Among women with T1D in the Uro-EDIC study we found UI to be highly prevalent with nearly 40% reporting monthly or more frequent incontinence. Furthermore, nearly 40% of these women were greatly bothered by their incontinence and 9% believed it affected their day-to-day activities. Incontinence was more prevalent than other commonly recognized diabetes associated complications such as retinopathy, nephropathy and neuropathy. Importantly women with T1D had a nearly 2-fold greater prevalence of weekly urge incontinence compared to women without diabetes.
Our finding of a 2-fold increased risk of urge incontinence among women with T1D is similar to several studies that have identified urge incontinence was increased among women with type 2 diabetes.8
Because women in these prior studies had mostly type 2 diabetes, it is likely that Uro-EDIC women using insulin had more severe diabetes with more advanced neurovascular complications affecting the innervation of the bladder which might present in the early stages as urge incontinence.10
Among women without diabetes parity is a well-known and major risk factor for development of UI in middle-aged women, and that risk increases with the number of births.17
Interestingly women in Uro-EDIC were more commonly nulligravid and had fewer births than those with normal glucose in the NHANES, yet the Uro-EDIC women had a 2-fold greater odds of urge incontinence and 50% greater odds of stress incontinence than those with normal glucose after adjustment for parity. This finding suggests that other factors, potentially those associated with diabetes, may explain the increased prevalence of incontinence in this cohort.
The biology of diabetes associated bladder complications can be due to an alteration in the detrusor smooth muscle, neuronal dysfunction and urothelial dysfunction. Specifically it is hypothesized that microvascular complications might damage the innervation of the bladder or alter bladder muscle function.18
Early evidence demonstrated that morphological changes in efferent and afferent pathways to the bladder were closely related to bladder dysfunction, and these periperhal axonopathies were specifically induced in diabetic animal studies.19
In later studies of patients with diabetes others have found significant associations between sympathetic skin response and bladder dysfunction suggesting that diabetic cystopathy may in fact be a manifestation of peripheral neuropathy induced by diabetes.20
Although our study provides information on the prevalence, level of bother and effect on daily activities of UI among women with T1D, there are several limitations that should be considered. The Uro-EDIC women participated in the DCCT and subsequently the EDIC study and, thus, may not be representative of the general population of women with T1D. It is likely that among participants in the DCCT/EDIC diabetic management was good, perhaps better than in a population based sample of women with T1D. If diabetes associated factors such as poorly controlled glycemic levels affect development of incontinence among women with T1D as with other complications (nephropathy, neuropathy and retinopathy) then our reported incontinence prevalence may be underestimated. In addition, it is possible Uro-EDIC participants may have been followed more closely and more likely treated for incident incontinence which would result in our reported estimate of prevalence in this cohort to be further underestimated. While measures of overall incontinence and its bother and impact were measured identically in both cohorts, the frequency of stress and urge incontinence was assessed during the last year in NHANES and during the last 7 days in Uro-EDIC, which may introduce the potential for measurement error in the comparison of differences between cohorts. Finally, because the participants in the current study are mostly white, generalizing the findings to persons of other races may not be appropriate.