Title: Born to Be Criminal? What to Make of Early Biological Risk Factors for Criminal Behavior
Abstract: Back to table of contents Previous article Next article EditorialFull AccessBorn to Be Criminal? What to Make of Early Biological Risk Factors for Criminal BehaviorPhillip Sterzer, M.D.Phillip Sterzer, M.D.Published Online:1 Jan 2010https://doi.org/10.1176/appi.ajp.2009.09111601AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail While the important role of psychosocial factors in the development of criminal behavior has long been acknowledged, there has been an increasing interest in the neurobiological basis of aggression and crime over the past decade, boosted by methodological advances in neuroimaging and molecular genetics (1, 2). Researchers recognized the potential role of biological factors in the etiology of criminal behavior some time ago, and in this vein an intriguing result of a long-term study is reported in this issue of the Journal. Gao and colleagues (3), using data rooted in a study that was initiated more than 20 years ago, tested whether abnormal fear conditioning predisposes to crime. Fear conditioning is a basic form of learning in which fear is associated with a previously neutral stimulus. Experimentally, this is done by pairing a neutral stimulus with an aversive one, such as an unpleasant loud noise. Eventually the previously neutral stimulus alone will evoke a fear response that can be quantified with physiological measurements such as electrodermal responses.The study by Gao et al. is based on the hypothesis that fear conditioning is the mechanism by which we learn to link antisocial acts with negative consequences such as punishment or social exclusion. By leading to a failure in such social learning, poor fear conditioning would thus predispose an individual to antisocial behavior. Crucially, if poor fear conditioning has a causal role in crime, it should be detectable early in life, before antisocial behavior becomes manifest. In the framework of a large birth cohort study, Gao et al. tested fear conditioning in children at age 3. Twenty years later, they probed the association of poor fear conditioning in early childhood with adult criminal behavior. A group of 137 individuals who had been convicted of committing crimes by age 23 was compared with a carefully matched group from the same cohort who showed no evidence of criminal behavior. Strikingly, skin responses to the conditioned stimulus were significantly smaller in children who became criminal later on. In fact, on average there was no evidence for any conditioning at all in the criminal group, as skin responses to the conditioned stimulus were statistically indistinguishable from responses to a stimulus that was not conditioned. The implications of this finding are at least twofold. First, it provides new insights into the etiology of criminal behavior; second, it may help to guide early therapeutic interventions in children at risk for antisocial behavior.The central brain structure in the circuitry underlying fear conditioning and the perception of threatening stimuli in the environment is the amygdala (4). Deficient amygdala function has been proposed to render individuals unable to recognize cues that signal threat, making them relatively fearless (5). Less sensitive to any negative consequences of their behavior, fearless individuals engage more readily in antisocial behavior. Indeed, the relationship between antisocial behavior and amygdala dysfunction is supported by a number of findings in adults and adolescents, including deficits in recognizing fearful facial expressions, poor fear conditioning, and reduced amygdala responses to negative emotional stimuli as measured with functional neuroimaging (2, 5, 6). While such findings in adults and adolescents are ambiguous as to whether they represent cause or consequence of repetitive antisocial behavior, the results reported here by Gao et al. now point to an early deficit in amygdala function as a causal mechanism. However, the notion of a generally hyporesponsive amygdala would be too simplistic. The amygdala is a small yet complex structure comprising a number of subnuclei with distinct functional properties (4). Moreover, some studies have shown increased amygdala responsiveness in antisocial individuals (2) and in those with a genetic predisposition to aggressive behavior (7). Contrasting with the fearlessness hypothesis outlined above, such findings point to a different pathomechanism whereby pathological aggression may be related to heightened anxiety. Increased amygdala responsiveness is a well-established finding in anxiety disorders and is thought to be the basis for exaggerated fear conditioning. This is nicely demonstrated by another study published in this issue. Using a simple but elegant modification of classical fear conditioning, Lissek et al. (8) show that in panic disorder fear responses are more easily generalized—that is, fear responses are evoked more easily by stimuli that resemble the conditioned stimuli in patients with panic disorder compared with healthy individuals.The heterogeneity of findings from neuroimaging studies suggests that the amygdala might be differentially involved in different etiologies of antisocial behavior. This exemplifies the necessity of taking into account the whole spectrum of possible pathogenetic factors and developmental pathways if we are to develop a more complete understanding