ADHD Psychopathy studies

NICE (2019)

Outlined diagnostic criteria, prevalence, and treatment guidelines for ADHD in children and adults in the UK.

BMJ Best Practice (2024)

Provided up-to-date clinical guidance on ADHD, including prevalence, subtypes, assessment, and management.

Verkuijl et al. (2015)

Identified three ADHD presentations: predominantly inattentive, predominantly hyperactive–impulsive, and combined presentation, and estimated their relative prevalence.

Matheiken et al. (2024)

Highlighted underdiagnosis of ADHD in women due to atypical symptom presentation and healthcare bias, and reported increased adult diagnoses post-COVID-19.

Young & Thome (2011)

Found high rates of childhood ADHD symptoms among youth and adult offenders, with persisting ADHD linked to earlier offending and higher recidivism.

Anns et al. (2023)

Reported that young adults with ADHD are significantly more likely to have contact with the criminal justice system.

Satterfield et al. (2017)

Showed that individuals with childhood ADHD tend to commit their first offence before age 15.

DeLisi et al. (2013)

Found that young offenders with ADHD had earlier police contact compared to non-ADHD peers.

DeSanctis et al. (2014)

Demonstrated that individuals with childhood ADHD were significantly younger at first arrest than controls.

Silva et al. (2014)

Reported earlier onset of criminal behaviour in men with ADHD but not women.

Rosler et al. (2009)

Found declining rates of ADHD in offender populations with increasing age, suggesting age-related normalisation.

Raaj et al. (2024)

Linked ADHD with increased risk of road traffic violations and motor vehicle accidents.

Mohr-Jensen & Steinhausen (2016)

Meta-analysis showing ADHD is associated with assault, theft, drug-related offences, and weapons possession.

Kelsey et al. (2023)

Found high prevalence of ADHD and traumatic brain injury (TBI) in secure psychiatric settings, with a significant association between ADHD, TBI, and interpersonal violence.

Young et al. (2009)

Scottish prison study showing higher ADHD symptoms were associated with increased verbal and physical aggression and critical incidents.

Retz et al. (2004)

Compared offenders with and without ADHD, finding earlier delinquency, poorer education, higher unemployment, and greater emotional and social difficulties in those with ADHD.

Chang et al. (2016)

Found that ADHD medication use was associated with reduced rates of criminal offending.

Boland et al. (2020)

Systematic review and meta-analysis showing ADHD medication was associated with reduced risks of criminality, substance use, depression, injuries, TBIs, and motor vehicle crashes.

Polanczyk et al. (2015)

Estimated global prevalence of conduct disorder and reported higher rates in boys than girls.

Ayano et al. (2024)

Suggested an increase in the prevalence of conduct disorder over recent decades.

Erskine et al. (2013)

Found minimal changes in CD prevalence over time and little variation between countries.

Merikangas et al. (2010)

Reported that ethnic differences in CD prevalence disappear when socioeconomic status is controlled.

US Department of Justice (2006)

Reported extremely high prevalence rates of conduct disorder in juvenile offender populations.

Moffitt & Lynam (1994)

Linked conduct disorder to executive function deficits, including poor planning, organisation, and task shifting.

Pennington & Bennetto (1993)

Proposed that cognitive deficits in CD interact with environmental risk factors to produce antisocial behaviour.

Raine (2011)

Identified structural and functional brain differences in CD, including reduced amygdala volume and orbitofrontal cortex dysfunction.

Fairchild et al. (2011)

Showed that individuals with CD have difficulties processing social and emotional stimuli regardless of age of onset.

Gelhorn et al. (2005)

Estimated heritability of conduct disorder at approximately .53, indicating a strong genetic contribution.

Wesseldijk et al. (2017)

Demonstrated that genetic influences on conduct disorder change across the lifespan.

Hinshaw & Lee (2003)

Highlighted the role of family adversity, inconsistent parenting, and peer rejection in the development and maintenance of CD.

Foley et al. (1996)

Showed that ADHD and CD frequently co-occur and jointly increase risk for juvenile delinquency and ASPD.

Spencer (2006)

Reported that around 50% of individuals diagnosed with ADHD also meet criteria for conduct disorder.

Deck et al. (2005)

Argued that ADHD with comorbid CD may represent a more severe subtype of ADHD rather than two distinct disorders.

Fergusson et al. (1993)

Found that CD predicted later offending, while ADHD predicted academic difficulties when comorbidity was controlled.

Satterfield et al. (2006)

Long-term follow-up showing increased criminality only when ADHD co-occurred with CD.

Mordre et al. (2011)

Norwegian longitudinal study replicating findings that CD, not ADHD alone, predicts later offending.

Christiansen et al. (2008)

Used genetic approaches to explore shared heritability between ADHD and conduct disorder.

Mulligan et al. (2008)

Provided molecular genetic evidence for overlap between ADHD and CD.

Azeredo et al. (2018)

Systematic review concluding that genetic factors primarily drive ADHD–CD comorbidity, with environmental factors moderating risk.

Holzer et al. (2020)

Showed that ASPD prevalence peaks in early adulthood and declines sharply in older age groups.

Goldstein (2022)

Estimated lifetime ASPD prevalence at 2–5% in general adult populations in the US and UK.

Kenan et al. (2000)

Proposed that ASPD symptoms may “burn out” or diminish with age.

