Nutrition and Epigenetics

Nutritionand Epigenetics

Nutritionand Epigenetics

Epigeneticshas emerged as an area of increased interest in recent scientificstudy. The study of epigenetics is closely related to nutrition.According to University of Utah, (n.d) unlike stress or behaviors,nutrition is one of the simply studied environmental aspects inepigenetic change. Epigenetics can be defined as the research ofheritable alterations in gene appearance caused by chemical processesdifferent from the original DNA sequence. The epigenome is acomposition of chemical mixtures that control the genome. Again, theepigenome contains both protein and chemical compounds that confer toDNA and control actions such as determining whether a gene is activeor inactive. The following paper aims at critically discussing howdiet can change the epigenome.

Thebasic concept of how diet can change the epigenome is based on thechemical components found in food that are part of the DNAcomposition. According to University of Utah, (n.d) the nutrients weremove from food find their way to metabolic passageways where theyare manipulated, altered, and shaped into molecules the body canutilize. In this case, one of the passageways is tasked withproducing methyl groups, which are significant epigenetic tags thathave the ability to silence genes. Common diet nutrients such asbetaine, B vitamins, and folic acid are main constituents of themethyl-producing passageways (Florean, 2014). Moreover, foods ordiets with increased methyl-producing nutrients can promptly changegene expression, specifically during early growth when the epigenomeis established for the first time. According to Wanjek, (2012) diethas the ability to induce changes in the cells whereby these changescan be inherited to offspring for generations to come. The mainexamples offered include susceptibility to cardiovascular diseasesand diabetes (Skinner &amp Jirtle, 2007). According to Wanjek,(2012) a mother’s diet during pregnancy can also alter the infant’sepigenome. These changes are inherited or sustained until the infantreaches adulthood.

Additionally,studies on animals such as mice and bees have illustrated how dietcan change the epigenome. One study illustrated that diet withreduced amounts methyl-giving choline or folate before or afterconceiving lead to certain regions of the genome to be deficient ofmethyl for the rest of their lives. The same case applies to adultsbecause consuming a diet low in methyl-giving nutrients makes the DNAhave reduced methyl, but the modifications can be changed when a dietwith methyl-giving nutrients is increased(Young, 2008). Sincedifferent foods or diets have different combinations of nutrients,the different nutrients cause differentiated changes to theepigenome. In this case, diet can alter the epigenome in numerousways depending on the type of nutrients found in the food. Diets richwith nutrients such as sulforaphane found in broccoli influence theepigenome based on their high histone acetylation that activatesanti-cancer genes. Therefore, people who consume such diets at anearly age help their genes to fight cancer more effectively thanpeople who do not consumer such diets. Another major nutrient withhigh histone acetylation is butyrate that is produced in theintestines during fermentation of dietary fiber (The Guardian, 2009).This nutrient has been illustrated to activate protective genes andenhance life span. Therefore, when one does not consume the rightfoods with a balanced nutritional context, it may result to life-longchanges to their genes. As it is popular said, one is what they eat,thus one’s diets makes them a unique individual in terms of theirgenes. According to Friso &amp Choi, (2010) during the Germanfamine, people starved and after a decade, their children were notedto be increasingly susceptible to health issues Skinner &ampJirtle,2007). Again, children who have also been born with altered andweakened genes illustrate increased health challenges during theiradult hood. The overall, explanation of how diet can change theepigenome is through instructing the genome to silence or turn oncertain genes. This is the reason for the study of epigenetics where“epi” is a borrowed Greek word for on or off.

Oneof the main breakthroughs in epigenetics is the fact that diet duringearly development or during pregnancy can change the epigenome for along time (Hessler&amp Gardner 2011). During infancy or earlychildhood development, what one eats may determine their epigenome inadulthood for decades and even passed on to generations later. Themost common example of how early diet can change the epigenome is thehoneybee. Honeybees feed a special diet to regular bees that altertheir genes to become queens. According to University of Utah, (n.d)the diet is known as royal jelly, which is a multifaceted,protein-rich matter that comes from glands located on the heads ofbees. During the early stage of a bee’s life, the larvae that ischosen to become the queen is fed on huge amounts of the royal jellyin special partitions known as queen cups.It is interesting to notequeen and worker bees are genetically similarUniversity of Utah,(n.d). However, due to the royal jelly diet, the larvae develops intoa queen that has unique features including a larger abdomen forlaying eggs and also develops ovaries to produce eggs. Additionally,the queen from infancy develops queen-like behaviors such as fightingrivals queens and communicating to the colony (University of Utah,n.d). Through the study of bees, researchers concluded that the royaljelly alters certain genes in the ordinary worker bees for them todevelop into queens during their infancy. The main gene in this caseis known as Dnmt that is responsible for directing an enzyme thatturn off a group of queen genes (University of Utah, n.d). However,chemical compounds in the diet of the bee turned off, the queen genesbecome active allowing the original worker bee to develop into aqueen.

Inthis case, diet during early development can change the epigenomethrough cell signals. According to University of Utah, (n.d) signalsoriginate from inside the cells. When a young child is developingchemical compounds in food produce signals. These signals are carriedinto the cells through proteins that act as signal relays. Thesesignals pass information to gene regulatory proteins that attachthemselves to a certain sequence of alphabets on the DNA. Each signalhas a certain set of messages that are aimed to change the geneexpression from one generation to another. This process involves thepresence of gene regulatory proteins that have two main functions,switching on and off. When a certain signal from a nutrient chemicalreaches the cell, the gene regulatory protein confines or attaches toa precise sequence of DNA.

