Effects of Diet on Sleep Quality

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.

Full text

REVIEW
Effects of Diet on Sleep Quality
1,2
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 describethe role of foodconsumption on sleep. Research has focused on theeffects of mixed meal patterns, such ashigh-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
Because studies have proposed a relation between sleep du-
ration and obesity (1–3), there has been much interest in assess-
ing the impact of sleep on energy intakes. Studies have
shown that short sleepers have higher energy intakes, notably
from fat (4, 5) and snacks (6), than do normal sleepers.
NHANES data in the United States showed that short sleepers,
generally defined as those who sleep <7 h/night, consume a
smaller variety of foods, with lower protein, carbohydrate, fiber,
and fat intakes relative to normal sleepers who report 7–8hof
sleep/night (7). These data are corroborated by clinical inter-
vention studies that also showed greater snack intakes during
periods of sleep restriction relative to habitual sleep in normal
sleepers (8). Fat was also highlighted as a macronutrient of choice
during periods of sleep restriction relative to habitual sleep
(9, 10).
Of note, however, is that epidemiologic studies cannot
address causality or the direction of the relation between
variables. Therefore, although those studies reported a link
between sleep and diet, it is unknown whether it is sleep
that affects dietary intakes or dietary intakes that affect sleep.
In this review, we sought to determine from clinical inter-
vention studies whether, and how, dietary intakes could
influence sleep variables, specifically duration, efficiency, and
architecture. We mainly focus on intervention studies that ex-
amined the effects of diets, meals, or foods on sleep at night,
not daytime napping, but we also report on more general ep-
idemiologic findings of associations between diet and sleep
quality. We did not include studies of single micronutrients
or dietary supplements.
Unlike sleep duration, which is clearly defined by the
amount of sleep one gets at night, sleep quality can be defined
in different ways. By using objective measures of sleep, such
polysomnography, sleep quality can be characterized by the
amount of slow wave sleep (SWS)
3
and rapid eye movement
(REM) sleep one gets at night. These 2 stages of sleep occur
with greater duration as the night progresses (11). SWS is
deep sleep and has a restorative function (12), whereas
both REM and SWS function toward memory consolidation
(11, 13). Of relevance to this review, we have shown that
these stages of sleep were inversely associated with fat and
carbohydrate intakes (14). By using polysomnography and
actigraphy, sleep quality can be defined by sleep efficiency
(SE), or the amount of time in bed spent asleep, as well as
sleep-onset latency (SOL), the amount of time one takes
to fall asleep at night. Low SE (generally <85%) and long
1
Supported in part by Columbia University R56HL119945 (M-PS-O) and New York Obesity
Research Center grant P30DK26687.
2
Author disclosures: M-P St-Onge, A Mikic, and CE Pietrolungo, no conflicts of interest.
*To whom correspondence should be addressed. E-mail: ms2554@cumc.columbia.edu.
3
Abbreviations used: GI, glycemic index; HC, high carbohydrate; HF, high fat; LC, low
carbohydrate; LCNAA, large-chain neutral amino acid; LF, low fat; NREM, nonrapid eye
movement; REM, rapid eye movement; SE, sleep efficiency; SOL, sleep-onset latency; SWS,
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.
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

SOL (>20–30 min depending on age) typically characterize
poor sleep. Finally, subjective measures of sleep quality can
be obtained by questionnaire. Typically, the Pittsburgh Sleep
Quality Index questionnaire is used.
Sleep duration and quality have been associated with obe-
sity, diabetes, hypertension, and cardiovascular disease risk
in cross-sectional and longitudinal studies (11). An excellent
review in this Journal covered some mechanistic explanations
for this association and provides recommendations for nu-
trition professionals with regard to sleep hygiene and its im-
portance in nutrition counseling (11).
Dietary Patterns and Sleep Quality
Epidemiologic findings
Associations between sleep quality and dietary patterns were
recently reported in a cross-sectional study (15) in female
Japanese workers who responded to lifestyle questionnaires.
A high intake of confectionary and noodles was associated
with poor sleep quality, as evidenced by a high global Pitts-
burg Sleep Quality Index score, whereas a high intake of fish
and vegetables was associated with good sleep quality. A sig-
nificant trend toward worse sleep quality with increasing
carbohydrate intake was found. The quality of carbohydrate
seemed to be more important than its quantity in mediating
this association. Poor sleepers with the highest carbohydrate
intake consumed more confectionary and noodles than rice
than did good sleepers with a similarly high carbohydrate in-
take. Moreover, frequent consumption ($1time/mo)of
energy drinks and sugar-sweetened beverages was associ-
ated with poor sleep quality. Other eating patterns indica-
tive of poor dietary habits were also related to sleep quality.
For example, skipping breakfast and eating irregularly were
strongly associated with poor sleep quality. Although relations
between sleep quality and dietary patterns were observed,
the directionality of the findings cannot be established from
this study. Furthermore, poor-quality sleepers were also short
sleepers, thus making sleep duration a likely confounding vari-
able that was not taken into account.
Other epidemiologic studies have found associations be-
tween disordered sleep and diet (16–18). Tanaka et al. (16)
reported a relation between macronutrient intakes and in-
somnia symptoms in a cross-sectional analysis of non–shift
workers who responded to a brief diet history questionnaire.
Low protein intake (<16% of energy from protein) was asso-
ciated with poor quality of sleep and marginally associated
with difficulty initiating sleep, whereas high protein intake
(>19% of energy from protein) was associated with difficulty
maintaining sleep. Low carbohydrate intake (<50% of energy
from carbohydrate) was marginally associated with difficulty
maintaining sleep. When stratified by sex, these associations
were significant in men but not in women.
Similar results were found with respect to the association
between carbohydrate intake and sleep quality in men (17).
Individuals with disordered sleep (insomnia, obstructive
sleep apnea, or a combination of the 2) assessed by question-
naires reported lower total carbohydrate intakes than did
normal-weight individuals who were free from sleep disorders.
Overweight individuals with insomnia also had lower carbo-
hydrate intakes than did healthy overweight counterparts. In
addition, they had higher fat intakes than individuals who
were free from sleep disorders.
The Mediterranean diet was associated with sleep quality
in older adults (18). On the basis of self-reported question-
naires evaluating sleep quality, lifestyle factors, and dietary in-
take, the Mediterranean diet was inversely associated with
insomnia symptoms (difficulty initiating sleep, difficulty main-
taining sleep, early morning awakening) in women but not
in men. Data from the 2007–2008 NHANES showed that
difficulty maintaining sleep was associated with lower food
variety and adhering to a special diet; however, this was no
longer significant after adjusting for covariates (19). Increased
caloric intake was associated with daytime sleepiness.
The epidemiologic studies that reported associations be-
tween dietary patterns and sleep quality are informative. In
general, those studies indicate higher fat intakes with sleep
disorders (17) and that following a Mediterranean dietary
profile is associated with fewer insomnia symptoms in
women (18). Information on the association between carbo-
hydrate intakes and sleep quality is conflicted (15–17), with
studies reporting low intakes in those with insomnia symp-
toms (16, 17) but high intakes of sweets (15). This would
suggest that carbohydrate quality may be important to con-
sider when examining the association between diet and sleep
quality. However, epidemiologic studies are limited by an
unclear direction of the associations and self-reported data.
Clinical trials that investigated the effect of individual macro-
nutrients on sleep architecture are more elucidative.
Experimental findings
High-carbohydrate diet. There is a substantial body of ev-
idence to indicate a role of carbohydrate intake on sleep indexes
(Table 1). Both high-carbohydrate (HC) and low-carbohydrate
(LC) diets are associated with changes in sleep architecture
(20–25). Carbohydrate manipulation has primarily been shown
to affect REM sleep and SWS; however, non-REM (NREM)
sleep, SOL, and REM-onset latency have also been affected.
