This new compendium is your source for trustworthy recommendations on quality care of children and adolescents with mental health issues.https://shop.aap.org/mental-health-a-compendium-of-aap-clinical-practice-guidelines-and-policies-paperback/
Peer-reviewed article·Dr. Jack P. Shonkoff (OpenAlex works)·
Sensitive periods to social adversity in immune and metabolic development: A systematic review
Childhood exposure to social adversity - including experiences such as poverty, discrimination, violence, family separation, household dysfunction, and maltreatment - is associated with cardiometabolic health problems across the life course. A key question in the field is whether the timing of social adversity matters. To better understand the developmental origins of cardiometabolic disease and the emergence of health disparities, we conducted a systematic review of human observational studies to synthesize the evidence for sensitive periods to social adversity in immune and metabolic development. To be included in the study, some form of social adversity had to be independently reported at two or more non-overlapping time points during the prenatal period or childhood (<21 years old) and studies were required to include an outcome relevant to immune and/or metabolic biomarkers measured at some time after the social adversity exposure. Of the 2440 unique records screened, 25 met criteria for inclusion. Twenty studies investigated sensitive periods in immune development and six in metabolic development. For immune development, studies identified sensitive periods to social adversity inconsistently from the prenatal period through age 18. However, the proportion of studies confirming sensitive periods was highest at the youngest stages of development and gradually decreased across the life course. 50 % of studies found significant sensitive period effects in the prenatal period, while only 20 % found significant effects in late adolescence. For metabolic development, studies identified sensitive periods more consistently from birth through age 12. The proportion of studies reporting sensitive periods peaked at 50 % in infancy and decreased to zero after preadolescence. Overall, we found insufficient evidence to identify precise periods during which specific social adversity exposures have been consistently associated with altered immune and metabolic development. More birth cohorts with repeated measures of both social exposures and immune and metabolic biomarkers are needed, as are studies leveraging causal inference methods to more robustly account for time-varying confounding. However, these limitations notwithstanding, our review finds evidence that early experiences matter for immune and metabolic functioning. Improving the social and economic circumstances of young children may benefit lifelong cardiometabolic health.
Logan Nicole Beyer, Seetha H. Davis, Michelle M. J. Mens et al.
BACKGROUND: Although investigations have begun to differentiate biological and neurobiological responses to a variety of adversities, studies considering both endocrine and immune function in the same datasets are limited. METHODS: Associations between proximal (family functioning, caregiver depression, and anxiety) and distal (SES-D; socioeconomic disadvantage) early-life adversities with salivary inflammatory biomarkers (IL-1β, IL-6, IL-8, and TNF-α) and hair HPA markers (cortisol, cortisone, and dehydroepiandrosterone) were examined in two samples of young U.S. children (N = 142; N = 145). RESULTS: Children exposed to higher SES-D had higher levels of TNF-α (B = 0.13, p = 0.011), IL-1β (B = 0.10, p = 0.033), and DHEA (B = 0.16, p = 0.011). Higher family dysfunction was associated with higher cortisol (B = 0.08, p = 0.033) and cortisone (B = 0.05, p = 0.003). An interaction between SES-D and family dysfunction was observed for cortisol levels (p = 0.020) whereby children exposed to lower/average levels of SES-D exhibited a positive association between family dysfunction and cortisol levels, whereas children exposed to high levels of SES-D did not. These findings were partially replicated in the second sample. CONCLUSIONS: Our results indicate that these biological response systems may react differently to different forms of early-life adversity. IMPACT: Different forms of early-life adversity have varied stress signatures, and investigations of early-life adversities with inflammation and HPA markers are lacking. Children with higher socioeconomic disadvantage had higher TNF-α, IL-1β, and DHEA. Higher family dysfunction was associated with higher hair cortisol and cortisone levels, and the association between family dysfunction and cortisol was moderated by socioeconomic disadvantage. Biological response systems (immune and endocrine) were differentially associated with distinct forms of early-life adversities.
Euclides José de Mendonça Filho, Irina Pokhvisneva, Christina Maria Maalouf et al.
