#neuroshit

This duality is also a puzzle to ourselves, at the heart of cosmologies, theologies and tragedies, the motor of moral codes and the tension at the heart of socio-political systems. We know light and we know dark. We are capable of doing terrible things, but also of asking ourselves contemplatively and creatively how that is. The self-consciousness that characterises the human mind is nowhere more baffling than in this problem of evil, which philosophers have been discussing since Plato. An obvious place to look for explanations of evil is in the patterns of behaviour that those who commit atrocities display.

This is what the neurosurgeon Itzhak Fried at the University of California, Los Angeles did with his article ‘Syndrome E’ (1997) in The Lancet. A syndrome is a group of biological symptoms that together constitute a clinical picture. And E stands for evil. With Syndrome E, Fried identified a cluster of 10 neuropsychological symptoms that are often present when evil acts are committed – when, as he puts it, ‘groups of previously nonviolent individuals’ turn ‘into repetitive killers of defenceless members of society’. The 10 neuropsychological symptoms are:

Repetition: the aggression is repeated compulsively.

Obsessive ideation: the perpetrators are obsessed with ideas that justify their aggression and underlie missions of ethnic cleansing, for instance that all Westerners, or all Muslims, or all Jews, or all Tutsis are evil.

Perseveration: circumstances have no impact on the perpetrator’s behaviour, who perseveres even if the action is self-destructive.

Diminished affective reactivity: the perpetrator has no emotional affect.

Hyperarousal: the elation experienced by the perpetrator is a high induced by repetition, and a function of the number of victims.

Intact language, memory and problem-solving skills: the syndrome has no impact on higher cognitive abilities.

Rapid habituation: the perpetrator becomes desensitised to the violence.

Compartmentalisation: the violence can take place in parallel to an ordinary, affectionate family life.

Environmental dependency: the context, especially identification with a group and obedience to an authority, determines what actions are possible.

Group contagion: belonging to the group enables the action, each member mapping his behaviour on the other. Fried’s assumption was that all these ways of behaving had underlying neurophysiological causes that were worth investigating.

Note that the syndrome applies to those previously normal individuals who become able to kill. It excludes the wartime, sanctioned killing by and of military recruits that leads many soldiers to return home (if they ever do) with post-traumatic stress disorder (PTSD); recognised psychopathologies such as sociopathic personality disorder that can lead someone to shoot schoolchildren; and crimes of passion or the sadistic pleasure in inflicting pain. When Hannah Arendt coined her expression ‘the banality of evil’ in Eichmann in Jerusalem (1963), she meant that the people responsible for actions that led to mass murder can be ordinary, obeying orders for banal reasons, such as not losing their jobs. The very notion of ordinariness was tested by social psychologists. In 1971, the prison experiment by the psychologist Philip Zimbardo at Stanford University played with this notion that ‘ordinary students’ could turn into abusive mock ‘prison guards’ – though it was largely unfounded, given evidence of flaws in the never-replicated experiment. Still, those afflicted with Syndrome E are indeed ordinary insofar as that they are not affected by any evident psychopathology. The historian Christopher Browning wrote of equally ‘ordinary men’ in the 1992 book of that name (referenced by Fried) who became Nazi soldiers. The soldier who killed my grandfather was very probably an ordinary man too.

Today, biology is a powerful explanatory force for much human behaviour, though it alone cannot account for horror. Much as the neurosciences are an exciting new tool for human self-understanding, they will not explain away our brutishness. Causal accounts of the destruction that humans inflict on each other are best provided by political history – not science, nor metaphysics. The past century alone is heavy with atrocities of unfathomable scale, albeit fathomable political genesis. But it was the advent of ISIS and the surge in youthful, enthusiastic recruits to it that gave Fried’s hypothesis a new urgency, and prompted him to organise, with the neurophysiologist Alain Berthoz at the Collège de France in Paris, three conferences around Syndrome E that between 2015 and 2017 gathered cognitive neuroscientists, social psychologists, neurophysiologists, psychiatrists, terrorism specialists and jurists, some of whose theories and insights I share here. Syndrome E is a useful provocation to an innovative, interdisciplinary discussion of this old problem – and a powerful example of how to frame neuroscientific output in human terms. Already this approach is giving rise to interesting hypotheses and explanations.

As the brain’s functional anatomy reveals itself in increasingly precise ways, neuroscience is growing in its ability to address the complexities underlying our behaviour, violence included. But since we are evolved animals, to investigate the biological bases for behaviour is to look both at the embodied results of evolutionary time and at historical time – at how the evolved circuits of the brain are recruited by cultures, as well as producing cultures. Given that we evolved as inherently social, interactive creatures, neuroscience requires dialogue with other disciplines – the brain has not evolved in isolation, and action always takes place at a moment in time in a particular place with particular meaning. The psychological and cultural environment is central in determining whether and how given biological processes will play out. The traits enumerated by Fried thus encompass a combination of neurological and environmental conditions.

Central to Syndrome E is the symptom of ‘diminished affect’. Most people – except, precisely, psychopaths – shy away from or are extremely reluctant to inflict pain, let alone kill. As the psychiatrist Robert Jay Lifton has shown, it takes brainwashing and coercion to dull our emotional response and to overcome our reticence to cross the line beyond which ‘habituation’ sets in – the Syndrome E symptom whereby the repetition of the act makes it easier to perform. Perpetrators of mass murder and torturers can also love and want the best for their children, while feeling nothing for their victims – an instance of the ‘compartmentalisation’ symptom of Syndrome E. This was probably the case for the anonymous Nazi soldier who killed my grandfather. Family belonging and social belonging are separate. When they meet, as happened in Bosnia and Rwanda when families turned on each other, the group identity prevails. Empathy is rarely universal.

The social neuroscientist Tania Singer at the Max Planck Institute in Leipzig in Germany defines empathy as the ability to ‘resonate’ with the feelings of the other. It develops from babyhood on – as imitation at first, then joint attention – into the ability to adopt the point of view of another, along with a shift in spatial perception from self to other, as if one were literally stepping into another’s shoes. This requires an ability to distinguish between self and other in the first place, an aspect of the so-called ‘theory of mind’ that one acquires over the first five years of life. The developmental psychologist Philippe Rochat at Emory University in Atlanta has shown how children develop an ethical stance by that time as well, and become aware of how their actions can be perceived by others.

But while empathy ensures the cohesion of a group or a society, it is also biased and parochial. Revenge thrives on it. The social psychologist Emile Bruneau at the University of Pennsylvania has demonstrated how it is easily directed at an ‘in-group’ at the expense of an ‘out-group’ that can then be targeted as an enemy, and dehumanised. Its selectivity also explains how we can walk by a homeless person without feeling the need to offer help, or rejoice in nasty gossip about a disliked absentee. Inevitably, we all practise selective empathy, its absence manifest in everyday, non-lethal instances of violence that occur in social and family life, in business and politics. What the psychologist Simon Baron-Cohen at the University of Cambridge calls ‘empathy erosion’ in The Science of Evil: On Empathy and the Origins of Cruelty (2011) is therefore not a sufficient ingredient in the outbreak of extreme violence. But it is a necessary one, opening the way to discrimination and ultimately genocide. As the social neuroscientist Jean Decety at the University of Chicago put it, ‘our hypersociality has a dark side’.

This developmental account can dispel, in part, the mystery of our two faces – of our ability at once to help each other and to kill each other, or to argue ourselves into ‘just wars’. In common with other hominins such as chimpanzees, we have evolved the capacity to cement relationships, communicate and cooperate with those in our immediate environment – and also to attack outsiders and members of other tribes. But our evolved self-consciousness is what defines our humanity even apart from other hominins. What remains puzzling is our continued ability to destroy even as we are able to understand ourselves and to create sophisticated scientific models of our own minds.

Neuroscience gives an interesting physiological model of the emotion of empathy as a complex, dynamic process that unites executive, premotor and sensorimotor functions. It recruits, in particular, the ventromedial prefrontal cortex (vmPFC) and the orbitofrontal context (OFC), with which the vmPFC overlaps in part, and which is crucial for the processing of emotions generated in the amygdala – an evolutionary ancient structure within the limbic system. Lesion to the OFC impairs emotional feeling – and with it, decision-making. With his ‘somatic marker hypothesis’, the neuroscientist Antonio Damasio at the University of Southern California in Los Angeles has shown how bodily feelings that participate in signalling emotions, processed in the OFC and vmPFC, enable appropriate, socially situated decision-making, thereby informing our evaluations of the world, including our moral sense.

In the phenomenon of diminished affect, hyperactivity in these same areas of the frontal lobe inhibits activation of the amygdala. Studies have shown dysfunctional activity of the OFC in people with obsessive-compulsive disorder. It thus might also be involved in the obsessive nature of ideas about one group that justify murderous intent against its members. And the sense of elated hyperarousal – such as that induced by cocaine – that entrains action upon these ideas involves processing in the medial prefrontal cortex (mPFC). In short, in cases of Syndrome E emotional pathways in the brain no longer regulate judgment and action. A breakdown occurs in the feedback between the amygdala and higher, cognitive cortical structures. The acting self splits away from the feeling self, a phenomenon that Fried calls ‘cognitive fracture’. He believes that, under given circumstances, about 70 per cent of the population can be subject to it and be able to take part in crimes as part of a group – as might have happened in the Stanford prison experiment, despite caveats regarding its results.

