COMMENTS: Authors suggest that successful sexual activity increases LH and testosterone in men treated for ED. None of the 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 testosterone levels.
Int J Impot Res. 2002 Apr;14(2):93-9; discussion 100.
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.
Male coital impotence, or erectile dysfunction (ED), is the chronic impossibility to have or to maintain a full erection in the presence of proper erotic stimuli.1 By the age of 75 y, at least 50% of men have developed impotence, the overall prevalence being about 20 million patients in the United States.2,3 ED is a symptom rather than a disease, and it is classified, on the basis of the etiology, into organic and nonorganic or psychogenic. However, the adjective psychogenic, even if widely used, is overtly inappropriate because, irrespective of the ultimate cause, impotence is per se stressful and source of psychological disturbances. Thus, all cases of ED are, or become, psychogenic.4
The organic causes of impotence are vascular (arteriogenic and venogenic), iatrogenic (medical and surgical), neurogenic (central and peripheral neuropathy), and, less frequently (with the exclusion of diabetes that causes arteriogenic and neurogenic impotence), endocrine. Primary or secondary hypogonadism, defined as subnormal levels of testosterone associated with high or, respectively, low levels of luteinizing hormone (LH), has been found in 15.6% of 268 impotent men,5 while others reported only a 2.1% prevalence (n=330).6 This puzzling discrepancy derives from differences in definition of impotence, age of the patients, diagnostic and inclusion criteria. We recently demonstrated that the reduction of sexual activity due to ED provokes a transitory decrease in serum testosterone levels.7 The pathogenesis of this reversible, relative hypotestosteronemia remains to be clarified.
The simultaneous measurement of bioactivity and immunoreactivity of LH has shown qualitative differences in the hormone that may be related to physiological processes. Since the LH secretion is pulsatile, the ratio of bioactive LH (as determined by androgen synthesis on Leydig cells) and immunoreactive LH (the ‘B/I ratio’) varies from 2 to 4 at the nadir of the serum LH pulsation, to values from 4 to 6 with LH peaks.8 The biochemical explanations of these differences are not clear, but post-translation modifications, such as the state of hormone glycosylation, are thought to play a role. A dichotomy between B- and I-LH has been demonstrated in many disorders of the hypothalamic-pituitary-gonadal axis.9,10 Thus, differences in the B/I ratio may reflect pathophysiological changes in the hypothalamo-pituitary complex involving GnRH secretion.11
The prospective, controlled study reported here has been undertaken to determine, in comparison with an aged-matched control group of sexually active volunteers, the quantity and quality of LH production, as measured by immunoradiometric and in vitro bioassay, respectively, in patients with organic and nonorganic impotence, before and after different nonhormonal treatments.
Subjects and methods
All experiments were conducted in accordance with the Declaration of Helsinki. The group of 83 patients with chronic ED reported in this study has been previously described.7 Patients were consecutive, ambulatory patients seen at our endocrine clinics who met all of the following inclusion criteria: (1) aged between 18 and 70 y at first examination (age 18-35: 37.3%; age 36-55: 48.2%; age 56-70: 14.5%); (2) ED of at least 1 y duration with or without loss of libido, as established by a clinical questionnaire;12 (3) stable relationship of at least 1 y; (4) return to the therapy follow-up.
We excluded from this study patients with: (1) history of cryptorchidism and varicocele; (2) clinically evident hypogonadism; (3) past or current use of illicit drugs; (4) previously defined etiology of ED.
The clinical questionnaire demonstrated that the majority of patients did not practice regular masturbation. However, eight subjects masturbated, with or without full erection, more than once a month. In all the patients the impotence was chronic and absolute, that is it was present with any partner.