Advances in science are fundamentally changing the way we understand how inextricable interactions among genetic predispositions, physical and social environments, and developmental timing influence early childhood development and the foundations of health and how significant early adversity can lead to a lifetime of chronic health impairments. This article and companion article illustrate the extent to which differential outcomes are shaped by ongoing interactive adaptations to context that begin at or even before conception and continue throughout life, with increasing evidence pointing to the importance of the prenatal period and early infancy for the developing brain, the immune system, and metabolic regulation. Although new discoveries in the basic sciences are transforming tertiary medical care and producing breakthrough outcomes in treating disease, this knowledge is not being leveraged effectively to inform new approaches to promoting whole-child development and preventing illness. The opportunity for pediatrics to serve as the leading edge of science-based innovation across the early childhood ecosystem has never been more compelling. In this article, we present a framework for leveraging the frontiers of scientific discovery to inform new strategies in pediatric practice and advocacy to protect all developing biological systems from the disruptive effects of excessive early adversity beyond providing information on child development for parents and enriched learning experiences for young children.
Jack P. Shonkoff, William Thomas Boyce, Pat R. Levitt et al.
BACKGROUND: Although systemic inequities, broadly defined, are associated with health disparities in adults, there is a dearth of research linking contextual measures of exclusionary policies or prejudicial attitudes to health impairments in children, particularly among Latino populations. In this study, we examined a composite measure of systemic inequities in relation to the cooccurrence of multiple health problems in Latino children in the United States. METHODS: Participants included 17 855 Latino children aged 3 to 17 years from the National Survey of Children's Health (2016-2020). We measured state-level systemic inequities using a factor score that combined an index of exclusionary state policies toward immigrants and aggregated survey data on prejudicial attitudes toward immigrants and Latino individuals. Caregivers reported on 3 categories of child health problems: common health difficulties in the past year, current chronic physical health conditions, and current mental health conditions. For each category, we constructed a variable reflecting 0, 1, or 2 or more conditions. RESULTS: In models adjusted for sociodemographic covariates, interpersonal discrimination, and state-level income inequality, systemic inequities were associated with 1.13 times the odds of a chronic physical health condition (95% confidence interval: 1.02-1.25) and 1.24 times the odds of 2 or more mental health conditions (95% confidence interval: 1.06-1.45). CONCLUSIONS: Latino children residing in states with higher levels of systemic inequity are more likely to experience mental health or chronic physical health conditions relative to those in states with lower levels of systemic inequity.
Natalie B. Slopen, Adriana J. Umaña‐Taylor, Jack P. Shonkoff et al.
As the science of adversity and resilience advances, and public awareness of the health consequences of stress grows, primary care providers are being increasingly asked to address the effects of adverse experiences on child wellbeing. Given limited tools for assessing these effects early in life, the authors explore how enhanced capacity to measure stress activation directly in young children could transform the role and scope of pediatric practice. When employed within a trusted relationship between caregivers and clinicians, selective use of biological measures of stress responses would help address the documented limitations of rating scales of adverse childhood experiences as a primary indicator of individual risk and strengthen the ability to focus on variation in intervention needs, assess their effectiveness, and guide ongoing management. The authors provide an overview of the potential benefits and risks of such expanded measurement capacity, as well as an introduction to candidate indicators that might be employed in an office setting. The ultimate value of such measures for both pediatricians and parents will require vigilant attention to the ethical responsibilities of assuring their correct interpretation and minimizing the harm of inappropriate labeling, especially for children and families experiencing the hardships and threats of racism, poverty, and other structural inequities. Whereas much work remains to be done to advance measurement development and ensure its equitable use, the potential of validated markers of stress activation and resilience to strengthen the impact of primary health care on the lives of young children facing significant adversity demands increased attention.
Jack P. Shonkoff, William Thomas Boyce, Nicole R. Bush et al.