The acting self of the individual with cognitive fracture feels no empathy. But empathy is not always a reliable guide to appropriate behaviour – we don’t feel empathy for the insects dying because of climate change, for instance, but we can decide rationally to act against the disaster. It can even lead to bad decisions with regard to those at whom it is directed – a surgeon who feels empathy for the patient under drapes should really not operate. There is such a thing as a surfeit of feeling. The psychologist Paul Bloom at Yale University has argued ‘against empathy’, in a 2016 book of that title and elsewhere, suggesting that ‘rational compassion’ is a better barometer with which to evaluate our environment and how we should act upon it. That is to say, members of a group whose mission is to kill its perceived enemies might have the ability for emotional empathy for their group, and no rational compassion for their perceived enemy.

An account of the inability to feel any emotion for such perceived enemies can take us closer to understanding what it is like to have crossed the line beyond which one can maim and kill in cold blood. Observers at the International Criminal Court (ICC) at the Hague note frequently the absence of remorse displayed by perpetrators. The clinical psychologist Françoise Sironi, who assesses perpetrators for the ICC and treats them and their victims, has directly seen what Lifton called the ‘murder of the self’ at work – notably with Kang Kek Iew, the man known as ‘Duch’, who proudly created and directed the Khmer Rouge S-21 centre for torture and extermination in Cambodia. Duch was one of those who felt absolutely no remorse. His sole identity was his role, dutifully kept up for fear of losing himself and falling into impotence. He did not comprehend what Sironi meant when she asked him: ‘What happened to your conscience?’ The very question was gibberish to him.

Along with what Fried calls this ‘catastrophic’ desensitisation to emotional cues, cognitive functions remain intact – another Syndrome E symptom. A torturer knows exactly how to hurt, in full recognition of the victim’s pain. He – usually he – has the cognitive capacity, necessary but not sufficient for empathy, to understand the victim’s experience. He just does not care about the other’s pain except instrumentally. Further, he does not care that he does not care. Finally, he does not care that caring does, in fact, matter. The emotionally inflected judgment that underlies the moral sense is gone.

Such a state involves the fusion of identity with a larger system within which occurs the splitting of the feeling self and the cognitive self, and the concomitant replacement of individual moral values with that system’s norms and rules. Chemistry is operative throughout, as it is in all cerebral and somatic functions – and tweakable by pharmaceuticals. The neuroscientist Trevor Robbins at the University of Cambridge has studied ‘pharmacoterrorism’, and how, for instance, the amphetamine Captagon – used, inter alia, by ISIS members – affects dopamine function, depletes serotonin in the OFC, and leads to rigid, psychopathic-like behaviour, increasing aggression and leading to the perseverance that Fried lists among the Syndrome E symptoms. It shuts off social attachment, and disables all emotional feeling (empathy included), a condition called alexithymia.

This is one simplified neurological account of how murderous action becomes possible. The neuroscience of value and action can help to further explain what might be going on. The OFC is exceptionally developed in humans and primates. As Edmund Rolls at the Oxford Centre for Computational Neuroscience has shown, it plays a crucial role in representing reward value in response to a stimulus: we make choices based on the assignation of value – to an object, an idea, an action, a norm, a person. Our emotions are value-rich, and our actions vary and can be updated according to how they are met in the world, in turn motivating us to seek or avoid a stimulus. Our behaviour can continue in the search of an absent reward – this would be one account of compulsive action, a Syndrome E symptom. The neuroscientist Mathias Pessiglione and his team in Paris have also shown a central role for vmPFC in value-attribution to a stimulus or an idea, whereby we choose to undertake an action based on its attractive reward or its aversive outcome. But when this function is overstimulated, new inputs – such as cries for mercy – have no impact on the attribution of value to the idea, for instance that ‘all you people deserve to die’, and action cannot change. It becomes automatic, controllable by an external agent or leader, independently of any sense of value.

But these neurological events signify criminal action only under particular environmental circumstances. The psychiatrist David Cohen and his team at the Pitié-Salpêtrière hospital in Paris evaluated teenage candidates for radicalisation. They found that certain socio-psychological conditions in childhood – such as an absent father or an unstable mother, and a history of foster care – affected the development of identity, in some cases eventually leading to the need to subsume it into a wider group with a transcendental message. Again, group trumps family. As the anthropologist Scott Atran has shown, conflicts are often intractable and non-negotiable because they are conducted in the name of absolute, spiritual values – secular or religious – and not for any utilitarian outcome. These values can seem highly attractive – stronger than family ties.

In her novel Home Fire (2017), the British Pakistani writer Kamila Shamsie showed how a loving, innocent but maladjusted and lost young man of Pakistani origin could fall prey to an ISIS recruiter’s siren call to rejoin a lost father and find fulfilment and belonging in a community depicted as devoted to a greater good. Our narratives, inner and outer, inform and justify the choices we make, conferring on them a coherence that is reassuring and can seem good and right. Coherence rides on the moral sense and masquerades as it, bringing on a cognitive dissonance ‘between what we think and what we do’, as Zimbardo once put it – between what we convince ourselves was an appropriate action, and our deeply held, prior beliefs. Shamsie’s character soon regrets his choice and tries to get away from a violence he cannot stomach, unable to withstand the cognitive dissonance. Not so Nazi doctors, say, who convinced themselves that they were acting for a greater good – in a perverse twist to the equivalence of morality with a concern for the good of others. Heinrich Himmler’s speech in Poznan in 1943 is a chilling instance of this high-minded justification of criminal behaviour: ‘We have the moral right, we had the duty to our people to do it, to kill this people who wanted to kill us.’ Once moral justification is divorced from an emotionally calibrated response to the other, violence can be deployed on rationalised grounds. This has happened time and again throughout history.

But ‘ordinary men’ must cross a line into that zone where the Syndrome E symptoms operate – pushed by circumstance. A noteworthy insight into what happens during the crossing is provided by the neuroscientist Patrick Haggard at University College London. He has shown how powerful is the initial coercion that allows us to step beyond the line. In the wake of the 1961 trial in Jerusalem of Adolf Eichmann, who invoked the ‘Nuremberg Defence’ that he was ‘just obeying orders’ – so-called because it was first used by the Nazi defendants in the Nuremberg Trials of 1945-46 – the psychologist Stanley Milgram at Yale University showed, or rather exaggeratedly claimed, that most people will obey orders from an authority even if the order is to harm another person. Milgram was interested in obedience. Haggard, who has been studying the sense of agency – the sense that we initiate and own our actions, which is central to our lives, and also to legal arguments about criminal accountability – asked instead what it feels like to be coerced and have one’s autonomy removed to some degree. Through an experiment that partly takes its cue from Milgram’s (but addresses some of its ethical and methodological issues) and uses the intentional binding effect, Haggard found that people do feel a notable reduction in their sense of agency when they are coerced into an action. Coercion switches off the sense of responsibility – a chilling finding.

The neurological correlates of what can lead to our worst actions do not indicate a clinical condition. Syndrome E is not a disease, nor quite a disorder eligible for integration into the Diagnostic and Statistical Manual of Mental Disorders or the International Statistical Classification of Diseases and Related Problems. If it were officialised as such, it would have intricate juridical ramifications: the use of neurological evidence in court is problematic, as the jurist Jean-Paul Costa, a former president of the European Court of Human Rights, has pointed out, because it requires the expert reading of imprecise and opaque data. It is hard to establish exactly which brain events – including those underlying the sense of agency – could or should constitute legally mitigating factors.

Introduction

The relationship between the mind and body remains one of the most fascinating and long-enduring puzzles facing philosophy, medicine, and many other disciplines. The nature of consciousness and subjective mental experiences, and their relationship to neurological structures and functions remain mysterious. The law, however, is not particularly concerned with the relationship between mental experiences and the physical brain even though legal institutions are involved every day in practical problems related to human behaviour and mental states. For example, in assigning blame and responsibility, the law is more interested in the functional effects of mental disorder, than on whether it is understood as a psychological disturbance of the mind or a physiological disturbance of the brain and body. In other words, the law is more interested in the effect on capacity of a mental disorder than on the causes – biological, psychological and/or social – of the mental disorder. In this article, however, I suggest that the dominant frame of reference adopted to understand mental disorder has a range of subtle effects on legal rules and practices, and that the increasingly sophisticated use of neuroscience in biological psychiatry is likely to enhance these socio-legal effects.

The article starts with a brief overview of biological psychiatry, showing that biological understandings of mental disorder have ancient origins in Western thought, but have ebbed and flowed in popularity over time, coexisting sometimes acrimoniously with other models of mental disorder. This section presents and explains the dominance today of neuroscientific approaches within a historical context. I then present ways in which I suggest that the neurobiological model of mental disorder will affect the law in five areas: evidence of mental states, the definition of disability in human rights law, criminal responsibility, the regulation of brain interventions, and the regulation of reproductive technologies. Some of these are admittedly speculative, but are advanced as suggestions for further attention as neuroscientific research proceeds and is incorporated within social institutions and practices, such as the law.

