Cannabis Usage and Blood Markers

not sure if this belongs in pharma but this was the closest category. question is there any long term cannabis users here that have seen (or felt for that matter) cannabis usage affecting their hormones in a negative manner? and if so is this shown in your bloods? I have recently begun using cannabis frequently(almost daily more as needed now), in the form of a tincture or edible. I generally use 50mg.

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Studies are conflicting; some say it hurts TT and others say it helps, both with varying methods of testing.

I’d imagine the stress reduction and better sleep associated with cannabis would increase TT about as much as if you’d reduced your stress and improved your sleep naturally though.

this was kindof what i was wondering. i wasn’t sure if the studies claiming it lowers tt or lh had a distinct chemical reason for it doing such or if its more a lifestyle issue.

From what I have read, it seems to lower TT/FT in short term users. I think it could be that they are more “messed” up, and sleep is impacted. I think long term users are statistically the same for TT/FT as non-users (based on an article I read that was about a study done).

makes sense i suppose

From what I’ve seen, smoking occasionally can lower stress and raise TT short term, but chronic use eventually lowers TT over time. Maybe one of those things where a little is ok but too much is bad

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i’m ideally going to be a short term user, and even though I feel good using it and think it could be helping, your body can lie and how you feel always isn’t the bodily reality

This contradicts what I have seen. They looked at Jamaican men that smoked at least daily for their long term users. They weren’t different than non-smokers in a statistically significant way.

There could be something about Jamaican men, that they have higher numbers than average, and they are experiencing a lowering effect, it just isn’t seen because they are inline with other users.

I’ll say I doubt it has anywhere near the impact of booze.

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The majority (66.2%) of the weighted study population reported ever using marijuana with 26.6% reporting current marijuana use. There was no difference in serum testosterone between ever users (adjusted mean = 3.69 ng/mL, 95% CI: 3.46, 3.93) and never users (adjusted mean = 3.70 ng/mL, 95% CI: 3.45, 3.98) upon multivariable analysis. However, serum testosterone was inversely associated with time since last regular use of marijuana ( p-value for trend = 0.02). When restricted to men aged 18 – 29 years, this relationship strengthened ( p-value for trend < 0.01) and serum testosterone was also inversely associated with time since last use ( p-value for trend < 0.01), indicating that recency of use, and not duration or frequency, had the strongest relationship with testosterone levels.


Serum testosterone concentrations were higher in men with more recent marijuana use. Studies are needed to determine the extent to which circulating testosterone concentrations mediate the relationship of marijuana use to male reproductive outcomes.


In this population-based study of U.S., men, there was no difference in serum testosterone levels among ever users of marijuana compared to never users. We observed, however, a dose-response relationship between increasing serum testosterone and decreasing time since last regular use indicating that recency of use, not duration or frequency of use, had the strongest relationship with testosterone levels. When we restricted the analysis to men aged 18 – 29, the inverse relationship to time since last regular use strengthened and serum testosterone was also inversely associated with time since last use.

Prior studies of marijuana use and testosterone levels have produced inconsistent results. An influential early study by Kolodny et al. reported a significant decrease in testosterone level for marijuana users in a small, highly-selected population (Kolodny et al., 1974). While a subsequent clinical study found a similar association (Cohen, 1976), most subsequent studies reported no association (Barnett et al., 1983; Block et al., 1991; Coggins et al., 1976; Cushman, 1975; Mendelson et al., 1978; Mendelson et al., 1974; Schaefer et al., 1975). Almost all studies, however, whether observational or clinical in design, had small samples sizes. In contrast, the recent Danish study by Gundersen et al., was based on a large sample of young, healthy men and reported higher testosterone levels with greater frequency of marijuana use (Gundersen et al., 2015). Our results were similar to those of Gundersen et al., however, recency of marijuana use was better correlated with testosterone level than was frequency of use.

The biologic mechanism by which marijuana exerts an effect on hormone production likely involves the response of cannabinoid receptors, CB1 and CB2, to THC. These receptors are functional in male reproductive organs, including the Leydig cells of the testis, the principle producer of testosterone in men. Leydig cell testosterone production decreases with age, but changes in testosterone production also occur as a result of alteration of the intracellular redox environment (Beattie et al., 2015), which can lead to oxidative stress and damage to cellular components. Environmental factors like marijuana use could play a role in this alteration. Further, Leydig cell aging may explain the more pronounced effect of marijuana among men aged 18 – 29 years compared to men ≥ 30 years. As Leydig cells age, they may be less resistant to the detrimental effects of oxidative stress.

Our results indicate that the relationship of marijuana use to serum testosterone is more pronounced among men aged 18 – 29 years, the age period of increased risk of nonseminoma. Nonseminoma has shown a stronger association with marijuana use than seminoma (Daling et al., 2009; Lacson et al., 2012; Trabert et al., 2011), however, the extent to which serum testosterone mediates this relationship is not possible without ascertainment of TGCTs in conjunction with serum testosterone and marijuana use.

A particular strength of our study is the use of a large population-based sample representative of the U.S. population with sufficient information on demographic and lifestyle factors. The use of a self-administered computer-assisted interview provided an ideal environment for collection of sensitive information, such as use of marijuana. Perhaps as a result of the confidential setting, 66.2% of the weighted study population reported ever using marijuana. The drug use questionnaire examined marijuana use in great detail, allowing differentiation of frequency, duration, and recency of marijuana use. Also, information on testosterone levels was determined using a standardized central assay with rigorous quality control measures (Botelho et al., 2013).

