The understanding of mental events and behaviour can be enhanced using the concept of bio-psychology. Peterson defined psychology in1996 as the scientific study of behaviour and mental process. Biology psychology is therefore, an extension of psychology, scientifically studying the biology of behaviour (Pinel 1997). It examines the physiological, evolutionary and developmental mechanisms of behaviour and experience and pays particular reference to the functions of the brain.
The area of the bio-psychology is a vast one, consisting of broad array of notions. A particular famous concept is that of Crick, who in 1990 developed the 'astonishing hypothesis theory'. He emphasised that identity and personal characteristics can be attributed to the make up of the individuals nerve cells and their associated molecules. Crick therefore believes that all mental events and behaviour can be explained as simply the construction or assembly of a person's genes. Mental events and behaviour are an amalgamation of a series of contributing factors such as dyslexia, depression, altruism, schizophrenia, aggression etc.
the areas that will be explored further will be depression and schizophrenia as these effect a large of proportion of the population and will make interesting examination.
Depression is the most common psychological problem people face therefor, therefore Seligman (1973) termed it as the "common cold" of psychological problems. The biological theory of depression emerged in the 1950's, when it was discovered that a certain class of drugs known as Trycyclic drugs, was effective in treating depression. Since then it has been proposed that depression is linked to a disturbance of amine metabolism (brain chemistry). There are two main categories of this mood disorder: unipolar depression and bipolar (manic) depression. Major unipolar depression occurs at lease five times more frequently than bipolar depression, and mania can occur on it's own ( although this is very rare).
The reasons for depression can be sub-divided into two main sections; genetic/neurological factors and social/psychological factors. There is very little substantial evidence for genetic factors in unipolar depression, but reasonable strong evidence in bipolar (manic) depression. Twin studies provide rather convincing evidence. Price (1968) looked at 7 twin studies and found a much higher concordance rates for manic depressive psychosis in identical (MZ) twins than in non-identical (DZ) twins. The most revealing factor was that the concordance rate for the (MZ) twins was almost the same for those reared together and those reared apart. These findings were reinforced in 1976 by Allen. In this study, it was reported that the concordance rate for the MZ twins was 72% and the DZ twins was 14%. This showed that there is strong genetic link. Another complementary study is that of Weissman (1987). It showed that people with first degree relatives (share 50% of the genes, i.e. parent, siblings) who have a mood disorder are ten times more likely to develop one then those with people with unaffected first degree relatives.
In alternative adoptive studies, the results were also corresponding. Wender et al (1986) discovered that adopted children who later develop a mood disorder are much more likely to have a biological parent who has been diagnosed as having a mood disorder, even though adopted children are raised in very different environments. Furthermore, Cockret (1978) looked at 126 adopted children, 8 of which were born to parents with manic depression but were adopted by a healthy couple. Three of those eight later developed a major affective disorder, compared to only eight of the remaining 118.
Although genetic evidence for bipolar depression is strong, no study has shown a 100% concordance rate which indicates that the genetic component might be a predisposing factor and there may be additional causes. Such as the Schildkraut (1965), whose neurological approach suggested that chemical imbalances in serotonin and norepinephrine play a causal role in affective disorders. He believed that too much norepinephrine resulted in mania and too little resulted in depression. Later research found this to be true of seretonin also.
Complementary research by Kety (1975) found abnormally high levels of norepinephrine-derived compounds in the urine of manic people. In conjunction with these findings, Teuting et al (1981) found that lower than normal levels of compounds that are produced when norepinephrine and seretonin are broken down by enzymes are found in the urine of depressed people. This suggest lower activity than normal of norepinephrine and seretonin, secreting neurons in the brain.
However, these approaches do not take into account the psychodynamic or social factors involved in depression. Freud argued that actual losses and symbolic losses lead us to re0experience parts of our childhood with depressed people becoming dependant, and in extreme cases regressing to a childlike state; both symptoms similar to depression. However, there is little evidence for direct connection between early loss and the risk of depression in adult life, (Crack and Elliot 1980). Freud also argued that unresolved hostility towards one's parents has been repressed so we are no longer consciously aware of it. When loss is experienced, anger is evoked and turned inward on the self. But yet if anger is turned inward, depressed people would not direct their hostility towards people who are close to them as they do, (Weissman and Paykel 1974).
Some psychologists believe major life events can cause depression, such as the death of a love done, divorce, illness, unemployment, etc. brown and Harris (1978) identified that severe life events and long term difficulties were two factors that contributed to women's depression. However, many people suffer psychosocial stresses but do not develop clinical depression. In addition, many people with depression do not report any severe life events.
Lewinsohn (1974) said depression is a consequence of a reduction in positive re-inforcement, for example if an individual loses a job. There is less opportunity for enjoying the pleasant experiences and receiving positive re-inforcement, therefore depression follows. He continued that depression often gives positive re-inforcement in the form of sympathy/concern from others. This does not however explain why depression does not cease long after sympathy has also stopped.
Dementia praecox (sensility of youth) was the original term used for schizophrenia by Kraeplin in 1902. He regarded it as a from of mental deterioration beginning in adolescence, resulting in typical symptoms such as hallucinations, attention deficits, delusions and bizarre motor activity. It was not until Bleuler observed in 1911, that symptom deterioration did not continue with patients and that adolescence was not the key time period for developing the illness, but in fact later, that the title 'schizophrenia' was implemented. With the literal meaning of 'divided self' or 'split mind' it describes a condition in which the personality loses its unity.
