Longitudinal Assessment of Childhood Dietary Patterns: Associations with Body Mass Index z-Score among Children in the Samoan Ola Tuputupua'e (Growing Up) Cohort.
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SUBMITTER: Choy CC
PROVIDER: S-EPMC7575349 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectivesGlobally, there is growing evidence of a double burden of malnutrition with obesity coexisting alongside micronutrient deficiencies across the life course. An emergent double burden poses a threat to health during childhood in Samoa: among 2-4-year-olds with overweight/obesity, 42.9% were anemic. Previous research suggests that obesity-related inflammation may increase the risk of iron deficiency or anemia in children. To test this hypothesis, we examined whether overweight/obesity at 2-4 is associated with anemia at 3.8-6 years old among Samoan children.MethodsData were obtained from the Ola Tuputupua'e "Growing Up" cohort study. Overweight/obesity at 2-4 years old was classified by body mass index-for-age Z-score > +2 SD. Anemia was defined as hemoglobin < 110 g/L for under 5-year-olds and < 115 g/L for 5-6-year-olds. Prevalence ratios (PRs) for anemia at 3.8-6 years old were estimated by fitting modified Poisson regression models.ResultsIn our sample of 197 children, 16.24% (n = 32) were affected by overweight/obesity at 2-4 years old and 26.90% (n = 53) had anemia at 3.8-6 years old. After covariate adjustment, the prevalence of anemia was 18% lower among children with overweight/obesity at 2-4 years old compared to those without (PR:0.82; 95% CI:0.42-1.63); however, the corresponding confidence interval was imprecise and inclusive of a higher prevalence.ConclusionsThere was not strong evidence to support a relationship between overweight/obesity and anemia in Samoan children, suggesting that obesity-related inflammation may not be related to iron deficiency nor anemia in this setting. Further investigation of the antecedents of overweight/obesity and anemia is critical to inform integrated action to improve health in Samoa.
| S-EPMC9636893 | biostudies-literature
Project description:Study Objectives:Having a regular, age-appropriate bedtime and sufficient sleep from early childhood may be important for healthy weight in adolescence. This study aimed to (1) identify heterogeneous groups of children by bedtime and sleep routines and (2) test longitudinal associations of childhood bedtime and sleep routine groups with adolescent body mass index (BMI). Methods:We analyzed longitudinal data from the Fragile Families and Child Wellbeing Study, a national birth cohort from 20 US cities (N = 2196). Childhood bedtime and sleep routines were assessed by mothers' reports of their children's presence and timing of bedtimes, adherence to bedtimes, and habitual sleep duration at ages 5 and 9. At age 15, these adolescents reported their height and weight, which were used to calculate BMI z-score. Results:Latent Class Analysis revealed four groups of childhood bedtime and sleep routines: No Bedtime Routine Age 5 (Group 1), No Bedtime Routine Age 9 (Group 2), Borderline Bedtimes Ages 5 and 9 (Group 3), and Age-Appropriate Bedtime and Sleep Routines Ages 5 and 9 (Group 4, reference). Compared with adolescents in the reference group, those in the No Bedtime Routine Age 9 (Group 2) had +0.38 SD greater BMI (95% CI = [0.13 to 0.63]), above the level for overweight (1.02 SD BMI/85th percentile). Associations persisted after adjusting for age 3 BMI and sociodemographic characteristics. Conclusions:Results demonstrate heterogeneity in childhood bedtime routine groups and their associations with adolescent BMI. Future studies should focus on whether childhood sleep behavior interventions promote healthier sleep and weight in later life course stages.
| S-EPMC6335870 | biostudies-literature
Project description:Given the importance of diet in early life, assessing children's diet is crucial to guide interventions. Using data from a nationally generalizable New Zealand (NZ) birth cohort we examined children's dietary patterns at 9- (n = 6259), 24- (n = 6292), and 54-months (n = 6131), and their association with maternal sociodemographic and health behaviours. At each time-point, children's dietary patterns were identified using principal components analysis. We then used multivariate linear regression to examine associations between each pattern and maternal variables. At 9-, 24- and 54-months, two dietary patterns were identified, explaining 36.4%, 35.3% and 33.6% of children's intake variability, respectively. Refined high in sugar, salt and fat dietary pattern, at all time-points, was characterized by high positive loadings in white/refined breads and cereals, and items with high sugar, sodium, and fat content. At 24-months, Refined high in sugar, salt and fat also included a high positive loading with protein food groups. Fruit and vegetables dietary pattern, at all time-points, had high positive loadings for fruits and vegetables (with type varying across time-points). Fruit and vegetables also included high loading in whole grain options of breads and cereals at 24-months and the protein food group was part of this dietary pattern at 9- and 54-months. Children's scores on the Refined high in sugar, salt and fat pattern had strong associations with maternal smoking habits, education level, ethnicity, and maternal scores in the "Junk" and "Traditional/White bread" dietary patterns (constructed from an antenatal interview). Children's scores on the Fruit and vegetables pattern had strong associations with the maternal scores in the dietary pattern "Health Conscious". Interventions to improve diet in early life in NZ need to be responsive to ethnicity and suitable for people of all education levels. Interventions that improve maternal health behaviours may also improve children's diet.
