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The Monoamine Oxidase A (MAOA) Genetic Predisposition to Impulsive Violence: Is It Relevant to Criminal Trials?

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Abstract

In Italy, a judge reduced the sentence of a defendant by 1 year in response to evidence for a genetic predisposition to violence. The best characterized of these genetic differences, those in the monoamine oxidase A (MAOA), were cited as especially relevant. Several months previously in the USA, MAOA data contributed to a jury reducing charges from 1st degree murder (a capital offence) to voluntary manslaughter. Is there a rational basis for this type of use of MAOA evidence in criminal court? This paper will review in context recent work on the MAOA gene–environment interaction in predisposing individuals to violence and address the relevance of such findings to murder trials. Interestingly, the MAOA genetic variants impact future violence and aggression only when combined with the adverse environmental stimuli of childhood maltreatment. Thus nature and nurture interact to determine the individual’s risk. Based on current evidence, I argue there is a weak case for mitigation. But should future experiments confirm the hypothesis that individual differences in impulse control and response to provocation found in MAOA-L men (without abuse) are significantly magnified when combined with childhood maltreatment, the case could turn into a stronger one.

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Notes

  1. This gene codes for the MAOA protein, which is important for the degradation of several neurotransmitters including serotonin, dopamine, and noradrenalin.

  2. Translated from the Italian. This quotation, with which the court concurs, is from the testimony of the psychological experts and is written in the court’s case report.

  3. 170,000 per year were estimated to die of collective violence [16].

  4. PET is an imaging technique that enables researchers to visualize the location and density of a protein of interest by labeling it with a tagged molecule that is injected into the blood.

  5. See [34]. Unfortunately, Bernet et al. does not identify the relevant trials by name, but codes them. Note also that Bernet provided the expert evidence in the Waldroup trial [5].

  6. Although different jurisdictions accept different criteria for mitigating factors, most of them resemble what I have outlined here. Mitigating factors are most relevant in jurisdictions that still permit capital punishment.

  7. I will leave discussion of Insanity and diminished capacity to another paper, for example.

  8. This comment seems to be reacting against notions of hard genetic determinism, a misinformed stance responsible for phrases like “crime genes.”

  9. A reasonable argument is that the jury might overweight this kind of evidence. The basis for overweighting would be a sort of “genetic exceptionalism,” or false belief that genetic evidence is in fact inherently different than other evidence. While there is gravity in this risk and it should be taken seriously, excluding genetic information will likely reinforce the very ideas of “genetic exceptionalism” that should be combated. Only by becoming comfortable with talking about and engaging with genetic information can we hope to overcome the specter of “genetic exceptionalism” and the risk of overweighting genetic evidence in trials if it is relevant to the case (see Parens 2010 [53] for “why talking about behavioral genetics is important and difficult”). During the transition period, juries should be guided about how to interpret genetic information.

  10. One might reasonably object to my conceptual re-organization by pointing out that a diagnosis of Schizophrenia or Epilepsy requires more than just a predisposition to certain behaviors; rather, it requires one to actually have exhibited those behaviors for some period of time. If the defense claims the first exhibition of the behavior is during or near the moment of the crime, however, a diagnosis—itself an inference made by the psychiatrist—should be investigated and if determined by further psychiatric evaluation to be warranted can further build support for the existence of the claimed mental state at the moment of the crime.

  11. Note that one does not need to have schizophrenia to have delusions or hallucinations.

  12. Some point menacingly to its statistical nature and the observation that a majority of those with MAOA-L and childhood maltreatment do not go on to commit violence (see [1]). While these things are important to remember, they do not form a sound basis upon which to argue that MAOA data should have no effect in criminal court. The majority of those with schizophrenia, epilepsy, etc. do not commit crimes. If they do, however, the court has a responsibility to investigate whether these markers are relevant to the crime. The same should be true in the MAOA case.

  13. The possibility of punishment based solely on risk to society hovers in the British skies where a person deemed to pose a greater than 50% risk to commit future violent crime is proposed to be diagnosed with Dangerous and Severe Personality Disorder (DSPD). DSPD would support an optional extension of a criminal sentence to life or permanent monitoring [54, 55].

  14. Modern research on epigenetics (in which environmental influences dynamically modify the accessibility and transcription rates of genes) shows that even genes themselves are less static than we had previously thought (see [24]). The MAOA gene–environment interaction itself may be mediated by such a mechanism: the MAOA promoter region contains sites for one mechanism (addition of a methyl group—methylation) of metaplasticity and has been shown to be methylated in response to components in tobacco smoke [56, 57].

  15. Mindfulness training is an adaptation of a type of Buddhist meditation that helps individuals recognize and tolerate impulses and seems especially suited to angry impulses [58]

  16. Omega-3 fatty acids are essential for proper development and function of the prefrontal cortex, the area of the brain most directly involved in impulse control, and supplementation shows promises of decreasing impulsive aggression [35, 59]

  17. Remember from the review of the science that MAOA-L subjects had increased activation of the perigenual anterior cingulate, which could be responsible for the aberrant coupling between the amygdala and prefrontal cortex. This region is rich in 5HT2a receptors and an antagonist applied to an animal model decreased aggression.

  18. [2] mistakenly claims that the victim was one of the defendant’s assailants.

  19. The details of the procedure were not provided in the legal document.

  20. This argument leaves itself open to a challenge that might arise if we continue down this road: courts may soon be faced with cases in which the defense presents whole genomes and points out thousands of genetic variants each with small but non-zero associations with violence (and with varying levels of empirical support).

  21. The possibility of discrimination exists with the MAOA data as well and should be safeguarded against in any application: the MAOA-L gene is differentially represented across ethnicities (see [60–62]).

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Acknowledgments

The author would like to thank Russell Perkins for aiding in the translation and understanding of the Italian Appeals Court trial, as well as Julian Savulescu, Mark Sheehan, Neil Levy, Owen Schaefer, Ben Edelstein, Paul Troop and one anonymous reviewer for thoughtful comment and discussion of the manuscript in its various stages.

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  1. The Ethox Centre, Division of Public Health and Primary Health Care, University of Oxford, Badenoch Building, Old Road Campus, Headington, Oxford, OX3 7LF, UK

    Matthew L. Baum

  2. Oxford Centre for Neuroethics, University of Oxford, Littlegate House, Suite 8, 16/17 St Ebbes St, Oxford, OX1 1PT, UK

    Matthew L. Baum

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Baum, M.L. The Monoamine Oxidase A (MAOA) Genetic Predisposition to Impulsive Violence: Is It Relevant to Criminal Trials?. Neuroethics 6, 287–306 (2013). https://doi.org/10.1007/s12152-011-9108-6

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