Biological Psychiatry

Over the years, the nature and causes of mental illnesses have been framed in supernatural, psychosocial and biological terms. The dominant paradigm is now that of biological psychiatry, an approach that understands mental experiences primarily in terms of the biological functioning of the nervous system.1 It may seem now that the biological approach is a modern idea, but nothing could be further from the truth. The 4th century BC Hippocratic text entitled “On the Sacred Disease” articulated a naturalistic biological explanation of mental states. Rather than resulting from divine punishment, the symptoms of mental disorder were the result of imbalances in bodily humours.2

“Men ought to know that from nothing else but the brain come joys, delights, laughter and sports, and sorrows, griefs, despondency, and lamentations…And by the same organ we become mad and delirious, and fears and terrors assail us, some by night, and some by day, and dreams and untimely wanderings, and cares that are not suitable, and ignorance of present circumstances, desuetude, and unskilfulness. All these things we endure from the brain, when it is not healthy, but is more hot, more cold, more moist, or more dry than natural, or when it suffers any other preternatural and unusual affection. And we become mad from its humidity.”3

While supernatural explanations of mental illness are now uncommon, the tension between biological and psychological theories has existed since the very beginning of psychiatry as a medical discipline in the late 19th century.

“Psychiatry has always been torn between two visions of mental illness. One vision stresses the neurosciences, with their interest in brain chemistry, brain anatomy, and medication, seeing the origin of psychic distress in the biology of the cerebral cortex. The other vision stresses the psychosocial side of patients’ lives, attributing their symptoms to social problems or past personal stresses to which people may adjust imperfectly.”4

In his History of Psychiatry, Shorter charts this tension between biological and psychological theories, identifying two main periods during which biological approaches were in the ascendancy, separated by the early to mid-20th century era of Freudian psychoanalysis.5 The second wave, emerging in the 1970s was fueled by psychiatric genetics research involving large twin and adoptee studies and the discovery of effective psychiatric drugs such as the anti-psychotic drug chlorpromazine.6 Walter suggests that we are in the midst of a third wave of biological psychiatry beginning in the 1980s and driven by progress in molecular neuroscience, and the development of cognitive neuroscience, neuroimaging and other techniques that enable the study of the interactions between genetics, experience and the environment.7 In Walter’s view, these developments are together leading to a much more complex and sophisticated picture of brain organization and the neurobiological changes associated with psychiatric disorders.

“The underlying model is that of systems medicine, understood as an interdisciplinary field of study that looks at the dynamic systems of the human body as part of an integrated whole, incorporating biochemical, physiological, and environmental interactions…”8

In Walter’s account, this third wave of biological psychiatry is an inclusive one that can incorporate multiple levels of information (e.g. genetic, molecular, cellular, circuit, physiological, behavioural and patients’ self-reported experience), can allow for multiple and complex causation of mental disorder (e.g. biological, psychosocial and cultural mechanisms), and does not entail that narrowly biological approaches (e.g. psychopharmacology) are necessarily the best therapies. 9

This being said, some may be sceptical about the apparent inclusiveness and neutrality regarding therapeutic modalities of this latest approach to biological psychiatry. There is evidence that clinicians are more likely to favour pharmacotherapy when patients’ conditions are framed in biological as opposed to psychosocial terms.10 Furthermore, some may harbour concerns that the apparently inclusive new biological psychiatry constitutes “lip service” to the mental or subjective experiences of patients or that it encourages inefficient allocation of resources to neurobiological approaches at the expense of addressing known psychosocial contributions to the development or maintenance of psychiatric disorders.11

Another concern that may exist with biological approaches to psychiatry is the unintended psychological impact of biological causal explanations on the attitudes of both clinicians and patients. Biological explanations for mental illnesses seem to encourage the belief that symptoms are immutable, leading to prognostic pessimism and a reduced sense among patients of personal ability to regulate symptoms, raising the risk of self-fulfilling beliefs in the immutability of mental illness.12 There is evidence, however, that educational interventions emphasizing the malleability of biological factors involved in mental illnesses may help to counteract these reactions.13 It is not just patients who may be affected by biological causal explanations of mental disorders, and there is considerable evidence that links these biological causal accounts to increased public perceptions of dangerousness and the desire to limit social interactions with people with mental illnesses.14 Furthermore, it appears that clinicians’ level of empathy for their patients is reduced by biological explanations of mental disorders, which is troubling given the importance of clinician empathy for the therapeutic relationship.15 Perhaps, as with the beneficial effects of educational interventions with patients, public and clinical education might overcome these potentially harmful side effects of biological causal accounts of mental disorders more broadly.

Research on mental health stigma is actively exploring the ideological impact of biological psychiatry on social behaviour and attitudes and in the therapeutic context. The purpose of the present article is to broaden the field of view to explore these same ideological effects in another important field of social behaviour – the law and legal decision-making. As the following sections suggest, there is reason to think that there may be fascinating and subtle effects of biological explanations of mental states and behaviours throughout the law.

Brain Imaging and Objective Evidence of Mental States

Courts are frequently intensely interested in subjective mental states. Yet, mental states such as the experience of pain, memories, deception, or sexual interests are private, directly accessible only to the person experiencing them. Yet, their existence is relevant to legal questions such as the quantum of damages to be awarded in personal injury litigation, entitlement to disability insurance benefits, the value of testimony about past experiences and observations, as well as forensic risk assessment in the criminal context. A witness’s veracity is frequently questioned because of the existence of powerful incentives to claim a particular mental state in court. As a result there is an omnipresent risk of accepting false claims as well as rejecting true claims.

One of the intriguing developments in recent years has been the rise of functional magnetic resonance imaging (fMRI), which detects patterns of blood flow in the brain. Relying on the assumption that these patterns of blood flow reflect brain activity, researchers are actively examining whether there are neurological “correlates” for particular mental experiences that might allow one to infer, from a particular pattern of brain activation, whether a person was experiencing a particular mental state. At present, it is not clear if or when this research will furnish evidence of mental states like pain, deception or memory that will satisfy tests of evidentiary admissibility.

Nevertheless, attempts have been made to introduce fMRI evidence of mental states in court. One of the first attempts to reach the courts has been fMRI-based lie detection. Based on research suggesting that deliberate deception can be identified by patterns of brain activation, several litigants have now attempted to submit in court fMRI evidence about a witness’s veracity.16 These efforts have so far been unsuccessful, as courts have not considered the technique to meet the standards for the admissibility of novel scientific evidence. One problem is whether tests on laboratory subjects can reliably be generalized to the very different “real-world” situation of an accused person.17 Another is that the possibility that a person may be able to defeat the fMRI lie-detection test using deliberate countermeasures.18

Another active area of research concerns memory, and there are now multiple studies in which researchers are able to distinguish certain types of true and false memories using fMRI and electroencephalography (EEG) under laboratory conditions.19 Given the known frailties of eyewitness memory and the risk that memory errors may lead to wrongful convictions,20 a technology that would help to detect when eyewitness memory is wrong would be useful. The research so far cannot be safely generalized to the real-world contexts at issue in the courtroom, although some leading experts predict that future advances in the neuroimaging technology and analysis will eventually address the problems that currently preclude its use.21

Another potential area for the detection of mental states relates to sexual interests, which form part of the risk assessment often at issue in criminal sentencing decisions involving sex offenders. At present, phallometry (or penile measurement to detect sexual arousal in response to sexual stimuli) is used in Canada for treatment and forensic risk assessment.22 The SORAG (Sex Offender Risk Appraisal Guide) is an actuarial forensic risk assessment tool that is used to assess sex offenders, which includes a range of risk factors including phallometric results showing “deviant sexual interests.”23 Researchers are now reporting that it is possible to distinguish between men with pedophilic and non-pedophilic sexual interests using fMRI techniques that measure brain responses to images of naked men, women and children.24 Most recently, Ponseti and colleagues have reported that they can discriminate between men with sexual interests in children versus adults, by looking at the brain response to images of the faces alone, which is preferable given the ethical concerns and legal barriers to using naked images of children in such tests. They note that their subjects admitted their sexual preferences, and so it was not possible to determine whether counter-measures could defeat this technique.

Pain is another private experience not accessible to others, and one that is of great importance in civil liability as well as workers’ compensation and disability insurance claims. In the case of chronic pain conditions, in which pain persists long after physical injuries have healed, the lack of some sort of visible reason for the pain combined with the legal incentive to claim pain leads to suspicion of malingering. Even if a plaintiff’s claim of pain is believed, defendants and clinicians sometimes take the position that chronic pain conditions are psychogenic (i.e. emerging for psychological reasons). In these cases, the challenge facing claimants is one of causation, as defendants may argue that the plaintiff had a “crumbling skull” – meaning that the psychogenic condition was a response in a vulnerable person to any number of stressful life events and would have occurred regardless of the defendants’ actions.25 While fMRI techniques to detect pain would not answer this second problem for claimants, attempts are now being made to use neuroimaging to address the first problem – suspicion of malingering. Although neuroimaging techniques appear to be effective at detecting acute pain caused in the laboratory in healthy volunteers, it is a different matter to detect chronic pain.26 As a result, neuroimaging techniques do not appear to be sufficiently reliable to be used as objective evidence of pain in a courtroom. Despite this, companies are already offering fMRI testing to detect the neurological signatures of pain.27 As Sara Reardon recounts in a recent news feature for Nature, this evidence appears to be influencing out of court settlements in civil litigation.28

The use of fMRI to draw inferences about mental states of specific individuals is currently subject to a variety of limitations, which may limit its uptake for legal purposes.29 If it does eventually offer evidence that meets tests of admissibility, a range of concerns arise. One possible risk is that it people may feel pressured to undergo these tests. For example, the failure to supply this evidence might be taken to suggest that a mental state such as pain is being faked.30 Another concern specific to pain detection is the possibility that it might be required to access certain prescription medications or insurance coverage.31 Another important issue if this evidence proves admissible is distributive justice, given that the cost of the test would make it inaccessible to many.

