Italian Court gives lighter sentence for murderer with ‘bad genes’
An Italian court has reduced the sentence given to a convicted murderer by a year because he has genes linked to violent behaviour. According to the journal Nature this is the first time that behavioural genetics has affected a sentence passed by a European Court.
Abdelmalek Bayout, an Algerian citizen who has lived in Italy since 1993, admitted in 2007 to stabbing and killing Walter Felipe Novoa Perez. Perez, a Colombian living in Italy, had, according to Bayout’s testimony, insulted him over the kohl eye make-up that he was wearing. Bayout, a Muslim, claims he wore the make-up for religious reasons.
Bayout’s lawyer, Tania Cattarossi, requested the court to take her client’s mental health into consideration, claiming he may have been mentally ill at the time of the crime. Judge Paolo Alessio Vernì considered three psychiatric reports and Bayout’s psychiatric illness as a mitigating factor before reaching his decision. Bayout was sentenced to 9 years and 2 months in prison, which is, as Nature reported, three years less than Bayout would have received had he been deemed to have been of sound mind. Consideration was then made by judge Pier Valerio Reinotti of the Court of Appeal in Trieste as to whether the sentence should be further commuted, following the commission of a new psychiatric report.
For this new commissioned report, Pietro Pietrini, a molecular neuroscientist at Italy’s University of Pisa, and Giuseppe Sartori, a cognitive neuroscientist at the University of Padova, conducted a series of tests. They found abnormalities in brain-imaging scans and in five genes that have been linked to violent behaviour — including the gene encoding the neurotransmitter MAOA. A 2002 study had found low levels of MAOA expression to be associated with aggressiveness and criminal conduct of young boys raised in abusive environments. The report concluded that if provoked, Bayout’s genes would make him ‘more prone to behaving violently’. In the light of this report and the genetic tests; Judge Reinotti reduced Bayout’s sentence by a further year.
This has provoked comment among the scientific community. Some fear that cases where MAOA deficits and other genetic evidence are offered in courtrooms could lead to the acceptance of genetic determinism in criminal cases; the idea that genes determine a person’s behaviour. Prosecutors could use the same genetic evidence to argue for tougher sentences by suggesting people with such genes are inherently ‘bad’.
2 Comments:
This is a note from the two court experts (Pietro Pietrini, molecular neuroscientisit from the University of Pisa and Giuseppe Sartori, Cognitive Neuroscientist from the University of Padova) involved in the Bayout case in Italy. (see Nature news: ttp://www.nature.com/news/2009/091030/full/news.2009.1050.html)
No es mi culpa: son mis genes
Bad genes get a ligther sentence
Strafmilderung wegen “schlechter Gene”
The “DNA Pardon”: Murder sentence genetically reduced
Un juge italien découvre le gène du meutre
These titles, used to summarise a decision from an Italian Criminal Court on a case of “diminuished capacity” due to psychiatric problems, are ill-posed and do not represent the core issue of this forensic case. Nowhere in our report or in the judge decision it is claimed a causal link between genes and criminal behaviour.
Dimisnuished responsibility was proved by a casual link (required by Italian criminal law) between a pathological mental state and and the criminal behaviour. The crime (homicide) resulted to be a symptom of the undelying psychiatric disorder. The defendant had a reduced capacity to “do otherwise” due to his mental illness.
Given that psychiatric symptoms may be easily faked as they are mostly based on the defendant’s verbal report, the objectivisation of the “disease of the mind” is therefore critical.
Evidence that the psychiatric phenomenology causally linked to the crime has a “hard” neural basis was investigated using neuropsychological assessment, MRI and fMRI (using the stop-signal as activation task) and molecular genetics. Cognitive and molecular neurosciences aìwere not used to causally explain the crime but to insturmentally prove the “hard” correlates of themental illness wichi symtpoms are acusally linked to the crime.
