Larger childhood body size and rapid growth have been associated with increased type 1 diabetes risk. We analyzed height, weight, body mass index (BMI), and velocities of growth in height, weight, and BMI, for association with development of islet autoimmunity (IA) and type 1 diabetes.
Since 1993, the Diabetes Autoimmunity Study in the Young (DAISY) has followed children at increased type 1 diabetes risk, based on HLA DR,DQ genotype or family history, for development of IA and type 1 diabetes. IA was defined as presence of autoantibodies to insulin, GAD or IA2 twice in succession, or autoantibody positive on one visit and diabetic at the next consecutive visit within one year. Type 1 diabetes was diagnosed by a physician. Height and weight were collected starting at age 2 years. Of 1,714 DAISY children < age 11.5 years, 143 children developed IA, and 21 progressed to type 1 diabetes. We conducted Cox proportional hazards analysis to explore growth velocities and size measures for association with IA and type 1 diabetes development.
Higher height growth velocity was associated with IA development (HR: 1.63, CI: 1.31-2.05) and type 1 diabetes development (HR: 3.34, CI: 1.73-6.42) for a 1 standard deviation difference in velocity.
Our study suggests that greater height growth velocity may be involved in the progression from genetic susceptibility to autoimmunity and then to type 1 diabetes in pre-pubertal children.
childhood height; height growth velocity; islet autoimmunity; type 1 diabetes
To examine whether delivery by caesarean section is a risk factor for childhood obesity.
Prospective pre-birth cohort study (Project Viva).
Eight outpatient multi-specialty practices based in the Boston, Massachusetts area.
We recruited women during early pregnancy between 1999 and 2002, and followed their children after birth. We included 1255 children with body composition measured at 3 years of age.
Main outcome measures
Body mass index (BMI) z-score, obesity (BMI for age and sex ≥ 95th percentile), and sum of triceps + subscapular skinfold thicknesses, at 3 years of age.
284 children (22.6 percent) were delivered by caesarean section. At age 3, 15.7% of children delivered by caesarean section were obese, compared with 7.5% of children born vaginally. In multivariable logistic and linear regression models adjusting for maternal pre-pregnancy BMI, birth weight, and other covariates, birth by caesarean section was associated with a higher odds of obesity at age 3 (OR 2.10, 95%CI 1.36 to 3.23), higher mean BMI z-score (0.20 units, 95% CI 0.07 to 0.33), and higher sum of triceps + subscapular skinfold thicknesses (0.94 mm, 95% CI 0.36 to 1.51).
Infants delivered by caesarean section may be at increased risk of childhood obesity. Further studies are needed to confirm our findings and to explore mechanisms underlying this association.
To examine perinatal and childhood risk factors for the presence of rheumatoid factor in healthy children.
The Diabetes Autoimmunity Study in the Young (DAISY) is a longitudinal study of children at increased risk of type 1 diabetes, based on possession of human leucocyte antigen (HLA)‐DR4 and DR3 alleles or a family history of diabetes. 651 children who participated in DAISY, with an average age of 6.4 (range 1–15) years, were tested for the presence of rheumatoid factor in their most recent serum sample. 23 children were positive for rheumatoid factor. Exposure data were collected prospectively by interview. HLA‐DR4 alleles were identified using polymerase chain reaction‐based Class II genotyping.
While exploring risk factors for rheumatoid factor positivity in a multivariate model, several important interaction terms involving HLA‐DR4 status suggested the need to evaluate risk factors in HLA‐DR4‐positive and HLA‐DR4‐negative children separately. In HLA‐DR4‐negative children, rheumatoid factor‐positive infants were less likely to have been breast fed for >3 months (odds ratio (OR) 0.18; 95% confidence interval (CI) 0.04 to 0.99), more likely to have been exposed to non‐parental tobacco smoke (OR 5.38; 95% CI 0.93 to 31.27) and more likely to be a race/ethnicity other than non‐Hispanic white (OR 6.94; 95% CI 1.10 to 43.88) compared with rheumatoid factor‐negative children, after adjusting for age, sex and maternal education. In HLA‐DR4‐positive children, there were no significantly associated risk factors for rheumatoid factor positivity.
Risk factors for rheumatoid factor positivity in children vary by HLA‐DR4 genotype. In HLA‐DR4‐negative children, breast feeding may decrease the risk, and environmental tobacco smoke may increase the risk, of autoimmunity.
