Prediction of childhood overweight and obesity at age 10-11: findings from the Studying Lifecourse Obesity PrEdictors and the Born in Bradford cohorts.

BACKGROUND: In England, 41% of children aged 10-11 years live with overweight or obesity. Identifying children at risk of developing overweight or obesity may help target early prevention interventions. We aimed to develop and externally validate prediction models of childhood overweight and obesity at age 10-11 years using routinely collected weight and height measurements at age 4-5 years and maternal and early-life health data. METHODS: We used an anonymised linked cohort of maternal pregnancy and birth health records in Hampshire, UK between 2003 and 2008 and child health records. Childhood body mass index (BMI), adjusted for age and sex, at 10-11 years was used to define the outcome of overweight and obesity (BMI ≥ 91st centile) in the models. Logistic regression models and multivariable fractional polynomials were used to select model predictors and to identify transformations of continuous predictors that best predict the outcome. Models were externally validated using data from the Born in Bradford birth cohort. Model performance was assessed using discrimination and calibration. RESULTS: Childhood BMI was available for 6566 children at 4-5 (14.6% overweight) and 10-11 years (26.1% overweight) with 10.8% overweight at both timepoints. The area under the curve (AUC) was 0.82 at development and 0.83 on external validation for the model only incorporating two predictors: BMI at 4-5 years and child sex. AUC increased to 0.84 on development and 0.85 on external validation on additionally incorporating maternal predictors in early pregnancy (BMI, smoking, age, educational attainment, ethnicity, parity, employment status). Models were well calibrated. CONCLUSIONS: This prediction modelling can be applied at 4-5 years to identify the risk for childhood overweight at 10-11 years, with slightly improved prediction with the inclusion of maternal data. These prediction models demonstrate that routinely collected data can be used to target early preventive interventions to reduce the prevalence of childhood obesity.

Exploring the associations between number of children, multi-partner fertility and risk of obesity at midlife: Findings from the 1970 British Cohort Study (BCS70).

BACKGROUND: Early parenthood, high parity, and partnership separation are associated with obesity. However, the emergence of non-marital partnerships, serial partnering and childbearing across unions, means that it is important to consider their association to obesity. This paper examined the associations between number of biological children and multi-partner fertility (MPF)-defined as having biological children with more than one partner, with obesity at midlife. METHOD: The sample consisted of 2940 fathers and 3369 mothers in the 1970 British Cohort Study. The outcome was obesity (BMI 30 or over) at age 46. Fertility and partnership histories ascertained the number of live biological children and MPF status by age 42. The associations were tested using logistic regression adjusting for confounders at birth, age 10 and age 16. Adult factors recorded at age 42 including age at first birth, smoking status, alcohol dependency, educational attainment and housing tenure were considered as mediators. RESULTS: For fathers, obesity odds did not differ according to number of children or MPF. In unadjusted models, mothers with one child (OR 1.24 95%CI 1.01-1.51), mothers who had two children with two partners (OR 1.45 95%CI 1.05-1.99), and mothers who had three or more children with two or more partners (OR 1.51 95%CI 1.18-1.93) had higher odds of obesity. In adjusted models, there remained an association between mothers with one child and odds of obesity (OR 1.30 95%CI 1.05-1.60). All other associations were attenuated when confounders were included. CONCLUSIONS: Mothers who had children with multiple partners had higher odds of obesity. However this association was completely attenuated when parental and child confounders were accounted for; suggesting that this association may be explained by confounding. Mothers who had one child only may be at increased odds of obesity, however this could be due to multiple factors including age at first birth.

Women's preconception health in England: a report card based on cross-sectional analysis of national maternity services data from 2018/2019.

OBJECTIVE: To present the first national-level report card on the state of women's preconception health in England. DESIGN: Cross-sectional population-based study. SETTING: Maternity services, England. POPULATION: All pregnant women in England with a first antenatal (booking) appointment recorded in the national Maternity Services Dataset (MSDS) from April 2018 to March 2019 (n = 652 880). METHODS: We analysed the prevalence of 32 preconception indicator measures in the overall population and across socio-demographic subgroups. Ten of these indicators were prioritised for ongoing surveillance based on modifiability, prevalence, data quality and ranking by multidisciplinary UK experts. RESULTS: The three most prevalent indicators were the proportion of the 22.9% of women who smoked 1 year before pregnancy who did not quit smoking before pregnancy (85.0%), those who had not taken folic acid supplementation before pregnancy (72.7%) and previous pregnancy loss (38.9%). Inequalities were observed by age, ethnicity and area-based deprivation level. The ten indicators prioritised were not taking folic acid supplementation before pregnancy, obesity, complex social factors, living in the most deprived areas, smoking around the time of conception, overweight, pre-existing mental health condition, pre-existing physical health condition, previous pregnancy loss and previous obstetric complication. CONCLUSIONS: Our findings suggest important opportunities to improve the state of preconception health and reduce socio-demographic inequalities for women in England. In addition to MSDS data, other national data sources that record further and possibly better quality indicators could be explored and linked to build a comprehensive surveillance infrastructure.

