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FAC T S B E H I N D T HE HE A D L I N E S

Can a poor nights sleep stop you from losing


body fat?
nbu_1875

99..101

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 71/4 h of sleep
on a daily basis (LSRC 2010). However, recommendations state that we should be getting 79 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 nights
sleep helps you stay slim (Daily Mail 2010) and Skipping sleep makes it harder to lose weight (Daily Telegraph 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 headlines 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; Bjorvatn et al. 2007; Stranges et al. 2008). While the mechanism 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.
Correspondence: Sarah Coe, Research Assistant, British Nutrition
Foundation, High Holborn House, 5254 High Holborn, London
WC1V 6RQ, UK.
E-mail: s.coe@nutrition.org.uk

2011 The Author


Journal compilation 2011 British Nutrition Foundation Nutrition Bulletin, 36, 99101

Studies investigating how sleep deprivation affects the


levels of these hormones have shown that leptin levels
(appetite suppressor) are lower and ghrelin levels (appetite 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 publication 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 different time periods and conditions in ten overweight,
sedentary, non-smoking adult volunteers (n = 3 female,
n = 7 male). The study population were aged 3549
with a body mass index (BMI) within the range of
2532 kg/m2; therefore, all participants were either
overweight (BMI 25 kg/m2) or obese (BMI 30 kg/
m2). Volunteers were excluded if they had a history of
sleep problems, night work, variable sleep habits, excessive 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

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S. Coe

allowed 5.5 h of sleep opportunity, resulting in an


average of 5 h and 14 min of sleep each night. Participants nightly sleep was measured by minutes spent in
the various stages of sleep, including slow-wave and
rapid eye movement sleep. The research outcomes measured included loss of fat and fat-free body mass, energy
expenditure, hunger ratings, 24-h hormone concentrations (ghrelin, leptin, cortisol, epinephrine, norepinephrine, growth hormone and thyroid hormone), and
change in substrate utilization (protein or fat), indicated
by measuring the respiratory quotient (RQ), which is
greater when protein is being metabolised for energy
rather than fat.
Although mean total weight loss was identical (3 kg)
between the two study periods, the findings showed
that, on average, subjects lost less weight as fat during
the reduced sleep phase compared with the period with
more 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 ghrelin
levels were found to be higher during the period of
reduced sleep, which is also supported by participants
reports of increased hunger during this phase. Sleep
deprivation was also found to induce a lower resting
metabolic rate and epinephrine levels, both of which
would reduce total energy expenditure and make it
more difficult to lose weight. RQ was measured both
before and after breakfast during both sleep conditions, and was found to be, on average, higher after
5.5 h of sleep opportunity compared with the longer
period of sleep. This suggests that the substrate being
metabolised for energy changed from fat to protein,
supporting the observation that less body fat was
lost.

Strengths and limitations of this study


The crossover design of this study was appropriate for
controlling selection bias, as all participants experienced
the same conditions in the same sequence. However, as
physical activity and daily calorie intake were controlled
during the laboratory study, the results are difficult to
extrapolate to a real-world setting where these variables could have a significant effect on the association
between sleep deprivation and body weight and fat distribution. The generalisability of the findings is also
limited by the studys short duration, small sample size,
and the study sample that was predominantly female
and had a limited age range.
Moreover, the findings cannot be extrapolated to
those with co-morbidities typically associated with
excess weight, such as type 2 diabetes, as subjects were

excluded if they suffered from any of these health conditions. A larger number of participants with equal representation of both genders from a wider age range need
to be studied to make the findings more generalisable,
although this is clearly difficult as these types of studies
are typically time consuming and expensive.
Although sleep duration was measured extensively,
any opportunity for sleep was within the confines of a
laboratory setting. Given that this was not the natural
sleep setting of the participants, the number of hours of
actual sleep obtained may have been much lower than
the average obtained during 5.5 h of sleep opportunity.
Furthermore, no comparisons were made regarding the
effects of different degrees of sleep deprivation on body
weight regulation. This therefore hampers any clear
guideline on the level of sleep needed to support fat loss.
Studies investigating the effects of a lack of sleep are
typically technically difficult to perform, particularly
as inducing long-term sleep deprivation is unethical
because of potential detrimental effects upon health and
wellbeing. For this reason, the feasibility of a larger,
more long-term study of this type is debatable. In addition, the criteria used for sleep deprivation in this study
(5.5 h of sleep opportunity) could be generally regarded
as a rare occurrence in UK adults, as evidence over the
past few decades has consistently shown that the
average amount of nightly sleep in adults is much
greater than this (LSRC 2010). Also, studies investigating sleep use varying criteria for the amount of sleep
classified as sleep deprivation; therefore, there is a need
for a formal definition.

