Effects of Diet On Sleep Quality

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REVIEW

Effects of Diet on Sleep Quality1,2


Marie-Pierre St-Onge,* Anja Mikic, and Cara E Pietrolungo
Institute of Human Nutrition and Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY

ABSTRACT

There is much emerging information surrounding the impact of sleep duration and quality on food choice and consumption in both children
and adults. However, less attention has been paid to the effects of dietary patterns and specific foods on nighttime sleep. Early studies have
shown that certain dietary patterns may affect not only daytime alertness but also nighttime sleep. In this review, we surveyed the literature
to describe the role of food consumption on sleep. Research has focused on the effects of mixed meal patterns, such as high-carbohydrate plus low-
fat or low-carbohydrate diets, over the short term on sleep. Such studies highlight a potential effect of macronutrient intakes on sleep
variables, particularly alterations in slow wave sleep and rapid eye movement sleep with changes in carbohydrate and fat intakes. Other studies
instead examined the intake of specific foods, consumed at a fixed time relative to sleep, on sleep architecture and quality. Those foods,
specifically milk, fatty fish, tart cherry juice, and kiwifruit, are reviewed here. Studies provide some evidence for a role of certain dietary patterns
and foods in the promotion of high-quality sleep, but more studies are necessary to confirm those preliminary findings. Adv Nutr 2016;7:938–49.

Keywords: diet, cherry, kiwi, dairy, carbohydrate, glycemic index, sleep, REM

Introduction influence sleep variables, specifically duration, efficiency, and


Because studies have proposed a relation between sleep du- architecture. We mainly focus on intervention studies that ex-
ration and obesity (1–3), there has been much interest in assess- amined the effects of diets, meals, or foods on sleep at night,
ing the impact of sleep on energy intakes. Studies have not daytime napping, but we also report on more general ep-
shown that short sleepers have higher energy intakes, notably idemiologic findings of associations between diet and sleep
from fat (4, 5) and snacks (6), than do normal sleepers. quality. We did not include studies of single micronutrients
NHANES data in the United States showed that short sleepers, or dietary supplements.
generally defined as those who sleep <7 h/night, consume a Unlike sleep duration, which is clearly defined by the
smaller variety of foods, with lower protein, carbohydrate, fiber, amount of sleep one gets at night, sleep quality can be defined
and fat intakes relative to normal sleepers who report 7–8 h of in different ways. By using objective measures of sleep, such
sleep/night (7). These data are corroborated by clinical inter- polysomnography, sleep quality can be characterized by the
vention studies that also showed greater snack intakes during amount of slow wave sleep (SWS)3 and rapid eye movement
periods of sleep restriction relative to habitual sleep in normal (REM) sleep one gets at night. These 2 stages of sleep occur
sleepers (8). Fat was also highlighted as a macronutrient of choice with greater duration as the night progresses (11). SWS is
during periods of sleep restriction relative to habitual sleep deep sleep and has a restorative function (12), whereas
(9, 10). both REM and SWS function toward memory consolidation
Of note, however, is that epidemiologic studies cannot (11, 13). Of relevance to this review, we have shown that
address causality or the direction of the relation between these stages of sleep were inversely associated with fat and
variables. Therefore, although those studies reported a link carbohydrate intakes (14). By using polysomnography and
between sleep and diet, it is unknown whether it is sleep actigraphy, sleep quality can be defined by sleep efficiency
that affects dietary intakes or dietary intakes that affect sleep. (SE), or the amount of time in bed spent asleep, as well as
In this review, we sought to determine from clinical inter- sleep-onset latency (SOL), the amount of time one takes
vention studies whether, and how, dietary intakes could to fall asleep at night. Low SE (generally <85%) and long

1 3
Supported in part by Columbia University R56HL119945 (M-PS-O) and New York Obesity Abbreviations used: GI, glycemic index; HC, high carbohydrate; HF, high fat; LC, low
Research Center grant P30DK26687. carbohydrate; LCNAA, large-chain neutral amino acid; LF, low fat; NREM, nonrapid eye
2
Author disclosures: M-P St-Onge, A Mikic, and CE Pietrolungo, no conflicts of interest. movement; REM, rapid eye movement; SE, sleep efficiency; SOL, sleep-onset latency; SWS,
*To whom correspondence should be addressed. E-mail: ms2554@cumc.columbia.edu. slow wave sleep; TST, total sleep time; WASO, wake after sleep onset.

