Genes play a powerful role in how our bodies process nutrients, but they’re only part of the story. A new study in Nature Genetics has created the largest genetic map of human metabolism to date, offering insights into how DNA influences health while underscoring the importance of diet and lifestyle.
Researchers from Queen Mary University of London and the Berlin Institute of Health analyzed data from 500,000 UK Biobank participants, measuring blood levels of 250 molecules including lipids and amino acids. They identified numerous genes tied to metabolism, many with previously unknown roles. Strikingly, results were consistent across ancestries and between men and women, suggesting wide applicability of the findings.
“We are now able to map systematically the genetic control of hundreds of blood molecules, at unprecedented scale,” said lead author Martijn Zoodsma, PhD. “This provides a powerful reference to understand disease risk and identify genes that contribute to variability in metabolism.”
The team also found genetic overlap between metabolites and diseases such as heart disease, raising the possibility of new treatment targets. One example: VEGFA, a gene that may help regulate cholesterol.
“The development of blood lipid-lowering medications, such as statins, has saved numerous lives, but heart diseases remain the major killer,” said senior author Maik Pietzner, PhD. “Our results highlight potential avenues that will hopefully lead to new medicines to prevent even more deaths.”
Still, genes are only part of the equation. The authors emphasized that lifestyle factors, including diet, physical activity and overall health behaviors, remain powerful drivers of metabolic health.
“Martijn’s work using these data has also revealed strong similarities between different ancestries or sexes of how our genes shape our metabolic individuality — a reminder that we are all human, and have much in common,” said Claudia Langenberg, PhD, senior author and director of Queen Mary’s Precision Health University Research Institute.
The findings provide a new foundation for studying how genetics and lifestyle interact, with the potential to improve prevention and treatment of metabolic and chronic diseases.
This work was supported by the German Centre for Cardiovascular Research, the German Ministry of Education and Research, the European Research Council and the Friede Springer Cardiovascular Prevention Center at Charité – Universitätsmedizin Berlin. Additional support came from the British Heart Foundation, the Imperial BHF Research Excellence Award and the VASCage Research Centre on Clinical Stroke Research in Austria, funded through the COMET programme of the Austrian Research Promotion Agency. Computational resources were provided by Charité – Universitätsmedizin Berlin. The authors also acknowledge Nightingale Health Plc for access to UK Biobank biomarker data.