as plausible but unquantified when counseling patients.

From a pharmacological standpoint, THC’s effects on the hypothalamic-pituitary-gonadal axis, including potential suppression of gonadotropin-releasing hormone and downstream testosterone, warrant attention in patients on concurrent hormonal therapies or those with baseline hypogonadism. Drug interactions between cannabinoids and phosphodiesterase-5 inhibitors used for erectile dysfunction have not been well characterized and deserve caution. The single most actionable recommendation from this evidence base is to include a standardized cannabis use history in male fertility evaluations, so that potential exposure is documented and can be factored into clinical decision-making as better evidence emerges.

Study at a Glance

Study Type

Narrative review (non-systematic)

Population

Preclinical models (animal and in vitro) and limited human observational cohorts; male reproductive health focus

Intervention

Endocannabinoid system signaling; exogenous cannabinoid (primarily THC) exposure

Comparator

Not applicable (no formal comparator structure)

Primary Outcomes

Spermatogenesis, erectile function, prostatic inflammation, hormonal parameters, prostate cancer cell proliferation

Sample Size

Not reported; no quantitative synthesis performed

Journal

Maturitas (Elsevier)

Year

2025 (accepted November 2024)

DOI

10.1016/j.maturitas.2024.108156

Funding Source

Not disclosed in available text

What Kind of Evidence Is This

This is a narrative review, which occupies a relatively low position in the evidence hierarchy compared to systematic reviews, meta-analyses, or randomized controlled trials. Narrative reviews synthesize literature based on the authors’ selection and interpretation rather than a preregistered, reproducible search and appraisal methodology. The most important inference constraint this imposes is that the conclusions reflect a qualitative, potentially selective synthesis of available studies, meaning the weighting of evidence behind any individual claim cannot be independently verified or reproduced.

How This Fits With the Broader Literature

This review is broadly consistent with prior work identifying endocannabinoid system components in reproductive tissues and with observational studies suggesting associations between heavy cannabis use and altered semen parameters. Earlier systematic reviews, including Payne et al. (2019) in Human Reproduction Update, similarly found that cannabis exposure was associated with changes in sperm morphology and concentration but noted that the clinical significance of these changes remained unclear. The current review extends this landscape by incorporating more recent preclinical work on CB2-mediated prostatic inflammation and FAAH/MAGL as therapeutic targets, though these additions are largely hypothesis-generating rather than confirmatory.

Notably, some epidemiological studies have reported paradoxical findings, including a 2019 Harvard study suggesting higher sperm counts among cannabis users, illustrating the inconsistency of the human evidence base that this narrative review does not fully reconcile.

Common Misreadings

The most likely overinterpretation of this review is reading it as evidence that cannabis use causes infertility or erectile dysfunction in men. The review aggregates mechanistic plausibility and associational data, but it does not establish causation for any reproductive outcome in humans. The preclinical findings, while biologically coherent, involve doses, routes of administration, and model organisms that may not reflect real-world human exposure patterns. Treating this narrative synthesis as a clinical evidence base for advising patients to stop cannabis use specifically to improve fertility outcomes goes beyond what the data, as presented here, can support.

Bottom Line

This narrative review usefully maps the endocannabinoid system’s involvement in male reproductive physiology and raises plausible concerns about chronic THC exposure. It does not, however, establish causal relationships between cannabis use and specific reproductive harms in humans, and its non-systematic methodology limits the reliability of its evidence synthesis. For clinical practice, it supports including cannabis use history in fertility evaluations and treating reproductive risk as biologically plausible but not yet quantified.

References

1. Endocannabinoid signaling in the male reproductive system. Maturitas. 2025. DOI: 10.1016/j.maturitas.2024.108156
2. Payne KS, Mazur DJ, Hotaling JM, Pastuszak AW. Cannabis and male fertility: a systematic review. J Urol. 2019;202(4):674-681. DOI: 10.1097/JU.0000000000000248
3. Nassan FL, Arvizu M, Minguez-Alarcon L, et al. Marijuana smoking and markers of testicular function among men from a fertility centre. Hum Reprod. 2019;34(4):715-723. DOI: 10.1093/humrep/dez002