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The reported associations between birth weight and childhood cardiovascular disease (CVD) risk factors have been inconsistent. In this study, we investigated the relationship between birth weight and CVD risk factors at 11 years of age. This study used longitudinally linked data from three cross-sectional datasets (N = 22,136) in West Virginia; analysis was restricted to children born full-term (N = 19,583). The outcome variables included resting blood pressure [systolic blood pressure (SBP), diastolic blood pressure (DBP)] and lipid profile [total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL, and triglycerides (TG)]. Multiple regression analyses were performed, adjusting for child’s body mass index (BMI), sociodemographics, and lifestyle characteristics. Unadjusted analyses showed a statistically significant association between birth weight and SBP, DBP, HDL, and TG. When adjusted for the child’s BMI, the association between birth weight and HDL [b = 0.14 (95% CI: 0.11, 0.18) mg/dl per 1000 g increase] and between birth weight and TG [b = –0.007 (–0.008, –0.005) mg/dl per 1000 g increase] remained statistically significant. In the fully adjusted model, low birth weight was associated with higher LDL, non-HDL, and TGs, and lower HDL levels. The child’s current BMI at 11 years of age partially (for HDL, non-HDL, and TG) and fully mediated (for SBP and DBP) the relationship between birth weight and select CVD risk factors. While effects were modest, these risk factors may persist and amplify with age, leading to potentially unfavorable consequences in later adulthood.
Both inadequate and excessive gestational weight gain (GWG) have been shown to increase the risk of adverse pregnancy outcomes, but the risk profiles of GWG rate are unclear. We aimed to examine the associations between GWG rate in the second/third trimester and a spectrum of pregnancy outcomes. This study consisted of 14 219 Chinese rural nulliparous women who participated in a randomised controlled trial of prenatal micronutrient supplementation during 2006–2009. The outcomes included stillbirth, neonatal and infant death, preterm birth, macrosomia, low birth weight (LBW) and large and small for gestational age (LGA and SGA, respectively). GWG rate was divided into quintiles within each BMI category. Compared with women in the middle quintile, those in the lowest quintile had higher risks of neonatal death (adjusted OR 2·27; 95 % CI 1·03, 5·02), infant death (adjusted OR 1·85; 95 % CI 1·02, 3·37) and early preterm birth (adjusted OR 2·33; 95 % CI 1·13, 4·77), while those in the highest quintile had higher risks of overall preterm birth (adjusted OR 1·28; 95 % CI 1·04, 1·59), late preterm birth (adjusted OR 1·25; 95 % CI 1·00, 1·56), LBW (adjusted OR 1·48; 95 % CI 1·02, 2·15), macrosomia (adjusted OR 1·89; 95 % CI 1·46, 2·45) and LGA (adjusted OR 1·56; 95 % CI 1·31, 1·85). In conclusion, very low and very high GWG rates in the second/third trimester appear to be associated with adverse pregnancy outcomes in Chinese nulliparous women, indicating that an appropriate GWG rate during pregnancy is necessary for neonatal health.
A mother's nutritional choices while pregnant may have a great influence on her baby's development in the womb and during infancy. There is evidence that what a mother eats during pregnancy interacts with her genes to affect her child's susceptibility to poor health outcomes including childhood obesity, pre-diabetes, allergy and asthma. Furthermore, after what an infant eats can change his or her intestinal bacteria, which can further influence the development of these poor outcomes. In the present paper, we review the importance of birth cohorts, the formation and early findings from a multi-ethnic birth cohort alliance in Canada and summarise our future research directions for this birth cohort alliance. We summarise a method for harmonising collection and analysis of self-reported dietary data across multiple cohorts and provide examples of how this birth cohort alliance has contributed to our understanding of gestational diabetes risk; ethnic and diet-influences differences in the healthy infant microbiome; and the interplay between diet, ethnicity and birth weight. Ongoing work in this birth cohort alliance will focus on the use of metabolomic profiling to measure dietary intake, discovery of unique diet–gene and diet–epigenome interactions, and qualitative interviews with families of children at risk of metabolic syndrome. Our findings to-date and future areas of research will advance the evidence base that informs dietary guidelines in pregnancy, infancy and childhood, and will be relevant to diverse and high-risk populations of Canada and other high-income countries.
