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Vulnerability to insomnia: the role of familial aggregation
Christopher L Drake1, Holly Scofield, Thomas Roth
1Sleep Disorders and Research Center, Henry Ford Hospital, 2799 West Grand Blvd, CFP3, Detroit, MI 48202, USA. cdrake1@hfhs.org
Background:
The goal of this study was to determine the degree of familial aggregation in vulnerability to stress-related sleep disturbance among siblings. One approach to investigating a potential "familial" predisposition to sleep disturbance is to examine the relationship between siblings on a standard measure of vulnerability to stress-related sleep disturbance.
Design:
Cross-sectional data on insomnia, vulnerability to stress-related sleep disturbance, sleepiness, habitual sleep, and additional demographic variables was collected separately from pairs of biological siblings. Data were collected during a 15-20min phone assessment.
Participants:
Interviews on a total of 62 individuals (31 sibling pairs) were completed. A total of 8 individuals and their respective siblings were excluded after meeting conservative criteria for Diagnostic and Statistical Manual of Mental Disorders, Fourth edition (DSM-IV)-based insomnia. The mean age of the sample was 51.1+/-12.1 years (range 18-70) and habitual nightly total sleep time averaged 6.91+/-1.42h/night.
Results:
Individuals completed the Ford Insomnia Response to Stress Test (FIRST), a standardized measure of individual vulnerability to stress-induced sleep disturbance. The intraclass correlation coefficient (ICC) was r =0.61, df=23, p =0.001 for the relationship between siblings in FIRST scores. This indicated that 37.2% of the variance in vulnerability to stress-related sleep disturbance can be accounted for by familial aggregation. This relationship remained after controlling for potential confounds including age, gender, shift schedule, and psychiatric history.
Conclusions:
Our data support the notion that vulnerability to stress-related sleep disturbance has a strong familial aggregation. Additional studies are needed to determine the genetic or environmental origins of this relationship and its underlying biological substrates.
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