International Journal of Impotence Research (2008) 20, 358–365; doi:10.1038/ijir.2008.9; published online 10 April 2008

Obesity and sexual dysfunction, male and female

K Esposito1, F Giugliano2, M Ciotola1, M De Sio2, M D'Armiento2 and D Giugliano2

  1. 1Division of Metabolic Diseases, Department of Geriatrics and Metabolic Diseases, University of Naples SUN, Naples, Italy
  2. 2Division of Urology, Department of Geriatrics and Metabolic Diseases, University of Naples SUN, Naples, Italy

Correspondence: Professor K Esposito, Division of Geriatrics and Metabolic Diseases, University of Naples SUN, Piazza L. Miraglia, Naples 80138, Italy. E-mail:

Received 3 February 2008; Accepted 18 February 2008; Published online 10 April 2008.



Obesity has become a worldwide public health problem of epidemic proportions, as it may decrease life expectancy by 7 years at the age of 40 years: excess bodyweight is now the sixth most important risk factor contributing to the overall burden of disease worldwide. Overweight and obesity may increase the risk of erectile dysfunction (ED) by 30–90% as compared with normal weight subjects. On the other hand, subjects with ED tend to be heavier and with a greater waist than subjects without ED, and also are more likely to be hypertensive and hypercholesterolemic. The metabolic syndrome, characterized by a clustering of risk factors associated with insulin resistance and abdominal obesity, associates with ED. Moreover, women with the metabolic syndrome have an increased prevalence of sexual dysfunctions as compared with matched control women. Lifestyle changes aimed at reducing body weight and increasing physical activity induce amelioration of both erectile and endothelial functions in obese men. Moreover, preliminary evidence suggests that a Mediterranean-style diet might be effective in ameliorating sexual function in women with the metabolic syndrome. Lifestyle changes, mainly focussing on regular physical activity and a healthy diet, are effective and safe ways to reduce cardiovascular diseases and premature mortality in all population groups; they may also prevent and treat sexual dysfunctions in both sexes.


obesity, erectile dysfunction, female sexual dysfunction, metabolic syndrome, lifestyle

Obesity has become nowadays a common condition and a worldwide public health problem of epidemic proportions.1 World Health Organization describes obesity as one of the most visible, yet most neglected, public-health problem that threatens to overwhelm both more and less developed countries.2 The problems of overweight and obesity have achieved global recognition only during the past decade, in contrast to underweight, malnutrition and infectious diseases, which have always dominated thinking. The International Obesity Task Force estimates that at present 1.1 billion adults are overweight, including 312 million who are obese. These estimates are conservative, however, as with the new Asian criteria of overweight at a lower cutoff of 23kg/m2 for body mass index (BMI), the number is even higher, reaching 1.7 billion people.3 For the first time, the number of overweight individuals in the world is equivalent to the number of underweight.

Obesity has been shown to decrease life expectancy by 7 years at the age of 40 years.4 Although there has been a trend over the last half century showing a general decline in the age-adjusted death rates of heart disease and stroke, the increasing epidemic of obesity, followed closely by type II diabetes, will likely slow the decline and reverse the trend.5 The increase in risk of death with each unit increase in BMI declines progressively with age but remains substantial until the age-group of 75 years and older. Intentional weight loss in obese individuals seems to prolong life and reduce risks: diabetes-related mortality was reduced by 30–40% with moderate weight loss (less than 10% of initial body weight);6 moreover, people with type II diabetes who lost 10kg in the first year after diagnosis gained a further 4 years of life.7


Metabolic consequences of obesity

In addition to being an independent risk factor for cardiovascular diseases, obesity also increases the incidence of other risk factors, notably diabetes, dyslipidemia, hypertension and the prothrombotic state.8 The risks of diabetes, hypertension and dyslipidemia increase from BMI of about 21kg/m2, thereby reducing life expectancy and increasing the health and societal economic burden; excess bodyweight is now the sixth most important risk factor contributing to the overall burden of disease worldwide.9

The risk of hypertension is up to five times higher among obese people than among those of normal weight,10 whereas more than 85% of hypertension arises in individuals with BMI values above 25kg/m2.11 The increase in blood pressure with excess weight is presumably linked to the release from adipocytes of angiotensinogen, the precursor of the well-known hypertensive molecule angiotensin, an increase in blood volume associated with the greater body mass and a rise in blood viscosity. Diets conductive to weight gain independently amplify blood pressure, as saturated fats and hypercholesterolemia induce a rise in systolic and diastolic blood pressure.12

Dyslipidemia progressively develops as BMI increases from 21kg/m2, with a rise in proatheromatous, dense, small-particle-sized low-density lipoprotein. With low high-density lipoprotein concentrations, as well as high concentrations of triglycerides, coronary heart disease risk increases.13 This particular dyslipidemia occurring in the obese people, especially in association with visceral obesity and insulin resistance, is also known as aterogenic dyslipidemia.

