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Wiki Education Foundation-supported course assignment[edit]

Sciences humaines.svg This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Akhamhoung. Peer reviewers: Kaw66, Cacioppo.j.

Above undated message substituted from assignment by PrimeBOT (talk) 01:45, 18 January 2022 (UTC)[reply]


Hi! I am a Northeastern student who is working on this page for my advanced writing in the sciences course. My main goal is to strengthen sections and get rid of a lot of the plagiarism, a lot of this page is quoted verbatim from various sources. I am also making it more concise, both out of time constraint and I do think certain sections are repetitive. I am focusing on definitions and background, and hopefully looking to add a cancer section to the applications section of the article and possibly ethics.Akhamhoung (talk) 14:47, 31 July 2017 (UTC)[reply]

Hi there, I'm UWO student who will be working on this page as my Wiki project for the AdGen course. I'm new to editing wiki so please point it out if I've done anything wrong while working on it. Million thanks :) Zkwan3 (talk) 22:02, 8 October 2015 (UTC)[reply]

Smells like spam -- Hu.

Spam isn't necessarily a recommended part of ones diet, regardless of genotype. Thincat 14:28, 18 November 2005 (UTC)[reply]

There is a little mixup between nutrigenomics and nutrigenetics in the article. --Wedian 19:20, 29 December 2005 (UTC)[reply]

I couldn't find any legitimate support for this topic. This article suggests this topic should be deleted: --Tim290280 17:48, 01 November 2012 (UTC)[reply]

Thanks for sharing the link... But actually what that article says is that nutrigenomics is a legitimate field of research equivalent to stem cell but unfortunately at risk of quackery ruining its reputation before sufficient research and findings have been made --Dakinijones (talk) 18:26, 29 January 2013 (UTC)[reply]
No, I'm afraid what that article says is that the current practice of using nutrigenomics for "treatment" is quackery. The article says that nutrigenomics is a valid field of research, but it also says that it is strictly in early stages, and that nothing in the research is yet applicable in the real world. As a result, all current talk of using nutrigenomics to address deficiencies and cure diseases is not just premature, it's quackery. To quote the author's conclusion: "There is no compelling evidence for any nutritional treatment for the above diseases, let alone for personalized nutritional treatment based on specific genetic types. How the practitioners of GBIM came by the knowledge they are claiming to have is a mystery... I would add “nutrigenomics” to the list of red flags for dangerous quackery. It is a shame because, like stem cells, it is a legitimate field of research, and the current quackery is likely to taint the reputation of what in the future might be a promising approach."
I think it is fairly clear that the current article is inappropriate and serves to legitimize a practice that does not have legitimacy. In my opinion, the article should be deleted, or should be re-written to make clear that it's describing dubious claims that are not scientifically validated by the medical and research communities. --The_Mental_Nomad — Preceding undated comment added 16:24, 16 January 2015 (UTC)[reply]
I agree. This needs a rewrite to make it clear this is pseudoscientific quackery. The bogus claims also need to be removed. StevenHirlston (talk) 01:51, 3 June 2017 (UTC)[reply]

This line from the article, for example, is bunk: "Ageing of cells occur because of the accumulation of excess free radicals formed due to the lack of proper nutrition to the cells and external factors like UV rays, pollution, stress, food, etc. DNA analysis is instrumental in identifying the right concoction of nutrients needed to eliminate the excess free radicals present in the cell." --The_Mental_Nomad

I am planning to add a section on application of nutrigenomics in obesity. However, there is an existing topic on the application on anti-aging. I am just wondering if anyone would mind if I just modify the section a little bit, and rename the section as 'Application of nutrigenomics', then move the existing content to subheading 'anti-aging' and add a new one 'obesity'? Zkwan3 (talk) 19:51, 15 October 2015 (UTC)[reply]

Wiki Education Foundation-supported course assignment[edit]

Sciences humaines.svg This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Zkwan3.

Above undated message substituted from assignment by PrimeBOT (talk) 05:30, 17 January 2022 (UTC)[reply]

predictions and successes[edit]

Could we add sections to address :

  • Does nutrigenomics make any falsifiable predictions ?
  • Is there any evidence of its success in treating diseases ? Rod57 (talk) 10:41, 6 July 2010 (UTC)[reply]

List of articles[edit]

Moved from the article. They don't seem to be sources. Quick look at additions: one initially, mostly here, another here. --Ronz (talk) 02:20, 20 December 2012 (UTC)[reply]


"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)
  • Brull, D.J., et al., Interleukin-6 gene -174g>c and -572g>c promoter polymorphisms are strong predictors of plasma interleukin-6 levels after coronary artery bypass surgery. Arterioscler Thromb Vasc Biol 21, 1458–1463 (2001)
  • 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)
  • Chen, W. et al., Combined effects of endothelial nitric oxide synthase gene polymorphism (G894T) and insulin resistance status on blood pressure and familial risk of hypertension in young adults: the Bogalusa Heart Study. Am J Hypertens 14, 1046–1052 (2001)
  • Dullaart, R.P., et al., Cholesteryl ester transfer protein gene polymorphism is a determinant of HDL cholesterol and of the lipoprotein response to a lipid-lowering diet in type 1 diabetes. Diabetes 46, 2082–2087 (1997)
  • Leeson, C.P., Glu298Asp endothelial nitric oxide synthase gene polymorphism interacts with environmental and dietary factors to influence endothelial function. Circ Res 90, 1153–1158 (2002)
  • Miyamoto, Y., et al., Endothelial nitric oxide synthase gene is positively associated with essential hypertension. Hypertension 32, 3-8 (1998)
  • Shoji, M., et al., Positive association of endothelial nitric oxide synthase gene polymorphism with hypertension in northern Japan. Life Sci 66, 2557–2562 (2000)
  • 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)
  • Hirvonen, A, et al., Association between manganese superoxide dismutase (MsSOD) gene polymorphism and breast cancer risk. Carcinogenesis 5(22), 827-829 (2001)
  • 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, TNFα:"

  • 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

Removed external links[edit]

Given the state of the article, I've moved the external links here, hoping they might be used to find sources or other information for improving the article. --Ronz (talk) 02:25, 20 December 2012 (UTC)[reply]

External links[edit]