Over the past 3 decades, scientific discoveries in epidemiology, neuroscience, epigenetics, and network and systems theory have created a new paradigm for understanding the origins and dynamics of social and health problems. The big question is how to translate that knowledge into effective and—also cost-effective and sustainable—solutions that can improve not just the health and well-being of individuals, but of communities as a whole. The landmark Adverse Childhood Experiences (ACEs) study established that accumulation of adversity during child development, including abuse, neglect, and household dysfunction, is the most powerful determinant of the public's health.1Anda R.F. Felitti V.J. Walker J. et al.The enduring effects of abuse and related adverse experiences in childhood: a convergence of evidence from neurobiology and epidemiology.Eur Arch Psychiatry Clin Neurosci. 2006; 256: 174-186Crossref PubMed Scopus (2645) Google Scholar We have also learned about the power of networks to carry information, connect like-minded people, and provide a flexible yet sustainable infrastructure for social movements. In this same time period we have experienced a fast-paced journey that transitioned from knowledge acquisition and management by experts, to distributed knowledge that is managed and shared by the population as a whole. Knowledge is changing so fast that detailed plans and programs can become obsolete before they can be implemented. In this new paradigm, it is becoming increasingly clear that direct-service interventions are necessary but not sufficient to produce transformative health improvements, generate population-based change, or catalyze the social movement necessary to address the scope of the problems generated by ACEs. Direct services reach only a small portion of the people affected, and the cost of direct services prohibits their use as a primary strategy for preventing ACEs, their intergenerational transmission, and the wide and complex array of serious health and social problems they cause. Addressing all of these challenges together is a tall order. The answer lies in helping communities develop the capacity to reshape their own culture, from one that perpetuates cycles of trauma to one that reduces the array of ACE-related problems simultaneously and promotes health. We call this approach the Self-Healing Communities Model (Fig).2Porter L, Martin K, Anda R. Self-healing communities, a transformational process model for improving intergenerational health. Robert Wood Johnson Foundation. Available at: http://www.rwjf.org/content/dam/farm/reports/reports/2016/rwjf430225. Accessed July 18, 2017.Google Scholar Culture comprises the abstract, learned, and shared rules/standards/patterns used to interpret experience and shape behavior.3Martin K. Naylor L. Diversity Orientations: Culture, Ethnicity and Race. Cultural Diversity in the United States. Bergin & Garvey, Westport, CT1997Google Scholar We are not consciously aware of most of our culture. Instead, culture becomes our autopilot. However, we have the ability to consciously take control of our perceptions, thoughts, and behaviors and generate a culture that promotes healing and health. To improve generational health and equity, we need to empower communities to recognize their own ability to make change, engender hope that what they do will make a difference, and challenge unexamined patterns that prevent realization of the community's aspirations. The processes communities use to improve hope and efficacy, examine patterns, and make cultural changes are community capacity-building processes. Community capacity refers to the ability of a geographically based group of people to come together, build authentic relationships and reflect honestly about things that matter, share democratic leadership, and take collective actions that assure social and health equity for all residents.4Morgan G.B. Building Community Capacity: A Qualitative Study. Seattle University, Seattle, Wash2015Google Scholar Increasing community capacity connects people so they can provide support and assistance for each other and generate solutions for locally prioritized issues.5Sandel M. Faugno E. Mingo A. et al.Neighborhood-level interventions to improve childhood opportunity and lift children out of poverty.Acad Pediatr. 2016; 16: S128-S135Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar Better adapted, more resilient communities with high community capacity have extensive, community-wide networks of relationships through which reciprocity can flow and foster the kind of collaboration that is needed to influence whole systems. In the early 1990s, Washington State passed legislation to create a statewide Family Policy Council, with the goal of addressing several social problems together: family violence, child abuse, youth violence, school dropouts, teen pregnancy, youth suicide, youth substance abuse, and child out-of-home placements. Because the Council had a limited budget and a statewide mandate, it was clear from outset that a direct-service approach would not be feasible. Instead, the Council opted to focus on capacity-building. The Council's approach evolved over time into an effective and replicable process for driving and measuring change: the Self-Healing Communities Model. From 1994 to 2012, the Council implemented the Self-Healing Communities Model in 42 communities. It assessed local community capacity using a specially designed index and controlled for other socioeconomic factors that might otherwise explain changes over time. Communities using the model for ≥8 years dramatically reduced the rates of 1 or more of 7 major social problems.6Hall J. Porter L. Longhi D. et al.Reducing adverse childhood experiences (ACE) by building community capacity: a summary of Washington Family Policy Council Research Findings.J Prev Interv Community. 2012; 40: 325-334Crossref PubMed Scopus (35) Google Scholar For example:•Births to teen mothers decreased nearly two-thirds.•Infant mortality decreased 43%.•Youth suicide and suicide attempts decreased 95%.•Youth arrests for violent crime were cut in half.•High school dropout rates were cut in half. The economic return on investment was as impressive as the social and health outcomes. The cost of implementing the Self-Healing Communities Model in Washington State averaged $3.4 million per year. Meanwhile, the avoided caseload costs in child welfare, juvenile justice, and public medical costs associated with births to teen mothers alone saved over $601 million, an average of $120 million per year.7Scheuler V. Goldstine-Cole K. Longhi D. Projected Cost Savings Due to Caseloads Avoided: Technical Notes. Washington State Family Policy Council, Wash2009Google Scholar The data from Washington State tell us what matters most when it comes to culture change and community capacity-building. Is the community inviting everyone to contribute to leadership, cultivating new leaders who think about the system as a whole even while they work within their own sector? Are those leaders working together in reciprocal ways to address problems? Do community members come together to generate a shared understanding of the dynamic factors that generate status quo outcomes? Is the community focused on a strategic body of work rather than single projects? Are they using a strategic framework, like ACEs, to get at root causes of an array of problems? Do they emphasize learning as a value? Do they bring in outside experts and question their own assumptions? Do they invest in iterative cycles of action and reflection that support changes to the way they work and the work they do? Is the community engaged in monitoring a wide enough set of indicators to see progress and unintended consequences clearly? Are positive results—small and large—used to nurture the community's sense of progress and accomplishment on what is inevitably a long journey? The health and social problems we are facing in many communities are highly complex. They are inter-related and intergenerational. If we have any chance of turning things around, we need right-fit solutions that address the complexity of problems and inspire emergent change in different community environments at a modest cost. Building the community capacity to create a culture of health for neighborhoods and families offers us the best hope for doing that in our time. Financial disclosure: Publication of this article was supported by the Promoting Early and Lifelong Health: From the Challenge of Adverse Childhood Experiences (ACEs) to the Promise of Resilience and Achieving Child Wellbeing project, a partnership between the Child and Adolescent Health Measurement Initiative (CAHMI) and Academy-Health, with support from the Robert Wood Johnson Foundation (#72512).

