Can Sleeping Make You Fat?

Knowing what we’re up against is the first step toward a healthier lifestyle and breaking that vicious cycle.
08/25/2016 12:52 pm ET Updated Nov 01, 2017

For years now, we’ve been told that too little sleep leads to weight gain. In fact, a study presented at last year’s Endocrine Society national meeting suggested that getting just 30 fewer minutes of sleep per weekday can increase your risk of obesity and Type 2 diabetes.

But what if the opposite were true? Would it surprise you to learn that sleeping can make you fatter as well?

If you suffer from sleep disturbances like sleep apnea, where sufferers actually stop breathing for up to 30-45 seconds at a time, often several times a night, you could be setting yourself up to gain weight. How so? Not to be confused with central sleep apnea secondary to brain dysfunction, this brand of sleep apnea correlates to the fatty enlargement of tissues in the nasal air passages and at the back and upper part of the throat. Studies have found there is a low-grade inflammation in the fat tissues and the fat cells of folks who are obese, and this inflammatory state can become chronic, leading to systemic insulin resistance and diabetes. Adenine nucleotide translocase 2 (ANT2a), a protein in fat cell membranes that is involved in cellular energy metabolism, can become activated in these people, increasing oxygen consumption, meaning less oxygen is available for the rest of the cell. This, in turn, leads to hypoxia, or low oxygen levels in the fat cell, creating an environment for even further weight gain.

I am not alone in believing this. The American Physiological Society concluded in a 2013 review, “Hypoxia and Adipose Tissue Function and Dysfunction in Obesity,” that: “Overall, hypoxia has pervasive effects on the function of adipocytes (fat cells) and appears to be a key factor in adipose tissue dysfunction in obesity.”

In layman’s terms: hypoxia itself is a major factor in weight gain.

Excess fat, particularly when located around the neck, can exacerbate obstructive sleep apnea, which is increasing in occurrence, thanks no doubt to the fact that more 93 million Americans are obese. Recent data from multiple U.S. and Canadian sleep centers show that obesity is the No. 1 cause of sleep apnea in children—rather than enlarged tonsils and adenoids, which was once the major cause of childhood sleep apnea. So the apnea, which is usually caused by obesity, causes hypoxia, which results in added pounds. It’s a vicious cycle.

There is another side effect of obesity affecting millions of people that the general public—and even many in the medical community—are unaware of. Research has shown that when fat settles in the central part of the abdomen, it also finds its way to internal organs, and to the omentum, the web of connective tissue supporting our intestines. All this excess fat prevents the chest, and therefore the lungs, from expanding fully. Compounding matters, fatty organs do not let the diaphragm descend fully, so the bottom parts of the lung don’t fully expand, decreasing the amount of air in the lungs, leading to hypoxia.

In Charles Dickens’ novel, The Posthumous Papers of the Pickwick Club, a character named Joe is described as “a wonderfully fat boy—habited as a serving-lad, standing upright on the mat, with his eyes closed as if in sleep.” Dickens may well have been describing someone living with another complication of obesity: Obesity Hypoventilation Syndrome (OHS), a condition sometimes called “Pickwikian Syndrome,” in which poor breathing—where too little air volume is moved—leads to lower oxygen and higher carbon dioxide levels in the blood. OHS is brain-related, meaning it “resets” the part of the brain that regulates the drive to breathe and subsequently leads to higher carbon dioxide levels. During hypoventilation, CO2 levels increase, changing the acidity of the blood and putting people at risk for serious health consequences such as pulmonary hypertension, a condition where the blood pressure in the pulmonary arteries is increased.

Pulmonary hypertension is difficult to diagnose, and the majority of heart specialists do usually not consider “mild or moderate” pulmonary hypertension to be a serious issue. But if left untreated, this condition overtaxes the right ventricle of the heart, eventually resulting in right heart failure (cor pulmonale), a defining feature of a condition I call lethal obesity. Cor pulmonale causes the right ventricle to enlarge and pump blood less effectively than it should. Once pushed to its limit, the right ventricle eventually fails. Just recognizing this potential complication of obesity, and treating it early, can lead to fewer patients developing lethal obesity.

A BMI (body mass index) chart is a useful tool anyone can use to assess their own risk of heart disease from obesity. Research has shown that a significant percentage of people with obesity hypoventilation syndrome who also have obstructive sleep apnea have extremely high BMIs, often greater than 50 (which is quite literally off the charts, as most indexes stop at 42). The higher your BMI, the greater the risk of lethal obesity.

Knowing what we’re up against is the first step toward a healthier lifestyle and breaking that vicious cycle. The importance of losing some of that fat takes on a whole new meaning, and preventing low oxygen levels associated with obesity becomes a priority in successful weight loss.

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