Inflammation in adulthood might be due to the exposure to environmental conditions in childhood. Aging, cardiovascular disease, diabetes, autoimmune disease, dementia are diseases that are due to inflammation.
‘Nutritional, microbial and psychosocial exposures early in development predict DNA methylation (DNAm) in nine genes involved in the regulation of inflammation.’
Drawing on prior research that links environmental exposures to inflammatory biomarkers, the research broke new ground in helping to understand:
‘Using data from a large birth cohort study in the Philippines, with a lifetime of information on the study participants, researchers found that nutritional, microbial and psychosocial exposures early in development predict DNA methylation (DNAm) in nine genes involved in the regulation of inflammation.
The researchers focused on DNAm — an epigenetic process that involves durable biochemical marks on the genome that regulate gene expression — as a plausible biological mechanism for preserving cellular memories of early life experiences.
In other words, epigenetic mechanisms appear to explain — at least in part — how environments in infancy and childhood are “remembered” and have lasting effects on inflammation and risk for inflammation-related diseases.
“Taking this a step further, the findings encourage us to reconsider the common view that genes are a ‘blueprint’ for the human body — that they are static and fixed at conception,” said Thomas McDade, lead author of the study.
The research suggests that altering aspects of the nutritional, microbial and psychosocial environment early in development can leave lasting marks on the epigenome, with the potential to reduce levels of chronic inflammation in adulthood.
Environmental exposures that leave their mark on the epigenome and shape inflammation over the course of development, include aspects of nutrition in infancy (breastfeeding duration), the intensity of microbial exposure in infancy (exposure to animal feces, season of birth) and exposure to adversity (socioeconomic status in infancy/childhood, extended parental absence) all leave their mark on the epigenome.
“If we conceptualize the human genome as a dynamic substrate that embodies information from the environment to alter its structure and function, we can move beyond simplistic ‘nature vs. nurture’ and ‘DNA as destiny’ metaphors that don’t do justice to the complexity of human development,” said McDade, also a faculty fellow with Northwestern’s Institute for Policy Research.