Erectile dysfunction (ED) is the inability to get or keep an erection firm enough for sex. In Ray Peat's framework it's often metabolic dysfunction rather than a standalone problem: erection depends on nitric oxide-driven vasodilation, which depends on cellular energy production, so anything that impairs metabolism tends to impair erections along with everything else.

Metabolic drivers

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Improving metabolic health enhances erection quality. Insulin resistance drives greater vasoconstriction (less nitric oxide production), higher stress hormones (raising blood pressure, reducing peripheral blood flow), and increased inflammation (worsening testosterone and dopamine). Giving men an insulin-sensitizing regimen led to better erections.[1] Endotoxin also lowers testosterone directly: a single endotoxin injection in mice significantly reduced serum testosterone within 2 hours, via testicular macrophages producing reactive oxygen species that disrupt Leydig cell mitochondria and inhibit steroidogenic proteins (StAR, 3beta-HSD).[2]

SSRIs

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In a prospective study of 1,022 outpatients with previously normal sexual function, overall sexual dysfunction incidence on antidepressants was 59% (604/1,022), including erectile dysfunction or decreased lubrication in 31%; incidence varied by drug from 58% (fluoxetine) up to 71-73% (paroxetine, citalopram).[3] See SSRIs for the full breakdown and PSSD (Post-SSRI Sexual Dysfunction) persistence data.

Mechanistically, SSRIs raise synaptic serotonin, which has a net inhibitory effect on sexual response: postsynaptic 5-HT2 (especially 5-HT2C) activation delays or blocks orgasm and can reduce desire, elevated serotonin tone inhibits dopamine release in mesolimbic and hypothalamic circuits that normally drive desire and arousal, and paroxetine specifically inhibits nitric oxide synthase, directly impairing the vasodilation an erection requires.

The rise in young men

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ED in men under 40 was rare before the mid-2000s. A 1999 study found ED in 5% of sexually active men aged 18-59, and a 2002 meta-analysis put the rate at 2% specifically in men under 40. A 2016 review found more recent reports putting ED prevalence in young men at 20-30%, a roughly tenfold increase, gathered after "porn tube" sites (offering unlimited free streaming video, unlike the static images and paid content that came before) proliferated starting in September 2006.[4] The review's authors propose habituation, tolerance, and altered reward-circuit sensitivity from a supply of novel sexual stimuli unlike anything available to earlier generations, not a hormonal mechanism.

This doesn't run through prolactin or acute hormone disruption from the sexual activity itself: Ray Peat, asked directly whether masturbation raises prolactin more than partnered sex, said he didn't think it did.[5] That points toward a learned, dopaminergic/reward-circuit habituation mechanism specific to the pattern of consumption (novelty, escalation, video) rather than a direct hormonal toxicity from orgasm or masturbation itself. See Pornography for that mechanism in more depth.

[Does masturbation or sex have positive or negative effects on the hormones or stress?] Generally positive, but intense arousal can have unwanted consequences, such as herpes virus outbreaks. [Masturbation: effect on prolactin] I don't think masturbation affects the hormones more than regular sex does.

— Ray Peat[6]

Gut microbiota

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Gut composition tracks with ED independent of the endotoxin mechanism above. Thirty ED patients showed significantly lower gut bacterial diversity than 30 healthy controls, with the genus Alloprevotella found only in the healthy group.[7] A larger Mendelian randomization study (using genetic variation to test causality, not just correlation) found six bacterial taxa causally linked to ED risk: family Lachnospiraceae and its subgroup Lachnospiraceae NC2004, plus genera Oscillibacter, Senegalimassilia, and Tyzzerella 3 all increased risk, while genus Ruminococcaceae UCG013 was protective.[8] This overlaps with SIBO and chronic bacterial prostatitis as a shared mechanism behind both ED and premature ejaculation; see Premature ejaculation for the prostatitis-specific literature.

Practice

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Address the metabolic basics first (insulin sensitivity, thyroid, endotoxin/gut health) rather than treating ED as an isolated plumbing problem. For the subset of cases tied to pornography use specifically, see Pornography for the reward-circuit mechanism and what the treatment-seeking literature shows. For cases tied to gut dysbiosis or SIBO/prostatitis, see Premature ejaculation and SIBO.

See also

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References

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  1. ↑ @Outdoctrination on X
  2. ↑ @lowmegatron on X
  3. ↑ Montejo AL, Llorca G, Izquierdo JA, Rico-Villademoros F. "Incidence of sexual dysfunction associated with antidepressant agents: a prospective multicenter study of 1022 outpatients," J Clin Psychiatry. 2001;62 Suppl 3:10-21. PMID 11229449.
  4. ↑ Park BY, Wilson G, Berger J, Christman M, Reina B, Bishop F, Klam WP, Doan AP. "Is Internet Pornography Causing Sexual Dysfunctions? A Review with Clinical Reports," Behav Sci (Basel). 2016;6(3):17. PMID 27527226.
  5. ↑ Ray Peat, email correspondence, "Sex & Masturbation," raypeatemails.com, https://raypeatemails.com/Topics/Sex+%26+Masturbation
  6. ↑ Ray Peat, email correspondence, "Sex & Masturbation," raypeatemails.com
  7. ↑ Geng Q, Chen S, Sun Y, et al. "Correlation between gut microbiota diversity and psychogenic erectile dysfunction," Transl Androl Urol. 2021;10(12):4412-4421.
  8. ↑ Zhu T, Liu X, Yang P, et al. "The Association between the Gut Microbiota and Erectile Dysfunction," World J Mens Health. 2024;42(4):772-786.