Overweight, obesity and weight gain have been shown to be major risk factors for the development of type II diabetes regardless of age and sex. In the Nurses' Health Study involving about 85000 US women free of diagnosed diabetes at baseline, a strong relation between overall obesity and the risk of incident diabetes was observed during the 16 years of follow-up:14 the relative risk of diabetes was amplified by 7.6 times for overweight, 20.1 times for obese and 39 times for severely obese (BMI >35kg/m2) women compared with lean women (BMI <23kg/m2). Similar results were noted in men.15


Obesity and erectile dysfunction

Epidemiological studies suggest that modifiable health behaviors are associated with a reduced risk for erectile dysfunction (ED). In the Health Professionals Follow-up Study,16 several modifiable lifestyle factors, including leanness, were associated with maintenance of good erectile function. For instance, men with a BMI (calculated as weight in kilograms divided by the square of height in meters) higher than 28.7 are likely to carry a 30% higher risk for ED than those with a normal BMI (25 or lower). Data from other surveys also indicate a higher prevalence of impotence in obese men.17, 18 For instance, the 9-year follow-up Massachusetts Male Aging Study19 and the 25-year follow-up Rancho Bernardo Study20 reported that body weight was an independent risk factor for ED, with a risk exceeding 90% of controls (odds ratio between 1.93 and 1.96, respectively). In general, subjects with ED tend to be heavier and with a greater waist than subjects without ED, and also are more likely to be hypertensive and hypercholesterolemic.21

Although the relation between obesity and ED may not be readily apparent, a growing body of evidence implicates central adiposity as key regulator of inflammation and endothelial functions.22 Insulin resistance, endothelial dysfunction and subclinical inflammation have been all demonstrated in the obese population and may contribute to increased cardiovascular risk in the population.23 Vascular endothelium plays a pivotal role in pathogenesis of numerous thrombotic and inflammatory disorders. Endothelial dysfunction is a predictor of future coronary events and may be detected clinically by determining the plasma levels of circulating soluble markers.24 According to a raising popular view, subjects with ED seem to have a vascular mechanism similar to that seen in atherosclerosis25 and therefore a diagnosis of ED may be seen as a sentinel event that should prompt investigation for coronary heart disease in asymptomatic men.26

We evaluated associations between erectile function, endothelial function and markers of systemic vascular inflammation in 80 obese men, aged 35–55 years, divided into two equal groups according to the presence/absence of ED.27 Compared with non-obese age-matched men, obese men had impaired indices of endothelial function and higher circulating concentrations of the proinflammatory cytokines interleukin-6, interleukin-8, interleukin-18, as well as C-reactive protein (CRP). Endothelial function showed a greater impairment in impotent obese men as compared with potent obese men, whereas circulating C-reactive protein levels were significantly higher in obese men with ED. The association between International Index of Erectile Dysfunction (IIEF) score and indices of endothelial dysfunction supports the presence of a possible common vascular pathway underlying both conditions in obese men. A defective nitric oxide activity, linked to reduced nitric oxide availability, could provide a unifying explanation for this association.


Endothelial microparticles and ED

Microparticles are small membrane vesicles that are released from cells upon activation or during apoptosis.28 The majority of in vivo microparticles in blood are derived from platelets, whereas microparticles from erythrocytes, granulocytes, monocytes, lymphocytes and endothelial cells usually circulate at lower numbers. Because of their procoagulant properties and capability to affect the endothelium functions, microparticles have been subjected to increasing attention during last years. An increase in endothelial microparticle (EMP) levels has been demonstrated in patients with cardiovascular disease, such as acute coronary syndromes, diabetes, hypertension and hypertriglyceridemia.29, 30, 31, 32, 33 Microparticles can also influence endothelial functions: microparticles from patients with acute coronary syndromes directly impaired endothelium-dependent vasodilatation in rat aorta-rings, presumably by inhibition of the nitric oxide-mediated signal transduction.34, 35 Although microparticles are elevated in condition of endothelial cell loss, as a consequence of inflammatory processes and the associated vascular damage, they may play a direct role in atherogenesis, also considering that EMPs can directly activate and stimulate cells to produce inflammatory mediators such as cytokines.36

Thirty overweight and obese diabetic men with ED and 20 age-matched control subjects without ED were assessed for circulating microparticles and endothelial dysfunction.37 Compared with non-diabetic subjects, diabetic men presented significantly higher numbers of EMPs (P=0.001), and reduced endothelial-dependent vasodilation (P=0.01), with a significant inverse correlation between the number of circulating EMP and the IIEF score (r=−0.457, P=0.01). Multivariate analysis correcting for age, anthropometric indices, glucose and lipid parameters, FMD and PMP identified EMP as the only independent predictor for IIEF score (P=0.03). The results demonstrate that circulating endothelial-derived microparticles are higher in impotent diabetic men as compared with age-matched non-diabetic potent men, and also negatively correlated with the severity of ED (Figure 1). As in multivariate analysis EMPs remained the only independent predictor of IIEF, it seems likely that EMP may represent a link between diabetes and ED.

Figure 1.
Figure 1 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact or the author

Relationship between EMPs and severity (mild: IIEF between 16 and 21; moderate: IIEF between 10 and 15; severe: IIEF <10) of ED in a sample of 30 overweight type II diabetic patients with ED. Each bar represents median and interquartile range. Adapted from Esposito et al.37 ED, erectile dysfunction; EMP, endothelial microparticle.

