Testosterone Research versus Testosterone Myths

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Testosterone spikes at day 7 after ejaculationCOMMENTS: We wrote this article to highlight possible mechanisms behind the benefits of rebooting. Below I address the most common misconceptions related to testosterone, abstinence and ejaculation:

  1. Testosterone levels do not decline from ejaculation or “too much masturbation”. This seems to be a myth with absolutely no scientific support.  However, there's evidence that ejaculation to the point of sexual satiation triggers multiple brain changes - including a decline in androgen receptors. and increases in estrogen receptors and dopamine-blocking opioids in several brain regions. Full recovery takes about 15 days and is quite apart from addiction-related brain changes. More below.
  2. There is no consistent correlation between sexual activity, or abstinence, and plasma testosterone levels – other than a one-day transient spike (46% above baseline) following seven days of abstinence. Wide fluctuations in male testosterone levels (10-40%) are normal.  
  3. There is no evidence for abstinence raising testosterone levels. Only two studies have measured T levels during a long-term abstinence - and both found no change:
    1.  The "famous" Chinese study measured T levels every day for 16 days, and found little increase until day 6 - and a return to baseline (slightly below) from day 8 through day 16 when the experiment ended.
    2. The study in #4
  4. This abstract - Endocrine response to masturbation-induced orgasm in healthy men following a 3-week sexual abstinence, where subjects didn't ejaculate for 3 weeks, is often cited as evidence that abstinence leads to increased testosterone. It doesn't. This sentence from the abstract is poorly worded and misleading: "although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence". In the full study, testosterone levels are the same in both groups. Examine the testosterone graph C on page 379. Notice testosterone levels at the start of the film (10-minute mark) were identical in both groups. End of story. The confusing language in the abstract refers to testosterone differences while masturbating. While watching the erotic film and masturbating, T-levels dropped for the pre-abstinence masturbation session. After 21 days of abstinence, T-levels stayed closer to the 10 minute baseline during masturbation. The statement - "higher testosterone concentrations were observed following the period of abstinence" - means that testosterone levels did not fall as much during the stimulus: masturbation & porn viewing. The authors suggest anticipation of watching a porno (perhaps augmented by the anticipation of finally masturbating) caused testosterone to remain elevated throughout the viewing.
  5. Rodent studies consistently find that ejaculation to "sexual exhaustion" has no effect on testosterone levels. These studies follow the animals for up to 15 days. However, they do find multiple changes within the limbic system, including a decline in androgen receptors, and increase in estrogen receptors & opioids (which block dopamine), and alterations in gene expression.
  6. Long-term studies on primates have shown no reliable correlation between ejaculation and blood testosterone levels.
  7. The authors of this study and this study suggest that abstinence may lead to chronically lower testosterone levels
  8. Viewing porn has little or no effect on testosterone or other hormones. See: The endocrine effects of visual erotic stimuli in normal men.
  9. Many men with porn-induced erectile dysfunction have seen doctors and had blood tests. Virtually all have reported normal testosterone levels.
  10. Many human and animal studies show that low testosterone has no effect on erections achieved through stimulation. See this discussion by a professor of reproductive endocrinology - Hypogonadal men and erections
  11. All evidence points to addiction processes in the brain as the primary cause of porn-induced ED, porn-induced loss of libido, or so called “sexual exhaustion”.
  12. Some men with porn-induced ED have tried testosterone supplementation, with no success. When these same men rebooted, their ED was cured.
  13. Reward circuitry dopamine is behind sexual desire, motivation, and erections.
  14. In short, the many improvements guys see in libido and confidence as they reboot are probably coming from changes in their brains, not their testosterone levels.

Men experience myriad benefits as they unhook from porn and compulsive masturbation. It's natural to assume positive changes such as more confidence, better mood, less anxiety, and greater motivation must have something to do with blood testosterone levels. Not so. While it’s possible that unidentified circulating hormones could be altered by excessive masturbation or porn addiction, testosterone levels are not affected.

For the science behind the benefits guys experience see - Porn, Masturbation and Mojo: A Neuroscience Perspective - Ex-porn users usually get their mojo back. Why?



