Effects of sleep on substance use in adolescents: a longitudinal perspective

Abstract

Substance use (SU) and sleep problems appear interrelated, but few studies have examined the influence of adolescent sleep patterns on development of SU disorders. This study prospectively examined the influence of sleep habits on subsequent SU in youth who later transitioned into heavy drinking. At time 1 (T1), participants (n = 95) were substance-naive 12- to 14-year-olds. Path-analytic models examined whether the effects of T1 risk factors (familial SU disorder, inhibition control, and externalizing and internalizing traits) on time 3 (M = 19.8 years old) tobacco, alcohol, and cannabis were mediated by time 2 (M = 15.1 years old) sleep chronotype, daytime sleepiness, and erratic sleep/wake behaviors. Significant direct path effects of T1 risk factors and time 2 sleep behaviors on time 3 SU were found, Ps < 0.05. In models that examined the effect of each individual sleep behavior separately on SU, more erratic sleep/wake and greater daytime sleepiness predicted higher lifetime use events for all substances (Ps < 0.01). Higher evening chronotype tendencies predicted lower tobacco and higher alcohol and cannabis lifetime use events (Ps < 0.01). Erratic sleep/wake behaviors mediated the effect of inhibitory control on subsequent SU; less erratic sleep/wake behaviors predicted better inhibition control ( β̂= -0.20, P < 0.05). Early-mid adolescent psychiatric health and sleep behaviors prior to drinking onset predicted greater SU 5 years later. Participants were substance-naïve at baseline, allowing for the examination of temporal order in the relationship between sleep problems and alcohol use. Early adolescent sleep problems may be an important risk factor for SU in later life.

Keywords: adolescence; sleep; substance use.

Figure 1

Conceptual path analytic model. Paths indicate hypothesized direct effects of time 1 (T1) risk factors (substance use disorder family history, inhibition control, and internalizing and externalizing traits) to outcome substance use. Dashed black lines indicate hypothesized indirect effects of T1 risk factors, mediated by sleep behaviors (chronotype, daytime sleepiness, and erratic sleep/wake behaviors), on outcome substance use. Solid black lines indicate biological (age and pubertal development) and environmental (hours playing video games and SES) factors that may influence and covary with sleep behaviors. All T1 risk factors were assessed at time 1, project entry; all sleep behaviors and covariates were assessed at time 2, and all outcome substance use measures were assessed at time 3.

Figure 2

Results of path analytic model. Note. SUD = Substance use disorder All paths shown are significant effects, ps<.05. Solid lines indicate significant positive effects of time 1 (T1) risk factors and time 3 sleep behaviors on outcome lifetime substance use events and dashed lines indicate significant negative effects of T1 risk factors and time 3 sleep behaviors on T3 lifetime substance use events. Unshaded boxes are indices measured at time 1 (age=13.4 [0.7]) grey boxes are indices measured at time 2 (age=15.1 [.9]), and black-shaded boxes are indices measured at time 3 (19.8 [.9]). In all models, better inhibitory control (lower time to completion score) predicted less erratic sleep/wake behaviors ( $\widehat{\mathrm{\beta }}$=.20). Note that higher Chronotype score indicates greater morningness tendency and higher SUD Family History indicates greater familial density of SUD. Shown are standardized path coefficients.