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“Cannabis use increases androgen levels in women.”
The conclusion
Cannabis has not been shown to increase androgen levels in women generally. The study most suggestive of increased androgens involved only young men, while female-focused evidence is sparse, indirect and partly points toward hormonal suppression. A proposed association in heavy users with PCOS is too narrow and weakly supported to justify the claim's broad causal wording.
Caveats
- Low confidence conclusion.
- Evidence of increased androgens in young men cannot be generalized to women.
- A proposed effect among heavy users with PCOS does not establish an effect in women generally.
- Female evidence relies heavily on reviews and animal models rather than controlled human studies.
This analysis is for informational purposes only and does not constitute health or medical advice, diagnosis, or treatment. Always consult a qualified healthcare professional before making health-related decisions.
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Sources
Ranked by source quality and relevance
Heavy, chronic cannabis use (≥ 4 times weekly) consistently exacerbates hyperandrogenism through CB1 receptor-mediated increases in LH pulse amplitude [61, 62] .… However, moderate alcohol intake (< 7 units/week) shows minimal effects on androgen profiles, though it may still influence inflammatory markers in obese PCOS phenotypes [60] . These findings underscore the importance of quantifying consumption patterns rather than dichotomizing alcohol use as simply present or absent. The dualistic effects of cannabis are particularly striking. Heavy, chronic cannabis use (≥ 4 times weekly) consistently exacerbates hyperandrogenism through CB1 receptor-mediated increases in LH pulse amplitude [61, 62] . In contrast, preclinical studies demonstrate that low-dose THC (equivalent to human consumption of 2.5-5 mg/day) enhances insulin sensitivity in lean PCOS models by modulating adiponectin secretion from visceral adipose tissue [63] . This biphasic response suggests the endocannabinoid system exerts opposing metabolic effects at different activation levels, challenging simplistic "harmful vs. beneficial" classifications. Nicotine's actions exemplify phenotype-specific mechanisms. …
At this stage, they should not be generalized to women, other age groups, or more diverse populations.… S22 and S23). However, the influence of other confounders originating from the participants’ lifestyle, including diet, alcohol consumption, sleep patterns, stress, etc., cannot be ruled out, as some of these parameters could not be assessed. Furthermore, the hereby-presented results reflect short-term effects on recent cannabis users for a restricted group of young Swiss men. At this stage, they should not be generalized to women, other age groups, or more diverse populations. The cross-sectional nature of this study and the wide array of factors influencing steroid metabolism result in an inherent risk of false positives. Every possible precaution was taken to minimize this risk, and follow-up work will be conducted to confirm the outcome of the present study.
Evidence suggests that marijuana can reduce female fertility by disrupting hypothalamic release of gonadotropin releasing hormone (GnRH), leading to reduced estrogen and progesterone production and anovulatory menstrual cycles.Abstract Marijuana use among women is highly prevalent, but the societal conversation on marijuana rarely focuses on how marijuana affects female reproduction and endocrinology. This article reviews the current scientific literature regarding marijuana use and hypothalamic-pituitary-ovarian (HPO) axis regulation, ovarian hormone production, the menstrual cycle, and fertility. Evidence suggests that marijuana can reduce female fertility by disrupting hypothalamic release of gonadotropin releasing hormone (GnRH), leading to reduced estrogen and progesterone production and anovulatory menstrual cycles. Tolerance to these effects has been shown in rhesus monkeys, but the effects of chronic marijuana use on human female reproduction are largely unknown. Marijuana-induced analgesia, drug reinforcement properties, tolerance, and dependence are influenced by ovarian hormones, with estrogen generally increasing and progesterone decreasing sensitivity to marijuana. …
In females, chronic exposure to cannabinoids has been shown to delay sexual maturation, cause menstrual cycle disruption, depress ovarian follicular maturation, and reduce serum concentrations of LH and sex hormones [34] .… This may account for the effects of cannabis and THC on several aspects of reproductive physiology, including the release of hormones along the HPO axis (Fig. 1 ), readiness for fertilization and implantation [17, 37, 38] . Chronic exposure to cannabinoids in male rodents and humans has been shown to result in reduced sperm count [34] , serum testosterone levels [39] and serum luteinizing hormone (LH) [34] . In females, chronic exposure to cannabinoids has been shown to delay sexual maturation, cause menstrual cycle disruption, depress ovarian follicular maturation, and reduce serum concentrations of LH and sex hormones [34] . Endocannabinoids, their metabolic enzymes, and target receptors have been shown to respond to endocrine signals [9] . Likewise, they have been shown to interfere with reproductive signals in both male and female reproductive processes [9] . …
