Women who gain excessive weight during pregnancy have an increased risk of post-partum obesity, and retention of gestational weight gain (GWG) post birth is a strong predictor of maternal overweight/obesity a decade or more after the birth. The aim of the current review was to identify, and evaluate the effect of key variables designed to modify risk factors for excessive weight gain in pregnant women that have been targeted in interventions over the last decade. The 10 interventions focused primarily on behavioural changes in relation to physical activity and/or to eating. While six studies reported significantly less weight gain in the intervention women, only three showed that women in the intervention were significantly more likely to gain within recommended guidelines. GWG was reduced in only normal-weight, low-income, obese, or overweight women, or not at all. Only one study reported a reduction in GWG in women with body mass indexes spanning the normal, overweight and obese categories. The findings were inconsistent in relation to what factors need to be targeted in intervention programmes to reduce GWG. Consideration of psychological factors relevant to pregnancy, in addition to behavioural changes in relation to eating and physical activity, is suggested for future intervention studies.

Background Distinctions between major depressive disorder (MDD) and perinatal depression (PND) reflect varying views of PND, from a unique etiological subtype of MDD to an MDD episode that happens to coincide with childbirth. This case–control study investigated genetic differences between PND and MDD outside the perinatal period (non‐perinatal depression or NPD). Methods We conducted a genome‐wide association study using PND cases (Edinburgh Postnatal Depression Scale score ≥ 13) from the Australian Genetics of Depression Study 2018 data (n = 3804) and screened controls (n = 6134). Results of gene‐set enrichment analysis were compared with those of women with non‐PND. For six psychiatric disorders/traits, genetic correlations with PND were evaluated, and logistic regression analysis reported polygenic score (PGS) association with both PND and NPD. Results Genes differentially expressed in ovarian tissue were significantly enriched (stdBeta = 0.07, p = 3.3e−04), but were not found to be associated with NPD. The genetic correlation between PND and MDD was 0.93 (SE = 0.07; p = 3.5e−38). Compared with controls, PGS for MDD are higher for PND cases (odds ratio [OR] = 1.8, confidence interval [CI] = [1.7–1.8], p = 9.5e−140) than for NPD cases (OR = 1.6, CI = [1.5–1.7], p = 1.2e−49). Highest risk is for those reporting both antenatal and postnatal depression, irrespective of prior MDD history. Conclusions PND has a high genetic overlap with MDD, but points of distinction focus on differential expression in ovarian tissue and higher MDD PGS, particularly for women experiencing both antenatal and postpartum PND.

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Findings indicate that the extra training of MCHN did not substantially assist in the detection and management of postnatal distress in these new mothers. Unexpected ecological conditions of workforce disruption and extra workloads may have mitigated against the success of the programme. Limitations of the study are examined and the implications for future research are discussed.