938 ã2016 American Society for Nutrition. Adv Nutr 2016;7:938–49; doi:10.3945/an.116.012336.
SOL (>20–30 min depending on age) typically characterize Overweight individuals with insomnia also had lower carbo-
poor sleep. Finally, subjective measures of sleep quality can hydrate intakes than did healthy overweight counterparts. In
be obtained by questionnaire. Typically, the Pittsburgh Sleep addition, they had higher fat intakes than individuals who
Quality Index questionnaire is used. were free from sleep disorders.
Sleep duration and quality have been associated with obe- The Mediterranean diet was associated with sleep quality
sity, diabetes, hypertension, and cardiovascular disease risk in older adults (18). On the basis of self-reported question-
in cross-sectional and longitudinal studies (11). An excellent naires evaluating sleep quality, lifestyle factors, and dietary in-
review in this Journal covered some mechanistic explanations take, the Mediterranean diet was inversely associated with
for this association and provides recommendations for nu- insomnia symptoms (difficulty initiating sleep, difficulty main-
trition professionals with regard to sleep hygiene and its im- taining sleep, early morning awakening) in women but not
portance in nutrition counseling (11). in men. Data from the 2007–2008 NHANES showed that
difficulty maintaining sleep was associated with lower food
Dietary Patterns and Sleep Quality variety and adhering to a special diet; however, this was no
Epidemiologic findings longer significant after adjusting for covariates (19). Increased
Associations between sleep quality and dietary patterns were caloric intake was associated with daytime sleepiness.
recently reported in a cross-sectional study (15) in female The epidemiologic studies that reported associations be-
Japanese workers who responded to lifestyle questionnaires. tween dietary patterns and sleep quality are informative. In
A high intake of confectionary and noodles was associated general, those studies indicate higher fat intakes with sleep
with poor sleep quality, as evidenced by a high global Pitts- disorders (17) and that following a Mediterranean dietary
burg Sleep Quality Index score, whereas a high intake of fish profile is associated with fewer insomnia symptoms in
and vegetables was associated with good sleep quality. A sig- women (18). Information on the association between carbo-
nificant trend toward worse sleep quality with increasing hydrate intakes and sleep quality is conflicted (15–17), with
carbohydrate intake was found. The quality of carbohydrate studies reporting low intakes in those with insomnia symp-
seemed to be more important than its quantity in mediating toms (16, 17) but high intakes of sweets (15). This would
this association. Poor sleepers with the highest carbohydrate suggest that carbohydrate quality may be important to con-
intake consumed more confectionary and noodles than rice sider when examining the association between diet and sleep
than did good sleepers with a similarly high carbohydrate in- quality. However, epidemiologic studies are limited by an
take. Moreover, frequent consumption ($1 time/mo) of unclear direction of the associations and self-reported data.
energy drinks and sugar-sweetened beverages was associ- Clinical trials that investigated the effect of individual macro-
ated with poor sleep quality. Other eating patterns indica- nutrients on sleep architecture are more elucidative.
tive of poor dietary habits were also related to sleep quality.
For example, skipping breakfast and eating irregularly were Experimental findings
strongly associated with poor sleep quality. Although relations High-carbohydrate diet. There is a substantial body of ev-
between sleep quality and dietary patterns were observed, idence to indicate a role of carbohydrate intake on sleep indexes
the directionality of the findings cannot be established from (Table 1). Both high-carbohydrate (HC) and low-carbohydrate
this study. Furthermore, poor-quality sleepers were also short (LC) diets are associated with changes in sleep architecture
sleepers, thus making sleep duration a likely confounding vari- (20–25). Carbohydrate manipulation has primarily been shown
able that was not taken into account. to affect REM sleep and SWS; however, non-REM (NREM)
Other epidemiologic studies have found associations be- sleep, SOL, and REM-onset latency have also been affected.
tween disordered sleep and diet (16–18). Tanaka et al. (16) Phillips et al. (20) showed that HC and LC diets have op-
reported a relation between macronutrient intakes and in- posite effects on SWS. In this study, healthy men were ran-
somnia symptoms in a cross-sectional analysis of non–shift domly assigned to consume a controlled diet, either LC plus
workers who responded to a brief diet history questionnaire. high fat [(HF) LC/HF] or HC plus low fat [(LF) HC/LF] for
Low protein intake (<16% of energy from protein) was asso- a period of 2 d after 2 d of a lead-in balanced diet. The LC/
ciated with poor quality of sleep and marginally associated HF and HC/LF diets provided 100 and 600 g carbohydrates
with difficulty initiating sleep, whereas high protein intake and 255 and 33 g fat, respectively. The lead-in diet contained
(>19% of energy from protein) was associated with difficulty 350 g carbohydrates and 140 g fat. Diets were designed to
maintaining sleep. Low carbohydrate intake (<50% of energy maintain weight and meals were administered at fixed times.
from carbohydrate) was marginally associated with difficulty SWS significantly decreased with the HC/LF diet relative to
maintaining sleep. When stratified by sex, these associations the LC/HF diet and the lead-in diets. REM sleep significantly
were significant in men but not in women. increased with both intervention diets relative to the lead-in
Similar results were found with respect to the association diet, with a significantly greater increase after consumption
between carbohydrate intake and sleep quality in men (17). of the HC/LF diet. Similarly, stage 1 sleep was reduced with
Individuals with disordered sleep (insomnia, obstructive both diets compared with the lead-in diet.
sleep apnea, or a combination of the 2) assessed by question- Yajima et al. (21) found similar changes in SWS after the
naires reported lower total carbohydrate intakes than did consumption of an HC test meal. In a similar fashion, healthy
normal-weight individuals who were free from sleep disorders. men underwent a 1-d randomized crossover intervention with

Food effects on sleep 939


TABLE 1 Summary of clinical studies that investigated the effect of dietary patterns on sleep architecture1
Study (ref) Diet pattern Subjects Duration Methods Treatment group results2
Phillips et al. (20) HC/LF diet vs. LC/HF diet 8 healthy men 4d Days 1–2: control diet (350 g carbohydrate, 140 g SWS: lower with the HC/LF diet (97.8 min) and
fat, 75 g protein) higher with the LC/HF diet (117.2 min) vs. the
control diet (115.5 min)
Days 3–4: HC/LF diet (600 g carbohydrate, 33 g REM: higher with the HC/LF diet (136.9 min) vs.

940 St-Onge et al.


fat, 75 g protein) or LC/HF diet (100 g carbo- the LC/HF (122.1 min) and control (103.6 min)
hydrate, 225 g fat, 75 g protein) diets
NREM 1: lower with both the HC/LF (319.5 min)
and LC/HF (331.5 min) diets vs. the control diet
(342.2 min)
Yajima et al. (21)3 HC vs. HF meals 10 healthy men 1d HC test meal: dinner consumed at 2000 (10% SWS: decreased during sleep cycle 1 with the HC
protein, 10% fat, 80% carbohydrate) diet vs. the HF diet
HF test meal: dinner consumed at 2000 (78% fat,
10% protein, 12% carbohydrate)
Lindseth et al. (22) High-protein vs. 44 healthy young 4d High-protein diet (56% protein, 22% carbohy- Wake episodes: decreased with the high-protein
HF vs. HC diets adults (19–22 y old) drate, and 22% fat) diet (13.5 times) vs. the control diet (16.7 times)
(between-group)
HC diet (56% carbohydrate, 22% protein, 22% fat) SOL: lower with the HC diet (9.1 min) vs. the
HF diet (56% fat, 22% carbohydrate, 22% protein) control diet (13.9 min)
Control diet (50% carbohydrate, 35% fat, 15%
protein)
Afaghi et al. (23) High- vs. low-GI 12 healthy men 1d 767 kcal/meal (8% protein, 1.6% fat, 90.4% SOL: lower with the high-GI diet at 4 h before
(18–35 y old) carbohydrate) bedtime (9.0 6 6.2 min) vs. both low-GI diet at
Low-GI diet [Mahatma rice (GI = 50) with meal 4 h 4 h before bedtime (17.5 6 6.2 min) and high-
before bedtime] GI diet at 1 h before bedtime (14.6 6 9.9 min)
High-GI diet 1 [jasmine rice (GI = 109) with meal 4
h before bedtime]
High-GI diet 2 [jasmine rice (GI = 109) with meal
1 h before bedtime]
Afaghi et al. (24) Very LC 14 healthy men 5d Control phase [3 d of mixed meals (15.5% protein, REM: percentage of TST lower during very LC
(18–35 y old) 12.5% fat, 72% carbohydrate) with 1 evening acute (17.6% 6 5.3%) and very LC ketosis
mixed test meal4] (17.7% 6 5.4%) phases vs. control (21.4% 6 6.3%)
Acute phase [night 3: very LC test meal4 (2400 SWS: higher during very LC acute (83.3 6 33.8
kcal; 38% protein, 61% fat, ,1% carbohydrate)] min) and very LC ketosis (80.4 6 628.0 min)
Ketosis phase (2 d of very LC diet) phases vs. control (66.2 6 30.1 min)
Kwan et al. (25) LC 6 healthy young 2 wk Week 1: weighing and recording habitual diet REM: onset latency increased from 66 6 8 min to
women (20–23 y old) Week 2: isoenergetic diet of 50-g/d carbohydrate 111 6 38 min
restriction
St-Onge et al. (9) Controlled vs. ad 26 healthy adults 1d Habitual sleep phase: 9 h/night in bed (2200– SWS: lower during the ad libitum food intake
libitum food intake (30–45 y old) 0700) period (24.6 6 12.8 min) than during con-
trolled intake period (29.3 6 13.9 min)
Test day: ad libitum food intake SOL: higher during the ad libitum food intake
period (29.2 6 23.1 min) than during con-
trolled intake period (16.9 6 11.1 min)

