Childhood Weight Gain Research Articles

Prevention of obesity in infancy and early childhood: a National Institutes of Health workshop.

Addressing the childhood obesity epidemic continues to be a challenge. Given that once obesity develops it is likely to persist, there has been an increasing focus on prevention at earlier stages of the life course. Research to develop and implement effective prevention and intervention strategies in the first 2 years after birth has been limited. In fall 2013, the National Institute of Diabetes and Digestive and Kidney Diseases convened a multidisciplinary workshop to summarize the current state of knowledge regarding the prevention of infant and early childhood obesity and to identify research gaps and opportunities. The questions addressed included (1) "What is known regarding risk for excess weight gain in infancy and early childhood?" (2) "What is known regarding interventions that are promising or have been shown to be efficacious?" and (3) "What are the challenges and opportunities in implementing and evaluating behavioral interventions for parents and other caregivers and their young children?"

DOHAD and early pubertal timing

Age at menarche varies widely between girls, is estimated to be highly heritable and is associated with long-term health outcomes, such as obesity and type 2 diabetes. Earlier pubertal maturation in boys and girls links rapid postnatal growth weight gain to later life metabolic and cardiovascular disease [1,2]. Genome-wide association studies (GWAS), which genotype hundreds of thousands of common genetic variants located across the entire genome, have been successful in identifying many specific genetic determinants of pubertal timing and these findings have informed the mechanisms that link earlier pubertal timing to increased risks of disease. The genetic signals indicate that both obesity-related and obesity-independent mechanisms may link pubertal timing to insulin sensitivity and diabetes risk. Our earlier findings [3] in the ReproGen international GWAS consortium identified substantial overlap between loci associated with menarche and those associated with body mass index, as had been predicted by analyses of data from twins, and in keeping with recognised associations between infancy and childhood weight gain and pubertal timing, and in turn between pubertal timing and obesity in adult life. However, the locus with the strongest individual effect size is in the gene LIN28B, which regulates microRNA processing and also insulin sensitivity. Our recent larger studies indicate further mechanisms that may link puberty timing to diabetes risk, and also suggest pubertal timing as a possible postnatal development target for the evolution of genomic imprinting [4].

Displaying parental responsibility for childhood obesity: aspects of care and family relationships

Childhood obesity is a much-debated health issue in Sweden as well as worldwide. Considerable emphasis is given to the prevention of excessive weight gain and obesity in early childhood, for example by providing lifestyle advice to parents. Based on interviews with Swedish parents of obese children aged between eight and 12, in this article parent narratives of everyday practices in relation to children’s diet and exercise habits are analysed as acts of ‘displaying normality’. The results show that explanations as to why it is difficult to manage the child’s weight appear to be connected to avoiding the risk of the child receiving negative attention and issues relating to the child’s own responsibility. These findings are discussed in terms of ‘displaying family normality’.

Does fetal smoke exposure affect childhood bone mass? The Generation R Study

We assessed the intrauterine influence of maternal smoking on childhood bone mass by comparing parental prenatal and postnatal smoking habits. We observed higher bone mass in children exposed to maternal smoking, explained by higher body weight. Maternal smoking or related lifestyle factors may affect childhood weight gain rather than skeletal growth. Maternal smoking during pregnancy may adversely affect bone health in later life. By comparing the associations of maternal and paternal smoking and of prenatal and postnatal exposure with childhood bone measures, we aimed to explore whether the suggested association could be explained by fetal programming or reflects confounding by familial factors. In 5565 mothers, fathers and children participating in a population-based prospective cohort study, parental smoking habits during pregnancy and current household smoking habits were assessed by postal questionnaires. Total body bone mineral content (BMC), bone area (BA) and bone mineral density (BMD) were measured by dual-energy X-ray absorptiometry (DXA) at the median age of 6.0 years (IQR 0.37). In confounder-adjusted models, maternal smoking during pregnancy was associated with a higher BMC of 11.6 g (95 % confidence interval (CI) 5.6, 17.5), a larger BA of 9.7 cm(2) (95 % CI 3.0, 16.4), a higher BMD of 6.7 g/cm(2) (95 % CI 2.4, 11.0) and a higher BMC of 5.4 g (95 % CI 1.3, 9.6) adjusted for BA of the child. Current weight turned out to mediate these associations. Among mothers who did not smoke, paternal smoking did not show evident associations with childhood bone measures. Also, household smoking practices during childhood were not associated with childhood bone measures. Our results do not support the hypothesis of fetal smoke exposure affecting childhood bone mass via intrauterine mechanisms. Maternal smoking or related lifestyle factors may affect childhood weight gain rather than skeletal growth.

