Lesson 2: Biological Explanations Of SZ Flashcards
Family studies
- Find individuals who have SZ and determine whether their biological relatives are similarly affected more often than non-biological relatives. Family studies have shown that the closer the genetic relatedness, the greater the risk. Gottesman (1991) found that if both parents were schizophrenic, then the likelihood of the offspring also having SZ was 46%, if one parent had SZ, then the likelihood dropped to 13% and if a sibling had SZ the likelihood was 9%.
Twin studies
- opportunity for researchers to explore the nature/nurture debate in terms of the contribution of heredity and environmental influences in having SZ
- as MZ twins share 100% of their genes whereas as DZ twins share 50% of their genes, if SZ is genetic, then the concordance rate should be much higher for MZ rather than DZ twins.
- Gottesman (1991) found a 48% concordance rate for MZ twins and 17% for DZ twins.
- shows that the more genetically similar you are, the more likely you are to get SZ
Joseph (2004)
- did a review on twin studies that were carried out up to 2001, and found an overall concordance rate for MZ twins as 40% but DZ twins as 7.4%.
Adoption studies
- difficult to separate genetic and environmental influences in twin and family studies so adoption students carried out
- Tienari et al (2001) carried out a study in Finland. 164 adoptees whose biological mothers had been diagnosed with SZ, 11 were also diagnosed with SZ compared to a control group of 197 adoptees where only 4 were diagnosed. This study shows that although the overall percentage of children having SZ were low, there is a small link between genes and SZ.
Candidate genes
Specific candidate genes associated with SZ e.g. PCM1.
- agreed that SZ is polygenic - means that there is a combination of different genes that have been implicated in SZ
- Gurling et al (2006) used evidence from family studies indicating that SZ was associated with chromosome 8p21-22 to identify a high-risk sample
- Using gene-mapping, the PCM1 gene was implicated in susceptibility to SZ, providing more evidence for genetics
- Benzel et al (2007) used gene mapping to find evidence suggesting that NRG3 gene variants interact with both NRG1 and ERBB4 gene variants to create susceptibility to developing SZ.
- Ripke et al (2014) compared the genetic makeup of 37000 SZ patients worldwide with 113,000 controls. They found that 108 separate genetic variations were associated with an increased risk of SZ. The genes that were particularly vulnerable were the ones that had some connection to the functioning of neurotransmitters such as dopamine.
Strength of genetic basis of SZ
- There is a wealth of research evidence to support the genetic basis explanation. For example with the findings of Gottesman, Joseph’s and Tienari’s thus there is a link between genes and SZ. This is a strength because it shows that if a child grows up in a family where both their biological parents has SZ, then the chances of the, getting it is heightened compared to if only one parent or none of the parents have it suggesting genetics is an important factor.
Weaknesses of genetic basis explanation (twin+ family and family history)
- Problem with twin and family students is separating nature from nurture. For example, MZ twins are normally reared together and sent to the same school, wear the same clothes this then makes it difficult to separate upbringing from genes. Even if we look at adoption students, children tend to be adopted by relatives who may still rear the child similarly to its biological parents, thus adoption studies may not always be a good comparison for the effects of nature and nurture.
- SZ can take place in the absence of family history. One explanation is that there may be a mutation in parental DNA, for example in paternal sperm cells. This can be caused by radiation, poison or infection. Evidence for role of mutation comes from Brown et al (2002) study which showed a positive correlation between paternal age and increased risk of SZ, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50. This suggests that although no direct genes are involved, a person can still get SZ if their father was older at the time of fertilisation. Role of nature and nurture may both play a part.
Weaknesses of genetic basis explanation (biologically reductionist and diathesis stress model)
- Genetic explanation is also biologically reductionist as it is stating that one cause of SZ is simply your genes. In other words, it is insinuating that if you possess the PCM1 gene, then you will have SZ. This means the explanation is ignoring factors such as psychological factors and family upbringing which could be more important in explaining SZ for example it has been found that certain parenting styles in an individual’s childhood could trigger symptoms of SZ in adulthood.
- Diathesis stress model states that there is a genetic vulnerability in schizophrenia but this vulnerability is only likely to be triggered if there is a stress trigger in the individual’s life. In other words, you may be born with a gene which makes you particularly vulnerable to SZ but if your life is relatively stress free, then you may not end up having the disorder at all. This we need to be cautious when looking at genetic factors since they alone may not trigger SZ. Therefore, taking a more holistic approach in understanding the causes of SZ may lead to more effective treatments.
Neural correlates
- Measurements of the structure or function of the brain that have a relationship with SZ especially different regions of the brain. Neural correlates also refers to how different neurotransmitters such as dopamine and serotonin are in different parts of the brain can also play a part in SZ.
Dopamine Hypothesis
- Neurotransmitters are the brain’s chemical messengers. They appear to work differently in the brains of schizophrenics. In particular, dopamine seems to have an important role since DA is necessary in the functioning of several brain systems. DA has also been implicated in SZ.
What is dopamine?
Dopamine is one of the brain’s neurotransmitters - a chemical that ferries information between neurons. Dopamine helps regulate movement, attention, learning and emotional responses. It also enables us not only to see rewards, but to take action to move toward them. Since dopamine contributes to feelings of pleasures and satisfaction as part of the reward system, the neurotransmitter also plays a part in addiction. Dopamine is involved in the motor system. When the brain fails to produce enough dopamine, it can result in Parkinson’s disease. A primary treatment for Parkinson’s disease therefore, is a drug called L-dopa which spurs the production of dopamine.
Dopamine and SZ
Thus, the dopamine hypothesis claims that an excess of dopamine in certain regions of the brain is associated with the positive symptoms of SZ. Thus messages from neurons that transmit dopamine fire too easily and often, leading to hallucinations and delusions.
Schizophrenics are thought to have particularly high levels of D2 receptors on receiving neurons resulting in more dopamine binding and more neurons firing.
Hyperdopaminergia (in the subcortex)
- Based on the original dopamine hypothesis is explaining SZ. This states that there are high levels of activity of dopamine in an area of the brain known as the subcortex. For example, an excess of dopamine receptors in the Broca’s area may be associated with problems in speech or auditory hallucinations.
Hypodopaminergia (in the cortex)
- recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex. Goldman-Rakic et al (2004) have focused on the role of low levels of dopamine in the prefrontal cortex on negative symptoms of SZ.
Strengths of neural correlates
- There is evidence from drug research to support the dopamine hypothesis. Dopamine agonists like amphetamines tends to increase dopamine and make schizophrenic symptoms worse in sufferers and can produce schizophrenic like symptoms in non sufferers thus supporting this idea of hyperdopaminergia.
- Anti-psychotic drugs work as antagonists - which act to reduce the levels of dopamine in SZ patients which usually reduce symptoms supporting the ides that dopamine levels are high in SZ and can be reduced by drugs (Tauscher et al 2014).
Lindstroem et al (1999) have found that chemicals needed to produce dopamine are taken up faster in the brains of schizophrenics compared controls, suggesting SZ patients produce more dopamine.
