Throughout the world, drug and alcohol use has a clear adolescent onset (Degenhardt et al., 2008). Alcohol continues to be the most popular drug among teens and emerging adults, with almost a third of 12th graders and 40% of college students reporting recent binge drinking (Johnston et al., 2009, 2010), and marijuana (MJ) is the second most popular drug in teens (Johnston et al., 2010). The initiation of drug use is consistent with an overall increase in risk-taking behaviors during adolescence that coincides with significant neurodevelopmental changes in both gray and white matter (Giedd et al., 1996a; Paus et al., 1999; Sowell et al., 1999, 2002, 2004; Gogtay et al., 2004; Barnea-Goraly et al., 2005; Lenroot and Giedd, 2006). Animal studies have suggested that compared to adults, adolescents may be particularly vulnerable to the neurotoxic effects of drugs, especially alcohol and MJ (see Schneider and Koch, 2003; Barron et al., 2005; Monti et al., 2005; Cha et al., 2006; Rubino et al., 2009; Spear, 2010). In this review, we will provide a detailed overview of studies that examined the impact of early adolescent onset of alcohol and MJ use on neurocognition (e.g., Ehrenreich et al., 1999; Wilson et al., 2000; Tapert et al., 2002a; Hartley et al., 2004; Fried et al., 2005; Townshend and Duka, 2005; Medina et al., 2007a; McQueeny et al., 2009; Gruber et al., 2011, 2012; Hanson et al., 2011; Lisdahl and Price, 2012), with a special emphasis on recent prospective longitudinal studies (e.g., White et al., 2011; Hicks et al., 2012; Meier et al., 2012). Finally, we will explore potential clinical and public health implications of these findings.

Thirty-six percent of high school seniors have used cannabis in the past year, and an alarming 6.5% smoked cannabis daily, up from 2.4% in 1993 (Johnston et al., 2013). Adolescents and emerging adults are undergoing significant neurodevelopment and animal studies suggest they may be particularly vulnerable to negative drug effects. In this review, we will provide a detailed overview of studies outlining the effects of regular (at least weekly) cannabis use on neurocognition, including studies outlining cognitive, structural and functional findings. We will also explore the public health impact of this research.

BackgroundRepeated CB1 binding due to THC results in downregulation of the endocannabinoid system in cortex and limbic regions, perhaps disrupting frontolimbic functioning. This is particularly a concern in young adults who are still undergoing neurodevelopment in frontal and limbic regions. Such disruptions may be linked to increased depressive symptoms, anxiety symptoms, and executive dysfunction, and decreased behavioral approach.ObjectivesHere we examine the influence of young adult marijuana use on anxiety, depressive symptoms, behavioral approach, and executive dysfunction. The influence of alcohol and gender were also assessed.Methods84 participants (42 MJ, 42 controls) aged 18–25 were balanced for gender (39 F). Exclusion criteria included: MRI contraindications, left handed, comorbid Axis-I disorders, major medical or neurologic disorders, prenatal issues, or prenatal alcohol/illicit drug exposure, or excessive other drug use. Participants completed the FrsBE, BIS/BAS, State-Trait Anxiety Inventory (State), and BDI-II. Multiple regressions were run to predict anxiety, depressive symptoms, behavioral approach, and executive dysfunction from MJ group status, past year alcohol use, gender, and MJ*gender interactions, controlling for cotinine and ecstasy.ResultsMJ group predicted increased depressive symptoms (p =.049). Decreased fun-seeking (p =.04), reward response (p =.01), and BAS total (p =.01) were predicted by MJ group. Gender predicted decreased reward responsiveness in females (p =.049) and decreased BIS in females (p =.03). Female marijuana users had increased anxiety symptoms (p =.04) and increased disinhibition (p =.04). Increased cotinine predicted increased drive (p =.046), reward responsiveness (p =.008) and BAS Total (p =.02). Apathy and Executive Dysfunction were not predicted by any measures. All results had small effect sizes.Conclusions/ImportanceDepressive symptoms were greater in MJ users, while behavioral approach was decreased. Cotinine levels predicted increased behavioral approach. Female MJ users also had greater anxiety and disinhibition. In sum, these findings suggest sub-clinical threshold deficits related to regular marijuana use that are indicative of a need to prevent marijuana use in adolescents and young adults.

ObjectiveEcstasy use is associated with memory deficits. Serotonin transporter gene (5-HTTLPR) polymorphisms have been linked with memory function in healthy samples. The present pilot study investigated the influence of 5-HTTLPR polymorphisms on memory performance in ecstasy users, marijuana-using controls, and non-drug-using controls, after a minimum of 7 days of abstinence.MethodData were collected from 116 young adults (18–25 years-old), including 45 controls, 42 marijuana users, and 29 ecstasy users, and were balanced for 5-HTTLPR genotype. Participants were abstinent seven days prior to completing memory testing. Three MANCOVAs and one ANCOVA were run to examine whether drug group, 5-HTTLPR genotype, and their interactions predicted verbal and visual memory after controlling for gender, past year alcohol use, other drug use, and nicotine cotinine levels.ResultsMANCOVA and ANCOVA analysis revealed a significant interaction between drug group and genotype (p = .03) such that ecstasy users with the L/L genotype performed significantly worse on CVLT-2 total recall (p = .05), short (p = .008) and long delay free recall (p = .01), and recognition (p = .006), with the reverse pattern found in controls. Ecstasy did not significantly predict visual memory. 5-HTTLPR genotype significantly predicted memory for faces (p = .02); short allele carriers performed better than those with L/L genotype.Conclusions 5-HTTLPR genotype moderated the effects of ecstasy on verbal memory, with L/L carriers performing worse compared to controls. Future research should continue to examine individual differences in ecstasy’s impact on neurocognitive performance as well as relationships with neuronal structure. Additional screening and prevention efforts focused on adolescents and emerging adults are necessary to prevent ecstasy consumption.

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