There are several contributing genetic, biological and environmental factors to take into consideration when discussing the causes of schizophrenia. Perhaps the most significant factor is genetic. Gottesman's twin study in 1987 reported that identical MZ twins has a concordance rate of 44% and DZ twins had a concordance rate of 12%, with parents and grandparents resulting in 9% and ÃÂ£% respectively. This indicates that the closer the genetic link a person has with an individual suffering from schizophrenia, the greater the likelihood of them suffering from the same illness too.
Heston (1996) carried out an adoption study with 47 children born to schizophrenic mothers but adopted within the first month of birth. These were compared with a control group of 50 children of non-schizophrenic mothers adopted into the same homes as the first group. All the children were followed up as adults and given intelligence and personality tests and interviewed by two 'blind' psychiatrists. Results of Heston's study recorded that in the experimental group of 47, 5 became schizophrenic compared to 0 out of the 50 in the control. Furthermore, 37 out of the experimental group developed some other form of psychiatric disorder compared to 9 from the control group. These results provide strong support for a genetic component, especially given that the environments of the two groups were identical.
In another major study, Kety et al (1968, 1976) looked at records of all children adopted in Denmark between 1927 and 1947. Those who were diagnosed as schizophrenic later in life were matched with a control group who were not. Records of the biological parents were then studies, and it was found that parents of the first group had a significantly higher incidence of schizophrenia that parents of the control group.
Twin and adoption studies indicate that genetic factors play an important role in influencing whether an individual will develop schizophrenia or not. However, in interpreting these findings, it must be noted that if genetic factors were the sole determinant of schizophrenia, we would expect 100% concordance rates in MZ twins and no study has found this. There genes cannot completely explain schizophrenia on their won, but they do seem to render some individuals more vulnerable to the illness.
Research into biological factors in schizophrenia has focused on the 'dopamine hypothesis'. Specifically, it is believed that excess activity of dopamine (DA - a neurotransmitter in the brain) causes schizophrenia. The evidence is supported by a number of sources. Firstly, the amphetamine psychosis. Large doses of amphetamines can cause symptoms which are virtually indistinguishable from acute, paranoid schizophrenia. In addition, amphetamines can exacerbate the symptoms of someone suffering from schizophrenia. Synder (1974) found that amphetamines increases the levels of dopamine in the synaptic cleft. This implies that excess dopamine causes at least some of the symptoms of schizophrenia. Secondly, the class of drugs which block dopamine receptors in the brain named phenothazines. They are an effective antidote to amphetamine psychosis and reduce some of the symptoms of schizophrenia. This confirms the role of dopamine activity in schizophrenia. To further re-inforce this theory, Mackay et al (9182) fond post mortems of schizophrenics brains revealed a greater number of dopamine receptors than normal. However, schizophrenics are often on drug treatment for long periods of time, and this could be the cause of brain abnormalities, rather than brain abnormalities being a cause of schizophrenia. Wong et al (1986) overcame this problem by studying PET scans of schizophrenics who had never been treated with drugs. These scans also revealed a greater than normal density of dopamine receptors in the brain, implying that this may be a biological cause of schizophrenia.
Methodological problems made it difficult to conclude that excess dopamine activity causes schizophrenia - it may be one of the symptoms, for example, rather than one of the causes. Nevertheless, Wong et al's study above is persuasive in indicating brain abnormality in untreated schizophrenics, although the problems above indicate the dopamine is only one piece of the puzzle and not the whole picture.
In addition to the genetic and biological evidence, a range of environmental factors have been reported to influence the development of schizophrenia. Bateson et al (1956) believed that families of schizophrenics are characterised by disturbed patterns of communication involving ambiguous or conflicting messages. He used the term "double-blind" to refer to the 'no-win' situation the individual is in within such a family. Although there is no specific evidence supporting Bateson's hypothesis, there are additional studies that have confirmed the influence of the family.
Davison and Neale (1990) reviewed the evidence and concluded that families of schizophrenics do show particularly vague patterns of communication and a higher that normal level of conflict. However, the evidence is only correlational. The link could be due to the disruptive influence of having a schizophrenic in the family, rather than the other way round! Therefore in 1982, Norton conducted a longitudinal study to overcome this problem. He found that communication problems in the families of adolescents were related to later incidence of schizophrenia.
In addition, all studies looking at family environments cannot rule out the possibility of genetic factors explaining the links between the maladjusted family life and schizophrenia. This factor was investigated further in an adoption study carried out by Tienari (1987). He found that individuals most at risk from developing schizophrenia were those with schizophrenic parents brought up in a maladjusted adoptive family. Those least at risk were control group of adoptees whose biological parents were not schizophrenic, even if the adoptive family environment was maladjusted.
This last study clearly shows that family influences are only linked to the development of schizophrenia in individuals whose genes render them vulnerable in the first place. Without this gender predisposition, it is unlikely that a person would become schizophrenic, whatever the family environment.
In conclusion, the bio-psychological approaches to understanding mental events and behaviour result in more conclusive findings than using a social approach and/or examining environmental factors. Recordings from a genetic or biological approach enables theories to be clearly proved or disproved. However, when adopting an environmental approach, ideas are often very abstract and merely symbolic. Social factors are also not as reliable, as they can suffer from possible variance in environment and are affected by the individual differences in each person. Therefore, the strengths of a bio-psychological approach to understanding the mental events and behaviour far outweigh the weaknesses. It will continue to be a powerful channel for research, with theorists repeatedly extending the boundaries of knowledge for years to come.