Sexual inactivity results in reversible reduction of LH bioavailability.

Int J Impot Res. 2002 Apr;14(2):93-9; discussion 100.

Carosa E, Benvenga S, Trimarchi F, Lenzi A, Pepe M, Simonelli C, Jannini EA.


We have recently documented significantly reduced serum testosterone (T) levels in patients with erectile dysfunction (ED). To understand the mechanism of this hypotestosteronemia, which was independent of the etiology of ED, and its reversibility only in patients in whom a variety of nonhormonal therapies restored sexual activity, we measured serum luteinizing hormone (LH) in the same cohort of ED patients (n=83; 70% organic, 30% nonorganic). Both immunoreactive LH (I-LH) and bioactive LH (B-LH) were measured at entry and 3 months after therapy. Based on outcome (ie number of successful attempts of intercourse per month), patients were categorized as full responders (namely, at least eight attempts; n=51), partial responders (at least one attempt; n=20) and non-responders (n=16). Compared to 30 healthy men with no ED, baseline B-LH (mean+/-s.d.) in the 83 patients was decreased (13.6+/-5.5 vs 31.7+/-6.9 IU/L, P<0.001), in the face of a slightly increased, but in the normal range, I-LH (5.3+/-1.8 vs 3.4+/-0.9 IU/L, P<0.001); consequently, the B/I LH ratio was decreased (3.6+/-3.9 vs 9.7+/-3.3, P<0.001). Similar to our previous observation for serum T, the three outcome groups did not differ significantly for any of these three parameters at baseline. However, outcome groups differed after therapy. Bioactivity of LH increased markedly in full responders (pre-therapy=13.7+/-5.3, post-therapy=22.6+/-5.4, P<0.001), modestly in partial responders (14.8+/-6.9 vs 17.2+/-7.0, P<0.05) but remained unchanged in non-responders (11.2+/-2.2 vs 12.2+/-5.1). The corresponding changes went in the opposite direction for I-LH (5.2+/-1.7 vs 2.6+/-5.4, P<0.001; 5.4+/-2.2 vs 4.0+/-1.7, P<0.05; 5.6+/-1.2 vs 5.0+/-1.2, respectively), and in the same direction as B-LH for the B/I ratio (3.7+/-4.1 vs 11.8+/-7.8, P<0.001; 4.2+/-4.3 vs 5.8+/-4.2, P<0.05; 2.1+/-0.7 vs 2.6+/-1.3, respectively). We hypothesize that the hypotestosteronemia of ED patients is due to impaired bioactivity of LH. This reduced bioactivity is reversible, provided that resumption of sexual activity is achieved regardless of the therapeutic modality. Because biopotency of pituitary hormones is controlled by the hypothalamus, LH hypoactivity should be due to the hypothalamic functional damage associated to the psychological disturbances which unavoidably follow sexual inactivity.

COMMENTS: Authors suggest that successful sexual activity increases LH and testosterone in men treated for ED. None of the men were treated with hormones, and low testosterone was not the cause of their ED. If true in healthy men, this suggests that sex/ejaculation may prevent a decline in testosterone levels.



Lack of sexual activity from erectile dysfunction is associated with a reversible reduction in serum testosterone.

Int J Androl. 1999 Dec;22(6):385-92.

Jannini EA, Screponi E, Carosa E, Pepe M, Lo Giudice F, Trimarchi F, Benvenga S.


