**2. Treatment**

CVD represents the paradigm of multi factorial disorders encompassing multiple genetic and non modifiable risk factors, for example older age and modifiable risk factors such as elevated total and LDL-cholesteroland and triglycerides concentrations, reduced HDLcholesterol concentrations (Ordovas & Corella., 2004; Ordovas., 2009; Perez-Martinez et al, 2011; Lovegrove & Gitau, 2008). The interactions of those modulate plasma lipid concentrations and potentially CVD risk (Ordovas., 2009; Lovegrove & Gitau., 2008).

Nutrigenetics and Dyslipidemia 43

baseline LDL-C levels, disease status and drug use. However, recent evidence strongly suggests that variations in a number of key genes may also be important (Lovegrove & Gitau., 2008). For example, individuals with specific of genetic variants in a gene may experience different type of lipoprotein changes when placed on a particular diet, whereas individuals with other variants in the gene may be resistant to the effects of the same diet. Although data is sparse in regard to whether such interactions exist, some limited work suggests that interactions may play an important role in determining lipoprotein profiles and may thus be informative for CVD risk prediction. For example, knowledge of a patient's genetic information may allow medical providers and nutritional counselors to predict what lipoprotein changes are likely to occur if the patient starts a particular dietary intervention and, thus, better advise the patient regarding lifestyle changes (Musunuru., 2010; Ordovas &

Lipoproteins are macromolecular complexes of lipids and proteins that originate mainly in the liver and intestine and are involved in transporting and redistributing lipids in the body. Lipid homeostasis is achieved by the coordinated action of numerous nuclear factors, enzymes, apolipoproteins, binding proteins, and receptors. Lipid metabolism is also linked with energy metabolism and is subject to many hormonal controls essential for adjusting to environmental and internal conditions. Genetic variability exists in humans for most of these components, and some of these mutations result in abnormal lipid metabolism and plasma lipoprotein profiles that may contribute to the pathogenesis of atherosclerosis. Many of these genes have been explored in terms of gene-diet interactions

So the shift towards personalized nutritional advice is a very attractive proposition, where, in principle, an individual can be given dietary advice specifically tailored to their genotype. However, the evidence-base for the impact of interactions between nutrients and fixed genetic variants on biomarkers of CVD risk is still very limited (Lovegrove & Gitau., 2008; Ordovas., 2006; Masson et al., 2003; Masson & Mc Neil., 2005; Fisler & Warden., 2005). With the advent of nutritional genomics, it's becoming clear that an individual's genetic makeup (genotype) is an important factor in this response and that dietary interventions must be matched to genotypes to effect the intended lipid-lowering responses (DeBusk.,

A number of such genes have already been identified and include those involved with postprandial lipoprotein and triglyceride responses, homocysteine metabolism, hypertension, blood-clotting, and inflammation (Ordovas & Corella., 2004; DeBusk., 2008). Genetic polymorphism in human populations is part of the evolutionary process that results from the interaction between the environment and the human genome. Recent changes in diet have upset this equilibrium, potentially influencing the risk of most common morbidities such as cardiovascular diseases, diabetes, and cancer. Reduction of these conditions is a major public health concern, and such a reduction could be achieved by improving our ability to detect disease predisposition early in life and by providing more personalized behavioral recommendations for successful primary prevention. In terms of cardiovascular diseases, polymorphisms at multiple genes have been associated with differential effects in terms of lipid metabolism. The integration of genetic and environmental complexity into current and future research will drive the field toward the implementation of clinical tools aimed at providing dietary advice optimized for the

Corella., 2004).

2008).

(Ordovas & Corella., 2004).

individual's genome (Ordovas., 2009; Engler., 2009).

The link between serum cholesterol and the development of atherosclerosis was established a few decades ago and is now widely accepted. The National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) publishes updated guidelines for treating lipid disorders. The latest version is the ATP III (Ordovas & Corella., 2004; Debra., 2008).

The current recommendations aim to reduce the classical modifiable risk factors, and much emphasis has been placed on controlling high-plasma cholesterol levels (Ordovas & Corella., 004).

Physicians are encouraged to refer patients to Registered Dietitians (RDs) to help patients meet goals for therapy (NCEP) based on LDL cholesterol levels. So the ATP III recommended the therapeutic lifestyle change (TLC) dietary pattern as the cornerstone for primary and secondary prevention of CHD. These guidelines consider dietary modification of treatment with emphasis on reducing the high saturated fat atherogenic diet and increased content of polyunsaturated fatty acid (PUFA) as well as controlling other behavioral factors. These therapies are used primarily to lower elevated blood levels of LDL-C, raise HDL –C and lower triglycerides (TGs) (Rubin & Berglund., 2002; Debra., 2008; Ordovas & Orella., 2004).
