Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Paper
  • Published:

Sexual inactivity results in reversible reduction of LH bioavailability

International Journal of Impotence Research volume 14, pages 93–99 (2002)Cite this article

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.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1
Figure 2
Figure 3

Similar content being viewed by others

References

  1. NIH Consensus Development Panel on Impotence. JAMA 1993 270: 83–90.

  2. Feldman HA et al . Impotence and its medical and psychological correlates: results of the Massachusetts Male Aging Study. J Urol 1994 151: 54–61.

    Article  CAS  Google Scholar 

  3. Krane RJ, Goldstein I, Sanz de Tejada I. . Impotence. New Engl J Med 1989 321: 1648–1659.

    Article  CAS  Google Scholar 

  4. Utiger RD. . A pill for impotence. Editorial. New Engl J Med 1998 338: 1458–1459.

    Article  CAS  Google Scholar 

  5. Govier FE, Dale McClure R, Kramer-Levien D. . Endocrine screening for sexual dysfunction using free testosterone determinations. J Urol 1996 156: 405–408.

    Article  CAS  Google Scholar 

  6. Johnson AR, Jarow JP. . Is routine endocrine testing of impotent men necessary? J Urol 1992 147: 1542–1543.

    Article  Google Scholar 

  7. Jannini EA et al . Lack of sexual activity from erectile dysfunction is associated with a reversible reduction in serum testosterone. Int J Androl 1999 22: 385–392.

    Article  CAS  Google Scholar 

  8. Dufau ML, Beitins IZ, McArthur JW, Catt KJ. . Effects of luteinizing hormone-releasing hormone (LHRH) upon bioactive and immunoreactive serum LH levels in normal subjects. J Clin Endocrinol Metab 1976 43: 658–667.

    Article  CAS  Google Scholar 

  9. Rich BH, Rosenfield RL, Moll GW, Lucky AW. . Bioactive luteinizing hormone pituitary reserves during normal and abnormal male puberty. J Clin Endocrinol Metab 1982 1: 140–146.

    Article  Google Scholar 

  10. Nagamani N, Osuampke C, Kelver ME. . Increased bioactive luteinizing hormone levels and Bio/Immuno ratio in women with hyperthecosis of the ovaries: possible role of hyperinsulinemia. J Clin Endocrinol Metab 1999 84: 1685–1689.

    CAS  PubMed  Google Scholar 

  11. Katt KJ, Dufau ML. . Gonadotropic hormones: biosynthesis, secretion, receptors, and action. In: Yen SSC, Jaffe RB (eds). Reproductive Endocrinology. Saunders Co: Philadelphia 1991 105–155.

    Google Scholar 

  12. Fabbri A et al . Endorphins in male impotence: evidence for naltrexone stimulation of erectile activity in patient therapy. Psychoneuroendocrinology 1989 14: 103–111.

    Article  CAS  Google Scholar 

  13. Heiman JR, Rowland DL. . Affective and psychological response patterns: the effect of instructions on sexually functional and dysfunctional men. J Psychosom Res 1983 27: 105–116.

    Article  CAS  Google Scholar 

  14. Korenman SG. . Advances in the understanding and management of erectile dysfunction. J Clin Endocrinol Metab 1995 80: 1985–1988.

    CAS  Google Scholar 

  15. Dufau ML, Pock R, Neubauer A, Catt KJ. . In vitro bioassay of LH in human serum: the rat interstitial cell testosterone (RICT) assay. J Clin Endocrinol Metab 1977 42: 958–969.

    Article  Google Scholar 

  16. Spratt D et al . WF. Bio- and immunoreactive luteinizing hormone responses to low doses of gonadotropin-releasing hormone (GnRH): dose–response curves in GnRH-deficient men. J Clin Endocrinol Metab 1986 63: 143–150.

    Article  CAS  Google Scholar 

  17. Fabbri A et al . Low bioactive luteinizing hormone in nonorganic male impotence: possible relationship with altered gonadotropin-releasing hormone. J Clin Endocrinol Metab 1988 67: 867–875.

    Article  CAS  Google Scholar 

  18. Linet OI, Ogrinc FG. . Efficacy and safety of intracavernosal alprostadil in men with erectile dysfunction. New Engl J Med 1996 334: 873–877.

    Article  CAS  Google Scholar 

  19. Padma-Nathan H et al . The Medical Urethral System for Erection (MUSE) Study Group Treatment of men with erectile dysfunction with transurethral alprostadil. New Engl J Med 1997 336: 1–7.

