The Identification of Essential Nutrients and Effects of Their Deficiencies - Essay Example

Nutritional Genomics Introduction One of the 20th century’s most momentous successes was the identification of essential nutrients and effects of their deficiencies. This has enhanced differential deficiency diagnosis with statistical norms informing public health recommendations and nutritional advice. However, viewing diet’s benefits only as a preventative measure for deficiency of nutrients limits its role, especially given its wider role in the prevention of disease and promotion of health. According to Kaput and Rodriguez, “new research includes the means to recognize and prevent diseases arising from consuming unbalanced diets and the resulting dysregulated metabolism” (Kaput & Rodriguez 86). This knowledge has been expanded on by the revolution in genomics. The ability for researchers to sequence genomes has driven branching of research into the characterization of the epigenome, the metabolome, and modifications after translation of genes that affect the expression of genes. In the 21st century, the major challenge will lie in using this knowledge to prevent disease and maintain health in individuals. Nutritional genomics, or nutrigenomics, investigates gene products and the way these products interact and function physiologically (Kaput & Rodriguez 86). This involves the impact of nutrients on their action and production, as well as how these products also affect the body’s response to nutrients. This paper will seek to identify nutrients metabolized in the body, their effect on genes, and the way the genetic products affect the body’s response to nutrients. Metabolism of Nutrients in Food Gene expression can be altered by dietary nutrients that act as ligands for receptors used in transcription of genes, alter pathways of signal transduction, and are metabolized to alter concentration of intermediaries and substrates (Kohlmeier 16). Metabolism is divided into catabolism and anabolism, which refer to breakdown and synthesis of nutrients respectively. One of the nutrients in food metabolized by the body is carbohydrates, involving the use, production, and storage of carbohydrates. Their metabolism begins in the intestines with breakdown of complex carbohydrates to simpler ones, which are absorbed. Glucose is the moist important carbohydrate in metabolism and its regulation is called glucoregulation. Glucose undergoes glycolysis to form pyruvate used for energy production. Excess glucose in the blood undergoes glycogenesis to form glycogen for storage (Kohlmeier 36). This glycogen is converted back to glucose after the latter’s levels fall. Another form of nutrient in food is lipids, which include cholesterols, glycolipids, fats, steroids, among others. Fatty acid oxidation is the main pathway for lipid catabolism while lipogenesis is the main one for lipid synthesis (Kohlmeier 56). The metabolism of lipids and fats are closely connected with excess carbohydrates also converted to fats. Lipids are first broken down in the cell to form fatty acids and glycerol. Glycerol enters the glycolytic pathway after conversion to DHAP, or is incorporated into gluconeogenesis to form glucose and glycogen. The fatty acids are transported to the mitochondria for oxidation to Acetyl CoA, which either enters the citric acid cycle for conversion to energy or the lipogenesis pathway. Metabolism of proteins, on the other hand, denotes various processes that synthesize and breakdown proteins from and into amino acids respectively. After dietary proteins are broken down into amino acids, further catabolism converts them to α-keto acids, which are used in production of energy and fat, glucose, and other amino acids (Kohlmeier 69). Effect of food on Genes One of nutrigenomics’ areas of study involves how the discussed nutrients affect genes and their expression. According to the tenets of nutrigenomics, diet could be a critical risk factor in various diseases, while common dietary nutrients act directly or indirectly on the genome to alter the structure and expression of some genes (Kaput 196). Therefore, it is possible to use knowledge of genotypes, nutritional status, and nutritional requirements as a basis of diet interventions to mitigate and prevent chronic illnesses. Health and diet interact in various areas, especially with macro-nutrients. As discussed, the main macro-nutrients in the human diet are proteins, fats, and carbohydrates. Diets that include a disproportionally big amount of one of these nutrients may develop serious illnesses related to gene expression. With regards to fats, diets that contain too much of saturated fats could be at increased risk of suffering from