Overweight and obesity in adulthood are established risk factors for adverse cardiovascular outcomes, but the contribution of overweight in childhood to later cardiovascular risk is less clear. Evidence for a direct effect of childhood overweight would highlight early life as an important target for cardiovascular disease prevention. The aim of this study was to assess whether overweight and obesity in childhood and adolescence contribute to excess cardiovascular risk in adults.
Methods and findings
Data from three British birth cohorts, born in 1946, 1958 and 1970, were pooled for analysis (n = 11,447). Individuals were categorised, based on body mass index (BMI), as being of normal weight or overweight/obese in childhood, adolescence and adulthood. Eight patterns of overweight were defined according to weight status at these three stages. Logistic regression models were fitted to assess the associations of patterns of overweight with self-reported type 2 diabetes, hypertension, and coronary heart disease (CHD) in adulthood (34–53 years). Compared to cohort members who were never overweight, those who were obese in adulthood had increased risk of all outcomes. For type 2 diabetes, the odds ratio was higher for obese adults who were also overweight or obese in childhood and adolescence (OR 12.6; 95% CI 6.6 to 24.0) than for those who were obese in adulthood only (OR 5.5; 95% CI 3.4 to 8.8). There was no such effect of child or adolescent overweight on hypertension. For CHD, there was weak evidence of increased risk among those with overweight in childhood. The main limitations of this study concern the use of self-reported outcomes and the generalisability of findings to contemporary child populations.
Type 2 diabetes and to a lesser extent CHD risk may be affected by overweight at all stages of life, while hypertension risk is associated more strongly with weight status in adulthood.
Overweight and obesity are steadily increasing worldwide with the greatest prevalence occurring in high-income countries. Many factors influence body mass index (BMI); however multiple influences assessed in families and individuals are rarely studied together in a prospective design. Our objective was to model the impact of multiple influences at the child (low birth weight, history of maltreatment, a history of childhood mental and physical conditions, and school difficulties) and family level (parental income and education, parental mental and physical health, and family functioning) on BMI in early adulthood.
We used data from the Ontario Child Health Study, a prospective, population-based study of 3,294 children (ages 4–16 years) enrolled in 1983 and followed up in 2001 (N = 1,928; ages 21–35 years). Using multilevel models, we tested the association between family and child-level variables and adult BMI after controlling for sociodemographic variables and health status in early adulthood.
At the child level, presence of psychiatric disorder and school difficulties were related to higher BMI in early adulthood. At the family level, receipt of social assistance was associated with higher BMI, whereas family functioning, having immigrant parents and higher levels of parental education were associated with lower BMI. We found that gender moderated the effect of two risk factors on BMI: receipt of social assistance and presence of a medical condition in childhood. In females, but not in males, the presence of these risk factors was associated with higher BMI in early adulthood.
Overall, these findings indicate that childhood risk factors associated with higher BMI in early adulthood are multi-faceted and long-lasting. These findings highlight the need for preventive interventions to be implemented at the family level in childhood.
Family and child level risk factors; Body mass index
Increasing evidence suggests exposure to adverse conditions in intrauterine life may increase the risk of developing attention-deficit/hyperactivity disorder (ADHD) in childhood. High maternal pre-pregnancy body mass index (BMI) has been shown to predict child ADHD symptoms, however the neurocognitive processes underlying this relationship are not known. The aim of the present study was to test the hypothesis that this association is mediated by alterations in child executive function.
A population-based cohort of 174 children (mean age = 7.3±0.9 (SD) yrs, 55% girls) was evaluated for ADHD symptoms using the Child Behavior Checklist, and for neurocognitive function using the Go/No-go task. This cohort had been followed prospectively from early gestation and birth through infancy and childhood with serial measures of maternal and child prenatal and postnatal factors. Maternal pre-pregnancy BMI was a significant predictor of child ADHD symptoms (F(1,158) = 4.80, p = 0.03) and of child performance on the Go/No-go task (F(1,157) = 8.37, p = 0.004) after controlling for key potential confounding variables. A test of the mediation model revealed that the association between higher maternal pre-pregnancy BMI and child ADHD symptoms was mediated by impaired executive function (inefficient/less attentive processing; Sobel Test: t = 2.39 (±0.002, SEM), p = 0.02).
