Sex
Sex is, in Ray Peat's framework, a direct expression of the same metabolic energy that drives growth and creativity generally: desire, orgasm, and pair bonding run on the same hormonal signals as health elsewhere in the body, not a separate domain with its own rules.
Sex as a driving and creative force
[edit]Sexual desire is one expression of a more general biological principle: an organism with abundant metabolic energy directs that surplus outward, into complexity, exploration, and connection with another organism, rather than holding it in reserve. Testosterone stimulates sexual desire in both sexes, and functions as one of the clearest hormonal signals of that outward-directed energy state.[1] On the Creativity page, the same principle is described as extending directly into pair formation: sustained pairing between two people is treated as the clearest biological example of that creative energy projecting itself into the future, rather than as a social obligation layered on top of biology.[2]
Wilhelm Reich made a version of the same claim central to his entire theory of health, under the name "sex-economy": the body's capacity to build up and then fully discharge sexual tension (what he called orgastic potency) was, for Reich, the central regulator of the organism's whole energy economy, with blocked or incomplete discharge diverting that energy into neurosis and physical illness instead.[3] Where Peat's framework starts from metabolic energy driving sexual behavior outward, Reich's starts from sexual discharge as the thing that keeps the rest of the energy economy in balance; the two describe the same coupling between sex and total body energy from opposite ends.
Libido
[edit]Libido is sexual desire. It depends on hormones, energy, relationship context, medications, and health.
Low thyroid, high stress hormones, SSRIs, and under-eating commonly suppress desire. Fixing metabolism and sleep helps more than exotic aphrodisiac stacks for many people.
See also: Testosterone, Estrogen, Prolactin, Depression.
Pair bonding
[edit]The social institution of lifelong sexual exclusivity is a cultural artifact rather than a biological necessity:
I think it's based on the property mentality.
— Ray Peat[4]
He extended the same analysis to sexual relationships generally, tying restrictive norms to artificial scarcity rather than to organismic need:
Our society is committed to creating artificial scarcity to maintain authoritarian relationships everywhere, especially sexual, interpersonal, reproductive relations. The basic sense of reality tends toward coherence, so one's sense of dutiful conforming affects the sense of erotic sensuality. The organism's well being is limited by all of the anti-empathic, exploitative institutions we interact with.
— Ray Peat[5]
This does not make the sexual pair itself an arbitrary or dispensable unit. Falling in love is a distinct physiological stage, the "Effect of Person," a shift toward parasympathetic dominance in which two people's perspectives on the world begin to merge into one, a process that continues, rather than starts, in the events that follow orgasm.[6] A stable pair bond, on this view, is what sustained mutual affirmation between two people builds over time, distinct from monogamy as an imposed social rule.
T3Uncoupled frames the ongoing bond in similar terms: two people who stay in a state of shared perceptual novelty, noticing and acting on the unexpected together rather than settling into routine, resist the stagnation that erodes a bond. One pattern offered in support: hypothyroid couples who pair up and then have one partner's thyroid normalized will often divorce, as if the shared low-energy state, not the relationship itself, had been holding them together.
Thyroid and progesterone can restore the bodily feeling of love itself after long deficiency:
A woman said, soon after she began using progesterone and thyroid, that, for the first time in her life she felt that her heart and abdomen were opening with feelings of love. Another said "thyroid is love." Since these women were using the hormones for problems that had developed gradually, over several years if not their entire life, the sudden change was dramatic. They had forgotten that life itself was pleasurable.
When the intercourse of the minds precedes the physical, when courageous play becomes a reflex upon confronting a synchronicity... only then can the sexual pair act as a "unit of invention".
— T3Uncoupled[8]
Sustained physical touch appears to support the bond directly: 10 minutes of hand-holding followed by a 20-second hug raised oxytocin and blunted the blood pressure and heart rate rise from a stress task in partnered women, a longer hold than the brief contact common in daily greetings.[9]
Romance
[edit]Romance and conception conditions leave a lasting mark on a child, an idea that predates and contradicts purely genetic models of inheritance.
Ultimately, what endows the future generation with the most adaptive and creative capacity is the mental, intellectual, and sexual friction of the fully differentiated pair, the mind guiding, with intention and direction, the potency and strength with which the gametes meet: a child who is desired and not an accident, whose future and character are visualized as the next evolutionary step in human development from the very start.
— T3Uncoupled[10]
Conception conditions and the child
[edit]A parent's emotional and energetic state at conception is held, in this framework, to shape a child's beauty, intellect, temperament, and health. Joy, love, mutual desire, and rapture at conception are described as producing superior offspring in centuries-old writing on the subject,[11] while drunkenness at conception has historically been linked to inferior outcomes: a Swiss census of 9,000 people classified as having low intellect reportedly found two annual conception peaks nine months after the yearly carnival and wine harvest, when drinking was heaviest.[12]
Preconception stress can alter germline epigenetics directly, producing heritable damage that persists across generations, a kind of biological hysteresis.[13] T3Uncoupled argues the conditions historically held to be optimal point toward the same pattern: physical union confined to daytime rather than night, in a natural setting rather than a city, prompted by desire rather than obligation, with female orgasm included, since the hormonal rise it brings is taken to protect the biological integrity of both partners rather than being incidental to conception.[14]
Marriage and mortality
[edit]Compared with married people, being unmarried associated with higher all-cause, cancer, CVD, and coronary heart disease mortality in both sexes across 21 studies (about 7.9 million people). The CVD and all-cause links were stronger in men. Divorced or separated status carried higher all-cause mortality in men and a stronger cancer and CVD mortality risk; never-married men had about 31% greater stroke mortality risk and 9% greater all-cause mortality risk than never-married women in the pooled women-to-men ratios.[15]
The lasting bond: telegony, xenia, and hormonal imprinting
[edit]Sex leaves a lasting biological mark on a woman beyond the immediate act, reviving old breeders' terms for the phenomenon:
These newer molecular approaches to the study of biology are vindicating some of the practical observations of plant and animal breeders, and terms such as telegony, heterosis, and xenia might come into common use again, along with genomic imprinting.
