Population vulnerability to heat: A case-crossover analysis of heat health alerts and hospital morbidity data in Victoria, Australia.

OBJECTIVE: From 2010 to 2022, the Victorian Department of Health operated a heat health alert system. We explored whether changes to morbidity occurred during or directly after these alerts, and how this differed for certain population groups. METHODS: We used a space-time-stratified case-crossover design and conditional logistic regression to examine the associations between heat health alerts and heat-related and all-cause emergency department (ED) presentations and hospital admissions at the state-wide level, with models created for the whole population and subgroups. Data were included for the warm season (November-March) from 2014 to 2021. RESULTS: Increases occurred in heat-related ED presentations (OR 1.73, 95% CI: 1.53-1.96) and heat-related hospital admissions (OR 1.23, 95% CI: 1.16-1.30) on days on or after heat health alerts. Effect sizes were largest for those 65 years and older, Aboriginal and Torres Strait Islander people, and those living in the most disadvantaged areas. CONCLUSIONS: We confirm that increases in morbidity occurred in Victoria during heat health alerts and describe which population groups are more likely to require healthcare in a hospital. IMPLICATIONS FOR PUBLIC HEALTH: These findings can inform responses before and during periods of extreme heat, data-driven adaptation strategies, and the development of heat health surveillance systems.

Early life adversity accelerates epileptogenesis and enhances depression-like behaviors in rats.

OBJECTIVE: Early life stressors are well-established risk factors for psychiatric disorders, and evidence also suggests that these promote vulnerability to epilepsy. Given the high prevalence of psychiatric disorders in epilepsy, early life stress may represent a common driver for these comorbidities. We used animal modelling to investigate the effects of early life stress on epileptogenesis and depressive behaviors, also exploring HPA axis programming as a potential associative mechanism. METHODS: From post-natal day 2-9, Wistar rat dams (n = 3) and their offspring were exposed to the Limited Bedding and Nesting (LBN) model of early life adversity. Control dams (n = 3) were undisturbed. Maternal care was video-recorded, and behavior scored. As adults, rats (n = 7/group) underwent kainic acid-induced status epilepticus (SE), to trigger epilepsy development. Spontaneous seizures, depression-like behavior and HPA axis function were quantified. RESULTS: LBN significantly altered aspects of maternal care, including markedly reducing the consistency of care (p < 0.05), compared to control conditions. Following SE, LBN rats exhibited significantly accelerated epileptogenesis (p = 0.01) and greater disease severity (p = 0.001), compared to control rats. Anhedonia and behavioral despair were observed in epileptic rats exposed to LBN. LBN rats showed significantly dampened HPA axis responsivity, but epileptic rats showed greater corticosterone responses to CRH administration (all p < 0.05). SIGNIFICANCE: Early life adversity promotes a vulnerability to experimental epileptogenesis. These two 'hits' (early life stress and epilepsy) interact to create a depressive-like phenotype, but effects on HPA axis are complex and contrasting. This has implications for the mechanisms underpinning the increased prevalence of psychiatric disorders observed in people with epilepsy.