The role of androgenic hormones in human sexuality, in the mechanism of erection and in the pathogenesis of impotence is under debate. While the use of testosterone is common in the clinical therapy of male erectile dysfunction, hypogonadism is a rare cause of impotence. We evaluated serum testosterone levels in men with erectile dysfunction resulting either from organic or non-organic causes before and after non-hormonal impotence therapy. Eighty-three consecutive cases of impotence (70% organic, 30% non-organic, vascular aetiology being the most frequent) were subjected to hormonal screening before and after various psychological, medical (prostaglandin E1, yohimbine) or mechanical therapies (vascular surgery, penile prostheses, vacuum devices). Thirty age-matched healthy men served as a control group. Compared to controls, patients with impotence resulting from both organic and non-organic causes showed reduced serum levels of both total testosterone (11.1 +/- 2.4 vs. 17.7 +/- 5.5 nmol/L) and free testosterone (56.2 +/- 22.9 vs. 79.4 +/- 27.0 pmol/L) (both p < 0.001). Irrespective of the different aetiologies and of the various impotence therapies, a dramatic increase in serum total and free testosterone levels (15.6 +/- 4.2 nmol/L and 73.8 +/- 22.5 pmol/L, respectively) was observed in patients who achieved normal sexual activity 3 months after commencing therapy (p < 0.001). On the contrary, serum testosterone levels did not change in patients in whom therapies were ineffective. Since the pre-therapy low testosterone levels were independent of the aetiology of impotence, we hypothesize that this hormonal pattern is related to the loss of sexual activity, as demonstrated by its normalization with the resumption of coital activity after different therapies. The corollary is that sexual activity may feed itself throughout the increase in testosterone levels.

COMMENTS: Authors suggest that lack of sexual activity leads to lower testosterone. In the above study they hypothesize that this may be related to the stress of ED, or may be due to the resumption of sexual activity itself. Hard to sort out as all the subjects suffered from ED, and had lower testosterone.



Jiang M, Xin J, Zou Q, Shen JW. J Zhejiang Univ Sci. 2003 Mar-Apr;4(2):236-40

The purpose of this study is to gain understanding of the relationship between ejaculation and serum testosterone level in men. The serum testosterone concentrations of 28 volunteers were investigated daily during abstinence periods after ejaculation for two phases.

The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak.

Ejaculation is the precondition and beginning of the special periodic serum testosterone level variations, which would not occur without ejaculation. The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum. These data are the first to document the phenomenon of the periodic change in serum testosterone level; the correlation between ejaculation and periodic change in the serum testosterone level, and the pattern and characteristics of the periodic change.

COMMENT: This is the only study that measured T level everyday, for 3 weeks, and they found no difference before or after the one day spike. This one day peak indicates a cycle initiated by orgasm. The experiment measured testosterone levels every day for 16 days following an ejaculation. Testosterone levels do not slowly rise over 7 days to reach 146% of baseline. Nor do levels slowly decline.  It’s a one day spike—up and back down. During other daily measurements, testosterone levels remain within normal ranges. Plasma testosterone levels are controlled by hormonal signals originating from the hypothalamus. It's common for spikes of hormones to activate other hormones or physiological events. No one yet knows the significance of this plasma-testosterone cycle initiated by ejaculation.

Note: This is one of the most cited studies on forums where men discuss bodybuilding, exercise, sex, health and the like. Please keep in mind the numerous factors that affect daily testosterone fluctuations, including type of activity or exercise, sexual stimulation, social status, mood, pheromones, stress, emotions, season, etc.



JournalArchives of Sexual Behavior April 23, 2005

Twenty males participated in a 2-month study examining the relationship between 8 a.m. plasma testosterone levels and orgasmic frequency. Within subjects, higher levels of testosterone are associated with periods of sexual activity. Over subjects, however, the direction of the relationship is reversed. Mean testosterone levels were higher for sexually less active individuals.

COMMENT: Average testosterone levels were higher in less sexually active men. But—sexual activity increased testosterone levels in individuals—on average.



Exton MS, Krüger TH, Bursch N, Haake P, Knapp W, Schedlowski M, Hartmann U. World J Urol. 2001 Nov;19(5):377-82

This current study examined the effect of a 3-week period of sexual abstinence on the neuroendocrine response to masturbation-induced orgasm. Hormonal and cardiovascular parameters were examined in ten healthy adult men during sexual arousal and masturbation-induced orgasm. Blood was drawn continuously and cardiovascular parameters were constantly monitored. This procedure was conducted for each participant twice, both before and after a 3-week period of sexual abstinence. Plasma was subsequently analysed for concentrations of adrenaline, noradrenaline, cortisol, prolactin, luteinizing hormone and testosterone concentrations. Orgasm increased blood pressure, heart rate, plasma catecholamines and prolactin. These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.