Medical research on adverse childhood experiences (ACEs) reveals a compelling relationship between the extent of childhood adversity, adult health risk behaviors, and principal causes of death in the United States. This article provides a selective review of the ACE Study and related social science research to describe how effective social work practice that prevents ACEs and mobilizes resilience and recovery from childhood adversity could support the achievement of national health policy goals. This article applies a biopsychosocial perspective, with an emphasis on mind-body coping processes to demonstrate that social work responses to adverse childhood experiences may contribute to improvement in overall health. Consistent with this framework, the article sets forth prevention and intervention response strategies with individuals, families, communities, and the larger society. Economic research on human capital development is reviewed that suggests significant cost savings may result from effective implementation of these strategies.

Medical research on “adverse childhood experiences” (ACEs) reveals a compelling relationship between the extent of childhood adversity, adult health risk behaviors, and principal causes of death in the United States. This article provides a selective review of the ACE Study and related social science research to describe how effective social work practice that prevents ACEs and mobilizes resilience and recovery from childhood adversity could support the achievement of national health policy goals. This article applies a biopsychosocial perspective, with an emphasis on mind–body coping processes to demonstrate that social work responses to adverse childhood experiences may contribute to improvement in overall health. Consistent with this framework, the article sets forth prevention and intervention response strategies with individuals, families, communities, and the larger society. Economic research on human capital development is reviewed that suggests significant cost savings may result from effective implementation of these strategies. Keywords: Health policypreventioninterventionfamily supportcommunity developmentmind–bodyintegrally informed

