Can inflammation during the prenatal and neonatal stages affect health in adulthood?

The Developmental Origins of Health and Disease (DOHaD) hypothesis has illuminated the profound influence of early-life experiences on lifelong health. This review synthesizes key findings and connections in the context of the DOHaD hypothesis, highlighting the impact of prenatal and neonatal inflammation on adult wellbeing. Evidence points to the presence of microplastics and nanoplastics (NPs) in the human placenta, raising concerns about their effects on fetal development and immune responses. These synthetic particles may incite immune responses, potentially interfering with fetal defenses against pathogens. Moreover, NPs have been shown to damage mitochondria and increase oxidative stress, accentuating the far-reaching impacts of environmental factors on early development. Even at low concentrations, such as those found in the environment, NPs have been demonstrated to exert these effects. The gut microbiota emerges as a central player, influencing gastrointestinal health, neuropsychiatric conditions, and cognitive functions through the microbiota-gut-brain axis. Within this complex web of interactions, the gut microbiota’s composition has been associated with cognitive function and behavior modulation by influencing neurotransmitter metabolism. In the context of psychiatric disorders, there is notable evidence of heightened gut inflammation in individuals with conditions such as schizophrenia and first-episode psychosis, which potentially influences systemic cytokine levels and, in turn, impacts brain function. Maternal factors, including cholesterol levels and microRNAs (miRNAs) in breast milk, play pivotal roles in shaping an individual’s health trajectory. The evolution of breast milk is intrinsically tied to its capacity to provide not only essential nutrients but also a sophisticated array of substances, including miRNAs. These miRNAs, discovered in extracellular vesicles in human milk, play indispensable roles in regulating various biological processes in infants. They wield influence over lipid and glucose metabolism, gut development, neurogenesis, immunity, and even tissue-specific gene expression throughout life. Furthermore, there is a burgeoning interest in the potential impact of these miRNAs on viral infections in infants. Moreover, neurodevelopmental disorders are linked to microglial dysfunction, while mitochondrial dysfunction and oxidative stress underlie aging and disease. Microglia develop from erythro-myeloid progenitors in the early embryonic yolk sac and migrate into the brain, where they remain throughout an individual’s life. Microglia’s association with various neuropsychiatric disorders, including schizophrenia, Rett syndrome, bipolar disorder, and major depressive disorder, underscores their critical role in synaptic modulation, learning, and memory processes. Microglia function and morphology may be altered in these conditions, potentially leading to imbalances in synaptic plasticity mechanisms. Proper synaptic pruning, vital for maintaining the balance between excitatory and inhibitory synapses in the brain, is necessary for healthy neurodevelopment. Despite some limitations, this review underscores the importance of early-life experiences and environmental factors in determining lifelong health, offering insights into potential preventive strategies and interventions.