Epigenetics and the Environment

Identical Twins:
Recent studies have been excessively focused on identical twins and the factors that make them unique, despite their label. Throughout the years, twins have been stereotyped to have an alike physique and mental capabilities. However, this is but a fantasy. Whether they are dressed the same for a family portrait does not decide which genes are turned on and off; that is a job for epigenetic tags. Imprinted tags are identical, thus giving twins their label. These determine what genes are active or not. The tags are placed on and off the genome in reality, which signals which trait to express or make dormant. So how do twins differ? And what causes this to occur?

The issue of nature versus nurture has been debated in Behavioral Genetics for over a century. From a genetic aspect, inherited traits from the maternal and paternal sources are researched, such as eye or hair color, are based on a biological component found in the DNA coding sequences. Other traits are coded from yet another origin: the environment. A study between two sets of twins (3 and 50 years old). Researchers hypothesized that certain diseases, handicaps, and traits are linked to their outside surroundings. In their research, dyed epigenetic samples were analyzed for epigenetic tag locations. Results yielded the 3 year old twins shared a generally common locale for their tags, whereas the 50 year old twins had the opposite effect. While running the study, scientists discovered that diseases such as arthritis are more environmentally-decided. However, dyslexia are more genetically influenced. This happens when the individual is allowed to make their own choices that may or may not impact their genetic makeup.

Fraternal twins are even more dissimilar in this case, speaking on a molecular level. Due to the fact that each stem from a different egg and sperm combination, they only share half the amount on similar genes that identical twins share. The rest of their pheno- and geno-type is based on their home lifestyle and the way they are raised. This also makes twins better role models for experiments when testing Molecular Genetics. To illustrate this point, take a set of identical twins. When one of them develops a disease such as lung cancer, scientists use newly advanced tools to pinpoint the mechanism of the event, whether it is environmental or genetic. In this case, the lung cancer is most likely caused by a physical activity that the particular twin chose to partake. Smoking, dietary decisions, exercise, and their overall routine influence the epigenome. These signals can be transferred from a number of sources, carried throughout the body on a cell, then copied onto a protein with the information to the genome, triggering the tags. Smoking must have been the main source of the twin's lung cancer.

Personal triggers on my specific epigenome most likely have been transforming my genotype through a semi-balanced diet, a fair amount of exercise, acceptable social behavior, the rate of the metabolic processes, fluctuating stress levels, environmental dust that provokes allergies/asthma, and the methods that may parents have chosen to raise me.

Lick your Rats:
Like many others in the animal kingdom, mother rats care for their young by grooming and licking their pups. These nurtured pups have been noted to develop a calmer personality, while opposing rats are more anxious. This trait is expressed in humans and bred dogs as well. These epigenetic tags that are established in the living organisms are almost as influential as the original imprinted tags. In the first week of the newborn's life, the Metho molecule (green) silences the GR gene (gold) in all rat pups. During the first week of licking, brain cells are stimulated and activate the GR gene, which makes the rat more calm in situations after stress hormones are released. This materializes in the hippocampus, where the GR protein energizes and binds to cortisol; this coordinates its fight-or-flight instinct. The nurturing that the pup receives in the first week may seem trivial at first glance, but the overall ramifications may conclude in breeding calmer rats, depending on how they were raised/licked.

As previously suggested, this occasion happens on a much larger and longer scale. Take humans and dogs, for example. The way a newborn is raised depends on how its parents are raised, which are based on how they were raised, and so on and so forth. The chain of reactions impact the way a human reacts to a situation, including stress. The all-too-common fight or flight instinct depends on whether he/she was raised to take a stand or flee from the combat zone. Social behavior is also a leading factor to how the individual nurtures his/her own offspring, if they even choose to have any. For example, the interaction with the opposite sex may take its toll on whether or not he/she will have an opportunity to produce progeny.

The interaction between dogs and humans are beneficial to biologist's studies because of their unique results that they have extracted. The chemical oxytocin is produced when an owner nurtures its dog. This occurs in both species, and has not been discovered in other relationships yet. This culminates in a more calm and nurturing second generation of dogs, and a convenience for humans that may live longer.

