Many factors, such as age, childbirth, fecal difficulties, obstetric complications, obesity, pelvic surgery, medications, functional impairment, chronic diseases, menstrual cycle, race, and family history, are associated with urinary incontinence and other lower urinary tract symptoms.1–9 A relationship to menopause has been postulated but never documented.1 Many of the factors are interrelated, so a full understanding of possible predisposing or inciting factors implies a model in which all potential associated factors are represented. However, many of the studies so far included only some factors, potentially overlooking confounding factors. Comparison between studies is impeded because varying definitions were applied. The aim of this study was to assess the association between various risk factors and the prevalence of lower urinary tract symptoms in women 40–60 years old.
Material and Methods
Four thousand women were asked at baseline to fill in a questionnaire concerning lower urinary tract symptoms. The women were selected at random from the Danish Civil Registration System, in which every person living in Denmark is identified by a unique ten-digit number assigned to them throughout life. The sample comprised women aged 40, 45, 50, 55, and 60 years old from one urban county (Copenhagen County) and one rural county (Storstrøms County), equally distributed with 400 in each age and county group. The sample was randomized by computer. Two thousand eight hundred sixty women (71.7%) returned completed questionnaires.10 Subsequently, 502 women with symptoms more than weekly and 742 with no symptoms (controls) completed a supplementary questionnaire concerning possible associated factors.
The symptom questionnaire was validated previously.11 For calibration we interviewed 13 women 45–55 years old admitted to our hospital for several lower urinary tract symptoms. A test-retest of the final questionnaire comprising a subsample of 100 women showed high reproducibility with kappa values of 0.31–1.00 (median 0.70).10 Construct validity was assessed in a subsample of 207 women using answers from interviews as the standard. Kappa values were between −0.02 and 0.52 (median 0.46).10 The final symptom questionnaire included data on age, urinary incontinence, daytime frequency, nighttime frequency, postmicturition dribble, straining, urgency, incomplete bladder emptying, and hesitancy. The definitions of stress and urge incontinence were those defined by the International Continence Society. Participants were asked to score symptoms on a four-point scale (never, sometimes, often, or weekly, or each time or daily/nightly). The supplementary questionnaire on associated factors included parity, episiotomy, anal sphincter defect, fetal weight, prior hysterectomy, prior anterior vaginal repair, prior operation for uterine prolapse, weight, height, hormonal status, stool habits, use of diuretics, physical activity, and medication (diuretics, antibiotics for cystitis, and non–antibiotics for non-infectious urinary symptoms).
For analysis data were transformed on a binary scale stating presence of absence of symptoms (symptoms: equal to or more than weekly or often). Body mass index (BMI) was stratified into quartiles for each symptom. Women were considered hormonally inactive if they did not menstruate, received no hormone replacement therapy (HRT), or (in case women had hysterectomies) had at least two of the following signs indicating hormonal insufficiency: hot flushes, dyspareunia, vaginal dryness, or nightly sweat. Constipation was defined as frequency of stool less than daily. A high level of physical activity was defined as conditions at work involving at least some heavy lifting or conditions in private life including activities such as running or gardening. The local ethics committee approved the study.
Descriptive data are presented as numbers or percentages of included women. A multivariable logistic regression model was used to analyze the relationship between potential associated factors, including age and lower urinary tract symptoms. Only factors in which a priori univariate χ2 test was significant were included in the model (forward inclusion). Factors were removed from the model according to results of logistic likelihood ratio tests and calculation of the deviance (backward elimination). Interactions between age and other associated factors were calculated. In all analyses a 5% significance level was used. A statistical model comprising inciting factors (all risk factors except gastrointestinal symptoms) were established, and associations between lower urinary tract symptoms and gastrointestinal symptoms adjusted for appropriate confounding factors were assessed.
