We replicated Bachhuber et al.’s (1) finding of a negative association between medical marijuana and opioid overdose deaths from 1999 to 2010. However, the association did not hold when more extensive data through 2017 were analyzed. Had the analysis’ endpoint been between 2008 and 2012, the results would have been comparable to those obtained by Bachhuber et al. (1). However, the association became equivocal in 2013; by 2017 it had reversed such that a study conducted in that year might lead some to conclude that medical cannabis laws were compounding opioid overdose mortality.
The mechanism theorized to describe a causal relationship between medical cannabis laws and opioid overdose mortality rests on several premises: (i) Cannabis is more available in states with medical cannabis laws; (ii) people in these states substitute cannabis for opioids, whether for pain management, intoxication, or both; and (iii) this substitution occurs on a large enough scale to impact the population-level overdose mortality estimates. Under this model, states with highly restrictive medical cannabis laws limited to low-THC products would be expected to have a weaker association than states with comprehensive medical cannabis, while states with recreational cannabis would be expected to have a stronger association. Our results do not support this, as after adjusting for more and less restrictive types of cannabis law (recreational and medical or low-THC only), states with comprehensive medical cannabis laws still had a positive association with opioid overdose mortality.
The Bachhuber et al. (1) study is one of several that find the rate of cannabis access and some index of opioid-related harm are negatively correlated in the aggregate (1, 5⇓-7). Policy that expands access to cannabis based on these findings assumes that (i) the same negative relationship is present at the individual level and (ii) the relationship is causal. The first conclusion is frequently incorrect across many research fields owing to the ecological fallacy (9). Ecological correlations cannot establish individual-level relationships and indeed may run in the directly opposite direction (e.g., higher rates of smoking in French regions with lower rates of esophageal cancer should not be interpreted as evidence of a protective effect of smoking) (10). In this case, compelling evidence exists that violates the first assumption: A study of a nationally representative sample of individuals shows that use of medical cannabis is positively correlated both with use and misuse of prescription pain relievers (11). This positive correlation does not at all prove that medical cannabis causes individuals to use opioids because correlation of nonexperimentally gathered data does not establish causation, a general principle that all parties to the current debate should bear in mind.
When multiple studies using similar methods generate a particular result, and for the first time one of those studies fails to replicate with more extensive data, there are multiple ways to explain the discrepancy. It could be that by bad luck the only one of those studies whose initial findings would not stand up to reanalysis with more recent data happened to be the one that was reexamined and every other similar study in that area would survive such an analysis (even though, as in this case, they explicitly build on the nonreplicated finding). However, we think a nonreplication should at least raise the possibility in the minds of scientists that the similar findings of other, similar studies in this area might also not replicate with a longer time series.
We are more cautious than others have been in drawing causal conclusions from ecological correlations and conclude that the observed association between these two phenomena is likely spurious rather than a reflection of medical cannabis saving lives 10 y ago and killing people today. Medical cannabis users are about 2.5% of the population, making it unlikely that they can significantly alter population-wide indices (12). Unmeasured variables likely explain both associations (e.g., state incarceration rates and practices, naloxone availability, and the extent of insurance and services) (2).
Our expanded analysis does not support the interpretation that broader access to cannabis is associated with lower opioid overdose mortality. The CIs for both recreational cannabis laws and low-THC laws are wide due to the comparatively small number of state/year combinations with these laws. Importantly, the CIs are compatible with a strong positive or strong negative correlation, as well as no correlation. Future estimates may be more precise (i.e., have narrower CIs) as data accumulate over time, and we caution scientists who conduct these analyses to note that, at present, states with recreational cannabis laws (Alaska, California, Colorado, Massachusetts, Maine, Oregon, Washington, Vermont, and the District of Columbia) form a group that is qualitatively different from the rest of the United States on a number of metrics that may confound estimates.
The nonrobustness of the earlier findings also highlights the challenges of controlling scientific messages in controversial policy areas. Corporate actors (e.g., the medical cannabis industry) with deep pockets have substantial ability to promote congenial results, and suffering people are desperate for effective solutions. Cannabinoids have demonstrated therapeutic benefits (13), but reducing population-level opioid overdose mortality does not appear to be among them.
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