Poverty and InequalitySexual and Reproductive HealthFamily, Maternal & Child HealthMethodology

Maternal distress and child neuroendocrine and immune regulation

TitleMaternal distress and child neuroendocrine and immune regulation
Publication TypeJournal Article
Year of Publication2016
AuthorsRiis, JL, Granger, DA, Minkovitz, CS, Bandeen-Roche, K, DiPietro, JA, Johnson, SB
JournalSoc Sci Med
Date PublishedFeb
ISBN Number0277-9536
Accession Number26808339
KeywordsAcute stress, anxiety, article, Baltimore, Child, child health, children, controlled study, copublication, cytokines, depression, endocrinology, Female, human, human experiment, hydrocortisone, hypothalamus hypophysis adrenal system, immune system, interleukin 1beta, interleukin 6, interleukin 8, Male, MARYLAND, Maternal mental health, maternal stress, Mental Health, neuroendocrine system, neurology, normal human, parental stress, psychological well being, psychology, saliva, saliva analysis, Salivary cortisol, sex difference, social status, tumor necrosis factor alpha, United States

RATIONALE: Neuroendocrine-immune regulation is essential for maintaining health. Early-life adversity may cause dysregulation in the neuroendocrine-immune network through repeated activation of the stress response, thereby increasing disease risk. OBJECTIVE: This paper examined the extent to which maternal psychological well-being moderates neuroendocrine-immune relations in children. METHODS: We used data from a laboratory-based study of mothers and their five-year old children (n = 125 mother-child pairs) conducted from 2011 to 2013 in Baltimore, Maryland. Child saliva was assayed for markers of immune function (i.e., cytokines: interleukin [IL]-1beta, IL-6, IL-8, tumor necrosis factor alpha [TNF-alpha]) and hypothalamic-pituitary-adrenal activity (i.e., cortisol). A composite score for depressive symptoms, anxiety, and parenting stress characterized maternal psychological distress. Multilevel mixed models examined the relationship between maternal psychological well-being and child neuroendocrine-immune relations. RESULTS: Significant cytokine x maternal distress interactions indicated that as maternal distress increased, expected inverse cytokine-cortisol relations within children became weaker for IL-1beta, IL-6, and TNF-alpha. Sex-stratified models revealed that these interactions were only significant among girls. Among boys, there were inverse cytokine-cortisol relations for all cytokines, and, while in the same direction as observed among girls, the cytokine x maternal distress interactions were non-significant. CONCLUSION: The findings suggest that maternal distress is associated with child neuroendocrine-immune relations in saliva and may alter the sensitivity of inflammatory immune processes to cortisol's inhibitory effects. This desensitization may place the child at risk for inflammatory diseases. The findings support efforts for the early detection and treatment of at-risk mothers to protect maternal and child health and well-being.