When talking about daily life, it’s hard to avoid the topic of intimate relationships; when discussing anti-aging, reproductive aging is equally unavoidable.
Last year, we covered Sinclair’s research, which turned the urban legend of "NMN boosting ovarian function and rejuvenating menopausal women" into a formal academic report.
But what about its effects on men?
To be honest, our assistant has received many positive feedbacks from male readers about "regaining sexual vitality"...
Among these readers are those who love life and advocate for science. They are curious about the mechanisms behind this phenomenon and hope we can provide a satisfying explanation.
Reader Question: "I heard taking NMN can improve sexual function—Is this true?"
Regrettably, there are currently no experimental studies specifically addressing this question (and unfortunately, we haven’t saved enough to build our own laboratory yet). We can only analyze it based on existing evidence and reasonable inferences:
01 Peering Into the Biological Secrets Behind "Sustained Erectile Function"
The primary manifestation of male sexual arousal and maintenance is penile erection[1]. Like all life activities, penile erection is regulated by both the nervous system (mental stimulation) and humoral factors (hormones)[2].
During intimate interactions with a partner, sensory stimulation, mechanical stimulation, and hormonal fluctuations work together. The parasympathetic nervous system instructs endothelial cells of the penile arteries to secrete nitric oxide (a vasodilator). This causes the corpus cavernosum to fill with blood; the swollen corpus cavernosum then compresses veins, trapping blood inside to maintain an erection[3].
Figure Note (translated by TIMEPIE): Anatomical basis of penile erection. (Source: OpenStax College - Anatomy & Physiology)
- Flaccid State: Penile venules, deep dorsal vein of the penis, corpus cavernosum, urethra, penile foreskin, corpus spongiosum.
-
Erectile Process:
① Corpus cavernosum arteries dilate, filling the corpus cavernosum with blood;
② Blood filling causes the corpus cavernosum to swell, leading to penile erection;
③ To maintain erection: The swollen corpus cavernosum compresses penile veins, preventing blood reflux.
Psychological factors play a significant role in inducing and maintaining erections. Negative emotions such as excessive excitement, tension, anxiety, depression, shock, or fear can easily lead to "failure"[4].
Joke Reference: "I was so scared I went soft."
Therefore, the best way to distinguish whether "erectile difficulty" stems from psychological or physical factors is to observe nocturnal erections ("morning wood")[5]:
During the REM (rapid eye movement) sleep phase, the locus coeruleus (the sympathetic nerve center) cannot be activated, losing its inhibitory effect on penile erections. Erections occurring at this time are entirely controlled by involuntary physiological processes[6].
During the REM (rapid eye movement) sleep phase, the locus coeruleus (the sympathetic nerve center) cannot be activated, losing its inhibitory effect on penile erections. Erections occurring at this time are entirely controlled by involuntary physiological processes[6].
Physiologically healthy men (except those with severe depression and physical disorders) experience 3–4 involuntary erections per night[7].

Figure Note: Stamp Test—Wrap a paper strip around the penis. If a nocturnal erection occurs, the strip will break the next day.
02 Investigating How the "Anti-Aging Supplement" Restores Male Sexual Vitality
On one hand, most vascular diseases—such as cardiovascular disease and diabetes—can cause erectile dysfunction (ED)[8]. NMN can help improve these conditions by increasing NAD+ levels[9], allowing some patients to regain a satisfying sex life.
On the other hand, in healthy men, the most important physiological factor affecting penile erection is testosterone levels[10].
Testosterone is crucial for maintaining nitric oxide synthase levels in the penis; testosterone deficiency directly triggers sexual dysfunction[11]. As age increases, testosterone levels decline, which is closely associated with a higher incidence of ED[12].
How Does NMN Affect Testosterone Levels to Restore Male Sexual Vitality? Possible Mechanisms Include:
1. Increasing DHEA Levels
Dehydroepiandrosterone (DHEA) is a precursor for synthesizing testosterone and estrone, and is also linked to various anti-aging benefits[13].
