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Nutrigenomics is an important field of study. It finds in roots in modern times, because of the direct relation to advances in science and technology. Nutrigenomics also straddles the nature vs. nurture divide. The publication of the relatively preliminary results of the Human Genome has given greater impetus to the idea of Nutrigenomics. One might assuredly say that the publication of the Human Genome is preliminary because the current versions of the genome are merely representatives of a very select group of individuals. (Lander et al., 2001; Venter et al., 2001) What makes individuals unique of course is the presence of single nucleotide polymorphisms or SNPs. It is these SNPs that give each of us our individuality. Hence each individual's genome is his or her genotype. A genotype is an individual's genome -- the genetic coding that identifies the character traits that govern existence. In the context of Nutrigenomics, a genotype is the identification of genetic makeup that codes a person's proclivities to diseases and how this code reexpreses with the environment, specifically the diet. Directly related to a person's genotype is how this encoded information translates into how a person lives. This involves voluntary and involuntary functions. This is called the phenotype. The phenotype is a reflection of how the cells, tissues, organs influence the functions and behavior of a person. Before arriving at a definition for Nutrigenomics, one must revisit the nature vs. nurture argument. The important question is if the genotype-phenotype relation is predetermined, does nutrition play an important role in a person's genome other than to serve as a source of energy?
Humankind has evolved to procure nourishment itself. This means that no matter what the location, we have evolved to make use of nature and the surroundings to obtain the basic food groups.
This good can come from animal or vegetal sources. Or it can come from a combination of animal and plant sources. The key definition of Nutrigenomics is in the identification of whether certain foods will affect the gene expression pattern of key genes that affect the metabolism or the genetic tendency towards certain disease. In other words, it is the correlation between the nutrition that a person receives and the cellular and genetic processes that take place in that person. (Gillies, 2003) A unit of nutrition therefore has to alter the expression of a gene. This has important consequences for the future. There is currently enough of a motivation from academia and the industry to eventually place that a person's genotypic information can be placed on a single card. This ensure that any time a person visits a doctor, his or her genotype will be the determinant as to how medication and nutrition can be tailored to help in the health of this person. Advances in Nutrigenomics will ensure that a person is not treated with one-size fits all medication. Advances in Nutrigenomics will preclude the use of medications, if the right nutrition supplement will aid in targeting the gene responsible for the disorder, metabolic malfunction or disease.
Nutrigenomics is based on certain basic tenets.
It embraces the nurture argument that substances in food, e.g. vitamins, have the ability to directly or indirectly change the structure of a gene and consequently its expression product -- proteins.
Nutrigenomics also assume that the dietary lifestyle can seriously impact a human being as a cause for a disease. An important concept of Nutrigenomics is that there are some genes that are directly regulated by diets. And that it is these genes that are responsible for diseases.
Nutrigenomics assumes that how harmful a diet can be also largely depends on a person's overall genotype. Nutrigenomics has as its final aims that when finally realized would result in customized nutritional programs that will address specific genotypes and help in the cure of diseases. (van Ommen & Stierum, 2002)
It has been mentioned earlier that nutrition evolved with humankind. This was to be expected; because, to eat was to live. While Nutrigenomics as a formal science has only been introduced relatively recently, the father of modern medicine, Hippocrates, had already addressed most of these issues. Hippocrates believed that the human body was susceptible to weaknesses in the absence of proper diets. And, weakness in the body was only a step away from diseases. Hippocrates believed that the quality of food also made a difference. He went as far as to say that bread made from grain that was ground differently or the amount of water that was mixed had an important effect on the cause of disease. This is important; eating food with adequate roughage is identified in avoiding colon cancer, today. It would be interesting to identify the gene which correlates with roughage and changes its expression to decrease the likelihood of colon cancer. This point then brings us to some of the possible drawbacks of pursuing Nutrigenomics. The definitions and associated concepts seek to identify the gene that can be targeted as susceptible to diets and related to the genes whose expression causes diseases. Unless genomic and genetic studies arrive at a point where the function of every gene is identified, it will set a very dangerous trend when the wrong nutrition from incomplete gene targeting will result in adverse health effects.
To date, approximately one thousand human diseases have been identified. A significant percentage of these diseases have been isolated as associated with one gene. (Jimenez-Sanchez, Childs, & Valle, 2001) However, the mechanisms for these diseases are far from being identified. Medications often treat the symptoms and let the body device its own methods for addressing the root cause of the disease. Also some of the more serious and commonplace diseases such as diabetes, cardiovascular disease, obesity and most cancers are due to several genes working together in concert. Besides, more than one gene contributing to a disease, there are additional environmental factors that might contribute. These effects cannot be quantified in terms of tendency to be afflicted by a disease. Also, the general makeup of the genotype is important. Two individuals exposed to the same risk factors will show distinctly different reactions. One might show symptoms of the disease, the other might not. One other factor that has not been discussed in the literature is the fact that emotional and mental aspects also determine whether a person will be more prone to a disease. The genetic aspects of a person's mental state are definite confounders in identifying genetic risk factors.
The common disease common variant (CD/CV) hypothesis states that more than one gene combines in the mechanism of a disease. (Collins, Guyer, & Charkravarti, 1997) These gene variants are responsible for the susceptibility to and progress of a disease, until corrective measures can be taken in terms of correcting the symptoms through medication or a lifestyle change. To be sure, there are associations with the intake of certain types of good and how much someone suffers from a disease. Indeed, the entire nutrition and diet concepts have been based on how certain foods might be used to ward of certain diseases. But one of the problems in furthering Nutrigenomics is the identification of not the item of food that helps against a disease but what constituent chemical or substance in the food that targets gene expression. Thus the problem is complex from the diet-intake side and also the gene expression/metabolic process side. This complexity is what makes identification of metabolic processes at the molecular level difficult. There are too many confounding aspects.
Another important confounder is allele frequencies that have changed with sub-populations depending on where a person resides. This is because in large part, the sub-populations remain isolated. For example, the acetylating gene N-acetyltransferase, NAT2 has polymorphic subtypes. (Risch, Wallace, Bathers, & Sim, 1995) Different subtypes are distributed in different people in different populations. These subtypes were perhaps due to environmental factors including certain diets. This also means that in identifying these situations it is going to be really difficult because any effort in identifying a trait for a disease and a corrective nutritional biomarker will be confounded by different subtypes in different populations. On the other hand, these allelic subtypes that are identified with specific populations can prove useful in designing nutritional remedies for specific diseases suffered by certain subpopulations. Or these same markers will prove useful in eliminating some populations from custom designed plans based on identification of specific polymorphic sub-types. And despite this, there is chance that a particular diet condition may be specific to a unique genotype.
The relationship between genomics and nutrition is not without precedence. In 1908, it was discovered that rabbits that were fed a fatty diet developed arterial lesions and cholesterol imbalances. Indeed, it has gotten greater exposure in the post-human genome era. In 1917, the disease of galactosemia was discovered. (Antshel & Waisbren, 2003) The deficiency in the enzyme that hydrolyzes the amino acid phenylalanine, phenylalanine hydroxylase results in the build of phenylalanine in children. This buildup, if not controlled, can result in neurological…[continue]
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