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FACTS BEHIND THE HEADLINES Can a poor night’s sleep stop you from losing body fat?S. Coe British Nutrition Foundation, London, UK Over the last 40 years, studies have consistently shown that adults in the UK obtain an average of 7 1 /4 h of sleep on a daily basis (LSRC 2010). However, recommenda- tions state that we should be getting 7–9 h of sleep a night (NSF 2009). Therefore, many adults may be accruing a ‘sleep debt’ if they are not getting enough sleep every night. Recent media headlines such as ‘A good night’s sleep helps you stay slim’ (Daily Mail 2010) and ‘Skip- ping sleep makes it harder to lose weight’ (Daily Tele- graph 2010) suggest that the amount of nightly sleep may be a particularly important factor for dieters to consider, as it may hinder any efforts to lose weight. This article therefore looks at the study that generated these head- lines to investigate the potential role that sleep may have in appetite and weight regulation. Sleep and weight regulation A number of cross-sectional studies have found short sleep duration to be associated with increased risk of obesity (Kohatsu et al. 2006; Moreno et al. 2006; Bjor- vatn et al. 2007; Stranges et al. 2008). While the mecha- nism by which sleep deprivation might affect weight regulation is still unclear, it has been suggested that the regulation of two appetite hormones may be involved: leptin and ghrelin. Leptin is a hormone secreted by adipose tissue that decreases appetite by signalling satiety, the feeling of fullness experienced after a meal. Ghrelin is a hormone secreted from the lining of the stomach that stimulates appetite. Consequently, these two hormones act in opposition to one another and have different cycles of secretion. A study of 31 healthy men and women found that leptin levels peaked on average at 01:20 am with the lowest levels at approximately 10:33 am (Saad et al. 1998). As ghrelin is known to have the reverse cycle of secretion to leptin, ghrelin levels normally peak during the day and are lowest at night. Studies investigating how sleep deprivation affects the levels of these hormones have shown that leptin levels (appetite suppressor) are lower and ghrelin levels (appe- tite stimulator) are higher in the morning after between 4 and 5 h of time in bed compared with longer periods of sleep (Spiegel et al. 2004; Taheri et al. 2004). The participants in Spiegel et al.’s study also reported feeling hungrier after sleep deprivation, which provides support for the altered levels of these hormones, in particular higher levels of ghrelin. The study behind the headlines The recent headlines regarding the association between sleep and weight loss were generated after the publica- tion of a study by scientists at the University of Chicago that investigated whether sleep restriction attenuates the effect of a reduced-calorie diet on excess adiposity (Nedeltcheva et al. 2010). The investigators conducted a randomised, crossover design study entailing two dif- ferent time periods and conditions in ten overweight, sedentary, non-smoking adult volunteers (n = 3 female, n = 7 male). The study population were aged 35–49 with a body mass index (BMI) within the range of 25–32 kg/m 2 ; therefore, all participants were either overweight (BMI 25 kg/m 2 ) or obese (BMI 30 kg/ m 2 ). Volunteers were excluded if they had a history of sleep problems, night work, variable sleep habits, exces- sive alcohol or caffeine intakes, use of medications that could affect sleep, physically demanding occupations or if they were pregnant. Participants spent two 14-day periods residing in a university sleep research centre. All participants spent their waking hours conducting home or office-like work or leisure activities in order to restrict their physical activity levels. Daily calorie intake was also restricted to 10% less than their daily calorie intake requirement to maintain weight (mean daily intake of 1450 calories). During the first phase of this experiment, participants were allowed the opportunity to sleep for 8.5 h, leading to an average of 7 h and 25 min of sleep each night. In the second period, participants were only Correspondence: Sarah Coe, Research Assistant, British Nutrition Foundation, High Holborn House, 52–54 High Holborn, London WC1V 6RQ, UK. E-mail: [email protected] © 2011 The Author Journal compilation © 2011 British Nutrition Foundation Nutrition Bulletin, 36, 99–101 99