Conclusions
Overall, this study found an association between sleep
deprivation and decreased fat mass loss illustrated by a
decreased loss of fat body mass after a 2-week period of
shortened sleep (5.5 h of sleep opportunity). However,
while the results from this study are a useful contributor
to the mounting evidence from studies investigating
potential contributors to weight gain, there are many
other factors involved in the development of overweight
and obesity that may have a much greater role to play
than quite simply a lack of sleep. For example, it may be
the case that adults who sleep less have more time to eat,
are too tired for physical activity or make up for a lack
of sleep by consuming more food for energy and therefore have an increased likelihood of weight gain. Moreover, given todays hectic lifestyles, it may also be easier
for some people to simply consume less energy rather
than to try to catch up on sleep. On the whole, there is
also little or no evidence to suggest that people with

2011 The Author


Journal compilation 2011 British Nutrition Foundation Nutrition Bulletin, 36, 99101

Poor nights sleep and weight management

short sleep cycles who simply change their sleep habits


so that they sleep longer will lose weight (Horne 2007).
More studies are therefore needed to investigate this
further.
The findings from this study build upon previous
evidence for the potential role of sleep in weight regulation. However, there is still insufficient evidence upon
which to make clinical recommendations that might be
used in weight-loss strategies. This study will hopefully
stimulate further research in this field to get a clearer
picture of the mechanisms behind the potential effect of
sleep 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 association
between sleep duration, body mass index and metabolic measures
in the Hordaland Health Study. Journal of Sleep Research 16:
6676.
Daily Mail (2010) A good nights sleep helps you stay slim. Daily
Mail, 5 October 2010.
Daily Telegraph (2010) Skipping sleep makes it harder to lose
weight. Daily Telegraph, 5 October 2010.
Horne J (2007) Short sleep is a questionable risk factor for obesity
and related disorders: statistical versus clinical significance.
Biological Psychology 77: 26676.

2011 The Author


Journal compilation 2011 British Nutrition Foundation Nutrition Bulletin, 36, 99101

101

Kohatsu ND, Tsai R, Young T et al. (2006) Sleep duration and


body mass index in a rural population. Archives of Internal
Medicine 166: 17015.
LSRC (Loughborough Sleep Research Centre) (2010) Ongoing
Research 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 is
associated with obesity among truck drivers. Chronobiology
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Nedeltcheva MD, Kilkus JM, Imperial J et al. (2010) Insufficient
sleep undermines dietary efforts to reduce adiposity. Annals of
Internal Medicine 153: 43541.
NSF (National Sleep Foundation) (2009) How Much Sleep Do We
Really Need? Available at: http://www.sleepfoundation.org/article/
how-sleep-works/how-much-sleep-do-we-really-need (accessed 18
November 2010).
Saad MF, Riad-Gabriel MG, Khan A et al. (1998) Diurnal and
ultradian rhythmicity of plasma leptin: effects of gender and adiposity. The Journal of Clinical Endocrinology & Metabolism 83:
4539.
Spiegel K, Leproult R, LHermite-Baleriaux M et al. (2004) Leptin
levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. The Journal of Clinical Endocrinology & Metabolism
89: 576271.
Stranges S, Cappuccio FP, Kandala NB et al. (2008) Cross-sectional
versus prospective associations of sleep duration with changes in
relative weight and body fat distribution. American Journal of
Epidemiology 167: 3219.
Taheri S, Lin L, Austin D et al. (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body
mass index. PLoS Medicine 1: 21017.

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