This study, comprising approximately 25 000 individuals, is the largest of its kind to report population-based prevalence rates of LUTS in young and middle-aged adults. In addition, the study design, using a large national cohort of twins, permits an evaluation of the relative importance of genetic, shared, and nonshared environmental factors for the occurrence of LUTS. The strongest genetic impacts were observed for conditions involving incontinence regardless of whether the involuntary loss of urine was caused by bladder overactivity or supposed pelvic floor weakness. Hence the incontinence reported here could be thought of as composed of its two main pathophysiologic expressions, urinary stress incontinence and urge UI, which together form mixed incontinence. The lowest heritability estimate was observed for OAB where environmental effects dominated. We also showed that LUTS are prevalent in young and middle-aged women but less so in men. The prevalence of LUTS increases with age. These findings are consistent with other large epidemiological studies of LUTS conducted in men and women of the same age, studies also reporting that the prevalence of symptoms increases linearly with age [1
The aetiology of LUTS is widely recognised to be multifactorial [10
], yet the importance of genetic and environmental influences is poorly understood. Evidence in support of a genetic influence on LUTS derives from studies on ethnic group diversity [20
], studies on familial transmission of disease [11
], and twin studies [26
]. Most of these studies have focused on the symptom of UI, and very few have evaluated the impact of genetic factors for susceptibility to other LUTS.
In the present study it was possible to quantify the importance of genetic liability to LUTS in >2000 female twin pairs of known zygosity. Our data indicate that the strongest genetic effects were observed for conditions involving incontinence. Genetic influences were also of importance for nocturia but of little importance for OAB syndrome for which environmental effects dominated. Our data indicate that nongenetic effects that are in common for family members (ie, the shared environmental estimate), such as toilet training and other lifestyle factors, may be involved in the causal mechanisms of OAB. The contention that childhood urinary symptoms may predict adult OAB symptoms was put forward previously [30
], and the results of our study tally with this hypothesis. However, it remains undecided exactly how dysfunctional voiding habits in childhood may give rise to OAB later in life. This study also showed that shared environmental effects contributed to the liability of developing SUI but were less pronounced. Our data are in line with family history studies reporting a two to three times higher prevalence of SUI among first-degree relatives of women with SUI compared with first-degree relatives of continent women [11
There are also some data regarding the heritability of pelvic floor disorders and UI from other twin studies [26
]. The data presented in the present paper suggest a genetic influence for the susceptibility to all subtypes of UI in contrast to a population-based Danish twin study comprising middle-aged and elderly twins that found evidence for significant heritability for urge but not for SUI [28
]. Another twin study showed that genetic factors accounted for nearly 60% of the variation in bladder neck descent as measured by ultrasound [29
]. However, it should be noted that twin studies based on small groups of volunteers are liable to bias because pairs who are concordant for the disease are more likely to participate [31
Several studies have suggested that the susceptibility of LUTS varies between different ethnic groups [20
]. It is not obvious, however, that this kind of data indicates genetic influences. Similarities between women of the same ethnic group might just as well be cultural differences that affect other potentially pathogenetic mechanisms (such as age at childbirth, number of children, etc), family influences, or similar environmental exposures. It is also a common misunderstanding that familial aggregation invariably is a result of genetic factors. Risk estimates derived from family members in most cases cannot distinguish between heritability and noninherited (environmental) factors in the family environment. Familial environmental influences (eg, lifestyle factors such as smoking habits, socioeconomic status, care-seeking behaviour, attitudes towards physical exercise, dietary and drinking habits, and toilet training) may also have a direct effect on the transmission of risk for LUTS.
A limitation of the present study is that the symptoms were not objectively demonstrated through physical examinations or micturition charts. In addition, the age of the twin pairs was not ideal for evaluating LUTS. Future longitudinal studies within this relatively young population would allow for an exclusive opportunity to track the onset of symptoms and to identify possible risk factors.