(Continued)
TABLE 1 (Continued )

Study (ref) Diet pattern Subjects Duration Methods Treatment group results2
3
Crispim et al. (26) Ad libitum food intake 52 healthy adults 3d Test days: ad libitum food intake recorded by Men:
(19–45 y old) using food diary NREM 2: negatively correlated with nocturnal
fat intake
SE: negatively correlated with nocturnal fat
intake
REM: negatively correlated with nocturnal fat
intake
SOL: negatively correlated with nocturnal fat
intake
WASO: negatively correlated with nocturnal fat
intake
Women:
SOL: positively correlated with nocturnal
caloric, protein, carbohydrate, and fat intake
SE: negatively correlated with nocturnal caloric,
carbohydrate, and fat intake
REM: negatively correlated with nocturnal fat
intake
Driver et al. (27) High-energy meal vs. 7 healthy men 1d Fast: evening fast beginning at 1300; maximum No effect of evening fast (10 h) or high-energy
evening fast vs. (20–24 y old) energy intake of 38 kcal consumed as fruit juice evening meal on sleep architecture
control meal and water
Control meal: administered at 2100 with a mac-
ronutrient ratio of 12:26:61 for fat, protein, and
carbohydrate
High-energy meal: administered at 2100 with a
macronutrient ratio of 37:21:42 for fat, protein,
and carbohydrate, with double the energy
content of the control meal
Lieberman et al. (28) Calorie deprivation 27 healthy young 2d All diets composed of hydrocolloid gels No effects of 2-d calorie deprivation on sleep
adults Carbohydrate diet: starch and maltodextrin gel
Carbohydrate+fat diet: starch, maltodextrin, and
polyunsaturated lipid gel
Calorie deprivation: hydrocolloid-based gel with
artificial sweeteners and flavors
Karacan et al. (29) Calorie deprivation 11 healthy men 3d Day 1: normal food intake with dinner meal as the REM: lower number of REM episodes (3.49 6 0.9
(22–25 y old) last meal before fast vs. 4.4 6 0.5 episodes) and higher percentage
Days 2–3: fasting days (no food intake) of stage 4 REM sleep (15% 6 7% vs. 11% 6
6%) on day 3 vs. day 1; higher percentage of
stage 4 REM sleep (15% 6 7% vs. 10% 6 7%)
and lower percentage of stage 2 REM sleep
(49% 6 9% vs. 53% 6 7%) on day 3 vs. day 2
1
GI, glycemic index; HC, high carbohydrate; HF, high fat; LC, low carbohydrate; LF, low fat; NREM, nonrapid eye movement; NREM 1, nonrapid eye movement stage 1; NREM 2, nonrapid eye movement stage 2; ref, reference; REM, rapid eye
movement; SE, sleep efficiency; SOL, sleep onset latency; SWS, slow wave sleep; WASO, wake after sleep onset.
2
Only significant results are reported, P , 0.05. Results are shown relative to the control group unless otherwise noted.
3
Numerical data not provided.
4

