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The relationship between nutrition and sleep may be considered in terms of a two-way interaction:
- the impact of sleep (timing and duration) on diet
- the impact of diet (both overall diet and specific nutrients) on sleep
This bi-directional relationship does not exist in a vacuum, and it is important to have a brief primer on the role of sleep and biological rhythms in human health. It is intrinsically obvious that sleep serves some vital functions for health, given that the state of sleep presents a significant evolutionary risk: i.e. we are unaware and unresponsive for one third of every 24 hour day. Our understanding of why this state is an evolutionary requirement has advanced substantially, with sleep serving vital roles in global cognitive function, from learning and memory to clearing metabolic waste accumulated during the waking state.
Virtually all organisms on the planet have evolved circadian rhythms (from the Latin ‘circa’, meaning ‘around’, and ‘dies’, meaning ‘day’: around the day). Circadian rhythms repeat on cycles that are roughly 24 hours in length, corresponding to the daily rotation of the Earth (which is primarily characterised by the light-dark cycle). Sleep occurs within this daily 24 hour cycle, and our drive to sleep is inherently driven by these internal circadian rhythms, and their alignment to the daily light-dark cycle (note, it is also driven by sleep drive, i.e., the homeostatic need to sleep after being awake for an extended period). In an entrained circadian rhythm, melatonin will begin to rise in the biological evening, providing a signal for the transition from the daytime, wakeful, active period, to the corresponding nighttime, restful, sleep phase.
Sleep itself is comprised of a series of repeating ultradian rhythms. An ultradian rhythm is a biological rhythm that repeats on cycles of less than 24 hours, and sleep is comprised of multiple repeating cycles of approximately 90 minutes in duration. There are two primary sleep states:
- Rapid-Eye Movement (REM)
- Non-REM sleep
Within the non-REM component, there are four sleep stages - Stage 1, 2, 3, and 4 - which are ordered according to the depth of sleep.
Stage 1 is the lightest phase of sleep, while Stage 2 is deeper and accounts for the majority of total sleep time. Stages 3 and 4 are known as “slow-wave sleep” (SWS), which is a deep phase of sleep associated with memory consolidation. Finally, REM sleep is characterised by rapid movement of the eyes, but temporary bodily paralysis which is believed to reflect the dream state that characterised this critical phase of sleep, which accounts for a quarter of total sleep time in a healthy sleep architecture.
For a long time, the general population has heard of the concept of approximately eight hours of sleep per night being desirable for health. But recently it has become popular to hear some people critisize "the myth of eight hours". However, the science-based reality is that this idea really is not a myth. While eight hours is of course a generalisation, the ultradian nature of sleep architecture (i.e. progressing from Stage 1 through REM in 90min cycles), means that the benefits of sleep are compounded over successive cycles. This means healthy sleep patterns are characterised by 5 to 7 sleep cycles; meaning anything from 7.5 to 10 hours of sleep. And whilst, indeed, emerging research indicates that there is a genetic basis for some to be "short-sleepers", such exceptions should not be used to inform the norm in this case.
With this broad overview of sleep, we’ll look at the relationship between sleep and nutrition by looking separately at:
- The influence of sleep on diet
- The influence of diet on sleep
The Influence of Sleep on Diet
There are distinct acute effects of sleep curtailment (restricted sleep time) on both:
- Food preferences, eating behaviour and energy intake
- Underlying metabolic physiology (e.g. glucose tolerance and appetite regulatory hormones like leptin)
1) Food preferences, eating behaviour and energy intake
There are significant effects of sleep curtailment on hunger and appetite regulation. As a reminder:
- Hunger is the physiological need to eat.
- Appetite is the is psychological desire to eat.
Five hours of sleep has been shown to result in a 28% increase in ghrelin (a gut-derived hunger-signalling hormone) and an 18% decrease in leptin (a hormone regulating energy balance). This decrease in leptin is equal to the drop in leptin that would occur from restricting calorie intake by 900kcal/d. And this percentage drop in leptin is reflected in an increased, compensatory calorie intake the following day, with sleep curtailment resulting in a 22% increase in calorie intake.
