The present paper aims at reviewing and commenting on the relationships between sleep and circadian phasing alterations and neurodegenerative/neuroprogressive processes in mood disorder. We carried out a systematic review, according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, in PubMed, PsycINFO, and Embase electronic databases for literature related to mood disorders, sleep disturbances, and neurodegenerative/neuroprogressive processes in relation to (1) neuroinflammation, (2) activation of the stress system, (3) oxidative stress, (4) accumulation of neurotoxic proteins, and (5) neuroprotection deficit. Seventy articles were collectively selected and analyzed. Experimental and clinical studies revealed that insomnia, conditions of sleep loss, and altered circadian sleep may favor neurodegeneration and neuroprogression in mood disorders. These sleep disturbances may induce a state of chronic inflammation by enhancing neuroinflammation, both directly and indirectly, via microglia and astrocytes activation. They may act as neurobiological stressors that by over-activating the stress system may negatively influence neural plasticity causing neuronal damage. In addition, sleep disturbances may favor the accumulation of neurotoxic proteins, favor oxidative stress, and a deficit in neuroprotection hence contributing to neurodegeneration and neuroprogression. Targeting sleep disturbances in the clinical practice may hold a neuroprotective value for mood disorders.

The present review investigates the role of sleep and its alteration in triggering metabolic disorders. The reduction of the amount of time sleeping has become an endemic condition in modern society and the current literature has found important associations between sleep loss and alterations in nutritional and metabolic aspects. Studies suggest that individuals who sleep less have a higher probability of becoming obese. It can be related to the increase of ghrelin and decrease of leptin levels, generating an increase of appetite and hunger. Sleep loss has been closely associated with problems in glucose metabolism and a higher risk for the development of insulin resistance and diabetes, and this disturbance may reflect decreased efficacy of the negative-feedback regulation of the hypothalamic–pituitary–adrenal axis. The period of sleep is also associated with an increase of blood lipid concentrations, which can be intensified under conditions of reduced sleep time, leading to disorders in fat metabolism. Based on a review of the literature, we conclude that sleep loss represents an important risk factor for weight gain, insulin resistance, type 2 diabetes and dyslipidaemia. Therefore, an adequate sleep pattern is fundamental for the nutritional balance of the body and should be encouraged by professionals in the area.

Sleep-related vehicle accidents are prevalent early morning, especially in younger drivers. In two independent studies following a night of either restricted or nil sleep, young experienced drivers drove for 2 hr (0600–0800h) continuously in an immobile car on an interactive, computer-generated, dull, and monotonous roadway. This exercise followed ingestion (at 0530h) of 200 mg caffeine (= 2–3 cups coffee) versus placebo, counterbalanced, double blind. Driving incidents (lane drifting), subjective sleepiness, and 4–11 Hz electroencephalogram (EEG) activity were logged. In Study 1 (sleeping 0000–0500h), caffeine significantly reduced incidents and subjective sleepiness throughout the 2-hr drive, and EEG power for the second 30-min period. In Study 2 (no sleep), sleepiness affected all measures profoundly, and driving was terminated after 1 hr. Nevertheless, caffeine reduced incidents significantly for the first 30 min and subjective sleepiness for the hour. This caffeine dose, feasibly taken via coffee, effectively reduces early morning driver sleepiness for about 30 min following nil sleep, and for around 2 hr after sleep restriction.