Kava, derived from the root of the Piper methysticum plant, has been used for centuries in the South Pacific for its calming and anxiety-reducing properties. Cannabis contains hundreds of compounds including the psychoactive tetrahydrocannabinol (THC) and non-intoxicating cannabidiol (CBD), known for its wide range of mood-altering and therapeutic effects. Combining any two substances that affect the central nervous system warrants caution, as their pharmacological actions may overlap or intensify one another in unpredictable ways. This article explores the specific risks associated with mixing kava and cannabis, focusing on their distinct mechanisms of action and the potential for dangerous biological synergy.
Understanding Kava and Cannabis Separately
Kava’s primary effects are attributed to active compounds called kavalactones, which interact with the central nervous system (CNS) to produce feelings of muscle relaxation and tranquility. The main mechanism involves the modulation of gamma-aminobutyric acid (GABA) receptors, the primary inhibitory neurotransmitter system in the brain. By enhancing GABAergic activity, kavalactones reduce neuronal excitability, leading to a calming effect similar to certain anti-anxiety medications. Some kavalactones have also been shown to bind to the cannabinoid CB1 receptor, though their affinity is considered weaker than that of THC.
Cannabis exerts its effects primarily through the Endocannabinoid System (ECS), a complex cell-signaling network that regulates functions like mood, pain, and sleep. THC is the compound responsible for the psychoactive “high,” achieving this by binding directly to and activating CB1 receptors, which are highly concentrated in the brain and nervous system. CBD and other cannabinoids interact with the ECS in more subtle ways, such as preventing the breakdown of the body’s own naturally produced endocannabinoids.
The Risks of Combined Central Nervous System Depression
Combining kava and cannabis carries a significant risk of additive or synergistic central nervous system (CNS) depression, as both substances function as relaxants and sedatives. Kava’s potentiation of GABA activity slows down brain activity, promoting drowsiness and anxiolysis. Simultaneously, the activation of CB1 receptors by THC can induce sedative effects, particularly at higher doses.
When these two depressants are taken together, the combined effect on the CNS can be far greater than the sum of their individual effects. This heightened CNS depression leads to severe drowsiness, confusion, and impaired motor coordination. Users experience increased dizziness, slower reaction times, and an elevated risk of accidental injury, especially when attempting to drive or operate machinery. The overlapping action on both the GABAergic system and the endocannabinoid system means the intoxicating effects of THC may be amplified, potentially leading to an overwhelming or uncomfortable experience.
The combined use increases the likelihood of becoming overly sedated. Due to the dual depressant action, the body’s ability to respond to stimuli is significantly diminished, making the combination a high-risk choice for immediate, acute impairment.
Metabolic Interactions and Liver Function
Both kava and many cannabinoids are metabolized in the liver by a group of enzymes known as the Cytochrome P450 (CYP) system. Kava’s kavalactones are known to inhibit the activity of several CYP enzymes, including CYP2C9 and CYP3A4.
Since cannabinoids like THC and CBD rely on these same CYP enzymes for clearance, kava acts as a metabolic bottleneck. The inhibition of CYP enzymes by kava means the liver breaks down the cannabinoids more slowly, causing the concentrations of THC and CBD to remain elevated for a prolonged period. This delayed clearance can intensify and lengthen the psychoactive and sedative effects of cannabis, increasing the chance of adverse reactions.
Kava has a historical association with liver injury (hepatotoxicity). The liver is responsible for detoxifying both kava and cannabis, and introducing a compound that actively stresses the organ by inhibiting its primary metabolic pathways compounds this risk, potentially increasing the risk of adverse liver-related events in susceptible individuals.