A broader question posed by the use of neuroimaging to find “objective” evidence of mental states is that it sets up a possible contest between subjective mental experiences and objective brain states. It is possible that the two may diverge, leading to a situation in which a person’s mental experience is at odds with what the fMRI results say it should be. For example, a person may subjectively remember something, only to be told that the brain imaging indicates that it is a false memory. In these circumstances, a contest of epistemic authority arises. Should the subjective experience be taken as reality, or should the objective brain evidence be taken to have successfully revealed that a person is delusional or lying? Some people, presented with this situation may refuse to believe the objective brain evidence, but others may instead come to doubt their own experiences. There are costs to doubting oneself, one of which might be vulnerability to suggestion, misinformation and manipulation by others.32

Defining Disability: Social Solidarity and Human Rights

The prevailing beliefs about the causes of a person’s behavior or condition affect feelings of social solidarity and willingness to help and protect the person. In essence, we are more likely to accept and protect people with disfavoured attributes and behaviours if those characteristics are perceived to be outside their causal control. As explained below, biological explanations of a behavioral problem increase the perception that it falls outside a person’s control. In this way, biological psychiatry may affect fundamental concepts in the area of human rights, where perceptions of control over one’s condition and behavior may affect the willingness to recognize it as a disability for the purposes of disability benefits and anti-discrimination protection under human rights law.

Social psychologists have long been interested in the impact of judgments about the causes of a person’s behavior or condition on social responses to that person.33 In particular, attribution theory looks at three dimensions of causal attributions – the locus, controllability and stability of the cause.34 Locus refers to whether or not the cause is internal to an actor (e.g. genetics, character, personal decisions) or external to the actor (e.g. bad luck, societal discrimination).

Controllability refers to the degree of control a person has over a particular cause. This is where biological causes may diverge from other types of internal causes such as those related to character or values. Some types of biological causes are apt to be interpreted as falling outside a person’s control (e.g. genes), such that states or behaviours understood as biologically caused are less likely to attract blame.35 A further layer complicates the relationship between control and blame, however. Even if a person has lost the ability to control a biological condition and so is not blamed for its continuation (due to a lack of “offset controllability”), the person may still be blamed because of perceived control over the development of the condition (due to perceived “onset controllability”). Conversely, even if a person is not responsible for the onset of a condition, the person may be blamed for the failure to take steps within his or her control to address it.36

The third dimension – stability – considers whether a cause is immutable or instead is amenable to change over time. Some biological causes such as genetics are understood as immutable, while others are considered modifiable.

Another important dimension in understanding the impact of a given causal explanation of a particular behavior or condition is the strength of that causal contribution. For example, some causes are understood as powerful - invariably leading to a given outcome - while others are weaker predisposing factors that may be counterbalanced or supplemented by other causal influences.

The reframing of historically stigmatized human characteristics as matters of unchosen and immutable biology is correlated with reduced blame and increased social solidarity. The shift from environmental or personal choice accounts of sexual orientation to biological explanations in the 1990s was framed in the US media as likely to have socially progressive effects such as reducing blame, and increasing acceptance and support for human rights protection.37 Dissenters were concerned that the biological explanations would instead generate eugenic practices by expecting parents or increase pressure to medicalize and “cure” homosexuality.38 Garretson and Suhay’s recent study of a set of American public opinion surveys from the 1980s, 1990s and 2000s explored the relationship between the rise in the 1990s of biological explanations of sexual orientation, attitudes to whether sexual orientation is innate or chosen, and support for gay rights. They conclude that “in the wake of the American media’s focus in the early 1990s on biological causes of homosexuality and their progressive implications, public opinion in the U.S. changed in substantial ways…Americans who believed homosexuality to be innate shortly after the spike in “born gay” messages became more progressive on gay rights over time, suggesting that altered causal attributions contributed to progressive changes in societal attitudes toward lesbians and gays during the 1990s.”39 The explanation of the linkage between changed attitudes and biological causal explanations of homosexuality is complex, however. Some have suggested that moral judgments of homosexuality might instead explain the adoption of particular causal accounts.40

In any event, the deliberate adoption of biological causal accounts of other stigmatized groups or conditions has been explored as a means to reduce stigma and discrimination. The brain disease model of mental illnesses such as schizophrenia has been deliberately invoked in an attempt to reduce stigma, although unfortunately this type of message may reduce one component of stigma (i.e., blame) while increasing others (i.e., pessimism about recovery, stereotypes about unpredictability and dangerousness, and social rejection or “othering”).41 The brain disease model has also been deployed in the context of addiction with similarly mixed results in reducing stigma.42

In addition to effects on social stigma, biological causal accounts of socially disfavoured behaviours may also affect the law. Proponents of the brain disease model of addiction argue that the widespread adoption of this model enabled the passage in 2008 of mental health parity legislation in the US requiring that medical insurance cover the costs of addiction treatment.43 The model of addiction as a chronic brain disease is now being expanded to other forms of compulsive behaviours including pathological gambling. Pathological gambling was formerly classified in the DSM-IV as an “impulse control disorder”44 but was recently reclassified in the DSM-5 within the section on “substance-related and addictive disorders.”45 The notes on the section indicate that gambling disorder has been added because of “evidence that gambling behaviors activate reward systems similar to those activated by drugs of abuse and produce some behavioral symptoms that appear comparable to those produced by the substance use disorders.”46 Tovino suggests that this neurobiologically-driven reclassification of pathological gambling may have legal implications in states like Nevada, which exclude health insurance coverage for “impulse control disorders” but make an exception for substance-related conditions (drug and alcohol use disorders).47 She argues that the claim that pathological gambling should not be treated like an “impulse control disorder” but instead like a substance-related disorder has been strengthened by the recent reclassification of pathological gambling as a form of addictive behavior in the DSM 5.

In recent work, I have examined the hypothesis that neurobiological accounts of problematic behaviours would affect human rights law by altering the scope of the legal definition of disability, or by limiting the scope of the protection available where the condition is accepted as a disability.48 The definition of disability is important as it sets the scope of entitlement to disability benefits, and the extent of protection from discrimination in employment, among other spheres of social activity. Consistent with the attribution theory described above, the case law reveals a reluctance to accept as protected disabilities behavioural conditions that are perceived to be within the control of the claimant. The case law also reveals attempts in some contexts to frame problematic behavioural conditions as brain disorders.

For example, employees dismissed for stealing from their employers have attempted to raise claims of disability discrimination based on the proposed disability of pathological gambling disorder. In these cases, they have argued for less severe disciplinary measures or accommodation of their disability by, for example, reassigning the employee to a position where theft is impossible. These cases are difficult for claimants as adjudicators often doubt that the claimant’s loss of self-control was sufficient to remove responsibility.49 For example, in Manitoba v. Manitoba Government and General Employees’ Union (2005), the arbitration panel doubted that gambling addiction made the decision to steal involuntary, despite evidence that gambling addictions “hijack the brain.”50

The importance of a finding of lack of control in establishing a behavioural condition as a disability is also revealed in the cases dealing with nicotine addiction. Even though addiction to nicotine is medicalized, some courts have refused to recognize it as a disability entitled to protection from discrimination on the basis that it is “a temporary condition that many people voluntarily overcome, albeit with varying levels of difficulty related to the strength of their will to discontinue smoking.”51 Another found that nicotine addiction was a disability, citing evidence that nicotine was as addictive as cocaine or heroin, and that smoking was a more direct method of delivering a drug to the brain than injecting it into the arm.52

In the different context of a recent class action lawsuit against tobacco companies, the experts engaged in a battle over whether nicotine dependence should be viewed as a “brain disease.”53 This was an important point in establishing liability because, if the claimants retained some self-control, then they would be solely or partly responsible for the health consequences of smoking if they persisted despite knowing it was harmful. The judge ultimately concluded that that “nicotine affects the brain in a way that makes continued exposure to it strongly preferable to ceasing that exposure. In other words, although it can vary from individual to individual, nicotine creates dependence. That is the point” (Letourneau 2015 para 179). The invocation of neurobiological explanations in these cases seems to produce a more sympathetic response to smokers, although the level of sympathy may vary by legal context. Courts may be more willing to find for smokers against tobacco companies, which are profiting from the alleged addiction, than for smokers against employees, who are being asked to accommodate an alleged addiction.

Although it is difficult to draw firm conclusions about the impact of biological explanations of compulsive behaviours from the fairly small number of available cases, the patterns are interesting. Future research looking at legal responses to current attempts to frame behaviours within the brain disease model of addiction, including Internet, sex, and food addictions, will be useful to explore this pattern further.