The famous "rhesus monkey experiment" in anti-aging research confirmed that calorie restriction (CR) can increase DHEA levels[14]; NMN shares many overlapping mechanisms with CR[15], suggesting it may also boost DHEA. However, no current studies confirm that NAD+ supplementation directly increases DHEA levels.
2. Promoting Testosterone Biosynthesis
Testosterone is biosynthesized from cholesterol, a process requiring multiple dehydrogenases and lyases—all of which use NAD+ or NADPH (derived from NAD+[16]) as coenzymes[17,18].

Figure Note (translated by TIMEPIE): Pathway of human steroid hormone synthesis. (Source: WikiJournal of Medicine)
Even for the same enzyme, there are multiple isoforms that perform different functions and are distributed in different organs/tissues[19]. This explains why NAD+ supplementation can promote "testosterone enhancement" in men and "ovarian maintenance" in women—two distinct effects.
03 Examining Why NMN "Fails" for Some Users
While most readers report improved sexual vitality, a small number have 反馈 ed the opposite: "I used to function well, but after taking NMN, I struggle."
After ruling out psychological factors, vascular diseases, and drowsiness (a common side effect in the first few weeks of NMN use due to circadian rhythm adjustments), if "erectile difficulty" persists, pay attention to the following factors:
Do You Exercise Regularly or Take Fitness Supplements?
Regular exercise can increase DHEA levels in both men and women[20], promoting a more youthful state; resistance training targeting large muscle groups is especially effective at boosting testosterone[21], enhancing male erectile duration and firmness.

Figure Note: As the body’s largest muscle group, training the legs may indeed "strengthen men"—this is not an unfounded claim.
However, more testosterone is not always better—"Excess leads to decline." Testosterone must bind to a limited number of androgen receptors (AR) to exert its physiological effects; free testosterone that cannot bind to receptors is converted into estradiol by aromatase[22]. Estradiol has a significant negative impact on male sexual activity[10].
If you are a well-trained bodybuilder, the combined testosterone increase from resistance exercise and NAD+ supplementation (via NMN) may exceed the capacity of your androgen receptors.
Solution: Adjust the ratio of resistance training ("weightlifting") to endurance exercise ("aerobics"). Endurance exercise can moderately lower testosterone levels[23], helping you find the optimal balance for both longevity and sexual vitality.
Taking fitness supplements adds complexity:
Studies confirm that in middle-aged and elderly men, additional protein intake (e.g., protein powder) after resistance training can counteract the testosterone-boosting effect of the exercise[24].
Studies confirm that in middle-aged and elderly men, additional protein intake (e.g., protein powder) after resistance training can counteract the testosterone-boosting effect of the exercise[24].

Injecting exogenous testosterone to aid fitness is far more problematic: Improper exogenous testosterone supplementation can easily cause feminization (e.g., gynecomastia), negatively feedback to the pituitary gland, reduce endogenous testosterone production, and in severe cases, lead to infertility[25].

Figure Note: Male breast feminization caused by anabolic steroid abuse (left: before plastic surgery; right: after surgery).
Current academic consensus holds that testosterone has "different effects on internal desire vs. external function" in men: Exogenous testosterone enhances libido but fails to improve physical (organic) function[10]. This leaves users with "desire outpacing physical capability"—a real-life example of "the contradiction between people’s longing for a better life and insufficient material conditions."
If you take fitness supplements, consider pausing them to observe improvements.
Do You Have Excess Body Fat?
Fat cells synthesize large amounts of aromatase, which promotes the conversion of NMN-boosted testosterone into estradiol. Losing weight can increase testosterone levels and improve sexual function[26].
Are You Deficient in Other Nutrients?
Besides NAD+, nutrients like vitamin A, vitamin D, and zinc[27–29] are also crucial for testosterone synthesis. Zinc even inhibits aromatase[30]; deficiency in any of these nutrients can become a "bottleneck" for testosterone levels, causing low libido and sexual dysfunction.
