Circadian Eating and Sleeping Patterns in the
Night Eating Syndrome
John P. O’Reardon,* Brenda L. Ringel,† David F. Dinges,‡ Kelly Costello Allison,* Naomi L. Rogers,‡
Nicole S. Martino,* Albert J. Stunkard*
Abstract
O’REARDON, JOHN P., BRENDA L. RINGEL, DAVID
F. DINGES, KELLY COSTELLO ALLISON, NAOMI L.
ROGERS, NICOLE S. MARTINO, ALBERT J.
STUNKARD. Circadian eating and sleeping patterns in the
night eating syndrome. Obes Res. 2004;12:1789 –1796.
Objective: To compare the eating and sleep-wake patterns
of persons with the night eating syndrome (NES) with those
of matched control subjects.
Research Methods and Procedures: Forty-six overweight/
obese NES subjects (mean age 43.3 ⫾ 9.8 years; 32 women)
and 43 similar controls (mean age 39.0 ⫾ 11.0 years; 28
women) wore wrist actigraphs for 7 days and completed
sleep and food diaries at home.
Results: There was no difference between the total energy
intake of the NES and the control subjects, but the pattern of
energy intake differed greatly. Relative to control subjects,
the temporal pattern of food intake of night eaters was
delayed. Food intake after the evening meal, as a proportion
of the 24-hour intake, was more than 3-fold greater in NES
subjects than in controls (34.6 ⫾ 10.1% vs. 10.0 ⫾ 6.9%,
p ⫽ 0.001). NES subjects had sleep onset, offset, and total
sleep duration times comparable with those of controls.
NES subjects reported more nocturnal awakenings than did
controls (1.5 ⫾ 1.0 per night vs. 0.5 ⫾ 0.5; p ⬍ 0.001), and
their actigraphically monitored arousals occurred earlier
during sleep (at 128 minutes after sleep onset vs. 193
minutes, p ⫽ 0.01). NES subjects consumed food on 74% of
Received for review December 5, 2003.
Accepted in final form July 21, 2004.
The costs of publication of this article were defrayed, in part, by the payment of page
charges. This article must, therefore, be hereby marked “advertisement” in accordance with
18 U.S.C. Section 1734 solely to indicate this fact.
*Weight and Eating Disorder Program, Department of Psychiatry, †Division of Sleep
Medicine, Department of Medicine, and ‡Division of Sleep and Chronobiology, Department
of Psychiatry, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Address correspondence to Albert J. Stunkard, 3535 Market Street, Suite 3024, Philadelphia,
PA 19104-3309.
E-mail: stunkard@mail.med.upenn.edu
Copyright © 2004 NAASO
the awakenings vs. 0% for the controls.
Discussion: The pattern of cumulative energy intake of the
night eaters suggests a phase delay in energy consumption
relative to sleep-wake times. NES may involve a dissociation of the circadian control of eating relative to sleep.
Key words: night eating, sleep, actigraphy, diaries
Introduction
The night eating syndrome (NES)1 is characterized by
morning anorexia, evening hyperphagia, insomnia, either
initial or midphase, and awakenings frequently accompanied by eating (1).
This outpatient study assessed the timing and distribution
of food intake, relative to sleep timing and continuity in
subjects with NES. The purpose of the study was to extend
our earlier behavioral observations of NES (2) to a larger
number of subjects and to evaluate the profile of caloric
intake in NES subjects relative to the circadian profile of the
sleep-wake cycle. Specifically, we sought to determine
whether NES involved either a temporal displacement of
both caloric intake and sleep-wake cycles or a delay of
caloric intake within a normally timed sleep-wake cycle.
Research Methods and Procedures
Ambulatory wrist actigraphy and daily diaries were used
to compare the pattern and timing of food intake and sleepwake profiles in patients diagnosed with NES relative to a
demographically comparable group of healthy control subjects.
Subjects
Subjects were recruited from printed advertisements, radio talk shows, and television interviews that described
NES. A total of 46 overweight/obese night eaters (32
women; 43.3 ⫾ 9.8 years old; BMI 34.9 ⫾ 7.1) and 43
1
Nonstandard abbreviations: NES, night eating syndrome; SCN, suprachiasmatic nucleus.