The aim of the study was to investigate how maternal dietary patterns and maternal/fetal cytokines are associated with birth weight and whether cytokines mediate the association. A total of 469 pregnant women and their children were recruited for this prospective study. Dietary patterns in pregnancy were identified using factor analysis of data from three consecutive 24 h dietary recalls. Maternal and umbilical blood serum cytokines (adiponectin (APN), IL-6 and interferon-γ) were measured via ELISA. Path analysis was used to explore the relationships between maternal diet, cytokines and birth weight. Four dietary patterns were identified: a mainly fruit, dairy products and poultry diet (FDP); a mainly vegetables, beans and pork diet (VBP); a mainly fish, shrimp and soup diet (FS) and a mainly tuber and egg diet (TE). Path analysis showed the order of effects of dietary patterns on birth weight was FS>FDP>TE>VBP (β=0·130, 0·109, –0·094 and 0·046, respectively). Only the TE pattern’s effect was negative. Maternal and fetal APN were positively associated with birth weight (β=0·045 and 0·226, respectively), and they mediated the association between the TE pattern and birth weight (indirect effect was 5·3 %). Maternal IL-6 was negatively associated with birth weight (β=–0·067) and mediated the association between maternal FDP and VBP patterns and birth weight (indirect effects were 10·1 and 100·0 %, respectively). All variables in the path explained 33·6 % of variation. These results suggested that maternal dietary patterns in pregnancy are associated with birth weight and mediated directly and indirectly through some maternal/fetal serum cytokines.
Maternal one-carbon metabolism during pregnancy is crucial for fetal development and programming by DNA methylation. However, evidence on one-carbon biomarkers other than folate is lacking. We, therefore, investigated whether maternal plasma methyl donors, that is, choline, betaine and methionine, are associated with birth outcomes. Blood samples were obtained from 115 women during gestation (median 26·3 weeks, 90 % range 22·7–33·0 weeks). Plasma choline, betaine, methionine and dimethylglycine were measured using HPLC-tandem MS. Multivariate linear and logistic regression models were used to estimate the association between plasma biomarkers and birth weight, birth length, the risk of small-for-gestational-age and large-for-gestational-age (LGA). Higher level of maternal betaine was associated with lower birth weight (–130·3 (95 % CI –244·8, –15·9) per 1 sd increment for log-transformed betaine). Higher maternal methionine was associated with lower risk of LGA, and adjusted OR, with 95 % CI for 1 sd increase in methionine concentration was 0·44 (95 % CI 0·21, 0·89). Stratified analyses according to infant sex or maternal plasma homocysteine status showed that reduction in birth weight in relation to maternal betaine was only limited to male infants or to who had higher maternal homocysteine status (≥5·1 µmol/l). Higher maternal betaine status was associated with reduced birth weight. Maternal methionine was inversely associated with LGA risk. These findings are needed to be replicated in future larger studies.
To analyse the relationship of altered birth weight with metabolic and cardiovascular outcomes among adolescents, as well as to identify if sports participation is able to attenuate or even eliminate the impact of birth weight on health outcomes.
Cross-sectional study (Analysis of Behaviours of Children During Growth [ABCD Growth Study]). Adolescents with age ranging from 11 to 18 years old (14.7±2.1) stratified according to normal (n = 230) and altered (n = 35) birth weight composed the sample. Birth weight was self-reported by adolescent’s parents. Sports participation was assessed by face-to-face interview. Carotid intima–media thickness (CIMT) and femoral intima–media thickness (FIMT) were measured using an ultrasound device. C-reactive protein levels were used to assess the inflammatory status. Blood pressure, Z score of metabolic risk (dyslipidemia and glucose), adiposity, and insulin resistance were covariates.
