Ever had that experience where you don’t agree with someone simply because you’re
coming at the problem from a different angle? You might even both be right about certain
aspects.
This is a situation that happens in science all the time. In this lecture and in the next one,
we’re going to take a look at two very different models of depression, both of which have a
lot of empirical support behind them. You’ll see that these two theories focus on very
different components of emotion, one highlights the role of cognition whereas the other
highlights the role of behaviour and learning. Both of them mention stimuli and the
environments that people find themselves in, but the role they see stimuli playing is quite
different.
Let’s start with the cognitive model of depression.
[intro]
The cognitive model of depression obviously focuses on cognitive components of emotions,
but the stimuli also feature highly too.
The original authors of this model, Aaron Beck and David Clark have also begun to integrate
physiological aspects into this model but they acknowledge that this integration is really in
its early stages. At the moment, their proposed relationships between cognitions and
physiology are hypotheses waiting to be tested!
At the heart of the cognitive model are dysfunctional attitudes that the authors refer to as
schemas. In this model, schemas become activated when a person experiences a negative
event in their life. The activated schema then starts a chain of negative thought patterns
that results in the symptoms of depression.
Ok, so what is a schema? Well, according to the authors, schemas are an abstract cognitive
construct that assign meaning to stimuli. They’re a bit like our conceptual understanding of
different things. They also contain our beliefs and attitudes towards that thing. So, for
instance, your self-schema contains all the knowledge and understanding that you have
about yourself as well as the beliefs and attitudes that you hold about yourself.
But sometimes our schemas are dysfunctional. They either may not accurately represent the
way things are. Like, part of my self-schema might be that I’m short, when in fact I’m
actually bang on average height. This would be an inaccuracy in my self-schema.
Dysfunctional schemas may also be maladaptive or just not very helpful. For example, if
someone held the belief “failure is terrible and absolute” then, if they ever experienced any
minor failure in their lives, the meaning that that schema might prompt the person to
extract from that situation could be that they are a failure as a person.
Beck and Clark argue that these negative and dysfunctional schemas lead people to pretty
black and white negative beliefs about themselves, the world and the future. This is
sometimes referred to as Beck’s cognitive triad.
One of the interesting things about schemas is that, when they’re activated, they change
how we perceive the world. They create what the authors term a “systematic cognitive
bias”. Activated negative schemas are a bit like the black cloud hanging over you that makes
everything around you seem dark. When activated, they literally change the way that we
perceive the world around us. They do this in a number of different ways.
It can affect which stimuli we pay attention to in the outside world. For example, people
with depression respond faster to negative stimuli like sad faces and sad words than they do
to happy stimuli. The sad stimuli captures their attention much, much faster. This is called
attention bias. Some other research suggests that the interpretation of stimuli is also
negatively biased when people are experiencing symptoms of depression. For example, one
study showed people with and without a history of depression pictures of neutral faces
[image]. These were images where people had no overt expression on their faces but
people with a history of depression interpreted these faces as being sad. This is called …???
And the negativity really is all encompassing. Even the valence of people’s current mood
influences the valence of memories they recall. This is called memory bias.
So, if schemas can affect us in such a negative way, then why do we have schemas at all?
Well, when the schemas are formed so that they accurately represent the world around us,
then schemas can be pretty useful. They allow us to do what’s known as automatic
appraisals. These are mental shortcuts that save cognitive resources and allow us to make
quick judgements. This is necessary in a threatening situation so that we can respond
rapidly. Without these automatic appraisals, we’d have to rely on a different system that
Beck and Clark refer to as the Cognitive control system. Where the automatic appraisal
system is quite reflexive, the cognitive control system is slower and more evaluative. It
allows us to reappraise situations, think about and weigh up alternatives. If you’re familiar
with some psychology terms the authors consider that problem solving and executive
functions are a part of this system. But the cognitive control system is much more mentally
demanding and effortful. It’s also suppressed during a depressive episode.
So, how do negative schemas get formed? People with moderate to severe depression are
more likely to have experienced significant traumatic events early in their life, like the loss
of a parent. According to Beck and Clark, the effect of these early negative experiences is
the creation of enduring attitudes and those attitudes create feelings like helplessness and
hopelessness if similar types of experiences ever happened again. And indeed the authors
found evidence that those events like early loss made the person more vulnerable to
depression if they then experienced another loss later on in their life. They call this effect
Cognitive vulnerability and it’s been seen in people of all ages from children to adolescents
to adults.
More recent research suggests that in vulnerable individuals, less severe events can also
trigger depressive episodes too. In addition, the authors found that this cognitive
vulnerability appears to be progressive in the sense that progressively less aversive events
can trigger subsequent episodes.
I mentioned right at the start of this lecture that the authors recognise that cognitions are
not an island all on their very own. They obviously interact with physiological and biological
components too. So, how do they do this?