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overweight/obese control subjects (28 women; 39.0 ⫾ 11.0
years old; BMI 36.7 ⫾ 6.2) completed a 10-day, outpatient
behavioral assessment period. BMI was similar between the
groups, whereas the NES subjects were slightly older [43.3
vs. 39.0 years; t(87) ⫽ 2.0, p ⫽ 0.05]. The NES group
consisted of 56.5% whites, 41.3% African Americans, and
2.2% Hispanic/Latinos. The control group consisted of
60.5% whites, 37.2% African Americans, and 2.3% Hispanic/Latinos.
Procedure
The screening procedure included: a structured clinical
interview, performed by a trained clinician, designed to
assess the presence or absence of NES; the Structured
Clinical Interview for the DSM-IV (3) to assess the presence of past or current psychiatric disorders; and the Eating
Disorder Examination (4) to assess the presence of concomitant eating disorders.
Eligible subjects were ⱖ18 years, met standard criteria
for NES as outlined by Birketvedt et al. (2), based on
assessment at the structured clinical interview, and had a
BMI ⱖ 27 kg/m2. Applicants were excluded if they: were
severely depressed, as determined by Structured Clinical
Interview for the DSM criteria; had a lifetime diagnosis of
bipolar disorder or any psychotic disorder; reported substance abuse or dependence within the last 6 months; were
currently taking psychotropic medications (including hypnotics); were working a night shift or swing shift schedule;
were in a weight reduction program; were diagnosed with
another eating disorder; or lacked awareness of their night
eating episodes. The latter criterion was used to exclude
subjects with nocturnal sleep-related eating disorder, in
which nocturnal eating is accompanied by a lack of awareness at the time and amnesia for the behavior the following
day (5). Eligible control subjects met the same inclusion and
exclusion criteria with the exception of not being diagnosed
with NES. Eligible subjects were enrolled in a 10-day
monitoring period that assessed patterns of food intake and
sleep-wake timing as described below.
Actigraphy
Sleep-wake timing was assessed using ambulatory wrist
actigraphy monitoring combined with twice daily diaries.
The study utilized the Actiwatch-L Mini-Logger Series
wristband dual-axis sensor with actillume (Mini-Mitter, Sun
River, OR), which was worn by all subjects 24 hours a day
for a period of 10 days and 11 nights. Recordings of the
amount of movement were made at 1-minute epochs. Of the
10 days recorded, the first 2 days were considered adaptation to the study procedures; the next 7 days were analyzed
for sleep-wake timing; and the last day was discarded because of the frequency of incomplete data. The Actiwatch-L
uses a motion sensor to detect bodily movement and, thus,
yields an objective measure of rest-activity cycles, which
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OBESITY RESEARCH Vol. 12 No. 11 November 2004
can serve as surrogates for sleep-wake activity. Several
studies have reported high correlations between actigraphy
and polysomnographic assessment of total sleep time, sleep
latency, and sleep termination in both healthy and patient
populations (6 –13). Together with a daily diary, actigraphy
data were used in the study to determine sleep onset and
sleep offset, and the sleep period duration (as defined by the
time difference between sleep onset and sleep offset), as
well as to detect awakenings accompanied by getting out of
bed.
Daily Diary
Subjects kept a daily food, sleep, and mood diary in
which they recorded all foods and beverage consumed, with
time, portion size, and brand noted. They recorded bedtime
and morning rising time, time and duration of all daytime
naps, ratings of depression and hunger on a visual analogue
scale before each ingestion, and all nocturnal awakenings
and whether they were accompanied by food intake. An
awakening was operationalized as an occasion when a subject awoke and got out of bed. Thus, we applied a more
stringent definition of awakening than that required by the
Birketvedt et al. criteria (2) because only awakenings where
the subject rose from bed were counted. We believed this
would provide a more accurate measure of the awakenings
more specifically tied to NES by not counting awakenings
where the subject might awake briefly before returning to
sleep. Caloric intake was averaged across 7 days in hourly
increments for each subject, and the 24-hour caloric intake
profile for NES and control groups was determined. These
mean values for each hour were then used to plot the
24-hour cumulative caloric intake curve for each group.
