背景:早期生活逆境与儿童时期许多不良健康结果有关;然而,促进敏感和响应性护理的二元干预措施可以保护儿童免受此类暴露的负面影响。迄今为止,准实验和随机对照试验(RCT)研究了二元干预对儿童个体生物标志物的影响,这可能会阐明早期压力暴露与前瞻性不良健康的综合诊断风险因素之间的关系。然而,干预的内容,分析策略,不同研究的发现差异很大,模糊了科学中的关键主题,阻碍了政策和研究工作。
方法:我们使用叙事方法来回顾来自方法上严格的(主要是RCT)研究的结果,该研究涉及二元干预对儿童不同生物标志物的影响,包括下丘脑-垂体-肾上腺(HPA)轴的指标,副交感神经(PNS)和交感神经系统(SNS),大脑发育,炎症,和细胞内DNA过程。我们通过整合生物系统中的发现并确定背景和机制因素来描述该领域的当前状态,为这一重要的研究领域做出了贡献。
结果:证据表明,二重干预可改善PNS功能和大脑成熟。一些研究表明干预措施降低了头发皮质醇浓度,全身性炎症,并导致DNA甲基化模式的差异。研究结果不支持HPA轴活动的唾液主要效应水平变化,SNS活动,或端粒长度。重要的是,综述的研究表明,在整个生物系统中的影响存在显著的异质性,强调上下文因素的重要性(例如,逆境子类型和严重性)作为影响的潜在调节剂。Further,研究结果表明,增强的育儿行为可能是二元干预对生物标志物起作用的一种机制。
结论:我们接近未来的政策和研究方向,强调生物知情的二元干预措施的承诺,以了解和改善早期逆境对健康诊断生物标志物的影响。
BACKGROUND: Early life adversity is related to numerous poor health outcomes in childhood; however, dyadic interventions that promote sensitive and responsive caregiving may protect children from the negative consequences of such exposures. To date, quasi-experimental and randomized controlled trials (RCTs) have examined the impact of dyadic interventions on a range of individual biomarkers in children, which may elucidate the relation between early stress exposure and transdiagnostic risk factors for prospective poor health. However, the content of interventions, analytic strategies, and findings vary widely across studies, obscuring key themes in the science and hindering policy and research efforts.
METHODS: We use a narrative approach to review findings from methodologically rigorous (predominantly RCT) studies of dyadic interventions\' impacts on different biomarkers in children, including indicators of the hypothalamic-pituitary-adrenal (HPA) axis, parasympathetic (PNS) and sympathetic nervous systems (SNS), brain development, inflammation, and intracellular DNA processes. We contribute to this important area of inquiry through integrating findings across biological systems and identifying contextual and mechanistic factors to depict the current state of the field.
RESULTS: Evidence suggests dyadic interventions improved PNS functioning and advanced brain maturation. Some studies indicated interventions reduced hair cortisol concentrations, systemic inflammation, and resulted in differences in DNA methylation patterns. Findings did not support main effect-level change in salivary measures of HPA axis activity, SNS activity, or telomere length. Importantly, reviewed studies indicated significant heterogeneity in effects across biological systems, underscoring the importance of contextual factors (e.g., adversity subtype and severity) as potential moderators of effects. Further, findings suggested enhanced parenting behaviors may be a mechanism through which dyadic interventions operate on biomarkers.
CONCLUSIONS: We close with future policy and research directions, emphasizing the promise of biologically-informed dyadic interventions for understanding and ameliorating the effects of early adversity on transdiagnostic biomarkers of health.