SL - Genetics and behaviour - genes and behaviour

Question 1

Beck (1967)

Answer 1

Theory based on trends in cognitive distortion between patients (Beck was a therapist).

Proposed a cognitive triad of depression: negative thoughts about themselves, negative thoughts about the future, negative views about the world.

Proposed cognitive vulnerability and reactivity. People who had early trauma had an increased likelihood of depression but not all react this way- there must be a biological factor to this difference in cognitive reactivity.

Question 2

Caspi (2003)

Answer 2

aim ->
To test if variations in the 5-HTT gene causes increased psychopathological reactions in stressful situations.

Method ->
Gathered participants with either S/S alleles, S/L alleles or L/L alleles of the 5-HTT gene and used life-history calendar from age 21-26 to identify an occurrence of certain stressful life events. Then the Diagnostic Interview Schedule at age 26 was used as a quantitative measure of symptoms of past-year depression, plus self-report of symptoms (and suicide attempts) and childhood maltreatment before age 10.

Results ->
Those with an S allele of the 5-HTT gene have an increased risk of depression, Those with an L allele had a lower risk (L/L > S/S). Additionally found that those with childhood trauma are more likely to have depression

Conclusion ->
There is a genetic component to having depression.

Evaluation ->

✔ 847 participants - good reliability (it is likely that he would find the same patterns if he were to do this again).
✔ Supported by Kobiella (2011), a piece of research that confirms the impact an S/S 5-HTTLPR allele combination can have on someone’s risk of developing depression.

❌ Correlational study, correlation does not mean causation
❌ Caspi gave no explanation for the findings, a different explanation might account for the reported relationship, including that the shorter alleles increase an individual’s tendency to get themselves into stressful situations.

Question 3

Kobiella (2011)

Answer 3

aim ->
To investigate whether variants of the 5-HTT gene affect amygdala reactivity by acting on serotonin transporter levels, or by influencing the brain’s development.

Method ->
Determined allele combinations for allocation to groups (S/S, S/L and L/L), used fMRI scans to measure amygdalae reactivity to emotionally pleasant, neutral and unpleasant pictures. Used MRI scans to measure the volumes of ppts’ amygdalae Used PET scans to measure availability (amount) of serotonin transporter protein (5-HTT)

5-HTTLPR = serotonin transporter protein
5-HTT = serotonin transporter gene
5-HT = serotonin

Results ->
confused - ask sir

Conclusion ->
The S-allele seems in some way related to increased activation in the left amygdala, specifically that it is linked to a greater degree of reactivity to negative stimuli than the L-allele is. This isn’t directly caused by different levels of serotonin transporter protein in the developed brain as there was no difference in the amount of SERT* in the different groups of ppts.
It is probable that there are other things going on as well.

Evaluation ->

✔ Supported by Caspi (2003) who has similar findings.

❌ Bad generalisability -> very small sample size of 54 people and there was unequal amounts of participants in each condition: there were a small amount of L/L allele participants.

Question 4

Kendler (2006)

Answer 4

aim ->
To determine the genetic and environmental contributions to depression in a large cohort of twins.

Method ->
Twins from the registry were contacted by telephone over a period of five years. Each was interviewed to determine:
Possible depression during previous twelve months,
zygosity (self-reported), biographical details regarding upbringing and life experiences, and other details. These findings were analysed

Results -> 
Concordance rates (likelihood of both the twins suffering from depression) were highest for monozygotic female twins, and they weren’t related to how long the twins had lived together in their “home of origin”.

Conclusion ->
As concordance rates weren’t affected by time spent together in childhood but were affected by whether twins were identical or non-identical, this points to a genetic component to depression.
The higher concordance rates for same-sex female sets of twins suggests that genes for sex might interact with genes related to depression - they suggest this might be hormone-related: women experience more hormonal fluctuations (and higher levels of some hormones) that might affect the way the genes influence depression.

Evaluation ->

✔ Good generalizability -> Enormous (42,161) sample gives robust reliability, and with a “nationally representative” wide range of ppts of different ages.
✔ Supported by Kobiella (2011) and Caspi (2003)
✔ The contributions of genetic and environmental factors remained stable across different generations, despite significant social change across that time.

❌ Correlational study -> correlation isn’t causation.
❌ The higher concordance rate for same-sex female sets of twins could be down to social differences rather than biological ones.
❌ Phone conversations might be more open to response biases than face-to-face interviews, which could mean that conclusions may lack validity.

Question 5

One gene affecting behaviour

Answer 5

Genes are sections of chromosomes that code for the production of specific proteins. These proteins affect certain physiological processes and, ultimately, can have an impact on behaviours, although the exact mechanism is not currently understood. One gene that seems to have an impact on human behaviour is the serotonin transporter (5-HTT) gene, which regulates the reuptake of the neurotransmitter serotonin from synapses within the brain. This gene has two variants (alleles) - long (L) and short (S) - that affect the amount of serotonin that is reclaimed from the synapse. Research has identified a correlation between the possession of S-allele and someone’s predisposition to develop depression.

Question 6

How 5-HTT could affect behaviour

Answer 6

Kobiella proposed that the S-allele, which leads to more efficient reuptake of serotonin (meaning that less ‘hangs around’ in synapses), could have an impact on the way the brain develops before birth. Serotonin is known to be important in brain development, and there will be less serotonin available in the developing brain of a foetus that carries an S-allele than in the brain of a foetus carrying only L-alleles. The impact of the allele on brain development might be observable only later in life, when S-allele carriers react more strongly to negative emotional stimuli (events/experiences) than others might.