Circadian Profiles of Infants from Families with a History of Autism

Saturday, May 14, 2016: 11:30 AM-1:30 PM
Hall A (Baltimore Convention Center)
G. L. Glickman1, E. M. Harrison1 and K. R. Dobkins2, (1)Center for Circadian Biology, University of California, San Diego, La Jolla, CA, (2)Department of Psychology, University of California, San Diego, La Jolla, CA
Background: Sleep problems and irregular hormone profiles are extremely common in children with Autism Spectrum Disorder (ASD), suggesting impairments in the circadian timing system. While sleep and circadian disturbances have also been observed in adolescents and adults with ASD, early development of these physiological functions has not yet been examined. Since ASD is only diagnosed reliably after 2-3 years of age, we are taking the innovative approach of examining sleep and hormone rhythms in infants at greater risk for developing ASD because they have an older sibling with the disorder. 

Objectives: Sleep and circadian rhythms are being rigorously characterized in these high-risk infants as well as in infant siblings of typical children at three different ages that represent important milestones in the early development of the circadian system: 3, 9 and 12 months.

Methods: At each age, sleep-wake patterns are examined with actigraphy, sleep diary and a modified version of the Sleep Habits Questionnaire, and fluctuations in melatonin and cortisol are examined across one mid-week day via assessment of saliva at 5 time points (8 AM, 9 AM, 10 AM, 6 PM and 9 PM). Patterns of light exposure, an important environmental factor that regulates both sleep and circadian rhythms, are also being measured, using both diary information and photosensors embedded within the actigraph devices.

Results: Thus far, seven consecutive days of sleep diaries and actigraphy as well as one day of serial salivary sampling have been collected for each infant (N=14, n=3 high-risk at mean±SD age=94.5±6.4 days; n=11 low-risk, mean±SD age= 95.3±10.5 days). Actigraphy data to date shows statistical differences between high- and low-risk infants in terms of mean sleep latency, with high-risk infants taking significantly longer to fall asleep (t=2.63, p<0.05). In addition, preliminary analysis of diary measures indicates that sleep is more asymmetrically distributed across the 24 h day in high-risk infants, with more sleep during morning hours, as compared with low-risk infants (t=4.24, p <0.01). Though still underpowered, the patterns of results also reveal greater light exposure and poorer sleep efficiency in high- versus low-risk infants. Salivary melatonin and cortisol assays are currently underway, providing data that will allow for the determination of phase angle relationships between sleep and hormone rhythms. 

Conclusions: Sleep and circadian rhythm abnormalities may be observed at even the earliest stages of development in infants with a family history of ASD. Ultimately, a better understanding of the sleep and circadian dysfunction that often co-occur with ASD may help guide treatment strategies and minimize the negative impact of these disturbances on both the children and their families.