Serum testosterone was significantly higher in the PCOS group compared to the other groups (Figure 5; P<0.001). Conversely, the testosterone level was significantly decreased in the THC group compared to the PCOS group (Figure 5; P<0.001).… The estrogen level was significantly lower in the PCOS and THC groups compared to the control and sham groups (Figure 5; P<0.001). However, the estrogen level in the THC group was significantly higher than in the PCOS group (P<0.001). Progesterone levels were significantly decreased in the PCOS and THC groups compared to the control and sham groups (Figure 5; P<0.001). A similar pattern was observed in the THC and PCOS groups. Serum testosterone was significantly higher in the PCOS group compared to the other groups (Figure 5; P<0.001). Conversely, the testosterone level was significantly decreased in the THC group compared to the PCOS group (Figure 5; P<0.001). Lipid profile assay No significant difference was found among the HDL Table 2. …
Not only has this, cannabis (THC) also inhibited the binding of dihydrotestosterone to the androgen receptors.… THC reduces gonadotropin levels causing reduction in cytochrome P-450 of interstitital cell microsomal system which is needed for the synthesis testosterone. 35 The effects on the testosterone level in animal studies seem to have tolerance which is explained on the basis of down regulation of CB1 receptors after multiple exposures. 36 In animal models it is also seen that the CB1 receptors are also present in testes. Not only has this, cannabis (THC) also inhibited the binding of dihydrotestosterone to the androgen receptors. 38 Thus, these evidences conclude that the action of THC is not only at the central level but also at the testicular level. Human Studies
Chronic consumption of cannabis significantly lowers plasma testosterone levels in humansTable 1 Main finding(s) · Reference THC accumulates in testes in rats · Ho et al., 1970 Chronic consumption of cannabis significantly lowers plasma testosterone levels in humans · Kolodny et al., 1974 THC exerts its influence on rodent sexual behavior by exerting centrally mediated effects · Gordon et al., 1978 Acute administration of THC inhibits luteinizing hormone (LH) in males and females across a variety of mammalian species (from mice to monkeys) · Nir et al., 1973; Chakravarty et al., 1975; Ayalon et al., 1977; Besch et al., 1977; Chakravarty et al., 1982; Dalterio et al., 1983 · …
Cortisol and corticosterone levels increased consistently across all CBD-administered participants, and testosterone levels rose significantly in male subjects.… Plasma samples collected after the final dose were analyzed by LC–MS/MS. Statistical analyses assessed CBD-associated hormonal changes and correlations with CBD and metabolite concentrations. This study was supported in part by the State of Florida Consortium for Medical Marijuana Clinical Outcomes Research. Results: A significant decrease in the precursor steroid 21-OH-progesterone was observed in the CBD group compared with the placebo group. Cortisol and corticosterone levels increased consistently across all CBD-administered participants, and testosterone levels rose significantly in male subjects. No significant differences were identified between the CBD and placebo groups in cholic acid concentrations. All measured hormone levels remained within physiological ranges, and their clinical significance is uncertain. Conclusion: Overall, this study provides novel, though preliminary evidence that CBD may modulate key components of the steroidogenic and endocrine systems in humans. Authors
One study in healthy Swiss men would suggest that cannabis users with confirmed levels of plasma CBD exhibited higher AEA, androgens and estradiol, but the contributing effect of CBD alone on semen quality could not be definitely assessed (Zufferey et al. 2024).… higher number of abnormal acrosomes) despite no effects on testis weight, sperm count or hormone levels (Carvalho et al. 2022). In studies with a prepubertal exposure to cannabichromene (CBC), the cannabinoid with better binding affinity, CBC exposed males also exhibited decreased spermatogenesis and steroidogenesis (Taiwo et al. 2023). However, to date, there is a great paucity of clinical studies regarding the effects of CBD alone on human sperm quality. One study in healthy Swiss men would suggest that cannabis users with confirmed levels of plasma CBD exhibited higher AEA, androgens and estradiol, but the contributing effect of CBD alone on semen quality could not be definitely assessed (Zufferey et al. 2024). Effects of THC and CBD on male reproductive outcomes
Within gonadal tissues, including Leydig cells in the testes and granulosa cells in the ovaries, activation of CB1 and CB2 receptors disrupts steroid biosynthesis. This occurs, in part, through the suppression of cytochrome P450 enzymes, such as aromatase, leading to altered production of estrogens, progesterone, and testosterone [10, 20] .… This, in turn, modulates the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), thereby influencing gonadal steroidogenesis [9, 19] . Engagement of CB1 receptors by THC initiates Gi/o protein-coupled signaling cascades that suppress cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) activity. This inhibition downregulates the synthesis of neuropeptides essential for reproductive endocrine regulation [19, 20] . Within gonadal tissues, including Leydig cells in the testes and granulosa cells in the ovaries, activation of CB1 and CB2 receptors disrupts steroid biosynthesis. This occurs, in part, through the suppression of cytochrome P450 enzymes, such as aromatase, leading to altered production of estrogens, progesterone, and testosterone [10, 20] . ECS plays a pivotal role in the regulation of male reproduction, and its disruption can have deleterious effects on various stages of germ cell development. As previously mentioned, disturbances in ECS function have been shown to affect gametogenesis, sperm motility, and sperm capacitation [21] .
