Erectile dysfunction and central obesity: an Italian perspective

Abstract

Erectile dysfunction (ED) is a frequent complication of obesity. The aim of this review is to critically analyze the framework of obesity and ED, dissecting the connections between the two pathological entities. Current clinical evidence shows that obesity, and in particular central obesity, is associated with both arteriogenic ED and reduced testosterone (T) levels. It is conceivable that obesity-associated hypogonadism and increased cardiovascular risk might partially justify the higher prevalence of ED in overweight and obese individuals. Conversely, the psychological disturbances related to obesity do not seem to play a major role in the pathogenesis of obesity-related ED. However, both clinical and preclinical data show that the association between ED and visceral fat accumulation is independent from known obesity-associated comorbidities. Therefore, how visceral fat could impair penile microcirculation still remains unknown. This point is particularly relevant since central obesity in ED subjects categorizes individuals at high cardiovascular risk, especially in the youngest ones. The presence of ED in obese subjects might help healthcare professionals in convincing them to initiate a virtuous cycle, where the correction of sexual dysfunction will be the reward for improved lifestyle behavior. Unsatisfying sexual activity represents a meaningful, straightforward motivation for consulting healthcare professionals, who, in turn, should take advantage of the opportunity to encourage obese patients to treat, besides ED, the underlying unfavorable conditions, thus not only restoring erectile function, but also overall health.

Implanted Muscle-Derived Stem Cells Ameliorate Erectile Dysfunction in a Rat Model of Type 2 Diabetes, but Their Repair Capacity Is Impaired by Their Prior Exposure to the Diabetic Milieu

“…It impairs the quality of life of patients and their partners and leads to considerable health costs (3,4). Erectile dysfunction is also prevalent in obese and metabolic syndrome patients (5–7). The risk factors and the histopathology that underlie erectile dysfunction are very similar to those affecting the media smooth muscle in the arterial tree in arteriosclerosis and hypertension (8,9).…”

Erectile dysfunction

“…Finally, meta-analysis of available evidence demonstrates that moderate and more frequent physical activity are associated with reduced risk of erectile dysfunction 90 . Accordingly, both cross-sectional and prospective epidemiological studies suggest that obesity and metabolic syndrome are associated with an increased risk of erectile dysfunction 91 . It is conceivable that obesity-associated hypogonadism and increased cardiovascular risk are correlated with the higher prevalence of erectile dysfunction in overweight and obese men (see below).…”

“…It is conceivable that obesity-associated hypogonadism and increased cardiovascular risk are correlated with the higher prevalence of erectile dysfunction in overweight and obese men (see below). However, recent clinical and experimental studies suggest that the association between erectile dysfunction and central obesity is independent from obesity-associated comorbidities and hypogonadism 91 . Although increased levels of tumour necrosis factor (TNF; also known as TNFα) — a cytokine involved in systemic inflammation — could be a mediator of these conditions 92 , further studies are needed to confirm this.…”

Metformin In Vitro and In Vivo Increases Adenosine Signaling in Rabbit Corpora Cavernosa

“…Although early evidence was against an endothelium dependency of ADO-induced relaxation of CC strips [32], recent studies suggest an involvement of NO in ADO signaling. Penile tissues from animals and humans receive a rich cholinergic innervation, which activates M3 muscarinic receptors on vascular endothelium and nicotinic receptors located on NANC nerves [44], promoting the synthesis and release of NO, which finally leads to the relaxation of arterial and trabecular smooth muscle in the CC [18,45]. NO is produced as the enzymatic by-product of molecular oxygen and L-arginine under the control of nNOS in NANC neurons, which is responsible for the immediate relaxation of CC and eNOS in the endothelium, which is essential for maintaining erection [18].…”