Higher Childhood Body Mass Index Research Articles

Associations between prenatal caffeine exposure and child development: Longitudinal results from the Adolescent Brain Cognitive Development (ABCD) Study.

Though caffeine use during pregnancy is common, its longitudinal associations with child behavioral and physical health outcomes remain poorly understood. Here, we estimated associations between prenatal caffeine exposure, body mass index (BMI), and behavior as children enter adolescence. Longitudinal data and caregiver-reported prenatal caffeine exposure were obtained from the ongoing Adolescent Brain and Cognitive Development (ABCD) SM Study, which recruited 11,875 children aged 9-11 years at baseline from 21 sites across the United States starting June 1, 2016. Prenatal caffeine exposure was analyzed as a 4-level categorical variable, and further group contrasts were used to characterize "any exposure" and "daily exposure" groups. Outcomes included psychopathology characteristics in children, sleep problems, and BMI. Potentially confounding covariates included familial (e.g., income, familial psychopathology), pregnancy (e.g., prenatal substance exposure), and child (e.g., caffeine use) variables. Among 10,873 children (5,686 boys [52.3%]; mean [SD] age, 9.9 [0.6] years) with nonmissing prenatal caffeine exposure data, 6,560 (60%) were exposed to caffeine prenatally. Relative to no exposure, daily caffeine exposure was associated with higher child BMI (β=0.08; FDR-corrected p=0.02), but was not associated with child behavior. Those exposed to two or more cups of caffeine daily (n=1,028) had greater sleep problems than those with lower/no exposure (β>0.92; FDR-corrected p<0.04). Daily prenatal caffeine exposure is associated with heightened childhood BMI, and when used multiple times a day greater sleep problems even after accounting for potential confounds. Whether this relationship is a consequence of prenatal caffeine exposure or its correlated factors remains unknown.

Mendelian randomization shows causal effects of birth weight and childhood body mass index on the risk of frailty

BackgroundThe association between birth weight and childhood body mass index (BMI) and frailty has been extensively studied, but it is currently unclear whether this relationship is causal.MethodsWe utilized a two-sample Mendelian randomization (MR) methodology to investigate the causal effects of birth weight and childhood BMI on the risk of frailty. Instrumental variables (p &amp;lt; 5E-08) strongly associated with own birth weight (N = 298,142 infants), offspring birth weight (N = 210,267 mothers), and childhood BMI (N = 39,620) were identified from large-scale genomic data from genome-wide association studies (GWAS). The frailty status was assessed using the frailty index, which was derived from comprehensive geriatric assessments of older adults within the UK Biobank and the TwinGene database (N = 175,226).ResultsGenetically predicted one standard deviation (SD) increase in own birth weight, but not offspring birth weight (maternal-specific), was linked to a decreased frailty index (β per SD increase = −0.068, 95%CI = −0.106 to −0.030, p = 3.92E-04). Conversely, genetically predicted one SD increase in childhood BMI was associated with an elevated frailty index (β per SD increase = 0.080, 95%CI = 0.046 to 0.114, p = 3.43E-06) with good statistical power (99.8%). The findings remained consistent across sensitivity analyses and showed no horizontal pleiotropy (p &amp;gt; 0.05).ConclusionThis MR study provides evidence supporting a causal relationship between lower birth weight, higher childhood BMI, and an increased risk of frailty.

Intrapartum antibiotic use is associated with higher child body mass index (BMI) z-score at 4 years of age

Early life antibiotic exposure may increase obesity risk. We investigated if prenatal, intrapartum, or childhood antibiotic use is associated with child zBMI score at 4 yrs of age. We included data from the Alberta Pregnancy Outcomes and Nutrition (APrON) study, a prospective cohort study, on maternal and child antibiotic exposure and clinic measures of height and weight at age 4 (n = 408). Prenatal and childhood antibiotic exposure was not associated with zBMI score. Maternal intrapartum antibiotic exposure was associated with a zBMI score increase of 0.12 (95 % CI; 0.04, 0.46) in children at 4 years of age compared to non-exposure intrapartum.