Phillips et al. (20) showed that HC and LC diets have op-
posite effects on SWS. In this study, healthy men were ran-
domly assigned to consume a controlled diet, either LC plus
high fat [(HF) LC/HF] or HC plus low fat [(LF) HC/LF] for
a period of 2 d after 2 d of a lead-in balanced diet. The LC/
HF and HC/LF diets provided 100 and 600 g carbohydrates
and 255 and 33 g fat, respectively. The lead-in diet contained
350 g carbohydrates and 140 g fat. Diets were designed to
maintain weight and meals were administered at fixed times.
SWS significantly decreased with the HC/LF diet relative to
the LC/HF diet and the lead-in diets. REM sleep significantly
increased with both intervention diets relative to the lead-in
diet, with a significantly greater increase after consumption
of the HC/LF diet. Similarly, stage 1 sleep was reduced with
both diets compared with the lead-in diet.
Yajima et al. (21) found similar changes in SWS after the
consumption of an HC test meal. In a similar fashion, healthy
men underwent a 1-d randomized crossover intervention with
Food effects on sleep 939
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

TABLE 1 Summary of clinical studies that investigated the effect of dietary patterns on sleep architecture
1
Study (ref) Diet pattern Subjects Duration Methods Treatment group results
2
Phillips et al. (20) HC/LF diet vs. LC/HF diet 8 healthy men 4 d Days 1–2: control diet (350 g carbohydrate, 140 g
fat, 75 g protein)
SWS: lower with the HC/LF diet (97.8 min) and
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
fat, 75 g protein) or LC/HF diet (100 g carbo-
hydrate, 225 g fat, 75 g protein)
REM: higher with the HC/LF diet (136.9 min) vs.
the LC/HF (122.1 min) and control (103.6 min)
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 1 d HC test meal: dinner consumed at 2000 (10%
protein, 10% fat, 80% carbohydrate)
SWS: decreased during sleep cycle 1 with the HC
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.
HF vs. HC diets
44 healthy young
adults (19–22 y old)
4 d High-protein diet (56% protein, 22% carbohy-
drate, and 22% fat)
Wake episodes: decreased with the high-protein
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
control diet (13.9 min)HF diet (56% fat, 22% carbohydrate, 22% protein)
Control diet (50% carbohydrate, 35% fat, 15%
protein)
Afaghi et al. (23) High- vs. low-GI 12 healthy men
(18–35 y old)
1 d 767 kcal/meal (8% protein, 1.6% fat, 90.4%
carbohydrate)
SOL: lower with the high-GI diet at 4 h before
bedtime (9.0 66.2 min) vs. both low-GI diet at
4 h before bedtime (17.5 66.2 min) and high-
GI diet at 1 h before bedtime (14.6 69.9 min)
Low-GI diet [Mahatma rice (GI = 50) with meal 4 h
before bedtime]
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
(18–35 y old)
5 d Control phase [3 d of mixed meals (15.5% protein,
12.5% fat, 72% carbohydrate) with 1 evening
mixed test meal
4
]
REM: percentage of TST lower during very LC
acute (17.6% 65.3%) and very LC ketosis
(17.7% 65.4%) phases vs. control (21.4% 66.3%)
Acute phase [night 3: very LC test meal
4
(2400
kcal; 38% protein, 61% fat, ,1% carbohydrate)]
SWS: higher during very LC acute (83.3 633.8
min) and very LC ketosis (80.4 6628.0 min)
phases vs. control (66.2 630.1 min)Ketosis phase (2 d of very LC diet)
Kwan et al. (25) LC 6 healthy young
women (20–23 y old)
2 wk Week 1: weighing and recording habitual diet REM: onset latency increased from 66 68 min to
111 638 minWeek 2: isoenergetic diet of 50-g/d carbohydrate
restriction
St-Onge et al. (9) Controlled vs. ad
libitum food intake
26 healthy adults
(30–45 y old)
1 d Habitual sleep phase: 9 h/night in bed (2200–
0700)
SWS: lower during the ad libitum food intake
period (24.6 612.8 min) than during con-
trolled intake period (29.3 613.9 min)
Test day: ad libitum food intake SOL: higher during the ad libitum food intake
period (29.2 623.1 min) than during con-
trolled intake period (16.9 611.1 min)
(Continued)
940 St-Onge et al.
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

TABLE 1 (Continued )
Study (ref) Diet pattern Subjects Duration Methods Treatment group results
2
Crispim et al. (26)
3
Ad libitum food intake 52 healthy adults
(19–45 y old)
3 d Test days: ad libitum food intake recorded by
using food diary
Men:
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.
evening fast vs.
control meal
7 healthy men
(20–24 y old)
1 d Fast: evening fast beginning at 1300; maximum
energy intake of 38 kcal consumed as fruit juice
and water
No effect of evening fast (10 h) or high-energy
evening meal on sleep architecture
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
adults
2 d All diets composed of hydrocolloid gels No effects of 2-d calorie deprivation on sleep
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
(22–25 y old)
3 d Day 1: normal food intake with dinner meal as the
last meal before fast
REM: lower number of REM episodes (3.49 60.9
vs. 4.4 60.5 episodes) and higher percentage
of stage 4 REM sleep (15% 67% vs. 11% 6
6%) on day 3 vs. day 1; higher percentage of
stage 4 REM sleep (15% 67% vs. 10% 67%)
and lower percentage of stage 2 REM sleep
(49% 69% vs. 53% 67%) on day 3 vs. day 2
Days 2–3: fasting days (no food intake)
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
Test meals 4 h before bedtime.
Food effects on sleep 941
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

either an HC or an HF evening test meal to investigate their
effects on sleep architecture. Participants were prescribed ei-
ther an HF (78% fat, 10% protein, 12% carbohydrate) or an
HC (10% protein, 10% fat, 80% carbohydrate) test meal to
be eaten at 2000. Breakfast and lunch on the test day were
the same for each intervention and provided 13–15% protein,
19–24% fat, and 60–63% carbohydrate. SWS decreased within
the first sleep cycle after the HC meal compared with the HF
meal. However, there was no difference in sleep architecture
between interventions over the entire sleep period. The au-
thors suggested that the reduction in SWS observed during
the first sleep cycle was related to the degree of carbohydrate
oxidation. Carbohydrate oxidation was higher after the HC
meal than after the HF meal, especially during the first half
of the sleep episode when SWS was markedly reduced with
the HC meal. In addition, they showed that carbohydrate ox-
idation was highest during REM sleep and lowest during SWS
(21), possibly indicating a greater reliance on carbohydrate for
energy during REM sleep. However, this study was limited by
the absence of a control (balanced) meal. Because of this, it is
not possible to determine whether SWS was, in fact, increased
with the HF meal or whether it was reduced with the HC meal.
Moreover, the clinical significance of a change in sleep architec-
ture in one sleep cycle, but not over the entire night, is unknown.
Another study (30) investigated the effects of a pre-bedtime
test meal on sleep architecture in men. Participants underwent
a 3-night intervention consisting of an HC, an LC, or a zero-
carbohydrate snack administered 45 min before bedtime. The
HC snack consisted of a glucose drink and fried potatoes (521
kcal or 130 g carbohydrate) and the LC snack consisted of
crispbread, salad, and butter (188 kcal or 47 g carbohy-
drate). Both the HC and LC snacks were similar in protein
and fat content but differed in carbohydrate content. The
carbohydrate-free snack consisted of a methyl-cellulose sup-
plement and contained no energy. Participants were allowed
8.5 h of sleep/night. NREM sleep decreased and the number
of REM periods increased during the HC relative to the no-
carbohydrate treatment over the entire sleep period. SWS de-
creased during the carbohydrate-free treatment relative to the
LC treatment over the entire sleep period. During only the first
half of the sleep period, REM sleep and stage 3 sleep increased
during the HC treatment. Persistent effects were observed on re-
covery nights after the 3-d intervention period. During the post-
HC conditions, stage 4 sleep decreased and the number of REM
periods increased relative to the other 2 treatments, whereas
stage 3 sleep increased relative to the no-carbohydrate condition
over the entire sleep period. REM latency increased after the LC
relative to the HC conditions over the entire sleep period. Con-
sistent with the findings of Phillips et al. (20), most of the
changes in sleep architecture occurred during the HC condition,
with a trend toward higher REM sleep and lower NREM sleep,
with the exception of stage 3 sleep. Although the direct mecha-
nisms mediating these changes are unclear, the authors pro-
posed that the effect of the HC condition on changes in sleep
stages is related to increased serotonin synthesis.
