Genetic factors in PTSD

True et al (1993) carried out a study of 4042 twins who fought in Vietnam. The researchers found that monozygotic twins had a significantly higher rate of concordance for the disorder than dizygotic twins. In addition to twin research, psychologists also find that PTSD runs in families. A study by Yehuda et al (2001) found that adult children of Holocaust survivors with PTSD had a higher risk of PTSD following trauma compared to adult children of Holocaust survivors without PTSD. Similarly, Sack et al (1995) found that Cambodian refugee children whose parents both had PTSD were five times more likely to receive the diagnosis than refugee children whose parents did not have PTSD. However, in both of these cases, the correlational nature of the data does not let us rule out environmental factors as the reason for the disorder.

Although early research on PTSD focused on twin studies, much of the research today is done through genetic mapping.  Psychologists who study PTSD are interested in the role of the α2b-adrenoceptor. It is found in the amygdala, a part of the brain involved in processing strong emotions such as fear. The role of the α2b-adrenoceptor is to promote memory formation when stimulated by adrenaline.  Obviously, when we experience a traumatic event, adrenaline plays an important role in that experience.  The gene that encodes this receptor comes in two varieties. The mutation of the gene appears to have difficulty in shutting off the stress response and returning the body to homeostasis.

Dominique de Quervain (2012), of the University of Zurich, wanted to know if having this genetic mutation would assist in recall of emotional memories. In his experiment, he showed students photographs of positive scenes such as families playing together, negative scenes such as car accidents, and neutral ones, such as people on the phone. Those students with at least one gene for the rarer version of the protein were twice as good at remembering details of emotionally charged scenes than were those with only the common version.

But as this was a laboratory experiment done under controlled conditions – and the task of looking at a series of unrelated photographs is rather artificial, we have to wonder if we can really link this mutation to PTSD. A study from the Rwandan genocide seems to confirm these findings.

The 1994 genocide in Rwanda resulted in the mass killing of up to one million people over the course of about 100 days. Many of the survivors of the genocide were living in refugee camps at the end of the crisis.  It was here that Kolassa et al (2010) carried out their study of 424 Rwandan genocide survivors – some with and some without symptoms of PTSD.

Using local people to help carry out interviews, they recorded how often people in the camp suffered flashbacks and nightmares about their wartime experiences. They also did blood testing to determine the version of the α2b-adrenoceptor genes in each of their volunteers. As predicted, those with the mutation of the gene had significantly more flashbacks than those with only the common version of the gene.

The role of neurochemistry in PTSD

Most biological research on the origins of PTSD focuses on the role of noradrenaline (also called norepinephrine), a neurotransmitter that plays an important role in the stress response. Noradrenaline helps to trigger the fight or flight response - increasing heart-rate, releasing glucose and increasing blood flow to the muscles. Noradrenaline also appears to be linked to a higher level of vigilance and concentration. Geracioti et al (2001) found that PTSD patients had higher levels of noradrenaline than average. In addition, stimulating the adrenal system in PTSD patients induced a panic attack in 70% of patients, and flashbacks in 40% of patients. No control group members experienced these symptoms.

Modern research seems to indicate that there could be another biochemical root of PTSD - neuropeptide Y (NPY). NPY is thought to have many functions, including reducing anxiety and stress, reducing pain perception and affecting the circadian rhythm. The hormone is released as part of a response to stress and works together with the amygdala, prefrontal cortex, hippocampus and brainstem to turn off the stress response. One hypothesis is that PTSD patients have lower levels of NPY. But how would psychologists test this hypothesis?

Morgan et al (2000) carried out a study of healthy US Army soldiers who participated in a survival course designed to simulate the conditions endured by prisoners of war, such as food and sleep deprivation, isolation and intense interrogations. Baseline levels of NPY were taken before the training and then the levels were measured after the training. The researchers found that NPY levels went up in the soldiers' blood within hours of the interrogations. Those soldiers who responded more negatively to the training experience were those with lower levels of NPY. It appears that NPY may play a key role in the alleviation of the stress response; low levels may mean that the stress response lasts longer, potentially leading to symptoms associated with PTSD.

Yehuda et al (2006) carried out a study that looked at soldiers exposed to combat that did not develop PTSD and soldiers exposed to combat who did develop PTSD. It was found that those that had PTSD had lower levels of NPY. Ideally, prospective, longitudinal studies will be carried out to test the predictive validity of this research.  Being able to predict which soldiers are more likely to develop PTSD as a result of combat would be an important finding for the military.

 Teacher only box

Do you think that this would be an appropriate application of the findings?  

This question usually leads to good debate with students  Some see this as a way for the military to avoid the problem of vets with PTSD - that cost the government a lot of money every year to treat.  Others will see it as a reductionist argument and argue that it denies people the chance to pursue a career in the military. It is easy to transfer the concept to other areas of life - e.g. should married couples have a test to show potential aggressive behaviour?

What problems would you predict could result from the application of this theory?

The most significant problem would be that some people that want to go on combat missions would be denied that choice. It could also, however, follow them to other jobs - e.g. if they were a doctor or wanted to work for the police.

Would the benefits to society potentially outweigh potential problems for the individual?  Should that matter?

This, of course, is the big question of preventative medicine.  If we know that you might be at higher risk than others for a physical or mental health problem, would it be better to inform you and to help you to take appropriate measures - or could this lead to a self-fulfilling prophecy? Is this a violation of one's rights?  Or is this necessary to protect the larger society?

Checking for understanding

Cognitive approaches to PTSD