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Is Depression Genetic?

The Biological Approach

Those who adopt the biological approach to the investigation of psychological disorders look for biological factors contributing to the development of psychological problems.  Investigators look for genetic predispositions to disorders, chemical imbalances in the brain, abnormalities in brain structure and infectious transmissions that may have contributed to the existence of a disorder. 

In relation to depression, over time it has been discovered that the prescribing of certain drugs (medicine) has brought about a certain amount of relief from symptoms of depression.  In times past, when less was know about brain functioning, medics were unaware of how these drugs helped alleviate symptoms of depression.  In recent decades, knowledge of brain functioning has become increasingly sophisticated. 

An example of how biological treatment has helped depression

It is now known that information is passed through the brain with the aid of chemicals known as neurotransmitters.  One class of drugs that are prescribed for the treatment of depression (such drugs are known as antidepressants) is monoamine oxidase (MOA) inhibitors.  Monoamine oxidase absorbs three important neurotransmitters, dopamine, noradrenaline, and serotonin (thereby stopping them from working).  Simply speaking, MOA inhibitors block the action of MOA.  This has the effect of increasing the activity of the three aforementioned neurotransmitters.  This appears to have positive effects in relation to the treatment of symptoms of depression. 

The question remains however (and this question is worth bearing in mind whenever considering the part played by biological factors in relation to psychological conditions), if depressed individuals exhibit abnormal levels of certain important neurotransmitters, do these imbalances occur as a result of depression, or do they cause depression, or is there perhaps a mixture of both scenarios operating in relation to depression?

Do our genes cause our psychological condition?

In relation to this question, I have chosen to use schizophrenia as an example of how the study of genetics has helped us understand the relative importance of genes in relation to the development of a psychological condition.  I have chosen to do this because since only around 1% of individuals in the UK suffer from schizophrenia during their lives, as oppose to around 10% or 15% of the UK population who will suffer from clinical depression at some point in their lives.  The relatively low incidence of schizophrenia in the general population makes schizophrenia a better example of how genetics may contribute to the occurance of schizopherenia in twin studies.  The study of genetics has been greatly aided by twin studies. 

Twin Studies of Schizophrenia

Without going into the details of why this is, I will begin by outlining the following:

Identical twins share 100% of their genes: they have an identical gene structure. 

However, non-identical twins are essentially like brothers and sisters born at the same time: they only share 50% of their genes on average, which is the same figure as that for any siblings. 

Gottesman (1991) surveyed 40 studies that had investigated the incidence of schizophrenia amongst twins. 

Identical Twins.  In 48% of pairs where at least one twin had schizophrenia, both twins had the condition whereas in 52% of such pairs, only one of the twins in the pair had the condition. 

Non-identical Twins.  In 17% of non-identical twins pair where at least one twin had schizophrenia, both twins exhibited the condition, whereas in 83% of such pairs, only one twin had the condition. 

Importantly, these figures are similar when twins are brought up apart, i.e. they have been adopted and brought up by different families. 

What is the relevance of these figures?

Since identical twins share 100% of their genes, whereas in non-identical twins around half of either twin's genes are different from their siblings', if genes play a part in bringing about schizophrenia, one might expect to see perhaps double the frequency of schizophrenia in identical twins as compared to the incidence found amongst non-identical twins.  This is because non-identical twins only have half the number of shared genes that identical twins have.  So they are half as likely to inherit the genes associated with schizophrenia.  The aforementioned figures appear to support this hypothesis. 

So is there nothing that can be done if we have the wrong genes?

You’ll notice that of the identical twin pairs where at least one of the pair had schizophrenia, in 52% of such pairs, one of the twins did NOT have schizophrenia.  This demonstrates that even for those twins who inherited the genes contributing to the development of schizophrenia, half of those twins did NOT develop schizophrenia.  It would be wrong, therefore, to say that if you have the genes contributing to schizophrenia, that you are predestined to get the condition.  Other factors must play a part. 

An example of how an environmental factor may contribute to the development of schizophrenia.

Brown and Birley (1968) found that schizophrenia appeared to often manifest in individuals after the occurrence of notable negative or positive life events.  Butzlaff and Hooley (1998) surveyed 22 studies concerning a phenomenon know as ‘high expressed emotion’ in families of those suffering from schizophrenia.  ‘High expressed emotion’ refers to individuals (or in this case families) being highly critical, hostile and overly interfering with the individual concerned.  Butzlaff and Hooley found a significant relationship between the incidence of high expressed emotion in the families of schizophrenics, and schizophrenic relapse in recovering schizophrenics. 

Psychological disorders are caused by a complex interaction between various factors

These findings suggest that schizophrenic symptoms may not develop exclusively due to biological preconditioning, but that there may exist a more complex interaction between biological predisposition, environmental factors, and individual emotional coping strategies. 


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