Diabetes, Obesity, and Erectile Dysfunction
Division of Endocrinology, Diabetes and Bone Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA. Gender Medicine
(Impact Factor: 2.26).
12/2009; 6 Suppl 1(Suppl 1):4-16. DOI: 10.1016/j.genm.2008.12.003
Diabetes mellitus (DM) and obesity affect large parts of the population in the United States and around the world. These disorders are among the most common risk factors for erectile dysfunction (ED), because of their effects on the vasculature and the hormonal milieu.
This article reviews the current literature on the connection between DM, obesity, and ED.
Using the search terms erectile dysfunction, endothelial dysfunction, hypogonadism, diabetes, and obesity, a systematic review of the available literature in the PubMed database was conducted. Relevant English-language publications (to August 2008) were identified.
ED is highly prevalent in men with both DM and obesity, and may act as a harbinger for cardiovascular disease (CVD) in this high-risk population. In addition to male hypogonadism and macrovascular disease, endothelial dysfunction is central to the connection between the metabolic syndrome and ED. Conversely, improved glycemic control and weight loss have been found to improve erectile function.
ED is very prevalent in men with DM and obesity. It is increasingly being recognized as an early clinical indicator and motivator for patients with CVD. The role of pharmacologic ED treatments in improving endothelial function is currently being investigated.
Available from: Kamla Kant Shukla
- "In particular, IL-6 and TNF-alpha disrupt the penile endothelium by creating high levels of ROS, which decrease Nitric Oxide Synthase (NOS) cofactor tetrahydrobiopterin and delay the hydrolysis of NOS inhibitor asymmetric dimethylarginine (ADMA). Obesity induced interference with such molecules cause erectile dysfunction because nitric oxide facilitates normal erection (Tamler, 2009). Another cytokine IL-18, a member of the IL-1 family is known for its role in inflammation as activation of inflammation leads to caspase 1 mediated cleavage of pro-IL-18 into mature IL-18. "
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ABSTRACT: The aim of this review was to provide current scenario linking obesity and male fertility. Obesity has been linked to male fertility because of lifestyle changes, internal hormonal environment alterations, and sperm genetic factors. A few studies assessing the impact of obesity on sperm genetic factor have been published, but they did not lead to a strong consensus. Our objective was to explore further the relationship between sperm genetic factor and obesity. There are emerging facts that obesity negatively affects male reproductive potential not only by reducing sperm quality, but in particular it alters the physical and molecular structure of germ cells in the testes and ultimately affects the maturity and function of sperm cells. Inhibition of microRNA in the male pronucleus of fertilized zygotes produces offspring of phenotypes of variable severity depending on miRNAs ratios. Hence, these RNAs have a role in the oocyte development during fertilization and in embryo development, fetal survival, and offspring phenotype. It has been reported that the miRNA profile is altered in spermatozoa of obese males, however, the impact of these changes in fertilization and embryo health remains as yet not known.
Available from: Durdane Aksoy
- "In this context, the psychological, hormonal, neurogenic and arterial pathologies, medications, iatrogenic causes, and also systemic and chronic diseases have been reported in the etiology of the ED. Chronic diseases include diabetes mellitus, chronic renal failure, chronic obstructive lung disease, arthrosis, collagen tissue diseases, chronic hepatitis and other chronic infections, hypertension, multiple sclerosis and Behçet's disease [4-7]. "
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Erectile dysfunction (ED), defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance, is a common condition. The psychological, hormonal, neurogenic and arterial pathologies, medications, chronic diseases have been reported in the etiology of the ED. This paper aims to study sexual dysfunction in the male patients with migraine and Tension type headache (TTH).
30 migraine cases (Group M), 31 TTH cases (Group T) and 30 control cases (Group C) were included in the study. Patients were evaluated with medical history, physical examination, body mass index (BMI), Beck Depression Inventory, biochemical analysis and hormone profiles. ED was evaluated via International Index of Erectile Function Scale (IIEF). In statistical analysis, variant analysis, post-hoc tukey test, Pearson correlation test, t-test, and fisher's exact chi-square test were used.
The patients' mean age was 34.96+/−1.30, 35.54+/−1.52 and 32.26+/−1.38 for group M,T and C, respectively. There was no significant difference between the groups in terms of testosterone levels. Mean IIEF scores was 19.83+/−2.2, 20.39+/−1.35 and 27.83+/−0.34 in groups M,T,C. When M and T groups were compared with group C, there were significant differences, and there was no statistical difference when T and M groups were compared to each other. Beck Depression Scores were not significantly different in groups M, T and C.
In this study, it was shown that, migraine and TTH affects the sexual functions negatively in male patients. Chronic diseases may cause sexual disorders in patients because of despair, guilt, and fear of death or pain. Our results suggest that, along with the effect of chronic disease and pain, there must be other complicated factors exist causing the development of SD in patients with migraine and TTH.
Available from: Johan Stranne
- "In this study other risk factors for ED, such as concomitant morbidity, use of medication and excessive alcohol intake also increased with age. Concomitant disease is a well-known risk factor for ED, especially diseases correlated with the metabolic syndrome such as CVD and type 2 diabetes mellitus . The correlation between ED and CVD is considered so strong that it is suggested that patients presenting with ED should be investigated for such conditions . "
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The aim was to explore how erectile dysfunction (ED) correlates with increasing age and a number of demographic, physical and lifestyle factors.
Material and methods:
A questionnaire was sent to a random sample (10,458) of men living in Gothenburg, Sweden, in 1992. The men were from the age cohorts 45, 50, 55 years, etc., up to the age of 85 or older. An analogous survey was sent to a random sample (10,845) of men of age cohorts 46, 51, 56 years, etc., in 2003. The prevalence of ED from the different age cohorts assessed on the two specific occasions 11 years apart was compared with a number of factors.
The response rates were 74.2% in 1992 and 68.7% in 2003. Within each survey the rate of ED increased with age at the same time as sexual activity decreased. This was paralleled by an increase in concomitant morbidity, intake of medications and alcohol consumption. The proportion of smokers and body mass index (BMI) decreased and the frequency of physical exercise increased until the age cohorts 70-71 years (1992) and 80-81 years (2003). Comparing the surveys, there was increased ED and decreased sexual activity over time despite an increase in exercise and decrease in smoking. In a multivariate analysis age, living alone, concomitant medication and smoking were the factors that significantly affected the risk of reporting ED.
Despite a seemingly healthier lifestyle in 2003 compared with 1992, the rate of ED increased in the population, highlighting the importance of assessing lifestyle factors when examining ED patients.
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