Lower methylation of glucocorticoid receptor gene promoter 1F in peripheral blood of veterans suffering from post-traumatic stress disorder
Lower methylation of glucocorticoid receptor gene promoter 1F in peripheral blood of veterans suffering from post-traumatic stress disorder.
Apropos to my recent post about depression and the HPA axis, this study has revealed for the first time a possible link between trauma, PTSD, and genetic change.
I said in the last post that a Stanford study identified a link between depression and the glucocorticoid receptor (GR). They showed that alterations in the GR receptor could lead to changes in cortisol levels in the body and brain, linked to everything from depression to anxiety to PTSD. They identified the gene NR3C1.
Well, in this study, the same gene is examined again; this time a group out of Mt. Sinai Hospital demonstrated that PTSD survivors had their gene altered–epigenetic modification–after trauma exposure (combat exposure in 122 veterans).
This is interesting: the gene promotor was LESS methylated (less CH3 functional groups are added onto the gene) leading to enhanced GR sensitivity. That is, the body and brain need less cortisol to feedback and regulate the HPA axis. The less methylation, the more the PTSD symptoms, and the lower the blood cortisol levels.
So this is very new and exciting. We can actually see how trauma changes the DNA in a very important part of brain physiology–the stress response system.
It appears too early to say what will happen with this finding, but it gives further direction. At the least, it may be a marker for diagnosis of PTSD (i.e. NR3C1–IF promotor methylation patterns: the less the methylation, the more likely the diagnosis).
I am curious how to draw a connection between PTSD and Depression through the HPA axis. The symptoms are very similar, but the HPA axis seems in opposite poles: PTSD, low cortisol; Depression, high cortisol. I know, I know–way too simplistic.
Let’s see what unfolds.