Biological Explanations of Depression

People with a relative diagnosed with bipolar disorder are 3 times more likely to be diagnosed with bipolar themselves.

Family Studies

Gershon (1980)

Reviewed 10 family studies and found that the rate of depressive disorder in first degree relatives ranged between 7% and 30%,, which is considerably higher than the general population. While this is a small percentage, it is statisically significant.

The younger someone is when they are diagnosed, the more likely it is that their relatives will also have depressive episodes.

Weissman et al (1984)

Relatives of people diagnosed before 20 were 8x more likely to be diagnosed with depression. This could be due to envrionmental factors, eg. parents could feel guilt for children who have depression.

Twin Studies

McGuffin et al (1996)

Found a 46% concordance rate in MZ twins and a 20% concordance rate with DZ twins with no evidence on the effect of shared environment.

Bierut et al (1999)

Used 2,662 twin pairs in Australia. They found a concordance rate between 36% and 44% in MZ twins. They claimed that environmental factors played a larger role. This study has a large sample size, but shows cultural bias.

Adoption Studies

Wender et al (1986)

Biological relatives are 8x more likely to have depression than adoptive relatives. This is the same result as Weissman's study which increases the reliability of both studies.

• Hard to separate environmental factors from genetic factors.
  • In most cases, those who are diagnosed same the same environment meaning it could be learned behaviours, this makes the biological approach reductionist. 
• There is a higher concordance rate for MZ twins, but it is only about 50% meaning there is other factors besides genetics.
• Not all aspects of depression are genetic, the 'negative' aspects of depression such as weight change and sleep disturbances are influenced by genetics, but the number of depressive episodes are linked to life events.
  • Kendler et al (1992), the way depression manifests may be genetics but the causation of depression is caused by external factors.
  • This is the diathesis-stress model where there are pre-disposing risk factors that are activated by stressful life events.
• If genetics play a part in depression, no one knows what mechanisms and genes code for depression so it is impossible to know how they code for biological structures and functions that produce depressive symptoms.

Carroll (1982)

High levels of cortisol have been found in those suffering from depression and techniques that reduce cortisol secretion are useful in depression. This suggests there is overactivtity in the HPAC pathway.

Nemeroff et al (1992)

There is a marked adrenal gland enlargement in those suffering from depression, which is not evident in those without depression. This suggests the adrenal gland has been overstimulated. 

Premenstrual Dysphoric Depression (not recognised disorder)

Depression can occur in the week prior to menstruation. This affects about 25% of women although most cases are not of a diagnosable severity.

Dalton (1964)

It is possible that this ia due to an oestrogen-progesterone imbalance where oestrogen levels are too high and progesterone levels are too low.

Post-natal depression (recognised disorder)

In cases of severe post-natal depression, psychotic episodes can occur with fantasies and loss of contact with reality. Sometimes this can result in harm or even death of the newborn.

Oestrogen and progesterone increase greatly during pregnancy and fall rapidly after birth which could explain post-natal depression.

Cooper (1988)

Found little difference between the number of women suffering from depression immediately after childbirth and a control group of non-pregnant women of a similar age. This is a bad control group, a better control group would be a group of non-depressed new mothers.

Menopausal Depression

During menopause, oestrogen levels drop. Hormone replacement therapy is useful in treating most cases of menopausal depression.

Abnormal levels and regulation of cortisol in people with depression suggests a link to the stress-response system. However, not everyone with depression has these irregularities and they are found in people with other mental disorders.

Clare (1985)

Research evidence into hormone imbalance theories of depression is inconclusive.

Females are more likely to be diagnosed with depression; female hormones could be the reason for this difference. But only a small number of women who suffer from depression have links to female only hormones so the difference can't be entirely contributed to hormones.

Seasonal Affective Disorder (SAD)

Rosenthal et al (1984)

• Some people have depressive eiposdes that start towards the end of Autumn and last until Spring. 
• One explanation for SAD is related to the change in daylight hours; the individual is not exposed to enough natural light, or they are exposed to too much artifical light.
• Special light bulbs can help people suffering from SAD.

Melatonin is released during dark conditions (winter), it has the effect of slowing us down and making us more fatigued. People with SAD Could be more sensitive to melatonin. This is supported by research and is very reliable.

Serotonin and noradrenaline

Lam et al (1996) found that antidepressants with serotonin are effective in treating SAD, but those with noradrenaline are not. He concluded SAD could be related to serotonergic mechanisms and this relationship is not casual as the depression returns when the treatment ceases.

Monoamine-oxidase inhibitors (MAOIs)

These block the actions of enzymes that break down noradrenaline and serotonin. This increased the availability of those neurotransmitters in the system. 

Tricycles (TCAs)

Most commonly used is Tofranil and works by blocking the reuptake of serotonin and noradrenaline. They do not start working for 10 days as they also slow down activity in nerve cells that use serotonin and noradrenaline are used in so less of them are released. It takes the nerve cells about 10 days to adapt to the drugs and release normal levels of the neurotransmitters.