COMMENT: The wording of the abstract is a mess. The full study completely contradicts what I have bolded. See #4 above



Psychoneuroendocrinology. 1998 May;23(4):401-11

Data regarding the neuroendocrine response pattern to sexual arousal and orgasm in man are inconsistent. In this study, ten healthy male volunteers were continuously monitored for their cardiovascular and neuroendocrine response to sexual arousal and orgasm. Blood was continuously drawn before, during and after masturbation-induced orgasm and analyzed for plasma concentrations of adrenaline, noradrenaline, cortisol, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, growth hormone (GH), beta-endorphin and testosterone. Orgasm induced transient increases in heart rate, blood pressure and noradrenaline plasma levels. Prolactin plasma levels increased during orgasm and remained elevated 30 min after orgasm. In contrast, none of the other endocrine variables were significantly affected by sexual arousal and orgasm.

COMMENT: Short-term testosterone levels not affected by orgasm—which opposes the following study.



Journal of Endocrinology, Vol 70, Issue 3, 439-444 1976 by Society for Endocrinology

The levels of pregnenolone, dehydroepiandrosterone (DHA), androstenedione, testosterone, dihydrotestosterone (DHT), oestrone, oestradiol, cortisol and luteinizing hormone (LH) were measured in the peripheral plasma of a group of young, apparently healthy males before and after masturbation. The same steroids were also determined in a control study, in which the psychological anticipation of masturbation was encouraged, but the physical act was not carried out. The plasma levels of all steroids were significantly increased after masturbation, whereas steroid levels remained unchanged in the control study. The most marked changes after masturbation were observed in pregnenolone and DHA levels. No alterations were observed in the plasma levels of LH. Both before and after masturbation plasma levels of testosterone were significantly correlated to those of DHT and oestradiol, but not to those of the other steroids studied. On the other hand, cortisol levels were significantly correlated to those of pregnenolone, DHA, androstenedione and oestrone. In the same subjects, the levels of pregnenolone, DHA, androstenedione, testosterone and DHT, androstenedione and oestrone. In the same subjects, the levels of pregnenolone, DHA, androstenedione, testosterone and DHT in seminal plasma were also estimated; they were all significantly correlated to the levels of the corresponding steroid in the systemic blood withdrawn both before and after masturbation. As a practical consequence, the results indicate that whenever both blood and semen are analysed, blood sampling must precede semen collection.

COMMENT: Short-term testosterone levels were elevated by orgasm, but less so than other steroids. However, this result is countered by several other studies.



J Clin Endocrinol Metab. 1975 Mar;40(3):492-500

The object of the study was to assess the lability of testosterone levels in plasma of normal human males over a long period of time and to search for periodicities in changing levels. Blood samples obtained from 20 healthy young men every second day for 2 months were assayed for total testosterone concentration by radioligand saturation analysis with late-pregnancy plasma. The flucturations of plasma testosterone levels over the total time span were substantial for most individuals; the coefficients of variation ranged from 14 to 42% (median 21%). The presence of periodic functions in these fluctuations was tested by 4 different, relatively independent methods. Close agreement among at least 3 analytic methods was found for 12 out of the 20 subjects. These 12 subjects had cycles of plasma testosterone levels with periods ranging between 8-30 days, with a cluster of periods around 20-22 days. The majority of such cycles were significant at least at the 5% level. The mean amplitudes of these cycles ranged from 9 to 28% of the subjects' mean testosterone levels (average 17%).

COMMENTS: "The fluctuations of plasma testosterone levels over the total time span were substantial for most individuals - ranged from 14 to 42% (median 21%)."  Not only that but many other things affects T levels, including type of exercise, mood, social rank, drugs, alcohol, etc.



