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From the * Division of Urology, Department of
Surgery, Tri-Service General Hospital, Taipei, Taiwan; the
Graduate Institute of Medical Informatics,
Taipei Medical University, Taipei, Taiwan; the
School of Public Health, National Defense
Medical Center, Taipei, Taiwan; and the Taipei
City Hospital, Taipei, Taiwan.
| Correspondence to: Tai-Lung Cha, Division of Urology, Department of Surgery, Tri-Service General Hospital, #325, Section 2, Cheng-Gung Road, Neihu 114, Taipei, Taiwan, R.O.C. (e-mail: tlcha{at}ndmctsgh.edu.tw). |
| Received for publication May 24, 2008; accepted for publication December 1, 2008. |
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Abstract |
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Key words: Central obesity, erectile dysfunction, young adults
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Materials and Methods |
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Erectile Function Assessment
Erectile function was assessed by completing questions 1 to 5 on the
International Index of Erectile Function–5 (IIEF-5), a multidimensional
questionnaire in which all 5 questions are similarly styled. The 5 questions
asked were: 1) How often were you able to get an erection during sexual
activity? 2) When you had erections with sexual stimulation, how often were
your erections hard enough for penetration? 3) When you attempted sexual
intercourse, how often were you able to penetrate (enter) your partner? 4)
During sexual intercourse, how often were you able to maintain your erection
after you had penetrated (entered) your partner? and 5) During sexual
intercourse, how difficult was it to maintain your erection to completion of
intercourse? The IIEF-5 score represents the sum of questions 1 to 5, with a
maximum score of 25; a score of 21 or less indicates ED. Subjects with a score
of less than 6 should be excluded because of lack of sexual intercourse
experience. Thus, the different forms of ED severity were classified by score
as moderate to severe (score 6 to 11), mild to moderate (score 12 to 16), mild
(score 17 to 21), and no ED (score > 21).
Body Measurements
BMI was calculated as weight in kilograms divided by height in meters
squared. WC was obtained from the midpoint between the iliac crest and costal
margin. Hip circumference (HC) was measured at the widest point around the
greater trochanter. Both WC and HC in centimeters were examined. WHR was
determined as WC divided by HC. To illustrate the real association between
sexual function and obesity, all subjects were categorized by quartiles
according to each anthropometric index, analyzing the severity of IIEF-5 score
with increasing obesity.
Statistical Analysis
Data are expressed as 
±
SD. Student's t test comparison was performed between the ED and
non-ED groups. The method of analysis of variance (ANOVA) was used to analyze
the association between IIEF-5 severity and obesity. A Pearson
2 test was performed for the association between obesity and
prevalence of each category of ED. P < 0.05 was considered
statistically significant. All analyses were conducted using SPSS statistical
software (version 13.0; SPSS Inc, Chicago, Illinois).
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Results |
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21). Among
these ED groups, the prevalences of moderate to severe (IIEF-5 6–11),
mild to moderate (IIEF-5 12–16), and mild ED (IIEF-5 17–21) were
1.3%, 3.4%, and 21.0%. For consideration of the association between sexual function and smoking, there were 569 smokers and 203 nonsmokers in the study. There was no statistical difference in IIEF-5 score between the smoking and nonsmoking groups (IIEF-5 = 22.30 and 22.49; Student's t test, P = .422). In addition, we analyzed the variables between each ED category and non-ED groups, which included age, height, weight, BMI, WC, and WHR, and all analyses revealed no significant difference (Table 1). To test the obesity-influence relationship, the severity of IIEF-5 and prevalence of each category of ED were examined by quartiles of the anthropometric indexes BMI, WC, and WHR. According to the ANOVA test, only the anthropometric indicator WC was shown to have a statistically significant correlation with IIEF-5 severity (P = .032; Table 2). An inverse relationship was noted between central obesity assessed by WC and sexual function. A borderline significant (P = .057) statistical result was followed between BMI and IIEF-5 score. An inverse trend seems to have been observed between general obesity and clinical sexual function.
