The maintenance of a healthy weight, or reductions in weight or waist size, to reduce morbidity and mortality is well known from international investigations. One of the largest prospective studies ever conducted was the European Prospective Investigation into Cancer and Nutrition (EPIC), which included a total of 359,387 participants, ages 25–70 years, from nine countries [4]. The mean follow-up in that study was 9.7 years, and a total of 14,723 participants died during this time period. The lowest risk of death was associated with a body mass index (BMI; in kg/m²) of approximately 24–25 for men and women. However, after adjustment for BMI, larger waist circumference (WC) measurements were also strongly associated with all-cause and disease-specific mortality, but both BMI and WC measurements provided better correlation than did one or the other measurement alone. Both measurements offer synergistic value for the patient attempting to lose weight [5]. Still, regardless of BMI, WC is becoming a significant predictor of mortality risk in men and women, as witnessed in the United States NIH-AARP Diet and Health Study of 154,776 men and 90,757 women aged 51–72 years at baseline [6]. A twofold or higher risk of mortality in men and women, regardless of BMI, was observed in the smaller US Cancer Prevention Study II Nutrition Cohort of 48,500 men and 56,343 women [7]. These and other studies provide the most accurate and realistic glimpse of the risk associated with BMI and WC and mortality. The only time I find that other studies question these findings that lower weight or waist is not associated with lower mortality is when a study does not adequately and precisely correct for specific smoking status and more specific comorbidity issues because reverse causation can occur in these studies [8]. In other words, it is not the low body weight that leads to morbidity and mortality, but morbidity (cancer, pulmonary disease) that leads to lower body weight and then mortality. Thus, it is critical to explain why there will always be some outliers in terms of the data on obesity and mortality risk, but overall the association of weight and waist increase and morbidity and mortality increase has become clear, regardless of race and ethnicity examined [9]. The correlation with BMI and WC and the increased risk of a variety of male and female cancers is also striking and has existed for some time [10, 11]. Table 5.1 summarizes the basic interpretation of the BMI and WC ranges of values for men and women [5].

Most men reporting ED symptoms (up to 70–80 %) are overweight or obese, and men who carry abnormal amounts of weight have a consistently higher risk of sexual dysfunction than do men with a normal BMI, especially with aging [12–16]. Interestingly, this correlation, albeit not as strong, is also observed in a large minority of women in terms of obesity and FSD [17]. Regardless, it is no longer difficult to conclude that in both sexes obesity is a risk factor for sexual dysfunction and that cardiovascular disease risk factors are predictive of sexual function and vice versa [18–20].

In the placebo group of the Prostate Cancer Prevention Trial (PCPT), men with incident or prevalent ED had a significant (p < 0.001) 45 % increased risk of a subsequent cardiovascular event during the study follow-up [19]. This risk was noted to be similar to the risk of a current smoker or that of a man with a family history of myocardial infarction. The average participant in the PCPT study was overweight (BMI 27.5), and increases in BMI were significantly associated with ED during the clinical trial and a subsequent cardiovascular event in the final multivariate statistical analysis. In women, the correlation between and FSD and obesity appeared to be greater in those with metabolic syndrome, which places postmenopausal women at a higher risk for a future cardiovascular event [21].

How strong is the correlation between weight gain and sexual function for men? In one of the largest meta-analyses (n = 6,800 men, 31 studies) of hormonal changes and obesity, researchers found that 18 of 20 studies measuring testosterone, 15 of 16 measuring sex hormone binding globulin (SHBG), and 10 of 12 investigating free testosterone found an inverse correlation between BMI and these parameters [22]. A total of 4 of 10 studies found a direct relationship between BMI and estradiol. The conclusion of this unique meta-analysis was the profound and unambiguous observation: “There was strong evidence of a negative relationship for testosterone, SHBG and free testosterone with increased BMI.” Studies continue to find significant inverse relationships between weight and testosterone and increases in estradiol in men [23, 24]. Additionally, a potential reduction in pregnancy rates with higher BMI is plausible because of sexual dysfunction, higher scrotal temperatures, and adipose hormone contributions [25]. Of concern, there is also recent evidence that this correlation is just as strong in boys aged 14–20 years with as much as a 40–50 % reduction in total testosterone compared to those with normal BMIs [26]. However, obesity in women increases androgen levels and also can result in hirsutism and reduced fertility [27, 28].

