In 1930s, cannabis was portrayed as an addictive drug capable of producing psychotic cravings in its users. These descriptions were exaggerated, and the reality is that true cannabis dependence appears to be rare except among the heaviest and most frequent users. Withdrawal symptoms appear mild when compared with drugs such as opiates and cocaine, but they have been confirmed experimentally using cannabinoid receptor antagonists, which force withdrawal symptoms when administered to dependent users.231

There is more to cannabis dependency than just cannabinoid receptor interaction. The mu-opioid receptor, which is directly responsible for one of the brain’s reward mechanisms underlying heroin addiction, is also involved. When a cannabinoid such as THC interacts with a CB1 cannabinoid receptor, it induces the release of opioid peptide molecules, which activate mu-opioid receptors. And the same mu-opioid receptor activation underlies the reward pathways associated with alcohol and nicotine dependency. It appears to be a primary brain receptor causing drug addiction.232 Additionally, recent studies indicate that there may be genetic, age, and sex differences associated with how cannabis affects brain structures in cannabinoid dependence among chronic users. For example, adolescent, cannabis-dependent males may suffer changes in the morphology of the amygdala, a brain structure that is primary in memory and emotional responses. These changes in the amygdala do not appear in cannabis-dependent adolescent females.233 Though some of these criteria have been discounted as being more indicative of cannabis prohibition than drug addiction, the appearance of three or more of the following is often considered evidence of cannabis dependency:

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