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By means of the Pearson 2 test, the prevalence of each
category of ED was shown to have no statistical correlation with BMI, WC, or
WHR (P = .074, .068, and .434; Tables
3,
4,
5). There was no significant
difference or trend identified between obesity and prevalence of each category
of ED.
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Discussion |
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TopAbstractMaterials and MethodsResultsDiscussionConclusionReferences |
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ED is defined as the persistent or recurrent inability to achieve or maintain an erection sufficient for satisfactory sexual intercourse. In men reporting symptoms of ED, 79% of the subjects are found to be overweight or obese (Feldman et al, 2000). In another survey of health professionals, obesity was associated with a relative risk of 1.3 for ED (Bacon et al, 2003). In a prospective study of risk factors for ED, the author found that obesity and smoking were positively associated, and physical activity was inversely associated with the risk of ED developing during the 14-year follow-up (Bacon et al, 2006).
Obesity might be in a proinflammatory state and result in the process of inflammation, inducing endocrine and endothelial dysfunction. A further hypothesis of these kinds of studies was that weight loss in obese patients would reduce serum concentration of markers (C-reactive protein [CRP], interleukin 6 [IL-6], and interleukin 8 [IL-8]) and would provide evidence of improved endothelial function (Meneilly et al, 2001). Obese men participating in weight loss programs with dietary modifications and increased physical activity experienced reduced oxidative stress associated with improved nitric oxide availability (Roberts et al, 2002). Another study (Esposito et al, 2004) demonstrated that lifestyle changes by means of reducing body weight and increasing physical activity would induce amelioration of erectile and endothelial function in obese men. The result of the study showed that the intervention group with weight loss improved erectile function significantly and had a better response to L-arginine. The effect of lifestyle changes caused not only decreases in biometric indicators (BMI and WHR) but also lower levels of biochemical factors including IL-6, IL-8, and CRP.
Specifically, the central obesity type has been associated with metabolic changes, diabetes mellitus, cerebrovascular disease, and ischemic heart disease (Brook et al, 2001). A study by Riedner et al (2006) revealed that central obesity is a predictor of ED among men 61 to 81 years old without known diabetes mellitus, hypertension, and other comorbidities. There have been several studies demonstrating the strong association between ED and metabolic syndrome (Bansal et al, 2005; Makhsida et al, 2005; Demir et al, 2006). On the other hand, Kupelian et al (2006) indicated that the occurrence of ED is a predictor of the development of metabolic syndrome, especially noticeable among men with a BMI less than 25, a group not usually considered at risk for cardiovascular disease or diabetes mellitus. Although our subjects were not fit for the criteria of metabolic syndrome, the possible condition of metabolic syndrome development should be considered. The pathogenesis of ED is likely multifactorial and may not be explained by endothelial dysfunction alone (Ferrini et al, 2004). Hypoandrogenism contributing to the sexual dysfunction has been found in obese males (Seftel, 2006). Whether obesity is coupled with ED independently or through cardiovascular risk factors or hypoandrogenism, it is evident that obese men have a high incidence of ED that affects their sexual life and fertility.
According to the results of our study, no significant difference is noted between smokers and nonsmokers. Only the anthropometric indicator of WC shows a statistical association with sexual function in the young adult population. In accordance with the conclusions of Riedner et al (2006), the aging process should have a major role in the process of endothelial dysfunction. Furthermore, our data support the opinion of Brook et al (2001) in that visceral obesity seems to be potentially more harmful to endothelial function than does obesity in general. On the other hand, ED subjects should consider the possibility of developing metabolic syndrome according to the study by Kupelian et al (2006), although the subjects were younger and with a lower BMI.
Some limitations of our study include that this is a cross-sectional study without a time serial association between obesity and sexual function. Because levels of testosterone and inflammatory cytokines are correlated with obesity, further study focusing on the analyses of endocrine and cytokine variations should be considered. Meanwhile, measurement of vessel quality could be assessed among young obese men; this is important to clarify the relationship with ED. Moreover, obesity-related infertility also could be taken into consideration in a future study.
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Conclusion |
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References |
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