Prenatal Healthy Dietary Patterns Are Associated with Reduced Behavioral Problems of Preschool Children in China: A Latent Class Analysis.

The relation between maternal dietary patterns during pregnancy and offspring behavioral problems is less verified. Therefore, we have aimed to assess the relationship between them and have hypothesized that children of mothers with healthy dietary patterns during pregnancy have better behavior. The 1612 mother-child pairs of the China-Anhui Birth Cohort Study (C-ABCS) have been enrolled as the study population. The dietary behaviors of mothers during early and mid-pregnancy have been investigated using a semi-quantitative food frequency questionnaire. Preschool child behavioral problems have been assessed. Clusters of maternal food groups intakes have been identified using latent class analysis, and the association between maternal dietary patterns and child behavioral problems has been subsequently analyzed using logistic regression. Maternal age at inclusion is 26.56 ± 3.51 years. There has been a preponderance of boys (53.3%). Maternal food groups intakes have been classified into four groups: "High-consumed pattern (HCP)", "Southern dietary pattern (SDP)", "Northern dietary pattern (NDP)", and "Low-consumed pattern (LCP)". The offspring with maternal SDP and NDP have lower emotional symptoms compared to the offspring with maternal LCP in the first trimester (p < 0.05). It has been reported to lower conduct problems in children with maternal SDP than the children with maternal LCP in the second trimester (p < 0.05). In boys, we have detected associations between first-trimester SDP and lower emotional symptoms (p < 0.05) and between second-trimester SDP with decreased peer relationship problems (p < 0.05). In girls, total difficulty scores are lower with second-trimester SDP (p < 0.05). Maternal SDP in early and mid-pregnancy predicts reduced behavioral problems in preschool children, while maternal HCP and NDP during pregnancy may result in fewer developmental benefits.

Perinatal low-dose bisphenol AF exposure impairs synaptic plasticity and cognitive function of adult offspring in a sex-dependent manner.

Bisphenol AF (BPAF), a kind of the ideal substitutes of Bisphenol A (BPA), has frequently been detected in environmental media and biological samples. Numerous studies have focused on the reproductive toxicity, cardiotoxicity and endocrine disrupting toxicity of BPAF. However, little evidence is available on neurodevelopmental toxicity of BPAF. Here, our study is to evaluate the effect of perinatal BPAF exposure (0, 0.34, 3.4 and 34 mg/kg body weight/day, correspond to Ctrl, low-, medium- and high-dose groups) on the cognitive function of adult mouse offspring. This study firstly found that perinatal BPAF exposure caused cognitive impairments of mouse offspring, in which male offspring was more sensitive than female offspring in low- and medium-dose BPAF groups. Furthermore, the dendritic arborization and complexity of hippocampal CA1 and DG neurons in male offspring were impaired in all BPAF groups, and these effects were only found in high-dose BPAF group for female offspring. The damage of BPAF to dendritic spines, and the structural basis of learning and memory, was found in male offspring but not in females. Correspondingly, perinatal BPAF exposure significantly downregulated the expressions of hippocampal PSD-95 and Synapsin-1 proteins, and male offspring was more vulnerable than female offspring. Meanwhile, we explored the alteration of hippocampal estrogen receptors (ERs) to explain the sex specific impairment of cognitive function in low- and medium-dose BPAF groups. The results showed that perinatal BPAF exposure significantly decreased the expression of ERα in male offspring in a dose-dependent manner, but not in female offspring. In addition, we found that perinatal BPAF exposure can disordered the balance of oxidation and antioxidation in hippocampus of male offspring. In summary, perinatal low-dose bisphenol AF exposure impairs synaptic plasticity and cognitive function of adult offspring in a sex-dependent manner. The present results provide a pierce of potential mechanism of BPAF-caused neurodevelopmental toxicity.