To the best of our knowledge this is the first study to report that maternal pre-pregnancy BMI-related alterations in child neurocognitive function may mediate its effects on ADHD risk. The finding is clinically significant and may extrapolate to an approximately 2.8-fold increase in the prevalence of ADHD among children of obese compared to those of non-obese mothers. These results add further evidence to the growing awareness that neurodevelopmental disorders such as ADHD may have their foundations very early in life.
The worldwide epidemic of childhood obesity is progressing at an alarming rate. Risk factors for coronary heart disease (CHD) are already identifiable in overweight children. The severity of the long-term effects of excess childhood weight on CHD, however, remains unknown.
We investigated the association between body-mass index (BMI) in childhood (7 through 13 years of age) and CHD in adulthood (25 years of age or older), with and without adjustment for birth weight. The subjects were a cohort of 276,835 Danish schoolchildren for whom measurements of height and weight were available. CHD events were ascertained by linkage to national registers. Cox regression analyses were performed.
In 5,063,622 person-years of follow-up, 10,235 men and 4318 women for whom childhood BMI data were available received a diagnosis of CHD or died of CHD as adults. The risk of any CHD event, a nonfatal event, and a fatal event among adults was positively associated with BMI at 7 to 13 years of age for boys and 10 to 13 years of age for girls. The associations were linear for each age, and the risk increased across the entire BMI distribution. Furthermore, the risk increased as the age of the child increased. Adjustment for birth weight strengthened the results.
Higher BMI during childhood is associated with an increased risk of CHD in adulthood. The associations are stronger in boys than in girls and increase with the age of the child in both sexes. Our findings suggest that as children are becoming heavier worldwide, greater numbers of them are at risk of having CHD in adulthood.
The transition between adolescence and young adulthood is a developmentally sensitive time where children are at an increased risk for becoming overweight and developing obesity. Twin studies have reported that body mass index [BMI] is highly heritable, however, it remains unclear whether the genetic influences are sex-limited and whether non-additive genetic influences contribute to body mass index [BMI] during these ages. In the current report, we examined self-reported data on BMI in same [n= 2744] and opposite-sex [n = 1178] siblings participating in the National Longitudinal Study on Adolescent Health [Add Health]. To investigate whether the same or different genes contributed to BMI for both sexes, we fit quantitative sex-limited genetic models to three waves of data collection. At each of the three Waves of assessment, models that included additive genetic, individual-specific environment, and no sex-limited genetic influences fit the data most parsimoniously. Heritable effects on BMI at each of the three Waves were large for both sexes and ranged between 0.75 and 0.86. While genetic contributions across the ages were highly correlated, longitudinal analyses indicated that the relevant individual-specific environmental influences on BMI in adolescence and young adulthood change sizably. These results underscore the importance of understanding early genetic influences on BMI and highlight the role environmental experiences have at later ages when new genetic influences appear to make a small contribution to individual variation in BMI.
People who were small at birth and had poor infant growth have an increased risk of adult cardiovascular disease, osteoporosis and type 2 diabetes, particularly if their restricted early growth is followed by increased childhood weight gain. These relations extend across the normal range of birth size in a graded manner, so reduced size is not a prerequisite. In addition larger birth size is associated with risks of obesity and type 2 diabetes. The associations appear to reflect developmental plastic responses made by the fetus and infant based on cues about the environment, influenced by maternal characteristics including diet, body composition, stress and exercise levels. These responses involve epigenetic processes which modify the offspring’s phenotype. Vulnerability to ill-health results if the environment in infancy, childhood and later life is mismatched to the phenotype induced in development, informed by the developmental cues. This mismatch may arise through unbalanced diet or body composition of the mother, or change in lifestyle factors between generations. These insights offer new possibilities for early diagnosis and prevention of chronic disease.
Nutrition; fetal growth; metabolic disease; epigenetics
The effect of childhood risk factors for cardiovascular disease on adult mortality is poorly understood.
In a cohort of 4857 American Indian children without diabetes (mean age, 11.3 years; 12,659 examinations) who were born between 1945 and 1984, we assessed whether body-mass index (BMI), glucose tolerance, and blood pressure and cholesterol levels predicted premature death. Risk factors were standardized according to sex and age. Proportional-hazards models were used to assess whether each risk factor was associated with time to death occurring before 55 years of age. Models were adjusted for baseline age, sex, birth cohort, and Pima or Tohono O'odham Indian heritage.