Food effects on sleep 941


Test meals 4 h before bedtime.
either an HC or an HF evening test meal to investigate their a controlled-feeding crossover study design. The dietary in-
effects on sleep architecture. Participants were prescribed ei- terventions included a high-protein diet (56% of energy
ther an HF (78% fat, 10% protein, 12% carbohydrate) or an from protein, 22% from carbohydrate, and 22% from fat),
HC (10% protein, 10% fat, 80% carbohydrate) test meal to an HC diet (56% of energy from carbohydrate, 22% from
be eaten at 2000. Breakfast and lunch on the test day were protein, and 22% from fat), an HF diet (56% of energy from
the same for each intervention and provided 13–15% protein, fat, 22% from carbohydrate, and 22% from protein), and a
19–24% fat, and 60–63% carbohydrate. SWS decreased within control diet (50% of energy from carbohydrate, 35% from
the first sleep cycle after the HC meal compared with the HF fat, and 15% from protein) that were each consumed for 4 d.
meal. However, there was no difference in sleep architecture Sleep was monitored continuously throughout each 4-d in-
between interventions over the entire sleep period. The au- tervention period by using actigraphy. A significant effect of
thors suggested that the reduction in SWS observed during diet on the number of wake episodes and SOL was observed.
the first sleep cycle was related to the degree of carbohydrate The consumption of the high-protein diet decreased the
oxidation. Carbohydrate oxidation was higher after the HC number of wake episodes compared with the control diet,
meal than after the HF meal, especially during the first half and SOL was significantly lower after the HC diet than after
of the sleep episode when SWS was markedly reduced with the control diet.
the HC meal. In addition, they showed that carbohydrate ox-
idation was highest during REM sleep and lowest during SWS Glycemic index. The glycemic index (GI) of carbohydrates
(21), possibly indicating a greater reliance on carbohydrate for has also been studied as a dietary factor related to sleep ar-
energy during REM sleep. However, this study was limited by chitecture. Afaghi et al. (23) investigated the effects of both
the absence of a control (balanced) meal. Because of this, it is GI and meal timing on sleep architecture in men. Sleep was
not possible to determine whether SWS was, in fact, increased measured on 3 separate test nights, which differed in the glyce-
with the HF meal or whether it was reduced with the HC meal. mic index of the pre-bedtime meal: either a low-GI (GI = 50)
Moreover, the clinical significance of a change in sleep architec- or a high-GI (GI = 109) meal was consumed 4 h before bed-
ture in one sleep cycle, but not over the entire night, is unknown. time or a high-GI meal was consumed 1 h before bedtime.
Another study (30) investigated the effects of a pre-bedtime SOL was significantly lower after the high-GI meal consumed
test meal on sleep architecture in men. Participants underwent 4 h before bedtime than after both the low-GI meal and the
a 3-night intervention consisting of an HC, an LC, or a zero- high-GI meal consumed 1 h before bedtime. Consistent with
carbohydrate snack administered 45 min before bedtime. The these findings, subjective ratings of sleepiness were significantly
HC snack consisted of a glucose drink and fried potatoes (521 higher after the high-GI meal ingested 4 h before bedtime.
kcal or 130 g carbohydrate) and the LC snack consisted of
crispbread, salad, and butter (188 kcal or 47 g carbohy- LC diet. Afaghi et al. (24) also investigated the effects of a
drate). Both the HC and LC snacks were similar in protein very LC diet on sleep architecture in men. The intervention
and fat content but differed in carbohydrate content. The consisted of a familiarization phase with 1 evening control
carbohydrate-free snack consisted of a methyl-cellulose sup- test meal for 3 d, an acute intervention phase (1 meal), and
plement and contained no energy. Participants were allowed a longer-term ketosis phase of 2 d. The familiarization phase
8.5 h of sleep/night. NREM sleep decreased and the number consisted of mixed, balanced meals (15% of energy from pro-
of REM periods increased during the HC relative to the no- tein, 25% from fat, and 60% from carbohydrate) provided on
carbohydrate treatment over the entire sleep period. SWS de- day 1 and for breakfast and lunch on day 2. The control test
creased during the carbohydrate-free treatment relative to the meal, altered to resemble an HC/LF diet (15.5% of energy
LC treatment over the entire sleep period. During only the first from protein, 12.5% from fat, 72% from carbohydrate), was
half of the sleep period, REM sleep and stage 3 sleep increased administered on the evening of day 2. The acute phase took
during the HC treatment. Persistent effects were observed on re- place on the third night, after consuming the familiarization
covery nights after the 3-d intervention period. During the post- diet for breakfast and lunch. The acute phase consisted of
HC conditions, stage 4 sleep decreased and the number of REM an evening test meal (38% of energy from protein, 61%
periods increased relative to the other 2 treatments, whereas from fat, <1% from carbohydrate). The ketosis phase was
stage 3 sleep increased relative to the no-carbohydrate condition followed over the next 2 d with maintenance of the very
over the entire sleep period. REM latency increased after the LC LC diet. Each participant was maintained on 2400 kcal/d
relative to the HC conditions over the entire sleep period. Con- for the 5-d intervention period, and test meals were admin-
sistent with the findings of Phillips et al. (20), most of the istered 4 h before bedtime. Participants were permitted to
changes in sleep architecture occurred during the HC condition, sleep at their discretion, and sleep was recorded by using
with a trend toward higher REM sleep and lower NREM sleep, polysomnography. REM sleep was reduced and SWS was in-
with the exception of stage 3 sleep. Although the direct mecha- creased during both the acute and ketosis phases relative to
nisms mediating these changes are unclear, the authors pro- the control phase. The arousal index was significantly in-
posed that the effect of the HC condition on changes in sleep creased during sleep stages 1 and 2 after the very LC acute
stages is related to increased serotonin synthesis. and ketosis phases compared with after the control phase.
Lindseth et al. (22) investigated the effect of individual In addition, there was a trend toward improved SE after
macronutrients on sleep indexes in adults with the use of the acute phase (P = 0.08) but not after the ketosis phase.

