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Prenatal and Early Life Fructose, Fructose-Containing Beverages, and Midchildhood Asthma.

ABSTRACT: RATIONALE:Cross-sectional studies have linked intake of high-fructose corn syrup-sweetened beverages with asthma in schoolchildren. OBJECTIVES:To examine associations of maternal prenatal and early childhood intake of sugar-sweetened beverages and fructose with current asthma in midchildhood (median age, 7.7 yr). METHODS:We assessed maternal pregnancy (first- and second-trimester average) and child (median age, 3.3 yr) intake of sugar-sweetened beverages and total fructose using food frequency questionnaires in 1,068 mother-child pairs from Project Viva, a prospective prebirth cohort. In a multivariable analysis, we examined associations of quartiles of maternal and child sugar-sweetened beverage, juice, and total fructose intake with child current asthma in midchildhood, assessed by questionnaire as ever having doctor-diagnosed asthma plus taking asthma medications or reporting wheezing in the past 12 months. RESULTS:Higher maternal pregnancy sugar-sweetened beverage consumption (mean, 0.6 servings/d; range, 0-5) was associated with younger maternal age, nonwhite race/ethnicity, lower education and income, and higher prepregnancy body mass index. Adjusting for prepregnancy body mass index and other covariates, comparing quartile 4 with quartile 1, higher maternal pregnancy intake of sugar-sweetened beverages (odds ratio, 1.70; 95% confidence interval, 1.08-2.67) and total fructose (odds ratio, 1.58; 95% confidence interval, 0.98-2.53) were associated with greater odds of midchildhood current asthma (prevalence, 19%). Higher early childhood fructose intake (quartile 4 vs. quartile 1) was also associated with midchildhood current asthma in models adjusted for maternal sugar-sweetened beverages (odds ratio, 1.79; 95% confidence interval, 1.07-2.97) and after additional adjustment for midchildhood body mass index z-score (odds ratio, 1.77; 95% confidence interval, 1.06-2.95). CONCLUSIONS:Higher sugar-sweetened beverage and fructose intake during pregnancy and in early childhood was associated with childhood asthma development independent of adiposity.

SUBMITTER: Wright LS

PROVIDER: S-EPMC5802621 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Prevention strategies that delay the onset of asthma may improve clinical outcomes. To identify early life environmental exposures associated with asthma age-of-onset and potential genetic modifiers of these exposures, we studied 1085 subjects with physician-diagnosed asthma and disease onset at or after age two. Subjects reported retrospectively on their exposure to 17 environmental factors before the age of two. The presence of individual or combinations of these early life exposures was then tested for association with variation in asthma age-of-onset. For exposures significantly associated with age-of-onset, we tested if 26 single nucleotide polymorphisms (SNP) with an established association with allergic disease significantly modified the effect of the exposure. Five environmental exposures were significantly associated with variation in asthma age-of-onset after correction for multiple testing: carpet at home (P = 6 × 10(-5)), a serious chest illness (P = 10(-4)), father a cigarette smoker (P = 6 × 10(-4)) and direct exposure to father's smoking (P = 3 × 10(-4)). Individuals with early childhood asthma onset, between the ages of two and six, were 1.4-fold (CI 1.1-1.9) more likely to report having lived in a house with carpet and 2.1-fold (CI 1.3-3.5) more likely to report suffering a serious chest illness before the age of two, than asthmatics with later disease onset. We further found these individual risks to increase to 3.2-fold (CI 1.7-6.0) if carpet exposure and suffering a serious chest illness co-occurred before age two. Paternal smoking exposures were less likely to be reported by asthmatics with early when compared to later disease onset (OR 0.5, CI 0.3-0.7). There were no significant SNP interactions with these environmental exposures after correction for multiple testing. Our results suggest that disease onset in individuals at a high-risk of developing asthma can potentially be delayed by avoiding exposure to carpet at home and preventing serious chest illnesses during the first 2 years of life.

Project description:OBJECTIVE: The obesigenic and related health effects of caloric sweeteners are subjects of much current research. Consumers can properly adjust their diets to conform to nutritional recommendations only if the sugars composition of foods and beverages is accurately measured and reported, a matter of recent concern. We tested the hypothesis that high-fructose corn syrup (HFCS) used in commercial carbonated beverages conforms to commonly assumed fructose percentages and industry technical specifications, and fulfills beverage product label regulations and Food Chemicals Codex-stipulated standards. DESIGN: A high-pressure liquid chromatography method was developed and verified for analysis of sugars in carbonated beverages sweetened with HFCS-55. The method was used to measure percent fructose in three carbonated beverage categories. Method verification was demonstrated by acceptable linearity (R(2)>0.99), accuracy (94-104% recovery) and precision (RSD < 2%). RESULT: Fructose comprised 55.58% of total sugars (95% confidence interval 55.51-55.65%), based on 160 total measurements by 2 independent laboratories of 80 randomly selected carbonated beverages sweetened with HFCS-55. The difference in fructose measurements between laboratories was significant but small (0.1%), and lacked relevance. Differences in fructose by product category or by product age were not statistically significant. Total sugars content of carbonated beverages showed close agreement within product categories (95% confidence interval = 0.01-0.54%). CONCLUSIONS: Using verified analytical methodology for HFCS-sweetened carbonated beverages, this study confirmed the hypothesis that fructose as a percentage of total sugars is in close agreement with published specifications in industry technical data sheets, published literature values and governmental standards and requirements. Furthermore, total sugars content of commercial beverages is consistent with common industry practices for canned and bottled products and met the US Federal requirements for nutritional labeling and nutrient claims. Prior concerns about composition were likely owing to use of improper and unverified methodology.

Project description:BACKGROUND:Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5??m (PM2.5) and ozone (O3) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES:We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM2.5 and O3 increase the risk of early developmental delays. STUDY DESIGN:Prospective cohort. SETTINGS:New York State excluding New York City. PARTICIPANTS:4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES:Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM2.5 and O3 estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES:Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM2.5 and O3, and for those living <1000?m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS:Compared to those >1000?m away from a major roadway, those resided 50-100?m [RR: 2.12 (1.00-4.52)] and 100-500?m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10??g/m3 increase in PM2.5 and 0.7%-1.7% for a 10?ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM2.5 exposures. CONCLUSIONS:In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 and O3 were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.

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Prenatal and Early Life Fructose, Fructose-Containing Beverages, and Midchildhood Asthma.

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