- Email: [email protected]
Is sleep duration associated with obesity—Where do U stand?
ARTICLE IN PRESS Sleep Medicine Reviews (2008) 12, 299–302
www.elsevier.com/locate/smrv
COMMENTARY
Is sleep duration associated with obesity—Where do U stand? Shahrad Taheria,b,, G. Neil Thomasa a
University of Birmingham, Birmingham, UK Birmingham Heartlands Hospital, Birmingham, UK
b
There is nothing either good or bad, but thinking makes it soyHamlet, Act 2, Scene 2, William Shakespeare. Despite Doll and Bradford-Hill first suggesting an association between smoking and lung cancer in the 1950s, smoking remains the leading preventable cause of death.1 Smoking continues to challenge public health physicians and, despite overwhelming evidence of its harmful effects, is likely to be a major contributor to morbidity and mortality for years to come. Obesity is an increasingly important public health challenge that is likely to replace smoking as the major global cause of premature death. Of concern, is the rising prevalence of childhood obesity, since childhood obesity causes early complications and tracks into adulthood. On the surface, stopping smoking or reducing calorie intake appears simple, but it is practically difficult because of the complex biopsychosocial factors involved in initiating and perpetuating smoking and unhealthy eating habits. While it is the imbalance between food intake and physical activity that leads to obesity, more information is needed about the various factors contributing to this imbalance. The medical approach has been concentrating on the molecular aspects of obesity with an emphasis on pharmaceutical solutions when a multi-faceted Corresponding author at: University of Birmingham and
Birmingham Heartlands Hospital, Birmingham, UK. E-mail address: [email protected] (S. Taheri).
approach is what is required. There is therefore a great need to improve our understanding of factors contributing to obesity in order to develop effective, acceptable and sustainable interventions to prevent and treat the condition. In a recent report, obesity was identified as a major threat to future health which should be tackled immediately.2 Additionally, because of the danger that obesity poses, it was stated that where evidence is lacking (e.g., effective preventive strategies for obesity) promising ideas should be piloted and evaluated followed by taking appropriate action. Recently, there has been great interest in the potential contribution of sleep duration to obesity and how sleep may alter both sides of the energy balance equation. This has captured not only the interest of sleep and metabolic researchers but also, like many other research areas, the interest of the media and the public. An immediate positive effect of the recent research interest in association between sleep duration and obesity has been a recognition that there are previously unexplored factors that could contribute to the development and perpetuation of obesity.3 A positive effect of the media and public interest has been the greater realisation that perhaps sleep is not a waste of time after all and could potentially have beneficial effects. When Doll and Bradford-Hill first highlighted the potential dangers of smoking to health, they faced a lot of scepticism from the scientific community
1087-0792/$ - see front matter & 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.smrv.2008.04.003
ARTICLE IN PRESS 300 and the general public. It took over 50 years since the publication of their report and an unprecedented body of evidence describing the harmful effects of tobacco for the first country to ban smoking in work and public places. It is therefore not surprising that Marshall4 and colleagues should now challenge the potential association between sleep duration and obesity. In their critical appraisal, Marshall and colleagues legitimately raised important issues that have a bearing on sleep research in general. According to these authors, there has been little emphasis on the evidence against an association between sleep duration and obesity. They argue that sleep researchers, whose raison d’e ˆtre is the promotion of sleep’s beneficial functions, have a conflict of interest. Furthermore, they also suggest that it is premature to give health advice regarding sleep as a potential measure against obesity. Certainly, there are questions to be answered regarding the association between sleep duration and obesity and additional studies are necessary to determine the importance of sleep to body weight regulation. It is, however, important to look at this association in the context of other research findings. For example, while it is common sense that increased calorie intake and reduced physical activity are important in the development of obesity, surprisingly, not all studies (including longitudinal studies) have shown that increased calorie intake and reduced physical activity cause obesity.5 Similar controversies exist regarding other health and cognitive associations with sleep duration. It is therefore not surprising that not all studies have shown an association between sleep duration and obesity (although a very clear majority have) and that while some studies have found a negative linear association, others have found a U-shaped relationship. Another