942 St-Onge et al.


In another study, Kwan et al. (25) investigated the effect of an effects of an HC diet on REM and SWS have been linked to
LC diet, 50 g/d for 1 wk, on sleep architecture in women. fuel utilization during the different sleep stages (21). Noctur-
REM-onset latency increased after the LC diet relative to the nal energy metabolism has been shown to differ between the
prestudy habitual diet. different sleep stages (31). Energy expenditure and fat oxida-
tion decline in the first 4 h of the sleep period and subse-
Mixed meals. The effect of various macronutrient intakes quently remain stable for the following 4 h of the night in
on sleep architecture was assessed by St-Onge et al. (9). Par- healthy men. Carbohydrate oxidation was higher during REM
ticipants consumed a fixed diet that provided 31% of energy sleep than in NREM sleep and highest in the last hour of
from fat, 53% from carbohydrate, and 17% from protein for the sleep episode before waking. The difference in carbohy-
4 d. On day 5, participants self-selected their food intake. On drate oxidation between sleep stages was greatest between
that night, SWS was lower and SOL was longer than sleep sleep stages 3 and 4 and REM sleep, indicating a higher en-
measured after the fixed diet. Higher fiber intakes on the ergy demand for REM sleep. Therefore, an HC meal or diet
ad libitum day were associated with more SWS and less could enhance nocturnal carbohydrate utilization and pro-
time spent in stage 1 sleep. A higher percentage of energy mote REM sleep.
consumed from saturated fat was associated with less time Although it cannot be confirmed, it has been hypothe-
spent in SWS. In addition, greater sugar and nonsugar, non- sized that carbohydrate oxidation also suppresses SWS (21,
fiber carbohydrate intakes were associated with more wake 31), which would support the findings of reciprocal changes
bouts during the sleep episode. These associations indicate in REM and SWS due to carbohydrate manipulation (20, 24).
that higher saturated fat and lower fiber intakes may pro- It was previously reported that an HC diet reduces growth
duce less SWS, more nighttime arousals, and a reduction hormone secretion in men, but not in women, after a 10-d
in overall sleep quality. dietary intervention (32). Because growth hormone has been
Crispim et al. (26) similarly investigated the effects of ad linked to SWS (20, 24), it is possible that a reduction in SWS
libitum food intake on sleep architecture. Over 3 nonconsec- with an HC diet may be mediated by a diet-induced reduc-
utive days, subjects recorded their food intake in a food diary tion in growth hormone secretion. However, additional re-
and reported to the sleep laboratory for polysomnography. search is warranted to confirm this hypothesis.
Nocturnal food intake (30–60 min before bedtime), but not The effect of an HC diet on SOL has been linked to ele-
total daily intake, was correlated with several sleep variables vated postprandial insulin and Trp response (23). Trp, a pre-
and differed by sex. In men, stage 2 sleep, REM sleep latency, cursor of serotonin (23), enters the brain in a competitive
SOL, and wake after sleep onset (WASO) were positively cor- manner with large-chain neutral amino acids (LCNAAs)
related with fat intake at night. In addition, fat intake at (33). An HC diet, low in protein, has been shown in animal
night was negatively correlated with SE and REM in men. models to elevate brain Trp concentrations relative to
In women, positive associations for evening intake included higher-protein diets (33). When the concentration of Trp
the following: SOL and energy, protein, carbohydrate, and is higher than that of LCNAAs, its entry into the brain is fa-
fat intakes; REM sleep latency and energy, carbohydrate, vored and serotonin production is upregulated (34, 35),
and fat intakes; stage 2 sleep and energy, carbohydrate, which would promote sleep (24). Because the Trp-to-LCNAA
and fat intakes; and WASO and energy and fat intakes. Neg- ratio is affected by dietary carbohydrate intake (33, 36), it is
ative associations for evening intake included REM sleep and possible that changes in sleep architecture as a result of carbo-
fat intake and SE and energy, carbohydrate, and fat intakes hydrate manipulation are mediated by the Trp-to-LCNAA
in women. Overall, the results of this study confirmed that ratio. An HC diet or meal would increase the Trp-to-LCNAA
diet quality, particularly closer to bedtime, influences sleep ratio and promote sleep through increased serotonin pro-
architecture. Nocturnal eating, considered in this study to duction (33, 34). Conversely, an LC diet would result in a
be any food intake 30–60 min before bedtime, was shown low ratio of Trp to LCNAA, thus limiting serotonin produc-
to negatively influence sleep quality, with a greater effect tion and prolonging SOL (25). With the consumption of an
in women than in men (26). This effect was proposed by HC diet, the resulting higher postprandial insulin enhances
the authors to be mediated by postprandial physical dis- the Trp-to-LCNAA ratio by facilitating uptake of LCNAA by
comfort and reduced digestive activity; however, this was muscle, further promoting Trp entry into the brain and en-
not confirmed. abling serotonin production (23). In support of this, a correla-
The studies to date point to an effect of carbohydrate in- tion between plasma glucose and insulin, and peak Trp:LCNAA
take on sleep, albeit with mixed results. Some found reduced has been reported (36). Therefore, an HC diet, especially one
SOL with the consumption of a higher carbohydrate diet with a high GI, would promote a higher Trp-to-LCNAA ra-
(22, 23) but others reported a trend for greater SE after an tio and have a greater serotonergic effect (36). Moreover, it
acute intake of a very LC meal (24). The findings from these has been reported that the Trp-to-LCNAA ratio peaks be-
studies support the idea that dietary carbohydrate intake or tween 2 and 4 h after the ingestion of an HC meal (36),
pre-bedtime meal also influence sleep architecture, particu- which likely accounts for shorter SOL after the consumption
larly REM and SWS. The consumption of an LC diet appears of an HC or high-GI meal 4 h compared with 1 h before bed-
to reduce REM sleep while increasing SWS (20, 24), with the time (23). This proposed mechanism must be explored further,
consumption of an HC diet having the opposite effect. The however, because the Trp-to-LCNAA ratio was not measured

