Abstract
Abstract
Assaults on sexuality in aging males result from changes in sexual physiology, psychosocial changes, irregular sexual activity, androgen deficiency, cardiovascular disease and risk factors, and lower urinary tract symptoms. Chronic illness, side effects of medications, and different kinds of surgery which the male may undergo during the aging process may all have its deleterious effects on sexual functions.
A healthy sexual attitude combined with lifestyle changes and addressing the physical problems provide a greater potential for enjoying a more fulfilled sexual life as one ages.
Introduction
Sexual dysfunction (SD) in aging males has only recently found widespread attention. Contrary to the previous conception of an asexual elderly, recent surveys show that the majority maintain sexual wishes and fantasies into old age.
Sexuality in elderly male has a significant Quality of Life (QOL) issue.. In the absence of any health-related issues, many elderly men show active sexual interest which is evident by their involvement in such activities.
SD in aging results from biological, psychosocial, lifestyle, and other physical changes. 1 Changes in sexual physiology adversely affect all components of sexual activity, including libido, erection, and ejaculation. Social isolation, nonavailability of partner or disinterest, emotional and relational stresses, all can lead to depression, further compounding sexual slowdown. The effects of androgen deficiency, associated lower urinary tract symptoms (LUTS), cardiovascular diseases and risk factors such as hypertension, diabetes, dyslipidemia, smoking, obesity, sedentary lifestyle, chronic illnesses, effects of various medications, and surgeries may further contribute to impairment of sexual functions.
Androgen Deficiency and Sexual Dysfunction in Aging Males
Androgens are essential for the growth and development of male external genitalia and, therefore, a reduction in the endogenous androgens is expected to have an adverse effect on the sexual functions in males. As the age advances, there is a reduction in the serum levels of testosterone. This is usually associated with rise in sex hormone–binding globulin further reducing the bioavailable testosterone. It is common knowledge that incidence of male SD increases with aging. Therefore, there is a correlation between reduction in serum levels of testosterone and increasing SD. This correlation has been found to be causal in nature rather than a mere coincidence. 2 A common clinical example is SD in men who have been treated with complete androgen deprivation for carcinoma of prostate.
Testosterone influences erectile function by both central and peripheral actions. Central action is related to facilitation of desire and arousal following stimulation via visual, auditory, olfactory, and tactile stimuli besides thoughts originating from the prefrontal region. This is seen as a progressive rise in the threshold for erection as the age advances. Peripheral action of testosterone is on the smooth muscle cells and the endothelial lining of the sinusoids in the corpora cavernosa. Testosterone plays a vital role in the RhoA/Rho kinase pathway and production of nitric oxide (NO) via the neuronal NO synthetase (nNOS). As a result, there is difficulty in initiating and maintaining erections. In addition to this, testosterone has been found to be acting as a maintenance fluid for the health of corpora cavernosa. There is evidence from animal studies indicating apoptosis of cavernosal smooth muscle and deposition of adipocytes in the subtunical region of corpora cavernosa consequent to androgen deprivation by orchidectomy. This causes suboptimal compression of tunical venules leading to venous leak and ill-sustained weak erections. This has been shown to reverse with administration of testosterone. This fact has been confirmed by clinical studies wherein hypogonadal men with erectile dysfunction (ED) have been shown to have venous leak documented with pharmaco cavernosography, which reversed upon testosterone administration.
Incidence of hypogonadism in men with ED is more than what is generally believed. 3 Using serum total testosterone as a marker, the incidence of hypogonadism in men with ED has been estimated to be 4.8%. However, when free testosterone levels were used, 17.6% of men with ED were found to be hypogonadal. 4 Hypogonadism causes diminished response to sildenafil in men with ED. The response rate of sildenafil rises when hypogonadism is treated suitably with testosterone replacement. Testosterone replacement alone is sufficient in treating ED in 40% of men with hypogonadism and ED.6, 6 Therefore, hypogonadal state must be excluded in men with initial poor response to sildenafil.
