530 research outputs found
Associations between Maternal Iron Supplementation in Pregnancy and Changes in Offspring Size at Birth Reflect Those of Multiple Micronutrient Supplementation.
It was previously observed that in a population of a high-income country, dietary multiple micronutrient supplementation in pregnancy was associated with an increased risk of gestational diabetes (GDM) and increased offspring size at birth. In this follow-up study, we investigated whether similar changes are observed with dietary iron supplementation. For this we used the prospective Cambridge Baby Growth Study with records of maternal GDM status, nutrient supplementation, and extensive offspring birth size measurements. Maternal iron supplementation in pregnancy was associated with GDM development (risk ratio 1.67 (1.01-2.77), p = 0.048, n = 677) as well as offspring size and adiposity (n = 844-868) at birth in terms of weight (Ξ²' = 0.078 (0.024-0.133); p = 0.005), head circumference (Ξ²' = 0.060 (0.012-0.107); p = 0.02), body mass index (Ξ²' = 0.067 (0.014-0.119); p = 0.01), and various skinfold thicknesses (Ξ²' = 0.067-0.094; p = 0.03-0.003). In a subset of participants for whom GDM statuses were available, all these associations were attenuated by adjusting for GDM. Iron supplementation also attenuated the associations between multiple micronutrient supplementation and these same measures. These results suggest that iron supplementation may mediate the effects associated with multiple micronutrient supplementation in pregnancy in a high-income country, possibly through the increased risk of developing GDM
Abdominal fat depots associated with insulin resistance and metabolic syndrome risk factors in black African young adults
Abstract
Background
Individuals of black African ethnicity tend to have less visceral adipose tissue (VAT) but more subcutaneous-abdominal adipose tissue (SCAT) than white Caucasians. However, it is unclear whether such distribution of abdominal fat is beneficial for metabolic disease risk in black individuals. Here we compared the associations between these specific abdominal fat depots, insulin sensitivity and metabolic syndrome risk.
Methods
A cross-sectional analysis of 76 black South African young adults (36 men; 40 women) aged 18β19 years participating in the Birth to Twenty Cohort Study had VAT and SCAT measured by MRI. The metabolic syndrome traits (blood pressure, lipid profile, fasting glucose and insulin) were measured and the values were combined into a metabolic syndrome risk score. Fasting glucose and insulin were used to derive the HOMA-index of insulin resistance (HOMA-IR).
Results
Compared to men, women had greater VAT (mean: 16.6 vs. 12.5Β cm2) and SCAT (median 164.0 vs. 59.9Β cm2). In men, SCAT (rβ=β0.50) was more strongly correlated to the metabolic syndrome score (MetS) than was VAT (rβ=β0.23), and was associated with both MetS (Pβ=β0.001) and HOMA-IR (Pβ=β0.001) after adjustment for VAT and total fat mass. In women, both abdominal fat compartments showed comparable positive correlations with MetS (rβ=β0.26 to 0.31), although these trends were weaker than in men.
Conclusions
In young black South African adults, SCAT appears to be more relevant than VAT to metabolic syndrome traits
The association between age at menarche and later risk of gestational diabetes is mediated by insulin resistance.
