Early life risk factors for obesity in childhood: cohort study

Objective To identify risk factors in early life (up to 3 years of age) for obesity in children in the United Kingdom.Design Prospective cohort study.Setting Avon longitudinal study of parents and children, United Kingdom.Participants 8234 children in cohort aged 7 years and a subsample of 909 children (children in focus) with data on additional early growth related risk factors for obesity.Main outcome measures Obesity at age 7 years, defined as a body mass index ³ 95th centile relative to reference data for the UK population in 1990.Results Eight of 25 putative risk factors were associated with a risk of obesity in the final models: parental obesity (both parents: adjusted odds ratio, 10.44, 95% confidence interval 5.11 to 21.32), very early (by 43 months) body mass index or adiposity rebound (15.00, 5.32 to 42.30), more than eight hours spent watching television per week at age 3 years (1.55, 1.13 to 2.12), catch-up growth (2.60, 1.09 to 6.16), standard deviation score for weight at age 8 months (3.13, 1.43 to 6.85) and 18 months (2.65, 1.25 to 5.59); weight gain in first year (1.06, 1.02 to 1.10 per 100 g increase); birth weight, per 100 g (1.05, 1.03 to 1.07); and short (< 10.5 hours) sleep duration at age 3 years (1.45, 1.10 to 1.89).Conclusion Eight factors in early life are associated with an increased risk of obesity in childhood.     

Childhood obesity and parental smoking as risk factors for childhood ADHD in Liverpool children

ADHD prevalence has risen in parallel with rising prevalence of pregnancy smoking and childhood obesity. The objective was to determine the epidemiological association of pregnancy smoking and childhood obesity with ADHD. A cross-sectional community study was conducted in 2006 using a parental questionnaire. A total of 1,074 schoolchildren aged 5-11 years were enrolled from 15 primary schools in a lower socio-economic area of Merseyside. ADHD was defined by the question "does your child have Attention Deficit Hyperactivity Disorder, (ADHD), which has been diagnosed by a doctor?" The prevalence estimates for childhood obesity, maternal smoking during pregnancy and childhood ADHD were 14.9% (116/777), 28.0% (269/955), and 3.4% (32/945), respectively. ADHD prevalence increased fivefold in children with obesity (RR, 4.80, 95% CI 2.2-10.4, P < 0.001) and more than twofold in children of mothers who smoked during pregnancy (RR, 2.44, 95% CI 1.2-4.9, P = 0.02). Regression analysis adjusting for obesity, overweight, maternal smoking during pregnancy, heavy maternal smoking, household member smoking during pregnancy, doctor-diagnosed asthma, preterm birth, and low birthweight showed significant independent associations of ADHD prevalence with obesity (AOR, 4.66, 95% CI 1.57-13.89, P = 0.006) and pregnancy smoking (AOR, 3.19, 95% CI 1.08-9.49, P = 0.04). There was a positive dose-response association of ADHD with the number of maternal cigarettes smoked during pregnancy. Measures to reduce both smoking among pregnant women and childhood obesity might reduce prevalence of childhood ADHD.     

Gene-diet interactions in childhood obesity

Childhood overweight and obesity have reached epidemic proportions worldwide, and the increase in weight-associated co-morbidities including premature type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease will soon become major healthcare and economic problems. A number of studies now indicate that the childhood obesity epidemic which has emerged during the past 30 years is a complex multi-factorial disease resulting from interaction of susceptibility genes with an obesogenic environment. This review will focus on gene-diet interactions suspected of having a prominent role in promoting childhood obesity. In particular, the specific genes that will be presented (FTO, MC4R, and NPC1) have recently been associated with childhood obesity through a genome-wide association study (GWAS) and were shown to interact with nutritional components to increase weight gain. Although a fourth gene (APOA2) has not yet been associated with childhood obesity, this review will also present information on what now represents the best characterized gene-diet interaction in promoting weight gain.     

