The Potential for Teacher‐Student Relationships and the Whole School, Whole Community, Whole Child Model to Mitigate Adverse Childhood Experiences

During the past 20 years there has been a dramatic increase in societal interest in preventing disability and death in the United States by changing individual behaviors linked to the risk of contracting chronic diseases. This renewed interest in health promotion and disease prevention has not been without its critics. Some critics have accused proponents of life-style interventions of promoting a victim-blaming ideology by neglecting the importance of social influences on health and disease. This article proposes an ecological model for health promotion which focuses attention on both individual and social environmental factors as targets for health promotion interventions. It addresses the importance of interventions directed at changing interpersonal, organizational, community, and public policy, factors which support and maintain unhealthy behaviors. The model assumes that appropriate changes in the social environment will produce changes in individuals, and that the support of individuals in the population is essential for implementing environmental changes.

Strong, graded relationships between exposure to childhood traumatic stressors and numerous negative health behaviors and outcomes, healthcare utilization, and overall health status inspired the question of whether these adverse childhood experiences (ACEs) are associated with premature death during adulthood. This study aims to determine whether ACEs are associated with an increased risk of premature death during adulthood. Baseline survey data on health behaviors, health status, and exposure to ACEs were collected from 17,337 adults aged >18 years during 1995-1997. The ACEs included abuse (emotional, physical, sexual); witnessing domestic violence; parental separation or divorce; and growing up in a household where members were mentally ill, substance abusers, or sent to prison. The ACE score (an integer count of the eight categories of ACEs) was used as a measure of cumulative exposure to traumatic stress during childhood. Deaths were identified during follow-up assessments (between baseline appointment date and December 31, 2006) using mortality records obtained from a search of the National Death Index. Expected years of life lost (YLL) and years of potential life lost (YPLL) were computed using standard methods. The relative risk of death from all causes at age < or =65 years and at age < or =75 years was estimated across the number of categories of ACEs using multivariable-adjusted Cox proportional hazards regression. Analysis was conducted during January-February 2009. Overall, 1539 people died during follow-up; the crude death rate was 91.0 per 1000; the age-adjusted rate was 54.7 per 1000. People with six or more ACEs died nearly 20 years earlier on average than those without ACEs (60.6 years, 95% CI=56.2, 65.1, vs 79.1 years, 95% CI=78.4, 79.9). Average YLL per death was nearly three times greater among people with six or more ACEs (25.2 years) than those without ACEs (9.2 years). Roughly one third (n=526) of those who died during follow-up were aged < or =75 years at the time of death, accounting for 4792 YPLL. After multivariable adjustment, adults with six or more ACEs were 1.7 (95% CI=1.06, 2.83) times more likely to die when aged < or =75 years and 2.4 (95% CI=1.30, 4.39) times more likely to die when aged < or =65 years. ACEs are associated with an increased risk of premature death, although a graded increase in the risk of premature death was not observed across the number of categories of ACEs. The increase in risk was only partly explained by documented ACE-related health and social problems, suggesting other possible mechanisms by which ACEs may contribute to premature death.