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Genetic markers of adult obesity risk are associated with greater early infancy weight gain and growth.

ABSTRACT: BACKGROUND:Genome-wide studies have identified several common genetic variants that are robustly associated with adult obesity risk. Exploration of these genotype associations in children may provide insights into the timing of weight changes leading to adult obesity. METHODS AND FINDINGS:Children from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were genotyped for ten genetic variants previously associated with adult BMI. Eight variants that showed individual associations with childhood BMI (in/near: FTO, MC4R, TMEM18, GNPDA2, KCTD15, NEGR1, BDNF, and ETV5) were used to derive an "obesity-risk-allele score" comprising the total number of risk alleles (range: 2-15 alleles) in each child with complete genotype data (n = 7,146). Repeated measurements of weight, length/height, and body mass index from birth to age 11 years were expressed as standard deviation scores (SDS). Early infancy was defined as birth to age 6 weeks, and early infancy failure to thrive was defined as weight gain between below the 5th centile, adjusted for birth weight. The obesity-risk-allele score showed little association with birth weight (regression coefficient: 0.01 SDS per allele; 95% CI 0.00-0.02), but had an apparently much larger positive effect on early infancy weight gain (0.119 SDS/allele/year; 0.023-0.216) than on subsequent childhood weight gain (0.004 SDS/allele/year; 0.004-0.005). The obesity-risk-allele score was also positively associated with early infancy length gain (0.158 SDS/allele/year; 0.032-0.284) and with reduced risk of early infancy failure to thrive (odds ratio = 0.92 per allele; 0.86-0.98; p = 0.009). CONCLUSIONS:The use of robust genetic markers identified greater early infancy gains in weight and length as being on the pathway to adult obesity risk in a contemporary birth cohort.

SUBMITTER: Elks CE

PROVIDER: S-EPMC2876048 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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Genetic markers of adult obesity risk are associated with greater early infancy weight gain and growth.

Elks Cathy E CE Loos Ruth J F RJ Sharp Stephen J SJ Langenberg Claudia C Ring Susan M SM Timpson Nicholas J NJ Ness Andrew R AR Davey Smith George G Dunger David B DB Wareham Nicholas J NJ Ong Ken K KK

PLoS medicine 20100525 5

<h4>Background</h4>Genome-wide studies have identified several common genetic variants that are robustly associated with adult obesity risk. Exploration of these genotype associations in children may provide insights into the timing of weight changes leading to adult obesity.<h4>Methods and findings</h4>Children from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were genotyped for ten genetic variants previously associated with adult BMI. Eight variants that showed in ...[more]

PMID: 20520848

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Project description:BackgroundPatterns of early growth are associated with later body composition and risk of adult noncommunicable disease but information from low-income countries is limited.ObjectivesThe aim of this study was to investigate early growth trajectories and later anthropometric and bone density outcomes among children born term low birth weight (LBW: 1.8-2.5 kg).MethodsWe used data from 902 children from the Delhi Infant Vitamin D Supplementation study of LBW term infants (which collected monthly anthropometry from birth to 6 mo) and who had height, weight, midupper arm circumference (MUAC), midupper arm muscle circumference (MUAMC), subscapular and triceps skinfold thicknesses, tibia and radius bone density measured at age 4-6 y. We investigated how growth in the first 6 mo of life, modeled using the SuperImposition by Translation and Rotation (SITAR) growth curve model, was related to these outcomes. SITAR summarizes each infant's weight and length trajectory in terms of a population mean curve and child-specific growth parameters: size, timing, and intensity. These were included as explanatory variables in linear regression models for the childhood outcomes.ResultsConsidering the infant weight and length SITAR parameters jointly, childhood weight was strongly associated with infant length timing [estimated regression coefficient β = 0.25 (95% CI: 0.10, 0.39)] and with weight size, timing, and intensity [β = 9.01 (6.75, 11.27), β = -0.25 (-0.43, -0.07), β = 5.03 (3.22, 6.84), respectively]. Childhood height was associated only with the length parameters [β = 0.97 (0.71, 1.23), β = -0.43 (-0.77, -0.09), β = 11.68 (8.60, 14.75), respectively]; childhood MUAC, MUAMC, and skinfolds with all parameters; and bone density with none. Overall, delayed and sustained growth in infant weight and length resulted in higher values of all outcomes except bone density, with the period up to 15 wk of age appearing critical for setting childhood anthropometry in this population.ConclusionsThe explanation for the effects of delayed growth and length of the period in which trajectories are set is unclear; however, sustained and delayed growth in early infancy appears to be beneficial for these LBW children at least in the short-term. The trial was registered at clinicaltrials.gov as BT/PR7489/PID/20/285/2006.

