Common chronic diseases such as coronary heart disease (CHD), diabetes, cancer, hypertension and obesity are significantly influenced by dietary and other behavioural habits. There is increasing scientific evidence that genetic factors (SNPs), conferring either protection or risk, also contribute importantly to the incidence of these diseases. SNPs are of particular interest because they influence disease in a complex but largely unknown manner by interacting with environmental and lifestyle factors. Because genetic factors also affect a person’s response to dietary habits, SNPs likely will be useful in helping to determine and understand why individuals differ in their response to diets. Therefore, the discovery of SNPs will likely revolutionize not only the diagnosis of disease but also the practice of preventative medicine. Other developments, like new biomarkers and noninvasive imaging techniques, might turn out to be highly sensitive and specific in order to identify patients at risk, especially in cases with asymptomatic coronary heart disease. Thus, further knowledge of such new risk factors and their interaction with nutrition, has the potential to provide a more precise and personalized approach to prevent and treat chronic diseases like coronary artery disease, myocardial infarction and stroke.
KeywordsMyocardial infarction Epidemiology Genetics Disease prevention Biomarkers Dietary recommendations
- 5.Williams RR, Hunt SC, Heiss G, Province MA, Bensen JT, Higgins M, Chamberlain RM, Ware J, Hopkins PN (2001) Usefulness of cardiovascular family history data for population-based preventive medicine and medical research (the Health Family Tree Study and the NHLBI Family Heart Study). Am J Cardiol 87:129–135PubMedCrossRefGoogle Scholar
- 8.Samani NJ, Burton P, Mangino M, Ball SG, Balmforth AJ, Barrett J, Bishop T, Hall A (2005) BHF Family Heart Study Research Group. A genomewide linkage study of 1,933 families affected by premature coronary artery disease: The British Heart Foundation (BHF) Family Heart Study. Am J Hum Genet 77:1011–1020PubMedCrossRefGoogle Scholar
- 9.Pajukanta P, Cargill M, Viitanen L, Nuotio I, Kareinen A, Perola M, Terwilliger JD, Kempas E, Daly M, Lilja H, Rioux JD, Brettin T, Viikari JS, Rönnemaa T, Laakso M, Lander ES, Peltonen L (2000) Two loci on chromosomes 2 and X for premature coronary heart disease identified in early- and late-settlement populations of Finland. Am J Hum Genet 67:1481–1493PubMedCrossRefGoogle Scholar
- 10.Francke S, Manraj M, Lacquemant C, Lecoeur C, Lepretre F, Passa P, Hebe A, Corset L, Yan SL, Lahmidi S, Jankee S, Gunness TK, Ramjuttun US, Balgobin V, Dina C, Froguel P (2001) A genome-wide scan for coronary heart disease suggests in Indo-Mauritians a susceptibility locus on chromosome 16p13 and replicates linkage with the metabolic syndrome on 3q27. Hum Mol Genet 10:2751–2765PubMedCrossRefGoogle Scholar
- 14.Helgadottir, Manolescu A, Thorleifsson G, Gretarsdottir S, Jonsdottir H, Thorsteinsdottir U, Samani NJ et al (2004) The gene encoding 5-lipoxygenase activating protein confers risk of myocardial infarction and stroke. Nat Genet 36:233–239Google Scholar
- 16.Heijmans BT, Beekman M, Putter H, Lakenberg N, van der Wijk HJ, Whitfield JB, Posthuma D, Pedersen NL, Martin NG, Boomsma DI, Slagboom PE (2005) Meta-analysis of four new genome scans for lipid parameters and analysis of positional candidates in positive linkage regions. Eur J Hum Genet 13:1143–1153PubMedCrossRefGoogle Scholar