Gut Health and Testosterone

There is a real connection between the gut and testosterone, and it is more interesting than the version being sold to you. Here is what the research actually shows — including the study that tested the whole idea in men, and what it found.

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Type "gut health and testosterone" into a search bar and you will get a lot of confident sentences. Most of them trace back to the same handful of studies, and a surprising number of those studies were done in mice.

This article goes through what is genuinely established, what is a hypothesis wearing a lab coat, and what the evidence says you can actually do about your testosterone. Some of that is unflattering to the category this company sells in. It is included anyway, because the alternative is writing something you cannot check.

What testosterone does, and how common low testosterone really is

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Testosterone is a sex hormone produced mainly in the testes, and it matters for muscle mass, bone density, red blood cell production, libido and sexual function. Both men and women make it; men make a great deal more.

The earlier version of this article said testosterone deficiency affects 30% of men aged 40–79. We went looking for the study behind that figure and there isn’t one. The number traces back through a 2014 review⁶ to a narrative review from 2004 — not to a prevalence survey. The actual numbers depend entirely on how you define the condition:

• A single blood test below 300 ng/dL, in men attending a doctor: 38.7% of men aged 45 and over.⁵
• Low total and free testosterone plus symptoms, in the general population: 5.6% of men aged 30–79 — between 3.1% and 7.0% under 70, rising to 18.4% at age 70.⁴
• Under the strictest research criteria (three sexual symptoms plus low total and free testosterone): 2.1% of men aged 40–79.³

That is a range from one man in fifty to one in three, depending on the definition. Note also what the largest of those studies found about symptoms: of the many complaints associated with low testosterone, only three sexual symptoms had a genuine syndromic association with it — poor morning erections, low sexual desire and erectile dysfunction.³ Fatigue, low mood and lost strength are real, and they are also caused by a hundred other things.

The 1–2% a year figure needs three footnotes

Testosterone does decline with age. The Massachusetts Male Aging Study measured it longitudinally: total testosterone fell about 1.6% a year, and bioavailable testosterone 2–3% a year.⁸ The Baltimore study found a similar picture.⁷

But: the decline starts around 30 to 40, not "as you reach your forties." Free testosterone falls faster than total, because the protein that binds it rises with age. And — the part almost nobody mentions — a large share of what looks like aging is not aging.

The gut connection: what is actually established

The idea goes like this. A compromised gut lining lets bacterial fragments — endotoxin, or LPS — into the bloodstream. Those fragments trigger inflammation. Inflammation suppresses testosterone production. Therefore: fix the gut, fix the testosterone.

It is a good hypothesis and there is real work behind the first two steps. It is worth being precise about how far that work goes.

The human experiment, and what it showed

Researchers gave 33 healthy lean men aged 18–40 either an intravenous dose of purified E. coli endotoxin or a saline placebo. Inflammatory markers spiked, peaking at two hours. Testosterone fell, significantly at six hours — and was back to baseline by 24 hours. LH and FSH did not change, which is the basis for inferring the effect was on the testes rather than the brain.¹⁰

That is genuine human evidence that acute endotoxin exposure lowers testosterone. What it is not: evidence that a slightly permeable gut in an otherwise well man produces sustained testosterone deficiency. The intervention was an injection of purified bacterial toxin into a vein, not a bad lunch. And in the same paper’s observational arm, when the researchers built their best statistical model of total testosterone, the endotoxin marker dropped out entirely — age, CRP, sex hormone binding globulin and estradiol did the explaining.¹⁰

The wider theory — that gut endotoxin drives late-onset hypogonadism in obese men — is set out in a 2016 paper the article used to cite as evidence. It is worth knowing what that paper is: a hypothesis paper. Its own author describes it as "a novel theory."¹¹ Theories are how science starts. They are not the same as findings.

What "leaky gut" does and does not mean

Intestinal permeability is a real, measurable thing. Whether it causes disease in humans is a separate question, and the answer is less settled than the wellness internet suggests.

