Lack of sleep results in a total increase in abdominal and visceral fat

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New research from Mayo Clinic shows that lack of sufficient sleep combined with free access to food increases calorie consumption and consequently fat accumulation, especially unhealthy fat inside the belly.

Findings from a randomized controlled crossover study led by Naima Covassin, Ph.D., a cardiovascular medicine researcher at Mayo Clinic, show that lack of sufficient sleep led to a 9% increase in total abdominal fat area and an 11% increase in abdominal visceral fat, compared to control sleep.

Visceral fat is deposited deep inside the abdomen around internal organs and is strongly linked to cardiac and metabolic diseases.

The findings are published in the Journal of the American College of Cardiology, and the study was funded by the National Heart, Lung and Blood Institute.

Lack of sufficient sleep is often a behavior choice, and this choice has become increasingly pervasive. More than one-third of adults in the U.S. routinely do not get enough sleep, in part due to shift work, and smart devices and social networks being used during traditional sleep times. Also, people tend to eat more during longer waking hours without increasing physical activity.

“Our findings show that shortened sleep, even in young, healthy and relatively lean subjects, is associated with an increase in calorie intake, a very small increase in weight, and a significant increase in fat accumulation inside the belly,” says Virend Somers, M.D., Ph.D., the Alice Sheets Marriott Professor of Cardiovascular Medicine, and principal investigator of the study.

“Normally, fat is preferentially deposited subcutaneously or under the skin. However, the inadequate sleep appears to redirect fat to the more dangerous visceral compartment. Importantly, although during recovery sleep there was a decrease in calorie intake and weight, visceral fat continued to increase.

“This suggests that inadequate sleep is a previously unrecognized trigger for visceral fat deposition, and that catch-up sleep, at least in the short term, does not reverse the visceral fat accumulation. In the long term, these findings implicate inadequate sleep as a contributor to the epidemics of obesity, cardiovascular and metabolic diseases,” says Dr. Somers.

The study cohort consisted of 12 healthy people who were not obese, each spending two 21-day sessions in the inpatient setting. Participants were randomly assigned to the control (normal sleep) group or restricted sleep group during one session and the opposite during the next session, after a three-month washout period.

Each group had access to free choice of food throughout the study. Researchers monitored and measured energy intake; energy expenditure; body weight; body composition; fat distribution, including visceral fat or fat inside the belly; and circulating appetite biomarkers.

The first four days were an acclimation period. During this time, all participants were allowed nine hours in bed to sleep. For the following two weeks, the restricted sleep group was allowed four hours of sleep and the control group maintained with nine hours. This was followed by three days and nights of recovery with nine hours in bed for both groups.

The participants consumed more than 300 extra calories per day during sleep restriction, eating approximately 13% more protein and 17% more fat, compared to the acclimation stage. That increase in consumption was highest in the early days of sleep deprivation and then tapered off to starting levels during the recovery period. Energy expenditure stayed mostly the same throughout.

“The visceral fat accumulation was only detected by CT scan and would otherwise have been missed, especially since the increase in weight was quite modest—only about a pound,” Dr. Covassin says.

“Measures of weight alone would be falsely reassuring in terms of the health consequences of inadequate sleep. Also concerning are the potential effects of repeated periods of inadequate sleep in terms of progressive and cumulative increases in visceral fat over several years.”

Dr. Somers says behavioral interventions, such as increased exercise and healthy food choices, need to be considered for people who cannot easily avoid sleep disruption, such as shift workers. More study is needed to determine how these findings in healthy young people relate to people at higher risk, such as those who are already obese, or have metabolic syndrome or diabetes.


Despite recent data suggesting that the dramatic increases in overweight and obesity seen over the past three decades have begun to plateau, rates remain alarmingly high [1, 2]. Concurrent with these increases has been a reduction in sleep duration [3, 4], raising the question of an association or even that short sleep duration could be a possible cause of obesity [5, 6•]. Factors responsible for this secular decline in sleep duration are not well understood, but this deficit has been ascribed to the modern way of living [7].

Interestingly, declines in children’s sleep duration have occurred as a result of progressive delays in children’s bedtimes, but unchanged wake times [8–10]. Delays in children’s bedtimes have been attributed to activities that keep children awake and contexts that allow them to do so such as technology use, schoolwork and part-time employment [11–13]. Similarly, artificial light, caffeine use and parental attitudes have been identified as contexts that allow children to have later bedtimes [14–16].

