SLEEP 2011 Abstract Supplement

B. Clinical Sleep Science II. Sleep Disorders – Circadian Rhythms
0470
DURATION RESPONSE CURVE TO BRIGHT LIGHT IN
HUMANS
Chang A 1,2 , Santhi N 1,2 , Bradstreet DS 1 , Lockley SW 1,2 , Duffy JF 1,2 ,
Kronauer RE 3 , Czeisler CA 1,2
1
Department of Medicine, Brigham & Women’s Hospital, Boston, MA,
USA, 2 Division of Sleep Medicine, Harvard Medical School, Boston,
MA, USA, 3 Department of Engineering and Applied Science, Harvard
University, Cambridge, MA, USA
Introduction: Light exposure at night has been shown to induce a phase
delay of the melatonin rhythm in humans. Previous studies have investigated
the effect of timing, intensity, wavelength, and pattern of light
stimuli on the human circadian timing system. Here we present results
from a study of the duration-response relationship to phase-delaying
bright light.
Methods: Thirty-seven healthy adults (18-30 years of age; 14 F) who
completed a 9-day inpatient protocol were included in this analysis. The
protocol consisted of 3 baseline days (16h wake/8h sleep) followed by a
50h constant routine (CR) to assess circadian phase. The dim light melatonin
onset (DLMO25%) was determined from hourly blood samples
collected throughout the CR. Following an 8h sleep episode, the next
16h wake episode included an experimental bright light exposure (LE)
which was scheduled during the early subjective night. This timing was
chosen because it is at a time when plasma melatonin levels are high
and when maximal phase delays of the endogenous circadian melatonin
rhythm occur. Subjects were assigned to receive an LE of 0.2h, 1.0h,
2.5h, or 4.0h in duration (n = 9, 10, 10, and 8, respectively). A 36h CR
on the following day was performed to reassess the DLMO25% so that
the phase shift induced by the LE could be determined.
Results: Mean ± SD phase delays induced by the 0.2h, 1.0h, 2.5h, and
4.0h LE were: 1.07 ± 0.36h, 1.37 ± 0.52h, 2.29 ± 0.28h, and 2.65 ±
0.25h, respectively. The magnitude of the phase delay shifts increased as
the duration of the LE increased; 0.44h of phase delay per hour of light
and R=0.984.
Conclusion: Brief exposure to bright light (0.2h) in humans can substantially
shift endogenous circadian melatonin phase, resetting the circadian
pacemaker much more efficiently per minute of light exposure
than longer durations of light.
Support (If Any): This study was supported by grants R01MH45130
and R01HL77453; and conducted in the BWH GCRC (M01 RR02635)/
Harvard Catalyst CTSC (UL1 RR025758).
0471
NIGHTLY MELATONIN SUPPLEMENTATION IMPROVES
TOTAL SLEEP TIME, SLEEP EFFICIENCY AND SLEEP
ONSET LATENCY IN HYPERTENSIVE PATIENTS TREATED
WITH β-BLOCKERS
Scheer FA 1,2 , Morris CJ 1,2 , Marks J 1 , Smales C 1 , Kelly EE 1 , Garcia JI 1 ,
Hahn M 1 , Xiong M 1 , Malhotra A 1,2 , Shea SA 1,2
1
Medical Chronobiology Program, Division of Sleep Medicine,
Brigham and Women’s Hospital, Boston, MA, USA, 2 Division of Sleep
Medicine, Harvard Medical School, Boston, MA, USA
Introduction: β-Blockers are often used in the treatment of hypertension,
angina, arrhythmia, and heart failure. However, β-blockers also
lower the levels of the soporific hormone melatonin, which may explain
some of the reported side-effects including nighttime insomnia and
daytime fatigue. Therefore, we tested whether or not nightly melatonin
supplementation improves sleep in hypertensive patients treated with
β-blockers.
Methods: Sixteen hypertensive patients (45-64 years of age; 9 women)
treated with the β-blocker Atenolol or Metoprolol were enrolled in a
randomized, double-blind, placebo-controlled, parallel-group trial. The
study included two 4-day in-laboratory visits during which their sleep
was assessed by polysomnography in a private, sound-attenuated, and
completely dark room during 8-h sleep opportunities. After the baseline
assessment during the first visit, patients were randomized to receive
melatonin 2.5 mg or placebo nightly for 3-4 weeks, after which their
sleep was assessed again during the second 4-day visit. One subject was
excluded from analysis due to unstable medication dose. Baseline-adjusted
values are reported.
Results: 3-4 Weeks of melatonin supplementation increased total sleep
time (placebo: 387 min vs. melatonin: 424 min; P=0.046), increased
sleep efficiency (81% vs. 88%; P=0.046), and decreased sleep onset latency
(16 min vs. 5 min; latency to Stage 1; P=0.007) as assessed by
polysomnography in the laboratory. Melatonin did not significantly affect
durations of different sleep stages, although the increase in Stage 2
approached significance (232 min vs. 271 min; P=0.051). Also throughout
the 3-4 weeks while on melatonin and sleeping at home, melatonin
significantly improved actigraphy-estimated total sleep time (377 min
vs. 390 min; P=0.011) and sleep efficiency (78% vs. 81%; P=0.007), but
not sleep onset latency.
Conclusion: In hypertensive patients treated with β-blockers, nighttime
melatonin supplementation significantly improves sleep quality as assessed
by polysomnography in the laboratory and as estimated by actigraphy
at home.
Support (If Any): NIH-R21 AT002713 and NIH-P30 HL101299 in
support of FAJLS; NSRBI fellowship in support of CJM; NCRR GCRC
M01 RR02635
0472
STAYING UP LATE AND EATING IN THE EVENING: RECIPE
FOR OBESITY?
Baron KG, Reid KJ, Zee P
Northwestern University, Chicago, IL, USA
Introduction: Alterations in circadian timing have been associated with
dysregulation of appetite hormones and insulin metabolism. Few studies
have evaluated the role of sleep timing and circadian rhythms on feeding
patterns and obesity. The goal of this study was to evaluate the associations
between sleep timing, timing of caloric intake, and BMI in adults.
Methods: Participants included 52 individuals (27 males, mean age 31
SD= 12). Diet was measured by a 7-day food diary. Caloric intake was
calculated through publicly available nutrition databases. Sleep timing
was defined a average midpoint of sleep based on 7 days of wrist actigraphy.
Data were analyzed using t-tests, correlations, and multivariate
regression. In categorical analyses, normal sleepers (n=23) were defined
as an average midpoint of sleep earlier than 5:30 am and late sleepers
were defined as a midpoint of sleep at or after 5:30 am.
Results: Late sleepers had later bedtimes (p