Project description:BACKGROUND:Rapid infant weight gain (RIWG) is a very strong predictor of childhood overweight and obesity (COO). Socioeconomic position (SEP) is also related to the risk of COO and parents of different SEP may differ in their reaction to accelerated infant weight gain. Together this could lead to differences in how weight gain and COO risk relate across SEP. This study aimed to analyse possible interaction of SEP and RIWG on COO risk. METHODS:A register-based longitudinal cohort study followed 19,894 healthy, term infants, born in Denmark between December 2011 and May 2015. Logistic regression models were used to estimate odds ratios (OR) of COO risk at 2 years (22-26 months) of age with 95% confidence intervals (95% CI) for categories of infancy weight gain based on changes in weight-for-age z-scores between 0 and 8-10 months of age (slow (<- 0.67), mean (- 0.67-0.67), rapid (> 0.67-1.34) and very rapid (> 1.34)). Possible multiplicative and additive interaction of SEP (based on household income and maternal education) on the relationship between infancy weight gain and COO were analysed. RESULTS:In total, 19.1 and 15.1% experienced rapid or very rapid weight gain, respectively, and 1497 (7.5%) children were classified with COO at follow-up. These prevalences were higher in those with lower levels of SEP. Adjusted OR for COO were 3.09 (95% CI [2.66-3.59]) and 7.58 (95% CI [6.51-8.83]) for rapid and very rapid weight gain, respectively, when household income was included in the model. Results were similar in the model including maternal education. No signs of interactions were detected on a multiplicative scale. Weak signs of additive interaction were present, but these values did not reach significance. CONCLUSION:Both rapid and very rapid weight gain were associated with substantially higher risks of COO but these associations were not modified by SEP. This indicates that promotion of healthy weight gain should take place in all population groups irrespective of their SEP.

Project description:Background:Excessive gestational weight gain and rapid infancy weight gain (RIWG) are associated with increased susceptibility to childhood obesity. Since low-income and minority children are particularly at risk, investigation of the associations between gestational weight gain and rate of infancy weight gain may inform childhood obesity prevention. This study investigated the associations between gestational weight gain and rate of infancy weight gain during the first four to six months postpartum in participants from the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) in Hawai'i and Puerto Rico. Methods:This was a cross-sectional secondary data analysis from a text message-based intervention in WIC participants in Hawai'i and Puerto Rico. The analysis included 80 mother/infant pairs from the control group who completed the follow-up visit when infants were four to six months old. Maternal weight, height, and gestational weight gain were self-reported. Infant weight was measured at baseline and follow-up. A proportional odds model was used to investigate the association between gestational weight gain and infancy weight gain rate (rapid or extremely rapid, on-track, or slow), adjusting for maternal age, pregravid body mass index (BMI) status, parity, and being up-to-date with infant vaccinations. Results:In comparison to recommended gestational weight gain, excessive and inadequate (under the recommended amount) gestational weight gain was associated with 77% decreased (adjusted odds ratio [AOR]?=?0.23; 95% confidence interval [CI]?=?0.08, 0.70; p?=?0.01) and 71% decreased (AOR?=?0.29; 95% CI?=?0.09, 0.94; p?=?0.04) odds of RIWG versus on-track or slow infant weight gain, respectively. In comparison to women with one child, women with two children (AOR?=?0.31; 95% CI?=?0.11, 0.87; p?=?0.03) or three or four children (AOR?=?0.24; 95% CI?=?0.07, 0.88; p?=?0.03) had significantly lower odds of RIWG versus on-track or slow infancy weight gain. Conclusions:Women with excessive or inadequate gestational weight gain had lower proportional odds of RIWG and were more likely to have slower infant weight gain than women who gained the recommended amount of weight. Trial registration:ClinicalTrials.gov Identifier; NCT02903186; September 16, 2016.

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Genetic markers of adult obesity risk are associated with greater early infancy weight gain and growth.

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Genetic markers of adult obesity risk are associated with greater early infancy weight gain and growth.

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