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Does time heal all wounds? Life course associations between child welfare involvement and mortality in prospective cohorts from Sweden and Britain.

ABSTRACT: Child welfare involvement reflects childhood adversity and is associated with increased adult mortality, but it remains unclear how this association changes over the life course. Drawing on the Stockholm Birth Cohort Multigenerational Study (Sweden) and the National Childhood Development Study (Great Britain) this study examines whether inequalities within these cohorts diverge or converge. Involvement with child welfare services (ICWS) is divided into two levels ('child welfare contact' and 'out-of-home care'). For each cohort, we quantify absolute health inequalities as differences in cumulative probabilities of death (18-58 years) and temporary life expectancy; and relative inequalities as hazard ratios in ten-year intervals and ratios of lifetime lost. Persistently, ICWS was associated with premature mortality. The strength of the association varied by age, sex and level of ICWS. Consistently across both countries, the most robust relationship was between out-of-home care and mortality, with statistically significant age-specific hazard ratios ranging between 1.8 and 3.4 for males and 1.8-2.1 for females. Child welfare contact that did not result in out-of-home placement showed less consistent results. Among females the mortality gap developed later compared to males. Estimates attenuate after controlling for family socioeconomic and other background variables but patterns remain intact. Our results show that absolute inequalities widen with increasing age, while relative inequalities might peak in early adulthood and then stabilize in midlife. The relative disadvantage among looked-after children in early adulthood is heightened by overall low rates of mortality at this age. Absolute inequality increases with age, highlighting the weight of the accumulation of disadvantage in mortality over time. The bulk of excess deaths that could be attributed to ICWS occurs from midlife onwards. Mechanisms that uphold the disadvantage after childhood experiences require further exploration. This study highlights that the association between out-of-home care and premature mortality seems to transcend welfare systems.

SUBMITTER: Jackisch J

PROVIDER: S-EPMC8010861 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND:Thalamic dysfunction has been implicated in overall chronic neurological dysfunction after traumatic brain injury (TBI), however little is known about the underlying histopathology. In experimental diffuse TBI (dTBI), we hypothesize that persisting histopathological changes in the ventral posteromedial (VPM) nucleus of the thalamus is indicative of progressive circuit reorganization. Since circuit reorganization in the VPM impacts the whisker sensory system, the histopathology could explain the development of hypersensitivity to whisker stimulation by 28days post-injury; similar to light and sound hypersensitivity in human TBI survivors. METHODS:Adult, male Sprague-Dawley rats underwent craniotomy and midline fluid percussion injury (FPI) (moderate severity; 1.8-2.0atm) or sham surgery. At 1d, 7d, and 28days post-FPI (d FPI) separate experiments confirmed the cytoarchitecture (Giemsa stain) and evaluated neuropathology (silver stain), activated astrocytes (GFAP), neuron morphology (Golgi stain) and microglial morphology (Iba-1) in the VPM. RESULTS:Cytoarchitecture was unchanged throughout the time course, similar to previously published data; however, neuropathology and astrocyte activation were significantly increased at 7d and 28d and activated microglia were present at all time points. Neuron morphology was dynamic over the time course with decreased dendritic complexity (fewer branch points; decreased length of processes) at 7d FPI and return to sham values by 28d FPI. CONCLUSIONS:These data indicate that dTBI results in persisting thalamic histopathology out to a chronic time point. While these changes can be indicative of either adaptive (recovery) or maladaptive (neurological dysfunction) circuit reorganization, they also provide a potential mechanism by which maladaptive circuit reorganization could contribute to the development of chronic neurological dysfunction. Understanding the processes that mediate circuit reorganization is critical to the development of future therapies for TBI patients.

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Does time heal all wounds? Life course associations between child welfare involvement and mortality in prospective cohorts from Sweden and Britain.

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