Analysis of Actigraphy and Diary Data
Diaries and Actiwatch-Ls were collected at the end of the
10-day period, when the Actiwatch data were downloaded
and the diary information was coded. Diary data were
analyzed for the same time period as actigraphy data. Two
raters analyzed the Actiwatch-L data manually in conjunction with the participants’ diary records so as to compare the
7 days of diary records with activity counts generated by the
Actiwatch-L (as described in the Appendix). They ascertained by each method the timing of sleep onset and sleep
offset, the sleep period duration, and the number of awakenings accompanied by getting out of bed. A research
dietitian analyzed food records for caloric intake.
Statistical Analysis
Means and SDs were calculated using descriptive statistics. Student’s t tests were performed to compare means
between groups for caloric intake, number of nocturnal
awakenings, and timing of sleep onset, offset, and sleep
duration with Satterthwaite adjustments when the variance
between groups was unequal. A repeated-measures
Eating and Sleeping Patterns in NES, O’Reardon et al.
Figure 1: Mean cumulative caloric curves and sleep timing profile for NES and control groups. Note the lack of evening plateau in food
intake and the more frequent arousals from sleep in the NES group compared with controls.
ANOVA was used to compare caloric intake between
groups across three 8-hour increments: day (6 AM to 1:59
PM), afternoon/evening (2 PM to 9:59 PM), and night (10 PM
to 5:59 AM). Correlations were used to compare the degree
of agreement between diary and actigraphy times, and frequencies were computed using ␹2 tests.
Results
Energy Intake
Total energy intake of the night eaters (2314.4 ⫾ 748
kcal) and that of the control subjects (2420 ⫾ 748 kcal) did
not differ significantly, but the pattern of cumulative energy
intake throughout the 24 hours differed markedly. As illustrated in Figure 1, the cumulative intake curve of the controls was characterized by upward inflections in the late
morning and early evening, reflecting the effects of midday
and evening meals. An evening plateau was observed from
9 PM in the controls, with no further food intake after that
time until the next morning at 6 AM. In contrast, the cumulative curve of NES subjects demonstrated lower energy
intake during most of the day without the acute meal-based
upward inflections observed in the control subjects. There
was also no late evening plateau in food intake but rather a
steady rise in the total calories ingested up until 6 AM. Initial
diagnosis of NES at screening required that the food intake
reported after the evening meal be at least one-half of the
total 24-hour caloric intake. Diary records, however, revealed a lower intake in the night eaters after the evening
meal during the monitoring period—34.6% (⫾10.1%) of
the total daily caloric intake compared with 10.0% (⫾6.9%)
by the control group.
The distribution of the 24-hour caloric intake, when assessed in eight hourly increments, is illustrated in Figure 2.
Caloric intake of NES subjects compared with controls was
significantly lower in the first 8 hours of the day [6 AM to
1:59 PM, t(87) ⫽ 8.4, p ⬍ 0.001], not different in the second
8-hour period [2 PM to 9:59 PM, t(87) ⫽ 0.87, p ⫽ 0.387],
and significantly greater during the last 8-hour period [10
PM to 5:59 AM, t(84.4) ⫽ 7.97, p ⬍ 0.001]. There were no
differences in either the cumulative 24-hour intake or in the
8-hour incremental intake between weekends and weekdays
for NES subjects. Controls had a higher 24-hour caloric
intake during weekends relative to weekdays [2690 vs. 2404
kcal, t(44) ⫽ 3.81, p ⬍ 0.001], due to a slightly higher
intake in the second 8-hour period of the day [2 PM to 10 PM,
1459 vs. 1227 kcal, t(44) ⫽ 4.21, p ⬍ 0.001]. Nevertheless,
the 24-hour intake over the weekends did not differ between
the groups (controls vs. NES means: 2690 vs. 2445 kcal,
t(80) ⫽ 1.1, p ⫽ 0.27).