Infant feeding practices and body mass index up to 7.5 years in the French nationwide ELFE study.

The infant diet represents one of the main modifiable determinants of early growth. This study aimed to investigate the associations of infant feeding practices with body mass index (BMI) until 7.5 years. Analyses were based on data from the French nationwide ELFE birth cohort. Data on breastfeeding (BF) and complementary feeding (CF) were collected monthly from 2 to 10 months. Infant feeding practices were characterized using principal component analyses (PCA) and hierarchical ascendant classification. BMI z-score was computed at 1, 2, 3, 5 and 7.5 years, from data collected in the child's health booklet; 7.5-year overweight was defined according to IOTF references. Associations between infant feeding practices and BMI were investigated by linear regression models adjusted for main confounders. Ever breastfeeding was not associated with BMI up to 7.5 years. Compared to intermediate breastfeeding duration (1 to <3 months), longer breastfeeding duration (≥6 months) was related to lower 1-year BMI, but not at older ages. Compared to the recommended age at CF introduction (4-6 months), early CF (<4 months) was related to higher BMI up to 5 years with a similar trend at 7.5 years, but not to the risk of overweight. The PCA patterns characterized by early baby cereal introduction and late food pieces introduction or by frequent intake of main food groups were related to a lower BMI up to 7.5 years. Breastfeeding was related with a lower BMI in infancy but not thereafter, whereas an early CF initiation (<4 months) was associated with a higher BMI in childhood.

Interpersonal Discrimination, Neighborhood Inequities, and Children's Body Mass Index: A Descriptive, Cross-Sectional Analysis.

Psychosocial stressors have been implicated in childhood obesity, but the role of racism-related stressors is less clear. This study explored associations between neighborhood inequities, discrimination/harassment, and child body mass index (BMI). Parents of children aged 5-9 years from diverse racial/ethnic backgrounds (n = 1307), completed surveys of their child's exposure to discrimination/harassment. Census tract data derived from addresses were used to construct an index of concentration at the extremes, a measure of neighborhood social polarization. Child's height and weight were obtained from medical records. Multiple regression and hierarchical models examined child's BMI and racism at the individual and census tract levels. Children residing in the most Black-homogenous census tracts had 8.2 percentage units higher BMI percentile (95% confidence interval, 1.5-14.9) compared with white-homogenous tracts (P = .03). Household income and home values were lower, poverty rates higher, and single parent households more common among Black-homogeneous census tracts. Almost 30% of children experienced discrimination/harassment in the past year, which was associated with a 5.28-unit higher BMI percentile (95% confidence interval, 1.72-8.84; P = .004). Discrimination and racial/economic segregation were correlated with higher child BMI. Longitudinal studies are needed to understand whether these factors may be related to weight gain trajectories and future health.

Infant effortful control predicts BMI trajectories from infancy to adolescence.

Effortful control, or the regulation of thoughts and behaviour, is a potential target for preventing childhood obesity. To assess effortful control in infancy through late childhood as a predictor of repeated measures of body mass index (BMI) from infancy through adolescence, and to examine whether sex moderates the associations. Maternal report of offspring effortful control and measurements of child BMI were obtained at 7 and 8 time points respectively from 191 gestational parent/child dyads from infancy through adolescence. General linear mixed models were used. Effortful control at 6 months predicted BMI trajectories from infancy through adolescence, F(5,338) = 2.75, p = 0.03. Further, when effortful control at other timepoints were included in the model, they added no additional explanatory value. Sex moderated the association between 6-month effortful control and BMI, F(4, 338) = 2.59, p = 0.03, with poorer infant effortful control predicting higher BMI in early childhood for girls, and more rapid increases in BMI in early adolescence for boys. Effortful control in infancy was associated with BMI over time. Specifically, poor effortful control during infancy was associated with higher BMI in childhood and adolescence. These findings support the argument that infancy may be a sensitive window for the development of later obesity.