Lindseth et al. (22) investigated the effect of individual
macronutrients on sleep indexes in adults with the use of
a controlled-feeding crossover study design. The dietary in-
terventions included a high-protein diet (56% of energy
from protein, 22% from carbohydrate, and 22% from fat),
an HC diet (56% of energy from carbohydrate, 22% from
protein, and 22% from fat), an HF diet (56% of energy from
fat, 22% from carbohydrate, and 22% from protein), and a
control diet (50% of energy from carbohydrate, 35% from
fat, and 15% from protein) that were each consumed for 4 d.
Sleep was monitored continuously throughout each 4-d in-
tervention period by using actigraphy. A significant effect of
diet on the number of wake episodes and SOL was observed.
The consumption of the high-protein diet decreased the
number of wake episodes compared with the control diet,
and SOL was significantly lower after the HC diet than after
the control diet.
Glycemic index. The glycemic index (GI) of carbohydrates
has also been studied as a dietary factor related to sleep ar-
chitecture. Afaghi et al. (23) investigated the effects of both
GI and meal timing on sleep architecture in men. Sleep was
measured on 3 separate test nights, which differed in the glyce-
mic index of the pre-bedtime meal: either a low-GI (GI = 50)
or a high-GI (GI = 109) meal was consumed 4 h before bed-
time or a high-GI meal was consumed 1 h before bedtime.
SOL was significantly lower after the high-GI meal consumed
4 h before bedtime than after both the low-GI meal and the
high-GI meal consumed 1 h before bedtime. Consistent with
these findings, subjective ratings of sleepiness were significantly
higher after the high-GI meal ingested 4 h before bedtime.
LC diet. Afaghi et al. (24) also investigated the effects of a
very LC diet on sleep architecture in men. The intervention
consisted of a familiarization phase with 1 evening control
test meal for 3 d, an acute intervention phase (1 meal), and
a longer-term ketosis phase of 2 d. The familiarization phase
consisted of mixed, balanced meals (15% of energy from pro-
tein, 25% from fat, and 60% from carbohydrate) provided on
day 1 and for breakfast and lunch on day 2. The control test
meal, altered to resemble an HC/LF diet (15.5% of energy
from protein, 12.5% from fat, 72% from carbohydrate), was
administered on the evening of day 2. The acute phase took
place on the third night, after consuming the familiarization
diet for breakfast and lunch. The acute phase consisted of
an evening test meal (38% of energy from protein, 61%
from fat, <1% from carbohydrate). The ketosis phase was
followed over the next 2 d with maintenance of the very
LC diet. Each participant was maintained on 2400 kcal/d
for the 5-d intervention period, and test meals were admin-
istered 4 h before bedtime. Participants were permitted to
sleep at their discretion, and sleep was recorded by using
polysomnography. REM sleep was reduced and SWS was in-
creased during both the acute and ketosis phases relative to
the control phase. The arousal index was significantly in-
creased during sleep stages 1 and 2 after the very LC acute
and ketosis phases compared with after the control phase.
In addition, there was a trend toward improved SE after
the acute phase (P= 0.08) but not after the ketosis phase.
942 St-Onge et al.
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

In another study, Kwan et al. (25) investigated the effect of an
LC diet, 50 g/d for 1 wk, on sleep architecture in women.
REM-onset latency increased after the LC diet relative to the
prestudy habitual diet.
Mixed meals. The effect of various macronutrient intakes
on sleep architecture was assessed by St-Onge et al. (9). Par-
ticipants consumed a fixed diet that provided 31% of energy
from fat, 53% from carbohydrate, and 17% from protein for
4 d. On day 5, participants self-selected their food intake. On
that night, SWS was lower and SOL was longer than sleep
measured after the fixed diet. Higher fiber intakes on the
ad libitum day were associated with more SWS and less
time spent in stage 1 sleep. A higher percentage of energy
consumed from saturated fat was associated with less time
spent in SWS. In addition, greater sugar and nonsugar, non-
fiber carbohydrate intakes were associated with more wake
bouts during the sleep episode. These associations indicate
that higher saturated fat and lower fiber intakes may pro-
duce less SWS, more nighttime arousals, and a reduction
in overall sleep quality.
Crispim et al. (26) similarly investigated the effects of ad
libitum food intake on sleep architecture. Over 3 nonconsec-
utive days, subjects recorded their food intake in a food diary
and reported to the sleep laboratory for polysomnography.
Nocturnal food intake (30–60 min before bedtime), but not
total daily intake, was correlated with several sleep variables
and differed by sex. In men, stage 2 sleep, REM sleep latency,
SOL, and wake after sleep onset (WASO) were positively cor-
related with fat intake at night. In addition, fat intake at
night was negatively correlated with SE and REM in men.
In women, positive associations for evening intake included
the following: SOL and energy, protein, carbohydrate, and
fat intakes; REM sleep latency and energy, carbohydrate,
and fat intakes; stage 2 sleep and energy, carbohydrate,
and fat intakes; and WASO and energy and fat intakes. Neg-
ative associations for evening intake included REM sleep and
fat intake and SE and energy, carbohydrate, and fat intakes
in women. Overall, the results of this study confirmed that
diet quality, particularly closer to bedtime, influences sleep
architecture. Nocturnal eating, considered in this study to
be any food intake 30–60 min before bedtime, was shown
to negatively influence sleep quality, with a greater effect
inwomenthaninmen(26).Thiseffectwasproposedby
the authors to be mediated by postprandial physical dis-
comfort and reduced digestive activity; however, this was
not confirmed.
The studies to date point to an effect of carbohydrate in-
take on sleep, albeit with mixed results. Some found reduced
SOL with the consumption of a higher carbohydrate diet
(22, 23) but others reported a trend for greater SE after an
acute intake of a very LC meal (24). The findings from these
studies support the idea that dietary carbohydrate intake or
pre-bedtime meal also influence sleep architecture, particu-
larly REM and SWS. The consumption of an LC diet appears
to reduce REM sleep while increasing SWS (20, 24), with the
consumption of an HC diet having the opposite effect. The
effects of an HC diet on REM and SWS have been linked to
fuel utilization during the different sleep stages (21). Noctur-
nal energy metabolism has been shown to differ between the
different sleep stages (31). Energy expenditure and fat oxida-
tion decline in the first4hofthesleepperiodandsubse-
quently remain stable for the following 4 h of the night in
healthy men. Carbohydrate oxidation was higher during REM
sleep than in NREM sleep and highest in the last hour of
the sleep episode before waking. The difference in carbohy-
drate oxidation between sleep stages was greatest between
sleep stages 3 and 4 and REM sleep, indicating a higher en-
ergy demand for REM sleep. Therefore, an HC meal or diet
could enhance nocturnal carbohydrate utilization and pro-
mote REM sleep.
Although it cannot be confirmed, it has been hypothe-
sized that carbohydrate oxidation also suppresses SWS (21,
31), which would support the findings of reciprocal changes
in REM and SWS due to carbohydrate manipulation (20, 24).