You can supplement these nutrients while taking NMN; if your condition improves, it indicates you may have had a deficiency.
Hormonal regulation is an extremely complex biological process. Beyond the above factors, it is also affected by genetic heterogeneity, environmental factors (e.g., plasticizers), special physical conditions, and even gut microbiota[31].
If you have ruled out the above factors but still experience persistent "erectile difficulty" after taking NMN, we recommend undergoing a blood sex hormone test to further analyze the specific cause.
References (Swipe to View)
[1] Cunningham GR, Rosen RC. Overview of male sexual dysfunction. In: UpToDate, Martin KA (Ed), UpToDate, Waltham, MA, 2018.
[2] Rosen, R.C., & Beck, J. G. Patterns of sexual arousal: Psychophysiological processes and clinical application, New York: Guilford Press.
[3] Drake, Richard, Wayne Vogl and Adam Mitchell, Grey's Anatomy for Students. Philadelphia, 2004.
[4] Krane RJ, Goldstein I, Saenz de Tejada I. Impotence. N Engl J Med 1989; 321:1648.
[5] Schmidt, Markus H; Schmidt, Helmut S (2004). Sleep-related erections: Neural mechanisms and clinical significance. Current Neurology and Neuroscience Reports. 4 (2): 170–178.
[6] Karacan I, Williams RL, Thornby JI, Salis PJ. Sleep-related penile tumescence as a function of age. Am J Psychiatry 1975; 132:932.
[7] Thase, Michael E.et al. (1988). Nocturnal penile tumescence is diminished in depressed men. Biological Psychiatry. 24 (1): 33–46.
[8] Sullivan ME, Keoghane SR, Miller MA. Vascular risk factors and erectile dysfunction. BJU Int 2001; 87:838.
[9] Xie, N., Zhang, L., Gao, W. et al. NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential. Sig Transduct Target Ther 5, 227 (2020).
[10] Bancroft, J (2005). The endocrinology of sexual arousal. Journal of Endocrinology. 186 (3): 411–427.
[11] Mills TM, Wiedmeier VT, Stopper VS. Androgen maintenance of erectile function in the rat penis. Biol Reprod 1992; 46:342.
[12] McVary KT. Clinical practice. Erectile dysfunction. N Engl J Med 2007; 357:2472.
[13] Cupp MJ, Tracy TS. Dietary Supplements: Toxicology and Clinical Pharmacology. Springer Science & Business Media. pp. 135–.
[14] Mattison JA, Lane MA, Roth GS, Ingram DK (2003). Calorie restriction in rhesus monkeys. Experimental Gerontology. 38 (1–2): 35–46.
[15] Lin, S.J., P.A. Defossez, and L. Guarente (2000). Requirement of NAD and SIR2 for life-span extension by calorie restriction in Saccharomyces cerevisiae. Science. 289 (5487): 2126–8.
[16] Kawai S, Murata K (2008). Structure and function of NAD kinase and NADP phosphatase: key enzymes that regulate the intracellular balance of NAD(H) and NADP(H). Bioscience, Biotechnology, and Biochemistry. 72 (4): 919–30.
[17] Lachance Y, Luu-The V, et al (1992). Characterization of human 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4-isomerase gene and its expression in mammalian cells. J. Biol. Chem. 267 (5): 3551.
[18] Moeller G, Adamski J (2009). Integrated view on 17beta-hydroxysteroid dehydrogenases. Mol. Cell. Endocrinol. 301 (1-2): 7-19.
[19] Mindnich R, Möller G, Adamski J (2004). "The role of 17 beta-hydroxysteroid dehydrogenases". Mol. Cell. Endocrinol. 218 (1–2): 7–20.
[20] Filaire E, Duché P, Lac G (1998). Effects of amount of training on the saliva concentrations of cortisol, dehydroepiandrosterone and on the dehydroepiandrosterone: cortisol concentration ratio in women over 16 weeks of training. European Journal of Applied Physiology and Occupational Physiology. 78 (5): 466–71.
