Green Chains: The Addictive Side of Cannabis
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- 2 days ago
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Written by: Manasa Kumar
Edited by: Fahad Hassan Shah
With the decriminalization of recreational cannabis in several states in the United States and in countries around the world, weed has become almost a household term (and item). It is the most commonly abused drug and accounts for half of all drug seizures by law enforcement (Hempel & Xi, 2022; WHO, 2021). Though its effects are mediated through the accumulation of several secondary metabolites, the two most-studied cannabinoids are Δ9-tetrahydrocannabinol (THC), the main psychoactive constituent and responsible for the “high” that comes with cannabis consumption, and cannabidiol (CBD), which is non-intoxicating and has shown anxiolytic and anti-inflammatory properties (Ferland et al., 2025; Mechoulam & Parker, 2013). While legalization of cannabis has reduced the stigma associated with it, it has given rise to the largely incorrect notion that its consumption is without harm. This is especially seen among teens, where data is contradictory to prevalent opinion, showing irreversible damage to cognition and decision-making abilities during these developmental years, and a higher risk of developing psychiatric conditions. Regular use also puts teens at risk of developing cannabis use disorder (CUD) (Bara et al., 2021; Ferland et al., 2023).
Why is cannabis addictive?
Before exploring the effects of cannabinoids from the cannabis plant, let's talk about cannabinoids in our bodies. The endocannabinoid system, or ECS, is a relatively recent discovery that plays a crucial role in maintaining homeostasis, as well as regulating other bodily functions, including mood, sleep, appetite, pain, temperature, and immune response. The cannabinoid receptors, CB1 and CB2, are found scattered throughout the body, with CB1 receptors predominantly localized in the central nervous system, whereas CB2 receptors are mostly found in the immune system and peripheral organs (Mechoulam & Parker, 2013; Skaper & Marzo, 2012).
So why isn’t cannabis considered as dangerous as “hard” drugs? Infrequent or occasional use of cannabis yields not-so-serious symptoms: predominantly a calming effect, distortions in motor coordination and time perception, and “the munchies.” While its effects are subjective, the symptoms do not have the euphoric rise and meteoric crash seen with the use of other drugs such as opioids. However, regular use has been proven to cause critical changes in cognition, memory, and decision-making. This effect is particularly pronounced in adolescents and pregnant women, affecting neural processes in developing brains (Bara et al., 2021). THC has a large hand in bringing about the compulsive use of cannabis, eventually leading to addiction. Addiction is characterized by compulsive intake of a drug, loss of control in limiting intake, and emergence of a negative emotional state when the rewarding effects of the drug wear off unless taken in high quantities (Koob and Volkow, 2009). CUD hijacks the brain’s reward system by targeting the ECS (Substance Abuse and Mental Health Services Administration, 2016).
Three regions in the brain primarily make up the addiction circuit. Each of these regions play a pivotal role in the three stages of the addiction cycle.
First, the Binge/Intoxication phase, involving the basal ganglia, occurs when the individual consumes cannabinoids. The cannabinoids activate dopaminergic neurons in the nucleus accumbens and the ventral tegmental area, taking over the ECS and affecting associated circuits and organs. Over time, external stimuli aid in building a habit of using cannabis for its pleasurable effects. Repeated activation of the habit circuitry, involving the dorsal striatum, contributes to compulsive drug seeking.
Next, the Withdrawal/Negative Affect stage follows the Binge/Intoxication Stage, often setting up a pathway back to the first. It is accompanied by physical symptoms such as irritability, depression, and sleep disturbances, though the intensity of cannabinoid withdrawal might be different compared to opioids. Withdrawal is brought about by two phenomena: the decrease in activity of the reward system through the basal ganglia, and the activation of the brain’s stress center, the amygdala.
Finally, the third stage, the Preoccupation/Anticipation Stage, occurs when the individual goes through a period of craving. In people with severe CUD, this may occur after a couple of hours. This stage recruits the prefrontal cortex (PFC), a region of the brain that is responsible for executive function and decision-making. Executive function is essential for making appropriate choices, determining whether or not to use cannabis, and resisting urges to do so. Without the PFC functioning properly, the brain’s innate “Stop and Go” system becomes dysfunctional, falling back into the cycle.
These three stages in CUD worsen over time and cause dramatic changes to the brain’s reward, stress, and executive function systems (Koob and Volkow, 2009; Substance Abuse and Mental Health Services Administration, 2016).
Thoughts to take home
Decriminalization and/or legalization of cannabis has alleviated some of the stigma associated with its consumption. However, this has also brought about unintended consequences, encouraging its use among teenagers and pregnant mothers, due to a drop in perception of its health risk. However, data from recent research shows that chronic cannabis users show poor decision-making, as well as an increased risk for the development of psychiatric disorders. Awareness about the risk of cannabis consumption is important among youths, especially considering its potency today and the resulting cognitive vulnerability experienced later in life.
References
Bara, A., Ferland, J.-M. N., Rompala, G., Szutorisz, H., & Hurd, Y. L. (2021). Cannabis and synaptic reprogramming of the developing brain. Nature Reviews Neuroscience, 22(7), 423–438. https://doi.org/10.1038/s41583-021-00465-5
Ferland, J.-M. N., Chisholm, A., Abdalla, J., Cinar, R., Johnson, C., Bradshaw, H. B., & Hurd, Y. L. (2025). Cannabidiol abrogates cue-induced anxiety associated with normalization of mitochondria-specific transcripts and linoleic acid in the nucleus accumbens shell. Molecular Psychiatry, 30(6), 2718–2728. https://doi.org/10.1038/s41380-024-02881-2
Ferland, J.-M. N., Ellis, R. J., Betts, G., Silveira, M. M., de Firmino, J. B., Winstanley, C. A., & Hurd, Y. L. (2023). Long-term outcomes of adolescent THC exposure on translational cognitive measures in adulthood in an animal model and computational assessment of human data. JAMA Psychiatry, 80(1), 66. https://doi.org/10.1001/jamapsychiatry.2022.3915
Hempel, B., & Xi, Z.-X. (2022). Receptor mechanisms underlying the CNS effects of cannabinoids: CB1 receptor and beyond. Advances in Pharmacology, 275–333. https://doi.org/10.1016/bs.apha.2021.10.006
Koob, G. F., & Volkow, N. D. (2009). Neurocircuitry of addiction. Neuropsychopharmacology, 35(1), 217–238. https://doi.org/10.1038/npp.2009.110
Mechoulam, R., & Parker, L. A. (2013). The endocannabinoid system and the brain. Annual Review of Psychology, 64(1), 21–47. https://doi.org/10.1146/annurev-psych-113011-143739
Substance Abuse and Mental Health Services Administration (US); Office of the Surgeon General (US). (2016). CHAPTER 2, THE NEUROBIOLOGY OF SUBSTANCE USE, MISUSE, AND ADDICTION. In Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. US Department of Health and Human Services. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK424849/.
Skaper, S. D., & Di Marzo, V. (2012). Endocannabinoids in nervous system health and disease: The big picture in a Nutshell. Philosophical Transactions of the Royal Society B: Biological Sciences, 367(1607), 3193–3200. https://doi.org/10.1098/rstb.2012.0313
World Health Organization. (2021). Cannabis. Alcohol, Drugs and Addictive Behaviours. https://www.who.int/teams/mental-health-and-substance-use/alcohol-drugs-and-addictive-behaviours/drugs-psychoactive/cannabis
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