Betrayal trauma theory (Freyd, 1996) postulates childhood abuse perpetrated by a caregiver or someone close to the victim results in worse mental health than abuse perpetrated by a noncaregiver. Using the Adverse Childhood Experiences (ACE) data, we tested whether adults with high betrayal (HB) abuse would report poorer functional and mental health than low betrayal (LB) abuse victims. Among those participants reporting childhood sexual abuse, 32% experienced HB abuse. HB victims had a higher average ACE score than LB victims (2.72 vs. 1.87, p < .001), had significantly lower functional health scores on 4 of the 7 SF-36 Health Survey scales (all p < .04), and reported higher depression, anxiety, suicidality, panic, and anger (all p < .05).

This introduction to the themed issue overviews the Adverse Childhood Experiences (ACE) Study and discusses prevention and intervention with ACE and their consequences in communities. A commentary by Dr. Robert Anda, an ACE Study Co-Principal Investigator, is incorporated within this introduction. Implications of articles within the issue are addressed, and next steps are explored.

Objective. Our objective was to examine the associations between adverse childhood experiences (ACEs) and smoking behavior among a random sample of adults living in five U.S. states.Methods. We used data from 25,809 participants of the 2009 Behavioral Risk Factor Surveillance System to assess the relationship of each of the 8 adverse childhood experiences and the adverse childhood experience score to smoking status.Results and conclusions. Some 59.4% of men and women reported at least one adverse childhood experience. Each of the eight adverse childhood experiences measures was significantly associated with smoking status after adjustment for demographic variables. The prevalence ratios for current and ever smoking increased in a positive graded fashion as the adverse childhood experience score increased. Among adults who reported no adverse childhood experiences, 13.0% were currently smoking and 38.3% had ever smoked. Compared to participants with an adverse childhood experience score of 0, those with an adverse childhood experience score of 5 or more were more likely to be a current smoker (adjusted prevalence ratio (aPR): 2.22, 95% confidence interval [CI]: 1.92-2.57) and to have ever smoked (aPR: 1.80, 95% CI: 1.67-1.93). Further research is warranted to determine whether the prevention of and interventions for adverse childhood experiences might reduce the burden of smoking-related illness in the general population. Published by Elsevier Inc.

Background: Sleep disturbances are associated with an increased risk for many chronic diseases and unhealthy behaviors. A history of adverse childhood experiences (ACEs) is also associated with similar adult health outcomes. We studied the relationship between multiple ACEs and the likelihood of experiencing self-reported sleep disturbances in adulthood.Methods: We used data from the adverse childhood experiences (ACE) study, a retrospective cohort study of 17,337 adult health maintenance organization members in California who completed a survey about eight ACEs, which included childhood abuse and growing up with various forms of household dysfunction. The self-reported sleep disturbances measured included ever having trouble falling or staying asleep and feeling tired after a good night's sleep. We used an integer count of the number of ACEs (the ACE score) to assess the cumulative impact of these experiences on the likelihood of self-reported sleep disturbances.Results: Thirty-three percent of the cohort reported trouble falling or staying asleep, while 24% reported feeling tired after sleeping. All eight ACE categories were associated with an increased likelihood of self-reported sleep disturbances (p < 0.05). Compared to persons with an ACE score of 0, those with an ACE score >= 5 were 2.1 (95% Cl: 1.8-2.4) times more likely to report trouble falling or staying asleep and 2.0 (95% Cl: 1.7-2.3) times more likely to report feeling tired even after a good night's sleep. The trend for increasing odds for both types of self-reported sleep disturbance with increasing ACE scores was statistically significant (p < 0.0001).Conclusions: Adverse childhood experiences were associated with self-reported sleep disturbances in adulthood, and the ACE score had a graded relationship to these sleep disturbances. A history of ACEs should be obtained for patients with self-reported sleep disturbances to coordinate services that ameliorate the long-term effects of these events. Published by Elsevier B.V.