high cholesterol and heart disease. Certain fats portend significant impacts on genes with their increase affecting genes that suppress anti-cancer activity of the immune system, thus causing breast, colorectal, and prostate cancers among others. For instance, corn oil that has high linoleic acid levels, lead to the over-expression of HER-2 gene, which is closely linked with increased aggressive breast cancer risks (Kaput 196). In addition, they were also linked with the promotion of faster tumor growth. However, omega-3 oil that is mainly found in fish slows down the progression of tumors. It has also been found that the amount and type of protein consumed by an individual is correlated to the prevalence of risk factors for bowel cancer, colorectal cancer, and type 2 diabetes (Kaput 196). It is believed that various genes, including glutathione-S-transferase and epoxide hydrolase, may impact the prevalence of risk factors if one eats meat. Micro-nutrients required by the body and present in foods also have a significant impact on gene expression and action. If, for example, folic acid is absent, it could cause the disentanglement and breakdown of nuclear and mitochondrial chromosomes, as well as brain dysfunction, heart disease, and colon cancer. In some cases, even addition of folic acid in dietary intakes, some individuals fail to get any additional benefits because the pathway the nutrient controls has been disabled. Niacin, another micro-nutrient, acts to enable DNA self-replicate during cell division by activating required enzymes and acting as a co-factor in enzymes required for DNA repair (Kaput 197). However, deficiency of the same could lead to poor DNA repair and resultant memory loss and neurological-associated symptoms. Nutrients are able to alter the expression and action of genes in order to create a positive health effect. For instance, genistein that is an isoflavone has the effect of deactivating, leading to fattening of offspring, although this has only been proven in pregnant mice and their offspring (Kaput 197). Therefore, it is possible that offspring of animals that are fed with isoflavone micro-nutrients will most likely develop diabetes and cancer because the genes affected code for proteins that are anti-carcinogenic. On the other hand, lack of isoflavone as a nutrient in diet will result in offspring that are leaner and will live for a longer period because their genes are not deactivated by genistein. Another dietary nutrient that has been investigated with regards to its ability to reduce disease risk factors is curcumin, which is a component of turmeric spices. When administered in animals, curcumin has been shown to decrease inflammation through its antioxidant properties. The genes involved in coding for inflammatory proteins are prevalent in cancer patients, and curcumin is believed to suppress its expression, thus slowing down the progression and development of tumors. Curcumin may also slow the tumor spread, whereas also suppressing genes responsible for the formation of new vascular tissue that is necessary for the replenishment of tumor cells; therefore, working to reduce the effects of tumors (Kaput 198). Effects of Genetic Makeup on Response to Nutrients Another two tenets of nutrigenomics is that the extent to which diet impacts on the balance between disease states and healthy state, may be reliant on a person’s genetic makeup. This is, in addition to, the fact that some genes regulated by diet play a possibly crucial role in the severity, progression, incidence, and even onset of some chronic diseases (Wittwer et al 345). Again, this makes the case for dietary interventions based on genomic knowledge and nutritional status to mitigate and prevent chronic diseases. Variations in genes have been known for a long time as having an impact on tolerance of food among various sub-populations. In addition, it has also been long suspected to influence an individual’s dietary requirements. This has been a keen area of research for nutrigenomics, while also increasing the probability that individualization of a person’s intake of nutrients may result in disease prevention and optimal health based on the individual’s genetic makeup (Wittwer et al 346). Nutrigenomics, in this sense, is a similar science to the much older pharmacogenomics that explores the impact of genes on the way an individual responds to medicines or drugs, especially with regards to the effective nature of cancer drugs based on the individual’s genes (Wittwer et al 346). Nutrigenomics has a similar role to play concerning diet and nutrients, pinpointing nutrient intake that could reduce risk factors associated with diabetes, Alzheimer’s, cancer, and other chronic