Biological Approach To Depression Essay
The Biological Approach to Unipolar Depression. Katie Evans
Abnormal behaviour was once thought to be caused by supernatural possession; this demonological model of abnormality was especially popular in the Middle Ages. It was not until the 18th century that psychologists began to argue that this behaviour should be treated as an illness and medical techniques could be used to treat it; and so emerged the medical model of abnormality. (Gross & McIlveen, 1996)1 The medical model of abnormal psychology treats mental disorders in the same way as a physical illness. Practitioners of this model believe mental illness to have a physical cause, therefore they treat mental disorders with somatic intervention such as medication, electroconvulsive therapy or in extreme cases, psychosurgery. It is largely believed that biological events have behavioural consequences and behavioural events have biological consequences. (Wickens, 2005)2
McLeod (2007)3 describes the assumptions of biological psychology:
Psychology should be seen as a science and should be studied scientifically. …show more content…
Illness is in the patient’s nature, not caused by nurturing. Behaviour can be explained largely by biology such as genes and hormones; mental disorders have a physical cause relating to the structure or functioning of the brain. Behaviours such as phobias, hallucinations or suicide attempts are symptoms of mental illness.
Genes evolve to adapt behaviour to the environment and as such behaviour will have an evolutionary purpose.
The International Classification of Diseases (ICD) is a diagnostic tool and framework published by the World Health Organisation (WHO) to classify diseases and health issues; it is used to analyse the general health of the population. (World Health Organisation, 2014)4 The Diagnostic and Statistical Manual of Mental Disorders (DSM) is a publication from the American Psychiatric Association (APA) containing the criteria and classification of mental disorders and is most commonly used for diagnostic and research purposes. (American Psychiatric Association, 2014)5 While the DSM covers mental disorders, the ICD contains information regarding all diseases and health problems; both are used throughout the world for the diagnosis of unipolar depression.
Unipolar depression is a severe, typically prolonged and fundamental disturbance of mood and emotions, presenting as feelings of despondency and dejection. It is defined by the ICD-10 as a mood (affective) disorder and as a mood disorder by the DSM-IV. Low amounts of monoamine neurotransmitters are apparent in depressed patients, particularly serotonin and norepinephrine; biological psychologists recommend chemotherapy in the first instance, to correct this.
Gross & McIlveen (1996)6 identify the symptoms of unipolar depression as a persistent low mood lasting at least two weeks plus any five of the following:
Poor appetite / weight loss
Increased appetite / weight gain
Difficulty sleeping or sleeping longer than usual
Loss of energy or tiredness that affects ability to make simple decisions
Slowing down or agitation
Loss of interest or pleasure in activities
Feelings of self-reproach
Excessive or inappropriate guilt
Diminished ability to concentrate
Recurrent thoughts of death or suicide
Biological psychologists argue there are several causes for depression, one such explanation is dysfunctional monoamines. The Biogenic Amine Hypothesis states that depression is associated with a functional deficit of monoamine neurotransmitters, predominantly noradrenaline and serotonin. Support for this theory came when MAOI’s were found to alleviate symptoms of depression and when depression was found to be a side effect of taking Reserpine, an antihypertensive drug which depletes levels of noradrenaline. However, as antidepressants have further effects on the brain beyond the alteration of neurotransmitters, we cannot conclude that depression is caused purely by neurotransmitter dysfunction; with this is mind, the Biogenic Amine Hypothesis is considered too simplistic. (Merrill Academy, 2012)7
Another cause argued biological psychologists is genetics. Gershon (1990)8 reviewed family studies and found that rates of unipolar depression in first degree relatives were 7-30%. The genetic argument is supported by twin studies; Allen (1976)9 has found the concordance rate of monozygotic twins to be 40% and 11% in dizygotic twins. Lastly, Wender et al (1986) 10 found that the biological parents of an adopted individual with depression were eight times more likely to suffer from the disorder than the adoptive parents providing strong evidence of a genetic link.