The Adverse Childhood Experiences (ACE) Study, a collaborative effort between Kaiser Permanente (San Diego, CA) and the Centers for Disease Control and Prevention (Atlanta, GA), was designed to examine the long-term relationship between adverse childhood experiences (ACEs) and a variety of health behaviors and outcomes in adulthood [1]. ACEs include childhood emotional, physical, or sexual abuse and household dysfunction during childhood. The ACE Study, based on chronic disease prevention and control models, proposes that ACEs influence social, emotional, and cognitive impairments which in turn increase the probability of adopting health risk behaviors that have been documented to influence the subsequent development of disease, disability, social problems, and ultimately premature death. We use the ACE pyramid to depict this concept (see www.cdc.gov/nccdphp/ace/pyramid.htm).

BACKGROUND:Few reports have addressed associations between family strengths during childhood and adolescent pregnancy and its consequences. We examined relationships among a number of childhood family strengths and adolescent pregnancy, risk behavior, and psychosocial consequences after adolescent pregnancy.METHODS:Our retrospective cohort of 4648 women older than 18 years (mean age, 56 years) received primary care in San Diego, CA. Outcomes included adolescent pregnancy and psychosocial consequences compared with number of the following childhood family strengths: family closeness, support, loyalty, protection, love, importance, and responsiveness to health needs.RESULTS:Of the cohort, 3082 participants (66%) reported 6 or 7 categories of childhood family strengths. Teen pregnancy occurred in 39%, 33%, 30%, 25%, 24%, 21%, and 19% of those with 0 or 1, 2, 3, 4, 5, 6, and 7 childhood family strengths, respectively (p for trend < 0.00001). When childhood abuse and household dysfunction were present, adjusted odds ratios (ORs) for adolescent pregnancy demonstrated an increasingly protective effect as numbers of childhood family strengths increased from 0 or 1 to 2 or 3, 4 or 5, and 6 or 7 (1.0 to 0.80), (1.0 to 0.80, 0.60, and 0.54, respectively). These findings were partly explained by progressive delays in initiation of sexual activity as the number of childhood family strengths increased. Adjusted ORs for psychosocial problem occurring decades later decreased as the number of childhood family strengths increased from 0 or 1 to 2 or 3, 4 or 5, and 6 or 7 (job problems, 1.0, 0.8, 0.6, 0.4; family problems, 1.0, 1.1, 0.7, 0.6; financial problems, 1.0, 0.9, 0.9, 0.6; high stress, 1.0, 1.1, 0.9, 0.8; uncontrollable anger, 1.0, 0.7, 0.7, 0.4).CONCLUSIONS:Childhood family strengths are strongly protective against adolescent pregnancy, early initiation of sexual activity, and long-term psychosocial consequences.

1. The result section needs more numbers in order to be self-explanatory to the reader. Please remove some of the last sentences and provide some extra numbers. RESPONSE: We thank the reviewer for the comment. While we disagree that the results section of the abstract is not self-explanatory, we are glad to work with the Editor to re-work this section. We have included the primary results of the analysis; namely, the presence of a graded relationship to the incidence of lung cancer based on hospital discharge records and mortality records, risk ratios comparing the risk of lung cancer for those with 6 or more ACEs to those without ACEs, a note on the early age at presentation for persons with 6 or more ACEs, and a note on the attributable risk percent. 2. Based on the small number of lung cancer cases and the findings of the study, your conclusion is too strong. There might be an association. RESPONSE: The conclusion has been toned down.

