Women who sleep poorly increase the risk of heart disease and obesity


Women who sleep poorly tend to overeat and consume a lower-quality diet, according to a new study from researchers at Columbia University Irving Medical Center.

The findings provide new insight into how poor sleep quality can increase the risk of heart disease and obesity and points to possible interventions for improving women’s heart health.

Previous studies have shown that people who get less sleep are more likely to develop obesity, type 2 diabetes, and heart disease–and that the relationship may be partially explained by diet.

But these studies were narrowly focused on specific foods or nutrients (such as fish, sweets, or saturated fat) or only measured sleep duration, not sleep quality.

The new study was designed to get a more comprehensive picture in women by examining associations between overall diet quality and multiple aspects of sleep quality.

“Women are particularly prone to sleep disturbances across the life span, because they often shoulder the responsibilities of caring for children and family and, later, because of menopausal hormones,” says Brooke Aggarwal, EdD, assistant professor of medical sciences at Columbia University Vagelos College of Physicians and Surgeons and senior author of the study.

The study of nearly 500 women was published online today in the Journal of the American Heart Association.

The researchers analyzed the sleep and eating habits of an ethnically diverse group of 495 women, ages 20 to 76.

The study looked at sleep quality, the time it took to fall asleep, and insomnia.

The women also reported on the types and amounts of foods they typically eat throughout the year, allowing researchers to measure their typical dietary patterns.

Similar to previous studies of sleep and diet, the study found that those with worse overall sleep quality consumed more of the added sugars associated with obesity and diabetes.

Women who took longer to fall asleep had higher caloric intake and ate more food by weight.

And women with more severe insomnia symptoms consumed more food by weight and fewer unsaturated fats than women with milder insomnia.

“Our interpretation is that women with poor-quality sleep could be overeating during subsequent meals and making more unhealthy food choices,” says Aggarwal.

The question remains: How might poor sleep contribute to poor eating?

“Poor sleep quality may lead to excessive food and calorie intake by stimulating hunger signals or suppressing signals of fullness,” says Faris Zuraikat, PhD, postdoctoral fellow at Columbia University Vagelos College of Physicians and Surgeons and lead author of the study.

“Fullness is largely affected by the weight or volume of food consumed, and it could be that women with insomnia consume a greater amount of food in an effort to feel full.

“However, it’s also possible that poor diet has a negative impact on women’s sleep quality,” adds Zuraikat.

“Eating more could also cause gastrointestinal discomfort, for instance, making it harder to fall asleep or remain asleep.”

The new study was designed to get a more comprehensive picture in women by examining associations between overall diet quality and multiple aspects of sleep quality.

“Given that poor diet and overeating may lead to obesity–a well-established risk factor for heart disease–future studies should test whether therapies that improve sleep quality can promote cardiometabolic health in women,” says Aggarwal.

About the Study

The women in the study were participants in the American Heart Association’s Go Red for Women Strategically Focused Research Network at Columbia University Irving Medical Center.

Two other research teams in Columbia’s Go Red for Women network are studying the impact of sleep restriction on risk factors for heart disease and on the cells that line blood vessels.

The study is titled “Measures of Poor Sleep Quality Are Associated with Higher Energy Intake and Poor Diet Quality in a Diverse Sample of Women from the Go Red for Women Strategically Focused Research Network.”

The other contributors (all at Columbia University Irving Medical Center) are Nour Makarem, Ming Liao, and Marie-Pierre St-Onge.

The research was supported by an AHA Go Red for Women Strategically Focused Research Network Award and an AHA Soter Collaborative Award, AHA postdoctoral fellowships, and a grant from the National Heart, Lung, and Blood Institute (T32HL007343-42).

Funding: The authors report no financial or other conflicts of interest.

Over two-thirds of adolescents are sleep deprived.1 

Sleep timing factors (eg, circadian phase delay), social factors (eg, bedtime autonomy, nighttime screen usage), and academic factors (eg, early school start times, academic pressure) place adolescents at increased risk of falling asleep late and waking up early.2,3 

Short or disrupted sleep has repeatedly been linked to increased risk of developing obesity in adolescence,4,5 though the mechanisms underlying these links remain unclear.

Previous reviews of the mechanisms driving the relationship between poor sleep (defined as too little, poor quality, poorly timed, or inconsistent sleep) and obesity in youth612 have reflected highly variable research findings.6 

Differences in child age across studies likely contribute to this variability. Adolescents are different from younger children in their cognitive abilities,13 brain development,14 desire for autonomy relating to health decision making,2 social context for eating,15 circadian phase timing and accumulation of homeostatic sleep drive,3 and overall prevalence of chronic sleep deprivation.3 

Further, risk for developing obesity is high during adolescence,16 and adolescent weight status is highly predictive of adult weight status.17,18 

This suggests that adolescence is a particularly important period to understand from a weight management perspective.

