Obesity-asthma association: is it explained by systemic oxidant stress?
BACKGROUND
The mechanism for the obesity-asthma association is unknown. This study evaluated the hypothesis that systemic oxidant stress explains this association.


METHODS
This cross-sectional study used year-20 follow-up evaluation data of 2,865 eligible participants in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. Current asthma was self-reported. Oxidant stress primarily was assessed by plasma F2-isoprostane concentrations. Obesity measures included categories of BMI and dual-energy x-ray absorptiometry-assessed fat mass index (FMI) and lean mass index (LMI). Logistic and linear regressions were used for analyses.


RESULTS
Asthma was associated with higher plasma F2-isoprostane concentrations (p = 0.049); however, this association was not significant when adjusted for either gender or BMI. The BMI-asthma association was seen only among women (p = 0.03; gender-specific interaction, p = 0.01), and this association was not explained by plasma F2-isoprostane levels. Similarly, both FMI and LMI were positively associated with asthma in women (p = 0.20 and 0.01, respectively). These associations also were not explained by plasma F2-isoprostane levels. Similar results were obtained when plasma levels of oxidized low-density lipoprotein were used instead of F2-isoprostane levels to study the BMI-asthma association at the year-15 evaluation.


CONCLUSIONS
Systemic oxidant stress, primarily assessed by plasma F2-isoprostane concentrations, was not independently associated with asthma and, therefore, may not explain the obesity-asthma association in women. The asthma-oxidant stress association is confounded by gender and obesity. This study is limited by the inability to measure airway oxidant stress. It is possible that another (as yet undetermined) measure of systemic oxidant stress may be more relevant in asthma.
Sood
Akshay
A
Department of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM. Electronic address: asood@salud.unm.edu.
Qualls
Clifford
C
Clinical Translational Sciences Center, University of New Mexico Health Sciences Center, Albuquerque, NM.
Arynchyn
Alexander
A
Department of Preventive Medicine, University of Alabama at Birmingham, Birmingham, AL.
Beckett
William S
WS
Department of Medicine, Mount Auburn Hospital, Cambridge, MA.
Gross
Myron D
MD
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN.
Steffes
Michael W
MW
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN.
Smith
Lewis J
LJ
Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL.
Holvoet
Paul
P
Department of Experimental Surgery and Anesthesiology, Katholieke Universiteit Leuven, Leuven, Belgium.
Thyagarajan
Bharat
B
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN.
Jacobs
David R
DR
Division of Epidemiology, University of Minnesota, Minneapolis, MN; Institute for Nutrition Research, University of Oslo, Oslo, Norway.
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000150:complications* / Q000503:physiopathology; D015992:Body Mass Index; D008078:Cholesterol, LDL / Q000097:blood; D003430:Cross-Sectional Studies; D028441:F2-Isoprostanes / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology*; D011446:Prospective Studies; D055815:Young Adult
D008078:Cholesterol, LDL; D028441:F2-Isoprostanes