Sugar and Childhood Asthma

  • Posted by Dr. Jay Gordon

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  • by Charles Bankhead
    Staff Writer, MedPage Today

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HOUSTON — A child’s risk of asthma increased significantly with maternal fructose intake during pregnancy, data from a longitudinal cohort study showed.

The odds ratio for asthma in mid-childhood increased 22% for children whose mothers consumed large quantities of fructose during the second trimester of pregnancy. A similar asthma association existed for the child’s fructose consumption at 2 years of age.

The mother’s intake of sugar-sweetened beverages during pregnancy and children’s juice consumption at 2 years appeared to drive the association with asthma, Lakiea Wright, MD, of Harvard and Brigham and Women’s Hospital in Boston reported here at the American Academy of Allergy, Asthma, and Immunology meeting.

“We found that sociodemographic factors, such as race and income, and measures of adiposity were associated with fructose intake,” said Wright. “Early-life exposure to fructose may influence asthma development in children.”

The ongoing obesity epidemic in the U.S. has its roots in increased caloric intake, which, in turn, has been linked to increased fructose consumption. Additionally, fructose has associations with multiple inflammatory conditions, including dyslipidemia, insulin resistance, diabetes, nonalcoholic fatty liver disease, hypertension, and gout, Wright said.

Few studies have examined the relationship between fructose intake and subsequent asthma risk, providing a rationale for investigation.

“We hypothesized that higher maternal prenatal and child fructose intake would be associated with childhood asthma,” said Wright.

To test this hypothesis, investigators analyzed data from 1,111 mother-child pairs in the Project Vivalongitudinal pre-birth cohort study. Wright and colleagues used self-reported information from food frequency questionnaires to estimate maternal fructose intake from beverages and foods during the first and second trimesters of pregnancy. They also estimated the children’s fructose intake at age 2.

Asthma prevalence was evaluated when the children had a median age of 7.7 years. Asthma status was based on the mother’s self-reported confirmation of physician diagnosis. Overall, 19.7% of the children had asthma diagnoses in mid-childhood.

The investigators stratified the study participants into quartiles of fructose intake. The primary analysis was the comparison of the lowest and highest quartiles of in intake.

Mothers in the highest quartile of fructose consumption had a lower family income, a higher body mass index (BMI, 25.4 versus 23.8), and were more likely to be black. Children of women in the highest fructose quartile had a higher mid-childhood BMI (z-score 0.46 versus 0.30) and a higher mid-childhood asthma prevalence (26% versus 14%).

Maternal fructose consumption during the first and second trimester of pregnancy had a significant association with asthma in mid-childhood (OR 1.22, 95% CI 1.03-1.44). An association of the same magnitude emerged from the analysis of the children’s fructose intake at age 2 (OR 1.22, 95% CI 1.02-1.46).

The investigators also examined the relationships of different types of fructose-containing beverages and asthma in mid-childhood. They found that sugar-sweetened beverages drove the association between maternal fructose intake and asthma (OR 1.20, 95% CI 1.01-1.42), whereas juice consumption by children at age 2 predicted the likelihood of asthma in mid-childhood (OR 1.34, 95% CI 1.12-1.61).

In this study, Wright hypothesized “that different sources of fructose at different stages of development may be contributing to inflammation and the development of asthma. The mechanism of action may be direct or indirect.”

In utero lung development is ongoing during the second trimester of pregnancy, and high fructose in a mother’s diet, in the form of sugar-sweetened drinks, might be contributing to asthma development through an indirect inflammatory pathway, she explained. Obesity could be the driver of the relationship, as adjustment for maternal BMI attenuated the association between fructose intake and asthma in mid-childhood.

At 2 years of age, a child’s lungs are still developing, and fructose in the form of juice might contribute to asthma development through a direct inflammatory pathway, Wright continued. The association between higher juice intake and mid-childhood asthma remained significant after controlling for maternal BMI and second-trimester intake of sugar-sweetened drinks.

Wright acknowledged limitations of the study: reliance on self-reported information, lack of adjustment for other dietary factors that could offset the pro-inflammatory effects of fructose (such as antioxidants), and lack of information on markers of inflammation (such as tumor necrosis factor, interleukin-6, and adipokines). The influence of balancing factors in the diet and levels of inflammatory markers on asthma risk will be assessed in future analyses.

The study was supported by the National Institutes of Health.

Wright and colleagues disclosed no relevant relationships with industry.

LAST UPDATED 02.26.2015