One hypothesis for this compensatory increase in energy intake, driven by impacts on underlying hunger and appetite regulatory mechanisms, is the additional energetic cost of extended wakefulness. However, the compensatory energy intake predictably exceeds these additional energy requirements. This may be due to the fact that while acute sleep curtailment increases energy requirements, there is a decrease in physical activity levels.
These additional energy requirements also appear to have an interaction with brain-reward circuitry which influences appetite. Neuroimaging studies have revealed that sleep curtailment results in:
- exaggerated food-reward
- increased appetite for high-calorie foods
- compromised inhibitory control of food intake
There are nutrient-specific changes, with a 30% increase in desire for high-carbohydrate refined foods in a sleep-deprived state. Research has also shown a preference for fat intake later in the night when sleep is curtailed to 4 hours per night. The lack of compensatory adjustment for energy intake, and preference for energy-dense foods, thus has a neural component in addition to an energetic component, and the interaction between the two results in increased calorie intake even following one acute night of sleep curtailment to 4.0-5.5 hours.
Sleep curtailment results in reduced dietary restraint and increased disinhibited eating. Conversely, extending sleep duration from 6.5 hours to 8.5 hours for two weeks led to significant improvements in appetite regulation, and decreased desire for hyperpalatable foods. There is an additional behavioural component, with a curtailment of sleep to 5 hours per night resulting in more calories being consumed after dinner (i.e. later in the biological night), than at any other individual meal. The relevance of this temporal eating pattern will be discussed further below.
2) Underlying Metabolic Physiology
Sleep duration also impacts on underlying metabolic physiology that govern responses to food intake. In otherwise healthy persons, the effect of acute sleep deprivation on glucose tolerance is comparable to a pre-diabetic state, with pronounced impairment of pancreatic beta-cell insulin secretion, and decreased peripheral insulin sensitivity, in particular skeletal muscle glucose uptake. This is somewhat compounded by the fact that the appetitive preferences during sleep curtailment are for high-carbohydrate, energy-dense foods.
There are implications of this metabolic disturbance for body composition. In a three-week free-living study in which participants continued their normal diet, but decreased nightly sleep time by 79mins (from a baseline habitual sleep duration of 7.5 hours), the sleep curtailment group had:
- reduced insulin sensitivity
- decreased leptin levels
- after initial weight loss in the first week, steadily regained weight to the end of the intervention
Another study in which participants consumed 90% of their RMR for two 14-day periods of either 5.5 hours or 8.5 hours a night, followed by the opposing condition. In this crossover study, both conditions led to the same absolute amount of weight over 14-days of the intervention (3kg), however the condition of sleeping 5.5 hours saw participants lose 55% less fat mass and lose 60% of lean mass. Using measures of carbohydrate and fat oxidation (respiratory quotient), the investigators showed that the condition of sleeping 5.5 hours led to impaired fat oxidation.
Conversely, increasing sleep duration may positively influence body composition, with a pooled analysis of three studies examining hypocaloric diets over 15-24 weeks showing that sleep duration and quality were associated with degree of fat mass lost, and percentage body fat loss. Increasing sleep duration by one hour, from a baseline of seven hours, was associated with a 0.7kg decrease in fat mass.
Impact of Chronotype
While the above-mentioned literature emphasises sleep duration as the variable impacting dietary intake and metabolism, recent research has brought scrutiny onto sleep timing. More specifically, the behavioural preference for going to bed earlier or later, and rising earlier or later. This behavioural preference is known as an individual’s “chronotype”, and is a behavioural expression of preference for ‘morningness’ or ‘eveningness’ that reflects the timing of their internal circadian rhythms.
Independent of sleep duration, a late/evening chronotype is associated with:
- increased risk for type-2 diabetes
- lower overall diet quality
- redistribution of energy and macronutrient intake to later in the day
- “social jetlag” (associated with increased metabolic disease risk)
The above-mentioned "social jetlag" relates to a disconnect between sleep timing on work days and free days. Late chronotypes naturally delay sleep timing, with later time-to-bed, than early chronotypes. However, our “social clocks” (i.e., timing of the work day, school start times, etc.) are generally timed for early in the day. This means that during work days, or days with social obligations, late chronotypes experience sleep curtailment, while on free days late chronotypes would have a later wake time. Hence leading to circadian phase shifts, and hence jetlag-like effects.