— Ray Peat[16]
The mechanism is intercellular and hereditary information transfer through mobile genetic elements and RNA-carrying particles, beyond the fertilizing sperm cell alone.[16] Asked directly whether this explains telegony, he answered:
A lab in Germany has published many papers showing that the DNA in our foods can be found in our cells... And autopsies on women who have had two or three husbands have demonstrated DNA from husbands one and two as well as the most recent one in her tissues, including brain tissue.
— Ray Peat[17]
He illustrated the same idea with a case he'd heard of directly: a white man's children by the same wife growing progressively paler with each successive birth, as if her body were accumulating and integrating his DNA over repeated exposures rather than starting fresh each pregnancy.[18]
More broadly, "hormonal imprinting" describes how a mother's hormonal state during pregnancy and nursing permanently sets her offspring's later sensitivity to those same hormones, an effect that can compound across generations of breeding.[16] In this framework, sex functions as an exchange of persistent biological information between partners and across generations, a lasting link rather than a contained, reversible event.
Peat extended this "nothing really disappears, it leaves a resonant trace" logic well past biochemistry, in a conversation that moved from reincarnation research directly to Persinger's work on electromagnetic resonance:
It's like memory. The things that you remember aren't there, but you can reconstruct them because they left a trace in your matter, and all matter is leaving a trace everywhere. That's why Michael Persinger, who analyzed interaction electronically, is interesting, because he showed that things resonate and the resonance can persist for a long time. He didn't explain how long, but the pattern is really, at any moment, very expansive if not universal.
— Ray Peat[19]
The question that prompted this answer was about Ian Stevenson's reincarnation research and whether a person leaves a "residue" behind after death; Telegony-style hormonal/DNA persistence, ordinary memory, and Persinger's resonance findings are instances of the same underlying phenomenon at different scales, rather than three unrelated topics.[20]
Physiology of orgasm
[edit]Hormone balance in women
[edit]A woman's ease or difficulty in reaching orgasm is a physiological signal, not just a psychological one.
Ease or difficulty in responding sexually, though, and perceptions of bodily emotions, might serve as a subtle indicator of hormone balance, especially thyroid sufficiency.
— Ray Peat[21]
He linked declining orgasmic capacity directly to oral contraceptives and rising estrogen, since estrogen is metabolically antagonistic to progesterone and testosterone; a pill-driven or IUD-driven ("luteolytic," suppressing progesterone) excess of estrogen relative to those hormones can blunt libido and orgasm.[1] He also flagged dietary copper as synergistic with estrogen in this effect, speculating it might explain reduced sexual interest among vegetarians eating copper-rich soy.[1]
Two distinct orgasm patterns track the estrogen/progesterone ratio: excessive estrogen tending to produce a series of small, incomplete orgasms in quick succession, and a lower estrogen-to-progesterone ratio tending to produce one large, complete orgasm followed by sleep.[22] For unsatisfying or absent orgasms he recommended correcting the underlying hormone imbalance and supporting liver function: high protein, B vitamins, vitamin A, vitamin C, vitamin E, zinc, and magnesium. Magnesium in particular has "a very powerful sedative" and even anesthetic effect, "which seems to be especially favorable to healthy sexuality," and may act as an anti-estrogenic mineral alongside zinc.[23] Vitamin E itself he called "the anti-estrogenic vitamin."[23]
Peat compared vitamin E and orgasm to breathing:
For certain nerve systems, both taking vitamin E and having an orgasm might be compared to taking a good deep breath. To continue the analogy between breathing and orgasm, having an orgasm without enough vitamin E would be like sneezing without first inhaling. Some people really do this, and the effect is a series of very small, quick sneezes.
— Ray Peat[24]
He tied this to ATP and the "ready state" of tissue: vitamin E preserves ATP, which stabilizes and relaxes tissue at the same time it energizes it, and it is this energized, relaxed "ready state" that lets tension resolve normally in orgasm. Without enough vitamin E and ATP, the nerve-muscle system cannot reach that ready state, and the tension discharges piecemeal instead, as a series of small, unsatisfying releases rather than one complete one.[25]
Prolactin and satiety
[edit]Orgasm produces a large, orgasm-specific rise in prolactin in both men and women, not seen with arousal alone.[26] Penile-vaginal intercourse produces a larger, longer post-orgasmic prolactin rise than masturbation does, interpreted as reflecting greater physiological satiety from partnered sex.[27] In a healthy person the surge declines back to baseline over a few hours, as part of the feedback loop that produces the normal post-orgasm refractory period.[26]
That decline depends on thyroid status. Georgi Dinkov (Haidut), discussing the topic directly with Ray Peat, described what happens when baseline prolactin is already elevated by hypothyroidism:
In a healthy person orgasm produces a very large rise in prolactin which then subsequently declines relatively over a matter of a few hours, but in a hypothyroid person their baseline prolactin is already elevated beyond optimal, and then when they have an orgasm, which is known to raise prolactin, it's going to raise it even more, but then, unlike a healthy person, it does not decline.