The Mayo Clinic review of the subject is direct: "Whereas inflammatory or ulcerating intestinal diseases result in leaky gut, no such disease can be cured by simply normalising intestinal barrier function. It is still unproven that restoring barrier function can ameliorate clinical manifestations in GI or systemic diseases."¹³ An earlier review puts the causal question plainly: "human and mouse studies show that intestinal barrier loss alone is insufficient to initiate disease… it is uncertain whether increased permeability in these patients is a cause or effect."¹⁴

One specific correction. The older version of this article said permeability comes "often from eating irritating foods." The things demonstrated to increase permeability in humans are endurance exercise, non-steroidal anti-inflammatories, pregnancy, bile acids and dietary emulsifiers.¹³ "Irritating foods" is precisely the framing that review singles out as unverified material circulating in the public domain.

And a second correction, because getting the mechanism right matters. The article previously said leaked particles cause immune cells to release histamine. That is the wrong pathway. Endotoxin is recognized by the TLR4 receptor complex, which switches on NF-κB and produces cytokines — TNF-α, IL-1β, IL-6. Those are exactly the markers the human endotoxin study measured.¹⁰ Histamine release is mast-cell degranulation, which in the relevant experiments is triggered by TLR2, not TLR4.¹⁵

The mechanism is inflammation and cytokines, not histamine. And an acute endotoxin injection is not the same thing as a permeable gut.

Does gut bacterial composition track testosterone in men?

A little, in small studies. One looked at 54 elderly Japanese men and found a modest correlation between relative Firmicutes abundance and serum testosterone — and no significant difference in overall diversity between higher and lower testosterone groups.¹² Fifty-four men, one center, cross-sectional, all attending a urology clinic. Hypothesis-generating, not conclusive, and heavily entangled with body weight.

The traffic runs the other way too

This is the genuinely interesting part, and the article previously undersold it.

Researchers found that adults with irritable bowel syndrome had lower free testosterone than healthy controls, and that the lower it was, the worse their symptoms. Then — and this next part is in mice — they removed gonadal androgens from adult animals and produced "a profound deficit in gastrointestinal transit," which restoring a single androgen reversed. Androgen receptors appear in a large group of enteric neurons at puberty, and signaling to those neurons turned out to be required for normal colonic motility.¹⁶

A 2026 follow-up in Nature Neuroscience traced a mechanism, and it is a proper gut–hormone loop: your liver packages used androgens for excretion, and gut bacteria carrying an enzyme called beta-glucuronidase unpack them again in the colon, regenerating usable androgen right where those neurons are. Wipe out the microbiome with antibiotics in mice and androgen receptor expression in enteric neurons disappears, serum testosterone falls and the gut slows down. Putting the bacterial enzyme back restores the signaling.¹⁷

Mostly mice, with a human component showing the same enzyme shifts across puberty in 506 males. It is a real microbiome-to-hormone mechanism — and note what it runs through: bacterial enzymes recycling your own hormones, not a probiotic supplement. Nobody has tested it as an intervention in people.

So it is fair to say androgens act on the nerves that move your colon, and that low free testosterone travels with worse IBS symptoms. It is not supported to say that raising testosterone improves transit or reduces gut pain in men — no human trial has shown that.

So — does a probiotic raise testosterone?

This is the question the whole article exists to answer, so here is the full sequence.

In 2014, researchers reported that aged male mice given Lactobacillus reuteri in their drinking water had larger testicles and higher serum testosterone than matched controls, with more Leydig cells and more spermatogenesis on histology.¹⁸ It is a striking result. It is also, as the title says, a study in mice. The previous version of this article hyperlinked that paper to a heading claiming research shows probiotics can prevent low testosterone in men. That heading is gone.