The importance of having a good night’s sleep for body weight stability and overall health is accumulating [17•]. A mounting body of epidemiological evidence associates insufficient sleep not only with obesity [18, 19], but also with type 2 diabetes [20, 21], coronary heart disease [22, 23], hypertension [24, 25], and premature death [26, 27]. It thus becomes clearer for researchers that multiple plausible causes of obesity exist outside of the conventional risk factors [28, 29]. Among them, there is robust evidence supporting the role of reduced sleep as contributing factor to the current obesity epidemic [30, 31]. Given that chronic sleep restriction is linked to the modern way of living, the maintenance of a healthy lifestyle appears to be more difficult for short-duration sleepers in the current obesogenic environment.

The objective of this paper is to highlight recent evidence on short sleep duration and its association with obesity. Furthermore, potential mechanisms by which insufficient sleep may predispose to weight gain are discussed.

Association Between Short Sleep Duration and Obesity
Observational Evidence

A growing body of epidemiologic evidence associates short sleep duration with obesity and weight gain [6•]. Using a cohort of children aged between 5 and 10 years, we reported that short sleep duration was the most important risk factor for overweight and obesity [32]. Excess body weight was predicted by short sleep duration, with odds ratios exceeding those of other well-known risk factors, including parental obesity, television viewing, socioeconomic status, and physical inactivity.

Likewise, we also showed that short sleep duration contributed more importantly to weight gain than other traditional risk factors, such as nonparticipation in high-intensity physical activity and high dietary fat intake in a prospective cohort of adults [33•]. A recent systematic review and meta-analysis by Cappuccio and colleagues reports that children who sleep less than 10 h per night are at 89 % greater risk of being obese than their peers who sleep more than 10 h/night [34].

Likewise, adults sleeping ≤5 h per night were 55 % more likely to be obese than those sleeping >5 h per night. A pooled regression analysis in adults also showed that a reduction in 1 h of sleep per day would be associated with a 0.35 kg/m2 increase in body mass index (BMI) [34]. For a person approximately 178 cm tall it would be equivalent to approximately 1.4 kg in weight. Thus, although most studies have found a significant association between inadequate sleep and obesity, the association appears stronger at younger ages, suggesting that children and adolescents may be more vulnerable to the effects of inadequate sleep.

We previously reported results in children showing that the association of sleep duration with waist circumference remained significant even after adjusting for BMI, indicating that short sleep duration is more strongly related to central fat deposition than to overall level of adiposity [35]. We recently corroborated this observation with the use of a 6-year longitudinal design in adults by showing that short sleep duration preferentially increases abdominal adiposity [36•].

This finding is of particular concern because abdominal adiposity is associated with a number of metabolic anomalies. The hyperactivity of the hypothalamo-pituitary-adrenal (HPA) axis associated with short sleep duration [37] is one possible source of explanation for our findings. Lack of sleep has been reported to constitute a metabolic stressor, with increased cortisol concentrations as the end product [38•]. Because abdominal adipose tissue has more cells per unit of mass, higher blood flow and more glucocorticoid receptors, glucocorticoids could affect abdominal fat to a greater extent than subcutaneous adipose tissue [39].

Of interest, it has been proposed that visceral obesity could represent a physiological adaptation to chronic exposure to stress, particularly when failure to cope is observed [40]. The Hervey’s hypothesis which suggests that fat cells take up and catabolize glucocorticoids is one of potential regulatory pathways by which abdominal fat may grow in response to chronic stress exposure [41]. This is also supported by other evidence showing that abdominal obesity is associated with an increased cortisol clearance [42]. Thus, one cannot exclude the possibility that abdominal fat accumulation represents a biological adaptation to chronic lack of sleep.

Although studies examining the relationship between sleep patterns and adiposity status tend to focus on sleep duration, it has recently been reported that sleep timing behavior may be a better predictor of obesity than sleep duration alone. Chronotype studies have shown that morning-type children tend to have a lower BMI than evening-type children [43, 44].

It is plausible that this may be due to differing opportunities for physical activity and sedentary behaviors in these time slots, with the evening offering relatively few opportunities for physical activity and relatively more opportunities for sedentary behaviors, such as television viewing and video game playing, which have been shown to increase food intake [45]. Results from a recent study involving 2,200 Australian children showed that those who went to bed late and woke up late were 2.2 times more likely to be obese than those who went to bed early and woke up early despite the same amount of sleep [46].

Furthermore, late sleepers were almost twice as likely to have low moderate-to-vigorous intensity physical activity and 2.9 times more likely to sit in front of the TV and computer or play video games for more hours than guidelines recommend. These results agree with those from a recent study in adults showing that late sleepers consumed on average 248 kcal more per day than normal sleepers, with the majority of the excess calories occurring at dinner and after 8:00 PM [47].

With regard to causality in the association between short sleep duration and weight gain using epidemiologic evidence, causal inference is difficult due to lack of control for important confounders in many studies (e.g. depression, psychosocial problems, chronic illness, use of hypnotics, etc.) and inconsistent evidence of temporal sequence in prospective studies.

