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Objectives. In 1999, New Zealand lowered the minimum purchasing age for alcohol from 20 to 18 years. We tested the hypothesis that this increased traffic crash injuries among 15- to 19-year-olds. Methods. Poisson regression was used to compute incidence rate ratios for the after to before incidence of alcohol-involved crashes and hospitalized injuries among 18- to 19-year-olds and 15- to 17-year-olds (20- to 24-year-olds were the reference). Results. Among young men, the ratio of the alcohol-involved crash rate after the law change to the period before was 12% larger (95% confidence interval [CI] = 1.00, 1.25) for 18- to 19-year-olds and 14% larger (95% CI = 1.01, 1.30) for 15- to 17-year-olds, relative to 20- to 24-year-olds. Among young women, the equivalent ratios were 51% larger (95% CI = 1.17, 1.94) for 18- to 19-year-olds and 24% larger (95% CI = 0.96, 1.59) for 15- to 17-year-olds. A similar pattern was observed for hospitalized injuries. Conclusions. Significantly more alcohol-involved crashes occurred among 15-to 19-year-olds than would have occurred had the purchase age not been reduced to 18 years. The effect size for 18- to 19-year-olds is remarkable given the legal exceptions to the pre-1999 law and its poor enforcement.

Objective: To estimate risk of fracture in men and women with recent diagnosis of type 2 diabetes compared with individuals without diabetes.Research Design and Methods: In this cohort study, we used routinely collected U.K. primary care data from The Health Improvement Network. In adults (>35 years) diagnosed with type 2 diabetes between 2004 and 2013, fractures sustained until 2019 were identified and compared with fractures sustained in individuals without diabetes. Multivariable models estimated time to first fracture following diagnosis of diabetes. Annual prevalence rates included at least one fracture in a given year.Results: Among 174,244 individuals with incident type 2 diabetes and 747,290 without diabetes, there was no increased risk of fracture among males with diabetes (adjusted hazard ratio [aHR] 0.97 [95% CI 0.94, 1.00]) and a small reduced risk among females (aHR 0.94 [95% CI 0.92, 0.96]). In those aged ≥85 years, those in the diabetes cohort were at significantly lower risk of incident fracture (males: aHR 0.85 [95% CI 0.71, 1.00]; females: aHR 0.85 [95% CI 0.78, 0.94]). For those in the most deprived areas, aHRs were 0.90 (95% CI 0.83, 0.98) for males and 0.91 (95% CI 0.85, 0.97) for females. Annual fracture prevalence rates, by sex, were similar for those with and without type 2 diabetes.Conclusions: We found no evidence to suggest a higher risk of fracture following diagnosis of type 2 diabetes. After a diagnosis of type 2 diabetes, individuals should be encouraged to make positive lifestyle changes, including undertaking weight-bearing physical activities that improve bone health. [ABSTRACT FROM AUTHOR]

Abstract Background Although many countries experience an increase in mortality during winter, the magnitude of this increase varies considerably, suggesting that some winter excess may be avoidable. Conflicting evidence has been presented on the role of gender, region and deprivation. Little has been published on the magnitude of excess winter mortality (EWM) in New Zealand (NZ) and other Southern Hemisphere countries. Methods Monthly mortality rates per 100,000 population were calculated from routinely collected national mortality data for 1980 to 2000. Generalised negative binomial regression models were used to compare mortality rates between winter (June–September) and the warmer months (October–May). Results From 1980–2000 around 1600 excess winter deaths occurred each year with winter mortality rates 18% higher than expected from non-winter rates. Patterns of EWM by age group showed the young and the elderly to be particularly vulnerable. After adjusting for all major covariates, the winter:non-winter mortality rate ratio from 1996–2000 in females was 9% higher than in males. Mortality caused by diseases of the circulatory system accounted for 47% of all excess winter deaths from 1996–2000 with mortality from diseases of the respiratory system accounting for 31%. There was no evidence to suggest that patterns of EWM differed by ethnicity, region or local-area based deprivation level. No decline in seasonal mortality was evident over the two decades. Conclusion EWM in NZ is substantial and at the upper end of the range observed internationally. Interventions to reduce EWM are important, but the surprising lack of variation in EWM by ethnicity, region and deprivation, provides little guidance for how such mortality can be reduced.