Childhood body mass index and the subsequent risk of anorexia nervosa and bulimia nervosa among women: A large Danish population-based study.

Evidence linking childhood body mass index (BMI) with subsequent eating disorders is equivocal. Potential explanations include different study populations and size, and that anorexia nervosa (AN) and bulimia nervosa (BN) should be studied separately. We examined whether birthweight and childhood BMI were associated with subsequent risk of AN and BN in girls. We included 68,793 girls from the Copenhagen School Health Records Register born between 1960 and 1996 with information on birthweight and measured weights and heights obtained from school health examinations at ages 6-15 years. Diagnoses of AN and BN were retrieved from Danish nationwide patient registers. We used Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). We identified 355 cases of AN (median age: 19.0) and 273 cases of BN (median age: 21.8). Higher childhood BMI was linearly associated with decreasing risk of AN and increasing risk of BN at all childhood ages. At age 6, the HR for AN was 0.85 (95% CI: 0.74-0.97) per BMI z-score and the HR for BN was 1.78 (95% CI: 1.50-2.11) per BMI z-score. Birthweight >3.75 kg was associated with increased risk of BN compared to a birthweight of 3.26-3.75 kg. Higher BMI in girls at ages 6-15 years was associated with decreasing risk of AN and increasing risk of BN. Premorbid BMI could be relevant for the etiology of AN and BN, and in identifying high risk individuals. Eating disorders are associated with elevated mortality, especially AN. Using a cohort of Copenhagen school children, we linked information on BMI at ages 6-15 years for 68,793 girls with nationwide patient registers. Low childhood BMI was associated with increased risk of AN, whereas high childhood BMI was associated with increased risk of BN. These findings may assist clinicians in identifying individuals at high-risk of these diseases.

Causal relationships between birth weight, childhood obesity and age at menarche: A two-sample Mendelian randomization analysis.

Observational studies suggest birth weight and childhood obesity are closely associated with age at menarche. However, the relationships between them are currently inconsistent and it remains elusive whether such associations are causal. Therefore, the aim of the study was to investigate whether there existed causal relationships between birth weight, childhood obesity and age at menarche. A two-sample Mendelian randomization (MR) study. The standard inverse variance weighted MR analyses were adopted to evaluate the causal effects of birth weight (n = 143,677), childhood body mass index (BMI) (n = 39,620) on age at menarche (n = 182,416) with summary statistics from large-scale genome-wide association studies(GWASs). Meanwhile, we validated our MR results with some sensitivity analyses including maximum likelihood, weighted-median and MR pleiotropy residual sum and outliermethods. The present study showed that each one standard deviation (1-SD) lower birth weight was predicted to result in a 0.1479 years earlier of age at menarche (β = .1479, 95% confidence interval [CI] = 0.0422-0.2535; p = 0.0061). We also found that genetically predicted 1-SD increase in childhood BMI was causally associated with early age at menarche (β = -.3966, 95%CI = -0.5294 to -0.2639; p = 4.73E-09). Our MR study suggests the causal effect of lower birth weight and higher childhood BMI on the increased risk of earlier menarche. It may be the opportune time to carry out weight control intervention in prenatal and early childhood development periods to prevent early menarche onset, thus decreasing the future adverse consequences.

Childhood BMI and other measures of body composition as a predictor of cardiometabolic non-communicable diseases in adulthood: a systematic review.

