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      Youth Experiencing Parental Death Due to Drug Poisoning and Firearm Violence in the US, 1999-2020

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          Abstract

          Importance

          Youth (those aged <18 years) parental death has been associated with negative health outcomes. Understanding the burden of parental death due to drug poisoning (herein, drugs) and firearms is essential for informing interventions.

          Objective

          To estimate the incidence of youth parental death due to drugs, firearms, and all other causes.

          Design, Setting, and Participants

          This cross-sectional observational study was conducted using vital registration, including all US decedents, and census data from January 1990 through December 2020. Data were analyzed from May 30, 2023, to March 28, 2024.

          Exposures

          Parental death due to drug poisoning or firearms.

          Main Outcomes and Measures

          A demographic matrix projection model was used to estimate the number and incidence of youth experiencing parental death, defined as the death of 1 or more parents, per 1000 population aged less than 18 years. Analyses evaluated parental deaths by drugs, firearms, and all other causes from 1999 through 2020 by race and ethnicity.

          Results

          Between 1999 and 2020, there were 931 785 drug poisoning deaths and 736 779 firearm-related deaths with a mean (SD) age of 42.6 (16.3) years. Most deaths occurred among males (73.8%) and White decedents (70.8%) followed by Black (17.5%) and Hispanic (9.5%) decedents. An estimated 759 000 (95% CI, 722 000-800 000) youth experienced parental death due to drugs and an estimated 434 000 (95% CI, 409 000-460 000) youth experienced parental death due to firearms, accounting for 17% of all parental deaths. From 1999 to 2020, the estimated number of youth who experienced parental death increased 345% (95% CI, 334%-361%) due to drugs and 39% (95% CI, 37%-41%) due to firearms compared with 24% (95% CI, 23%-25%) due to all other causes. Black youth experienced a disproportionate burden of parental deaths, based primarily on firearm deaths among fathers. In 2020, drugs and firearms accounted for 23% of all parental deaths, double the proportion in 1999 (12%).

          Conclusions and Relevance

          Results of this modeling study suggest that US youth are at high and increasing risk of experiencing parental death by drugs or firearms. Efforts to stem this problem should prioritize averting drug overdoses and firearm violence, especially among structurally marginalized groups.

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          Most cited references17

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          Psychological stress in childhood and susceptibility to the chronic diseases of aging: moving toward a model of behavioral and biological mechanisms.

          Among people exposed to major psychological stressors in early life, there are elevated rates of morbidity and mortality from chronic diseases of aging. The most compelling data come from studies of children raised in poverty or maltreated by their parents, who show heightened vulnerability to vascular disease, autoimmune disorders, and premature mortality. These findings raise challenging theoretical questions. How does childhood stress get under the skin, at the molecular level, to affect risk for later diseases? And how does it incubate there, giving rise to diseases several decades later? Here we present a biological embedding model, which attempts to address these questions by synthesizing knowledge across several behavioral and biomedical literatures. This model maintains that childhood stress gets "programmed" into macrophages through epigenetic markings, posttranslational modifications, and tissue remodeling. As a consequence these cells are endowed with proinflammatory tendencies, manifest in exaggerated cytokine responses to challenge and decreased sensitivity to inhibitory hormonal signals. The model goes on to propose that over the life course, these proinflammatory tendencies are exacerbated by behavioral proclivities and hormonal dysregulation, themselves the products of exposure to early stress. Behaviorally, the model posits that childhood stress gives rise to excessive threat vigilance, mistrust of others, poor social relationships, impaired self-regulation, and unhealthy lifestyle choices. Hormonally, early stress confers altered patterns of endocrine and autonomic discharge. This milieu amplifies the proinflammatory environment already instantiated by macrophages. Acting in concert with other exposures and genetic liabilities, the resulting inflammation drives forward pathogenic mechanisms that ultimately foster chronic disease.
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            Tracking the reach of COVID-19 kin loss with a bereavement multiplier applied to the United States

            Significance COVID-19 has created a mortality shock throughout the world, and it may yield a second wave of population health concerns tied to bereavement and social support reductions. We created the COVID-19 bereavement multiplier, an indicator that clarifies one downstream impact of COVID-19 mortality and can be applied to different epidemiological projections of death counts: How many people are at risk for losing a grandparent, parent, sibling, spouse, or child for each COVID-19 death. In the United States, we estimate that on average, under diverse epidemiological circumstances, every death from COVID-19 will leave approximately nine bereaved. Studying how acute mortality crises reverberate through a population in the form of bereavement multipliers expands understandings of the social impacts of health crises.
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              Current Causes of Death in Children and Adolescents in the United States

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                Author and article information

                Journal
                JAMA
                JAMA
                American Medical Association (AMA)
                0098-7484
                May 04 2024
                Affiliations
                [1 ]Statistical Sciences, University of Toronto, Toronto, Ontario, Canada
                [2 ]Kinship Inequalities Research Group, Max Planck Institute for Demographic Research, Rostock, Mecklenburg-Vorpommern, Germany
                [3 ]Editor in Chief, JAMA and the JAMA Network, Chicago, Illinois
                [4 ]Epidemiology and Biostatistics, University of California, San Francisco
                [5 ]Sociology, University of Toronto, Toronto, Ontario, Canada
                [6 ]Epidemiology and Population Health, Stanford University, Stanford, California
                Article
                10.1001/jama.2024.8391
                c6d63c02-7163-401e-ac6b-f2ecce764f51
                © 2024
                History

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