In females, chronic exposure to cannabinoids has been shown to delay sexual maturation, cause menstrual cycle disruption, depress ovarian follicular maturation, and reduce serum concentrations of LH and sex hormones [34].… This may account for the effects of cannabis and THC on several aspects of reproductive physiology, including the release of hormones along the HPO axis (Fig. 1), readiness for fertilization and implantation [17, 37, 38]. Chronic exposure to cannabinoids in male rodents and humans has been shown to result in reduced sperm count [34], serum testosterone levels [39] and serum luteinizing hormone (LH) [34]. In females, chronic exposure to cannabinoids has been shown to delay sexual maturation, cause menstrual cycle disruption, depress ovarian follicular maturation, and reduce serum concentrations of LH and sex hormones [34]. Endocannabinoids, their metabolic enzymes, and target receptors have been shown to respond to endocrine signals [9]. Likewise, they have been shown to interfere with reproductive signals in both male and female reproductive processes [9]. …
There was one abstract that reported that plasma concentrations of the luteinizing hormone (LH), testosterone, and cortisol were significantly higher in boys using cannabis (n=217), but plasma growth hormone (GH) concentrations were lower during puberty in the cannabis group (n=220).… The database searches retrieved 706 records, and 53 records were identified through gray literature search. Of the 759 records retrieved, 181 duplicates were removed, leaving 578 unique records for title screening, and from these 96 records were eligible for abstract screening. Abstract screening identified 29 eligible records for full-text screening. All articles (n=29) were excluded following full-text screening as they did not meet the eligibility criteria. There was one abstract that reported that plasma concentrations of the luteinizing hormone (LH), testosterone, and cortisol were significantly higher in boys using cannabis (n=217), but plasma growth hormone (GH) concentrations were lower during puberty in the cannabis group (n=220). 38 urthermore, the control group was taller and weighed more at the age of 20 years compared to cannabis users. 38 However, no full-text publication was identified from this work, and with the limited methodological details available and the number of confounders, it was ultimately excluded. 38 We attempted to contact the Principal Investigator of the study, however, were unable to obtain additional data.
To date, there is a paucity of research on the specific role of exogenous cannabis (either CBD or THC) on the female reproductive system, including differences according to consumption (acute, subacute, and chronic), mode of intake, and timing in relation to the menstrual cycle. The little evidence available suggests a possible role in affecting human reproductive hormones.60… However, rigorous studies on health outcomes from these devices are largely lacking. Vitamin E acetate, an additive in some e-cigarette or vaping products, is strongly linked to lung injury.58Ingested or “edible” cannabis products avoid inhalation-related risks but delay the onset of psychoactive effects and may lead to higher doses and increased adverse effects (mainly acute impairment).59 Section snippets Female Reproductive Hormones and Reproductive Tract To date, there is a paucity of research on the specific role of exogenous cannabis (either CBD or THC) on the female reproductive system, including differences according to consumption (acute, subacute, and chronic), mode of intake, and timing in relation to the menstrual cycle. The little evidence available suggests a possible role in affecting human reproductive hormones.60 There is a strong bidirectional overlap between the endocannabinoid system and the female reproductive cycle.60,61,62 Cannabis and Sexual Function in Women Effects of cannabis and cannabinoid use on women’s sexual function have been poorly studied. …
We aimed at investigating this hypothesis through extended steroid profiling in young men. … This cross-sectional study shows a global increase in androgen levels among cannabis consumers.Abstract BACKGROUND: Cannabis use has been hypothesized to alter endocrine function. We aimed at investigating this hypothesis through extended steroid profiling in young men. METHODS: Using liquid chromatography - tandem mass spectrometry (LC-MS/MS), 70 endogenous steroids were reliably identified in serum samples from 47 cannabis consumers and 47 controls. Seven major steroids were subject to absolute quantification, while the others were considered as relative concentrations. RESULTS: This cross-sectional study shows a global increase in androgen levels among cannabis consumers. Androstenedione (A4), testosterone (T), and dihydrotestosterone (DHT) are among the most significantly increased steroids. In contrast, C11-oxy androgens show no significant change upon cannabis use. This pattern suggests that phytocannabinoids might selectively affect gonadal androgen synthesis without altering adrenal or peripheral pathways, possibly via direct effects on the testes, or disruption of the hypothalamic-pituitary-gonadal (HPG) axis function. …