Food effects on sleep 943


in the studies reported in the current review. However, urine 6- architecture. In fact, prolonged fasting (60–67 h) decreased
sulfatoxymelatonin, a metabolite of melatonin, was highest af- the number of REM episodes but increased the percentage of
ter the consumption of the high-GI meals (23). This finding REM sleep compared with baseline (29). A comparison of
may also be related to the plasma concentration of Trp (23). fasting periods of 30–37 h and 60–67 h showed an increase
Therefore, an increase in plasma Trp after a high-GI meal in the percentage of stage 4 REM sleep with a compensatory
may influence both melatonin and serotonin, thus promoting decrease in stage 2 REM sleep.
sleep onset. However, subsequent sleep quality, such as duration Although Karacan et al. (29) were the only authors, to
of SWS and arousals during sleep, may be adversely affected our knowledge, to report an effect of calorie restriction on
by HC intakes, particularly of simple sugars. sleep variables, it is surprising that there was no effect of
The fat content of the meal has been suggested to mediate the other dietary interventions (27, 28). In the study per-
the observed changes in REM and SWS (24) due to an LC diet. formed by Driver et al. (27), neither the control meal nor
This effect may be mediated through the postprandial release the high-energy meal resulted in the acute changes in sleep
of cholecystokinin, a satiety hormone released by the duode- architecture that had been previously shown (23). Similarly,
num after an HF meal (24). The role of cholecystokinin in me- the study by Lieberman et al. (28) failed to show an effect of
diating changes in sleep architecture in humans has not yet been the carbohydrate or carbohydrate+fat gel preparations on
defined; however, an animal study showed that injection of cho- sleep. It is possible that a longer adaptation period to the di-
lecystokinin into rats promoted SWS and NREM sleep (37). In etary interventions is required for changes in sleep variables
humans, both subjective ratings of fatigue and cholecystokinin to be observed, although acute changes in sleep have been
concentrations were significantly higher after an HF/LC meal reported after one evening test meal (23). Overall, it is rea-
than after an LF/HC meal in 18 healthy adults (25). Further- sonable to suggest that calorie restriction influences sleep
more, cholecystokinin was reported to be predictive of and pos- architecture over longer durations; nevertheless, research is
itively correlated with fatigue (25). Although clinical trials directly limited on this topic and further investigation is warranted.
investigating the effect of cholecystokinin concentrations on
sleep architecture are lacking, the association between cholecys- Sleep-Promoting Foods and Sleep Quality:
tokinin and fatigue in response to an HF/LC meal suggests that Experimental Findings
sleep architecture may be mediated by this satiety hormone. Despite the availability of anecdotal evidence, scientific re-
search on the effects of various foods on sleep enhancement
Calorie Restriction and Sleep Quality: Experi- is limited (Table 2). Daily incorporation of sleep-promoting
mental Findings foods, such as milk, fatty fish, cherries, and kiwifruit, has
In a study by Driver et al. (27), the effect of short-term (10 h) been studied for their potential benefits for immediate and
calorie restriction on sleep indexes was investigated. Partic- acute sleep improvement without large changes in dietary
ipants consumed food ad libitum until 1300 when they patterns.
reported to the laboratory. A test meal was provided at
2100. The test meals consisted of no meal, a control meal, Milk. The first studies to examine the sleep-inducing effects
or a high-energy meal. The fast (no meal) allowed only the of a specific food date to the 1970s, when Horlicks, a malted
consumption of fruit juice and water, with a maximum energy milk drink, was tested. Southwell et al. (38) used time-lapse
intake of ;38 kcal. The control meal had a macronutrient ra- cinematography to record sleep movements after the con-
tio of 13:26:61 for fat:protein:carbohydrate and provided ;1370 sumption of 350 mL warm water, 350 mL warm milk with
kcal, whereas the high-energy meal had a ratio of 37:21:42 with 5 teaspoons Horlicks powder, or no beverage (control). Par-
double the energy content, resembling a higher-fat meal. Bed- ticipants with no history of sleep disorders consumed the
time was set between 2250 and 2306, and sleep was monitored drink ;30 min before bedtime, which was fixed at mid-
by polysomnography. The authors found no effect of diet on night. The authors reported fewer small movements during
sleep variables. sleep after consumption of the Horlicks drink, particularly
Another study investigated the effects of 2.5 d of calorie from 0400 to 0700, than after consumption of water and
deprivation on sleep, cognition, activity, and blood glucose the control. In support of these findings, another study
concentrations (28). Participants underwent 3 test periods: (39) also found that young adults experienced fewer move-
near-complete fasting, carbohydrate only, and carbohydrate+fat ments during sleep in the latter half of the night after the
diets. Diets were composed exclusively of hydrocolloid gels consumption of a Horlicks drink 30 min before bedtime.
to maintain blinding. The carbohydrate diet (940 kcal/meal) con- The study used polysomnography recordings to assess the
sisted of a starch and maltodextrin gel; the carbohydrate+fat sleep quality of healthy young and middle-aged adults after
diet (940 kcal/meal) consisted of starch, maltodextrin, and the consumption of Horlicks relative to an inert capsule.
polyunsaturated lipid gel; and the calorie-deprivation diet Compared with the younger participants, the older adults ex-
(61 kcal/meal) consisted of an artificial sweetener and artifi- perienced increased total sleep time (TST) and greater sleep
cial flavor gel. There was no effect of dietary intervention continuity after the consumption of Horlicks.
on sleep variables or other outcome measures. The effect of Horlicks on sleep quality and duration ap-
The short duration of the above studies suggests that pro- pears to be partially mediated by age. Aging is associated
longed calorie restriction may be required to influence sleep with a decline in nighttime sleep quality (47) as well as with

944 St-Onge et al.


TABLE 2 Summary of clinical studies that assessed effects of food on sleep quality1
Study (ref) Food Subjects Methods Treatment group results2
Southwell et al. (38) MM, Horlicks 4 healthy men No drink (control), 350 mL warm water, or 350 mL Less movement after MM (412 frames of movements) vs.
MM drink 30 min before bedtime control (500 frames of movements)
Brezinová et al. (39) MM, Horlicks Group 1: 10 subjects (4 women), MM drink (32 g Horlicks powder + 250 mL hot Group 1:
aged 20–30 y milk) or inert capsule (control) at night for 10 d, Wake episodes: decreased (11.6 times) vs. control
Group 2: 8 subjects (5 women), 30 min before bedtime (14.5 times) in the seventh hour of sleep
aged 42–66 y Group 2:
TST: higher (450.5 min) vs. control (439.6 min)
WASO: lower (3.6 min) vs. control (15.5 min) in the
second 3 h of sleep
Adam (40) MM, Horlicks 16 subjects Inert capsule (control), MM drink (32 g Horlicks TST: higher in those who habitually eat before bedtime
powder + hot milk), flavored drink (devoid of after MM (463.8 min) and milk alone (471.2 min) vs.
milk and cereal), or milk alone at night for 5 d control (452.0 min)
Valtonen et al. (41) Melatonin-enriched milk 70 elderly subjects with a chronic 17 oz melatonin-enriched milk for 8 wk Increased morning and evening physical activity (within
illness groups)
Yamamura et al. (42) Fermented milk, Lactobacillus 29 subjects, aged 60–81 y 100 g fermented milk or artificially acidified milk SE: higher after intervention (91.18% 6 1.08%) vs. control
helveticus (control) 1 time/d at any time for 3 wk (91.37% 6 0.98%)
Wake episodes: decreased after intervention (8.31 6 0.62
times) vs. control (8.85 6 0.75 times)
Pigeon et al. (43) TCJ, Montmorency 15 subjects (7 women), aged .65 y, 8 oz TCJ or cherry-flavored drink (control) for 2 wk ISI: lower after TCJ (13.2 6 2.8) vs. control (14.9 6 3.6)
with insomnia in morning and evening WASO: lower after TCJ (62.1 6 37.4 min) vs. control (79.1 6
38.6 min)
Garrido et al. (44) Jerte Valley cherries (7 cultivars) M group: 6 subjects, aged 35–55 y; 200 g cherries for 3 d as lunch and dinner desserts TST: increased after consumption of 6 of the 7 cultivars in
E group: 6 subjects, aged 65–85 y (no control) M group (1.15- to 1.45-fold increase vs. control) and
after all 7 cultivars in E group (1.14- to 1.33-fold in-
crease vs. control)
SE: increased 1.12- 6 0.02-fold in Van cultivar in M group
SOL: decreased 0.54- 6 0.10-fold with consumption of
Navalinda cultivar in M group and 0.51- 6 0.07-fold
with consumption of Pico Negro cultivar in E group
Howatson et al. (45) TCJ, Montmorency 20 subjects, aged 18–40 y 8 oz TCJ or cherry-flavored drink (control) for 1 wk TIB: higher after TCJ (514.7 6 17.0 min) vs. control (492.2 6
within 30 min of awakening and 30 min before 40.6 min)
the evening meal TST: higher after TCJ (419 6 22 min) vs. control (380 6
49 min)
SE: higher after TCJ (86.8 6 3.6%) vs. control (84.1 6
5.8%)
Lin et al. (46) Kiwifruit 24 subjects (2 men), aged 20–55 y 2 kiwifruits 1 h before bedtime for 4 wk (no TST: higher with kiwifruit intake (395.3 6 17.4 min) vs.
control) control (354.5 6 17.1 min)
SE: higher with kiwifruit intake (91.2 6 1.53%) vs. control
(86.9 6 1.94%)
WASO: lower with kiwifruit intake (12.8 6 3.49 min) vs.
control (18.9 6 4.31 min)
SOL: lower with kiwifruit intake (20.4 6 3.53 min) vs.
control (34.3 6 3.86 min)
1
E, elderly; ISI, Insomnia Severity Index; M, middle-aged; MM, malted milk; oz, ounce; ref, reference; SE, sleep efficiency; SOL, sleep onset latency; TCJ, tart cherry juice; TIB, time in bed; TST, total sleep time; WASO, wake after sleep onset.
2
Only significant results are reported, P , 0.05. Results are shown relative to the control group unless otherwise noted.