It was previously reported that an HC diet reduces growth
hormone secretion in men, but not in women, after a 10-d
dietary intervention (32). Because growth hormone has been
linkedtoSWS(20,24),itispossiblethatareductioninSWS
with an HC diet may be mediated by a diet-induced reduc-
tion in growth hormone secretion. However, additional re-
search is warranted to confirm this hypothesis.
The effect of an HC diet on SOL has been linked to ele-
vated postprandial insulin and Trp response (23). Trp, a pre-
cursor of serotonin (23), enters the brain in a competitive
manner with large-chain neutral amino acids (LCNAAs)
(33). An HC diet, low in protein, has been shown in animal
models to elevate brain Trp concentrations relative to
higher-protein diets (33). When the concentration of Trp
is higher than that of LCNAAs, its entry into the brain is fa-
vored and serotonin production is upregulated (34, 35),
which would promote sleep (24). Because the Trp-to-LCNAA
ratio is affected by dietary carbohydrate intake (33, 36), it is
possible that changes in sleep architecture as a result of carbo-
hydrate manipulation are mediated by the Trp-to-LCNAA
ratio. An HC diet or meal would increase the Trp-to-LCNAA
ratio and promote sleep through increased serotonin pro-
duction (33, 34). Conversely, an LC diet would result in a
low ratio of Trp to LCNAA, thus limiting serotonin produc-
tion and prolonging SOL (25). With the consumption of an
HC diet, the resulting higher postprandial insulin enhances
the Trp-to-LCNAA ratio by facilitating uptake of LCNAA by
muscle, further promoting Trp entry into the brain and en-
abling serotonin production (23). In support of this, a correla-
tion between plasma glucose and insulin, and peak Trp:LCNAA
has been reported (36). Therefore, an HC diet, especially one
with a high GI, would promote a higher Trp-to-LCNAA ra-
tio and have a greater serotonergic effect (36). Moreover, it
has been reported that the Trp-to-LCNAA ratio peaks be-
tween 2 and 4 h after the ingestion of an HC meal (36),
which likely accounts for shorter SOL after the consumption
of an HC or high-GI meal 4 h compared with 1 h before bed-
time (23). This proposed mechanism must be explored further,
however, because the Trp-to-LCNAA ratio was not measured
Food effects on sleep 943
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

in the studies reported in the current review. However, urine 6-
sulfatoxymelatonin, a metabolite of melatonin, was highest af-
ter the consumption of the high-GI meals (23). This finding
may also be related to the plasma concentration of Trp (23).
Therefore, an increase in plasma Trp after a high-GI meal
may influence both melatonin and serotonin, thus promoting
sleep onset. However, subsequent sleep quality, such as duration
of SWS and arousals during sleep, may be adversely affected
by HC intakes, particularly of simple sugars.
The fat content of the meal has been suggested to mediate
the observed changes in REM and SWS (24) due to an LC diet.
This effect may be mediated through the postprandial release
of cholecystokinin, a satiety hormone released by the duode-
num after an HF meal (24). The role of cholecystokinin in me-
diating changes in sleep architecture in humans has not yet been
defined; however, an animal study showed that injection of cho-
lecystokinin into rats promoted SWS and NREM sleep (37). In
humans, both subjective ratings of fatigue and cholecystokinin
concentrations were significantly higher after an HF/LC meal
than after an LF/HC meal in 18 healthy adults (25). Further-
more, cholecystokinin was reported to be predictive of and pos-
itively correlated with fatigue (25). Although clinical trials directly
investigating the effect of cholecystokinin concentrations on
sleep architecture are lacking, the association between cholecys-
tokinin and fatigue in response to an HF/LC meal suggests that
sleep architecture may be mediated by this satiety hormone.
Calorie Restriction and Sleep Quality: Experi-
mental Findings
In a study by Driver et al. (27), the effect of short-term (10 h)
calorie restriction on sleep indexes was investigated. Partic-
ipants consumed food ad libitum until 1300 when they
reported to the laboratory. A test meal was provided at
2100. The test meals consisted of no meal, a control meal,
or a high-energy meal. The fast (no meal) allowed only the
consumption of fruit juice and water, with a maximum energy
intake of ;38kcal.Thecontrolmealhadamacronutrientra-
tio of 13:26:61 for fat:protein:carbohydrate and provided ;1370
kcal, whereas the high-energy meal had a ratio of 37:21:42 with
double the energy content, resembling a higher-fat meal. Bed-
time was set between 2250 and 2306, and sleep was monitored
by polysomnography. The authors found no effect of diet on
sleep variables.
Another study investigated the effects of 2.5 d of calorie
deprivation on sleep, cognition, activity, and blood glucose
concentrations (28). Participants underwent 3 test periods:
near-complete fasting, carbohydrate only, and carbohydrate+fat
diets. Diets were composed exclusively of hydrocolloid gels
to maintain blinding. The carbohydrate diet (940 kcal/meal) con-
sisted of a starch and maltodextrin gel; the carbohydrate+fat
diet (940 kcal/meal) consisted of starch, maltodextrin, and
polyunsaturated lipid gel; and the calorie-deprivation diet
(61 kcal/meal) consisted of an artificial sweetener and artifi-
cial flavor gel. There was no effect of dietary intervention
on sleep variables or other outcome measures.
The short duration of the above studies suggests that pro-
longed calorie restriction may be required to influence sleep
architecture. In fact, prolonged fasting (60–67 h) decreased
the number of REM episodes but increased the percentage of
REM sleep compared with baseline (29). A comparison of
fasting periods of 30–37 h and 60–67 h showed an increase
in the percentage of stage 4 REM sleep with a compensatory
decrease in stage 2 REM sleep.
Although Karacan et al. (29) were the only authors, to
our knowledge, to report an effect of calorie restriction on
sleep variables, it is surprising that there was no effect of
the other dietary interventions (27, 28). In the study per-
formed by Driver et al. (27), neither the control meal nor
the high-energy meal resulted in the acute changes in sleep
architecture that had been previously shown (23). Similarly,
the study by Lieberman et al. (28) failed to show an effect of
the carbohydrate or carbohydrate+fat gel preparations on
sleep. It is possible that a longer adaptation period to the di-
etary interventions is required for changes in sleep variables
to be observed, although acute changes in sleep have been
reported after one evening test meal (23). Overall, it is rea-
sonable to suggest that calorie restriction influences sleep
architecture over longer durations; nevertheless, research is
limited on this topic and further investigation is warranted.
Sleep-Promoting Foods and Sleep Quality:
Experimental Findings
Despite the availability of anecdotal evidence, scientificre-
search on the effects of various foods on sleep enhancement
is limited (Table 2). Daily incorporation of sleep-promoting
foods, such as milk, fatty fish, cherries, and kiwifruit, has
been studied for their potential benefits for immediate and
acute sleep improvement without large changes in dietary
patterns.
Milk. The first studies to examine the sleep-inducing effects
of a specific food date to the 1970s, when Horlicks, a malted
milk drink, was tested. Southwell et al. (38) used time-lapse
cinematography to record sleep movements after the con-
sumption of 350 mL warm water, 350 mL warm milk with
5 teaspoons Horlicks powder, or no beverage (control). Par-
ticipants with no history of sleep disorders consumed the
drink ;30 min before bedtime, which was fixed at mid-
night. The authors reported fewer small movements during
sleep after consumption of the Horlicks drink, particularly
from 0400 to 0700, than after consumption of water and
the control. In support of these findings, another study
(39) also found that young adults experienced fewer move-
ments during sleep in the latter half of the night after the
consumption of a Horlicks drink 30 min before bedtime.
The study used polysomnography recordings to assess the
sleep quality of healthy young and middle-aged adults after
the consumption of Horlicks relative to an inert capsule.