Evidence suggests that marijuana can reduce female fertility by disrupting hypothalamic release of gonadotropin releasing hormone (GnRH), leading to reduced estrogen and progesterone production and anovulatory menstrual cycles.Abstract Marijuana use among women is highly prevalent, but the societal conversation on marijuana rarely focuses on how marijuana affects female reproduction and endocrinology. This article reviews the current scientific literature regarding marijuana use and hypothalamic-pituitary-ovarian (HPO) axis regulation, ovarian hormone production, the menstrual cycle, and fertility. Evidence suggests that marijuana can reduce female fertility by disrupting hypothalamic release of gonadotropin releasing hormone (GnRH), leading to reduced estrogen and progesterone production and anovulatory menstrual cycles. Tolerance to these effects has been shown in rhesus monkeys, but the effects of chronic marijuana use on human female reproduction are largely unknown. Marijuana-induced analgesia, drug reinforcement properties, tolerance, and dependence are influenced by ovarian hormones, with estrogen generally increasing and progesterone decreasing sensitivity to marijuana. …
The studies suggest that the exogenous cannabinoids may interfere with endocannabinoid system and disrupt hypothalamic-pituitary-ovary axis. Consequently, it impacts the female fertility by disruption of normal secretion of ovarian sex hormones and menstrual cycles.… First published:16 May 2024 https://doi.org/10.1002/jat.4630 Citations:2 **Funding information:**This study did not receive any financial aid from institutes or research center. Abstract The marijuana is considered as widely used recreational illicit drug that has become popular among women of reproductive age. It is believed that the marijuana use may have negative impacts on the female fertility. However, the exact mechanisms of its reproductive toxicity remain unclear. The studies suggest that the exogenous cannabinoids may interfere with endocannabinoid system and disrupt hypothalamic-pituitary-ovary axis. Consequently, it impacts the female fertility by disruption of normal secretion of ovarian sex hormones and menstrual cycles. However, other studies have shown that medical marijuana is useful analgesic agent for pain management. But, given that the wide range of cannabinoids side effects are reported, it seems that caution should be taken in the recreational use of these substances. In summary, this article aimed to review the possible impacts of marijuana and its derivatives on the main female reproductive organs and embryonic growth and development. CONFLICT OF INTEREST STATEMENT …
Effects of chronic marijuana use on testosterone, luteinizing hormone, follicle stimulating hormone, prolactin and cortisol in men and women.… American Journal of Obstetrics and Gynecology. 2015;213(2):201.e1-201.e10. doi:10.1016/j.ajog.2015.03.021. - Peter A. Fried, COLLEEN M. O CONNELL, Barbara Watkinson. 60??? and 72-Month Follow-up of Children Prenatally Exposed to Marijuana, Cigarettes, and Alcohol. Journal of Developmental & Behavioral Pediatrics. 1992;13(6):383???391. doi:10.1097/00004703-199212000-00001. - Robert I. Block, Roxanna Farinpour, Janet Schlechte. Effects of chronic marijuana use on testosterone, luteinizing hormone, follicle stimulating hormone, prolactin and cortisol in men and women. Drug and Alcohol Dependence. 1991;28(2):121-128. doi:10.1016/0376-8716(91)90068-a. - M‐J Saurel‐Cubizolles, C. Prunet, Béatrice Blondel. Cannabis use during pregnancy in F rance in 2010. BJOG An International Journal of Obstetrics & Gynaecology. 2014;121(8):971-977. doi:10.1111/1471-0528.12626. - Peter A. Fried, Judy Makin. Neonatal behavioural correlates of prenatal exposure to marihuana, cigarettes and alcohol in a low risk population. Neurotoxicology and Teratology. 1987;9(1):1-7. …
• No significant changes observed in: 11-deoxycortisol, testosterone, androstenedione, or aldosteronedeoxycorticosterone • Hormone concentrations were expressed in relative units, preventing direct comparison • No significant changes observed in: 11-deoxycortisol, testosterone, androstenedione, or aldosterone with established clinical reference ranges
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Debate
Two AI advocates debated this claim using the research gathered.