Blame and Criminal Responsibility

The use of biological causal accounts of behavior to deflect moral blame by suggesting a lack of control may also affect our practices of criminal justice. The question of capacity is central to criminal responsibility. The standard for exculpation set out in s.16 of the Criminal Code is very high, excluding most cases in which mental disorder is a contribution to the commission of a crime. However, less severe degrees of impaired capacity are often considered at the stage of sentencing a convicted offender. The fundamental principle of sentencing is that a sentence must be proportionate to the gravity of the offence and the degree of responsibility of the offender. Diminished capacity due to mental disorder is frequently taken to reduce the degree of moral blameworthiness and so serves as a mitigating factor in deciding on sentence.54 However, at the same time, where prospects for successful treatment and rehabilitation are considered poor and a person is judged to be dangerous, mental disorder may instead lead to a longer sentence because public safety via incapacitation is also an objective of sentencing.

In recent years, there has been a considerable amount of attention paid to biological explanations of mental disorders associated with criminal offending and whether this should affect our judgments of moral responsibility. For example, Glenn, Raine and Laufer argue that evidence that brain regions critical for emotional and moral capacity are impaired in psychopaths means that those severely affected should not be held criminally responsible for their antisocial actions.55 Evidence that an offender possessed a gene associated with impulsive aggression has also resulted in lowered sentences in a number of Italian cases.56 Some have argued that evidence of the neurobiological causes of behaviour call into question our practices of punishment based on moral blame, and that we should move to a system based solely on consequentialist objectives such as deterrence, rehabilitation and incapacitation.57

“Intuitively, we want to punish those people who truly deserve it, but whenever the causes of someone’s bad behaviour are made sufficiently vivid, we no longer see that person as truly deserving of punishment. This insight is expressed by the old French proverb: ‘to know all is to forgive all’. It is also expressed in the teachings of religious figures, such as Jesus and Buddha, who preach a message of universal compassion. Neuroscience can make this message more compelling by vividly illustrating the mechanical nature of human action.”58

This debate, which becomes rapidly embroiled within the ancient philosophical problems of whether we have free will, and whether the concept of moral responsibility necessarily relies upon the existence of free will, continues to roll onward. In some ways these recent genetic and neurobiological challenges to punishment based on moral blame are updated versions of suggestions such as that of Lady Barbara Wootton in the 1960s to abandon retributivism in favour of a purely preventive role for criminal justice – one that abandons useless or incoherent concepts of moral responsibility and focuses on rehabilitative treatment or, failing that, incapacitation.59

Despite this, systems of criminal justice continue to be based to a large degree on judgments of moral blameworthiness. Forensic psychiatric evidence related to mental disorder has long been a part of assessing mental capacity and responsibility, and an intriguing question posed by the emerging biologically-oriented accounts of criminal behavior is whether these biological accounts are more likely than the typical non-biological psychiatric evidence to reduce attributions of control and blame.

A growing body of experimental research is examining whether effects of neurobiological explanations of criminal behavior differ from those of psychiatric explanations. The results are inconsistent so far, perhaps reflecting the different methodologies adopted.60 One survey of nearly 200 American state trial judges found that evidence supporting a neurobiological cause of an offender’s psychopathy reduced the sentence imposed as well as the extent to which the psychopathy was viewed as an aggravating factor.61 The judges considered a vignette in which a psychiatrist provided expert testimony that a man who committed a violent assault was a psychopath. Half of the participants also received the expert testimony of a neurobiologist who presented a neurobiological explanation of the psychopathy. The participants were able to provide explanatory comments on their responses. One judge wrote that “[t]he evidence that psychopaths do not have the necessary neural connections to feel empathy is significant. It makes possible an argument that psychopaths are, in a sense, morally ‘disabled’ just as other people are physically disabled.”62 The neurobiological explanation of psychopathy appears to have reduced perceived moral blame but at the same time may have increased the perception of increased dangerousness. Another judge wrote that “[p]sychopathy may make the defendant less morally culpable, but it increases his future dangerousness to society. In my mind, these factors balance out…”63 In a similar study with a group of German judges, Fuss and colleagues found that the neurobiological explanation slightly reduced the judgment of legal responsibility, but it did not significantly affect the prison sentence imposed. However, the presentation of the neurobiological evidence by the prosecution did greatly increase the decision to order involuntary commitment in a psychiatric hospital, which could lead to a longer detention time.

As research in behavioural genetics and neuroscience proceeds, evidence suggesting biological causal influences on criminal behaviour will be identified. This evidence fits fairly seamlessly into existing sentencing practices in which a broad range of biological, social and environmental causes of behaviour are proposed in an attempt to mitigate blame. Another possibility is that biological causal explanations of behaviour may be more likely than other explanations to imply an offender is dangerous, producing an aggravating effect on sentencing decisions. As the scientific research is taken up by courts, key questions will be whether a neurobiological work-up is likely to improve legal decision-making or not, when it is likely to be in an offender’s interest to pursue this type of evidence, and whether the right to make a full answer and defence might sometimes require the collection and presentation of this type of evidence.

The Regulation of Brain Interventions: Mind-Brain Dualism

Biological psychiatry, and particularly the accumulation of information at the biological levels about mental illnesses, will challenge laws that purport to distinguish between the mind or mental properties on one hand, and the brain and its physical properties on the other hand. Put another way, biological psychiatry is monist – (treating the mind and brain as aspects of the same thing) and also materialist (regarding mental states as reflections of states of physical matter).64 The law, on the other hand, is often dualistic – positing a distinction between mental and physical phenomena, or between psychiatric and neurological treatments. This dualism will be increasingly unstable as the neurobiological underpinnings of psychiatric disorders are discovered.

A good example is furnished by section 49 of Ontario’s Mental Health Act, which sets specific rules to govern “psychosurgery.”65 The special and restrictive rules are explained by the backlash against the prefrontal lobotomy that garnered its inventor the 1949 Nobel prize, but went on to be applied in widespread and highly questionable way in the mid-20th century.66 Section 49 states that psychosurgery cannot be administered to people who are incapable to consent for themselves, as well as to people detained involuntarily in a psychiatric facility under mental health legislation or the Criminal Code.67 The purpose of this restriction is to protect people who are vulnerable by reason of incapacity or because they are being detained in a psychiatric facility.

However, it is the definition of “psychosurgery” that reveals the legal impact of biological psychiatry. The Act defines psychosurgery as follows:

49(2) Psychosurgery is any procedure that, by direct or indirect access to the brain, removes, destroys or interrupts the continuity of histologically normal brain tissue, or that inserts indwelling electrodes for pulsed electrical stimulation for the purpose of altering behaviour or treating psychiatric illness, but does not include neurological procedures used to diagnose or treat organic brain conditions, intractable physical pain or epilepsy, if these conditions are clearly demonstrable.

This definition is a problem on many levels. It is not clear that those whose symptoms are due to demonstrable organic brain conditions are any less vulnerable than those whose symptoms are ascribed to a psychiatric condition. The definition thus fails to accord with the apparent objective of the legislation.

Second, how should we classify interventions that target the behavioural consequences of what is clearly an organic brain disorder? Should this be understood as an intervention to address an organic brain condition or an intervention to alter behaviour? For example, a surgical intervention to address intractable aggression after a traumatic brain injury will not remedy the brain injury but may address the behavioural consequence of that injury.68

Third, intractable physical pain is sometimes ascribed to psychiatric somatoform disorders,69 and so it is necessary to decide whether neurosurgical treatment of such cases should be excluded from the regulation as a “neurological procedure used to…treat…intractable physical pain,” or included as a treatment for “psychiatric illness.”

Finally, Ontario’s dualistic definition of psychosurgery, which distinguishes psychiatric “mental” conditions and organic “brain” conditions is inherently unstable. In psychiatry, the “organic brain disorders” are understood to include “a range of mental disorders grouped together on the basis of their having in common a demonstrable etiology in cerebral disease, brain injury, or other insult leading to cerebral dysfunction…”70 Psychiatric conditions, on the other hand, are those mental and behavioural disorders that lack this demonstrable physical etiology. History is filled with examples of mental conditions that are now regarded as organic brain disorders, such as epilepsy, neurosyphilis, and certain vitamin deficiencies. As Insel and Quirion have noted, “in the past, mental disorders were defined by the absence of a so-called organic lesion. Mental disorders became neurological disorders at the moment a lesion was found.”71

It is an explicit objective of today’s biological psychiatry to uncover the biological nature of psychiatric conditions, and to find biomarkers that help to move away from nosologies based on symptoms to those based on underlying biology. If and when biomarkers are identified for other psychiatric conditions that are currently poorly understood, the category of “organic brain disorders” will grow and the scope of the regulation of “psychosurgery” will shrink.

Regulation of Reproductive Technologies: The “New Eugenics?”

Biological psychiatry is interested in understanding psychiatric disorders at multiple levels of biological focus spanning genes, molecules, cells, circuits and structures in the brain. Some conditions such as aneuploidies like Down Syndrome have a clear and determining genetic causal explanation. For other conditions, such as schizophrenia or bipolar disorder, heritability studies suggest a genetic contribution although causation is complex and multifactorial.72 If and when biological psychiatry uncovers these genetic contributions, and particularly if they are found to substantially raise the risk of developing mental illness, we may need to contend with what has come to be known as the “new eugenics” or the screening out of affected embryos or foetuses prior to birth.

