Relationship between social support during pregnancy and postpartum depressive state: a prospective cohort study.

Although the association between social support and postpartum depression has been previously investigated, its causal relationship remains unclear. Therefore, we examined prospectively whether social support during pregnancy affected postpartum depression. Social support and depressive symptoms were assessed by Japanese version of Social Support Questionnaire (J-SSQ) and Edinburgh Postnatal Depression Scale (EPDS), among 877 pregnant women in early pregnancy and at one month postpartum. First, J-SSQ was standardized among peripartum women. The J-SSQ was found to have a two-factor structure, with Number and Satisfaction subscales, by exploratory and confirmatory factor analyses. Analysis of covariance was performed to examine how EPDS and J-SSQ scores during pregnancy affected the EPDS score at postpartum. Significant associations were found between postpartum EPDS score and both EPDS and total scores on the Number subscales during pregnancy (ß = 0.488 and -0.054, ps < 0.001). Specifically, this negative correlation was stronger in depressive than non-depressive groups. Meanwhile, total score on Satisfaction subscales was not significantly associated with postpartum EPDS score. These results suggest that having a larger number of supportive persons during pregnancy helps protect against postpartum depression, and that this effect is greater in depressive than non-depressive pregnant women. This finding is expected to be vitally important in preventive interventions.

The postpartum depressive state in relation to perceived rearing: a prospective cohort study.

BACKGROUND: The relationship between perceived rearing and the postpartum depressive state remains unclear. We aimed to examine whether perceived rearing is a risk factor for postpartum depression as measured by the Edinburgh Postnatal Depression Scale (EPDS), and whether the score of perceived rearing is affected by depressive mood (the state dependency of perceived rearing). METHODS: Pregnant women (n = 448, mean age 31.8 ± 4.2 years) completed the EPDS as a measure of depressive state in early pregnancy (T1), late pregnancy (around 36 weeks), and at 1 month postpartum (T2), and the Parental Bonding Instrument (PBI) at T1 as a measure of perceived rearing. Changes in the EPDS and the PBI scores from T1 to T2 were compared between the non depressive (ND) group and the postpartum depressive (PD) group. RESULTS: There were no significant differences in any PBI category for perceived rearing between the ND and PD groups at T1. EPDS scores did not change significantly from T1 to T2 in the ND group but increased significantly in the PD group. The PBI maternal care score increased significantly in the ND group (p<0.01), while decreasing in the PD group (p<0.05). Additionally, in both the ND and PD groups, significant negative correlation was observed regarding change in the EPDS and PBI maternal care scores from T1 to T2 (r = -0.28, p = 0.013). CONCLUSIONS: The present study suggests that perceived rearing is not a strong risk factor for postpartum depression as measured by the EPDS. Furthermore, the results indicated the state dependency of the PBI maternal care score.

Prospective study on the association between harm avoidance and postpartum depressive state in a maternal cohort of Japanese women.

BACKGROUND: Recent studies have displayed increased interest in examining the relationship between personality traits and the onset, treatment response patterns, and relapse of depression. This study aimed to examine whether or not harm avoidance (HA) was a risk factor for postpartum depression measured by the Edinburgh Postnatal Depression Scale (EPDS) and the state dependency of HA. METHODS: Pregnant women (n=460; mean age 31.9±4.2 years) who participated in a prenatal program completed the EPDS as a measure of depressive state and the Temperament and Character Inventory (TCI) as a measure of HA during three periods: early pregnancy (T1), late pregnancy (around 36 weeks), and 1 month postpartum (T2). Changes in EPDS and HA scores from T1 to T2 were compared between the non depressive (ND) group and the postpartum depressive (PD) group. RESULTS: There was no significant difference in the level of HA between the ND and PD groups at T1. In the ND group, EPDS and HA scores did not change significantly from T1 to T2. In the PD group, both scores increased significantly from T1 to T2 (EPDS, p<0.0001; HA, p<0.048). In the ND and PD groups, a significant positive correlation was observed in changes in EPDS and HA scores from T1 to T2 (r=0.31, p=0.002). CONCLUSIONS: These results suggest that HA cannot be considered a risk factor for the development of postpartum depression measured by EPDS. Furthermore, HA may be state dependent.