Although in our study each patient serves as his own control, to evaluate the hormone profile at baseline (pre-therapy) we recruited 30 control volunteers upon informed consent. They were three groups of 10 men for each of the age classes 18-35, 36-55, and 56-70. Subjects were asked to complete the Personal History Questionnaire and Sexual History Form,13 with slight modifications, to provide information on the volunteer’s background, sexual experience, and sexual functioning. Exclusion criteria were the same as for patients. Entry criteria were: (1) good general health, (2) stable relationship with at least two successful attempts of sexual intercourse per week.
Diagnostic evaluation and study design
The impotent men admitted to the study were classified into two groups (organic and nonorganic) on the basis of the following data:14 results of laboratory (glycemic, hepatic, lipidic, and renal profiles), psychiatric (Minnesota Multiphasic Personality Inventory and State trait Anxiety Index), neurological (bulbocavernous reflex latency time), and vascular (penile-brachial pressure index before and after exercise; two dimensional Doppler assessment before and after vasodilator infusion) parameters. Pharmacocavernosometry, pharmaco-cavernosography, and angiography were used when indicated to study patency of major vessels and the veno-occlusive mechanism.
Reproductive axis was evaluated by the use of commercial kits for Immunoreactive Luteinizing Hormone (I-LH; n.r.: 1.5-10.0 IU/L). Finally, to demonstrate variations in the regulation of qualitative aspects of LH production, LH biopotency (B-LH) was studied by the Rat Interstitial Cell Testosterone (RICT) assay, as described by Dufau et al,15 with minor modifications.16 The B/I-LH ratio was calculated as previously described,17 with the only difference that I-LH levels were assessed by IRMA instead of RIA. The standard used was LH 78/549, generously provided by the National Biological Standard Board (London, UK). This standard was also calibrated using the 2nd IRP hMG. The results are expressed in IU/L of this standard. The sensitivity of the assay was 0.4 IU/L, and the intra- and interassay CV were 9 and 14%, respectively.
Since gonadotropins are secreted episodically and vary both diurnally and seasonally, FSH, I-LH, and B-LH were measured in duplicate both at entry and after 3 months from the beginning of the various impotence therapies on serum collected every 15 min for 90 min, starting at 0800 h. Samples were pooled using the same volume of serum and stored at -70°C. For each hormone, including B-LH, each pair of serum samples (ie pre- and post-therapy) of a given patient were assayed in the same run. Because patient treatments were scattered throughout the year, seasonal variations of pituitary-testicular axis did not affect the results.
The major cause of impotence in our cohort of unselected patients was the vascular etiology, being the venous leak (34%, considered on a basis of 91 cases since eight patients had two etiologies) equally represented with respect to the arterial pathology (31%). The lowest prevalence was found in the neurogenic group (8%). In 27% of cases it was impossible to demonstrate an organic cause for the symptom.
Major endocrine abnormalities in 83 subjects were not found. In fact, basal serum values of prolactin (PRL), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and urinary free cortisol (as determined by commercial kits) did not significantly differ from controls. However, metabolic alterations were discovered in 28 patients, with the higher frequency in subjects with arteriogenic impotence.
The global therapy efficacy was evaluated by asking the patient and the partner, in separate rooms: ‘After 3 months of therapy, did the treatment improve your/his erections?’ (R.: ‘yes, partially, no’). Furthermore, it has been evaluated how often full sexual intercourse has been performed in the past month on the basis of the patient and partner’s logs. Subjects were designed as ‘full responders’ when they had eight or more successful attempts of sexual intercourse per month, ‘partial responders’ when they had at least one successful sexual intercourse per month, and ‘non responders’ when they did not have sexual intercourse.
The results are expressed as mean±s.d. Mean differences in hormone levels were analyzed with the paired and unpaired t-test as appropriate, by setting the level of significance at P values <0.05.
Hormone profile at entry
Figure 1 shows that I-LH was slightly but significantly higher in the whole group of patients with ED with respect to controls (5.3±1.8 vs 3.4±0.9 IU/L, P<0.001; Figure 1A), but always in the normal range. On the contrary, mean LH biopotency, as measured by the RICT assay (Figure 1B), was significantly lower (13.6±5.5 vs 31.7±6.9 IU/L, P<0.001). Thus, the B/I-LH ratio was dramatically reduced in patients with absent sexual activity for impotence (3.6±3.9 vs 9.7±3.3, P<0.001; Figure 1C).