Energy imbalance underlying the development of childhood obesity

Objective: To develop a model based on empirical data and human energetics to predict the total energy cost of weight gain and obligatory increase in energy intake and/or decrease in physical activity level associated with weight gain in children and adolescents. Research Methods and Procedures: One‐year changes in weight and body composition and basal metabolic rate (BMR) were measured in 488 Hispanic children and adolescents. Fat‐free mass (FFM) and fat mass (FM) were measured by DXA and BMR by calorimetry. Model specifications include the following: body mass (BM) = FFM + FM, each with a specific energy content, cff (1.07 kcal/g FFM) and cf (9.25 kcal/g FM), basal energy expenditure (EE), kff and kf, and energetic conversion efficiency, eff (0.42) for FFM and ef (0.85) for FM. Total energy cost of weight gain is equal to the sum of energy storage, EE associated with increased BM, conversion energy (CE), and diet‐induced EE (DIEE). Results: Sex‐ and Tanner stage–specific values are indicated for the basal EE of FFM (kff) and the fat fraction in added tissue (fr). Total energy cost of weight gain is partitioned into energy storage (24% to 36%), increase in EE (40% to 57%), CE (8% to 13%), and DIEE (10%). Observed median (10th to 90th percentile) weight gain of 6.1 kg/yr (2.4 to 11.4 kg/yr) corresponds at physical activity level (PAL) = 1.5, 1.75, and 2.0 to a total energy cost of weight gain of 244 (93 to 448 kcal/d), 267 (101 to 485 kcal/d), and 290 kcal/d (110 to 527 kcal/d), respectively, and to a total energy intake of 2695 (1890 to 3730), 3127 (2191 to 4335), and 3551 (2487 to 4930) kcal/d, respectively. If weight gain is caused by a change in PAL alone and PAL₀ = 1.5 at baseline t = 0, the model indicates a drop in PAL of 0.22 (0.08 to 0.34) units, which is equivalent to 60 (18 to 105) min/d of walking at 2.5 mph. Discussion: Halting the development or progression of childhood obesity, as observed in these Hispanic children and adolescents, by counteracting its total energy costs will require a sizable decrease in energy intake and/or reciprocal increase in physical activity.     

Examining the temporal relationships between childhood obesity and asthma

Childhood obesity has become an issue of increasing concern to health researchers and policymakers in the United States. One important chronic health condition linked to obesity is pediatric asthma. Although researchers have speculated that both conditions may have common origins, the majority of research in this area has focused on a unidirectional relationship between obesity and later asthma. However, much of the literature is limited by its reliance on cross-sectional data and its failure to examine the possibility that asthma may influence weight fluctuations through changes in physical and sedentary activity. Using data from the Early Childhood Longitudinal Study-Kindergarten Cohort (ECLS-K), I explore the bidirectional relationships between childhood obesity and asthma. The results in this paper suggest that past asthma levels are positively correlated with changes in BMI and the onset of obesity. However, only new onset asthma is positively correlated with subsequent changes in BMI. The potential mechanisms are unclear, as I find little evidence that asthma is structurally related to changes in physical or sedentary activity over time. When testing the prevailing hypothesis that obesity is related to subsequent asthma, I find that lagged weight status is strongly related to asthma prevalence levels but that the onset of overweight or obesity is not associated with the subsequent onset of asthma. These results suggest that the onset of asthma may be related to subsequent weight gain over time.     

Maternal employment and childhood obesity in Russia

Existing research on childhood obesity shows that rising maternal employment is associated with increases in child weight. This paper aims to estimate the effect of maternal employment on childhood obesity in Russia, where obesity has been spreading quickly over the last 20 years. To address the endogeneity of maternal employment and estimate its effect on the weight outcomes of older siblings, I use plausibly exogenous variation in childcare enrolment for the youngest child in the household as an instrumental variable for maternal employment. Based on the Russian Longitudinal Monitoring Survey (RLMS-HSE), the results show that maternal employment leads to an increase in children’s BMI and in their probabilities of becoming overweight and obese. In exploring the potential underlying mechanisms, I find that maternal employment is related to less physical activity, to a higher probability of either watching TV or playing video games, and to poorer dietary habits among children.     