Food effects on sleep 945


changes in the circadian regulation of the sleep-wake cycle in both young and old populations, although the mechanisms
(48). It has been suggested that the age-related changes in sleep remain unclear. However, studies indicate that the timing of
are partly due to a decrease in circadian amplitude (47). It has consumption may play an additional role as to whether the
also long been known that endogenous melatonin production consumption of a malted milk beverage before bedtime en-
declines with increasing age (48). This may offer an explana- hances sleep. More research with the use of objective measure-
tion as to why the effects of Horlicks are more effective after ments is necessary to confirm these findings.
serial administration in older adults but not in younger adults. There are several mechanisms by which malted milk may
In an effort to distinguish the sleep-enhancing factors of affect sleep quality. Horlicks is composed of wheat, malt bar-
the Horlicks drink, one study (40) compared the consump- ley, sugar, milk, and 14 vitamins and minerals, including
tion of Horlicks to inert capsules, milk alone, and a flavored vitamin D and several B-group vitamins. Emerging clinical
drink with energy and macronutrient contents similar to evidence supports the association between vitamin and min-
Horlicks. Of note, the participants in this study (40) were eral deficiencies and disrupted sleep. In individuals with low
older than those in the other Horlicks studies: 52–67 y old serum concentrations, 3 mo of vitamin D supplementation
compared with 20–66 y old for the other studies (38, 39). of either 1200 IU/d or 50,000 IU/wk improved SOL and in-
TST was not different between the 4 treatments (40); how- creased sleep duration (51). However, the mechanisms by
ever, as in previous studies (38, 39), the authors noted fewer which vitamin D may affect sleep are not yet clear.
sleep disturbances after the consumption of Horlicks. The There is also substantial evidence with regard to the influ-
authors also examined habitual dietary habits and divided ence of B vitamins on sleep. A small clinical crossover study
participants into those who usually ate within 1 h of bedtime (52) showed that vitamin B-12 affects plasma melatonin con-
(eaters) and those who did not (noneaters) (40). The noneat- centrations and contributes to the entrainment of the light-dark
ers slept best after consuming the inert capsules, whereas the cycle. Vitamin B-12 was also associated with improvements
eaters slept best after consuming the Horlicks drink, leading in sleep quality and alertness assessed by using visual analog
the authors to conclude that an individual’s dietary habits pri- scales (53). Furthermore, vitamin B-6 serves as a cofactor in
marily influence their sleep response to bedtime foods. This is the synthesis of serotonin from 5-hydroxytryptophan and
supported by others (26), who showed that nocturnal food in- thus indirectly affects the synthesis of melatonin. However,
take negatively influences sleep quality, which may be medi- supplementation of 100 mg vitamin B-6 had no effect on mel-
ated by postprandial discomfort due to reduced digestive atonin secretion or sleep duration and architecture in a study
activity. It is possible that pre-bedtime food consumption, of in 12 healthy men (54).
any kind, in those who typically do not eat before bedtime Higher Trp and melatonin concentrations appear to be
negatively influences sleep. However, in those who eat before mainly responsible for the sleep-promoting effect of night-
bedtime, choosing the right nighttime snack may be impor- time milk. An analysis of milk content in one study revealed
tant in modifying their sleep quality. that nighttime milk contained higher amounts of Trp (4.66 mg/g)
In addition to malted milk, natural melatonin-enriched and melatonin (85.5 pg/g) than daytime milk (3.75 mg/g and
milk, obtained by milking cows at nighttime (nighttime milk) 8.8 pg/g, respectively) (50). Another study used nighttime
as opposed to daytime (daytime milk), is of scientific interest. milk with a melatonin concentration of 10.2–18.3 pg/mL,
A long-term crossover study in 70 elderly patients with demen- with subjects consuming 0.5 L milk/d (41). This amount
tia examined the effect of daily nighttime milk consumption on did not increase the subjects’ blood melatonin concentrations.
sleep quality and circadian activity. The study found no ef- However, the consumption of nighttime milk with a mela-
fect of nighttime milk over 8 wk on sleep quality in patients tonin concentration of 39.43 pg/mL, ;10 times the concen-
when compared with the consumption of normal milk from tration found in daytime milk, was associated with increased
cows milked during the day (41). However, in this study, the circulating melatonin concentrations in rats (55). Thus, it ap-
elderly participants experienced greater morning and even- pears that high milk melatonin concentrations are necessary to
ing physical activity after the consumption of nighttime milk, affect blood concentrations.
which was seen as beneficial. To further corroborate the poten-
tial sleep-inducing effects of nighttime milk, another study Fatty fish. Fatty fish (>5% fat) is a good source of vitamin D
showed that melatonin-enriched milk improved sleep effi- and omega-3 FAs, nutrients important for the regulation of
ciency and reduced the number of awakenings in middle- serotonin and therefore sleep regulation. Hansen et al. (56)
aged adults diagnosed with insomnia (49). Nighttime milk, investigated the effects of fatty fish consumption on sleep
which is abundant in Trp and melatonin, shortens the onset variables in inmates with limited daylight exposure. The fish
and prolongs the duration of sleep in mice (50) and has a sedat- group consumed 300 g Atlantic salmon 3 times/wk for 6 mo,
ing effect. In mice, motor balance and coordination are reduced whereas the control group consumed an equivalent amount
to a level comparable to known sedatives with the administra- of meat (chicken, pork, or beef); however, the portions were
tion of nighttime milk. reduced to 150 g during the last 4 wk of the study. Participants
Clinical trials that examined the influence of malted milk wore wrist actigraphy monitors and kept sleep diaries for 1 wk
and related nutrients on sleep are limited by small study pop- before and during the last week of the intervention. From pre-
ulations and short interventions. The current available evi- to post-test, SOL and actual wake time increased in the control
dence suggests that malted milk promotes less restless sleep group and SE decreased in both the control and fish groups. By