Because the obvious next step was taken. In 2024, a team ran a 12-week randomized, double-blind, placebo-controlled trial of the very same organism — Limosilactobacillus reuteri ATCC PTA 6475 — in healthy men aged 55 to 65, at a high dose and a low dose, with blood drawn at baseline, six weeks and twelve.¹⁹

The result, in the authors’ words: "The supplementation had no effect on testosterone levels, neither using high- or low dose, nor placebo." And their conclusion: "The present study does not support the hypothesis that a probiotic supplementation can increase testosterone levels in ageing men."¹⁹

One detail makes that harder to dismiss rather than easier: one of the authors is an employee of the company that owns the strain. A manufacturer running a trial on its own product and publishing a null result is about as credible as evidence of absence gets.

The mouse finding was tested in men, by the strain’s own manufacturer, and it did not replicate.

We looked for any other human trial of any probiotic with testosterone as an outcome, published between 2022 and 2026, and found none. As of today, no probiotic has been shown in a controlled human trial to raise testosterone.

And the gut-barrier evidence?

The article previously cited a 2023 review as showing "with the highest amount of scientific evidence" that probiotics fortify the gut barrier. That review is real — 26 randomized human trials, 1,891 people.²⁰ Its contents are more mixed than the title suggests.

Every validated in-vivo measure of intestinal permeability came out null: the lactulose/mannitol ratio (p=0.06), lactulose/rhamnose (p=0.33), diamine oxidase (p=0.39), D-lactate (p=0.15), LPS-binding protein (p=0.63) and fecal zonulin (p=0.80). The significant results were in blood markers, with heterogeneity between studies running as high as 92–97% — and no certainty-of-evidence grading was performed at all.²⁰

There is a further wrinkle worth knowing. The cleanest positive finding was serum zonulin — and the commercial assay used to measure zonulin has been shown not to detect the protein it is supposed to detect. A 2018 paper, co-authored by the researcher who discovered zonulin, concluded that "the zonulin ELISA does not recognize pre-haptoglobin2, rather structural (and possibly functional) analog proteins."²¹

The honest version: in some clinical populations, some probiotic formulations have shifted some laboratory markers related to the gut barrier, inconsistently, while the most direct measures generally showed nothing. The trial populations were largely hospital patients — intensive care, pancreatitis, cirrhosis, colorectal surgery — and not one of those studies measured testosterone.^20,22

What actually raises testosterone

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Here is the list with human evidence behind it. None of it is a supplement.

1. Losing weight, if you carry extra

The best-evidenced non-drug intervention there is. A meta-analysis of 24 studies found a low-calorie diet raised total testosterone by 2.87 nmol/L — roughly 83 ng/dL — and bariatric surgery raised it by 8.73 nmol/L, about 252 ng/dL. Both highly significant, and "the degree of body weight loss is the best determinant of TT rise."²³

For scale: the diet effect alone is comparable to reversing about two decades of age-related decline. And it corrects exactly the hypothalamic-pituitary pattern that the European study identified as the obesity signature.⁹

2. Sleeping

Ten healthy young men were restricted to five hours in bed for eight nights in a laboratory. Daytime testosterone fell from 18.4 to 16.5 nmol/L — a 10 to 15% drop.²⁴ The researchers made the comparison themselves, and it is the most quotable line in the whole field: "normal aging is associated with a decrease of testosterone levels by 1% to 2% per year."²⁴

One week of short sleep cost these men roughly what a decade of getting older would have. Small study, young men, short duration — but it was a controlled experiment, and it is more relevant to a 45-year-old than any probiotic paper in this article.

3. Exercise — for the right reasons

Here the honest answer is counter-intuitive. A meta-analysis of 11 randomized trials in 421 previously inactive men found exercise training had a negligible effect on resting total testosterone — a standardized mean difference of 0.00, and it did not vary by training type, age or body weight.²⁵

The post-workout testosterone spike after heavy lifting is real and it lasts about an hour. It does not raise your resting level. Train anyway — for body composition, insulin sensitivity, bone, mood and the fact that it helps you lose the weight in point one. Just not because a set of squats is going to move your blood work.