The assumption that behaviour is caused by faulty genes and the assumption that mental disorders have a physical cause has caused the heavy use of antidepressants as a treatment. Antidepressant medications are a type of psychotropic drug, they are the most cost effective way to treat depression; they offer a quick biological fix to the problem by altering the amount of affected neurotransmitters. For these reasons the National Institute of Clinical Excellence (NICE) recommend them as a first-line treatment. (NICE, 2009)11 There are several forms of antidepressant, most fit into one of the following categories:
SSRI’s – Selective Serotonin Reuptake Inhibitors work by blocking the reabsorption of serotonin into the presynaptic terminal which increases the extracellular level of serotonin. (Helicon, 2006)12 SSRI’s are the most commonly prescribed of all antidepressants, (National Health Service, 2013)13 due in part to their high tolerance levels; of this type Fluoxetine (Prozac) is the most commonly prescribed. Fluoxetine and other SSRI’s have been shown to be effective in severe depression. (Kroenke et al, 2001)14
MAOI’s – Monoamine Oxidase inhibitors.
Monoamine oxidase (MAO) is a group of enzymes bound to the mitochondria; they regulate neurochemistry by degrading monoamine neurotransmitters. (Edmondson et al, 2004)15 Too much MAO activity is thought to be a cause of depression (Meyer et al, 2006)16; therefore MAOI’s are used by biological psychologists to block the function of MAO, preventing the breakdown of monoamine neurotransmitters thereby increasing their availability. They are an older variety of antidepressant which are usually the last type of antidepressant prescribed as they have potentially serious drug and dietary interactions. (Grady & Stahl, 2012)17 Isocarboxazid is a commonly prescribed MAOI which has had good results in controlled trials. A response rate of 50-70% has been recorded and is especially effective in atypical depression and treatment-resistant depression. (Davidson et al,
1988)18
NaSSA’s – Noradrenergic and Specific Serotonergic Antidepressants enhance the neurotransmission of noradrenaline and serotonin in the brain by antagonising specific adrenergic and serotonin receptors. As these target specific receptors, there are fewer side effects than those associated with the use of SSRI’s. (Robert, 2004)19 One such antidepressant is Mirtazapine, a 2001 study showed Mirtazapine to be effective in 48% of patients who had not responded to SSRI treatment, showing it to be an effective alternative. (Fava et al, 2001)20
Biological psychologists recommend psychotropic medications because they believe an imbalance of neurotransmitters causes abnormal behaviour; by altering the amount of neurotransmitters in the brain, they hope to alter the behaviour of the patient. In depression, biological psychologists may use an SSRI to increase the amount of extracellular serotonin in the brain to normal levels, thereby normalising the patient’s mood and behaviour.
The biological psychologist’s recommendation of antidepressants is based on thorough, mature research. Antidepressants as a whole are an effective biological treatment, while they do not treat the root cause, they offer the fastest relief of symptoms. (National Health Service, 2013)21 They have several advantages including: they are well tolerated, non-addictive, they can aid sleep and they are effective in relieving moderately severe depression in 50-65% of people. (Royal College of Psychiatrists, 2012)22 However, they do not treat the root cause so depression is more likely to return, they may not be as effective for mild depression as once thought (NHS, 2013)21, they increase volition which can increase the risk of suicide, they have a large, varied array of side effects and it can take more than six weeks for their effect to be felt.
As it takes so long for antidepressants to have an effect, some patients who are at a very high risk of suicide and those who are experiencing severe psychosis or catatonia may be prescribed electroconvulsive therapy (ECT) to prevent serious damage. Patients with severe depression who have tried many types of antidepressant over a long period of time with no effect can also be prescribed ECT. (Hauser, 2006)23 A 2004 study found that 34% of patients receiving ECT were in remission within 6 sessions and 65% within 10 sessions. This can be achieved in less than 4 weeks, for high risk or treatment resistant patients this can be an effective, alternative treatment to alleviate their depression quickly. (Husain et al, 2004)24
While objective, the biological assumption that psychology is a science has made the approach nomothetic and reductionist; behaviour is explained in terms of brain structure and chemicals, it is broken down into the smallest component parts. Over-simplifying behaviour in this way disregards the possibility that emotions or experience can be a cause of mental disorders. This has led to the development of humanism, which views the patient individually, as a whole instead of physiological pieces. This gives the treating psychologist the opportunity to discover the root cause and treat it appropriately rather than making assumptions based purely on biology.