[21] Vingren JL, Kraemer WJ, Ratamess NA, Anderson JM, Volek JS, Maresh CM (2010). Testosterone physiology in resistance exercise and training: the up-stream regulatory elements. Sports Medicine. 40 (12): 1037–53.
[22] Mooradian AD, Morley JE, Korenman SG (1987). Biological actions of androgens. Endocrine Reviews. 8 (1): 1–28.
[23] Hackney AC, Moore AW, Brownlee KK (2005). Testosterone and endurance exercise: development of the exercise-hypogonadal male condition. Acta Physiologica Hungarica. 92 (2): 121–37.
[24] Hulmi JJ, Ahtiainen JP, Selänne H, Volek JS, Häkkinen K, Kovanen V, Mero AA (2008). Androgen receptors and testosterone in men-effects of protein ingestion, resistance exercise and fiber type. The Journal of Steroid Biochemistry and Molecular Biology. 110 (1–2): 130–37.
[25] World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia and oligozoospermia in normal men. Fertil Steril 1996; 65:821.
[26] Håkonsen LB, et al (2011). Does weight loss improve semen quality and reproductive hormones? Results from a cohort of severely obese men. Reproductive Health. 8 (1): 24.
[27] Livera G, Rouiller-Fabre V, Pairault C, Levacher C, Habert R (2002). Regulation and perturbation of testicular functions by vitamin A. Reproduction. 124 (2): 173–80.
[28] Pilz S, Frisch S, Koertke H, Kuhn J, Dreier J, Obermayer-Pietsch B, Wehr E, Zittermann A (2011). Effect of vitamin D supplementation on testosterone levels in men. Hormones et Métabolisme. 43 (3): 223–25.
[29] Prasad AS, Mantzoros CS, Beck FW, Hess JW, Brewer GJ (1996). Zinc status and serum testosterone levels of healthy adults. Nutrition. 12 (5): 344–48.
[30] Om AS, Chung KW (1996). Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver. The Journal of Nutrition. 126 (4): 842–8.
[31] Fernanda Pace, Paula I. Watnick. The Interplay of Sex Steroids, the Immune Response, and the Intestinal Microbiota. Trends in Microbiology, 2020.
[2] Rosen, R.C., & Beck, J. G. Patterns of sexual arousal: Psychophysiological processes and clinical application, New York: Guilford Press.
[3] Drake, Richard, Wayne Vogl and Adam Mitchell, Grey's Anatomy for Students. Philadelphia, 2004.
[4] Krane RJ, Goldstein I, Saenz de Tejada I. Impotence. N Engl J Med 1989; 321:1648.
[5] Schmidt, Markus H; Schmidt, Helmut S (2004). Sleep-related erections: Neural mechanisms and clinical significance. Current Neurology and Neuroscience Reports. 4 (2): 170–178.
[6] Karacan I, Williams RL, Thornby JI, Salis PJ. Sleep-related penile tumescence as a function of age. Am J Psychiatry 1975; 132:932.
[7] Thase, Michael E.et al. (1988). Nocturnal penile tumescence is diminished in depressed men. Biological Psychiatry. 24 (1): 33–46.
[8] Sullivan ME, Keoghane SR, Miller MA. Vascular risk factors and erectile dysfunction. BJU Int 2001; 87:838.
[9] Xie, N., Zhang, L., Gao, W. et al. NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential. Sig Transduct Target Ther 5, 227 (2020).
[10] Bancroft, J (2005). The endocrinology of sexual arousal. Journal of Endocrinology. 186 (3): 411–427.
[11] Mills TM, Wiedmeier VT, Stopper VS. Androgen maintenance of erectile function in the rat penis. Biol Reprod 1992; 46:342.
[12] McVary KT. Clinical practice. Erectile dysfunction. N Engl J Med 2007; 357:2472.
