L3 - Genetic Influences on Antisocial and Violent Behaviours Flashcards

1
Q

Briefly describe the case of Jeffrey Landrigan

A

Jeffrey was adopted into a loving middle class professional family, but ended up in a life of crime. He was sentenced to death after committing his second murder. His father, Darrel Hill was locked up in the same prison, after also killing two people. Landrigan’s grandfather was also a career criminal having been shot to death by police, and Landrigan’s great grandfather was a notorious bootlegger (seller of illegal goods)

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2
Q

What are the 3 lines of evidence in behavioural genetics?

A
  • adoption studies
  • identical and fraternal twin studies
  • identical twins separated at birth
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3
Q

What are the two lines of evidence in molecular genetics?

A
  • XXY

- Candidate genes

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4
Q

What are MZ twins and how much genetic material do they share?

A

Monozygotic/Identical twins - share virtually 100% of their genes

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5
Q

What are DZ twins and how much genetic material do they share?

A

Dizygotic/fraternal twins - share about 50% of their genes

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6
Q

What percentage of the population are twins?

A

2%

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7
Q

What is the proportion of MZ and DZ twins?

A

DZ/Fraternal - 92%

MZ/Identical - 8%

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8
Q

The variance in antisocial behaviour between MZ and DZ twins can be divided into which elements?

A
  • Genetic factors
  • Shared environmental factors
  • Non-shared environmental factors
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9
Q

When analysing the variance in ASB between MZ and DZ twins, how do we tell if genes influence the ASB?

A

If genes do influence ASB, the degree of similarity in ASB between twins that are MZ will be greater than that between twins that are DZ.

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10
Q

Name 3 shared environmental factors

A

Persoanlity of parents
SES of family
Number of books in the family

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11
Q

Name non shared environmental factors

A

Friends
School
Birth order (and parenting style for each)
Way the child acts, influencing parenting style

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12
Q

When analysing the variance in ASB between MZ and DZ twins, how do we tell if the environment influences the ASB?

A

There will be a greater degree of similarity in ASB between DZ twins than MZ twins.

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13
Q

In the twin study design where does error get included? What does this mean for the other factors?

A

In the non-shared environmental factors - therefore the genetic factors are always underestimated.

Why? If there is more variance assigned to the non-shared, just because it is unknown, there is less being assigned to genetic influence if/when it should be.

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14
Q

What is the range of heritability for ASB?

A

Ranges between .4 and .5

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15
Q

What is the percentage contribution of the shared environment to ASB?

A

Between 15 and 20%

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16
Q

What is the percentage contribution of the non-shared environment to ASB?

A

30%

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17
Q

What is the difference in heritability between reactive and proactive aggression?

A

Reactive - .39

Proactive - .50

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18
Q

What is the difference in heritability between aggressive and non-aggressive ASB?

A

.Aggressive - .65

Non-aggressive - .48

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19
Q

What is the difference in contribution of the shared environment between aggressive and non-aggressive ASB?

A

Shared influence on:

Aggressive - .50
Non-aggressive - .18

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20
Q

Heritability is strongest for which forms of ASB?

A

Early-onset, persists and occurs across different settings, and involves psychopathic tendencies (CU traits)

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21
Q

What did Viding, Frick and Plomin (2007) study about the heritability of CU traits at early ages?

A

Looked at 7 year olds’ CU traits. Selected extreme end of the sample to look at heritability of those CU traits. Twin sample included DZ and MZ twins.

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22
Q

What did Viding, Frick and Plomin (2007) find about the heritability of CU traits at early ages?

A

2/3rds of CU traits at 7 years old is under genetic influence.

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23
Q

How did Viding, Jones, Frick, Moffitt & Plomin, (2009) study the heritability for ASB between a high CU group and low CU group

A

Of the youths that were in the top 10% for ASB, two subgroups were created based on top 10% for CU traits and bottom 10% for CU traits.

Assessed for heritability of ASB at 7 years and 9 years.

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24
Q

What did Viding, Jones, Frick, Moffitt & Plomin, (2009) find about the heritability for ASB between a high CU group and low CU group

A

Heritability for ASB in the high CU group was .81 - ASB is mostly explained by genetic influence, for both age groups.

Genetic influence is much lower for group with ASB and low CU traits (.3), for both age groups

No shared influence for high CU group, but a third influence for low CU group, at 7.

So authors seem to have found that, within children with ASB, two different subtypes exist based on their level of callous-unemotional traits, and seem to have distinct/differing etiologies.

