Risk prediction using our genes and gut bacteria can improve early detection of diseases

Publicly released:
Australia; VIC
iStock: Beneficial healthy intestinal bacterium microflora
iStock: Beneficial healthy intestinal bacterium microflora

A new study has shown that risk scores based on our genes and gut bacteria can improve the prediction of diseases such as type 2 diabetes and prostate cancer over traditional risk factors alone. And when it comes to prediction of a person’s risk of common chronic diseases, combining traditional risk factors that are used by doctors today with new technologies that quantify our genetic risk (polygenic risk scores) and gut bacteria (gut microbiome) resulted in the most powerful predictors.

Media release

From: Baker Heart and Diabetes Institute

A new study has shown that risk scores based on our genes and gut bacteria can improve the prediction of diseases such as type 2 diabetes and prostate cancer over traditional risk factors alone.

And when it comes to prediction of a person’s risk of coronary artery disease, type 2 diabetes, Alzheimer's disease and prostate cancer, combining traditional risk factors that are used by doctors today with new technologies that quantify our genetic risk (polygenic risk scores) and gut bacteria (gut microbiome) resulted in the most powerful predictors of common chronic diseases.

The study, led by Dr Yang Liu, is one of the first to look at the combined impact of genetics and the gut microbiome on disease risk and paves the way for a more refined, powerful and personalised approach to disease prediction.

Published today in Nature Aging and based on the data of more than 5670 adults, the study is a collaboration by the Baker Heart and Diabetes Institute, the University of Cambridge and the Finnish Institute of Health and Welfare.

While traditional risk factors typically rely on age, sex, and measurements like body mass index, blood pressure, non-HDL cholesterol and HbA1c, this study highlights how large-scale analysis of a person’s genetics and gut bacteria can improve predictive performance.

In this study, researchers investigated the individual and combined predictive performance of polygenic risk scores, the gut microbiome and traditional risk factors for development of future coronary artery disease, type 2 diabetes, Alzheimer's disease and prostate cancer over a median of ~18 years of follow-up, using the population-based FINRISK 2002 cohort.

The recent emergence of multi-omics means that it is now possible to measure and integrate who classes of biomolecular and cellular factors for the purpose of building multi-omic risk scores.

Multi-omic technologies, which are powering discovery across multiple aspects of biology from the genome, proteome and transcriptome to epigenome and microbiome, have uncovered new biomarkers for various common age-related diseases. If diseases such as coronary artery disease, Alzheimer’s Disease, prostate cancer and type 2 diabetes can be predicted early, prevention strategies can also be applied.

Dr Liu says these personalised risk scores, combined with traditional risk factors, open up new avenues for non-invasive risk profiling and early detection of disease.

“This study shows the potential of integrating a person’s multiple omes in advancing understanding of the development and prediction of diseases,” says Dr Liu.  “Multi-omics has come a long way, but data integration and translation into benefits for clinical decision-making remain challenging.”

About the Cambridge Baker Systems Genomics Initiative
This work forms part of the Baker Heart and Diabetes Institute's partnership with the University of Cambridge to harness big data to target approaches in disease prediction and personalised medicine. Last year, the Baker Institute announced an extension of the Cambridge Baker Systems Genomics Initiative to 2030 which will build on the Institute's exciting work in this area.

Journal/
conference:
Nature Aging
Research:Paper
Organisation/s: Baker Heart and Diabetes Institute, University of Cambridge, Finnish Institute of Health and Welfare.
Funder: YL was supported by funding from the Cambridge Baker Centre for Systems Genomics. SR was supported by a British Health Foundation programme grant (RG/18/13/33946). MOR was funded by the Research Council of Finland (grant no. 338818). LL was supported by the European Union’s Horizon 2020 research and innovation program (grant no. 952914). TN was supported by the Finnish Foundation for Cardiovascular Research, the Sigrid Jusélius Foundation, the Southwestern Finland Hospital District, and the Research Council of Finland (grants no. 321351 and 354447). VS was supported by the Finnish Foundation for Cardiovascular Research and by the Juho Vainio Foundation. ASH was supported by the Research Council of Finland, grant no. 321356. MI was supported by the Munz Chair of Cardiovascular Prediction and Prevention and the NIHR Cambridge Biomedical Research Centre (BRC-1215-20014; NIHR203312) [*]. MI was also supported by the UK Economic and Social Research Council (ES/T013192/1). This study was supported by the Victorian Government’s Operational Infrastructure Support (OIS) program and by core funding from the British Heart Foundation (RG/18/13/33946) and the NIHR Cambridge Biomedical Research Centre (BRC-516 1215-20014; NIHR203312) [*]. This work was supported by Health Data Research UK, which is funded by the UK Medical Research Council, Engineering and Physical Sciences Research Council, Economic and Social Research Council, Department of Health and Social Care (England), Chief Scientist Office of the Scottish Government Health and Social Care Directorates, Health and Social Care Research and Development Division (Welsh Government), Public Health Agency (Northern Ireland), British Heart Foundation and Wellcome.
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