The Role of Nutrigenetics/Nutrigenomics in Dietary Control of Type 2 Diabetes - Essay Example

www.academia-research.com Sumanta Sanyal Nutrigenetics/Nutrigenomics d: 6th November, 2005 The Role of Nutrigenetics/Nutrigenomics in DietaryControl of Type 2 Diabetes Introduction Nutrigenetics, also commonly called nutrigenomics, is a recent development of nutritional science that matches nutritional requirements of an individual to his or her personal genetic makeup. The individual’s DNA is tested for common SNPs (single nucleotide polymorphisms) and a specific diet is suggested to help the person stay healthy. Human evolution as well as survival, which primarily involves health and disease, is an effect of interaction between genetics and the environment. The most primary environmental factor is nutrition and recent advanced studies have shown that nutrition and genetics are interlinked in the following two ways: genetic variation, especially presence of certain common SNPs, can cause variation in dietary response: e.g.: polymorphisms causing variance in levels of serum cholesterol and blood pressure can cause variance in dietary response (Artemis P. Simopolous, 2002, Genetic Variation and Dietary Response: Nutrigenetics/Nutrigenomics), and dietary nutrients, as chemicals and as primary environmental factors that influence evolution, influence gene expression: e.g.: polyunsaturated fatty acids suppress fatty acid synthase (mRNA) gene expression (Artemis P. Simopolous, 2002, Genetic Variation and Dietary Response: Nutrigenetics/Nutrigenomics). Dietary intake, by influencing gene expression, can become the associative cause of certain chronic diseases like atherosclerosis, diabetes, obesity, cancer, and others (Nutritional genomics: the next frontier in the post-genomic era, Jim Kaput and Raymond L. Rodriguez, 2003). The first definition of nutrigenomics this research paper starts out with presents the science as being more effective for interactions of the first kind – genetic variation affecting dietary response – but in the light of the primary objective of this paper which is to maintain that nutrigenomics can be effective as a means to preventing, mitigating and curing a chronic disease - type 2 diabetes – the following definition, though it is succinct, will be more appropriate. The science of the dietary interface and the cellular/genetic processes is known as nutrigenomics. The science explores ways and means by which dietary intakes can change a healthy phenotype to a chronic disease phenotype by changes in gene expression or variance in activities of proteins and enzymes, which can secondarily cause changes in gene expression (Nutritional genomics: the next frontier in the post-genomic era, Jim Kaput and Raymond L. Rodriguez, 2003). Ignatovski first noticed this association between dietary intake and chronic disease in 1908. He observed development of arterial lesions in mice fed on a special variant diet. Type 2 Diabetes Though type 2 diabetes was considered as mild in the past it is today an almost endemic disease. Sedentary lifestyles, increased obesity and higher average age of populations have had the combined effects of increased incidence of the disease. Today, even young people are diagnosed with it (Initial Management of Glycemia in Type 2 Diabetes Mellitus, David M. Nathan, MD, 2002). A WHO 2002 report presented at the Third World Congress on the Prevention of Diabetes suggested that the worldwide incidence of diabetes would exceed 450 million by 2025. More recent WHO studies estimate that over 1 billion people are obese and over 400 million clinically obese (MR Green and F van der Ouderaa, 2003). Causes of Diabetes Diet genotype X interaction is clearly responsible for type 2 diabetes. Sedentary, obese individuals and members of certain minority groups are prone to it (Nutrigenomics, University of California at Davis, 2004). This last suggests involvement of certain SNPs specific to such minority groups. Nevertheless, genetic risk assays, which can accurately reveal which individuals are prone to the disease by disclosing susceptible genotypes, are not possible at present (MR Green and F van der Ouderaa, 2003). This preempts any attempts at accurate dietary preventive measures based on nutrigenomics. It is found that certain dietary habits are a risk. Total and saturated fat intake is associated with a higher risk of the disease, though this is not independent of BMI (Body Mass Index: an independent measure used almost exclusively to