The impact of early childhood experiences and parent-child relationships on our neurodevelopment and psychological health is popularly known. However, research has shown that there is a deeper link between the nature of our early childhood life and adult immune function.
Early life stress or childhood adversity can include child abuse, parental conflict or neglect, low socioeconomic conditions, and poor parent-child relationships among a multitude of other scenarios that might put undue stress on a child. Researchers investigating the physiological implications of such early-life stress found that these children grew up to have elevated levels of pro-inflammatory immune biomarkers. Adults diagnosed with depression who experienced childhood adversity have higher levels of C-reactive protein (CRP) than those who did not.
Early life stress can increase sympathetic activity and decrease parasympathetic activity in the nervous system. These processes in early life can cause increased hypothalamic-pituitary-adrenal (HPA)-axis activity in the body upon facing stress, either physiological or psychological. This can cause an increase in cortisol levels to enormous amounts, leading to insensitivity to glucocorticoids that are important for regulating the effects of stress, such as the production of messenger molecules that promote inflammation, including interleukin 6, TNF-alpha, and CRP. Early life stress can also cause certain immune cells such as monocytes and macrophages to have an excessive inflammatory response to microbial antigens. Another mechanism is increased systemic inflammation due to elevated transcription of NF-kB, a molecule that regulates the expression of pro-inflammatory molecules. This is proposed to occur through epigenetic processes.
Childhood adversity-related systemic, chronic inflammation is associated with increased morbidity, mortality, and lower quality of adult life. Our DNA is packed into dense structures called chromosomes. These chromosomes have protective caps at their ends called ‘telomeres’. Telomere shortening is a direct indication of aging and a predictor of lifespan. Adults who reported having faced childhood adversity had shorter telomeres than the adults who did not. While childhood adversity was correlated with shorter telomere lengths in adults, current social adversity was not. Moreover, researchers estimate a 7 to 15-year reduction in lifespan in older adults if they faced early life stress or any form of childhood adversity.
The beginnings of these studies were in animal models where scientists found that rats that were lifted, held, and/or touched by scientists before weaning had slower development of tumors and showed better anti-microbial responses upon challenge. It has also been shown that the negative effects of childhood adversity due to low socioeconomic status can be ameliorated to a significant extent by the presence of maternal warmth. Interestingly, some studies show strong associations between childhood adversity and inflammatory biomarkers in girls but no association in boys. This hints towards complex sex effects in different facets of this psychosomatic link.
The long-lasting impact of childhood adversity on the immune landscape and inflammatory status of the adult sheds light on the lesser-known impacts of pediatric psychological health and urges the implementation of better systems in our society that help children feel seen, heard, and above all, safe.
Manjula Kamath
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