This review focuses on the mechanisms of dietary intervention improving ED, dietary intervention modalities, and dietary recommendations, aiming to provide some guidance to ED patients in developing healthy dietary habits, so as to prevent and improve ED and promote overall health.
Humans ; Erectile Dysfunction/diet therapy* ; Male ; Diet ; Feeding Behavior

PURPOSE: To evaluate the combined effect of type 2 dimethylarginine dimethylaminohydrolase (DDAH) gene therapy with vitamin E treatment for the treatment of erectile dysfunction in atherosclerotic rats. Our previous study showed that penile accumulation of asymmetric dimethylarginine (ADMA) which was due to decreased DDAH activity, was responsible for the impairment of erectile function in atherosclerotic rats. MATERIALS AND METHODS: Fourty adult male Sprague-Dawley rats (3 months old) were placed in 5 groups (n=8 per group) as follows: 1) healthy control (C) 2) atherosclerotic (AS) 3) vitamin E daily treatment (E, 30 IU/day) 4) injection of pcDNA3/DDAH2 (G) 5) vitamin E+injection of pcDNA3/DDAH2 (E+G). Except group C, all rats received a 1% cholesterol diet for 6 weeks and an initial 2 weeks of N(G)-nitro-L-arginine methyl ester (L-NAME, 3 mg/ml) treatment to promote systemic atherosclerosis. After induction of the atherosclerosis, pcDNA3/DDAH2 was intracavernosally injected in the G and E+G groups. Also, 2 weeks of daily vitamin E treatment was carried out for E and E+G groups. Erectile function was assessed with cavernous nerve electrostimulation. Penile levels of ADMA and protein expression and activity of DDAH2 were assayed. RESULTS: Compared to the C group, AS rats showed significantly impaired erectile function. No single treatment was enough to maintain their erectile function. Only E+G group maintained their erectile function. As a result?of gene transfection, overexpression of DDAH2 was observed in G and E+G groups. However, only the combination arm showed elevated DDAH activity and normalized penile ADMA level. Systemic antioxidant monotherapy enhanced DDAH activity, though not enough to normalize penile ADMA level. CONCLUSIONS: Penile ADMA accumulation, caused by altered metabolic activity of DDAH was responsible for the erectile impairment of atherosclerotic rats. Gene therapy with DDAH2, when combined with antioxidant treatment, effectively suppressed the increase in penile ADMA level and preserved erectile function in atherosclerotic rats.
Adult ; Animals ; Arm ; Atherosclerosis ; Cholesterol ; Diet ; Erectile Dysfunction* ; Genetic Therapy* ; Humans ; Male ; Models, Animal* ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Rats* ; Rats, Sprague-Dawley ; Transfection ; Vitamin E ; Vitamins