CannaTrials adheres to evidence-based medicine – making statements based on medical evidence.
This page is excerpted and quoted from the National Academies of Science, Engineering, and Medicine. A Committee of over 40 experts, researchers, and reviewers in The Health and Medicine Division published a 486 page report in 2017 entitled “The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research.”
If you would like to access the entire report you may do so by clicking this link.
Medical Marijuana and Stroke
“Stroke is the fifth leading cause of death in the United States, accounting for 133,000 deaths annually (Kochanek et al., 2016). A stroke is the death of a portion of brain tissue due to a disruption of the blood supply. Strokes may be ischemic (inadequate blood/oxygen supply) or hemorrhagic (bleeding into the brain) in origin. Each year, approximately 795,000 people experience a new or recurrent stroke. Approximately 610,000 of these are first stoke occurrences and 185,000 are recurrent stroke events (Mozaffarian et al., 2016). The committee responsible for the IOM report Marijuana and Medicine: Assessing the Science Base (1999) did not make any conclusions or recommendations regarding cannabis use and stroke.
Numerous reports have suggested that smoking cannabis increases the risk of stroke, including case series (Phillips et al., 2011) and studies describing cannabis-associated vascular changes that may be associated with stroke (Herning et al., 2001; Wolff et al., 2011, 2015). Several reports have indicated a close temporal relationship between cannabis smoking and stroke (Wolff et al., 2013). The cardiovascular effects of cannabis that have been proposed as a possible mechanism in the etiology of stroke include orthostatic hypotension with secondary impairment of the autoregulation of cerebral blood flow, altered cerebral vasomotor function, supine hypertension and swings in blood pressure, cardioembolism with atrial fibrillation, other arrhythmias, vasculopathy, vasospasm, reversible cerebral vasoconstriction syndrome, and multifocal intracranial stenosis (Wolff et al., 2015).
The studies by Rumalla et al. (2016a,b) and Westover et al. (2007) were cross-sectional studies using administrative data consisting of ICD-9 codes. Cross-sectional studies do not allow one to assess temporality between exposure and outcome. The miscoding of strokes does occur, although the reliability is probably reasonable for epidemiological studies. The classification of exposure status using ICD-9 is particularly concerning, given the likelihood that the percentage of cannabis users appears to be low compared to population norms in each of these studies, most notably the Westover et al. (2007) study.
With the exception of the Sidney (2002) study, none of the studies have data on the temporal relation between the cannabis or tobacco use and the stroke. A general problem was the analytic treatment of tobacco use. Given the much longer duration and frequency of tobacco smoking than of cannabis smoking for most people and the very common co-use of both substances, it is not appropriate to assume that an adjustment for tobacco use in a multivariable model will provide an accurate assessment of the risk associated with cannabis use. Additional analytic approaches, when feasible, may include testing the interaction between cannabis and tobacco use and performing stratified analyses to test the association of cannabis use with clinical endpoints in nonusers of tobacco. Other general limitations beyond those already mentioned in the description of the studies include the absence of the impact of the route of consumption (e.g., smoked, edible, etc.); the absence of information on dose, including accounting for the content of THC and other cannabinoids and potential additives or contaminants; and the lack of information on the total lifetime duration/dose of cannabis use.
All the articles were judged to be of fair quality for assessing the risk of stroke associated with cannabis use. With the exception of Sidney (2002) and Barber et al. (2013), all showed an increased risk of stroke associated with cannabis use but had significant limitations. For ischemic stroke, two of the studies indicated an increased risk while one showed a nonsignificant finding in the direction of increased risk. For subarachnoid hemorrhage, the single study found an increased risk. For the combined hemorrhagic stroke endpoint assessed by Westover et al. (2007), the study showed no association of cannabis use with the risk of this endpoint.
CONCLUSION 6-2 There is limited evidence of a statistical association between cannabis use and ischemic stroke or subarachnoid hemorrhage. “
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