Neurobiological bases to risk factors for offending- Part 2.

Question 1

What does behavioural genetic research do?

Answer 1

It looks at the contribution of genetics and the contribution of the environment to antisocial behaviour.

Question 2

Classical twin design:

Who do classical twin studies compare?

Say some information about mono-zygotic twins.

Say some information about dizygotic twins.

Using these two groups, what can you establish?

Answer 2

Mono-zygotic and dizygotic twins.

Identical- share 100% of their genes + common environment.

Fraternal- share 50% of their genes + common environment.

Can establish what extent of a behaviour is more driven by genes or the environment or both.

Question 3

Continuation from classical twin design:

How is this done?

What happens if the correlation is higher in the two pairs?

Answer 3

Measure the antisocial behaviour of identical twins- will get a correlation- do the same for non-identical twins- correlation would be less, share less genes.

Tells us how heritable a trait or specific behaviour is.

Question 4

Genetic contribution - antisocial behavior:

By comparing the measures of antisocial behaviour between monozygotic and dizygotic twins, what three things is the variance of antisocial behavior divided into?

Answer 4

1) Genetic factors (or heritability, h2).
2) Shared environmental factors (c2).
3) Non-shared environmental factors (e2).

Question 5

What is a shared environment?

What is a non-shared environment?

Answer 5

Environmental experiences that make family members similar like the same school.

Unique environmental experiences that make family members dissimilar to each other- e.g. one twin having a accident leading to a brain injury and the other twin not having this.

Question 6

What can a shared environment have on different siblings?

Give an example.

Answer 6

Different effects.

Being brought up in poverty will have a different effect on both siblings (have some differences in genes).

Question 7

Who did a study based on twins?

What kind of study was it?

What did they look at?

What can non-aggressive be?

What did they look at?

Answer 7

Burt et al.

A meta-analysis- lots of twin studies.

Antisocial behaviour- split into aggressive + non-aggressive.

Rule breaking but not engaging in physical aggression.

The genetic contribution of aggressive and non-aggressive behaviour.

Question 8

What did they find? 2 findings.

What contributes equally?

Answer 8

1) Aggressive behaviour- genetic contribution (heritable)- not due to shared environment.
2) Opposite for rule-breaking- less genetically driven- more driven by shared environmental characteristics.

Non-shared environmental characteristics.

Question 9

What are psychopathic traits in youths and adults split into? 2 things.

What is the affective dimension often termed as?

What is this a central feature to?

What aspect of psychopathy does callous-unemotional traits refer to?

Answer 9

Affective (lack of stuff like empathy) and interpersonal deficits (e.g. superficial charm).

Overt impulsive, irresponsible, and antisocial behavior.

Psychopathy.

Affective aspect.

Question 10

What can callous unemotional traits do?

What does the DSM-5 include callous-uemotional traits as?

Answer 10

Distinguish a subgroup of youths with conduct problems- they show more severe and stable patterns of antisocial behavior (psychopathic like traits).

An indicator of conduct disorder.

Question 11

What are youths with AB and high CU like? 4 things.

What are youths with AB and low CU like?

Answer 11

1) Planned violent behaviour.
2) Do not react emotionally to others distress.
3) Do not think of punishment.
4) Genetically vulnerable to antisocial behavior.

The opposite- do not lack things like empathy + understand the consequences of their behaviour.

Question 12

Where have twin studies which examine the causes of callous-unemotional traits been done?

What varies here?

What do the studies focus on?

When is heritability inferred?

Answer 12

Youth in USA+ Sweden + UK.

Size of the sample + ages.

Genes.

When greater resemblance on a trait/behaviour is seen in identical rather than non-identical twins.

Question 13

How are the findings from studies on callous-unemotional traits like?

What do the studies show?

What does data from TEDs also show?

When was high heritability still found?

Answer 13

Consistent.

Youth have moderate to strong heritability of callous-unemotional traits- 40-78% is due to genes.

High level of callous-unemotional traits- under genetic influences- 67% accounted for heritability.

Still found when combined with high levels of antisocial behaviour (CD).

Question 14

What is one thing you need to keep in mind about callous-unemotional traits?

Answer 14

Measured with different tools + differences exist between tools.

Question 15

The warrior gene:

What is the warrior gene also called?

What does this look at?

What is there a connection between?

What does warrior gene comprise of?

Are there different variants of the gene?

Answer 15

Monoamine oxidase A (MAO-A) gene (3R).

Specific genes, not heritability of twin studies.

Version of warrior gene + different types of antisocial behaviour.

Variations in X chromosome- produces monoamine oxidase- this enzyme affects dopamine, norepinephrine and serotonin.

Yes- low and high expression.

Question 16

What did Caspi et al (2002) do?

What did they find?

Answer 16

Identified people with low + high MAO-A activity + whether they had been abused as a child.

Evidence of strong interaction between low MAO-A activity and childhood maltreatment (in terms of likelihood of developing conduct disorder).

Question 17

What did another study look at?

What did they find?

What do these studies show?

Answer 17

Violent offences (16-30) + maltreatment (physical and sexual abuse).

Significant interactions between sexually abused and the low version- they also committed more violent offences.

That you should keep genetic contributions in mind.

Question 18

What are the 3 prenatal factors?

What are the perinatal risk factors?

What are the postnatal risk factors?

