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Background: Exposure to maternal postpartum depression (PPD) increases the risk for emotion regulatory and psychiatric problems in offspring. This study aimed to determine if maternal cognitive behavioral therapy (CBT) for PPD improves infant emotion regulatory capacity. Methods: Participants were 40 infants of mothers with a primary diagnosis of major depressive disorder matched 1:1-40 healthy control infants of nondepressed mothers on infant age, sex, and socioeconomic status. Mothers with PPD received nine weeks of group CBT. Dyads were tested at two time points. Visit 1 occurred following the first CBT session (baseline visit for control infants). Visit 2 took place after CBT (nine weeks post-baseline for controls). At both visits, infant emotion regulation was assessed using resting-state frontal electroencephalography alpha asymmetry (FAA), heart rate variability (HRV), and maternal and partner ratings of orientation or regulation behaviors (infant behavior questionnaire-revised [short form]). Changes in maternal characteristics (depression, bonding, and emotion regulation) from pretreatment to posttreatment were examined to determine if they explained infant changes. Results: At Visit 1, infants of women with PPD exhibited poorer emotion regulation relative to the healthy control infants. At Visit 2, following maternal PPD treatment, infants exhibited improved emotion regulation (shifted from right to left FAA [p = .01, d = 0.60], increased HRV [p = .003, d = 0.56], mother [p = .015, d = 0.29] and partner [p = .049, d = 0.35] reported orientation or regulation behaviors) such that they no longer differed from the healthy control infants. Changes in maternal characteristics did not appear to account for these changes. Conclusion: Treating PPD may promote adaptive changes in physiological and behavioral systems underlying infant emotion regulation. [ABSTRACT FROM AUTHOR]

[Display omitted] • This is the first study to examine associations between prenatal fluoride exposure and disruptions to visual acuity and cardiac autonomic function in infants. • In this Canadian pregnancy cohort, prenatal fluoride exposure was linked to poorer visual acuity. • Prenatal fluoride exposure was linked to lower heart rate variability (root mean square of successive differences) • Results suggest that prenatal fluoride exposure may be associated with poorer central and peripheral markers of nervous system functioning in infant offspring. Prenatal fluoride exposure can have adverse effects on children's development; however, associations with visual and cardiac autonomic nervous system functioning are unknown. We examined associations between prenatal fluoride exposure and visual acuity and heart rate variability (HRV) in 6-month-old infants. We used data from Canadian mother-infant pairs participating in the Maternal-Infant Research on Environmental Chemicals (MIREC) cohort. We estimated prenatal fluoride exposure using: i) fluoride concentration in drinking water (mg/L), ii) maternal urinary fluoride adjusted for specific gravity (MUF SG ; mg/L) and averaged across pregnancy, and iii) maternal fluoride intake (µg/kg/day) from consumption of water, tea, and coffee, adjusted for maternal body weight (kg). We used multivariable linear regression to examine associations between each measure of fluoride exposure and Teller Acuity Card visual acuity scores (n = 435) and assessed HRV (n = 400) using two measures: root mean square of successive differences (RMSSD) and the standard deviation of N-N intervals (SDNN) measured at 6-months of age. Median (IQR) values for water fluoride, MUF SG , and daily fluoride intake were 0.20 (IQR: 0.13–0.56) mg/L; 0.44 (0.28–0.70) mg/L and 4.82 (2.58–10.83) µg/kg/day, respectively. After adjustment for confounding variables, water fluoride concentration was associated with poorer infant visual acuity (B = - 1.51; 95 % CI: −2.14,-0.88) and HRV as indicated by lower RMSSD (B = -1.60; 95 % CI: −2.74,-0.46) but not SDNN. Maternal fluoride intake was also associated with poorer visual acuity (B = -0.82; 95 % CI: −1.35,-0.29) and lower RMSSD (B = -1.22; 95 % CI: −2.15,-0.30). No significant associations were observed between MUF SG and visual acuity or HRV. Fluoride in drinking water was associated with reduced visual acuity and alterations in cardiac autonomic function in infancy, adding to the growing body of evidence suggesting fluoride's developmental neurotoxicity. [ABSTRACT FROM AUTHOR]

Background: Many pregnant women are consuming diets of poor overall quality. Although many studies have linked poor prenatal diet quality to an increased risk of specific diseases in offspring, it is not known if exposure to poor prenatal diet affects core neurophysiological regulatory systems in offspring known to lie upstream of multiple diseases.Objective: We aimed to examine the association between prenatal diet quality and autonomic nervous system (ANS) function in infants at 6 mo of age.Methods: Data from 400 women (aged >18 y, with uncomplicated pregnancies) and their infants participating in the Maternal-Infant Research on Environmental Chemicals-Infant Development cohort were used to investigate links between prenatal diet quality and infant ANS function at 6 mo of age. Prenatal diet quality was assessed using the Healthy Eating Index (2010), calculated from a validated FFQ completed by women during the first trimester. Infant ANS function was measured using 2 assessments of heart rate variability (HRV) including root mean square of successive differences (RMSSD) and SD of N-N intervals (SDNN). Associations were analyzed before and after adjustment for socioeconomic status, maternal depression symptoms, maternal cardiometabolic dysfunction, breastfeeding, and prenatal smoking.Results: Poorer prenatal diet quality was associated with lower infant HRV assessed using RMSSD (B: 0.07; 95% CI: 0.01, 0.13; R2 = 0.013) and SDNN (B: 0.18; 95% CI: 0.02, 0.35; R2 = 0.011). These associations remained significant after adjustment for confounding variables [RMSSD: B: 0.09; 95% CI: 0.003, 0.18; squared semipartial correlation (sp2) = 0.14 and SDNN B: 0.24; 95% CI: 0.0, 0.49; sp2 = 0.13].Conclusions: In a large cohort study, poorer prenatal diet quality was associated with lower offspring HRV, a marker of decreased capacity of the ANS to respond adaptively to challenge. Therefore, poor prenatal diet may play a significant role in the programming of multiple organ systems and could increase general susceptibility to disease in offspring. [ABSTRACT FROM AUTHOR]