Probiotics may help to prevent symptoms of anxiety and depression through several putative mechanisms. The aim of this study was to evaluate the effect of Lactobacillus rhamnosus HN001 (HN001) given in pregnancy and postpartum on symptoms of maternal depression and anxiety in the postpartum period. This was a secondary outcome, the primary outcome being eczema in the offspring at 12months of age. A randomised, double-blind, placebo-controlled trial of the effect of HN001 on postnatal mood was conducted in 423 women in Auckland and Wellington, New Zealand. Women were recruited at 14-16weeks gestation. Women were randomised to receive either placebo or HN001 daily from enrolment until 6months postpartum if breastfeeding. Modified versions of the Edinburgh Postnatal Depression Scale and State Trait Anxiety Inventory were used to assess symptoms of depression and anxiety postpartum. Australia NZ Clinical Trials Registry: ACTRN12612000196842. 423 women were recruited between December 2012 and November 2014. 212 women were randomised to HN001 and 211 to placebo. 380 women (89.8%) completed the questionnaire on psychological outcomes, 193 (91.0%) in the treatment group and 187 (88.6%) in the placebo group. Mothers in the probiotic treatment group reported significantly lower depression scores (HN001 mean=7·7 (SD=5·4), placebo 9·0 (6·0); effect size -1·2, (95% CI -2·3, -0·1), p=0·037) and anxiety scores (HN001 12·0 (4·0), placebo 13·0 (4·0); effect size -1·0 (-1·9, -0·2), p=0·014) than those in the placebo group. Rates of clinically relevant anxiety on screening (score>15) were significantly lower in the HN001 treated mothers (OR=0·44 (0·26, 0·73), p=0·002). Women who received HN001 had significantly lower depression and anxiety scores in the postpartum period. This probiotic may be useful for the prevention or treatment of symptoms of depression and anxiety postpartum. Health Research Council of New Zealand (11/318) and Fonterra Co-operative Group Ltd.

To measure sleep duration in 7-year-old children; identify the determinants of sleep duration; and assess the association between short sleep duration and obesity, cognitive functioning, and behaviour. Longitudinal study with disproportionate sampling of the participants. Community. 591 seven-year-old children, of whom 519 had complete sleep data. Not applicable. Sleep duration was assessed by actigraphy. Other measurements included height, weight, BMI, percentage body fat as assessed by bioimpedance assay, intelligence (WISC-III) and behaviour (Strengths & Difficulties questionnaire, parent and teachers Conners Rating Scales). Mean time in bed according to parental report was 10.9 hours (SD 0.8). Mean sleep duration by actigraphy was 10.1 (SD 0.8) hours. In multivariable analysis, sleep duration was longer on weekdays vs. weekend nights (31.5 min, P = 0.002), in winter (40.5 min), autumn (31.1 min), and spring (14.8 min) compared with summer (P <0.0001), and in those with younger siblings (11.7 min, P = 0.03). Sleep duration was shorter when bedtime was after 21:00 (−41.1 min, P <0.0001). In multivariable analysis, sleep duration <9 hours was associated with being overweight/ obese (BMI: OR = 3.32; 95% CI = 1.40, 7.87) with an increase of 3.34% body fat (P = 0.03), and this was not explained by physical activity or television watching. Short sleep duration was also associated with higher emotional lability scores (Conners Rating Scale Parent Form; P = 0.03). IQ (WISC-III) and attention deficit / hyperactivity disorder scores (both parent and teachers Conners Rating Scales) did not differ with sleep duration. Sleep duration in 7-year-old children varies considerably among individuals. The duration is affected by weekday, season, and having younger siblings. Importantly, short sleep duration was shown to be an independent risk factor for obesity/overweight.

The aims of this review are (a) to critically examine the epidemiologic evidence for a possible association between smoking and the sudden infant death syndrome (SIDS), (b) to review the pathology and postulated physiological mechanism(s) by which smoking might be causally related to SIDS, and (c) to provide recommendations for SIDS prevention in relation to tobacco smoking. Over 60 studies have examined the relation between maternal smoking during pregnancy and risk of SIDS. With regard to prone-sleep-position intervention programs, the pooled relative risk associated with maternal smoking was RR = 2.86 (95% CI = 2.77, 2.95) before and RR = 3.93 (95% CI = 3.78, 4.08) after. Epidemiologically, to distinguish the effect of active maternal smoking during pregnancy from involuntary tobacco smoking by the infants of smoking mothers is difficult. Clear evidence for environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking when the mother is a non-smoker. Seven such studies have been carried out. The pooled unadjusted RR was 1.49 (95% CI = 1.25, 1.77). Consideration of the pathological and physiological effects of tobacco suggests that the predominant effect from maternal smoking comes from the in utero exposure of the fetus to tobacco smoke. Assuming a causal association between smoking and SIDS, about one-third of SIDS deaths might have been prevented if all fetuses had not been exposed to maternal smoking in utero.

Objective To examine whether the prone sleeping position may increase the risk for sudden infant death syndrome (SIDS), particularly in infants unused to prone sleep. Design A 3-year (1987-1990) case-control study. Setting Nationwide study in New Zealand. Subjects Four hundred eighty-five infants who died of SIDS and 1800 controls. Main Outcome Measures Infants were classified asunaccustomed to proneif their usual sleep position was nonprone and they were placed prone for the last sleep.Secondary pronewas used to describe infants placed nonprone but found prone. Results Infants usually and last placed nonprone were at the lowest risk for SIDS (odds ratio [OR], 1.0); those usually and last placed prone were at increased risk (adjusted OR, 4.6; 95% confidence interval, 3.4-6.3). Risk was greatly increased among infants unaccustomed to the prone position (adjusted OR, 19.3; 95% confidence interval, 8.2-44.8). These infants accounted for 8% (31/386) of all SIDS deaths. Ninety percent (28/ 31) of infants in this group were found prone, and 71% (20/28) of those found prone were found with their faces turned down into bedding—a position in which asphyxia has been implicated as a mechanism of death. In addition, 138 infants who died of SIDS were last placed nonprone. Forty-seven infants (34%) in this group were found prone (secondary prone), and 60% (28/47) of those found prone were found with their faces turned down into the bedding. This group accounted for 12% of all SIDS deaths. Most of these infants (91% [43/47]) were usually placed nonprone. Conclusions Infants placed supine to sleep were at the lowest risk of SIDS, which supports the recommendation that this is the preferred sleeping position for healthy infants. In New Zealand, 20% of SIDS deaths involved lack of experience with the prone sleeping position. Our findings suggest the possibility that an infant's competence in escaping from potentially lethal situations during prone sleep (eg, the face-down position) may be impaired by inexperience in prone sleeping. Great caution should be exercised in placing infants unaccustomed to the prone sleeping position in the prone position.