Obesity is associated with lower quality and shorter duration of sleep (here). As sleep levels drop from around 8 hours to around 4 to 5 hours a night, energy intake increases. This energy increase has been given as an explanation for the association between obesity and sleep quality. However, the association may be more complex than this because it is not clear what type of foods are ingested to provide this increased energy consumption. For example, changes to macronutrient intakes may occur following sleep deprivation. This may result from stimulation of the appetite regulatory centres of the brain which result in increases plasma levels of the hunger hormone ghrelin. If sleep deprivation does stimulate appetite, this may lead to an over consumption of low quality foods containing processed fat, sugar and refined carbohydrates. Such low quality foods are drivers of weight gain because they cause metabolic dysfunction including non-alcoholic fatty liver, insulin and leptin resistance.
As well as increases in energy intake, sleep deprivation may also cause increases in energy expenditure. For example, in a recent study1, researchers assessed the energy expenditure of subjects who were deprived of sleep. The subjects were kept in a metabolic ward where their sleep duration was curtailed prematurely at 4 hours, or allowed their normal 8 hour sleep duration. The respiratory quotient and total 24-hour energy expenditure were measured. All subjects were female with body mass indices between 23.4 and 27.5 which suggests that the subjects were healthy but some were overweight. When sleep was curtailed early for the subjects the total 24-hour energy expenditure increased by around 92 kcals per day, which the authors calculated to be around 5 % of total energy expenditure. However, this increase in energy expenditure was less than the increase in energy intakes seen in previous studies investigating the effect of sleep deprivation on energy intake.
These results occurred after just two nights sleep suggesting that the effects of sleep deprivation on energy expenditure are acute in nature. Interestingly the increase in energy expenditure was due mainly to the increase energy expended at night while being awake, with only a small contribution from the day time. The respiratory quotient was unaffected by the sleep deprivation suggesting that substrate metabolism did not change due to lack of sleep. The fact that energy expenditure increases with sleep deprivation may suggest that compensatory changes occur to eating behaviour that result in the increased energy intake during the day. If these mechanisms overcompensate, or result in a higher intake of a particular type of macronutrient, this could explain the association between obesity and sleep deprivation. However, as the obese are more likely to suffer from sleep apnea, it could be that the cause and effect of the association are opposite, with obesity being the cause of a lack of sleep.
Dr Robert Barrington’s Nutritional Recommendation: Clearly the associations between sleep and being overweight are complex. However, a few conclusions can be drawn from research on the effects of sleep deprivation. Firstly sleep deprivation is metabolically disruptive and leads eventually to disease and death. Getting enough sleep is therefore pivotal in any strategy for health. Secondly, if sleep is deprived, it is important not to increase intakes of obesogenic foods. Eating a high quality diet is likely to protect from any effects of sleep deprivation, if higher intakes of refined carbohydrates and sugar are the cause of the association between sleep and obesity. Thirdly, if sleep deprivation is sustained through unforeseen and uncontrollable factors, it is important to consider nutritional strategies to combat the stress associated with sleep deprivation. This can include the use of L-tyrosine to support the production of stress hormones, levels of which can become depleted during chronic stress episodes.
RdB