This particular hormonal pattern has been found in all four etiological subgroups, demonstrating that it is not due to the disease underlying the impotence (Table 1, column ‘All’, row ‘Pre’). These changes mirror those previously found in testosterone levels.7 These differences hold true even when patients and controls are compared by age (data not shown).
Hormone changes after therapy
To test whether recovery of the sexual activity by a variety of non-hormonal therapeutic interventions affects the reduced B/I-LH ratio of impotent patients, we repeated the B- and I-LH assays 3 months after the beginning of each therapy and correlated hormone values with the sexual performance achieved over this period. Considering our patient group as a whole, 15% of the total did not improve its sexual performance after 3 months of therapy, 24% obtained a partial recovery, while a full recovery was found in 61%. Luteinizing hormone biopotency, immunoreactivity and their ratio changed significantly after 3 months of different impotence therapies in the whole group of 83 patients (B-LH: 13.6±5.5 vs 19.8±6.9 IU/L; I-LH: 5.3±1.8 vs 3.3±1.7 IU/L; B/I-LH: 3.6±3.9 vs 9.0±7.4; P<0.001 for each difference). However, in the subgroup with persistent impotence and no resumption of sexual activity because of therapy failure, B-LH (11.2±2.2 vs 12.2±5.1 IU/L), I-LH (5.6±1.2 vs 5.0±1.2 IU/L), and their ratio (2.1±0.7 vs 2.6±1.3) were unchanged after the therapy. When recovery was complete, serum values of these hormones significantly increased, with the exception of I-LH levels that significantly decreased (B-LH: 13.7±5.3 vs 22.6±5.4 IU/L, P<0.001; I-LH: 5.2±1.7 vs 2.6±5.4 IU/L, P<0.001; B/I-LH: 3.7±4.1 vs 11.8±7.8, P<0.001). Finally, in partially responding patients the same pattern was seen, even if to a lower, but significant, extent (B-LH: 14.8±6.9 vs 17.2±7.0 IU/L, P<0.05; I-LH: 5.4±2.2 vs 4.0±1.7 IU/L, P<0.05; B/I-LH: 4.2±4.3 vs 5.8±4.2, P<0.05).
These differences may be due to the various etiological causes of ED and/or to the different impotence therapies. In response to the first possibility, hormonal values before and after treatments were divided on the basis of the etiological category. Irrespective of the etiology, patients in whom therapies failed (Table 1, column 0) showed no increment in B/I-LH ratio. Patients who recovered completely (Table 1, column 2+) showed for each etiological group a significant increase of B/I-LH values. A comparable pattern was demonstrated for testosterone levels in the same patients.7
The second possibility is that the hormonal changes found in our patients are due to the different therapies. Thus, we divided the various impotence treatments into three therapeutic subgroups: psychological, medical (prostaglandin E1, yohimbine), and mechanical (vacuum devices, penile prostheses, vascular surgery) therapies (Figure 2). Statistical significance of the increases in total testosterone and in the B/I ratio of LH was found only in the patients who fully recovered in all three therapeutic subgroups and in some who partially recovered, demonstrating that the normalization of hormonal values is not due to the differences in impotence therapy.
Hence, resumption of sexual activity per se, within 3 months from beginning of the successful therapy, restores LH biopotency. In contrast, persistent ED, and related sexual inactivity, maintains a low B-LH.
In this study we show that the B/I ratio of LH of impotent patients is significantly reduced with respect to healthy men. We also demonstrate the reversibility of this endocrine pattern upon the resumption of sexual activity obtained with both etiological or symptomatic therapies.
