NMN and Testosterone: Does NAD+ Affect Male Hormones?

Interest in NMN and testosterone has grown as men look for ways to support energy, body composition, and hormonal health with age. The connection is not direct: NMN raises NAD+, a coenzyme central to cellular metabolism, and researchers are now asking whether restoring NAD+ can influence the hormonal environment that supports testosterone production. The evidence is early, mostly indirect, and worth examining carefully before drawing conclusions.

What the Research Actually Shows

There are currently no large randomized controlled trials (RCTs) testing whether NMN supplementation raises testosterone in men. The human data we have focuses on NAD+ metabolism, muscle function, and metabolic markers rather than direct hormonal endpoints. This is an important limitation to state upfront.

Igarashi et al. (2022) conducted a randomized trial in healthy older men (65 years and older) using 250 mg per day of NMN for 12 weeks. The study measured blood NAD+ levels, gait speed, and grip strength. NAD+ rose significantly, and muscle function improved in the NMN group compared to placebo. However, testosterone and other sex hormones were not reported as outcomes. The study tells us NMN can restore NAD+ and benefit muscle in aging men, but it does not tell us whether testosterone changed.

Irie et al. (2020) ran an open-label study in healthy Japanese men, testing doses from 100 to 500 mg per day of NMN over a single day and then over 5 weeks. They tracked clinical safety parameters and nicotinamide metabolite levels. Again, testosterone was not a measured endpoint. The study confirmed NMN is well tolerated and raises NAD+ metabolites in serum, but it offers no direct evidence for a hormonal effect.

Yoshino et al. (2021) studied NMN in prediabetic women, not men, so the data are not directly applicable to male testosterone biology. Liao et al. (2021) tested NMN in amateur runners for aerobic capacity, and Niu et al. (2023) examined telomere length and gut microbiota in a pre-aging cohort. None of these trials measured testosterone. The gap is real: the existing human NMN literature is broad in metabolic outcomes but narrow in endocrine endpoints.

Study	Population	Dose & Duration	Testosterone Measured?	Key Outcome
Igarashi et al. (2022)	Healthy older men (65+)	250 mg/day, 12 weeks	No	Increased NAD+, improved gait speed and grip strength
Irie et al. (2020)	Healthy Japanese men	100–500 mg/day, 5 weeks	No	Elevated serum NMN metabolites; well tolerated
Yoshino et al. (2021)	Prediabetic women	250 mg/day, 10 weeks	No	Improved muscle insulin sensitivity
Liao et al. (2021)	Amateur runners	300–1200 mg/day, 6 weeks	No	Enhanced aerobic capacity (VO2-related)
Niu et al. (2023)	Pre-aging adults	300 mg/day, 8 weeks	No	Changes in serum metabolism and telomere length

Because no human NMN trial has measured testosterone, any claim that NMN directly raises testosterone is unsupported. What we can discuss is the mechanistic rationale and indirect evidence from related fields.

How NAD+ Might Connect to Testosterone Biology

Testosterone synthesis in the Leydig cells of the testes is an energy-intensive process. It requires cholesterol transport, mitochondrial steroidogenesis, and enzymatic cascades that depend on redox balance. NAD+ is the central electron carrier in these reactions. Without adequate NAD+, the efficiency of mitochondrial respiration drops, and cells may enter a state of functional hypoxia even when oxygen is present.

Gomes et al. (2013) demonstrated that declining NAD+ during aging disrupts nuclear-mitochondrial communication, creating what they termed a "pseudohypoxic state." In this condition, the cell behaves as if it is oxygen-deprived because the NAD+/NADH ratio has shifted, altering the activity of sirtuins and hypoxia-inducible factors. For steroidogenic tissues like the Leydig cells, this could theoretically reduce the capacity to produce testosterone, though this specific tissue has not been studied in that paper.

Sirtuins, particularly SIRT1 and SIRT3, are NAD+-dependent deacetylases that regulate mitochondrial biogenesis, oxidative stress, and inflammation. In animal models, sirtuin activation in the testes has been associated with preserved steroidogenic enzyme activity and reduced oxidative damage. However, human data is limited. Whether raising NAD+ via NMN translates into measurable sirtuin-mediated protection of testosterone production in men remains an open question.

Another indirect link is metabolic health. Low testosterone is associated with insulin resistance, visceral adiposity, and chronic inflammation. Yoshino et al. (2021) showed that NMN improves muscle insulin sensitivity in prediabetic women. If NMN improves metabolic health in men, it could theoretically support a hormonal environment more conducive to healthy testosterone levels, but this is speculative and not a direct pharmacological effect.