There is growing evidence that childhood malnutrition is associated with non-communicable diseases (NCD) in adulthood and that body composition mediates some of this association. This review aims to determine if childhood body composition can be used to predict later-life cardiometabolic NCD and which measures of body composition predicts future NCD. Electronic databases were searched for articles where: children aged under 5 years had body composition measured; cardiometabolic health outcomes were measured a minimum of 10 years later. The databases Embase, Medline and Global Health were searched through July 2020. Children aged under 5 years with a follow-up of minimum 10 years. Twenty-nine studies met the inclusion criteria. Though a poor proxy measure of body composition, body mass index (BMI) was commonly reported (n 28, 97 %). 25 % of these studies included an additional measure (ponderal index or skinfold thickness). Few studies adjusted for current body size (n 11, 39 %). Many studies reported that low infant BMI and high childhood BMI were associated with an increased risk of NCD-related outcomes in later life but no conclusions can be made about the exact timing of child malnutrition and consequent impact on NCD. Because studies focussed on BMI rather than direct measures of body composition, nothing can be said about which measures of body composition in childhood are most useful. Future research on child nutrition and long-term outcomes is urgently needed and should include validated body composition assessments as well as standard anthropometric and BMI measurements.

Growth pattern during early infancy, body mass index during childhood and childhood asthma.

There is a lack of longitudinal studies of associations between growth from infancy to childhood and asthma development. The objective of the study was to investigate the effects of weight change during infancy, body mass index (BMI) and the interaction of these factors on the risk of childhood asthma. We enrolled children born in 2008 and 2009 at full-term and with normal birth weight. The weight change in infancy was grouped into slow, on-track and rapid. BMI status in childhood was stratified into low, normal and high groups and used as a time-varying variable. The outcome was asthma, defined as two or more diagnoses of asthma separated by at least 1year after 2 years of age. The risk of asthma was assessed using Cox proportional hazard regression, with adjustment for sex, residence area at birth, economic status and feeding types in infancy. Of 917,707 children born in Korea in 2008 and 2009, 271,871 were eligible for analysis. The risk of asthma was greater in groups with low birth weight (aHR 1.06, 95% CI 1.04 to 1.08), rapid body weight change during early infancy (aHR 1.08, 95% CI 1.07 to 1.10) and high BMI during childhood (aHR 1.06, 95% CI 1.04-1.08). The interaction of weight change during early infancy with BMI during childhood was significant for asthma (p < .01). Rapid weight gain in infancy was associated with lower risk of asthma in those with low BMI during childhood; had no association with asthma in those with normal BMI during childhood; and was associated increased asthma risk in those with high BMI during childhood-aHR 1.26 (95% CI 1.19 to 1.33) and aHR 1.33 (95% CI 1.12 to 1.56) compared with on-track and slow infant weight gain, respectively. Low birth weight, high BMI during childhood and, in those with high childhood BMI, rapid weight gain during early infancy are associated with increased risk of childhood asthma.

Household food insecurity and obesity risk in preschool-aged children: A three-year prospective study

BackgroundHousehold food insecurity (FI) is a pressing social, economic and public health issue. However, little is known regarding the effect of FI exposure during the first few years of life, the most active postnatal time for neurobiological and physiological development, on patterns of weight gain during early childhood. It is also unknown whether dietary quality would serve as a pathway through which FI affects children's weight development. MethodThis was a secondary data analysis from a three-year randomized clinical trial with five hundred and thirty-four parent/child dyads. Household FI in the past year was reported by parents at baseline when children were 2–4 years of age using the USDA Household Food Security Survey Module-Six Item Short Form. Children's dietary quality at baseline was measured by the US Department of Agriculture Healthy Eating Index (HEI). Child body mass index (BMI) was measured following standardized protocols at baseline and 12-, 24-, and 36-month follow-up. A latent growth curve model was used to examine 1) the association between baseline FI and sex-and-age-adjusted BMI z-scores in children and 2) the HEI pathway between the FI- BMI association. ResultsFI early in life was associated with higher baseline BMI z-scores. Children who had higher BMI at baseline maintained their higher BMI status over the next three years. Children's dietary intake quality did not explain the association between baseline FI and BMI z-scores. ConclusionEarly exposure to FI was associated with higher BMI in children as early as two years of age, setting them up for an increased likelihood of persistently high BMI-for-age in later childhood. These data suggest that the first few years may be a critical time for developing obesity risk, calling for policy and practices designed for early intervention of food insecurity.