To our knowledge, no recent research has proposed a mechanistic model to explain the relationship between sleep and obesity in an exclusively adolescent population. Such a mechanistic model could identify novel intervention targets for adolescents and areas where future research is needed.

This paper presents recent research within a multisystemic conceptual framework to highlight the pathways that may connect poor sleep to increased obesity risk in adolescents.

As illustrated in Figure 1, the model includes biological, cognitive, emotional, and behavioral mechanisms that impact the balance of energy intake and expenditure, which in turn affect weight regulation.

This paper first reviews how poor sleep could impact energy intake, including increased food reward, decreased inhibitory control, metabolic disturbances, and emotional reactivity, all of which may influence food selection and portion control.

Next, we outline how poor sleep could limit energy expenditure via increased sedentary behavior and decreased physical activity.

We posit that, in combination, these various mechanisms contribute to an energy imbalance, subsequently intensifying the overall risk for obesity.

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Potential mechanisms driving the relationship between poor sleep and increased obesity risk in adolescence.

Proposed mechanisms impacting energy intake

Food reward processes and hunger

Food reward processes, or how rewarding an individual perceives or experiences food, may be impacted by poor sleep. On the neurological level, this would be reflected in sleep-related changes in the activity of reward centers of the brain.

For example, studies using monetary rewards have shown alterations in reward-related neural activation in adolescents with poor sleep quality19 and variability in their sleep schedules,20 though the nature of these alterations has varied.

More recently, Jensen et al21 examined reward-related neural activation following experimentally shortened sleep and healthy sleep using a task involving food images in samples of normal weight and overweight adolescents.

Regardless of weight class, adolescents had amplified activation in brain regions associated with food reward when experiencing shortened sleep, compared to when undergoing healthy sleep.21

Other, more phenomenological aspects of food reward include food appeal (ie, how appetizing a food appears) and food desire (ie, how strongly one desires to consume the food).22 

Regarding food appeal, healthy adolescents rated sweets/desserts as more appetizing after experimentally shortened sleep than after healthy sleep.23 

Another study found that weight status may affect how sleep interacts with appetitive cues; specifically, adolescents of normal weight increased their appetite ratings during experimental sleep restriction compared to healthy sleep, whereas adolescents who were overweight or obese showed high appetite ratings regardless of sleep condition.21 

An intervention trial targeted to shift adolescents with habitually late bedtimes to a healthier sleep schedule also resulted in decreases in food desire for high glycemic index foods.24

Hunger is a similar construct to food reward but is more related to the physiological sensations (often discomfort or feelings of weakness) that trigger the desire to consume food.

Studies evaluating relationships between sleep duration and adolescents’ self-reported hunger ratings have been mixed.

Experimentally shortened sleep has been associated with lower self-reported motivation to eat in adolescent boys,25 though another experimental study including both male and female youth found no change in hunger ratings based on sleep duration.23

In sum, poor sleep in adolescents appears to increase neural activation in brain regions associated with food reward, appeal, and desirability, but may not increase adolescent’s subjective sensation of hunger or motivation to seek out these foods.

Furthermore, preliminary evidence suggests that some aspects of food reward may be improved following interventions tailored to improve sleep. Even so, all of these studies have been conducted within the past decade.

Given the limited research in this area, replication is needed to draw more confident and nuanced conclusions.

Most studies have used a limited range of types of foods (eg, sweets/desserts compared to fruits and vegetables) or fail to differentiate types of foods at all, so we suggest specifying additional food categories (eg, fast food, meats, snack foods) to better understand food-specific reward responses relating to sleep outcomes.

Finally, recent research in the adult literature has begun to examine the relative reinforcing value of food (ie, how and when a food item is reinforcing) as an additional facet of food reward;26,27 similar methods have not yet been published in the adolescent sleep research literature.

Sleep and inhibitory control

Whereas reward processes increase appetitive drive, inhibitory control (ie, one’s ability to withhold an automatic response in order to meet one’s goals) can reduce dietary intake. Adolescents in developed countries often have easy access to appealing, high-calorie foods.

If inadequate sleep results in diminished ability to inhibit eating such foods, this could lead to weight gain over time.

