Is there a link between PTSD and our body’s immune response?
Well, research published in the Journal of Brain, Behavior, and Immunity has stretched beyond focusing on what happens to the body’s nervous and endocrine systems after trauma. . .
. . . and researchers have discovered a connection between trauma and the body’s immune system. More specifically, researchers have become curious about how trauma affects inflammation – as well as whether inflammation influences the development of PTSD.
Mark Miller, PhD and his team from the Boston University School of Medicine took this one step further. They wanted to look at how epigenetics might influence the link between PTSD and inflammation.
In a study from January 2018, Dr. Miller and his team were able to pinpoint how traumatic stress influences one important gene associated with inflammation, the AIM2 gene.
You see, previous research had identified the protein CRP, C-reactive protein, as a major player in our response to inflammation. CRP can act like an internal firefighter – it puts out the blaze of inflammation in the central and peripheral nervous system.
And the gene most responsible for producing CRP is AIM2.
Now when the immune system is at rest and there is no inflammation, a specific part of AIM2 is methylated – that means the genes are tightly bound together and are turned “off.” And when AIM2 is off, CRP is not being made because there are no fires to put out in the body.
So what can cause AIM2 to switch “on”?
Well, stress can be a big factor – and as we know, stress can contribute to inflammation.
But when AIM2 switches on, it also raises CRP levels in the blood to reduce inflammation.
So these researchers wanted to find out two things. First, did traumatic stress contribute to turning this gene “on?” And second (and perhaps more importantly), if AIM2 didn’t turn on and CRP levels remained low – would that influence the development of PTSD?
In this study, Miller and the team took blood tests of 288 post-9/11 US military veterans who had experienced traumatic stress during deployment in Iraq and/or Afghanistan.
After analyzing their blood samples for CRP levels and doing a clinical assessment of the veterans, the researchers’ findings were two-fold.
They concluded that after traumatic stress, CRP levels are elevated. This means that trauma has an epigenetic influence that turns AIM2 “on.” So trauma can lead to inflammation in the body. But CRP helps to reduce that inflammation.
Now here’s the other implication of the researchers’ findings – people who have experienced trauma but have low CRP levels (either due to a failure in epigenetic control of AIM2 or some other genetic mutation) might be at a higher risk for developing PTSD.
While it’s still too early for these findings to have any immediate clinical application, researchers are hopeful that this study is a step forward in identifying how PTSD impacts gene expression and the body.
Of course, we do need to keep in mind some limitations of this study. The research could have been strengthened by using a control group.
Given that you could not use a randomized design in this study, it would be nice to see a future effort conducted with a prospective design.
If you’d like to read this study for yourself, you can find it in the Journal of Brain, Behavior, and Immunity, volume 67, pp. 194-202.
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Now I’d like to hear from you. What have you found helpful in working with clients who struggle with PTSD?
Please leave a comment below.
This study is just the kind of research that will support my PhD which is specifically looking at the intergenerational transference of trauma through epigenetics
Very promising research, leads me to believe that in the future we could have a blood sample and be able to determine diagnosis. It is amazing how stress affects genetic constitution.
CRP is a protein made mostly in the liver in response to immune system activation anywhere in the body. It is measured frequently along with other routine blood tests to get an idea of how activated the immune system is. It is an “acute phase reactant”, and a “non-specific marker of inflammation”. It functions to INCREASE inflammation and support immune system activity. If your CRP is high, your “inflammation” is high.
CRP supports an effective immune response. We use it in primary care mostly to put cholesterol levels into context, because atherosclerosis is an inflammatory process that itself raises CRP levels, and CRP can be high for other reasons (like infection, injury, autoimmune disease (such as rheumatoid arthritis), obesity, cigarette smoking, sleep disturbance, and other stress states), and high ambient CRP accelerates atherosclerosis, increasing risk.
Inflammation (immune system activation) is the body’s response to actual or perceived danger of any kind. You are getting ready for an attack, getting ready to fight off infection in case you get injured, etc. Or you are already injured and responding to that. The nervous system and the immune system run in parallel. Stress of any kind can increase CRP.
We need the immune system to respond decisively and effectively to problems, then to switch into repair/restore mode and then into resting readiness mode. So, this article is affirming the concept that we need CRP to go up acutely (and then to go back down again, when we switch modes). The article is also making the point that maybe individuals who don’t make a decisive, strong CRP response, (reflected by low CRP level), don’t manage to resolve the problem and end up with a lingering chronic problem instead of healing.
I would not go so far as to say that “when AIM2 switches on it also raises CRP levels in the blood to reduce inflammation”. CRP does not directly reduce inflammation.
CRP RAISES inflammation. CRP indicates inflammation is present. It feels bad. (When you have the flu, your CRP is high and part of its function is making you feel bad so you will rest.). This is a good thing, we need it, but we don’t want to get stuck there. Inflammation, when it is working well, runs up and down an orderly sequence to healing and actually you can’t get to healing without having the initial inflammatory fire (with all the collateral damage) happen first. So, yes, CRP indirectly reduces inflammation but only because it is a big part of the inflammatory fire at the beginning.
This article gets at that ambiguity, which is lost in a lot of discussion of inflammation, which generally sees inflammation as “bad”. You need that strong immune response, but generally you want your CRP to be low at baseline.
The article is looking at a genetic basis for some people being more vulnerable than others– I like to believe that environment is more important than genes; genes are not destiny; maybe knowing there is a certain vulnerability can increase compassion and self-compassion; knowing our vulnerabilities may help us take appropriate action; everybody can heal.
In order to maintain or regain the dynamic flexibility to effectively fight off (or escape from) danger and then exit out of that acute stress state to rest and repair and heal— this process is supported by all of the things we know that are healing– which everyone has listed below.
Body and mind are not separate and never have been.
Thank you. Important clarification and clear explanation.
Great clarification, thank you.
Yes, thank you very much for this clearly stated information!
We run a 5 week group using art materials and psycho-education to teach skills for lowering arousal and interrupting PTSD symptoms in active ways participants can then fine tune individually. This is usually used as the start of a pathway through treatment. Achieving some sense managing and lowering arousal and symptoms often lowers the desperation associated with acute PTSD symptoms.
The research you feature further supports the importance appearing in so many different forms for all the approaches which focus on ‘resetting’ physiological states, and practicing finding the moments and longer spaces of settled and engaged states. Creative activities have a role to play in helping to access and sustain such states.
Nadija Corcos Art Psychothdrapist