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Bedoya, G.

Publications and source records attributed to Bedoya, G..

2 recordsLinked to original sources

Gut microbiota composition explains more variance in the host cardiometabolic risk than genetic ancestry

BackgroundCardiometabolic affections greatly contribute to the global burden of disease. The susceptibility to these conditions associates with the ancestral genetic composition and gut microbiota. However, studies explicitly testing associations between genetic ancestry and gut microbes are rare. We examined whether the ancestral genetic composition was associated with gut microbiota, and split apart the effects of genetic and non-genetic factors on host health.\n\nResultsWe performed a cross-sectional study of 441 community-dwelling Colombian mestizos from five cities. We characterized the host genetic ancestry using 40 ancestry informative markers and gut microbiota through 16S rRNA gene sequencing. We measured variables related to cardiometabolic health (adiposity, blood chemistry and blood pressure), diet (calories, macronutrients and fiber) and lifestyle (physical activity, smoking and medicament consumption). The ancestral genetic composition of the studied population was 67{+/-}6% European, 21{+/-}5% Native American and 12{+/-}5% African. While we found limited evidence of associations between genetic ancestry and gut microbiota or disease risk, we observed a strong link between gut microbes and cardiometabolic health. Multivariable-adjusted linear models indicated that gut microbiota was more likely to explain variance in host health than genetic ancestry. Further, we identified 9 OTUs associated with increased disease risk and 11 with decreased risk.\n\nConclusionsGut microbiota seems to be more meaningful to explain cardiometabolic disease risk than genetic ancestry in this mestizo population. Our study suggests that novel ways to control cardiometabolic disease risk, through modulation of the gut microbial community, could be applied regardless of the genetic ancestry of the intervened population.

microbiology

Contribution of common and rare variants to bipolar disorder susceptibility in extended pedigrees from population isolates

Current evidence from case/control studies indicates that genetic risk for psychiatric disorders derives primarily from numerous common variants, each with a small phenotypic impact. The literature describing apparent segregation of bipolar disorder (BP) in numerous multigenerational pedigrees suggests that, in such families, large-effect inherited variants might play a greater role. To evaluate this hypothesis, we conducted genetic analyses in 26 Colombian (CO) and Costa Rican (CR) pedigrees ascertained for BP1, the most severe and heritable form of BP. In these pedigrees, we performed microarray SNP genotyping of 856 individuals and high-coverage whole-genome sequencing of 454 individuals. Compared to their unaffected relatives, BP1 individuals had higher polygenic risk scores estimated from SNPs associated with BP discovered in independent genome-wide association studies, and also displayed a higher burden of rare deleterious single nucleotide variants (SNVs) and rare copy number variants (CNVs) in genes likely to be relevant to BP1. Parametric and non-parametric linkage analyses identified 15 BP1 linkage peaks, encompassing about 100 genes, although we observed no significant segregation pattern for any particular rare SNVs and CNVs. These results suggest that even in extended pedigrees, genetic risk for BP appears to derive mainly from small to moderate effect rare and common variants.

genetics