There were 166 deaths from endogenous causes (3.4% of the cohort) during a median follow-up period of 23.9 years. Rates of death from endogenous causes among children in the highest quartile of BMI were more than double those among children in the lowest BMI quartile (incidence-rate ratio, 2.30; 95% confidence interval [CI], 1.46 to 3.62). Rates of death from endogenous causes among children in the highest quartile of glucose intolerance were 73% higher than those among children in the lowest quartile (incidence-rate ratio, 1.73; 95% CI, 1.09 to 2.74). No significant associations were seen between rates of death from endogenous or external causes and childhood cholesterol levels or systolic or diastolic blood-pressure levels on a continuous scale, although childhood hypertension was significantly associated with premature death from endogenous causes (incidence-rate ratio, 1.57; 95% CI, 1.10 to 2.24).
Obesity, glucose intolerance, and hypertension in childhood were strongly associated with increased rates of premature death from endogenous causes in this population. In contrast, childhood hypercholesterolemia was not a major predictor of premature death from endogenous causes.
The purpose of this study was to investigate the association between large-for-gestational age (LGA) infants and the development of childhood obesity in an inner-city, primarily African-American population.
Maternal, neonatal, socioeconomic and nutritional histories were collected for mothers with children age 2–5 years old. Associations between Alexander and customized birth weight (BW) percentiles and body mass index (BMI)-for-age of the child were examined.
195 mother-child pairs were enrolled; childhood obesity rate was 18%. Increasing Alexander and customized BW percentiles were related to increasing obesity. LGA newborns were 2.5 times more likely to be obese in childhood than average size newborns. Maternal smoking was also associated with childhood obesity.
LGA infants have the highest likelihood of childhood obesity in this inner-city, predominantly African-American population. Customized growth percentiles perform best in identifying the highest risk population.
Childhood obesity; Customized growth percentiles; Large-for-gestational age infants; Maternal smoking
Background and Objectives
Obesity is a chronic disease that requires good eating habits and an active life style. Obesity may start in childhood and continue until adulthood. Severely obese children have complications such as diabetes, hypercholesterolemia, hypertension and atherosclerosis. The goal of this study was to determine the effects of exercise programs on anthropometric, metabolic, and cardiovascular parameters in obese children.
Subjects and Methods
Fifty four obese children were included. Anthropometric data such as blood pressures, body mass index (BMI) and obesity index (OI) were measured. Blood glucose, total cholesterol, triglycerides, low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), aspartate aminotransferase (AST), alanine aminotransferase (ALT), high sensitive-CRP (hs-CRP), brachial-ankle pulse wave velocity (BaPWV) and ankle brachial index (ABI) were measured. Physical fitness measurements were done. Obese children were divided into three groups: an aerobic exercise group (n=16), a combined exercise group (n=20), and a control group (n=18). Obese children exercised in each program for 10 weeks while those in the control group maintained their former lifestyle. After 10 weeks, anthropometric data and cardiovascular parameters were compared with the data obtained before the exercise program.
LDL-C, waist circumference, and systolic blood pressure decreased significantly in the aerobic exercise group compared to the control group (p<0.05). Waist circumference and systolic blood pressure decreased significantly in the combined exercise group compared to controls (p<0.05). Physical fitness level increased significantly after the exercise programs (p<0.05 vs. control). PWV did not show a significant change after exercise.
A short-term exercise program can play an important role in decreasing BMI, blood pressure, waist circumference, LDL-C and in improving physical fitness. Future investigations are now necessary to clarify the effectiveness of exercise on various parameters.
Obesity; Exercise; Cardiovascular disease
While many studies have demonstrated positive associations between childhood obesity and adult metabolic risk, important questions remain as to the nature of the relationship. In particular, it is unclear whether the associations reflect the tracking of body mass index (BMI) from childhood to adulthood or an independent level of risk. This systematic review aimed to investigate the relationship between childhood obesity and a range of metabolic risk factors during adult life.
To perform an unbiased systematic review to investigate the association between childhood BMI and risk of developing components of metabolic disease in adulthood, and whether the associations observed are independent of adult BMI.
Electronic databases were searched from inception until July 2010 for studies investigating the association between childhood BMI and adult metabolic risk. Two investigators independently reviewed studies for eligibility according to the inclusion/exclusion criteria, extracted the data and assessed study quality using the Newcastle–Ottawa Scale.