In the crude model, FIMT (p value = 0.037) and C-reactive protein (p value = 0.029) were affected by altered birth weight. In the adjusted models, altered birth weight affected FIMT (p value = 0.048; small effect size of 1.7%), independently of sports participation. For C-reactive protein, previous time of engagement in sports (p value = 0.001; small effect size of 4.8%) affected C-reactive protein, independently of birth weight.
Vascular structure seems to be affected by birth weight in adolescents, while its impact on inflammation seems to be attenuated by the regular engagement in sports.
We assessed whether paternal demographic, anthropometric and clinical factors influence the risk of an infant being born large-for-gestational-age (LGA). We examined the data on 3659 fathers of term offspring (including 662 LGA infants) born to primiparous women from Screening for Pregnancy Endpoints (SCOPE). LGA was defined as birth weight >90th centile as per INTERGROWTH 21st standards, with reference group being infants ⩽90th centile. Associations between paternal factors and likelihood of an LGA infant were examined using univariable and multivariable models. Men who fathered LGA babies were 180 g heavier at birth (P<0.001) and were more likely to have been born macrosomic (P<0.001) than those whose infants were not LGA. Fathers of LGA infants were 2.1 cm taller (P<0.001), 2.8 kg heavier (P<0.001) and had similar body mass index (BMI). In multivariable models, increasing paternal birth weight and height were independently associated with greater odds of having an LGA infant, irrespective of maternal factors. One unit increase in paternal BMI was associated with 2.9% greater odds of having an LGA boy but not girl; however, this association disappeared after adjustment for maternal BMI. There were no associations between paternal demographic factors or clinical history and infant LGA. In conclusion, fathers who were heavier at birth and were taller were more likely to have an LGA infant, but maternal BMI had a dominant influence on LGA.
In Australia, there are two distinct populations, each with vastly disparate health outcomes: Aboriginal and Torres Strait Islander People and non-Aboriginal Australians. Aboriginal Australians have significantly higher rates of health and socioeconomic disadvantage, and Aboriginal babies are also more likely to be born low birth weight or growth restricted. The Developmental Origins of Health and Disease (DOHaD) hypothesis advocates that a sub-optimal intrauterine environment, often manifested as diminished foetal growth, during critical periods of foetal development has the potential to alter the risk of non-communicable disease in the offspring. A better understanding of the role of the intrauterine environment and subsequent developmental programming, in response to both transgenerational and immediate stimuli, in Aboriginal Australians remains a relatively unexplored field and may provide insights into the prevailing health disparities between Aboriginal and non-Aboriginal children. This narrative review explores the role of DOHaD in explaining the ongoing disadvantage experienced by Aboriginal People in today’s society through a detailed discussion of the literature on the association between foetal growth, as a proxy for the quality of the intrauterine environment, and outcomes in the offspring including perinatal health, early life development and childhood education. The literature largely supports this hypothesis and this review therefore has potential implications for policy makers not only in Australia but also in other countries that have minority and Indigenous populations who suffer disproportionate disadvantage such as the United States, Canada and New Zealand.
Birth weight and early growth have been associated with later blood pressure. However, not all studies consistently find a significant reduction in blood pressure with an increase in birth weight. In addition, the relative importance of birth weight and of other lifestyle and environmental factors is often overlooked and the association is rarely studied in adolescents. We investigated early life predictors, including birth weight, of adolescent blood pressure in the Gateshead Millennium Study (GMS). The GMS is a cohort of 1029 individuals born in 1999–2000 in Gateshead in Northern England. Throughout infancy and early childhood, detailed information were collected, including birth weight and measures of height and weight. Assessments of 491 returning participants at age 12 years included measures of body mass and blood pressure. Linear regression and path analysis were used to determine predictors and their relative importance on blood pressure. Birth weight was not directly associated with blood pressure at the age of 12. However, after adjustment for contemporaneous body mass index (BMI), an inverse association of standardized birth weight on systolic blood pressure was significant. The relative importance of birth weight on later systolic blood pressure was smaller than other contemporaneous body measures (height and BMI). There was no independent association of birth weight on blood pressure seen in this adolescent population. Contemporaneous body measures have an important role to play. Lifestyle factors that influence body mass or size, such as diet and physical activity, where interventions are directed at early prevention of hypertension should be targeted.