Additionally, the findings suggest that there may be bidirectional effects, shortened sleep causing weight gain and weight gain causing shortened sleep, hence creating a setting for a vicious cycle [6•]. Another concern is the rarity of objective measurements of sleep duration (including sleep quality). Although polysomnography is not feasible in large cohorts and the recording instrumentation may itself interfere with sleep, other methods of objectively measuring sleep exist. Wrist actigraphy is definitively one of them and has been validated against polysomnography [48].

Unfortunately, only few studies of sleep duration and obesity to date have utilized actigraphy. The fact that many investigators reported retrospective analysis in this new field of research can explain why many studies have relied on questionnaires to assess sleep. In a population-based sample of middle-aged adults, subjective reports of habitual sleep are moderately correlated with actigraph-measured sleep, but are biased by systematic over-reporting [49].

The wording of these sleep questions varies greatly across studies and few questions have been validated. For example, many studies asked only about nocturnal sleep which may substantially underestimate sleep duration in populations where napping or shift-working is common. Additionally, the large night to night variability in sleep duration may also lead to substantial measurement error. Of particular concern is the fact that sleep habits vary greatly between weekdays and weekends [50]. These differences are even larger in those who have more severe sleep restriction during the week.

It is unclear how accurately individuals are able to average their sleep habits over weekdays and weekends to answer a single question about usual sleep habits. Finally, other aspects have the potential to hamper the interpretation of the evidence in terms of causality, such as the body weight history and the possibility of common or upstream underlying causes; however, the preponderance of the evidence taken as a whole points toward an effect of shortened sleep on body weight. Future epidemiologic research from large prospective cohort studies with objective measurement of sleep habits and repeated measures of both sleep duration and adiposity is needed to more definitively establish a causal link and to better define the magnitude of any causal effect.

Experimental Evidence

Many short-term intervention studies aimed at investigating the effects of sleep restriction on energy balance have been published over the last 10 years and have contributed to our understanding of the potential physiological mechanisms underpinning the short sleep–obesity association. This field of research has certainly been fueled by the apparent paradox that an increase in the time spent in the most sedentary of all activities (i.e., sleep) is associated with leanness.

The group of Eve Van Cauter in Chicago has certainly helped to clarify this paradox several years ago, when they experimentally tested the acute effects of sleep restriction on feeding behavior and key appetite-related hormones. The seminal study by Spiegel et al. [51] showed that two consecutive nights of sleep restriction to 4 h instead of 10 h induced an 18 % decrease in the circulating concentrations of the anorexigenic hormone leptin and a 28 % increase in the concentrations of the orexigenic hormone ghrelin in conjunction with increased sensations of hunger and appetite.

This is concordant with the analysis that we have performed in the Quebec Family Study, which has revealed that short sleepers are characterized by plasma leptin levels that are lower than predicted by their fat mass [52]. Furthermore, these findings concur with some other intervention studies showing that sleep is an important modulator of neuroendocrine function and metabolism. Indeed, sleep restriction has been shown to decrease glucose tolerance, decrease insulin sensitivity, increase evening concentrations of cortisol, increase levels of ghrelin, decrease levels of leptin, and increase the drive to eat [53–56].

However, other intervention studies have not been able to reproduce these findings [57–59], leaving the question open as to whether the connection between short sleep duration and obesity can be explained by changes in homeostatic feeding behavior (i.e., the hormones that trigger hunger and food intake).

An important limitation of experimental studies is that they are short-term, lasting a few weeks at most. This raises the question of whether these effects will persist outside the laboratory when sleep restriction is chronic. Experimental evidence that sleep restriction induces obesity is not possible in humans for both ethical and logistic reasons.

The best evidence to show a cause-and-effect association between shortened sleep and weight gain would be to conduct a randomized controlled trial in which we would have to restrict sleep duration in a group of lean people in order to be able to compare them with a control group. However, the slow development of obesity implies that such a study would have to run for years in a large sample of individuals.

This means that we need to rely on short-term intervention studies and epidemiologic studies. As recently addressed [6•], short-term experiments may elucidate biological mechanisms supposedly inducing continuous weight gain, but whether they produce obesity in the long run is unknown. Likewise, observations of obesity development in non-obese population groups over time after exposure to short sleep duration can be addressed with the use of various epidemiological methods, each of which have pros and cons.

Although the proof-of-concept will never be complete in this field of investigation, the preponderance of the evidence taken as a whole points toward an effect of sleep duration on the vulnerability to weight gain. It is also important to remember that a good night’s sleep is the “normal” biological condition and no one can effectively argue that lack of sleep is healthy. Therefore, there is minimal risk in taking a pragmatic approach and encouraging a good night’s sleep as an adjunct to other health promotion measures [7, 60, 61].

