Neurobiology of Crime
48 important questions on Neurobiology of Crime
What did Murray et al. (2016) find?
Specific to childhood-onset (means it is more pervasive, more long-term and massive detrimental effects long term) - Moffet et al showed that 30 years later, these individuals are more likely to be incarcerated for a violent offence, more likely to unemployed, remarried several times
As well as prenatal exposure to alcohol consumption, does the influence of antisocial parents contribute to antisocial behaviour?
What are examples of perinatal risk factors?
= all of these things in sum are related offending and antisocial behaviour; they are peripheral markers of development
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What postnatal factor is associated with antisocial behaviour? What are the mechanisms behind this association?
Nutrient deficiencies lead to impaired brain functioning, and a predisposition for antisocial behaviour in childhood and adolescences (Lister et al. 2005)
--> Poor nutrition affects neuropsychological development e.g. executive function, IQ, which in turn impacts behaviour
What did Jackson et al. (2016) study?
Found that factors that are predictive of antisocial behaviour include:
- antisocial behaviour of the parents
- poor quality nutrition
- low vegetable consumption
- low fruit consumption
- high sweets consumption
What did Raine et al. (2015) find?
Over the 12-month period:
40% reduction in externalizing behaviours
68% reduction in internalizing behaviours
Omega-3 strengthens neurological function
What disorder would display externalising and internalising behaviours?
- Omega-3 a treatment?
Having a head injury increases the risk of offending by at least...
What percentage of adults in prison and young offenders have a history of head injury?
30% of young offenders
To what extent does a head injury increase the risk of developing a mental health problem?
What did Vaughn et al. (2015) find?
Limitation of study - the researchers didn't look at where the brain injury was from - would have been interesting, e.g. did the head injury come from when they were exposed to violence?
Where was Charlie Whitman's brain tumour? What was his crime? What was he like before his crime?
He killed his wife, mother and open fired on a university campus
Charlie Whitman had no history of antisocial behaviour, showed a good academic record, won a scholarship at his university. Hen then started feeling very hostile, had aggressive thoughts and disgust towards other people
How does secure attachment affect behaviour?
- high levels of self-esteem
- positive relations with others
- accepting intimacy and close relations
How does dismissive (avoidant) attachment affect behaviour?
- minimal reliance on others
- desire for independence (often appears as an attempt to avoid attachment altogether)
- deals with problems by social withdrawal
- aggressive and suspicious of others
- maintains distance from partners
How does preoccupied attachment affect behaviour?
- seek high levels of intimacy
- become dependent on attachment figures
- less positive self-perception
- high levels of emotionality, emotional dysregulation, worry, and impulsiveness in relationships
- immense fear of abandonment
How does disorganised attachment affect behaviour?
- child is caught in conflict which is frightening and lacks security
- individuals may act passive-aggressive
- most often associated with psychiatric disorders
- they develop maladaptive strategies for friendships
- predictive of hostile behaviours and psychosocial problems
What is Mitchell & Beech's (2011) definition of attachment?
Regarding neurochemistry of attachment, are we born a level of predisposition for attachment style? What other factors may affect this?
--> this is influenced by environmental factors and biological factors
Note: Environmental factors can influence biological factors and vice versa --> it is important to understand that while these are unique factors, they are intertwined
- which can then ultimately affect our type of attachment
What is the ACE model?
C = shared family environment (common/shared experience)
E = environmental risk factors unique to the individual (non-shared experiences)
Using the ACE model, what did Larson et al. (2006) find in its prediction of psychopathy?
C = 0% of the variance
E = 37% of the variance
The best predictors of psychopathy in terms of genes, family environment, and individual environment risk factors are the A and E
Psychopathy is largely influenced by genetics
Using the ACE model, how does psychopathy compare to aggressive behaviour? Who studied this?
= A and E were equally important in explaining aggression = less of an emphasis on genetics - this makes sense as aggression is not a disorder, it's a behaviour
Using the ACE model, how does psychopathy and aggressive behaviour compare to antisocial behaviour? Who studied this?
A = 40-50% of the variance
C = 15-20% of the variance
E = 30% of the variance
---> for antisocial behaviour, there seems to be more factors at play - this make sense because psychopathy is a disorder whereas antisocial behaviour is a behaviour and is therefore influenced by more things
What is the multiplicative effect? According to which researchers?
(Cloninger et al. 1982)
What is the warrior gene?
Regarding the MAO-A gene, what did Caspi et al. (2002) find?
--> shows gene by environment interaction
Antisocial personality disorder is similar to psychopathy; however there are some differences. What are these differences?
What did Raine at al. (2000) study?
--> they looked at the white and grey matter volumes in the prefrontal cortex
Results:
The grey matter volume is a lot lower in individuals with antisocial personality disorder (reported an 11% reduction) --> suggests something to do with the prefrontal cortex that is affecting these individuals. Suggests PFC is a biological marker for these individuals
PFC has a role in inhibition, executive function --> may explain why someone with APSD has difficulty with responses , such as theft, getting into arguments and fights
This is neuroimaging evidence
How does the neurobiology of people with ASPD differ?
