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BackgroundAccelerated infant weight gain in individuals born full term is linked to cardiovascular risk in adulthood, but data in those born preterm are inconsistent.ObjectiveTo investigate the association between weight gain in infancy and childhood with later markers of the metabolic syndrome in adolescents who were born preterm.Study designLongitudinal cohort study.SettingChildren born preterm with regular assessments of infant growth had auxology, body composition (dual X-ray absorptiometry), blood pressure, insulin sensitivity and lipid profile determined in adolescence.ResultsWe reviewed 153 children (mean gestation 30.8 weeks, median birth weight 1365 g) of whom 102 consented to venepuncture at a median age of 11.5 years. Adolescent height and weight standard deviation scores (SDS) were similar to population averages (0.01±0.92 and 0.3±1.2, respectively) and did not differ between infants when grouped according to degree of catch-up in weight gain in the immediate postdischarge period to 12 weeks of age. There were no significant associations between infant weight gain (change in weight SDS adjusted for length) and later metabolic outcome. However, there were strong associations between more rapid childhood weight gain (after 1 year of age) and subsequent body composition (higher fat mass %, fat mass index and waist circumference) and metabolic markers (higher fasting insulin, blood pressure and lower insulin sensitivity).ConclusionsThe association of rapid weight gain on health is time critical in those born preterm; in early infancy, this does not impact on metabolic status in adolescence, in contrast to rapid weight gain in childhood, which should be discouraged. However, given the critical importance of brain growth in the neonatal period and infancy, further research is needed before strategies that discourage infant weight gain or catch-up can be recommended for infants born preterm.

AimIntrauterine growth restriction (IUGR) is associated with poorer outcomes in later life. We used a monochorionic twin model with IUGR in one twin to determine its impact on growth and neurocognitive outcomes.MethodsMonochorionic twins with ≥20% birth weight discordance born in the north of England were eligible. Cognitive function was assessed using the British Ability Scales. The Strength and Difficulties Questionnaire was used to identify behavioural problems. Auxological measurements were collected. Generalised estimating equations were used to determine the effects of birth weight on cognition.ResultsFifty-one monochorionic twin pairs were assessed at a mean age of 6.3 years. Mean birth weight difference was 664 g at a mean gestation of 34.7 weeks. The lighter twin had a General Conceptual Ability (GCA) score that was three points lower (TwinL −105.4 vs TwinH −108.4, 95% CI −0.9 to −5.0), and there was a significant positive association (B 0.59) of within-pair birth weight differences and GCA scores. Mathematics and memory skills showed the largest differences. The lighter twin at school age was shorter (mean difference 2.1 cm±0.7) and lighter (mean difference 1.9 kg±0.6). Equal numbers of lighter and heavier twins were reported to have behavioural issues.ConclusionsIn a monochorionic twin cohort, fetal growth restriction results in lower neurocognitive scores in early childhood, and there remain significant differences in size. Longer term follow-up will be required to determine whether growth or cognitive differences persist in later child or adulthood, and whether there are any associated longer term metabolic sequelae.

Background The UK Newborn Screening Programme Centre recommends that a blood spot thyroid stimulating hormone (TSH) cut-off of 10 mU/l is used to detect congenital hypothyroidism (CHT). As the value used varies from 5 to 10 mU/l, we examined the implications of altering this threshold. Methods Our regional blood spot TSH cut-off is 6 mU/l. Positive or suspected cases were defined as a TSH >6 mU/l throughout the study period (1 April 2005 to 1 March 2007). All term infants (>35 weeks) whose first TSH was 6–20 mU/l had a second TSH measured. The biochemical details of infants with a TSH between 6.1 and 10.0 mU/l and then >6 mU/l on second sampling were sent to paediatric endocrinologists to determine approaches to management. Results 148 of 65 446 infants (0.23%) had a first blood spot TSH >6.0 mU/l. 120 were term infants with 67 of these (0.1% of all infants tested) having a TSH between 6.1 and 10.0 mU/l and 53 a TSH >10.0 mU/l. Of the 67 term infants with a TSH between 6.1 and 10.0 mU/l on initial testing, four continued to have a TSH >6 mU/l. One with a TSH >10 mU/l and one infant with a TSH <10 mU/l on the second blood spot have been diagnosed with CHT. The survey of endocrinologists highlighted significant differences in practice. Conclusions A reduced threshold of 6 mU/l will increase the number of false positive term infants by 126%, but abnormalities of thyroid function requiring treatment will be detected. We suspect that the additional expense involved in setting a lower threshold is justified.