Patients are often surprised to learn that exercise is not needed to lose weight. Of course, it should be encouraged to promote overall and cardiovascular health, but weight loss can be achieved in men and women with strict caloric restriction. Weight loss-only studies of short- and/or long-term duration that do not include a rigid exercise component (again only caloric modification or restriction) are demonstrating increases in testosterone and sexual function in men. A pilot study of 43 obese men followed for just 14 weeks on a weight-loss program found significant (p = 0.02), graded improvements in total testosterone with weight loss [29]. Median baseline testosterone was approximately 7–9 nmol/L, and men losing 3.5–12.1 %, 12.2–17.1 %, and 17.2–25.4 % of their body weight experienced adjusted mean increases in testosterone levels of 0.7, 3.3, and 3.7 nmol/L, respectively. The free androgen index (FAI) also increased significantly in the group with the largest weight reduction. Total sperm count, semen volume, and anti-Müllerian hormone significantly increased.

Bariatric surgical series of women demonstrate significant reductions in androgen levels and cardiovascular markers in pre- and postmenopausal women [30]. Significant reductions were also observed for DHEA-S in premenopausal women. These changes are also found in dietary restriction studies of obese women when following a high-protein (30 %+ of daily energy) and low glycemic index diet [31] or by adhering to a low-calorie diet (500–600 cal per day) over an 8-week period [32]. The hormonal benefits of weight loss in women are occurring in those with and without polycystic ovarian syndrome (PCOS) [31, 32].

Rapid weight loss also appears to be an effective method for rapidly improving lower urinary tract symptoms (LUTS), libido, and/or ED [33]. An 8-week low-calorie diet (approximately 900 cal per day) was given to nondiabetic and diabetic men with a BMI >30 and a WC >102.1 cm versus a control group. This was a nonrandomized intervention study and a dietitian communicated with these men and monitored their progress throughout the study period. A total of 68 men completed the study, and the mean age of the participants was 50 years. Weight loss of approximately 10 % or greater was correlated with significant improvements in insulin sensitivity, testosterone, erectile function, and sexual desire, as well with decreases in WC and LUTS, in both diabetic and nondiabetic men. Improvement in LUTS was associated with a significant increase in erectile function, sexual desire, and testosterone. Similar improvements were noted in nondiabetic and diabetic individuals on the sexual function score of the International Index of Erectile Function (IIEF-5) but not in the International Prostate Symptom Score (IPSS) (−6.4 vs. −2.1). In the nondiabetic men, the mean weight and waist losses in 8 weeks were over 12 kg and approximately 12.5 cm. Thus, profound weight loss is plausible in motivated individuals utilizing severe caloric restriction without any initial change in physical activity levels. Reductions in LUTS with weight loss could be another mechanism of action that improves erectile function, similar to what is touted in conventional medicine with pharmacologic agents [34, 35].

A study that analyzed short- and long-term data and different caloric modifications or diet options continues to espouse the notion that weight loss can be achieved with diverse programs and more practical changes [36]. An 8-week study of 31 obese (mean BMI of 35 and WC of 122 cm) men with type 2 diabetes (mean age 60 years) who received a 1,000 cal/day meal replacement low-calorie (LC) diet (n = 19) or a high-protein (HP), low-fat, reduced-carbohydrate (n = 12) diet reduced total daily energy or caloric consumption by approximately 600 cal per day. After 8 weeks, all subjects were then placed on the HP (600 cal per day reduction) diet for an additional 44 weeks. After 8 weeks, the total weight and waist size of men in the LC diet group was reduced by 10 % compared with 5 % for men in the HP diet group. Both diets resulted in significant improvements in glucose, LDL, SHBG, IIEF-5, sexual desire inventory (SDI), IPSS, and endothelial function. ED, sexual desire, and urinary symptoms improved by approximately equal amounts with both diets. C-reactive protein (CRP) and interleukin-6 (IL-6) were lowered with the HP diet. At 52 weeks, the metabolic benefits were maintained, and sexual and urinary parameters continued to improve. Men switching to a more moderate diet after an 8-week caloric restriction challenge showed that results and compliance were sustainable up to 52 weeks. Mean weight loss after 1 year was approximately 9 kg, and mean reductions in the IPSS from 9 to 4 occurred after 52 weeks. The mean SDI score increased over 20 points. The IIEF-5 was 11 and improved to 18. Changes in total and free testosterone were not significant, but men were eugonadal at baseline.