Compared with the younger participants, the older adults ex-
perienced increased total sleep time (TST) and greater sleep
continuity after the consumption of Horlicks.
The effect of Horlicks on sleep quality and duration ap-
pears to be partially mediated by age. Aging is associated
with a decline in nighttime sleep quality (47) as well as with
944 St-Onge et al.
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

TABLE 2 Summary of clinical studies that assessed effects of food on sleep quality
1
Study (ref) Food Subjects Methods Treatment group results
2
Southwell et al. (38) MM, Horlicks 4 healthy men No drink (control), 350 mL warm water, or 350 mL
MM drink 30 min before bedtime
Less movement after MM (412 frames of movements) vs.
control (500 frames of movements)
Brezinová et al. (39) MM, Horlicks Group 1: 10 subjects (4 women),
aged 20–30 y
MM drink (32 g Horlicks powder + 250 mL hot
milk) or inert capsule (control) at night for 10 d,
30 min before bedtime
Group 1:
Group 2: 8 subjects (5 women),
aged 42–66 y
Wake episodes: decreased (11.6 times) vs. control
(14.5 times) in the seventh hour of sleep
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
powder + hot milk), flavored drink (devoid of
milk and cereal), or milk alone at night for 5 d
TST: higher in those who habitually eat before bedtime
after MM (463.8 min) and milk alone (471.2 min) vs.
control (452.0 min)
Valtonen et al. (41) Melatonin-enriched milk 70 elderly subjects with a chronic
illness
17 oz melatonin-enriched milk for 8 wk Increased morning and evening physical activity (within
groups)
Yamamura et al. (42) Fermented milk, Lactobacillus
helveticus
29 subjects, aged 60–81 y 100 g fermented milk or artificially acidified milk
(control) 1 time/d at any time for 3 wk
SE: higher after intervention (91.18% 61.08%) vs. control
(91.37% 60.98%)
Wake episodes: decreased after intervention (8.31 60.62
times) vs. control (8.85 60.75 times)
Pigeon et al. (43) TCJ, Montmorency 15 subjects (7 women), aged .65 y,
with insomnia
8 oz TCJ or cherry-flavored drink (control) for 2 wk
in morning and evening
ISI: lower after TCJ (13.2 62.8) vs. control (14.9 63.6)
WASO: lower after TCJ (62.1 637.4 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;
E group: 6 subjects, aged 65–85 y
200 g cherries for 3 d as lunch and dinner desserts
(no control)
TST: increased after consumption of 6 of the 7 cultivars in
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- 60.02-fold in Van cultivar in M group
SOL: decreased 0.54- 60.10-fold with consumption of
Navalinda cultivar in M group and 0.51- 60.07-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
within 30 min of awakening and 30 min before
the evening meal
TIB: higher after TCJ (514.7 617.0 min) vs. control (492.2 6
40.6 min)
TST: higher after TCJ (419 622 min) vs. control (380 6
49 min)
SE: higher after TCJ (86.8 63.6%) 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
control)
TST: higher with kiwifruit intake (395.3 617.4 min) vs.
control (354.5 617.1 min)
SE: higher with kiwifruit intake (91.2 61.53%) vs. control
(86.9 61.94%)
WASO: lower with kiwifruit intake (12.8 63.49 min) vs.
control (18.9 64.31 min)
SOL: lower with kiwifruit intake (20.4 63.53 min) vs.
control (34.3 63.86 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
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

changes in the circadian regulation of the sleep-wake cycle
(48). It has been suggested that the age-related changes in sleep
are partly due to a decrease in circadian amplitude (47). It has
also long been known that endogenous melatonin production
declines with increasing age (48). This may offer an explana-
tion as to why the effects of Horlicks are more effective after
serial administration in older adults but not in younger adults.
In an effort to distinguish the sleep-enhancing factors of
the Horlicks drink, one study (40) compared the consump-
tion of Horlicks to inert capsules, milk alone, and a flavored
drink with energy and macronutrient contents similar to
Horlicks. Of note, the participants in this study (40) were
older than those in the other Horlicks studies: 52–67 y old
compared with 20–66 y old for the other studies (38, 39).
TST was not different between the 4 treatments (40); how-
ever, as in previous studies (38, 39), the authors noted fewer
sleep disturbances after the consumption of Horlicks. The
authors also examined habitual dietary habits and divided
participants into those who usually ate within 1 h of bedtime
(eaters) and those who did not (noneaters) (40). The noneat-
ers slept best after consuming the inert capsules, whereas the
eaters slept best after consuming the Horlicks drink, leading
the authors to conclude that an individual’s dietary habits pri-
marily influence their sleep response to bedtime foods. This is
supported by others (26), who showed that nocturnal food in-
take negatively influences sleep quality, which may be medi-
ated by postprandial discomfort due to reduced digestive
activity. It is possible that pre-bedtime food consumption, of
any kind, in those who typically do not eat before bedtime
negatively influences sleep. However, in those who eat before
bedtime, choosing the right nighttime snack may be impor-
tant in modifying their sleep quality.
In addition to malted milk, natural melatonin-enriched
milk, obtained by milking cows at nighttime (nighttime milk)
as opposed to daytime (daytime milk), is of scientific interest.
A long-term crossover study in 70 elderly patients with demen-
tia examined the effect of daily nighttime milk consumption on
sleep quality and circadian activity. The study found no ef-
fect of nighttime milk over 8 wk on sleep quality in patients
when compared with the consumption of normal milk from
cows milked during the day (41). However, in this study, the
elderly participants experienced greater morning and even-
ing physical activity after the consumption of nighttime milk,
which was seen as beneficial. To further corroborate the poten-
tial sleep-inducing effects of nighttime milk, another study
showed that melatonin-enriched milk improved sleep effi-
ciency and reduced the number of awakenings in middle-
aged adults diagnosed with insomnia (49). Nighttime milk,
which is abundant in Trp and melatonin, shortens the onset
and prolongs the duration of sleep in mice (50) and has a sedat-
ing effect. In mice, motor balance and coordination are reduced
to a level comparable to known sedatives with the administra-
tion of nighttime milk.
Clinical trials that examined the influence of malted milk
and related nutrients on sleep are limited by small study pop-
ulations and short interventions. The current available evi-
dencesuggeststhatmaltedmilkpromoteslessrestlesssleep
in both young and old populations, although the mechanisms
remain unclear. However, studies indicate that the timing of
consumption may play an additional role as to whether the
consumption of a malted milk beverage before bedtime en-
hances sleep. More research with the use of objective measure-
ments is necessary to confirm these findings.
There are several mechanisms by which malted milk may
affect sleep quality. Horlicks is composed of wheat, malt bar-
ley, sugar, milk, and 14 vitamins and minerals, including
vitamin D and several B-group vitamins. Emerging clinical
evidence supports the association between vitamin and min-
eral deficiencies and disrupted sleep. In individuals with low
serum concentrations, 3 mo of vitamin D supplementation
of either 1200 IU/d or 50,000 IU/wk improved SOL and in-
creased sleep duration (51). However, the mechanisms by
which vitamin D may affect sleep are not yet clear.
There is also substantial evidence with regard to the influ-
ence of B vitamins on sleep. A small clinical crossover study
(52) showed that vitamin B-12 affects plasma melatonin con-
centrations and contributes to the entrainment of the light-dark
cycle. Vitamin B-12 was also associated with improvements
in sleep quality and alertness assessed by using visual analog
scales (53). Furthermore, vitamin B-6 serves as a cofactor in
the synthesis of serotonin from 5-hydroxytryptophan and
thus indirectly affects the synthesis of melatonin. However,
supplementation of 100 mg vitamin B-6 had no effect on mel-
atonin secretion or sleep duration and architecture in a study
in 12 healthy men (54).