Role of foetal kidney size on kidney function in childhood: the born in bradford cohort renal study.

BACKGROUND: Foetal and early childhood development contributes to the risk of adult non-communicable diseases such as hypertension and cardiovascular disease. We aimed to investigate whether kidney size at birth is associated with markers of kidney function at 7-11 years. METHODS: Foetal kidney dimensions were measured using ultrasound scans at 34 weeks gestation and used to derive kidney volume (cm3) in 1802 participants in the Born in Bradford (BiB) birth cohort. Blood and urine samples were taken from those who participated in the BiB follow-up at 7-11 years (n = 630) and analysed for serum creatinine, cystatin C, urea, and urinary albumin to creatinine ratio (ACR), protein to creatinine ratio (PCR) and retinol binding protein (RBP). Estimated glomerular filtration rate (eGFR) was calculated using Schwartz creatinine only and combined with cystatin C, and cystatin C only Zappitelli and Filler equations. Linear regression was used to examine the association between foetal kidney volume and eGFR, ACR, PCR and blood pressure, unadjusted and adjusted for confounders. RESULTS: Kidney volume was positively associated in adjusted models with eGFR calculated using Schwartz combined (0.64 ml/min diff per unit increase in volume, 95% CI 0.25 to 1.02), Zappitelli (0.79, 95% CI 0.38 to 1.20) and Filler (2.84, 95% CI 1.40 to 4.28). There was an association with the presence of albuminuria but not with its level, or with other urinary markers or with blood pressure. CONCLUSION: Foetal kidney volume was associated with small increases in eGFR in mid-childhood. Longitudinal follow-up to investigate the relationship between kidney volume and markers of kidney function as children go through puberty is required.

Trajectory of long covid symptoms after covid-19 vaccination: community based cohort study.

OBJECTIVE: To estimate associations between covid-19 vaccination and long covid symptoms in adults with SARS-CoV-2 infection before vaccination. DESIGN: Observational cohort study. SETTING: Community dwelling population, UK. PARTICIPANTS: 28 356 participants in the Office for National Statistics COVID-19 Infection Survey aged 18-69 years who received at least one dose of an adenovirus vector or mRNA covid-19 vaccine after testing positive for SARS-CoV-2 infection. MAIN OUTCOME MEASURE: Presence of long covid symptoms at least 12 weeks after infection over the follow-up period 3 February to 5 September 2021. RESULTS: Mean age of participants was 46 years, 55.6% (n=15 760) were women, and 88.7% (n=25 141) were of white ethnicity. Median follow-up was 141 days from first vaccination (among all participants) and 67 days from second vaccination (83.8% of participants). 6729 participants (23.7%) reported long covid symptoms of any severity at least once during follow-up. A first vaccine dose was associated with an initial 12.8% decrease (95% confidence interval -18.6% to -6.6%, P<0.001) in the odds of long covid, with subsequent data compatible with both increases and decreases in the trajectory (0.3% per week, 95% confidence interval -0.6% to 1.2% per week, P=0.51). A second dose was associated with an initial 8.8% decrease (95% confidence interval -14.1% to -3.1%, P=0.003) in the odds of long covid, with a subsequent decrease by 0.8% per week (-1.2% to -0.4% per week, P<0.001). Heterogeneity was not found in associations between vaccination and long covid by sociodemographic characteristics, health status, hospital admission with acute covid-19, vaccine type (adenovirus vector or mRNA), or duration from SARS-CoV-2 infection to vaccination. CONCLUSIONS: The likelihood of long covid symptoms was observed to decrease after covid-19 vaccination and evidence suggested sustained improvement after a second dose, at least over the median follow-up of 67 days. Vaccination may contribute to a reduction in the population health burden of long covid, although longer follow-up is needed.

