In this series, I dig a little deeper into the meaning of psychological terms. This week’s term is diathesis-stress model.
This week’s term may sound a bit obscure, but bear with me, because it’s actually quite relevant. A diathesis-stress model, also known as stress-vulnerability model, is used to explain the course of a mental disorder based on the interaction between biological vulnerability and the stress caused by the environment and life experience. The concept was first described by psychologist Marvin Zuckerman in his 1999 book Vulnerability to Psychopathology.
Diathesis meets stress
This model recognizes the interplay between underlying vulnerability (i.e. diathesis) that predisposes someone to illness and environmental stressors. There’s a certain threshold or critical level at which a psychological disorder will develop.
Reaching that threshold requires both a stressor and a diathesis, with the proportions depending on the individual. Someone with greater vulnerability would require a much less significant stressor to reach that threshold than someone with minimal vulnerability. This provides an explanation for why two people might be exposed to the same situational stressors yet respond quite differently. It also means there’s no single root cause; there’s a combination of factors.
Vulnerabilities
Because vulnerability is latent until a disorder develops, it’s difficult to measure. Vulnerability can involve both biological and psychological factors, including genetics, biology, physiology, cognitive styles, and personality. Some disorders may have a window of vulnerability, a period of life during which environmental stressors are most likely to activate latent biological vulnerability.
Stressors
Environmental stressors can be acute or chronic. A single stressful event may not be enough to trigger illness, but the accumulation of multiple stressful life events may trigger activation of the latent vulnerability. The accumulation of stressors in combination with vulnerability doesn’t just have an additive effect, it has a multiplicative effect, so people can become essentially powder kegs ready to blow.
Applying the model
Diathesis-stress models have been used to describe a number of mental disorders, including depression and schizophrenia. It’s also part of dialectical behaviour therapy (DBT) developer Marsha Linehan’s biosocial model of borderline personality disorder.
I think this is a really interesting way of looking at the development of mental illness. My first episode of depression came after a significant interpersonal conflict with my ex-boyfriend. He had remained my best friend after I broke up with him, right up until he started dating someone and decided we shouldn’t be friends anymore. It was a significant life event, for sure, but it’s far from the biggest life stressor I’ve had, and it certainly didn’t seem bad enough in proportion to how sick I was.
That happened in my late 20s, and there was no clear indication of depression before that. From a diathesis-stress perspective, that would be latent vulnerability. That stressor at that time was enough to activate that latent vulnerability. That makes a lot of sense, especially since the prominent symptoms in my illness tend to be more biological.
How do you think this model fits with your own illness?
References
- Colodro-Conde, L., Couvy-Duchesne, B., Zhu, G., et al. (2018). A direct test of the diathesis-stress model for depression. Molecular Psychiatry, 23(7), 1590-1596.
- OpenTextBC: Psychology: Perspectives on Psychological Disorders
- Wikipedia: Diathesis-stress model
The Psychology Corner has an overview of terms covered in the What Is… series, along with a collection of scientifically validated psychological tests.
Ashley L. Peterson
BScPharm BSN MPN
Ashley is a former mental health nurse and pharmacist and the author of four books.
This makes a lot of sense. I’d been thinking along those lines about myself. I think my autism makes me vulnerable, and some difficult childhood events are in there too as long-term stressors, but the actual triggering events for my depression were fairly trivial and my depression seemed really out of proportion; later episodes of depression didn’t even have any obvious triggers.
It’s very interesting to think in my own case. 4 out of 5 immediate family members have developed a mental illness. I wonder why that is? And why only 1 did not develop an illness.
Fascinating
My own illness is complex. I found this post interesting though, because it pin-points a possible CAUSE. I have had various ‘stressors’ (trauma) since I was four years old. I was in care as a child with a couple who had their own massive problems who damaged my self-esteem and psyche further. There is a history of mental illnesses in my biologic family, some diagnosed, others not. Depression is intertwined with all of them to a degree. My own ‘breaking’ point I believe was when puberty hit. Perhaps the traumas suffered previously were enough to make me vulnerable to the hormonal changes that puberty brings. Perhaps it was biology. Or it was my broken self esteem coupled with the angst that teenagers often have, that provoked a home environment that further triggered the mental illness.
I have two siblings, neither of which developed the same (or any at all) mental illness issues that I did. But some of their children have a milder form of the familial depression and all of one sibling’s children have had therapy.
You have given me some things to consider when discussing my problems NOW (forty five years after the onset). Thanks Ashleyleia!
It’s such an interesting topic, and so incredibly complex I wonder if we’ll ever have a full understanding.
It fits very well with my illness. Strong genetic tendency toward depression (my mother and 2 of her 3 sisters, me, my sister and my daughter) plus some earlier life stresses which contributed to vulnerability and less flexible coping strategies, but it wasn’t until the major life stress of having a baby which is when the cracks really started to show.
There’s a lot of research from the Dunedin Study (a lifelong cohort study of 1000 people born in Dunedin in one particular year which is a prolific generator of academic papers) which supports this model. There was a great documentary made about this study and its implications for public provision and funding of support for families with small children and early intervention programs (unfortunately it was geo-blocked outside of NZ and Australia and they haven’t made a DVD available for sale 😕 otherwise I’d provide a link).
Sounds very interesting! I found a Canadian network site that streams it – I’ll watch it this weekend!