No-one knows why Steven Kazmierczak snapped. When he kicked his way into a packed lecture hall in Northern Illinois University, shooting dead five students and injuring 21 more, those who knew him expressed surprise that he was capable of such brutal violence.
He killed himself at the end of the spree, meaning his motives remain unknown, but the legacy of this tragic event may be more than just the actions of a lone unfathomable killer.
Because when Kazmierczak attacked, a team of psychologists and neuroscientists had already assessed a large group of students who had been recruited as non-affected participants for a study on the effects of victimisation, giving the researchers an unwanted opportunity to better understand how sudden trauma affects the innocent.
Since the 1980s we have recognised a trauma-specific mental disorder. Its name, ‘post-traumatic stress disorder,’ seems to suggest that trauma alone causes the condition but we have known for years that genetics play a large part in determining who does and who doesn’t develop PTSD.
Not everyone who experiences a violent attack, disaster or sexual assault will develop PTSD. In fact, the single most common outcome after tragedy is not mental illness, but recovery. That’s not to say that we wouldn’t feel shaken up or distressed after such events but most people can return to their everyday lives, perhaps changed, but unimpaired.
What we still don’t know is how people who recover are different. Why is it that some individuals develop the disorder following trauma while others appear to be relatively resilient?
We’ve known since studies on Vietnam veterans that genetics accounts for up to 30% of the difference in PTSD symptoms but researchers have been keen to find to specific genes that confer the biggest vulnerability.
Normally these types of studies look at people with and without PTSD and compare the presence of specific genes known to be linked to brain function, to see if they appear more in one group than another. Although helpful, one problem with these sorts of studies is that it is difficult to say whether the genes might directly contribute to the condition or to a general difficulty with mood or behaviour.
In scientific terms, the reason this can be a problem is because people who are already, for example, low in mood or impulsive, are on average more likely to be victimised, attacked or abused. This means it’s difficult to know exactly which genes are most important for explaining the reaction to trauma, rather than the chance of being victimised.
Psychologist Kristina Mercer was leading a study on trauma before the shooting occurred. She had been interviewing female students about their life histories and experience of trauma at Northern Illinois University, originally planning to re-interview the students over time to see which characteristics made them more likely to experience sexual assault.
Clearly motivated to make sure that something more than grief and pain would come from the event, she switched focus to better understand what made some people more likely to develop PTSD after the shooting.
The team re-interviewed the participants in the weeks following the tragedy, assessing their exposure to the violence, any PTSD symptoms present and their level of support from friends and family. A similar interview was conducted 8 to 12 months later and at the end of the study, the researchers took saliva samples to look at the DNA of each participant.
As PTSD is largely a disorder of anxiety accompanied by an intrusive reexperiencing of the event that doesn’t fade with time, the team focused on genes for the serotonin transporter system or SERT.
Serotonin is one of the brain’s neurotransmitters that provide chemical signalling between brain cells. The serotonin transporter system is responsible for removing the used serotonin from the synaptic cleft, the signalling space between the neurons, and putting it back in place, ready to be used again.
This is important because if not removed from the synaptic cleft, the serotonin will keep on signalling. In other words, the efficiency of the serotonin transport system in cleaning-up stray neurotransmitter determines the strength of the signal as much as the original message.
We know that many of the key circuits involved in anxiety are reliant on the serotonin neurotransmitter, so the research team suspected that people with genes differing in how they control transport system could be differently susceptible to anxiety and, perhaps, trauma.
In line with their thinking, the results showed a similar picture. A transport gene called rs25531 was identified as directly linked to the chance of developing PTSD after the shooting. Interestingly, a commonly mentioned serotonin gene, 5-HTTLPR, was only linked to PTSD risk when it was also present with rs25531, suggesting the importance of looking at genetic interactions and not just single genes.
Because of nature of the shootings – a lone gunman who randomly attacked anyone in range – the results are more directly tied to reaction to trauma, rather than a possible vulnerability to being victimised, meaning this is one of the few studies that gives us an unambiguous insight into the post-trauma process.
Now it’s common at this point to say that a discovery of specific genes raising the risk of mental illness should lead to a better treatment for trauma, but this is usually nothing more than a hopeful twist on the scientific details, and this case is no different.
The results suggest no direct treatment and no immediate cure because mind, brain and trauma are too complex for simple solutions.
But the study is no less important. It’s still an essential part of our understanding and provides an essential thread in a tapestry of knowledge.
And fittingly, it shows that even from the shadow of tragedy, light emerges.
3 thoughts on “A thread of hope from a shooting”
Good story, and I appreciate the post, but here to tsk tsk about some sloppiness. Rs25531 is not a gene, it is the designation for a single nucleotide polymorphism. Likewise, 5-httpr is not a gene, it’s the name given to a region of a serotonin transporter gene that is polymorphic. The ‘short’ polymorphism of this region has been linked to anxiety and depression. 5-httpr genotype refers to whether this region has more (long) or less (short) repeats. rs53321 is a SNP, so a single base pair change, in this region.
PTSD and traumatic events will need to be studied so much more…but it’s a good start. So what gene is it anyway? How are they testing for this? It will be interesting to see if PTSD is over-diagnosed in a significant number of people simply how they may describe the events…but truly do not exhibit the number of symptoms required to qualify. Is it because insurance covers certain diagnosis and not others? Just some thoughts. Great article though.
I wonder what the implications are for everyday stress. I mean, if extreme events can cause enduring anxiety what would even minimal stress do when repeatedly experienced over years do?
I suppose a lot of research is done in this area, but are there anyone looking into whether PTSD and chronic symptoms of repetitive stress have genetic overlaps?