    Article  CAS  Google Scholar 

  20. Anonymous. . Yohimbine for male sexual dysfunction. Med Lett Drug Ther 1994 36: 115–116.

    Google Scholar 

  21. Kaplan HS. . The New Sex Therapy Brunner/Mazel: New York 1974

  22. Levine FJ, Goldstein I. . Vascular reconstructive surgery in the management of erectile dysfunction. Int J Impot Res 1990 2: 59–78.

    Google Scholar 

  23. Glibert P et al . Venous surgery in erectile dysfunction. Urol Int 1992 49: 40–47.

    Article  Google Scholar 

  24. Petrou SP, Barret DM. . The use of penile prostheses in erectile dysfunction. Sem Urol 1990 8: 138–152.

    CAS  Google Scholar 

  25. Meinhardt W et al . The negative pressure device for erectile disorders: when does it fail? J Urol 1993 149: 1285–1287.

    Article  CAS  Google Scholar 

  26. Segre GV, Brown EN. . Measurement of hormones. In: Williams Textbook of Endocrinology, IX edition. Saunders Co: Philadelphia 1998 43–54.

    Google Scholar 

  27. Veldhuis JD, Johnson ML, Dufau ML. . Preferential release of bioactive luteinizing hormone in response to endogenous and low dose exogenous gonadotropin-releasing hormone pulses in man. J Clin Endocrinol Metab 1987 64: 1275–1282.

    Article  CAS  Google Scholar 

  28. Sherwood N. . The GnRH family of peptides. Trends in Neurosci 1987 10: 129–132.

    Article  CAS  Google Scholar 

  29. Goldstein JA. . Erectile function and naltrexone. Ann Intern Med 1986 105: 799.

    Article  Google Scholar 

  30. Brannemann W et al . Treatment of idiopathic erectile dysfunction in men with the opiate antagonist naltrexone—a double-blind study. J Androl 1993 14: 407–410.

    Google Scholar 

  31. Veldhuis JD, Rogol AD, Samojlik E, Ertel NH. . Role of endogenous opiates in the expression of negative feedback actions of androgen and estrogen on pulsatile properties of luteinizing hormone secretion in man. J Clin Invest 1984 74: 47–55.

    Article  CAS  Google Scholar 

  32. Lightman SL et al . Constancy of opioid control of luteinizing hormone in different pathophysiological states. J Clin Endocrinol Metab 1981 52: 1260–1263.

    Article  CAS  Google Scholar 

  33. Plourde PV, Dufau ML, Plourde N, Santen RJ. . Impotence associated with low biological to immunological ratio of luteinizing hormone in a man with a pituitary stone. J Clin Endocrinol Metab 1985 60: 797–802.

    Article  CAS  Google Scholar 

  34. Warner BA, Dufau ML, Santen RJ. . Effects of aging and illness on the pituitary–testicular axis in men: qualitative as well as quantitative changes in luteinizing hormone. J Clin Endocrinol Metab 1985 60: 263–268.

    Article  CAS  Google Scholar 

  35. Carani C et al . Changes in the bioactivity to immunoreactivity ratio of circulating luteinizing hormone in impotent men treated with testosterone undecanoate. Acta Endocrinol 1989 120: 284–288.

    Article  CAS  Google Scholar 

Download references

Acknowledgements

The authors wish to thank Drs Massimino D'Armiento and Susanna Dolci for the critical reading of the manuscript. Our compliments and gratitude to Paola Minelli for her secretarial work and to Dr Rosaria Caruso for adapting her English expertise to our needs. This paper has been partially supported by the Italian Ministry of University and Scientific Research grants.

Author information

Authors and Affiliations

  1. Division of Endocrinology and Reproductive Medicine, Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy

    E Carosa & E A Jannini

  2. Division of Endocrinology, University of Messina, Messina, Italy

    S Benvenga & F Trimarchi

  3. Department of Medical Pathophysiology, University of Rome ‘La Sapienza’, Rome, Italy

    A Lenzi & M Pepe

  4. Department of Psychology, Division of Psychology and Psychopathology of Sexual Behavior, University of Rome ‘La Sapienza’, Rome, Italy

    C Simonelli

Authors
  1. E Carosa
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. S Benvenga
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. F Trimarchi
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. A Lenzi
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. M Pepe
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. C Simonelli
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. E A Jannini
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to E A Jannini.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Carosa, E., Benvenga, S., Trimarchi, F. et al. Sexual inactivity results in reversible reduction of LH bioavailability. Int J Impot Res 14, 93–99 (2002). https://doi.org/10.1038/sj.ijir.3900832

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.ijir.3900832

Keywords

Search

Advanced search

Quick links