A short while ago I was asked to take part in an Open University day about mental health for tutors. It was a good chance to give a workshop about self care and why that might be useful for both students and staff. But I was also given a lecture slot in the day. I decided to share some of my thoughts on mental health more broadly. I was nervous because this was the first time I had spoken on this topic specifically and I know that my ideas on it can be challenging to hear. However, the talk seemed to go well and led to some great discussions, so I've decided to share it here too.
The talk preceding mine set the scene very well as Saroj Datta gave us an update on the latest evidence regarding the interactions between genes and the environment in relation to mental health. Saroj was involved in the OU science course on mental health which takes a 'biopsychosocial' approach to the issue, and her talk demonstrated just how impossible it is to tease apart those elements: bio, psycho, and social (which is why they are combined into one word).
I already knew about 'neuroplasticity': the fact that the way our brains connect up changes over the course of our lives depending on the experiences we have (this is the way that we learn, of course, but we often forget this and regard brains as static and unchanging). Saroj presented evidence that there is also flexibility on a genetic level. Whilst the set of genes in every cell in our body remains fixed, whether they are 'switched on' or 'express themselves' is not. Animal studies have shown, for example, that a glucocorticoid receptor gene tends to remain switched off, leading the animal to be fearful and anxious, unless the mother displays nurturing behaviours (due to not being anxious herself) in which case it is switched on, leading to pups who are calmer and less stressed. This research is in its early stages, and needs to be treated with caution when applied to humans of course.
Human research supports the genetic-envionmental interaction, finding that, for example, rates of depression are high when a particular allele of a gene is present and someone has experienced three or more stressful life events, but lower if just that allele, or just the life events, are present. It is the interaction between genes and environment that is vital. There have been similar findings in relation to childhood maltreatment. However, it is important to remember that some people were still depressed without those particular elements in the place (either that gene allele, those life events, or the two together): so this is not the whole picture. Also there is unlikely to be any one single gene involved in any element of human behaviour, but rather many.
Saroj suggested that such 'epigenetic' changes are potentially reversible and it has been suggested that this, and neuroplasticity, may explain why there are multiple different routes to repair and recovery.
My own interest has been mainly about the social end of the biopsychosocial composite, but it is vital to remember that this is as impossible to tease apart from the rest of it as the bio end is. The ways in which the society in which we live understands, and treats, people, is vital to the way in which we understand and treat ourselves. And one of the main things our society currently does is to split apart the biopsychosocial in a deeply problematic way when understanding issues of distress or 'mental health'. This is something I will explore, in detail, in the next post.