— Georgi Dinkov (Haidut)[28]
In hypothyroid people, the failure of that post-orgasm decline is functionally the same state some now call "post-sexual stress disorder": ordinary chronic hyperprolactinemia that does not resolve because the underlying hypothyroidism does not resolve, linked to a higher rate of alcoholism, gambling, and other compulsive behaviors driven by the resulting low-dopamine, high-cortisol, high-prolactin/estrogen state.[29] Baseline prolactin has also risen across generations, and Ray Peat's reaction to the rise follows:
I remember years ago telling Ray that most people I talked to had a prolactin of about 10, and he immediately interjected and said, "yeah, that's high." A childhood average used to be around four or five, back in the 60s and 70s. Then they kept raising the reference range gradually; today it's 22. And there's a paper on women where they say 14 is associated with hypothyroidism... it's also associated with nymphomania — they just cannot get any sort of satisfaction.
— Georgi Dinkov (Haidut)[30]
This produces a distinction worth stating plainly: a high sex drive looks the same from the outside whether it comes from health or from its opposite. A prolactin/estrogen-dominant person compulsively pursuing sex without ever reaching satisfaction, and a metabolically healthy, thyroid-sufficient person in a stable relationship with a normal drive toward reproduction, can present identically as "high libido" to an outside observer. Only the physiology underneath, and whether real satiation follows, tell the two apart: prolactin that surges and declines normally after orgasm marks the healthy case; prolactin that stays elevated, driving the person back toward sex without resolving the underlying hormone state, marks the other.[29] Lowered interest after taking something estrogen-lowering (e.g. aspirin or T3) is often misread as "low libido" in this same discussion, when it is really the loss of an unhealthy, estrogen-driven preoccupation rather than a loss of health.[29]
In men, chronically excess prolactin is a recognized, underdiagnosed cause of reduced libido and impotence outside of any hypothyroid framing as well, estimated as the cause in 20 to 25 percent of male impotence cases in one review, often presenting only as prostate discomfort or tender, atrophied testes rather than the breast changes usually associated with high prolactin.[31] A separate, more severe men's-only pattern is post-orgasmic illness syndrome (POIS): debilitating flu-like symptoms beginning shortly after ejaculation. Case reports describe relief with thyroid or testosterone therapy, and one published case achieved full, sustained resolution with 500 mg/day of niacinamide over five months, which points to an energetic/metabolic origin.[32]
Oxytocin and vasopressin
[edit]Oxytocin rises during sexual arousal in both sexes and peaks sharply at orgasm.[33] Endocrinology literature Peat drew on ties this to the uterine contractions of female orgasm, stimulated "by oxytocin released from the pituitary during orgasm or by substances in the seminal fluid."[34] Oxytocin's close pituitary relative vasopressin was reported, in a 1982 review, to intensify and prolong orgasm when administered as a nasal spray shortly before sex, an effect attributed to vasopressin's action in the brain rather than any local genital effect; the same source describes histamine release as a physiological requirement for reaching orgasm at all, which is why supplemental niacin (which triggers histamine release) is reported to help some people who otherwise have difficulty reaching orgasm.[35]
Health correlates
[edit]Two population studies quantify the health correlates of sexual frequency directly. A 10-year follow-up of 918 Welsh men aged 45-59 found:
Mortality risk was 50% lower in the group with high orgasmic frequency than in the group with low orgasmic frequency, with evidence of a dose-response relation across the groups... Death from coronary heart disease and from other causes showed similar associations with frequency of orgasm.
— Davey Smith G, Frankel S, Yarnell J.[36]
A separate, smaller study of sexual frequency and mucosal immunity found a curvilinear, not linear, relationship: college students having sex once or twice a week had roughly a third higher salivary IgA than students who were abstinent, less frequent, or having sex three or more times a week, all three of which were comparable to each other.[37] Neither study establishes causation on its own, but both point the same direction: moderate, satisfying sexual activity correlates with better measured health outcomes, while neither abstinence nor excess shows the same benefit.
Semen as an active tissue
[edit]Semen is not biologically inert. Human semen is one of the richest known sources of prostaglandins (the compounds were in fact isolated from, and named for, prostatic/seminal fluid before their wider role was understood), and these prostaglandins can stimulate contraction of the uterus.[38] Marian Diamond's survey of reproductive endocrinology states this plainly:
Uterine contractions, perhaps enhanced by prostaglandins present in the seminal plasma, may hasten the transport of the uterine contents toward the oviduct.
— Marian Cleeves Diamond, Carol Cleaves Korenbrot[39]
Semen also carries zinc at a higher concentration than blood plasma, along with citric acid, fructose, and other secretions from the prostate and seminal vesicles.[40]
Because a healthy pregnancy depends on the uterus staying quiescent under sustained progesterone tone, and because seminal prostaglandins are a recognized uterotonic (the same class of compound used medically to ripen the cervix and induce labor), intercourse late in pregnancy is not hormonally neutral: it delivers a dose of contraction-stimulating prostaglandin directly to the tissue that must stay relaxed for the pregnancy to continue. This is the physiological basis for caution around intercourse, and particularly around ejaculation, in a woman with a threatened or late-term pregnancy.