Maternal glucose during pregnancy and after delivery in women with gestational diabetes mellitus on overweight status of their children.

Objective. To examine the association of maternal glycemia during pregnancy and after delivery with anthropometry in the offspring of mothers with gestational diabetes mellitus (GDM). Methods. A total of 1,263 GDM mothers and their children finished the health survey at 1–5 years after delivery. Results. Offspring of GDM mothers who were diagnosed with diabetes during pregnancy had higher prevalence of overweight, higher mean weight for height Z scores, and higher mean BMI for age Z scores at 1–5 years old than the offspring of GDM mothers who were diagnosed with impaired glucose tolerance (IGT) during pregnancy. Offspring of GDM mothers who developed diabetes 1–5 years after delivery had higher mean values of Z scores for weight for height and BMI for age at 1–5 years old than the offspring of GDM mothers who had normal glucose or prediabetes after delivery. Conclusions. Offspring of GDM mothers who were diagnosed with diabetes during pregnancy or after delivery had an increased risk of childhood overweight or weight gain at 1–5 years old compared with children of GDM mothers with IGT during pregnancy or with normal glucose or prediabetes after delivery.

A WORLD OF SUFFERING? BIOCULTURAL APPROACHES TO FAT STIGMA IN THE GLOBAL CONTEXTS OF THE OBESITY EPIDEMIC

Even as obesity rates rise, weight‐related stigma remains widespread in the United States and leads to many documented social, economic, and health disparities. These include lower wages, less academic achievement, social exclusion as early as childhood, psychosocial stress, depression, and additional weight gain. Recent research documents the proliferation of antifat beliefs across the globe, but we know little about how this fat stigma varies across cultures. A clearer empirical and theoretical understanding of fat stigma in cultural context is essential to gauging its likely biocultural impacts across populations. Using data from Paraguay, Bolivia, India, and students and Muslim women in the United States (N = 414 women), we show that psychometric scales suggest high levels of stated or expressed fat stigma in all these samples, capturing globalizing anti‐fat norms. However, when we assess what people think implicitly through reaction‐time implicit association tests, we find marked variation across sites in the degree to which people are internalizing these stigmatized ideas around obesity. In India and among U.S. university students, women tend to internalize the idea of “fat” negatively. Paraguay women present, on average, fat‐neutral internalized views. In Bolivia and among Muslim women in the United States, average assessments suggest fat‐positive internalized views. This indicates fat stigmatizing norms are not always internalized, even as explicit fat stigma otherwise appears to be globalizing. Our findings indicate that the proposed biocultural relationships between fat stigma and health disparities may be complex and very context specific.

Weight in Infancy and Obesity in Children Born Preterm

Excessive weight gain in infancy may lead to obesity and its sequelae later in life. Children born preterm have higher associated risk of becoming obese than full term babies. The goal of the study was to examine early weight gain among preterm infants, who later in life became obese. In a retrospective chart review of 37 preterm infants, 27 grew to support a normal weight and 10 became obese. We demonstrated differences in early childhood weight gain dynamics with weight differences between groups noted at 6 months of age that persisted later in life. Increased risk of obesity could be identified very early in infancy among preterm children. Early nutritional consult and attention to weight gain in infancy and early childhood are important steps in obesity prevention.

What Can Providers Learn From Childhood Body Mass Index Trajectories: A Study of a Large, Safety-Net Clinical Population