Overall, biological psychologists have satisfied their theory with the use of antidepressant therapy; it is effective and is one of the most commonly used of all methods in the treatment of depression. Biological psychology has contributed significant research to discover and treat the causes of mental illness but it cannot provide a complete answer; genetics, brain structure and monoamines are a factor but these things cannot tell us what triggers metal health issues, they can only show us patterns where they have occurred, so unless a biological trigger can be identified this approach, or any other, cannot help to prevent depression. Researchers are not yet in a position to say whether low amounts of monoamines are caused by depression, or if depression causes there to be low amounts of monoamines in the patient’s brain. With further research and co-operation between perspectives, the depression puzzle may one day be solved.
References
Allen, M. (1976) “Twin studies of affective illness”. Archives of General Psychiatry, vol. 33 no. 12 pp. 1476 – 1478.
American Psychiatric Association (2014) DSM [online] Available at: http://www.psychiatry.org/practice/dsm [Accessed 10th April 2014]
Davidson, J. R. T. et al (1988) An efficacy study of Isocarboxazid and placebo in depression, and its relationship to depressive nosology. Chicago, IL, USA: American Medical Association.
Edmondson, D. E. et al (2004) “Structure and mechanism of monoamine oxidase”. Current Medicinal Chemistry, vol. 11 no. 15 pp. 1983 - 1993.
Fava, M. et al (2001) “Efficacy and safety of Mirtazapine in major depressive disorder patients after SSRI treatment failure: an open label trial”. The Journal of Clinical Psychiatry, vol. 62 no. 6 pp. 413 - 420.
Gershon, E. S. (1990) Genetics. FK Goodwin, KR Jamison (Eds.), Manic-depressive illness. Oxford: Oxford University Press.
Grady, M. M. & Stahl, S. M. (2012) "Practical guide for prescribing MAOIs: debunking myths and removing barriers". CNS Spectrums, vol. 17 no. 17 pp. 2 – 10.
Gross, R. & McIlveen, R. (1996) Abnormal Psychology. London, UK: Hodder & Stoughton.
Hauser, J. (2006) An Overview of Electroconvulsive Therapy (ECT). Psych Central. [online] Available at: http://psychcentral.com/lib/an-overview-of-electroconvulsive-therapy-ect/00053 [accessed 16th April 2014]
Helicon (2006) Hutchinson Encyclopedia of Science. Abingdon, UK: Helicon Publishing.
Husain, M. M. (2004) “Speed of response and remission in major depressive disorder with acute electroconvulsive therapy (ECT): a Consortium for Research in ECT (CORE) report”. The Journal of Clinical Psychiatry, vol. 65 no. 4 pp. 485 - 491
Kirsch, I. et al (2008) Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration. [online] available at: http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0050045 [accessed 7th April 2014]
Koenke , K. et al (2001) Similar Effectiveness of Paroxetine, Fluoxetine, and Sertraline in Primary Care: A Randomized Trial. Chicago, IL, USA: The Journal of American Medical Association.
McLeod, S. A. (2007) Biological Psychology. [online] available at: http://www.simplypsychology.org/biological-psychology.html [Accessed 5th April 2014]
Meyer, J. H. (2006) “Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major depression”. Archives of General Psychiatry, vol 63 no. 11 pp. 1209 - 1216.
National Health Service (2013) Antidepressants. [online] available at: http://www.nhs.uk/conditions/Antidepressant-drugs/Pages/Introduction.aspx [accessed 7th April 2014]
NICE (2009) Depression: The Treatment and Managemnet of Depression in Adults. [online] Available at: http://www.nice.org.uk/nicemedia/pdf/CG90NICEguideline.pdf [Accessed 15th April 2014]
Robert M. J. (2004) A Primer Of Drug Action: A Comprehensive Guide To The Actions, Uses, And Side Effects Of Psychoactive Drugs. New York, USA: Worth Publishers.
Royal College of Psychiatrists (2012) Antidepressants: key facts from the Royal College of Psychiatrists [online] Available at: http://www.rcpsych.ac.uk/pdf/antidepressants.pdf [accessed 16th April 2014]
Wender, P. et al (1986) “Psychiatric disorders in the biological and adoptive families of adopted individuals with affective disorders”. Archives of General Psychiatry, vol. 43 no. 10 pp. 923 - 929.
Wickens, A. (2005) Foundations of Biopsychology. 2nd edn. Upper Saddle River, NJ: Prentice- Hall.