AIMS: Associations have been reported between age at menarche and the later risk of gestational diabetes. However, it is not known whether these associations reflect differences in insulin sensitivity and/or pancreatic Ξ²-cell function in pregnancy. METHODS: We examined this question in women enrolled in the prospective Cambridge Baby Growth Study who recalled their age at menarche in questionnaires during pregnancy. Polynomial logistic and linear regression models were used to relate menarche timing to the risk of gestational diabetes, both unadjusted and adjusted for the Homeostasis Model Assessments of insulin resistance (HOMA IR) and pancreatic Ξ²-cell function (HOMA B) at week 28 of pregnancy. RESULTS: Age at menarche showed a U-shaped association with gestational diabetes risk (linear term: pβ=β9.5βΓβ10-4; quadratic term: pβ=β1.0βΓβ10-3; nβ=β889; overall model pβ=β8.1βΓβ10-3). Age at menarche showed a negative linear association with insulin resistance (HOMA IR: Ξ²β=β-0.13, pβ=β5.2βΓβ10-4, nβ=β771), which explained the relationship between age at menarche and gestational diabetes risk (adjusted linear term going from pβ=β0.03-0.08; adjusted quadratic term going from pβ=β0.04-0.08; nβ=β771). Age at menarche also showed a negative linear association with Ξ²-cell function (HOMA B: Ξ²β=β-0.11, pβ=β2.8βΓβ10-3, nβ=β771) but this did not attenuate the relationship between age at menarche and gestational diabetes (adjusted linear term pβ=β0.02; adjusted quadratic term pβ=β0.03, nβ=β771). CONCLUSIONS: These results suggest that the associations between age at menarche and risk of gestational diabetes and raised pregnancy glucose concentrations may be mediated by insulin resistance.Funding for this study has come from the Wellbeing of Women (the Royal College of Obstetricians and Gynaecologists, UK) (RG1644). Other core funding has come from the Medical Research Council (7500001180, G1001995, U106179472), European Union Framework 5 (QLK4-1999-01422), the Mothercare Charitable Foundation (RG54608), Newlife Foundation for Disabled Children (07/20), and the World Cancer Research Fund International (2004/03). In addition, there has been support from National Institute for Health Research Cambridge Biomedical Research Centre. KO is supported by the Medical Research Council (Unit Programme number: MC_UU_12015/2)
Lipidomic analyses, breast- and formula-feeding, and growth in infants.
OBJECTIVE: To evaluate lipidomic differences between breast- and formula-fed infants. STUDY DESIGN: We utilized high-resolution mass-spectrometry methods to analyze 3.2 mm dried blood spot samples collected at ages 3 months (n = 241) and 12 months (n = 144) from a representative birth cohort study. Lipidomic profiles were compared between infants exclusively breast-fed, formula-fed, or mixed-fed, and related to 12-month infancy weight. Data analysis included supervised multivariate statistics (partial least squares discriminant analysis), and univariate analysis with correction for multiple testing. RESULTS: Distinct differences in 3-month lipidomic profiles were observed between exclusively breast-fed and formula-fed infants; mixed-fed infants showed intermediate profiles. Principle lipidomic characteristics of breast-fed infants were lower total phosphatidylcholines (PCs), with specifically lower short chain unsaturated PC but higher long chain polyunsaturated PC; higher cholesterol esters; and variable differences in sphingomyelins. At 12 months, lipidomic profiles were markedly different to those at 3 months, and differences between the earlier breast/formula/mixed-feeding groups were no longer evident. However, several specific lipid species, associated with breast-feeding at 3 months, also correlated with differences in 3- to 12-month weight. CONCLUSIONS: State-of-the-art dried blood spot sample lipidomic profiling demonstrated striking differences between breast-fed and formula-fed infants. Although these changes diminished with age, breast-fed lipidomic profiles at 3 months were associated with infancy weight and could potentially represent biomarkers of infant nutrition.PP was supported by a UK MRC Clinical Training Fellowship (G1001995). The Cambridge Baby Growth Study has been supported by the European Union, the World Cancer Research Foundation International, the Medical Research Council (including a centenary award), and the NIHR Cambridge Comprehensive Biomedical Research Centre. The lipidomics assays were supported by the Medical Research Council (UD99999906 and Cambridge Lipidomics Biomarker Research Initiative G0800783).This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.jpeds.2014.10.02
Age at Weaning and Infant Growth: Primary Analysis and Systematic Review.
