Reframing stimulant‐involved mortality: Counting—and preventing—fentanyl ± stimulant deaths as opioid deaths

Chang and colleagues [1] show that in San Francisco, 2013 to 2023, deaths attributed to fentanyl—whether or not stimulants are detected—share similar cause-of-death profiles and are distinct from stimulant-only deaths. This distinction should reshape surveillance and prevention. First, use mutually exclusive, mechanism-aligned categories. When stimulants co-occur with fentanyl, the pattern tracks acute opioid toxicity (high odds of no additional cause; far lower cardiovascular/cerebrovascular contributors), not the chronic-disease phenotype seen in stimulant-only deaths. Collapsing everything as ‘stimulant-involved’ double counts and obscures mechanisms, and other jurisdictions echo this. In Ontario, >80% of accidental stimulant toxicity deaths also involved an opioid and most occurred in private residences—settings where naloxone, medications for opioid use disorder (MOUD) and take-home overdose education are the relevant tools [2]. In Quebec, toxicology shifted toward non-pharmaceutical fentanyl in opioid deaths and toward novel benzodiazepines as frequent co-detected depressants, illustrating how ‘any-listed-substance’ attribution can mislead mechanistic inference [3]. Second, account for stimulant heterogeneity and geography. Pooling methamphetamine and cocaine masks risk. United States poison-center data show sharp increases in fentanyl–cocaine co-exposures in the Northeast, with higher odds of major effects than fentanyl–methamphetamine, and the latter rose more in the Midwest/South/West [4]. Among patients receiving MOUD in Ontario, stimulant use rose over time, driven by crystal methamphetamine, and was independently associated with daily fentanyl use and injection [5]. Surveillance and models should stratify by stimulant type and region to target responses (e.g. cocaine-focused drug checking and messaging versus methamphetamine-specific supports). Third, strengthen attribution by addressing documentation artifacts and co-depressants. ‘No additional cause’ likely mixes true acute respiratory failure with information availability that varies by setting and certifier. Models should include year, location of death (scene vs. hospital) and certifier type with sensitivity analyses excluding hospital deaths. Crucially, adjust for alcohol and benzodiazepines, (e.g. Quebec data document a rapid rise of novel benzodiazepines in opioid deaths since 2019) [3]. Without this, the opioid signal can be conflated with unmeasured sedative co-toxicity. Taken together, the evidence supports counting and preventing fentanyl ± stimulant deaths as opioid deaths, while reserving a separate category for stimulant-only mortality. Mechanism-based classification will clarify metrics and sharpen prevention—scaling naloxone, low-threshold MOUD and sedative-risk messaging for fentanyl-driven deaths—while different strategies address stimulant-only mortality. Yu Chieh Wu: Conceptualization; investigation; writing—original draft. Lien-Chung Wei: Conceptualization; supervision; project administration; writing—review and editing. None.