Arguably, one of the more overt arguments to consistently demonstrate to healthcare professionals and patients that weight loss is critical to immediate overall and sexual health in men and women are the short- and long-term data on bariatric surgery [37–39]. This is not used to advocate for more bariatric procedures in obese men and women, but to provide a tangible example of how weight loss alone can profoundly and rapidly change disease risk and multiple health parameters over short and long time periods. Past studies evaluating bariatric surgery and changes in male sex hormones found improvements in sexual health or testosterone levels in almost every investigation completed. Testosterone increases would have been tantamount to receiving prescription androgen replacement therapy in some cases for men [38]. A notable study by Hammoud et al. found a mean significant increase in total testosterone of 15.3–47.6 ng/mL (increase of 310 ng/dL) and free testosterone (45.2 pg/mL) 2 years after a Roux-en-Y gastric bypass [40]. Dissatisfaction with sexual quality of life was associated with increases in obesity, and difficult sexual performance and low libido were inversely correlated with total and free testosterone. Other series demonstrate improvements in IIEF-5 scores 2 years after bariatric surgical weight loss of 30 % [41]. Significant improvements in all domains (drive, erectile, ejaculatory, problem assessment, and satisfaction) of the Brief Sexual Function Inventory (BSFI) were also demonstrated in a 2-year study of bariatric weight loss [42]. Mean age in this study was 48 years (range 19–75 years), and multivariate analysis demonstrated that the amount of weight loss was predictive of the amount of improvement in every BSFI domain. Few studies of women and bariatric surgery outcomes with a focus on sexual health have been completed, but the preliminary results also suggest the potential for noteworthy benefits. A US case series of reproductive-aged women (n = 29) not utilizing confounding medications and followed up to 12–24 months found a significant increase in the Female Sexual Function Index (FSFI) by 28 % [39]. In a study from Greece, 59 obese females were given an FSFI 1 week before surgery and again at 1 year postoperatively [43]. Significant reductions in depression and sexual pain levels (p = 0.01) and improvements in sexual desire (p = 0.005), arousal (p = 0.001), lubrication (p = 0.003), satisfaction (p = 0.01), and total sexual function (p = 0.003) were observed. A US study of 54 sexually active women (mean age 43 years) with a FSFI and 6 months postoperatively found women with FSD (n = 34) actually resolved in 68 % of these participants [44]. All domains of the FSFI significantly (p < 0.05) improved and in regression analysis marriage, younger age, and worse preoperative sexual issues were associated with greater improvements in sexual function. The improvements in sexual function in women with FSD to that of the level of women without FSD in this study again suggest that improvements in women can be as notable as what is observed in men with sexual dysfunction. This is important because in some surgical series the rate of FSD is as high as 60 % and any domain of the FSFI, for example, can be impacted (desire, arousal, lubrication, orgasm, satisfaction, and pain) [45].

Critics of lifestyle changes may focus on a few select studies of men and women that demonstrated no benefit or even negative impacts on sexual health with significant weight loss regardless of the method used to accomplish that weight loss (diet, surgery, etc.) [46–48]. Yet, what needs to be highlighted is that these rare negative studies found other diverse quality-of-life benefits with weight loss [49]. An inability to improve some aspect of sexual health via lifestyle should be just another clinical indicator to begin to introduce other conventional medicine options to improve sexual function [46], which is no different than what is suggested in other medical specialties, such as cardiology, rheumatology, or orthopedics [1, 2].

It appears that weight loss alone of 5–10 % that does not include aerobic or resistance exercise in overweight or obese nondiabetic or diabetic men and women can result in improvements in sexual, reproductive, and urinary function in a short period of time. One of the first meta-analyses to review the correlation between weight loss and endocrine health in men was published and reviewed data from the past 40+ years [50]. A total of 24 studies met the inclusion criteria that examined diet or bariatric surgery. Researchers found that both low-calorie diets and bariatric surgery were associated with statistically significant (p < 0.001) increases in SHBG and unbound total testosterone. Bariatric surgery was significantly more effective compared to caloric-restriction diets in raising testosterone (8.73 nmol/or 252 ng/dL vs. 2.87 nmol/L or 83 ng/dL; p < 0.001) in men. Androgen levels were increased by greater amounts in those that lost more weight, and more so in younger patients and nondiabetics. Reductions in estradiol and an increase in gonadotropins also occurred with weight loss. I look forward to being able to cite a similar meta-analysis for women in the near future; again, there is a paucity of data for women, but I am optimistic that it will be profoundly positive.

One of the only meta-analyses of exercise and ED included seven cross-sectional studies, and there was an estimate of a 40–60 % reduction in ED risk with moderate to higher levels of exercise [51]. Another meta-analysis of randomized controlled trials and ED of arteriogenic origin identified five (n = 385) randomized controlled studies utilizing the International Index of Erectile Function (IIEF) and found significant improvement of ED with aerobic activity [52].

