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Nutrigenomics is the study of the effects of foods and food constituents on gene expression. It is about how our DNA is transcribed into mRNA and then to proteins and provides a basis for understanding the biological activity of food components. [1] Nutrigenomics has also been described by the influence of genetic variation on nutrition by correlating gene expression or single-nucleotide polymorphisms with a nutrient's absorption, metabolism, elimination or biological effects. By doing so, nutrigenomics aims to develop rational means to optimise nutrition, with respect to the subject's genotype.

By determining the mechanism of the effects of nutrients or the effects of a nutritional regime, nutrigenomics tries to define the causality|relationship between these specific nutrients and specific nutrient regimes (diets) on human health. Nutrigenomics has been associated with the idea of personalized nutrition based on genotype. While there is hope that nutrigenomics will ultimately enable such personalised dietary advice, it is a science still in its infancy and its contribution to public health over the next decade is thought to be major. [2]


[edit] Definitions

Nutrigenomics is applying the sciences of genomics, transcriptomics, proteomics, and metabolomics to human nutrition in order to understand the relationship between nutrition and health. Nutrigenomics is a new science and has several different definitions. Nutrigenomics has been defined as the application of high-throughput genomic tools in nutrition research.[2]It can also be seen as research to provide people with methods and tools who are looking for disease preventing and health promoting foods that match their lifestyles, cultures and genetics. Nutritional genomics is a systems approach to understanding the relationship between diet and health and will ensure that everyone benefits from the genomic revolution. [3]

The term "high throughput tools" in nutrigenomics refers to genetic tools that enable literally millions of genetic screening tests to be conducted at a single time. When such high throughput screening is applied in nutrition research, it allows the examination of how nutrients affect the thousands of genes present in the human genome. Nutrigenomics involves the characterization of gene products and the physiological function and interactions of these products. This includes how nutrients impact on the production and action of specific gene products and how these proteins in turn affect the response to nutrients. [4]

[edit] Background and preventive health

Throughout the 20th century, nutritional science focused on finding vitamins and minerals, defining their use and preventing the deficiency diseases that they caused. As the nutrition related health problems of the developed world shifted to overnutrition, obesity and type two diabetes, the focus of modern medicine and of nutritional science changed accordingly.

In order to address the increasing incidence of these diet-related-diseases, the role of diet and nutrition has been and continues to be extensively studied. To prevent the development of disease, nutrition research is investigating how nutrition can optimize and maintain cellular, tissue, organ and whole body homeostasis. This requires understanding how nutrients act at the molecular level. This involves a multitude of nutrient-related interactions at the gene, protein and metabolic levels. As a result, nutrition research has shifted from epidemiology and physiology to molecular biology and genetics[2] and nutrigenomics was born.

The emergence and development of nutrigenomics has been possible due to powerful developments in genetic research. Inter-individual differences in genetics, or genetic variability, which have an effect on metabolism and on phenotypes were recognized early in nutrition research, and such phenotypes were described. With the progress in genetics, biochemical disorders with a high nutritional relevance were linked to a genetic origin. Genetic disorders which cause pathological effects were described. Such genetic disorders include the polymorphism in the gene for the hormone Leptin which results in gross obesity. Other gene polymorphisms were described with consequences for human nutrition. The folate metabolism is a good example, where a common polymorphism exists for the gene that encodes the methylene-tetrahydro-folate reductase (MTHFR).

It was realized however, that there are possibly thousands of other gene polymorphisms which may result in minor deviations in nutritional biochemistry, where only marginal or additive effects would result from these deviations. The tools to study the physiological impact were not available at the time and are only now becoming available enabling the development of nutrigenomics. Such tools include those that measure the transcriptome - DNA microarray, Exon array, Tiling arrays, single nucleotide polymorphism arrays and genotyping. Tools that measure the proteome are less developed. These include methods based on gel electrophoresis, chromatography and mass spectrometry. Finally the tools that measure the metabolome are also less developed and include methods based on nuclear magnetic resonance imaging and mass spectrometry often in combination with gas and liquid chromatography.