context is the emergence of data regarding sleep deprivation and changes in appetite and appetite-regulating hormones. These studies and their drawbacks have been previously discussed, but together with epidemiological findings6 help us to get closer in completing the jigsaw for the association between sleep duration and obesity.7 The lack of suitable animal models is likely to delay our understanding of all potential neuro-hormonal mechanisms. What is clear from the majority of population studies quoted by Marshall and colleagues, and other studies not included in their critique, is that there is a relationship between sleep duration and obesity that requires further investigation. This is strengthened by recent meta-analyses that have also examined the potential contribution of publication bias.8,9 These findings have been reported
S. Taheri, G.N. Thomas from several countries and ethnicities and should not be dismissed off-hand. A significant body of the current data was collected by researchers whose focus was not purely sleep research negating any conflict of interest by sleep researchers. Scientific publications in this research area, including reviews, have been peer-reviewed and balanced in highlighting the available knowledge base including potential weaknesses of research findings. Some of the publications have been accompanied by editorials from sleep and non-sleep researchers discussing both positive and negative aspects of findings. While maintaining objectivity, it is vital for sleep researchers to highlight the sleep–obesity association and to investigate it through collaboration with obesity and metabolic researchers. Although a separate debate, sleep or any other researchers have no control on what the media does or does not report and how this is reported, or any influence on recent scientifically suspect lay books promoting sleep as a panacea to obesity. Not unlike the relationship of several risk factors, such as obesity with morbidity and mortality, the association between sleep duration and obesity has been reported to be U-shaped in adults, with both short and long sleep duration being associated with obesity. This could be related to the complex mechanisms through which individuals reach the obese phenotype, but could also reflect the potential role of sleep duration as a marker for development of unhealthy lifestyles or for confounding as a result of existing unrecognised morbidity rather than being causal for obesity. Future studies should aim to bring greater clarity in understanding the factors contributing to the Ushape just as smoking has been identified as a contributor to the association between low-body mass index and mortality. Additionally, as previously alluded to,7 the association between short and long sleep duration and obesity may not necessarily reflect the causal effect of sleep loss or excess sleep per se, but could be a marker highlighting that naturally short and long sleepers are at-risk populations for obesity, diabetes, cardiovascular disease and mortality. The relationship between sleep duration and obesity is more straightforward in children in that short sleep duration is consistently associated with obesity and there is no U-shaped relationship. Of note, there is a potentially interesting difference between males and females reported by some studies that needs further evaluation. It has to be considered that sleep duration and patterns may have different health effects in different age groups. The majority of studies reporting an association between sleep duration and obesity have been
ARTICLE IN PRESS Is sleep duration associated with obesity? cross-sectional and were not designed to specifically study this association. On the other hand, some studies have perhaps over-controlled for various potential confounding factors thus dimishing the association between sleep duration and obesity. For instance, if sleep duration modulates dietary intake thus predisposing to obesity, adjustment for diet would effectively attenuate the direct effect of sleep duration. Few studies have used more objective measures of sleep and the validity and reliability of self-reported sleep duration have been questioned.10 While polysomnography interferes with sleep and cannot be carried out over a prolonged period, actigraphy is less intrusive. But even actigraphy will only provide a snapshot of sleep behaviour. Future studies should concentrate on collecting more objective repeated sleep data. Careful longitudinal studies will help to determine causality, but these will require sufficient numbers and objective measures of sleep. Large studies such as the US National Children’s Study may provide helpful information, but notwithstanding funding problems for such large studies, it will take a significant amount of time before there is a definitive answer. Marshall and colleagues argue that no study has shown that changes in sleep duration are associated with weight loss. It would be difficult to make such an observation in population studies since it is unlikely that individuals will have static behaviours. It is not uncommon for individuals to go through periods where they try to lose weight (by reducing calorie intake, altering macronutrient intake, and/or increasing physical activity) and periods where