Summary
A large analysis of more than 4 million adults found that those with a history of cannabis-related diagnoses had almost four times the risk of developing type 2 diabetes over five years compared with people without cannabis- or other substance-use histories. The findings raise concerns about potential long-term metabolic harms as cannabis use increases globally, though the study cannot prove cause and effect.
Study design
Investigators at Boston Medical Center used the TriNetX Research Network to examine electronic health records from 54 health organizations in the U.S. and Europe. They reviewed data from 2010 to 2018 for adults aged 18 to 50. Nearly 97,000 people had cannabis-related diagnoses (from occasional use or intoxication to dependence and withdrawal) and were matched to more than 4 million individuals without substance-use diagnoses or major chronic conditions. Matching adjusted for common diabetes risk factors such as age, sex, and underlying medical conditions. All participants were followed for five years to identify new cases of type 2 diabetes.
Key results
– During follow-up, 2.2% of people with cannabis-related diagnoses developed type 2 diabetes versus 0.6% of matched non-users, an increase of nearly fourfold in relative risk.
– Diabetes-free (survival) rates were 96.82% among the cannabis-diagnosis group and 99.15% among non-users; while the percentage difference is modest, it corresponds to thousands of additional cases given the study’s large sample.
– The multisite, real-world clinical dataset strengthens the findings’ relevance to routine care, but the observational design precludes causal conclusions.
Possible mechanisms
Lead author Ibrahim Kamel, MD, suggested several mechanisms that could link cannabis use to higher diabetes risk. Overactivation of the endocannabinoid system—particularly the CB1 receptor—may promote abdominal and liver fat accumulation and insulin resistance. Other potential contributors include increased caloric intake (the “munchies”), low-grade inflammation, oxidative stress, and impaired pancreatic β-cell function affecting glucose regulation. Lifestyle factors associated with cannabis use—such as lower physical activity and concurrent alcohol or tobacco use—could further increase risk.
Expert practical advice
Kamel noted that the study population was relatively healthy and without many typical diabetes risk factors, implying that even otherwise healthy adults might face elevated risk. He recommended further research to clarify mechanisms and whether occasional versus heavier use differs in risk, and suggested that reducing use while maintaining healthy diet and attention to calories could be prudent pending more data.
An independent clinician, Chad Larson, NMD, DC, advised practical monitoring and prevention steps: track waist circumference as an early sign of insulin resistance (thresholds often cited are >40 inches in men and >35 inches in women), consider an evening protein snack of about 25 grams to stabilize overnight blood sugar and curb cravings, and add brief daily exercise (for example, a 20-minute brisk walk) to improve muscle glucose uptake.
Limitations and implications
Because the study relied on observational clinical records, it cannot establish causation and may be affected by residual confounding despite matching and adjustments. The data do not clarify whether risk varies by frequency, dose, or mode of cannabis use, or whether occasional use is safer. Nevertheless, the association observed in a large, diverse cohort suggests clinicians and people who use cannabis should be aware of possible metabolic risks. The authors and commentators call for prospective studies to confirm these findings and to explore mechanisms and dose–response relationships.