| S-EPMC10733397 | biostudies-literature
Project description:Background & aimsMaternal hyperglycemia during pregnancy is an important risk factor for childhood adiposity. Maternal dietary glycemic index during pregnancy directly influences maternal and fetal glucose concentrations. We examined the associations of maternal early-pregnancy dietary glycemic index with offspring general, abdominal and ectopic fat accumulation among normal weight and overweight or obese pregnant women and their offspring.MethodsIn a population-based cohort study among 2488 Dutch pregnant women and their children, we assessed maternal dietary glycemic index by food frequency questionnaire at median 13.4 (95% range 10.7; 21.1) weeks gestation. Dietary glycemic index was used continuously and categorized into low (≤55), normal (56-69) and high (≥70) glycemic index diet. We measured offspring BMI, total fat mass and android/gynoid fat mass ratio by DXA, and visceral fat mass and liver fat fraction by MRI at 10 years.ResultsNo associations of maternal early-pregnancy dietary glycemic index with offspring adiposity were present among normal weight women and their children. Among overweight and obese women and their children, 1-Standard Deviation Score (SDS) increase in maternal early-pregnancy dietary glycemic index was associated with higher childhood BMI (0.10 SDS, 95% Confidence Interval (CI) 0.01; 0.19), total fat mass index (0.13 SDS, 95% CI 0.05; 0.22), visceral fat mass index (0.19 SDS, 95% CI 0.07; 0.32) and tended to be associated with a higher android/gynoid fat mass ratio (0.09 SDS, 95% CI -0.01; 0.19) and higher risk of childhood overweight (Odds Ratio (OR) 1.20, 95% CI 0.97; 1.48). Overweight and obese women consuming an early-pregnancy low-glycemic index diet, as compared to an early-pregnancy normal-glycemic index diet, had children with lower BMI, total fat mass index, visceral fat mass index and android/gynoid fat mass ratio at 10 years (p-values<0.05). No women consumed a high-glycemic index diet. No associations were explained by maternal socio-economic, lifestyle and dietary characteristics, birth or childhood characteristics. No associations with liver fat fraction were present.ConclusionsIn overweight or obese women and their children, a higher maternal early-pregnancy dietary glycemic index is associated with childhood general, abdominal and visceral fat accumulation, but not with liver fat. Intervention studies among overweight and obese pregnant women may need to target the dietary glycemic index to prevent childhood adiposity.
| S-EPMC7613756 | biostudies-literature
Project description:scores provide an alternative approach to measuring dietary quality. The Growing Up Milk-Lite (GUMLi) Trial was a multi-centre, double-blinded, randomised controlled trial of children randomised to receive a reduced protein GUM (GUMLi) or unfortified cow's milk (CM). In a secondary analysis of the GUMLi Trial, we used the Probability of Adequate Nutrient Intake (PANDiet) to determine the nutritional adequacy of the diets of participating children living in Auckland. The PANDiet was adapted to the New Zealand Nutrient Reference Values and data from four 24 h Recalls (24HR) collected at months 7, 8, 10, and 11 post-randomisation were used. Differences between randomised groups (GUMLi vs. CM) of the PANDiet and its components were made. Eighty-three Auckland participants were included in the study (GUMLi n = 41 vs. CM n = 42). Total PANDiet scores were significantly higher in the GUMLi group (p < 0.001), indicating better overall nutrient adequacy and diet quality. Dietary intakes of children in both groups met the recommendations for fat, total carbohydrates and most micronutrients; however, protein intakes exceeded recommendations. Consumption of GUMLi was associated with higher nutritional adequacy, with an increased likelihood of meeting nutrient requirements; however, the impact of the family diet and GUMLi on dietary diversity requires further evaluation.
