Sex Increases Testosterone
by Gisela Henriques
Sex before a game can actually improve an athlete's performance, say researchers.
A recent study conducted by Italian researcher Emmnuele Jannini, from the University of L'Aquila proves that the levels of the testosterone hormone rise after having sexual intercourse.
This study tears apart the previous belief that if players were deprived from sex before a match they would have a better performance on the field because testosterone is often related to aggressiveness.
Researchers from the University of L'Aquila measured the levels of testosterone in the blood of more than 80 patients that suffered from long-term impotence. The results were to show that the amount of that hormone was two thirds of those with sexual active lives. After several months of therapy - that did not include hormone treatments-, the researchers found that the men that were treated with a reasonable success had an increase of their testosterone level, while the ones that did not respond to the treatments continued to have low production of testosterone.
The increase in the sexual activity made the researchers believe that the raise in the level of that hormone is related to the amount of sexual activity one has. Jannini told the English scientific journal New Scientist that he believes that in men " the body adjusts testosterone levels to match sexual drive to the sexual activity. If he [athlete] needs to be more aggressive it's better to have sex", he concludes.
Although it was known that inadequate levels of testosterone may cause depressed mood, lack of motivation on men and decreased energy, it was never established a correlation between the amount of sexual activity and its direct impact on the testosterone levels. Doctor David Handelsman, who studies reproductive medicine in the University of Sidney, also told New Scientist that Jannini's research was the " first clear evidence in the vexed relationship between male sexuality and testosterone", and that the previous researches did not provided any evidence of the levels of this hormone before and after treatments were induced in patients.
It is still fresh in our memories the controversy surrounding the Portuguese football coach's decision to prevent his players to have any contact with their wives during the 1996 European football tournament. His argument was led by the belief that his team would have a good performance if they did have any sexual activity on the nights previous to the games. On the opposite side were the Scandinavian coaches, who encouraged their players to go on with their conjugal duties. The overall final scores proved that perhaps the Danish and Swedish were right, and now scientific proof makes it even clearer why they had better results. On the verge of the classification to the Euro-2000, surely the Portuguese coaches will take these facts into consideration for a far better result.
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Here is an abstract of the above mentioned study.
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Paper
Sexual inactivity results in reversible reduction of LH bioavailability
E Carosa1, S Benvenga2, F Trimarchi2, A Lenzi3, M Pepe3, C Simonelli4 and E A Jannini1
1.Division of Endocrinology and Reproductive Medicine, Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy
2.Division of Endocrinology, University of Messina, Messina, Italy
3.Department of Medical Pathophysiology, University of Rome 'La Sapienza', Rome, Italy
4.Department of Psychology, Division of Psychology and Psychopathology of Sexual Behavior, University of Rome 'La Sapienza', Rome, Italy
Correspondence to: E A Jannini, Department of Experimental Medicine, University of L'Aquila, Coppito, Bldg. 2, Room A2/54, 67100, L'Aquila, Italy. E-mail:
[email protected]
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.
International Journal of Impotence Research (2002) 14, 93-99. DOI:10.1038/sj/ijir/3900832
Continued.....
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 [etiology; the set of factors that contributes to the occurrence of a disease; red] 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.