ObjectiveTo describe childhood weight gain using body mass index (BMI) z-score trajectories in a low-income urban safety-net population and identify among gender- and race/ethnicity-specific groups any trends for increased risk. MethodsA retrospective cohort study was conducted among 2- to 12-year-old patients (2006–2013) visiting a safety-net provider. BMI z-score trajectories were calculated overall, for gender- and race/ethnicity-specific groups, and for peak BMI percentile subgroups to describe weight gain longitudinally. ResultsFrom 2006 to 2013, a total of 26,234 eligible children were followed for an average of 3.7 years. At baseline (mean age, 4.2 years), 74% of patients were at a normal weight compared to 65% at most recent observation (mean age, 7.8 years). All gender and race/ethnicity subgroups showed increasing average BMI z-scores during childhood. Children consistently under the 50th percentile and those of white race had the most stable BMI z-score trajectories. BMI z-score increased with increasing age in all subgroups. Hispanic boys and black girls had the most significant increase in BMI z-score during this observation period. Children observed in early childhood and whose BMI exceeded the 95th percentile at any time were often already overweight (20%) or obese (36%) by 3 years of age. ConclusionsThe entire population demonstrated an upward trend in BMI z-score trajectory. This trend was most notable among black girls and Hispanic boys. Many obese children were already overweight by age 3, and persistence of obesity after 3 years of age was high, suggesting that intervention before age 3 may be essential to curbing unhealthy weight trajectories.

Protein intake and nutritional programming: metabolic consequences

According to recent epidemiological evidence, early protein intakes that exceeds metabolic requirements (>15% of energy) may increase weight gain during infancy and the risk of developing obesity in childhood: the so-called “early protein hypothesis” [1]. A high protein intake, indeed, especially milk’s protein [2,3], may enhance the secretion of insulin and insulin-like growth factor-I (IGF-I), associated with increased weight gain during the first 2 years of life, increase of adipocyte differentiation and adipogenic activity [4]. In a large number of studies increased weight gain in infancy and early adiposity rebound have been associated with the development of later obesity [4]. The presence of a positive strong association between early protein intake and increased weight gain in early childhood has been recently demonstrated in the European Childhood Obesity Project (CHOP): a multicenter, double-blind intervention trial involving both formula fed infants, randomly assigned to receive, during the first year of life, infant and follow-on formulas with different protein content (high or low), and breastfed infants as control group. This trial showed that both weight-for-length and BMI z-scores were significantly higher in the high protein (HP) compared with the low protein (LP) group at 12 and 24 months [5]. Moreover the body composition analysis at 6 months of life showed that weight gain velocity from baseline to 6 months was significantly associated with fat mass, proving that higher early protein intakes may influence adiposity [6]. Concerning metabolic data, HP group compared with LP group showed higher plasma concentrations of branched chain aminoacids, IGF-I and insulin at 6 months. Moreover, IGF-I concentrations have been associated with weight gain in the first 6 months of life [7]. Additionally IGF-I could partly mediate protein-induced kidney growth in healthy children [8]. This phenomenon was observed in the HP group: children at 6 months of life showed a significantly greater kidney volume compared with the LP group [9]. However the long-term consequences of these results should be further evaluated. Lastly it has been recently published that protein content of infant formulas may influence not only the growth pattern in the first two years, but also the risk of developing obesity at school-age, showing a 2.43 increased risk of obesity at 6 years of age in the HP vs LP group [10]. In conclusion these results suggest that early nutritional intervention programs are needed to avoid negative long-term consequences on health, especially to prevent “non-communicable diseases”in adult age.

Association of early childhood abdominal circumference and weight gain with blood pressure at 36 months of age: secondary analysis of data from a prospective cohort study

ObjectivesTo assess whether changes in measures of fat distribution and body size during early life are associated with blood pressure at 36 months of age.DesignAnalysis of data collected from a...

Overweight in early adulthood, adult weight change, and risk of type 2 diabetes, cardiovascular diseases, and certain cancers in men: a cohort study.