LUTS and Sexual Dysfunction in Aging Males
In aging men, both SD and LUTS are highly prevalent. The most common cause of LUTS is benign prostatic hyperplasia (BPH). A total of 26% men aged 40-79 years in Olmsted County were found to have LUTS while the Baltimore Longitudinal Study found the prevalence of BPH/LUTS to be up to 79% in the eighth decade. 7 The Massachusetts Male Aging Study showed that greater than 50% of men above the age of 40 years have ED and this was strongly related to age among other factors.
It has now been epidemiologically demonstrated that these two conditions do not simple co-exist in the similar population of older men but are related to each other. The Multinational Survey of the Aging Male studied the relationship between LUTS and SD and found LUTS to be a major risk factor in both erectile and ejaculatory disorders, independent of other risk factors. Another cross-sectional study of Spanish men (EDEM study) found LUTS to be the strongest risk factor for ED in elderly men.
A number of theories have been propounded to explain the physiologic reason for association between LUTS and SD. The NOS/NO hypothesis suggests that both conditions result from a decrease in the NOS/NO level in the smooth muscle with age. The autonomic hyperactivity and metabolic syndrome theory believes that LUTS is a part of the metabolic syndrome and both LUTS and ED are a result of autonomic hyperactivity. Increased smooth muscle contraction mediated by elevated Rho kinase activity may be another common pathway for the two conditions. Finally, pelvic atherosclerosis may account for chronic ischemia and resultant LUTS and ED.
Apart from hypothesis, a few recent studies suggest that the two conditions may also be amenable to common therapy. Therapy for LUTS also results in improvement in sexual function. Surgical therapy with transurethral resection of the prostate resulted in lower pain during ejaculation and improved erectile function in a study of 340 men. An open label trial of alfuzosin for six months in men with LUTS found that the drug facilitated significant improvement not only in LUTS but also in quality of life and sexual function. Two randomized, double blind placebo controlled studies demonstrated improvement in baseline sexual function including ED in men receiving doxazosin.
These epidemiologic, theoretical, and trial data suggests a relationship between LUTS and SD which merits further study and may be amenable to a common combination therapy. 8
Drugs-Disease-Surgery and Sexual Dysfunction in Aging Males
Sexuality is a vital component of a healthy emotional and physical relationship, and its importance does not decline with increasing age. While two-thirds of aging men express interest in maintaining sexual activity, there ability to do so depends upon their health status and the availability of a partner. Although aging and functional decline may affect sexual function, the urologist should rule out disease or side effects of medications and surgery in all such patients presenting with SD.
Sexual function may be adversely affected by common conditions such as diabetes, dyslipidemia, obesity, cardiovascular disease, alcohol abuse, arthritis and depression. Management of cardiovascular risk factors may reduce sexual dysfunction by improving endothelial function. Obesity may cause endothelial dysfunction and hypogonadism by elevating the levels of pro-inflammatory cytokines. Lifestyle changes to reduce weight have been shown to have a positive effect on sexual function by reducing the levels of C reactive protein and IL-6. ED is common in diabetic men, present in about 75% of diabetic men over 60 years. 9 Similarly, high total and low-density lipoprotein cholesterol and hypertension are other factors which when adequately controlled can potentially reverse the associated decline in sexual function.
Aging men are more likely to be on one or more chronic medication for an associated comorbidity. Moreover, with increasing age there is also a decline in renal and hepatic clearance of drugs. This leads to a greater likelihood of sexual adverse reactions in this age group, which can be reversed with diligent enquiry and intelligent substitution. Medications responsible for SD include selective serotonin reuptake inhibitors, tricyclic antidepressants, alpha and beta blockers, antipsychotics, diuretics and antihyperlipidemic drugs.
Surgery is also a potential cause of SD in aging men. Transurethral resection of the prostate invariably leads to retrograde ejaculation, which can be quite distressing for the patient unless he has been adequately forewarned. Other pelvic surgeries such as radical prostatectomy, radical cystectomy, and abdominoperineal resection also have an adverse impact on both ejaculatory and erectile functions. Rehabilitation of such patients involves a stepladder approach starting with sildenafil and going up to the use of penile prosthesis.
In conclusion, the evaluation and treatment of SD in aging men require a multifactorial approach. Simple measures such as control of risk factors, rationalization of medications, and rehabilitation after surgery can result in significant improvement in their sexual function.