In this respect, late chronotypes appear to be at a more significant risk for negative influences of sleep on diet, given our current social timing in society. In response to sleep curtailment, energy intake has been shown to occur to a greater degree in the evening after dinner than at any other meal, indicating a behavioural effect of sleep duration. Sleep timing also influences eating behaviour in the evening, with later sleep timing associated with eating in closer proximity to sleep, later clock time of calorie intake, and eating occasions occurring after dinner. This pattern of energy intake is associated with increased total daily energy intake, and energy intake after 8pm associated with increased body mass index (BMI). These associations may relate to the nocturnal, pre-sleep rise in melatonin, a hormone which is inversely associated with insulin sensitivity, i.e., when melatonin is elevated, insulin secretion is exaggerated and insulin sensitivity is impaired.
Several recent cross-sectional studies have shown that calorie intake in close proximity to melatonin onset is associated with increased body fat, and adverse effects on glucose tolerance. This relationship may also not be evident when looking at calorie intake relative to clock time, indicating that it is the relationship with an individual’s internal, biological time, that explains the relationship.
The practical significance of this is that late chronotypes, with a tendency for later sleep timing in the evening, and thus later timed energy intake, may be at a greater risk for the adverse metabolic effects of later sleep timing. Persons with later midpoint of sleep during the biological night need to sleep until later in the morning for a full, rested nights sleep. Such individuals have been shown to have significantly higher calorie intake compared to persons with an earlier sleep midpoint, an association that was independent of sleep duration. In type-2 diabetics, each 1 hour later the midpoint of sleep occurs has been associated with a significant 2.5% increase in haemoglobin A1c (HbA1c), a marker of long-term blood glucose regulation.
These relationships between sleep timing and duration, and diet-health outcomes, are particularly important in children and adolescents. A salient feature of adolescence is a delay in chronotype, leading to a general behavioural tendency for later sleep timing and later morning sleeping. Therefore the typical enforced waking from early school start times interrupts sleep timing and duration during this critical developmental period. Despite this general delay in chronotype during this period, there remain chronotype differences in adolescents which are associated with weight outcomes in children: “morning-type” children tend to have lower BMI than “evening-type” children.
Similar to late chronotype adults and work start times, adolescents with an late chronotype may be more vulnerable to the disconnect between school start times and their internal clocks, and late sleep timing is associated with increased consumption of fast foods and lower diet quality, predisposing this population to increased adiposity. Morning-type adolescents have been shown to benefit to a greater degree than evening-types from extending sleep duration by 2.5 hours with an earlier bedtime, resulting in reduced calorie intake the following days. The curtailment in energy intake in morning-types began in the early evening, before the onset of sleep, implying a circadian effect of increased sleep timing and duration, and not merely a decreased propensity to eat. Conversely, earlier sleep timing and duration had no effect on calorie intake in evening-types, who continued to increase energy steadily through the evening before plateauing prior to sleep onset.
What this indicates is that the behavioural effects of early enforced wake times, resulting in a disconnect in sleep timing from sleep needs, poses a significant risk factor to metabolic health in adolescent evening-types. Late-bed/late-rise adolescent chronotypes have been shown to be 1.5 times more likely to be obese than than early-bed/early-rise chronotypes, despite both groups averaging approximately the same nightly sleep duration, suggesting that sleep pattern is a more significant factor associated with risk for unfavourable weight outcomes, independent of sleep duration.
In relation to the influence of sleep on diet, the following broad conclusions may be drawn:
- Sleep curtailment per se negatively impacts on hunger and appetite regulation, precipitating overconsumption of energy the following day;
- Sleep curtailment negatively impacts on glycaemic control, with impaired glucose tolerance and insulin secretion. In addition, fat oxidation is impaired;
- Sleep curtailment has deleterious effects on body composition, with proportionally greater lean body mass, and less fat mass, lost during weight loss;
- Chronotype is emerging as an important mediator of the relationship between sleep, diet, and health outcomes. Later chronotypes tend toward lower diet quality, later evening energy intake, and increased risk for metabolic disease that are independent of sleep duration;
- Later midpoint of sleep, as an indication of the relationship between chronotype and sleep timing, is associated with increased energy intake in persons with obesity, and impaired long-term blood glucose regulation in persons with T2DM;
- In adolescents with a natural phase delay in biological rhythms, later chronotype remains a factor associated with late sleep timing, curtailed sleep with enforced morning waking, poor diet quality, and increased risk for obesity.
