Overall the evidence for a biochemical theory of schizophrenia is inconclusive, there exists no consistent difference in dopamine levels between drug-free schizophrenics and non-schizophrenics, similarly, there is no evidence of higher levels of other metabolites indicating any greater dopamine activity. (Richard Gross 2010).
In respect of biochemical factors for the treatment of depression anti-depressant drugs work by increasing the availability of serotonin at the synapses by preventing its reuptake or breakdown suggesting that it’s the low levels of serotonin that lead to depressive disorders, however because anti depressants relieve some of the symptoms associated with depression doesn’t mean they treat the cause; low levels of serotonin could be a symptom of depression. Post mortems carried out on people who have committed suicide have revealed abnormally low levels of serotonin suggesting that this may have caused their depression, however psychological research has discovered that there are alternative and often complex explanations for the cause of depression. (Coordination Group Publications 2009; Richard Gross 2010).
Alternative Explanations
There exists a strong probability that other factors play a part in the potential causes of schizophrenia, being genetically related to someone with schizophrenia can significantly increase a person’s chances of developing it. Gottesman (1991) reviewed forty twin studies and found that with identical (MZ) twins there was a 48% chance of both being schizophrenic; with non-identical (DZ) twins that percentage had reduced but was still a significant 17%. The same can be said of depression as it would appear that genetics equally plays a significant part in potential offspring developing endogenous depression or depression caused by internal factors, however, for both schizophrenia and depression other factors need to be considered such as neurological, behavioural, psychological and socio-cultural. (Coordination Group Publications 2009; Richard Gross 2010).
There are theories to suggest that abnormal brain structure caused by abnormal development could be the cause of schizophrenia. Johnstone et al (1976) compared the size of the ventricles in schizophrenics’ brains, they discovered that people with schizophrenia had enlarged ventricles which suggest that schizophrenia is linked to a loss of brain tissue, however non-schizophrenics can also have enlarged ventricles which is in direct opposition to Johnstones evidence. Buchsbaum (1990) carried out MRI scans on schizophrenics’ brains and found abnormalities in the prefrontal cortex, however these findings are inevitably correlational as they don’t display cause and effect; it may be that abnormal brain structure is a symptom of schizophrenia rather than a cause of it. (Coordination Group Publications 2009; Richard Gross 2010).
Behaviourists argue that schizophrenia is learnt through operant conditioning; someone may do something that gets a positive reaction or reward from others, this encourages the person to repeat the behaviour thus reinforcing it; token economies which use reinforcement to encourage supposed normal behaviours can help treat schizophrenia, suggesting that some of the behaviour could be learnt. Behaviourists believe that depression develops when stressors such as bereavement or being made redundant lead to a lack of positive reinforcement, the attention that depressive behaviour then draws can then provide positive reinforcement, meaning the person learns to continue being depressed; it may also be influenced by learned helplessness, occurring when individuals learn not to try as they believe they will never succeed. Most biological and psychological research suggests that schizophrenia and depression are not merely learnt behaviours. (Coordination Group Publications 2009; Richard Gross 2010).
The social causation hypothesis states that people with low social status are more likely to suffer from either schizophrenia or depression, equally factors such as poverty and discrimination cause higher stress levels which are thought to be potential triggers. Harrison et al (2001) found that people who were born in deprived areas were more likely to develop schizophrenia, suggesting that factors such as poverty, unemployment and over-crowding may have an impact. (Coordination Group Publications 2009; Richard Gross 2010).
Freud claimed that schizophrenia is caused by over-whelming anxiety, it’s a defence mechanism involving regression into an earlier stage of development; Freud believed hallucinations are the ego’s attempt to restore contact with reality. Laing (1967) also argued that schizophrenics lose contact with reality as a way of coping with social pressure; Laing claimed that it was wrong to encourage schizophrenics to conform. Freud also claimed that depression occurs when a child feels unloved by its parents and becomes angry, such anger then creates guilt so the anger is redirected towards the self; these feeling are eventually repressed but later return following a stressful and/or traumatic life event causing depression. Brown and Harris (1978) found that the women they interviewed were more likely to have depression if they experienced disrupted childhood attachments especially if their mother had died; unfortunately their isn’t sufficient research to support Freud’s theory, psychoanalysis isn’t an effective treatment for schizophrenia and is unfalsifiable in the treatment of depression. (Coordination Group Publications 2009; Richard Gross 2010).
It is possible that any numbers of factors in immeasurable quantities are potentially responsible for either schizophrenia or depression; any potential treatment is primarily dependent upon individual circumstances which in essence are almost impossible to pigeon hole or stereotype.
Reference List:
Coordination Group Publications 2009 AS & A2 Psychology Exam Board AQA A
Richard Gross 2010 Psychology: The Science of Mind and Behaviour Sixth Edition
Kieron Walsh 2008 Biological Explanations of Schizophrenia and Dopamine Hypothesis accessed on the 27th February 2011 at 09:29 hrs
Bibliography:
Richard Gross 1996 Third Edition Psychology: The Science of Mind and Behaviour
Atypical Psychology: Symptoms, causes and explanations of psychological disorders
In this assignment the author intends to write an essay by identifying the symptoms and potential causes of three psychological disorders other than schizophrenia and depression.