OBJECTIVE: To test whether earlier age at weaning (age 3-6 months) may promote faster growth during infancy. STUDY DESIGN: Weaning at age 3.0-7.0 months was reported by 571 mothers of term singletons in a prospective birth cohort study conducted in Cambridge, UK. Infant weight and length were measured at birth and at age 3 months and 12 months. Anthropometric values were transformed into age- and sex-adjusted z-scores. Three linear regression models were performed, including adjustment for confounders in a stepwise manner. Measurements at age 3 months, before weaning, were used to consider reverse causality. RESULTS: Almost three-quarters (72.9%) of infants were weaned before age 6 months. Age at weaning of 3.0-7.0 months was inversely associated with weight and length (but not with body mass index) at 12 months (both P β€ .01, adjusted for maternal and demographic factors). These associations were attenuated after adjustment for type of milk feeding and weight or length at age 3 months (before weaning). Rapid weight gain between 0 and 3 months predicted subsequent earlier age at weaning (P = .01). Our systematic review identified 2 trials, both reporting null effects of age at weaning on growth, and 15 observational studies, with 10 reporting an inverse association between age at weaning and infant growth and 4 reporting evidence of reverse causality. CONCLUSION: In high-income countries, weaning between 3 and 6 months appears to have a neutral effect on infant growth. Inverse associations are likely related to reverse causality.European Union, World Cancer Research Foundation International, Medical Research Council, Newlife Foundation, NIHR Cambridge Comprehensive Biomedical Research Center, and University of California San Francisco Pathways Explore GrantThis is the final version. It first appeared at http://www.sciencedirect.com/science/article/pii/S0022347615004710
The influence of maternal pregnancy glucose concentrations on associations between a fetal imprinted gene allele score and offspring size at birth
Abstract
Objective
Previously we found that certain fetal imprinted genes represented as an allele score are associated with maternal pregnancy glucose concentrations. Recently it was reported that fetal polymorphisms with strong associations with birth weight tend to mediate these independently of increases in maternal pregnancy glucose concentrations. We therefore investigated whether potential associations between the fetal allele score and birth weight were related to maternal glucose concentrations in the Cambridge Baby Growth Study.
Results
The fetal imprinted gene allele score was positively associated with birth weight (Ξ²β=β63 (17β109) g/risk allele, Ξ²β²β=β0.113, pβ=β7.6βΓβ10β3, nβ=β405). This association was partially attenuated by adjusting for maternal glucose concentrations (Ξ²β=β50 (4β95) g/risk allele, Ξ²β²β=β0.089, pβ=β0.03, nβ=β405). The allele score was also positively associated with risk of being large for gestational age at birth (odds ratio 1.60 (1.19β2.15) per risk allele, pβ=β2.1βΓβ10β3, nβ=β660) and negatively associated with risk of being small for gestational age at birth (odds ratio 0.65 (0.44β0.96) per risk allele, pβ=β0.03, nβ=β660). The large for gestational age at birth association was also partially attenuated by maternal glucose concentrations. These results suggest that associations between the fetal imprinted gene allele score and size at birth are mediated through both glucose-dependent and glucose-independent mechanisms
Anogenital distance from birth to 2 years: a population study.
BACKGROUND: Anogenital distance (AGD) is sexually dimorphic in rodents and humans, being 2- to 2.5-fold greater in males. It is a reliable marker of androgen and antiandrogen effects in rodent reproductive toxicologic studies. Data on AGD in humans are sparse, with no longitudinal data collected during infancy. OBJECTIVE: This study was designed to determine AGD from birth to 2 years in males and females and relate this to other anthropometric measures. MATERIALS AND METHODS: Infants were recruited from the Cambridge Baby Growth Study. AGD was measured from the center of the anus to the base of the scrotum in males and to the posterior fourchette in females. Measurements were performed at birth and at 3, 12, 18, and 24 months of age. RESULTS: Data included 2,168 longitudinal AGD measurements from 463 male and 426 female full-term infants (median = 2 measurements per infant). Mean AGD (+/- SD) at birth was 19.8 +/- 6.1 mm in males and 9.1 +/- 2.8 mm in females (p < 0.0001). AGD increased up to 12 months in both sexes and in a sex-dimorphic pattern. AGD was positively correlated with penile length at birth (r = 0.18, p = 0.003) and the increase in AGD from birth to 3 months was correlated with penile growth (r = 0.20, p = 0.001). CONCLUSION: We report novel, longitudinal data for AGD during infancy in a large U.K. birth cohort. AGD was sex dimorphic at all ages studied. The availability of normative data provides a means of utilizing this biological marker of androgen action in population studies of the effects of environmental chemicals on genital development
Postnatal penile growth concurrent with mini-puberty predicts later sex-typed play behavior: Evidence for neurobehavioral effects of the postnatal androgen surge in typically developing boys.