Early life body size, pubertal timing, and risks of benign breast disease in a large cohort of Danish female adolescents and women

A high childhood body mass index (BMI) may be protective against benign breast disease (BBD), but little is known about the effects of other early life body size measures. Thus, we examined associations between birthweight, childhood BMI, height, and pubertal timing and BBD risks. We included 171,272 girls, born from 1930 to 1996, from the Copenhagen School Health Records Register, which contains information on birthweight, childhood anthropometry (7-13years), age at onset of the growth spurt (OGS), and peak height velocity (PHV). During follow-up, 9361 BBD cases (15-50years) were registered in the Danish National Patient Register. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated by Cox regressions. At all childhood ages, BMI was inversely but non-linearly associated with BBD. The association was slightly stronger in magnitude for BMI z-scores above 0 (HRage 7 = 0.86; 95%CI: 0.83-0.90 per z-score) than below 0 (HRage 7 = 0.95; 95%CI 0.91-0.99 per z-score). Associations between childhoodheight and BBD differed by age; at 7years the association was an inverted U-shape, whereas at 13years height was not associated with BBD. Ages at OGS and PHV were positively associated with BBD. Low and high birthweights were associated with lower BBD risks. Conclusion: A high childhood BMI, a short or tall stature at young childhood ages, an early pubertal onset, and low or high birthweights are associated with reduced risks of BBD. These complex associations suggest that the role of these factors in breast tissue development during early life warrants further investigation in relation to BBD etiology. What is Known: •Benign breast disease (BBD) is common and may be an intermediary marker of breast cancer risks. •Early life body size may relate to the development of BBD, but currently little is known. What is New: •Girls with a high body mass index at school ages or with an early pubertal timing have decreased risks of BBD. •Short and tall heights at young childhood ages and low and high birthweights are associated with lower BBD risks.

The Association Between Puberty Timing and Body Mass Index in a Longitudinal Setting: The Contribution of Genetic Factors

We analyzed the contribution of genetic factors on the association between puberty timing and body mass index (BMI) using longitudinal data and two approaches: (i) genetic twin design and (ii) polygenic scores (PGS) of obesity indices. Our data were derived from Finnish cohorts: 9080 twins had information on puberty timing and BMI and 2468 twins also had genetic data. Early puberty timing was moderately associated with higher BMI in childhood in both boys and girls; in adulthood these correlations were weaker and largely disappeared after adjusting for childhood BMI. The largest proportion of these correlations was attributable to genetic factors. The higher PGSs of BMI and waist circumference were associated with earlier timing of puberty in girls, whereas weaker associations were found in boys. Early puberty is not an independent risk factor for adult obesity but rather reflects the association between puberty timing and childhood BMI contributed by genetic predisposition.

Pathways of Parental Education on Children's and Adolescent's Body Mass Index: The Mediating Roles of Behavioral and Psychological Factors.

AimThe increasing body mass index (BMI) often followed by overweight and obesity is a global health problem of the 21st century. Children and adolescents with lower socioeconomic status are more affected than their counterparts. The mechanisms behind these differences must be well understood to develop effective prevention strategies. This analysis aims at examining the association of parental education as an indicator of the socioeconomic status on children's and adolescent's body mass index and the role of behavioral and psychological risk factors for a higher BMI longitudinally.MethodsThe analysis was based on a nationwide sample of N = 460 children and adolescents, aged 11 to 17 at baseline (2009–2012), who took part in the representative BELLA study, the mental health module of the German National Health Interview and Examination Survey among Children and Adolescents (KiGGS). A follow-up was conducted 5 years later. Using mediation analyses, the mediating effects of breakfast consumption, consumption of sugar-sweetened beverages, screen time, physical activity, mental health problems (Strengths and Difficulties Questionnaire), and health-related quality of life (KIDSCREEN-10) on the association of parent's years of education on their children's BMI were investigated.ResultsA lower level of parental education was significantly associated with a higher BMI in children and adolescents 5 years later. The association was partially mediated by breakfast consumption and total screen time, with breakfast consumption mediating 16.7% and total screen time 27.8% of the association. After controlling for age, gender, and migration status, only breakfast consumption remained a partial mediator (8.5%). Other included variables had no mediating effects.ConclusionsPreventive measures should be mainly targeted at children and adolescents of parents with lower educational levels. Tailored strategies to prevent the development of overweight and obesity in this population among children and adolescents should promote daily breakfast consumption at home and reducing screen time.

