| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
ORIGINAL RESEARCH |
From the Division of Urogynecology, Department of Obstetrics and Gynecology, Brown University School of Medicine, Providence, Rhode Island.
Address reprint requests to: Lily A. Arya, MD, MS, 100 Dudley Street, Providence, RI 02905, E-mail: larya{at}wihri.org
 |
Abstract |
|---|
Top
 Abstract Materials and MethodsResultsDiscussionReferences |
|---|
Methods: Women were included if they had symptoms of urinary incontinence, completed a 48-hour voiding diary detailing fluid and caffeine intake, and had undergone standardized multichannel urodynamics. The study group had 131 women with detrusor instability on provocative cystometry and maximum urethral closure pressure greater than 20 cm of water. The control group had 128 women without detrusor instability on provocative cystometry and maximum urethral closure pressure greater than 20 cm of water. For statistical comparison, women were divided into the following three groups on the basis of caffeine intake: minimal (< 100 mg/day), moderate (100–400 mg/day), and high (> 400 mg/day).
Results: The mean caffeine intake of women with detrusor instability (484 ± 123 mg/day) was significantly higher than that of controls (194 ± 84 mg/day, P = .002). On univariate analysis, significant risk factors for detrusor instability were age, smoking status, and caffeine intake. On multivariate analysis, the statistically significant association between high caffeine intake and detrusor instability persisted after controlling for age and smoking (odds ratio [OR] 2.4, 95% confidence interval [CI] 1.1, 6.5, P = .018). When women with moderate caffeine intake were compared with those with minimal caffeine intake, the risk for detrusor instability was lower and did not reach significant levels (OR 1.5, 95% CI 0.1, 7.2, P = .093).
Conclusion: An association between high caffeine intake and detrusor instability was seen in this population. Larger studies are required to determine whether the association is causal.
Detrusor instability, ie, unstable bladder, is an important cause of urinary incontinence, especially in older women. The prevalence of detrusor instability has been reported to be as high as 38% in women 65 years or older and 27% in women less than 65 years old.1 However, relatively little is known about the etiology of this condition. Neurologic disease,2 inflammation,3 prior bladder surgery,4 and smoking5 are some of the known risk factors of detrusor instability. Most cases, however, are considered to be idiopathic.6
Reduced consumption of caffeinated beverages has been shown to improve urinary incontinence.7 In a series of 20 women with confirmed bladder instability, 200 mg of oral caffeine citrate provoked a statistically significant increase in detrusor pressure on bladder filling during cystometry, but no abnormality was noted in ten continent women.8 However, a clear relationship between caffeine intake and detrusor instability is not recognized in the medical literature. The purpose of this retrospective case-control study was to determine whether excessive dietary caffeine intake in women was associated with an increased risk for detrusor instability.
|
Materials and Methods |
|---|
|
Top
AbstractMaterials and MethodsResultsDiscussionReferences |
|---|
Detrusor instability was diagnosed if a woman had symptoms of urge incontinence and had objective demonstration of a bladder contraction and urinary leakage, spontaneously or on provocation, during cystometry when she was attempting to inhibit micturition.9 Women with urethral closure pressure of less than 20 cm of water, diabetes, known neurologic disorders, and women on anticholinergic or alpha-adrenergic agonist and antagonist medications were excluded.
All women completed a 48-hour voiding diary before urodynamic testing. The voiding diary consisted of a structured intake and output diary to record the type and amount of fluid intake in mL or ounces during a 48-hour period. Women were asked to record their intake of coffee (caffeinated or decaffeinated, instant or brewed), tea, cola (with brand name), and cocoa using a measuring cup. The reproducibility of this diary in assessing caffeine intake was examined by retesting, after an interval of 1 week, 50 women randomly selected by using a random number table. The intraclass correlation coefficient for the voiding diary in assessing caffeine intake was 0.63 (95% confidence interval [CI] 0.54, 0.73, P = .007).
Total caffeine intake was calculated by multiplying the average milligram content of each beverage by the quantity of the beverage consumed and then summing across all beverage categories.10 An average of the 2-day intake was used to obtain the daily (24-hour) caffeine intake. The caffeine content was calculated as follows: 128 mg per 5-ounce cup of brewed coffee with caffeine, 66 mg per 5-ounce cup of instant coffee with caffeine, 3 mg per 5-ounce cup of decaffeinated coffee, 38 mg per 5-ounce cup of hot nonherbal tea, 4 mg per 5-ounce cup of hot cocoa, 47 mg per 8-ounce glass of iced tea, 24 mg per 8-ounce glass of cola soft drinks, and 24 mg per 8-ounce glass of diet cola drinks.11 For statistical comparisons, women were divided into three groups depending on their amount of caffeine intake, ie, minimal intake was less than 100 mg/day, moderate intake was 100–400 mg/day, and high intake was greater than 400 mg/day.