Ethnic differences in kidney function in childhood: the Born in Bradford Cohort Renal Study.

Background: Endstage kidney failure rates are higher in South Asians than in White Europeans. Low birth weight is associated with adult chronic kidney disease and is more common in South Asians. Foetal kidney size was smaller in South Asians in the Born in Bradford (BiB) birth cohort. As part of BiB follow up, we aimed to investigate if there were ethnic differences in kidney function and blood pressure in early childhood and whether this was different by foetal kidney size. Methods: Serum creatinine, cystatin C, urea, and urinary albumin to creatinine ratio (ACR), protein to creatinine ratio (PCR) and retinol binding protein (RBP) were analysed in blood and urine samples from those who participated in the BiB follow-up at 7-11 years. Ethnicity was categorised by parental self-report as White European and South Asian. Estimated glomerular filtration rate (eGFR) was calculated using Schwartz, and cystatin C Zappitelli and Filler equations. Linear regression was used to examine the association between ethnicity and eGFR, PCR and blood pressure. Results: 1591 children provided blood (n=1403) or urine (n=625) samples. Mean eGFR was 92 ml/min/1.73m 2 (standard deviation (SD) 9) using Schwartz (n=1156) and 94 (SD 11) using Zappitelli (n=1257). CKD prevalence was rare (1 with eGFR <60 ml/min/1.73m 2, 14 (2.4%) had raised ACR (>2.5 mg/mmol in boys/3.5 mg/mmol in girls). Diastolic blood pressure was higher in South Asian children (difference 2.04 mmHg, 95% CI 0.99 to 3.10) but was not significant in adjusted analysis. There was no evidence of association in adjusted models between ethnicity and any eGFR or urinary measure at this age. Conclusions: There was no evidence of significant ethnic differences in kidney function at pre-pubertal age despite differences in kidney volume at birth. Longitudinal follow-up is required to track ethnic patterns in kidney function and blood pressure as children develop through puberty.

Characterising and monitoring preconception health in England: a review of national population-level indicators and core data sources.

Initiatives to optimise preconception health are emerging following growing recognition that this may improve the health and well-being of women and men of reproductive age and optimise health in their children. To inform and evaluate such initiatives, guidance is required on indicators that describe and monitor population-level preconception health. We searched relevant databases and websites (March 2021) to identify national and international preconception guidelines, recommendations and policy reports. These were reviewed to identify preconception indicators. Indicators were aligned with a measure describing the prevalence of the indicator as recorded in national population-based data sources in England. From 22 documents reviewed, we identified 66 indicators across 12 domains. Domains included wider (social/economic) determinants of health; health care; reproductive health and family planning; health behaviours; environmental exposures; cervical screening; immunisation and infections; mental health, physical health; medication and genetic risk. Sixty-five of the 66 indicators were reported in at least one national routine health data set, survey or cohort study. A measure of preconception health assessment and care was not identified in any current national data source. Perspectives from three (healthcare) professionals described how indicator assessment and monitoring may influence patient care and inform awareness campaign development. This review forms the foundation for developing a national surveillance system for preconception health in England. The identified indicators can be assessed using national data sources to determine the population's preconception needs, improve patient care, inform and evaluate new campaigns and interventions and enhance accountability from responsible agencies to improve preconception health.

Maternal smoking behaviour across the first two pregnancies and small for gestational age birth: Analysis of the SLOPE (Studying Lifecourse Obesity PrEdictors) population-based cohort in the South of England.

Maternal smoking is established to cause adverse birth outcomes, but evidence considering maternal smoking change across successive pregnancies is sparse. We examined the association between self-reported maternal smoking during and between the first two pregnancies with the odds of small for gestational age (SGA) birth (<10th percentile) in the second infant. Records for the first two pregnancies for 16791 women within the SLOPE (Studying Lifecourse Obesity PrEdictors) study were analysed. This is a population-based cohort of prospectively collected anonymised antenatal and birth healthcare data (2003-2018) in Hampshire, UK. Logistic regression was used to relate maternal smoking change to the odds of SGA birth in the second infant. In the full sample, compared to never smokers, mothers smoking at the start of the first pregnancy had higher odds of SGA birth in the second pregnancy even where they stopped smoking before the first antenatal appointment for the second pregnancy (adjusted odds ratio (aOR) 1.50 [95% confidence interval 1.10, 2.03]). If a mother was not a smoker at the first antenatal appointment for either her first or her second pregnancy, but smoked later in her first pregnancy or between pregnancies, there was no evidence of increased risk of SGA birth in the second pregnancy compared to never smokers. A mother who smoked ten or more cigarettes a day at the start of both of her first two pregnancies had the highest odds of SGA birth (3.54 [2.55, 4.92]). Women who were not smoking at the start of the first pregnancy but who subsequently resumed/began smoking and smoked at the start of their second pregnancy, also had higher odds (2.11 [1.51, 2.95]) than never smokers. Smoking in the first pregnancy was associated with SGA birth in the second pregnancy, even if the mother quit by the confirmation of her second pregnancy.

