Two Key Studies of Genetic Similarity: McGuffin (1996) & Brunner et al. (1993) (HL IB Psychology)

Key Study: McGuffin (1996)

Aim: To investigate concordance rates for depression in MZ and DZ twins.

Participants:  177 twin probands and who were registered between 1948 and 1986 with the Maudsley Hospital in London as suffering from depression. Their same-sex twin siblings were used as comparison participants. 

Procedure: The twins were assessed by clinicians via a series of tests and interviews by blind researchers i.e. the researchers were unaware as to whether the twin was MZ or DZ and whether they had depression or not. The data also consisted of the twins’ medical records.

Results: MZ twins showed a 46% concordance rate for depression compared to 20% in DZ twins. Shorter periods of depression in one MZ twin was matched by depression in their twin sibling. MZ twins aged 65 showed heightened levels of depression compared to the general population.

Conclusion: Depression may be highly heritable rather than a product of environmental factors. Short-term depression in one MZ twin appears to increase the probability of their MZ twin sibling also developing depression, which reinforces the idea that depression is genetic.

Evaluation of McGuffin et al. (1996)

Strengths

• This was a longitudinal study, conducted over decades which means that it is high in validity as the participants could be tracked over time to look for real differences in behaviour

• The use of a blind interviewer means that the study was free from bias which increases the validity of the findings

Limitations

• The concordance rate for MZ twins was 46% - if depression is entirely genetic then it should show a 100% concordance rate

• This research was conducted prior to DNA testing was available so it is possible that some of the MZ twins may actually have been DZ i.e. they may have looked identical but in fact have been biologically non-identical

Key terms:

• MZ

• DZ

• Proband 

Key Study: Brunner et al. (1993)

Aim: To investigate the violent, anti-social behaviour of specific male members of a large family in the Netherlands. The behaviour exhibited by the males in the family was borderline mental retardation (their average IQ was around 85), and violent behaviour. 

Participants: 5 males from a family in the Netherlands, all of whom had the same genetic condition, transmitted via the X chromosome on the MAOA gene. The family lived in a remote rural region of the Netherlands. Two carrier females and one non-carrier female were used as a control and compared with 3 clinically affected males.

(Carrier means that some of the females carried the faulty gene in their genotype but it was not expressed in the phenotype i.e. their behaviour)

All of the affected males acted aggressively when angry, fearful, or frustrated. Examples of their violent, anti-social behaviour included attempted rape of one of the female members of the family, arson, attacking a mental institute warden with a pitchfork, voyeurism (spying on the females in the family at night), exhibitionism (appearing naked in public). Only one of the males in the family with the faulty gene finished primary education.

Procedure: A case study (close study of a small group of individuals from one family) and quasi-experiment. A quasi-experimentis one in which the IV is naturally occurring i.e. it can’t be manipulated by the researcher – in this case the individuals involved either had the faulty gene or they didn’t have the faulty gene. Brunner conducted DNA analysis, obtained via urine samples. Observations of the males and interviews with the family provided qualitative data.

Results: None of the affected males had dysmorphic signs of the genetic mutation i.e. they didn’t ‘look abnormal’ or different physically to the unaffected males. Unaffected males in this family attended normal schools, and most had steady jobs. All the females (including several carriers) also functioned normally.

A base change in the DNA structure was identified in all 5 affected males. This in turn resulted in flawed monoamine metabolism, which is linked with a deficit of the enzyme monoamine oxidase A (MAOA) – an enzyme which (among other functions) regulates the supply of serotonin levels to the brain. The reason only males are affected is because it is specifically the single X chromosome which is responsible for the production of MAOA.

Conclusion: The dysfunctional MAOA gene may be linked to irregular serotonin metabolism which could in turn be responsible for the mental retardation and aggressive behaviour of the affected males. MAOA deficiency may account for an individual’s inability to regulate their aggression. This MAOA deficiency is now known as ‘Brunner syndrome’

Evaluation of Brunner et al. (1993)

Strengths

• This research was highly influential and resulted in the faulty MAOA gene being known as ‘Brunner Syndrome’

• By using one extended family the researchers were able to directly test their theory by using family members as control samples rather than an unrelated general population, thus validating the idea that the males’ behaviour was genetic rather than as a result of their environment

Limitations

• There are some ethical concerns arising from this study e.g. could the affected males give fully informed consent considering their low IQ? 

• The affected males may have encountered more adverse reactions from others e.g. hostility, aggression, confrontations due to their reduced IQ and lack of impulse-control which could have exacerbated their anti-social tendencies i.e. nurture may have influenced their behaviour as well as nature

Key terms:

• X Chromosome

• MAOA gene

• Serotonin