Sleep is among the most essential of human needs, but one that is often neglected. Many studies have shown that sleep deprivation puts people at risk of obesity and immune dysfunction. A new study provides insights into how experimentally-induced sleeplessness affects body fat when the subject is provided access to food.
Study: Effects of Experimental Sleep Restriction on Energy Intake, Energy Expenditure, and Visceral Obesity. Image Credit: Photographee.eu/Shutterstock
Introduction
It is estimated that one in three Americans have less than required sleep daily. This has been related to the incidence of obesity, morbidity, and early death. The current study, published in the Journal of the American College of Cardiology, aimed to determine whether too little sleep-induced obesity and where the extra fat was stored.
The study was designed in a randomized controlled design. Over 21 days, the investigators looked at how prolonged sleep deprivation acted on the intake and expenditure of energy and the storage of fat in healthy people who were of a healthy weight. The subjects were allowed to be in bed for only four hours a night during the two weeks of the experiment – the remaining week was for acclimation and recovery.
Like controls, the subjects were allowed 9 hours in bed during the latter phases. For both groups, subjects had unlimited access to food and were sedentary.
What did the study show?
All subjects had altered sleep patterns during the sleep restriction phase, with greater sleep efficiency and a change in the duration of various sleep stages. Rebound sleep was seen during the recovery phase.
Sleep-deprived subjects ate on average >300 kilocalories per day more than the controls during the sleep-restricted stage. Both protein and fat intake increased during this stage, by 13% and 17%, respectively, with about 11 g and 22 g more of protein and fat being ingested daily.
Carbohydrate intake showed no significant increase, however. The biggest increase was early in sleep deprivation but decreased towards the levels in the first three acclimation days of the study.
The way in which the body handles food, as seen by the basal metabolic rate, thermic effect of food, energy expenditure during ordinary activities vs. exercise, and physical activity, did not show any alteration. The body weight increased during sleep in both groups, but the gain was higher in the sleep-deprived group. During the study, participants in the sleep-restricted group gained half a kilogram.
The increase was steepest during the middle of the experimental phase and tapered towards normal during recovery. Significantly, no change was observed in the body fat percentage, total fat mass, or total lean mass. Total abdominal fat did increase during the sleep-deprived phase by almost a tenth. The increase, compared to controls, was 15 square cm.
The subcutaneous fat area also went up during sleep in both groups, by 4% for controls and 8% for sleep-deprived subjects, but the highest increase was in the sleep-restricted group. Visceral fat went up by 11% during sleep restriction, but this was not seen in controls, accounting for an 8 sq. cm difference between sleep-deprived and normal-sleep subjects.
It is important to note that both subcutaneous and visceral fat accumulation began early in the study and continued throughout the recovery phase in the sleep-restricted group. Conversely, controls showed later increases in subcutaneous fat.
What are the implications?
The study showed that energy intake increased over 14 days of sleep restriction when allowed free access to food, causing weight gain. The novel finding was that the excess fat accumulated in the abdominal area, especially visceral fat.
The increase in energy intake by over 300 kcal/day, on average, with sleep restriction, was lower than expected but led to increased body weight and visceral fat deposition. This agrees with earlier studies on the effect of shortened sleep on eating. The tendency to overeat was highest earlier in the sleep restriction part of the study and went down with continued sleep deprivation to finally return to normal eating patterns during recovery.
This may indicate that people take time to adjust to sleep loss, initially tending to eat more but returning to lower food intake patterns as shorter sleep patterns continue. However, “this defense response appears insufficient to entirely dissipate such effects, with consequent detrimental implications for weight gain and obesity.”
Not only do people eat more when sleep-deprived, but they eat more protein and fat. The reasons for overeating and choosing these nutrients over others remain to be elucidated. However, from prior research, it seems that the endocrine factors modulating appetite change with sleep loss. Some studies suggest increases in the levels of appetite-inducing hormones like ghrelin and endogenous cannabinoids increase, while leptin goes down, but these remain to be validated.
The current study also failed to show any changes in these hormones. This may mean that central brain areas fail to regulate appetite, perhaps providing excessive rewards when confronted with visual food cues, especially with energy-dense foods like junk foods. The failure of the body to regulate energy intake even though more food is being ingested than energy spent may indicate a dysregulation shift in appetite regulation.
Also, there was no increase in the energy spent during waking, despite the increase in wakeful periods. It would appear that “overeating is not simply a compensatory response to augmented energy output or daily movements with sleep truncation.” Instead, the positive energy balance is due to excess intake, uncorrected by appetite-regulatory endocrine changes, eventually causing weight gain.
The use of supplementary methods showed that both visceral and subcutaneous abdominal fat increased during sleep restriction but did not control sleep. Only a small increase occurred in subcutaneous fat in the control group. The increase in visceral fat continued in the recovery phase, even after sleep patterns and energy intake had returned to normal.
These data show, for the first time, that experimentally induced sleep curtailment affects regional fat accumulation, favoring abdominal adiposity, specifically centralized partitioning of fat into the visceral depot.”
In healthy individuals, fat storage with a positive energy balance occurs first in the subcutaneous region. The upsetting of this pattern during sleep deprivation occurs due to altered fat storage mechanisms that direct fat preferentially to visceral fat.
Abdominal fat increases are linked to poor health outcomes, probably because this fat depot contains lipids with less insulin sensitivity, greater metabolic activity, and a more pro-inflammatory profile. Visceral fat predicts cardiometabolic disease, other illnesses, and early death, far better than body mass index or subcutaneous fat.
Short periods of recovery sleep were unable to reverse visceral fat deposition. The catch-up sleep behavior that is often adopted currently to make up for lost sleep over the week may not, therefore, compensate for the metabolically risky visceral fat accumulation. These findings underline the public health importance of ensuring proper sleep in relation to excess fat deposition and alleviating cardiometabolic risk.
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