Potential Mechanisms by Which Short Sleep Duration May Predispose to Weight Gain
Effects of Short Sleep Duration on Energy Intake

In order to produce weight gain, reduced sleep must either increase energy intake and/or reduce energy expenditure. The potential mechanisms by which short sleep duration may influence body weight are shown in Fig. 1. The most plausible explanation as to why short sleepers have a higher risk of becoming obese is through an increased food intake. Indeed, many recent intervention studies have reported an increase in food intake after short-term sleep restriction [59, 62–64]. Among the possible explanations, short sleep duration might increase the risk of weight gain by preventing the restoration of a hormonal profile facilitating appetite control (homeostatic drives to eat). As mentioned above, inadequate sleep has been reported in some studies to decrease leptin levels, increase ghrelin level and cortisol levels, alter glucose homeostasis, and activate the orexin system [65, 66]. However, recent studies have not been able to reproduce these findings and it suggests that the explanation of an up-regulation of appetite as a result of sleep restriction is not as robust as previously reported [57–59].

figure 1
Potential mechanisms by which insufficient sleep may predispose to weight gain. The symbol (?) denotes a lack of scientific support

Shortened sleep could also lead to weight gain and obesity by increasing the time available for eating and by making the maintenance of a healthy lifestyle more difficult. In an environment in which energy-dense food is highly palatable and readily available, caloric intake may be directly proportional to the time spent awake, especially if most of wakefulness is spent in sedentary activities, such as watching television in which snacking is common [45]. This concept is supported by recent data showing that recurrent bedtime restriction under free-living conditions did not down-regulate the satiety hormone leptin nor upregulate the appetite-stimulating hormone ghrelin, but increased intake of calories from snacks, which suggests hedonic rather than homeostatic mediators of the shift in food selection [57]. Results from another study showed that habitual short sleepers (average of 6 h/night) ate more often (i.e., >3 meals/day with more frequent nibbling) than did long sleepers [67]. Likewise, the recent study by Weiss and colleagues [68] provides further evidence to support the theory of reward seeking behaviors associated with short sleep duration. The authors observed that objectively measured shorter sleep duration in adolescents was associated with a relatively higher caloric intake derived from fat and a 2-fold increased risk of consuming ≥475 kcal/day from snacks. Accordingly, future studies should put more efforts in investigating the non-homeostatic, reward-driven eating behavior associated with inadequate sleep [69].

The functional magnetic resonance imaging (fMRI) has recently been instrumental in documenting food-related reward activation in the brain after sleep restriction. Interestingly, a recent study in adolescents reports that impaired sleep was associated with less reactivity of reward-related brain systems, suggesting that more exciting rewards are required to create the same level of neuronal activation [70]. Furthermore, two other recent studies reported that sleep restriction leads to increased activation of brain regions sensitive to food stimuli [71, 72]. These new studies provide evidence that inadequate sleep enhances hedonic stimulus processing in the brain underlying the drive to consume food and are consistent with the notion that reduced sleep may lead to greater propensity to overeat.

The fact that studies are not all consistent in showing an effect of shortened sleep on food intake [57, 58] highlights the need for a better characterization of short-duration sleepers. In order to further explain the inter-individual variations in weight gain among short-duration sleepers, we explored this issue by measuring disinhibition eating behavior trait in short- (≤6 h), average- (7–8 h) and long-duration sleepers (≥9 h) over a 6-year follow-up period in adults. We observed that having a high disinhibition eating behavior trait significantly increases the risk of overeating and gaining weight in those with short sleep duration (Fig. 2) [73•]. These novel results emphasize the need to include a disinhibition eating behavior score in the personalized risk assessment of weight gain and obesity of short-duration sleepers. Furthermore, these results suggest that short sleep duration alone may not be sufficient in and of itself to predict weight gain.

figure 2
(a) Six-year weight gain and (b) energy intake according to sleep duration group and disinhibition eating behavior trait (high vs. low). Values are mean ± SEM. LDEB: low disinhibition eating behavior trait tertile (score ≤ 3). HDEB: high disinhibition eating behavior trait tertile (score ≥ 6). Short sleepers (≤6 h/night), average sleepers (7–8 h/night) and long sleepers (≥9 h/night). Statistical significance was assessed by analysis of covariance, followed by a Tukey HSD post-hoc test. The model was adjusted for age, sex, baseline body weight, length of follow-up, employment status, highest educational level, total annual family income, menopausal status, shift-working history, and alcohol intake as covariates. *Significantly different from all other groups (P < 0.05). Figure adapted from Chaput et al. [73•]

reference link :https://link.springer.com/article/10.1007/s13679-012-0026-7


Original Research: Closed access.
Effects of Experimental Sleep Restriction on Energy Intake, Energy Expenditure, and Visceral Obesity” by Naima Covassin et al. Journal of the American College of Cardiology

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