Cardiac Risk and Sexual Dysfunction in Aging Males
Sexual dysfunction and cardiovascular diseases share common risk factors and are often associated with each other as both result from endothelial dysfunction. The Princeton guidelines provide a strategy for assessing cardiac risk and planning a safe return to sexual activity. Men at low cardiac risk include less than 3 cardiac risk factors, controlled hypertension, stable angina, congestive heart failure-grade-1, mild valvular disease, post–myocardial infarction (MI > 6 weeks). These can be treated for ED and can be sexually active without further untoward cardiac event. Men at high risk include unstable angina, uncontrolled hypertension, CHF (gr.3-4), MI (<2 weeks), recent stroke, moderate to severe valvular disease, and arrhythmias. These need to have their primary disease controlled and should be stabilized before treating ED and planning to resume sexual activity. Men at intermediate risk include more than 2 risk factors, moderate angina, MI ( >2, <6 weeks), CHF (GR-2), and stroke. These are candidates for restratification as either low or high risk and treated accordingly. 10
The close correlation between ED and cardiovascular disease (CVD) is a signal to evaluate sexual histories of all men who present for cardiac evaluation. Early detection of ED may allow for early diagnosis and management of CVD.
ED is an early marker of CVD as they share common risk factors and pathophysiology related to endothelial dysfuncton. Any person who has no cardiac symptoms but presents with ED should be screened for diabetes, dyslipidemia, cardiovascular diseases and hypertension. All patients with risk factors but asymptomatic for cardiac disease should undergo stress test for risk stratification. Lifestyle changes like reducing weight and increased physical activity may prove beneficial in ED. The recognition of ED as an early marker for CVD has led to the belief that any man with ED should be considered a cardiac patient until proved otherwise. These patients should be counselled for lifestyle modification.
Phosphodiesterase type 5 (PDE-5) inhibitors are well tolerated by most patients with stable cardiac disease who are not on nitrates or nitric oxide donors as the coprescription may result in life-threatening hypotension. So before treating such patients for ED they should be evaluated for any cardiac risk during sexual activity and treatment should begin only after stabilising cardiac condition (low-risk group).
Conclusion
With the expanding geriatric population and general attitudinal change towards sexuality, SD in the aging has recently found profound interest and has become an important QOL issue in the old age.
Recent surveys have shown that 60% of the elderly population continue to express their interest for maintaining sexual activity.
Besides normal biological changes and psychosocial factors, the other causes that impair sexual function in the aging include androgen deficiency, LUTS, cardiovascular risk, chronic illnesses, medications, and postsurgical effects.
Hypogonadism or androgen deficiency should be ruled out in patients with suggestive clinical features. The response rate of PDE-5 inhibitors rises when hypogonadism is treated suitably with testosterone replacement.
LUTS has recently been found to be a major risk factor for SD in aging. Epidemiologic and trial data have shown a clear relationship between them and both could be amenable to a common combination therapy.
Cumulative effect of chronic illness, side effects of various medications, and surgery is an important contributory factor for sexual decline in old age. Controlling such illnesses with rationalization of medications and rehabilitation after surgery can significantly improve the sexual function in them.
Cardiovascular disease and ED share common risk factors with endothelial dysfunction as the basic pathophysiology. Smaller penile arteries suffer obstruction from plaque earlier than larger coronary arteries. Thus, ED may be a marker for latent coronary artery disease. Treating these diseases and modifying the risk factors may help prevent SD in the elderly. It is also important to assess the adverse events of drugs and sexual activity in patients with coronary artery disease. Exercise stress testing is recommended for risk stratification to establish that patients with significant cardiac risk factors and known cardiac diseases can safely tolerate the physical work of sex before starting treatment of ED. Men with low cardiac risk can safely tolerate ED treatment and sexual activity, whereas those with high cardiac risk should get stable before resuming sexual activity and any treatment for it. In general, PDE-5 inhibitors and other treatment options are well tolerated in these patients. However, nitrates and NO donors are contraindicated for producing a potentially life-threatening hypotension.
Declaration of Conflicting Interests
The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author received no financial support for the research, authorship, and/or publication of this article.