Sleep Disorders - Primary Insomnia
Primary Sleep disorders are divided into two subcategories: Dyssomnias are those disorders relating to the amount, quality, and timing of sleep. Parasomnias relate to abnormal behaviour or physiological events that occur during the process of sleep. The cause of primary insomnia can be different for each individual but often involves a preoccupation with the inability to sleep or excessive worry about sleep, which in turns causes the individual to not sleep. The criteria for a diagnosis of primary insomnia include a difficulty falling asleep, remaining asleep, or receiving restorative sleep for a period no less than one month. This disturbance in sleep must cause significant distress or impairment in social, occupational, or other important functions and does not appear exclusively during the course of another mental or medical disorder or during the use of alcohol, medication, or other substances. (DSM-IV 1999 – 2003).
‘For all the advantages of modern society, we cannot afford to ignore the rhythms of the animal brain within us, any more than we can neglect our need to breathe or eat. Without the biological clocks in our brains, our lives would be chaotic, our actions disorganised. The brain has internalised the rhythms of nature, but can tick on for months without sight of the sun.’ (Blackmore, 1988). (Richard Gross 2010).
Insomnia and Mental Disorder
Young (2009) cites a 1987 American study of 1053 male medical students who’d been followed for an average of 34 years after graduation, during that time 101 had developed clinical depression, 13 of whom had committed suicide, those that had reported suffering from insomnia were twice as likely to become depressed as those with no sleep problems; one conclusion to this data is that insomnia can predispose people to depression. Impaired sleep can also induce the manic episodes involved in bipolar disorder as well as failure of a sleep-dependant component of procedural learning, associated with schizophrenia. (Stickgold, 2004; Young, 2009). (Richard Gross 2010).
Both Stickgold and Young believe that during REM sleep the visceral component of our memories is stripped away from the more cognitive component. This happens because the neurotransmitters associated with stress, fear and the fight or flight response, serotonin and noradrenaline are shut down. Although dreams can be emotional, they gradually alleviate the emotional edge to our memories thus serving us in many positive psychological and pathological areas. (Richard Gross 2010).
Bipolar Disorder (Manic-Depression)
Research has shown a strong biological component for this disorder, with environmental factors playing a role in the exacerbation of symptoms; Bipolar Disorder has been broken down into two types. . (DSM-IV 1999 – 2003).
For a diagnosis of Bipolar I disorder, a person must have at least one manic episode. Mania is sometimes referred to as the other extreme to depression. Mania is an intense high where the person feels euphoric, almost indestructible in areas such as personal finances, business dealings, or relationships. They may have an elevated self-esteem, be more talkative than usual, have flight of ideas, a reduced need for sleep, and be easily distracted. Depression is often experienced as the high quickly fades and as the consequences of their activities becomes apparent, the depressive episode can be exacerbated. For Bipolar II Disorder there are periods of highs as described above and often followed by periods of depression. Bipolar II Disorder however is different in that the highs are hypo manic, rather than manic. In other words, they have similar symptoms but they are not severe enough to cause marked impairment in social or occupational functioning and typically do not require hospitalization in order to assure the safety of the person. . (DSM-IV 1999 – 2003).
There are definitely varying degrees of this illness and it is not difficult to misdiagnose due to it's similarity to other mood disorders. If the illness is not severe, often time’s medication and therapy can do very well in terms of treatment. And, life experience, strong support, and an openness to improve can be enough sometimes to make a difference in outcome. . (DSM-IV 1999 – 2003)
Anorexia Nervosa
Much research has been completed on this disorder, and results indicate a strong familial undercurrent. Many individuals with Anorexia come from over controlling families where nurturance is lacking. Studies suggest that sexual abuse survivors are more prone to the disorder, as are fraternal twins and first degree relatives of those who have anorexia, the latter suggesting a biological component as well. . (DSM-IV 1999 – 2003).
Most often diagnosed in females (up to 90%), Anorexia is characterized by failure to maintain body weight of at least 85% of what is expected, fear of losing control over your weight or of becoming ‘fat.’ There is typically a distorted body image, where the individual sees themselves as overweight despite overwhelming evidence to the contrary. (DSM-IV 1999 – 2003).
If caught in time, Anorexia is very treatable, but can easily lead to severe physical problems and death if it is allowed to continue. In many cases, an individual with anorexia is very reluctant to get treatment as this would mean giving up control. Inpatient or other hospitalization is often needed when health is at risk. . (DSM-IV 1999 – 2003).
In the past 30 years eating disorders or (EDs) have become widespread in western industrialised societies; this may be related to the over-abundance of food but it’s more likely to be influenced by societal norms that link human attractiveness to being thin or waif-like. The popular and scientific assumption is that the preoccupation with thinness and dieting rampant in western societies is a direct cause of eating disorders. (Richard Gross 2010).
‘According to Fedoroff and McFarlane (1998) it is well established that eating disorders are multidetermined and that culture is only one of many factors that contribute to the development of eating disorders. Furthermore, cultural factors can only be understood as they interact with the psychology and biology of the vulnerable individual; a culture cannot cause a disorder.’ (Richard Gross 2010).
According to the dimensional viewpoint, the full blown ED is the end point along a continuum that begins with normal dieting, advances to excessive concern about weight and the emergence of some clinical symptoms, and finally a severe, pathological illness. (Richard Gross 2010).
Reference List:
DSM-IV 1999 – 2003 accessed at 01:01 hrs on the 12th March 2011
Richard Gross 2010 Psychology: The Science of Mind and Behaviour Sixth Edition
Gary Wheadon. Access to Higher Education Page
