Abstract:
BACKGROUND:High fructose corn syrup (HFCS) sweetened soft drink intake has been linked with asthma in US high-schoolers. Intake of beverages with excess free fructose (EFF), including apple juice, and HFCS sweetened fruit drinks and soft drinks, has been associated with asthma in children. One hypothesis for this association is that underlying fructose malabsorption and fructose reactivity in the GI may contribute to in situ formation of enFruAGEs. EnFruAGEs may be an overlooked source of advanced glycation end-products (AGE) that contribute to lung disease. AGE/ RAGEs are elevated in COPD lungs. EFF intake has increased in recent decades, and intakes may exceed dosages associated with adult fructose malabsorption in subsets of the population. Intestinal dysfunction has been shown to be elevated in COPD patients. The objective of this study was to investigate the association between HFCS sweetened soft drink intake and chronic bronchitis (CB), a common manifestation of COPD, in adults. METHODS: DESIGN:In this cross sectional analysis, the outcome variable was self-reported existing chronic bronchitis or history of CB. Exposure variable was non-diet soda. Rao Scott Ҳ(2) was used for prevalence differences and logistic regression for associations, adjusted for age, sex, race-ethnicity, BMI, smoking, exposure to in-home smoking, pre-diabetes, diabetes, SES, total energy and total fruits and beverages consumption. SETTING:Data are from the National Health and Nutrition Examination Survey 2003-2006. SUBJECTS:2801 adults aged 20-55 y. RESULTS:There was a statistically significant correlation between intake of non-diet soft drinks and greater prevalence and odds of chronic bronchitis (p < 0.05). Independent of all covariates, intake of non-diet soda ≥5 times a week (vs. non/low non-diet soda) was associated with nearly twice the likelihood of having chronic bronchitis (OR = 1.80; p = 0.047; 95% CI 1.01-3.20). CONCLUSIONS:HFCS sweetened soft drink intake is correlated with chronic bronchitis in US adults aged 20-55 y, after adjusting for covariates, including smoking. Results support the hypothesis that underlying fructose malabsorption and fructose reactivity in the GI may contribute to chronic bronchitis, perhaps through in situ formation of enFruAGEs, which may contribute to lung disease. Longitudinal and biochemical research is needed to confirm and clarify the mechanisms involved.
journal_name
Nutr Jjournal_title
Nutrition journalauthors
DeChristopher LR,Uribarri J,Tucker KLdoi
10.1186/s12937-015-0097-xsubject
Has Abstractpub_date
2015-10-16 00:00:00pages
107issn
1475-2891pii
10.1186/s12937-015-0097-xjournal_volume
14pub_type
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pub_type: 杂志文章
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pub_type: 临床试验,杂志文章,随机对照试验
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更新日期:2013-07-10 00:00:00
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pub_type: 杂志文章,随机对照试验
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pub_type: 杂志文章,多中心研究,随机对照试验
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