Rationale Adiposity is associated with low lung function, but the longitudinal relationship between lung function and adiposity is inadequately studied.
Objective To examine the bidirectional longitudinal associations between rapid decline in lung function and adiposity phenotypes in healthy adults.
Methods This secondary analysis used a 25-year longitudinal dataset from the Coronary Artery Risk Development in Young Adults (CARDIA) study that enrolled 5115 participants.
Measurements In the first analysis, metabolic syndrome at or before CARDIA year (Y) 10 (Y10) was the predictor, and subsequent rapid decline in forced vital capacity (FVC) or forced expiratory volume in 1 s (FEV1) between Y10 and Y20 was the outcome. In the second analysis, rapid decline was the predictor, and incident metabolic syndrome at Y20 and/or Y25 was the outcome. In the third analysis, rapid decline was the predictor, and subsequent CT-assessed regional fat depots at Y25 were the outcome.
Results Metabolic syndrome at or before Y10 is temporally associated with rapid decline in FVC between Y10 and Y20 (adjusted p=0.04), but this association was explained by body mass index (BMI) at Y10. Rapid decline in FVC or FEV1 is temporally associated with greater incident metabolic syndrome at Y20 and/or Y25 (adjusted OR 2.10 (1.69, 2.61); p<0.001, and 1.56 (1.26, 1.94); p<0.001, respectively) and greater CT-assessed intrathoracic visceral adiposity at Y25 (adjusted standardised β 0.09; p<0.001 for both analyses). These associations were not explained by BMI levels prior to the outcome measurement.
Conclusions Healthy adults with rapid decline in lung function are at risk for developing metabolic syndrome and for disproportionate accumulation of intrathoracic visceral fat. Metabolic abnormalities may be an early extrapulmonary manifestation of lung impairment that may be preventable by improving lung health.
- Body mass index
- metabolic syndrome
- visceral fat
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Contributors AS, MM, BT, RK, LJS and DRJ made substantial contributions to the conception or design of the work, and CQ, JJC and AA made substantial contributions to the acquisition, analysis or interpretation of data for the work. AS, MM, BT, RK, LJS, DRJ, CQ, JJC and AA made substantial contribution towards drafting the work or revising it critically for important intellectual content. AS, MM, BT, RK, LJS, DRJ, CQ, JJC and AA provided the final approval of the version to be published. AS, MM, BT, RK, LJS, DRJ, CQ, JJC and AA agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Funding The Coronary Artery Risk Development in Young Adults Study (CARDIA) is conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the University of Alabama at Birmingham (HHSN268201300025C & HHSN268201300026C), Northwestern University (HHSN268201300027C and R01 HL122477), University of Minnesota (HHSN268201300028C), Kaiser Foundation Research Institute (HHSN268201300029C), and Johns Hopkins University School of Medicine (HHSN268200900041C). CARDIA is also partially supported by the Intramural Research Program of the National Institute on Aging (NIA) and an intra,agency agreement between NIA and NHLBI (AG0005). This manuscript has been reviewed by CARDIA for scientific content.
Competing interests None declared.
Ethics approval CARDIA study was approved by each of the four participating institutions.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement Additional unpublished data are available on request from the CARDIA Study Publications and Presentations Committee.
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