World Health Organisation (2014) International Classification of Diseases (ICD) [online] Available at: http://www.who.int/classifications/icd/en/ [accessed: 10th April 2014]
Abnormal behaviour was once thought to be caused by supernatural possession; this demonological model of abnormality was especially popular in the Middle Ages. It was not until the 18th century that psychologists began to argue that this behaviour should be treated as an illness and medical techniques could be used to treat it; and so emerged the medical model of abnormality. (Gross & McIlveen, 1996)1 The medical model of abnormal psychology treats mental disorders in the same way as a physical illness. Practitioners of this model believe mental illness to have a physical cause, therefore they treat mental disorders with somatic intervention such as medication, electroconvulsive therapy or in extreme cases, psychosurgery. It is largely believed that biological events have behavioural consequences and behavioural events have biological consequences. (Wickens, 2005)2
McLeod (2007)3 describes the assumptions of biological psychology:
Psychology should be seen as a science and should be studied scientifically. …show more content…
Illness is in the patient’s nature, not caused by nurturing. Behaviour can be explained largely by biology such as genes and hormones; mental disorders have a physical cause relating to the structure or functioning of the brain. Behaviours such as phobias, hallucinations or suicide attempts are symptoms of mental illness.
Genes evolve to adapt behaviour to the environment and as such behaviour will have an evolutionary purpose.
The International Classification of Diseases (ICD) is a diagnostic tool and framework published by the World Health Organisation (WHO) to classify diseases and health issues; it is used to analyse the general health of the population. (World Health Organisation, 2014)4 The Diagnostic and Statistical Manual of Mental Disorders (DSM) is a publication from the American Psychiatric Association (APA) containing the criteria and classification of mental disorders and is most commonly used for diagnostic and research purposes. (American Psychiatric Association, 2014)5 While the DSM covers mental disorders, the ICD contains information regarding all diseases and health problems; both are used throughout the world for the diagnosis of unipolar depression.
Unipolar depression is a severe, typically prolonged and fundamental disturbance of mood and emotions, presenting as feelings of despondency and dejection. It is defined by the ICD-10 as a mood (affective) disorder and as a mood disorder by the DSM-IV. Low amounts of monoamine neurotransmitters are apparent in depressed patients, particularly serotonin and norepinephrine; biological psychologists recommend chemotherapy in the first instance, to correct this.
Gross & McIlveen (1996)6 identify the symptoms of unipolar depression as a persistent low mood lasting at least two weeks plus any five of the following:
Poor appetite / weight loss
Increased appetite / weight gain
Difficulty sleeping or sleeping longer than usual
Loss of energy or tiredness that affects ability to make simple decisions
Slowing down or agitation
Loss of interest or pleasure in activities
Feelings of self-reproach
Excessive or inappropriate guilt
Diminished ability to concentrate
Recurrent thoughts of death or suicide
Biological psychologists argue there are several causes for depression, one such explanation is dysfunctional monoamines. The Biogenic Amine Hypothesis states that depression is associated with a functional deficit of monoamine neurotransmitters, predominantly noradrenaline and serotonin. Support for this theory came when MAOI’s were found to alleviate symptoms of depression and when depression was found to be a side effect of taking Reserpine, an antihypertensive drug which depletes levels of noradrenaline. However, as antidepressants have further effects on the brain beyond the alteration of neurotransmitters, we cannot conclude that depression is caused purely by neurotransmitter dysfunction; with this is mind, the Biogenic Amine Hypothesis is considered too simplistic. (Merrill Academy, 2012)7
Another cause argued biological psychologists is genetics. Gershon (1990)8 reviewed family studies and found that rates of unipolar depression in first degree relatives were 7-30%. The genetic argument is supported by twin studies; Allen (1976)9 has found the concordance rate of monozygotic twins to be 40% and 11% in dizygotic twins. Lastly, Wender et al (1986) 10 found that the biological parents of an adopted individual with depression were eight times more likely to suffer from the disorder than the adoptive parents providing strong evidence of a genetic link.
