A recent study trying to explain the epidemiological relationship between the metabolic syndrome and LUTS hypothesized that the metabolic syndrome is associated with an overactivity of the autonomic nervous system [
9,
10] for which hyperinsulinemia, a key element of the metabolic syndrome might be responsible [
9,
10]. This overactivity of the autonomic nervous system is supposedly not responsible for the development of LUTS, but plays a key role in increasing the severity of LUTS above an intrinsic basal intensity that is determined by the genitourinary anatomical/pathophysiological characteristics of other ailments leading to LUTS [
11,
12]. Another recent study provided evidence that stress conditions could be associated with the development and aggravation of prostatic disease. It was found that body mass index, and age, greater diastolic blood pressure reactivity were associated with a greater transition zone volume, greater total prostate gland volume, greater postvoid residual bladder volume, and more severe LUTS [
13]. Inflammatory infiltrates are frequently found in and around nodules in benign prostate hyperplasia (BPH) and in symptomatic BPH [
14]. The presence of the metabolic syndrome might be a mediator of this association because it is associated with elevated serum C-reactive protein concentration, a non-specific marker of inflammation [
15], thus linking the metabolic syndrome to LUTS and elevated circulating C-reactive protein concentrations might be an indicator of intraprostatic inflammation in symptomatic BPH [
14,
15]. (Central) obesity is a hallmark of the metabolic syndrome of which the other components are dyslipidemia, hypertension, impaired glucose metabolism, with insulin resistance and diabetes type 2. Particularly if poorly controlled, there is a significant association between low level of total testosterone or DHEA-S and indices of poorly controlled type 2 diabetes [
16].
Insulin resistance is associated with hyperinsulinemia and insulin, particularly in excess, has due to its biochemical similarities with insulin-like growth factor, growth promoting properties [
17]. This might be a factor in the growth of the prostate in aging men [
18]. It has become clear that normal levels of T improve insulin resistance [
19].
All the above-mentioned elements of the metabolic syndrome are conducive to the development not only of erectile dysfunction but also of LUTS. Risk factors and medical co-morbidities of erectile dysfunction were prevalent among patients with LUTS [
20] (El-Sakka 2006b) and it is, therefore, not surprising that a larger number of studies have established a relationship between LUTS and erectile dysfunction [
21‐
23], particularly since an underlying vascular association between LUTS and erectile dysfunction could be demonstrated [
24].
As indicated earlier, with a more integrative approach to the ailments of the aging male, the age-related decline of plasma testosterone levels has been found to be a feature of erectile failure and central obesity in elderly men with proven successes of administration of testosterone to correct lower-than-normal levels [
25‐
29]. So, it is time to review the relationship between late onset hypogonadism (LOH) and LUTS, which like the other ailments mentioned earlier, manifest themselves concurrently in the lives of elderly men.