they put on excessive weight and this will confound findings. Additionally, it may be argued that the body weight difference with fewer sleep hours is small. What is clear is that as little as a daily excess of 100 kcal (the near equivalent of a slice of bread) can result in obesity over time. Also, weight reduction of as little as 5–10% of body weight could significantly reduce the risk of developing obesity complications such as diabetes mellitus and ameliorates obstructive sleep apnoea. Obesity treatment options in children in particular are limited necessitating a preventive approach. Attempts to reduce or prevent obesity by interventions only focussed on food intake or activity levels have been unsuccessful. Thus, there is an urgent need to implement additional potential measures quickly to halt obesity. It would be unethical to experimentally manipulate sleep in children or adults to induce obesity. The randomised controlled trial designed using the UK Medical Research Council’s framework for the evaluation of complex interventions11 aiming to
301 alter sleep in specific sleep duration cohorts, would provide useful information, but whether the preparatory work and the trial itself will be funded in societies that do not recognise the value of sleep, remain to be determined. Furthermore, it would be argued that there will be confounding effects of several factors, e.g., physical activity which appears to have a synergistic interaction with sleep. It is recognised that sleep duration alone is not the answer to the obesity pandemic.12 However, while further evidence is awaited, including potential specific strategies that may be used in certain populations to extend or reduce sleep duration that may be tested in randomised controlled trials, there is little risk in taking a pragmatic approach and encouraging adequate sleep as an adjunct to other lifestyle measures in prevention of obesity in children. Indeed, Marshall and colleagues are comfortable with recommending adequate sleep for other potentially beneficial reasons. The question is how long should ‘‘adequate’’ sleep be. One approach is to ensure that there is no interference with sleep such as a lack of bedtime routines, and television viewing and use of electronic devices near bedtimes and in bedrooms.12 By providing the appropriate circumstances and environment for sleep, children may benefit from not only a reduced risk of obesity, but there are also other potential benefits. While it is important to approach the sleep-obesity relationship with the utmost scientific rigour, a major drawback of being prematurely over critical of this fledgling research area is that much needed funding to investigate the association between sleep and obesity will not be provided. Thus, the association could be ignored with potential negative health consequences. In fact, the US National Institute of Health and other funding bodies should be applauded for recognising the importance of understanding all potential factors, including sleep duration, that could influence body weight. No plausible avenues should remain unexplored in developing strategies to tackle the obesity pandemic. Hopefully, it will take less time to understand the implications of sleep duration, including its potential impact on obesity than for the realisation of the health dangers related to smoking. For this to happen, the glass should be seen as half full, as the majority of the evidence purports, rather than half empty.
References 1. Doll R, Hill AB. Smoking and carcinoma of the lung preliminary report. Br Med J 1950;2(4682):739–48.
ARTICLE IN PRESS 302 2. Wanless D, Appleby J, Harrison A, Patel D. Our future health secured? The King’s Fund 2007 /http://www.kingsfund. org.uk/media/the_nhs_will.htmlS. 3. Keith SW, Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC, Benca RM, et al. Putative contributors to the secular increase in obesity: exploring the roads less traveled. Int J Obes (Lond) 2006;30(11):1585–94 [Epub 2006 June 27]. 4. Marshall NS, Glozier N, Grunstein RR. Is sleep duration related to obesity? A critical review of the epidemiological evidence. Sleep Med Rev 2008;12:289–98. 5. Slyper AH. The pediatric obesity epidemic: causes and controversies. J Clin Endocrinol Metab 2004;89(6): 2540–7. 6. Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med 2004;1(3):e62 [Epub 2004 December 7].
S. Taheri, G.N. Thomas 7. Taheri S. Sleep and metabolism: bringing pieces of the jigsaw together. Sleep Med Rev 2007;11:159–62. 8. Cappuccio FP, Taggart FM, Kandala N-B, et al. Meta-analysis of short sleep duration and obesity in children and adults. Sleep 2008;31:619–26. 9. Chen X, Beydoun MA, Wang Y. Is sleep duration associated with childhood obesity? A systematic review and metaanalysis. Obesity (Silver Spring) 2008;16(2):265–74. 10. Bliwise DL, Young TB. The parable of parabola: what the U-shaped curve can and cannot tell us about sleep. Sleep 2007;30(12):1614–5. 11. A framework for development and evaluation of RCTs for complex interventions to improve health. The Medical Research Council (UK) 2000. /http://www.mrc.ac.uk/ Utilities/Documentrecord/index.htm?d=MRC003372S. 12. Taheri S. The link between short sleep duration and obesity: we should recommend more sleep to prevent obesity. Arch Dis Child 2006;91(11):881–4.
