To date, the precise prevalence of co-morbidity of anxiety and depression in the perinatal period is not well known. We aimed to estimate the prevalence of co-morbid anxiety and depression in the antenatal and postnatal periods. Systematic searches of multiple electronic databases were conducted for studies published between January 1950 and January 2016. We included 66 (24 published and 42 unpublished) studies incorporating 162 120 women from 30 countries. Prevalence of self-reported antenatal anxiety symptoms and mild to severe depressive symptoms was 9.5% [95% confidence interval (CI) 7.8–11.2, 17 studies, n = 25 592] and of co-morbid anxiety symptoms and moderate/severe depressive symptoms was 6.3% (95% CI 4.8–7.7, 17 studies, n = 27 270). Prevalence of a clinical diagnosis of any antenatal anxiety disorder and depression was 9.3% (95% CI 4.0–14.7, 10 studies, n = 3918) and of co-morbid generalized anxiety disorder and depression was 1.7% (95% CI 0.2–3.1, three studies, n = 3085). Postnatally between 1 and 24 weeks postpartum, the prevalence of co-morbid anxiety symptoms and mild to severe depressive symptoms was 8.2% (95% CI 6.5–9.9, 15 studies, n = 14 731), while co-morbid anxiety symptoms and moderate/severe depressive symptoms was 5.7% (95% CI 4.3–7.1, 13 studies, n = 20 849). The prevalence of a clinical diagnosis of co-morbid anxiety and depression was 4.2% (95% CI 1.9–6.6, eight studies, n = 3251). Prevalence rates did not differ with regard to year of publication, country income, selection bias and attrition bias. The results suggest that co-morbid perinatal anxiety and depression are prevalent and warrant clinical attention given the potential negative child developmental consequences if left untreated. Further research is warranted to develop evidence-based interventions for prevention, identification and treatment of this co-morbidity.

Epigenetic studies suggest that diseases that develop in adulthood are related to certain conditions to which the individual is exposed during the initial stages of life. Experimental evidence has demonstrated that offspring born to mothers maintained on high-Na diets during pregnancy have higher mean arterial pressure (MAP) in adulthood. Although these studies have demonstrated the importance of prenatal phases to hypertension development, no evidence regarding the role of high Na intake during postnatal phases in the development of this pathology has been reported. Therefore, in the present study, the effects of Na overload during childhood on induced water and Na intakes and on cardiovascular parameters in adulthood were evaluated. Experiments were carried out in two groups of 21-d-old rats: experimental group, maintained on hypertonic saline (0·3 m-NaCl) solution and food for 60 d, and control group, maintained on tap water and food. Later, both groups were given water and food for 15 d (recovery period). After the recovery period, chronic cannulation of the right femoral artery was performed in unanaesthetised rats to record baseline MAP and heart rate (HR). The experimental group was found to have increased basal MAP (98·6 (sem 2·6) v. 118·3 (sem 2·7) mmHg, P< 0·05) and HR (365·4 (sem 12·2) v. 398·2 (sem 7·5) beats per min, P< 0·05). There was a decrease in the baroreflex index in the experimental group when compared with that in the control group. A water and Na intake test was performed using furosemide. Na depletion was found to induce an increase in Na intake in both the control and experimental groups (12·1 (sem 0·6) ml and 7·8 (sem 1·1), respectively, P< 0·05); however, this increase was of lower magnitude in the experimental group. These results demonstrate that postnatal Na overload alters behavioural and cardiovascular regulation in adulthood.