Prospective study of maternal depressive symptomatology among Japanese women.

BACKGROUND: The primary objective of this study was to analyze the pattern of depressive moods related to pregnancy and postpartum in a dataset collected prospectively. A secondary objective was to assess the association between (1) low moods during pregnancy and postpartum depressive symptoms, and (2) maternity blues and postpartum depressive symptom. METHOD: Three hundred eighty-seven women completed self-administered questionnaires. The participants were asked to respond to Stein's Maternity Blues Scale (Stein's Scale) on five consecutive days after delivery and to the Edinburgh Postnatal Depression Scale (EPDS) during both pregnancy and postpartum. RESULTS: 32.0% of the women were identified as having a score of more than 9 on EPDS during pregnancy and postpartum. 21.6% of the women scored above the Stein's Scale cut-off point for at least 1 day during the 5-day period following delivery. The odds ratio (95% CI) for postpartum low mood if the women experienced low mood during pregnancy was 4.46 (2.48-8.04), while the odds ratio for postpartum depressive symptoms if the women experienced symptoms of maternity blues was 5.48 (2.74-10.98). In logistic regression analysis, the number of days in which women scored over the cut-off point by Stein's Scale proved to be the more significant predictor of scoring over the EPDS cutoff (8/9) [OR (95% CI)=2.74 (1.89-3.96)]. CONCLUSION: The rate of maternity blues in our findings was similar to the rates previously reported in Japan, but lower than the rates observed in Western countries. Furthermore, our longitudinal study confirms the likelihood of subsequent postpartum depressive symptoms if low moods during pregnancy and/or maternity blues are present.

Association analysis of the GDNF gene with methamphetamine use disorder in a Japanese population.

Methamphetamine (MAP) dependence is a highly heritable and aberrant dopaminergic signaling that has been implicated in the disease. Glial cell line-derived neurotrophic factor (GDNF), which plays an important role in the survival of dopaminergic neurons, may be involved in this disorder. In this study, we examined the association between GDNF and MAP dependence using a Japanese population-based sample. We selected eight single nucleotide polymorphisms (SNPs) in the GDNF locus for the association analysis. When patients with MAP dependence were divided into two subgroups consisting of multi-substance and MAP-only users, we detected a significant association between these two groups and the tagging SNP, rs2910704 (after Bonferroni's correction; allele P=0.034). Thus, GDNF is likely to be related to the severity of MAP use in the Japanese population.

Gene-wide association study between the methylenetetrahydrofolate reductase gene (MTHFR) and schizophrenia in the Japanese population, with an updated meta-analysis on currently available data.

Methylenetetrahydrofolate reductase (MTHFR) is a critical molecule for single-carbon transfer reactions. Recent evidence suggests that polymorphisms of MTHFR are related to neural tube deficits and the pathogenesis of schizophrenia. While several studies have demonstrated associations between the gene encoding the MTHFR (MTHFR) polymorphisms and schizophrenia, these studies lack consistency. Therefore, we conducted a gene-wide association study (patients with schizophrenia = 696, control subjects = 747) and performed imputation analysis. Additionally, we performed meta-analysis on currently available data from 18 studies for two common functional polymorphisms (rs1801131 and rs1801133). There were no significant associations with schizophrenia in the single marker analysis for the seven tagging SNPs of MTHFR. In the haplotypic analysis, a nominally significant association was observed between the haplotypes, which included four SNPs (rs1801133, rs17421511, rs17037396, and rs9651118) and the schizophrenic patients. Additionally, the imputation analysis demonstrated there were several associated markers on the MTHFR chromosomal region. However, confirmatory analyses of three tagging SNPs (rs1801133, rs17037396, and rs9651118) and the top SNP (rs17421511) for the imputation results (patients with schizophrenia = 797, control subjects = 1025) failed to replicate the haplotypic analysis and the imputation results. These findings suggest that MTHFR polymorphisms are unlikely to be related to the development of schizophrenia in the Japanese population. However, since our meta-analysis results demonstrated strong support for association of rs1801133 with schizophrenia, further replication studies based on a gene-wide approach need to be considered.

