Background: Lower socioeconomic status is often thought to be associated with an elevated risk of postpartum depression; however, this relationship exhibits noticeable heterogeneity between studies. The present study examined this relationship in Japan. Methods: Data were obtained from 90,194 mothers in an ongoing birth cohort of the Japan Environment and Children’s Study. Socioeconomic status was assessed based on the mothers’ highest education level during pregnancy. Postpartum depression was identified at 1 and 6 months postpartum based on an Edinburgh Postnatal Depression Scale score of ≥9, and analyses were also performed based on the sub-scores for anxiety, depression, and anhedonia symptoms. Logistic and generalized linear regression model analyses were used to calculate odds ratios for postpartum depression according to education level with the highest education group (≥16 years of education) defined as the reference group, while controlling for covariates in a stepwise fashion. Results: Univariate analysis revealed that a lower education level was associated with a higher prevalence of postpartum depression and related symptoms. Although these relationships weakened in the fully adjusted models, odds ratios for cases and related symptoms remained significant at 1 and 6 months postpartum. Among three symptom dimensions, the relationship was strongest and weakest in the depressive and anxiety symptoms, respectively. Conclusions: A lower education level was an independent risk factor for postpartum depression. In view of the low mobility of the education level, this finding suggests the potential importance of collecting information regarding education levels at the earliest opportunity.

The endocrine disrupting chemical bisphenol A (BPA) is widely used in the production of polycarbonate plastics and epoxy resins. The use of BPA-containing products in daily life makes exposure ubiquitous, and the potential human health risks of this chemical are a major public health concern. Although numerous in vitro and in vivo studies have been published on the effects of BPA on biological systems, there is controversy as to whether ordinary levels of exposure can have adverse effects in humans. However, the increasing incidence of developmental disorders is of concern, and accumulating evidence indicates that BPA has detrimental effects on neurological development. Other bisphenol analogues, used as substitutes for BPA, are also suspected of having a broad range of biological actions. The objective of this review is to summarize our current understanding of the neurobiological effects of BPA and its analogues, and to discuss preventive strategies from a public health perspective.

Because the prevalence of obesity has increased dramatically in recent years, one of the key targets of public health is obesity and its associated pathological conditions. Obesity occurs as a result of white adipose tissue enlargement, caused by adipocyte hyperplasia and/or hypertrophy. Recently, endocrine aspects of adipose tissue have become an active research area and these adipose tissue-derived factors are referred to as adipokines. These adipokines interact with a range of processes in many different organ systems and influence a various systemic phenomena. Therefore, dysregulated production of adipokines has been found to participate in the development of metabolic and vascular diseases related to obesity. The obese state is also known to be associated with increased local and systemic inflammation. Adipokines influence not only systemic insulin resistance and have pathophysiological roles in the metabolic syndrome and cardiovascular disease, but also contribute toward an increase in local and systemic inflammation. Thus, circulating levels of adipokines can be used as high-throughput biomarkers to assess the obesity-related health problems, including low grade inflammation. This review focuses on the usefulness of measuring circulating adipokine levels for the assessment of obesity-related health problems.

Obesity is a leading risk factor for impaired glucose tolerance and type 2 diabetes (T2D). Although the cause of the obesity epidemic is multi-factorial and not entirely clear, the recent acceleration in incidence is too rapid to be accounted for only by genetics, the wide availability of calorie-rich foods, and increasingly sedentary lifestyles. Accumulating data suggest that the important causes of the obesity epidemic may be related to developmental and early life environmental conditions. The concept of the developmental origins of health and disease (DOHaD) suggests that adverse influences early in development, particularly during intrauterine life, may result in permanent changes in the physiology and metabolism of the infant, which in turn result in an increased risk of non-communicable diseases in adulthood. For example, undernutrition during pregnancy and rapid postnatal weight gain are associated with obesity and T2D in the adult offspring. Moreover, increasing evidence suggests that early-life exposure to a wide range of chemicals has a significant impact on the causes of metabolic disorders. Although the underlying molecular mechanisms remain to be determined, these factors can affect epigenetic processes, such as DNA methylation, allowing the developmental environment to modulate gene transcription. The objective of this review article was to summarize recent progress in the biomedical implications of the DOHaD concept, focusing on the pathogenesis of obesity and T2D, and to discuss a future direction for preventive strategies from a public health perspective.

Background: Postpartum depression is a major mental health issue. It not only adversely affects the mother's quality of life, but also mother-infant bonding. However, the relationship between postpartum depression (at multiple points after childbirth) and mother-infant bonding failure one year after birth is not well understood. This study investigates the relationship between postpartum depression at 1-month and 6-month after birth and mother-infant bonding failure at 1 year after birth with a large cohort.Methods: Data from 83 109 mothers from the Japan Environment and Children's Study were analyzed. Mother-infant bonding 1-year after delivery was assessed using the Mother-to-Infant Bonding Scale Japanese version (MIBS-J). Postpartum depression was measured using the Edinburgh Postnatal Depression Scale (EPDS) at 1-month and 6-month after delivery. Twenty covariates during pregnancy and one month after delivery were controlled for deriving the odds ratios (ORs) describing postpartum depression to mother-infant bonding.Results: EPDS Total Score crude ORs and adjusted ORs against the MIBS-J Total Score at 1-month and 6-month after delivery were calculated. Crude ORs were 1.111 (95% CI 1.110–1.112) and 1.122 (95% CI 1.121–1.124) respectively. In the fully adjusted model, ORs were 1.088 (95% CI 1.086–1.089) and 1.085 (95% CI 1.083–1.087), respectively.Conclusions: This study demonstrated prospectively, in a large-scale cohort, that depression at multiple postpartum points, including associations with each EPDS and MIBS-J factors, may be a robust predictor of mother-infant bonding failure 1-year after birth.