Smoking during pregnancy is associated with child overweight independent of maternal pre-pregnancy BMI and genetic predisposition to adiposity

High maternal body mass index (BMI) and smoking during pregnancy are risk factors for child overweight. Maternal smoking tends to reduce her BMI and the association of smoking with child overweight may be confounded by or interacting with maternal genetic predisposition to adiposity. In the Danish National Birth Cohort, we investigated whether smoking during pregnancy is associated with child BMI/overweight independent of pre-pregnancy BMI and maternal genetic predisposition to adiposity estimated as total, transmitted and non-transmitted genetic risk scores (GRSs) based on 941 common genetic variants associated with BMI. Smoking during pregnancy was associated with higher child BMI and higher odds of child overweight in a dose–response relationship. The odds ratio (95% CI) for smoking 11 + cigarettes in third trimester versus no smoking was 2.42 (1.30; 4.50), irrespective of maternal BMI and maternal GRSs (total, transmitted or non-transmitted). There were no statistically significant interactions between maternal GRSs and smoking (all p-values for interactions > 0.05). In conclusion, in this study, smoking during pregnancy exhibits a dose–response association with increased child BMI/overweight, independent of maternal pre-pregnancy BMI, maternal transmitted, and non-transmitted genetic predisposition to adiposity. Avoidance of smoking during pregnancy may help prevent childhood obesity irrespective of the mother–child genetic predisposition.

Prevalence of High Body Mass Index in Children with Sickle Cell Disease and Its Correlation of Disease Severity

▪BackgroundChildren with sickle cell disease (SCD), particularly those with the homozygous form designated HbSS, have frequently been reported to suffer from impaired growth, delayed onset of puberty and poor nutritional status (1). However, improvement in healthcare of children with SCD in more economically developed countries, along with increased use of SCD-directed therapies such as hydroxyurea and chronic transfusions along with the recent rise in childhood obesity rates may have influenced growth of children with SCD. Two recent reports in the US found that 19-22% of children with SCD were overweight or obese (2, 3) . It is not known whether high body mass index (BMI) in children with SCD results in a worse clinical phenotype. Known association of childhood obesity with obstructive sleep apnoea (OSA) raises the potential of worsening clinical phenotype of SCD by increasing the incidence of nocturnal hypoxaemia which in turn may give rise to increased vaso-occlusive episodes (4). This study aimed to determine the prevalence of high body mass index (BMI) in an urban population of children in the UK with SCD and assess if there is correlation between BMI and disease severity.MethodsA retrospective chart review was performed on all patients aged 2-18 years with SCD who attended an outpatient clinic at Kings College Hospital, London between April 2015 and April 2017. Acute sickle cell-related emergency department (ED) attendances and hospital admissions in this period were recorded. BMI percentile, demographic information and laboratory markers of disease were recorded from the most recent clinic visit. Age and gender specific definitions of BMI percentiles were used, based on the British 1990 growth reference charts. Patients were assigned to 1 of 3 groups based on their BMI percentile: low, normal and high BMI. A high BMI was defined as >85th percentile for age and gender, whilst underweight was defined as <5th percentile.ResultsData was collected on 385 children with SCD in a single tertiary Paediatric Haemoglobinopathy centre in London. 16.6% children with SCD were overweight or obese and 5.2% were underweight. In contrast, government figures indicate that in the South London Borough of Southwark, up to 28% children aged 10-11 years were overweight or obese and 0.9% children were underweight in 2016-2017 (data.london.gov.uk). A high BMI among our SCD patients was associated with HbSC genotype (P= 0.006) and females (P=< 0.001). HbSS patients taking hydroxycarbamide had a significantly higher mean BMI compared to those not taking it (P=0.006). No association was found between BMI group and the number of acute sickle cell-related A&E attendances or hospital admissions for HbSS patients (P=0.450 and 0.780 respectively) or HbSC patients (P=0.838 and P=0.750 respectively). Patients with HbSS SCD in the high BMI group had a significantly higher haemoglobin (Hb) and fetal Hb (HbF) than those in the normal BMI group (P=<0.001 and P=0.010 respectively). HbSS patients in the high BMI group had a significantly lower absolute reticulocyte count (ARC) than those in the normal BMI group (P=0.022), see Table 1. These results suggest that HbSS patients with a high BMI may have a less severe disease than those with a normal BMI. These associations were not demonstrated in patients with HbSC disease.ConclusionsNearly one-sixth of children and adolescents with SCD in this urban population were overweight or obese. The association of hydroxycarbamide therapy and higher BMI in children with HbSS has been demonstrated in this study for the first time. There was no association between BMI group and the number of acute sickle cell-related A&E attendances or hospital admissions. In patients with HbSS disease, laboratory markers of disease severity, including Hb, HbF and ARC, suggest than patients with a high BMI may have a less severe disease than those with a normal BMI. Longitudinal studies monitoring BMI of children over time and markers of severity in SCD would produce greater evidence of the impact of a high BMI on disease severity. [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Causal association of childhood obesity with cancer risk in adulthood: A Mendelian randomization study.

