Sexual inactivity results in reversible reduction of LH bioavailability

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/1 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.