Answer 18

1) Abnormalities in foetal development.
2) Maternal alcohol (FAS + FASD), tobacco and drug use.
3) Prenatal malnutrition.

Birth complications and maternal rejection.

Adverse childhood experiences, poor nutrition and head injury- also attachment and substance abuse.

Question 19

Abnormalities in foetal development:

Where do minor physical anomalies (MPAs) arise from?

What are MPAs characterised by? 3.

Answer 19

From abnormalities in foetal development (genetic) also anoxia, bleeding, or infection during pregnancy.

Curved pinky, low-seated ears and furrowed tongue.

Question 20

Continuation of abnormalities in foetal development:

What have studies show about MPAs?

Who has increased MPAs?

Answer 20

Correlation between MPAs and aggressive behaviors in children as young as 3.

School-aged boys- have behavioral problems also.

Question 21

Continuation of abnormalities in foetal development:

When MPAs were identified at 14, what does this predict?

What does MPAs interacting with adverse life experiences (like marital conflict) lead to?

Answer 21

Violence at 17.

Physical neglect + predicts conduct problems in adolescence.

Question 22

Continuation of abnormalities in foetal development:

Who did a study on MPAs and when?

Who did they do this study on?

What did they find?

What kind of studies is this?

Answer 22

Brennan, Mednick, and Raine (1997).

Male children of psychiatrically ill parents.

Having both MPAs and family adversity = high rates of adult violent offending.

Correlational studies.

Question 23

Maternal alcohol, tobacco and drug use:

What causes fetal alcohol syndrome (FAS) or fetal alcohol spectrum disorder (FASD)?

What is alcohol considered?

What can a high concentration of alcohol prevent?

What areas of the brain are most vulnerable to alcohol?

When is alcohol consumption most harmful?

Answer 23

Excessive alcohol use in pregnancy.

A teratogen.

Nutrition and oxygen getting to the fetus’ vital organs, like the brain.

Hippocampus, basal ganglia and the corpus callosum.

During the first trimester- can still be harmful throughout.

Question 24

Continuation from maternal alcohol, tobacco and drug use:

What is alcohol harmful to?

What is one physical effect of FASD?

What else has FASD been linked to?
4 things.

Answer 24

Brain and development.

When in-between nose and mouth it is totally flat.

Psychological problems like:

• Behavioural and emotional regulation problems.
• Language delays.
• Memory issues.
• Executive functioning issues.

Question 25

Continuation from maternal alcohol, tobacco and drug use:

What is it difficult to do sometimes?

What does FASD do?

Answer 25

Making a differential diagnosis between CD and this syndrome- can interact.

Predisposes individuals to antisocial behavior.

Question 26

Continuation from maternal alcohol, tobacco and drug use:

Who did a study based on this?

Who did they look at?

What did they find? 3 things.

Answer 26

Streissguth, et al (1996).

400 adolescents + adults with FASD.

1) 60%- trouble with the law.
2) 50%- showed unwanted sexual behavior.
3) 30%- alcohol/drug problems.

Question 27

Continuation from maternal alcohol, tobacco and drug use:

Do those with FASD have high recidivism rates (as victims and offenders)?

What percentage of the incarcerated populations-adolescences- have FASD?

What percentage of the incarcerated populations- adults- have FASD?

Answer 27

Yes.

32%- adolescences.

42%- Adults.

Question 28

Maternal smoking:

What is maternal smoking a risk factor for? 4 things.

How do cigarette smoke affect the baby?

What essentially happens?

Answer 28

Miscarriages, perinatal mortality, low birth weight and premature birth.

Interferes normal placental function- Acts as a vasoconstrictor, reducing uterine blood flow- Causes fetal hypoxia-ischemia and malnutrition.

Foetal- deprived of oxygen + nutrients- Impacts brain development.

Question 29

Continuation of maternal smoking:

What does nicotine do?

What else does it do?

Answer 29

Targets nicotinic acetylcholine receptors- changes the the pattern of cell proliferation and differentiation (synaptogenesis/synaptic pruning).

Causes abnormalities in the development of synaptic activity.

Question 30

Continuation of maternal smoking:

Studies by Fergusson, Woodward, & Horwood (1998) + Orlebeke, Knol, & Verhulst, 1997; Wakschlag et al., (1997) showed prenatal smoking predicted what?

What does evidence from- Brennan, Grekin, & Mednick, 1999; Maughan, Taylor, Caspi, & Moffitt (2004)- show?

Answer 30

Bad behaviors in childhood + criminal behavior in adolescence.

A dose-dependent relationship between smoking and later criminal behaviour- High levels of smoking = higher risks of criminality.

Question 31

Use of illicit drugs in pregnancy and pre-natal malnutrition:

How many women use illicit drugs?

What do they also do?

Does it make it harder to show the sole effect of the illegal drugs?

A study by Lester et al (2004) showed cocaine-exposed children in the utero are more likely to have what?

Answer 31

32%.

Also use cigarettes and alcohol during pregnancy.

Yes.

Poor sustained attention, more disorganization and less abstract thinking than peers- Leads to offending.

Question 32

Continuation of the use of illicit drugs in pregnancy and pre-natal malnutrition:

What did Hibbeln et al. (2007) do?

What did they find?

Answer 32

Looked at 11,875 pregnant women + their consumption of fatty acids.

Eating foods less rich in omega-3 fatty acids = children with lower scores on many neurodevelopmental outcomes + had more antisocial behaviour.