In observational studies of children and adolescents, higher body weight has been associated with distinct disease outcomes, including cancer, in adulthood. Therefore, we performed a two-sample Mendelian randomization (MR) study to evaluate the causal effect of childhood obesity on long-term cancer risk. Single-nucleotide polymorphisms associated with higher childhood body mass index (BMI) from large-scale genome-wide association studies were used as genetic instruments. Summary-level data for 24 site-specific cancers were obtained from UK Biobank. We found that a 1-SD increase in childhood BMI (kg/m2 ) was significantly associated with a 60% increase in risk of pancreatic cancer (odds ratio [OR]: 1.60; 95% confidence interval [CI]: 1.12-2.28; P< 0.01) and a 47% increase in risk of esophageal cancer (OR: 1.47; 95% CI: 1.09-1.97; P< 0.01) in adults. In contrast, there was an inverse association of genetic predisposition to childhood obesity with throat (OR: 0.46; 95% CI: 0.27-0.79; P< 0.01) and breast cancer (OR: 0.77; 95% CI: 0.64-0.94; P< 0.01) in adult life. For the other 20 cancers studied, no statistically significant association was observed. Our MR analyses found causal effects of childhood obesity on several cancers. Maintaining a healthy weight should be emphasized during childhood and adolescence to prevent cancer risk later in life.

Phenome-wide investigation of the causal associations between childhood BMI and adult trait outcomes: a two-sample Mendelian randomization study