Nutrition and the Epigenome:
One can better understand something if they can easily relate to it, such as diet. Maintaining a healthy, balanced diet is a struggle for many, especially in America, and countless individuals succumb to temptation. Methyl groups, extracted from the metabolic pathways in a human being, silence genes with their epigenetic tag abilities. Owing to the known actuality that the epigenome commences life as a blank slate, it is vulnerable to any rapidly altering chemical such as folic acids, SAM-e, or B vitamins. The earlier the intake is increased, the quicker the epigenome is manipulated. Studies show that methyl or choline deficient mothers deny their child of a methylated-healthy adulthood.

Yet again, mice were tested in the lab for agouti-linked dietary impacts. Those that were prone to obesity, cancer, diabetes, and a yellow coat, lacked in the gene. All the while, the contrasting experiment cluster supported their brown hue, immunity to common diseases, and smaller framework. Even though there is such a significant difference, the two sets of rats are still generically homogeneous. In a separate, yet related investigation, pregnant mutated rats with a high income dosage of methyl produced "normal" brown mice. Scientists connected the dots and concluded that your epigenome isn't based on your specific diet, rather, your prenatal diet.

When the mutated mothers were supplied with a Bisphenol-A-rich exposure status, the ratio of yellow to brown mice increased with a steep incline. BPA, being toxic in addition to a polycarbonate plastic component, altered the genetics in the maternal DNA and therefore passed on the unhealthy lineage to her infants. Even so, when a test was done to dictate whether the diet or contamination exposure level outweighs one another or if they were co-dominant, the BPA capitulated to the methyl-rich diet, consequentially resulting in a primarily brown generation.

Analogous in many other categories, a one-size-fits-all procedure is not in the least helpful when considering factors of obesity, reduce stress levels, or mapping out a successful diet in order to achieve a balanced lifestyle. Just as mapping the genome did to biology, the same may be said for charting unique epigenomes for solitary patients in dire need of guidance.

Epigenetics and the Human Brain

The human brain, thought to be sacred because of its overindulgence in functions and hippocampus minor existence, features innumerable roles that support our actuality and continuation. Recent inquiries have stumbled upon an association between the brain and the epigenome, as well as its DNA methylation stability, basic chromatin protein mutations, long-term memory, and chiefly suicide rates. Dr. Moshe Szyf described the methods of epigenetic researching and the link between child abuse, suicide, and the epigenome. Those who were neglected or abused as a child showed a 100% rate of suicide, with a 70% methylation level in the hippocampus minor, identical DNA sequence as non-suiciders, and an environmental stamp on their brain. Their "twin" who did not commit self-murder expressed little to no differences in methylation levels in the cerebellum, overall methylation levels, and a significant GR peak difference. What codes for this variation? The ribosomal RNA which acts as a scaffold which determines the quantity of expressed genes, regulated by methylation. This allows for an identical twin, at 50 years old who has been raised separately to contain less active ribosomal rRNA genes, to have less protein production, than their twin. A common pattern is also found in Alzheimer's disease.

Abuse is not the only cause of suicide, despite what some may think. Mental disabilities such as Rubinstein-Taybi syndrome is caused by the CPB protein malfunctioning to reduce acetyl tags on histones. Other mentally handicapped patients may suffer from REELIN deficiency, which shapes the brain for infantile development. The 60 connector genes that differentiate unstable and healthy human beings from one another are chiefly signals between brain cells being mistranslated or intercepted. This can be modified by drugs given to patients with these types of illnesses may change gene expression, therefore stabilizing DNA methylation in order to reverse the symptoms of the particular disease. Other drugs that are received by the patient may be abused, resulting in the mutation of hundreds of genes at a certain point in time. This misuse ad possible addiction has the possibility of rewriting the epigenome to a point of no return. Notwithstanding, modern technology has been able to operate a process in which specific genes are pulled down and the methylation levels are measured. This translates which specific section of the brain is being affected, leading to gateways of solutions in the genetic field.