Assessing screening policies for childhood obesity

To address growing concerns over childhood obesity, the United States Preventive Services Task Force (USPSTF) recently recommended that children undergo obesity screening beginning at age 6. An Expert Committee recommends starting at age 2. Analysis is needed to assess these recommendations and investigate whether there are better alternatives. We model the age- and sex-specific population-wide distribution of BMI through age 18 using National Longitudinal Survey of Youth (NLSY) data. The impact of treatment on BMI is estimated using the targeted systematic review performed to aid the USPSTF. The prevalence of hypertension and diabetes at age 40 are estimated from the Panel Study of Income Dynamics (PSID). We fix the screening interval at 2 years, and derive the age- and sex-dependent BMI thresholds that minimize adult disease prevalence, subject to referring a specified percentage of children for treatment yearly. We compare this optimal biennial policy to biennial versions of the USPSTF and Expert Committee recommendations. Compared to the USPSTF recommendation, the optimal policy reduces adult disease prevalence by 3% in relative terms (the absolute reductions are <1%) at the same treatment referral rate, or achieves the same disease prevalence at a 28% reduction in treatment referral rate. If compared to the Expert Committee recommendation, the reductions change to 6 and 40%, respectively. The optimal policy treats mostly 16-year olds and few children under age 14. Our results suggest that adult disease is minimized by focusing childhood obesity screening and treatment on older adolescents.     

The association between childhood obesity and tooth eruption

Obesity is a growth-promoting process as evidenced by its effect on the timing of puberty. Although studies are limited, obesity has been shown to affect the timing of tooth eruption. Both the timing and sequence of tooth eruption are important to overall oral health. The purpose of this study was to examine the association between obesity and tooth eruption. Data were combined from three consecutive cycles (2001-2006) of the National Health and Nutrition Examination Survey (NHANES) and analyzed to examine associations between the number of teeth erupted (NET) and obesity status (BMI z-score >95th percentile BMI relative to the Centers for Disease Control and Prevention (CDC) growth reference) among children 5 up to 14 years of age, controlling for potential confounding by age, gender, race, and socioeconomic status (SES). Obesity is significantly associated with having a higher average NET during the mixed dentition period. On average, teeth of obese children erupted earlier than nonobese children with obese children having on average 1.44 more teeth erupted than nonobese children, after adjusting for age, gender, and race/ethnicity (P < 0.0001). SES was not a confounder of the observed associations. Obese children, on average, have significantly more teeth erupted than nonobese children after adjusting for gender, age, and race. These findings may have clinical importance in the area of dental and orthodontic medicine both in terms of risk for dental caries due to extended length of time exposed in the oral cavity and sequencing which may increase the likelihood of malocclusions.     

Parental employment,family routines and childhood obesity

Using the Early Childhood Longitudinal Survey-Kindergarten Class of 1998–1999 (ECLS-K) data from kindergarten through eighth grade, this paper investigate the relationships among maternal employment, family routines and obesity. More hours worked by the mother tend to be negatively related to positive routines like eating meals as a family or at regular times, or having family rules about hours of television watched. Many of these same routines are significantly related to the probability of being obese, implying that family routines may be a mechanism by which maternal employment intensity affects children's obesity. However, inclusion of family routines in the obesity regression does not appreciably change the estimated effect of maternal employment hours. Thus, the commonly estimated deleterious effect of maternal employment on children's obesity cannot be explained by family routines, leaving the exact mechanisms an open question for further exploration.     

Parental obesity moderates the relationship between childhood appetitive traits and weight

Objective:

In this study, the independent and combined associations between childhood appetitive traits and parental obesity on weight gain from 0 to 24 months and body mass index (BMI) z‐score at 24 months in a diverse community‐based sample of dual parent families (n = 213) were examined.

Design and Methods:

Participants were mothers who had recently completed a randomized trial of weight loss for overweight/obese postpartum women. As measures of childhood appetitive traits, mothers completed subscales of the Children's Eating Behavior Questionnaire, including Desire to Drink (DD), Enjoyment of Food (EF), and Satiety Responsiveness (SR), and a 24‐h dietary recall for their child. Heights and weights were measured for all children and mothers and self‐reported for mothers' partners. The relationship between children's appetitive traits and parental obesity on toddler weight gain and BMI z‐score were evaluated using multivariate linear regression models, controlling for a number of potential confounders.

Results:

Having two obese parents was related to greater weight gain from birth to 24 months independent of childhood appetitive traits, and although significant associations were found between appetitive traits (DD and SR) and child BMI z‐score at 24 months, these associations were observed only among children who had two obese parents. When both parents were obese, increasing DD and decreasing SR were associated with a higher BMI z‐score.

Conclusions:

The results highlight the importance of considering familial risk factors when examining the relationship between childhood appetitive traits on childhood obesity.