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FACTS BEHIND THE HEADLINES

Can a poor night’s sleep stop you from losingbody fat?nbu_1875 99..101

S. CoeBritish Nutrition Foundation, London, UK

Over the last 40 years, studies have consistently shownthat adults in the UK obtain an average of 71/4 h of sleepon a daily basis (LSRC 2010). However, recommenda-tions state that we should be getting 7–9 h of sleep a night(NSF 2009). Therefore, many adults may be accruing a‘sleep debt’ if they are not getting enough sleep everynight. Recent media headlines such as ‘A good night’ssleep helps you stay slim’ (Daily Mail 2010) and ‘Skip-ping sleep makes it harder to lose weight’ (Daily Tele-graph 2010) suggest that the amount of nightly sleep maybe a particularly important factor for dieters to consider,as it may hinder any efforts to lose weight. This articletherefore looks at the study that generated these head-lines to investigate the potential role that sleep may havein appetite and weight regulation.

Sleep and weight regulation

A number of cross-sectional studies have found shortsleep duration to be associated with increased risk ofobesity (Kohatsu et al. 2006; Moreno et al. 2006; Bjor-vatn et al. 2007; Stranges et al. 2008). While the mecha-nism by which sleep deprivation might affect weightregulation is still unclear, it has been suggested that theregulation of two appetite hormones may be involved:leptin and ghrelin. Leptin is a hormone secreted byadipose tissue that decreases appetite by signallingsatiety, the feeling of fullness experienced after a meal.Ghrelin is a hormone secreted from the lining of thestomach that stimulates appetite. Consequently, thesetwo hormones act in opposition to one another and havedifferent cycles of secretion. A study of 31 healthy menand women found that leptin levels peaked on average at01:20 am with the lowest levels at approximately 10:33am (Saad et al. 1998). As ghrelin is known to have thereverse cycle of secretion to leptin, ghrelin levels normallypeak during the day and are lowest at night.

Studies investigating how sleep deprivation affects thelevels of these hormones have shown that leptin levels(appetite suppressor) are lower and ghrelin levels (appe-tite stimulator) are higher in the morning after between4 and 5 h of time in bed compared with longer periodsof sleep (Spiegel et al. 2004; Taheri et al. 2004). Theparticipants in Spiegel et al.’s study also reported feelinghungrier after sleep deprivation, which provides supportfor the altered levels of these hormones, in particularhigher levels of ghrelin.

The study behind the headlines

The recent headlines regarding the association betweensleep and weight loss were generated after the publica-tion of a study by scientists at the University of Chicagothat investigated whether sleep restriction attenuatesthe effect of a reduced-calorie diet on excess adiposity(Nedeltcheva et al. 2010). The investigators conducteda randomised, crossover design study entailing two dif-ferent time periods and conditions in ten overweight,sedentary, non-smoking adult volunteers (n = 3 female,n = 7 male). The study population were aged 35–49with a body mass index (BMI) within the range of25–32 kg/m2; therefore, all participants were eitheroverweight (BMI � 25 kg/m2) or obese (BMI � 30 kg/m2). Volunteers were excluded if they had a history ofsleep problems, night work, variable sleep habits, exces-sive alcohol or caffeine intakes, use of medications thatcould affect sleep, physically demanding occupationsor if they were pregnant. Participants spent two 14-dayperiods residing in a university sleep research centre. Allparticipants spent their waking hours conducting homeor office-like work or leisure activities in order to restricttheir physical activity levels. Daily calorie intake wasalso restricted to 10% less than their daily calorie intakerequirement to maintain weight (mean daily intake of1450 calories). During the first phase of this experiment,participants were allowed the opportunity to sleep for8.5 h, leading to an average of 7 h and 25 min of sleepeach night. In the second period, participants were only