[edit] Rationale and aims of nutrigenomics

In nutrigenomics, nutrients are seen as signals that tell a specific cell in the body about the diet. The nutrients are detected by a sensor system in the cell. Such a sensory system works like sensory ecology whereby the cell obtains information through the signal, the nutrient, about its environment, which is the diet. The sensory system that interprets information from nutrients about the dietary environment include transcription factors together with many additional proteins. Once the nutrient interacts with such a sensory system, it changes gene, protein expression and metabolite production in accordance with the level of nutrient it senses. As a result, different diets should elicit different patterns of gene and protein expression and metabolite production. Nutrigenomics seeks to describe the patterns of these effects which have been referred to as dietary signatures. Such dietary signatures are examined in specific cells, tissues and organisms and in this way the manner by which nutrition influences homeostasis is investigated. Genes which are affected by differing levels of nutrients need first to be identified and then their regulation is studied. Differences in this regulation as a result of differences in genes between individuals are also studied. [2]

It is hoped that by building up knowledge in this area, nutrigenomics will promote an increased understanding of how nutrition influences metabolic pathways and homeostatic control, which will then be used to prevent the development of chronic diet related diseases such as obesity and type two diabetes. Part of the approach of nutrigenomics involves finding markers of the early phase of diet related diseases; this is the phase at which intervention with nutrition can return the patient to health. As nutrigenomics seeks to understand the effect of different genetic predispositions in the development of such diseases, once a marker has been found and measured in an individual, the extent to which they are susceptible to the development of that disease will be quantified and personalized dietary recommendation can be given for that person.

The aims of nutrigenomics also includes being able to demonstrate the effect of bioactive food compounds on health and the effect of health foods on health, which should lead to the development of functional foods that will keep people healthy according to their individual needs.

Nutrigenomics is a rapidly emerging science still in its beginning stages. It is uncertain whether the tools to study protein expression and metabolite production have been developed to the point as to enable efficient and reliable measurements. Also once such research has been achieved, it will need to be integrated together in order to produce results and dietary recommendations. All of these technologies are still in the process of development.

[edit] References

  1. ^ Rawson, N. (October 24, 2008). Nutrigenomics Boot Camp: Improving Human Performance through Nutrigenomic Discovery. A Supply Side West VendorWorks Presentation. Las Vegas, Nevada 
  2. ^ a b c d MĂĽller M, Kersten S. (2003). Nutrigenomics: Goals and Perspectives.. Nature Reviews Genetics 4. 315 -322. 
  3. ^ "Nutritional Genomics: Home". http://nutrigenomics.ucdavis.edu/?page=Home. Retrieved 2010-07-02. 
  4. ^ Trayhurn P. (2003). Nutritional genomics-"Nutrigenomics". British Journal Nutrition. 89:1-2. 

[edit] Articles

"Genes associated with cholesterol metabolism, triglyceride balance, vascular flow and tissue development: APOC3, IL-6, eNOS, LPL, CETP, MTHFR:"

  • Brousseau, M.E., et al, Cholesteryl ester transfer protein TaqI b2b2 Genotype is associated with higher HDL cholesterol levels and lower risk of coronary heart disease end points in men with HDL deficiency: Veterans Affairs HDL Cholesterol Intervention Trial. Arterioscler Thromb Vasc Biol 22, 1148-1154 (2002) http://atvb.ahajournals.org/cgi/content/full/22/7/1148
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  • Brull, D.J., et al, The effect of the Interleukin-6-174G > C promoter gene polymorphism on endothelial function in healthy volunteers. Eur J Clin Invest 32, 153-157 (2002)
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  • Brown, C.A., et al, A common polymorphism in methionine synthase reductase increases risk of premature coronary artery disease. J Cardiovasc Risk 7, 197-200 (2000)
  • Christensen, B., et al, Genetic polymorphisms in methylenetetrahydrofolate reductase and methionine synthase, folate levels in red blood cells, and risk of neural tube defects. Am J Med Genet 84, 151-157 (1999)
  • Chen, J, et al, A methylenetetrahydrofolate reductase polymorphism and the risk of colorectal cancer. Cancer Res 56, 4862-4864 (1996)
  • Jacques, P.F., et al, Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation 93, 7-9 (1996)
  • Ma, J., et al, Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer. Cancer Res 57, 1098-1102 (1997)
  • Martinez de Villarreal, L.E., et al, Folate levels and N(5),N(10)-methylenetetrahydrofolate reductase genotype (MTHFR) in mothers of offspring with neural tube defects: a case-control study. Arch Med Res 32, 277-282 (2001)
  • Slattery, M.L., et al, Methylenetetrahydrofolate reductase, diet, and risk of colon cancer. Cancer Epidemiol Biomarkers Prev 8, 513-518 (1999)
  • Brown, S., et al. Interaction between the APOC3 gene promoter polymorphisms, saturated fat intake and plasma lipoproteins. Atherosclerosis. 170: 307-313, 2003.
  • Fisher, R., et al. Common variation in the lipoprotein lipase gene effects on plasma lipids and risk of atherosclerosis. Atherosclerosis. 135: 145-159, 1997.
  • Guzik, T., et al. Relationship between the G894T (Glu298Asp variant) in endothelial nitric oxide synthase and nitric oxide-mediated endothelial function in human atherosclerosis. American Journal of Medical Genetics. 100: 130-137, 2001.
  • Wallace, A., et al. Variants in the cholesterol ester transfer protein and lipoprotein lipase genes are predictors of plasma cholesterol response to dietary change. Atherosclerosis. 152: 327-336, 2000