The search process identified 11 articles that fulfilled the inclusion and exclusion criteria. Although several identified weak positive associations between childhood BMI and adult total cholesterol, low-density lipo protein-cholesterol, triglyceride and insulin concentrations, these associations were ameliorated or inversed when adjusted for adult BMI or body fatness. Of the four papers that considered metabolic syndrome as an end point, none showed evidence of an independent association with childhood obesity.
Little evidence was found to support the view that childhood obesity is an independent risk factor for adult blood lipid status, insulin levels, metabolic syndrome or type 2 diabetes. The majority of studies failed to adjust for adult BMI and therefore the associations observed may reflect the tracking of BMI across the lifespan. Interestingly, where adult BMI was adjusted for, the data showed a weak negative association between childhood BMI and metabolic variables, with those at the lower end of the BMI range in childhood, but obese during adulthood at particular risk.
childhood obesity; metabolic syndrome; cardiovascular disease
Although recent trends in obesity have been well documented, generational patterns of obesity from early childhood through adulthood across birth cohorts, which account for the recent epidemic of childhood obesity, have not been well described. Such trends may have implications for the prevalence of obesity-associated conditions among population subgroups, including type 2 diabetes.
Our objective was to evaluate trajectories of obesity over the life course for the US population, overall and by gender and race.
Design, Setting, and Participants
We conducted an age, period, and birth cohort analysis of obesity for US individuals who participated in the National Health and Nutrition Examination Surveys (1971-2006).
Main Outcome Measures
Obesity was defined as a body mass index ≥ 95th percentile for individuals aged 2-16 years or ≥ 30 kg/m2 among individuals older than 16 years. Age was represented by the age of the individual at each NHANES survey, period was defined by the year midpoint of each survey, and cohort was calculated by subtracting age from period.
Recent birth cohorts are becoming obese in greater proportions for a given age, and are experiencing a greater duration of obesity over their lifetime. For example, whereas the 1966-75 and 1976-85 birth cohorts had reached an estimated obesity prevalence of at least 20% by 20-29 years of age, this level was only reached by 30-39 years for the 1946-55 and 1956-65 birth cohorts, by 40-49 years for the 1936-45 birth cohort, and by 50-59 years of age for the 1926-35 birth cohort. Trends are particularly pronounced for female compared with male, and black compared with white cohorts.
The increasing cumulative exposure to excess weight over the lifetime of recent birth cohorts will likely have profound implications for future rates of type 2 diabetes, and mortality within the US population.
obesity; trends; birth cohort; childhood; life course
Exposures during fetal life may have long-term health consequences including risk of childhood overweight. We investigated the associations between maternal recreational exercise during early and late pregnancy and the children's body mass index (BMI) and risk of overweight at 7 years. Data on 40,280 mother-child pairs from the Danish National Birth Cohort was used. Self-reported information about exercise was obtained from telephone interviews around gestational weeks 16 and 30. Children's weight and height were reported in a 7-year follow-up and used to calculate BMI and overweight status. Data was analyzed using multiple linear and logistic regression models. Recreational exercise across pregnancy was inversely related to children's BMI and risk of overweight, but all associations were mainly explained by smoking habits, socioeconomic status, and maternal pre-pregnancy BMI. Additionally, we did not find exercise intensity or changes in exercise habits in pregnancy related to the children's BMI or risk of overweight.
Low birth weight and high childhood body mass index (BMI) is each associated with an increased risk of coronary heart disease (CHD) in adult life. We studied individual and combined associations of birth weight and childhood BMI with the risk of CHD in adulthood.
Birth weight and BMI at age seven years were available in 216,771 Danish and Finnish individuals born 1924–1976. Linkage to national registers for hospitalization and causes of death identified 8,805 CHD events during up to 33 years of follow-up (median = 24 years) after age 25 years. Analyses were conducted with Cox regression based on restricted cubic splines. Using median birth weight of 3.4 kg as reference, a non-linear relation between birth weight and CHD was found. It was not significantly different between cohorts, or between men and women, nor was the association altered by childhood BMI. For birth weights below 3.4 kg, the risk of CHD increased linearly and reached 1.28 (95% confidence limits: 1.13 to 1.44) at 2 kg. Above 3.4 kg the association weakened, and from about 4 kg there was virtually no association. BMI at age seven years was strongly positively associated with the risk of CHD and the relation was not altered by birth weight. The excess risk in individuals with a birth weight of 2.5 kg and a BMI of 17.7 kg/m2 at age seven years was 44% (95% CI: 30% to 59%) compared with individuals with median values of birth weight (3.4 kg) and BMI (15.3 kg/m2).
