Chronic sleep deprivation and seasonality: implications for the obesity epidemic

Abstract

Sleep duration has progressively fallen over the last 100 years while obesity has increased in the past 30 years. Several studies have reported an association between chronic sleep deprivation and long-term weight gain. Increased energy intake due to sleep loss has been listed as the main mechanism. The consequences of chronic sleep deprivation on energy expenditure have not been fully explored. Sleep, body weight, mood and behavior are subjected to circannual changes. However, in our modern environment seasonal changes in light and ambient temperature are attenuated. Seasonality, defined as cyclic changes in mood and behavior, is a stable personality trait with a strong genetic component. We hypothesize that the attenuation in seasonal changes in the environment may produce negative consequences, especially in individuals more predisposed to seasonality, such as women. Seasonal affective disorder, a condition more common in women and characterized by depressed mood, hypersomnia, weight gain, and carbohydrate craving during the winter, represents an extreme example of seasonality. One of the postulated functions of sleep is energy preservation. Hibernation, a phenomenon characterized by decreased energy expenditure and changes in the state of arousal, may offer useful insight into the mechanisms behind energy preservation during sleep. The goals of this article are to: a) consider the contribution of changes in energy expenditure to the weight gain due to sleep loss; b) review the phenomena of seasonality, hibernation, and their neuroendocrine mechanisms as they relate to sleep, energy expenditure, and body weight regulation.

Fig. 1

The pineal-adipose tissue-β cell endocrine loop. A new endocrine axis? Melatonin is synthesized in the pineal gland starting from the aminoacid L-tryptophan that is converted to serotonin. Serotonin in turn is converted to N-acetyl-5-hydroxytryptamine by the rate limiting enzyme arylalkylamine N-acetyltransferase (AA-NAT) to N-acetyl 5-hydroxytryptamine and finally converted to melatonin. Melatonin is under a constant inhibitory effect exercised by daylight. Via the retino-hypothalamic trait light inhibits melatonin production. In darkness melatonin is produced by the pineal gland and rises in plasma. Melatonin receptors type 1 (MT-1) and 2 (MT-2) are G-protein coupled receptors. They are present in the brown adipose tissue (BAT), in the white adipose tissue (WAT), where they exert a stimulatory role, and in the β cell of the pancreas where they have an inhibitory role. Via these receptors the rise in melatonin in darkness can stimulate heat production from the BAT and expend energy, induce lypolisis from the WAT and decrease insulin production during the night from the beta cell in the pancreas. To close this loop insulin receptors are present on the pinealocyte. Not indicated in the figure, MT receptors are present both in the central nervous system (CNS) and in the periphery. In the CNS they are present in the suprachiasmatic nucleus, retina, cerebellum, and hippocampus. In the periphery they are represented in the skin, cardiovascular system, the reproductive system, and the immune system where they modulate the immune response.