The masculinizing effects of prenatal androgens on human neurobehavioral development are well established. Also, the early postnatal surge of androgens in male infants, or mini-puberty, has been well documented and is known to influence physiological development, including penile growth. However, neurobehavioral effects of androgen exposure during mini-puberty are largely unknown. The main aim of the current study was to evaluate possible neurobehavioral consequences of mini-puberty by relating penile growth in the early postnatal period to subsequent behavior. Using multiple linear regression, we demonstrated that penile growth between birth and three months postnatal, concurrent with mini-puberty, significantly predicted increased masculine/decreased feminine behavior assessed using the Pre-school Activities Inventory (PSAI) in 81 healthy boys at 3 to 4years of age. When we controlled for other potential influences on masculine/feminine behavior and/or penile growth, including variance in androgen exposure prenatally and body growth postnally, the predictive value of penile growth in the early postnatal period persisted. More specifically, prenatal androgen exposure, reflected in the measurement of anogenital distance (AGD), and early postnatal androgen exposure, reflected in penile growth from birth to 3months, were significant predictors of increased masculine/decreased feminine behavior, with each accounting for unique variance. Our findings suggest that independent associations of PSAI with AGD at birth and with penile growth during mini-puberty reflect prenatal and early postnatal androgen exposures respectively. Thus, we provide a novel and readily available approach for assessing effects of early androgen exposures, as well as novel evidence that early postnatal aes human neurobehavioral development.We thank the participating families and the Cambridge Baby Growth Study team. Data were presented at Erasmus Medical Centre, Rotterdam, where suggestions were integrated into analyses. The study was supported by the European Union Fifth Framework Programme) (Grant #QLK4-CT-1999-01422, World Cancer Research Fund International, Mothercare Foundation, Newlife Foundation for Disabled Children and Medical Research Council (UK). We also thank the Wellcome Trust Clinical Research Facility and the National Institute for Health Research β Biomedical Research Centre Cambridge.This is the final published version. It first appeared at http://www.sciencedirect.com/science/article/pii/S0018506X15000033#
Earlier Mother's Age at Menarche Predicts Rapid Infancy Growth and Childhood Obesity
Earlier age at menarche may be a transgenerational marker of faster growth, particularly during infancy, leading to taller childhood stature but earlier maturation and hence shorter adult stature
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Raised late pregnancy glucose concentrations in mice carrying pups with targeted disruption of H19delta13.
OBJECTIVE: We have hypothesized that variation in imprinted growth-promoting fetal genes may affect maternal glucose concentrations in pregnancy. To test this hypothesis we evaluated the effects of fetal disruption of murine H19(Delta13) on maternal glucose concentrations in pregnancy. RESEARCH DESIGN AND METHODS: Experimental mice were pregnant females that had inherited the disrupted H19(Delta13) from their fathers and were therefore phenotypically wild type due to imprinting; approximately half of their litters were null for H19(Delta13) through maternal inheritance of the disrupted gene. In control mice approximately half the litter paternally inherited the disrupted H19(Delta13), so the pups were either genetically wild type or phenotypically wild type due to imprinting. Blood glucose concentrations were assessed by intraperitoneal glucose tolerance tests on days 1, 16, and 18 of pregnancy. RESULTS: There were no differences in the glucose concentrations of control and experimental pregnant mice at day 1. However, at day 16 mothers carrying H19(Delta13)-null pups had a significantly higher area under the glucose tolerance test curves than controls (1,845 +/- 378 vs. 1,386 +/- 107 mmol * min * l(-1) [P = 0.01]) in association with increasing pregnancy-related insulin resistance. Although this difference lessened toward term, overall, mothers of maternally inherited H19(Delta13) mutants had significantly higher glucose concentrations during the last trimester (1,602 +/- 321 [n = 17] vs. 1,359 +/- 147 [n = 18] mmol * min * l(-1) [P = 0.009]). CONCLUSIONS: This study provides evidence that maternal glucose concentrations in pregnant mice can be affected by targeted disruption of fetal H19(Delta13). This implies that variable fetal IGF2 expression could affect risk for gestational diabetes
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