Models of Understanding Depressive and Bipolar Disorders

Welcome back to module 2 mood disorders. This is Lecture 3. In this lecture, we're going to talk about the prevailing models used to understand

depressive and bipolar disorders. Think back to module 1, when we spent a

great deal of time talking about the major models of psychological abnormality. The dominant model for

understanding both depressive and bipolar disorders is the biological model. Let's begin by considering

depressive disorders. There is a large research base suggesting

that depression is caused by low levels of two specific neurotransmitters,

serotonin and norepinephrine. This connection was discovered by accident

in the 1950s when scientists observed that certain medications used to

treat high blood pressure caused depressive symptoms in

the people who took them. These medications,

in addition to lowering blood pressure, suppressed serotonin and

norepinephrine activity in the brain. This finding led to the theory that

depressive disorders are associated with low serotonin and

low epinephrine activity in the brain. And it launched research into the

development of medications that increase serotonin and norepinephrine activity

in the brains of depressed people. Not all research into the biological

basis of depression has investigated neurotransmitter activity. There's been a great deal of research

into the genetic basis of depression. This research has investigated the extent

to which depression can be passed from parent to child. Studies have shown that depression

does in fact run in families. Studies of identical and fraternal twins have also demonstrated

a strong genetic component. If one identical twin has

a depressive disorder, there's a 38% chance the other

twin will develop it too. Among fraternal twins if

one twin has the disorder, the other twin has a 20%

chance of developing it. Let's turn now to the biological

model of bipolar disorders. Scientific research into the biological

basis of bipolar disorders has also investigated the roles played by

neurotransmitters and genetic factors. The findings are very interesting,

like people with depression, people with bipolar disorder have

also been found to have low serotonin activity in their brains. However, unlike depression,

bipolar disorder has been found to be associated with high levels

of norepinephrine activity. These findings have led researchers to

believe that the interactions between these two neurotransmitters influence

whether a person will experience uni polar depressive disorder or

bipolar disorder. And what of the research into

the genetic basis of bipolar disorder? As you may recall from the last lecture, bipolar disorder effects between 1% and

2.6% of the world's population. In families however,

the prevalence is very different. If an identical twin has bipolar disorder, there is a 40% to a 70% chance

the other twin will develop it too. Among fraternal twins and non twin

siblings, if one sibling has the illness, the other siblings each have a 5%

to 10% chance of developing it. Clearly, there is strong evidence for

the heritability of bipolar disorder. Are there any other models that are in

wide use to understand these disorders? For bipolar illness, the answer's no. A biological model is the only

accepted framework for understanding the origins

of this disorder. The same cannot be said for

depression however. Several other models are used to

understand depressive disorders, the most prevalent of which is

the cognitive behavioral model. Let's consider it briefly. As you may recall from the first module,

the cognitive behavioral model asserts that psychological abnormality occurs

when a person's thought patterns become significantly distorted and

impact both emotions and behavior. Aaron Beck is widely known for his

cognitive behavioral theory of depression. According to this theory, depressed people have identifiable

patterns of negative thinking. Beck developed the concept

of the cognitive triad, which is the notion that depressed

people interpret their life experiences, themselves and their futures and

consistently negative ways. And this is what causes the depression. Beck asserted, the cognitive triad leads

depressed people to make errors and thinking which are logical errors

that worsen their depression. For example, a depressed person with a

negative view of their future may receive a poor grade on an exam and think I'm

not smart enough to pass this class, I'm going to be a failure forever. I may as well give up. In fact, it is not logical to assume

future failure based upon one poor grade. Beck's theory also emphasizes

automatic thoughts, which our beliefs about the self world and

future that are so fundamental and so deeply ingrained that we do not

notice them, they're automatic. Beck theorized that depressed people

demonstrate a pattern of deeply negative automatic thoughts. For example, I will never succeed

no matter how hard I try or no one would ever want to be with me or

I'm not as smart as other people. Another well known cognitive behavioral

theory of depression was developed by martin Seligman and

based in early animal learning studies. This is called the learned

helplessness model. The learned helplessness model asserts

that a feeling of helplessness is fundamental to the development and

experience of depression. If a person has repeated

experiences in which they try and fail to effect change in themselves,

their external world or their personal future,

they become depressed. There's been a great deal of research

conducted into the validity of a CBT model of depression and there's an impressive

body of data supporting it. The question of cause and effect remains. However, does a pattern of negative

thinking cause depression or does depression lead to

a pattern of negative thinking? In our next lecture, will take a look

at treatment interventions for mood disorders.