Schwartz MF, Kolodny RC, Masters WH. Arch Sex Behav. 1980 Oct;9(5):355-66

Plasma testosterone levels in a group of 341 men with sexual dysfunction were compared to those in 199 men with normal sexual function. All subjects were participants in a 2-week intensive conjoint sex therapy program at the Masters & Johnson Institute. Testosterone determinations were made using radioimmunoassay methods after column chromatography; all blood samples were obtained on the second day of therapy between 8:00 and 9:00 a.m. after an overnight fast. Circulating levels of testosterone in men with normal sexual function (mean 635 ng/dl) were not significantly different from testosterone values in sexually dysfunctional men (mean 629 ng/dl). However, men with primary impotence (N = 13) had significantly higher testosterone levels than men with secondary impotence (N = 180), with mean levels of 710 and 574 ng/dl, respectively (p < 0.001). The mean testosterone level for men with ejaculatory imcompetence was 660 ng/dl (N = 15), while for men with premature ejaculation the mean was 622 ng/dl (N = 91). Plasma testosterone concentrations were not related to therapy outcome but were correlated negatively with age of patients.

COMMENTS: As it says—not much difference in testosterone levels between impotent and normal guys. Conclusion should be that many of the impotent men are not having orgasms. Further conclusion is that testosterone levels are not significant players in post-ejaculatory experience—including a post-ejaculatory hangover—since long term differences between ejaculators and non-ejaculators do not occur. 




1) The endocrine effects of visual erotic stimuli in normal men.

 Psychoneuroendocrinology. 1990;15(3):207-16.

 Carani C, Bancroft J, Del Rio G, Granata AR, Facchinetti F, Marrama P.


Endocrine responses to erotic stimulation in the laboratory were assessed in eight normal subjects. Each subject was tested on two occasions. On one occasion only neutral stimuli were involved. After 15 min baseline, 30 min of films were shown. For the erotic condition on the other occasion, two 10-min erotic films were interspersed with 10 min of neutral film. Fifteen-minute blood samples were taken from the start of each test and continued for 5 hr after the films. Plasma was assayed for testosterone, LH, prolactin, cortisol, ACTH and beta-endorphin. Urine was collected for 4 hr before and 4 hr after the films; this was assayed for adrenaline, noradrenaline and dopamine. Sexual arousal occurred in response to the erotic films in all subjects, as shown by erectile and subjective responses. There were no significant changes in hormone or catecholamine levels following either the erotic or the neutral stimuli, except for a rise in cortisol during the neutral but not the erotic film. These results indicate that in the laboratory, substantial sexual response can occur without accompanying endocrine or biochemical changes.


2) Neuroendocrine and cardiovascular response to sexual arousal and orgasm in men.

Psychoneuroendocrinology. 1998 May;23(4):401-11.


Data regarding the neuroendocrine response pattern to sexual arousal and orgasm in man are inconsistent. In this study, ten healthy male volunteers were continuously monitored for their cardiovascular and neuroendocrine response to sexual arousal and orgasm. Blood was continuously drawn before, during and after masturbation-induced orgasm and analyzed for plasma concentrations of adrenaline, noradrenaline, cortisol, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, growth hormone (GH), beta-endorphin and testosterone. Orgasm induced transient increases in heart rate, blood pressure and noradrenaline plasma levels. Prolactin plasma levels increased during orgasm and remained elevated 30 min after orgasm. In contrast, none of the other endocrine variables were significantly affected by sexual arousal and orgasm.

COMMENTS: I've seen a few "sciencey" articles claim that porn use increases testosterone levels 100%. The take away is that porn use is agreat way to keep your T levels high. However, I have yet to find a study to verify such claims. Below are studes where guys masturbated to porn as their hormones where monitored:




Scand J Psychol. 2003 Jul;44(3):257-63.

Fernández-Guasti A, Rodríguez-Manzo G.

Departamento de Farmacobiología, Cinvestav, Mexico. jfernand@mail.cinestav.mx


The present article reviews the current findings on the interesting phenomenon of sexual satiety. Knut Larsson in 1956 reported on the development of sexual exhaustion in the male rat after repeated copulation. We have studied the process and found the following results.

(1) One day after 4 hours of ad libitum copulation, two-thirds of the population showed complete inhibition of sexual behavior, while the other third displayed a single ejaculatory series from which they did not recover.