The relative importance of overweight after childhood and excess weight gain during adulthood remains unclear. In 39,909 male participants of the Health Professionals Follow-Up Study who were 40-75 years of age in 1986 and were followed until 2008, we documented 8,755 incident cases of obesity-related chronic diseases (type 2 diabetes mellitus, cardiovascular diseases, and colorectal, renal, pancreatic, and esophageal cancers). We calculated composite and cause-specific hazard ratios using a model that included body mass index (BMI; weight (kg)/height (m)(2)) at 21 years of age, weight change since age 21 years, smoking, alcohol consumption, and family histories of myocardial infarction, colon cancer, and diabetes. Compared with a BMI at 21 years of 18.5-22.9, the composite hazard ratio for a BMI of 23-24.9 was 1.22 (95% confidence interval (CI): 1.16, 1.29), that for a BMI of 25.0-27.4 was 1.57 (95% CI: 1.48, 1.67), that for a BMI of 27.5-29.9 was 2.40 (95% CI: 2.17, 2.65), and that for a BMI ≥30.0 was 3.15 (95% CI: 2.76, 3.60). The composite hazard ratios for adult weight gain compared with a stable weight were 1.12 (95% CI: 1.03, 1.22) for a gain of 2.5-4.9 kg, 1.41 (95% CI: 1.31, 1.52) for a gain of 5-9.9 kg, 1.72 (95% CI: 1.59, 1.86) for a gain of 10-14.9 kg, and 2.45 (95% CI: 2.27, 2.63) for a gain ≥15 kg. Adiposity in early adulthood and adult weight gain were both associated with marked increases in the risk of major chronic diseases in middle-aged and older men, and these associations were already apparent at modest levels of overweight and weight gain.

Excess weight in preschool children with a history of severe bronchiolitis is associated with asthma.

The relationship between excess weight gain and asthma in childhood remains inadequately defined. The aim of this study was to evaluate, as part of a prospective post-bronchiolitis follow-up, whether there is a link between earlier or current overweight or obesity and asthma or asthma symptoms at 5-7 years of age. In all, 151 former bronchiolitis patients were followed-up until the mean age of 6.45 years. At the control visit, the weights and heights were measured, and the asthma symptoms and medications for asthma were recorded. The weight status was expressed as body mass index (BMI) z-scores (zBMI). There were 10 obese and 31 overweight (zBMI over national references) children. In adjusted analyses, presence of current asthma at 6-7 years of age (aOR 3.05, 95% CI 1.02-9.93) differed between overweight and normal weight children. Further, asthma ever, asthma at age 4-5 years, asthma at age 5-6 years, use of bronchodilators ever and use of ICSs during the last 12 months were more common in currently overweight than in normal weight children. Obesity was associated only with current asthma and asthma ever. Instead, there were no significant associations between birth weight, excess weight gain in infancy, or overweight at age 1.5 years, and later asthma, asthma symptoms or use of asthma medication. Asthma was more common in currently overweight than in normal weight former bronchiolitis patients at preschool age and early school age.

Appetite and Growth

Identifying early markers of future obesity risk can help target preventive interventions. Several studies have shown that a heartier appetite in infancy is a risk factor for more rapid weight gain, but to date no investigations have been able to rule out familial confounding. To use a sibling design (data from same-sex, dizygotic twin pairs) to test the hypothesis that sibling differences in infant appetite predicted differential weight gain during childhood. Gemini is a population-based twin cohort among the general United Kingdom population born between March 1, 2007, and December 15, 2007. Growth trajectories were analyzed from birth to age 15 months. Appetite-discordant pairs were selected from 800 nonidentical, same-sex twin pairs. Appetite during the first 3 months of life was assessed with the food responsiveness (FR) and satiety responsiveness (SR) subscales from the Baby Eating Behaviour Questionnaire. Discordance was defined as a within-pair difference of at least 1 SD. A mean of 11.5 weight measurements per child were available between birth and age 15 months. Multilevel models, adjusted for sex and birth weight, compared growth curves for the higher-appetite vs lower-appetite twins. In total, 172 pairs were discordant for SR and 121 pairs for FR. Within-pair analyses showed that those with higher FR and those with lower SR grew faster than their sibling. At age 6 months, those with higher FR were 654 (95% CI, 395-913) g heavier and at age 15 months were 991 (95% CI, 484-1498) g heavier. For sibling pairs discordant for SR, the weight differences between siblings were 637 (95% CI, 438-836) g at age 6 months and 918 (95% CI, 569-1267) g at age 15 months. A heartier appetite (indexed with higher FR or lower SR) in early infancy is prospectively associated with more rapid growth up to age 15 months in a design controlling for potential familial confounding, supporting a causal role for appetite in childhood weight gain. Appetite could be an early marker for risk of weight gain in the current obesogenic environment and might be a potential target for preventive interventions.