Sleep
Subjects’ reported bedtimes (diary data) correlated highly
with actigraphy quiescence (NES, r ⫽ 0.95, p ⬍ 0.001;
OBESITY RESEARCH Vol. 12 No. 11 November 2004
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Figure 2: Caloric intake in 8-hour increments for NES and control groups. Note that food intake is lower in the first part of the day and
higher in the evening and night in the NES group. **p ⬍ 0.01.
controls, r ⫽ 0.93, p ⬍ 0.001). Similarly, diary entries for
sleep termination correlated significantly with activity on
the Actiwatches (NES, r ⫽ 0.93, p ⬍ 0.001; controls, r ⫽
0.85, p ⬍ 0.001). Actigraphy confirmed the diary record of
awakenings within 30 minutes of the recorded time for
94.2% of the events in NES subjects compared with 87% of
the events in the control group. The mean difference between diary-recorded nocturnal out-of-bed periods and increased activity counts from actigraphy was 2 ⫾ 9 minutes
for night eating subjects and 4 ⫾ 17 minutes for controls
(p ⬍ 0.06).
Complete and analyzable actigraphy and diary data were
available for 90.7% of all nights for NES subjects and
80.0% of all nights for controls. Some nights were not
analyzable because of incomplete diary data or because the
subject removed the actigraph overnight. In 3.1% of the
arousals noted by actigraphy in NES subjects, there was a
failure to record the actual time of the arousal in the diary
(but not the event itself), compared with none in the controls.
Table 1 shows the similarity of sleep patterns of NES and
control subjects in the timing of sleep onset by actigraphy
and diary records. The sleep offset time in NES subjects
compared with control subjects was marginally later by both
actigraphy (29 minutes later, p ⫽ 0.07) and diary (25
minutes later, p ⫽ 0.09). The sleep duration did not differ
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significantly between the two groups either by actigraphy or
diary measures, as shown in Table 1. Both groups slept
longer by diary and actigraphy criteria during weekends
compared with weekdays, but they did not differ from each
other in the total sleep duration either during the weekdays
or weekends (Table 2).
Nocturnal Arousals and Activity
NES subjects reported significantly more nocturnal
arousals than did controls (1.5 ⫾ 1.0 per night vs. 0.5 ⫾ 0.5,
p ⬍ 0.001). The mean number of arousals found in the NES
group in this study was lower than that reported by the
Birketvedt et al. study (4) (1.5 ⫾ 1.0 vs. 3.6 ⫾ 0.9), as might
be expected by virtue of methodological differences between the studies. A more stringent requirement was applied
to operationalize an awakening in this study, namely an
arousal followed by getting out of bed. These arousals, as
determined by actigraphy, commenced 2 hours and 8 minutes (⫾1:08) after quiescence among NES subjects, compared with 3 hours and 13 minutes (⫾2:07) after quiescence
among control subjects, about an hour earlier in the sleep
period (p ⫽ 0.04). During the 7-day recording period, NES
subjects not only had more nocturnal awakenings than did
controls, but also a larger percentage of them had multiple
awakenings. Figure 3a shows that all of the night eaters
Eating and Sleeping Patterns in NES, O’Reardon et al.
Table 1. Diary and actigraphy data for NES vs. control subjects
Mean and SD of time (hours:minutes)
Time of diary-recorded sleep onset
Time of actigraphy quiescence
Amount of time elapsed (in minutes)
between diary sleep onset and
first awakening
Amount of time elapsed (in minutes)
between quiescence and first
period of increased actigraphy
activity
Time of diary first awakening
Time of actigraphy first period of
increased activity
Time of diary-recorded sleep offset
Time of actigraphy AM increase in
activity
Duration of sleep period by diary
(in hours and minutes)
Duration of sleep period duration by
actigraphy (in hours and minutes)
Awakenings/night
Ingestions/night
NES
Controls
Significance
23:31 (1:40)
23:57 (1:33)
149 (68)
23:32 (1:06)
23:47 (1:07)
211 (127)
t(78.4) ⫽ 0.06, p ⫽ 0.96*
t(73.8) ⫽ 0.52, p ⫽ 0.6*
t(42.1) ⫽ 2.5, p ⫽ 0.02*
128 (68)
193 (127)
t(41.9) ⫽ 2.6, p ⫽ 0.01*
01:58 (1:51)
02:05 (1:51)
03:03 (1:54)
03:01 (1:56)
t(74) ⫽ 2.5, p ⫽ 0.02
t(74) ⫽ 2.1, p ⫽ 0.04
07:24 (1:07)
07:35 (1:11)
06:59 (1:12)
07:06 (0:59)
t(87) ⫽ 1.7, p ⫽ 0.09
t(74) ⫽ 1.9, p ⫽ 0.07
7 hours and 53 minutes
duration (1 hour and
13 minutes)
7 hours and 37 minutes
duration (1 hour and
26 minutes)
1.5 (1.03)
1.2 (0.94)
7 hours and 26 minutes
duration (1 hour and
20 minutes)
7 hours and 18 minutes
duration (1 hour and
23 minutes)
0.5 (0.46)
0 (0)
t(87) ⫽ 1.6, p ⫽ 0.11
t(74) ⫽ 0.97, p ⫽ 0.34
t(63.3) ⫽ 5.9, p ⬍ 0.001*
t(86) ⫽ 8.0, p ⬍ 0.001
* Tests were performed with Satterthwaite adjustment for unequal variances.
