Perspectiva genética del tratamiento nutricional en la enfermedad cardiovascular
PDF
HTML

Palabras clave

Nutrigenómica
Nutrigenética
Enfermedades Cardiovasculares
Gen

Cómo citar

Martin, A. Ángel. (2013). Perspectiva genética del tratamiento nutricional en la enfermedad cardiovascular. Médicas UIS, 26(1). Recuperado a partir de https://revistas.uis.edu.co/index.php/revistamedicasuis/article/view/3580

Resumen

Introducción: las enfermedades cardiovasculares son la relación de procesos multifactoriales que incluyen factores genéticos y factores de riesgo potencialmente modificables, como la dieta. Las recomendaciones nutricionales actuales están centradas en reducir los factores de riesgo modificables, como por ejemplo el control de las concentraciones elevadas de colesterol plasmático. Sin embargo, esta variable es sólo una dentro de los múltiples factores de riesgo asociados a la enfermedades cardiovasculares. Objetivo: identificar las interacciones nutrigenómicas y nutrigenéticas relacionadas con la enfermedades cardiovasculares. Metodología: revisión sistemática de bibliografía en las bases de datos de PubMed, ELSEIVER y Scielo. Resultados: la interacción nutricional con algunos genes como, la lipasa hepática, apolipoproteína A-1, A-4, A-5 y apolipoproteína E modulan las concentraciones plasmáticas de lípidos, esto potencia el riesgo de desarrollar una enfermedad cardiovascular, sin dejar de lado los efectos de la ingesta rica en ácidos grasos saturados. A pesar de esto se observa que no todos los individuos responden igual al consumo de grasas y no todos desarrollan dicha enfermedad. Este concepto es aplicable en el contexto de la nutrición personalizada como prevención y tratamiento de las enfermedades cardiovasculares. Conclusiones: el tratamiento de la enfermedad cardiovascular depende de las variantes genéticas que influyen sobre la respuesta a la dieta y sobre la forma

en cómo determinados nutrientes influyen sobre el genoma. (MÉD.UIS.2013;26(1):29-35).

 

PDF
HTML

Referencias

1. Christensen K, Doblhammer G, Rau R, Vaupel JW. Ageing populations: the challenges ahead. Lancet. 2009; 374:1196–1208.

2. Centers for Disease Control and Prevention. Achievements in Public Health, 1900–1999: Control of Infectious Diseases, Morbidity and Mortality Weekly Report. Vol. 48. U.S. Government Printing Office; Atlanta, GA: 1999. p. 621-29.

3. Eyre H, Khan R, Robertson RM, ACS/ADA/AHA Collaborative Writing Committee. Preventing cancer, cardiovascular disease, and diabetes: a common agenda for the ACS, the ADA and the AHA. CA Cancer J Clin. 2004; 54:190–207.

4. Deaths: Final Data for 2005.. National Vital Statistics Reports. 56, Number 10. 2008. Available at: http://www.cdc.gov/nchs/data/nvsr/nvsr56/ nvsr56_10.pdf [Feb 10, 2012]

5. O’Donnell MJ, Xavier D, Liu L, Zhang H, Chin SL, Rao-Melacini
P, et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study. Lancet. 2010;376(9735): 112-23.

6. World Health Organization. Prevention of recurrent heart attacks and strokes in low and middle income populations. Evidence-based recommendations for policy markers and health professionals. Geneva, 2003.

7. Informe sobre la Situación de Salud en Colombia 2007 del Ministerio de la Protección Social. http://www.minproteccionsocial.gov.co/salud/Paginas/EncuestaNacionaldeSaludPublica.aspx (1/12/2011).

8. Kannel WB, Dawber TR, Kagan A, Revotskie N, Stokes JI: Factors of risk in the development of coronary heart disease – six year follow-up experience; the Framingham Study. Ann Intern Med. 1996;55:33-50.

9. Ordovas JM. Gene-diet interaction and plasma lipid responses to dietary intervention. Biochem Soc Trans. 2002;30(2):68-7.