The GnRH pulses of adequate amplitude and frequency are critical determinants of the normal processing of LH by the gonadotrophs and the secretion of LH with a normal B/I-LH ratio.26,27 In fact, LH bioassay has been regarded as sensitive parameters of endogenous GnRH secretion. We have extended earlier studies on 23 impotent males aged 25-50 y in whom immunoassayble LH was measured by RIA.17 Importantly, these early series consisted of purely psychogenic impotent patients, while the present series included nonorganic, vascular and neurological patients. Moreover, the early patients were studied only at baseline showing a low serum testosterone and a low bioactivity of serum LH associated with impotence. It was concluded that the psychogenic impotence is characterized by a dysfunction concerning the hypothalamic GnRH pulse generator. Gonadotropic Releasing Hormone is thought to play a pivotal role in the neuroendocrine control of reproductive and sexual activity.28
We have shown here that the biological hypoactivity of LH is not irreversible. No matter how ED is successfully treated, within 3 months after commencement of treatment, LH bioactivity increases towards normality (and, as a result, testosterone returns towards normality).7 Partial therapeutic success restores the hormone pattern to a lower extent, while therapeutic failure leaves the hormone pattern unchanged. Thus, we may hypothesize that psychological stress associated with lasting impotence (that is, lasting lack of sexual activity) causes an hypothalamic disturbance of the GnRH pulse generator which, in turn, causes pituitary to secrete LH molecule with reduced bioactivity. This is suggested by the role of stress-induced endogenous opiates in erectile failure,7,17,29,30 substances that have been demonstrated to control the hypothalamic pulse generator of GnRH as well as LH levels.31,32 In fact, it has been demonstrated that nonorganic impotence is associated with pulsatile GnRH secretion of lower than normal amplitude.17 Since the low B-LH levels are indeed associated with diminished testosterone production17,33,34 and testosterone is able to increase significantly the B/I-LH ratio,35 the low androgen levels found in ED7 may in turn amplify the disruption of a correct GnRH discharge. The close parallelism between serum testosterone and B-LH levels leads to the conclusion that the decreased LH bioactivity is principally, if not exclusively, responsible for the inhibition of testicular androgen secretion found in subjects with absent sexual activity.7
The vicious circle triggered by the ED is illustrated in Figure 3(A). This may represent an adaptive mechanism. In other words, sexual activity feeds itself through activation of the hypothalamic-pituitary axis, and the impossibility to have a regular sexual activity resets the hormonal reproductive axis to a lower level. The vicious circle is disrupted (and the LH-testosterone axis restored) by the resumption of sexual activity, regardless of the modality of the nonhormonal treatment (Figure 3B). It will be now of interest to see whether a similar impairment of LH bioactivity exists in the equivalent sexual dysfunction of women.
In conclusion, we have demonstrated that the loss of sexual activity is characterized by low B/I LH ratio, and that resumption of normal sexual behavior can restore this endocrine pattern. For this reason, we suggest that sexual activity is able to feed itself throughout the activation of hypothalamic-pituitary axis, prepares for the next sexual meeting and for the re-activation of the same endocrine axis.
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.
|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. MEDLINE
3 Krane RJ, Goldstein I, Sanz de Tejada I. Impotence. New Engl J Med 1989; 321: 1648-1659. MEDLINE
4 Utiger RD. A pill for impotence. Editorial. New Engl J Med 1998; 338: 1458-1459. MEDLINE
5 Govier FE, Dale McClure R, Kramer-Levien D. Endocrine screening for sexual dysfunction using free testosterone determinations. J Urol 1996; 156: 405-408. MEDLINE
6 Johnson AR, Jarow JP. Is routine endocrine testing of impotent men necessary? J Urol 1992; 147: 1542-1543. MEDLINE
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. MEDLINE
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.
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. MEDLINE
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.