awakened on at least 1 night per week, compared with 70%
of the control subjects [␹2 (1) ⫽ 16.3, p ⬍ 0.001], and 44%
awakened on 6 or more nights, compared with only 9.3% of
the control subjects [␹2 (1) ⫽ 13.2, p ⬍ 0.001]. Figure 3b
shows that night eaters consumed food on 74% of their
awakenings, whereas no control subject ate on awakening.
The frequency with which awakenings were followed by
ingestions declined during the night from 88.6% the first
time to 65.8% the second time, 60.4% the third time, and
41.2% the fourth time, if it occurred at all.
Table 2. Sleep period duration (by diary) (⫾SD) during the weekend vs. weekdays in NES and control subjects
Weekends
Weekdays
Significance within groups
NES
(hours:minutes)
Controls
(hours:minutes)
Significance
between groups
8:21 (1:33)
7:45 (1:09)
p ⫽ 0.04
7:54 (1:10)
7:26 (1:10)
p ⫽ 0.03
p ⫽ NS*
p ⫽ NS
* Not significant.
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Figure 3:(a) Percentage of NES and control participants who
awakened (by diary, confirmed by actigraphy) at least 1 night per
week, at least 3 nights per week, and 6 or more nights per week.
All three frequency indices were significantly higher for NES than
for control subjects (p ⬍ 0.001). (b) Mean number (⫾SE) of
awakenings and ingestions (by diary) per night by NES and control
groups (for awakenings p ⬍ 0.001). **p ⬍ 0.01.
Discussion
This controlled study showed evidence of an abnormal
circadian phase relationship between the timing of sleepwake cycles and the timing of food intake in patients diagnosed with NES. Although nocturnal sleep onset, offset, and
duration in NES participants were comparable with those of
a demographically similar control group (Table 1), food
ingestion profiles differed greatly between the two groups
(Figures 1, 2, and 3). The results of the study suggest that
the NES may be characterized by a circadian phase delay in
the timing of food intake relative to a normally timed (phase
appropriate) nocturnal sleep-wake cycle.
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The circadian rhythms of eating and sleep are ordinarily
synchronized with each other in humans such that food
intake does not occur nocturnally. The synchronization of
these rhythms is performed by a central pacemaker in the
suprachiasmatic nucleus (SCN) of the hypothalamus, which
is believed to be responsible for the tight coordination of
most, if not all, rhythms of behavior and physiology (14,15),
including locomotor rhythms (16). It also coordinates the
activity of peripheral circadian oscillators, which are present
in tissues such as the liver, and are believed to have a role
in the signaling of food intake (17). Results from the behavioral methods used in the current study suggest that the
phase delay between cumulative caloric intake and sleepwake timing ranges in duration from 2 to as much as 6 hours
(Figure 1), depending on how it is measured.
The NES and control participants did not differ in their
total 24-hour energy intake (2314.4 ⫾ 748 kcal vs. 2420 ⫾
748 kcal), which suggests that the central feature of NES is
primarily the abnormal timing of food intake. Further evidence in support of this observation comes from published
reports of NES from other countries such as Italy (18,19).
NES is recognized in these settings even though the Mediterranean lifestyle dictates a much later time for the
evening meal. From these reports, it is evident that the food
intake pattern is out of phase with the sleep rhythm. Thus,
NES appears to be a transcultural syndrome where the
disordered rhythm of food intake is able to manifest itself
clinically despite widely varying meal schedules across
cultures.