- smaller temporal lobe (Dolan et al. 2002)
- reduction in dorsolateral prefrontal cortex, medial prefrontal cortex, and the orbital prefrontal cortex (Laakso et al. 2002)
= diminished activity in the PFC
People with ASPD show diminished activity in the PFC. How is the similar to conduct disorder? Why is this not surprising?
- reduced grey matter volume in orbital prefrontal cortex (Huebner et al. (2008)
- reduced grey matter volumes in the amygdala (Sterzer et al. (2005)
- reduced right temporal lobe volume (including amygdala; Krusi et al. 2004)
CD is a precursor for ASPD (ASPD = only diagnosed in adults)
Who was Herbert Weinstein?
= he had a large cist putting pressure on his PFC which would effect his impulsive behaviour
--> Before, Weinstein had no history of violence
--> This neuroimaging evidence shortened his sentence from 25 to 7 years
What neuroactivity do psychopaths typically display less of?
What is the role of the amygdala? What can be said about the amygdala function of murderers?
--> murders amygdala’s don’t function normally. They may recognise that someone is afraid but they do not have any concern for that person – they would take advantage of this i.e. pretend to help a crying child but then kidnap/murder them
Why is the orbitofrontal cortex important?
--> if this cortex isn’t working, the person does not have this breaking system and will go ahead a commit a crime
What is the role of the anterior cingulate?
Involved in modulation of emotional responses, motivation, error detection
What is the social-push theory and who was it proposed by?
The theory states that biological factors may more likely explain antisocial behaviour in the absence of predispositional social factors
The effect of the gene-environment interaction is embedded in the social-push theory
How did Goldman & Ducci (2007)'s study contribute to neurobiological research?
Findings:
1) Most genetic effects upon antisocial behaviour increase with age while shared environmental effects decrease with age
2) Early-onset antisocial behaviour is more heritable than later-onset conduct disorder
3) Family environment is relevant for the initiation and early maintenance of aggression (particularly in men), but its effect fades
4) Some genes influence antisocial behaviour across the entire lifespan, and others only in adolescence and adulthood
(p. 74 textbook)
What are the 2 prefrontal regions most consistently found to be impaired in antisocial, violent individuals?
dorsolateral prefrontal cortex (DLPFC)
(p. 75 textbook)
What is the role of the orbitofrontal cortex?
(p. 75 textbook)
What is the role of the dorsolateral prefrontal cortex?
(p. 75 textbook)
How may the temporal lobe be linked to violent criminal behaviours?
(p. 75 textbook)
What study supports Soderstrom et al's. (2000) finding that the temporal lobe is associated with violent behaviour?
--> reduced activity in the left anterior temporal cortex in individuals convicted of impulsive violent offensive
(p. 75 textbook)
How may deficits in the amygdala-hippocampal complex be associated with violent behaviour?
Note: the amygdala-hippocampal complex is within the temporal region, so in an essay you could say that the temporal cortex is also linked with violent criminal behaviour, particularly the amygdala-hippocampal complex
(p. 75 textbook)
What is a limitation of neuroimaging evidence?
(p. 75 textbook)
So far these neurological evidence suggest that impairments in frontal lobe functioning may be involved in the development of antisocial behaviour. However, in some cases, brain damage has not produced behavioural changes and even reduced aggression in previously aggressive individuals. What were these studies? What does this suggest?
This may suggest that frontal lobe impairment, particularly in the orbitofrontal cortex, is merely a risk factor for antisocial behaviour, but does not necessarily result in antisocial behaviour in all cases
(p. 76 textbook)
What is low levels of cortisol associated with in children and adolescents?
- Aggression (McBurnett et al. 2000)
- Externalising behaviour and low anxiety (van Goozen et al. 1998)
- Conduct disorder symptomatology (Oosterlaan et al. 2005)
- Callous-unemotional traits (Loney et al. 2006)
(p. 81 textbook)
What did Shoal et al. (2003) find?
Results: reduced cortisol in pre-adolescent boys is associated with low harm-avoidance, low self-control and increased aggression later in adolescence
- Low level cortisol may suggest reduced responsivity to stressors which in turn leads to decreased fear of negative consequences
(p. 81 textbook)
What brain regions associated with moral decision making have also been found impaired in antisocial individuals? What does this suggest? What study found this?
- orbitofrontal cortex
- posterior cingulate
- angular gyrus
- amygdala
(p. 81 textbook)
How does our life experiences (environmental/biological factors) affect our neurochemistry?
--> this tells us how much we get out of being kind to people, hugging people, having healthy relationships
= there is a neurobiological feedback of attachment i.e. attachment has biological underpinnings
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