Study: Marijuana Use Associated With Lower Risk of Non-Alcoholic Fatty Liver Disease

According to a new study, those with a history of marijuana use are less likely to develop the non-alcoholic fatty liver disease (NAFLD) than those who haven’t used cannabis.

The study, titled “Cannabis consumption and non-alcoholic fatty liver disease: A three years longitudinal study in first-episode non-affective psychosis patients”, was published in the journal Progress in Neuro-Psychopharmacology and Biological Psychiatry.

For the study researchers examined the relationship between cannabis use and liver steatosis over a three-year period in 390 patients, determining that those “who reported continuing cannabis use were at lower risk for developing NAFLD.”

Researchers conclude by stating: “Our results suggest that using cannabis could have a protective effect on liver steatosis. The beneficial effect of cannabis at the level of the development of steatosis seems to be secondary to its modulation effect on weight gain and the reduced development of obesity. … These results are in line with previous studies in the general population, in which cannabis showed significantly lower NAFLD prevalence compared to non-users.”

The full abstract of the study can be found below:


Increased incidence of obesity and excess weight lead to an increased incidence of non-alcoholic fatty liver disease (NAFLD). Recent evidence indicates a protective effect of cannabis consumption on weight gain and related metabolic alterations in psychosis patients. Overall, patients are at greater risk of presenting fatty diseases, such as NAFLD, partly due to lipid and glycemic metabolic disturbances. However, there are no previous studies on the likely effect of cannabis on liver steatosis. We aimed to explore if cannabis consumption had an effect on hepatic steatosis, in a sample of first-episode (FEP) non-affective psychosis.


A total of 390 patients were evaluated at baseline and after 3 years of initiating the antipsychotic treatment. Anthropometric measurements and liver, lipid, and glycemic parameters were obtained at both time points. All but 6.7% of patients were drug-naïve at entry, and they self-reported their cannabis use at both time points. Liver steatosis and fibrosis were evaluated through validated clinical scores (Fatty Liver Index [FLI], Fibrosis-4 [FIB-4], and NAFLD).


At 3-year follow-up, cannabis users presented significantly lower FLI scores than non-users (F = 13.874; p < .001). Moreover, cannabis users less frequently met the criteria for liver steatosis than non-users (X2 = 7.97, p = .019). Longitudinally, patients maintaining cannabis consumption after 3 years presented the smallest increment in FLI over time, which was significantly smaller than the increment in FLI presented by discontinuers (p = .022) and never-users (p = .016). No differences were seen in fibrosis scores associated with cannabis.


Cannabis consumption may produce a protective effect against liver steatosis in psychosis, probably through the modulation of antipsychotic-induced weight gain.

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