Comorbid Cannabis and Tobacco Use in Adolescents and Adults

Abstract

The prevalence of comorbid cannabis and tobacco use has been increasing among adolescents and adults and has been shown to be associated with a range of changes or deficits in physical, psychological and behavioral outcomes. Moreover, comorbid use has been shown to have a differential effect on the structure and function of the brain, especially as it relates to the reward circuitry and learning and memory. This interaction might be mediated by the involvement of the endocannabinoid system and alterations in dopamine signaling in regions associated with reward and cognitive functioning. While current findings demonstrate a differential effect of comorbid use on neurobiological and behavioral correlates compared with single substance use, additional studies are needed controlling for potential psychiatric comorbidities, age of onset of use and use of other substances. Understanding the neurobiological mechanisms associated with comorbid cannabis and tobacco use will be important in developing successful treatment outcomes in the future.

Differential associations of combined vs. isolated cannabis and nicotine on brain resting state networks

“…A widely utilized approach of looking at the brain’s resting state networks (RSNs) provides baseline information on the brain’s functional network architecture based on the temporal correlations of spatially distributed brain regions in the absence of a task (Biswal et al 1997). Existing studies in primarily cannabis and nicotine users indicate opposing effects of each substance (Subramaniam et al 2016), including in RSNs (Vergara et al 2018). For example, increased connectivity has been reported in cannabis users (Pujol et al 2014; Filbey et al 2014), whereas reduced connectivity has been observed in nicotine users (Weiland et al 2015).…”

Chronic nicotine exposure attenuates the effects of Δ9‐tetrahydrocannabinol on anxiety‐related behavior and social interaction in adult male and female rats

“…Evidence shows that illicit drug use (i.e., cannabis, cocaine, and heroin) is often preceded by tobacco and alcohol use, which supports the well‐known gateway hypothesis of drug use; however, cannabis use is a strong predictor for the onset and lifetime use of tobacco use, which supports the reverse gateway hypothesis (Agrawal et al, ; Becker et al, ; Fergusson, Boden, & Horwood, ; Kandel & Kandel, ; Keyes et al, ; Subramaniam et al, ; Wagner & Anthony, ). Thus, several neurobiological mechanisms for comorbid tobacco and cannabis have been proposed to explain the association, for example, synergistic mechanisms, involving central nervous system nicotinic acetylcholine receptors (nAChRs) and cannabinoid receptors (CBRs), and compensatory mechanisms, involving attenuation of withdrawal symptoms (Rabin & George, ; Subramaniam et al, ). Both of these mechanisms involve changes in the opposing physiological processes of reward and aversion learning which are mediated by neural circuits in the brain's mesolimbic dopaminergic system (MDS; Kandel & Kandel, ; Scherma et al, ).…”

“…The burden of disease attributable to substance use and the rates of comorbid tobacco and cannabis use are increasing, particularly for adolescents and young adults (Becker, Schaub, Gmel, & Haug, 2015;Degenhardt, Stockings, Patton, Hall, & Lynskey, 2016;Keyes, Hamilton, & Kandel, 2016;Patton, Coffey, Carlin, Sawyer, & Lynskey, 2005;Ramo, Liu, & Prochaska, 2012;Rubinstein, Rait, & Prochaska, 2014;Subramaniam, McGlade, & Yurgelun-Todd, 2016). Tobacco use is the primary preventable cause of death with an estimated mortality rate of 5 to 6 million people per year globally (World Health Organization [WHO], 2008[WHO], , 2009[WHO], , 2013.…”

“…Both of these mechanisms involve changes in the opposing physiological processes of reward and aversion learning which are mediated by neural circuits in the brain's mesolimbic dopaminergic system (MDS; Kandel & Kandel, 2015;Scherma et al, 2016). After nicotine exposure, neurons in the MDS become sensitized to the effects of other drugs, particularly THC and cocaine (Kandel & Kandel, 2015;Rabin & George, 2015;Subramaniam et al, 2016). Nicotine's effects on the endocannabinoid system include the release of endocannabinoids in the MDS, affecting dopamine levels and thus the rewarding effects of nicotine (González et al, 2002;Scherma et al, 2008); these effects can be blocked by administration of CBR antagonists, such as SR141716 (Cheer et al, 2007;Scherma et al, 2008).…”

Lower total and regional grey matter brain volumes in youth with perinatally-acquired HIV infection: Associations with HIV disease severity, substance use, and cognition

“…Differing patterns found in our study may be due to dose-related effects; we examined ever-use, not frequency or duration of use. Moreover, concurrent marijuana and alcohol could have complex and perhaps interacting effects on brain structure (Price et al, 2015; Squeglia et al, 2014, 2009; Subramaniam et al, 2016). …”