The assumption that behaviour is caused by faulty genes and the assumption that mental disorders have a physical cause has caused the heavy use of antidepressants as a treatment. Antidepressant medications are a type of psychotropic drug, they are the most cost effective way to treat depression; they offer a quick biological fix to the problem by altering the amount of affected neurotransmitters. For these reasons the National Institute of Clinical Excellence (NICE) recommend them as a first-line treatment. (NICE, 2009)11 There are several forms of antidepressant, most fit into one of the following categories:
SSRI’s – Selective Serotonin Reuptake Inhibitors work by blocking the reabsorption of serotonin into the presynaptic terminal which increases the extracellular level of serotonin. (Helicon, 2006)12 SSRI’s are the most commonly prescribed of all antidepressants, (National Health Service, 2013)13 due in part to their high tolerance levels; of this type Fluoxetine (Prozac) is the most commonly prescribed. Fluoxetine and other SSRI’s have been shown to be effective in severe depression. (Kroenke et al, 2001)14
MAOI’s – Monoamine Oxidase inhibitors.
Monoamine oxidase (MAO) is a group of enzymes bound to the mitochondria; they regulate neurochemistry by degrading monoamine neurotransmitters. (Edmondson et al, 2004)15 Too much MAO activity is thought to be a cause of depression (Meyer et al, 2006)16; therefore MAOI’s are used by biological psychologists to block the function of MAO, preventing the breakdown of monoamine neurotransmitters thereby increasing their availability. They are an older variety of antidepressant which are usually the last type of antidepressant prescribed as they have potentially serious drug and dietary interactions. (Grady & Stahl, 2012)17 Isocarboxazid is a commonly prescribed MAOI which has had good results in controlled trials. A response rate of 50-70% has been recorded and is especially effective in atypical depression and treatment-resistant depression. (Davidson et al,
1988)18
NaSSA’s – Noradrenergic and Specific Serotonergic Antidepressants enhance the neurotransmission of noradrenaline and serotonin in the brain by antagonising specific adrenergic and serotonin receptors. As these target specific receptors, there are fewer side effects than those associated with the use of SSRI’s. (Robert, 2004)19 One such antidepressant is Mirtazapine, a 2001 study showed Mirtazapine to be effective in 48% of patients who had not responded to SSRI treatment, showing it to be an effective alternative. (Fava et al, 2001)20
Biological psychologists recommend psychotropic medications because they believe an imbalance of neurotransmitters causes abnormal behaviour; by altering the amount of neurotransmitters in the brain, they hope to alter the behaviour of the patient. In depression, biological psychologists may use an SSRI to increase the amount of extracellular serotonin in the brain to normal levels, thereby normalising the patient’s mood and behaviour.
The biological psychologist’s recommendation of antidepressants is based on thorough, mature research. Antidepressants as a whole are an effective biological treatment, while they do not treat the root cause, they offer the fastest relief of symptoms. (National Health Service, 2013)21 They have several advantages including: they are well tolerated, non-addictive, they can aid sleep and they are effective in relieving moderately severe depression in 50-65% of people. (Royal College of Psychiatrists, 2012)22 However, they do not treat the root cause so depression is more likely to return, they may not be as effective for mild depression as once thought (NHS, 2013)21, they increase volition which can increase the risk of suicide, they have a large, varied array of side effects and it can take more than six weeks for their effect to be felt.
As it takes so long for antidepressants to have an effect, some patients who are at a very high risk of suicide and those who are experiencing severe psychosis or catatonia may be prescribed electroconvulsive therapy (ECT) to prevent serious damage. Patients with severe depression who have tried many types of antidepressant over a long period of time with no effect can also be prescribed ECT. (Hauser, 2006)23 A 2004 study found that 34% of patients receiving ECT were in remission within 6 sessions and 65% within 10 sessions. This can be achieved in less than 4 weeks, for high risk or treatment resistant patients this can be an effective, alternative treatment to alleviate their depression quickly. (Husain et al, 2004)24
While objective, the biological assumption that psychology is a science has made the approach nomothetic and reductionist; behaviour is explained in terms of brain structure and chemicals, it is broken down into the smallest component parts. Over-simplifying behaviour in this way disregards the possibility that emotions or experience can be a cause of mental disorders. This has led to the development of humanism, which views the patient individually, as a whole instead of physiological pieces. This gives the treating psychologist the opportunity to discover the root cause and treat it appropriately rather than making assumptions based purely on biology.