www.elsevier.com/locate/smrv
COMMENTARY
Is sleep duration associated with obesity—Where do U stand? Shahrad Taheria,b,, G. Neil Thomasa a
University of Birmingham, Birmingham, UK Birmingham Heartlands Hospital, Birmingham, UK
b
There is nothing either good or bad, but thinking makes it soyHamlet, Act 2, Scene 2, William Shakespeare. Despite Doll and Bradford-Hill first suggesting an association between smoking and lung cancer in the 1950s, smoking remains the leading preventable cause of death.1 Smoking continues to challenge public health physicians and, despite overwhelming evidence of its harmful effects, is likely to be a major contributor to morbidity and mortality for years to come. Obesity is an increasingly important public health challenge that is likely to replace smoking as the major global cause of premature death. Of concern, is the rising prevalence of childhood obesity, since childhood obesity causes early complications and tracks into adulthood. On the surface, stopping smoking or reducing calorie intake appears simple, but it is practically difficult because of the complex biopsychosocial factors involved in initiating and perpetuating smoking and unhealthy eating habits. While it is the imbalance between food intake and physical activity that leads to obesity, more information is needed about the various factors contributing to this imbalance. The medical approach has been concentrating on the molecular aspects of obesity with an emphasis on pharmaceutical solutions when a multi-faceted Corresponding author at: University of Birmingham and
Birmingham Heartlands Hospital, Birmingham, UK. E-mail address: [email protected] (S. Taheri).
approach is what is required. There is therefore a great need to improve our understanding of factors contributing to obesity in order to develop effective, acceptable and sustainable interventions to prevent and treat the condition. In a recent report, obesity was identified as a major threat to future health which should be tackled immediately.2 Additionally, because of the danger that obesity poses, it was stated that where evidence is lacking (e.g., effective preventive strategies for obesity) promising ideas should be piloted and evaluated followed by taking appropriate action. Recently, there has been great interest in the potential contribution of sleep duration to obesity and how sleep may alter both sides of the energy balance equation. This has captured not only the interest of sleep and metabolic researchers but also, like many other research areas, the interest of the media and the public. An immediate positive effect of the recent research interest in association between sleep duration and obesity has been a recognition that there are previously unexplored factors that could contribute to the development and perpetuation of obesity.3 A positive effect of the media and public interest has been the greater realisation that perhaps sleep is not a waste of time after all and could potentially have beneficial effects. When Doll and Bradford-Hill first highlighted the potential dangers of smoking to health, they faced a lot of scepticism from the scientific community
1087-0792/$ - see front matter & 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.smrv.2008.04.003
ARTICLE IN PRESS 300 and the general public. It took over 50 years since the publication of their report and an unprecedented body of evidence describing the harmful effects of tobacco for the first country to ban smoking in work and public places. It is therefore not surprising that Marshall4 and colleagues should now challenge the potential association between sleep duration and obesity. In their critical appraisal, Marshall and colleagues legitimately raised important issues that have a bearing on sleep research in general. According to these authors, there has been little emphasis on the evidence against an association between sleep duration and obesity. They argue that sleep researchers, whose raison d’e ˆtre is the promotion of sleep’s beneficial functions, have a conflict of interest. Furthermore, they also suggest that it is premature to give health advice regarding sleep as a potential measure against obesity. Certainly, there are questions to be answered regarding the association between sleep duration and obesity and additional studies are necessary to determine the importance of sleep to body weight regulation. It is, however, important to look at this association in the context of other research findings. For example, while it is common sense that increased calorie intake and reduced physical activity are important in the development of obesity, surprisingly, not all studies (including longitudinal studies) have shown that increased calorie intake and reduced physical activity cause obesity.5 Similar controversies exist regarding other health and cognitive associations with sleep duration. It is therefore not surprising that not all studies have shown an association between sleep duration and obesity (although a very clear majority have) and that while some studies have found a negative linear association, others have found a U-shaped relationship. Another context is the emergence of data regarding sleep deprivation and changes in appetite and appetite-regulating hormones. These studies and their drawbacks have been previously discussed, but together with epidemiological findings6 help us to get closer in completing the jigsaw for the association between sleep duration and obesity.7 The lack of suitable animal models is likely to delay our understanding of all potential neuro-hormonal mechanisms. What is clear from the majority of population studies quoted by Marshall and colleagues, and other studies not included in their critique, is that there is a relationship between sleep duration and obesity that requires further investigation. This is strengthened by recent meta-analyses that have also examined the potential contribution of publication bias.8,9 These findings have been reported
