Intelligent Nutrition and Personalized Diets
Source: http://nutrigenomics.ucdavis.edu/intelligentnutrition.htm

Humans can metabolize a wide variety and range of amounts of food chemicals. The flexibility in metabolic response to changes in type and concentration of dietary chemicals demonstrates an important clue for understanding the effects of diet on health. It is the interactions of dietary chemicals with genetic machinery and information, (diet X genotype interactions) that play a key role in maintaining health and preventing diet-influenced chronic diseases ([1, 2]).

The advances and concepts of pharmacogenomics underscore the importance of genotype X environment interactions by showing how individual genetic variation in human populations can effect a drug's efficacy and severity of undesirable side effects [3,4]. Genotyping is now being incorporated into clinical trails in order to predict drug safety, toxicity, and efficacy. By relating phenotype to genotype, drug companies are designing and developing better drugs with fewer adverse side affects. By identifying the non-responding sub-populations, pharmacogenomics can also develop new drugs from compounds previously thought too toxic for human use.

The concept of "personalized" medicine is now being extended to the field of nutrition [5, 6]. It is now accepted that nutrients (i.e., macronutrients, micronutrients and antinutrients) alter molecular processes such as DNA structure, gene expression, and metabolism, and these in turn may alter disease initiation, development, or progression. Individual genetic variation can influence how nutrients are assimilated, metabolized, stored, and excreted by the body.

The interface between the nutritional environment and human cellular/genetic processes is being referred to as "nutrigenomics." The same tools and methods used in pharmacogenomics (SNP analysis, gene expression profiling, proteomics, metabolomics, bioinformatics, and biocomputation) are being used to examine an individual's response to his or her nutritional environment. The desired outcome of nutrigenomics is the use of personalized diets or intelligent nutrition (i.e., knowledge of nutritional status, nutritional requirement and genotype) to prevent or delay the onset of disease and optimize and maintain human health.

Understanding the molecular mechanisms that maintain health or generate chronic diseases will require new scientific strategies that account for genetic variation, environmental factors, and social and economic factors that may influence expression of genetic information. The results of such research may lead to altering guidelines of recommended dietary allowances (RDA) established by the National Research Council to specific genetic populations, and some day, to individuals.

References
1. Ames, B.N. and L.S. Gold, The causes and prevention of cancer: the role of environment. Biotherapy, 1998. 11(2-3): p. 205-20.

2. Ames, B.N., DNA damage from micronutrient deficiencies is likely to be a major cause of cancer. Mutat Res, 2001. 475(1-2): p. 7-20.

3. Kaput, J., et al., Diet-disease interactions at the molecular level: an experimental paradigm. J Nutr, 1994. 124(8 Suppl): p. 1296S-1305S.

4. Park, E.I., et al., Lipid level and type alter stearoyl CoA desaturase mRNA abundance differently in mice with distinct susceptibilities to diet-influenced diseases. J Nutr, 1997. 127(4): p. 566-73.

5. McCarthy, J.J. and R. Hilfiker, The use of single-nucleotide polymorphism maps in pharmacogenomics. Nat Biotechnol, 2000. 18(5): p. 505-8.

6. Park, E.I., et al., Lipid level and type alter stearoyl CoA desaturase mRNA abundance differently in mice with distinct susceptibilities to diet-influenced diseases. J Nutr, 1997. 127(4): p. 566-73.