A controlled study of sleep-deprived young adults has provided the first causal evidence linking the lack of sleep to abdominal obesity and harmful visceral, or “belly” fat. In what the researchers claim is the first-ever study evaluating the relationship between sleep restriction and body fat distribution, they’ve reported the novel finding that the expansion of abdominal adipose tissue, and especially visceral fat, occurred as a function of shortened sleep.
Naima Covassin, PhD, a researcher in cardiovascular medicine at Mayo Clinic in Rochester, Minn., led the randomized, controlled study of 12 healthy, nonobese people randomized to controlled sleep restriction — 2 weeks of 4 hours of sleep a night — or controlled sleep of 9 hours a night, followed by a 3-day recovery period. The study was conducted in the hospital, monitored participants’ caloric intake, and used accelerometry to monitor energy expense. Participants ranged in age from 19 to 39 years.
“What we found was that at the end of 2 weeks these people put on just about a pound, 0.5 kg, of extra weight, which was significant but still very modest,” senior author Virend K. Somers, MD, PhD, said in an interview. “The average person who sleeps 4 hours a night thinks they’re doing OK if they only put on a pound.” Somers is the Alice Sheets Marriott Professor in Cardiovascular Medicine at Mayo Clinic.
“The problem is,” he said, “that when you do a more specific analysis you find that actually with the 1 pound the significant increase of the fat is in the belly area, particularly inside the belly.”
The study found that the patients on curtailed sleep ate on average an additional 308 calories a day more than their controlled sleep counterparts (95% confidence interval, 59.2 – 556.8 kcal/day; P = .015), and while that translated into a 0.5-kg weight gain (95% CI, 0.1 – 0.8 kg; P = .008), it also led to a 7.8-cm2 increase in visceral adipose tissue (VAT) (95% CI, 0.3 – 15.3 cm2; P = .042), representing an increase of around 11%. The study used CT on day 1 and day 18 (1 day after the 3-day recovery period) to evaluate the distribution of abdominal fat.
VAT Findings Post Recovery
After the recovery period, however, the study found that VAT in the sleep-curtailed patients kept rising, yet body weight and subcutaneous fat dropped, and the increase in total abdominal fat flattened. “They slept a lot, they ate fewer calories and their weight came down, but, very importantly, their belly fat went up even further,” Somers said. On average, it increased another 3.125 cm2 by day 21.
The findings raised a number of questions that need further exploration, Somers said. “There’s some biochemical message in the body that’s continuing to send fat to the visceral compartment,” he said. “What we don’t know is whether repetitive episodes of inadequate sleep actually accumulate over the years to give people a preponderance of belly fat.”
The study also showed that the traditional parameters used for evaluating cardiovascular risk are not enough, Somers said. “If we just did body weight, body mass index, and overall body fat percentage, we’d completely miss this,” he said.
Future investigations should focus on two points, he said: identifying the mechanisms that cause VAT accumulation with less sleep, and whether extending sleep can reverse the process.
“The big worry is obviously the heart,” Somers said. “Remember, these are not sick people. These are young healthy people who are doing the wrong thing with their body fat; they’re sending the fat to the completely wrong place.”
In an invited editorial, endocrinologist Harold Bays, MD, wrote that the study confirmed the need for evaluating sleep disorders as a potential cause of accumulated VAT. Bays, of the University of Louisville (Ky.), is medical director and president of the Louisville Metabolic and Atherosclerosis Research Center.
“The biggest misconception of many clinicians, and some cardiologists, is that obesity is not a disease,” Bays said in an interview. “Even when some clinicians believe obesity is a disease, they believe its pathogenic potential is limited to visceral fat.” He noted that subcutaneous fat can lead to accumulation of VAT and epicardial fat, as well as fatty infiltration of the liver and other vital organs, resulting in increased epicardial adipose tissue and indirect adverse effects on the heart.
“Thus, even if disruption of sleep does not increase body weight, if disruption of sleep results in fat dysfunction — “sick fat” or adiposopathy — then this may result in increased CVD risk factors and unhealthy body composition, including an increase in visceral fat,” Bays said.
The study received funding from the National Institutes of Health. Somers disclosed relationships with Baker Tilly, Jazz Pharmaceuticals, Bayer, Sleep Number, and Respicardia. Coauthors had no disclosures. Bays is medical director of Your Body Goal and chief science officer of the Obesity Medical Association.
This article originally appeared on MDEdge.com.