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Lactation is a critical time in mammalian development, where maternal factors shape offspring outcomes. In this scoping review, we discuss current literature concerning maternal factors that influence lactation biology and highlight important associations between changes in milk composition and offspring outcomes. Specifically, we explore maternal nutritional, psychosocial, and environmental exposures that influence non-nutritive bioactive components in milk and their links to offspring growth, development, metabolic, and behavioral outcomes. A comprehensive literature search was conducted using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Extension for Scoping Reviews (PRISMA-ScR) guidelines. Predetermined eligibility criteria were used to analyze 3,275 papers, and the final review included 40 primary research articles. Outcomes of this review identify maternal obesity to be a leading maternal factor influencing the non-nutritive bioactive composition of milk with notable links to offspring outcomes. Offspring growth and development are the most common modes of programming associated with changes in non-nutritive milk composition due to maternal factors in early life. In addition to discussing studies investigating these key associations, we also identify knowledge gaps in the current literature and suggest opportunities and considerations for future studies.
Obesity rates among children are rapidly rising internationally and have been linked to noncommunicable diseases in adulthood. Individual preventive strategies have not effectively reduced global obesity rates, leading to a gap in clinical services regarding the development of early perinatal interventions. The objective of this scoping review is to explore the relationship between maternal BMI and breastfeeding behaviors on child growth trajectories to determine their relevance in developing interventions aimed at preventing childhood obesity.
The scoping review was guided and informed by the Arksey and O’Malley (2005) framework. A systematic search was performed in four databases. Studies included in the final review were collated and sorted into relevant themes. A systematic search yielded a total of 5831 records (MEDLINE: 1242, EMBASE: 2629, CINAHL: 820, PubMed: 1140). Results without duplicates (n = 4190) were screened based on relevancy of which 197 relevant-full-text articles were retrieved and assessed for eligibility resulting in 14 studies meeting the inclusion criteria. Data were extracted and charted for the studies and six themes were identified: (1) healthy behaviors, lifestyle, and social economic status; (2) parental anthropometrics and perinatal weight status; (3) genetics, epigenetics, and fetal programming; (4) early infant feeding; (5) infant growth trajectories; and (6) targeted prevention and interventions. Early life risk factors for child obesity are multifactorial and potentially modifiable. Several at-risk groups were identified who would benefit from early preventative interventions targeting the importance of healthy weight gain, exclusive breastfeeding to 6 months, and healthy lifestyle behaviors.
Effects of stresses associated with extremely preterm birth may be biologically “recorded” in the genomes of individuals born preterm via changes in DNA methylation (DNAm) patterns. Genome-wide DNAm profiles were examined in buccal epithelial cells from 45 adults born at extremely low birth weight (ELBW; ≤1000 g) in the oldest known cohort of prospectively followed ELBW survivors (Mage = 32.35 years, 17 male), and 47 normal birth weight (NBW; ≥2500 g) control adults (Mage = 32.43 years, 20 male). Sex differences in DNAm profiles were found in both birth weight groups, but they were greatly enhanced in the ELBW group (77,895 loci) versus the NBW group (3,424 loci), suggesting synergistic effects of extreme prenatal adversity and sex on adult DNAm profiles. In men, DNAm profiles differed by birth weight group at 1,354 loci on 694 unique genes. Only two loci on two genes distinguished between ELBW and NBW women. Gene ontology (GO) and network analyses indicated that loci differentiating between ELBW and NBW men were abundant in genes within biological pathways related to neuronal development, synaptic transportation, metabolic regulation, and cellular regulation. Findings suggest increased sensitivity of males to long-term epigenetic effects of extremely preterm birth. Group differences are discussed in relation to particular gene functions.
This study examined the link between two biological markers of stress vulnerability at 22–26 years of age and telomere length at 30–35 among extremely low birth weight (ELBW; <1000 g) survivors and normal birth weight (NBW; >2500 g) control participants. Sixteen ELBW and 22 NBW participants provided baseline afternoon salivary cortisol samples and resting frontal electroencephalogram (EEG) alpha asymmetry data at 22–26 years. Buccal cells were assayed for telomere length at 30–35 years. Analyses controlled for sex, postnatal steroid exposure, childhood socioeconomic status, time of cortisol sample collection, and body mass index at 22–26 years. Salivary cortisol and frontal asymmetry at age 22–26 independently predicted telomere length at age 30–35, such that relatively higher cortisol and greater relative right frontal asymmetry at rest predicted telomere shortening among NBW controls, but not among ELBW survivors. However, similar associations were not noted in ELBW survivors, suggesting that ELBW survivors may have different mechanisms of stress coping as a result of their early-life exposures. These findings offer preliminary evidence in support of the role of stress in the genesis of cellular senescence at least among those born at NBW, but that these links may differ in those born preterm.
This article highlights the defining principles, progress, and future directions in epigenetics research in relation to this Special Issue. Exciting studies in the fields of neuroscience, psychology, and psychiatry have provided new insights into the epigenetic factors (e.g., DNA methylation) that are responsive to environmental input and serve as biological pathways in behavioral development. Here we highlight the experimental evidence, mainly from animal models, that factors such as psychosocial stress and environmental adversity can become encoded within epigenetic factors with functional consequences for brain plasticity and behavior. We also highlight evidence that epigenetic marking of genes in one generation can have consequences for future generations (i.e., inherited), and work with humans linking epigenetics, cognitive dysfunction, and psychiatric disorder. Though epigenetics has offered more of a beginning than an answer to the centuries-old nature–nurture debate, continued research is certain to yield substantial information regarding biological determinants of central nervous system changes and behavior with relevance for the study of developmental psychopathology.
Early life events both before and after birth have a long-lasting impact on physical and mental health trajectories later in life. Several lines of evidence point to the early origin of adult-onset diseases and psychiatric disorders. For example, nutritional restriction or maternal stress during pregnancy has been correlated with an increased risk of developing obesity, type 2 diabetes, and coronary heart disease (Ozanne & Constancia, 2007). Postnatally, adverse socioeconomic status during early childhood has been firmly linked to a susceptibility to the same conditions, as well as autoimmune disease, whereas childhood abuse is a major risk factor in the development of mood and anxiety disorders (Heim & Nemeroff, 2001; Kendler, Kuhn, & Prescott, 2004; see also Seraphin et al.; Nater & Heim, this volume). The critical question is, what are the mechanisms that mediate the effects of the early environment on our health and mental well-being, producing stable, long-lasting changes? It is now widely believed that epigenetics may constitute the mechanism that binds nurture and nature. “Epigenetics” is a polysemous term that in the present context refers to various mechanisms in the cell's nucleus that control genetic activity without altering the DNA sequence. The “epigenome” refers to the configuration of epigenetic modifiers of gene activation around the genome. Recent data suggest that epigenetic programming of gene expression profiles represented in the epigenome is sensitive to the early-life environment and that both the chemical and social environment early in life could affect the manner by which the genome is programmed by the epigenome.
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