There’s a myth that PTSD is all in our heads, that it only affects people who are not emotionally equipped to handle trauma. It’s understandable why some people may think this. After all, why doesn’t everyone who is exposed to trauma develop PTSD? However, in recent years we’ve begun to develop a better understanding of the physiological factors that are involved in PTSD.
Given the interplay between cognitive effects and healthy emotional regulation, researchers hypothesize that major parts of the brain are also involved. The amygdala and hypothalamus, for example, are vital to processing memories and modulating fear and anxiety, and likely play a significant role in the symptomatology of PTSD.
In 2013 a team — comprised of researchers from the schools of medicine at NYU, Yale, Harvard, and the University of California at Irvine — discovered that individuals with PTSD have an endocannabinoid deficiency. Researchers used brain imagery to compare PTSD patients with healthy individuals (with and without lifetime histories of trauma). They found that the PTSD group, on average, had anandamide levels that were 53.1% lower than individuals who had been exposed to trauma at some point in their lives (but were otherwise healthy). More strikingly, they had 58.2% lower anandamide levels than healthy individuals with no history of trauma.
The PTSD patients also had lower cortisol levels and a higher density of CB1 receptors. The reason for the increase in receptors is likely that the body’s endocannabinoids (our naturally produced cannabinoids) produce an adaptive response to more efficiently exploit the depressed levels of anandamide. The researchers’ findings support the growing body of evidence implicating alterations of CB1 receptor-mediated anandamide signaling in PTSD.
Further, their findings may help explain one of the reasons many PTSD patients find relief in cannabis (given the fact THC mimics anandamide). The researchers provide a promising neurological model to help us develop cannabinoid-derived medications to treat PTSD. Likewise, that we have biomarkers that can help us diagnose PTSD is a tremendous advance in science. (Researchers were able to correctly identify nearly 85% of the PTSD cases based on brain imagery.)
It certainly seems plausible. In the same study, researchers found that women — even under non-stress conditions — have more densely populated CB1 receptors than men. This might provide a neurobiological explanation for why women experience PTSD at nearly twice the rate as men following traumatic exposure.
Thus far, there hasn’t been any research to compare anandamide levels and CB1 receptor density before and after exposure to combat, which could help determine if those who later develop PTSD had an endocannabinoid deficiency prior to combat. This type of research would help validate speculation that an endocannabinoid deficiency increases a soldier’s PTSD risk.