Full figure and legend (7K)


The metabolic syndrome and ED

The metabolic syndrome, characterized by a clustering of risk factors associated with insulin resistance and abdominal obesity, is associated with an increased risk of coronary heart disease and cardiovascular disease mortality. The prevalence of this condition in developed and developing countries continues to increase. The initial report documenting the prevalence of the metabolic syndrome based on US adults surveyed in 1988–1994 showed approximately one-fourth of US adults or 47 million to have this condition,38 whereas more recent estimates from 1999 to 2002 place the US adult prevalence between 34 and 40% in men and between 35 and 38% in women, depending on the definition used to define the syndrome.39

Common features are central obesity, insulin resistance, hypertension and dyslipidemia. Patients with the metabolic syndrome also are at increased risk for type II diabetes. The ATP-III guideline also suggests a working definition of the metabolic syndrome that includes the presence of at least three of the following characteristics: abdominal obesity, elevated triglycerides, reduced levels of high-density lipoprotein cholesterol, high blood pressure and high fasting glucose.40 In particular, the cutoff values are the following: waist circumference >102cm in men and >88cm in women; triglycerides >150mg per 100ml; high-density lipoprotein-cholesterol <40mg per 100ml in men and <50mg per 100ml in women; blood pressure >130/85mmHg; and fasting glucose >110mg per 100ml.

As four of the five components of the metabolic syndrome are risk factors for ED, we postulated an association between ED and the metabolic syndrome, and tested the hypothesis that ED was more prevalent in men with the metabolic syndrome.41 In uncontrolled prospective studies, 43% of men presenting with ED met the US National Cholesterol Education Program criteria for metabolic syndrome;42 29% of men presenting with sexual dysfunction had metabolic syndrome: 96% had ED, 40% hypoactive sexual desire, 23% premature ejaculation and 5% delayed ejaculation.43 In a case–control study,41 compared with age- and weight-matched control subjects (n=50), patients with the metabolic syndrome (n=100) had increased prevalence of ED (26.7 vs 13%, P=0.03); moreover, there was an increase in ED prevalence (IIEF <21), as the number of components of the metabolic syndrome increased, suggesting that the cumulative burden of cardiovascular risk may be central to the pathogenesis of ED.


Hypogonadism and the metabolic syndrome

Hypogonadism in men has been associated with increased risk of metabolic syndrome,44, 45, 46 cardiovascular disease47 and sexual dysfunction. Metabolic syndrome is associated with endothelial dysfunction, penile vascular compromise and the autonomic neuropathy of diabetes, which underlie ED in men.48 An uncontrolled prospective study of men for the assessment of sexual dysfunction reported that the presence of hypogonadism in men with metabolic syndrome was associated with worse sexual dysfunction and anxiety than in men with metabolic syndrome but without hypogonadism.43 For example, in 864 men (mean age 52 years) participating in two lipid treatment studies,49 testosterone decreased with increasing BMI (P<0.0001). Mean baseline total serum testosterone levels in obese and severely obese aging men with the metabolic syndrome were around 150 and 300ng per 100ml, respectively, less than that in aging, lean men with no metabolic syndrome. Based on these analyses, the presence of diabetes or fasting serum glucose greater than 110mg per 100ml, BMI 30kg/m2 or greater, and triglycerides 150mg per 100ml or greater each appeared to have a clinically relevant association with low serum testosterone. Aging men with obesity and the metabolic syndrome have a significant decrease in total serum testosterone levels compared to aging, metabolically healthy men.


Obesity, metabolic syndrome and female sexual function

Female sexual dysfunction (FSD) is characterized by disturbances in the psychophysiological changes associated with the sexual response cycle in women, including disorders of sexual desire, arousal, orgasm and pain.50 Sexual difficulties in women appear to be widespread in society, influenced by both health-related and psychosocial factors, and are associated with impaired quality of life and interpersonal relationships.51 Older data reveal that up to 76% of women had some type of sexual dysfunction.52 Data from the National Health and Social Life Survey (NHSLS), a study of adult sexual behavior, showed that 43% of women in the United States had at least one of sexual problem, in relation with age, marital status, education, race or ethnicity.53 These figures have recently been confirmed by the results of GSSAB (Global Study of Sexual Attitudes and Behaviors), an international survey of various aspects of sex and relationships among adults aged 40–80 years.54 However, well-designed, random-sample, community-based epidemiological studies are limited and hampered by low response rate, the use of different tools to assess FSD and the underlying complexity of female sexuality.

Both overweight and obesity have been identified as risk factors for sexual dysfunction in men,55 but the relationship between female sexual function and amount of body fat is still obscure.56, 57 The discrepancy that still exists among the few reports may mainly be due to the different instruments used to assess sexual function in women. The FSFI (female sexual function index) is a brief, validated 19 items self-report instrument proposed to decode information on specific sexual dysfunction symptoms.58 This clinical tool has the advantage of being standardized, easy to administer and score, and provides normal values in general and pathological populations.59

Previous evidence linking FSD to obesity is very scanty. In 171 postmenopausal women, Kirchengast et al.56 reported that body weight and BMI were significantly related to the degree of reduced sexual interest. In 59 healthy women aged 19–40 years, Brody57 found that hip size was negatively associated with a lower frequency of penile–vaginal intercourse. However, both studies focused upon single aspects of women sexuality, and used different tools for investigating sexual function. Also for diabetes mellitus, which represents an important causes of ED in men,60 the data about the prevalence of FSD are controversial.61, 62, 63