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25
Q

Viding, Frick and Plomin (2007) found that there is a degree of genetic overlap between ASB and CU traits. What does this mean?

A

The causal mechanisms for ASB and CU could well be similar. It tells us that an individual with a high level of CU traits is also likely to have a high level of ASB.

26
Q

What did Sariaslan, Larsson and Farzel (2016) find about the heritability of violent crime and other major disorders, using twin study designs?

A

Used just under a million twin-sibling pairs from Sweden, gathered over a 30-year period.

Found that the heritability of violent crime was .54.

The heritability of other disorders were as follows:

Schizophrenia: .71
Bipolar disorder: .62
Substance misuse: .53

27
Q

What did Langstrom et al., (2015) find about the heritability of sexual offending, in a Swedish population?

A

Familial aggregation of sexual crime. Combined nationwide Swedish crime records, and multigenerational family registers.

Increased aggregation of sexual offences in brothers of convicted sex offenders.

Genetic factors (40%) and non shared environmental factors (58%) explained the liability to offend sexually.

Genetic effect varied depending on the type of sexual offending, such as rape (19%) and child molestation (46%).

28
Q

Why might identical twins be more similar than fraternal twins, in terms of the shared environment?

A

People may treat identical twins more similarly than people treat fraternal twins - making the shared environment more shared for MZ twins than DZ twins.

29
Q

Why did twin studies begin to evolve into studies of identical twins separated at birth?

A

To overcome the problem of more similar treatment for MZ twins than DZ twins. By comparing the behaviour and antisocial outcomes of MZ twins reared apart, we can see the true effect of genetics while accounting for environmental factors

30
Q

What did Gove et al., (1990) find about the heritability of ASB in MZ twins separated shortly after birth?

A

Heritability in:

Children: .42
Adults: .28

31
Q

What is the rationale for using adoption studies instead of using twin studies?

A

twin studies:

  • overestimate the genetic influence due to the assumption that MZ twins and DZ twins are treated the same by others (have smaller shared environment than actually is the case)
  • underestimate the genetic influence because unknown variance, error, is attributed to the non-shared environment.

Adoption studies simply compare levels of ASB in children sent to foster families between those with criminal biological parents and non-criminal biological parents - therefore, the two above assumptions are not made.

32
Q

In adoption studies, how can we tell the extent of genetic influence?

A

Experimental group have criminal biological parents, control group have non-criminal biological parents. Both groups/all children are sent to foster families.

–> if the level of ASB is higher than the control group, a genetic influence has been demonstrated.

33
Q

What did Mednick et al.’s (1984) adoption study show about the genetic influence of property crime and violent crime?

A

Significant positive correlation between children and biological parents for convictions of property crime, but not for violent crime.

34
Q

What did Kendler (2014) show about the environmental and genetic contribution to criminal behaviour?

A

Environmental risk index and genetic risk index both strongly predicted the probability of criminal behaviour. Contributed additively.

Criminal behaviour is etiologically complex and influenced by a range of genetic risk factors.

Genetic risk factors for violent and non violent criminal behaviour may be partially distinct

35
Q

Findings in adoption studies have been consistent, and are regardless of:

A
  • age of participants
  • study period
  • countries
  • measures of ASB
  • study design
36
Q

What is the percentage of men with XYY in clinical samples?

A

Around 4%

Jacobs et al., (1965)
Scottish high security hospital for patients with severe mental disabilities - 4% had the XYY makeup

Telfer et al., (1968)
4 different institutions in Pennsylvania
5/129 were XYY - 3.9%

37
Q

What is the prevalence of the XYY in the general population?

A

1 in 1000

38
Q

What is XYY syndrome?

A

A condition in men where they have an extra Y chromosome. Typically leads to tall men, with acne and an increased risk of learning problems.

39
Q

What did Witkin et al., (1976) show about associated outcomes with XYY?

A

XYY is associated with crime, but not violent crime.

40
Q

What did Ross et al., (2012) compare and find about XYY?

A

Control men vs XYY men vs Kleinfeld syndrome (XXY)

Childhood behavioural checklist . XYY and XXY scored higher than controls, but they are still within 2 SDs of healthy individuals.

Only a few with the syndrome that are scoring highly and are driving the group mean.

41
Q

What are polymorphisms?

A

Genetic variations of chromosomes.

42
Q

What are candidate genes?

A

A gene or variation in a gene that may relate to the construct/disorder of interest.

Physically, genetic variants that bias the functioning of several brain regions and hormonal circuity, which mediate the body’s stress responses.

43
Q

What are neurotransmitters?

