Looking at The Epigenetics of Pain
An old, cursory, exploratory interest piece (68)
--
With the exception of certain conditions, nearly every person is familiar with the sensation of pain. While it is true that there are several ailments plaguing society such as cardiovascular disease and cancer, pain is something that is reportedly understudied. Chronic pain affects approximately one-third of Americans and comes at a large economic cost to society (“Health and Economic Costs of Chronic Disease | CDC”). The breadth of chronic pain’s impact is stunning. It affects more people than cancer, heart disease and diabetes combined. In this brief paper, we will explore a potential way of approaching the problem of pain as it pertains to these under treated populations.
The epigenome holds a great deal of potential for our discussion of chronic pain treatment. The epigenome is comprised of chemicals and proteins that is unique to every individual and interact with the human genome (Campbell & Wood 2019). Epigenetic mechanisms can be considered as changing chromatin structure while leaving the nucleotide sequence of the genome intact (Campbell & Wood 2019). Modulating expression by exercising control over such mechanisms could result in more efficacious treatment options. Changes in the epigenetic level are in reference to the stable alterations in gene expression potential (over long periods of time) due to the aforementioned chemicals and proteins (Louwies, Ligon, Johnson, & Meerveld 2018).
Much of epigenetic regulation is accomplished through the process of histone acetylation and deacetylation. Acetylation of a histone relaxes the strong binding interactions between it and DNA (Campbell & Wood 2019; Kim & Kaang 2017). This looser, relaxed form is more conducive to expression of the underlying genome (Campbell & Wood 2019). Proteins called histone acetyltransferases and histone deacetylases work in tandem to thus regulate expression from this level (Campbell & Wood 2019; Kim & Kaang 2017). These proteins specifically act by chemically altering lysine residues on the histones (Campbell & Wood 2019; Kim & Kaang 2017). Other mechanisms for altering the epigenome also include the presence non-coding RNAs and DNA methylation (Campbell & Wood 2019; Louwies, Ligon, Johnson, & Meerveld 2018).
