Erectile dysfunction and central obesity： an Italian perspective

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.

How to recognize late-onset hypogonadism in men wit sexual dysfunction

Late-onset hypogonadism （LOH） has been considered the most common form of male hypogonadism with a prevalence of approximately 1 in 100 men. Diagnosis of LOH should be made in symptomatic men with unequivocally low serum testosterone （T） levels. However, its clinical presentation is often insidious and difficult to recognize because it is characterized by nonspecific symptoms that make differential diagnosis with physiological ageing problematic. Sexual dysfunction is the most important determinant for medical consultation and the most specific symptom associated with low T. We therefore analysed a consecutive series of 1734 subjects who attended our unit for sexual dysfunction to investigate the associations between low T （different thresholds）, sexual parameters, medical history data （delayed puberty, pituitary disease or cryptorchidism） and their physical exam results. Metabolic parameters, in particular waist circumference, display the greatest accuracy in detecting low T. We found that only the association of several symptoms and signs could significantly raise the clinical suspicion of low T. Structured inventories, which cluster together symptoms and signs of hypogonadism, can help clinicians suspect androgen deficiency. In particular, structured interviews, such as ANDROTEST, have been demonstrated to have a greater accuracy when compared to self reported questionnaires in detecting low T levels.

Clinical correlates of enlarged prostate size in subjects with sexual dysfunction

Digito-rectal examination （DRE） of the prostate provides useful information on the state of prostate growth and on the presence of suspected peripheral nodules. The aim of this study is to describe the clinical and biochemical correlates of finding an enlarged prostate size at DRE in subjects with sexual dysfunction （SD）. A consecutive series of 2379 patients was retrospectively studied. The analysis was focused on a subset of subjects （n = 1823; mean age 54.7± 11.4） selected for being free from overt prostatic diseases. Several parameters were investigated. After adjusting for confounders, the presence of an enlarged prostate size at DRE was associated with a higher risk of metabolic syndrome （HR = 1.346 （1,129-1.759）; P = 0.030）, type 2 diabetes mellitus （HR = 1.489 （1.120-1.980）; P = 0.006）, increased LDL cholesterol （〉100mgdl^-1; HR = 1.354 （1.018-1.801）; P = 0.037） and increased mean blood pressure （BP） values （HR = 1.017 （1.007-1.027） for each mmHg increment; P = 0.001）. Accordingly, enlarged prostate size was also associated with a higher risk of arteriogenic erectile dysfunction （ED）, as well as with other andrological conditions, such as varicocele and premature ejaculation （PE）. PSA levels were significantly higher in subjects with enlarged prostate size when compared to the rest of the sample （HR = 3.318 （2.304; 4.799） for each log unit increment in PSA levels; P 〈 0.0001）. Arteriogenic ED, according to different criteria, was also associated with increased PSA levels. In conclusion, our data support the need to examine prostate size either by clinical （DRE） or biochemical （PSA） inspection in subjects with SD, in order to have insights into the nature of the SD and the metabolic and cardiovascular （CV） background of the patient.

Association between resting energy expenditure, psychopathology and HPA-axis in eating disorders

AIM: To investigate the complex relationships between resting energy expenditure(REE), eating psychopathology, and Hypothalamus Pituitary Adrenal axis functioning in patients with eating disorders. METHODS: The study was designed as a crosssectional survey, and it was planned by the Clinic for Eating Disorders of the University of Florence(Italy). The protocol was approved by the Ethics Committee of the Institution. Twenty two anorexia nervosa and twenty one Bulimia Nervosa patients were assessed by means of a clinical interview and the structured clini-cal interview for diagnostic and statistical manual of mental disorders, fourth edition. Eating attitudes and behaviour were specifically investigated by means of the eating disorder examination questionnaire(EDE-Q). Patients were also evaluated by means of the symptom checklist(SCL 90-R), REE was measured by means of indirect calorimetry, and blood cortisol morning levels were evaluated. RESULTS: Both anorexia nervosa and bulimia nervosa patients showed a reduced REE as compared with predicted REE. Body mass index(BMI) was positively associated with resting energy expenditure in Bulimics, whereas a strong, negative association between BMI and REE was observed in Anorectics. The pattern of associations between variables supported a mediation model, where shape concern accounted for variations in REE and cortisol levels(mediator), and variations in the mediator significantly accounted for variations in REE. When these associations where taken into account together, the relationship between shape concern and REE was no longer significant, whereas the association between cortisol levels and REE retained its significance, showing strong evidence for a single, dominant mediator. Anorectics and Bulimics showed an opposite pattern of association between BMI and REE. In Anorectics only, a higher REE was associated with a more severe eating disorder specific psychopathology, and cortisol levels represent a possible mediating factor for this relationship. CONCLUSION: The data supported a mediation model where cortisol levels mediated the relationship between eating psychopathology(concern about body shape) and REE.