There is no necessary association between a biological psychiatry and eugenic impulses. What matters is the social response to the mental condition in question. A society that devalues these conditions will respond differently from one that accommodates or celebrates the diversity in terms of mental and behavioural types. The neurodiversity movement, which originated with the autistic community and has now broadened to include a range of other conditions or “neurotypes” shows that a eugenic response is not a necessary result of biological psychiatry.73 However, one cannot ignore the connection between biological theories of mental disorders and the 20th century state-sanctioned eugenic policies in multiple countries including Canada.

As is well-known, eugenic ideologies led to programs of the most profound human rights violations in the 20th century in Nazi Germany as well as in North America. These ideologies originated in mid to late 19th century in the confluence of the social disruption brought about by industrialization, the publication of Darwin’s On the Origin of Species by Means of Natural Selection, and the rediscovery of Mendel’s experiments on heredity.74 The idea of eugenics was to improve humanity through selective reproduction, much as was done with livestock. By 1934, the Nazis passed the “Law for the Prevention of Hereditarily Diseased Progeny” which forced sterilization of people diagnosed with a range of mental illnesses and cognitive disabilities.75 Similar laws were passed in Canada and the United States. Among the subsequent outrages committed by the Nazi government were the programs of “special treatment” (i.e., murder) of children with mental disabilities and adults with mental illness and mental disabilities.76

Eugenic ideologies also drove law and policy in North America, where the objective of improving the fitness of the population led first to the ideas of isolating or segregating those with mental illness and cognitive disabilities to prevent reproduction and then to the idea of contraceptive sterilization as a cheaper alternative.77 The constitutionality of the American state compulsory sterilization laws was upheld in Buck v. Bell78 and they remained in some places until the 1970s.79 Canada too adopted legislation authorizing the forced contraceptive sterilization of people with mental illnesses.80 In fact, Alberta’s 1928 Sexual Sterilization Act was the first of its kind in the British Commonwealth, allowing a Eugenics Board to authorize sterilization of those about to be discharged from mental institutions in order to eliminate the “danger of procreation with its attendant risk of multiplication of the evil by transmission of the disability to progeny.”81

Although these statutes have been repealed, and Alberta has apologized and paid compensation to some of those forcibly sterilized under its legislation,82 some have suggested that we are now in a era of “laissez-faire,” “liberal,” or “new” eugenics in which parents take up the tools of prenatal diagnosis and pre-implantation genetic diagnosis to avoid the birth of children at risk of particular condition.83 Prenatal screening for Down syndrome has been available since the early 1970s and is now commonplace, and the vast majority of cases diagnosed prenatally result in abortion.84

While the genetic contributions to most major mental health conditions are extremely complex, and are unlikely to be the complete etiological story, the identification of psychiatric genetic risk factors is likely to enter a new world in which mental health stigma, social structures, and economic constraints will put pressure on parents to avoid conditions perceived as disabling and costly.

A good example of the possible impact of these developments as psychiatric genetics develops is furnished by the recent application to the UK’s Human Fertility and Embryology Authority (HFEA) to approve pre-implantation genetic screening for autism spectrum disorder (ASD). Pre-implantation genetic diagnosis (PGD) involves the testing of embryos created through in vitro fertilization to detect genes associated with various conditions. Under UK law, PGD may only be performed to detect conditions licensed by the HFEA.85 While this testing was developed for fully penetrant, monogenic, severe pediatric conditions, use has now expanded to a range of other heritable conditions.86

In 2014, the HFEA considered whether to approve an application to license screening out male embryos to avoid the inheritance of ASD.87 The applicants argued that this should be available for families with at least two severely affected male children on the basis that ASD was a “gender-related serious medical condition.” The Committee rejected the application because there was no “specific conclusive test for autism,” and stated that applications could not be approved “unless and until there is more scientific certainty on the genetic cause(s) of Autism Spectrum Disorder.”88 Despite the uncertain genetics of ASD, other jurisdictions such as the Australian States of Western Australia and Victoria have authorized the screening out of male embryos in families with a prior history of the condition.89

Research into the attitudes of families affected by mental health conditions to hypothetical genetic tests shows some receptiveness to use them to avoid or terminate affected pregnancies. This is noteworthy given that these families are likely to be better informed about the reality of living with these conditions than the general public. A recent study of the attitudes of parents of children with ASD toward prenatal genetic testing and pregnancy termination found that 57% of the 42 participating parents would use a hypothetical prenatal test for autism, and 20% of the group that was willing to take the test of unsure about taking the test said they would have terminated affected pregnancies.90 Research into the attitudes of extended families affected by multiple cases of bipolar disorder to a hypothetical genetic test for the condition showed 54% endorsed prenatal testing, and 27% endorsed termination if the test indicated that bipolar disorder would definitely develop.91 Among those diagnosed with a psychiatric condition, 25% endorsed termination and among unaffected family members 29% endorsed termination.

This research supports the suggestion of Lakhan and colleagues that “[i]t is only a matter of time before psychiatric biomarkers are added to the list of conditions routinely screened for prenatally.”92 Whether or not these screening tests are likely to lead to abortion probably depends upon the predictive value of the test, as well as on whether the condition itself varies in severity (as is the case with ASD). Nevertheless, it is important to note that the move toward embryo screening prior to implantation, and even to gene editing of affected embryos, avoids the likely more difficult decision of whether to terminate an established pregnancy.

Biological psychiatry intersects here with the law by raising the challenging issue of whether regulatory regimes should attempt to limit the use of prenatal or pre-implantation genetic diagnosis, as is done in the UK, or leave decision-making to parents and clinicians. This contentious issue pits concerns about the devaluation and disappearance of certain classes of people through a form of new eugenics against the reproductive liberty of parents. The debate is likely to become only more difficult with the increasing understanding of psychiatric genetics.

Conclusion

Biological theories of mental illness are not new, although they are increasing in sophistication. There are many reasons to celebrate this new knowledge, particularly as better understanding of all of the causal contributions to mental illnesses (psychosocial and biological) will help in designing preventive strategies and more effective ways to help. At the same time, biological psychiatry seems to encourage certain patterns of thought that have social, political and legal consequences. These consequences may be helpful or harmful, or perhaps both, as the example of how the brain disease model of mental illness both increases and decreases different components of stigma shows. The ultimate ideological consequences of biological psychiatry on the law and other social institutions are difficult to predict. Attention to these topics over the coming years is advisable in order to ensure the benefits of the accumulating knowledge are seized and the social, political and economic risks are avoided.

Footnotes

GE Berrios and IS Markova, “Conceptual Issues” in H D’Haenen, JA den Boer and P Willner Eds. Biological Psychiatry (Chichester: John Wiley & Sons Ltd.,2002) at p. 3; J Gach “Thoughts toward a critique of biological psychiatry” in ER Wallace and J Gach eds. History of Psychiatry and Medical Psychology (New York: Springer 2008) at p. 685; E Shorter A History of Psychiatry: From the Era of the Asylum to the Age of Prozac, (John Wiley & Sons, 1997) at p. 26.

R Porter, Madness: A Brief History (Oxford: Oxford University Press, 2002) at p. 41; B Simon, “Mind and madness in classical antiquity” in ER Wallace and J Gach eds. History of Psychiatry and Medical Psychology (New York: Springer, 2008 at p. 181; T Millon Masters of the Mind: Exploring the story of mental illness from ancient times to the new millennium (Hoboken: John Wiley & Sons, 2004), at p. 16.

Hippocrates, On the Sacred Disease Trans. Francis Adams (MIT Internet Classics Archive, 400 BCE) <http://classics.mit.edu/Hippocrates/sacred.html>.

4 Supra note 1, Shorter at p. 26.

Ibid.

Ibid.

H Walter “The third wave of biological psychiatry” (2013) 4(582) Frontiers in Psychology 1 at 2.

Ibid.

Ibid.

MS Lebowitz and W Ahn “Effects of biological explanations for mental disorder on clinicians’ empathy” (2014) 111(50) PNAS 17786.

Supra note 7 at p.5; Gach, supra note 1 at p. 688.

MS Lebowitz and W Ahn. “Emphasizing malleability in the biology of depression: Durable effects on perceived agency and prognostic pessimism” (2015) 71 Behaviour Research and Therapy 125; NR Farrel, AA Lee, BJ Deacon “Biological or psychological? Effects of eating disorder psychoeducation on self-blame and recovery expectations among symptomatic individuals” (2015) 74 Behavior Research and Therapy 32. 

Farrel et al., ibid.

Supra note 10.

Ibid.

Wilson v. Corestaff Services L.P. 900 N.Y.S. 2d 639 (N.Y. Sup. Ct. 2010); United States v. Semrau 693 F.3d 510 (6th Cir. 2012).

HJ Greely “Neuroscience, mindreading and the courts: The example of pain” (2015) 18 J Health Care L & Pol’y 171.

G Ganis et al. “Lying in the scanner: Covert countermeasures disrupt deception detection by funcational magnetic resonance imaging” (2011) 55 Neuroimage 312.

DL Schachter and E Loftus. “Memory and law: What can cognitive neuroscience contribute?” (2013) 16(2) Nature Neuroscience 119.