Well, one way that the authors propose that negative schemas are formed is when a person
has a genetic disposition that causes certain brain structures like the amygdala to become
hyperactive. The amygdala is a pair of almond shaped structures deep in the brain and it
plays a really big role in emotions like sadness. Another biological predisposition that people
can inherit is an underactive prefrontal cortex. Now, remember that the prefrontal cortex is
involved in those cognitive control activities like weighing up different alternatives and
reappraisal. Beck and Clark argue that an inherited tendency for the prefrontal cortex to be
a bit sluggish is that the person experiences “diminished cognitive appraisal”.
An overactive stress response can also play a really big role in depression and the authors
speculate that it may also contribute to the formation of dysfunctional schemas. Some
people will have a inherited predisposition to release lots of stress hormones when they’re
in a challenging situation. This is called hypercortisolemia. Now, we won’t get into the fine
details because they’re really complex, but when the body is flooded with too much cortisol
over and over again, it can disrupt other chemicals in the body including serotonin which we
know plays a role in regulating our moods.
Serotonin levels can also be disrupted in a more roundabout way too. What many people
don’t realise is that serotonin gets transported on little structures called serotonin
transporters. Now there are different variants of the gene that codes for these serotonin
transporters. Some of the variants code for long serotonin transporters and another variant
of the gene codes for short serotonin transporters.
Think of these transporters a bit like trucks. Some people have a whole fleet of just long
trucks, some people have a mixed fleet of long and short trucks and other people have only
got short trucks. I want you to pause the video and write down what you think the
implications of having a whole fleet of long trucks, so all long serotonin transporters, versus
only having access to short trucks. How would this affect serotonin transportation and in
turn, how might that affect someone’s mood? Pause the presentation and jot down some
ideas.
So, as you might have guessed, just like a long truck, the long serotonin transporters can
carry much, much more serotonin. Having access to more serotonin means that people with
two copies of the long serotonin transporter allele gives them some emotional protection if
they ever experienced a serious adverse event in their lives. On the other hand, people with
two copies of the short serotonin transporter allele are much more likely to experience a
major depressive episode after a significant life stressor.
What’s interesting too is that, even in children who have only short serotonin transporters,
even when they’re not clinically depressed, they are more likely to evaluate themselves
negatively when their mood is low.
Ok so how does the activation of a dysfunctional schema actually translate to a major
depressive episode?
Well, according to this model, like we’ve already said, the activated schemas influence the
appraisal of stressful life events. And those life events can be big or small. And I think that
we as science communicators can often focus so much on those big life stressors like losing
a loved one or losing a job, that we tend to gloss over the effect that smaller everyday
stressors plays. When Clark and Beck reviewed the literature they found that “the daily
negative appraisals of daily stressors predicted daily depressive symptoms.” What they’re
saying is that people who appraise everyday stressors in a negative way are more likely to
feel symptoms like low mood more often. And what’s more, the tendency to react
negatively to everyday stressors is strongly associated with an increased risk of depression.
So how does this happen?
Well, according to the model, the negative life event or lots of smaller events, activates the
dysfunctional schemas. Once the schema has been activated, it skews the person’s
information processing. Their attention, memory and interpretation of ambiguous events is
all negative too, so the person’s lived experience becomes negatively skewed as well. This
global cognitive bias towards negativity leads to those recognizable symptoms of depression
like sadness, hopelessness and withdrawing from society. This in turn leads to negative
evaluations about what all this means. The authors use example phrases like “My poor
functioning is a burden on my family” and “My loss of motivation shows how lazy I am.”
One of the side effects of repeated activation of depressive schemas is that they become
hypersensitive so, increasingly less stressful events can trigger the depressive episode. This
is because repeated activation of those maladaptive schemas makes the maladaptive
processing more ingrained and easily triggered. It’s almost like the pessimism starts
becoming the person’s default setting.
Now, just like every other model that we’ve discussed so far, Beck and Clark acknowledge
that this model is not all encompassing. It’s not the full story. Some of the future work
they’d like to see to develop their model is for other scientists to integrate the information
that has been gathered from areas such as genetics, neurosciences and social psychology.
This integration of established scientific knowledge is, in my mind at least, how science
makes its biggest leaps.
Thanks for watching! In this lecture we talked about the cognitive model of depression. We
discussed how Beck and Clark conceptualise depression with maladaptive schemas at the
heart. They outline how these schemas influence how we appraise ourselves and the world
around us and how this negative appraisal can lead to the symptoms characteristic of a
major depressive episode. We also covered how the repeated activation of negative
schemas can make them hypersensitive to future activation and could explain the recurrent
depressive episodes seen in major depressive disorder.
In the next lecture we’ll talk about one aspect that Beck and Clark virtually neglect in all of
their discussions; behaviour. Catch you next time when we talk about the Behavioural
Activation model of depression.