GENES AND BEHAVIOUR
Theory:
Nature of the gene:
* Genes are made up of DNA which provides the blueprint for the structure and function of the human body. An individual’s genome refers to all the genes an individual possesses.
Gene regulation and gene expression:
* Not all genes an individual possesses are expressed at all times. Genes expression can be regulated, and results in differential gene expression. Therefore having a gene for a particular behaviour does not necessarily mean an individual will exhibit that behaviour.
Factors which influence gene expression:
* Genes are switched on and off by signals from inside and outside the body
* Internal signals include the presence of hormones, other chemicals, or other genes.
* The nature and nurture debate is often entangled with this topic. That is because we can see that environmental events can trigger hormones which regulate gene expression
* Environmental events may also signal special proteins, which can promote or block gene expression.
* Genes are constantly being switched on and off!
* The diathesis-stress model explains how the environment triggers the genes we have inherited which predispose behaviour. It argues that our inherited genetic predispositions are not the sole cause of certain behaviours, but that stressful environments can trigger illnesses such as depression
Sometimes, however, genes may be permanently switched off. This is achieved by DNA molecule methylation as part of the developmental process. This effect in genes is referred to as epigenetics.
* Epigenetics do not alter the DNA structure but limit DNA transcription, which may result in the genes not being expressed.
* Epigenetic changes can be passed down through generations. Since the expression of genesis can be altered we can see how our genetics may not be fully deterministic
* Mutations occur when there is a permanent alteration in the DNA sequence of genes.
Why is it important to study:
* Many genes have been linked to severe disabilities and have been strongly linked with predisposed mental illnesses which are becoming more relevant to modern studies. Genetics are thought to increase the likelihood of inheriting a disease or certain distinguishable characteristics and they are important to consider in tandem with our environment. This would allow us to be able to find modifications that can be made to promote or manage certain predispositions to improve our quality of life
Study 1: Caspi et al 2003
Aim:
* The main aim was to see why stressful experiences lead to depression in some people but not others.
* The researchers wanted to investigate the role of a gene involved with serotonin to see if it contributed to depression
Procedure:
Research Method: a longitudinal study - with each participant completing a questionnaire that measures the life events that occurred during their 21st and 26th birthdays
Sample: investigated participants at ages 3, 5, 7, 9, 11,13, 15, 18, 21 and virtually all again at age 26
Group 1:two copies of the short (s) allele of the 5-HTTLPR genotype
Group 2: one copy of the short (s) allele, and one copy of the long (l) allele of the 5-HTTLPR genotype
Group 3: two copies of the long (l) allele of the 5-HTTLPR genotype
Measure 1:stressful life events
For each of the groups, the stressful life events occurring after their 21st but before their
26th birthdays were recorded using a life-history calendar. The 14 life events included
employment, financial, housing, health and relationship stressors.
Measure 2: depression
For each of the groups at age 26, the depressive symptoms for the past year were assessed using the Diagnostic Interview Schedule.
For each of the groups at age 26, an informant (someone who knew them well) was asked via questionnaire about depressive symptoms for the past year for 96% of the participants.
Findings:
* Individuals carrying an (s) allele had a significantly stronger interaction between life events and self-reported depression at age 26.
* Individuals carrying an (s) allele whose life events occurred after their 21st birthday experienced increases in depressive symptoms from 21 to 26 years old.-
* Life events that occurred after their 21st birthday predicted more cases of new depression at 26 years old for those individuals carrying an (s) allele.-
* Stressful life events predicted major depression among carriers of an (s) allele.
* Stressful life events predicted informant reports of depression among carriers of an (s) allele (ruling out self-report bias).
* Stressful life events predicted suicide ideation among carriers of an (s) allele.
Conclusion:
* While there is no direct relation between short versions of the 5-HTT gene and depression, there is a relationship between these and incidences of stress and subsequent depression.
* The long versions of 5-HTT seem to protect against suffering from depression because of stress. The effects of gene adaptation are dependent on environmental exposure to stress.