Maternal iodine status in a multi-ethnic UK birth cohort: Associations with child cognitive and educational development.

BACKGROUND: Maternal iodine requirements increase during pregnancy to supply thyroid hormones critical for fetal neurodevelopment. Iodine insufficiency may result in poorer cognitive or child educational outcomes but current evidence is sparse and inconsistent. OBJECTIVES: To quantify the association between maternal iodine status and child educational outcomes. METHODS: Urinary iodine concentrations (UIC) and iodine/creatinine ratios (I:Cr) were measured in 6971 mothers at 26-28 weeks' gestation participating in the Born in Bradford cohort. Maternal iodine status was examined in relation to child school achievement (early years foundation stage (EYFS), phonics, and Key Stage 1 (KS1)), other learning outcomes, social and behavioural difficulties, and sensorimotor control in 5745 children aged 4-7 years. RESULTS: Median (interquartile range) UIC was 76 µg/L (46, 120), and I:Cr was 83 µg/g (59, 121). Overall, there was no strong or consistent evidence to support associations between UIC or I:Cr and neurodevelopmental outcomes. For instance, predicted EYFS and phonics scores (primary outcomes) at the 25th vs 75th I:Cr percentiles (99% confidence intervals) were similar, with no evidence of associations: EYFS scores were 32 (99% CI 31, 33) and 33 (99% CI 32, 34), and phonics scores were 34 (99% CI 33, 35) and 35 (99% CI 34, 36), respectively. CONCLUSIONS: In the largest single study of its kind, there was little evidence of detrimental neurodevelopmental outcomes in children born to pregnant women with iodine insufficiency as defined by World Health Organization-outlined thresholds. Alternative functional biomarkers for iodine status in pregnancy and focused assessment of other health outcomes may provide additional insight.

Maternal iodine status, intrauterine growth, birth outcomes and congenital anomalies in a UK birth cohort.

BACKGROUND: Severe iodine insufficiency in pregnancy has significant consequences, but there is inadequate evidence to indicate what constitutes mild or moderate insufficiency, in terms of observed detrimental effects on pregnancy or birth outcomes. A limited number of studies have examined iodine status and birth outcomes, finding inconsistent evidence for specific outcomes. METHODS: Maternal iodine status was estimated from spot urine samples collected at 26-28 weeks' gestation from 6971 mothers in the Born in Bradford birth cohort. Associations with outcomes were examined for both urinary iodine concentration (UIC) and iodine-to-creatinine ratio (I:Cr). Outcomes assessed included customised birthweight (primary outcome), birthweight, small for gestational age (SGA), low birthweight, head circumference and APGAR score. RESULTS: There was a small positive association between I:Cr and birthweight in adjusted analyses. For a typical participant, the predicted birthweight centile at the 25th percentile of I:Cr (59 µg/g) was 2.7 percentage points lower than that at the 75th percentile of I:Cr (121 µg/g) (99% confidence interval (CI) 0.8 to 4.6), birthweight was predicted to be 41 g lower (99% CI 13 to 69) and the predicted probability of SGA was 1.9 percentage points higher (99% CI 0.0 to 3.7). There was no evidence of associations using UIC or other birth outcomes, including stillbirth, preterm birth, ultrasound growth measures or congenital anomalies. CONCLUSION: Lower maternal iodine status was associated with lower birthweight and greater probability of SGA. Whilst small, the effect size for lower iodine on birthweight is comparable to environmental tobacco smoke exposure. Iodine insufficiency is avoidable, and strategies to avoid deficiency in women of reproductive age should be considered. TRIAL REGISTRATION: ClinicalTrials.gov NCT03552341. Registered on June 11, 2018.

Predicting the risk of childhood overweight and obesity at 4-5 years using population-level pregnancy and early-life healthcare data.