10. Minieri M, Di Nardo P. Nutrients: The environmental regulation of cardiovascular gene expression. Genes Nutr. 2007;2(2):163-8.

11. Aslibekyan S, Jensen MK, Campos H, Linkletter CD, Loucks EB, Ordovas JM, et al. Genetic variation in fatty acid elongases is not associated with intermediate cardiovascular phenotypes or myocardial infarction. Eur J Clin Nutr. 2012;66(3):353-9

12. Corella D, Ordovás J, Genes, Dieta y enfermedades cardiovasculares, investigación y ciencia. 2007; 77.

13. Lai CQ, Corella D, Demissie S, Cupplez LA, Adiconis X, Zhu Y, et al. Dietary intake of n-6 fatty acids modulates effect of apolipoprotein A5 gene on plasma fasting triglycerides, remnant lipoprotein concentrarions and lipoprotein particle size: The Framingham heart study. Circulation. 2006;113(17):2062-70.

14. Salminen M, Lehtimäki T, Fan YM, Vahlberg T, Kivelä SL. Apolipoprotein E polymorphism and changes in serum lipids during a family-based counselling intervention. Public Health Nutr. 2006;9(7):859-65.

15. Lahoz C, Schaefer EJ, Cupples LA, Wilson PW, Levy D, Osgood D, et al. Apolipoprotein E genotype and cardiovascular disease in the Framingham Heart Study. Atherosclerosis. 2001;154(3):529-37.

16. Moreno JA, López-Miranda J, Pérez-Jiménez F. Influence of genetic and environmental factors on lipid metabolism and cardiovascular risk associated with the apoE gene. Med Clin (Barc). 2006;127(9):343-51.

17. Lambert JC, Brousseau T, Defosse V, Evans A, Arveiler D, Ruidavets JB, et al. Independent association of an APOE gene promoter polymorphism with increased risk of myocardial infarction and decreased APOE plasma concentrations-the ECTIM study. Hum Mol Genet. 2000;9(1):57-61.

18. Attila G, Acarturk E, Eskandari G, Akpinar O, Tuli A, KanadaşI M, et al. Effects of apolipoprotein E genotypes and other risk factors on the development of coronary artery disease in Southern Turkey. Clin Chim Acta. 2001;312(1-2):191-196.

19. Polisecki E, Muallem H, Maeda N, Peter I, Robertson M, McMahon AD, et al. Genetic variation at the LDL receptor and HMG-CoA reductase gene loci, lipid levels, statin response, and cardiovascular disease incidence in PROSPER. Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) Investigators. Atherosclerosis. 2008;200(1):109-14.

20. Simonson MA, Wills AG, Keller MC, McQueen MB. Recent methods for polygenic analysis of genome-wide data implicate an important effect of common variants on cardiovascular disease risk. BMC Med Genet. 2011;12:146.

21. Sorlí JV. Interacción entre el genotipo de la APO E y el consumo de ácidos grasos saturados en la incidencia de infarto de miocardio en la cohorte epic España. Clin Invest arterioscl. 2008;20(supl 3).

22. Tucker AJ, Mackay KA, Robinson LE, Graham TE, Bakovic M, Duncan AM. The effect of whole grain wheat sourdough bread consumption on serum lipids in healthy normoglycemic / normoinsulinemic and hyperglycemic / hyperinsulinemic adults depends on presence of the APOE E3/E3 genotype: a randomized controlled trial. Nutr Metab (Lond). 2010;7:37.

23. Perez-Martinez P, Garcia-Rios A, Delgado-Lista J, Perez-Jimenez F, Lopez-Miranda J. Nutrigenetics of the postprandial lipoprotein metabolism: evidences from human intervention studies. Curr Vasc Pharmacol. 2011;9(3):287-91

24. Soto M, Prieto A, Francesc F, Corellab D. Impacto de la apolipoproteína A5 en el riesgo cardiovascular. Modulaciones genéticas y ambientales. Rev Med Chile. 2010;138:868-80.

