Life on earth has evolved during the past several billion years under relatively bright days and dark night conditions. The wide-spread adoption of electric lights during the past century exposed animals, both human and non-human, to significant light at night for the first time in their evolutionary history. Endogenous circadian clocks depend on light to entrain to the external daily environment and seasonal rhythms depend on clear nightly melatonin signals to assess time of year. Thus, light at night can derange temporal adaptations. Indeed, disruption of naturally evolved light–dark cycles results in several physiological and behavioural changes with potentially serious implications for physiology, behaviour and mood. In this review, data from night-shift workers on their elevated risk for metabolic disorders, as well as data from animal studies will be discussed. Night-shift workers are predisposed to obesity and dysregulated metabolism that may result from disrupted circadian rhythms. Although studies in human subjects are correlative, animal studies have revealed several mechanisms through which light at night may exert its effects on metabolism by disrupting circadian rhythms that are associated with inflammation, both in the brain and in the periphery. Disruption of the typical timing of food intake is a key effect of light at night and subsequent metabolic dysregulation. Strategies to avoid the effects of light at night on body mass dysregulation should be pursued.

Presently, about 12% of the population is 65 years or older and by the year 2030 that figure is expected to reach 21%. In order to promote the well-being of the elderly and to reduce the costs associated with health care demands, increased longevity should be accompanied by ageing attenuation. Energy restriction, which limits the amount of energy consumed to 60–70% of the daily intake, and intermittent fasting, which allows the food to be available ad libitum every other day, extend the life span of mammals and prevent or delay the onset of major age-related diseases, such as cancer, diabetes and cataracts. Recently, we have shown that well-being can be achieved by resetting of the circadian clock and induction of robust catabolic circadian rhythms via timed feeding. In addition, the clock mechanism regulates metabolism and major metabolic proteins are key factors in the core clock mechanism. Therefore, it is necessary to increase our understanding of circadian regulation over metabolism and longevity and to design new therapies based on this regulation. This review will explore the present data in the field of circadian rhythms, ageing and metabolism.

Use of artificial light resulted in relative independence from the natural light–dark (LD) cycle, allowing human subjects to shift the timing of food intake and work to convenient times. However, the increase in artificial light exposure parallels the increase in obesity prevalence. Light is the dominant Zeitgeber for the central circadian clock, which resides within the hypothalamic suprachiasmatic nucleus, and coordinates daily rhythm in feeding behaviour and metabolism. Eating during inappropriate light conditions may result in metabolic disease via changes in the biological clock. In this review, we describe the physiological role of light in the circadian timing system and explore the interaction between the circadian timing system and metabolism. Furthermore, we discuss the acute and chronic effects of artificial light exposure on food intake and energy metabolism in animals and human subjects. We propose that living in synchrony with the natural daily LD cycle promotes metabolic health and increased exposure to artificial light at inappropriate times of day has adverse effects on metabolism, feeding behaviour and body weight regulation. Reducing the negative side effects of the extensive use of artificial light in human subjects might be useful in the prevention of metabolic disease.

The human circadian system anticipates and adapts to daily environmental changes to optimise behaviour according to time of day and temporally partitions incompatible physiological processes. At the helm of this system is a master clock in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus. The SCN are primarily synchronised to the 24-h day by the light/dark cycle; however, feeding/fasting cycles are the primary time cues for clocks in peripheral tissues. Aligning feeding/fasting cycles with clock-regulated metabolic changes optimises metabolism, and studies of other animals suggest that feeding at inappropriate times disrupts circadian system organisation, and thereby contributes to adverse metabolic consequences and chronic disease development. ‘High-fat diets’ (HFD) produce particularly deleterious effects on circadian system organisation in rodents by blunting feeding/fasting cycles. Time-of-day-restricted feeding, where food availability is restricted to a period of several hours, offsets many adverse consequences of HFD in these animals; however, further evidence is required to assess whether the same is true in humans. Several nutritional compounds have robust effects on the circadian system. Caffeine, for example, can speed synchronisation to new time zones after jetlag. An appreciation of the circadian system has many implications for nutritional science and may ultimately help reduce the burden of chronic diseases.

The putative neural pacemaker controlling circadian rhythms in mammals is contained in the suprachiasmatic nuclei of the hypothalamus. These nuclei receive a projection, the geniculo-hypothalamic tract (GHT), from neurons in the intergeniculate leaflet (IGL) and portions of the ventral lateral geniculate nucleus (vLGN) of the thalamus. We examined the responses of putative GHT neurons to diffuse illumination using extracellular electrophysiological recordings. The great majority of IGL neurons showed sustained ON responses to diffuse retinal illumination; vLGN neurons showed more variation in their responses. Discharge rates of sustained ON neurons increased monotonically as light intensity was increased and saturated over 2–3 log units of intensity changes. Many IGL neurons had binocular input, and input from the ipsilateral eye was often inhibitory. These results indicate that GHT neurons may provide information about ambient light intensity to the suprachiasmatic nuclei.