Abstracts

Rationale: People with epilepsy have fewer children than others, and improved understanding of their reproductive decisions is important. This study assessed the impact of genetic causal attribution, i.e., the degree to which people with epilepsy believe that genetics was a cause of their disorder, on reported number of children.

Methods: A self-administered survey was completed by 457 adults (63% women, average age 41 years, range 19-79) treated for epilepsy at Columbia University Irving Medical Center. Genetic attribution was assessed by a scale based on survey items. First, participants rated 17 factors for the likelihood that they “caused you to have epilepsy,” with four possible responses for each (very unlikely, somewhat unlikely, somewhat likely, very likely). Two other questions asked participants to rate, from 0 to 10, “the chance that one of your genes was a big part of the reason you have epilepsy” and “how big a role did your genes play in causing you to have epilepsy.” Responses to these four questions were highly consistent (Cronbach’s alpha=0.90) and were averaged to compute the GA scale. Participants were also asked how many children they had, and to rate the influence on their reproductive decisions of perceived offspring epilepsy risk (“the chance of having a child with epilepsy”). Poisson regression models were used to estimate rate ratios (RRs) for number of offspring per unit increase in GA, and by increasing influence on reproductive decisions of the chance of having a child with epilepsy, controlling for age, education, race/ethnicity, and religion.

Results: GA scores averaged 4.6 (range 0-10) and declined with advancing age. Findings differed by age; thus, all analyses were carried out within three age categories: 19-35 (mean 0.3 offspring), 36-50 (mean 1.1 offspring), 51-79 (mean 1.6 offspring). Among participants aged 19-35, number of offspring decreased significantly, by about 10%, for each 1-unit increase in GA score (Table: RR=0.9, p=0.02). In this age group, number of offspring was not associated with participants’ reports of the influence on their reproductive decisions of the chance of having a child with epilepsy. Among participants in the two older age groups, number of offspring was not associated with GA scores. However, those who reported a “strong or very strong” influence on their reproductive decisions of the chance of having a child with epilepsy had only half as many offspring as those who reported no influence (age 36-50: RR=0.5, p=0.04; age 51-79: RR=0.5, p=0.03).

Conclusions: Among people with epilepsy aged 35 or younger, stronger belief in a genetic cause of their illness may lead to reduced or delayed childbearing. Among those aged 36 or older, many of whom are likely to have completed their families, concerns about having affected children may have made an important contribution to reduced childbearing. The lack of association with genetic attribution in these older age groups suggests its effects, if any, may be completely mediated by concerns about having an affected child.

Funding: Please list any funding that was received in support of this abstract.: Supported by: NIH R01NS104076.