Whenattached to the DNA, it takes the role of a switch activating genesor hindering them from copying genes or their features. Additionally,the gene regulatory proteins also help in recruiting enzymes that addand eliminate epigenetic tags. The epigenetic tags act as kinds ofcellular memory whereby a cell comprises of numerous epigenetic tagsthat can alter or instruct a gene to be active or silent. In thiscase, diet intakes that have a variety of nutrients can alter orinstruct the epigenome numerous times in a life time. In this case,the epigenetic tags allow the cell to remember what it should bedoing even after a long time. According to Utah, just as a fertilizedegg grows into a baby, numerous signals received over certainduration either day, months, or years can increasingly causealterations in gene expression configurations or patterns. Diets ordifferent chemicals have chemicals that have the ability to sendsignals. As the cells develop and divide, the whole structure andfunctioning copies the epigenetic tags together with the DNA.Therefore, it is important for mother during their pregnancy sincewhat they consume will be translated or copied through to theiroffspring. Overall, the idea of early development and nutrition cancause increased changes in the genome (Pilcher, 2013). In humans,this may promote development or suppression of certain genes and genecharacteristics. People who do not follow a balanced diet may facereduced immune systems that hamper their ability to resist numerousdiseases.

Anothermajor area in nutrition and epigenetics is pregnancy and obesity ininfants. Obesity is a major challenge in developing countries(Pilcher, 2013). Nonetheless, when a child is born they are notalways obese and may eventually become obese as they grow up (Wanjek,2012). People have a tendency of blaming their obesity on genes,which has been of increased controversy. Nonetheless, currently whata mother consumers during pregnancy may contribute to her infantbeing obese later in life (The Tech Museum of Innovation, 2009). Themain research that has illustrated this is in terms of animal study.Researchers used mice to investigate the effects of mother’s dieton their infancy especially in terms of obesity (Wanjek, 2012).Nonetheless, diet solely has not illustrated any evidence thatfeeding mice on different diets or foods may result in obesity.

Nonetheless,in one study, it was determined that mice fed on toxic chemicals thatmay find their way in the diet may result in obesity. In this case,the mice were fed on bisphenol, which is a compound used inmanufacturing polycarbonate plastics (University of Utah, n.d). Theeffect of the chemical compound was an alteration in the geneexpression of the mice. One of the mice was added supplementarynutrient compounds such as the B vitamins and folate that resulted ina healthy offspring (University of Utah, n.d). Nonetheless, the othermouse was fed with the same toxin and ordinary mice diet thatresulted in an obese offspring. What can be concluded is thatdifferent nutrients in diet can help alter genes that may seek toactivate obesity. In this case, when women are pregnant, their dietscan predict if their children will obese (University of Utah, n.d).When mother choose to eat junk food and leave out fruits andvegetables, they tend to turnoff some genes that may help in burningfat, thus leading to inherited obesity genes(University of Utah,n.d).

Theoverall implications point out to the fact that mother can indeedinfluence if their offspring will be obese. Nonetheless, currentresearch only relies on animal studies and has not focused on humanresearch especially in terms of obesity. Despite this fact, it isclear that environmental issues also contribute to gene changes orchange in the genome. Issues such as social interaction and stresscan alter one’s genes, thus diet during pregnancy may contribute tochances of obesity in later life. Although it has not beenscientifically proven, what has been proven tends to show a strongrelationship between diet during pregnancy and the health status ofchildren (The Tech Museum of Innovation, 2009). When cells aredeprived of methylation, which is needed for their proper functioninganything can happen. The cells will develop without the rightstructure or framework, thus may lead to obesity or a certaindisease. Pregnant women are already encouraged to consume foods richin folic acid and B Vitamins to avoid defects in their children(University of Leicester, n.d). When women fail to consume such kindsof food, the likelihood of their offspring being unhealthy is high,thus the effect of diet takes effect quickly and directly.

Toillustrate this, the paper will offers an example of a case studythat illustrates how diet changes the epigenome. During the end ofthe Second World War, a famine broke out in Europe. Due to increasedwar and conflict, there were food shortages (Kinner, 2014). Thewinter season was defined by increased lack of a balanced diet andenough supplements. During the famine people died while babies wereborn severely underweight (Kinner, 2014). Researchers analyzedmedical reports after ten years in the worst hit areas. The effectsdiscovered were associated to perennial disclosure to famine tenyears before. Infants who survived and also gave birth to otheroffspring were susceptible to health challenges. This means thatchildren born even after a decade still inherited the same healthchallenges as their parents. It was concluded that the famine damagedthe victims DNA for generations (Kinner, 2014).

Inconclusion, the study of epigenetics is closely related to nutrition.According to National Human Genome Research Institute, (n.d) unlikestress or behaviors, nutrition is one of the simply studiedenvironmental aspects in epigenetic change. Epigenetics can bedefined as the research of heritable alterations in gene appearancecaused by chemical processes different from the original DNAsequence. The epigenome is a composition of chemical mixtures thatcontrol the genome. Again, the epigenome contains both protein andchemical compounds that confer to DNA and control actions such asdetermining whether a gene is active or inactive. The basic conceptof how diet can change the epigenome is based on the chemicalcomponents found in food that are part of the DNA composition.According to Utah, the nutrients we remove from food find their wayto metabolic passageways where they are manipulated, altered, andshaped into molecules the body can utilize.In this case, one of thepassageways is tasked with producing methyl groups, which aresignificant epigenetic tags that have the ability to silence genes.Common diet nutrients such as betaine, B vitamins, and folic acid aremain constituents of the methyl-producing passageways. Moreover,foods or diets with increased methyl-producing nutrients can promptlychange gene expression, specifically during early growth when theepigenome is established for the first time.


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