Correspondence: Sarah Coe, Research Assistant, British NutritionFoundation, High Holborn House, 52–54 High Holborn, LondonWC1V 6RQ, UK.E-mail: [email protected]

© 2011 The AuthorJournal compilation © 2011 British Nutrition Foundation Nutrition Bulletin, 36, 99–101

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allowed 5.5 h of sleep opportunity, resulting in anaverage of 5 h and 14 min of sleep each night. Partici-pants’ nightly sleep was measured by minutes spent inthe various stages of sleep, including slow-wave andrapid eye movement sleep. The research outcomes mea-sured included loss of fat and fat-free body mass, energyexpenditure, hunger ratings, 24-h hormone concentra-tions (ghrelin, leptin, cortisol, epinephrine, norepine-phrine, growth hormone and thyroid hormone), andchange in substrate utilization (protein or fat), indicatedby measuring the respiratory quotient (RQ), which isgreater when protein is being metabolised for energyrather than fat.

Although mean total weight loss was identical (3 kg)between the two study periods, the findings showedthat, on average, subjects lost less weight as fat duringthe reduced sleep phase compared with the period withmore sleep opportunity (0.6 kg vs. 1.4 kg, respectively;P = 0.043) but lost more weight as fat-free mass (i.e.muscle) (2.4 kg vs. 1.5 kg; P = 0.002). Serum ghrelinlevels were found to be higher during the period ofreduced sleep, which is also supported by participants’reports of increased hunger during this phase. Sleepdeprivation was also found to induce a lower restingmetabolic rate and epinephrine levels, both of whichwould reduce total energy expenditure and make itmore difficult to lose weight. RQ was measured bothbefore and after breakfast during both sleep condi-tions, and was found to be, on average, higher after5.5 h of sleep opportunity compared with the longerperiod of sleep. This suggests that the substrate beingmetabolised for energy changed from fat to protein,supporting the observation that less body fat waslost.

Strengths and limitations of this study

The crossover design of this study was appropriate forcontrolling selection bias, as all participants experiencedthe same conditions in the same sequence. However, asphysical activity and daily calorie intake were controlledduring the laboratory study, the results are difficult toextrapolate to a ‘real-world’ setting where these vari-ables could have a significant effect on the associationbetween sleep deprivation and body weight and fat dis-tribution. The generalisability of the findings is alsolimited by the study’s short duration, small sample size,and the study sample that was predominantly femaleand had a limited age range.

Moreover, the findings cannot be extrapolated tothose with co-morbidities typically associated withexcess weight, such as type 2 diabetes, as subjects were

excluded if they suffered from any of these health con-ditions. A larger number of participants with equal rep-resentation of both genders from a wider age range needto be studied to make the findings more generalisable,although this is clearly difficult as these types of studiesare typically time consuming and expensive.

Although sleep duration was measured extensively,any opportunity for sleep was within the confines of alaboratory setting. Given that this was not the naturalsleep setting of the participants, the number of hours ofactual sleep obtained may have been much lower thanthe average obtained during 5.5 h of sleep opportunity.Furthermore, no comparisons were made regarding theeffects of different degrees of sleep deprivation on bodyweight regulation. This therefore hampers any clearguideline on the level of sleep needed to support fat loss.

Studies investigating the effects of a lack of sleep aretypically technically difficult to perform, particularlyas inducing long-term sleep deprivation is unethicalbecause of potential detrimental effects upon health andwellbeing. For this reason, the feasibility of a larger,more long-term study of this type is debatable. In addi-tion, the criteria used for sleep deprivation in this study(5.5 h of sleep opportunity) could be generally regardedas a rare occurrence in UK adults, as evidence over thepast few decades has consistently shown that theaverage amount of nightly sleep in adults is muchgreater than this (LSRC 2010). Also, studies investigat-ing sleep use varying criteria for the amount of sleepclassified as sleep deprivation; therefore, there is a needfor a formal definition.