We found64 a negative relationship between body weight and sexual function in 52 women with abnormal values of FSFI (score less than or equal to23) (Figure 2). We also showed that obesity affects several aspects of sexual function in otherwise healthy women with FSD, including arousal, lubrication, satisfaction and orgasm, but not desire and pain. Central fat distribution, as evaluated by the waist-to-hip ratio, showed no correlation with FSFI score or with any individual sexual domains, suggesting that the amount of fat is more important than its distribution. Interestingly enough, desire was the only domain showing a positive yet not significant relation with BMI, supporting the hypothesis that the domains of women's sexual function (desire, arousal, lubrication and orgasm) may not represent a linear progression.65 The lack of relation between BMI and FSFI in women without FSD (r=0.2, P=0.09) seems to suggest that obesity may be an important factor once FSD is manifested, but prospective studies are needed to answer this question. At present, we can only speculate that the increasing number of circulating factors produced by the fat cell may probably play a role,66 although specifically addressed studied are needed.

Figure 2.
Figure 2 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact or the author

Relationship between female sexual function and BMI in a sample of 52 women with abnormal (less than or equal to23) value of FSFI. Adapted from Esposito et al.64 BMI, body mass index; FSFI, female sexual function index.

Full figure and legend (11K)

In a preliminary observation, we showed that women with the metabolic syndrome have an increased prevalence of sexual dysfunctions as compared with matched control women, although the association remained not easily explained.67 Compared with the control group, women with the metabolic syndrome had reduced mean full FSFI score (23.9±5.4 vs 29.9±4.8, P<0.001). We considered the functional results to be good when the FSFI score was 30 or more, intermediate between 23 and 29, and poor below 23. The percentages of women falling within these three categories of FSFI score were for control women 77, 21 and 2%, respectively, and for women with the MS 55, 36 and 9%, respectively (P<0.01). Individual analysis of the different domains demonstrated that women with the metabolic syndrome reported significantly lower arousal, orgasm and lubrication scores (P<0.01) in comparison with controls (Figure 3). Satisfaction rate was 3.5±1.1 in patients and 4.7±1.2 in controls (P<0.001). There was a decrease in full FSFI score as the number of components of the metabolic syndrome increased (three components, N=65: 24±3.8; four components, N=23: 19±3.1 and five components, N=12: 16±2.7, P<.01). Women with the metabolic syndrome have an increased prevalence of sexual dysfunctions as compared with matched control women; however, the inverse relation between the FSFI score and the numbers of components of the syndrome is intriguing but at present not easily explained.

Figure 3.
Figure 3 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact or the author

Individual domains of female sexual function in women with the metabolic syndrome (SM) and in control women. Adapted from Esposito et al.67

Full figure and legend (41K)


Lifestyle and sexual function

Erectile and endothelial dysfunction may have some shared pathways, through a defect in nitric oxide activity, which may be inhibited through age-, disease- and behavior-related pathways. Intervention on modifiable health behaviors, especially reducing body weight and increasing physical activity, may in theory be a safe strategy to reduce the risk of both erectile and endothelial dysfunction. In the Massachusetts Male Aging Study, for example, Derby et al.68 found that men who were overweight at baseline were at an increased risk of developing ED regardless of whether they lost weight during the follow-up records. Moreover, epidemiological evidence suggests that physical activity is associated with a 30% lower risk of ED.16 A more recent assessment of the association between physical activity and ED comes from a meta-analysis of population-based studies demonstrating the existence of a simple dose–response relationship, with higher physical activity conferring lower risks. The adjusted reduction of the risk of having ED was 58% for high activity and 37% for moderate activity, as compared with men with low physical activity.69

We hypothesized that lifestyle changes aimed at reducing body weight and increasing physical activity would induce amelioration of erectile and endothelial functions in obese men. We conducted a randomized controlled trial involving 110 obese men with ED.70 Men assigned to the intervention group were entered in an intensive weight loss program, involving personalized dietary counseling and exercise advice and regular meetings with a nutritionist and personal trainer. Men assigned to the control group received general guidance on weight loss at each visit. After 2 years, men randomized to the intervention had lost significantly more weight, increased their physical activity, experienced favorable changes in physiologic measures of endothelial dysfunction and had significant improvement in their ED score compared with men in the control group. In particular, erectile function score was improved from 13.9 to 17 (P<0.001) after the intervention: 17 men in the intervention group and 3 men in the control group reported having IIEF score 22 or more (that is returned to normal). Multivariate analysis found that physical activity, BMI and C-reactive protein independently predicted IIEF score and almost explained 68% of the variance.

This study provided evidence that sustained lifestyle changes can partially ameliorate erectile function in obese men. Additionally, men in the intervention program showed improvement in the number of surrogate traditional and novel cardiovascular risk factors, which were better than those seen in control men. Although the findings may not be totally generalizable to primary care clinics as the intervention was very intensive and involved many contacts with the study team, this should not detract from the potential importance of the findings for the public health, in the light of the mounting evidence that sustained lifestyle modifications have profound impact on diseases.