Endotoxin content depends on the man's gut health
[edit]Semen is not a fixed substance; it reflects the health of the man producing it. Human sperm express both TLR4 and the CD14 co-receptor for LPS (bacterial endotoxin), and semen is a documented carrier of both LPS and leukocytes.[41] In men with obesity, a high-PUFA/high-endotoxin diet, or leaky gut, circulating LPS reaches the testes directly, raises seminal leukocyte reactive oxygen species, damages sperm DNA and motility, and correlates with elevated seminal plasma neopterin (a marker of local macrophage activation).[41] The endotoxin load a man's semen carries is not constant; it tracks his own gut permeability and diet, the same variables that govern endotoxin exposure everywhere else in the body. There is no published evidence that the endotoxin content of semen is transferred to a female partner in amounts large enough to matter systemically; the documented harm is to the man's own sperm and testicular function.[41]
Repeated exposure and immune tolerance
[edit]Separately from endotoxin, there is a substantial reproductive-immunology literature running in the opposite direction from "exposure is the danger": cumulative exposure to the same partner's semen, across a relationship, is associated with lower rates of preeclampsia and recurrent miscarriage, not higher. Semen carries soluble HLA class I antigens and TGF-β that appear to tolerize the mother's immune system to the father's antigens, the same antigens the fetus will carry.[42] In a case-control study, women with unexplained recurrent miscarriage reported oral sex with their partner less often than matched controls. The finding hints at, without proving, an immunomodulatory role for pre-conception seminal exposure via the oral mucosa.[43] The preeclampsia literature more broadly finds risk is highest with a new or short-term partner and with barrier-contracepted, low cumulative sperm exposure before conception, and lowest with long, condom-free exposure to one partner.[42]
Direct cohort data quantify this. In consecutive deliveries, pregnancy-induced hypertension was about five times as common in repeat pregnancies with a new father as in repeat pregnancies with the same father, and longer cohabitation before conception was strongly protective.[44] In a California cohort of women with two consecutive births, changing partners between pregnancies raised the risk of preeclampsia/eclampsia by about 30% in women without a prior preeclamptic pregnancy, but lowered it by about 30% in women with one, i.e. a new partner reset the risk profile in both directions.[45] In the Calcium for Preeclampsia Prevention Trial, a prior abortion was protective against preeclampsia only when the woman conceived again with the same partner, cutting the risk roughly in half. With a new partner, the protection disappeared and her risk matched that of a woman with no prior pregnancy.[46] A Swedish population-based cohort found that in women with a prior affected pregnancy, a new partner cut the recurrence of preterm preeclampsia by about three-quarters and also lowered small-for-gestational-age (SGA) birth, while in women without that history, partner change instead raised SGA risk.[47] Cumulative vaginal exposure to a partner's semen shows the same gradient outside of pregnancy-spacing studies: one case-control study found roughly 70% lower odds of preeclampsia in the highest-exposure group, and a systematic review found lower risk with sexual cohabitation over 12 months and with paternal sperm exposure in nulliparous women; barrier contraception that blocks semen contact tracked with higher risk in the same body of work.[48]
Read together with the endotoxin point above, the two lines of evidence are not in conflict: the risk factor is a man's metabolic/gut health (which determines his semen's endotoxin and inflammatory cargo) and a woman's lack of prior immune exposure to a given partner (which determines whether his antigens are tolerated or attacked), not exposure to semen as such. Established exposure to a metabolically healthy partner is the profile associated with the best outcomes in this literature; novel-partner exposure or exposure from an endotoxemic partner are the profiles flagged as risk factors, for different reasons.
Orgasm, consciousness, and rival theories
[edit]Mind and Tissue treats orgasm as a fusion of two people's perspectives, using the same brain-hemisphere/"dominant" framework (after the physiologist Ukhtomskii) that explains how a person comes to see the world through someone else's eyes:
In the loving interaction of perspectives, a similar generation and amplification of consciousness can occur... If our brain "forms a dominant for" the other person, that person has really come into us, and we can see the world from their perspective... The sudden turning of perception at orgasm seems to involve a transformation of both people, each achieving a synthesis of the two dominants.
— Ray Peat[49]
He located this in the same physiology as heartbeat and breathing, and tied its intensity directly to thyroid status:
This would presumably apply not only to heart-beat and respiration, but to other reflex actions such as orgasm. The thyroid hormone keeps the cellular energy high, the adrenaline low, and reflexes strong.
— Ray Peat[50]
Wilhelm Reich, writing decades earlier, insisted the orgasm itself was not a psychic phenomenon:
The orgasm is not a psychic phenomenon. On the contrary, it is a phenomenon which comes about only by the reduction of all psychic activity to the basic vegetative function, that is, precisely by the elimination of psychic activity.
— Wilhelm Reich[51]
Asked directly about this years later, Peat read Reich's position as compatible with his own, distinguishing a merely local, genital release from what Reich called full "orgastic potency":
Wilhelm Reich called it the genitalization, the localization of the orgasm and losing the whole organism's function of the orgasm. He saw the real orgasm as a cosmic thing in which your whole view of your partner and the universe is undergoing a change, so that both of your personalities and position in the world change. The orgasm is a discovery rather than a sneeze in the loins.
— Ray Peat[52]
On this reading, "the orgasm is not a psychic phenomenon" describes Reich's account of the bioelectric mechanism producing it, not a claim that a complete, whole-organism orgasm has no psychological consequences: the "sneeze in the loins" is what Reich's genital-only, blocked version reduces to, and the "discovery" is what happens when nothing is blocking the full-organism version. Both writers located the health question in the same place, whether the discharge is complete, not whether it happens at all.