of antisocial behavior. Especially when it comes to developing targeted preventive or therapeutic interventions, it will be crucial to identify subgroups of at-risk individuals in whom different neurobiological mechanisms underlie antisocial behavior (5, 9). The Gao et al. study (3) is an important step toward this goal, as it identifies a biological marker that may help to identify subgroups with a distinct neurobiological profile even in early childhood. Clearly, the scope for changing behavior will be greatest in the early years because of the greater plasticity of the brain in childhood.Is poor fear conditioning at age 3 likely to represent an innate trait? While this question cannot be answered with certainty, it is clear that a wealth of environmental influences can already have taken effect during the first 3 years and even in utero. Reduced fear conditioning in 3-year-olds may thus represent not just a genetic predisposition but rather the early manifestation of gene-environment interactions (9). The authors of the study aimed to minimize the chances that differences in fear conditioning were due to adverse environmental factors by matching the two groups for social adversity. However, some important issues were not systematically assessed and may have gone unnoticed, such as differences in nutrition, parenting style, and maternal stress during infancy. The latter is indeed associated with behavioral problems later in childhood, as shown in another carefully conducted longitudinal study published in this issue (10).There are a number of caveats when it comes to drawing conclusions from and considering the potential consequences of findings such as those reported by Gao et al. First, there is a tendency, not only among scientific laypersons, to mistake neurobiological findings for evidence of a fateful and unchangeable condition. It is of the utmost importance that this view be acknowledged as wrong. One of the most stupendous characteristics of the nervous system is its plasticity, and neurobiological measures thus often represent little more than a snapshot at one stage in development. Just as longitudinal assessment of behavior elucidates developmental pathways to psychological problems (10), longitudinal studies of neurobiological factors could help us better understand their contribution to long-term behavioral outcome. Second, while poor fear conditioning can be seen as a predisposing factor for criminal behavior, it can by no means be used to predict future behavior. Such markers can only be applied at the group level and are far from being selective or specific enough to be used as diagnostic or screening tools in individuals. Finally, crime is a multifaceted behavioral outcome of complex interactions among multiple biological and environmental factors and cannot possibly be explained by a single neurobiological factor such as fear conditioning.If not handled with great caution, neurobiological markers can easily be misused to stigmatize individuals who are perceived as a potential threat to society. With the increasing availability of data that help us prevent, diagnose, and treat antisocial behavior early in life, we also need a public debate on how to use this information and, even more important, how to avoid its misuse. Neurobiological research offers a great chance to further our understanding of antisocial and criminal behavior. This understanding should be used to benefit those children who are at greatest risk for a criminal career and to design interventions that are tailored to their needs.Address correspondence and reprint requests to Dr. Sterzer, Department of Psychiatry, Campus Charité Mitte, Charitéplatz 1, D-10117 Berlin, Germany; philipp.[email protected]de (e-mail). Editorial accepted for publication November 2009.Dr. Sterzer reports no financial relationships with commercial interests.References1 Dressing H , Sartorius A , Meyer-Lindenberg A : Implications of fMRI and genetics for the law and the routine practice of forensic psychiatry. Neurocase 2008; 14:7–14 Crossref, Medline, Google Scholar2 Sterzer P , Stadler C : Neuroimaging of aggressive and violent behaviour in children and adolescents. Front Behav Neurosci 2009; 3:1–8 Crossref, Google Scholar3 Gao Y , Raine A , Venables PH , Dawson ME , Mednick SA : Association of poor childhood fear conditioning and adult crime. Am J Psychiatry 2010; 167:56–60 Link, Google Scholar4 Phelps EA , LeDoux JE : Contributions of the amygdala to emotion processing: from animal models to human behavior. Neuron 2005; 48:175–187 Crossref, Medline, Google Scholar5 van Goozen SH , Fairchild G : How can the study of biological processes help design new interventions for children with severe antisocial behavior? Dev Psychopathol 2008; 20:941–973 Crossref, Medline, Google Scholar6 Lorber MF : Psychophysiology of aggression, psychopathy, and conduct problems: a meta-analysis. Psychol Bull 2004; 130:531–552 Crossref, Medline, Google Scholar7 Meyer-Lindenberg A , Buckholtz JW , Kolachana B , Hariri AR , Pezawas L , Blasi G , Wabnitz A , Honea R , Verchinski B , Callicott JH , Egan M , Mattay V , Weinberger DR : Neural mechanisms of genetic risk for impulsivity and violence in humans. Proc Natl Acad Sci USA 2006; 103:6269–6274 Crossref, Medline, Google Scholar8 Lissek S , Rabin S , Heller RE , Lukenbaugh D , Geraci M , Pine DS , Grillon C : Overgeneralization of conditioned fear as a pathogenic marker of panic disorder. Am