s have found that in girls, but not boys, the onset of pubertal maturation is a significant risk factor in the development of insomnia and is associated with increased symptom severity [ , ]. Therefore, another possible mechanism underlying gender differences in pretreatment symptoms is hormonal fluctuations associated with the onset of puberty in girls. The menstrual cycle is a major source of hormonal fluctuations in estradiol and progesterone over a 4-week period. Estradiol and progesterone levels are initially low (follicular phase), with a midcycle peak in estradiol indicating ovulation, followed by a rise in both estradiol and progesterone during the second half of the cycle before declining to the initial low levels (luteal phase). In support of this notion, adult women self-report poorer sleep quality during periods of hormonal flux, including the luteal phase of the menstrual cycle, perinatal period and menopause [ , , ]; however, the association between sex hormones and more objectively measured sleep variables (eg, via polysomnography) is more contentious [ ]. The nature of the association between pubertal maturation and insomnia prevalence and disturbed sleep characteristics, including the potential role of fluctuating sex hormones, requires further examination.
Despite pretreatment differences in symptom severity, boys and girls responded comparably to CBT-I, as evidenced by comparable reductions in symptom severity. On the one hand, it is encouraging that despite greater pretreatment symptom severity, girls gain the same benefits from treatment as boys. On the other hand, equivalent treatment-elicited symptom reduction would suggest gender differences in symptom severity at baseline are maintained posttreatment, which we speculate may render girls more vulnerable to relapse than boys. More work in this area is required to determine if differences remain between boys’ and girls’ posttreatment symptom levels. We were unable to adequately analyze this here due to participant attrition and therefore an incomparable sample at baseline and posttreatment. Future studies could also examine if there are gender differences in responsiveness to certain treatment elements. For example, as girls engage in more rumination and worry [, ], which are perpetuating features of insomnia (as discussed above), they may benefit from extending the cognitive aspect of CBT-I to reduce the frequency of these cognitive maintaining factors and thus limit ongoing sleep disturbance. These ideas require further investigation to refine gender-specific delivery of CBT-I.
Our study had several limitations, namely the lack of a nontreatment control group to exclude the possibility that participants responded to some nontherapeutic aspect of CBT-I. Our study also relied on subjectively reported sleep diary variables. The inclusion of polysomnography or actigraphy would help establish gender differences in objectively measured sleep parameters. However, the presence of gender differences on some sleep characteristics but not others in the current study suggests that our results are not merely driven by a bias for girls to overreport (or boys to underreport) symptoms in general. A disproportionate number of girls participated in this study. This is consistent with male to female participant ratios reported in similar studies evaluating CBT-I in adolescents that use a range of recruitment strategies (eg, community recruitment via a study website  and outpatient mental health clinics [ ]). This suggests gender disparity in participation is representative of the increased prevalence of sleep problems in girls compared to boys in the community. The small sample size, particularly the small sample of boys, should also be taken into consideration when interpreting the current results. It is possible that a lack of power to detect significant effects concealed true differences between boys and girls in treatment response (particularly in reductions in sleep quality, in which there was a trend, though it was not statistically significant) and baseline s