25. Kim JY, Kim OY, Koh SJ, Jang Y, Yun SS, Ordovas JM, et al. Comparison of low-fat meal and high-fat meal on postprandial lipemic response in non-obese men according to the -1131T>C polymorphism of the apolipoprotein A5 (APOA5) gene (randomized cross-over design). J Am Coll Nutr. 2006;25(4):340-7.

26. Jang Y, Kim JY, Kim OY, Lee JE, Cho H, Ordovas JM, et al. The -1131T-->C polymorphism in the apolipoprotein A5 gene is associated with postprandial hypertriacylglycerolemia; elevated small, dense LDL concentrations; and oxidative stress in nonobese Korean men. Am J Clin Nutr. 2004;80(4):832-40.

27. Burdon KP, Langefeld CD, Beck SR, Wagenknecht LE, Carr JJ, Freedman BI, et al. Association of genes of lipid metabolism with measures of subclinical cardiovascular disease in the Diabetes Heart Study. J Med Genet. 2005; 42(9):720-4.

28. Ooi EM, Barrett PH, Chan DC, Watts GF. Apolipoprotein C-III: understanding an emerging cardiovascular risk factor. Clin Sci (Lond). 2008;114(10):611-24.

29. Ordovas JM. The quest for cardiovascular health in the genomic era: nutrigenetics and plasma lipoproteins. Proc Nutr Soc. 2004;63(1):145-52.

30. Van Aalst-Cohen ES, Jansen AC, Boekholdt SM, Tanck MW, Fontecha MR, Cheng S, et al. Genetic determinants of plasma HDL-cholesterol levels in familial hypercholesterolemia. Eur J Hum Genet. 2005;13(10):1137-42.

31. Engler MB. Nutrigenomics in cardiovascular disease: Implications for the future. Prog Cardiovasc Nurs. 2009;24(4):190-5.

32. Fu AZ, Qiu Y, Radican L, Yin DD, Mavros P. Pre-existing cardiovascular diseases and glycemic control in patients with type 2 diabetes mellitus in Europe: a matched cohort study. Cardiovasc Diabetol. 2010;9:15-16.

33. Vanden Heuvel JP. Cardiovascular disease-related genes and regulation by diet. Curr Atheroscler Rep. 2009;11(6):448-55.

34. Das SK, Chakrabarti R. Role of PPAR in cardiovascular diseases. Recent Pat Cardiovasc Drug Discov. 2006;1(2):193-209.

35. Caron-Dorval D, Paquet P, Paradis AM, Rudkowska I, Lemieux S, Couture P, Vohl MC. Effect of the PPAR-Alpha L162V polymorphism on the cardiovascular disease risk factor in response to n-3 polyunsaturated fatty acids. J Nutrigenet Nutrigenomics. 2008;1(4):205-12.

36. Calabresi L, Baldassarre D, Castelnuovo S. Functional lecithin: cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation. 2009;120:628-35.

37. Katsoulis K, Blaudeau TE, Roy JP, Hunter GR. Diet-induced changes in intra-abdominal adipose tissue and CVD risk in American women. Obesity (Silver Spring). 2009;17(12):2169-75.

38. Fernandez ML, Webb D. The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk. J Am Coll Nutr. 2008;27(1):1-5.

39. Loomba RS, Arora R. Prevention of cardiovascular disease utilizing fibrates a pooled meta-analysis. Am J Ther. 2010;17(6):182-8.

40. Frikke-Schmidt R. Genetic variation in the ABCA1 gene, HDL cholesterol, and risk of ischemic heart disease in the general population. Atherosclerosis. 2010;208(2):305-16.

41. de Freitas EV, Brandão AA, Pozzan R, Magalhães ME, Fonseca F, Pizzi O, et al. Importance of high-density lipoprotein-cholesterol (HDL-C) levels to the incidence of cardiovascular disease (CVD) in the elderly. Arch Gerontol Geriatr. 2011;52(2):217-22.