"Genes associated with antioxidant function and detoxification: MnSOD, SOD3, GSTM1, GSTT1, GSTP1:"

  • Ambrosone, C.B., et al, Manganese superoxide dismutase 9MsSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer. Cancer Res 59(3), 602-606 (1999)
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  • Kimura, K.Y., et al, Genetic association of manganese superoxide dismutase with exudative age-related macular degeneration. Am J Ophthalmol 130(6), 769-73 (2000)
  • Stoehlmacher, J., et al, A genetic polymorphism of manganese superoxide dismutase (9MnSOD) predicts for risk of colorectal cancer in young individuals. Annals of Oncology 11(Suppl 4), 59 (2000)
  • Wang, X.L., et al, Plasma extracellular cuperoxide dismutase levels in an Australian population with coronary artery disease. Arterioscler Thromb Vasc Biol 18, 1915-1921 (1998)
  • Purdie, D., et al, Dietary antioxidants, manganese superoxide dismutase (MnSOD), and risk of epithelial ovarian cancer. Proc. American Assoc. for Cancer Res. 43, 4227 (2002)
  • Cotton, S.C., et al, Glutathione S-transferase polymorphisms and colorectal cancer: a HuGE review. Am J Epidemiol 151(1), 7-32 (2000)
  • Lampe, J.W., et al, Modulation of human glutathione S-transferases by botanically defined vegetable diets. Cancer Epidemiol Biomarkers Prev 8, 787-93
  • Lin, H.J., et al, Glutathione transferase GSTT1, broccoli, and prevalence of colorectal adenomas. Pharmacogenetics 12, 175-179
  • Mitrunen, K.N., et al, Glutathione S-transferase M1, M3, P1, and T1 genetic polymorphisms and susceptibility to breast cancer. Cancer Epidemiol Biomarkers Prev 10(3), 229-36 (2001)
  • Pool-Zobul, B, et al, Mechanisms by which vegetable consumption reduces genetic damage in humans. Cancer Epidemiol. Biomarkers Prev. 7, 891-99 (1998)
  • Rock, C.L., et al, Nutrition genetics and risks of cancer. Annu Rev Public Health 21, 47-64 (2000)
  • Steinkellner, H., et al, Effects of crusiferous vegetables and their constituents on drug metabolizing enzymes involved in the bioactivation of DNA-reactive dietary carcinogens. Mutation Research, 480-481,285-297 (2001)
  • Ambrosone, C., et al. Manganese superoxide dismutase (MnSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer. Cancer Research. 59(3): 602-606, 1999.
  • Chistyakov, D. A., et al. Polymorphisms in the Mn-SOD and EC-SOD genes and their relationship to diabetic neuropathy in type 1 diabetes mellitus. BMC Medical Genetics. 2(1): 4, 2001.
  • Parke, D.V. “Antioxidants and disease prevention: mechanisms of action”. Antioxidants in Human Health. CABI Publishing, 1999.
  • Gaudet, M., et al. Diet, GSTM1, and GSTT1 and head and neck cancer. Carcinogenesis. 25(5): 735-740, 2003
  • Lampe, J.W., et al. Modulation of human glutathione S-transferases by botanically defined vegetable diets. Cancer Epidemiology Biomarkers Preview. 9(8):787-793, 2000.
  • Verhoeff, B., et al. The effect of a common methylenetetrahydrofolate reductase mutation on levels of homocysteine, folate, vitamin B12 and on the risk of premature atherosclerosis. Atherosclerosis. 141(1): 161-166, 1998
  • Change, A., et al. The effect of 677 C T and 1298 A C mutations on plasma homocysteine and 5,10- methylenetetrahydrofolate reductase activity in healthy subjects. British Journal of Nutrition. 83(6): 593-596, 2000.
  • Jacques, P., et al. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation. 93(1): 7-9, 1996.
  • Miller M., and Mohrenweiser, H. Genetic variability in susceptibility and response to toxicants. Toxicology Letters. 120(1-3): 269-280, 2001.
  • Cosma, G., et al. Relationship between genotype and function of the human CYP1A1 gene. Journal of Toxicology and Environmental Health. 40(2-3): 309-316, 1993.
  • Bosron, W. and Ting-Kai, L. Genetic polymorphism of human liver alcohol and aldehyde dehydrogenases, and their relationship to alcohol metabolism and alcoholism. Hepatology. 6(3):502 - 510, 1986.
  • Takeshita, T. and Morimoto, K. Accumulation of hemoglobin-associated acetaldehyde with habitual alcohol drinking in the atypical ALDH2 genotype. Alcohol Clinical and Experimental Research. 24(1): 1-7, 2000