(2) Several pharmacological treatments, including 8-OH-DPAT, yohimbine, naloxone and naltrexone, reverse this sexual satiety, indicating that the noradrenergic, serotonergic and opiate systems are involved in this process. Indeed, direct neurochemical determinations showed changes in various neurotransmitters during sexual exhaustion.

(3) Given enough stimulation, by changing the stimulus female, sexual satiety was prevented, suggesting that there are motivational components of the sexual inhibition that characterizes sexual exhaustion.

(4) The GABA antagonist bicuculline, or the electrical stimulation of the medial preoptic area, did not reverse sexual exhaustion. These data suggest, on the one hand, that sexual exhaustion and the postejaculatory interval (which is shortened by bicuculline administration) are not mediated by similar mechanisms and, on the other, that the medial preoptic area does not regulate sexual satiety.

(5) The androgen receptor density in brain areas closely related to the expression of masculine sexual behavior, such as the medial preoptic nucleus, was drastically reduced in sexually exhausted animals. Such reduction was specific to certain brain areas and was not related to changes in the levels of androgens. These results suggest that changes in brain androgen receptors account for the inhibition of sexual behavior present during sexual exhaustion.

(6) The recovery process of sexual satiety after 4 hours of ad libitum copulation reveals that, after 4 days, only 63% of the males are able to show sexual behavior while after 7 days all animals display copulatory activity.

COMMENTS: The part of the brain where the receptor drop occurred tends to be very similar in all mammals. If this drop in testosterone receptors occurs in human males, it could explain why some men feel like their testosterone is low after too frequent ejaculation, and why they feel like their testosterone levels rise with a period of abstinence.

NOTE: This temporary effect is being measured in normal brains. If your brain has changed due to addiction, your dopamine is also dysregulated, quite apart from a temporary decline in testosterone receptors, and you will need longer to return to normal libido.

Also: #4 - Sexual exhaustion was prevented by introducing a novel female (that's what porn does).



Increased estrogen receptor alpha immunoreactivity in the forebrain of sexually satiated rats.

Horm Behav. 2007 Mar;51(3):328-34. Epub 2007 Jan 19.

Phillips-Farfán BV, Lemus AE, Fernández-Guasti A.


Department of Pharmacobiology, CINVESTAV, México City, México.


Estrogen receptor alpha (ERalpha) participates in the neuroendocrine regulation of male sexual behavior, primarily in brain areas located in the limbic system. Males of many species present a long-term inhibition of sexual behavior after several ejaculations, known as sexual satiety. It has been shown that androgen receptor density is reduced 24 h after a single ejaculation or mating to satiety, in the medial preoptic area, nucleus accumbens and ventromedial hypothalamus. The aim of this study was to analyze if the density of ERalpha was also modified 24 h after a single ejaculation or mating to satiety. Sexual satiety was associated with an increased ERalpha density in the anteromedial bed nucleus of the stria terminalis (BSTMA), ventrolateral septum (LSV), posterodorsal medial amygdala (MePD), medial preoptic area (MPA) and nucleus accumbens core (NAc). A single ejaculation was related to an increase in ERalpha density in the BSTMA and MePD. ERalpha density in the arcuate (Arc) and ventromedial hypothalamic nuclei (VMN), and serum estradiol levels remained unchanged 24 h after one ejaculation or mating to satiety. These data suggest a relationship between sexual activity and an increase in the expression of ERalpha in specific brain areas, independently of estradiol levels in systemic circulation.

COMMENTS: Estrogen receptors density increases in several regions following a single ejaculation, and sexual satiety. In the full study they suggest this change lasts longer than 24 hrs.


Relationship Between Sexual Satiety And Brain Androgen Receptors.

Romano-Torres M, Phillips-Farfán BV, Chavira R, Rodríguez-Manzo G, Fernández-Guasti A.

Neuroendocrinology. 2007;85(1):16-26. Epub 2007 Jan 8.

Department of Pharmacobiology, Centro de Investigación y Estudios Avanzados, Mexico City, Mexico.