The Innocence Project investigated the causes of wrongful convictions revealed by DNA exonerations. Of the 325 DNA exonerations studied, 235 or 72% involved eyewitness misidentification. This was the most frequently cited contributing cause of the wrongful conviction. See Innocence Project, The Causes of Wrongful Convictions (visited June 13, 2016) <http://www.innocenceproject.org/causes-wrongful-conviction/>; JB Gould and RA Leo. “One hundred years later: Wrongful convictions after a century of research” (2010) 100(3) J. Crim Law and Criminology 825.

Supra note 19; NS Werner and HJ Markowitsch, “The neuroscience of face processing and identification in eyewitnesses and offenders” (2013) 7(189) Frontiers in Behav. Neurosci. 1 at p. 8.

MS Purcell, JA Chandler, JP Fedoroff “The use of phallometric evidence in Canadian criminal law” (2015) 43(2) J Am Acad Psych Law 141.

V Quinsey, “Sex Offender Risk Appraisal Guide” in BL Cutler ed. Encyclopedia of Psychology and Law (Thousand Oaks: SAGE Publications Inc., 2008); Purcell, ibid.

J Ponseti et al. “Assessing pedophilia based on the haemodynamic brain response to face images” (2016) 17(1) World Journal of Biological Psychiatry 39; C Wiebking and G Northoff, “Neuroimaging in pedophilia” (2013) 15 Curr Psychiatry Rep. 351.

See e.g. Hunt v. Ugre 2012 BCSC 1704; M Finch “Law and the problem of pain” (2005-2006) 74 U. Cin. L. Rev. 285; SA Pate “Litigating chronic pain syndrome in the Canadian court system” (1996) 5 Health L. Rev. 19.

A Pustilnik “Imaging brains, changing minds; How pain neuroimaging can inform the law” (2014) 66 Ala. L. Rev. 1099, citing T Wager et al., “An fMRI-Based Neurologic Signature of Physical Pain” (2013) 368 New Engl. J. Med. 1388.

S. Reardon “Neuroscience in court: the painful truth” 2 March 2015. Nature news. <http://www.nature.com/news/neuroscience-in-court-the-painful-truth-1.16985>; Pustilnik, ibid.

Reardon, ibid.

M Farah “Brain images, babies, and bathwater: Critiquing critiques of functional neuroimaging” (2014) 44 Hastings Center Report S19.

Reardon, supra note 27; N Salmanowit “The case for pain neuroimaging in the courtroom: lessons from deception detection” (2015) Journal of Law and the Biosciences doi:10.1093/jlb/lsv003; S. Cassin, “Eggshell minds and invisible injuries: Can neuroscience challenge longstanding treatment of tort injuries” (2013) 50 Houston L. Rev 929; Greely, supra note 17.

Reardon, supra note 27.

S Van Bergen et al. “Memory distrust and acceptance of misinformation” (2010) 24 Applied Cognitive Psychology 885.

J Garretson and E Suhay, “Scientific communication about biological influences on homosexuality and the politics of gay rights” (2016) 69(1) Political Res. Q. 17.

34 B Weiner “On sin versus sickness: A theory of perceived responsibility” (1993) 48(9) American Psychologist 957; B Weiner, D Osborne, U Rudolph “An attributional analysis of reactions to poverty: The political ideology of the giver and the perceived morality of the receiver” (2011) 15(2) Pers. and Soc. Psych. Rev. 199.

35 Garretson and Suhay, supra note 33.

36 PW Corrigan “Mental health stigma as social attribution: Implications for research methods and attitude change” (2000) 7(1) Clinical Psychology: Science and Practice 48.

Garretson and Suhay, supra note 33.

Ibid.

Ibid at p. 25.

GB Lewis, “Does believing homosexuality is innate increase support for gay rights?” (2009) 37(4) Policy Studies Journal 669.

PW Corrigan and AC Watson. “Stop the stigma: call mental illness a brain disease” (2004) 30(3) Schizophrenia Bulletin 477; AA Lee, et al. “Genetic attributions and mental illness diagnosis: Effects on perceptions of danger, social distance, and real helping decisions” (2014) 49 Soc. Psych. Psychiatr. Epidemiol. 781; EP Kvaale, WH Gottdiener and N Haslam “Biogenetic explanations and stigma: A meta- analytic review of associations among laypeople” (2013) 96 Soc. Sci. & Med. 95.

B Pescosolido et al. “A disease like any other”? A decade of change in public reactions to schizophrenia, depression and alcohol dependence (2010) 167(11) American J. Psychiatry 1321; ND Volkow and G Koob “The brain disease model of addiction: why is it so controversial?” (2015) 2(8) Lancet Psychiatry 677.

Volkow and Koob, ibid; K Roy and M Miller “Parity and the medicalization of addiction treatment” (2010) 42(2) Journal of Psychoactive drugs 115.

American Psychiatric Association, 2000. DSM-IV TR 4th ed. (Arlington:, APA, 2000), section 312.31.

American Psychiatric Association, 2013 DSM-5 5th ed. (Arlington: APA, 2013), “Substance-related and addictive disorders”

Ibid.

SA Tovino, “Will neuroscience redefine mental injury? Disability benefit law, mental health parity law, and disability discrimination law” (2015) 12(2) Indiana Health L Rev. 695.

JA Chandler “The impact of neuroscience in the law: How perceptions of control and responsibility affect the definition of disability” forthcoming in J Illes and S Hossain eds. Neuroethics: Defining the Issues in Theory, Practice and Policy, 2nd ed. (Oxford: Oxford University Press, forthcoming).

Canada Safeway Ltd. and RWDSU (MacNeill) Re [1999] S.L.A.A. No. 1 (Sask. Labour Arbitration).

Manitoba v. Manitoba Government and General Employees’ Union 2005 MGAD No. 14 at paras 48, 59, 85.

McNeill v. Ontario Ministry of the Solicitor General and Correctional Services [1998] O.J. No. 2288 (Ont. Ct. J. – Gen Div.). See also R. v. Ample Annie’s Itty Bitty Roadhouse [2001] O.J. No.5968 (Ont. C.J.); Yellowknife (City) v. Denny 2004 NWTTC 2.

Cominco Ltd. v. United Steelworkers of America, Local 9705, [2000] B.C.C.A.A.A. No. 62 at para 180.

Letourneau v. JTI-MacDonald Corp. 2015 QCCS 2382.

C Ruby, Sentencing 6th ed (Markham: LexisNexis, 2004) at para 5.246.

AL Glenn et al. “Is it wrong to criminalize and punish psychopaths?” (2011) 3 Emot. Rev. 302.

M Farisco and C Petrini, “The impact of neuroscience and genetics on the law: A recent Italian case” (2012) 5 Neuroethics 317.

J Greene and J Cohen J. “For the law, neuroscience changes nothing and everything” (2004) 359 Phil. Trans. R. Soc. Lond B. 1775.

Ibid at p. 1783

C Slobogin “The civilization of the criminal law” (2005) 58 Vanderbilt Law Review 121; S Morse “Gene- Environment Interactions, Criminal Responsibility, and Sentencing” in K Dodge & M Rutter Eds., Gene- Environment Interactions in Developmental Psychopathology (New York: Guilford Press, 2011) at pp. 207- 234; AR Cashmore “The Lucretian swerve: The biological basis of human behaviour and the criminal justice system” (2010) 107(10). Proc. Nat Acad. Sci. 4499.

LG Aspinwall, TR Brown and J Tabery, “The double-edged sword: Does biomechanism increase or decrease judges’ sentencing of psychopaths?” (2012) 337 Science 846; J Fuss J, H Dressing and P Briken “Neurogenetic evidence in the courtroom: a randomized controlled trial with German judges” (2015) 42 J Med. Genet 730; BY Cheung and SJ Heine, “The double-edged sword of genetic accounts of criminality: Causal attributions from genetic ascriptions affect legal decision making” (2015) 41(12) Personality and Social Psychology Bulletin 1723; PS Appelbaum and N Scurich, “The impact of behavioral genetic evidence on the adjudication of criminal behavior” (2014) 42 J. Am Acad Psych Law 91; N Scurich and P Appelbaum “The blunt-edged sword: genetic explanations of misbehavior neither mitigate nor aggravate punishment” (2016) 3(1) J. Law and Biosci. 140.

Aspinwall et al, ibid.

Ibid. at p. 847.

Ibid at p. 848.

Gach, supra note 1 at p. 685.

Mental Health Act, R.S.O. 1990 c.M.7, s. 49.

ES Valenstein Great and Desperate Cures: The rise and decline of psychosurgery and other radical treatments for mental illness (New York: Basic Books, 1986).

67 Supra note 65 at s. 49(1).

68 See M Lévêque, Psychosurgery: New techniques for brain disorders (Springer, 2014) “Disorders for which psychosurgery is relevant today” at p. 230 for a discussion of the use of psychosurgery in aggressive disorders.

Supra note 44 at p. 485.

World Health Organization, “F00-09 Organic, including symptomatic, mental disorders” in International Statistical Classification of Diseases and Related Health Problems, 10th revision (ICD-10) (2016) available at <http://apps.who.int/classifications/icd10/browse/2016/en#/F00-F09>.

TR Insel and R Quirion, “Psychiatry as a clinical neuroscience discipline” (2005) 294(17) JAMA 2221.

