International Life Sciences Institute's First International Conference on nutrigenomics: opportunities in Asia. Singapore 7-9 December 2005.

Nutrigenomics is the study of the interaction between gene expression and nutrients or food components. This focused conference, held in collaboration with the Commonwealth Scientific and Industrial Research Organisation, was attended by around 400 delegates from over 20 countries, about half from Asia, who heard from over 50 scientists and experts in the field. Three and a half packed days included plenary sessions on molecular epidemiology, nutrient-gene interactions and nutrigenomics in relation to cancer, immunity and wellbeing. These were supplemented with symposia on genomic technologies in nutrition research generally, and in the development of functional foods specifically. Highlights of the conference, at least for this attendee, are reported here.

John Milner from the National Institutes of Health provided numerous personal insights into the topic. Noting that 90% of deaths appear related to genomics, and there was wide variability in risk and in response to dietary intervention, nutrigenomics provided a form of health promotion strategy that could be described as nutritional pre-emption. The complexity of the task was extensive, however, with a daily exposure of individuals to some 25 000 dietary components. Key questions were, what is the process by which nutrients influence phenotype, and what are the most important for diseases such as cancer, osteoporosis and cardiovascular disease. One of the principles emerging from the study of nutrigenomics was that some individuals may benefit from higher intakes of nutrients, but others may be at increased risk. At the very least, research has shown that responses to nutritional interventions such as changes in dietary fat were dependent on genetic profiles. The ability to identify polymorphisms was improving but severely limited, with 30 000 genes to consider overall. This underpinned a second major principle, that the mapping exercise was enormous, requiring a systems approach to managing massive amounts of data, and effective collaboration between researchers to mount the task.

Other speakers provided ideas for effective ways forward. Edison Liu from the Genomics Institute of Singapore argued that it may be more important to understand the gene signature than the gene sequence, and that the expression profile may give an indication of the environmental exposure. There may be benefit in nutritional science moving from being an observational science to an interventionist science, and better value in studying cohorts rather than cases and controls. Multiple throughput technologies are now allowing for the examination of multiple factors in health and disease, enabling a systems approach to research. Recounting the theme of collaboration, researchers need to think on how their work might fit in with that of others. Carl Keen from UC Davis argued the point for optimising health through diet. The success of nutrigenomics lay in the determination of goals, how the score is kept and how successes are communicated. Industry is already taking up some of the concepts. Risk-benefit ratios need to be considered, bearing in mind that diet has the ability to modulate the progression of disease. On this point, other speakers commented on the need to consider variation between ethnic groups in the significance of lipid biomarkers in cardiovascular disease and the impact of diet on these biomarkers.

One of the outstanding areas for dietary intervention is India, which is showing an alarming increase in the prevalence of diabetes, with predictions for 2030 almost overwhelming in proportion (see recent articles in Diabetes Care). Dr Mohan Viswanathan from the Madras Diabetes Research Foundation outlined how the Asian Indian phenotype demonstrated an increased ethnic susceptibility to the disease. Noting increased urbanisation with decreased physical activity Dr Mohan argued how genes and environment were colluding to produce diabetes through a synergistic effect of family history, reduced activity and diet.

In contrast, osteoporosis was described as a disease where multiple genes interact with each other and the environment. Candidate genes carried varied prevalence in different populations and calcium supplementation produced varying effects, appearing more efficacious in those with low calcium intakes. The impact of polymorphisms associated with longevity also varied depending on the environment and appeared to be linked to pathways associated with caloric restriction.

The conference then heard that one of the explanations for the differences seen may lie in the foetal origins of health. Studies of micronutrient deficiencies in animal model studies suggest that the maternal diet may be linked to the future health of the next two generations. Future research will benefit from the identification of genetic polymorphisms that are associated with toxicity and deficiencies, studies of the effects of epigenetics and mild micronutrient deficiency, and how these relate to the development of chronic diseases and ageing. John Mathers from the University of Newcastle, UK, noted that epigenetic markings influence gene expression and are affected by nutrition. Epigenetic change reflects how the gene learns from its environment, evidenced by the comparison of epigenetic markings in monzygous twins as children compared with that at middle age. The balance between health and disease equates to a balance within and between genetic types, nutritional options and lifestyle factors.

At the practice level, Graeme Young from Australia presented a model for diet and cancer, and using examples of food components, demonstrated how diet may influence the steps between the gene and the development of cancer. A number of presentations addressing components of food demonstrated how the food component may interact with the genetic environment, highlighting in a number of ways the benefits of foods of plant origin. Lynette Ferguson's work on selenium in New Zealand confirmed the principle that the amount required depends on the genotype, whereas, from Wageningen, Muller's rendition on polyunsaturated fatty acid and inflammation argued that gene upregulation was seen as more potent in drug therapy, then fasting states, and then nutritional intervention, positioning the nutritional effect in the scheme of events. The conference was also reminded of the significance of iodine in mental wellbeing, and of antioxidants in eye health. Peter Weber from DSM Nutritional Products acknowledged the 'technology pull' of nutrigenomics in industry noting the movement in nutrition from a focus on single components (preventing deficiency) to dietary strategies (health promotion of populations) to personalised nutrition (genome-lifestyle balance in individuals). The challenge will be in how to apply the technology, and a new kind of expertise will be required to deliver on it. From Toronto, El-Sohemy's presentation on how genotype may impinge on taste preferences added another interesting dimension to this challenge. The symposium on functional foods heard that the science of nutrigenomics would be able to deliver on the knowledge base for mechanisms, biomarkers and safety assessments.

Overall, this conference demonstrated the intricate tapestry of nutrigenomics research and touched on its applications to nutrition practice. A main challenge will be in establishing the collaborations required to build the knowledge base and to this end Lynette Ferguson from New Zealand called for the establishment of a regional network. For dietitians, the important issue will be to remain aware of developments in nutrigenomics1 and keep up-to-date on opportunities for valid applications in practice and research.

Linda C. Tapsell, PhD, FDAA 

Professor, Director

National Centre of Excellence in Functional Foods, University of Wollongong, Wollongong, New South Wales, Australia

REFERENCES

1 Corthesy-Theulaz I, den Dunnen JT, Free P et al. Nutrigenomics: The impact of biomics technology on nutrition research. Ann Nutr Metab 2005; 49: 355-65.