At last the RDI’s are under scrutiny as to be more about optimum nutrition then just prevention of disease. Mounting evidence on the effect of micronutrients on DNA damage calls for a re-evaluation of recommended dietary intake values, say researchers.
Professor Michael Fenech of CSIRO’s Food and Nutritional Sciences Division in Adelaide lays out his argument in a paper accepted for publication in the journal American Journal of Clinical Nutrition.
DNA damage accumulates naturally as we age, but a lack or excess of antioxidants and trace elements, involved in DNA replication and repair, could exacerbate the problem.
Fenech says current recommended dietary intake levels (RDIs) for micronutrients are not defined in terms of preventing DNA damage – the fundamental basis of diseases such as cancer.
“RDIs are the minimum amounts needed to prevent diseases caused by nutrient deficiencies,” says Fenech. “We now need to define optimal dietary reference values for DNA damage prevention.”
“The issue is how we do this for genetic subgroups of people, because supplements of a particular nutrient may be beneficial for some and harmful to others”.
Professor Lynn Ferguson, Head of Nutrition at the University of Auckland, agrees, likening nutrient profiles to shoes.
“You can’t have a different range of shoes for everybody, but you could have a group of sports shoes in one corner and a group of designer heels in another,” says Ferguson.
“What we might end up with is some less rigid recommended amount that is then individually optimised by more precise techniques.”
Fenech is currently investigating the use of biomarkers to develop personalised nutritional advice for “genome health”.
For the last three years, Fenech and colleagues have been working with Adelaide’s Reach 100 genome health clinic to analyse the amount of DNA damage in blood samples from approximately 200 patients.
They use a technique called the ‘cytokinesis-blocked micronucleus’ (CBMN) assay, pioneered by Fenech, to assess DNA damage.
Each person’s results were combined with their medical history, to develop dietary and lifestyle advice that aims to reduce DNA damage.
The cost of the process is $1150 and is a labour-intensive and time-consuming process. But Dr Jane Alderman of the Reach 100 clinic believes it is essential for preventative health.
“Approximately a third of patients who were in the middle or higher risk group in terms of their DNA damage rates have had a significant improvement [four months later] with our suggestions,” she says.
Alderman says it “is a pleasing result”, but points out that the research is still in its early stages.
“At the moment we are only making recommendations based on the levels of vitamin B12, folate and lifestyle,” she says.
“In the next few years we look forward to being able to use additional biomarkers to refine our recommendations so that we can advise on supplementation of other micronutrients.”
The scientists have identified other biomarkers in the laboratory.
“The CBMN assay has proven to be more versatile than we originally thought”, says Fenech. “There are now six biomarkers which measure three types of DNA damage, such as breaks, the rate of cell division and two forms of cell death”.
The researchers believe segregating the type of DNA damage will yield further clues as to its cause. This could lead to intervention measures that could be used to improve genome health and prevent onset of disease.
“Ten years ago we didn’t have the data or the methods to be able to do this, we are really just at the beginning”, says Fenech.
Ferguson, whose research interest is Crohn’s disease and Inflammatory Bowel Disease, hopes the technology may one day be used to stop genetically-prone infants from developing these disorders.
Source: Branwen Morgan in ABC, 9 March 2010, http://www.abc.net.au/science/articles/2010/03/09/2839781.htm