Increased Maternal Prenatal Adiposity, Inflammation, and Lower Omega-3 Fatty Acid Levels Influence Child Negative Affect.

OBJECTIVE: Increased maternal adiposity during pregnancy is associated with offspring risk for psychiatric disorders. Inflammation secondary to adiposity is believed to be an important mechanism through which this effect occurs. Although increased adiposity introduces risk, not all children of overweight mothers develop these problems. Gestational factors that modify this risk are not well-understood. If maternal increased adiposity exerts its effects on offspring outcomes by increasing inflammation in the gestational environment, then anti-inflammatory inputs such as omega-3 fatty acids may be one protective factor. The goal of this study was to investigate whether maternal pre-pregnancy body mass index (BMI) and omega-3 fatty acid levels independently and/or interactively predicted offspring infant negative affect, an early life marker of risk for psychopathology. METHODS: Data came from a prospective study of women recruited during pregnancy and their 6 month old infants (N = 62; 40% female). Maternal pre-pregnancy BMI was pulled from medical charts and third trimester omega-3 fatty acid concentrations were assessed in plasma. Child negative affect was assessed using observer- and maternal-ratings at 6 months of age. Maternal inflammation was indexed by third trimester plasma levels of interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1. RESULTS: Maternal pre-pregnancy BMI was associated with increased infant negative affect whereas eicosapentaenoic acid was associated with less infant negative affect. Maternal omega-3 fatty acid levels moderated the effect of BMI on infant negative affect, such that omega-3 fatty acids buffered children against the negative consequences of increased adiposity. Supporting the role of maternal inflammation in these associations, maternal BMI and omega-3 fatty acid levels interacted to predict maternal third trimester inflammation. Further, maternal inflammation was associated with increased infant negative affect. CONCLUSION: Results suggest that omega-3 supplementation during pregnancy may protect against offspring behavioral risk associated with increased maternal adiposity.

Maternal prenatal depression predicts infant negative affect via maternal inflammatory cytokine levels.

Maternal depressive symptoms during pregnancy are associated with risk for offspring emotional and behavioral problems, but the mechanisms by which this association occurs are not known. Infant elevated negative affect (increased crying, irritability, fearfulness, etc.) is a key risk factor for future psychopathology, so understanding its determinants has prevention and early intervention potential. An understudied yet promising hypothesis is that maternal mood affects infant mood via maternal prenatal inflammatory mechanisms, but this has not been prospectively examined in humans. Using data from a pilot study of women followed from the second trimester of pregnancy through six months postpartum (N = 68) our goal was to initiate a prospective study as to whether maternal inflammatory cytokines mediate the association between maternal depressive symptoms and infant offspring negative affect. The study sample was designed to examine a broad range of likely self-regulation and mood-regulation problems in offspring; to that end we over-selected women with a family history or their own history of elevated symptoms of attention-deficit/hyperactivity disorder. Results supported the hypothesis: maternal pro-inflammatory cytokines during the third trimester (indexed using a latent variable that included plasma interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 concentrations as indicators) mediated the effect, such that higher maternal depressive symptoms were associated with higher maternal inflammation, and this mediated the effect on maternal report of infant negative affect (controlling for maternal affect during the infant period). This is the first human study to demonstrate that maternal inflammatory cytokines mediate the association between prenatal depression and infant outcomes, and the first to demonstrate a biological mechanism through which depressive symptoms impact infant temperament.

Early identification of ADHD risk via infant temperament and emotion regulation: a pilot study.

BACKGROUND: Attention deficit hyperactivity disorder (ADHD) is theorized to have temperamental precursors early in life. These are difficult to identify because many core features of ADHD, such as breakdowns in executive function and self-control, involve psychological and neural systems that are too immature to reliably show dysfunction in early life. ADHD also involves emotional dysregulation, and these temperamental features appear earlier as well. Here, we report a first attempt to utilize indices of emotional regulation to identify ADHD-related liability in infancy. METHODS: Fifty women were recruited in the 2nd trimester of pregnancy, with overselection for high parental ADHD symptoms. Measures of maternal body mass index, nutrition, substance use, stress, and mood were examined during pregnancy as potential confounds. Offspring were evaluated at 6 months of age using LABTAB procedures designed to elicit fear, anger, and regulatory behavior. Mothers completed the Infant Behavior Questionnaire about their child's temperament. RESULTS: After control for associated covariates, including maternal depression and prenatal stress, family history of ADHD was associated with measures of anger/irritability, including infant negative vocalizations during the arm restraint task (p = .004), and maternal ratings of infant distress to limitations (p = .036). In the regulation domain, familial ADHD was associated with less parent-oriented attention seeking during the still face procedure (p < .001), but this was not echoed in the maternal ratings of recovery from distress. CONCLUSIONS: Affective response at 6 months of age may identify infants with familial history of ADHD, providing an early indicator of ADHD liability. These preliminary results provide a foundation for further studies and will be amplified by enlarging this cohort and following participants longitudinally to evaluate ADHD outcomes.