BACKGROUND: Nearly a third of children in the UK are overweight, with the prevalence in the most deprived areas more than twice that in the least deprived. The aim was to develop a risk identification model for childhood overweight/obesity applied during pregnancy and early life using routinely collected population-level healthcare data. METHODS: A population-based anonymised linked cohort of maternal antenatal records (January 2003 to September 2013) and birth/early-life data for their children with linked body mass index (BMI) measurements at 4-5 years (n = 29,060 children) in Hampshire, UK was used. Childhood age- and sex-adjusted BMI at 4-5 years, measured between September 2007 and November 2018, using a clinical cut-off of ≥ 91st centile for overweight/obesity. Logistic regression models together with multivariable fractional polynomials were used to select model predictors and to identify transformations of continuous predictors that best predict the outcome. RESULTS: Fifteen percent of children had a BMI ≥ 91st centile. Models were developed in stages, incorporating data collected at first antenatal booking appointment, later pregnancy/birth, and early-life predictors (1 and 2 years). The area under the curve (AUC) was lowest (0.64) for the model only incorporating maternal predictors from early pregnancy and highest for the model incorporating all factors up to weight at 2 years for predicting outcome at 4-5 years (0.83). The models were well calibrated. The prediction models identify 21% (at booking) to 24% (at ~ 2 years) of children as being at high risk of overweight or obese by the age of 4-5 years (as defined by a ≥ 20% risk score). Early pregnancy predictors included maternal BMI, smoking status, maternal age, and ethnicity. Early-life predictors included birthweight, baby's sex, and weight at 1 or 2 years of age. CONCLUSIONS: Although predictive ability was lower for the early pregnancy models, maternal predictors remained consistent across the models; thus, high-risk groups could be identified at an early stage with more precise estimation as the child grows. A tool based on these models can be used to quantify clustering of risk for childhood obesity as early as the first trimester of pregnancy, and can strengthen the long-term preventive element of antenatal and early years care.

Change in modifiable maternal characteristics and behaviours between consecutive pregnancies and offspring adiposity: A systematic review.

Causal evidence links modifiable maternal exposures during the periconceptional period with offspring obesity. The interconception period may be an important time to intervene. We systematically identified studies examining change in modifiable maternal exposures between pregnancies and offspring adiposity. We searched for longitudinal studies published between 1990 and 2019, which included measurements taken on at least two occasions in the period from 1 year prior to the conception of the first birth to the time of the second birth, and which included a measure of adiposity in second, or higher order, siblings. Age, ethnicity and genetics were not considered modifiable; all other factors including length of the interpregnancy interval were. Eleven studies satisfied the inclusion criteria. Higher interpregnancy weight gain or loss, maternal smoking inception, mothers smoking in their first pregnancy and quitting, increasing the number of cigarettes smoked and longer interpregnancy intervals were positively associated with adiposity in second or higher order children. Vaginal birth after caesarean delivery was protective. Further research is needed to ascertain whether the risk of adiposity is fixed based on first pregnancy exposures or if interpregnancy change alters the risk for a subsequent child. This can inform the type and effectiveness of interventions for mothers prior to a subsequent pregnancy.

Are environmental area characteristics at birth associated with overweight and obesity in school-aged children? Findings from the SLOPE (Studying Lifecourse Obesity PrEdictors) population-based cohort in the south of England.

BACKGROUND: Geographical inequalities in overweight and obesity prevalence among children are well established in cross-sectional research. We aimed to examine how environmental area characteristics at birth are related to these outcomes in childhood. METHODS: Anonymised antenatal and birth data recorded by University Hospital Southampton linked to school-measured weight and height data for children within Southampton, UK, were utilised (14,084 children at ages 4-5 and 5637 at ages 10-11). Children's home address at birth was analysed at the Lower and Middle layer Super Output Area (LSOA/MSOA) levels (areas with average populations of 1500 and 7000, respectively). Area-level indices (walkability, relative density of unhealthy food outlets, spaces for social interaction), natural greenspace coverage, supermarket density and measures of air pollution (PM2.5, PM10 and NOx) were constructed using ArcGIS Network Analyst. Overweight/obesity was defined as a body mass index (BMI; kg/m2) greater than the 85th centile for sex and age. Population-average generalised estimating equations estimated the risk of being overweight/obese for children at both time points. Confounders included maternal BMI and smoking in early pregnancy, education, ethnicity and parity. We also examined associations for a subgroup of children who moved residence between birth and outcome measurement. RESULTS: There were mixed results between area characteristics at birth and overweight/obesity at later ages. MSOA relative density of unhealthy food outlets and PM10 were positively associated with overweight/obesity, but not among children who moved. LSOA greenspace coverage was negatively associated with the risk of being overweight/obese at ages 10-11 in all children (relative risk ratio 0.997, 95% confidence interval 0.995-0.999, p = 0.02) and among children who moved. CONCLUSIONS: Local access to natural greenspaces at the time of birth was inversely associated with becoming overweight or obese by age 10-11, regardless of migration. Increased access/protection of greenspace may have a role in the early prevention of childhood obesity.