Four hundred eighty-seven (97.0%) women with symptoms and 564 (76.0%) controls completed the questionnaire on associated factors and were included. Demographic data are given in Table 1. At the time of the questionnaire, eight women received antibiotics for cystitis. Four women received other medical treatment for non–infectious lower urinary tract symptoms. Stress incontinence was associated with parity (primipara OR 2.2, 95% CI 1.0, 4.9; para 2 OR 3.9, 95% CI 1.9, 8.0; para 3 OR 4.5, 95% CI 2.1, 9.5), use of diuretics (OR 2.2, 95% CI 1.2, 3.9), hysterectomy (OR 2.4, 95% CI 1.6, 3.7), and increased BMI (Table 2). Urge incontinence was associated with diuretics (OR 4.0, 95% CI 2.2, 7.1) and BMI, and urgency was associated with parity (primipara OR 1.9, 95% CI 0.9, 4.2; para 2 OR 3.0, 95% CI 1.5, 5.9; para 3 OR 3.1, 95% CI 1.5, 6.5), use of diuretics (OR 2.7, 95% CI 1.5, 4.7) and BMI (Table 2). Associations between non–incontinence symptoms (except for urgency) and risk factors were weak and inconsistent (Tables 2 and 3). Straining at stool and constipation was positively associated with most lower urinary tract symptoms. Lesion of sphincter ani, episiotomy, fetal weight, physical activity, and hormonal status showed little association with lower urinary tract symptoms (Tables 2 and 3). An almost uniform positive association between straining at stool and constipation and lower urinary tract symptoms was observed (Table 4). No interaction between age and any items was found.
Lower urinary tract symptoms are common and increase in women 40–60 years old.10 The cause of lower urinary tract symptoms is multifactorial. Clinical implications are obvious because most associated factors can be prevented, reversed, or predicted. It was important to incorporate all possible associated factors into a statistical model that dealt with the effect of confounding, ie, logistic regression. Some otherwise appropriate studies did not do this.1,12
As in retrospective studies, this study found a positive association between hysterectomy and stress incontinence and other non–incontinence lower urinary tract symptoms.3,8 The uterus probably supports part of the pelvic floor; therefore, removal of it might compromise pelvic floor function. However, it is well known that in some cases hysterectomy tended to decrease the risk of urinary incontinence.8 Any biologic model to explain an association between hysterectomy and lower urinary tract symptoms so far remains speculative.
An association between parity and stress incontinence is well established.1,9,12 Our data and those of others showed a dose-response effect that indicates a cause-effect relationship between parity and stress incontinence.9,13 The mechanism is probably muscular or neuromuscular pelvic lesions.14 Non–incontinence lower urinary tract symptoms are clinically less well delineated than those of urinary incontinence. However, if etiology were similar one would expect at least some association between parity and non–incontinence lower urinary tract symptoms. Except for urgency, we did not find such association.
Obesity is well established as a risk factor for urinary incontinence.7,9 Our study confirmed a positive and almost linear association between them,7 and a similar association between other lower urinary tract symptoms and obesity (Tables 2 and 3). The association between urinary incontinence and obesity was probably a consequence of comparatively higher intrapelvic pressure. Mechanisms that link obesity and other types of lower urinary tract symptoms are less evident.
Our findings support a hypothesis that excessive load on the bladder after treatment with diuretics possibly causes not only urgency and urge incontinence, but also stress incontinence. Estrogen and progesterone receptors are present in the vagina, urethra, bladder, and pelvic floor. Urodynamic changes have been found during the menstrual cycle, during pregnancy, and after menopause.15 A significant effect of estrogen replacement therapy on urinary incontinence has not been found. The relationship between onset of symptoms and menopause appears to be an important confounder because only symptoms that originated during or after menopause are likely to benefit from hormonal treatment. That confounder has seldom been investigated.
History of abortion was negatively associated with prevalence of daytime frequency but positively associated with the feeling of an empty bladder. Those haphazard findings are inconsistent with biologic models. Obstetric complications (episiotomy, lesion of anal sphincter, delivery of a large fetus, and prolonged delivery) might predispose women to postpregnancy urinary incontinence,2 but in our population, obstetric complications had no demonstrable effect. Those findings indicate that obstetric complications have little if any long-lasting influence on prevalence of urinary incontinence or other lower urinary tract symptoms.
