Perinatal Origins of Adult Disease and Opportunities for Health Promotion: A Narrative Review

Abstract

The “developmental origins of health and disease” (DOHaD) hypothesis refers to the influence of early developmental exposures and fetal growth on the risk of chronic diseases in later periods. During fetal and early postnatal life, cell differentiation and tissue formation are influenced by several factors. The interaction between genes and environment in prenatal and early postnatal periods appears to be critical for the onset of multiple diseases in adulthood. Important factors influencing this interaction include genetic predisposition, regulation of gene expression, and changes in microbiota. Premature birth and intrauterine growth restriction (IUGR) are other important factors considered by the DOHaD hypothesis. Preterm birth is associated with impaired or arrested structural or functional development of key organs/systems, making preterm infants vulnerable to cardiovascular, respiratory, and chronic renal diseases during adulthood. Growth restriction, defined as impaired fetal growth compared to expected biological potential in utero, is an additional negative factor increasing the risk of subsequent diseases. Environmental factors implicated in the developmental programming of diseases include exposure to pollution, stress, drugs, toxic agents, nutrition, and exercise. The DOHaD may explain numerous conditions, including cardiovascular, metabolic, respiratory, neuropsychiatric, and renal diseases. Potential antenatal and postnatal preventive measures, interventions, and future directions are discussed.

Environmental influences on child health outcomes: cohorts of individuals born very preterm

“…This priority aligns with the burgeoning field of the developmental origins of health, which hypothesizes that early-life exposures can program metabolic, immunologic, epigenetic, or physiologic responses that have persisting effects on health. 61 , 62 To facilitate mechanistic studies of the developmental origins of health, ECHO preterm cohorts have collected data on biomarkers of potential mechanisms linking early-life exposures and later-life outcomes, such as epigenetic markers in the placenta 52 , 53 , 63 and neonatal tissues, 12 biomarkers of neonatal inflammation, 64 , 65 and chemical exposures during neonatal intensive care in the first several postnatal months. 18 Like the “canary in the coal mine,” it seems likely that at least some of the findings from mechanistic studies will pertain not just to individuals born preterm but also to those born at term.…”

Folic acid supplementation in pregnant women with hepatitis B surface antigen improves infant hepatitis B surface antibody mediated by infant IL-4

“…None of the 195 neonates were born with any malformations. The mean age (range) of the infants at follow-up was 12 (11)(12)(13) 6.…”

“…Furthermore, the possible causes of this phenomenon remain largely unknown. Similar to the "developmental origins of health and disease" theory (12) , some scholars have noted that normal development of the foetal immunity as a potential advantageous intermediate outcome of adequate intrauterine folate might facilitate protective levels of immune response to vaccines after birth (13) . Previous work has shown that FAS is associated with an increase in levels of markers related to immunity, such as B lymphocyte response markers, innate immune proinflammatory pathways (14) , antigen processing and presentation markers, nuclear factor-k-gene binding signalling pathways, tumor necrosis factor signalling (15) , interleukin-8 (16) and interleukin-4 (IL-4) (17,18) .…”

Psychosocial adversity experienced in utero and early life is associated with variation in gut microbiota: a prospective case-control study

“…Health inequities experienced by socially disadvantaged populations is an increasing and urgent societal issue [1,2]. The psychosocial factors contributing to these disparities often begin early in life and include the prenatal environment which has profound effects on fetal and infant outcomes that can last a lifetime [3][4][5]. How social disadvatage (SD) and psychological stress (PS) becomes biologically embedded, and then leads to disparete health outcomes remains unclear.…”