4. Reviewing what you take

Several extremely common exposures suppress testosterone far more reliably than anything gut-related:

• Opioids — chronic opioid therapy is a well-recognized cause of central hypogonadism.
• Long-term corticosteroids — the urology guideline lists chronic corticosteroid use as a specific reason to check testosterone.¹
• Anabolic steroids and "prohormone" supplements — these shut down your own production, and recovery afterwards can take many months. If you are shopping in the testosterone-booster aisle, this is the one that can actually leave you worse off.
• Obesity and type 2 diabetes — the dominant modifiable drivers.^5,9

5. Alcohol, honestly

Heavy and chronic alcohol use clearly suppresses the whole hormonal axis. The evidence that moderate drinking meaningfully lowers testosterone in healthy men is weaker than usually claimed: a meta-analysis of 17 studies found no significant overall effect, with the moderate-intake subgroup pointing very slightly the other way — almost certainly confounding rather than benefit.²⁶ Drink less if you drink a lot. Do not expect two fewer beers a week to move a blood test.

6. One thing that does not work, despite what you have read

Treating sleep apnea with CPAP does not raise testosterone. A meta-analysis of 12 studies in 388 patients found "CPAP use was not associated with a significant change in total testosterone levels", and concluded that "strategies other than CPAP should therefore be considered in managing hypogonadism in patients with OSA."²⁷ The low testosterone in men with sleep apnea appears to be driven mainly by the weight they share, not the apnea. Treat the apnea — it is worth treating for its own substantial reasons. Just not for this.

If you think your testosterone is low, get it measured properly

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The American Urological Association guideline — published 2018, reviewed and validity confirmed in 2024 — is clear about how this is done.¹

• Total testosterone below 300 ng/dL is "a reasonable cut-off in support of the diagnosis of low testosterone." In support of — not the diagnosis on its own.
• Two measurements, both early morning, on separate days. "The diagnosis of low testosterone should be made only after two total testosterone measurements are taken on separate occasions with both conducted in an early morning fashion." Strong recommendation, Grade A evidence. An afternoon sample is not interpretable.
• If it is low, LH must be measured. Strong recommendation, Grade A.
• If LH is low or low-normal, prolactin must be measured. Strong recommendation, Grade A.

The Endocrine Society takes the same approach, adding that the diagnosis should be made "only in men with symptoms and signs consistent with testosterone deficiency and unequivocally and consistently low serum T concentrations."²

Two more things worth knowing before anyone starts treatment. Testosterone therapy suppresses sperm production and can cause infertility — the guideline requires this to be discussed with any man interested in future fertility, and a great many men do not know it.¹ And on cardiovascular safety: the TRAVERSE trial randomized 5,246 men with hypogonadism and cardiovascular risk to testosterone gel or placebo, and found testosterone noninferior to placebo for major cardiac events. But the testosterone group had "a higher incidence of atrial fibrillation, of acute kidney injury, and of pulmonary embolism."³⁰ Reassuring on the headline question, not a green light.

About "testosterone boosters"

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A systematic review looked at 52 studies covering 27 ingredients marketed as testosterone boosters. Its assessment of the category: "Lax industry regulation has allowed sales of supplements to thrive in the absence of verification of their purported benefits… Our findings indicate that most fail to increase total testosterone."²⁸

Specifically not supported for raising testosterone: Tribulus terrestris, D-aspartic acid, maca, isoflavones and creatine. Vitamin D has its own meta-analysis of eight randomized trials, which found "no significant effect" on total testosterone.²⁹ A small number of ingredients were rated possibly effective in narrow populations, on small trials.²⁸

We are a supplement company telling you that most supplements in this category do not do what they say. Take that for what it is worth — and apply the same skepticism to us.