From the totality of evidence, it is possible to conclude that both sleep timing and duration have strong influences on diet, and related health outcomes. However, it is evident that this relationship is a complex interaction of physiological, genetic, environmental, and behavioural factors, and our understanding of certain factors - in particular chronotype and social jetlag - is only beginning to emerge.
The Influence of Diet on Sleep
Specific Foods & Nutrients
The ability of certain foods or nutrients to influence sleep is often rooted in more folklore than scientific evidence, and the body of scientific evidence is generally weak in this area. A common proposition advanced is that a physiological connection between a nutrient and a mechanism must translate into an effect on sleep, but there is often a disconnect between the proposed mechanism and actual outcomes.
For example, a number of studies have suggested that consumption of foods rich in tryptophan, an amino acid precursor to serotonin and melatonin, can increase brain concentrations of tryptophan, suggesting an improvement of sleep parameters. However, while tryptophan concentrations may be shown to increase from tryptophan-rich foods, the putative mechanism of enhancing sleep has not been shown with any consistency. It should be stated that pharmacological doses of supplemental tryptophan may improve sleep, however, this should not be conflated with the role of tryptophan-rich protein source foods, which do not contain levels of tryptophan comparable to pharmaceutical grade supplemental interventions.
Similarly, the use of melatonin-enriched milks or foods naturally high in melatonin, like tart cherries, suggests that these foods provide a dietary source of melatonin, however the levels of melatonin in these food sources are a fraction of the therapeutic doses of supplemental melatonin which have been shown to have effects on sleep parameters in controlled trials. A couple of small trials have found improvements in sleep from concentrated tart cherry juice intake, but the improvements were modest and not clinically relevant. Although urinary melatonin was found to be elevated, tart cherries also contain numerous bioactive phenolic compounds, which may have an effect.
Similarly, a single trial in healthy sleepers found that consumption of two kiwi fruits, a natural source of serotonin, an hour before bedtime led to improved sleep by objective measurements, albeit the study was uncontrolled. However, these studies are largely in non-clinical populations and it is difficult to extrapolate the small effect sizes and questionable clinical relevance to populations with sleep issues.
While early research 50 years ago suggested that consumption of cow’s milk may enhance sleep, recent research has been mixed, with certain studies finding a benefit to fermented milk on sleep efficacy, while other studies have found no effect. Cumulatively, the evidence for effects of specific foods in promoting sleep is confined to isolated studies, which have yet to be replicated, with small sample sizes, small effect sizes, and tenuous links between the food-based intervention and the proposed biological mechanisms.
Caffeine & Alcohol
The exceptions to the focus on isolated dietary constituents are caffeine and alcohol, globally the most widely consumed drugs, which have strong negative interactions with sleep. The drive to sleep is influenced by the build-up of adenosine in the brain, however, caffeine acts as an adenosine antagonist (which is how it promotes wakefulness and delays fatigue perception), preventing the accumulation of adenosine and sleep-promoting effects. In addition, the half-life of caffeine (i.e., the time for the levels of the compound in circulation to be reduced by 50%) is 5-6 hours, meaning caffeine consumption earlier in the day may still negatively interfere with sleep quality later in the day. Further, the capacity of the liver to clear caffeine appears to have two broad genetic types, those who metabolise caffeine quickly, and those who slowly metabolise caffeine; the latter may have a longer circulating half-life of the compound, and may be more predisposed to sleep disturbances from caffeine intake.
Alcohol results in pronounced reductions of time spent in deep stages of sleep, in particular REM sleep, and while it exerts a sedative effect - hence the colloquial ’nightcap’ - alcohol results in less restorative sleep, and more time spent in light-stage sleep. The dose for acute effects of alcohol on sleep architecture is relative small, equivalent to one standard lager or glass of wine. Both caffeine and alcohol, despite their ubiquitous consumption, are the two dietary constituents with the strongest evidence for effects on sleep.