[13] Cupp MJ, Tracy TS. Dietary Supplements: Toxicology and Clinical Pharmacology. Springer Science & Business Media. pp. 135–.
[14] Mattison JA, Lane MA, Roth GS, Ingram DK (2003). Calorie restriction in rhesus monkeys. Experimental Gerontology. 38 (1–2): 35–46.
[15] Lin, S.J., P.A. Defossez, and L. Guarente (2000). Requirement of NAD and SIR2 for life-span extension by calorie restriction in Saccharomyces cerevisiae. Science. 289 (5487): 2126–8.
[16] Kawai S, Murata K (2008). Structure and function of NAD kinase and NADP phosphatase: key enzymes that regulate the intracellular balance of NAD(H) and NADP(H). Bioscience, Biotechnology, and Biochemistry. 72 (4): 919–30.
[17] Lachance Y, Luu-The V, et al (1992). Characterization of human 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4-isomerase gene and its expression in mammalian cells. J. Biol. Chem. 267 (5): 3551.
[18] Moeller G, Adamski J (2009). Integrated view on 17beta-hydroxysteroid dehydrogenases. Mol. Cell. Endocrinol. 301 (1-2): 7-19.
[19] Mindnich R, Möller G, Adamski J (2004). "The role of 17 beta-hydroxysteroid dehydrogenases". Mol. Cell. Endocrinol. 218 (1–2): 7–20.
[20] Filaire E, Duché P, Lac G (1998). Effects of amount of training on the saliva concentrations of cortisol, dehydroepiandrosterone and on the dehydroepiandrosterone: cortisol concentration ratio in women over 16 weeks of training. European Journal of Applied Physiology and Occupational Physiology. 78 (5): 466–71.
[21] Vingren JL, Kraemer WJ, Ratamess NA, Anderson JM, Volek JS, Maresh CM (2010). Testosterone physiology in resistance exercise and training: the up-stream regulatory elements. Sports Medicine. 40 (12): 1037–53.
[22] Mooradian AD, Morley JE, Korenman SG (1987). Biological actions of androgens. Endocrine Reviews. 8 (1): 1–28.
[23] Hackney AC, Moore AW, Brownlee KK (2005). Testosterone and endurance exercise: development of the exercise-hypogonadal male condition. Acta Physiologica Hungarica. 92 (2): 121–37.
[24] Hulmi JJ, Ahtiainen JP, Selänne H, Volek JS, Häkkinen K, Kovanen V, Mero AA (2008). Androgen receptors and testosterone in men-effects of protein ingestion, resistance exercise and fiber type. The Journal of Steroid Biochemistry and Molecular Biology. 110 (1–2): 130–37.
[25] World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia and oligozoospermia in normal men. Fertil Steril 1996; 65:821.
[26] Håkonsen LB, et al (2011). Does weight loss improve semen quality and reproductive hormones? Results from a cohort of severely obese men. Reproductive Health. 8 (1): 24.
[27] Livera G, Rouiller-Fabre V, Pairault C, Levacher C, Habert R (2002). Regulation and perturbation of testicular functions by vitamin A. Reproduction. 124 (2): 173–80.
[28] Pilz S, Frisch S, Koertke H, Kuhn J, Dreier J, Obermayer-Pietsch B, Wehr E, Zittermann A (2011). Effect of vitamin D supplementation on testosterone levels in men. Hormones et Métabolisme. 43 (3): 223–25.
[29] Prasad AS, Mantzoros CS, Beck FW, Hess JW, Brewer GJ (1996). Zinc status and serum testosterone levels of healthy adults. Nutrition. 12 (5): 344–48.
[30] Om AS, Chung KW (1996). Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver. The Journal of Nutrition. 126 (4): 842–8.
[31] Fernanda Pace, Paula I. Watnick. The Interplay of Sex Steroids, the Immune Response, and the Intestinal Microbiota. Trends in Microbiology, 2020.