The short version

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The gut and testosterone are connected, in both directions, and some of the mechanism is genuinely elegant.^10,16,17 What has not been shown is that taking a probiotic changes a man’s testosterone — the one trial that tested it in men found nothing.¹⁹

Meanwhile the things with real human evidence are unglamorous and free: lose weight if you are carrying it, sleep properly, drink less if you drink a lot, review your medications, and get a proper two-sample morning blood test rather than guessing.^1,23,24

If your testosterone is genuinely low, that is a medical conversation with real options and real trade-offs. It is not a shopping problem.

A note about Flourish

Flourish is a living liquid probiotic taken daily by adults for general digestive and microbiome support — eleven species from five genera, fermented together as one culture, third-party lab tested every batch.

It is not a testosterone product. No probiotic has been shown in a controlled human trial to raise testosterone in men, including the specific strain that worked in mice.^18,19 If your energy, libido or strength have changed, the useful next step is a blood test and a conversation with your doctor, not a bottle of anything.

What Flourish is for is digestive wellness, taken daily, as an ordinary habit. That is a smaller claim than this category usually makes, and it is the one we can stand behind.

Flourish is a dietary supplement intended to support digestive and microbiome health. It is not a treatment for testosterone deficiency, hypogonadism, or any other condition, and it is not intended to raise testosterone levels. Speak to your healthcare provider before starting any supplement. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

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A few questions we hear a lot

Will taking a probiotic raise my testosterone?

On the current evidence, no. A 12-week double-blind placebo-controlled trial of the strain that raised testosterone in mice found no effect in men aged 55–65, and no other human trial of any probiotic has shown one.^18,19

But I read that gut health affects testosterone. Was that wrong?

Not wrong — oversold. Acute endotoxin exposure does lower testosterone in men, transiently, and androgens do act on the nerves controlling the gut.^10,16 What has not been shown is that improving gut health in a well man raises his testosterone.

Is 30% of men over 40 really testosterone deficient?

No. That figure traces to a review, not a prevalence study. Requiring both low levels and symptoms gives about 5.6% of men aged 30–79; the strictest criteria give 2.1% of men aged 40–79. About a third of men over 45 fall below 300 ng/dL on a single test, but many of them have no symptoms at all.^3,4,5

What is the single most effective thing I can do?

If you are carrying extra weight, lose some. A low-calorie diet raised total testosterone by around 83 ng/dL across 24 studies, and the amount of weight lost was the best predictor of the rise.²³ After that, sleep.²⁴

Does lifting weights raise testosterone?

Not your resting level. A meta-analysis of 11 randomized trials found a negligible effect on resting total testosterone.²⁵ The acute post-workout spike is real and short-lived. Lift for every other reason.

How should I get tested?

Two total testosterone measurements, both early morning, on separate days — a strong, Grade A recommendation. If it comes back low, insist on LH, and prolactin if LH is low or low-normal, because that combination can point to a pituitary problem.¹

Are "testosterone booster" supplements worth trying?

A systematic review of 52 studies covering 27 ingredients found most fail to raise total testosterone.²⁸ Vitamin D, Tribulus, D-aspartic acid and maca all came out unsupported.^28,29 Be especially careful with anything containing prohormones, which can suppress your own production.

Important information

This article is for general education and is not a substitute for professional medical advice, diagnosis, or treatment. Symptoms of low testosterone overlap with many other conditions, some of them serious, and diagnosis requires proper testing by a clinician. Guideline recommendations are summarized here in brief; the linked documents contain the full wording and the strength of each recommendation. Where findings come from animal studies, that is stated in the text. Probiotic effects are specific to the strain, the dose and the population studied, and evidence for one product does not transfer to another. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Sources