Conclusions

Overall, this study found an association between sleepdeprivation and decreased fat mass loss illustrated by adecreased loss of fat body mass after a 2-week period ofshortened sleep (5.5 h of sleep opportunity). However,while the results from this study are a useful contributorto the mounting evidence from studies investigatingpotential contributors to weight gain, there are manyother factors involved in the development of overweightand obesity that may have a much greater role to playthan quite simply a lack of sleep. For example, it may bethe case that adults who sleep less have more time to eat,are too tired for physical activity or make up for a lackof sleep by consuming more food for energy and there-fore have an increased likelihood of weight gain. More-over, given today’s hectic lifestyles, it may also be easierfor some people to simply consume less energy ratherthan to try to catch up on sleep. On the whole, there isalso little or no evidence to suggest that people with

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short sleep cycles who simply change their sleep habitsso that they sleep longer will lose weight (Horne 2007).More studies are therefore needed to investigate thisfurther.

The findings from this study build upon previousevidence for the potential role of sleep in weight regu-lation. However, there is still insufficient evidence uponwhich to make clinical recommendations that might beused in weight-loss strategies. This study will hopefullystimulate further research in this field to get a clearerpicture of the mechanisms behind the potential effect ofsleep on the regulation of body mass.

Conflict of interest

The author has no conflict of interest to disclose.

References

Bjorvatn B, Sagen IM, Oyane N et al. (2007) The associationbetween sleep duration, body mass index and metabolic measuresin the Hordaland Health Study. Journal of Sleep Research 16:66–76.

Daily Mail (2010) A good night’s sleep helps you stay slim. DailyMail, 5 October 2010.

Daily Telegraph (2010) Skipping sleep makes it harder to loseweight. Daily Telegraph, 5 October 2010.

Horne J (2007) Short sleep is a questionable risk factor for obesityand related disorders: statistical versus clinical significance.Biological Psychology 77: 266–76.

Kohatsu ND, Tsai R, Young T et al. (2006) Sleep duration andbody mass index in a rural population. Archives of InternalMedicine 166: 1701–5.

LSRC (Loughborough Sleep Research Centre) (2010) OngoingResearch – How Much Sleep Do We Need? Available at: http://www.lboro.ac.uk/departments/ssehs/research/centres-institutes/sleep/research1.html (accessed 18 November 2010).

Moreno CRC, Louzada FM, Teixeira LR et al. (2006) Short sleep isassociated with obesity among truck drivers. ChronobiologyInternational 23: 1295–303.

Nedeltcheva MD, Kilkus JM, Imperial J et al. (2010) Insufficientsleep undermines dietary efforts to reduce adiposity. Annals ofInternal Medicine 153: 435–41.

NSF (National Sleep Foundation) (2009) How Much Sleep Do WeReally Need? Available at: http://www.sleepfoundation.org/article/how-sleep-works/how-much-sleep-do-we-really-need (accessed 18November 2010).

Saad MF, Riad-Gabriel MG, Khan A et al. (1998) Diurnal andultradian rhythmicity of plasma leptin: effects of gender and adi-posity. The Journal of Clinical Endocrinology & Metabolism 83:453–9.

Spiegel K, Leproult R, L’Hermite-Baleriaux M et al. (2004) Leptinlevels are dependent on sleep duration: relationships with sym-pathovagal balance, carbohydrate regulation, cortisol, and thy-rotropin. The Journal of Clinical Endocrinology & Metabolism89: 5762–71.

Stranges S, Cappuccio FP, Kandala NB et al. (2008) Cross-sectionalversus prospective associations of sleep duration with changes inrelative weight and body fat distribution. American Journal ofEpidemiology 167: 321–9.

Taheri S, Lin L, Austin D et al. (2004) Short sleep duration is asso-ciated with reduced leptin, elevated ghrelin, and increased bodymass index. PLoS Medicine 1: 210–17.

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