| S-EPMC6356321 | biostudies-literature
Project description:BackgroundAssociations have been observed among genetic variants, dietary patterns, and metabolic syndrome (MetS). A gap in knowledge is whether a genetic risk score (GRS) and dietary patterns interact to increase MetS risk among African Americans. We investigated whether MetS risk was influenced by interaction between a GRS and dietary patterns among Whites and African Americans. A secondary aim examined if molecular genetic clusterings differed by racial ancestry.MethodsWe used longitudinal data over 4-visits (1987-1998) that included 10,681 participants aged 45-64y at baseline from the Atherosclerosis Risk in Communities study (8451 Whites and 2230 African Americans). We constructed a simple-count GRS as the linear weighted sum of high-risk alleles (0, 1, 2) from cardiovascular disease polymorphisms from the genome-wide association studies catalog associated with MetS risk. Three dietary patterns were determined by factor analysis of food frequency questionnaire data: Western, healthy, and high-fat dairy. MetS was defined according to the 2016 National Cholesterol Education Program Adult Treatment Panel III criteria but used 2017 American Heart Association/American College of Cardiology criteria for elevated blood pressure. Analyses included generalized linear model risk ratios (RR), 95% confidence intervals (CI), and Bonferroni correction for multiple testing.ResultsThe Western dietary pattern was associated with higher risk for MetS across increasing GRS tertiles among Whites (p < 0.017). The high-fat dairy pattern was protective against MetS, but its impact was most effective in the lowest GRS tertile in Whites (RR = 0.62; CI: 0.52-0.74) and African Americans (RR = 0.67; CI: 0.49-0.91). Among each racial group within GRS tertiles, the Western dietary pattern was associated with development and cycling of MetS status between visits, and the high-fat dairy pattern with being free from MetS (p < 0.017). The healthy dietary pattern was associated with higher risk of MetS among African Americans which may be explained by higher sucrose intake (p < 0.0001). Fewer genes, but more metabolic pathways for obesity, body fat distribution, and lipid and carbohydrate metabolism were identified in African Americans than Whites. Some polymorphisms were linked to the Western and high-fat dairy patterns.ConclusionThe influence of dietary patterns on MetS risk appears to differ by genetic predisposition and racial ancestry.
| S-EPMC8088631 | biostudies-literature
Project description:BackgroundNinety-seven independent single nucleotide polymorphisms (SNPs) are robustly associated with adult body mass index (BMI kg/m2) in Caucasian populations. The relevance of such variants in African populations at different stages of the life course (such as childhood) is unclear. We tested whether a genetic risk score composed of the aforementioned SNPs was associated with BMI from infancy to early adulthood. We further tested whether this genetic effect was mediated by conditional weight gain at different growth periods. We used data from the Birth to Twenty Plus Cohort (Bt20+), for 971 urban South African black children from birth to 18 years. DNA was collected at 13 years old and was genotyped using the Metabochip (Illumina) array. The weighted genetic risk score (wGRS) for BMI was constructed based on 71 of the 97 previously reported SNPs.ResultsThe cross-sectional association between the wGRS and BMI strengthened with age from 5 to 18 years. The significant associations were observed from 11 to 18 years, and peak effect sizes were observed at 13 and 14 years of age. Results from the linear mixed effects models showed significant interactions between the wGRS and age on longitudinal BMI but no such interactions were observed in sex and the wGRS. A higher wGRS was associated with an increased relative risk of belonging to the early onset obese longitudinal BMI trajectory (relative risk = 1.88; 95%CI 1.28 to 2.76) compared to belonging to a normal longitudinal BMI trajectory. Adolescent conditional relative weight gain had a suggestive mediation effect of 56% on the association between wGRS and obesity risk at 18 years.ConclusionsThe results suggest that genetic susceptibility to higher adult BMI can be tracked from childhood in this African population. This supports the notion that prevention of adult obesity should begin early in life. The genetic risk score combined with other non-genetic risk factors, such as BMI trajectory membership in our case, has the potential to be used to screen for early identification of individuals at increased risk of obesity and other related NCD risk factors in order to reduce the adverse health risk outcomes later.