Higher Trp and melatonin concentrations appear to be
mainly responsible for the sleep-promoting effect of night-
time milk. An analysis of milk content in one study revealed
that nighttime milk contained higher amounts of Trp (4.66 mg/g)
and melatonin (85.5 pg/g) than daytime milk (3.75 mg/g and
8.8 pg/g, respectively) (50). Another study used nighttime
milk with a melatonin concentration of 10.2–18.3 pg/mL,
with subjects consuming 0.5 L milk/d (41). This amount
did not increase the subjects’blood melatonin concentrations.
However, the consumption of nighttime milk with a mela-
tonin concentration of 39.43 pg/mL, ;10 times the concen-
tration found in daytime milk, was associated with increased
circulating melatonin concentrations in rats (55). Thus, it ap-
pears that high milk melatonin concentrations are necessary to
affect blood concentrations.
Fatty fish. Fatty fish (>5% fat) is a good source of vitamin D
and omega-3 FAs, nutrients important for the regulation of
serotonin and therefore sleep regulation. Hansen et al. (56)
investigated the effects of fatty fish consumption on sleep
variables in inmates with limited daylight exposure. The fish
group consumed 300 g Atlantic salmon 3 times/wk for 6 mo,
whereas the control group consumed an equivalent amount
of meat (chicken, pork, or beef); however, the portions were
reducedto150gduringthelast4wkofthestudy.Participants
wore wrist actigraphy monitors and kept sleep diaries for 1 wk
before and during the last week of the intervention. From pre-
to post-test, SOL and actual wake time increased in the control
groupandSEdecreasedinboththecontrolandfishgroups.By
946 St-Onge et al.
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

the end of the intervention, the men consuming fatty fish dur-
ing the study had higher concentrations of vitamin D and n–3
fatty acids (EPA and DHA) than the control group, which may
partially mediate the reported differences in sleep quality be-
tween the groups. Consistent with previous studies (51, 57),
vitamin D status was positively correlated with sleep efficiency
and sleep quality. Given that SOL and wake time did not
change in the fish group but rather worsened in the control
group, the conclusion that fatty fish is beneficial for sleep qual-
ity is not appropriate. It would be more adequate to state that
meat consumption may worsen sleep quality. This, however,
deserves further exploration.
Fruit. Other studies have looked at the consumption of fruit
on sleep promotion. The consumption of 2 kiwifruits/d, 1 h
before bedtime for 4 wk, significantly increased TST and SE
as measured by sleep actigraphy in adults with self-reported
sleep disorders (46). In addition, sleep diary data showed a
significant reduction in WASO and SOL compared with
baseline values. Daily consumption of kiwifruit before bed-
time thus appears to be beneficial in increasing TST and SE
in adults with sleep disturbances but warrants additional re-
search, particularly with studies that include a control food.
More recent studies have examined the effect of tart
cherries on sleep regulation. The consumption of 8 ounces
of tart cherry juice in the morning and nighttime for 2 wk
was associated with a significant reduction in insomnia se-
verity and WASO in adults with chronic insomnia (43). Ho-
watson et al. (45) later replicated the study in a population of
young, healthy adults. One week of tart cherry juice supple-
mentation increased urinary melatonin concentrations,
TST, and SE compared with a placebo juice.
Other varieties of cherries were also assessed for their ef-
fects on sleep variables (44). Participants consumed 200 g of
7 different Jerte Valley cherry cultivars (not including the
Montmorency cherry) as lunch and dinner desserts for 3 d
each with a 1-wk washout period between cultivars. Com-
pared with baseline values, there was an increase in urinary
melatonin, antioxidant capacity, and TST after the consump-
tion of each of the 7 cherry cultivars in both middle-aged
and elderly individuals. However, other sleep variables varied
depending on the age group (middle-aged compared with el-
derly) and cherry cultivar consumed. The number of night-
time awakenings decreased significantly after the consumption
of the Pico Limón cultivar in the middle-aged group, whereas
the elderly group saw a similar decrease after the consumption
of the Pico Colorado cultivar. In addition, SOL decreased in
both age groups after the consumption of Navalinda cherries
and after intake of the Pico Negro cultivar in the elderly group.
Although Jerte Valley cherries naturally have higher concentra-
tions of melatonin and Trp (46), it is possible that the melatonin
concentrations vary between the different cultivars. Differences
in melatonin concentrations may explain why the consumption
of specific cherry cultivars resulted in sleep improvements in
certain age groups and others did not. However, the study did
not include a control group, and additional studies on Jerte Val-
ley cherries are necessary.
In summary, clinical evidence supports the sleep-promoting
effects of tart cherries and kiwifruit. The consumption of 2 ki-
wifruits 1 h before bedtime appears to enhance the sleep of
individuals with self-reported sleep disorders and may also
promote sleep in healthy individuals, although this has not
been confirmed. It is also uncertain if the timing of consump-
tionplaysanimportantroleindeterminingwhetherkiwifruit
consumption will enhance sleep. Tart cherries are an additional
fruit that has been shown to improve sleep quality and increase
urinary melatonin concentrations. However, the effects of
cherries on sleep variables appear to be partially mediated by
age as well as the cherry cultivar consumed. Clinical evidence
for both cherries and kiwifruit is based on individual studies
and the mentioned observations have yet to be confirmed.
The melatonin and phytonutrient profile of tart cherries
is often associated with their health and sleep benefits. Tart
cherries have a high dietary melatonin concentration, and
the consumption of tart cherry juice has been shown to in-
crease urinary melatonin concentrations (43). However, this
remains to be confirmed. Tart cherries have also been shown
to exhibit anti-inflammatory characteristics that may be
beneficial in improving sleep quality. In studies that exam-
ined the impact of Montmorency tart cherry juice supplemen-
tation on exercise-induced inflammation, tart cherry juice
attenuated circulating inflammatory markers and increased
the antioxidant capacity of cyclists and marathon runners
(58, 59). Because patients with sleep and psychiatric disorders
exhibit increased levels of oxidative stress (60), the abundance
of antioxidants in cherries may mediate improvements in
sleep quality by minimizing oxidative damage.
Although further research into the sleep-promoting
mechanisms of kiwifruit is needed, several explanations
for the effects of kiwifruit on sleep exist. Lin et al. (46) hy-
pothesized that the high antioxidant capacity and serotonin
and folate content of kiwifruit may contribute to the observed
sleep benefits of kiwifruit consumption. Kiwifruit is a good
source of vitamins C and E (46), both of which protect against
the damaging effects of free radicals, and is a source of folate.
Previous studies reported an association between disordered
sleep and oxidative stress (60), and folate deficiency has been
linked to insomnia and restless leg syndrome (61). Folic acid
supplementation has been shown to alleviate these symptoms
(62). The high antioxidant capacity of kiwifruit may also re-
duce oxidative damage and consequently improve sleep qual-
ity. In addition, kiwifruit is one of the few fruits that has a
high serotonin concentration (63), which may be another pos-
sible sleep-promoting mechanism of kiwifruit. However, the
authors did not measure any of these biological compounds
and therefore the mechanism of action remains unclear. Al-
though the study did not have a control group and participants
could not be blinded to the intervention, the objective nature
of the sleep measurements helps to moderate such biases.
Conclusions
In conclusion, there is evidence to suggest that dietary pat-
terns that favor HC intakes are associated with reduced SOL
and SWS and increased REM, whereas HF intakes promote
Food effects on sleep 947
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

lower SE and REM and higher SWS and arousals. However,
longer-term effects have not been examined in randomized
controlled studies. Some foods, such as milk products, fish,
fruit, and vegetables, also show sleep-promoting effects, but
studies have been too diverse, short, and small to lead to
firm conclusions. This review thus finds that some dietary
patterns and foods show promise as sleep modulators, but
more research is necessary to draw definitive conclusions.
