Sexual inactivity results in reversible reduction of LH bioavailability

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 ¼ 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 ¼ 51), partial responders (at least one attempt; n ¼ 20) and non-responders (n ¼ 16). Compared to 30 healthy men with no ED, baseline B-LH (mean AE s.d.) in the 83 patients was decreased (13.6 AE 5.5 vs 31.7 AE 6.9 IU=L, P < 0.001), in the face of a slightly increased, but in the normal range, I-LH (5.3 AE 1.8 vs 3.4 AE 0.9 IU=L, P < 0.001); consequently, the B=I LH ratio was decreased (3.6 AE 3.9 vs 9.7 AE 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 ¼ 13.7 AE 5.3, post-therapy ¼ 22.6 AE 5.4, P < 0.001), modestly in partial responders (14.8 AE 6.9 vs 17.2 AE 7.0, P < 0.05) but remained unchanged in non-responders (11.2 AE 2.2 vs 12.2 AE 5.1). The corresponding changes went in the opposite direction for I-LH (5.2 AE 1.7 vs 2.6 AE 5.4, P < 0.001; 5.4 AE 2.2 vs 4.0 AE 1.7, P < 0.05; 5.6 AE 1.2 vs 5.0 AE 1.2, respectively), and in the same direction as B-LH for the B=I ratio (3.7 AE 4.1 vs 11.8 AE 7.8, P < 0.001; 4.2 AE 4.3 vs 5.8 AE 4.2, P < 0.05; 2.1 AE 0.7 vs 2.6 AE 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.

Using Ecological Momentary Assessment to Investigate Associations between Ejaculatory Latency and Control in Partnered and Non-Partnered Sexual Activities

“…In turn, this means that increased (or decreased) ejaculatory control at one event did not appear to affect ejaculatory control at a later event (and, thus, did not appear to affect confidence in one's ejaculatory performance in this context). This has some implications for the ''vicious circle'' hypothesis (Carosa et al, 2002;Hedon, 2003) in that the presence of a partner is required for this effect to take place. Therefore, it seems appropriate to clearly underline the interpersonal aspect of the vicious circle, rather than contextualize it as a feedback loop between strictly psychological states and sexual failures.…”

“…Also, indirect evidence for long-term temporal stability is indicated in studies in which PE patients have reported long durations for the dysfunction (e.g., Pryor, Althof, et al, 2006, who found that patients reported a mean PE duration of $16 years). It has also been suggested that sexual dysfunctions, including PE, may actually get worse over time, with the patient becoming stuck in a ''vicious circle'' of, for example, performance anxiety and rapid ejaculations (Carosa et al, 2002;Hedon, 2003;Jern et al, 2010).…”

Sexual Symptoms in Endocrine Diseases: Psychosomatic Perspectives

“…We have previously demonstrated, in open-label prospective studies, that men suffering from impotence, irrespective of its etiology, have significantly lower androgen levels than normal controls, although still in the normal range [7,8,9]. We hypothesized that this is due to reduced luteinizing hormone (LH) bioactivity, a marker of impaired GnRH secretion [7, 9].…”

“…We hypothesized that this is due to reduced luteinizing hormone (LH) bioactivity, a marker of impaired GnRH secretion [7, 9]. All successful therapies, such as psychological (behavioral therapy), pharmacological (prostaglandin, yohimbine, sildenafil, tadalafil), and mechanical (penile prostheses, surgery, vacuum device) therapies are able to restore testosterone (T) levels and LH bioactivity [8,9,10]. …”

The impact of sexual activity on serum hormone levels after penile prosthesis implantation

“…healthy men (1,2). Testosterone, which has androgenic and anabolic effects on human body, decline gradually with aging in males.…”