Last week I attended a seminar on nutritional genomics organised by the Nutrition Society of Australia. Presenters were Prof. Michael Fenech from CSIRO, Dr Jennifer Cropley from Victor Chang, Cardiac Research Institute and Melissa Adamski from Nutted Out Nutrition. Here’s a summary of their presentations.Embed from Getty Images
The OMICS and ETICS of personalised nutrition and lifestyle recommendations
Prof. Michael Fenech
- Nutrigenomics refer to the impact of diet in nutrition and medicine. Nutrigenetics refer to what has been programmed in our DNA.
- Diet has an impact in our DNA (the blueprint and its stability), RNA (the transcript) and proteins (the products), the way genes are expressed.
- Exposomes are things we’re exposed to that can cause DNA damage. These include: malnutrition, lifestyle toxins (e.g. alcohol), psychological stress, environmental toxins. There’s a higher risk earlier in life.
- Some nutrients that are important to make good DNA are folate, methionine, vitamin B12, zinc. However, elevated doses can be as harmful, e.g. folate exposure can be as harmful as X-ray exposure.
- DNA repair can be performed by homologous recombination (error free) or non-homologous recombination (error prone, i.e. repair happens but introduces errors in the genome).
- DNA damage can be decreased by dietary intake (not supplementation) of iron, vitamin E, calcium, folate, retinol and nicotinic acid. It can be decreased by dietary intake (not supplementation) of riboflavin, pantothenic acid, biotin. Beta-carotene has a U-shaped effect.
- Telomeres are important in DNA damage. Currently the main focus is on length but quality is also important. Longer telomeres are found in association with folate, vitamin E, vitamin D, omega-3 fatty acids, cereal fibre, multivitamin use. Shorter telomeres are found in association with polyunsatured fatty acids, oxidative stress, obesity, psychological stress.
- Cancer growth can be controlled by methionine restriction.
- Alzheimer’s and other neurodegenerative diseases can be improved by acetyl-L-carnitine, choline, omega-3 fatty acids.
- Carriers of the APOe4 gene are better adapted to famine, and so may be respond better to a paleolithic-type diet.
Influence of parental obesity on offspring
Dr Jennifer Cropley
- Experiments with mice where the mother is predisposed to metabolic disease via a Western-type diet, this predisposition is inherited in the second and third generations.
- When the father is the carrier of the predisposition, it’s carried up to the grandchildren. miRNAs and tRNAs in sperm that encode transcription factors are different in obese vs non-obese fathers.
- The predisposition, even with a healthy phenotype (not displaying signs of metabolic disease) can be passed on.
- Genetic variations have been included in the NRVs (nutrient reference values) of 2006 (e.g. folate, vitamin D).
- There are popular genetic tests that are offered to determine everything from micro-nutrient status to salt sensitivity.
- Personal care businesses are advertising their products as able to cause changes in gene expression. Should we believe the hype?
- Commercial nutrigenetic testing can be direct to consumer or through a healthcare professional. In either case, it’s important to consider the quality and accuracy of the test analysis, how the data is going to be used (ethics, privacy), etc. For dietitians it’s also important to work closely with a genetic counselor.
- Some resources:
- The regulation of nutrigenetic tests in Australia
- International Society of Nutrigenetics / Nutrigenomics
- PEN: Practice-based Evidence in Nutrition
- Academy of Nutrition and Dietetics
- The book Nutrigenomics and Nutrigenetics in Functional Foods and Personalized Nutrition by Lynette Ferguson
- Genome Web
It was a great seminar with plenty of useful information and not a bunch of conventional wisdom thrown at us. I was also glad that catering in charge of About Life.