Future studies should include a larger sample size, including
both men and women, and focus on individuals with sleep
disorders. In addition, studies should test whether the timing
of the intake of specific foods is important in modulating sleep
at night and in determining the most appropriate dose. Finally,
it is unknown at this time if an overall diet approach, rather
than inclusion or exclusion of specific foods, can improve
sleep and, if it does, within what time frame benefits should
be observed. Nevertheless, as nutrition professionals, it is im-
portant to educate patients on the role of sleep on dietary in-
takes and health but also to initiate discussions about how diet
could be modified to improve sleep quality. It is comforting to
note that the findings reported herein are in line with other di-
etary recommendations for health in the general population:
increasing fruit and vegetable intakes, choosing whole grains
(higher in fiber), and favoring vegetable oils (low in saturated
fat) (64).
Acknowledgments
M-PS-O, AM, and CEP designed and conducted the litera-
ture search and wrote the manuscript; and M-PS-O had pri-
mary responsibility for the final content. All authors read
and approved the final manuscript.
References
1. Patel SR. Reduced sleep as an obesity risk factor. Obes Rev 2009;10
(Suppl 2):61–8.
2. Patel SR, Hu FB. Short sleep duration and weight gain: a systematic re-
view. Obesity (Silver Spring) 2008;16:643–53.
3. Keith SW, Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC,
Benca RM, Ruden D, Pietrobelli A, Barger JL, Fontaine KR, et al. Pu-
tative contributors to the secular increase in obesity: exploring the
roads less traveled. Int J Obes (Lond) 2006;30:1585–94.
4. Weiss A, Xu F, Storfer-Isser A, Thomas A, Ievers-Landis CE, Redline S.
The association of sleep duration with adolescents’fat and carbohy-
drate consumption. Sleep 2010;33:1201–9.
5. Imaki M, Hatanaka Y, Ogawa Y, Yoshida Y, Tanada S. An epidemiolog-
ical study on relationship between the hours of sleep and life style fac-
tors in Japanese factory workers. J Physiol Anthropol Appl Human Sci
2002;21:115–20.
6. Grandner MA, Kripke DF, Naidoo N, Langer RD. Relationships among
dietary nutrients and subjective sleep, objective sleep, and napping in
women. Sleep Med 2010;11:180–4.
7. Grandner MA, Jackson N, Gerstner JR, Knutson KL. Dietary nutrients
associated with short and long sleep duration: data from a nationally
representative sample. Appetite 2013;64:71–80.
8. Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller DA, Penev
PD. Sleep curtailment is accompanied by increased intake of calories
from snacks. Am J Clin Nutr 2009;89:126–33.
9. St-Onge MP, Roberts AL, Chen J, Kelleman M, O’Keeffe M, RoyChoudhury
A, Jones PJ. Short sleep duration increases energy intakes but does not
change energy expenditure in normal-weight individuals. Am J Clin
Nutr 2011;94:410–6.
10. Schmid SM, Hallschmid M, Jauch-Chara K, Wilms B, Benedict C,
Lehnert H, Born J, Schultes B. Short-term sleep loss decreases physical
activity under free-living conditions but does not increase food intake
under time-deprived laboratory conditions in healthy men. Am J Clin
Nutr 2009;90(6):1476–82.
11. Golem DL, Martin-Biggers JT, Koenings MM, Davis KF, Byrd-Bredbenner
C. An integrative review of sleep for nutrition professionals. Adv Nutr
2014;5:742–59.
12. Dijk DJ. Regulation and functional correlates of slow wave sleep. J Clin
Sleep Med 2009;5(2 Suppl):S6–15.
13. Walker MP. The role of slow wave sleep in memory processing. J Clin
Sleep Med 2009;5(2 Suppl):S20–6.
14. Shechter A, O’Keeffe M, Roberts AL, Zammit GK, RoyChoudhury
A, St-Onge MP. Alterations in sleep architecture in response to ex-
perimental sleep curtailment are associated with signs of positive
energy balance. Am J Physiol Regul Integr Comp Physiol 2012;
303:R883–9.
15. Katagiri R, Asakura K, Kobayashi S, Suga H, Sasaki S. Low intake of
vegetables, high intake of confectionary, and unhealthy eating habits
are associated with poor sleep quality among middle-aged female Jap-
anese workers. J Occup Health 2014;56:359–68.
16. Tanaka E, Yatsuya H, Uemura M, Murata C, Otsuka R, Toyoshima H,
Tamakoshi K, Sasaki S, Kawaguchi L, Aoyama A. Associations of pro-
tein, fat, and carbohydrate intakes with insomnia symptoms among
middle-aged Japanese workers. J Epidemiol 2013;23:132–8.
17. Tan X, Alen M, Cheng SM, Mikkola TM, Tenhunen J, Lyytikainen A,
Wiklund P, Cong F, Saarinen A, Tarkka I, et al. Associations of disor-
dered sleep with body fat distribution, physical activity and diet among
overweight middle-aged men. J Sleep Res 2015;24:414–24.
18. Jaussent I, Dauvilliers Y, Ancelin ML, Dartigues JF, Tavernier B,
Touchon J, Ritchie K, Besset A. Insomnia symptoms in older adults: as-
sociated factors and gender differences. Am J Geriatr Psychiatry 2011;
19:88–97.
19. Grandner MA, Jackson N, Gerstner JR, Knutson KL. Sleep symptoms
associated with intake of specific dietary nutrients. J Sleep Res 2014;
23:22–34.
20. Phillips F, Chen CN, Crisp AH, Koval J, McGuinness B, Kalucy RS,
Kalucy EC, Lacey JH. Isocaloric diet changes and electroencephalo-
graphic sleep. Lancet 1975;2:723–5.
21. Yajima K, Seya T, Iwayama K, Hibi M, Hari S, Nakashima Y, Ogata H,
Omi N, Satoh M, Tokuyama K. Effects of nutrient composition of din-
ner on sleep architecture and energy metabolism during sleep. J Nutr
Sci Vitaminol (Tokyo) 2014;60:114–21.
22. Lindseth G, Lindseth P, Thompson M. Nutritional effects on sleep.
West J Nurs Res 2013;35:497–513.
23. Afaghi A, O’Connor H, Chow CM. High-glycemic-index carbohydrate
meals shorten sleep onset. Am J Clin Nutr 2007;85:426–30.
24. Afaghi A, O’Connor H, Chow CM. Acute effects of the very low carbo-
hydrate diet on sleep indices. Nutr Neurosci 2008;11:146–54.
25. Kwan RM, Thomas S, Mir MA. Effects of a low carbohydrate isoener-
getic diet on sleep behavior and pulmonary functions in healthy female
adult humans. J Nutr 1986;116:2393–402.
26. Crispim CA, Zimberg IZ, dos Reis BG, Diniz RM, Tufik S, de Mello
MT. Relationship between food intake and sleep pattern in healthy in-
dividuals. J Clin Sleep Med 2011;7(6):659–64.
27. Driver HS, Shulman I, Baker FC, Buffenstein R. Energy content of the
evening meal alters nocturnal body temperature but not sleep. Physiol
Behav 1999;68:17–23.
28. Lieberman HR, Caruso CM, Niro PJ, Adam GE, Kellogg MD, Nindl
BC, Kramer FM. A double-blind, placebo-controlled test of 2 d of cal-
orie deprivation: effects on cognition, activity, sleep, and interstitial
glucose concentrations. Am J Clin Nutr 2008;88:667–76.
29. Karacan I, Rosenbloom AL, Londono JH, Salis PJ, Thornby JI, Williams
RL. The effect of acute fasting on sleep and the sleep-growth hormone
response. Psychosomatics 1973;14:33–7.
30. Porter JM, Horne JA. Bed-time food supplements and sleep: effects of
different carbohydrate levels. Electroencephalogr Clin Neurophysiol
1981;51:426–33.