Montomery et al (1993)

You  must continue to take the drugs for a number of months after the symptoms have gone. About 50% of users relapse if they stop taking the drug too soon after symtoms have vanished.

Selective Serotonin Re-uptake Inhibitors (SSRIs)

This includes Prozac and works by inhibiting the re-uptake of serotonin. A new type of SSRIs work also work noradrenaline and are called SNRIs.

Sir et al (2005), these drugs are seen as more effective in treating depression, although they have more severe side effects.

Users should not stop taking these drugs abruptly or they risk symptoms such as dizziness, nausea, lethargy and headaches.

Taking drugs only treats the symptoms of depression, rather than the underlying causes. This means they only provide short term relief.

It is more useful to combine pyschological and biological treatments rather than just one type, eg. CBT and drugs is the most effective treatment for depression.

Side effects of MAOIs and TCAs:

• MAOIs can have serious side effects. Patients have to stick to strict diet regimes and avoid food/medication that could interfere with the drug to produce a potentionally fatal reaction.
• Julien (2005), a recently introduced MAOI in the form of a skin patch allows for slow continuous absorption of the drug and is less likely to produce dangerous food reactions.
• Jarrett et al (1999), MAOIs are much more effective at treating depression than TCAs.
• TCAs are prescribed more often as they are milder and cause few adverse effects, although their most serious possible side effect is cardiac problems.

Prien (1988) and Gitlin (2002), Anti-depressants have been tested in trials with placebos and found to be effective in reducing symptoms in around 65%-75% of cases compared to about 33% of placebo cases.

Prozac (SSRI) is the most frequently prescribed anti-depressant drug. It was known as a 'wonder drug' when it was first introduced as it has less side effects and is less dangerous in terms of an overdose compared to TCAs. 

Steiner (1991), it has connotations with violence and suicide as a study was released reporting that increased violence and suicidal behaviour were a side effect of the drug. 

Geoffrey (1991) A notorious case incolving Prozac is the case of Joseph Wesbecker in America in 1991. He shot 20 people at his former workplace beofre shooting himself.

Other studies have concluded that any very small risk of suicide or violent behaviour should be weighed against the benefits of taking SSRIs to reduce the symptoms of depression.

Orginal procedure included passing very high currents of electricity through both hemisphere of the brain (bi-lateral). It was known to lead to severe memory loss, speech disorders and irreversible brain damage. Its use declined with the introduction of drugs in the 1950s. It was seen as barbaric because of the serious side effects. It was soon realised that drugs weren't as effective so it was brought back into use.

Current procedure:

• Given muscle relaxant and short-acting anesthetic before the treatment
• 70-130 volts are passed through the brain for 0.5 seconds
• Can be unilateral or bilateral
• Convulsion similar to a seizure occurs for about a minute
• Patient remembers nothing about the treatment afterwards
• Most patients are treated 2-3 times a week for 3-6 weeks

It is not understood how ECT works in reducing symptoms of depression. Heather (1976), an analogy has been given to compare ECT with banging the side of a TV to make it work.

• It is likely that ECT increases the amount of available serotonin or noradrenaline in the brain, but as it is such an invasive technique, it is difficult to isolate the element that brings about the change.

It is effective in reducing depression in patients where other treatments have failed. Richard and Lyness (2006), 60-70% of patients who undergo ECT will witness a decrease of depressive symptoms. Sackeim et al (2001), however, a large proportion of these patients will become depressed again the following year.

It has a history of abuse as it was used as punishment and a method of control in mental hospitals.

Comer (2007), applying electrical currents to the brain is frightening and is a forceful method of intervention.

It requires consent from either the patient or a close relative.

Mental Health Act (2007), should only be administered if anti-depressant drugs have no effect and there is a risk the patient will commit suicide. It works more rapidly than drugs or psychological therapies, which is why it is used for people who are a suicide risk.

When it was first introduced, possible side effects included bone fractures, memory loss, language impairments, eg. There are still concerns that ECT can impair memory, especially if bi-lateral treatment is used. 

There are no dectable changes in brain structures with newer procedures and new types of ECT are reducing side effects, for example Transcranial Magnetic Stimulation.

Involves stimulating brain cells using magnetic fields, but without direct contact.

It is painless and does not use anestheics, electrodes or surgery.

It is not clear how TMS works but it is thought to increase the availability of serotonin and other neurotransmitters within the brain. 

Schulze-Rauschenbach et al (2050), compared TMS and ECT in the treatment of major depressiec disorder and found 44% of TMS patients showed a significant improvement comapared to 46% of ECT patients. But, people in the ECT group showed some signs of memory impairements after treatment, whereas those in the TMS group did not. This suggests that TMS is a safer alternative to ECT.