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The Dangerous Metabolic Consequences of Sleep Deprivation

Monday, June 29, 2020 3:16 AM
 
When it comes to metabolism, most people focus on nutrition and exercise. Sleep is just as important. Emerging research shows that adequate sleep may be the most powerful behavior for supporting metabolic health because of how it impacts appetite, fat burning hormones, and energy levels.
 
There are three harmful metabolic effects that occur when we skimp on sleep:
 
1. Increased hunger and appetite
2. Decreased insulin sensitivity and glucose tolerance
3. Decreased basal metabolic rate and a tendency to be lazy
 
This article will help you understand the mechanisms behind the dangerous metabolic consequences of sleep deprivation.
 
#1: Increase in Hunger & Appetite
Lack of sleep makes people feel hungrier and more likely to make poor food choices. In one study, normal-weight volunteers had their sleep reduced from 9 hours to 4 hours a night (1, 5). As a group, the subjects increased calorie intake by 300 calories a day, with women experiencing the greatest increase in food intake, clocking a 15.2 percent increase in calories compared to a 9.2 percent increase in men. Participants also favored fatty, high-carb foods when they were sleep deprived, increasing their saturated fat consumption by 61 percent. If sustained, this behavior could result in gaining more than two pounds of fat a month. 
 
Scientists theorize that lack of sleep can lead to higher levels of the hunger hormone ghrelin and decrease sensitivity  to the hormone leptin (2). Leptin helps regulate appetite by giving an “I’m full” message to the brain. When leptin levels are altered they negatively impact release of other metabolic hormones, including melatonin, insulin, and thyroid function. The stress hormone cortisol is also elevated, which impairs glucose tolerance and insulin sensitivity.
 
#2: Decreased Insulin Sensitivity and Glucose Tolerance
The uptick in cortisol that follows a night of poor sleep leads to lower insulin sensitivity so that glucose metabolism is impaired, meaning the body isn’t able to use the sugar in the blood effectively and it is more likely to get stored as body fat. Over time, this develops into full blown type 2 diabetes in which the body is no longer able to safely regulate glucose levels and cells don’t readily bind to insulin.
 
Scientists theorize that lack of sleep directly impacts insulin health by stimulating the sympathetic nervous system, decreasing both insulin release from the pancreas and binding of cells to insulin. Glycemic control is reduced and circulating glucose levels trend higher, leading to inflammation. For example, one study of type 2 diabetics found that a sleep debt of 3 hours per night led to a 1.1 percent increase in HBA1C levels (3). HBA1C is a measure of glycated hemoglobin, which occurs when red blood cells attach to glycation proteins. It reflects glucose levels over the past three months and is indicative of a high degree of oxidative stress and inflammation.
 
#3: Decreased Metabolic Rate & Lower Energy Expenditure
Lack of sleep has a markedly negative effect on energy expenditure, lowering the number of calories your body burns at rest.
 
Researchers theorize that sleep loss impacts resting energy expenditure by lowering leptin and ghrelin, which impact thermogenesis in brown adipose tissue (a type of fat tissue that is highly metabolically active). 
 
Of course, lack of sleep is exhausting, impacting motivating chemicals in the brain such that people become lazier and burn fewer calories during spontaneous physical activity. Known as NEAT (standing for non-exercise activity thermogenesis), spontaneous physical activity includes all the movement you do outside of regular workouts. It has been shown to have a greater effect on the number of calories you burn than exercise.
 
The reduction in physical activity from poor sleep leads to poorer body composition and less fat loss. For example, in a study conducted at the University of Chicago, overweight volunteers went on a calorie restricted diet that supplied 1,450 calories daily for two weeks (4). They were put into either a “normal” sleep group in which they got 8.5 hours a night or a “short” sleep group in which they got 5.5 hour night.
 
Results showed that both groups lost roughly the same amount of weight, decreasing body mass by 3 kg. However, the “normal” sleep group lost significantly more body fat, whereas the “short” sleep group had most of their weight loss come from muscle. Lack of sleep decreased the fraction of weight lost as body fat by an incredible 55 percent:
 
The “normal” sleep group lost 1.4 kg of fat but the “short” sleep group lost only 0.6 kg of fat, while also losing 2.4 kg of lean mass. This unfavorable change in body composition sets the stage for rebound weight gain because lean mass drives the metabolism and plays a role in strength and the subjects’ ability to move with ease.
 
The take away is that whether you’re battling Type II diabetes or simply want to lose body fat, healthy sleep is an essential part of your routine. If you are struggling with obesity or trying to lean up, making an effort to adopt good sleep habits is critical. Use this Checklist of Healthy Sleep Habits  to support metabolism and set yourself up to manage hunger and food cravings.
 
References:
1.  Benedict, C., Brooks, S., et al. Acute Sleep Deprivation Enhances the Brain’s Response to Hedonic Food Stimuli. Journal of Clinical Endocrinology and Metabolism. 2012. 97(3), E443-E447. 
 
2. Chaput, J., et al. Sleeping Habits Predict the Magnitude of Fat Loss in Adults Exposed to Moderate Calorie Restriction. Obesity Facts. 2012. 5(4), 561-566.
 
3.  Knutson, K., et al. The Metabolic Consequences of Sleep Deprivation. Sleep Medicine Reviews. 2007. 11(3), 163-167.
 
4. Nedeltcheva, A., et al. Insufficient sleep undermines dietary efforts to reduce adiposity. Annals of Internal Medicine. 2010. 153(7): 435–441.
 
5.  St-Onge, M., et al. Short Sleep Duration Increases Energy Intakes but Does not Change Energy Expenditure in Normal-Weight Individuals. The American Journal of Clinical Nutrition. 2011. 94, 410-416.

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