370The Impact of Early Life Antibiotic Exposure on Childhood Weight Gain

370The Impact of Early Life Antibiotic Exposure on Childhood Weight Gain

Displaying parental responsibility for childhood obesity: aspects of care and family relationships

Childhood obesity is a much-debated health issue in Sweden as well as worldwide. Considerable emphasis is given to the prevention of excessive weight gain and obesity in early childhood, for example by providing lifestyle advice to parents. Based on interviews with Swedish parents of obese children aged between eight and 12, in this article parent narratives of everyday practices in relation to children’s diet and exercise habits are analysed as acts of ‘displaying normality’. The results show that explanations as to why it is difficult to manage the child’s weight appear to be connected to avoiding the risk of the child receiving negative attention and issues relating to the child’s own responsibility. These findings are discussed in terms of ‘displaying family normality’.

Distinct Genetic Backgrounds in Quantitative Traits Preceding Type 2 Diabetes: One Reason for Missing Heritability

Genome-wide association studies (GWAS) have identified variants associated with type 2 diabetes (T2D), but less than five percent of the genetic variance associated with T2D is accounted for in GWAS studies performed using T2D as endpoint. These findings suggest relevance of assessing preceding quantitative traits (QTs) or sub-phenotypes and their respective markers for contributing to the appearance of glycemic thresholds defining T2D. The QTs first appear in gestation and childhood when birth weight and childhood weight gain have an influence on T2D. Changes in fetal growth are associated with metabolic programming for T2D in adulthood. Subsequently gains in body fat leading to obesity, ectopic lipid deposition in liver and muscle, dyslipidemia and hypertension express in the β-cells, hypothalamus, adipocytes, myocytes, liver and kidney, and are associated with worsening insulin resistance and β-cell failure preceding overt T2D. Obesity, an increasingly common trait is associated with gene variants that regulate energy balance but have no association with T2D with few exceptions. For instance, FTO gene variants are associated with early onset of obesity and have also been associated with T2D and hypertension suggesting pleiotropism. Non-alcoholic fatty liver disease (NAFLD) has an independent genetic background and is considered as a new addition to the metabolic syndrome. Association of NAFLD with dyslipidemia, Review Article British Journal of Medicine & Medical Research, 4(2): 590-620, 2014 591 cardiovascular disease and hepatic insulin resistance contributes to progression to T2D. The classic dyslipidemia encountered in insulin resistant states consisting of increased triglyceride, low high-density lipoprotein cholesterol (HDL-C) and molding of triglyceridecontaining lipoproteins to form atherogenic LDL particles and dysfunctional HDL particles, has strong environmental and genetic association. In addition evidence is accumulating to show that the abnormal lipoproteins have a direct effect on β-cells leading to failure and possible acceleration of diabetes onset. Consequently known variants affecting either the dyslipidemia or β-cell function have a compound effect on T2D. Like other preceding traits the genetic background for commonly encountered hypertension is independent of diabetes although it remains a predictive trait. However, increasing evidence supports a role for the renin-angiotensin system in causing oxidative stress and insulin resistance. Finally when glucose intolerance has progressed to overt T2D, reversibility is usually no longer possible; therefore recognition of preceding prediabetic glycemic thresholds and both their genetic and environmental associations may facilitate and serve as signals for prevention. Thus a better understanding of the sequential expression of the respective QTs and genetic variation affecting their metabolic effects leading to T2D could initiate more effective prevention strategies.

Developing Prediction Equations and a Mobile Phone Application to Identify Infants at Risk of Obesity

BackgroundAdvancements in knowledge of obesity aetiology and mobile phone technology have created the opportunity to develop an electronic tool to predict an infant’s risk of childhood obesity. The study aims were to develop and validate equations for the prediction of childhood obesity and integrate them into a mobile phone application (App).Methods and FindingsAnthropometry and childhood obesity risk data were obtained for 1868 UK-born White or South Asian infants in the Born in Bradford cohort. Logistic regression was used to develop prediction equations (at 6±1.5, 9±1.5 and 12±1.5 months) for risk of childhood obesity (BMI at 2 years >91st centile and weight gain from 0–2 years >1 centile band) incorporating sex, birth weight, and weight gain as predictors. The discrimination accuracy of the equations was assessed by the area under the curve (AUC); internal validity by comparing area under the curve to those obtained in bootstrapped samples; and external validity by applying the equations to an external sample. An App was built to incorporate six final equations (two at each age, one of which included maternal BMI). The equations had good discrimination (AUCs 86–91%), with the addition of maternal BMI marginally improving prediction. The AUCs in the bootstrapped and external validation samples were similar to those obtained in the development sample. The App is user-friendly, requires a minimum amount of information, and provides a risk assessment of low, medium, or high accompanied by advice and website links to government recommendations.ConclusionsPrediction equations for risk of childhood obesity have been developed and incorporated into a novel App, thereby providing proof of concept that childhood obesity prediction research can be integrated with advancements in technology.

