Restricted (Penn State Only)
Baker, Joshua Henry
Graduate Program:
Master of Science
Document Type:
Master Thesis
Date of Defense:
March 24, 2017
Committee Members:
  • Edward Bixler, Thesis Advisor
  • Julio Fernandez-Mendoza, Committee Member
  • Patricia McLaughlin , Committee Member
  • Insomnia
  • Adolescence
  • Inflammation
  • C-reactive protein
  • Penn State Child Cohort
Sleep is a behavior essential to healthy development. Insomnia, which is characterized by difficulty falling and/or staying asleep and associated daytime functioning impairment, is the most prevalent sleep disorder. Insomnia is not just a disruption of an individual’s normal sleep but rather impacts both physical and mental health and, in adults, insomnia with objective short sleep duration has shown to be a more biologically severe form of the disorder. This insomnia phenotype has been associated with activation of the stress system, inflammation and adverse cardiometabolic, neurocognitive and psychiatric outcomes. It is also known that this insomnia phenotype is highly persistent throughout adulthood; therefore, it is important for clinicians to identify this phenotype early during development. Our primary aim in this project was to test whether objective short sleep duration, as measured by polysomnography (PSG), played a key role in predicting the association of insomnia symptoms with inflammation in adolescents. Given that PSG is not readily available for clinicians, we examined in secondary analyses whether the persistence of insomnia symptoms since childhood also helped predict the association of insomnia symptoms with inflammation in adolescents. Subjects were participants in the Penn State Child Cohort (PSCC), a population-based sample of 421 adolescents who underwent 9-h PSG followed by a single fasting blood draw to assess plasma levels of C-reactive protein (CRP) and other inflammatory markers via ELISA. Insomnia symptoms were defined by a self-report of difficulty falling and/or staying asleep on the Pediatric Sleep Questionnaire, while objective sleep duration was defined as ≥ 8 hours, 7-8 hours, ≤ 7 hours of sleep based on the quartiles of PSG-measured total sleep time. Multivariable-adjusted general linear models tested the association between insomnia symptoms, objective sleep duration and their interaction on CRP levels. Adolescents reporting insomnia symptoms had significantly higher CRP levels compared to controls and a significant interaction (p<0.01) showed that objective sleep duration modified this association. Elevated CRP was present in adolescents with insomnia symptoms who slept ≤ 7 hours (1.8 mg/L) as compared to controls or adolescents with insomnia symptoms who slept ≥ 8 hours (0.9 mg/L and 1.0 mg/L, respectively) or controls who slept ≤ 7 hours (0.74mg/L; all p-values <0.01). These findings indicated that, as in adults, objective short sleep duration identifies a phenotype of insomnia at greater risk of morbidity via chronic low-grade inflammation. Secondary analyses based solely on self- and parent-reported data revealed that adolescents whose parents reported persisting insomnia symptoms since childhood had significantly higher CRP levels (1.2 mg/L, p=0.046) compared to controls or to adolescents with new-onset insomnia symptoms (1.0 and 0.8 mg/L, respectively). This finding suggests that a childhood onset of insomnia symptoms may be a useful tool to screen for those adolescents at greater risk of inflammation. Together, our findings indicate that chronic low-grade inflammation may be a common final pathway towards morbidity in adulthood in the insomnia with objective short sleep duration phenotype as early as adolescence.