Younger sedentary men (<40 years of age) appear to experience a significantly increased risk of ED in the domains of erectile function, orgasm function, and intercourse satisfaction. Increased amounts of exercise improve sexual function in younger men even after control for multiple confounding variables [53]. Sedentary lifestyles have also been associated with an increased risk of ED in multiple well-known, diverse prospective epidemiologic studies regardless of age or age range, such as the Massachusetts Male Aging Study [54], the Health Care Professionals’ Follow-up Study [55], and a Vienna Health Screening Project [56]. Cardiovascular fitness and exercise frequency also appear to provide reductions in risk or severity of ED of 40–50 % and even higher in men with diabetes and in men with hypertension and other comorbidities [57, 58].

There are a dearth of studies overall for the risk of FSD and lifestyle changes but especially in terms of exercise as an isolated intervention. Still, in populations with higher rates of FSD, such as diabetics, a large sampling of 595 women found a 10 % lower risk in those that reported greater amounts of physical activity [59]. This may not seem impressive, but the average age of the study participants (58 years) and the mean duration of diabetes was 5 years, which is still a noteworthy benefit. Just 20 min of exercise before sexual stimuli has been shown to increase genital arousal in women reporting antidepressant sexual arousal issues (n = 47) and appeared to do this by increasing sympathetic nervous system activity [60].

How much exercise should be recommended, or is needed for some form of tangible impact? A population-based cross-sectional study of ED in Hong Kong that included 1,506 men aged 26–70 years found that being physically active by expending at least 1,000 kcal/week or more reduced the risk of ED in obese men [61]. Moderate-intensity exercise of 150 min/week or more was associated with maintaining healthy erectile function, and both a low physical activity level and a high WC were independently associated with ED in an analysis of 3,941 men [62]. A smaller study of 674 men aged 45–60 years found an 83 % reduction in severe ED in those who engaged in at least 3,000 kcal/week of physical activity compared with those doing less [63]. A metabolic syndrome comparative case–control study found a significant 88 % reduction in the risk of ED for middle-aged men who engaged in greater than 400 kcal/day of exercise [64].

Lifestyle changes could also significantly enhance the benefits of conventional medical prescription ED pill options [65] and perhaps other therapies if they were tested. One unique randomized, open-label study of 60 patients with ED allowed half of the participants on PDE-5 inhibitors alone, and the other half combined the pill with regular exercise for 3 months. Men were overall inactive at baseline and were instructed to choose any form of exercise and to include intensity and duration information. Men with a history of radical pelvic surgery were excluded. The mean age and BMI of the participants were 50 years and 27 (overweight), respectively. A significant improvement was observed in all aspects of the IIEF-15 except the orgasm domain for men who exercised 3 or more hours a week compared with the non-exercise, pill-only group. Erectile function, confidence, sexual desire, intercourse satisfaction, and total satisfaction were all significantly improved in the exercise group over the PDE-5 alone group. No significant difference in testosterone levels occurred between the groups, but within the exercise group only, there was an increase in testosterone. Intercourse frequency was nonsignificantly greater in the exercise group than in the pill-alone group. It is interesting that no single PDE-5 inhibitor has ever demonstrated a consistent benefit on libido [66, 67], but when combined with exercise, this precise benefit occurred [65]. And the synergism that has occurred in women’s studies of adding caloric reduction to exercise has demonstrated more profound health benefits in terms of the potential for favorable hormonal changes and disease reduction [68]. Thus, recommending at least 30 min of aerobic exercise per day on average with a minimum of 300–500 cal utilized during each physical activity session should be discussed with patients. If any intervention had this kind of preliminary data to reduce or improve ED, would it be included in sexual health guidelines or recommended in most medical clinics as a legitimate treatment option for ED?

A variety of mechanisms of action have been suggested as to how exercise could improve sexual function, and these benefits revolve around heart-healthy parameters [55, 64, 66, 69–71]. Improved cardiovascular fitness, endothelial function, and neurotransmitter release reduced sympathetic overdrive, but improved sympathetic tone, inflammatory response, and fibrinogen and psychological benefit have all been demonstrated with exercise in laboratory and human studies. Improved resting heart rate and heart rate recovery may also be novel factors associated with ED [72, 73]. Increases in resting heart rate over time may also be associated with a higher rate of mortality from heart disease and all causes in non-, former, and current smokers [74, 75]. Novel cardiovascular risk marker reductions that may improve erectile function appear to get adequate attention [76, 77], but more simplistic markers, such as resting heart rate, are low cost and appear to be needed to monitor the success of an exercise program. Patients should be encouraged to include daily exercise that is adequate to maintain a healthy sexual function, weight, WC, and heart rate.