948 St-Onge et al.
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from

31. Katayose Y, Tasaki M, Ogata H, Nakata Y, Tokuyama K, Satoh M. Met-
abolic rate and fuel utilization during sleep assessed by whole-body in-
direct calorimetry. Metabolism 2009;58:920–6.
32. Merimee TJ, Pulkkinen AJ, Burton CE. Diet-induced alterations of
hGH secretion in man. J Clin Endocrinol Metab 1976;42:931–7.
33. Fernstrom JD, Wurtman RJ. Brain serotonin content: physiological reg-
ulation by plasma neutral amino acids. Science 1972;178:414–6.
34. Wurtman RJ, Wurtman JJ, Regan MM, McDermott JM, Tsay RH, Breu
JJ. Effects of normal meals rich in carbohydrates or proteins on plasma
tryptophan and tyrosine ratios. Am J Clin Nutr 2003;77:128–32.
35. Fernstrom JD, Wurtman RJ. Brain serotonin content: physiological de-
pendence on plasma tryptophan levels. Science 1971;173:149–52.
36. Lyons PM, Truswell AS. Serotonin precursor influenced by type of car-
bohydrate meal in healthy adults. Am J Clin Nutr 1988;47:433–9.
37. Kapás L, Obal F Jr., Alfoldi P, Rubicsek G, Penke B, Obal F. Effects of
nocturnal intraperitoneal administration of cholecystokinin in rats:
simultaneous increase in sleep, increase in EEG slow-wave activity,
reduction of motor activity, suppression of eating, and decrease in
brain temperature. Brain Res 1988;438:155–64.
38. Southwell PR, Evans CR, Hunt JN. Effect of a hot milk drink on move-
ments during sleep. BMJ 1972;2:429–31.
39. Brezinová V, Oswald I. Sleep after a bedtime beverage. BMJ 1972;2:
431–3.
40. Adam K. Dietary habits and sleep after bedtime food drinks. Sleep
1980;3:47–58.
41. Valtonen M, Niskanen L, Kangas AP, Koskinen T. Effect of melatonin-
rich night-time milk on sleep and activity in elderly institutionalized
subjects. Nord J Psychiatry 2005;59:217–21.
42. Yamamura S, Morishima H, Kumano-go T, Suganuma N, Matsumoto
H, Adachi H, Sigedo Y, Mikami A, Kai T, Masuyama A, et al. The effect
of Lactobacillus helveticus fermented milk on sleep and health percep-
tion in elderly subjects. Eur J Clin Nutr 2009;63:100–5.
43. Pigeon WR, Carr M, Gorman C, Perlis ML. Effects of a tart cherry juice
beverage on the sleep of older adults with insomnia: a pilot study.
J Med Food 2010;13:579–83.
44. Garrido M, Paredes SD, Cubero J, Lozano M, Toribio-Delgado AF,
Munoz JL, Reiter RJ, Barriga C, Rodriguez AB. Jerte Valley cherry-enriched
diets improve nocturnal rest and increase 6-sulfatoxymelatonin and
total antioxidant capacity in the urine of middle-aged and elderly
humans. J Gerontol A Biol Sci Med Sci 2010;65:909–14.
45. Howatson G, Bell PG, Tallent J, Middleton B, McHugh MP, Ellis J. Ef-
fect of tart cherry juice (Prunus cerasus) on melatonin levels and en-
hanced sleep quality. Eur J Nutr 2012;51:909–16.
46. Lin HH, Tsai PS, Fang SC, Liu JF. Effect of kiwifruit consumption on
sleep quality in adults with sleep problems. Asia Pac J Clin Nutr
2011;20:169–74.
47. Cajochen C, Munch M, Knoblauch V, Blatter K, Wirz-Justice A. Age-
related changes in the circadian and homeostatic regulation of human
sleep. Chronobiol Int 2006;23:461–74.
48. Reiter RJ, Paredes SD, Korkmaz A, Manchester LC, Tan DX. Melatonin
in relation to the “strong”and “weak”versions of the free radical the-
ory of aging. Adv Med Sci 2008;53:119–29.
49. Campbell AN. A randomized placebo controlled trial of melatonin en-
riched milk—can it improve symptoms of insomnia? Sleep 2015;38:A232.
50. dela Peña IJ, Hong E, de la Pena JB, Kim HJ, Botanas CJ, Hong YS,
Hwang YS, Moon BS, Cheong JH. Milk collected at night induces sed-
ative and anxiolytic-like effects and augments pentobarbital-induced
sleeping behavior in mice. J Med Food 2015;18:1255–61.
51. Huang W, Shah S, Long Q, Crankshaw AK, Tangpricha V. Improve-
ment of pain, sleep, and quality of life in chronic pain patients with vi-
tamin D supplementation. Clin J Pain 2013;29:341–7.
52. Hashimoto S, Kohsaka M, Morita N, Fukuda N, Honma S, Honma K.
Vitamin B12 enhances the phase-response of circadian melatonin
rhythm to a single bright light exposure in humans. Neurosci Lett
1996;220:129–32.
53. Mayer G, Kroger M, Meier-Ewert K. Effects of vitamin B12 on perfor-
mance and circadian rhythm in normal subjects. Neuropsychopharma-
cology 1996;15:456–64.
54. Luboshitzky R, Ophir U, Nave R, Epstein R, Shen-Orr Z, Herer P. The
effect of pyridoxine administration on melatonin secretion in normal
men. Neuroendocrinol Lett 2002;23:213–7.
55. Milagres MP, Minim VP, Minim LA, Simiqueli AA, Moraes LE, Martino
HS. Night milking adds value to cow’s milk. J Sci Food Agric 2014;94:
1688–92.
56. Hansen AL, Dahl L, Olson G, Thornton D, Graff IE, Froyland L, Thayer
JF, Pallesen S. Fish consumption, sleep, daily functioning, and heart
rate variability. J Clin Sleep Med 2014;10:567–75.
57. Massa J, Stone KL, Wei EK, Harrison SL, Barrett-Connor E, Lane NE,
Paudel M, Redline S, Ancoli-Israel S, Orwoll E, et al. Vitamin D and
actigraphic sleep outcomes in older community-dwelling men: the
MrOS sleep study. Sleep 2015;38:251–7.
58. Bell PG, Walshe IH, Davison GW, Stevenson E, Howatson G. Montmorency
cherries reduce the oxidative stress and inflammatory responses to
repeated days high-intensity stochastic cycling. Nutrients 2014;6:829–43.
59. Howatson G, McHugh MP, Hill JA, Brouner J, Jewell AP, van Someren
KA, Shave RE, Howatson SA. Influence of tart cherry juice on indices of
recovery following marathon running. Scand J Med Sci Sports 2010;20:
843–52.
60. Tsaluchidu S, Cocchi M, Tonello L, Puri BK. Fatty acids and oxidative
stress in psychiatric disorders. BMC Psychiatry 2008;8(Suppl 1):S5.
61. Kelly GS. Folates: supplemental forms and therapeutic applications.
Altern Med Rev 1998;3:208–20.
62. Patrick LR. Restless legs syndrome: pathophysiology and the role of
iron and folate. Altern Med Rev 2007;12:101–12.
63. Feldman JM, Lee EM. Serotonin content of foods: effect on urinary ex-
cretion of 5-hydroxyindoleacetic acid. Am J Clin Nutr 1985;42:639–43.
64. USDA. Dietary guidelines for Americans. 8th ed. [cited 2016 Jan].
Available from: http://health.gov/DietaryGuidelines/2015/guidelines.
Food effects on sleep 949
at COLUMBIA UNIVERSITY HEALTH SCIENCE LIBRARY on September 15, 2016advances.nutrition.orgDownloaded from