A limitation of this study is the cross-sectional nature of data collection in NHANES. Although there is likely a minimal effect of response bias given the frequency at which marijuana use was reported, questions about the timing and frequency of past marijuana use may be difficult to recall. Also, forms of marijuana consumption other than smoking were not captured. Factors such as the amount of sleep the previous night (Auyeung et al., 2015) and physical activity immediately before blood draw (Hakkinen & Pakarinen, 1995; Kraemer et al., 1998) may affect testosterone levels. Adjustment for these variables could not be conducted as NHANES did not collect this information. In addition, NHANES has not measured serum concentrations of other sex steroid hormones thus it was not possible to examine whether they were associated with marijuana use.

This study is the largest to examine the relationship of marijuana use to serum testosterone levels and the first study to examine the effects by age group. As marijuana use continues to rise in the US, further elucidation of its relationship to male reproductive health is warranted.


thank you

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In the adjusted model, there was no difference in serum testosterone between ever users (adjusted mean = 3.69 ng/mL, 95% CI: 3.46, 3.98) and never users (adjusted mean = 3.70 ng/mL, 95% CI: 3.45, 3.98). Slightly higher serum testosterone concentrations persisted in current users (adjusted mean = 3.96 ng/mL, 95% CI: 3.55, 4.42) and ever regular users (adjusted mean = 3.90 ng/mL, 95% CI: 3.56, 4.29) after adjustment, but 95% CIs of mean estimates overlapped widely with those of never users. In a dose-response analysis, serum testosterone increased with decreasing time since regular use of marijuana ( p-value for trend = 0.02). There was no dose-response relationship between serum testosterone and time since last use, frequency during regular use, number of joints / pipes smoked per day during regular use, and years of regular use. All estimates were similar when obtaining predictive margins (results not shown).

Table 4 shows the weighted associations between marijuana use and testosterone levels, stratified by age group. Among men aged 18 – 29 years, the adjusted analysis found that serum testosterone levels among ever users were lower than among never users (adjusted mean = 4.03 ng/mL, 95% CI: 3.26, 4.97 vs. adjusted mean = 4.35 ng/mL, 95% CI: 3.40, 5.58). Among ever users, levels in current users were higher than past users (adjusted mean = 4.15 ng/mL, 95% CI: 3.77, 4.58 vs. adjusted mean = 3.86 ng/mL, 95% CI: 3.51, 4.25) and levels among ever regular users were higher than never regular users (adjusted mean = 4.12, 95% CI: 3.68, 4.61 vs. adjusted mean = 3.81, 95% CI: 3.27, 4.44) but neither current users or ever regular users had higher levels than never users. When restricted to men aged 18 – 29 years, the inverse relationship to time since last regular use strengthened ( p-value for trend < 0.01) and serum testosterone was also inversely associated with time since last use ( p-value for trend < 0.01). Among men aged ≥ 30 years, there was a slight increase in ever users relative to never users (adjusted mean = 3.51 ng/mL, 95% CI: 3.25, 3.77 vs. adjusted mean = 3.41 ng/mL, 95% CI: 3.12, 3.73). Among current users (adjusted mean = 3.81 ng/mL, 95% CI: 3.32, 4.39), and ever regular users (adjusted mean = 3.71 ng/mL, 95% CI: 3.33, 4.13), testosterone levels were slightly higher, but 95% CIs overlapped with never users. The dose-response relationship between testosterone level and time since last regular was weaker in this age group ( p-value for trend = 0.10).

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Do you think this:


Could have to do with the user group having a higher baseline than the non-users? Higher TT is correlated to taking risks, which drug use would probably fall under.

I have heard the saying before “bodybuilders like drugs”. I think that doesn’t just apply to PEDs. I think some of the personality traits associated with using PEDs are the same as the ones for rec. drugs, and perhaps those personality traits are influenced by TT?

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To your point:



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thank you for taking the time to find the snippets and diagrams that answer all the questions. i appreciate it.


Anecdotally, I feel no obvious negative hormonal effects (I have no quantitative way to assess this) while using at low dosages (usually 5-10mg) and relatively high frequency (not quite every day) over a 5ish year span.

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if you don’t mind me asking, do you get high from 5-10mg ingested??

Yea, I’m not like Snoop Dogg high but it definitely takes the edge off. I use stuff from dispensaries, which makes a significant difference. I bought some stuff from a sticker store (they’re trying to sell in a grey space by giving you weed and selling you stickers) in NY recently, they were allegedly selling 500mg of gummies, 50mg per gummy, those had about an equivalent effect as the normal 5mg edible I take from a regulated dispensary.

Weird, maybe it’s individual or yeah just Jamaicans are different? IDK.

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I meant to mention earlier…
When I went to my primary to discuss low T symptoms, she mentioned a few of her other younger patients and talked about why they were low T.

One admitted to abusing AAS, which caused his hypogonadism
The other was a heavy marijuana smoker, which she said caused his chronically low testosterone.

Though my primary doesn’t know too much about testosterone (what primaries ever do?), I think she’s likely right about weed induced hypogonadism. Still, hard to find studies to support this.

lol I quit kratom due to fear of kratom induced hypogonadism. didn’t know cannabis could do the same.