The evidence that short sleep duration is a determinant of obesity is accumulating (1–3). Prospective cohort studies have repeatedly shown that short sleep duration is associated with weight gain and an increased incidence of obesity in children and adults. Intervention studies have provided a mechanistic explanation, i.e. that sleep restriction impacts hormonal regulation of appetite. Ongoing research is assessing whether sleep extension in sleep deprived obese individuals can influence appetite control and/or reduce body fat (4). Given that chronic sleep restriction is highly tied to the modern way of living, studies aiming to investigate the possible causal association between short sleep duration and obesity are of particular importance from a public health standpoint.
In this issue of Obesity Reviews, Professor Jim Horne critically addressed the link between habitual short sleep duration and obesity from a sleep perspective (5). The author argued that the clinical significance of short sleep as a risk factor for obesity is very little, with weight gains attributed to short sleep of <2 kg over a year. Additionally, the author mentioned that the growing interest in short sleep as a determinant of obesity has the potential to focus attention on sleep rather than to exercise and diet as behaviours to promote weight loss and healthy body weight. Globally, the review paper is interesting and provides a different view point that can generate new studies on the field. However, some aspects need to be put into perspective.
First, many people fail to realize that obesity has a complex causation. The underlying causes and paths to obesity are manifold and one should thus expect the effect of any single factor to be relatively small. In this context, I would rather argue that a weight gain of as little as 1 kg over a year attributed to short sleep is clinically important on a population level. Second, it is important to realize that the main issue is not to determine whether or not short sleep is a cause of obesity (likely impossible to prove), but to understand the implications of chronic short sleep duration on energy balance. Time pressure is a reality of the modern way of living and many people prefer to reduce the time allocated to sleep in order to improve their quality of life. Such a strategy is understandable, but few realize that there might be a price to pay in the long run. Any influence of short sleep duration on food intake and physical activity participation is of importance in our understanding of the different pathways to obesity. Additionally, recent results have shown that sleep might be an important factor in successful weight loss, emphasizing that a narrow focus on diet and exercise might not be enough (6). Third, the objective in studying the association between short sleep duration and obesity should not be to neglect diet and physical activity in promoting healthy body weights, but rather to understand the interactions between short sleep duration and energy balance. In particular, we have recently realized that many factors (e.g. vitamins and minerals, chemical pollutants, sleep duration, etc.) can influence energy balance despite the fact that they do not have any caloric value per se(7,8). Finally, the author elegantly indicated in its review that ‘sleep-related obesity might even be protective’. This argument is interesting and agrees with the physiological perception of obesity that considers fat gain as a biological adaptation that ultimately permits the person gaining weight to reach a new homeostatic state (9). For the short sleeper, adipose tissue may at least provide an increased leptinemia.
It is obvious that the causal relation between short sleep duration and obesity will be difficult to obtain, if at all possible. Experimental evidence that sleep restriction induces obesity is not possible in humans for both ethical and logistic reasons. The best evidence 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 longitudinal studies. As recently addressed (2), short-term experiments may elucidate biological mechanisms supposedly inducing continuous weight gain, but whether they do 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. As mentioned by Professor Horne in his article, ‘the case for short sleep as a cause rather than just a correlate of obesity has yet to be established’. This is perhaps true, but the main message is that sleep quality/quantity still needs to be assessed if we want to adequately address the obesity problem; the preponderance of the evidence taken as a whole points towards an effect of sleep duration on body composition.
In summary, the review paper by Professor Horne is timely and brings about an interesting vision to the issue of short sleep duration as a possible cause of obesity. This again highlights the complex aetiology of obesity and the need for a personalized approach in both the prevention and treatment of this condition. Understanding the root causes of weight gain is crucial in the road to success. In the modern obesogenic environment, lack of sleep renders the maintenance of a healthy lifestyle more difficult for some people. I argue that the solution for obese short sleepers is not as simple as eating less and exercising more. As well, it is not as simple as telling them to sleep more. However, as long as short sleep is linked to our westernized lifestyle, it will be very difficult for short sleepers to swim upstream against the tide of obesogenic pressures.