BackgroundChildhood obesity is reported to be associated with the risk of many diseases in adulthood. However, observational studies cannot fully account for confounding factors. We aimed to systematically assess the causal associations between childhood body mass index (BMI) and various adult traits/diseases using two-sample Mendelian randomization (MR).MethodsAfter data filtering, 263 adult traits genetically correlated with childhood BMI (P < 0.05) were subjected to MR analyses. Inverse-variance weighted, MR-Egger, weighted median, and weighted mode methods were used to estimate the causal effects. Multivariable MR analysis was performed to test whether the effects of childhood BMI on adult traits are independent from adult BMI.ResultsWe identified potential causal effects of childhood obesity on 60 adult traits (27 disease-related traits, 27 lifestyle factors, and 6 other traits). Higher childhood BMI was associated with a reduced overall health rating (β = − 0.10, 95% CI − 0.13 to − 0.07, P = 6.26 × 10−11). Specifically, higher childhood BMI was associated with increased odds of coronary artery disease (OR = 1.09, 95% CI 1.06 to 1.11, P = 4.28 × 10−11), essential hypertension (OR = 1.12, 95% CI 1.08 to 1.16, P = 1.27 × 10−11), type 2 diabetes (OR = 1.36, 95% CI 1.30 to 1.43, P = 1.57 × 10−34), and arthrosis (OR = 1.09, 95% CI 1.06 to 1.12, P = 8.80 × 10−9). However, after accounting for adult BMI, the detrimental effects of childhood BMI on disease-related traits were no longer present (P > 0.05). For dietary habits, different from conventional understanding, we found that higher childhood BMI was associated with low calorie density food intake. However, this association might be specific to the UK Biobank population.ConclusionsIn summary, we provided a phenome-wide view of the effects of childhood BMI on adult traits. Multivariable MR analysis suggested that the associations between childhood BMI and increased risks of diseases in adulthood are likely attributed to individuals remaining obese in later life. Therefore, ensuring that childhood obesity does not persist into later life might be useful for reducing the detrimental effects of childhood obesity on adult diseases.

Childhood obesity and multiple sclerosis: A Mendelian randomization study

Background: Higher childhood body mass index (BMI) has been associated with an increased risk of multiple sclerosis (MS). Objective: To evaluate whether childhood BMI has a causal influence on MS, and whether this putative effect is independent from early adult obesity and pubertal timing. Methods: We performed Mendelian randomization (MR) using summary genetic data on 14,802 MS cases and 26,703 controls. Large-scale genome-wide association studies provided estimates for BMI in childhood (n = 47,541) and adulthood (n = 322,154). In multivariable MR, we examined the direct effects of each timepoint and further adjusted for age at puberty. Findings were replicated using the UK Biobank (n = 453,169). Results: Higher genetically predicted childhood BMI was associated with increased odds of MS (odds ratio (OR) = 1.26/SD BMI increase, 95% confidence interval (CI): 1.07–1.50). However, there was little evidence of a direct effect after adjusting for adult BMI (OR = 1.03, 95% CI: 0.70–1.53). Conversely, the effect of adult BMI persisted independent of childhood BMI (OR = 1.43; 95% CI: 1.01–2.03). The addition of age at puberty did not alter the findings. UK Biobank analyses showed consistent results. Sensitivity analyses provided no evidence of pleiotropy. Conclusion: Genetic evidence supports an association between childhood obesity and MS susceptibility, mediated by persistence of obesity into early adulthood but independent of pubertal timing.

Risk of gestational diabetes mellitus in nulliparous women – Associations with early life body size and change in body mass index from childhood to adulthood

AimsWe examined whether a woman’s birthweight, childhood height, body mass index (BMI), and BMI changes from childhood to pregnancy were associated with risks of gestational diabetes mellitus (GDM). MethodsWe studied 13,031 women from the Copenhagen School Health Records Register born 1959–1996 with birthweight and measured anthropometric information at ages 7 and/or 13. The diagnosis of GDM (n = 255) was obtained from a national health register. Risk ratios (RR) were estimated using log-linear binomial regression. ResultsOwn birthweight and childhood height were inversely associated with GDM. Girls with overweight at age 7 had a higher risk of GDM than girls with normal-weight (RR: 1.79, 95% CI: 1.31, 2.47). Compared to women with normal-weight in childhood and adulthood, risks of GDM were higher in women who developed overweight from age 7 to pregnancy (RR: 4.62; 3.48, 6.14) or had overweight at both times (RR: 4.71; 3.24, 6.85). In women whose BMI normalized from age 7 to pregnancy the RR for GDM was 1.08 (0.47, 2.46). ConclusionsLower birthweight, shorter childhood height, and higher childhood BMI are associated with increased risks of GDM. Efforts to help girls maintain a normal BMI before pregnancy may be warranted to minimize risks of GDM.