"Genes associated with bone structure: VDR, COL1A1, IL6, TNFî±:"

  • Chen, H.Y., et al, Relation of vitamin D receptor FokI start codon polymorphism to bone mineral density and occurrence of osteoporosis in postmenopausal woman in Taiwan. Acta Obstet Gynecol Scan 81, 93-98 (2002)
  • Dennison, E.M., at al, Birthweight, vitamin D receptor genotype and the programming of osteoporosis. Paediatr Perinat Epidemiol 15, 211-219 (2001)
  • Eastell, R. and Lambert, H., Diet and healthy bones., Calcif Tissue Int 70, 400-404 (2002)
  • Ferrari, S., et al, Bone mineral mass and calcium and phosphate metabolism in young men: relationships with vitamin D receptor allelic polymorphisms. J Clin Endocrinol Metab 84, 2043-2048 (1999)
  • Ferrari. S.L., Osteoporosis, vitamin D receptor gene polymorphisms and response to diet. World Rev Nutr Diet 89, 83-92 (2001)
  • Garnero, P., et al, Association between a functional interleukin-6 gene polymorphism and peak bone mineral density and postmenopausal bone loss in women: the ofely study. Bone 31, 43-50 (2002)
  • Gong, G., et al, The association of bone mineral density with vitamin D receptor gene polymorphisms. Osteoporos Int 9, 55-64 (1999)
  • Lorentzon, M., et al, Vitamin D receptor gene polymorphism is related to bone density, circulating osteocalcin, and parathyroid hormone in healthy adolescent girls. J Bone Miner Metab 19, 302-307
  • MacDonald, H.M., et al, COL1A1 Sp1 polymorphism predicts perimenopausal and early postmenopausal spinal bone loss. J Bone Miner Res 16, 1634-1641 (2001)
  • Mann, V., et al, A COL1A1 Sp1 binding site polymorphism predisposes to osteoporotic fracture by affecting bone density and quality. J Clin Invest 107, 899-907 (2001)
  • Prentice, A., The relative contribution of diet and genotype to bone development. Proc Nutr Soc 60, 45-52 (2001)
  • Ralston, S.H., Genetic control of susceptibility to osteoporosis. J Clin Endocrinol Metab 87, 2460-2466 (2002)
  • Grant, S., et al. Reduced bone density and osteoporosis associated with a polymorphic Sp1 binding site in the collagen type 1 alpha 1 gene. Nature Genetics. 14: 203-205, 1996.
  • Ortlepp, J., et al. The vitamin D receptor gene variant and physical activity predicts fasting glucose levels in healthy young men. Diabetic Medicine. 20: 451-454, 2003.
  • Uitterlinden, A., et al. Interaction between the vitamin D receptor gene and collagen type 1alpha1 gene susceptibility for fracture. Journal of Bone and Mineral Research. 16: 379-385, 2001

"Genes associated with inflammatory response: TNF, IL-6:"

