Recreational cannabis use may trigger stroke, says study

CANNABIS use outside of what is medically prescribed, including recreational purposes, is associated with a 37-percent higher overall risk of stroke, with evidence pointing to chronic, long-term exposure rather than casual consumption as the primary driver of this cardiovascular danger, according to a landmark global study led by researchers at the University of Cambridge.

The comprehensive study, titled “Does illicit drug use increase stroke risk? A systematic review, meta-analyses, and Mendelian randomization analysis,” was published in the International Journal of Stroke by a research team including from the Cambridge Department of Clinical Neurosciences.

Responding to questions from The Manila Times, Megan Ritson, a post-doctoral research associate with the Cambridge Stroke Research Group and lead author of the study, provided crucial context regarding how these findings apply to different usage patterns, substance types, and global populations. She is joined Eric Harshfield and professor Hugh Markus.

Regarding the 37-percent risk increase for cannabis, Ritson noted that a sensitivity analysis focusing strictly on recent or occasional exposure caused the statistical link to lose significance.

“This may suggest the risk reflects longer-term use rather than occasional exposure,” Ritson said, though she cautioned that current data limitations prevent a definitive conclusion.

The team conducted a systematic review and meta-analysis of 32 international studies comprising more than 100 million total participants across hospital-based, population-based, and administrative registries. The research evaluated the cerebrovascular impacts of several substances used outside of regulated medical contexts, finding that while stimulant drugs like amphetamines (122 percent increased risk) and cocaine (96 percent increased risk) roughly doubled overall stroke risk, cannabis consumption presented a distinct threat of its own.

In contrast, the meta-analysis found no statistically significant association between opioid use or nicotine dependence and stroke risk, underscoring that stroke danger is driven by specific vascular mechanisms unique to stimulants and cannabis.

To determine whether these substances directly trigger strokes or merely correlate with unhealthier overall lifestyles, the research team employed Mendelian randomization, a statistical technique that examines naturally occurring genetic variants to establish direct cause-and-effect relationships.

The genetic validation revealed distinct mapping between specific substances and stroke subtypes. First, cannabis use disorders were specifically linked to large artery strokes, driven by the drug’s propensity to heighten blood clotting tendencies, induce vessel spasms, and trigger sudden blood pressure surges.

Interestingly, the research revealed that cocaine dependence was strongly linked to cardioembolic strokes — where a blood clot forms in the heart and travels to the brain — and intracerebral hemorrhages (bleeding within brain tissue). Overall genetically predicted substance use disorder carried an almost eightfold increased risk (OR = 7.79) for intracerebral hemorrhage.

In a separate sub-analysis focusing on individuals under the age of 55, cannabis use was associated with a 14-percent elevated stroke risk, while amphetamine and cocaine usage showed risk spikes of 174 percent and 97 percent, respectively.

Ritson also acknowledged major geographic and demographic limitations in the dataset, particularly for non-Western populations. Of the 32 cohort studies analyzed, 27 originated in the United States due to data availability, leaving Asian and Southeast Asian populations underrepresented. Furthermore, the Mendelian randomization analysis was restricted entirely to individuals of European ancestry.

“The mechanisms through which these drugs cause harm are unlikely to be dramatically different across populations, however, we cannot assume that the magnitude of risk will be the same,” Ritson explained. “Variables such as genetic background, pattern of use, substance type and cardiovascular risk factors can vary across populations.”

Addressing substance categories prevalent in Southeast Asia, Ritson clarified that the underlying studies categorized drugs broadly as “amphetamine-type stimulants” rather than isolating specific synthetic derivatives like methamphetamine. She added that genome-wide association study (GWAS) data suitable for analyzing amphetamines or methamphetamines via Mendelian randomization is not currently available.

On the challenge of polysubstance use — where individuals consume cannabis alongside alcohol, tobacco, or other illicit drugs — Ritson stated that the meta-analysis specifically selected studies that reported adjusted odds ratios to account for concurrent substance misuse. The genetic instruments used in the Mendelian randomization phase further isolated specific substances to prevent confounding variables.