diseases based on genetic makeup. For example, an individual could lose more weight if their calorie-restricted diets were created with the aim of taking advantage of their makeup genetically compared to those whose diets are non-genetic factor based (Wittwer et al 347). Although nutrigenomics is still a young field, it is possible that in the next decade, especially with the improvement of mass gene sequencing technologies, dietary changes can be made based on the genetic makeup of individuals. This, in turn, will result in the effective reduction of risk factors contributing to chronic illnesses. Various genes and alleles are proven to have a significant effect on the utilization of nutrients. A study of MTHFR gene showed that polymorphism of the specific gene led to significantly severe alterations in the metabolism of folic acid (Wittwer et al 347). This leads to increased risk factors for cardiovascular disease and neural tube defects, although the risk factors for colon cancer decrease. Because folic acid cannot be metabolized in the body, it is necessary to take folic acid as a nutritional supplement to reduce risk factors for disease and bypass the biochemical disruptions that prevent its metabolism. This is a good example genetic variation that influence an individual’s required daily intake, while also supporting the concept that variation in genetic makeup modifies the utilization of nutrients and the potential diet needs of an individual. Another example is the effect that polymorphism of the gene involved in homocysteine metabolism is altered to interfere with, and possibly curtail, the uptake and transport of folic acid (Wittwer et al 348). Genetic variation for enzymes requiring vitamin B-12 for their metabolic activity are widely linked to the development of colon cancer and Down syndrome, which is suggestive of their potential to affect an individual’s nutrient requirements. Genetic variation in the gene coding for vitamin D receptors are also associated with adult and childhood asthma because the body is unable to bind vitamin D, which is required in responding to steroids that relax air passage muscles (Wittwer et al 350). The HFE gene also has significant importance in the metabolism and storage or iron nutrients in the body and poor or no expression of the gene leads to poor metabolism and storage of the nutrient, such as in hemochromatosis. This also affects the body’s upper limit for intake of iron. Other gene variations may lead to lipid and lactose metabolism, pathway effects. These gene variations are interestingly associated with geographical and particular ethnic groups subpopulations. These variations are, or were beneficial to these individuals in their ancestral environments because of the diet they took. The aldolase B enzyme, which is responsible for the metabolism of fructose, has very many gene variants that for a long time have been thought to be silent (Wittwer et al 351). However, these polymorphisms become active as disease genes when fructose is used in excess as a sweetener to interfere with the manner in which the body responds to fructose, especially when it is in excess. Conclusion Nutrigenomics offers the promise of a personalized program for health and medicine anchored on the knowledge provided by the individual’s nutritional status and needs, and his/her genetic makeup. It will have a significant impact with regards to dietary practices and medicine, as well as public and social policies, whereas its application could be even more significant than the characterization of the human genome. Chronic illnesses could be prevented or mitigated through the use of a sensible and balanced diet. The knowledge that can be gained from comparison between interactions of genes and diet will provide information required to solve the effects of genetic variations that impair nutrient metabolism. In addition, this knowledge can also be used to control specific diets that interfere with the production and metabolic activity of important gene products. Works Cited Kaput, Jim. "Book Review: Molecular Nutrition and Genomics: Nutrition and the Ascent of Humankind." American Journal of Human Biology. 20.2 (2012): 196-199. Print. Kaput, Jim. & Rodriguez, Raymond. L. Nutritional Genomics: Discovering the Path to Personalized Nutrition. Hoboken, N.J: Wiley-Interscience, 2006. Print. Kohlmeier, Martin. Nutrient Metabolism. London: Academic Press, 2013. Print. Wittwer, Jonas. Rubio-Aliaga, Isabel. Hoeft, Birgit. Bendik, Igor. Weber, Peter. & Daniel, Hannelore. "Nutrigenomics in Human Intervention Studies: Current Status, Lessons Learned and Future Perspectives." Molecular Nutrition & Food Research. 55.3 (2011): 341-358. Print. Read More