Erectile dysfunction
[edit]Erectile dysfunction (ED) is the inability to get or keep an erection firm enough for sex. An erection is a vascular event: penile arteries relax when the second messenger cyclic GMP (cGMP) rises, and testosterone raises cGMP directly.[53] Anything that impairs metabolism, thyroid function or testosterone production tends to impair erections along with everything else. In a randomized trial of 30 insulin-resistant men who responded poorly to sildenafil, adding metformin raised erectile-function scores from 14.3 to 19.8 within four months.[54]
Nitric oxide, cGMP and Viagra
[edit]In the late 1980s and early 1990s nitroglycerin was sold as a topical treatment for impotence. The nitrate converts to nitric oxide, which raises cGMP by activating guanylyl cyclase, the same enzyme that testosterone, DHEA and other steroid precursors activate.[55][53] Sildenafil (Viagra) was first developed as a heart drug and works by blocking the breakdown of cGMP. Its commercial success turned nitric oxide, until then studied mainly as a toxic free radical, into a symbol of virility.[55]
Tadalafil blocks cyclic GMP breakdown the same way, by inhibiting phosphodiesterase type 5 (PDE5), and has no effect without sexual stimulation, because stimulation triggers the local nitric oxide release that starts cyclic GMP synthesis.[56]
Even though Viagra acts on cGMP which is also increased by testosterone, the culture that developed after the mid-1990s began treating nitric oxide the way the drug industry had earlier taught researchers to treat estrogen--if something good happens in the body, it must be caused by NO, and if NO has an effect in the body, that effect must be good.
Supplements sold to raise nitric oxide, such as arginine and concentrated beet products, carry the same risks as the drugs: heart attacks, cardiovascular accidents and atrophy of the testicles.[58] Testosterone raises the same cGMP through the body's own route.
Metabolic drivers
[edit]Insulin resistance damages the lining of blood vessels and lowers their release of nitric oxide. In the metformin trial above, 17 men took metformin and 13 took placebo. Erectile-function scores in the metformin group rose from 14.3 to 17.0 by month 2 and 19.8 by month 4, while insulin resistance (HOMA) fell from 5.5 to 4.5. The placebo group did not change. Side effects were mild and mostly digestive (61.5% of metformin patients against 7.7% on placebo).[54]
Endotoxin suppresses testosterone at its source. A single endotoxin injection in mice lowered serum testosterone within 2 hours, cut the steroid-making proteins StAR and 3beta-HSD, and disrupted the mitochondria of the testosterone-producing Leydig cells through oxidative damage.[59]
Thyroid function sets the tone for the whole system of sex hormones.
Thyroid is the best way to regulate the system, keeping libido up, making orgasms satisfying.
In 40 men with arterial erectile dysfunction and subclinical hypothyroidism, randomized to levothyroxine or no treatment for six months, the treated men had lower TSH, better penile blood flow and higher erectile function scores, while the untreated men showed no significant change.[61]
Serotonin and SSRIs
[edit]Excess serotonin works against testosterone in the brain centers that drive sexual behavior. In men with impotence and normal blood testosterone, lowering serotonin with parachlorophenylalanine and raising testosterone produced vivid sexual stimulation in about half of otherwise untreatable cases.
Sexual deficiency or frank impotence in man could be due to an imbalance of monoamines, particularly 5-HT, at the mating center level. An absolute or relative excess of 5-HT seems to antagonize testosterone at the level of the mating center receptors in the brain. Plasma testosterone levels in so-called psychological impotence are normal.
— Sicuteri F, Del Bene E, Fonda C[62]
In a prospective study of 1,022 outpatients with previously normal sexual function, overall sexual dysfunction on antidepressants reached 59% (604/1,022), including erectile dysfunction or decreased lubrication in 31%. Rates varied by drug from 58% (fluoxetine) up to 71-73% (paroxetine, citalopram).[63] Paroxetine also inhibits nitric oxide synthase: in 17 heart patients treated for depression, it significantly lowered serum nitrite and nitrate, which the comparison drug nortriptyline did not.[64] See SSRIs for the full breakdown and PSSD (Post-SSRI Sexual Dysfunction) persistence data.
The rise in young men
[edit]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% 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 spread from September 2006 onward.[65] The review's authors attribute the rise to habituation, tolerance and altered reward-circuit sensitivity from an endless supply of novel sexual stimuli.
Orgasm itself is not the hormonal problem. Masturbation affects prolactin and other hormones no more than partnered sex does, which leaves the pattern of consumption (novelty, escalation, video) as the likely driver. See Pornography for that mechanism in more depth.
Generally positive, but intense arousal can have unwanted consequences, such as herpes virus outbreaks. [...] I don't think masturbation affects the hormones more than regular sex does.
Gut microbiota
[edit]Gut composition tracks with ED separately from 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.[67] A larger Mendelian randomization study, which uses genetic variation to test cause and effect, linked six bacterial taxa 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.[68] This overlaps with SIBO and chronic bacterial prostatitis, a shared mechanism behind both ED and premature ejaculation.
Practice
[edit]Address the metabolic basics first: insulin sensitivity, thyroid, and endotoxin and gut health. Aspirin is a low-cost option with trial support. In 336 men with vascular ED, 100 mg/day aspirin improved erectile-function scores by 7.2 points, against 7.3 for 5 mg/day tadalafil, 7.5 for both together and 2.0 for placebo.[69] Avoid nitric-oxide boosters. For cases tied to pornography use, see Pornography. For cases tied to gut dysbiosis or SIBO and prostatitis, see Premature ejaculation and SIBO.
Pornography
[edit]Pornography use is near-universal in the Western world, and a meaningful share of users report it as problematic, with a smaller share seeking treatment to stop. Ray Peat didn't write specifically about internet pornography (streaming video sites postdate most of his published work), but his framework on masturbation, prolactin, and reward-driven stress applies directly.