BACKGROUND AND OBJECTIVES: Research has linked neighborhood opportunity to health outcomes in children and adults; however, few studies have examined neighborhood opportunity and mortality risk among children and their caregivers. The objective of this study was to assess associations of neighborhood opportunity and mortality risk in children and their caregivers over 11 years. METHODS: Participants included 1 025 000 children drawn from the Mortality Disparities in American Communities study, a cohort developed by linking the 2008 American Community Survey to the National Death Index and followed for 11 years. Neighborhood opportunity was measured using the Child Opportunity Index, a measure designed to capture compounding inequities in access to opportunities for health. RESULTS: Using hazard models, we observed inverse associations between Child Opportunity Index quintile and deaths among child and caregivers. Children in very low opportunity neighborhoods at baseline had 1.30 times the risk of dying over follow-up relative to those in very high opportunity neighborhoods (95% confidence interval [CI], 1.15-1.45), and this excess risk attenuated after adjustment for household characteristics (hazard ratio, 1.15; 95% CI, 0.98-1.34). Similarly, children in very low opportunity neighborhoods had 1.57 times the risk of experiencing the death of a caregiver relative to those in very high opportunity neighborhoods (95% CI, 1.50-1.64), which remained after adjustment (hazard ratio, 1.30; 95% CI, 1.23-1.38). CONCLUSIONS: Our analyses advance understanding of the adverse consequences of inequitable neighborhood contexts for child well-being and underscore the potential importance of place-based policies for reducing disparities in child and caregiver mortality.
Natalie B. Slopen, Candace M. Cosgrove, Dolores Acevedo‐García et al.
Advances in science are fundamentally changing the way we understand how inextricable interactions among genetic predispositions, physical and social environments, and developmental timing influence early childhood development and the foundations of health and how significant early adversity can lead to a lifetime of chronic health impairments. This article and companion article illustrate the extent to which differential outcomes are shaped by ongoing interactive adaptations to context that begin at or even before conception and continue throughout life, with increasing evidence pointing to the importance of the prenatal period and early infancy for the developing brain, the immune system, and metabolic regulation. Although new discoveries in the basic sciences are transforming tertiary medical care and producing breakthrough outcomes in treating disease, this knowledge is not being leveraged effectively to inform new approaches to promoting whole-child development and preventing illness. The opportunity for pediatrics to serve as the leading edge of science-based innovation across the early childhood ecosystem has never been more compelling. In this article, we present a framework for leveraging the frontiers of scientific discovery to inform new strategies in pediatric practice and advocacy to protect all developing biological systems from the disruptive effects of excessive early adversity beyond providing information on child development for parents and enriched learning experiences for young children.
Jack P. Shonkoff, William Thomas Boyce, Pat R. Levitt et al.
Exposures to adverse environments, both psychosocial and physicochemical, are prevalent and consequential across a broad range of childhood populations. Such adversity, especially early in life, conveys measurable risk to learning and behavior and to the foundations of both mental and physical health. Using an interactive gene-environment-time (GET) framework, we survey the independent and interactive roles of genetic variation, environmental context, and developmental timing in light of advances in the biology of adversity and resilience, as well as new discoveries in biomedical research. Drawing on this rich evidence base, we identify 4 core concepts that provide a powerful catalyst for fresh thinking about primary health care for young children: (1) all biological systems are inextricably integrated, continuously "reading" and adapting to the environment and "talking back" to the brain and each other through highly regulated channels of cross-system communication; (2) adverse environmental exposures induce alterations in developmental trajectories that can lead to persistent disruptions of organ function and structure; (3) children vary in their sensitivity to context, and this variation is influenced by interactions among genetic factors, family and community environments, and developmental timing; and (4) critical or sensitive periods provide unmatched windows of opportunity for both positive and negative influences on multiple biological systems. These rapidly moving frontiers of investigation provide a powerful framework for new, science-informed thinking about health promotion and disease prevention in the early childhood period.
William Thomas Boyce, Pat R. Levitt, Fernando D. Martínez et al.
Inequalities in health outcomes impose substantial human and economic costs on all societies-and the relation between early adversity and lifelong well-being presents a rich scientific framework for fresh thinking about health promotion and disease prevention broadly, augmented by a deeper focus on how racism influences disparities more specifically. This review begins with an overview of advances in the biology of adversity and resilience through an early childhood lens, followed by an overview of the unique effects of racism on health and a selective review of findings from related intervention research. This article presents a framework for addressing multiple dimensions of the public health challenge-including institutional/structural racism, cultural racism, and interpersonal discrimination-and concludes with the compelling need to protect the developing brain and other biological systems from the physiological disruptions of toxic stress that can undermine the building blocks of optimal health and development in the early childhood period.
Jack P. Shonkoff, Natalie B. Slopen, David R. Williams