Genetics Flashcards

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1
Q
  1. Genetic similarities (MZ & DZ twins used to study genetic heritability)
A

Falconer model → calculate heritability of trait / behaviour from observed similarities b/w MZ & DZ twins by accounting for heredity, shared env, & individual env

What are DZ, MZ twins? Concordance rate higher for MZ twins = genetics

Gottesman & Goldsmith (1994)

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2
Q

Gottesman & Goldsmith (1994)

A

→ concordance rate of juvenile delinquency in MZ & DZ twins
→ 85 sets of young twins - likelihood of committing crime
→ 91% for MZ, 73% for DZ
→ genetics is a factor in aggression/delinquency but not 100%

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3
Q

Evaluation of Gottesman & Goldsmith (1994)

A
  • TRIANGULATION → studied over 500 ADULT twins, 0.52 MZ, 0.23 DZ for criminality
  • Large sample, significant results → generalisability
  • EQUAL ENVIRONMENT ASSUMPTION
  • Twin research not highly representative of general populace
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4
Q
  1. Genetic Similarities (DZ & MZ twins along with other types of kinship studies)
A
  • Making comparisons based on genetic relatedness
  • Drawing conclusions about genes & behaviour

Natsuaki et al (2009)
- Externalising antisocial problems in children (Whit, middle class)
- Longitudinal study, 390 sibling pairs, antisocial behaviours towards others
- MZ twins (0.59), DZ (0.21), then full, half, & genetically unrelated siblings
- Also found deviancy training (social learning) e.g. of environmental factor → behaviour of 1 could influence other

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5
Q

Natsuaki et al (2009)

A
  • Longitudinal → same group of participants followed throughout entire study so less participant variables
  • Developmental trends
  • Did not identify a specific gene
  • Issues w/ bidirectional ambiguity → correlation only
  • No direct observational data → used a quantitative behavioural genetic design. May be able to pinpoint specific genes if DNA data collected
  • Increased complexity in family structures = need to replicate findings w/ other samples
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6
Q
  1. Genetic Similarities & Genes (Counterclaim → environmental factors more impactful than genes)
A

Brendgen et al (2006)
→ teacher-rated reactive & proactive aggression in 6-year old twins pairs (172)
→ genes = 39% of variance for reactive, 41% of variance for proactive
→ rest explained by unique env. factors
→ aggression influenced by socialisation experiences specific to each type of aggression

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7
Q
A
  • future studies aimed at isolating specific genes + env. variables
  • Implications for preventative interventions → tailored to specific temperamental & socialisation needs of child
  • Physical aggression only
  • Other methods needed besides teacher ratings
  • Parent ratings might be better - kids act dif at school
  • research → genetic effects decrease w/ age, non-shared env. influences increases
  • possible that heritable factors may play a larger role initially in placing a child at risk for reactively or proactively aggressive behaviour but that later socialisation experiences determine whether the child overcomes this risk
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8
Q

What is MAOA? (1st body paragraph of genes)

A
  • MAOA functions in neuronal mitochondria
  • regualtes levels of dopamines + serotonin
  • in absence of sufficient levels of MAOA, neurotransmitters / hormones accumulate in neurons
  • normal people = MAOA-H, others have MAOA-L
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9
Q

Meyer Lindenberg et al (2008)

A
  • How differences in MAOA gene affects brain activity when exposed to threat
  • fMRI, 1 group MAOA-H, MAOA-L, both shown angry / fearful faces
  • MAOA-L = more activity in amygdala, less in vmPFC
  • More emotional arousal (amygdala) & impulsivity (less activity in vmPFC) for MAOAL
  • Low ecological validity + low operationalization of aggression
  • Viewing only angry faces
  • Lying in magnetic tube & not seeing real humans
  • Didn’t account for other factors influencing aggression (e.g. testosterone)
  • Only investigates 1 type of aggression (responsive)
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10
Q

Body paragraph 2 for Genes & Behaviour – environmental factors can influence expression on MAOA-L gene

Caspi et al (2002)

A
  • interaction b/w MAOA & env = antisocial behaviour - over 1000 children, Dunedin (NZ), over 25 years (longitudinal) - MALES ONLY
  • Sample genotyped, env. factors assessed (maltreatment)
  • antisocial behaviour measured by clinical diagnosis of conduct disorder, personality checklists, official conviction records
  • Participants w/ MAOA-l gene variant who were abused as children more likely to be antisocial + aggressive compared w/ just those w/ gene alone
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11
Q

Evaluation of Caspi et al (2002)

A
  • High ecological validity + longitudinal
  • Genetics & environmental interactions
  • Low internal val since study did not take into account many confounding variables + major life events
  • Partial cultural bias (NZ)
  • Ethical considerations (assessed from birth) + stigmatisation
  • Only focused on MALES → another study by -Sjoberg et al (2007) showed teenage females did not have the same effects
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