The prenatal development of cattle has influence on productive performance throughout postnatal life. The number of muscle and fat cells that the animal will have throughout its life is determined in the foetal stage and is influenced by nutrition of the pregnant cow. A systematic review and meta-analysis was performed to evaluate the effect of different energy levels (total digestible nutrient, TDN) and crude protein (CP) supplied to pregnant cows on foetal weight at 4 (FW4) and 8 months (FW8) and calf birth weight (CBW). Four studies and six trials involving 170 animals were assessed for FW4; four studies, four trials and 156 animals for FW8 and 48 studies, 125 trials and 9053 animals for CBW. High heterogeneity across studies was presented in FW4 (I2 = 94.4%), FW8 (I2 = 91.08%) and CBW (I2 = 96.9%). Dietary TDN and CP levels did not influence FW4. The FW8 was reduced by 2.24 kg when cows were fed 100% of their CP and TDN requirements (I2 = 0%), relative to those fed 70% of their requirements during the first and second trimesters. The CBW was reduced by 0.45 kg (I2 = 96.9%) when cows were fed 130% of their CP requirements relative to other dietary CP levels. When cows were fed 140% of their TDN requirements, CBW decreased by 2.71 kg (I2 = 98.3%) relative to other TDN levels. Dietary energy or CP levels fed above the requirements to pregnant cows restrict foetal development and CBW.
The Barker hypothesis states that low birth weight (BW) is associated with higher risk of adult onset diseases, including mental disorders like schizophrenia, major depressive disorder (MDD), and attention deficit hyperactivity disorder (ADHD). The main criticism of this hypothesis is that evidence for it comes from observational studies. Specifically, observational evidence does not suffice for inferring causality, because the associations might reflect the effects of confounders. Mendelian randomization (MR) — a novel method that tests causality on the basis of genetic data — creates the unprecedented opportunity to probe the causality in the association between BW and mental disorders in observation studies. We used MR and summary statistics from recent large genome-wide association studies to test whether the association between BW and MDD, schizophrenia and ADHD is causal. We employed the inverse variance weighted (IVW) method in conjunction with several other approaches that are robust to possible assumption violations. MR-Egger was used to rule out horizontal pleiotropy. IVW showed that the association between BW and MDD, schizophrenia and ADHD is not causal (all p > .05). The results of all the other MR methods were similar and highly consistent. MR-Egger provided no evidence for pleiotropic effects biasing the estimates of the effects of BW on MDD (intercept = -0.004, SE = 0.005, p = .372), schizophrenia (intercept = 0.003, SE = 0.01, p = .769), or ADHD (intercept = 0.009, SE = 0.01, p = .357). Based on the current evidence, we refute the Barker hypothesis concerning the fetal origins of adult mental disorders. The discrepancy between our results and the results from observational studies may be explained by the effects of confounders in the observational studies, or by the existence of a small causal effect not detected in our study due to weak instruments. Our power analyses suggested that the upper bound for a potential causal effect of BW on mental disorders would likely not exceed an odds ratio of 1.2.
