Sleeping too little is correlated with obesity and non-obesity extra "love handle" weight. Does sleep debt 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 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 results in added fat.
Sleep debt increases the appetite, and particularly increases the desire for high-calorie, carbohydrate-rich foods. Functional MRI 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.
Why the connection between sleep duration and excessive weight? 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 supressor. 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. (Ref)
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.
It is hypothesized that there are evolutionary reasons for this connection. 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 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.
A Cleveland Family Study looked into this issue found that adipokines and sleep duration. Leptin and visfatin are hormones released by adipose tissue (they are called adipokines) and they are higher in people with high insulin resistance, meaning they 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.
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".
Scientific American: Sleep might help dieters shed more fat