These findings in NES highlight an apparent dissociation
between the circadian patterns of eating and sleeping. A
possible explanation is that patients with NES may have
circadian oscillators that signal food intake at a different
phase relationship from that normally signaled by the SCN.
In the laboratory, alteration in the timing of food intake has
been shown in mice to uncouple the food intake rhythm
from that of the central circadian pacemaker in the brain
(20 –24). Thus, when nocturnally active rodents are fed
during a light period, the peripheral circadian gene cycle in
the liver shifts (22), in one study in as little as 2 days (23).
In persons afflicted with NES, there is also alteration in
the timing of food intake relative to the circadian regulation
of the sleep-wake cycle. There seem to be three possible
mechanisms: a dysfunction in either the central or peripheral circadian clocks, a problem of central to peripheral
clock coupling, or inappropriately timed entrainment of
peripheral oscillators (through eating at night). The NES
may be an important clinical example, possibly the first in
humans, of a dissociation of the patterns of eating and
sleeping.
As discussed above, the dissociation may be maintained
by inappropriately timed ingestive behavior. There are links
between stress and the onset of NES, and elevated levels of
serum cortisol have been reported in the disorder (2). A
Eating and Sleeping Patterns in NES, O’Reardon et al.
stress event might serve to precipitate nocturnal awakenings
(i.e., sleep maintenance insomnia) in susceptible individuals. The act of eating during these awakenings (perhaps as
a form of self-soothing stress management) might entrain
the peripheral oscillators responsible for circadian signals
for energy intake to a delayed phase relative to the sleepwake cycle. Continued nocturnal ingestions would then
perpetuate the syndrome by delayed phase entrainment of
these peripheral clocks. Once an abnormal phase relationship between eating and sleeping is established in NES, it
might contribute to the association between NES and the
development of obesity. High rates of the syndrome have
been found in obese patients in bariatric surgery clinics (25).
Limitations of this study include the reliance on selfreported food intake, which may have been influenced by
self-monitoring. The timing of sleep onset and offset was
based on diary records and actigraph readouts, each of
which is subject to error. The convergence of the diary
records and actigraphy, however, suggests that the measures
captured the basic behavioral aspects of NES.
The dissociation of circadian rhythms of eating and sleeping in the NES participants observed in this study warrants
further investigation. The dissociation produced experimentally in nocturnally active rodents by feeding during the
light period may serve as an animal model for this key
characteristic of the NES. Sertraline, a serotonin selective
reuptake inhibitor, has been reported to restore a normal
food intake pattern in patients with NES (26). The dorsal
raphe nucleus of the midbrain (site of origin of serotonin
neurons in the brain) projects a significant modulatory input
to the SCN (27). It would be useful to test whether sertraline
might also restore a normal food intake phase in nocturnal
rodents entrained to eat at an adverse circadian phase.
Acknowledgments
We thank Greg Maislin and Jacqueline Cater (Biomedical
Statistical Consulting, Wynnewood, PA) for statistical assistance and Lisa Basel-Brown for dietary analysis. This
study was supported by NIH Grant R01-DK56735 and by
Pfizer Pharmaceuticals.
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Appendix 1
Rules for the Analysis of Activity
“Quiescence” was defined for the actigraph as onset of an
unequivocal period of at least 10 minutes of reduced activity
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that began no earlier than 15 minutes before the bedtime
recorded in the diary. If the patient did not record a bedtime,
no onset of quiescence was determinable.
When the participants responded affirmatively to the
question “Did you get up during the night?”, the actigraphic
record was investigated for a period of unequivocally increased activity of at least 3 minutes in length, within 30
minutes of the time recorded that the subject got out of bed.
We chose the more conservative route of comparing only
the time that the patient reported having gotten out of bed
rather than the entire range of time that they spent out of
bed. This did mean, however, that we probably underestimated the incidence of nocturnal awakening periods.
“AM increase in activity” was defined as the first period
of 10 sequential minutes of increased activity on the
actigraphic record, which followed the rise time recorded
in the diary. Out-of-bed periods were times when diary
reports of the subject being out of bed were confirmed by
actigraphy.