Recently we showed that 24 h after copulation to satiety, there is a reduction in androgen receptor density (ARd) in the medial preoptic area (MPOA) and in the ventromedial hypothalamic nucleus (VMH), but not in the bed nucleus of the stria terminalis (BST).

The present study was designed to analyze whether the ARd changes in these and other brain areas, such as the medial amygdala (MeA) and lateral septum, ventral part (LSV), were associated with changes in sexual behavior following sexual satiety.

Males rats were sacrificed 48 h, 72 h or 7 days after sexual satiety (4 h ad libitum copulation) to determine ARd by immunocytochemistry; additionally, testosterone serum levels were measured in independent groups sacrificed at the same intervals. In another experiment, males were tested for recovery of sexual behavior 48 h, 72 h or 7 days after sexual satiety. The results showed that 48 h after sexual satiety 30% of the males displayed a single ejaculation and the remaining 70% showed a complete inhibition of sexual behavior. This reduction in sexual behavior was accompanied by an ARd decrease exclusively in the MPOA-medial part (MPOM). Seventy-two hours after sexual satiety there was a recovery of sexual activity accompanied by an increase in ARd to control levels in the MPOM and an overexpression of ARd in the LSV, BST, VMH and MeA. Serum testosterone levels were unmodified during the post-satiety period. The results are discussed on the basis of the similarities and discrepancies between ARd in specific brain areas and male sexual behavior.

COMMENTS: According to other studies androgen receptors increase on day 4, but have declined once more by day 7



Sexual behavior correlates with the diurnal plasma testosterone range in intact male rhesus monkeys

Biol Reprod. 1984 Apr;30(3):652-7.

Michael RP, Zumpe D, Bonsall RW.


There is evidence that androgens are necessary for the full expression of sexual behavior in male primates, but it has proved difficult to relate sexual activity to circulating androgens levels in comparisons between intact males. In the present study, 4423 behavior tests of 32 pairs of rhesus monkeys were conducted in a constant photoperiod over a 2-year period, and there was no significant relationship between the frequency of ejaculation and plasma testosterone levels in samples collected at 0800, 1600 or 2200 h. However, the magnitude of the diurnal range between the lowest and highest levels correlated negatively with sexual behavior. As the seasonal increase in sexual activity occurred, there was a corresponding decrease in the diurnal range of plasma testosterone. Furthermore, those males with the highest numbers of ejaculations showed the smallest diurnal plasma testosterone ranges. An additional experiment with 32 males revealed that neither behavior testing nor the occurrence of ejaculation influenced the diurnal testosterone range. Consequently, we have concluded that if any causality operated it would be in the direction of a hormonal influence on behavior. These findings suggest that increased nocturnal levels of testosterone do not enhance behavior and that a threshold level maintained throughout the 24 h may be a critical endocrine factor.

COMMENTS: Again, testosterone levels and ejaculation have little correlation


The post-orgasmic prolactin increase following intercourse is greater than following masturbation and suggests greater satiety (2006)

Biol Psychol. 2006 Mar;71(3):312-5. Epub 2005 Aug 10.

Brody S, Krüger TH.


Division of Psychology, School of Social Sciences, University of Paisley, Scotland, UK. stuartbrody@hotmail.com


Research indicates that prolactin increases following orgasm are involved in a feedback loop that serves to decrease arousal through inhibitory central dopaminergic and probably peripheral processes. The magnitude of post-orgasmic prolactin increase is thus a neurohormonal index of sexual satiety. Using data from three studies of men and women engaging in masturbation or penile-vaginal intercourse to orgasm in the laboratory, we report that for both sexes (adjusted for prolactin changes in a non-sexual control condition), the magnitude of prolactin increase following intercourse is 400% greater than that following masturbation. The results are interpreted as an indication of intercourse being more physiologically satisfying than masturbation, and discussed in light of prior research reporting greater physiological and psychological benefits associated with coitus than with any other sexual activities.

COMMENTS: This may be the only study comparing the hormonal differences between sexual intercourse and masturbation. It concluded that intercourse raised prolactin 400% more than masturbation. Prolactin rises at orgasm, and functions as a sexual satiationmechanisms - it inhibits dopamine.