CHAPTER ONE

INTRODUCTION

The etiology of complex chronic diseases involves both environmental and genetic factors, with environmental influences such as diet exerting a greater effect among individuals with certain genetic profiles (David, 2005). Nutrition is clearly one of the most important determinants of health. Too much or too little of a nutrient can result in metabolic disturbances that predispose individuals to various diseases such as osteoporosis, diabetes, rheumatoid arthritis, cardiovascular disease (CVD) and certain types of cancer. Non-nutritive food bioactive can also affect the risk of developing various chronic diseases. Functional foods that are enriched with certain food bioactive have been suggested to play an important role in combating CVD and other chronic ill- nesses (David, 2005).

However, inconsistencies among epidemiological studies have yielded conflicting advice on the optimal level of intake for nutrients and specific food bioactive. These inconsistencies may be due, in part, to genetic difference between populations that are studied. 

Nutrigenomics is the science that uses genomic information along with high-throughput ‘omics’ technologies to address issues important to nutrition and health (David, 2005).

Nutrigenomics is sometimes called nutritional genomics, which is increasingly being used as an umbrella term to refer to both the study of how diet affects genes and how genes affect diet (Kaptur et al., 2004).

One approach used to explore how dietary and genetic factors interact to influence various health outcomes is to examine how diet alters the function of genes or their protein products such as enzymes, receptors, transporters and ion channels that are known to regulate important biochemical pathways and cellular processes.

Another approach is to examine how variations in genes affect responsiveness to Specific dietary factors, an area that is sometimes referred to as nutrigenetics (David et al., 2005).

Candidate genes that are studied tend be those that are the targets of a nutrient or food bioactive, or those that impact the metabolism of the bioactive compound, including its absorption, biotransformation, distribution or elimination. For example, how efficiently we absorb fat, how rapidly we digest starch, or how slowly we eliminate caffeine from our circulation all determine the levels of a food bioactive that a target cell would be exposed to. Knowledge of the genetic basis for the variability in response to food bioactive should result in a more accurate measure of exposure of target tissues of interest to these compounds and their metabolites (David et al., 2005).

It has been demonstrated that numerous genetic polymorphisms can influence protein structure function. The Nutritional genomic area includes two parts: first Nutrigenomics that is the study of interaction between dietary components and the genome, and the regulating changes in proteins and other metabolism; second Nutrigenetics that identify the response to dietary components with regard to genetic differences (Subbiah, 2007).  Nutrients are as environmental factors can interact with genetic material. It has been clearly demonstrated that DNA metabolism and repair depend on a wide range of dietary factors that act as cofactors or substrates in metabolic pathway, but much less is known about the impact of cofactors and/or micronutrients deficiency or excess on the fidelity of DNA replication and repair (Bull, 2008). Although the nutrients can influence the development of a particular phenotype, the response to a specific nutrient that determined by the individual genotype has also to be considered. The central role of genetic code in determining genome stability and related health outcomes such as developmental defects, degenerative diseases, and cancer is well-established (Fenech, 2008). The etiology of complex chronic diseases obviously relates to both environmental and genetic factors (El-Sohemy, 2007). Specifically, the “fetal basis of adult disease” or “early origins hypothesis” postulates that nutrition and other environmental factors during prenatal and early postnatal development influence gene expression and cellular plasticity, which can alter susceptibility to adult diseases (cardiovascular diseases, diabetes, obesity. etc) (El-Sohemy, 2007). The concept of nutrients effects on DNA stability, repair and on the different gene expression processes, recently became more prominent in nutritional science (Paoloni-Giacobino, 2003). Numerous dietary components can alter genetic and epigenetic events and therefore influence health (Trujillo, 2006). SNPs (single nucleotide polymorphisms) are the most common genetic variation, occur at about 500-2000 bp throughout the human genome, and normally found in at least 1% of the population (Ferguson, 2006). Many human studies have demonstrated the evidence for interaction between SNPs in various genes and the metabolic response to the diet. Moreover, SNPs analysis provides a potential molecular tool for investigating the role of nutrition in human health, diseases and identification of optimal diets (Ferguson, 2006).  Nutrients and genome interact at two levels:

·                    Nutrients can induce or repress gene expression thereby altering individual phenotype.

·                     Conversely, single nucleotide polymorphisms can alter the bioactivity of important metabolic pathways and mediators and influence the ability of nutrients to interact with them