Search PubMed⌕ Search

Biomedical subjects

Ruth Morley

Publications and source records attributed to Ruth Morley.

26 records · Page 2Linked to original sources
PubMed2003

Studies of twins: can they shed light on the fetal origins of adult disease hypothesis?

There has been much interest in evidence that people with lower birthweight have higher risk of adult cardiovascular disease, but the causal pathways underlying such observations are uncertain. Study of twins offers an opportunity to shed light on these pathways, in three different ways. First, in a twin pregnancy maternal nutritional resources and the "supply line" to the fetuses will be more "stretched". We hypothesise that study of twin pregnancies is a more efficient way to identify modifiable maternal factors that influence later health than studies of singleton pregnancies. Second, twins have lower birthweight than singletons. Comparison of cardiovascular disease risk in twins versus that in singletons will provide insight into whether birthweight per se is in the underlying causal pathway of interest, and whether factors constraining fetal growth of twins (versus singletons) affect later outcome. Third, twin cohorts provide an opportunity to investigate the role of "shared" factors versus factors affecting each individual fetus, by comparing results of within-cohort versus within-pair analyses. Generalisability of findings in twins is debated. We suggest that findings in monochorionic twins (or in the absence of chorionicity data, those from monozygotic twins) need to be interpreted with caution.

Animals↗
PubMed2003

Blood pressure in late adolescence and very low birth weight.

OBJECTIVES: To determine whether blood pressure (BP) differed between very low birth weight (VLBW; birth weight 2499 g) subjects in late adolescence, and to determine whether growth restriction in utero was related to BP in VLBW survivors at this age. METHODS: This was a cohort study of 210 preterm survivors with birth weights <1501 g born from January 1, 1977, to March 31, 1982, and 60 randomly selected NBW subjects from the Royal Women's Hospital, Melbourne. BP was measured at 18+ years of age in 156 (74%) VLBW subjects and 38 (63%) NBW subjects with both a standard mercury sphygmomanometer and an ambulatory BP monitor. RESULTS: VLBW subjects had higher sphygmomanometer systolic and diastolic BPs than NBW subjects (mm Hg; mean difference [95% confidence interval]; systolic, 8.6 [3.4, 13.9]; diastolic, 4.3 [1.0, 7.6]). VLBW subjects also had significantly higher mean systolic ambulatory BPs (mm Hg; mean difference [95% confidence interval]) for the 24-hour period (4.7 [1.4, 8.0]), and for both the awake (5.0 [1.6, 8.5]) and asleep (3.6 [0.04, 7.1]) periods. There were no significant differences between the birth weight groups for any ambulatory diastolic BPs. Within the VLBW subjects, there was no significant relationship between birth weight standard deviation score and any measure of BP. CONCLUSIONS: BP was significantly higher in late adolescence in VLBW survivors than in NBW subjects. Growth restriction in utero was not significantly related to BP in VLBW survivors.

Adolescent↗
PubMed2002

Is birthweight a good marker for gestational exposures that increase the risk of adult disease?

There is much evidence of a link between low birthweight and elevated risk of adult cardiovascular disease, from humans and experimental animals. However, if one relies on data linking birthweight to coronary heart disease to estimate the public health implications of this association, the effects are likely to be modest. The focus on birthweight may be misplaced, because reduced size at birth may not be in the causal pathway linking gestational factors to disease in adult offspring. We need to know more about this before we can estimate the public health implications of gestational factors and assess the potential for intervention. The most studied gestational factor is maternal nutrition. We review here evidence for and against birthweight being in the causal pathways between suboptimal maternal nutrition and increased risk of adult disease in the offspring and provide evidence suggesting that birthweight is not in all of them. From a public health point of view, we suggest that future research in this field should focus on modifiable gestational exposures that may be linked to adult disease, whether or not they influence size at birth.

Adult↗
PubMed2002

Double-blind, randomized trial of long-chain polyunsaturated fatty acid supplementation in formula fed to preterm infants.

OBJECTIVE: We tested the hypothesis that balanced addition of long-chain polyunsaturated fatty acid (LCPUFA) to preterm formula during the first weeks of life would confer long-term neurodevelopmental advantage in a double-blind, randomized, controlled trial of preterm formula with and without preformed LCPUFA. METHODS: The participants were 195 formula-fed preterm infants (birth weight <1750 g, gestation <37 weeks) from 2 UK neonatal units and 88 breast milk-fed infants. Main outcome measures were Bayley Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) at 18 months and Knobloch, Passamanick and Sherrard's Developmental Screening Inventory at 9 months' corrected age. Safety outcome measures were anthropometry at 9 and 18 months, tolerance, infection, necrotizing enterocolitis, and death. RESULTS: There were no significant differences in developmental scores between randomized groups, although infants who were fed LCPUFA-supplemented formula showed a nonsignificant 2.6-point (0.25 standard deviation) advantage in MDI and PDI at 18 months, with a greater (nonsignificant) advantage (MDI: 4.5 points; PDI: 5.8 points) in infants below 30 weeks' gestation. LCPUFA-supplemented infants were shorter than control infants at 18 months (difference in length standard deviation score: 0.44; 95% confidence interval: 0.08-0.8). No other significant short- or long-term differences in safety outcomes were observed. Breastfed infants had significantly higher developmental scores at 9 and 18 months than both formula groups and were significantly heavier and longer at 18 months than LCPUFA-supplemented but not control infants. CONCLUSIONS: With the dose, duration, and preparation of LCPUFA used, efficacy was not demonstrated, although an advantage in later neurodevelopment cannot be excluded by global tests of development up to 18 months, particularly in infants below 30 weeks' gestation. The surprising effect of LCPUFA-supplemented formula on growth 18 months beyond the intervention period needs to be confirmed in other studies using similar supplementation strategies. Additional follow-up of this cohort is critical at an age when more specific tests of cognitive function are possible.

Age Factors↗