Indeed, inadequate sleep has been correlated with a range of adolescent risk-taking behaviors,28 suggesting broadly decreased inhibitory control. However, findings from the few experimental studies of the impact of poor sleep on inhibitory control have been mixed.29 

For example, despite having a marked effect on mood and attention, experimentally restricting healthy adolescents’ sleep has been found to have minimal effect on parent- or self-reported impulsive behaviors.30,31 

Amongst adolescents with attention-deficit/hyperactivity disorder, experimentally shortened sleep was found to result in greater hyperactivity/impulsivity by adolescent self-report but not by parent-report or on a computerized test.32

Computerized testing has also indicated no significant effect of a sleep treatment on response inhibition for adolescents with insomnia, despite significant benefits for attention.33

Even so, it remains possible that broad measures of inhibitory control are insensitive to specific effects of sleep on dietary inhibition or one’s ability to refrain from eating a highly palatable food.

Duraccio et al21 found that adolescents were less effective at discriminating healthy from unhealthy foods in a computerized inhibitory control task when they were sleep-restricted compared to when well-rested.

While a direct mediation model has not been tested in adolescents, in adults, the association between weight and self-reported sleep quality is statistically mediated by self-reported dietary disinhibition.34 Furthermore, experimental sleep deprivation diminishes inhibitory control on a food-related computerized task in adults.35

Interestingly, functional neuroimaging studies have found that sleep restriction increases activation of inhibition-related cortical regions in response to food cues both in young adults36 and in normal-weight adolescents.37

 On the surface, such findings might suggest paradoxically better food-related inhibitory control during sleep restriction. However, Demos et al36 caution that such activation patterns reflect increased attempts at inhibiting hedonic/reward drive but do not address whether such attempts translate to actual inhibition in day-to-day eating.

Further, some individuals may not have such a compensatory attempt at inhibition; Jensen et al found that, unlike their normal-weight counterparts, adolescents who were overweight failed to show increased recruitment of inhibitory brain regions during sleep restriction.37

Thus, while the role of sleep in broadly defined behavioral inhibition remains unclear, there is at least preliminary evidence that it has more salient effects on dietary inhibition.

Even so, much of that evidence is based on studies of young adults (not adolescents) that used correlational methods and indirect outcome measures (eg, food proxies such as pictures presented on a computer screen).

Although generally in line with the hypothesis that inadequate sleep diminishes adolescents’ ability to inhibit consumption in an obesogenic environment, more research is needed on relevant samples using real-world outcome measures.

Emotional reactivity

Emotional eating, or eating in response to negative affect, may also increase dietary intake in adolescents with poor or short sleep. Short sleep has consistently been found to worsen affective functioning in adolescents in experimental studies.31,38,39 

This is consistent with neuroimaging studies in adults which have found increased amygdala activation and limbic activity in response to negative stimuli following sleep deprivation.40 

Beyond worsened mood, shortened sleep worsens adolescent’s ability to modulate emotion swings.31 Studies outside of the sleep research literature have found correlations between depressive and emotional symptoms and increased preference for, and consumption of, unhealthier foods.41,42 

Eating may, at least in the short term, help stabilize emotions and improve mood, particularly for foods that heavily impact the reward centers of the brain (eg, sugary, energy-dense foods).43

Considering these findings, it is possible that adolescents may consciously or unconsciously increase their food intake as a way to regulate negative emotions experienced as a result of poor sleep.

However, the few studies in adolescents that have directly examined the relationship between sleep and emotional eating have produced inconsistent results. In a large sample of adolescents from Finland, shorter sleep was associated with an increased likelihood of self-reporting eating as a way to manage stress in females but not males.44 

Adolescent males from Iran who were emotional eaters had worse sleep quality, greater sleep disturbance, and worse sleep-related daytime dysfunction than those with lower levels of emotional eating.45 

However, in a study comparing both pre-adolescents and adolescents who had experienced child sexual abuse with those with no abuse history, there was no relationship between emotional eating and insomnia symptoms in either group.46

 Constructs closely related to emotional eating have also been examined in relation to sleep in adolescents.

Disordered eating attitudes and food preoccupation have been found to be related to sleep variability in adolescents47 as well as increased sleep disturbance and daytime sleepiness in youth aged 8–17.48 

Finally, greater daytime sleepiness has been associated with increased odds of binge eating in adolescent girls at-risk for developing type 2 diabetes.49

Eating as a way to regulate emotions may contribute to the relationship between poor sleep and greater dietary intake, but much research is needed before definitive conclusions can be made.

In particular, there is a need for experimental sleep research and more consistent measurement of emotional eating including the use of objective, behavioral tasks in addition to self-report questionnaires.

