Has too much masturbation decreased my testosterone levels?

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Answer: The preponderance of evidence says this is highly unlikely.

Read this article for a synopsis on the effects of ejaculation: Men: Does Frequent Ejaculation Cause A Hangover?

It's not surprising that many heavy porn users who develop erectile dysfunction suspect that masturbation has lowered their testosterone levels. Men posting on forums usually say something like, "All my lab tests came back normal, including T levels, so the doctor gave me Viagra."

First, it's quite rare for ED in young men to be caused by low testosterone. Second, men with porn-induced ED consistently report normal testosterone levels, yet they have clearly engaged in a lot of ejaculation. In addition, studies report similar testosterone levels in healthy men and men with chronic ED (1, 2, 3, 4). From these, the many studies discussed below, and the anecdotal evidence, we can conclude that:

  • low testosterone is rarely involved in youthful ED
  • frequency of ejaculation has no effect on testosterone levels.

Put simply, we know of no research evidence (yet) that implicates low testosterone in the reported negative effects of heavy porn use/masturbation. In fact, evidence generally points to the brain's reward circuitry and hypothalamus as central players in porn-related symptoms, and porn-induced sexual dysfunction. See this video for details.

This doesn't mean that other porn-induced brain changes cannot alter circulating hormones. It's quite likely they do, as addictions do alter the reward circuitry, which may affect downstream hormonal control systems. The current state of the science:

  1. Testosterone is not "used up" by ejaculation or masturbation, although testosterone receptors may decline for 3-4 days after ejaculation.
  2. Studies on both abstinence and "ejaculation to sexual exhaustion" demonstrate that neither have any effect on testosterone levels.
  3. In fact, the authors of this study and this study suggest that abstinence may lead to chronically lower testosterone levels.
  4. 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. After the single day spike testosterone returned to baseline until the end of the experiment at day 16.
  5. However, there's evidence that ejaculation to the point of sexual satiation triggers multiple brain changes - including a decline in androgen receptors and an increase in estrogen receptors in several brain regions. Recovery of full sexual appetite takes from 7-15 days and is quite apart from addiction-related brain changes.
  6. Porn-induced ED has nothing to do with blood testosterone levels. Anecdotal evidence, countless ED studies, and erectile physiology all refute this. See this discussion by a professor of reproductive endocrinology - Hypogonadal men and erections
  7. 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.  
  8. 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
  9. 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.
  10. 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.
  11. Long-term studies on primates have shown no reliable correlation between ejaculation and blood testosterone levels.
  12. By the way, testosterone levels normally fluctuate from 10-40%.
  13. This single study from 1974 reported less sexual activity correlating with higher testosterone - for some subjects, but not all. However, the study also found that higher levels of testosterone were associated with periods of sexual activity. A bit contradictory. Let's place this study in context: It has never been replicated and contains countless uncontrolled variables. All other animal and human studies examining testosterone and high ejaculation frequency, abstinence, various levels of sexual activity, along with erectile dysfunction refute its findings.

Close, trusted relationships and bonding behaviors, such as intercourse itself, increase overall wellbeing, so isolation or other lifestyle aspects of heavy porn use may possibly indirectly suppress testosterone levels, via epigenetics or other factors that alter cell performance.


 

Here's part of an exchange about testosterone levels and anabolic steroids that may be of interest to bodybuilding visitors. Note: A steroid user can become addicted to steroids. Even a few experiments with rats, which don't care about how they look, show addiction to anabolic steroids. So it's not only a psychological need to maintain muscle gained that hooks users. High levels also inhibit your own testosterone production. Be careful.

  • Question: How long have you been on HRT? There is a growing body of literature that suggests that low testosterone results in changes in the structure of the erectile tissue, leading to erectile dysfunction. If your testosterone was confirmed to be low, this is a likely cause of your current difficulties. Fortunately, it has been shown that these changes in erectile tissue are largely reversible with HRT. It would be reasonable to expect it to take slightly longer for your erections to improve than it would take for your testosterone to reach normal levels, since that's an actual physical change in the smooth muscle, not a simple matter of blood hormone levels. Out of curiosity, might I ask your age, how long you've been experiencing erectile problems, and how long you've undergone therapy so far?
  • Answer: I am on HRT now for 2 years. I am 40 years old now. I have been a semi-professional strength athlete for 20 years. During that time I frequently used anabolic steroids (AAS). This is probably the reason why my testosterone was to low when I stopped using AAS 3 years ago. After one year of recovery my endogenous testosterone levels were still nonexistent, so that was when I went on HRT. The last 8 years, the quality of my erections has been bad. So, that was when I was on and off the AAS and during HRT as well. There are so many factors involved that it is hard to say what is causing my ED. I hoped that a reboot could help me with this problem. Right now I don't know what other options I have.

 


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.

Abstract

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 succesful sexual activity increases LH and testosterone in men treted for ED. None of tye 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 testoterone levels.


 

PHARMACOLOGICAL AND PHYSIOLOGICAL ASPECTS OF SEXUAL EXHAUSTION IN MALE RATS

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

Fernández-Guasti A, Rodríguez-Manzo G.

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

Abstract

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.

Source

Department of Pharmacobiology, CINVESTAV, México City, México.

Abstract

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.