determine overweight and obesity in adults). Consumption of processed meat on a regular basis also poses as a higher risk (Dietary Fat and Meat Intake in Relation to Risk of Type 2 Diabetes in Men, Rob M. van Dam et al, 2002). Since glycemia and dyslipidemia are symptoms for type 2 diabetes, diets that enhance the GI (glycemic index: a quantitative measure of foods based on the postprandial blood glucose response) also pose as a higher risk of the disease (Initial Management of Glycemia in Type 2 Diabetes Mellitus, David M. Nathan, MD, 2002). Prevention and Therapy Once diagnosed with type 2 diabetes some individuals can control symptoms by increasing physical activity and reducing calorific intakes, specifically in the form of fat. Other individuals may have to take drug therapy. This is because irreversible complications have become evident in them through loss of phenotypic plasticity. Such irreversible changes may be caused by chromatin remodeling and changes in DNA methylation (Nutritional genomics: the next frontier in the post-genomic era, Jim Kaput and Raymond L. Rodriguez, 2003). Such irreversible changes become increasingly incident because type 2 diabetes is often diagnosed late, 4 to 7 years after onset of disease. Also, affected persons with greater longevity gradually acquire these irreversible changes. In both cases continuous incidence of above-average level of the glycemic index cause these irreversible changes to phenotypic factors (physiological changes caused by changes in gene expression) that are responsible for incidence of the disease (Initial Management of Glycemia in Type 2 Diabetes Mellitus, David M. Nathan, MD, 2002). Green and Ouderaa propose in their article on nutrigenetics that consumer-attractive (tasty) low glycemic index food products containing biologically effective natural ingredients combined with improved communications and advertising conveying advice on lifestyles can significantly influence the incidence of diabetes. This is true for type 2 diabetes as well. Conclusion The exact mechanism by which gene expression is altered to cause incidence of type 2 diabetes has still not been fully unraveled. Neither have all the particular components of the human genetic makeup whose mutation cause the disease though Jean Marx’s article “Unraveling the Causes of Diabetes” in Science magazine, 2002 April issue, does contain a number of pointers in this direction. Under these circumstances, as Green and Ouderaa suggest, a population strategy based partly on dietary responses rather than an individual strategy based wholly on nutrigenomics is more compelling for providing therapy for type 2 diabetes. Individual dietary prescriptions based on nutrigenomics is at present not fully feasible in treatment of the disease though any dietary recommendations must be based on nutrigenomics as a lot of information generating such a recommendation is based on the understanding of how gene expression affected by diet cause the disease. References Dietary Fat and Meat Intake in Relation to Risk of Type 2 Diabetes in Men, Rob M. van Dam et al, Diabetes Care, 25: 417-424, 2002. Extracted on 26th October, 2005, from: http://care.diabetesjournals.org/cgi/content/full/25/3/417 Genetic variation and dietary response: Nutrigenetics/nutrigenomics, Artemis P. Simopoulos, Asia Pacific J Clin Nutr (2002) 11 (S6): S117-S128. Extracted on 26th October, 2005, from: http://www.healthyeatingclub.com/APJCN/Volume11/vol11sup6/S117.pdf#search=Artemis P. Simopoulos Nutrigenetics/nutrigenomics Initial Management of Glycemia in Type 2 Diabetes Mellitus, David M. Nathan, The New England Journal of Medicine, Vol. 347: 1342-1349, 2002. Extracted on 26th October, 2005, from: http://content.nejm.org/cgi/content/full/347/17/1342#R1 Nutrigenomics, Diabetes section, NCMHD Center of Excellence for Nutritional Genomics, University of California at Davis Website. Extracted on 25th October, 2005, from: http://nutrigenomics.ucdavis.edu/dietarychemicals.htm#top Nutritional genomics: the next frontier in the post-genomic era, Jim Kaput and Raymond L. Rodriguez, Physiological Genomics, 16: 166-177 (2004). Extracted on 26th October, 2005 from: http://physiolgenomics.physiology.org/cgi/content/full/16/2/166#top Nutrigenetics: where next for the food industry? MR Green and F van der Ouderaa, The Pharmacogenomics Journal, 0, 1-3, 2003. Extracted on 26th October, 2005, from: http://www.unilever-colworth.co.uk/Nurigenomic.pdf#search=Nutrigenetics%20Green%20and%20Ouderaa Read More