Prevalence and problematic use
[edit]Estimates of how many pornography users find their own use problematic vary widely by what's being measured. A survey of 84 college-age men found 20-60% considered their use problematic, depending on the specific domain asked about (time spent, effect on relationships, guilt, control).[70] The amount of viewing itself didn't predict how problematic it felt; how someone responded to the urge to view did.[70]
Among 1,298 male pornography users surveyed online, 14% reported being interested in seeking treatment for their pornography use, though only 6.4% had actually sought treatment before. Interest in treatment tracked with clinically significant hypersexuality (9.5x more likely) and with more past attempts to cut back or quit.[71]
Erectile dysfunction link
[edit]ED in men under 40 rose from roughly 2-5% in studies from 1999-2002 to 20-30% in more recent reports, a rise that tracks the spread of "porn tube" streaming sites after 2006 more closely than any change in the usual metabolic risk factors for ED at that age.[65] See Erectile dysfunction for the full mechanism discussion and the metabolic side of ED that applies regardless of cause.
Not a hormone-dose problem
[edit]It's tempting to frame the effect as a direct hormonal one, prolactin spiking with each session and gradually suppressing testosterone and libido, but Ray Peat didn't think masturbation itself does anything to hormones that partnered sex doesn't:
[Masturbation: effect on prolactin] I don't think masturbation affects the hormones more than regular sex does.
— Ray Peat[72]
The mechanism fits the pattern of consumption specific to streaming pornography: constant novelty, an endless supply of new partners/scenarios on demand, and rapid escalation, features that drive dopamine-mediated reward-circuit habituation regardless of what prolactin or testosterone are doing on any given day. This is the same general category of compulsive, escalating pattern described for stimulants and stress-hormone-driven behavior more broadly (see OCD's stimulant section for the parallel with dopaminergic overstimulation).
Practice (pornography)
[edit]Treat it as a behavioral/reward-circuit pattern rather than a hormonal one specifically, ordinary metabolic support (thyroid, adequate protein and sugar, low stress) still matters for the libido and mood side of things, but won't by itself reverse habituation built by the consumption pattern. ERP-style approaches (deliberately not acting on the urge until it passes) and Acceptance and Commitment Therapy have direct trial evidence for reducing problematic use.[73]
Premature ejaculation
[edit]Premature ejaculation (PE) affects 30-40% of sexually active men in an age-dependent manner, making it the most common male sexual disorder.[74] A substantial fraction of cases have a bacterial, treatable organic cause rather than a purely psychological one. See Prostatitis for the condition itself and Erectile dysfunction for the related problem.
Chronic bacterial prostatitis
[edit]A cohort of 153 men with PE, compared against 100 healthy controls, found prostatic inflammation in 64% and chronic bacterial prostatitis specifically in 52% of PE patients, both significantly elevated over controls.[74]
Treating the infection improved PE in most treated men. In a follow-up study, 145 men with secondary PE were tested for chronic bacterial prostatitis; 94 (64.8%) tested positive. Of those, 74 received one month of antibiotics matched to their culture and sensitivity results, while 20 went untreated as controls. All 74 treated patients had sterile cultures afterward, and 62 (83.9%) showed increased ejaculatory latency time and good ejaculatory control, sustained through a 4-month follow-up with no PE recurrence in patients whose cultures stayed negative. None of the untreated control patients improved.[75]
Prostatic inflammation (64% of PE patients) was more common than a positive bacterial culture (52%).[74] Standard cultures can also miss fungal causes, and SIBO turns up in most chronic prostatitis patients. See Prostatitis for the Candida case report, the SIBO breath-test and rifaximin studies, and the gut origin of prostate inflammation.
Gut bacterial diversity is also reduced in men with erectile dysfunction.[67] Gut and prostate infection are worth ruling out as a shared driver in men with both PE and ED. See Erectile dysfunction § Gut microbiota for the studies.
Practice (premature ejaculation)
[edit]For PE that doesn't have an obvious psychological driver, a urine and prostatic fluid culture (and, if negative, a SIBO breath test) is worth ruling out before assuming the cause is purely psychogenic. Antibiotics matched to the actual culture result, not a generic broad-spectrum course, is what the treatment studies above actually tested.
References
[edit]- ↑ 1.0 1.1 1.2 Ray Peat, "Nutrition for Women", p. 12
- ↑ See Creativity.
- ↑ Wilhelm Reich, "The Function of the Orgasm," 1973 (orig. 1927).
- ↑ Ray Peat, "Monogamy and Property," Q&A, Ray Peat Forum, in Ephemera: Ray's Email Exchanges.
- ↑ Ray Peat, "Polyamory, Sexual Relationships," Q&A, Ray Peat Forum, in Ephemera: Ray's Email Exchanges.
- ↑ Ray Peat, "Mind and Tissue", p. 141
- ↑ Ray Peat, "Nutrition for Women", p. 7
- ↑ Synchronicity as a Fountain for Novelty, t3uncoupled.substack.com
- ↑ Grewen KM, Girdler SS, Amico J, Light KC. "Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact," Psychosom Med. 2005;67(4):531-538. PMID 16046364.
- ↑ Great Loves Make Great People, t3uncoupled.substack.com
- ↑ Anonymous, Procreation refin'd: A New Method For the Begetting Children With Handsome Faces, Richard Griffin, 1710.
- ↑ Auguste Forel, The Sexual Question, 1908.
- ↑ Duffy KA, Bale TL, Epperson CN, "Germ Cell Drivers: Transmission of Preconception Stress Across Generations," Frontiers in Human Neuroscience, 2021;15:642762. https://doi.org/10.3389/fnhum.2021.642762
- ↑ T3Uncoupled, "Great Loves Make Great People," t3uncoupled.substack.com.