It will also be important to examine the moderating effect of individual differences beyond sex, particularly focusing on adolescents from disadvantaged backgrounds who may be at increased risk for sleep problems and obesity.

Metabolic disturbances

Metabolic processes may also be disturbed in adolescents with poor sleep. The two most studied hormones associated with appetite regulation are ghrelin (ie, a peptide hormone that stimulates appetite) and leptin (ie, a hormone that suppresses hunger).50

Although adult studies have found some evidence linking short sleep with altered profiles of leptin and ghrelin, this does not appear to generalize well to the adolescent literature. Only one observational study of adolescent females has linked shorter sleep duration to higher levels of ghrelin.51 

This relationship has not been found in observational studies10 nor in an experimental sleep restriction study of adolescent males.25 Most adolescent research has also found no consistent association between sleep and leptin levels.25,52,53

 However, there may be a sex-dependent effect as one study found shorter sleep duration was associated with decreased leptin levels in adolescent boys but not girls.52

Another pathway by which sleep may impact weight may be insulin resistance or the process in which the cells in the human body become less responsive to insulin (thereby hampering the regulation of blood glucose).

Although often thought of as a consequence of obesity (evident in roughly two-thirds of adolescents with obesity),54 insulin resistance has also been shown to contribute to increased dietary intake.55 

Adolescents are at increased risk for developing insulin resistance simply by going through puberty.56

There is also consistent evidence that poor sleep further increases the risk of insulin resistance in adolescents.5761 

Cross-sectional research shows that adolescents who slept less than eight hours/night had higher insulin resistance compared to those who slept for eight or more hours/night.58,61 

However, in an earlier adolescent study, sleeping less than eight hours/night was also associated with higher body mass index (BMI) and central distribution of fat, two markers found to attenuate the relationship between sleep and insulin sensitivity.62 

Another study of adolescents with overweight/obesity found that earlier weekday bedtimes and less circadian misalignment were positively related to decreased insulin resistance, suggesting an independent effect of sleep.61 

Longitudinal research also demonstrates an effect of pre-pubertal sleep duration and sleep efficiency on insulin sensitivity in females.59 

Experimentally induced sleep restriction also increased fasting insulin levels and insulin resistance in normal-weight adolescent boys.60

In sum, adolescent sleep does not appear to be consistently linked with leptin and ghrelin levels.

It does seem likely to impact insulin sensitivity, but no publications have tested the mediating role of insulin resistance on the relationship between poor sleep and obesity. Additional areas to explore include the potential moderating impact of sex, given the wide variability of leptin and ghrelin alterations across sexes.

Importantly, future studies should be careful to control for potential nuisance or confounding variables (eg, time-of-day of blood draws, BMI, or adiposity) as hormone levels are highly sensitive to circadian effects and other difficult to control influences.

See Hagan et al63 for a thorough discussion of these concerns and future directions.

Conclusions and limitations

Poor sleep – variably defined as too little, poor quality, poorly timed, or inconsistent sleep – is related to increased obesity risk in adolescents, though the mechanisms driving this relationship are unclear.

In proposing a multisystem mechanistic model specific to adolescence, we highlight several pathways by which poor sleep might increase adolescent obesity. Specifically, increased food reward and emotional reactivity, decreased inhibitory control, metabolic disturbances (eg, insulin sensitivity), and poorer dietary quality and meal timings likely increase overall energy intake.

Simultaneously, we discuss how poor sleep limits vigorous physical activity and increases sedentary activity, particularly screen time, limiting overall energy expenditure.

We elected a narrative review format for this paper to allow for greater conceptual discussion than is typical of more structured systematic reviews, which are often dominated by methodological details of the review process itself and large, detailed reference tables.

This choice was also motivated by the wide variety of methods employed in this relatively small and emerging research literature, which precluded a formal meta-analysis or even a less sophisticated “vote count” procedure.

Even so, it is acknowledged that this review does not conform to the well-defined methodologies associated with systematic reviews (eg, PRISMA guidelines). Readers interested in a systematic review that covers similar ground but with less conceptual emphasis are directed to Krietsch et al.6 

Beyond the limitations of the narrative review format, it is important to acknowledge that all reviews are dependent upon the quality of the existing empirical literature.

The current paper highlights limitations in this emerging literature area, highlighting the most promising and speculative proposed mechanisms for the sleep-obesity link in adolescents.

Future research needs to explore these relationships in more detail to help elucidate both the strength and the conditional relationships between these various mechanisms, as well as explore external moderators (eg, race, SES, sex, maternal obesity).

These relationships can help inform current preventative and weight-loss intervention efforts in adolescent populations.

Columbia University Irving Medical Center


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