Obesity and urinary incontinence in women: is the black box becoming grayer?

Abstract

The prevalence of obesity is increasing worldwide and has lately reached epidemic proportions in many countries. Epidemiological studies have consistently shown that both overweight and obesity are important risk factors for the development of various female pelvic floor disorders including urinary incontinence, pelvic organ prolapse, and fecal incontinence, as well as resistance to treatment [1]. The relationship between obesity and urinary incontinence will be discussed here. Strong associations between obesity and stress urinary incontinence (SUI) in women had been frequently reported in the urogynecologic literature [1, 2]. The pathophysiologic basis for this relationship is the significant correlation between body mass index (BMI) and intra-abdominal pressure suggesting that obesity may stress the pelvic floor secondary to a chronic state of increased pressure [2]. Obesity has also been confirmed as an important risk factor for failure of continence surgery in the first follow-up year. Patients with BMI>30 were 3.7 times more likely to be incontinent 1 year after colposuspension compared to nonobese patients [1]. Weight loss has been proven to be an effective treatment of SUI in obese women. Weight reduction of only 5% of initial body weight has been shown to reduce UI severity enough to result in significant improvement in quality of life measures in obese women [3]. Moreover, surgically induced weight loss had been shown to significantly improve various urodynamic and bladder/urethral imaging parameters during coughing, e.g., the magnitude of vesical pressure increase, bladder-tourethra pressure transmission, and urethral axial mobility. More recently, overweight and obesity were found to be an independent risk factor for overactive bladder (OAB) in women [4]. The most likely explanation is the occurrence of chronic low-grade inflammation in the bladder of obese women indicated by increased urinary chemokines [5]. In fact, dietinduced obesity was shown to be associated with infiltration of macrophages into adipose tissue [6]. Adipocytes surrounding the human bladder can be affected, thus leading to inflammation and triggering OAB symptoms. The waist–hip ratio has been advocated as a measure of “central” obesity because BMI does not describe the distribution of obesity. This measurement, however, was found to be associated with SUI but not with OAB or mixed urinary incontinence, further suggesting a nonmechanical mechanism for OAB in obese women [7]. The association between urinary incontinence and diabetes mellitus, a disease that is closely linked to obesity, is well established [1, 2]. It has been suggested that the most likely reason for the increased risk is a microvascular compromise in diabetic women leading to damage to the urethral sphincter mechanism and bladder “sensitivity” with increased risk of developing SUI and OAB, respectively. Stricter glycemic control may reduce the risk or severity of urinary incontinence [2]. Some studies have also found that women who used insulin were more likely to be incontinent than women who did not require insulin, but the mechanisms are unclear. W. Agur (*) Department of Obstetrics and Gynecology, Crosshouse Hospital, Kilmarnock, Scotland, UK e-mail: waelagur@nhs.net