Are socioeconomic inequalities in the incidence of small-for-gestational-age birth narrowing? Findings from a population-based cohort in the South of England.

OBJECTIVES: To investigate socioeconomic inequalities, using maternal educational attainment, maternal and partner employment status, and lone motherhood indicators, in the risk of small-for-gestational-age (SGA) births, their time trend, potential mediation by maternal smoking and body mass index, and effect modification by parity. DESIGN: Population-based birth cohort using routine antenatal healthcare data. SETTING: Babies born at University Hospital Southampton, UK, between 2004 and 2016. PARTICIPANTS: 65 909 singleton live births born to mothers aged ≥18 years between 24-week and 42-week gestation. MAIN OUTCOME MEASURES: SGA (birth weight <10th percentile for others born at the same number of completed weeks compared with 2013/2014 within England and Wales). RESULTS: Babies born to mothers educated up to secondary school level (adjusted OR (aOR) 1.32, 99% CI 1.19 to 1.47), who were unemployed (aOR 1.27, 99% CI 1.16 to 1.38) or with unemployed partners (aOR 1.27, 99% CI 1.13 to 1.43), were at greater risk of being SGA. There was no statistically significant change in the magnitude of this risk difference by these indicators over time between 2004 and 2016, as estimated by linear interactions with year of birth. Babies born to lone mothers were not at higher risk compared with partnered mothers after adjusting for maternal smoking (aOR 1.05, 99% CI 0.93 to 1.20). The inverse association between maternal educational attainment and SGA risk appeared greater in multiparous (aOR 1.40, 99% CI 1.10 to 1.77) compared with primiparous women (aOR 1.28, 99% CI 1.12 to 1.47), and the reverse was true for maternal and partner's unemployment where the association was stronger in primiparous women. CONCLUSIONS: Socioeconomic inequalities in SGA risk by educational attainment and employment status are not narrowing over time, with differences in association strength by parity. The greater SGA risk in lone mothers was potentially explained by maternal smoking. Preventive interventions should target socially disadvantaged women, including preconception and postpartum smoking cessation to reduce SGA risk.

Maternal Fatty Fish Intake Prior to and during Pregnancy and Risks of Adverse Birth Outcomes: Findings from a British Cohort.

Fish is an important source of the essential fatty acids contributing to foetal growth and development, but the evidence linking maternal fatty fish consumption with birth outcomes is inconsistent. In the UK, pregnant women are recommended to consume no more than two 140 g portions of fatty fish per week. This study aimed to investigate the association between fatty fish consumption before and during pregnancy with preterm birth and size at birth in a prospective birth cohort. Dietary intake data were acquired from a cohort of 1208 pregnant women in Leeds, UK (CARE Study) to assess preconception and trimester-specific fatty fish consumption using questionnaires. Multiple 24-h recalls during pregnancy were used to estimate an average fatty fish portion size. Intake was classified as ≤2, >2 portions/week and no fish categories. Following the exclusion of women taking cod liver oil and/or omega-3 supplements, the associations between fatty fish intake with size at birth and preterm delivery (<37 weeks gestation) were examined in multivariable regression models adjusting for confounders including salivary cotinine as a biomarker of smoking status.. The proportion of women reporting any fatty fish intake decreased throughout pregnancy, with the lowest proportion observed in trimester 3 (43%). Mean intakes amongst consumers were considerably lower than that recommended, with the lowest intake amongst consumers observed in the 1st trimester (106 g/week, 95% CI: 99, 113). This was partly due to small portion sizes when consumed, with the mean portion size of fatty fish being 101 g. After adjusting for confounders, no association was observed between fatty fish intake before or during pregnancy with size at birth and preterm delivery.

Relationships between Maternal Obesity and Maternal and Neonatal Iron Status.