946 St-Onge et al.


the end of the intervention, the men consuming fatty fish dur- In summary, clinical evidence supports the sleep-promoting
ing the study had higher concentrations of vitamin D and n–3 effects of tart cherries and kiwifruit. The consumption of 2 ki-
fatty acids (EPA and DHA) than the control group, which may wifruits 1 h before bedtime appears to enhance the sleep of
partially mediate the reported differences in sleep quality be- individuals with self-reported sleep disorders and may also
tween the groups. Consistent with previous studies (51, 57), promote sleep in healthy individuals, although this has not
vitamin D status was positively correlated with sleep efficiency been confirmed. It is also uncertain if the timing of consump-
and sleep quality. Given that SOL and wake time did not tion plays an important role in determining whether kiwifruit
change in the fish group but rather worsened in the control consumption will enhance sleep. Tart cherries are an additional
group, the conclusion that fatty fish is beneficial for sleep qual- fruit that has been shown to improve sleep quality and increase
ity is not appropriate. It would be more adequate to state that urinary melatonin concentrations. However, the effects of
meat consumption may worsen sleep quality. This, however, cherries on sleep variables appear to be partially mediated by
deserves further exploration. age as well as the cherry cultivar consumed. Clinical evidence
for both cherries and kiwifruit is based on individual studies
Fruit. Other studies have looked at the consumption of fruit and the mentioned observations have yet to be confirmed.
on sleep promotion. The consumption of 2 kiwifruits/d, 1 h The melatonin and phytonutrient profile of tart cherries
before bedtime for 4 wk, significantly increased TST and SE is often associated with their health and sleep benefits. Tart
as measured by sleep actigraphy in adults with self-reported cherries have a high dietary melatonin concentration, and
sleep disorders (46). In addition, sleep diary data showed a the consumption of tart cherry juice has been shown to in-
significant reduction in WASO and SOL compared with crease urinary melatonin concentrations (43). However, this
baseline values. Daily consumption of kiwifruit before bed- remains to be confirmed. Tart cherries have also been shown
time thus appears to be beneficial in increasing TST and SE to exhibit anti-inflammatory characteristics that may be
in adults with sleep disturbances but warrants additional re- beneficial in improving sleep quality. In studies that exam-
search, particularly with studies that include a control food. ined the impact of Montmorency tart cherry juice supplemen-
More recent studies have examined the effect of tart tation on exercise-induced inflammation, tart cherry juice
cherries on sleep regulation. The consumption of 8 ounces attenuated circulating inflammatory markers and increased
of tart cherry juice in the morning and nighttime for 2 wk the antioxidant capacity of cyclists and marathon runners
was associated with a significant reduction in insomnia se- (58, 59). Because patients with sleep and psychiatric disorders
verity and WASO in adults with chronic insomnia (43). Ho- exhibit increased levels of oxidative stress (60), the abundance
watson et al. (45) later replicated the study in a population of of antioxidants in cherries may mediate improvements in
young, healthy adults. One week of tart cherry juice supple- sleep quality by minimizing oxidative damage.
mentation increased urinary melatonin concentrations, Although further research into the sleep-promoting
TST, and SE compared with a placebo juice. mechanisms of kiwifruit is needed, several explanations
Other varieties of cherries were also assessed for their ef- for the effects of kiwifruit on sleep exist. Lin et al. (46) hy-
fects on sleep variables (44). Participants consumed 200 g of pothesized that the high antioxidant capacity and serotonin
7 different Jerte Valley cherry cultivars (not including the and folate content of kiwifruit may contribute to the observed
Montmorency cherry) as lunch and dinner desserts for 3 d sleep benefits of kiwifruit consumption. Kiwifruit is a good
each with a 1-wk washout period between cultivars. Com- source of vitamins C and E (46), both of which protect against
pared with baseline values, there was an increase in urinary the damaging effects of free radicals, and is a source of folate.
melatonin, antioxidant capacity, and TST after the consump- Previous studies reported an association between disordered
tion of each of the 7 cherry cultivars in both middle-aged sleep and oxidative stress (60), and folate deficiency has been
and elderly individuals. However, other sleep variables varied linked to insomnia and restless leg syndrome (61). Folic acid
depending on the age group (middle-aged compared with el- supplementation has been shown to alleviate these symptoms
derly) and cherry cultivar consumed. The number of night- (62). The high antioxidant capacity of kiwifruit may also re-
time awakenings decreased significantly after the consumption duce oxidative damage and consequently improve sleep qual-
of the Pico Limón cultivar in the middle-aged group, whereas ity. In addition, kiwifruit is one of the few fruits that has a
the elderly group saw a similar decrease after the consumption high serotonin concentration (63), which may be another pos-
of the Pico Colorado cultivar. In addition, SOL decreased in sible sleep-promoting mechanism of kiwifruit. However, the
both age groups after the consumption of Navalinda cherries authors did not measure any of these biological compounds
and after intake of the Pico Negro cultivar in the elderly group. and therefore the mechanism of action remains unclear. Al-
Although Jerte Valley cherries naturally have higher concentra- though the study did not have a control group and participants
tions of melatonin and Trp (46), it is possible that the melatonin could not be blinded to the intervention, the objective nature
concentrations vary between the different cultivars. Differences of the sleep measurements helps to moderate such biases.
in melatonin concentrations may explain why the consumption
of specific cherry cultivars resulted in sleep improvements in Conclusions
certain age groups and others did not. However, the study did In conclusion, there is evidence to suggest that dietary pat-
not include a control group, and additional studies on Jerte Val- terns that favor HC intakes are associated with reduced SOL
ley cherries are necessary. and SWS and increased REM, whereas HF intakes promote

Food effects on sleep 947


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