Calories & Macronutrients
Overall energy balance may influence sleep, but the evidence suggests that acute calorie restriction does not impact on sleep quality parameters, while more extended duration calorie restriction may decrease REM cycles. However, the body of evidence in this area is very small. Some research has found that extended fasting of up to 67 hours in duration has an impact on sleep architecture, suggesting that negative influences of negative energy balance on sleep occurs from more extended calorie restriction.
The effect of specific macronutrients, and balance of macronutrients in a diet, appears to relate to the absolute level of intake. Polysomnography studies (objective recording of sleep in a lab setting), have indicated oppositional effects of high-fat or high-carbohydrate meals on REM sleep:
- high-fat meals resulting in reduced REM sleep and more slow-wave sleep
- high-carb meals result in less slow-wave sleep and increased time in REM
The increased protein ratio from manipulating carbohydrate and fat may be a factor influencing outcomes in these studies, as increasing protein has been associated with less waking episodes, with either a high-fat or high-carb intake. A study inducing ketosis with <1% carbohydrate intake for two weeks found reduced REM sleep and increased slow-wave sleep, suggesting that the main effect of high-fat diets on sleep architecture is to reduce REM and result in more time spent in slow-wave sleep. A hypothesis for this effect is derived from animal studies, which indicate that the satiety hormone, cholecystokinin (CCK), which is released in response to dietary fat intake, increases time spent in slow-wave sleep and non-REM sleep. However, this relationship between dietary fat, CCK, and sleep, has not yet been directly investigated in humans. Interestingly, in contrast to the main apparent effect of high-fat diets overall, saturated fat intake is associated with less time spent in slow-wave sleep.
Conversely, studies investigating varying degrees of higher carbohydrate intake (56-80%) suggest an effect that is inverse to the effect of high-fat diets, namely:
- increasing time spent in REM
- reduced REM latency
- decreased slow-wave sleep
One putative mechanism for this effect, for which there is some mechanistic support in the literature, relates to the ratio of tryptophan to long-chain amino acids (LCAA), which outcompete tryptophan for transport across the blood-brain barrier. A higher carbohydrate intake could divert LCAA to skeletal muscle, increasing the availability for tryptophan transport into the brain. However, this specific mechanism has not been directly investigated, and remains hypothetical at this juncture.
Dietary fibre intake is associated with less time spent in light, Stage 1 sleep, and increased slow-wave sleep. Glycaemic-index (GI) may also influence sleep parameters, with a high-GI meal consumed 4 hours before bedtime found to significantly reduce sleep onset latency, with correlated with subjective sleepiness after the meal, compared to either a low-GI meal 4 hours before bedtime or the high-GI meal 1 hour before bedtime.
There are certain specific nutrients which have become popular as sleep supplements, despite varying levels of evidence in support of their efficacy:
- Magnesium citrate may improve sleep in persons with deficient magnesium levels, however, this trial was in a population aged over 60 years old, and is difficult to extrapolate beyond that. As a central nervous system sedative, there is popular interest in magnesium in athletic populations as a sleep aid, but there remains a lack of research specifically investigating this intervention.
- Administration of vitamin B3 in the form of niacin, which is synthesised from dietary tryptophan and may increase tryptophan availability with exogenous supplementation, in one study found increased REM sleep in persons without sleep problems, and improved sleep efficacy in persons with mild-moderate insomnia.
- Vitamin B6, which acts as a cofactor in the synthesis of serotonin, has been shown to increase dream content and vividness, but without measures of objective sleep quality.
- The amino acid glycine, which acts as an inhibitory neurotransmitter, has been shown to reduce sleep onset latency, measured objectively by polysomnography, and to improve subjective sleep quality.
- Valerian root has some evidence for improving subjective sleep quality, however, the apparent supplemental quality of 450mg root extract standardised to 0.8-1% valeneric acid, is often not present in commonly available supplements.
- Finally, notwithstanding the various availability of supplemental melatonin in different jurisdictions, melatonin supplementation in the range 1-5mg has been shown to correct sleep and entrain circadian rhythms in the short-term, resulting in reduced sleep onset latency, and increased sleep time. In this regard, supplemental melatonin is best utilised to overcome jet-lag, or for athletes travelling to new time zones who need to correct circadian alignment quickly.
Implications for Nutrition Practitioners
Due to the clear role of sleep health in impacting on diet quality, energy balance, and body composition, nutrition professionals should consider sleep in dietary assessments. However, at this time the evidence for improving sleep favours consideration of sleep hygiene over any specific dietary interventions.
