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Sleeping too little is correlated with obesity and non-obesity extra “love handle” weight. Does sleep restriction make you fat or does extra weight make it hard to sleep? Both. Like most things involving sleep, the interactions are complex and the causal relationship runs both ways.
Higher BMI (body mass index) is correlated with shorter sleep time. It is also correlated with later sleep than normal (going to bed late and getting up late.) Not enough sleep results in a tendency to gain weight. This isn’t true for everybody (some people actually lose weight when they don’t sleep enough), but over the population as a whole it has repeatedly been shown that less sleep is correlated with added fat.
Population and laboratory studies have found that a persistent pattern of shortened sleep results in insulin resistance and cardiovascular disease.
Sleep debt increases the appetite, and particularly increases the desire for high-calorie, carbohydrate-rich foods. Advanced medical imaging scans show higher activation in an area of the brain involved with appetite. This is one obvious reason for weight gain, although the deeper picture is more complex. In some situations, researchers have found sleep-restricted subjects did not have an increased appetite, but they still gained weight.
Although even one night of short sleep can result in a desire to eat more, the second night of a very short sleep left participants in a controlled study reaching for cookies and cake and eschewing fruit and vegetables.
Public health minded authorities who worry about the obesity pandemic look at both sides of the energy balance – people eat too many calories and burn off too few calories with physical activity. Too little sleep affects both. When you are tired from insufficient sleep, you might fidget less and burn fewer calories, but a more likely explanation is the effect of sleep deprivation on hormones.
Adipocytes (your “fat cells”) release leptin to the bloodstream to signal sufficient fat stores; leptin therefore acts as a natural appetite suppressor. The stomach releases ghrelin when it is empty signal hunger. (That’s oversimplified; ghrelin is suspected to be associated with the body’s long-term weight regulation – levels are higher in obese people than lean people.)
Sleep deprivation lowers the levels of leptin and raises levels of grehlin. It’s a double whammy hormone hit that makes you want to eat more. The brain is getting signals that the body is starving, so you crave food.
Lack of sleep affects leptin and ghrelin; short sleep time (4 hours per night or less) results lower leptin levels and higher ghrelin levels in the blood plasma. With sleep loss, low leptin and high ghrelin can give powerful dual signals that the body has an energy deficit, thus increasing food intake.
Leptin levels in the body follow a circadian rhythm although unlike the sleep circadian cycle the leptin one is not correlated with daylight and night. The cycle is more tied to habitual meal patterns. Exercise also makes leptin levels fall.
Other hormones are intimately tied up with both sleep and weight. A reciprocal interaction of the growth hormone releasing hormone (GHRH) and corticotropin-releasing hormone play a role in sleep patterns. Ghrelin, galanin and neuropeptide Y have been shown to promote sleep
Additionally, the orexin (hypocretin) system in the hypothalamus plays a part in the interaction between sleep and appetite. Orexin levels influence leptin release, which in turn regulates appetite and weight and tells the brain how much energy the body has. Scientists do not fully understand all these interactions. There are many competing systems and cycles in the body. A better understanding of these system might result in new avenues for addressing the sleep disorder epidemic and the obesity epidemic. Researchers recently found that oxerin appears to increase the body’s sensitivity to leptin, leading to the promise that ways to boost oxerin levels may eventually become a therapy for obesity.
Poor sleep results in daytime lethargy, lower energy levels, drowsiness – all of which lead to less exercise – both formal and informal. Poor sleep also leads to an increased appetite – they eat more food and more calorie-dense food.
So shortened sleep times makes us fatter through several channels. It is hypothesized that there are evolutionary reasons for this connection between weight and sleep times. Mother Nature may have set us up to store fat in summer in anticipation of scarcer food in the winter. Summertime has shorter nights and longer days – people tend to sleep less during the summer – so the body interprets these circadian signals as a time to increase fat deposits.