: Obesity in pregnancy may negatively influence maternal and infant iron status. The aim of this study was to examine the association of obesity with inflammatory and iron status in both mother and infant in two prospective studies in pregnancy: UPBEAT and SCOPE. Maternal blood samples from obese (n = 245, BMI ≥ 30 kg/m²) and normal weight (n = 245, BMI < 25 kg/m²) age matched pregnant women collected at approximately 15 weeks' gestation, and umbilical cord blood samples collected at delivery, were analysed for a range of inflammatory and iron status biomarkers. Concentrations of C- reactive protein and Interleukin-6 in obese women compared to normal weight women were indicative of an inflammatory response. Soluble transferrin receptor (sTfR) concentration [18.37 nmol/L (SD 5.65) vs 13.15 nmol/L (SD 2.33)] and the ratio of sTfR and serum ferritin [1.03 (SD 0.56) vs 0.69 (SD 0.23)] were significantly higher in obese women compared to normal weight women (P < 0.001). Women from ethnic minority groups (n = 64) had higher sTfR concentration compared with white women. There was no difference in maternal hepcidin between obese and normal weight women. Iron status determined by cord ferritin was not statistically different in neonates born to obese women compared with neonates born to normal weight women when adjusted for potential confounding variables. Obesity is negatively associated with markers of maternal iron status, with ethnic minority women having poorer iron statuses than white women.

Lifestyle interventions for the treatment of women with gestational diabetes.

BACKGROUND: Gestational diabetes (GDM) is glucose intolerance, first recognised in pregnancy and usually resolving after birth. GDM is associated with both short- and long-term adverse effects for the mother and her infant. Lifestyle interventions are the primary therapeutic strategy for many women with GDM. OBJECTIVES: To evaluate the effects of combined lifestyle interventions with or without pharmacotherapy in treating women with gestational diabetes. SEARCH METHODS: We searched the Pregnancy and Childbirth Group's Trials Register (14 May 2016), ClinicalTrials.gov, WHO International Clinical Trials Registry Platform (ICTRP) (14th May 2016) and reference lists of retrieved studies. SELECTION CRITERIA: We included only randomised controlled trials comparing a lifestyle intervention with usual care or another intervention for the treatment of pregnant women with GDM. Quasi-randomised trials were excluded. Cross-over trials were not eligible for inclusion. Women with pre-existing type 1 or type 2 diabetes were excluded. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures expected by the Cochrane Collaboration. All selection of studies, data extraction was conducted independently by two review authors. MAIN RESULTS: Fifteen trials (in 45 reports) are included in this review (4501 women, 3768 infants). None of the trials were funded by a conditional grant from a pharmaceutical company. The lifestyle interventions included a wide variety of components such as education, diet, exercise and self-monitoring of blood glucose. The control group included usual antenatal care or diet alone. Using GRADE methodology, the quality of the evidence ranged from high to very low quality. The main reasons for downgrading evidence were inconsistency and risk of bias. We summarised the following data from the important outcomes of this review. Lifestyle intervention versus control groupFor the mother:There was no clear evidence of a difference between lifestyle intervention and control groups for the risk of hypertensive disorders of pregnancy (pre-eclampsia) (average risk ratio (RR) 0.70; 95% confidence interval (CI) 0.40 to 1.22; four trials, 2796 women; I2 = 79%, Tau2 = 0.23; low-quality evidence); caesarean section (average RR 0.90; 95% CI 0.78 to 1.05; 10 trials, 3545 women; I2 = 48%, Tau2 = 0.02; low-quality evidence); development of type 2 diabetes (up to a maximum of 10 years follow-up) (RR 0.98, 95% CI 0.54 to 1.76; two trials, 486 women; I2 = 16%; low-quality evidence); perineal trauma/tearing (RR 1.04, 95% CI 0.93 to 1.18; one trial, n = 1000 women; moderate-quality evidence) or induction of labour (average RR 1.20, 95% CI 0.99 to 1.46; four trials, n = 2699 women; I2 = 37%; high-quality evidence).More women in the lifestyle intervention group had met postpartum weight goals one year after birth than in the control group (RR 1.75, 95% CI 1.05 to 2.90; 156 women; one trial, low-quality evidence). Lifestyle interventions were associated with a decrease in the risk of postnatal depression compared with the control group (RR 0.49, 95% CI 0.31 to 0.78; one trial, n = 573 women; low-quality evidence).For the infant/child/adult:Lifestyle interventions were associated with a reduction in the risk of being born large-for-gestational age (LGA) (RR 0.60, 95% CI 0.50 to 0.71; six trials, 2994 infants; I2 = 4%; moderate-quality evidence). Birthweight and the incidence of macrosomia were lower in the lifestyle intervention group.Exposure to the lifestyle intervention was associated with decreased neonatal fat mass compared with the control group (mean difference (MD) -37.30 g, 95% CI -63.97 to -10.63; one trial, 958 infants; low-quality evidence). In childhood, there was no clear evidence of a difference between groups for body mass index (BMI) ≥ 85th percentile (RR 0.91, 95% CI 0.75 to 1.11; three trials, 767 children; I2 = 4%; moderate-quality evidence).There was no clear evidence of a difference between lifestyle intervention and control groups for the risk of perinatal death (RR 0.09, 95% CI 0.01 to 1.70; two trials, 1988 infants; low-quality evidence). Of 1988 infants, only five events were reported in total in the control group and there were no events in the lifestyle group. There was no clear evidence of a difference between lifestyle intervention and control groups for a composite of serious infant outcome/s (average RR 0.57, 95% CI 0.21 to 1.55; two trials, 1930 infants; I2 = 82%, Tau2 = 0.44; very low-quality evidence) or neonatal hypoglycaemia (average RR 0.99, 95% CI 0.65 to 1.52; six trials, 3000 infants; I2 = 48%, Tau2 = 0.12; moderate-quality evidence). Diabetes and adiposity in adulthood and neurosensory disability in later childhoodwere not prespecified or reported as outcomes for any of the trials included in this review. AUTHORS' CONCLUSIONS: Lifestyle interventions are the primary therapeutic strategy for women with GDM. Women receiving lifestyle interventions were less likely to have postnatal depression and were more likely to achieve postpartum weight goals. Exposure to lifestyle interventions was associated with a decreased risk of the baby being born LGA and decreased neonatal adiposity. Long-term maternal and childhood/adulthood outcomes were poorly reported.The value of lifestyle interventions in low-and middle-income countries or for different ethnicities remains unclear. The longer-term benefits or harms of lifestyle interventions remains unclear due to limited reporting.The contribution of individual components of lifestyle interventions could not be assessed. Ten per cent of participants also received some form of pharmacological therapy. Lifestyle interventions are useful as the primary therapeutic strategy and most commonly include healthy eating, physical activity and self-monitoring of blood glucose concentrations.Future research could focus on which specific interventions are most useful (as the sole intervention without pharmacological treatment), which health professionals should give them and the optimal format for providing the information. Evaluation of long-term outcomes for the mother and her child should be a priority when planning future trials. There has been no in-depth exploration of the costs 'saved' from reduction in risk of LGA/macrosomia and potential longer-term risks for the infants.