1. American Urological Association (2018; reviewed and validity confirmed 2024). Evaluation and management of testosterone deficiency: AUA guideline. Source
2. Bhasin, S., Brito, J. P., Cunningham, G. R., et al. (2018). Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism, 103(5), 1715–1744. Source
3. Wu, F. C., Tajar, A., Beynon, J. M., et al.; EMAS Group (2010). Identification of late-onset hypogonadism in middle-aged and elderly men. New England Journal of Medicine, 363(2), 123–135 — only three sexual symptoms had a syndromic association with low testosterone. Source
4. Araujo, A. B., Esche, G. R., Kupelian, V., et al. (2007). Prevalence of symptomatic androgen deficiency in men. Journal of Clinical Endocrinology & Metabolism, 92(11), 4241–4247 — 1,475 men aged 30–79; 5.6%. Source
5. Mulligan, T., Frick, M. F., Zuraw, Q. C., Stemhagen, A., & McWhirter, C. (2006). Prevalence of hypogonadism in males aged at least 45 years: the HIM study. International Journal of Clinical Practice, 60(7), 762–769 — 38.7% on a biochemical threshold alone. Source
6. Miner, M., Barkin, J., & Rosenberg, M. T. (2014). Testosterone deficiency: myth, facts, and controversy. Canadian Journal of Urology, 21(Suppl. 2), 39–54 — the source of the widely repeated "30%" figure, which it attributes to a 2004 narrative review rather than a prevalence study. Source
7. Harman, S. M., Metter, E. J., Tobin, J. D., Pearson, J., & Blackman, M. R. (2001). Longitudinal effects of aging on serum total and free testosterone levels in healthy men (Baltimore Longitudinal Study of Aging). Journal of Clinical Endocrinology & Metabolism, 86(2), 724–731. Source
8. Feldman, H. A., Longcope, C., Derby, C. A., et al. (2002). Age trends in the level of serum testosterone and other hormones in middle-aged men: longitudinal results from the Massachusetts Male Aging Study. Journal of Clinical Endocrinology & Metabolism, 87(2), 589–598. Source
9. Wu, F. C., Tajar, A., Pye, S. R., et al.; EMAS Group (2008). Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study. Journal of Clinical Endocrinology & Metabolism, 93(7), 2737–2745 — 3,200 men; the age-versus-obesity partition. Source
10. Tremellen, K., McPhee, N., Pearce, K., Benson, S., Schedlowski, M., & Engler, H. (2018). Endotoxin-initiated inflammation reduces testosterone production in men of reproductive age. American Journal of Physiology: Endocrinology and Metabolism, 314(3), E206–E213 — 75 men observational plus 33 men given intravenous endotoxin or placebo. Source
11. Tremellen, K. (2016). Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING) — a novel theory for the development of late onset hypogonadism in obese men. Basic and Clinical Andrology, 26, 7 — a hypothesis paper, described by its author as "a novel theory." Source
12. Matsushita, M., Fujita, K., Motooka, D., et al. (2022). Firmicutes in gut microbiota correlate with blood testosterone levels in elderly men. The World Journal of Men’s Health, 40(3), 517–525 — cross-sectional, n=54. Source
13. Camilleri, M. (2019). Leaky gut: mechanisms, measurement and clinical implications in humans. Gut, 68(8), 1516–1526. Source
14. Odenwald, M. A., & Turner, J. R. (2013). Intestinal permeability defects: is it time to treat? Clinical Gastroenterology and Hepatology, 11(9), 1075–1083. Source
15. Supajatura, V., Ushio, H., Nakao, A., et al. (2002). Differential responses of mast cell Toll-like receptors 2 and 4 in allergy and innate immunity. Journal of Clinical Investigation, 109(10), 1351–1359 — a mouse study; TLR2, not TLR4, triggers degranulation. Source
16. Rastelli, D., Robinson, A., Lagomarsino, V. N., et al. (2022). Diminished androgen levels are linked to irritable bowel syndrome and cause bowel dysfunction in mice. Journal of Clinical Investigation, 132(2), e150789 — human association, mouse causation. Source