BACKGROUND: Intestinal fibrosis is a common and potentially serious complication of inflammatory bowel disease (IBD).In addition to mesenchymal cells, endothelial cells can contribute to fibrosis through the recently described process of EndoMT.We investigated whether i) human intestinal microvascular endothelial cells (HIMEC) can undergo EndoMT and contribute to fibrosis in IBD, and ii) epigenetic changes are involved in mediation of EndoMT.MATERIALS AND METHODS: HIMEC exposed to TGF-β1, IL-1β and TNF-α or supernatants of lamina propria mononuclear cells (LPMC) were evaluated for morphological, phenotypic and functional changes compatible with EndoMT.Microarray genomic analysis was used to identify transcription factors controlling the transformation process.Evidence of in situ and In Vivo EndoMT was sought in human and experimental IBD tissues.Chromatin immunoprecipitation (ChIP) assays were performed to identify specific histone modification changes on the promoters of von Willebrand factor (vWF) and collagen1 alpha2 (Col1α2) genes (markers of endothelial cells and fibroblasts, respectively) during EndoMT.RESULTS: The combination of TGF-β1, IL-1β and TNF-α induced morphologic and phenotypic changes in HIMEC consistent with EndoMT, and these were reproduced using supernatants of activated LPMC.Transformed HIMEC exhibited loss of acetylated LDL-uptake, enhanced extracellular matrix secretion, and acquisition of de novo collagen synthesis capacity.These functional alterations persisted at 10 days after removal of the inducing agents, and then still were associated with an approximate 8-fold upregulation of Col1α2 gene expression and 1.6-fold downregulation of vWF gene expression.EndoMT was detected in inflamed microvessels of human IBD mucosa and TNBS-induced colonic fibrosis of Tie2-GFP reporter mice.Genomic analysis uncovered Sp1 as the dominant transcriptional regulator of EndoMT.Finally, ChIP analysis revealed increased methylation of lysines 9 and 27 in histone H3 associated with repression of vWF gene expression, while increased acetylation of histone H4 accompanied activation of Col1α2 gene expression.CONCLUSIONS: Inflammatory stimuli induce trans-differentiation of mucosal microvascular cells into mesenchymal cells In Vitro and In Vivo, supporting the notion that the microvasculature undergoes EndoMT in IBD and contributes to fibrogenesis.These events involve epigenetic changes such as histone modifications crucial to regulation of EndoMT, and define unique pro-fibrotic epigenotypes that could become targets of selective anti-fibrotic therapies in IBD.

In May 2009, the WHO and the National Center for Chronic Disease Prevention and Health Promotion (CDC, Atlanta GA) met in Geneva, Switzerland, to begin a collaborative effort to build a framework for public health surveillance that can be used to define the global health burden of adverse childhood experiences (ACEs). In addition to WHO and CDC staff, meeting participants included people working in the fields of public health and early child development from Canada, China, the former Yugoslav Republic of Macedonia, Philippines, Saudi Arabia, South Africa, Switzerland, and Thailand.

BACKGROUND: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. PURPOSE:This study aims to determine whether ACEs are associated with an increased risk of premature death during adulthood. METHODS: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. RESULTS: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. CONCLUSIONS: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.

Objective: To examine whether childhood traumatic stress increased the risk of developing autoimmune diseases as an adult. Methods: Retrospective cohort study of 15,357 adult health maintenance organization members enrolled in the Adverse Childhood Experiences (ACEs) Study from 1995 to 1997 in San Diego, California, and eligible for follow-up through 2005. ACEs included childhood physical, emotional, or sexual abuse; witnessing domestic violence; growing up with household substance abuse, mental illness, parental divorce, and/or an incarcerated household member. The total number of ACEs (ACE Score range = 0-8) was used as a measure of cumulative childhood stress. The outcome was hospitalizations for any of 21 selected autoimmune diseases and 4 immunopathology groupings: T- helper 1 (Th1) (e.g., idiopathic myocarditis); T-helper 2 (Th2) (e.g., myasthenia gravis); Th2 rheumatic (e.g., rheumatoid arthritis); and mixed Th1/Th2 (e.g., autoimmune hemolytic anemia). Results: Sixty-four percent reported at least one ACE. The event rate (per 10,000 person-years) for a first hospitalization with any autoimmune disease was 31.4 in women and 34.4 in men. First hospitalizations for any autoimmune disease increased with increasing number of ACEs (p < .05). Compared with persons with no ACEs, persons with ≥2 ACEs were at a 70% increased risk for hospitalizations with Th1, 80% increased risk for Th2, and 100% increased risk for rheumatic diseases (p < .05). Conclusions: Childhood traumatic stress increased the likelihood of hospitalization with a diagnosed autoimmune disease decades into adulthood. These findings are consistent with recent biological studies on the impact of early life stress on subsequent inflammatory responses. ACE = adverse childhood experience; AD = autoimmune disease; Th1 = T-helper 1; Th2 = T-helper 2; CRP = C-reactive protein; CRH = corticoid releasing hormone.

To assess the association between adverse childhood experiences (ACEs), including childhood abuse and neglect, and serious household dysfunction, and premature death of a family member. Because ACEs increase the risk for many of the leading causes of death in adults and tend to be familial and intergenerational, we hypothesized that persons who report having more ACEs would be more likely to have family members at risk of premature death.