S. Taheri, G.N. Thomas from several countries and ethnicities and should not be dismissed off-hand. A significant body of the current data was collected by researchers whose focus was not purely sleep research negating any conflict of interest by sleep researchers. Scientific publications in this research area, including reviews, have been peer-reviewed and balanced in highlighting the available knowledge base including potential weaknesses of research findings. Some of the publications have been accompanied by editorials from sleep and non-sleep researchers discussing both positive and negative aspects of findings. While maintaining objectivity, it is vital for sleep researchers to highlight the sleep–obesity association and to investigate it through collaboration with obesity and metabolic researchers. Although a separate debate, sleep or any other researchers have no control on what the media does or does not report and how this is reported, or any influence on recent scientifically suspect lay books promoting sleep as a panacea to obesity. Not unlike the relationship of several risk factors, such as obesity with morbidity and mortality, the association between sleep duration and obesity has been reported to be U-shaped in adults, with both short and long sleep duration being associated with obesity. This could be related to the complex mechanisms through which individuals reach the obese phenotype, but could also reflect the potential role of sleep duration as a marker for development of unhealthy lifestyles or for confounding as a result of existing unrecognised morbidity rather than being causal for obesity. Future studies should aim to bring greater clarity in understanding the factors contributing to the Ushape just as smoking has been identified as a contributor to the association between low-body mass index and mortality. Additionally, as previously alluded to,7 the association between short and long sleep duration and obesity may not necessarily reflect the causal effect of sleep loss or excess sleep per se, but could be a marker highlighting that naturally short and long sleepers are at-risk populations for obesity, diabetes, cardiovascular disease and mortality. The relationship between sleep duration and obesity is more straightforward in children in that short sleep duration is consistently associated with obesity and there is no U-shaped relationship. Of note, there is a potentially interesting difference between males and females reported by some studies that needs further evaluation. It has to be considered that sleep duration and patterns may have different health effects in different age groups. The majority of studies reporting an association between sleep duration and obesity have been
ARTICLE IN PRESS Is sleep duration associated with obesity? cross-sectional and were not designed to specifically study this association. On the other hand, some studies have perhaps over-controlled for various potential confounding factors thus dimishing the association between sleep duration and obesity. For instance, if sleep duration modulates dietary intake thus predisposing to obesity, adjustment for diet would effectively attenuate the direct effect of sleep duration. Few studies have used more objective measures of sleep and the validity and reliability of self-reported sleep duration have been questioned.10 While polysomnography interferes with sleep and cannot be carried out over a prolonged period, actigraphy is less intrusive. But even actigraphy will only provide a snapshot of sleep behaviour. Future studies should concentrate on collecting more objective repeated sleep data. Careful longitudinal studies will help to determine causality, but these will require sufficient numbers and objective measures of sleep. Large studies such as the US National Children’s Study may provide helpful information, but notwithstanding funding problems for such large studies, it will take a significant amount of time before there is a definitive answer. Marshall and colleagues argue that no study has shown that changes in sleep duration are associated with weight loss. It would be difficult to make such an observation in population studies since it is unlikely that individuals will have static behaviours. It is not uncommon for individuals to go through periods where they try to lose weight (by reducing calorie intake, altering macronutrient intake, and/or increasing physical activity) and periods where they put on excessive weight and this will confound