Development of My Understanding of Epigenetics

Introduction to Genetics and Epigenetics

My understanding of epigenetics is directly linked to my understanding of how basic genetics itself works. Cells, which are popularly known as the “building blocks of life” or the “smallest unit of life,” are like little workers in every human being that play a major part in how the body functions. The activities of cells are directed by deoxyribose nucleic acid (DNA), which is made up of four nucleotide bases: adenine, guanine, cytosine, and thymine, each pairing with one specific other base. The structure of the nucleotide bases determines what our genes are, and genes are specific sequences of bases that provide directions on how to make proteins that control how we function.

Development of My Understanding of Epigenetics

Epigenetics is the study of changes in gene expression, a change in phenotype without a change in genotype, that can be inherited or caused by certain lifestyles. The epigenetics video opened my eyes to how gene expression affects us, those around us, and those who come after us. It also enlightened me on how identical twins develop and change over time, leading to discoveries about the effect age has on gene expression. The mice research helped me understand how epigenetics itself can cause certain gene expressions that may negatively affect health, but at the same time, reverse it, meaning repair the unhealthy gene expression. In the video, scientists were able to alter tags that manipulate gene expression in offspring by altering the diet of a pregnant mouse, which can regulate the gene that causes a mouse to be fat or skinny. This is caused by an epigenetic fix which can be inherited by the next generation of mice offspring, regardless of whether the mother's diet was altered. Environmental toxins also reversed the epigenetic fix, making skinny mice fat again. This was mind-blowing to me because being able to manipulate gene expression like this in humans would be revolutionary for modern medicine. The lifestyle of our parents and grandparents can help make predictions about health and determine or prevent health issues in our children.

This is all possible due to the fact that we have what is called an epigenome, which tells our cells what kind of cells they should be—for example, heart, bone, or skin. They all have the same genes, but the epigenome silences the unneeded ones to make cells diverse. Epigenetic instructions pass on as cells divide but are not necessarily lasting. Researchers believe that they can change during critical periods like puberty or pregnancy. There is mind-blowing and groundbreaking research that aids disease and cancer treatments. Epigenetic therapy aims to change instructions rather than killing the cell, in a way re-activating or reprogramming it. Our epigenome is more vulnerable, so we have a responsibility to take care of our bodies and treat them like a temple. But it allows us to invent drugs to correct and reprogram cells.

Family Health History and Epigenetics

Upon interviewing my family about their health history, I came upon some interesting finds. First, the disease I am most at risk for is high blood pressure/hypertension, which can be the leading cause of more serious implications like stroke, kidney disease, and heart failure. Less dangerous health issues I am at risk for are cataracts and arthritis. My grandmother (age 80), mother (age 49), sister (age 29), and I (age 21) all have eye conditions; we have all worn glasses, my older sister has had corrective eye surgery, and my grandmother had surgery years ago to remove cataracts. At a premature age (6), my optometrist noticed I had small cataracts, which led him to believe it was hereditary. This was when I got my first pair of glasses, younger than most, and my doctors over the years have monitored the condition to ensure they weren’t growing. It’s fascinating how the condition skipped both my mother and older sister. My grandmother and mother, who is significantly younger, have severe arthritis joint pains. My mother has told me in the past that she developed some of her pain in her 20’s, which is why she was not surprised by my occasional wrist pain. Connecting these dots can be frightening but at the same time keeps me alert about my health and future treatment and prevention.

Since hypertension is popular in my family, and I have an uncle who suffered three strokes in a year and died, I decided to investigate what might have caused it in my family and what scientists believe and have discovered. What I learned from research is that scientists are not exactly sure about the specific cause of essential hypertension, but there are certain factors that play a role, including smoking, obesity, lack of exercise, too much salt or fatty foods consumption, drinking too much alcohol, stress, age, genetics, family history of hypertension, kidney disease, thyroid disorders, and sleep apnea. This is a long list, but in my opinion, things anyone can easily suffer from. My family is African American, who are two times more at risk for hypertension in the United States than Caucasians. Black women over the age of sixty-five are observed to have the highest occurrence of high blood pressure, meaning age and race also play a role. According to Wise & Charchar (2016), “Essential hypertension (EH) is a complex, polygenic condition with no single causative agent. Despite advances in our understanding of the pathophysiology of EH, hypertension remains one of the world’s leading public health problems. Furthermore, there is increasing evidence that epigenetic modifications are as important as genetic predisposition in the development of EH.” What I believe this means regarding epigenetics and the health of my family is that the cause of hypertension could have been either genetics, lifestyle, and diet solely or a combination of all these factors. With tens of thousands of genes in the human body, there could be many combinations of genes being switched on and off, causing many different modifications.

There isn’t a way to single out which factor may have predominantly caused our hypertension occurrences, but what we eat may have played the most significant role. My family is Jamaican; in the Caribbean, we cook with a lot of herbs and spices, some of which are unhealthy. There is a direct link between salt and hypertension; many individuals who suffer from symptoms of high blood pressure are sensitive to salt, meaning that intaking more than the minimum amount of salt needed for the body to function increases their blood pressure. I know for a fact that I am salt-sensitive because if something I am eating has too much salt or more than I am used to, I cannot swallow it all. This is the same for my mother, while my grandmother can cook with and consume more salt, although it is not necessarily healthy. This is probably because she has a higher tolerance for it due to more years consuming it. Wise and Charchar (2016) stated, “Epigenetic modifications can be provoked by a variety of factors, including environmental influences during fetal and childhood development, chemical exposure, aging, dietary habits, and the use of recreational drugs and some prescription medications.”

Conclusion and Personal Reflection

After completing the Living to 100 Questionnaire and using the resources on the Sharecare website, I learned my estimated life expectancy is ninety years old, and that my estimated true age is sixteen, five years younger than I am. Knowing what I know now with my understanding of epigenetics and knowledge of my family history, I can improve my health and longevity by increasing and continuing my daily exercise and refraining from activities that contribute to hypertension, like smoking and eating unhealthy foods. The connection between lifestyle choices and epigenetic modifications is profound, emphasizing the importance of making informed decisions for both present and future generations.

References

Wise, I. A., & Charchar, F. J. (2016). Epigenetic Modifications in Essential Hypertension. International Journal of Molecular Sciences, 17(4), 451. https://doi.org/10.3390/ijms17040451