Previous studies of congenital hypothyroidism (CHT) have reported an increasing incidence which may suggest that environmental factors play an aetiological role. If so, then cases may exhibit space-time clustering, where cases occur at similar times and close proximities to other cases. In this study we investigated whether space-time clustering of elevated thyroid stimulating hormone (TSH) in newborns exists. All infants born in the Northern Region of England are screened by measuring levels of circulating TSH using a blood spot assay. Data on 207 cases of elevated TSH values, as a proxy for CHT, in newborns born from 1994 to 2006 inclusive were available and analysed using rigorous space-time clustering statistical methods. Analysis showed statistically significant evidence of space-time clustering. The strength of clustering was most marked for cases born within 0.1-0.7 year (1-8 months) of one another. This is the first study to find significant space-time clustering of cases of elevated TSH levels in newborns, a surrogate for space-time clustering of CHT. Whilst the reasons for the clustering are unclear, it would appear from this analysis that transient environmental exposures are likely to be involved, although environmental determinants of genetic mutations and epigenetic factors cannot be ruled out. Further research is required to a) validate these results in other populations and b) to assess in more detail the potential environmental determinants of increased CHT risk.

Background Preterm infants represent up to 10% of births worldwide and have an increased risk of adverse metabolic outcomes in later life. Early life exposures are key factors in determining later health but current lifestyle factors such as diet and physical activity are also extremely important and provide an opportunity for targeted intervention. Methods/Design This current study, GROWMORE, is the fourth phase of the Newcastle Preterm Birth Growth Study (PTBGS), which was formed from two randomised controlled trials of nutrition in early life in preterm (24–34 weeks gestation) and low birthweight infants. 247 infants were recruited prior to hospital discharge. Infant follow-up included detailed measures of growth, nutritional intake, morbidities and body composition (Dual X Ray Absorptiometry, DXA) along with demographic data until 2 years corrected age. Developmental assessment was performed at 18 months corrected age, and cognitive assessment at 9–10 years of age. Growth, body composition (DXA), blood pressure and metabolic function (insulin resistance and lipid profile) were assessed at 9–13 years of age, and samples obtained for epigenetic analysis. In GROWMORE, we will follow up a representative cohort using established techniques and novel metabolic biomarkers and correlate these with current lifestyle factors including physical activity and dietary intake. We will assess auxology, body composition (BODPOD™), insulin resistance, daily activity levels using Actigraph™ software and use 31 P and 1 H magnetic resonance spectroscopy to assess mitochondrial function and intra-hepatic lipid content. Discussion The Newcastle PTBGS is a unique cohort of children born preterm in the late 1990’s. The major strengths are the high level of detail of early nutritional and growth exposures, and the comprehensive assessment over time. This study aims to examine the associations between early life exposures in preterm infants and metabolic outcomes in adolescence, which represents an area of major translational importance.

Low birth weight is associated with hypothyroidism and an adverse metabolic profile in later life. Our aim was to examine the relationship between neonatal TSH and birth weight, gestational age and sex. We compared blood spot filter paper TSH levels with birth weight, gestational age and sex in a 10% sample of infants screened for congenital hypothyroidism at a single centre in Northern England. All gestational ages were included with infants suspected of having congenital hypothyroidism excluded. Data on 1,728 male and 1,662 female infants were analysed. The distribution of TSH was significantly different between males and females, with males having a higher median TSH (0.7 vs. 0.6). Correlations were shown between TSH and birth weight (rho = -0.07, p = 0.0001) and gestational age (rho = -0.05, p = 0.008), with the birth weight association remaining independent of gestational age. The functional form of the model suggested that higher TSH in the lowest birth weight categories was responsible for the association between TSH and birth weight. Low birth weight is related to neonatal TSH levels. Further research is required to assess whether this association explains the relationship between higher TSH and an adverse metabolic profile in later life.

Preterm infants represent up to 10% of births worldwide and have an increased risk of adverse metabolic outcomes in later life. Early life exposures are key factors in determining later health but current lifestyle factors such as diet and physical activity are also extremely important and provide an opportunity for targeted intervention. This current study, GROWMORE, is the fourth phase of the Newcastle Preterm Birth Growth Study (PTBGS), which was formed from two randomised controlled trials of nutrition in early life in preterm (24-34 weeks gestation) and low birthweight infants. 247 infants were recruited prior to hospital discharge. Infant follow-up included detailed measures of growth, nutritional intake, morbidities and body composition (Dual X Ray Absorptiometry, DXA) along with demographic data until 2 years corrected age. Developmental assessment was performed at 18 months corrected age, and cognitive assessment at 9-10 years of age. Growth, body composition (DXA), blood pressure and metabolic function (insulin resistance and lipid profile) were assessed at 9-13 years of age, and samples obtained for epigenetic analysis. In GROWMORE, we will follow up a representative cohort using established techniques and novel metabolic biomarkers and correlate these with current lifestyle factors including physical activity and dietary intake. We will assess auxology, body composition (BODPOD[TM]), insulin resistance, daily activity levels using Actigraph[TM] software and use .sup.31P and .sup.1H magnetic resonance spectroscopy to assess mitochondrial function and intra-hepatic lipid content. The Newcastle PTBGS is a unique cohort of children born preterm in the late 1990's. The major strengths are the high level of detail of early nutritional and growth exposures, and the comprehensive assessment over time. This study aims to examine the associations between early life exposures in preterm infants and metabolic outcomes in adolescence, which represents an area of major translational importance.