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Nutrigenomics pp 195-208 | Cite as

Hypertension, Atherosclerosis and Dyslipidemias

  • Carsten Carlberg
  • Stine Marie Ulven
  • Ferdinand Molnár
Chapter

Abstract

Hypertension is the most important preventable risk factor for pre-mature death. Chronically elevated blood pressure increases the risk of ischemic heart disease, stroke, peripheral vascular disease and other CVDs, such as heart failure, aortic aneurysms, diffuse atherosclerosis and pulmonary embolism. The high consumption of saturated fat, low intake of fruit and vegetables and whole grain fiber high-cholesterol diets, i.e. Western-type diet, can lead to hypercholesterolemia and atherosclerosis, especially in genetically predisposed individuals. Atherosclerosis is a chronic inflammatory disease caused by the accumulation of cholesterol-laden macrophages in the artery wall, i.e it is based on dyslipidemia and an overeaction of the immune system. Central cells in atherosclerosis are macrophages and their phenotype, i.e. their programming to M1 and M2 type, which influences both disease progression and regression.

In this chapter, we will link three important risk factors for heart disease, hypertension, atherosclerosis and dyslipidemia, in a combined mechanistic model. We will understand that the susceptibility to CVD is associated with levels of plasma lipids and lipoproteins. Like in obesity and T2D, the genetic basis of the cardiometabolic traits, such as plasma lipoprotein levels, can be explainable to a minor part on a monogenetic basis causing a large effect and to a larger part by common genetic variants with minor effects on the trait. This will provide another example how molecular medicine is applied, in order to diagnose and treat the basis of a disease.

Keywords

Hypertension CHD Stroke Renal disease Atherosclerosis Chronic inflammation Foam cells ER stress LXR Cholesterol Triacylglycerols Lipoproteins LDL HDL Apolipoproteins Dyslipidemia 

Additional Reading

  1. Hegele RA (2009) Plasma lipoproteins: genetic influences and clinical implications. Nat Rev Genet 10:109–121CrossRefPubMedGoogle Scholar
  2. Jensen MK, Bertoia ML, Cahill LE, Agarwal I, Rimm EB, Mukamal KJ (2014) Novel metabolic biomarkers of cardiovascular disease. Nat Rev Endocrinol 10:659–672CrossRefPubMedGoogle Scholar
  3. Moore KJ, Sheedy FJ, Fisher EA (2013) Macrophages in atherosclerosis: a dynamic balance. Nat Rev Immunol 13:709–721CrossRefPubMedPubMedCentralGoogle Scholar
  4. Swirski FK, Nahrendorf M (2013) Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Science 339:161–166CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  • Carsten Carlberg
    • 1
  • Stine Marie Ulven
    • 2
  • Ferdinand Molnár
    • 3
  1. 1.Institute of BiomedicineUniversity of Eastern FinlandKuopioFinland
  2. 2.Department of NutritionUniversity of OsloOsloNorway
  3. 3.School of PharmacyUniversity of Easterm FinlandKuopioFinland

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