We have found that the psychosis was also accompanied by other severe cognitive disorders, by a dysfunctional frontal lobe and a sfavorable genetics. We have assessed the defendant, previously evaluated only with a psychiatric interview, also with a full neuropsychological, imaging (morphological and functional) and genetic evaluation. The psychiatric interview may be may be easily faked by the defendant and it has a unsatisfacory inter-rated concordance. Neuroscience methods may, therefore, be used to better picture the “disease of mind” but can say nothing, contrary to what seems attributed to us, about the direct proximal causal link with the crime.The symptoms which, by incontrovertible evidence, are linked to the crime are a fully blown untreated psychotic state characterised by delusions of persecuzione, lowIQ, a very poor “theory of mind”, and control of impulse. THESE ARE THE DIRECT CAUSES OF THE CRIME NOT THE BRAIN OR THE GENETIC.
In order to better characterise the required “disease of the mind” there is the legal requirement to show that the disease has a biological basis.Altered brain functioning in controlling behaviour and genetics are the required biological markers of the “disease of the mind”. The only methods that can respond to this requirements are the methods of neuroscience that we have applied. THE CRITICAL ISSUE IS WHETHER THERE ARE BETTER TECHNIQUES, TO ADDRESS THIS ISSUES OTHER THAN THE ONE USED BY US? WE BELIEVE THE RESPONSE IS NO.
As regards to moleculasr genetics, we sequenced 5HTTLPR, STin2 – VNTR (Variable Number of Tandem Repeats) , rs4680, MAOA, DRD4-1/7. Results showed that for each of the examined genes the Defendant had one or both the alleles found to be significantly associated with aggressive and violent behavior.In our specific case, as I said above, for each of the candidate genes examined the subject had one or even both the alleles associated with a significantly greater risk for abnormal aggression, impulsivity and violence. This is a very sensitive issue and there is a need to be absolutely clear. To date there is NO indication of any DETERMINISTIC effect, that is, there is no genetic variant that determines abnormally aggressive behavior (no cause-effect relationship). What the studies reported in the literature have shown is that possessing one or more specific allele(s) is associated with a significantly greater probability of having abnormal aggressive behavior. That is, possessing such a variant is neither necessary nor sufficient to have abnormal aggressive behavior. However, the incidence of individuals with abnormal aggressive behavior is significantly greater in the group of people with such a variant than in the group without.
It is important to clarify that results from association studies have shown that possessing one or more of these genetic variants makes the individual more vulnerable to the effects of an unfavourable environment, such as childhood abuse and maltreatment or social exclusion (see for instance Caspi et al., Science, 2002; Eisenberger et al., Biol Psychiatry, 2006). Indeed, some of these environmental features were present in the case of our Proband.
In no way the conclusions reported in our evaluation of the defendant can be interpreted in a way that denies free will in favour of a genetic determinism (“I did not do it, my genes made me do it”, like a couple of newspaper titled). Indeed, our conclusion was based on the whole evaluation of the defendant, who showed a limited cognitive development (IQ= 70), a history of psychotic disorder with delusional ideation, a history of social exclusion, abnormal performance on cognitive testing for impulse control, abnormal pattern of brain activity in response to inhibition tasks and, finally, a genetic background associated with a statistically significant higher risk of impulsivity and aggressive behavior, especially in response to provocation. Considered each and all these pieces of evidence, we concluded that the defendant at a greatly diminished capacity, which must be considered, by law, as a mitigating factor.