Birth weight and BMI at age seven years appeared independently associated with the risk of CHD in adulthood. From a public health perspective we suggest that particular attention should be paid to children with a birth weight below the average in combination with excess relative weight in childhood.
OBJECTIVE: To update the 1979 Canadian Task Force on the Periodic Health Examination recommendation on screening for childhood obesity by reviewing any new evidence concerning health risks in childhood and adulthood, and effective preventive or therapeutic interventions. OPTIONS: Detection: routine measurement of height and weight, use of skinfold thickness measurements, calculation of body mass index (BMI). Intervention: diet, exercise, behaviour modification and comprehensive family-based weight-reduction programs. Components of these interventions could be offered routinely or reserved for children and families who perceive obesity to be a present or potential problem. OUTCOMES: The task force reviewed the probability of obese children become obese adults as a risk factor for adult heart disease and overall related illness and death in adult life as well as obesity as a risk factor for physical and psychologic illness in childhood. EVIDENCE: A MEDLINE search for relevant articles published between January 1981 and February 1991 was undertaken. VALUES: The task force's evidence-based rules for recommendations were used. BENEFITS, HARMS AND COSTS: If weight reduction in childhood were shown to prevent physical or psychologic illness in childhood, or illness and death in adult life, screening and treatment should be recommended. Screening for obesity may cause anxiety on the part of the child and family; malnutrition in children as a result of parents becoming overly anxious about the health risks of obesity has been reported. Most weight reduction programs have limited long-term effectiveness and can be costly. RECOMMENDATIONS: There is insufficient evidence of short-term or long-term benefits from screening for or treatment of childhood obesity to recommend such screening or recommend against it. There is fair evidence to recommend against very-low-kilojoule diets for preadolescents. There is insufficient evidence to recommend for or against exercise programs or intensive family-based programs for most obese children. VALIDATION: These recommendations are similar to those of the American Academy of Pediatrics and the US Preventive Services Task Force. SPONSOR: These guidelines were developed and endorsed by the Canadian task force, which is funded by Health Canada.
To evaluate the cross-sectional relationship between asthma and pre-gravid body mass index (BMI); and to assess the risk of adult weight change among women with history asthma diagnosed in childhood or adulthood, respectively.
Study participants were 3,737 pregnant women enrolled in a cohort study. Information on history of asthma, pre-gravid BMI, adult weight change (difference between BMI at age 18 and pre-gravid BMI) and other socio demographic characteristics was collected using interviewer-administered questionnaires. Pre-gravid BMI was categorized into lean (BMI <18.5 kg/m2), overweight (BMI 25–24.9 kg/m2) and obese (BMI ≥30 kg/m2). Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI).
Approximately 13.1% of study participants reported history of asthma. Compared with the reference group (BMI 18.5–24.9 kg/m2), the odds of asthma was higher among overweight (OR=1.51; 95%CI 1.18–1.93) and obese (OR=1.47; 95% CI 1.06–2.03) women while it was lower among lean women (OR=0.42; 95% CI 0.21–0.84) (trend p-value <0.001). Women who gained ≥20 kg, compared with those who maintained their weight (±2.5 kg) had a 2.7-fold increased odds of asthma (95% CI 1.02–7.00).
Overweight and obese women were more likely to have history of asthma. Adult weight gain was positively associated with asthma diagnosis. Longitudinal studies designed to prospectively assess patterns of adult weight change in relation to asthma are warranted.
Asthma; Pediatric Asthma; Body Mass Index; Obesity; Adult Weight Change
Hyperhomocysteinemia is regarded as a risk factor for cardiovascular diseases, diabetes and obesity. Manifestation of these chronic metabolic disorders starts in early life marked by increase in body mass index (BMI). We hypothesized that perturbations in homocysteine metabolism in early life could be a link between childhood obesity and adult metabolic disorders. Thus here we investigated association of common variants from homocysteine metabolism pathway genes with obesity in 3,168 urban Indian children.
