Cannabis linked to liver enzyme changes in new study

Impact of cannabis, benzodiazepines, and methamphetamine use on inflammatory and hepatic biomarkers in Benin City, Nigeria: a case-control study.

Naunyn-Schmiedeberg's archives of pharmacology • • Moderately Relevant
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AI Summary

This case-control study from Nigeria examined how cannabis use—alone and in combination with benzodiazepines and methamphetamine—affects liver function and immune markers in 83 adults. Researchers measured liver enzymes and inflammatory markers in control groups and users of various substance combinations. The findings revealed elevated liver enzyme levels (specifically AST and ALT) in cannabis users and those combining cannabis with other drugs, suggesting subclinical stress on liver cells. Notably, THC users showed higher AST levels compared to non-users, indicating potential hepatic strain.

An unexpected finding emerged regarding immune function: IL-6, a key inflammatory marker, was significantly reduced in cannabis users and polysubstance users compared to controls. This counters assumptions that cannabis simply increases inflammation and instead suggests selective modulation of immune signaling pathways. However, IL-10 levels showed no significant differences. The research provides concrete evidence of biochemical changes associated with cannabis use, particularly when combined with other substances, pointing to complex interactions between THC and hepatic metabolism pathways.

The authors conclude that these findings warrant further investigation to understand whether these changes are reversible and what the long-term health implications might be. While the study is relatively small and specific to a Nigerian population, it contributes important clinical data from an understudied geographic region and highlights that cannabis effects on the body are more nuanced than commonly understood. Future longitudinal studies could clarify whether these biochemical alterations resolve with abstinence and identify the specific mechanisms by which cannabinoids interact with liver metabolism.

📄 Original Abstract

Cannabis (tetrahydrocannabinol, THC), benzodiazepines (BZO), and methamphetamine (MET) exert diverse pharmacodynamic effects on hepatic metabolism and immune signaling pathways. While experimental studies suggest that these agents modulate cytochrome P450 activity, oxidative stress pathways, and cytokine production, comparative clinical data particularly in African populations remain limited. This study investigated the association between single and polysubstance use and alterations in hepatic and inflammatory biomarkers. In a case-control design, 83 adults (19-59 years) from Benin City, Nigeria, were categorized as controls (n = 20) or users of THC only (n = 27), THC/BZO (n = 12), THC/MET (n = 10), BZO/MET (n = 5), or THC/BZO/MET (n = 9). Substance exposure was confirmed by urine immunochromatographic screening. Plasma levels of aspartate aminotransferase (AST, U/L), alanine aminotransferase (ALT, U/L), alkaline phosphatase (ALP, U/L), gamma-glutamyl transferase (GGT, U/L), total bilirubin (mg/dL), direct bilirubin (mg/dL), interleukin-6 (IL-6, pg/mL), and interleukin-10 (IL-10, pg/mL) were measured using standardized biochemical and ELISA methods. Group differences were assessed using ANOVA with Bonferroni correction. AST levels were significantly elevated in the THC-only (79.07 ± 59.60 U/L) and THC/BZO (73.58 ± 46.11 U/L) groups compared with controls (36.90 ± 11.05 U/L; p = 0.002 and p = 0.027, respectively). ALT was higher in the THC/MET group (54.30 ± 51.15 U/L) versus controls (33.60 ± 12.31 U/L; p = 0.037). IL-6 concentrations were significantly reduced in THC-only, THC/BZO, and THC/BZO/MET users compared with controls (p = 0.002), an unexpected finding discussed further below, whereas IL-10 showed no significant intergroup differences. Cannabis, benzodiazepine, and methamphetamine exposure particularly in combination is associated with biochemical patterns consistent with subclinical hepatocellular and cholestatic stress, alongside selective modulation of IL-6-mediated inflammatory signaling. These findings support pharmacologically plausible interactions affecting hepatic metabolism and immune regulation and warrant longitudinal investigation to clarify mechanistic pathways and reversibility.

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