Objectives: The aim of this study was to investigate the effects of infant and toddler head growth on intelligence scores from early childhood to adulthood in very preterm (<32 weeks gestational age; VP) and/or very low birth weight (<1500 g; VLBW) and term born individuals. Methods: 203 VP/VLBW and 198 term comparisons were studied from birth to adulthood as part of the prospective geographically defined Bavarian Longitudinal Study (BLS). Head circumference was assessed at birth; 5, 20 months; and 4 years of age. Intelligence was assessed with standardized tests in childhood (6 and 8 years: K-ABC) and at 26 years (Wechsler Adult Intelligence Scale, WAIS). Structural equation modeling (SEM) was used to model the effect of head growth on IQ. Results: On average, VP/VLBW had lower head circumference at birth (27.61 cm vs. 35.11 cm, mean difference 7.49, 95% confidence interval [7.09–7.90]) and lower adult intelligence scores (88.98 vs. 102.54, mean difference 13.56 [10.59–16.53]) than term born comparison individuals. Head circumference at birth (e.g., total effect β=.48; p<.001 for adult IQ) and head growth in childhood predicted intelligence development from age 6 to 26 years in both VP/VLBW and term born individuals (70% of variance in adult IQ explained by full model). Effects of gestation and birth weight on intelligence were fully mediated by head circumference and growth. Conclusions: This longitudinal investigation from birth to adulthood indicates head growth as a proxy of brain development and intelligence. Repeated early head circumference assessment adds valuable information when screening for long-term neurocognitive risk. (JINS, 2019, 25, 48#x2013;56)
Low birth weight has been shown to be related to increased risk of depression later in life – but the evidence is not conclusive. We examined the association of size at birth with repeatedly measured depressive symptoms in 947 individuals from the Northern Swedish Cohort, a community-based age-homogeneous cohort born in 1965, and followed with questionnaires between ages 16 and 43 (participation rate above 90% in all the surveys). Information on birth size was retrieved from archived birth records. Length of gestation was known for a subsample of 512 individuals (54%). We studied the association of birth weight and ponderal index with self-reported depressive symptoms at ages 16, 21, 30 and 43; with the life-course average of depressive symptoms score and with longitudinal trajectories of depressive symptoms retrieved by latent class growth analysis. Socioeconomic background, mental illness or alcohol problems of a parent, exposure to social adversities in adolescence and prematurity were accounted for in the analyses. We did not find any relationship between weight or ponderal index at birth and our measure of depressive symptoms between ages 16 and 43 in a series of different analyses. Adjustment for length of gestation did not alter the results. We conclude that size at birth is not associated with later-life depressive symptoms score in this cohort born in the mid-1960s in Sweden. The time and context need to be taken into consideration in future studies.
Evidence suggests that both high and low birth weight children have increased the risk for obesity and the metabolic syndrome in adulthood. Previously we have found altered feeding behaviour and food preferences in pre-school children and adults born with low birth weight. In this study, we investigated if birth weight was associated with different intake of fat, carbohydrate and/or protein at 6–12 years of age. This is a cross-sectional study where 255 guardians answered online and telephone questions including anthropometrics and demographic data, parental family food rules (food control, encouragement and restriction) and a complete web-based FFQ for their children (130 boys and 125 girls). Baseline demographic and parental food rules characteristics did not differ accordingly to sex. Linear regression models were conducted separately for each sex, adjusted for income, age and maternal age. There were no differences in total energy intake, but energy density (ED, energy content/g) was negatively associated with birth weight in boys. Macronutrient analysis showed that ED intake was from a greater intake of fat. Birth weight was not a significant predictor of protein and carbohydrate intake in boys. In girls, we saw a positive correlation between fat intake and cholesterol intake v. birth weight, but no association with ED intake (results did not remain after adjustment). The study shows that low birth weight is associated with altered fat intake in childhood in a sex-specific manner. It is likely that biological factors such as fetal programming of homoeostatic and/or hedonic pathways influencing food preferences are involved in this process.
Recent findings highlight that there are prenatal risks for affective disorders that are mediated by glucocorticoid mechanisms, and may be specific to females. There is also evidence of sex differences in prenatal programming mechanisms and developmental psychopathology, whereby effects are in opposite directions in males and females. As birth weight is a risk for affective disorders, we sought to investigate whether maternal prenatal cortisol may have sex-specific effects on fetal growth. Participants were 241 mothers selected from the Wirral Child Health and Development Study (WCHADS) cohort (n=1233) using a psychosocial risk stratifier, so that responses could be weighted back to the general population. Mothers provided saliva samples, which were assayed for cortisol, at home over 2 days at 32 weeks gestation (on waking, 30-min post-waking and during the evening). Measures of infant birth weight (corrected for gestational age) were taken from hospital records. General population estimates of associations between variables were obtained using inverse probability weights. Maternal log of the area under the curve cortisol predicted infant birth weight in a sex-dependent manner (interaction term P=0.029). There was a positive and statistically significant association between prenatal cortisol in males, and a negative association in females that was not statistically significant. A sex interaction in the same direction was evident when using the waking (P=0.015), and 30-min post-waking (P=0.013) cortisol, but not the evening measure. There was no interaction between prenatal cortisol and sex to predict gestational age. Our findings add to an emerging literature that suggests that there may be sex-specific mechanisms that underpin fetal programming.