We genotyped 90 common variants from 18 genes in 1,325 children comprising of 862 normal-weight (NW) and 463 over-weight/obese (OW/OB) children in stage 1. The top signal obtained was replicated in an independent sample set of 1843 children (1,399 NW and 444 OW/OB) in stage 2. Stage 1 association analysis revealed association between seven variants and childhood obesity at P<0.05, but association of only rs2796749 in AMD1 [OR = 1.41, P = 1.5×10-4] remained significant after multiple testing correction. Association of rs2796749 with childhood obesity was validated in stage 2 [OR = 1.28, P = 4.2×10-3] and meta-analysis [OR = 1.35, P = 1.9×10-6]. AMD1 variant rs2796749 was also associated with quantitative measures of adiposity and plasma leptin levels that was also replicated and corroborated in combined analysis.
Our study provides first evidence for the association of AMD1 variant with obesity and plasma leptin levels in children. Further studies to confirm this association, its functional significance and mechanism of action need to be undertaken.
Adult cholesterol concentrations might be influenced by early-life factors, such as breastfeeding and birth weight, referred to as “early programming”. How such early factors exert their influence over the life course is still poorly understood. Evidence from studies in children and adolescents is scarce and conflicting. We investigated the influence of 6 different perinatal risk factors on childhood total and HDL cholesterol concentrations and total-to-HDL cholesterol ratio measured at 8 years of age, and additionally we studied the role of the child's current Body Mass Index (BMI).
Anthropometric measures and blood plasma samples were collected during a medical examination in 751 8-year-old children participating in the prospective Prevention and Incidence of Asthma and Mite Allergy (PIAMA) birth cohort study. Linear and logistic regression were performed to estimate associations of total and HDL cholesterol concentrations with breastfeeding, birth weight, infant weight gain, maternal overweight before pregnancy, gestational diabetes and maternal smoking during pregnancy, taking into account the child's current BMI.
Linear regressions showed an association between total-to-HDL cholesterol ratio and maternal pre-pregnancy overweight (β = 0.15, Confidence Interval 95% (CI): 0.02, 0.28), rapid infant weight gain (β = 0.13, 95%CI: 0.01, 0.26), and maternal smoking during pregnancy (β = 0.14, 95%CI: 0.00, 0.29). These associations were partly mediated by the child's BMI.
Total-to-HDL cholesterol ratio in 8-year-old children was positively associated with maternal pre-pregnancy overweight, maternal smoking during pregnancy and rapid infant weight gain.
Rates of weight gain in infancy and early childhood can influence later neurocognitive, metabolic, and cardiovascular health. We studied the relationship of weight gain during infancy and early childhood to intelligence quotient (IQ), blood pressure (BP), and body mass index (BMI) at age 9 in children born with very low birth weight (VLBW). Sixty-five children born prematurely with VLBW were followed longitudinally and at 9 years IQ, BP, and BMI were measured. The mean weight z scores at birth, neonatal intensive care discharge, 1 year corrected for prematurity, 5, and 9 years were −0.17, −2.09, −1.3, −0.68, 0.06, respectively. Weight gain during infancy (discharge to 1 year corrected for prematurity) and early childhood (1 year corrected age to 5 years) was expressed as rate of change in weight, rate of change in weight z score, and interval change in weight z score. In multiple regression analyses that adjusted for race, gender, maternal education, antenatal steroids, birth weight z score, major intracranial lesions on ultrasound, and chronic lung disease, rates of weight gain in infancy and early childhood were predictive of BMI z score at 9 years, regression coefficients (95% confidence intervals); 0.19 (0.02, 0.36) and 0.37 (0.11, 0.63), respectively, expressed as change in BMI z score per 10 g/week weight increase. Rates of weight gain were not predictive of systolic BP z score, Verbal IQ or Performance IQ. In VLBW infants, more rapid weight gain during infancy, and especially early childhood, is associated with higher BMI at school age.
prematurity; growth; follow-up; outcomes
Identifying adults at increased risk of cardiovascular disease (CVD) from childhood BMI could be informative for disease prevention, but depends on the utility of childhood BMI cut-offs.
We aimed to establish how well the International Obesity Task Force (IOTF) and population-specific cut-offs for childhood BMI predict CVD risk factors in mid-adulthood.
We used the 1958 British birth cohort, whose BMI measures were collected at 7, 11, 16y and CVD risk factors (obesity, hypertension, adverse lipid levels, type 2 diabetes risk) at 45y. Sensitivity and specificity of IOTF and population-specific cut-offs for childhood BMI were calculated for each CVD risk factor.
