Hello everyone, I would you’ve having a good week.
Today’s post is related to abnormal and clinical psychology in the form of the biological explanations for Major Depression Disorder.
This is an extract from my book: Abnormal Psychology
Extract from Abnormal Psychology
Chapter 2: Biological explanations
Now, we’re starting to get to what I call proper psychology and my favourite parts of psychology because to this and the next two chapters are some of the most interesting pieces of psychology.
As we start to explore the why and the reasons behind why Major Depressive Disorder develops.
Firstly, we are starting with a biological basis for MDD.
There are two theories for why MDD develops within the biological world. The first is called the serotonin hypothesis.
This theory states that MDD is caused by an imbalance of serotonin in the brain. Serotonin is a neurotransmitter associated with many functions in the body and it’s sometimes referred to as the happiness chemical. As it’s associated with happiness as well as well-being.
There are two pieces of evidence supporting this hypothesis:
· Supported by: certain drugs known to decrease serotonin are known to have depressive side effects.
· Drugs that increase serotonin levels can relieve depression symptoms. Like: Selective Serotonin Reuptake Inhibitors (SSRIs)
However, a major criticism and a problem that I personally have with this theory is that once you take an SSRI the level of serotonin in your blood increases within an hour. However, depressive symptoms don’t decrease until a month later.
Therefore, it begs the question: is it actually the increase in serotonin that cures your depression?
Or does that increase start another bodily process and that process takes a month to finish and that process cures your depression?
I know that it sounds strange or not thought out but if the serotonin hypothesis is true, then surely your depression could be cured within an hour of you taking the SSRI as within that hour the serotonin imbalance is gone or reduced?
The neurogenesis hypothesis:
On the other hand, modern research has been focusing on the Neurogenesis theory of depression. The theory states that depression is the result of a lack of neuron birth in the hippocampus (this is the part of the brain responsible for emotion) and in other places in the brain that is related to serotonin, dopamine and norepinephrine.
In addition, cortisol appears to be the reason for this lack of neurogenesis. (the birth of neurons in the brain) Patients with MDD show a symptom called HPA-axis hyperactivity. This results in the over-secretion of cortisol. (too much cortisol is being released) This leads to reduced levels of serotonin as well as other neurotransmitters in the brain, including dopamine. This has been linked to depression. Demonstrating how complex the brain’s chemistry is, and why the treatment for depression remains problematic. As we will explore later.
There are a few pieces of evidence that support this theory as well.
· Depressed people tend to have smaller hippocampi that the rest of the general population.
· Stress hormones are increased in MDD patients and this appears to stop neurogenesis in the hippocampus, as shown in rodents and other primates.
· Finally, anti-depressants can increase neurogenesis in the hippocampus in rodents.
Caspi et al (2003):
The 5-HTT gene is responsible or the production of serotonin.
A longitudinal study of 1,037 children from New Zealand. Divided into three groups: people with two short alleles of the 5-HTT gene, one long and short alleles, two long alleles.
They were assessed from the age of 3 to 25.
A life history calendar was used to assess stressful life events.
Subjects were assessed for depression with an interview and information from someone who knew them well.
Results showed that there were no differences in the number of stressful life events.
People with two short alleles managed life events with more depressive symptoms.
The study effective looks at the genetic argument for the serotonin hypothesis.
Nonetheless, this study does have ethical concerns. For example, the distress that knowing that you’re genetically more likely to develop depression.
Therefore, the costs and benefits of research must always be calculated before research is done.
Kendler et al (2006):
Over 42,000 twins were recruited for the study across a 60-year age span for the purpose of generational comparison.
They used a computer-assisted telephone interview that was conducted using DSM-4 criteria for MDD.
Informed consent was got before the interview. Trained interviewers were used with a lot of medical training to collect data.
The aim was to reach both pairs within a month.
Results showed prior studies got similar results. Heritability of depression is 38% on average.
Didn’t differ very much across the generations.
No evidence was found that the shared environment was a factor in developing depression.
In conclusion, major depression is moderately inherited.
The study is highly reliability as a number of studies have supported its findings that depression is about 37% inherited.
However, this study is open to population fallacy; were your sample does actually represent the general population; because most of the population aren’t twins.
The serotonin hypothesis states the depression is caused by a serotonin imbalance in the brain.
The neurogenesis theory states that depression is caused by a lack of neuron birth in the brain.
Capsi et al (2003) shows that there is a clear genetic basis for depression.
Kendler et al (2006) shows that depression is moderately inherited.
I hope that you found today’s blog post interesting and if you want to find out about the causes and treatment of depression. Please check out my Abnormal Psychology book.
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Have a great week everyone!