Can a Greenhouse Gas Emissions Tax on Food also Be Healthy and Equitable? A Systemised Review and Modelling Study from Aotearoa New Zealand.

Policies to mitigate climate change are essential. The objective of this paper was to estimate the impact of greenhouse gas (GHG) food taxes and assess whether such a tax could also have health benefits in Aotearoa NZ. We undertook a systemised review on GHG food taxes to inform four tax scenarios, including one combined with a subsidy. These scenarios were modelled to estimate lifetime impacts on quality-adjusted health years (QALY), health inequities by ethnicity, GHG emissions, health system costs and food costs to the individual. Twenty-eight modelling studies on food tax policies were identified. Taxes resulted in decreased consumption of the targeted foods (e.g., -15.4% in beef/ruminant consumption, N = 12 studies) and an average decrease of 8.3% in GHG emissions (N = 19 studies). The "GHG weighted tax on all foods" scenario had the largest health gains and costs savings (455,800 QALYs and NZD 8.8 billion), followed by the tax-fruit and vegetable subsidy scenario (410,400 QALYs and NZD 6.4 billion). All scenarios were associated with reduced GHG emissions and higher age standardised per capita QALYs for Maori. Applying taxes that target foods with high GHG emissions has the potential to be effective for reducing GHG emissions and to result in co-benefits for population health.

Linking the heart and the brain: Neurodevelopmental disorders in patients with catecholaminergic polymorphic ventricular tachycardia.

BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an uncommon inherited arrhythmia disorder characterized by adrenergically evoked ventricular arrhythmias. Mutations in the cardiac calcium release channel/ryanodine receptor gene (RYR2) are identified in the majority of patients with CPVT. RyR2 is also the major RyR isoform expressed in the brain. OBJECTIVE: The purpose of this study was to estimate the prevalence of intellectual disability (ID) and other neurodevelopmental disorders (NDDs) in RYR2-associated CPVT (CPVT1) and to study the characteristics of these patients. METHODS: We reviewed the medical records of all CPVT1 patients from 12 international centers and analyzed the characteristics of all CPVT1 patients with concomitant NDDs. We functionally characterized the mutations to assess their response to caffeine activation. We did not correct for potential confounders. RESULTS: Among 421 CPVT1 patients, we identified 34 patients with ID (8%; 95% confidence interval 6%-11%). Median age at diagnosis was 9.3 years (interquartile range 7.0-14.5). Parents for 24 of 34 patients were available for genetic testing, and 13 of 24 (54%) had a de novo mutation. Severity of ID ranged from mild to severe and was accompanied by other NDDs in 9 patients (26%). Functionally, the ID-associated mutations showed a markedly enhanced response of RyR2 to activation by caffeine. Seventeen patients (50%) also had supraventricular arrhythmias. During median follow-up of 8.4 years (interquartile range 1.8-12.4), 15 patients (45%) experienced an arrhythmic event despite adequate therapy. CONCLUSION: Our study indicates that ID is more prevalent among CPVT1 patients (8%) than in the general population (1%-3%). This subgroup of CPVT1 patients reveals a malignant cardiac phenotype with marked supraventricular and ventricular arrhythmias.