Prevalence of overweight or obesity was low in childhood (<11%, using IOTF cut-offs) compared to adulthood (75% men; 56% women). IOTF cut-offs had high specificities (91.6-97.9%) but low sensitivities (7.1-31.5%) for predicting adult outcomes. In comparison, population-specific cut-offs identified large groups of children (e.g. >38% for predicting adult obesity) that had improved sensitivities (17.3-67.3%), but lower specificities (52.9-84.6%) than IOTF cut-offs. Accelerated BMI gains in childhood predicted adult obesity and type 2 diabetes risk, but prediction was no greater than for childhood BMI at one age (AUC 0.55-0.65 vs 0.59-0.75). Childhood BMI and BMI gain were weak predictors for adult hypertension and adverse lipid levels.
Neither the IOTF nor our population-specific cut-offs for childhood BMI provided adequate diagnostic tools for adult CVD risk factors in a population experiencing rapid change in obesity prevalence over their lifetime.
Child body mass index cut-offs; Overweight and obesity; IOTF; Cardiovascular risk factors; Great Britain
Background and aim: Childhood obesity represents a rising threat in southern Europe. It is widely accepted that childhood obesity is an important risk factor for the appearance of obesity in adulthood. Our aim was to estimate the prevalence of obesity in school aged children living in one of the poorest districts of Europe, as well as to estimate the association between the frequency of obesity observed in these children and their parents.
Material and methods: We examined and calculated the body mass index (BMI) in 107 children aged 12.2 ±0.78 years. BMI was adjusted for age and sex and it was correlated with children parents' weight status.
Results: Obesity was diagnosed in 16% of the children. The relationship between childrens and their parents weight status was very strong. In 40% of the obese parents, their children were found to be obese also (p<0.001).
Conclusion: In the present study a strong relationship between children weight status and their parents' weight status was confirmed. Additionally, this correlation was proven at a district with very low house income. Knowing that it is easier to prevent obesity, rather than to cure it, our aim should be, when a child is brought to the doctor, independently of the cause, to assess both the child as well as its parents' weight status.
obesity; children; childhood obesity; children's parent obesity; BMI
We investigated early childhood disparities in high body mass index (BMI) between Black and White US children.
We compared differences in Black and White children’s prevalence of sociodemographic, prenatal, perinatal, and early life risk and protective factors; fit logistic regression models predicting high BMI (≥ 95th percentile) at age 4 to 5 years to 2 nationally representative samples followed from birth; and performed separate and pooled-survey estimations of these models.
After adjustment for sample design–related variables, models predicting high BMI in the 2 samples were statistically indistinguishable. In the pooled-survey models, Black children’s odds of high BMI were 59% higher than White children’s (odds ratio [OR] = 1.59; 95% confidence interval [CI]= 1.32, 1.92). Sociodemographic predictors reduced the racial disparity to 46% (OR = 1.46; 95% CI = 1.17, 1.81). Prenatal, perinatal, and early life predictors reduced the disparity to nonsignificance (OR = 1.18; 95% CI = 0.93, 1.49). Maternal prepregnancy obesity and short-duration or no breastfeeding were among predictors for which racial differences in children’s exposures most disadvantaged Black children.
Racial disparities in early childhood high BMI were largely explained by potentially modifiable risk and protective factors.
Prepregnant obesity has been shown to be related to several birth defects, most notably neural tube defects. We investigated the previously observed association between obesity and spina bifida and also possible associations between obesity and other birth defects.
We conducted a case-control study of fetuses and liveborn infants among California births, July 1999 and June 2004. Of those eligible, 80% of case mothers (n = 659) and 77% of control mothers (n = 700) were interviewed. Cases were 147 infants with anencephaly, 191 with spina bifida, 142 with d-transposition of great arteries, and 181 with tetralogy of Fallot. Maternal body mass index (BMI) was based on prepregnant weight and height.
The odds ratios of birth defects with obesity (BMI ≥30 relative to normal BMI) were 1.6 for anencephaly (95% confidence intervals = 1.0 –2.6); 1.4 for spina bifida (0.8–2.2); 0.7 for d-transposition of great arteries (0.4–1.4); and 0.8 for tetralogy of Fallot (0.4–1.4). Modestly elevated odds ratios were observed with obesity among women who reported weight gain in their waist before pregnancy—for anencephaly, 2.4 (1.2–5.1) and for spina bifida, 1.8 (0.9–3.6).
These data do not fully support earlier findings with respect to the relationships of obesity with anencephaly and spina bifida.