17. Lagomarsino, V. N., Robinson, A., Mitchell, P. E., et al. (2026). Microbial reactivation of host androgens directs enteric neuronal regulation of gut motility. Nature Neuroscience, 29(8), 1791–1800 — mostly mouse work, with a human component in 506 males. Source
18. Poutahidis, T., Springer, A., Levkovich, T., et al. (2014). Probiotic microbes sustain youthful serum testosterone levels and testicular size in aging mice. PLOS ONE, 9(1), e84877 — an animal study. Source
19. Ljunggren, L., Butler, E., Axelsson, J., Åström, M., & Ohlsson, L. (2024). Effects of probiotic supplementation on testosterone levels in healthy ageing men: a 12-week double-blind, placebo-controlled randomized clinical trial. Contemporary Clinical Trials Communications, 39, 101300 — the same strain as the mouse study; no effect in men. Source
20. Zheng, Y., Zhang, Z., Tang, P., et al. (2023). Probiotics fortify intestinal barrier function: a systematic review and meta-analysis of randomized trials. Frontiers in Immunology, 14, 1143548 — 26 trials, 1,891 participants; validated permeability measures null; no certainty grading performed. Source
21. Scheffler, L., Crane, A., Heyne, H., et al. (2018). Widely used commercial ELISA does not detect precursor of haptoglobin2, but recognizes properdin as a potential second member of the zonulin family. Frontiers in Endocrinology, 9, 22. Source
22. Chaiyasut, C., Sivamaruthi, B. S., Lailerd, N., et al. (2022). Probiotics supplementation improves intestinal permeability, obesity index and metabolic biomarkers in elderly Thai subjects: a randomized controlled trial. Foods, 11(3), 268 — did not measure testosterone. Source
23. Corona, G., Rastrelli, G., Monami, M., et al. (2013). Body weight loss reverts obesity-associated hypogonadotropic hypogonadism: a systematic review and meta-analysis. European Journal of Endocrinology, 168(6), 829–843 — 24 studies. Source
24. Leproult, R., & Van Cauter, E. (2011). Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA, 305(21), 2173–2174 — n=10; daytime testosterone fell 10–15%. Source
25. Potter, N. J., Tomkinson, G. R., Dufner, T. J., et al. (2021). Effects of exercise training on resting testosterone concentrations in insufficiently active men: a systematic review and meta-analysis. Journal of Strength and Conditioning Research, 35(12), 3521–3528 — 11 RCTs, 421 men. Source
26. Moosazadeh, M., Heydari, K., Rasouli, K., et al. (2024). Association of the effect of alcohol consumption on LH, FSH, and testosterone hormones in men: a systematic review and meta-analysis. International Journal of Preventive Medicine, 15, 75. Source
27. Cignarelli, A., Castellana, M., Castellana, G., et al. (2019). Effects of CPAP on testosterone levels in patients with obstructive sleep apnea: a meta-analysis study. Frontiers in Endocrinology, 10, 551 — 12 studies, 388 patients; no significant change. Source
28. Morgado, A., Tsampoukas, G., Sokolakis, I., Schoentgen, N., Urkmez, A., & Sarikaya, S. (2024). Do "testosterone boosters" really increase serum total testosterone? A systematic review. International Journal of Impotence Research, 36(4), 348–364 — 52 studies, 27 proposed ingredients. Source
29. Hosseini Marnani, E., Mollahosseini, M., Gheflati, A., Ghadiri-Anari, A., & Nadjarzadeh, A. (2019). The effect of vitamin D supplementation on the androgenic profile in men: a systematic review and meta-analysis of clinical trials. Andrologia, 51(9), e13343. Source
30. Lincoff, A. M., Bhasin, S., Flevaris, P., et al.; TRAVERSE Study Investigators (2023). Cardiovascular safety of testosterone-replacement therapy. New England Journal of Medicine, 389(2), 107–117 — 5,246 men. Source

The original version of this article also linked to a Healthline consumer page on the causes of low testosterone, and cited the 2016 GELDING theory paper twice under two different URLs. The duplicate has been consolidated at reference 11, and the consumer page has been replaced by the primary sources above.