* Environmental stressors don’t always lead to depression
Evaluation + TEACUP:
It was a natural experiment, the IV (length of the alleles) was not manipulated by the researcher. It would be impossible for demand characteristics to bias this aspect of the study. It allows us to see that the relationship between genes and behaviour is one that can only be observed, and can mean that we may not be able to form clear cause and effect relationships but rather identify correlation and positive trends allowing us to identify whether our genes impact our behaviour to some extent. Furthermore, it allows us to bypass and ethical considerations as altering ones genome it not only difficult but can be cionsidere dunethicasl in relation to this study as the gene studied it what is assumed to be deeply intertwined with depression.
Attempting to isolate the action of one gene is difficult and may not have been accurate in the study. Psychologists still do not know the exact gene that is responsible for depression as many have been identified due to the complexity of the disorder.This allows us to see the diffulty in testing the theory between genes and behviour as we do not fully know teh origins of depression and are mostly able to identify thsi by observable behviors and action carries out by people. THis means that at most we can create correlations between genes, behviour and our environments, espoecially in relation to the diathesis stress model
Study 2: Kendler et al 2006
Kendler and his team wanted to investigate three questions in their study:
1. Past studies suggest a 35 - 45% heritability of major depression. Would this be true in a large Swedish sample?
2. Are there significant gender differences in the heritability of major depression?
3. Is there evidence that genetic and environmental factors in major depression differ over time?
The sample was made up of 15,493 complete twin pairs listed in the national Swedish Twin Registry. Only twins whose zygosity could be verified were used in the study.
Procedure:
To gather their data, the researchers used a team of trained interviewers to carry out telephone interviews. Interviews were carried out between March 1998 and January 2003. The interviewers assessed lifetime major depression by using modified DSM-IV criteria. 8056 twins met the criteria for a diagnosis of major depression at some point in their life - and 322 twins voluntarily discussed a history of antidepressant treatment.
In addition to this information, the interviewers also asked questions about the twins' "shared environment" - that is when they were living in the same household - and their "individual-specific environment" - that is, adult personal life events that may make members of the twin pair more susceptible to depression.
Findings
The results indicate that the concordance rates for major depression were significantly higher in women than men. In addition, the correlations were significantly higher in monozygotic than in dizygotic twins. They also found no correlation between the number of years that the twins had lived together and lifetime major depression. The estimated heritability of major depression was 0.38, in line with previous research.
There were also no significant differences seen in the roles of genetic and environmental factors in major depression in the three cohorts spanning birth years 1900-1958. Even when they split the entire cohort into pre and post-World War II, there was no significant difference.
Conclusions:
This study suggests both that the heritability of major depression is higher in women than in men and that some genetic risk factors for major depression are sex-specific. In addition, the study confirms the level of heritability of major depression found in other studies, strengthening the reliability of European twin studies.
Evaluation + TEACUP:
Please evaluate for me !
Additional TEACUP
T- hard to isolate and conclude that specific genes are caused/ correlate to different behaviours and illnesses such as depression. This is because our behaviour is often a combination of multiple genes in tandem with various usually uncontrollable environmental factors
E- /evidence from Caspi et al 2003 highlights how the relationship between the 5-HTT gene and the number of depressive episodes people experience throughout their lives. This enunciated how strong the correlation between genetics and behaviour can truly be.
C&U - other factors such as past trauma and experiences play a major role in our behaviour and this is not emphasized in the theory, showing the bias towards the deterministic standpoint of investigating behaviour.
LAQ PLAN:
Theory:
→ define DNA and Genetics
→ influences of genes on behaviour
→ Diathesis-stress Model
Topic sentence 1: one way we can test to see the influence of generics on our behaviour is through twin studies, This is because by having the same genes, we can see if twins display similar behaviour and draw conclusions about the influence of certain genes on our behaviour
→ Study 1: Kendler et al 2015
Topic sentence 2: Another way in which we can see the effect of genetics, is through how genes affect our behaviour in response to environmental triggers
→ Study 2: Caspi et al (2003)
Additional TEACUP
conclusion