Overall, biological psychologists have satisfied their theory with the use of antidepressant therapy; it is effective and is one of the most commonly used of all methods in the treatment of depression. Biological psychology has contributed significant research to discover and treat the causes of mental illness but it cannot provide a complete answer; genetics, brain structure and monoamines are a factor but these things cannot tell us what triggers metal health issues, they can only show us patterns where they have occurred, so unless a biological trigger can be identified this approach, or any other, cannot help to prevent depression. Researchers are not yet in a position to say whether low amounts of monoamines are caused by depression, or if depression causes there to be low amounts of monoamines in the patient’s brain. With further research and co-operation between perspectives, the depression puzzle may one day be solved.
References
Allen, M. (1976) “Twin studies of affective illness”. Archives of General Psychiatry, vol. 33 no. 12 pp. 1476 – 1478.
American Psychiatric Association (2014) DSM [online] Available at: http://www.psychiatry.org/practice/dsm [Accessed 10th April 2014]
Davidson, J. R. T. et al (1988) An efficacy study of Isocarboxazid and placebo in depression, and its relationship to depressive nosology. Chicago, IL, USA: American Medical Association.
Edmondson, D. E. et al (2004) “Structure and mechanism of monoamine oxidase”. Current Medicinal Chemistry, vol. 11 no. 15 pp. 1983 - 1993.
Fava, M. et al (2001) “Efficacy and safety of Mirtazapine in major depressive disorder patients after SSRI treatment failure: an open label trial”. The Journal of Clinical Psychiatry, vol. 62 no. 6 pp. 413 - 420.
Gershon, E. S. (1990) Genetics. FK Goodwin, KR Jamison (Eds.), Manic-depressive illness. Oxford: Oxford University Press.
Grady, M. M. & Stahl, S. M. (2012) "Practical guide for prescribing MAOIs: debunking myths and removing barriers". CNS Spectrums, vol. 17 no. 17 pp. 2 – 10.
Gross, R. & McIlveen, R. (1996) Abnormal Psychology. London, UK: Hodder & Stoughton.
Hauser, J. (2006) An Overview of Electroconvulsive Therapy (ECT). Psych Central. [online] Available at: http://psychcentral.com/lib/an-overview-of-electroconvulsive-therapy-ect/00053 [accessed 16th April 2014]
Helicon (2006) Hutchinson Encyclopedia of Science. Abingdon, UK: Helicon Publishing.
Husain, M. M. (2004) “Speed of response and remission in major depressive disorder with acute electroconvulsive therapy (ECT): a Consortium for Research in ECT (CORE) report”. The Journal of Clinical Psychiatry, vol. 65 no. 4 pp. 485 - 491
Kirsch, I. et al (2008) Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration. [online] available at: http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0050045 [accessed 7th April 2014]
Koenke , K. et al (2001) Similar Effectiveness of Paroxetine, Fluoxetine, and Sertraline in Primary Care: A Randomized Trial. Chicago, IL, USA: The Journal of American Medical Association.
McLeod, S. A. (2007) Biological Psychology. [online] available at: http://www.simplypsychology.org/biological-psychology.html [Accessed 5th April 2014]
Meyer, J. H. (2006) “Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major depression”. Archives of General Psychiatry, vol 63 no. 11 pp. 1209 - 1216.
National Health Service (2013) Antidepressants. [online] available at: http://www.nhs.uk/conditions/Antidepressant-drugs/Pages/Introduction.aspx [accessed 7th April 2014]
NICE (2009) Depression: The Treatment and Managemnet of Depression in Adults. [online] Available at: http://www.nice.org.uk/nicemedia/pdf/CG90NICEguideline.pdf [Accessed 15th April 2014]
Robert M. J. (2004) A Primer Of Drug Action: A Comprehensive Guide To The Actions, Uses, And Side Effects Of Psychoactive Drugs. New York, USA: Worth Publishers.
Royal College of Psychiatrists (2012) Antidepressants: key facts from the Royal College of Psychiatrists [online] Available at: http://www.rcpsych.ac.uk/pdf/antidepressants.pdf [accessed 16th April 2014]
Wender, P. et al (1986) “Psychiatric disorders in the biological and adoptive families of adopted individuals with affective disorders”. Archives of General Psychiatry, vol. 43 no. 10 pp. 923 - 929.
Wickens, A. (2005) Foundations of Biopsychology. 2nd edn. Upper Saddle River, NJ: Prentice- Hall.
World Health Organisation (2014) International Classification of Diseases (ICD) [online] Available at: http://www.who.int/classifications/icd/en/ [accessed: 10th April 2014]