Factors influencing early development such as birth weight, nest competition, and the diet received during rearing have been proposed as elements conditioning the future reproductive performance of European rabbit (Oryctolagus cuniculus) females. To evaluate their effects, we followed the life of 1513 females from birth to time of death, culling or censoring (animals alive at a fixed date). Between 0 and 63 days of age 353 females died. From the remaining 1160 females, 864 were chosen based on their birth weight to be transferred from the selection to the production farm. At this farm, 431 females received the control diet (184 g of CP, 381 g of NDF and 11.8 MJ of DE per kg DM), while the other 433 received the fibrous diet (134 g of CP, 436 g of NDF and 10.0 MJ of DE per kg DM). Throughout the rearing period, we checked for the individual live weight and body condition (perirenal fat thickness) at first artificial insemination. Reproductive lifespan was defined as the number of days between the first parturition and the time of death, culling or censoring. Birth weight affected the survival of newborn females during lactation and the presence of a milk spot at birth (related to nest competition) increased the survivability of newborns weighing <45 g (P<0.001). Rearing diet altered the growth curve of females and their body condition at first insemination. The diet also altered the relative risk of death during the rearing period, which was lower among females fed on the fibrous diet (−12.5%; P<0.001). Therefore, a higher number of females fed with this diet reached their reproductive life, directly affecting the productivity measured per housed female. Fatter females at first insemination had smaller litter sizes and a higher risk of being culled than lean ones (P<0.05). In general, the fibrous diet reduced the risk of leaving the herd at early rearing, and both birth weight and perirenal fat thickness affected female’s reproductive lifespan. An excess of fat (positive change in one unit of perirenal fat) at their first insemination represented an increased the risk of death or elimination of 13%.
In the present study we investigated gender-specific associations of low birth weight (LBW) and shorter relative leg length with metabolic syndrome (MetS) after adjusting for sociodemographic characteristics and health-related behaviours. We also investigated whether these associations are independent of age at menarche and BMI at 20 years old.
Baseline data from 12 602 participants (35–74 years) of the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), 2008–2010.
MetS was defined according to the revised National Cholesterol Education Program Adult Treatment Panel III guidelines. LBW (<2·5 kg) and age- and sex-standardized relative leg length (high, medium and low) were the explanatory variables studied. The strength of the associations between the explanatory variables and MetS was estimated by Poisson regression with robust variance.
MetS prevalence was 34·2 %; it was more prevalent in men (36·8 %) than in women (32·2 %). In multivariate analysis, LBW was associated (prevalence ratio; 95 % CI) with MetS only in women (1·28; 1·24, 1·45). Shorter leg length was associated with MetS in both men (1·21; 1·09, 1·35 and 1·46; 1·29, 1·65 for low and medium lengths, respectively) and women (1·12; 1·00, 1·25 and 1·40; 1·22, 1·59 for low and medium lengths, respectively). Additional adjustments for age at menarche and BMI at 20 years old did not change the associations.
Poor nutritional status as estimated by LBW and lower leg length in childhood was associated with a higher prevalence of MetS, although LBW was a significant factor only among women.
