The prostate cancer 68ga-psma aim of this review is to delineate lifestyle choices which may impose an increased risk prostate cancer 68ga-psma of developing ED, present relevant studies addressing behavioral factors correlated with ED, as well as prostate cancer 68ga-psma highlight proposed mechanisms for intervention aimed at improving erectile function in men with ED. Go to: Smoking Smoking has been shown in several studies to be positively associated with an increased risk of ED. Longitudinal epidemiologic studies have reported a relative risk of developing ED 1.Prostate cancer 68ga-psma prostate cancer 68ga-psma 5–2 times more in smokers in comparison to non-smokers (7,8,26,27).
In the Boston prostate cancer 68ga-psma Area Community Health survey, a cross-sectional study Prostate cancer 68ga-psma of 2,301 men, a dose-response relationship was Prostate cancer 68ga-psma demonstrated between smoking and ED (28). Significance was achieved at 20-pack years cumulative exposure after Prostate cancer 68ga-psma adjusting for risk factors of age, CVD, and diabetes.
Though not found to be significant, passive Prostate cancer 68ga-psma smoking exposure trended toward a significant risk Prostate cancer 68ga-psma of ED.
While this study design is subject to recall bias, it may provide important information when quantifying risk of ED due to smoking exposure. Positive dose-response association between quantity and Prostate cancer 68ga-psma duration of smoking with risk of ED was confirmed in a meta-analysis of observational epidemiologic studies (29). The investigators found an incremental increased Prostate cancer 68ga-psma risk of ED per 10 cigarettes smoked per day and 10 years of smoking, by 14% and 15%, respectively. An individualized inverse dose-response relationship was seen in male smokers undergoing polysomnographic assessment of nocturnal penile tumescence (NPT), where the highest consumers of cigarettes (>40 cigarettes per day) had the fewest minutes of nocturnal tumescence and detumesced fastest (30). At a molecular and cellular level in the animal model, cigarette smoking (CS) is linked to significantly higher markers of oxidative stress and cavernosal tissue apoptosis (31). CS exposed rats were noted to have significantly lower expression of cavernosal neuronal nitric oxide synthase (nNOS) and decreased endothelial and smooth muscle content, supporting the role of endothelial dysfunction prostate cancer 68ga-psma in pathophysiology of ED (12). The effect of smoking cessation on erectile function has also been examined.
Prospectively studied a sample of men with ED and smoking as their only risk prostate cancer 68ga-psma factor; excluded were men with other risk factors for ED such as diabetes, hypertension, dyslipidemia, peripheral vascular disease, psychiatric disorders, and renal failure. At Prostate cancer 68ga-psma baseline, severity of ED was found Prostate cancer 68ga-psma to be significantly correlated to duration of exposure prostate cancer 68ga-psma in pack-years (32).
At follow-up 1 year after smoking cessation, patients who successfully stopped smoking (ex-smokers) had a 25% improvement in erectile function, Prostate cancer 68ga-psma while men who continued (current smokers) did not improve. Additionally, a larger proportion of current smokers (7%) than ex-smokers (2.5%) had worsening of their baseline ED.
This study suggests a large degree of stabilization or improvement in ED after smoking cessation. These results were corroborated in a randomized controlled study of Chinese men enrolled in a nicotine replacement therapy (NRT) Prostate cancer 68ga-psma Prostate cancer 68ga-psma program with or without counseling. Six months after enrollment, patients who successfully quit smoking were more likely to have improvement in erectile function compared to persistent smokers (53.8% vs. 28.1%, P3,000 kcal/week significantly reduced the likelihood Prostate cancer 68ga-psma of severe ED (IIEF-5 600 mL/week) (6). Furthermore, prostate cancProstate cancer 68ga-psma er 68ga-psma in a large, multi-national epidemiologic study, heavy and no alcohol consumption were associated with higher risk of ED as compared to moderate alcohol intake (1 to 7 drinks per week), Prostate cancer 68ga-psma though not significantly (48).
On the contrary, in the HPFS study, there was no change Prostate cancer 68ga-psma in relative risk of ED across all categories of alcohol consumption (8). In the rat model, chronic alcohol consumption leads to an upregulation of endothelin-1 (ET-1) which acts as a vasoconstrictor Prostate cancer 68ga-psma in the corpora cavernosa (CC). Following electrical stimulation of the major Pelvic ganglion, ethanol treated Prostate cancer 68ga-psma rats demonstrated significantly reduced erectile response as measured prostate cancer 68ga-psma by maximal intracavernosal pressure/mean arterial pressure (ICP/MAP) (49). These prostate cancer 68ga-psma results Provide some basis for investigation in human subjects. Whether changes in CC ET-1 Prostate cancer 68ga-psma levels are sustained after ethanol cessation warrants investigation. Illicit prostate cancer 68prostate cancer 68ga-psma ga-psma drug use was studied in a cross-sectional trial of Taiwanese detainees (N=701, mean age 33.8 years) with a history of drug abuse versus controls (N=196) (50). Heroin, amphetamine prostate cancer 68ga-psma and MDMA (“ecstasy”) were the most commonly reported drugs of abuse in this detainee population. Over one third (36.4%) of drug abusers were found to have ED as reported by IIEF-5 score, with 10% reporting severe ED. Drug abusers were found to have significantly lower mean IIEF scores in each domain as compared to controls. Additionally, multiple logistic regression analysis proved dosing frequency to be a predictor of ED.
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