Association between metabolic syndrome (MetS) at baseline and incidence of major adverse cardiovascular events (MACE) during a mean follow-up of 4.3 years. Panel A represents the Kaplan Meier curves for incidence of MACE in a population of 211 men aged 18–52 years having or not MetS at baseline. This group represents the first tertile of age of a sample of patients (n=619) consulting the Sexual Medicine and Andrology Unit of the University of Florence for erectile dysfunction and followed-up for a mean of 4.3 years for the occurrence of MACE. Panel B represents the Cox analyses for the age- and smoking habit-adjusted incidence of MACE associated with the number of MetS components at baseline (glycaemia ≥100 mg/dL, triglycerides ≥150 mg/dL, HDL <40 mg/dL; blood pressure ≥135/80 mmHg, waist circumference >102 cm), according to the tertile of age, in the same population, during the same follow-up. The first, second and third tertile include 211, 199 and 209 patients aged 18–52, 53–60 and 61–88 years, respectively.
If you suffer from erectile dysfunction and you can’t blame it on underlying health conditions, you might feel like your problems are all in your head. While psychological issues may be at the root of your problem, they are just as valid as many physiological causes for ED. Keep reading to learn more about the psychological causes of ED and what you can do to resolve them.
To avoid the dreaded whiskey d---, you don’t necessarily have to stop drinking alcohol. Just drink in moderation. The National Institute on Alcohol Abuse and Alcoholism defines moderate drinking as no more than two drinks a day for men, and one drink a day for women. The liver can only process 1 ounce of liquor or one standard drink in one hour. Consuming more than this will lead the system to become saturated, where extra alcohol will increase in the blood and body tissues, until the liver is ready to metabolize it again. Until then, high blood alcohol concentration will last for several hours and affect you physiologically.
For patients who have ED related to hypertonic cavernous smooth muscle and excessive sympathetic discharge, we recommend a trial of a low-dose alpha adrenergic blocker, such as terazosin 1 mg PO at bedtime nightly. We typically increase the dosage as needed every 2–3 weeks for 3–5 months until the patient experiences improvement of the erection or we determine that treatment is ineffective. We explain the potential side effects of orthostasis, dizziness, and retrograde ejaculation in detail. We also take great care and time in explaining to the patient, and his family/partner if present, the pathophysiologic mechanism of their erectile dysfunction and the biological basis of the treatment plan. This detailed discussion helps to engage the patient in the treatment plan and provides encouragement regarding the potential for response to treatment and recovery. During these encounters, we utilize teaching tools, such as diagrams, drawings, printed handouts, and other visual aids to ensure that the discussion is patient-focused and patient-friendly. Patient education is critical to exploring treatment options and developing confidence in our ability to treat the ED, and their own ability to overcome and eventually resolve the problem of ED.
If the patient complains of loss of sensation on his penile shaft or glans, it is useful to perform hot and cold perception testing and/or additional vibratory sensory testing with biothesiometer. These are tests that can be performed quickly during the office visit and provide useful information about the function of the dorsal nerve of the penis (Table 3).
And be aware that the vast majority of physical or psychological causes of erectile dysfunction are temporary. They may go away as quickly as they occurred. But if anything is bothering you or your partner, you should seek out confidential, professional advice. There is no point in worrying and not doing anything about it. It may just make the situation worse.
When we say it’s a barometer of men’s health, it’s a signal. It’s an indicator that things may be right or not. And so when a man develops an erectile problem– and we’re talking about something that is occurring over time. It’s not something that just occurred overnight. When it occurs overnight, it’s more often than not a psychogenic, an anxiety reaction.
Similar to the general population (58), in subjects consulting for sexual dysfunction, T deficiency is progressively more prevalent as a function of age (50). In a series of 4,890 subjects consulting our Sexual Medicine and Andrology Unit for sexual dysfunction, one in five (19.6%) and one in three (29.4%) patients have total T below 10.4 and 12 nmol/L, respectively (60). Clinical correlates of T deficiency show different figures according to patient’s age. In fact, we previously demonstrated that in the youngest quartile (17–42 years old), but not in the oldest one (62–88 years old), severity of reported ED and penile blood flow impairment (dynamic peak systolic velocity) were not associated to decreasing testosterone levels (50). It is possible to speculate that, in young individuals, intercourse-related penile erection is such a complex phenomenon that other determinants (i.e., intrapsychic or relational) might mask its androgen regulation and that T deficiency produces greater sexual disturbances in subjects with greater frailty, such as older individuals. However, reported frequency of spontaneous erection and sexual thoughts were significantly decreased as a function of T decline even in younger subjects (50). Moreover, in young individuals low T was associated with a worse metabolic profile, including hypertriglyceridemia and increased waist circumference (50). Accordingly, the prevalence of MetS in the youngest quartile was clearly associated with T deficiency, as it was in the older quartiles (50). Therefore, T deficiency must be accurately verified in all subjects consulting for sexual dysfunction, even in the youngest ones.
Sildenafil (Viagra) was the first oral phosphodiesterase type 5 (PDE5) inhibitor approved by the FDA in the United States for the treatment of erectile dysfunction (it is not approved for women). Sildenafil inhibits PDE5, which is an enzyme that destroys cGMP. By inhibiting the destruction of cGMP by PDE5, sildenafil allows cGMP to accumulate. The cGMP in turn prolongs relaxation of the smooth muscle of the corpora cavernosa. Relaxation of the corpora cavernosa smooth muscle allows blood to flow into the penis resulting in increased engorgement of the penis. In short, sildenafil increases blood flow into the penis and decreases blood flow out of the penis.
In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).