Delayed sleep phase cases and controls

Daniel F Kripke¹^,2 , Katharine M Rex¹ , Sonia Ancoli-Israel¹^,3 , Caroline M Nievergelt¹^,4 , Walt Klimecki⁵ and John R Kelsoe¹^,3

¹Department of Psychiatry, University of California, San Diego, La Jolla, California 92093-0667, USA

²Scripps Clinic Sleep Center, 10666 North Torrey Pines Road, La Jolla, California 92037, USA

³Department of Psychiatry 116A, VA San Diego Health System, 3350 La Jolla Village Drive, San Diego, CA 92161, USA

⁴The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA

⁵Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, PO Box 210207, Tucson, Arizona, 85721-0207, USA

author email corresponding author email

Journal of Circadian Rhythms 2008, 6:6doi:10.1186/1740-3391-6-6


Published:	29 April 2008

Abstract

Background

Delayed sleep phase disorder (DSPD) is a condition in which patients have difficulty falling asleep before the early morning hours and commonly have trouble awakening before late morning or even early afternoon. Several studies have suggested that variations in habitual bedtime are 40–50% heritable.

Methods

We recruited a case series of 205 participants, along with 221 controls (DSPD-C) with normal sleep, roughly matched for age, gender, and ancestry. A representative sample of San Diego adults recruited some years before was already available to confirm the control group. Both DSPD and DSPD-C provided blood or saliva samples for DNA and completed extensive questionnaires about sleep habits, sleep history, family history, sleep quality, morningness-eveningness traits, depression, mania, and seasonality of symptoms. The DSPD group wore wrist actigraphs for a median of 13.2 days. The representative sample collected previously had undergone actigraphic recordings, from which 48 hours of data were generally available.

Results

The DSPD and DSPD-C samples showed almost no overlap on morningness-eveningness scores. DSPD cases went to bed and arose about 3 hours later than the DSPD-C and the representative sample. DSPD cases reported more difficulties with sleep, poorer sleep quality, and more depression, but there was no significant difference in a history of mania. DSPD cases reported more family history of late bedtimes, but female DSPD reported that their fathers' bedtimes were later than the fathers of male DSPD.

Conclusion

These results indicate a DSPD phenotype is familial and associated with unipolar depression.