J Psychiatry 2010; 167:47–55 Link, Google Scholar9 Moffitt TE : The new look of behavioral genetics in developmental psychopathology: gene-environment interplay in antisocial behaviors. Psychol Bull 2005; 131:533–554 Crossref, Medline, Google Scholar10 Essex MJ , Klein MH , Slattery MJ , Goldsmith H , Kalin NH : Early risk factors and developmental pathways to chronic high inhibition and social anxiety disorder in adolescence. Am J Psychiatry 2010; 167:40–46 Link, Google Scholar FiguresReferencesCited byDetailsCited ByPerspectives on the success rate of current antidepressant pharmacotherapy24 October 2022 | Expert Opinion on Pharmacotherapy, Vol. 125Major Cardiac–Psychiatric Drug–Drug Interactions: a Systematic Review of the Consistency of Drug Databases19 May 2020 | Cardiovascular Drugs and Therapy, Vol. 35, No. 3The Brain as a Protagonist: Without the Brain, All Is Nothing22 May 2021Risk Factors of Relapse After Successful Electroconvulsive Therapy for Taiwanese Patients With Major Depression24 July 2019 | The Journal of ECT, Vol. 36, No. 2A randomized, double-blind study comparing the efficacy and safety of trazodone once-a-day and venlafaxine extended-release for the treatment of patients with major depressive disorderInternational Clinical Psychopharmacology, Vol. 35, No. 3Difficult-to-treat depression: A clinical and research roadmap for when remission is elusive31 October 2018 | Australian & New Zealand Journal of Psychiatry, Vol. 53, No. 2CNS Spectrums, Vol. 24, No. 03Psychology, Crime & Law, Vol. 25, No. 6Journal of Women's Health, Vol. 28, No. 2Guidelines for the evaluation and treatment of perimenopausal depression: summary and recommendationsMenopause, Vol. 25, No. 10Changes in healthcare resource use and costs associated with early versus delayed initiation of atypical antipsychotic adjunctive treatment in major depressive disorder19 June 2018 | Journal of Medical Economics, Vol. 21, No. 9The Neurobiological Underpinnings of Psychopathy16 February 2018The Neurodevelopmental Basis of Early Childhood Disruptive Behavior: Irritable and Callous Phenotypes as ExemplarsLauren S. Wakschlag, Ph.D., Susan B. Perlman, Ph.D., R. James Blair, Ph.D., Ellen Leibenluft, M.D., Margaret J. Briggs-Gowan, Ph.D., Daniel S. Pine, M.D.17 November 2017 | American Journal of Psychiatry, Vol. 175, No. 2, Vol. 250Journal of Palliative Medicine, Vol. 21, No. 8Rapid-Acting Antidepressant Effect of Ketamine and Its Clinical ApplicationJournal of Korean Neuropsychiatric Association, Vol. 57, No. 2US public views toward biosocial risk factors for criminality: a brief reportJournal of Criminological Research, Policy and Practice, Vol. 3, No. 4Jury-Eligible Public Attitudes Toward Biological Risk Factors for the Development of Criminal Behavior and Implications for Capital Sentencing11 July 2017 | Criminal Justice and Behavior, Vol. 44, No. 8Brexpiprazole15 December 2016 | Annals of Pharmacotherapy, Vol. 51, No. 4MAOIs – does the evidence warrant their resurrection?10 July 2016 | Australasian Psychiatry, Vol. 24, No. 4Community Mental Health Journal, Vol. 52, No. 3Genes, Brain and Behavior, Vol. 15, No. 1Scientific Reports, Vol. 5, No. 1A review of the evidence supporting the use of lithium augmentation therapy for the reduction of suicidal behavior in patients with unipolar depression: Revisiting an overlooked benefit of an older medicationMental Health Clinician, Vol. 4, No. 5Use of Augmentation Agents for Treating Depression: Analysis of a Psychiatric Electronic Medical Record Data SetKenneth R. Gersing, M.D., John J. Sheehan, Ph.D., Bruce Burchett, Ph.D., Ling Zhu, Ph.D., John A. Bates, Ph.D., Ross A. Baker, Ph.D., and Iftekhar D. Kalsekar, Ph.D.1 August 2014 | Psychiatric Services, Vol. 65, No. 8Generalizability of Findings From Efficacy Trials for Chronic Depression: An Analysis of Eligibility CriteriaAlessa von Wolff, M.A., Malte Jansen, M.A., Lars P. Hölzel, Ph.D., Annika Westphal, B.A., Martin Härter, M.D., Ph.D., and Levente Kriston, Ph.D.1 July 2014 | Psychiatric Services, Vol. 65, No. 7Biological Psychiatry, Vol. 75, No. 1BioSocieties, Vol. 9, No. 1Low Skin Conductance Activity in Infancy Predicts Aggression in Toddlers 2 Years Later16 April 2013 | Psychological Science, Vol. 24, No. 6Burglary Crime Analysis Using Logistic RegressionSocial Neuroscience, Vol. 8, No. 2Developmental Science, Vol. 16, No. 1Annals of the New York Academy of Sciences, Vol. 1299, No. 1Suicide bereavement and complicated grief1 April 2022 | Dialogues in Clinical Neuroscience, Vol. 14, No. 2Archives of Women's Mental Health, Vol. 15, No. 3Forensische Psychiatrie, Psychologie, Kriminologie, Vol. 6, No. 2Brain, Vol. 135, No. 7Japanese Journal of Clinical Oncology, Vol. 42, No. 12Schizophrenia Bulletin, Vol. 38, No. 5Journal of Medical Economics, Vol. 15, No. 1Postdischarge Care for Depression in Ontario1 August 2011 | The Canadian Journal of Psychiatry, Vol. 56, No. 8Combination Antidepressants in Australia: A Right or Wrong?1 August 2011 | Australian & New Zealand Journal of Psychiatry, Vol. 45, No. 8 Volume 167Issue 1 January 2010Pages 1-3 Metrics PDF download History Accepted 1 November 2009 Published online 1 January 2010 Published in print 1 January 2010
Publication Year: 2010
Publication Date: 2010-01-01
Language: en
Type: letter
Indexed In: ['crossref', 'pubmed']
Access and Citation
Cited By Count: 127
AI Researcher Chatbot
Get quick answers to your questions about the article from our AI researcher chatbot