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Sleep deprivation: an important cardiometabolic risk factor

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The association between obesity and sleep deprivation has been demonstrated by multiple studies. The experiment conducted at the Mayo Clinic by Covassin and colleagues shows how sleep deprivation is associated with a higher energy intake and, consequently, with an increase in abdominal adipose tissue. Excess abdominal fat is an important cardiometabolic risk factor.

It is known from observational population-based data, that poor sleep may be a factor that can promote obesity. However, before the results of the study by Covassin et al., it was not known where excess fat was stored. Indeed, the study shows that poor sleep leads to an increase in abdominal adipose tissue. Visceral obesity is defined as an increase in intra-abdominal fat (visceral fat) and it’s much more dangerous than excess of subcutaneous adipose tissue, since it is associated with a reduction of insulin sensitivity, with a pro-inflammatory state and therefore with a risk of developing cardiovascular and metabolic diseases such as diabetes, hypertension and stroke

In this study, 12 non-obese participants, predominantly males, age between 19 and 39 years, were recruited. One week before the beginning of the study each participant was asked to sleep at least 8 hours per night (these data have been confirmed by wrist actigraphy) and to refrain from alcohol consumption, coffee and vigorous exercise. These subjects were randomly divided into an experimental and a control group, and they were hospitalized for 21 days. In the control group, a 9-hour time in bed (22:00-7:00) was allowed throughout the entire 21-day experiment. In the experimental group, during the acclimation phase (first 4 days) and the recovery phase (last 3 days) a 9-hour time in bed was allowed, as in the control group. During the 14-day/14-night experimental phase, in which sleep restriction occurred, participants could stay in bed only 4 hours (00:30-4:30). Participants were studied in a sedentary setting with ad libitum food access.

The study shows that experimental subjects ingested significantly more calories, especially protein and fat, during sleep deprivation. Excessive energy intake was reduced during the recovery period. However, there was no significant difference in energy consumption in the two groups and this metabolic imbalance between energy intake and consumption resulted in a weight gain of more than 0.5 kg in the experimental subjects. By examining participants body composition, it was evident that abdominal fat was increased in the experimental group compared to controls, while subcutaneous adipose tissue increased equally in both groups.

In conclusion, sleep deprivation is a very important cardiometabolic risk factor because it is associated with an increased energy intake, resulting in weight gain and excess of abdominal fat. Visceral obesity leads to insulin resistance and pro-inflammatory state, and it can contribute to explain the premature mortality and morbidity secondary to cardio-metabolic conditions.

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Giulia GIovannini

Covassin N, Singh P, McCrady-Spitzer SK, St Louis EK, Calvin AD, Levine JA, Somers VK. Effects of Experimental Sleep Restriction on Energy Intake, Energy Expenditure, and Visceral Obesity. J Am Coll Cardiol. 2022 Apr 5;79(13):1254-1265. doi: 10.1016/j.jacc.2022.01.038. PMID: 35361348; PMCID: PMC9187217.

LINK: Effects of Experimental Sleep Restriction on Energy Intake, Energy Expenditure, and Visceral Obesity – ScienceDirect