Dietary considerations relate more to timing and distribution over the course of the day from the perspective of circadian alignment (details here), and the relationship with sleep timing. One factor that warrants consideration in this context is individual time-of-day preference, or ‘chronotype’, which can be assessed by the Munich Chronotype Questionnaire (which can also provide an estimate of social jetlag). For late chronotypes, dietary factors to consider would be the tendency for later distribution of energy, energy intake after dinner and in close proximity to bedtime, and delayed eating initiation. Modifying patterns of evening energy intake may be beneficial dietary interventions for later chronotypes.
In the overall sleep hygiene context, caffeine consumption and timing would be the primary dietary constituent that warrants attention, due to the well-established interaction between caffeine and sleep. Alcohol also warrants attention, due to the suppression of deep-stage and REM sleep which occurs with low dose alcohol in close proximity to bedtime.
While caffeine and alcohol may both broadly be considered under the umbrella of dietary factors, of the environmental factors influencing sleep, artificial bright light exposure - particularly of the shortwave blue light spectrum - in the evening prior to bed results in suppressed melatonin levels, and increased physiological arousal. Thus, consideration of evening light exposure is a positive step in improving sleep hygiene. As a corollary, encouraging outdoor light exposure in the early part of the day may help to regulate circadian rhythms (or use of an artificial blue light box in latitudes with extended morning darkness during winter months).
Consideration of ’state and trait’ is also important in the context of sleep hygiene, engaging in stress reduction techniques or deliberate relaxation modalities before bed.
Beyond the primary dietary factors influencing sleep, namely caffeine and alcohol, however, the evidence for any specific macronutrient manipulations at this juncture remains weak, and thus no definitive recommendations can be made regarding the role of dietary proteins, or varying ratios of carbohydrate to fat in the diet, as strategies to influence sleep quality. There may be some support for carbohydrate intake with evening meals to support increased REM sleep, and carbohydrate restriction may reduce deep-stage sleep and REM sleep.
Long-term energy restriction may result in impaired sleep, and consideration should be given to athletes or physique competitors in this regard. Although suggestive evidence exists for the roles of specific foods or isolated supplemental nutrients to enhance sleep, the strength of the evidence is weak, as trials are typically standalone studies in small, non-clinical populations, with weak effect sizes. Cumulatively, the weight of evidence favours consideration of sleep hygiene factors in order to improve sleep quality in non-clinical populations.
Summary of Key Points
Impact of Sleep on Diet
- Sleep curtailment negatively impacts on hunger and appetite regulation, leading to increased calorie intake the following day.
- Sleep curtailment negatively impacts on glycaemic control (impaired glucose tolerance and insulin secretion).
- Sleep curtailment impairs fat oxidation.
- Sleep curtailment has deleterious effects on body composition, with proportionally greater lean body mass, and less fat mass, lost during weight loss.
- Later chronotypes tend toward lower diet quality, later evening energy intake, and increased risk for metabolic disease (with these effects being independent of sleep duration).
- Whilst both sleep timing and duration have strong influences on diet, and related health outcomes, this relationship is a complex interaction of physiological, genetic, environmental, and behavioural factors.
Impact of Diet on Sleep
- No definitive recommendations can be made regarding the role of dietary proteins, or varying ratios of carbohydrate to fat in the diet, as strategies to influence sleep quality.
- Long-term energy restriction may result in impaired sleep.
- Although suggestive evidence exists for the roles of specific foods or isolated supplemental nutrients to enhance sleep, the strength of the evidence is weak.
- At this time the evidence for improving sleep favours consideration of sleep hygiene over any specific dietary interventions.
Statement Author: Alan Flanagan, PhD (c)
Alan is the Research Communication Officer here at Sigma Nutrition. Alan is currently pursuing his PhD in nutrition at the University of Surrey, UK, with a research focus in chrononutrition. Alan previuosly completed a Masters in Nutritional Medicine at the same institution.
Originally a lawyer by background in Dublin, Ireland, Alan combines an investigative and logical approach to nutrition together with advocacy skills to communicate the often complicated world of nutrition science, and is dedicated to guiding healthcare professionals and the lay public in science-based nutrition.