The overarching goal of our research is to understand the role of nutrition and its interaction with the genome in the etiology of chronic disease. Our past studies provided evidence that nutrients with antioxidant properties play a role in the etiology of lung disease, and this line of research culminated in a randomized controlled trial of vitamin E and selenium supplementation to study effects on rate of decline in lung function and risk of COPD. The trial found a protective effect of selenium on a marker of lung function decline in cigarette smokers, and evidence that vitamin E was protective in a subset of participants. Given important contributions of genetic susceptibility to major chronic diseases, and the hypothesis that dietary exposures interact with genomic variation in the causation of chronic disease, we also study whether genomic variation contributes to differential responses to diet in relation to lung phenotypes. Understanding the role of genetic variation, and the interaction between genes and nutrients, is important to identify prevention targets and to provide the best advice for dietary guidance to avoid chronic disease.

We work in collaboration with the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium and the SpiroMeta consortium to directly investigate gene-by-nutrient interactions in relation to pulmonary function and chronic obstructive pulmonary disease, with studies on plasma omega 3 fatty acids, serum vitamin D, dietary patterns, and the dietary intake of fiber and omega 3 fatty acids.

Current projects include:

  • Randomized controlled trial of selenium and/or vitamin E effects on rate of decline in lung function and risk of COPD, including genome-wide association studies of response to supplementation
  • Genome-wide association studies of lung function, with CHARGE pulmonary working group, using 1000 Genomes and Exome chip data