What the Evidence Does Not Show

It is important to separate what is plausible from what is proven. No human study has reported that NMN increases serum total testosterone, free testosterone, or luteinizing hormone. No study has examined NMN in men with documented low testosterone (hypogonadism). No dose-response data exists for hormonal outcomes. The entire connection between NMN and testosterone rests on mechanistic inference and preclinical models, not clinical demonstration.

Preclinical studies in rodents have shown that NAD+ precursors can influence spermatogenesis and Leydig cell markers, but rodent steroidogenesis differs substantially from human physiology. Translating those findings to men requires caution. The absence of direct evidence does not mean NMN is ineffective; it means we do not know.

Supplement marketers sometimes cite NAD+ restoration as a proxy for hormonal rejuvenation. This is misleading. NAD+ supports cellular metabolism broadly. It is not a testosterone booster in the way that clomiphene or hCG act on the hypothalamic-pituitary-gonadal axis. NMN does not stimulate luteinizing hormone release, block estrogen feedback, or directly activate steroidogenic acute regulatory protein (StAR). Any effect on testosterone, if it exists, would be indirect and likely modest.

Who Benefits Most

Men most likely to see meaningful effects from NMN are those with age-related NAD+ decline and associated metabolic or functional impairment. Igarashi et al. (2022) found that older men (mean age in the 70s) showed improved muscle function with NMN supplementation. This population is also the one most likely to experience declining testosterone, though the trial did not measure it. The overlap suggests that NMN may be a useful adjunct for aging men focused on energy and physical performance, not as a testosterone replacement but as a metabolic support strategy.

Younger men with normal NAD+ and testosterone levels are less likely to benefit from NMN in terms of hormonal output. Irie et al. (2020) studied healthy men across a wide age range and found metabolite changes but no dramatic clinical shifts in the short term. For athletes, Liao et al. (2021) showed aerobic benefits, yet again with no hormonal data. If your primary goal is to raise testosterone, NMN is not the right tool based on current evidence. If your goal is to support cellular energy and recovery as you age, the rationale is stronger.

Men considering NMN alongside testosterone testing should track baseline and follow-up labs if they hope to observe any personal correlation. Individual variation in NAD+ metabolism, absorption, and baseline status means responses will differ. This is why standardized trial data matters more than anecdotal reports.

When selecting a product, dose and form matter. Most human trials used 250–500 mg per day, with some athletic studies going higher. Bio:sudo NMN 1000mg provides a dose at the upper end of the studied range, which may appeal to men who want to align their intake with the higher doses used in exercise research. The 1000 mg dose is split across servings in most regimens, and the capsule form offers consistent absorption compared to sublingual powders with unverified bioavailability claims.

Practical Takeaways

• No human trial has directly tested whether NMN raises testosterone; the link is mechanistic and indirect.
• NMN reliably increases blood NAD+ levels and improves muscle function in older adults, based on Igarashi et al. (2022).
• The pseudohypoxic state caused by NAD+ decline may impair energy-intensive tissues, including steroidogenic cells, but human Leydig cell data is absent.
• Men with age-related metabolic decline and low energy are the most plausible beneficiaries, not young men seeking hormonal enhancement.
• If you track testosterone, do not expect NMN to act like a direct androgenic intervention; it is a metabolic cofactor, not a hormone analog.
• Choose doses with human evidence behind them. Products supplying 250–1000 mg per day fit the studied range, though higher doses do not guarantee better hormonal outcomes.

Bottom Line

The question of whether NMN and testosterone are meaningfully linked in humans remains unanswered. NMN restores NAD+, supports muscle function, and may improve metabolic health in aging men, but no clinical study has shown it directly increases testosterone. The mechanism is biologically plausible, yet plausible is not the same as proven. For now, NMN is best viewed as a cellular energy support tool, not a hormonal therapy. If you are concerned about testosterone, test your levels, address sleep, body composition, and training first, and consider NMN as an adjunct with realistic expectations.

References

1. Yoshino M, et al. "Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women." Science. 2021;372(6547):1224–1229. [Source]
2. Igarashi M, et al. "Chronic nicotinamide mononucleotide supplementation elevates blood nicotinamide adenine dinucleotide levels and alters muscle function in healthy older men." npj Aging. 2022;8(1):5. [Source]
3. Irie J, et al. "Effect of oral administration of nicotinamide mononucleotide on clinical parameters and nicotinamide metabolite levels in healthy Japanese men." Endocrine Journal. 2020;67(2):153–160. [Source]
4. Liao B, et al. "Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners: a randomized, double-blind study." Journal of the International Society of Sports Nutrition. 2021;18(1):54. [Source]
5. Gomes AP, et al. "Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging." Cell. 2013;155(7):1624–1638. [Source]
6. Niu KM, et al. "The impacts of short-term NMN supplementation on serum metabolism, fecal microbiota, and telomere length in pre-aging phase." Nutrients. 2023;15(3):755. [Source]

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