findings. Additionally, it may be argued that the body weight difference with fewer sleep hours is small. What is clear is that as little as a daily excess of 100 kcal (the near equivalent of a slice of bread) can result in obesity over time. Also, weight reduction of as little as 5–10% of body weight could significantly reduce the risk of developing obesity complications such as diabetes mellitus and ameliorates obstructive sleep apnoea. Obesity treatment options in children in particular are limited necessitating a preventive approach. Attempts to reduce or prevent obesity by interventions only focussed on food intake or activity levels have been unsuccessful. Thus, there is an urgent need to implement additional potential measures quickly to halt obesity. It would be unethical to experimentally manipulate sleep in children or adults to induce obesity. The randomised controlled trial designed using the UK Medical Research Council’s framework for the evaluation of complex interventions11 aiming to
301 alter sleep in specific sleep duration cohorts, would provide useful information, but whether the preparatory work and the trial itself will be funded in societies that do not recognise the value of sleep, remain to be determined. Furthermore, it would be argued that there will be confounding effects of several factors, e.g., physical activity which appears to have a synergistic interaction with sleep. It is recognised that sleep duration alone is not the answer to the obesity pandemic.12 However, while further evidence is awaited, including potential specific strategies that may be used in certain populations to extend or reduce sleep duration that may be tested in randomised controlled trials, there is little risk in taking a pragmatic approach and encouraging adequate sleep as an adjunct to other lifestyle measures in prevention of obesity in children. Indeed, Marshall and colleagues are comfortable with recommending adequate sleep for other potentially beneficial reasons. The question is how long should ‘‘adequate’’ sleep be. One approach is to ensure that there is no interference with sleep such as a lack of bedtime routines, and television viewing and use of electronic devices near bedtimes and in bedrooms.12 By providing the appropriate circumstances and environment for sleep, children may benefit from not only a reduced risk of obesity, but there are also other potential benefits. While it is important to approach the sleep-obesity relationship with the utmost scientific rigour, a major drawback of being prematurely over critical of this fledgling research area is that much needed funding to investigate the association between sleep and obesity will not be provided. Thus, the association could be ignored with potential negative health consequences. In fact, the US National Institute of Health and other funding bodies should be applauded for recognising the importance of understanding all potential factors, including sleep duration, that could influence body weight. No plausible avenues should remain unexplored in developing strategies to tackle the obesity pandemic. Hopefully, it will take less time to understand the implications of sleep duration, including its potential impact on obesity than for the realisation of the health dangers related to smoking. For this to happen, the glass should be seen as half full, as the majority of the evidence purports, rather than half empty.
References 1. Doll R, Hill AB. Smoking and carcinoma of the lung preliminary report. Br Med J 1950;2(4682):739–48.
ARTICLE IN PRESS 302 2. Wanless D, Appleby J, Harrison A, Patel D. Our future health secured? The King’s Fund 2007 /http://www.kingsfund. org.uk/media/the_nhs_will.htmlS. 3. Keith SW, Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC, Benca RM, et al. Putative contributors to the secular increase in obesity: exploring the roads less traveled. Int J Obes (Lond) 2006;30(11):1585–94 [Epub 2006 June 27]. 4. Marshall NS, Glozier N, Grunstein RR. Is sleep duration related to obesity? A critical review of the epidemiological evidence. Sleep Med Rev 2008;12:289–98. 5. Slyper AH. The pediatric obesity epidemic: causes and controversies. J Clin Endocrinol Metab 2004;89(6): 2540–7. 6. Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med 2004;1(3):e62 [Epub 2004 December 7].
S. Taheri, G.N. Thomas 7. Taheri S. Sleep and metabolism: bringing pieces of the jigsaw together. Sleep Med Rev 2007;11:159–62. 8. Cappuccio FP, Taggart FM, Kandala N-B, et al. Meta-analysis of short sleep duration and obesity in children and adults. Sleep 2008;31:619–26. 9. Chen X, Beydoun MA, Wang Y. Is sleep duration associated with childhood obesity? A systematic review and metaanalysis. Obesity (Silver Spring) 2008;16(2):265–74. 10. Bliwise DL, Young TB. The parable of parabola: what the U-shaped curve can and cannot tell us about sleep. Sleep 2007;30(12):1614–5. 11. A framework for development and evaluation of RCTs for complex interventions to improve health. The Medical Research Council (UK) 2000. /http://www.mrc.ac.uk/ Utilities/Documentrecord/index.htm?d=MRC003372S. 12. Taheri S. The link between short sleep duration and obesity: we should recommend more sleep to prevent obesity. Arch Dis Child 2006;91(11):881–4.