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Review
. 2018 Jun 15;83(12):987-996.
doi: 10.1016/j.biopsych.2017.11.035. Epub 2017 Dec 15.

Impact of Sleep and Circadian Rhythms on Addiction Vulnerability in Adolescents

Affiliations
Review

Impact of Sleep and Circadian Rhythms on Addiction Vulnerability in Adolescents

Ryan W Logan et al. Biol Psychiatry. .

Abstract

Sleep homeostasis and circadian function are important maintaining factors for optimal health and well-being. Conversely, sleep and circadian disruptions are implicated in a variety of adverse health outcomes, including substance use disorders. These risks are particularly salient during adolescence. Adolescents require 8 to 10 hours of sleep per night, although few consistently achieve these durations. A mismatch between developmental changes and social/environmental demands contributes to inadequate sleep. Homeostatic sleep drive takes longer to build, circadian rhythms naturally become delayed, and sensitivity to the phase-shifting effects of light increases, all of which lead to an evening preference (i.e., chronotype) during adolescence. In addition, school start times are often earlier in adolescence and the use of electronic devices at night increases, leading to disrupted sleep and circadian misalignment (i.e., social jet lag). Social factors (e.g., peer influence) and school demands further impact sleep and circadian rhythms. To cope with sleepiness, many teens regularly consume highly caffeinated energy drinks and other stimulants, creating further disruptions in sleep. Chronic sleep loss and circadian misalignment enhance developmental tendencies toward increased reward sensitivity and impulsivity, increasing the likelihood of engaging in risky behaviors and exacerbating the vulnerability to substance use and substance use disorders. We review the neurobiology of brain reward systems and the impact of sleep and circadian rhythms changes on addiction vulnerability in adolescence and suggest areas that warrant additional research.

Keywords: Addiction; Adolescence; Circadian; Circuitry; Reward; Sleep.

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Conflict of interest statement

Disclosures:

All other report no biomedical financial interests or potential conflicts of interest.

Figures

Figure 1
Figure 1
Factors contributing to sleep deprivation in adolescents are compounded by the consequences of sleep and circadian disruptions.
Figure 2
Figure 2
Working model of the interplay between circadian rhythms, sleep, ‘reward’, and vulnerability to substance use during adolescence. Developmental changes in neural circuitry controlling reward function occurs during adolescence and seems to be altered by sleep deprivation and circadian misalignment, potentially leading to risk-taking, impulsivity, and poor decision making. These changes likely contribute to vulnerability to substance use particularly in adolescents. Rodent studies have demonstrated associations between certain circadian variants, striatal dopamine, and brain response to reward stimuli. Interventions to phase shift, resynchronize, and/or improve sleep timing may be effective for treating mood and substance issues often experienced during adolescence.
Figure 3
Figure 3
Sagittal sections of a representative human (A) and rodent (B) brain illustrating major pathways of ‘reward’ neural circuitry. Sleep deprivation and/or circadian misalignment leads to reduced activity of the PFC (in humans, both DLPFC and mPFC) and increased activity of the ventral striatum (VS) or nucleus accumbens (NAc) in response to reward anticipation in adolescents. The imbalance of excitatory and inhibitory signaling is hypothesized to lead to poor executive function, academic performance, and decision making, while increasing impulsivity, risk-taking behavior, all of which likely contribute to a vulnerability to substance use and abuse. In rodents, sleep deprivation and/or circadian disruptions, whether environmental or genetic, usually lead to poor cognitive performance, working memory, and increased impulsivity, risk-taking behavior, and drug self-administration. Yellow pathways represent ascending dopaminergic pathways from the ventral tegmental area (VTA), and blue pathways represent descending glutamatergic pathways from the prefrontal cortex (PFC). AMY, amygdala; DS, dorsal striatum; HIPP, hippocampus; LHb, lateral habenula; LH, lateral hypothalamus; mPFC, medial prefrontal cortex; SNc, substantia nigra.

Comment in

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