There is hardly a bodily system that is not affected when an organism is stressed, but finding which pathologies connect to which biological processes is very difficult. With the support of the Canadian Institutes of Health Research (CIHR), one Carleton University professor is trying to connect the dots.
Hymie Anisman, a professor in the Department of Neuroscience and the Canada Research Chair in Neuroscience, is examining if and how stressful events are related to specific symptoms of pathology. His recent CIHR-funded research looks particularly at depression in relation to stressful life events.
“Treatments for depression aren’t all that effective; however, if you isolate particular symptoms and biomarkers of depression, it may be possible to identify who would be responsive to a particular treatment and who might not be,” Anisman explains.
Anisman and his team have broken down depression into sub-components based on biomarkers. This allows them to identify which people are more prone to depressive disorders based on their life experiences and/or particular gene mutations, and also to determine whether genetic factors like polymorphisms or epigenetic effects result in a particular phenotype occurring, and if they are moderated further by stressors.
“For example, it is known that if you inherit a particular gene related to serotonin you are more prone to depression, provided that you also encounter either an adult stressor or an early life stressor. But one or the other alone might not be enough to become depressed. We’re looking at how several other genes interact.”
One gene Anisman is looking at in particular is related to BDNF, or Brain Derived Neurotrophic Factor, which ensures neurons in the brain are healthy. There are interesting interactions that occur in an adult with polymorphisms for BDNF in relation to environmental stressors, he says.
Another aspect of Anisman’s research is concerned with the link between stressors and immune activation. In previous research also funded by CIHR, the neuroscience professor found that stressful events affect immune factors. In subsequent studies, however, his team came to the conclusion that a set of molecules called cytokines, which serve to prevent damage by being present in both the immune cells and the brain, can have damaging effects at high levels. This led him to shift his focus to how cytokines might be related to stressors, and how they may influence the manifestation of depressive illnesses.
Discrimination, a very profound stressor, is another area of focus for the veteran researcher. In examining a number of different groups affected by discrimination and putting into context how they associate with their self and group identities, Dr. Anisman has discovered intergenerational effects connected to group-associated cultural and historical trauma.
In addition, Dr. Anisman’s is looking at a population that he calls “highly vulnerable” to depression: first-year undergraduate university students. His research in this regard examines what social and hormonal factors make one student more or less able to cope with stressful events. Anisman points out the importance of the hormone oxytocin, which is involved with social behaviours such as bonding, trust, making friends, and love. Those with the proper genes for oxytocin seem to be better off dealing with stressors and seeking support than those with oxytocin systems that are not working well.
“There are some surprising results with this; it’s not as simple as you might think. I would have expected that those with the wrong genes who were placed in the wrong environment would be very badly off. But we’re seeing that sometimes those with certain genes do not react to negative events in the same way one might otherwise. In a sense, they are deficient in being able to react negatively.”
Hymie Anisman has been researching the area of stress and depression for almost forty years. His original intent, he says, was not to find out how stressful events came to make you ill. His original intent was something quite different.
“There are some people that even in the greatest trauma come out alright. The real question was: what made them resilient while so many other people around them fall by the way-side? It’s easier to find out what breaks the person than to find out what keeps them whole. It’s like anything else — easy to break but hard to repair. If we know what makes people resilient, I thought maybe we could help those who aren’t so resilient. That’s still my goal.”