  • Abraham, L.J., et al, Impact of the -308 TNF promoter polymorphism on the transcriptional regulation of the TNF gene: relevance to disease. J Leukoc Biol 66, 552-566 (1999)
  • Chung, H.Y., et al, The inflammation hypothesis of aging: molecular modulation by calorie restriction. Ann NY Acad Sci 928, 327-335 (2001)
  • Grimble, R.F., Nutritional modulation of immune function. Proc Nutr Soc 60, 389-397 (2001)
  • Nakajima, T., et al, Allelic variants in the interleukin-6 gene and essential hypertension in Japanese women. Genes Immun 1, 115-119 (1999)
  • Terry, C.F., et al, Cooperative influence of genetic polymorphisms on interleukin 6 transcriptional regulation. J Biol Chem 275, 18138-18144 (2000)
  • Vickers, M.A., et al, Genotype at a promoter polymorphism of the interleukin-6 gene is associated with baseline levels of plasma C-reactive protein. Cardiovasc Res 53, 1029-1034 (2002)
  • Ferrari, S., et al. Two promoter polymorphisms regulating interleukin-6 gene expression are associated with circulating levels of C-reactive protein and markers of bone resorption in postmenopausal women. Journal of Clinical Endocrinology & Metabolism. 88: 255-259, 2003.
  • Grimble R., et al. The ability of fish oil to suppress tumor necrosis factor alpha production by peripheral blood mononuclear cells in healthy men is associated with polymorphisms in genes that influence tumor necrosis factor alpha production. American Journal of Clinical Nutrition. 76(2): 454-459, 2002.
  • Terry, c., et al. Cooperative influence of genetic polymorphisms on interleukin 6 transcriptional regulation. Journal of Biological Chemistry. 275: 18138-18144, 2000.
  • Vendrell, J., et al. A polymorphism in the promoter of the tumor necrosis factor-alpha gene (-308) is associated with coronary heart disease in type 2 diabetic patients. Atherosclerosis. 167: 257-264, 2003.
  • Witte, J.S., et al, Relation between tumour necrosis factor polymorphism TNFalpha-308 and risk of asthma. Eur J Hum Genet 10, 82-85 (2002)

"Genes associated with glucose balance: VDR, PPARg2, ACE, TNF:"

  • Chiu, K.C., et al, The vitamin D receptor polymorphism in the translation initiation codon is a risk factor for insulin resistance in glucose tolerant Caucasians. BMC Med Genet 2,2 (2001)
  • Dalziel, B., et al, Association of the TNF-alpha -308G/A promoter polymorphism with insulin resistance in obesity. Obes Res 10, 401-407 (2002)
  • Deeb, S.S., et al, A Pro12Ala substitution in PPARgamma2 associated with decreased receptor activity, lower body mass index and improved insulin sensitivity. Nat Genet 20, 284-287 (1998)
  • Dengel, D.R., et al, Exercise-induced changes in insulin action are associated with ACE gene polymorphisms in older adults. Physiol Genomics 11, 73-80 (2002)
  • Kadowaki, T., et al, The role PPARgamma in high-fat diet-induced obesity and insulin resistance. J Diabetes Complications 16, 41-45 (2002)
  • Nicaud, V., et al, The TNF alpha/G-308A polymorphism influences insulin sensitivity in offspring of patients with coronary heart disease: the European Atherosclerosis Research Study II. Atherosclerosis 161, 317-325 (2002)
  • Paolisso, G., et al, ACE gene polymorphism and insulin action in older subjects and healthy centenarians. J Am Geriatr Soc 49, 610-614 (2001)
  • Li, S., et al. The peroxisome proliferator-activated receptor-gamma2 gene polymorphism (Pro12Ala) beneficially influences insulin resistance and its tracking from childhood to adulthood: the Bogalusa Heart Study. Diabetes. 52: 1265-1269, 2003.
  • Ostgren, C., et al. Peroxisome proliferator-activated receptor-gammaPro12Ala polymorphism and the association with blood pressure in type 2 diabetes: Skaraborg hypertension and diabetes project. Journal of Hypertension. 21: 1657-1662, 2003.
  • Paolisso, G., et al. ACE gene polymorphism and insulin action in older subjects and healthy centenarians. Journal of American Geriatric Society. 49: 610-614, 2001.
  • Perticone, F., et al. Relationship between angiotensin-converting enzyme gene polymorphism and insulin resistance in never-treated hypertensive patients. Journal of Clinical Endocrinology & Metabolism. 86: 172-178, 2001

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