Maternal iron status in early pregnancy and birth outcomes: insights from the Baby's Vascular health and Iron in Pregnancy study.

Fe deficiency anaemia during early pregnancy has been linked with low birth weight and preterm birth. However, this evidence comes mostly from studies measuring Hb levels rather than specific measures of Fe deficiency. The present study aimed to examine the association between maternal Fe status during the first trimester of pregnancy, as assessed by serum ferritin, transferrin receptor and their ratio, with size at birth and preterm birth. In the Baby VIP (Baby's Vascular health and Iron in Pregnancy) study, we recruited 362 infants and their mothers after delivery in Leeds, UK. Biomarkers were measured in maternal serum samples previously obtained in the first trimester of pregnancy. The cohort included sixty-four (18 %) small for gestational age (SGA) babies. Thirty-three babies were born preterm (9 %; between 34 and 37 weeks). First trimester maternal Fe depletion was associated with a higher risk of SGA (adjusted OR 2·2, 95 % CI 1·1, 4·1). This relationship was attenuated when including early pregnancy Hb in the model, suggesting it as a mediator (adjusted OR 1·6, 95 % CI 0·8, 3·2). For every 10 g/l increase in maternal Hb level in the first half of pregnancy the risk of SGA was reduced by 30 % (adjusted 95 % CI 0, 40 %); levels below 110 g/l were associated with a 3-fold increase in the risk of SGA (95 % CI 1·0, 9·0). There was no evidence of association between maternal Fe depletion and preterm birth (adjusted OR 1·5, 95 % 0·6, 3·8). The present study shows that depleted Fe stores in early pregnancy are associated with higher risk of SGA.