We tested the effect of a Mediterranean-style diet on sexual function in women with the metabolic syndrome (unpublished data). Thirty-one women with a diagnosis of FSD and metabolic syndrome were assigned to the Mediterranean-style diet and 28 to a standard control diet. After 2 years, women on the Mediterranean diet consumed more fruits, vegetables, nuts, whole grain and olive oil as compared with men on the control diet. FSFI improved in the intervention group, from a mean basal value of 19.7±3.1 to a mean post-treatment value of 26.1±4.1 (P=0.01), and remained stable in the control group. No single sexual domain (desire, arousal, lubrication, orgasm, satisfaction, pain) was significantly ameliorated by the dietary treatment, suggesting that the whole female sexuality may find benefit from lifestyle changes. A Mediterranean-style diet might be effective in ameliorating sexual function in women with the metabolic syndrome.



Dietary energy restriction and increasing physical activity still represent the cornerstone of prevention and therapy of obesity. Regular exercise can reduce body weight and fat mass without dietary caloric restriction in overweight individuals. An increase in total energy expenditure appears to be the most important determinant of successful exercise-induced weight loss. The best long-term results may be achieved when physical activity produces an energy expenditure of at least 2500kcal per week. The optimal approach in weight reduction programs appears to be a combination of regular physical activity and caloric restriction. A minimum of 60min but most likely 80–90min of moderate-intensity physical activity per day may be needed to avoid or limit weight regain in formerly overweight or obese individuals. Sustained lifestyle changes, including regular moderate-intensity physical activity, a healthy diet and avoiding unhealthy weight gain are effective and safe ways to reduce cardiovascular diseases and premature mortality in all population groups,71, 72, 73 and to prevent and treat ED.

As overweight and obesity represent important risk factors for the development of type II diabetes, which is one main cause of ED, it is fundamental to avoid or limit those nutritional factors that have been associated with the risk of type II diabetes in epidemiological studies. A pattern characterized by higher intake of fruits and vegetables (prudent pattern) was associated with a reduced risk of type II diabetes, whereas a pattern characterized by higher intake of foods typical of Western diets, including processed meat, French fry, sugar-sweetened beverages, food with high glycemic load, was associated with an increased risk.74, 75 To combat the epidemic of overweight at a population level, it is important to develop strategies to increase habitual physical activity and to prevent overweight and obesity in collaboration with communities, families, schools, work sites, health-care professionals, media and policymakers.