No association between physical activity and lower urinary tract symptoms was found. Women who know that physical activity precipitates lower urinary tract symptoms avoid such activities. The optimal approach to assessing any relationship between physical activity and lower urinary tract symptoms is unknown. A hypothetical question that assesses the degree to which women avoid physical activities is a possibility.
Chronic constipation and repeated prolonged straining efforts are believed to induce progressive neuropathy and continued gastrointestinal dysfunction.16 The anatomic close relationship between pelvic floor neuropathy and constipation and straining at stool might explain increased incidence of lower urinary tract symptoms in this and other studies.5
1. Thomas TM, Plymat KR, Blannin J, Meade TW. Prevalence of urinary incontinence. BMJ 1980;281:1243–5.
2. Viktrup L, Lose G, Rolff M, Barfoed K. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 1992;79:945–9.
3. Milsom I, Ekelund P, Molander U, Arvidsson L, Areskoug B. The influence of age, parity, oral contraception, hysterectomy and menopause on the prevalence of urinary incontinence in women. J Urol 1993;149:1459–62.
4. Elving LB, Foldspang A, Lam GW, Mommsen S. Descriptive epidemiology of urinary incontinence in 3,100 women age 30–59. Scand J Urol Nephrol 1989;125(Suppl):37–43.
5. Spence-Jones C, Kamm MA, Henry MM, Hudson CN. Bowel dysfunction: A pathogenic factor in uterovaginal prolapse and urinary stress incontinence. Br J Obstet Gynaecol 1994;101:147–52.
6. Bump RC, Sugerman HJ, Fantl JA, McClish DK. Obesity and lower urinary tract function in women: Effect of surgically induced weight loss. Am J Obstet Gynecol 1992;167:392–7; discussion 397–9.
7. Mommsen S, Foldspang A. Body mass index and adult female urinary incontinence. World J Urol 1994;12:319–22.
8. Vervest HA, van Venrooij GE, Barents JW, Haspels AA, Debruyne FM. Non-radical hysterectomy and the function of the lower urinary tract. I: Urodynamic quantification of changes in storage function. Acta Obstet Gynecol Scand 1989;68:221–9.
9. Brown JS, Grady D, Ouslander JG, Herzog AR, Varner RE, Posner SF. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Heart & Estrogen/Progestin Replacement Study (HERS) Research Group. Obstet Gynecol 1999;94:66–70.
10. Møller LA, Lose G, Jørgensen T. The prevalence and bothersomeness of lower urinary tract symptoms in women 40–60 years of age. Acta Obstet Gynecol Scand 2000;79:298–305.
11. Jackson S, Donovan J, Brookes S, Eckford S, Swithinbank L, Abrams P. The Bristol Female Lower Urinary Tract Symptoms Questionnaire: Development and psychometric testing. Br J Urol 1996;77:805–12.
12. Sommer P, Bauer T, Nielsen KK, Kristensen ES, Hermann GG, Steven K, et al. Voiding patterns and prevalence of incontinence in women. A questionnaire survey. Br J Urol 1990;66:12–5.
13. Foldspang A, Mommsen S, Lam GW, Elving L. Parity as a correlate of adult female urinary incontinence prevalence. J Epidemiol Community Health 1992;46:595–600.
14. Tetzschner T, Sorensen M, Jonsson L, Lose G, Christiansen J. Delivery and pudendal nerve function. Acta Obstet Gynecol Scand 1997;76:324–31.
15. Cardozo L. Role of estrogens in the treatment of female urinary incontinence. J Am Geriatr Soc 1990;38:326–8.
16. Jorge J, Wexner S, Ehrenpreis E, Nogeuras J, Jagelman D. Does perineal descent correlate with pudendal neuropathy? Dis Colon Rectum 1993;36:475–83.