Background And Aim: Effective policies to reduce drug-related overdoses remain a public health priority. We aimed to estimate the causal effects of a national opioid agonist treatment (OAT) program on population level drug fatalities.
Design: Population-based prospective cohort study exploiting supply driven variation in treatment uptake across cohort-age groups generated by the introduction and scale-up of a national OAT program. A Poisson difference-in-differences model with an intention-to-treat design was used to assess how treatment uptake altered the age profile of risks and infer treatment effects on drug fatalities.
Setting: Norway, from 1996 through 2016.
Cases: The data include a total of 5634 drug-related overdose deaths and cover the introduction of the Norwegian OAT program in 1998 and its initial growth period, reaching 12 286 ever-treated recipients by 2016.
Measurements: Fatal opioid-related overdoses were defined as deaths with a primary cause assigned an International Classification of Diseases 10th Revision (ICD-10) code F11, or X42, X44, X62 or X64 in combination with T40.0-T40.4. Other non-opioid related fatal overdoses were defined by a primary cause registered as F12, F14, F15, F16 or F19, or X42, X44, X62 or 64 in combination with T40.5-T40.9.
Findings: An additional 887 deaths (95% credibility interval [CI] = 265-1563) would have been expected in the absence of OAT, which implies one death avoided per 111 (95% CI = 61-342) treatment-exposed person-years. At scale, the program reduced annual overdose mortality by 27% in 2016 (95% CI = 10%-41%) relative to a no-OAT counterfactual, corresponding to 99 fewer expected fatal overdoses (95% CI = 28-180) in 2016. Analysing fatal opioid-related and other drug overdoses separately found similar numbers for avoided opioid-related fatalities (921, with 95% CI = 373-1526) and no treatment effects on non-opioid related fatalities (-38, with 95% CI = -193-154).
Conclusion: The introduction and rapid scale-up of a national opioid agonist treatment program in Norway was associated with substantial and plausibly causal reductions in drug fatalities.
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