Nutrigenetics the relation between Genes and nutrition APOA2 concerning cardiovescular diseases - Dissertation Example

Nutrigenetics the relation between Genes and nutrition APOA2 concerning cardiovescular diseases Introduction Since the ancient ages, nutrition has been found to have a recognizable and predominant role towards health management. The advent of science resulted in the knowledge of essential nutrients together with their quantities in promoting optimal health, and this led to dietary recommendations, and the knowledge of food being a direct contributor to the onset of certain diseases experienced today (Ordovas and Mooser, 2004). Human genes exhibit variations in the general population. Since the responses to nutrition are multigenic in nature, it is normal that individuals that are not related could exhibit varied responses. Within the nutrition-related disorder context, the variations in genetics underline the varying risks of the diseases, in response to interventions or treatments, as well as in the successful prevention chances. In addition to knowledge of the specific responsible genes, nutrigenetics provides an explanation on how and to which level the nutrition-related disorders and traits are determined by the variations in genetics (Wang and Oram, 2002). Therefore, the major concern in this is the need to answer the question of which particular genes are responsible for a trait, as well as the particular variation in functional identity by which individuals exhibit differences for trait, and the ideal way through which the gained knowledge can be beneficial to the population. Nutrigenetics refers to the effect of variations in genetics on an individual’s optimal dietary requirements. Therefore, nutrigenetics can be regarded as the retrospective study of how variations in genetics, which include single nucleotide polymorphisms (SNPs) in individuals, result in varied responses to particular nutrients. Nutrigenetics has been found to be instrumental in facilitating understanding of the excessive adiposity in the body, as evaluated in terms of Body Mass Index. A nutrigenetics search for genes Researchers have always defined the candidate genes for a given disorder or trait and eventually went ahead to search for the variation in genes, and the approach has been referred to as ‘hypothesis-driven’ method, since the gene selection is done based on their respective functions, just like the lipoprotein genes is regarded as candidates for obesity disorder; whereas the genes for signaling insulin are considered to be candidates for diabetes (Mendes, 2002). In addition to the physiological or biochemical approaches, Jump (2002) observes that the orthologous genes that underlie animal models that exhibit Mendelian trait segregation have been found to be attractive candidates for similar candidates in human. For instance, a diabetes model, db/db mouse, from which leptin receptor genes were identified, presents a perfect example of this. Rabilloud (2002) establishes that a particular gene is linked to a specific trait if one allele demonstrates significantly higher frequency in individuals with the identified trait compared to the general human population. Other techniques depend on the preferred allele segregation from the parents of the affected children, most commonly through the transmission disequilibrium test (Kaput and Rodriguez, 2004). When a gene is established to be associated to a particular trait, it should be proven whether the linked or associated allele is a risk factor by itself, or if it behaves as a mere marker for a close causative variation that together form the linkage-disequilibrium (Lapillonne, Clarke and Heird, 2004). On the other hand, if the variations in genes correspond to a variation in amino acids in a protein, there is a functional test by which the comparison of the allelic genes can be done to determine their affinity for binding DNA, as well as their enzymatic activities. However, when the variation is in regulatory sequences for the expression of genes, a biological effect would occur due to the difference in production of protein between the allelic gene forms (Cahill and Nordhoff, 2003). Despite the fact that it is difficult to proof functional relevance of the gene variant, the associated genes could be employed as markers in identification of carriers of the enhanced trait risk. Another method by which the risk-conferring genes for a particular disorder or trait can be searched is the total scan for genome, which is a holistic approach (Arab, 2004). Selection for hundreds of polymorphs is done using a random distribution in all genome, but with known location for chromosome. For each polymorphic site, the above method is used in determination of linkage or association of whether there is a relation to the trait. In this case, several loci across the genome could be established with at least a risk-contributing gene on each locus (Mooser and Ordovas, 2003). The use of this method has led to description of numerous disorders related to nutrition, including diabetes and obesity. Rye and Barter (2004) observe that carrying out a study on a trait within different populations results in a partially identical loci. This shows that the trait risk is defined using a limited combination of common genes with an extra set of genes that are population-specific. This partially explains the differences exhibited among individuals at risk in different geographical regions. Curtiss, Valenta and Rye (2006) propose that a backcross of a strain free from a trait enables segregation of contributing genes into variable offspring lines encompassed in a given piece of genetic material from a parent that carries the trait. Through determination of the chromosomal location of the parental DNA, it is possible to trace the risk locus, and the technique is termed as ‘quantitative trait locus mapping’ (Movva and Rader, 2008). Upon finding the risk-locus, the next task involves identification of the real risk-conferring gene together with the causative variation. Hausenloy and Yellon (2008) caution that there still exists a problem here, since every locus could have to cover millions of the base pairs, thus a big gene population. In order to establish the real risk-gene, there would be a need to put significant effort for functional testing. To aid in disease gene identification from genetic loci, there is the construction of a ‘haplotype map’ in place, specifically for a human genome, which includes a dense polymorphism network (Singh, Shishehbor and Ansell, 2007). Personalized diet Genetic experiments in different populations, together with investigations of in vitro and animal model systems have already indicated that several hundred genes are associated with certain nutrition-related disorders and traits such as diabetes and obesity (Kontush and Chapman, 2006). Eventually, it is expected that nutrigenetic and nutrigenomics studies result in comprehensive understanding of the trait etiology and disorders in relation to the interacting genes, the components of the diet, and the related risk as demonstrated through variation in genes and diet combination (Edgar, Domrachev and Lash, 2002). The combined knowledge is instrumental in enabling genetic profiling of all individuals thus assessing an individual’s risk or acquiring a disorder related to nutrition. On the basis of risk profiles of genetic factors, there could be prescription of personalized diet, which could prevent or delay a disorder onset. Watts, Barrett and Chan (2008) report that currently certain enterprises provide genetic testing services for the alleles that were initially discovered to associate with particular traits, amongst which is the ApoE allele, which is a cardiovascular disorder risk factor, as well as the allele for an alcohol dehydrogenase gene that is associated with alcohol use and sensitivity (Lewis and Rader, 2005). Despite the popularity of the genetic testing in the modern practices, Meigs, Panhuysen, Wilson and Cupples (2002) caution of the demerits of the tests, particularly in terms of their specificity. For instance, conducting a test for one genetic factor could result in a wrong or incomplete view of the prevailing situation. In some individuals, the risk that is increased by a single factor could be compensated by a protective factor, hence giving wrong advice and conclusion (Escola-Gil, Blanco-Vaca and Julve, 2002). Current research does not provide a comprehensive knowledge of all genetic factors together with their manner of interaction. Ideally, Nutrigenetics is aimed at understanding the manner in which genetic individual’s makeup coordinates diet responses. In this case, were the human population identical genetically and stayed within an environment that was constant, then their responses to drugs and diets would be similar (de Hoog and Mann, 2004). However, the complete human genome sequencing, s. rstanding how Read More