The Science Journal of the Lander College of Arts and Sciences


The origins of adult disease have been a prime topic for research, as deciphering causes can lead to strategies for preventions and cures. There has been recent intrigue focused on the environment in the womb. Records from England and Wales in 1911 show that those who suffered from cardiovascular disease were geographically correlated with regions high in infant mortality in the past, seventy years before the study. When looking into the cause of the neonatal death rates, low birth weight, poor maternal health, and high maternal death rates during childbirth were clearly associated. Barker inferred that there is much happening in the intrauterine environment that ultimately affects our quality of life. This research helps support the concept that rather than looking at childhood adversity and socioeconomic circumstances to help explain adult disease, we might need to reach further back (Barker,1990).

Through epigenetic mechanisms, alterations to the physical expression of our DNA can take place without changing the sequences of the actual DNA. Epigenetics is what is responsible during fetal development for the differentiation of stem cells to specific cells by adding or subtracting methyl groups to silence or activate particular genes. When an egg and sperm unite all previous methylation patterns are stripped from the newly formed diploid. However, by the time it becomes a blastocyst, new patterns have already formed. It is during this crucial stage of development that new patterns and changes to our epigenome our founded and passed down (Powledge, 2009).

The purpose of this paper is to determine if chronic health issues in adulthood have their roots in the environment and changes experienced by the fetus in the womb. Environmental exposures like nutrition, stress, and toxicants are evaluated and tested for their potential hand in setting the course for adult disease. Many studies show correlation between malnutrition and the development of metabolic diseases like obesity, type II diabetes, and even hypertension. Likewise, stress during gestation has been linked to anxiety, depression, and posttraumatic stress disorder (PTSD) in offspring. Toxicants like bisphenol-A are the likely culprit for genetically expressed abnormalities that range from cancers of the reproductive system to attention/deficit hyperactive disorder (ADHD) in exposed offspring. The “how” and the “why” are explored in this paper. If we can better understand the origins of adult disease then we are better equipped to defend our future generations against it. Furthermore, the notion that our DNA is not at fault for these outcomes, but rather epigenetic adjustments written on top of our DNA, provides hope that just as easily as it can be added on, we can take it off (Powledge, 2009).



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