- ↑ Wang Y, Jiao Y, Nie J, et al. "Sex differences in the association between marital status and the risk of cardiovascular, cancer, and all-cause mortality: a systematic review and meta-analysis of 7,881,040 individuals," Glob Health Res Policy. 2020;5:4. doi:10.1186/s41256-020-00133-8. PMID 32161813.
- ↑ 16.0 16.1 16.2 Ray Peat, "Estrogen, Memory and Heredity: Imprinting and the Stress Response," raypeat.com.
- ↑ Ray Peat, "Hormonal Imprinting, Fake History, Aristotelian Philosophy, Marx, Lenin, Stalin, and Lysenko", Danny Roddy, 34:25
- ↑ Ray Peat, "Hormonal Imprinting, Fake History, Aristotelian Philosophy, Marx, Lenin, Stalin, and Lysenko", Danny Roddy, 35:37
- ↑ Ray Peat, "Lost Conversations with Ray Peat #3," Danny Roddy's Substack, recorded August 26, 2019.
- ↑ Ray Peat, "Lost Conversations with Ray Peat #3," Danny Roddy's Substack, recorded August 26, 2019.
- ↑ Ray Peat, "Nutrition for Women", p. 104
- ↑ Ray Peat, "Nutrition for Women", p. 12
- ↑ 23.0 23.1 Ray Peat, "Nutrition for Women", p. 13
- ↑ Ray Peat, "Nutrition for Women", p. 14
- ↑ Ray Peat, "Nutrition for Women", p. 14
- ↑ 26.0 26.1 Krüger THC, Haake P, Hartmann U, Schedlowski M, Exton MS. "Orgasm-induced prolactin secretion: feedback control of sexual drive?" Neurosci Biobehav Rev. 2002;26(1):31-44; Krüger THC, et al. "Specificity of the neuroendocrine response to orgasm during sexual arousal in men." J Endocrinol. 2003;177(1):57-64.
- ↑ Brody S, Krüger THC. "The post-orgasmic prolactin increase following intercourse is greater than following masturbation and suggests greater satiety." Biol Psychol. 2006;71(3):312-315.
- ↑ Ray Peat, "#88: Escalation to World War 3, Low-Carb Diets, Thyroid, Stress, and Digestive Disease", Danny Roddy
- ↑ 29.0 29.1 29.2 Ray Peat, "#88: Escalation to World War 3, Low-Carb Diets, Thyroid, Stress, and Digestive Disease", Danny Roddy
- ↑ Ray Peat, "#88: Escalation to World War 3, Low-Carb Diets, Thyroid, Stress, and Digestive Disease", Danny Roddy
- ↑ Durk Pearson, Sandy Shaw, "Life Extension: A Practical Scientific Approach," 1982, ch. 5.
- ↑ Haidut, "may treat post-orgasmic illness syndrome (POIS)," haidut.me, discussing a case report at Post-orgasmic Illness Syndrome: A Case Report.
- ↑ Carmichael MS, Humbert R, Dixen J, Palmisano G, Greenleaf W, Davidson JM. "Plasma oxytocin increases in the human sexual response." J Clin Endocrinol Metab. 1987;64(1):27-31.
- ↑ "1972 - Biology Today (Part 2)."
- ↑ Durk Pearson, Sandy Shaw, "Life Extension: A Practical Scientific Approach," 1982, ch. 5, p. 204.
- ↑ "Sex and death: are they related? Findings from the Caerphilly cohort study." BMJ. 1997;315(7123):1641-1644.
- ↑ Charnetski CJ, Brennan FX. "Sexual frequency and salivary immunoglobulin A (IgA)." Psychol Rep. 2004;94(3 Pt 1):839-844.
- ↑ Clarence Donnell Turner, Joseph T. Bagnara, "General Endocrinology," 1971.
- ↑ Diamond, Korenbrot, "Hormonal Contraceptives, Estrogens, and Human Welfare," 1978.
- ↑ Clarence Donnell Turner, "General Endocrinology," 1966.
- ↑ 41.0 41.1 41.2 Haidut, "has a G.E.L.D.I.N.G effect, causes obesity and hypogonadism," haidut.me, quoting Tremellen K, "Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING), a novel theory for the development of late onset hypogonadism in obese men," Basic Clin Androl. 2016;26:7.
- ↑ 42.0 42.1 Koelman CA, et al. "Correlation between oral sex and a low incidence of preeclampsia: a role for soluble HLA in seminal fluid?" J Reprod Immunol. 2000;46(2):155-166.
- ↑ Meuleman T, et al. "Oral sex is associated with reduced incidence of recurrent miscarriage." J Reprod Immunol. 2019;133:1-6. Oral sex reported by 56.9% of cases vs 72.9% of controls.
- ↑ Robillard PY, et al. "Association of pregnancy-induced hypertension with duration of sexual cohabitation before conception." Lancet. 1994;344(8928):973-975. 1,011 consecutive deliveries; pregnancy-induced hypertension 11.9% first pregnancies, 4.7% repeat with same father, 24.0% repeat with new father; cohabitation effect.
- ↑ Li DK, Wi S. "Changing paternity and the risk of preeclampsia/eclampsia in the subsequent pregnancy." Am J Epidemiol. 2000;151(1):57-62. 140,147 women.
- ↑ Saftlas AF, et al. "Abortion, changed paternity, and risk of preeclampsia in nulliparous women." Am J Epidemiol. 2003;157(12):1108-1114. Same partner adjusted OR 0.54; new partner adjusted OR 1.03 (not significant).