  1. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trend in obesity among US adults, 1999–2000. JAMA 2002; 288: 1723–1727. | Article | PubMed | ISI |
  2. WHO. Obesity: preventing and managing the global epidemic. WHO Technical Report Series Number 894. WHO: Geneva, 2000.
  3. James WTP, Rigby N, Leach R. The obesity epidemic, metabolic syndrome and future prevention strategies. Eur J Cardiovasc Prev Rehabil 2004; 11: 3–8. | Article | PubMed | ISI |
  4. Peeters A, Barendregt JJ, Willekens F, Mackenbach JP, Al Mamun A, Nonneux L. NEDCOM, the Netherlands epidemiology and demographic compression on morbidity research group. obesity in adulthood and its consequences for life expectancy: a life-table analysis. Ann Intern Med 2003; 138: 24–32. | PubMed | ISI |
  5. Preston HP. Deadweight? The influence of obesity on longevity. N Engl J Med 2005; 352: 1135–1137. | Article | PubMed |
  6. Williamson DF, Parnuk E, Thues M, Flanders D, Byers T, Heath C. Modest intentional weight loss increases life expectancy in overweight women. Am J Epidemiol 1995; 141: 1128–1145. | PubMed | ISI | ChemPort |
  7. Lean ME, Powrie JK, Anderson AS, Garthwaite PH. Obesity, weight loss and prognosis of type 2 diabetes. Diabet Med 1990; 7: 228–233. | PubMed | ChemPort |
  8. Kopelman PG. Obesity as a medical problem. Nature 2000; 404: 635–643. | Article | PubMed | ISI | ChemPort |
  9. Ezzati M, Lopez AD, Rodgers A, Vander Hoorn S, Murray CJ. Comparative risk assessment collaborative group. Selected major risk factors and global and regional burden of disease. Lancet 2002; 360: 1347–1360. | Article | PubMed | ISI |
  10. Wolf HK, Tuomilehto J, Kuulasmaa K, Domarkiene S, Cepaitis Z, Molarius A et al. Blood pressure levels in the 41 populations of the WHO MONICA project. J Hum Hypertens 1997; 11: 733–742. | Article | PubMed | ChemPort |
  11. Kastarinen MJ, Nissinen AM, Vartiainen EA, Jousilahti PJ, Korhonen HJ, Puska PM et al. Blood pressure levels and obesity trends in hypertensive and normotensive Finnish population from 1982 to 1997. J Hypertens 2000; 18: 255–262. | Article | PubMed | ChemPort |
  12. Appel LJ, Moore TG, Obarzanek R, Vollmer WM, Svetkey LP, Sacks FM et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. A clinical trial of effects of dietary patterns on blood pressure. N Engl J Med 1997; 336: 117–124. | Article |
  13. Wannamethee SG, Shaper AG, Durrington PN, Perry IJ. Hypertension, serum insulin, obesity and the metabolic syndrome. J Hum Hypertens 1998; 12: 735–741. | Article | PubMed | ChemPort |
  14. Hu FB, Manson JE, Stampfer MJ, Colditz J, Liu S, Solomon CG et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med 2001; 345: 790–797. | Article | PubMed | ISI | ChemPort |
  15. Hu G, Lindstrom J, Valle TT, Eriksson GJ, Jousilahti P, Silventoinen K et al. Physical activity, body mass index, and risk of type 2 diabetes in patients with normal or impaired glucose regulation. Arch Intern Med 2004; 164: 892–896. | Article | PubMed | ISI |
  16. Bacon CG, Mittleman MA, Kawachi I, Giovannucci E, Glasser DB, Rimm EB. Sexual function in men older than 50 years of age: results from the health professionals follow-up study. Ann Intern Med 2003; 139: 161–168. | PubMed | ISI |
  17. Pinnock CB, Stapleton AM, Marshall VR. Erectile dysfunction in the community: a prevalence study. Med J Aust 1999; 171: 353–357. | PubMed | ISI | ChemPort |
  18. Chung WS, Sohn JH, Park YY. Is obesity an underlying factor in erectile dysfunction? Eur Urol 1999; 36: 68–70. | Article | PubMed | ISI | ChemPort |
  19. Feldman HA, Johannes CB, Derby CA, Kleinman KP, Mohr BA, Araujo. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts male aging study. Prev Med 2000; 30: 328–338. | Article | PubMed | ISI | ChemPort |
  20. Fung MM, Bettencourt R, Barrett-Connor H. Heart disease risk factors predict erectile dysfunction 25 years later. J Am Coll Cardiol 2004; 43: 1405–1411. | Article | PubMed | ISI |
  21. Esposito K, Giugliano F, De Sio M, Carleo D, Di Palo C, D'Armineto M et al. Dietary factors in erectile dysfunction. Int J Impot Res 2006; 18: 370–374. | Article | PubMed | ChemPort |
  22. Esposito K, Giugliano D. The metabolic syndrome and inflammation: association or causation? Nutr Metab Cardiovasc Dis 2004; 14: 228–232. | Article | PubMed | ISI | ChemPort |
  23. Esposito K, Pontillo A, Di Palo C, Giugliano G, Masella M, Marfella R et al. Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial. JAMA 2003; 289: 1799–1804. | Article | PubMed | ISI | ChemPort |
  24. Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. Arterioscler Thromb Vasc Biol 2003; 23: 168–175. | Article | PubMed | ISI | ChemPort |
  25. Cheitlin MD. Erectile dysfunction. The earliest sign of generalized vascular disease? J Am Coll Cardiol 2004; 43: 185–186. | Article | PubMed | ISI |
  26. Blumentals WA, Gomez-Caminero A, Joo S, Vannapagari V. Should erectile dysfunction be considered as a marker for acute myocardial infarction? Int J Imp Res 2004; 16: 350–353. | Article | ChemPort |
  27. Giugliano F, Esposito K, Di Palo C, Ciotola M, Giugliano G, Marfella R et al. Erectile dysfunction associates with endothelial dysfunction and raised proinflammatory cytokines levels in obese men. J Endocrinol Invest 2004; 27: 665–669. | PubMed | ISI | ChemPort |
