Microbiome-mediated chemical communication in insects: Implications for pest management.

Experiences of early life adversity, including poverty [], abuse [], neglect [], and family dysfunction [], are associated with an increased risk of cardiometabolic diseases across the life course, contributing to a growing public health burden []. These experiences perpetuate health disparities, as children from racially and ethnically minoritized groups [] and lower socioeconomic backgrounds [] are disproportionately exposed to higher levels of adversity and experience worse long-term health outcomes. Despite this, the biological pathways linking early life adversity to later life cardiometabolic health are not fully understood. Chronic or repeated exposure to early life adversity requires constant adaptation by regulatory systems, leading to cumulative “wear and tear,” often referred to as allostatic load []. While these short-term responses may be adaptive, prolonged activation can disrupt hypothalamic–pituitary–adrenal (HPA) axis function and hormone regulation (e.g., cortisol, leptin, neuropeptide Y), alter brain development, and activate the sympathetic nervous system []. These processes, in turn, can impair arterial circulation, glucocorticoid metabolism, and insulin sensitivity, thereby contributing to adverse cardiometabolic profiles, including obesity, insulin resistance, and hypertension []. At the cellular level, sustained childhood trauma has been linked to accelerated leukocyte telomere shortening [], a hallmark of biological aging associated with earlier stroke, myocardial infarction, and type 2 diabetes [,]. In addition, childhood trauma has been associated with elevated C-reactive protein, a marker of systemic inflammation that predicts higher risk of coronary heart disease, ischemic stroke, and vascular mortality [,]. Together, this evidence suggests that early life adversity becomes biologically embedded through multisystem physiological dysregulation, with growing support that these effects are mediated at the molecular level by epigenetic modifications that regulate gene regulation []. One widely studied epigenetic modification is DNA methylation (DNAm), the addition of a methyl group (CH) to the fifth carbon atom of a cytosine base, primarily at cytosine-phosphate-guanine (CpG) dinucleotides []. This modification can impact transcription factor binding and gene expression without altering the underlying DNA sequence. The effects of DNAm on gene expression vary by genomic context (, promotor regions, gene bodies, other regulatory sites), with DNAm capable of both silencing or enhancing transcription depending on the region []. Due to this regulatory role, variation in DNAm has been implicated in biological pathways underlying a broad range of disease domains, including cardiometabolic health, through genes involved in inflammation, oxidative stress []. DNAm variation occurs both as part of normal development and aging, as well as in response to social and environmental stressors []. The fetal period has been extensively studied as a window for epigenetic programming, during which DNAm is completely erased and reestablished to enable cell differentiation []. Childhood, though comparatively understudied, represents another biologically dynamic window for epigenomic change, driven by rapid growth and developmental plasticity []. In human studies, a growing number of candidate gene and epigenome-wide association studies (EWAS) have examined whether early life adversity is linked to changes in DNAm []. Candidate gene studies of childhood maltreatment and stressful life events have primarily focused on genes involved in glucocorticoid signaling [], serotonin and oxytocin uptake [], and inflammatory processes [], with mixed findings. EWAS have identified associations between early life adversity and widespread variation in DNAm in children and adults [], though these studies have largely failed to identify commonly studied candidate genes. Key gaps remain, as most of these existing studies rely on retrospective, self-reported measures of early life adversity, single timepoint measurements of DNAm, and analyses limited to a single omics layer (, DNAm alone, without integration of transcriptomic, proteomic, or other omics data). Additionally, many EWAS examining psychosocial adversity have focused on adult samples, limiting insight into how DNAm patterns associated with adversity emerge and evolve earlier in development. To address these research gaps, we leveraged data from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a longitudinal cohort of low-income Latino families living in an agricultural community, to prospectively examine associations between multiple types of early life adversity and repeated measures of DNAm from childhood (age 7) through adolescence (ages 9, 14) and into young adulthood (age 18). We chose to focus on adversity exposure from pregnancy through mid-childhood (age 7), a biologically sensitive period marked by rapid neurodevelopment