Birth weight and growth from infancy to late adolescence in relation to fat and lean mass in early old age: findings from the MRC National Survey of Health and Development

Objective:High birth weight and greater weight gain in infancy have been associated with increased risk of obesity as assessed using body mass index, but few studies have examined associations with direct measures of fat and lean mass. This study examined associations of birth weight and weight and height gain in infancy, childhood and adolescence with fat and lean mass in early old age.Subjects:A total of 746 men and 812 women in England, Scotland and Wales from the MRC National Survey of Health and Development whose heights and weights had been prospectively ascertained across childhood and adolescence and who had dual energy X-ray absorptiometry measures at age 60–64 years.Methods:Associations of birth weight and standardised weight and height (0–2 (weight only), 2–4, 4–7, 7–11, 11–15, 15–20 years) gain velocities with outcome measures were examined.Results:Higher birth weight was associated with higher lean mass and lower android/gynoid ratio at age 60–64 years. For example, the mean difference in lean mass per 1 standard deviation increase in birth weight was 1.54 kg in males (95% confidence interval=1.04, 2.03) and 0.78 kg in females (0.41, 1.14). Greater weight gain in infancy was associated with higher lean mass, whereas greater gains in weight in later childhood and adolescence were associated with higher fat and lean mass, and fat/lean and android/gynoid ratios. Across growth intervals greater height gain was associated with higher lean but not fat mass, and with lower fat/lean and android/gynoid ratios.Conclusion:Findings suggest that growth in early life may have lasting effects on fat and lean mass. Greater weight gain before birth and in infancy may be beneficial by leading to higher lean mass, whereas greater weight gain in later childhood and adolescence may be detrimental by leading to higher fat/lean and android/gynoid ratios.

A randomised controlled trial and mediation analysis of the ‘Healthy Habits’, telephone-based dietary intervention for preschool children

BackgroundConsumption of non-core foods in childhood is associated with excessive weight gain in childhood. Parents play a vital role in establishing healthy diet behaviours in young children. The aim of this study was to assess the effectiveness of a telephone-based intervention in reducing child consumption of non-core foods, and to examine parent and home food environment mediators of change in child consumption.MethodsThe ‘Healthy Habits’ trial utilised a clustered randomised controlled design.Setting/participantsParents were recruited from 30 preschools (N = 394 participants, mean age 35.2±5.6 years). Parents randomized to the intervention group received four telephone contacts and print materials. Parents allocated to the control condition receive generic print materials only. Non-core food consumption was assessed using a validated child dietary questionnaire at baseline, 2 and 6 months post recruitment in 2010.ResultsThe intervention was effective in reducing child consumption of non-core foods at 2 months (intention to treat analysis: z=-2.83, p<.01), however this effect was not maintained at 6 months. Structural equation modelling using 2 month data indicated that child access to non-core foods in the home and child feeding strategies mediated the effect of the intervention.ConclusionThe telephone-based intervention shows promise in improving short term dietary behaviour in preschool age children, however further development is needed to sustain the effect in the long-term.Trial registrationAustralian Clinical Trials Registry: ACTRN12609000820202

Determinantes nutricionais precoces da massa livre de gordura no início da vida adulta: revisão sistemática da literatura

Early childhood nutritional factors can play a crucial role in the development of body composition in later phases of life. A systematic literature review was conducted to identify studies on the association between early nutritional determinants and fat-free mass in adulthood. The PubMed and Virtual Health Library electronic databases were used. Nine articles were included after a peer review of the 576 references initially found, published from 2003 to 2009, with healthy subjects and longitudinal analysis. Birth weight and birth length and variations across childhood were strong predictors of fat-free mass at later ages. The studies showed that higher birth weight and greater weight gain in early childhood were associated with greater fat-free mass in adulthood. However, the available data are limited and inconclusive in relation to eating in early childhood as a predictor of fat-free mass at later ages.