Depression and other psychological issues and their conventional treatments have been correlated with sexual dysfunction [78, 79]. Approximately 60–70 % of patients (men and women) on antidepressants experience adverse sexual effects [79]. Yet, meta-analyses have demonstrated that exercise reduces depressive scores with and without conventional medicine [80–82]. A Cochrane review evaluated 32 randomized controlled trials in 1,858 patients diagnosed with Major Depressive Disorder (MDD) and found a potential clinical impact on depression scores that in some cases mirrored the impact with conventional drug treatment and behavioral therapies, but the pooled effect in more rigorous trials was smaller [81]. There appear to be no age limits on the impact of exercise and mood. A meta-analysis of nine randomized trials in older individuals (approximately 60–90 years of age, majority were female) found that exercise was correlated with significantly lower depression severity regardless if the individual was clinically diagnosed or identified based on a symptom checklist [83]. These results suggest that 63 % of those that engaged in exercise had a lower severity of depression compared to the average control participant. The pooled impact of exercise on depression severity was actually comparable to the effects predicted for different classes of antidepressant medication and psychotherapy.

A multitude of mechanisms as to how exercise reduces depression have been postulated: cortisol reduction, favorable neurotransmitter alterations, diversion from negative thoughts, social contact, improved sleep quality, and reductions in sympathetic overload that can reduce anxiety and agitation [80–82, 84]. Still, limitations with exercise and depression are arguably compliance, more strict methodology of trials, whether or not tachyphylaxis can occur in the short- or long-term and negative effects of excessive physical activity. An emerging limitation may simply be the lack of this treatment to be embraced and emphasized in clinical practice as an acceptable form of ancillary therapy.

Exercise is recommended to only one in three patients during a visit with a healthcare professional [85]. Psychological interventions, at the very minimum, without even considering physical health changes, appear to be effective for the treatment of certain forms of ED [86]. This must be kept in mind with any patient who seeks treatment for ED or who is trying to prevent ED. When exercise is truly considered, a standard treatment in most major ED and FSD clinical recommendation guidelines, enhancing medication compliance and treatment, improving quality of life, and reducing sexual dysfunction should be the standard expected outcomes of the patient and the clinician.

Numerous other lifestyle changes that could impede sexual function in men and women are further discussed in detail from other sources [66]. For example, something as simple as a small caloric meal or even glucose or sugar before a testosterone blood test could cause short-term and, at times, profound (15 % of men becoming temporarily hypogonadal, or up to 47 % drop) reductions in total testosterone [118], which can last from 30 min to 2 h after consumption [118, 119]. This is due to insulin release that can acutely reduce pulsatile LH and then testosterone levels. Overnight fasting has been shown to be associated with higher testosterone levels in men 40 years and older [120]. Collectively, these findings could profoundly impact a sexual dysfunction work-up or evaluations and should be discussed with male patients. It is well known that chronic hyperglycemia (or hypoglycemia) or long-term fasting (several days) inhibits the male gonadal axis [118], but soon it should be well known that caloric intake also could block the same path acutely, which I could now argue should result in the requirement for fasting before drawing male testosterone blood levels. Other dietary factors also could impact hormone levels and more gender-specific disease risk. For example, low-fat and high-fiber diets may also acutely and slightly suppress testosterone levels [121], and similar healthy diets can reduce estradiol in women [122]. Again, more intensive research on lifestyle changes and sexual health markers are needed, but in the meantime fasting before androgen level determination makes sense. Other factors, such as lean muscle mass, strength, and frailty, that can be associated with lifestyle changes are just beginning to receive adequate attention in the area of sexual health [123].

A truly novel and rare 2-year randomized trial of regular exercise and multiple dietary changes, which followed a Mediterranean diet, to improve ED in obese men should receive more clinical attention, discussion, and awareness, despite being initially published in 2004 [124]. A total of 110 obese men with a mean BMI of 36–37, waist-to-hip ratio (WHR) of 1.01–1.02, and age of 43 years were included. The mean IIEF score at baseline ranged from 13 to 14 out of 25, and men in this trial were without diabetes, high cholesterol, or high blood pressure. A total of 55 men were included in an intensive intervention group that reduced calories and increased physical activity via personalized dietary counseling, exercise advice, dietary changes, and regular appointments with a nutritionist and personal trainer. Another group of 55 men were in the control group and received basic and general information about exercise and healthy food choices. After 2 years, multiple, diverse, and significant mean changes occurred in the intervention group compared with the placebo group. These are summarized in Table 5.2 [124] in regard to the profound changes observed in the intervention arm. This should give the clinician and patient an overview of what may be needed comprehensively to achieve adequate or tangible effects in the area of ED improvement or even prevention.