Scientists have now definitely established the link. There are genes controlled by the circadian clock that regulates sleeping/waking and some of the same genes also contribute to fat deposits.
This result comes from animal tests. When researchers turned off the clock gene in mice (through genetic engineering), the the mice did not gain weight on a high calorie diet compared with a control group. The glucose and lipid metabolic pathways were disrupted. The genetically modified mice did not store fat in the same quantities.
Leptin and visfatin are hormones released by adipose tissue (they are called adipokines) and they are higher in people with high insulin resistance, meaning those individuals have or are at risk for diabetes. When subjects were deprived of sleep, the blood levels of these hormones rose. Each hour of short sleep caused a 6% increase in leptin and a 14% increase in visfatin. Another adipokine, retinol-binding protein 4, which is also strongly suspected to contribute to insulin resistance, did not vary with sleep duration.
Nature magazine reports scientists have found “disrupted circadian rhythm leads people to crave high-fat foods.”
There is some indication that the body reacts differently to sleep restriction during times of stress versus other times. Sleep loss due to stress may lead to more food consumption the next day than sleep loss due to other causes. The calorie-rich food people crave in such periods is often referred to as “comfort food”.
A study of children found a U-shaped relationship between weight and time spent in stages 3 and R of sleep. Moderately overweight kids spent more time in deep sleep and REM sleep, but obese kids had reductions in both deep and REM sleep.
A British study found the in children as young as 30 months, short sleep duration was correlated with obesity at age 7. Plenty of other investigators have found a link between insulin sensitivity and sleep loss.
We can see the effect of diet and consumption on sleep by noting how unusual eating patterns affect sleep timing and circadian cycles. The old punishment of sending someone to bed without their supper is instructive: it is unpleasant to skip a meal during a day, but it is really difficult to go to sleep on an empty stomach.
Muslims who observe dietary restrictions in Ramadan show how moving eating and drinking around the day affects even our unconscious lives. Ramadan fasting produces a decrease in slow-wave sleep and REM sleep and an increase in sleep latency. A shift in body temperature fluctuations indicates the circadian cycle is shifted, too. Another study also found a decrease in REM time but NREM time and total sleep time unchanged.
It also turns out the causal arrow can go the other direction. Experiments in mice found type of diet and timing of eating can affect the circadian cycle. The molecular mechanism for this is not known and it is not clear whether the percentage of fat in the diet made a difference or the fact that the mice were eating when they would otherwise be sleeping, or both.
The evidence showing many short sleepers are obese does not prove cause and effect in either direction, of course, and for years it was debated whether doctors should try to intervene to get people to sleep more. But we are getting more evidence that the metabolic hormone levels are directly affected by sleep duration.
Some observers look at the long-term trends to support the idea of a cause-and-effect. Sleep times have been declining for the past 100 years (some say) rates of obesity and higher BMI have been rising for the past four decades. Both are hallmarks of modern life. From what we know about the relationship between sleep deprivation and over a few years for individuals, it must be true for society as a whole. Right? The evidence is not really strong. It is not clear that sleep times have declined over the decades and there are plenty of reasons for increased weight – automation and machines taking over tasks humans used to do with their muscles and availability of cheap food.
Looking at the coincidence of the obesity/metabolic syndrome and sleepless some are calling for widespread effort to get people to sleep more. (What this effort would involve and how effective it would be are other questions.) Of course, there are plenty of reasons to get people to sleep more. Some call for more study of the question – but researchers are forever calling for more study.
The well respected sleep scientist Jim Horne raises skepticism about working on increasing sleep times as a way to lose weight. He thinks the evidence that inadequate sleep leads to weight gain on a wide scale is scant, and that there are other reasons to worry about short sleep times. “The real health risk of inadequate sleep comes from a sleepiness-related accident” – not weight gain. He concedes that extremely short sleep times – 4 hours per night – lead to glucose intolerance, but points out that only a small fraction of obese people would be classified as “short sleepers”.