12 Fabbri A et al. Endorphins in male impotence: evidence for naltrexone stimulation of erectile activity in patient therapy. Psychoneuroendocrinology 1989; 14: 103-111. MEDLINE
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. MEDLINE
14 Korenman SG. Advances in the understanding and management of erectile dysfunction. J Clin Endocrinol Metab 1995; 80: 1985-1988. MEDLINE
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.
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. MEDLINE
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. MEDLINE
18 Linet OI, Ogrinc FG. Efficacy and safety of intracavernosal alprostadil in men with erectile dysfunction. New Engl J Med 1996; 334: 873-877. MEDLINE
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. MEDLINE
20 Anonymous. Yohimbine for male sexual dysfunction. Med Lett Drug Ther 1994; 36: 115-116.
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.
23 Glibert P et al. Venous surgery in erectile dysfunction. Urol Int 1992; 49: 40-47. MEDLINE
24 Petrou SP, Barret DM. The use of penile prostheses in erectile dysfunction. Sem Urol 1990; 8: 138-152.
25 Meinhardt W et al. The negative pressure device for erectile disorders: when does it fail? J Urol 1993; 149: 1285-1287. MEDLINE
26 Segre GV, Brown EN. Measurement of hormones. . In: Williams Textbook of Endocrinology, IX edition. Saunders Co: Philadelphia, 1998, 43-54.
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. MEDLINE
28 Sherwood N. The GnRH family of peptides. Trends in Neurosci 1987; 10: 129-132.
29 Goldstein JA. Erectile function and naltrexone. Ann Intern Med 1986; 105: 799. MEDLINE
30 Brannemann W et al. Treatment of idiopathic erectile dysfunction in men with the opiate antagonist naltrexone¾a double-blind study. J Androl 1993; 14: 407-410. MEDLINE
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. MEDLINE
32 Lightman SL et al. Constancy of opioid control of luteinizing hormone in different pathophysiological states. J Clin Endocrinol Metab 1981; 52: 1260-1263. MEDLINE
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. MEDLINE
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. MEDLINE
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. MEDLINE
|Figure 1 Serum values of immunoreactive LH (A); bioactive LH (B) levels; and bio/immuno-LH ratio (B/I-LH, C) in 83 impotent patients. Values are expressed as mean±s.d. vs 30 healthy controls.|
|Figure 2 Comparison of circulating bio/immuno LH ratio (B/I LH) concentrations in 83 impotent men prior (pre) and after (post) 3 months from the beginning of the specified therapies (indicated in bold). Patients are classified according to the outcome: ‘full responders’ when they had eight or more successful attempts of sexual intercourse per month (2+), ‘partial responders’ when they had at least one successful sexual intercourse per month (1+), and ‘non responders’ when they did not have sexual intercourse (0). Subtotals of etiological groups do not add up, because eight patients have two etiological causes. Initial diagnoses are also indicated. Prostaglandin E1 was administered at a dose of 10-20 µg by intracavernosal injection18 or at a dose of 500 µg by transurethral; administration;19 yohimbine hydrochloride was given orally, at a dose of 5.4 mg three times a day.20 Psychological therapy was applied using standard therapeutic protocols of HS Kaplan (a time limited format and an assignment of specific, graduated erotic exercises to be carried out at home and discussed in subsequent therapy sessions).21 Vascular surgery consisted in both arterial reconstructive surgery22 or venous surgery such as Selective Vein Ligation (SVL) of veins identified as incontinent.23 Penile prostheses used in this study were inflatable self-contained prostheses.24 Finally, commercial vacuum constriction devices were used.25 *P<0.05; **P<0.001.|
|Figure 3 Physiopathology of low LH biopotency during erectile dysfunction (A); and normal autofeeding of sexual activity throughout activation of the hypothalamus-pituitary-testis axis (B). The hypothesized stressful reduction of sexual activity for impotence of any cause may alter a correct GnRH discharge, leading to a low testosterone production. This may, in turn, amplify the alteration of the hypothalamus-pituitary communication as well as the impairment of sexual drive.|