A subject was defined as a current smoker if she smoked at the time of urodynamic testing. She was defined as a past smoker if she had quit smoking for at least 2 months, and as a never smoker if she had smoked regularly for less than 2 months in the past and was not smoking currently.5
Medical charts were reviewed to obtain information on age at the time of urodynamic testing, parity, weight, smoking history, prior anti-incontinence surgery, and estrogen status. Women were classified as hypoestrogenic if they had undergone spontaneous or surgical menopause, were not taking hormone replacement, and had vaginal atrophy.
Complex urodynamics was performed using a Dantec UD 5500 (Dantec Inc., Copenhagen, Denmark) and included uroflowmetry with determination of postvoid residual urine volume, multichannel cystometry, and urethral profilometry. All testing was performed in the sitting erect position in a Century birthing chair (Century Mfg. Co., Tampa, FL). A Millar 8F dual microtip transducer (Millar Instruments, Houston, TX) was used for the multichannel urethrocystogram and urethral profilometry. The urethrocystogram was performed using sterile water at 22C at a filling rate of 50 mL/minute. Provocative measures such as water stimulation and cough were used to provoke detrusor instability. Urethral profilometry was performed with the dual microtip sensor at the 9 o’clock position using a mechanical puller at a rate of 1 mm/second. Both static and dynamic (coughing at maximum effort) profiles were performed at cystometric capacity (with a minimum bladder volume of 200 mL). Maximum urethral closure and functional urethral length were assessed.
Data were analyzed using SAS (SAS Institute Inc., Cary, NC). Within the study group and the control group, we summarized age, weight, parity, prior surgeries, and mean caffeine intake by using means and standard deviation (SD) and then compared the two groups using two-sample t test for independent samples. Estrogen status and smoking were summarized using proportions, then the 
2 test was used to compare the two groups. Crude odds ratios (OR) with 95% CIs were calculated to quantify the increased risk for detrusor instability for women with moderate and high caffeine intake compared with minimal caffeine intake. To control for the possible confounding effect of age and smoking, logistic regression analysis was used to determine adjusted ORs.
Sample size calculations were done using Epi Info, Version 6.0 (Centers for Disease Control and Prevention, Atlanta, GA). We fixed the type I error rate (alpha) at .05 and power at 80%. A preliminary survey of our study population showed that 15% of women with genuine stress incontinence (controls) had high caffeine intake. On the basis of this information, we estimated that 125 women were needed in each group to detect a risk of 2.5 or greater for detrusor instability.
|
Results |
|---|
|
Top
AbstractMaterials and MethodsResultsDiscussionReferences |
|---|
). There was no significant difference in the parity, weight, estrogen status, or number of prior surgical procedures of the two groups. Women with detrusor instability were more likely to be current smokers compared with women without detrusor instability (P = .04). The number of past smokers was higher in the control group compared with the study group, although this difference was not statistically significant (P = .1). The mean caffeine intake of women with detrusor instability (484 ± 123 mg/day) was higher than that of women without detrusor instability (194 ± 84 mg/day, P = .002).
|
Univariate analysis was performed to identify risk factors for detrusor instability. The OR for detrusor instability for women older than 55 years compared with women less than 55 years was 1.7 (95% CI 1.03, 2.9, P = .028). Women with high caffeine intake had significantly higher odds for detrusor instability than women with minimal caffeine intake (OR 2.7, 95% CI 1.2, 5.8, P = .006) (Table 2). The odds for detrusor instability for women with moderate caffeine intake did not reach significant levels (OR 2.0, 95% CI 0.9, 4.5, P = .066). The OR for detrusor instability for women with high caffeine intake compared with moderate caffeine intake was 1.3 (95% CI 0.8, 2.4, P = .29). The OR for detrusor instability was also significantly higher for current smokers compared with never smokers, although a similar relationship was not seen for past smokers (Table 2).
|
). The adjusted OR for detrusor instability was 2.4 for women with high caffeine intake compared with women with minimal caffeine intake (95% CI 1.1, 6.5, P = .018). For women with moderate caffeine intake, the risk for detrusor instability was 1.5 compared with women who had minimal caffeine intake (95% CI 0.1, 7.2, P = .093).
|
|
Discussion |
|---|
|
Top
AbstractMaterials and MethodsResultsDiscussionReferences |
|---|
The association between dietary caffeine intake and detrusor instability has not been investigated adequately. In our study, the 2.4-fold increased risk for detrusor instability in women with high caffeine intake persisted even after controlling for two confounding variables, age and smoking. It is unlikely that this was due to recall bias because subjects completed the 48-hour voiding diary before their first visit to the urodynamics laboratory. For women with moderate caffeine intake, the increased risk for detrusor instability compared with minimal caffeine intake was lower than that for high caffeine intake and it did not reach statistical significance, which could have been due to a small sample size.
