In this video I describe the diathesis-stress model. This model suggests that development of mental illness can be explained by two main factors – a genetic predisposition (diathesis) and environment (stress). Individuals vary for both of these factors and these variations can help us to understand why some people develop a mental illness and others don’t. Next I discuss how this model is an oversimplification because it ignores the potential interaction between genes and environment and how experiences may alter gene expression. This can be seen in a study by Caspi et al (2003) which found a relationship between versions of a serotonin transporter gene and depression, but only when accompanied by stressful life events.
Caspi et al (2003) – Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene http://sci-hub.tw/10.1126/science.1083968
Video Transcript
Hi, I’m Michael Corayer and this is Psych Exam Review. In this video, we’re going to talk about the diathesis stress model and this is a model that helps us to answer the question of what the role of genes is in the development of mental illness. What the diathesis stress model proposes is that there are two main factors, a diathesis and stress.
So the diathesis refers to a genetic predisposition for a particular mental illness and the stress refers to the environmental and psychological events that the individual experiences. And so it’s the combination of this predisposition and stress that leads to the expression, or not, of a particular mental illness. And so what this diathesis stress model helps us to understand is why it is that some individuals might suffer from particular mental illness while others don’t.
The idea is that they’ll have different levels of predisposition for that illness, but also different levels of environmental stress that might influence the expression of that illness. So here’s a diagram that I’ve made to help explain this diathesis stress model. And what you can see here is we have this idea of a hypothetical threshold for a particular disorder. So this is not an actual threshold but the idea is that if you cross this hypothetical threshold, then you develop the disorder. And if you don’t, then you don’t develop the disorder. So what we can see with individuals 1 and 2 here on this chart is that they have differing predispositions for whatever disorder might be represented here. And so they have different predispositions and in the face of the same amount of environmental stress, so the gray section here is the stress, so these two individuals have the same environmental stress, but because they have different predispositions, only individual 2 will develop this mental illness. Individual 1 will not cross this hypothetical threshold and therefore does not develop the disorder.
Now if we look at individuals 3 and 4 on this chart, we see that these two individuals have the same predisposition. So maybe these are monozygotic twins who share their genes. And so they have the same predisposition for a particular illness, but they face different amounts of environmental stress. So individual 3 here is experiencing more stress in this greater amount of stress just pushes this person over the hypothetical threshold. And so individual 3 would develop this mental illness whereas individual 4 with the same genetic previous position has a lower amount of stress and as a result doesn’t develop the mental illness. So this is a way of trying to understand why it is that some people might develop an illness while other people don’t. And this could be due to either differences in the predisposition or differences in the levels of environmental stress that they experience.
Now it’s important to remember that this is a model and like all models, it’s an oversimplification and the assumption here is that your predisposition and your environmental stress, that these are fixed entities. But that’s not necessarily the case because it might be the case that your predisposition actually changes depending on your experiences. So there could be environmental effects on gene expression. So even though your genes aren’t necessarily changing, your gene expression could change as a result of the environment.
And this can be demonstrated in a study by Avshalom Caspi and colleagues in 2003. And this was a longitudinal study that looked at young adults in New Zealand over the course of five years. And what Caspi and colleagues were looking at were different versions of a promoter section of a serotonin transporter gene, 5 HTT gene, and the influence in this gene on responsiveness to stress. And so what they found was that particular versions of this gene were associated with an increased risk of depressive symptoms and an increased risk of diagnosis of depression. And so they looked at three different versions of this gene. So you can have two long alleles, you can have one short and one long allele, or you can have two short alleles for this particular gene associated with this serotonin transporter.
What they found was that if people had the short allele, this was associated with an increased risk of diagnosis of depression and with depressive symptoms. But it was only associated with this increased risk when the short allele was accompanied by stressful life events. So what this means is that if you have the short allele either short and long or too short, which about 43% of people have, then this only increases your risk of depression if you also have the stressful life events So here we can see it’s an interaction between the genetic predisposition and the environment and the person’s life experiences, and that these together influence each other. They interact and this can change a person’s risk for the development of particular disorder. In this case depression and I’ll post a link to the paper so you can read in more detail in the video description box. OK, I hope you found this helpful. If so, please like the video and subscribe to the channel for more. Thanks for watching!