| S-EPMC6090951 | biostudies-literature
Project description:BackgroundThe ageing population poses a tremendous challenge in understanding the sources of inequalities in health. Though they appear to be far removed, childhood conditions are known to be inextricably linked with adult health, and in turn on health in later life. The long arm of childhood conditions hypothesis is often tested using recollection of childhood circumstances, but such subjective recall can yield potentially inaccurate or possibly biased inferences. We tested the long arm hypothesis on three outcomes in later life, arrayed from objective to subjective health, namely: gait speed, episodic memory and mental health.Methods and findingsWe used the English Longitudinal Study of Ageing 2006 enriched with retrospective life history (N = 5,913). To deal with recall problems two solutions, covariate measurement and endogenous treatment models, were applied. Retrospective childhood material lack includes growing up without running hot or cold water, fixed bath, indoor lavatory and central heating. Adjustment is made for an extensive set of confounders including sex, age, adult health, wealth, education, occupation, social support, social connections, chronic conditions, smoking, drinking, and physical exercise. It is found that material poverty when growing up shows no association with health when growing old, assuming accurate recall. Once recall problems are controlled, we found that childhood material poverty changes inversely with later life health.ConclusionA poorer childhood goes with slower gait, poorer memory and more depression in later life. This result provides a further impetus to eliminate child poverty.
| S-EPMC4682716 | biostudies-literature
Project description:OBJECTIVE:Childhood disadvantage is associated with a higher risk of adult obesity, but little is known about its associations with body mass index (BMI) trajectories during adulthood. This study aimed first to identify adulthood BMI trajectories, and second to investigate how childhood disadvantage is associated with trajectory group membership. METHODS:Data from the Helsinki Health Study, a longitudinal cohort study of initially 40- to 60-year-old employees of the City of Helsinki in Finland, were used. The baseline survey was conducted in 2000-2002, and similar follow-up surveys in 2007, 2012, and 2017. Based on self-reported BMI, participants' (n =5,266; 83% women) BMI trajectories, including their retrospectively reported BMI at the age of 25 years, were examined. Data on childhood disadvantage, including parental education and 7 types of childhood adversity (their own serious illness; parental divorce, death, mental disorder, or alcohol problems; economic difficulties at home; and peer group bullying) before the age of 16 years, were obtained from the baseline survey. Group-based trajectory modeling was used to identify BMI trajectories, and multinomial logistic regression to analyze the odds for trajectory group membership for the disadvantage variables. RESULTS:Four ascending BMI trajectories in women and men were found: persistent normal weight (trajectory 1; women 35% and men 25%), normal weight to overweight (trajectory 2; women 41% and men 48%), normal weight to class I obesity (trajectory 3; women 19% and men 23%) and overweight to class II obesity (trajectory 4; women 5% and men 4%). Compared to trajectory 1, women with multiple adversities and repetitive peer bullying in childhood had greater odds of belonging to trajectories 3 and 4, whereas men with parental alcohol problems had greater odds of belonging to trajectory 4. For women and men, a low level of parental education was associated with a higher-level BMI trajectory. CONCLUSIONS:Low parental education for both genders, multiple adversities and repetitive peer bullying in childhood among women, and parental alcohol problems among men increased the odds of developing obesity during adulthood. Further studies are needed to clarify how gender differences modify the effects of childhood disadvantage on adult BMI trajectories.
| S-EPMC6876612 | biostudies-literature
Project description:BackgroundEvidence suggests that childhood near-roadway air pollution (NRAP) exposures contribute to increased body mass index (BMI); however, effects of NRAP exposure during the vulnerable periods including in utero and first year of life have yet to be established. In this study, we examined whether exposure to elevated concentrations of NRAP during in utero and/or first year of life increase childhood BMI growth.MethodsParticipants in the Children's Health Study enrolled from 2002 to 2003 with annual visits over a four-year period and who changed residences before study entry were included (n = 2318). Annual height and weight were measured and lifetime residential NRAP exposures including in utero and first year of life periods were estimated by nitrogen oxides (NOx) using the California line-source dispersion model. Linear mixed effects models assessed in utero or first year near-road freeway and non-freeway NOx exposures and BMI growth after adjusting for age, sex, race/ethnicity, parental education, Spanish questionnaire, and later childhood near-road NOx exposure.ResultsA two-standard deviation difference in first year of life near-road freeway NOx exposure was associated with a 0.1 kg/m2 (95% confidence interval (CI): 0.03, 0.2) faster increase in BMI growth per year and a 0.5 kg/m2 (95% CI: 0.02, 0.9) higher attained BMI at age 10 years.ConclusionsHigher exposure to early life NRAP increased the rate of change of childhood BMI and resulted in a higher attained BMI at age 10 years that were independent of later childhood exposures. These findings suggest that elevated early life NRAP exposures contribute to increased obesity risk in children.
| S-EPMC6137930 | biostudies-literature