  28. Diamant M, Tushuizen ME, Sturk A, Nieuwland R. Cellular microparticles: new players in the field of vascular disease. Eur J Clin Invest 2004; 34: 392–401. | Article | PubMed | ISI | ChemPort |
  29. Ferreira AC, Peter AA, Mendez AJ, Jiemenez JJ, Mauro LM, Chirinos JA et al. Postprandial hypertriglyceridemia increases circulating levels of endothelial cell microparticles. Circulation 2004; 110: 3599–3603. | Article | PubMed |
  30. Sabatier F, Darmon P, Hugel B, Combes V, Sanmarco M, Velut JG et al. Type 1 and type 2 diabetic patients display different patterns of cellular microparticles. Diabetes 2002; 51: 2840–2845. | Article | PubMed | ISI | ChemPort |
  31. Bernal-Mizrachi L, Jy W, Fierro C, Macdonough R, Velazques HA, Purow J et al. Endothelial microparticles correlate with high-risk angiographic lesions in acute syndrome. Int J Cardiol 2004; 97: 439–446. | Article | PubMed |
  32. Koga H, Sugiyama S, Kugiyama K, Watanabe K, Fukushima H, Tanaka T et al. Elevated levels of VE-Cadherin-positive endothelial microparticles in patients with type 2 diabetes mellitus and coronary artery disease. J Am Coll Cardiol 2005; 45: 1622–1630. | Article | PubMed | ISI | ChemPort |
  33. Werner N, Wassmann S, Ahlers P, Kosiol S, Nickening G. Circulating CD31+/Annessin V+ apoptotic microparticles correlate with coronary endothelial function in patients with coronary artery disease. Arterioscler Thromb Vasc Biol 2006; 26: 112–116. | Article | PubMed | ChemPort |
  34. Boulanger CM, Scoazec A, Ebrahimian T, Henry P, Mathieu E, Tedgui A et al. Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction. Circulation 2001; 104: 2649–2652. | Article | PubMed | ChemPort |
  35. Brodsky SV, Zhang F, Nasjletti A, Goligorsky MS. Endothelium-derived microparticles impair endothelial function in vitro. Am J Physiol Circ Heart Physiol 2004; 286: H1910–H1915. | Article | ChemPort |
  36. Mesri M, Altieri DC. Leukocyte microparticles stimulate endothelial cells cytokine release and tissue factor induction in JNK-1 signaling pathway. J Biol Chem 1999; 274: 23111–23118. | Article | PubMed | ISI | ChemPort |
  37. Esposito K, Ciotola M, Giugliano F, Schisano B, Improta L, Improta MR et al. Endothelial microparticles correlate with erectile dysfunction in diabetic men. Int J Impot Res 2007; 19: 161–166. | Article | PubMed | ChemPort |
  38. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA 2002; 287: 356–359. | Article | PubMed | ISI |
  39. Ford ES. Prevalence of the metabolic syndrome defined by the International Diabetes Federation among adults in the US. Diabetes Care 2005; 28: 2745–2749. | Article | PubMed | ISI |
  40. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP). Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 2001; 285: 2486–2497. | Article | PubMed | ISI |
  41. Esposito K, Giugliano F, Martedì E, Feola G, Marfella R, D'Armiento M et al. High proportions of erectile dysfunction in men with the metabolic syndrome. Diabetes Care 2005; 28: 1201–1203. | Article | PubMed | ISI |
  42. Bansal TC, Guay AT, Jacobson J, Woods BO, Nesto RW. Incidence of metabolic syndrome and insulin resistance in a population with organic erectile dysfunction. J Sex Med 2005; 2: 96–103. | Article | PubMed |
  43. Corona G, Mannucci E, Schulman C, Petrone L, Mansani R, Cilotti A et al. Psychobiologic correlates of the metabolic syndrome and associated sexual dysfunction. Eur Urol 2006; 50: 595–604. | Article | PubMed |
  44. Laaksonen DE, Niskanen L, Punnonen K, Nyyssonen K, Tuomainen TP, Valkonen VP et al. The metabolic syndrome and smoking in relation to hypogonadism in middle-aged men: a prospective cohort study. J Clin Endocrinol Metab 2005; 90: 712–719. | Article | PubMed | ISI | ChemPort |
  45. Kupelian V, Page ST, Araujo AB, Travison TG, Bremner WJ, McKinlay JB. Low sex hormone-binding globulin, total testosterone, and symptomatic androgen defi ciency are associated with development of the metabolic syndrome in nonobese men. J Clin Endocrinol Metab 2006; 91: 843–850. | Article | PubMed | ChemPort |
  46. Braga-Basaria M, Dobs AS, Muller DC, Carducci MA, John M, Egan J et al. Metabolic syndrome in men with prostate cancer undergoing long-term androgendeprivation therapy. J Clin Oncol 2006; 24: 3979–3983. | Article | PubMed |
  47. Hak AE, Witteman JC, de Jong FH, Geerlings MI, Hofman A, Pols HA. Low levels of endogenous androgens increase the risk of atherosclerosis in elderly men: the Rotterdam study. J Clin Endocrinol Metab 2002; 87: 3632–3639. | Article | PubMed | ChemPort |
  48. Billups KL. Sexual dysfunction and cardiovascular disease: integrative concepts and strategies. Am J Cardiol 2005; 96: 57–61. | Article | ChemPort |
  49. Kaplan SA, Meehan AG, Shah A. The age related decrease in testosterone is significantly exacerbated in obese men with the metabolic syndrome. What are the implications for the relatively high incidence of erectile dysfunction observed in these men? J Urol 2006; 176(4 Part 1): 1524–1527. | Article | PubMed | ChemPort |
  50. Basson R, Berman J, Burnett A, Derogatis L, Ferguson D, Fourcroy J et al. Report of international consensus development conference on female sexual dysfunction: definitions and classifications. J Urol 2000; 163: 888–893. | Article | PubMed | ISI | ChemPort |
  51. Edwards WM, Coleman E. Defining sexual health: a descriptive overview. Arch Sex Behav 2004; 33: 189–195. | Article | PubMed | ISI |
