Diet and nutrition play a key influence on our health. We also know that nutrition and other influences from our lifestyles and environment act in combination with our genetic make-up to affect health and disease risk. Due to recent advances in gene discovery and big data methodologies, it is now possible to examine the joint effects of genes and environment. Importantly, this will help us to establish whether making changes where we can (e.g. diet, lifestyle) can ameliorate adverse influences caused by susceptibility genes, which we cannot alter.
The Nutritional and Genetic Epidemiology group, headed by ACPreH Director Elina Hyppönen, uses tools from observational and genetic epidemiology to investigate the role of nutrition, lifestyles and other modifiable influences on public health. We seek to understand gene-environment interactions, and use genetic markers in causal modelling often looking across the full spectrum of human diseases.
Work in this research area includes projects examining intergenerational and genetic influences on growth and disease risk, as well as the short and long-term health effects of Vitamin D, coffee consumption, obesity and other lifestyle factors. Much of the work is done using large-scale population data collections, often in the context of large-scale international collaborations.
Researchers
- Professor Elina Hyppönen
- Dr Catherine King
- Dr Ang Zhou
- Dr Anwar Mulugeta
- Dr Mandy Lumsden
- Joshua Sutherland
- Kitty Pham
- Muktar Ahmed
Current research projects
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Genome-wide association studies to identify factors affecting nutrition and growth
(PI: Professor Elina Hyppönen)
Genetic variants affect every aspect of our health and well-being, and Professor Hyppönen's team plays an important role in contributing to genetic risk factor discovery with respect to nutrition related phenotypes, including Vitamin D, coffee, obesity and other growth related traits. Related work has been supported by funding from the Medical Research Council (UK), Department of Health (UK), Academy of Finland, and the British Heart Foundation. We contribute actively to many international large scale consortia working on related topics, including Early Growth Genetics (EGG), SUNLIGHT Consortium (Study of Underlying Genetic Determinants of Vitamin D and Highly Related Traits), and others.
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Vitamin D and Health
(PI: Professor Elina Hyppönen)
Vitamin D deficiency is prevalent in adults, and it has been suggested to contribute to the development of cardiovascular diseases, diabetes, mood disorders, cognitive decline and eventually, mortality risk. However, causality for many of the observed associations has not been demonstrated, with much of the evidence arising from observational studies potentially affected by confounding and reverse causality. With funding from the NHMRC, Professor Hyppönen leads the international D-CarDia collaboration, and a body of work to establish the causality and safety of Vitamin D and calcium in relation to cardiovascular risk. Currently D-CarDia consists of over 40 studies from all around the world with a total of >150,000 individuals.
The effects of our lifestyle behaviours on cognitive function remain poorly understood and there is no effective prevention for dementia. With funding from the Mason-Williams foundation we are working to establish effective dietary approaches to prevent cognitive decline and reduce dementia risk. This work is led by Professor Hyppönen, and includes in aggregate over 100,000 participants from various studies around the world.
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Discovering and using genetic variations affecting biochemical markers for disease
(PI: Dr Beben Benyamin)
Biochemical markers measured in blood are widely-used indicators of a current disease, or predictors of disease risk in the future. In collaboration with Dr John Whitfield (QIMR Berghofer Medical Research Institute), the project focuses on identifying genetic variants associated with biochemical markers for cardiovascular diseases and metabolic syndrome (high-density and low-density lipoprotein cholesterol, triglycerides, C-reactive protein and urate); liver function (alanine aminotransferase, albumin, alkaline phosphatase, aspartate aminotransferase, bilirubin, cholinesterase, gamma-glutamyl transferase and total protein), renal function (creatinine, urea), carbohydrate deficient transferrin (marker for chronic alcohol intake) and iron status (serum iron, transferrin and ferritin). We also use the identified genetic information to infer the causal effect of biochemical markers on disease and to test for the genetic and environmental interaction.