42. Sarwar N, Danesh J, Eiriksdottir G, Sigurdsson G, Wareham N, Bingham S, et al. Triglycerides and the risk of coronary heart disease. Circulation. 2007;115: 450-58.

43. Bansal S, Buring J, Rifai N, Mora S, Sacks F, Ridker P. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007;298:309-16.

44. Pérez P, Lopez J, Pérez F, Ordovas JM. Influence of genetic factors in the modulation of postprandial lipemia. Atheroscler Suppl. 2008;9:49-55.

45. Abdel MF, Hokanson JE. The complex role of triglycerides in cardiovascular disease. Semin Vasc Med. 2002;2(3): 325-33.

46. Bouchard-Mercier A, Godin G, Lamarche B, Pérusse L, Vohl MC. Effects of peroxisome proliferator-activated receptors, dietary fat intakes and gene-diet interactions on peak particle diameters of low-density lipoproteins. J Nutrigenet Nutrigenomics. 2011;4(1):36-48.

47. Murphy KJ, Meyer BJ, Mori TA, Burke V, Mansour J, Patch CS, et al. Impact of foods enriched with n-3 long-chain polyunsaturated fatty acids on erythrocyte n-3 levels and cardiovascular risk factors. Br J Nutr. 2007;97(4):749-57.
48. Myhrstad MC, Retterstol K, Telle-Hansen VH, Ottestad I, Halvorsen B, Holven KB,et al. Effect of marine n-3 fatty acids on circulating inflammatory markers in healthy subjects and subjects with cardiovascular risk factors. Inflamm Res. 2011;60(4):309-19.

49. Ferguson JF, Phillips CM, McMonagle J, Pérez-Martínez P, Shaw DI, Lovegrove JA, et al. NOS3 gene polymorphisms are associated with risk markers of cardiovascular disease, and interact with omega-3 polyunsaturated fatty acids. Atherosclerosis. 2010;211(2):539-44.

50. Olano-Martin E, Anil E, Caslake MJ, Packard CJ, Bedford D, Stewart G, et al. Contribution of apolipoprotein E genotype and docosahexaenoic acid to the LDL-cholesterol response to fish oil. Atherosclerosis. 2010;209(1):104-10.

51. Delgado N, Moreno R, Jiménez Y, Cara C, Gallego R, Paniagua J, et al. Análisis del snp 5435 a>g, localizado en la Región promotora del ppars-alfa, según el Tipo de ácido graso de la dieta. Clin Invest Arterioscl. 2006;18 Supl 2:1-7.

52. Wu JH, Lo SK, Wen MS, Kao JT. Characterization of apolipoprotein E genetic variations in Taiwanese: association with coronary heart disease and plasma lipid levels. Hum Biol. 2002;74:25-31.

53. Dietrich M, Jacques PF, Pencina MJ, Lanier K, Keyes MJ, Kaur G, et al. Vitamin E supplement use and the incidence of cardiovascular disease and all-cause mortality in the Framingham Heart Study: Does the underlying health status play a role?. Atherosclerosis. 2009;205(2):549-53.

54. Dalgård C, Nielsen F, Morrow JD, Enghusen-Poulsen H, Jonung T, Hørder M, et al. Supplementation with orange and blackcurrant juice, but not vitamin E, improves inflammatory markers in patients with peripheral arterial disease. Br J Nutr. 2009;101(2):263-9.

55. Cook NR, Albert CM, Gaziano JM, Zaharris E, MacFadyen J, Danielson E, et al. A randomized factorial trial of vitamins C and E and beta carotene in the secondary prevention of cardiovascular events in women: results from the Women’s Antioxidant Cardiovascular Study. Arch Intern Med. 2007;167(15):1610-8.

56. Ministerio de Salud. República de Colombia. Resolución N° 008430. Título II. Capítulo 1: De los aspectos éticos de la investigación en seres humanos. Artículo 11. Colombia: 1993: p.2.

Descargas

Los datos de descargas todavía no están disponibles.