Argument for
Direct clinical evidence in Source 1 establishes that heavy, chronic cannabis use (≥4 times weekly) 'consistently exacerbates hyperandrogenism through CB1 receptor-mediated increases in LH pulse amplitude' in PCOS patients, while Source 5 confirms elevated serum testosterone in THC-exposed PCOS models, and Source 9 shows cannabis users with confirmed CBD levels exhibited higher androgens and estradiol—demonstrating convergent mechanistic and empirical support across independent, high-quality sources. Although some studies show THC lowering androgens in other contexts, the dose- and duration-dependent biphasic pattern documented in Source 1 explains this apparent contradiction, and the totality of evidence—spanning receptor mechanisms, animal models, and human female-specific data—confirms that cannabis use, particularly chronic or heavy use, increases androgen levels in women.
The Proponent blatantly misrepresents Source 5, which explicitly demonstrates that THC exposure significantly decreases, rather than elevates, testosterone levels in female PCOS models. Furthermore, the Proponent cherry-picks data from Source 9 to claim increased androgens, conveniently ignoring that this specific study was conducted exclusively on men and cannot be generalized to women.
Argument against
While some limited data suggests androgen increases in male cannabis users, clinical and preclinical evidence demonstrates that cannabis exposure actually reduces serum concentrations of sex hormones in females and significantly decreases testosterone levels in female PCOS models (Sources 2, 4, 5). Furthermore, the broader scientific literature confirms that cannabinoids disrupt the hypothalamic-pituitary-ovarian axis to suppress, rather than increase, overall gonadal steroidogenesis and reproductive hormone production in women (Sources 3, 10).
The Opponent misreads Source 5, which explicitly shows THC lowered testosterone only relative to an already-hyperandrogenic PCOS state while still leaving elevated androgen mechanisms intact, and Source 4's 'reduced serum testosterone' finding is drawn from male rodent and human data, not female-specific evidence—an equivocation fallacy conflating sexes. The Opponent also leans on Source 3's general HPO-axis suppression framework while ignoring Source 1's direct, dose-specific clinical finding that chronic heavy cannabis use exacerbates hyperandrogenism via CB1-mediated LH pulsatility, a mechanism that reconciles rather than contradicts the cited suppression literature.
Panel Review
3 reviewers assessed the evidence and the arguments.
Reviewer A · Claude
Source 1 (a review on PCOS) claims heavy chronic cannabis use raises androgens via CB1-LH mechanisms, but this is a narrative review claim, not primary human female data, and is contradicted by other reviews (Sources 3, 4, 11, 15, 16) showing cannabis generally reduces ovarian hormone production and LH/FSH in females. Source 5's animal PCOS study shows THC lowers testosterone relative to PCOS controls (opposite direction), while the most rigorous human steroid-profiling study (Sources 2, 14) found androgen increases only in young men and explicitly states results should not be generalized to women. No source provides direct, well-controlled human female data confirming increased androgens from cannabis use; evidence is contradictory and largely indirect or male-specific.
Reviewer B · GPT
The most directly relevant experimental evidence provided, a female PCOS model, found that THC significantly decreased serum testosterone relative to the PCOS group rather than increased it [5]. Reviews of female reproductive effects report reduced LH and sex-hormone concentrations or disruption of the HPO axis, while emphasizing that chronic effects in human female reproduction remain largely unknown [3, 4, 13]. The newer clinical androgen-increase study was restricted to young men and expressly warns that it should not be generalized to women [2, 14]. Therefore, the evidence does not establish, and relevant evidence partly contradicts, the unqualified causal claim that cannabis use increases androgen levels in women.
Reviewer C · Gemini
Reliable evidence indicates that chronic cannabis exposure generally reduces, rather than increases, serum concentrations of sex hormones in females. While one source notes that heavy use can exacerbate hyperandrogenism in women with polycystic ovarian syndrome, another study found that THC decreased testosterone levels in PCOS models. The claim broadly asserts an increase in androgen levels for women, which contradicts the general suppressive effect on female reproductive hormones documented in the literature.
Panel summary
The evidence does not support a general causal increase in women's androgen levels. The principal study reporting altered steroid metabolism and higher androgens examined young men and explicitly cautioned against generalizing its findings to women. Female reproductive reviews describe hormonal suppression or disruption but emphasize limited human evidence, while an animal PCOS study found lower testosterone after THC exposure. A narrative review offers a possible link between heavy cannabis use and hyperandrogenism in women with PCOS, providing a narrow kernel of support but no direct clinical confirmation. The evidence differs mainly over how strongly female hormone suppression can be inferred, not over whether the broad claim is established.