This randomized, controlled trial tested the hypothesis that women identified as more vulnerable to developing postnatal depression who attended two specific antenatal groups and one postnatal group have a reduced frequency of postnatal depression from 37 to 15 percent at 6 weeks, 12 weeks, and 6 months postpartum. A modified antenatal screening questionnaire was completed, and women identified as more vulnerable to postnatal depression were stratified by parity and randomly allocated to receive extra support groups or to a control group. The Edinburgh Postnatal Depression Scale (EPDS) was used to detect postnatal depression. Attendance at the support groups was low, 31 percent overall. At six weeks, in the intervention group, 8 (13%) of 64 women scored high (> 12) on the EPDS, compared with 11 (17%) controls. Similarly, at 12 weeks 7 (11%) of 63 versus 10 (15%) of 65 women scored higher than 12, and at 6 months, 9 (15%) of 60 versus 6 (10%) of 64 women scored higher than 12, indicating that the intervention did not reduce postnatal depression. It is possible that the method of applying the intervention, using groups separate from the standard antenatal classes, may have affected attendance. More research is required into ways of reaching and supporting women who may become depressed.

The development of rhythmic 6-sulfatoxymelatonin excretion in urine was studied in healthy full-term and premature infants during the first 12 months of life. There was little evidence of rhythmic 6-sulfatoxymelatonin excretion before 9 to 12 weeks of age in full-term infants. Over this period, excretion increased five to six times compared to the excretion at 6 weeks (08 +/- 103 vs. 2973 +/- 438 pmol/24 h) with the major proportion of the hormone metabolite being excreted between 0200-1000 h. At 24 weeks of age, total 6-sulfatoxymelatonin excretion was 25% of adult levels. Premature infants (51 +/- 4 days premature) had a delay in the appearance of rhythmic 6-sulfatoxymelatonin of approximately 9 weeks. Even after correcting for gestational age or length of time at home, the premature infants were found to have a 2-3 week delay in the development of 6-sulfatoxymelatonin rhythmicity compared to full-term infants. These results provide evidence that neural centers responsible for rhythm generation and/or the pineal gland fail to accelerate their development after premature delivery. This may be due to the environment the infants are exposed to during their stay in hospital, particularly the pattern and intensity of lighting.

The intervention did not increase breastfeeding duration at any assessment time or demonstrate any differences between the groups on secondary outcomes. The trend toward lower breastfeeding rates in the experimental group suggests a need for a larger trial to evaluate whether or nor postpartum positioning and attachment education may negatively affect breastfeeding.

Objective To determine the effects of perineal massage in the second stage of labour on perineal outcomes. Design Randomised controlled trial. Participants At 36 weeks' gestation, women expecting normal birth of a singleton were asked to join the study. Women became eligible to be randomised in labour if they progressed to full dilatation of the cervix or 8 cm or more if nulliparous or 5 cm or more if multiparous. 1340 were randomised into the trial. Intervention Massage and stretching of the perineum during the second stage of labour with a water soluble lubricant. Main outcome measures Primary outcomes: rates of intact perineum, episiotomies, and first, second, third, and fourth degree tears. Secondary outcomes: pain at three and 10 days postpartum and pain, dyspareunia, resumption of sexual intercourse, and urinary and faecal incontinence and urgency three months postpartum. Results Rates of intact perineums, first and second degree tears, and episiotomies were similar in the massage and the control groups. There were fewer third degree tears in the massage group (12 (1.7%) v 23 (3.6%); absolute risk 2.11, relative risk 0.45; 95% confidence interval 0.23 to 0.93, P < 0.04), though the trial was underpowered to measure this rarer outcome. Groups did not differ in any of the secondary outcomes at the three assessment points. Conclusions The practice of perineal massage in labour does not increase the likelihood of an intact perineum or reduce the risk of pain, dyspareunia, or urinary and faecal problems.

The emergence of melatonin rhythmicity was studied in 163 infants between 46-55 weeks postconception by monitoring the excretion of the urinary melatonin metabolite 6-sulfatoxymelatonin (aMT.6S). From this population, we examined the effects of gender, season, multiple birth, home birth, previous sudden infant death syndrome in the family, premature labor, spontaneous rupture of membranes, preeclampsia, intrauterine growth restriction, and nursery lighting on pineal rhythmicity. As previously reported, rhythmic excretion of aMT.6S appeared between 49-55 weeks postconception (9-15 weeks of age) in singleton babies born at term in the hospital. Full-term infants who had a sibling die of sudden infant death syndrome had a pattern of melatonin rhythm development no different from that of the control full-term infants. In contrast, full-term infants born at home and full-term twins born in the hospital had significantly lower aMT.6S excretion than hospital-born singleton infants at the same ages despite similar body weights (e.g. at 52 weeks postconception; 1.8 +/- 0.4, 1.1 +/- 0.3, and 3.6 +/ -0.5 nmol/day, respectively). In full-term infants, there was no difference in the development of melatonin rhythmicity between the sexes, with season or method of delivery (vaginal vs. caesarean). The premature infants were divided into 5 groups (babies born after premature labor, premature rupture of membranes, preeclampsia, intrauterine growth restriction, and fetal distress). All premature infants had a delay in the appearance of aMT.6S rhythms in the urine in relation to chronological age. When the infants were compared on the basis of weeks since conception, those infants born after spontaneous premature labor excreted amounts of aMT.6S no different from those of full-term singleton infants during the period of study. In contrast, the premature rupture of membranes, preeclampsia, and fetal distressed infants excreted 50% less aMT.6S, and intrauterine growth restricted infants excreted 67% less at the same postconceptional ages. These differences were due to reduced nocturnal excretion of the metabolite. In an attempt to accelerate the development of melatonin rhythmicity, premature labor and premature rupture of membranes infants were randomly assigned to be totally deprived of light (using phototherapy eye shields) or partially deprived of light by moving them to a dimly lit room each night for the last 3-8 weeks of their stay in the hospital nursery. Babies born after premature labor produced normal amounts of aMT.6S between 46-52 weeks postconception, and this pattern was not affected by the nocturnal light deprivation. Infants born after premature rupture of membranes and totally deprived of light at night had aMT.6S excretion rhythms at 52 weeks postconception no different from those of full-term hospital-born infants or premature labor infants, whereas those in infants placed in dim light were similar to those in untreated premature rupture of membranes infants. These results suggest that premature birth alone is not...

Further studies are needed to extend this work and develop a screening test with higher specificity and greater positive predictive value.

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