Rockford For Safe Access: DNA, PTSD, Abused Children, And Cannabis

At Cannabis For PTSD I had some videos on the uses of cannabis for those who suffer from PTSD. I thought it might be a good idea to go into the subject a little deeper from the aspect of abused children.

from Genome Advance of the Month - Child abuse leaves epigenetic marks By Roseanne Zhao, Ph.D. - NIH Medical Scientist Training Program Track 3 Scholar

In addition to harming the immediate wellbeing of the child, maltreatment and extreme stress during childhood can impair early brain development and metabolic and immune system function, leading to chronic health problems. As a consequence, abused children are at increased risk for a wide range of physical health conditions including obesity, heart disease, and cancer, as well as psychiatric conditions such as depression, suicide, drug and alcohol abuse, high-risk behaviors and violence.

They are also more susceptible to developing post-traumatic stress disorder (PTSD)-a severe and debilitating stress-related psychiatric disorder-after experiencing other types of trauma later in life.

Part of the explanation is that child abuse can leave marks, not only physically and emotionally, but also in the form of epigenetic marks on a child's genes. Although these epigenetic marks do not cause mutations in the DNA itself, the chemical modifications-including DNA methylation-change gene expression by silencing (or activating) genes. This can alter fundamental biological processes and adversely affect health outcomes throughout life.

New research, published in the May 14, 2013, issue of the Proceedings for the National Academy of Sciences, shows that PTSD patients who were abused as children have different patterns of DNA methylation and gene expression compared to those who were not.

Another good article on the subject: The Road to Post Traumatic Stress Disorder Begins at the Intersection of DNA and Childhood Trauma

Our genetic predispositions are only part of the equation when it comes to determining our risk for developing psychiatric disorders. Exposure to stressful environments during critical periods of brain development plays a dramatic role in changing gene function and influencing response to traumatic events in adulthood.

The National Institute of Mental Health defines post-traumatic stress disorder (PTSD) as an anxiety disorder arising in the aftermath of living through a dangerous or traumatic event. In PTSD the “fight-or-flight” response to fearful stimuli is activated in situations where it is not necessary for the body to defend itself from harm. It does not affect every individual who has been exposed to trauma. A major question in the field is how variations at the molecular level alter the likelihood that a person will develop PTSD.

In an insightful paper recently published in Nature Neuroscience, Klengel et al. shed light on the mystery of how genetic variability and life experiences alter our chances for developing neuropsychiatric disorders later in life. The authors identified single nucleotide polymorphisms (SNPs) (DNA sequence variations that differ across members of the population) in the FKBP5 gene. Variations in this gene alone were not enough to predict adult PTSD, but if the individual had been exposed to trauma as a child and had the genetic variation, the chances increased. Gene-environment interaction is a term used to explain situations where an individual’s likelihood of having a particular disorder or disease is dependent on a risk allele that arises from exposure to a specific environment early in life.

The researchers continued their quest by pinpointing the specific DNA change underlying the increased risk for developing PTSD later in life. During development, our DNA undergoes changes that result in the addition or removal of methyl groups. Methylation modifies DNA and can result in increased expression of a particular gene or gene silencing. Traumatic events can change DNA methylation beginning during development and continuing through adulthood. The researchers observed that FKBP5, which is a risk allele for a stress response regulator, had an altered methylation state in children exposed to trauma.