A two-stage case-control association study of the dihydropyrimidinase-like 2 gene (DPYSL2) with schizophrenia in Japanese subjects.

We examined the association of schizophrenia (SCZ) and dihydropyrimidinase-like 2 (DPYSL2), also known as collapsin response mediator protein 2, which regulates axonal growth and branching. We genotyped 20 tag single nucleotide polymorphisms (SNPs) in 1464 patients and 1310 controls. There were two potential associations in a screening population of 384 patients and 384 controls (rs2585458: P=0.046, rs4733048: P=0.014). However, we could not replicate these associations in a confirmatory population of 1080 patients and 926 controls (rs2585458: P=0.39, rs4733048: P=0.70) or a joint analysis (rs2585458: P=0.72, rs4733048: P=0.10). We conclude that DPYSL2 does not have a major function in SCZ in Japanese subjects.

An association study of tachykinin receptor 3 gene with schizophrenia in the Japanese population.

The tachykinin receptor 3 (TACR3) gene encodes the neurokinin3 (NK3) receptor. Animal studies showed that agonist-induced stimulation of the NK3 receptor leads to the excessive release of dopamine in the ventral and dorsal striatal and prefrontal cortical regions. Data from clinical trials of selective NK3 receptor antagonists in schizophrenia have shown significant improvement in positive symptoms. We performed an association study of the TACR3 gene in the Japanese population of 384 schizophrenic patients and 384 controls. Nine single nucleotide polymorphisms were genotyped using TaqMan assays and polymerase chain reaction-restriction fragment length polymorphism method. No significant association between schizophrenia and these single nucleotide polymorphisms was observed in single-marker and haplotype analyses. Our results suggest that TACR3 is unlikely to be related to the development of schizophrenia in the Japanese population.

Genetic analysis of the gene coding for DARPP-32 (PPP1R1B) in Japanese patients with schizophrenia or bipolar disorder.

Several lines of evidence, including genome-wide linkage scans and postmortem brain studies of patients with schizophrenia or bipolar disorder, have suggested that DARPP-32 (dopamine- and cAMP-regulated phosphoprotein, 32 kDa), a key regulatory molecule in the dopaminergic signaling pathway, is involved in these disorders. After evaluating the linkage disequilibrium pattern of the gene encoding DARPP-32 (PPP1R1B; located on 17q12), we conducted association analyses of this gene with schizophrenia and bipolar disorder. Single-marker and haplotypic analyses of four single nucleotide polymorphisms (SNPs; rs879606, rs12601930, rs907094, and rs3764352) in a sample set (subjects with schizophrenia=384, subjects with bipolar disorder=318, control subjects=384) showed that PPP1R1B polymorphisms were not significantly associated with schizophrenia, whereas, even after Bonferroni corrections, significant associations with bipolar disorder were observed for rs12601930 (corrected genotypic p=0.00059) and rs907094 (corrected allelic p=0.040). We, however, could not confirm these results in a second independent sample set (subjects with bipolar disorder=366, control subjects=370). We now believe that the significant association observed with the first sample set was a result of copy number aberrations in the region surrounding these SNPs. Our findings suggest that PPP1R1B SNPs are unlikely to be related to the development of schizophrenia and bipolar disorder in the Japanese population.

The 2',3'-cyclic nucleotide 3'-phosphodiesterase and oligodendrocyte lineage transcription factor 2 genes do not appear to be associated with schizophrenia in the Japanese population.

Several lines of evidence suggest that disturbance of myelin-related genes is associated with the etiology of schizophrenia. Recently, the 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP) gene and the oligodendrocyte lineage transcription factor 2 (OLIG2) gene were reported to be related to the development of schizophrenia, based on the results of genetic association and microarray studies. In the present study, no significant association with schizophrenia was observed by single-marker or haplotype analysis for 6 tag SNPs of these genes (759 cases, 757 controls). These findings suggest that CNP and OLIG2 are unlikely to be related to the development of schizophrenia in the Japanese population.