Skeptics say that behavioral genetics studies are mostly based on correlations in groups of people so these data is hardly applicable to single individuals. This is false logic. Such a statement, infact, applies to every aspect of medical science. What I mean is that there is no test in medicine that has a sensitivity nor a specificity of 100%. Not even for a diagnosis of hyperglicemia you can rely on a clear-cut reference value, simply because what we call “normal reference values” are obtained through a statistical evaluation of data collected from hundreds of subjects. Thus, such objections are a too simple way to disguise the question. Data are data. In medicine, there is increasing evidence showing that having certain genetic variants increases the susceptibility to certain disease or may affect the likelihood to respond to specific drug treatment. Oncologists already take into account the genetic features of their patients in deciding for the best treatment strategy. In neuroscience, genetic and molecular studies are offering a powerful tool to understand the complex interaction between genetic characteristics and environmental factors in shaping our personality and behavior. This is with no doubt a great step forward. We need to avoid oversimplification as well as mystification. The titles of some news reports I read about this case around the world are simply misleading and untrue. In no way the conclusions reported in our evaluation of the defendant can be interpreted in a way that denies free will in favour of a genetic determinism (“I did not do it, my genes made me do it”, like a couple of newspaper titled). Indeed, our conclusion was based on the whole evaluation of the defendant, who showed a limited cognitive development (IQ= 70), a history of psychotic disorder with delusional ideation, a history of social exclusion, abnormal performance on cognitive testing for impulse control, abnormal pattern of brain activity in response to inhibition tasks and, finally, a genetic background associated with a statistically significant higher risk of impulsivity and aggressive behavior, especially in response to provocation. Considered each and all these pieces of evidence, we concluded that the defendant at a greatly diminished capacity, which is the requisite by law for a judge to cut the sentence.
The Court recognised all these further data as more convincing than a previous court evaluation based solely on the clinical interview and applied the maximum sentence reduction for “diminuished capacity”. This further reduction was worth 8 months.
Thank you very much for this clarification on the case that indeed has received a surprising amount of international attention; perhaps you might want to consider to submit it also as a comment to the actual report of Nature such that more readers are able to learn your clarifying opinion.
There are, however, a few questions that came to my mind when reading your comment. For example:
(1) You emphasize that you made claims about the background of the mental disorder, not of the crime directly. Yet, the evidence you quote (at least partially) associates the genotypes you investigated with aggressive behavior or violence, not with mental disorders. It appears that this evidence is thus directly related to the crime (which was a crime of aggression and violence) and not just to the (alleged) mental disorder.
(2) At least some of the genotypes you investigated are not only related to aggressive behavior, but to a number of mental conditions. The enzyme that is influenced by the MAOA gene probably affects a number of neurotransmitter systems which each can be associated with some mental disorders. The 5HTTLPR gene, for example, is frequently associated with a gene x environment interaction of depression. You criticize the objections referring to these data as merely correlational and that they cannot be applied to individual cases. Yet, to my knowledge, the available evidence primarily comes from cross-sectional studies, not prospective studies which actually tested the predictive validity for individuals; and, furthermore, the environmental effects are many times much stronger than the genetic effects; and if the genetic effects are significant (sometimes they aren’t, but just the gene x environment interaction, as in some of Caspi’s investigations), the effect sizes are usually very very small, making it extremely difficult to draw any inferences about individual cases. The neurogenetic evidence is usually not comparable to the predictive value of, for example, a common DNA test of parenthood. Besides the question of the individual predictive value which we, according to my opinion, cannot answer yet in lack of unequivocal empirical data, the interpretation only in terms of aggression in violence appears to be selective and might be related to what is called the “reverse inference problem” in neuroscience (e.g. R. Poldrack, Trends in Cognitive Sciences, 2006).
(3) You write that “there is the legal requirement to show that the disease has a biological basis.” I have to admit that I do not know anything about Italian law but I find this statement very surprising. As a matter of fact, no or almost no psychiatric disorder (unlike neurologic disorders) in the DMS-IV or ICD-10 is defined by a biological basis but just by behavioral data, observations, reports etc. Of course, the previous decades of neuroscientific and genetic research have produced a vast amount of theories and hypotheses about the biological basis of mental disorders but, to my knowledge, no such disorder can today be reliably diagnosed by neuroscientific or genetic evidence. Surely, this might change in the future, but if the Italian law had such a requirement, then it would appear to me that psychiatric disorders cannot ever play a role in actual cases given our current limited knowledge.
Stephan Schleim
Theory and History of Psychology
University of Groningen
The Netherlands