The topic of marijuana addiction is emotionally charged. The two aspects of addiction—withdrawal symptoms unique to marijuana and alterations in the brain’s reward mechanism common to all addictive drugs—must be approached separately. THC’s stimulation of CB1 receptors causes a homeostatic reduction of receptor density, called downregulation. When THC stimulation wanes, the resultant relative lack of receptors leads to a transient deficiency of endocannabinoid activity. Hirnoven found a 20% reduction in endocannabinoid receptors in the cortex of individuals regularly using marijuana requiring 4 weeks of abstinence to be reversed. The effects of cannabinoid deficiency outlined by Budney include withdrawal symptoms of restlessness, anxiety, insomnia, boredom and irritability. Relapse to marijuana use often occurs to abort withdrawal symptoms. The influx of dopamine in the reward center (nucleus accumbens) caused by excessive cannabinoid stimulation is the sine qua non for addiction and leads to a neurologically based increase in the salience of marijuana. Modification of reward mechanisms increases the motivation to use marijuana to the point that cognitive rationality is clouded and denial is produced.

People use marijuana for nonmedical reasons because they like how it affects the brain, and therefore their mind and subjective experience. However, regular use of marijuana alters brain structure and function in ways that persist well beyond the period of acute intoxication. Progressively more powerful research tools are documenting effects in high risk populations with considerably less than daily use. These impacts are generally reversible but may be permanent if they occur during stages of rapid neurodevelopment typical of early adolescence. The volume of gray matter and the number of synaptic connections can be reduced by marijuana use, most importantly in the hippocampus, amygdala, and frontal lobes. Gender differences exist in the impact of marijuana on cortical thickness during adolescence. The functional integrity of white matter interconnecting areas of the brain can also be reduced by chronic marijuana use, which interferes with the endogenous cannabinoid system’s formation of the microtubule skeleton within axons.

Every clinician encounters patients compromised by marijuana, whether fully addicted or not and whether recognized by the individual or not. While adult heavy users usually seek help themselves (often in response to a partner’s pressure or for reasons seemingly unrelated to marijuana use), the parents of heavy adolescent users usually make the initial contact. The Cannabis Youth Treatment Study (CYT) demonstrated that several manualized brief treatment protocols have similar, but limited, success treating adolescents and recommended greater focus on long term monitoring and care. Although CYT established an evidence base for treatment, it was unable to evaluate the skill of individual therapists to engage patients and develop mutual ground for discussion. A motivational interviewing (MI) framework is presented emphasizing engagement and nonjudgmental exploration of patients’ experience and attachment to marijuana. The clinician’s curiosity about each individual’s favorite subjective experiences when high is used to discuss explanations for marijuana’s effects. Scientific information paves the way for introducing the concept of downregulation and potential negative side effects that create cognitive dissonance. The goal is to avoid evoking defensiveness and to help patients struggle with their own internal doubts about marijuana’s ability to help reach their life goals.