As in any case-control study, the selection of the control group can introduce bias. We recognize that the ideal control group for this study would have been age-matched continent women from the general population; however, women in the control group had genuine stress incontinence. It is unlikely that this accounts for the lower caffeine intake in this group compared with the study group; an association between low caffeine intake and genuine stress urinary incontinence has not been reported. It is also unlikely that women in the control group were selectively counseled about lowering their caffeine intake by their primary care physician before referral to the urodynamics laboratory compared with the study group. Even though we do not have data on the mean caffeine intake for our population, the mean caffeine intake of our control group (194 ± 94 mg/day) is almost identical to the mean caffeine intake estimated for the general population in the United States (200 mg/day).12 Hence, the selection of our control group, though not perfect, does not in itself account for the increased risk of detrusor instability in women with excessive caffeine intake.
The theory that caffeine might cause detrusor instability is biologically plausible because caffeine has been shown to have an excitatory effect on detrusor smooth muscle and could cause an increased rise during bladder filling.7 In vitro animal studies have shown that smooth muscle contraction in strips of detrusor muscle is mediated by an increase in the concentration of cytoplasmic free calcium.13 Caffeine has been shown to induce transient contraction of smooth muscle through the release of intracellular calcium from intracellular storage sites.14 Further studies are required to determine the effect of caffeine on the human detrusor muscle.
Our study also did not determine whether a decrease in caffeine intake would be associated with improvement in detrusor instability. Based on the present findings, it would be prudent to advise women to avoid excessive caffeine intake, ie, more than 400 mg/day (equivalent to four cups of brewed coffee). For women with bladder symptoms, even moderate intake such as 200–400 mg/day (equivalent to two cups of brewed coffee) could result in an increased risk for detrusor instability.
|
Footnotes |
|---|
Received July 19, 1999. Received in revised form November 15, 1999. Accepted December 2, 1999.
|
References |
|---|
|
Top
AbstractMaterials and MethodsResultsDiscussionReferences |
|---|
2. Beck RP, Warren KG, Whitman P. Urodynamic studies in female patients with multiple sclerosis. Am J Obstet Gynecol 1981;139: 273–6.[Medline]
3. Bhatia NN, Bergman A. Cystometry: Unstable bladder and urinary tract infection. Br J Urol 1986;58:134–7.[Medline]
4. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress urinary incontinence. Br J Urol 1979;51:204–7.[Medline]
5. Bump RC, McClish DK. Cigarette smoking and urinary incontinence in women. Am J Obstet Gynecol 1992;167:1213–8.[Medline]
6. Kinder RB, Mundy AR. Pathophysiology of idiopathic detrusor instability and detrusor hyperreflexia: In-vitro study of human detrusor muscle. Br J Urol 1987;60:509–15.[Medline]
7. Creighton SM, Stanton SL. Caffeine: Does it affect your bladder? Br J Urol 1990;66:613–4.[Medline]
8. Tomlinson BU, Dougherty MC, Pendergast JF, Boyington AR, Coffman MA, Pickens SM. Dietary caffeine, fluid intake and urinary incontinence in older rural women. Int Urogynecol J 1999;10:22–8.
9. Abrams P, Blaivas JG, Stanton SL, Anderson JT. The standardization of terminology of the lower urinary tract function recommended by the International Continence Society. Int Urogynecol J 1990;1:45–58.
10. Boyle CA, Berkowitz GS, LiVolsi MD, Ort S, Merino MJ, White C, et al. Caffeine consumption and fibrocystic breast disease: A case-control epidemiologic study. J Natl Cancer Inst 1984;72: 1015–9.
11. Bunker ML, McWilliams M. Caffeine content of common beverages. J Am Diet Assoc 1979;74:28–32.[Medline]
12. Lamarine RJ. Selected health and behavioral effects related to the use of caffeine. J Community Health 1994;19,449–66.[Medline]
13. Shenfeld OZ, Morgan CW, Ratz PH. Bethanecol activates a post-receptor negative feedback mechanism in rabbit urinary bladder smooth muscle. J Urol 1998;159:252–7.[Medline]
14. Lee JG, Wein AJ, Levin RM. The effect of caffeine on the contractile response of the rabbit urinary bladder to field stimulation. Gen Pharmacol 1993;24:1007–11.[Medline]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