- ↑ Wikström AK, et al. "Changing paternity and time since last pregnancy: the impact on pre-eclampsia risk." BMJ Open. 2012;2(4):e001178. Prior affected pregnancy: preterm preeclampsia recurrence OR 0.24, SGA OR 0.75.
- ↑ Systematic review, sexual cohabitation, sperm exposure, and preeclampsia risk. Eur J Obstet Gynecol Reprod Biol. 2020. Cohabitation over 12 months OR 0.73; paternal sperm exposure in nulliparous women OR 0.63.
- ↑ Ray Peat, "Mind and Tissue", p. 143
- ↑ Ray Peat, "Mind and Tissue", p. 140
- ↑ Wilhelm Reich, "Character Analysis," 1950.
- ↑ Ray Peat, "Generative Energy, Thyroid Function and Pulse Rate, Weaponized Culture, Finasteride as an Insane Decision", Danny Roddy, 1:11:11
- ↑ 53.0 53.1 Vesely DL. "Testosterone and its precursors and metabolites enhance guanylate cyclase activity," Proc Natl Acad Sci U S A. 1979;76(7):3491-4. PMID 40226.
- ↑ 54.0 54.1 Rey-Valzacchi GJ, Costanzo PR, Finger LA, Layus AO, et al. "Addition of metformin to sildenafil treatment for erectile dysfunction in eugonadal nondiabetic men with insulin resistance. A prospective, randomized, double-blind pilot study," J Androl. 2012;33(4):608-14. doi:10.2164/jandrol.111.013714. PMID 22016348.
- ↑ 55.0 55.1 Ray Peat, "Nitric Oxide, Degenerative Processes, and the Medical Marketplace," Ray Peat's Newsletter, 2015.
- ↑ "CIALIS (tadalafil) tablets, for oral use: full prescribing information," Eli Lilly and Company, NDA 021368, section 12.1 Mechanism of Action. DailyMed, label revised June 2026.
- ↑ Nitric Oxide, Degenerative Processes, and the Medical Marketplace, Ray Peat's Newsletter, 2015
- ↑ Ray Peat, "Nitric Oxide, Nitrates, Nitrites, and Fluoride", KMUD
- ↑ Allen JA, Diemer T, Janus P, Hales KH, Hales DB. "Bacterial endotoxin lipopolysaccharide and reactive oxygen species inhibit Leydig cell steroidogenesis via perturbation of mitochondria," Endocrine. 2004;25(3):265-75. doi:10.1385/ENDO:25:3:265. PMID 15758255.
- ↑ Ray Peat, email correspondence, "Sex & Masturbation," raypeatemails.com
- ↑ Is There a Role for Levo-Thyroxine for the Treatment of Arterial Erectile Dysfunction? The Clinical Relevance of the Mean Platelet Volume doi:10.3390/jcm9030742 Levothyroxine 1 µg/kg/day, 20 men per group, no placebo. Treated group: TSH 6.5 to 2.26 µIU/mL, PSV 26.5 to 40.0 cm/s, IIEF-5 8.2 to 20.2.
- ↑ Sicuteri F, et al., "Sex, migraine and serotonin interrelationships," Monogr Neural Sci 1976;3:94-101, cited in Ray Peat, "Tryptophan, serotonin, and aging"
- ↑ Montejo AL, Llorca G, Izquierdo JA, Rico-Villademoros F. "Incidence of sexual dysfunction associated with antidepressant agents: a prospective multicenter study of 1022 outpatients. Spanish Working Group for the Study of Psychotropic-Related Sexual Dysfunction," J Clin Psychiatry. 2001;62 Suppl 3:10-21. PMID 11229449.
- ↑ Finkel MS, Laghrissi-Thode F, Pollock BG, Rong J. "Paroxetine is a novel nitric oxide synthase inhibitor," Psychopharmacol Bull. 1996;32(4):653-8. PMID 8993087.
- ↑ 65.0 65.1 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.
- ↑ Ray Peat, email correspondence, "Sex & Masturbation," raypeatemails.com
- ↑ 67.0 67.1 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.
- ↑ 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.
- ↑ Bayraktar Z, Albayrak S. "Efficacy and safety of combination of tadalafil and aspirin versus tadalafil or aspirin alone in patients with vascular erectile dysfunction: a comparative randomized prospective study," Int Urol Nephrol. 2019;51(9):1491-1499. doi:10.1007/s11255-019-02211-4. PMID 31230261.
- ↑ 70.0 70.1 Twohig MP, Crosby JM, Cox JM. "Viewing Internet Pornography: For Whom is it Problematic, How, and Why?" Sexual Addiction & Compulsivity. 2009;16(4):253-266.
- ↑ Kraus SW, Martino S, Potenza MN. "Clinical Characteristics of Men Interested in Seeking Treatment for Use of Pornography," J Behav Addict. 2016;5(2):169-178. PMID 27348557.
- ↑ Ray Peat, email correspondence, "Sex & Masturbation," raypeatemails.com
- ↑ Twohig MP, Crosby JM. "Acceptance and commitment therapy as a treatment for problematic internet pornography viewing," Behav Ther. 2010;41(3):285-295. PMID 20569778.
- ↑ 74.0 74.1 74.2 Shamloul R, el-Nashaar A. "Chronic prostatitis in premature ejaculation: a cohort study in 153 men," J Sex Med. 2006;3(1):150-154. PMID 16409229.
- ↑ El-Nashaar A, Shamloul R. "Antibiotic treatment can delay ejaculation in patients with premature ejaculation and chronic bacterial prostatitis," J Sex Med. 2007;4(2):491-496. PMID 17367444.