A

Chemicals in the brain that allow communication between neurons

44
Q

What percentage of genes are expressed in the brain?

A

70%

45
Q

What did Brunner et al., (1993) find about men in a family showing signs of extreme violent behaviour?

A

Tracked down the men, urine- and blood-sampled them to genotype them.

5 brothers showed based change in the DNA structure on the MAOA gene.

Thought to contribute to the extreme aggressiveness they showed when angry, fearful or frustrated.

46
Q

What does the MAOA gene do?

A

Degrades amine neurotransmitters such as dopamine, serotonin and epinephrine.

47
Q

What does the low activity of the MAOA gene lead to, synaptically?

A

Less effective at clearing serotonin at the pre-synapse.

48
Q

What percentage of the population have the low activity allele of the MAOA gene, and why do they not all show abnormally aggressive behaviour?

A

30%

Low activity allele needs to interact with the environment to develop behaviour such as that seen in Brunner syndrome

49
Q

What did Caspi et al (2002) show about being a carrier of the high/low activity allele of MAOA interacted with level of childhood maltreatment?

A

No significant difference between the high and low activity allele if there was no childhood maltreatment.

Those carrying the low activity allele were much more likely to show a high level of antisocial behaviour than those with the high activity allele, at the extreme end of childhood maltreatment.

First demonstration gene vs environment risk factor interaction, and it was observed regardless of how antisocial behaviour/outcomes was defined.

50
Q

What did Eisenberger et al., (2007) find about students with the low-activity MAOA allele?

A

Students with the low-activity allele show greater brain responses following social exclusion, than students with the high-activity allele.

51
Q

What did McDermott et al., (2009) find about the associations with the low activity allele of the MAOA gene?

A

In lab settings, MAOA-low was associated with higher levels of aggression following provocation.

52
Q

What did Holtz et al., (2014) study and find about sex differences in the relationship between the MAOA-activity polymorphism and aggression?

A

The relationship between MAOA activity and aggression shown in males is the opposite in females.

Measured childhood life stress, and then later genotyped for the MAOA gene (establishing high or low activity allele). Measured response to emotional faces.

3-way interaction:

In males, high CLS, higher amygdala response if carrying the low-activity allele. In females, the higher CLS, the greater the amygdala activity if they were carrying the high-activity allele.

Males - low activity allele, positive relationship between amygdala activity and aggression later in life.
Females - positive relationship between amygdala reactivity and later aggression, but for the high-activity allele.

53
Q

What is a genetic polymorphism?

A

The inheritance of a trait controlled by a single genetic locus with two alleles.

(the least common allele has to have a frequency of at least 1%)

54
Q

What is the role of dopamine, and the specific relation to aggression?

A

Involved in reward-seeking behaviour - acts as the driver/motivator.

Evidence showing aggression associated with high level of dopamine

55
Q

What is the role of serotonin, and its specific relation to aggression?

A

Mood stabiliser, biological brake for impulsive behaviour. Affects mood and social behaviour

High level of aggression associated with low serotonin turnover/removal from synapses - higher level of build-up.

56
Q

What are the two versions of the serotonin transporter gene

A

Short and long.

Short version is associated with higher levels of serotonin in the synaptic cleft, higher emotional response, impulsivity and affective dysregulation.

57
Q

Those with a high level of childhood maltreatment, and the short version of the serotonin transporter gene (5-HTTLPR) have a greater risk of what?

A

Higher risk of depression

Externalising behaviour

58
Q

What did Weeland et al., (2015) find about the association of the short or long version of the serotonin transporter gene (5-HTTLPR) with externalising behaviour?

A

Both the short and long version of the serotonin transporter gene (5-HTTLPR) can lead to increased externalising behaviour - what matters is the environment in which you are raised.

59
Q

What did Sadeh et al., (2010) find about the relationship between the serotonin transporter gene, economic status and level of CU traits?

A

Showed, in 2 separate samples, that carrying the long version allele, and living in low area of SES, is associated with CU traits.

60
Q

What did Glenn (2011) claim about the link between the polymorphism in the serotonin transporter gene and psychopathy?

A

Claims that, if you carry the long version, you might be at increased risk of carrying callous-unemotional traits in psychopathy. Therefore, we need to look at the effects of the long version allele, rather than focusing on the short allele so much.

61
Q

What did Cicchetti et al., (2012) find about the link between maltreatment, serotonin transporter gene and levels of CD symptoms/delinquent behaviour?

A

Maltreatment and short version of the serotonin transporter gene leads to higher self-reported levels of conduct disorder symptoms.

Also associated with an increased level of delinquent behaviour.