Mattar & Khan (2017)

Suggested individuals may age out of ASPD symptomatology across adulthood.

Fridell et al. (2008)

Identified ASPD as a strong predictor of criminal behaviour.

Shepherd et al. (2018)

Reported higher recidivism rates among offenders diagnosed with ASPD.

Black et al. (2010)

Found ASPD in around one-third of incarcerated offenders, linked to earlier offending, substance misuse, poor mental health, and higher recidivism.

Harris et al. (2017)

Demonstrated increased risk of repeat offending in adults with ASPD.

Moffitt (1993)

Proposed the dual taxonomy theory distinguishing life-course persistent offenders from adolescence-limited offenders.

Blair et al.

Defined psychopathy as a refinement of CD and ASPD characterised by emotional impairment, particularly deficits in empathy and guilt.

Frick et al. (1994; 2014)

Identified callous-unemotional traits in childhood as predictors of later psychopathy and violent behaviour.

Boduszek & Debowska (2016)

Reviewed literature identifying core psychopathic traits such as callousness, lack of empathy, and manipulativeness.

Patrick & Drislane (2015)

Estimated prevalence of psychopathy in the general population and noted higher rates in males.

Lilienfeld & Arkowitz (2007)

Estimated psychopathy prevalence in prison populations at 15–25%.

Hare (1980; 1991; 2003)

Developed the Psychopathy Checklist and Psychopathy Checklist–Revised (PCL-R), the most widely used assessment tools.

Hart et al. (1988)

Found higher recidivism rates among psychopathic offenders.

Serin & Amos (1995)

Reported increased reconviction rates among psychopathic individuals.

Valdez et al. (2000)

Found higher psychopathic traits, particularly lack of empathy, among gang-involved youth.

Dupere et al. (2007)

Reported that adolescents with psychopathic traits were significantly more likely to join gangs.

Ray et al. (2016)

Showed that a small group with high psychopathic traits accounted for disproportionate substance use and delinquency.

Lejuez et al. (2010)

Demonstrated that substance use facilitates risky decision-making and aggression in psychopathic individuals.

Blonigen et al. (2003)

• Twin study examining genetic influences on psychopathy

• Found moderate heritability, particularly in male twins

• Suggests psychopathic traits are partly genetically influenced, but not fully determined

• Supports a biopsychosocial rather than purely environmental explanation

Flor et al. (2002)

• Examined aversive conditioning responses

• Psychopaths showed reduced emotional conditioning to negative stimuli

• Supports the idea that punishment is a weak deterrent for psychopaths

Levenston et al. (2000)

• Replicated findings of reduced startle response in psychopaths

• Suggests deficits in fear processing systems

• Supports amygdala-related explanations of psychopathy

Newman & Kosson (1986)

• Studied passive avoidance learning

• Psychopaths failed to avoid behaviours that led to punishment

• Indicates difficulty learning to suppress antisocial responses

• Relevant to persistent offending despite sanctions

Blair (2003)

• Proposed the Violence Inhibition Mechanism (VIM) deficit

• Failure to respond to others’ distress cues (fear/sadness)

• Explains lack of guilt, empathy, and moral learning

Gregg & Siegel (2001)

• Showed the orbitofrontal and ventrolateral frontal cortex regulate threat responses

• These regions modulate the amygdala and hypothalamus

• Dysfunction linked to reactive aggression

Blair et al. (2006)

• Psychopathy linked to instrumental aggression (goal-directed harm)

• Amygdala dysfunction disrupts stimulus–reinforcement learning

• Victims’ distress does not function as a deterrent

• Makes standard parental punishment less effective

Oxford et al. (2003)

• Inconsistent parenting increases aggression in typical children

• BUT children with early psychopathic traits benefit less from parenting interventions

• Suggests reduced environmental malleability

Finger et al. (2011)

• fMRI study of youths with conduct disorder + psychopathic traits

• Reduced orbitofrontal cortex responsiveness to reinforcement

• Poor learning from mistakes and emotional feedback

• Explains persistent harmful decision-making

Frick & Viding (2009)

• Distinguished CD with CU traits vs CD without CU traits

• CU traits: proactive aggression, low anxiety, lack of remorse

• Non-CU: reactive aggression, higher anxiety, guilt present

• Important for diagnosis and intervention

Viding et al. (2005)

• Large twin study (3,500 pairs)

• High callous–unemotional (CU) traits strongly heritable

• 73% similarity in MZ twins vs 39% in DZ twins

• ~⅔ of variance in high CU explained genetically

Frick et al. (2014)

• Children with CD + CU traits:

  • Poor fear/sadness recognition

  • Less fear themselves

  • Reduced sensitivity to punishment

• Twin designs confirm substantial genetic influence

Johnson et al. (2006)

• Longitudinal study of 593 families (ages 6 → 33)

• Low parental warmth predicted personality disorders, including ASPD

• Effects remained after controlling for confounders

• Shows environmental risk even across adulthood

Byrd & Manuck (2013)

• For children with high CD but low CU, maltreatment predicts worsening conduct problems

• Suggests environmental sensitivity differs by CU level

Pasalich et al. (2011)

• Parental warmth may reduce antisocial behaviour even in high-CU children

• Indicates some scope for protective environmental effects

McCrory et al. (2012)

• Review of maltreatment and neurodevelopment

• Early trauma alters emotional processing systems

• Supports developmental and neurobiological pathways to antisocial behaviour