An inverse association between offspring birth weight (BW) and higher risk of parental cardiovascular disease (CVD) mortality and morbidity has been reported. Shared environmental, genetic and intrauterine factors may be responsible for explaining these associations. We studied the role of parental CVD risk factors in the association between offspring BW and CVD mortality among mothers and fathers. All births registered in Medical Birth Registry Norway (1967–2012) were linked to three health surveys, National Educational Registry and Cause of Death Registry. Number of births with information of parental CVD risk factors available for the analyses was 1,006,557 (520,670 for mothers and 485,887 for fathers). Cox proportional hazards regression models were used, following CVD deaths in parents from 1974 to 2012. An inverse association between offspring BW and CVD mortality was observed among both parents: hazard ratio 1.60 (1.44–1.75) for mothers and 1.16 (1.10–1.23) for fathers. Among mothers, adjustment for smoking, triglycerides and diabetes reduced the risk to 1.36 (1.25–1.52), 1.57 (1.43–1.73) and 1.58 (1.43–1.79), respectively. Adjustment for diastolic blood pressure (DBP) and systolic blood pressure (SBP) both reduced the risk to 1.53 (1.37–1.66). Among fathers, adjustments for smoking, DBP, SBP reduced the risk to 1.08 (1.02–1.15), 1.13 (1.06–1.19) and 1.14 (1.08–1.22), respectively. Triglycerides and diabetes both reduced the risk to 1.15 (1.09–1.12). Our results indicate that shared environmental factors might be important in the association. A stronger association in mothers suggest that intrauterine factors also are at play.
Low and high birth weight have been associated with increased risk of type 2 diabetes and CVD. Diet could partly mediate this association, e.g. by intra-uterine programming of unhealthy food preferences. We examined the association of birth weight with diet in Finnish children.
Birth weight standard deviation score (SDS) was calculated using national birth register data and Finnish references. Dietary factors were assessed using 4 d food records. Diet quality was defined by the Finnish Children Healthy Eating Index (FCHEI).
The Physical Activity and Nutrition in Children (PANIC) study.
Singleton, full-term children (179 girls, 188 boys) aged 6–8 years.
Birth weight was inversely associated (standardized regression coefficient β; 95 % CI) with FCHEI (−0·15; −0·28, −0·03) in all children and in boys (−0·27; −0·45, −0·09) but not in girls (−0·01; −0·21, 0·18) after adjusting for potential confounders (P=0·044 for interaction). Moreover, higher birth weight was associated with lower fruit and berries consumption (−0·13; −0·25, 0·00), higher energy intake (0·17; 0·05, 0·29), higher sucrose intake (0·19; 0·06, 0·32) and lower fibre intake (−0·14; −0·26, −0·01). These associations were statistically non-significant after correction for multiple testing. Children with birth weight >1 SDS had higher sucrose intake (mean; 95 % CI) as a percentage of energy intake (14·3 E%; 12·6, 16·0 E%) than children with birth weight of −1 to 1 SDS (12·8 E%; 11·6, 14·0 E%) or <−1 SDS (12·4 E%; 10·8, 13·9 E%; P=0·036).
Higher birth weight may be associated with unhealthy diet in childhood.
Previous studies suggest that Ramadan exposure during pregnancy might affect the health of women and their babies, particularly through the effect of fasting. This study aimed to evaluate the association between Ramadan exposure and fasting during pregnancy on the birth weight of newborns. This study concerned 1351 pregnant women from a prospective cohort in Jakarta, Indonesia. Ramadan exposure was based on the actual overlap between Ramadan and pregnancy. Women's fasting behaviour was recorded among 139 women who came for antenatal care between 10 July 2013 and 7 August 2013, and those who had fasted for at least 1 d (n 110) were classified as exposed to Ramadan fasting. Furthermore, a 24 h dietary recall was performed and repeated 1 month later. Birth weight of newborns who were exposed to Ramadan during pregnancy did not significantly differ from those who were not, both in the total and trimester-specific analysis. Maternal fasting did not seem to affect the birth weight of newborns (−72 (95 % CI −258, 114) g; P = 0·44), although there was a non-significant trend towards lower birth weight with fasting in the second and third trimester. Women who fasted had significantly lower total energy, macronutrient and water intake as compared with women who did not. Women's intake was also lower during Ramadan (regardless of their fasting behaviour) as compared with 1 month later. Lifestyle changes that occur with Ramadan and fasting during pregnancy are associated with lower reported energy intake. We cannot conclude on the effect of fasting on birth weight due to low statistical power.