  52. Frank E, Anderson C, Rubinstein D. Frequency of sexual dysfunction in normal couples. N Engl J Med 1978; 299: 111–115. | PubMed | ISI | ChemPort |
  53. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA 1999; 281: 537–544. | Article | PubMed | ISI | ChemPort |
  54. Laumann EO, Nicolosi A, Glasser DB, Paik A, Gingell C, Moreira E et al. Sexual problems amomg women and men aged 40–80 y: prevalence and correlates identified in the Global Study of Sexual Attitudes and Behaviors. Intern J Impot Res 2005; 17: 39–57. | Article | ChemPort |
  55. Esposito K, Giugliano D. Obesity, the metabolic syndrome, and sexual dysfunction. Int J Impot Res 2005; 17: 391–398. | Article | PubMed | ISI | ChemPort |
  56. Kirchengast S, Hartmann B, Gruber D, Huber J. Decreased sexual interest and its relationship to body build in postmenopausal women. Maturitas 1996; 23: 63–71. | Article | PubMed | ChemPort |
  57. Brody S. Slimness is associated with greater intercourse and lesser masturbation frequency. J Sex Marital Ther 2004; 30: 251–261. | Article | PubMed |
  58. Rosen R, Brown C, Heiman J, Leiblum S, Meston C, Shabsign R et al. The female sexual function index (FSFI): a multidimensional self-report instrument for the assessment of female sexual function. J Sex Marit Ther 2000; 26: 191–208. | Article | ISI | ChemPort |
  59. Corona G, Jannini EA, Maggi M. Inventories for male and female sexual dysfunction. Int J Impot Res 2006; 18: 236–250. | Article | PubMed | ChemPort |
  60. Corona G, Mannucci E, Mansani R, Petrone L, Bartolini M, Giommi R et al. Organic, relational and psychological factors in erectile dysfunction in men with diabetes mellitus. Eur Urol 2004; 46: 222–228. | Article | PubMed | ISI | ChemPort |
  61. Enzlin P, Mathieu C, Van den Bruel A, Bosteels J, Vanderschueren D, Demyttenaere K. Sexual dysfunction in women with type 1 diabetes. Diabetes Care 2002; 25: 672–677. | Article | PubMed | ISI |
  62. Duby JJ, Campbell RK, Setter SM, White JR, Rasmussen KA. Diabetic neuropathy: an intensive review. Am J Health Syst Pharm 2004; 61: 160–173. | PubMed | ISI | ChemPort |
  63. Salonia A, Lanzi R, Scavini M, Postillo M, Gatti E, Putrella G et al. Sexual function and endocrine profile in fertile women with type 1 diabetes. Diabetes Care 2006; 29: 312–316. | Article | PubMed | ISI |
  64. Esposito K, Ciotola M, Giugliano F, Bisogni C, Schisano B, Autorino R et al. Association of body weight with sexual function in women. Int J Impot Res 2007; 19: 353–357. | Article | PubMed | ChemPort |
  65. Basson R. Women's sexual dysfunction: revised and expanded definitions. CMAJ 2005; 172: 1327–1333. | PubMed |
  66. Esposito K, Giugliano G, Scuderi N, Giugliano D. Role of adipokines in the obesity-inflammation relationship: the effect of fat removal. Plast Reconstr Surg 2006; 118: 1048–1057. | Article | PubMed | ChemPort |
  67. Esposito K, Ciotola M, Marfella R, Di Tommaso D, Cobellis L, Giugliano D. The metabolic syndrome: a cause of sexual dysfunction in women. Int J Impot Res 2005; 17: 224–226. | Article | PubMed | ISI | ChemPort |
  68. Derby CA, Mohr BA, Goldstein I, Feldman HA, Johannes CB, McKinlay JB. Modifiable risk factors and erectile dysfunction: can lifestyle changes modify risk? Urology 2000; 56: 302–306. | Article | PubMed | ISI | ChemPort |
  69. Cheng JYW, Ng EML, Chen RYL. Physical activity and erectile dysfunction: meta-analysis of population-based studies. Int J Impot Res 2007; 19: 245–252. | Article | PubMed | ChemPort |
  70. Esposito K, Giugliano F, Di Palo C, Giugliano G, Marfella R, D'Andrea F et al. Effect of lifestyle changes on erectile dysfunction in obese men: a randomized trial. JAMA 2004; 291: 2978–2984. | Article | PubMed | ISI | ChemPort |
  71. Willett WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999; 341: 427–434. | Article | PubMed | ISI | ChemPort |
  72. Katzmarzyk PT, Janssen I, Ardem CI. Physical inactivity, excess adiposity and premature mortality. Obes Rev 2003; 4: 257–271. | Article | PubMed | ChemPort |
  73. Hu G, Tuomilehto J, Silventoinen K, Barengo NC, Peltonen M, Jousilahti P. The effects of physical activity and body mass index on cardiovascular, cancer and all-cause mortality among 47 212 middle-aged Finnish men and women. Int J Obes Relat Metab Disord 2005; 29: 894–902. | Article | PubMed | ChemPort |
  74. Fung TT, Schulze M, Manson JE, Willett WC, Hu FB. Dietary patterns, meat intake, and the risk of type 2 diabetes in women. Arch Intern Med 2004; 164: 2235–2240. | Article | PubMed | ISI |
  75. Montonen J, Knekt P, Harkanen T, Jarvinen R, Heliovaara M, Aromaa A et al. Dietary patterns and the incidence of type 2 diabetes. Am J Epidemiol 2005; 161: 219–227. | Article | PubMed |


These links to content published by NPG are automatically generated


Sexual function and obesity

International Journal of Obesity Review

See all 19 matches for Reviews


Metabolomic study of cisplatin-induced nephrotoxicity

Kidney International Original Article

Association of body weight with sexual function in women

International Journal of Impotence Research Original Article

Mediterranean diet improves sexual function in women with the metabolic syndrome

International Journal of Impotence Research Original Article

Mediterranean diet improves erectile function in subjects with the metabolic syndrome

International Journal of Impotence Research Original Article

See all 32 matches for Research

Extra navigation