KR Merikangas and A Cravchik, “Contribution of genetic epidemiology to our understanding of psychiatric disorders” in JI Nurnberger and W Berrettini eds Principles of Psychiatric Genetics (Cambridge: Cambridge Univ. Press, 2012) at p.1.

S Baron-Cohen, “Neuroethics of neurodiversity” in J Clausen and N Levy Handbook of Neuroethics (Dordrecht: Springer, 2015) at p.1757. A Fenton and T Krahn, “Autism, neurodiversity and equality beyond the “normal”” (2009) 2(2) J Ethics Mental Health 1.

BA Fischer “Maltreatment of people with serious mental illness in the early 20th century: A focus on Nazi Germany and Eugenics in America” (2012) 200(12) J. Nervous and Mental Disease 1096; NA Nind “Solving an “appalling” problem: Social reformers and the campaign for the Alberta Sexual Sterilization Act” (2000) 38 Alta. L. Rev. 536.

Fischer, ibid.

Ibid.

Ibid.

Buck v. Bell 274 U.S. 200 (1927).

Fischer, supra note 74; Nind, supra note 74.Sexual Sterilization Act, SA 1928, c 37; Sexual Sterilization Act, SBC 1933, c 59; see also Muir v Alberta (1996), 36 Alta LR (3d) 305 (Alta Q.B.)

Nind, supra note 74.

CBC News “Alberta apologizes for forced sterilization” CBCNews.com 9 November 1999, <http://www.cbc.ca/news/canada/alberta-apologizes-for-forced-sterilization-1.169579>.

N Agar “Liberal eugenics” (1998) 12(2) Public Affairs Quarterly 137; T Caulfield and G Robertson “Eugenic policies in Alberta: From the systematic to the systemic?” (1996) 35 Alta L. Rev. 59.

AL Caplan “Chloe’s Law; A powerful legislative movement challenging a core ethical norm of genetic testing” (2015)13(8) PLoS Biol. e1002219.

UK Human Fertility and Embryology Authority. “PGD conditions licensed by the HFEA” <http://guide.hfea.gov.uk/pgd/> (visited 10 June 2016).

KJ Abbate et al. “Views of preimplantation genetic diagnosis (PGD) among psychiatrists and neurologists” (2014) 59 J. Reprod. Med. 385.

UK Human Fertility and Embryology Authority “Statutory Approvals Committee Minutes. Centre 0044 (The Centre for Reproductive and Genetic Health (CRGH)) PGD application for Autism Spectrum Disorder OMIM #209850” (30 January 2014) available at <http://guide.hfea.gov.uk/guide/ShowPDF.aspx?ID=5518>.

Ibid at para 18.

A Ne’eman “Screening sperm donors for autism? As an autistic person, I know that’s the road to eugenics” The Guardian 30 December 2015, available at <http://www.theguardian.com/commentisfree/2015/dec/30/screening-sperm-donors-autism-autistic-eugenics>

LS Chen et al. “Autism spectrum disorders: A qualitative study of attitudes toward prenatal genetic testing and termination decisions of affected pregnancies” (2015) 88 Clinical Genetics 122.

B Meiser et al. “Attitudes to genetic testing in families with multiple cases of bipolar disorder” (2008) 12(2) Genetic Testing 233.

Keeping the Science in Neuroscience

In a world of increasing specialization, the number of scientific disciplines seems to increase every day. However, there is a central tenet that underlies all of science: the requirement that knowledge be based on systemic observations of the world that result in predictions that can be tested and falsified. This focus on empiricism is the defining feature of the scientific method, and it is what allows scientists to differentiate between scientific knowledge and mere conjecture, opinion, and speculation. This is not to say that conjecture, opinion, and speculation cannot help the scientific process advance, but that every scientist worth her salt can differentiate between the two and guards the line zealously.

A common misunderstanding about science is that it results from the use of technologically advanced techniques. This misunderstanding, in my opinion, drives a great deal of confusion about what science is all about. Advanced technology is often used to assist scientists and is often developed by scientists. But the use of advanced technology is akin to the use of a word processor; it is a tool that assists the work scientists do, but is orthogonal to the concept and demands of scientific discovery itself. To be sure, this is not a misunderstanding that is only held by laypersons. Even scientists often become complacent in their application of the scientific method when advanced―some might say ‘sexy’―technologies are used. For example, it is well known that studies in the early years of fMRI research were plagued with basic mistakes in scientific inference.7Despite being peer-reviewed, these methodological mistakes were, by most people's understanding, elementary even at the time.

The contrast between the use of science and the use of technology figures prominently in the four Journal of Law and the Biosciences studies. The methods employed―which were largely homogenous across the studies―did not isolate cases where neuroscience was introduced insomuch as they isolated cases where brain imaging technology or neurojargon was used. Each study defined a case as ‘involving neuroscience’ if it contained at least one of a family of key words, such as Brain, EEG, fMRI, and CT Scan. No study examined whether the use of these technologies was consistent with the rigors of the scientific method, or in other words, actually constituted ‘neuroscience’. The commentary of at least one author suggests that this determination was based on the belief that the use of a brain scan is indisputably sufficient to conclude that the evidence is neuroscientific in nature: ‘Brain scan evidence might be accepted by all or virtually all commentators as being neuroscientific evidence.’8 But this conclusion is far from obvious. By itself, a brain scan is no more scientific than the careful measurements of the bumps on an individual's skull―a practice called phrenology that was once considered cutting edge brain science, but now widely considered bizarre.

Even though these studies’ search methods did not target evidence having scientific rigor, it is certainly possible that the identified cases were based on science nonetheless. It is impossible for me to examine all the cases identified, since only a few representative cases are presented in the manuscripts. However, a cursory examination of these representative cases provides no indication that the technology was used with anything approaching the demands of scientific inference. In the article examining English and Welsh courts, the authors describe testimony of a Dr Reeves, who links a defendant's childhood head injury to his behavior as an adult. That testimony concludes that the childhood injury may have caused damage to the defendant's temporal lobe―the part of the brain, the doctor claims, that governs temper control and learning. The article examining the American courts highlights a case where a man was diagnosed, via PET, of abnormalities in the left lateral frontal area. These abnormalities were used to support a conclusion of legal insanity at the time he assaulted people on a street with a large metal pipe. By any definition of the term, the evidence provided in these cases, and the others described in the four articles, is not rooted in science but mere speculation.

Not Repeating the Mistakes of the Past

Being careful with the use of the term neuroscience is not merely a matter of semantics or usage. In my estimation it could be a matter of life or death for the future of neuroscience in the law. While that diagnosis is easy to characterize as hyperbole, an examination of the tumultuous history of forensic psychology is instructive.

It is impossible to thoroughly review the history of forensic psychology and its use in the law within the confines of this commentary. There is, however, no better example than that of Dr James Grigson. Up through 1990, Dr Grigson testified in 127 cases where prosecutors sought the death penalty. In each of these cases, Dr Grigson's testimony took the same form, as described by one person who researched his work:

He'll take the stand, listen to a recitation of facts about the killing and the killer, and then―usually without examining the defendant, without ever setting eyes on him until the day of the trial―tell the jury that, as a matter of medical science, he can assure them the defendant will pose a continuing danger to society.9

Of the 127 cases where he provided testimony, juries provided death sentences in all but nine.10 Forensic psychiatrists and psychologists like Grigson did not limit their commentary to diagnoses of future dangerousness. During the last half of the century, it is reported that psychiatrists and psychologists were participating in up to 1 million cases annually, providing expert scientific opinions on the issues of defendants’ prior mental states, their ability to comprehend the charges against them, and whether they were legally insane at the time of their conduct, to name a few.11

Unfortunately for everyone, in the late 20th century it became apparent that the scientific foundation for these experts’ conclusions simply did not exist. It is not that they were imperfect in making their conclusions; they were a complete fraud. To wit, a number of large studies revealed that, irrespective of education or experience, expert psychologists were no better than high school children, office secretaries, or random persons off the street at making the types of diagnoses being made under the color of science in the courts.12 It is important to note that in these cases the science was not wrong; rather there was simply no science involved in the first place. These revelations cast a shadow of disrepute over the use of these experts in legal proceedings that maintains today.

Our experience with psychology and psychiatry in the law does not only provide a cautionary tale of what generally happens to a field when testimony is no longer bound by the science. It also useful because the majority of the purported ‘neuroscience’ presented in courts today is actually the same junk psychology and psychiatry of yesteryear repackaged with the allure of neuroimaging and neurojargon. But the allure is unfounded. While it can seem almost self-evident that abnormalities in a brain scan would be the cause of deviant behavior, it is critical to recognize that this is based almost purely on intuition. Two questions can make this fact clear. First, would the reader similarly rely on an expert that supported his conclusion with measurements of the size of the bumps on different parts of the subject's skull, as commonly done in the 19th century? And if not, why not? What does the neuroimaging provide that is more informative than the phrenology? Second, consider a recent conversation I had with a criminal defense attorney that made scanning of his clients’ brains part of his standard operating procedure. The expert performing the scans found brain ‘abnormalities’ in ‘every single one’ of the attorney's clients (over 100 cases in total). Given the complexity of the brain, this is hardly surprising; there truly is no such thing as a normal brain. Thus we must ask whether abnormality, by itself, provides useful information for the law. In both of these points we see the same thing; intuitively we want to create a connection between the results of a brain scan and criminal behavior but, as a matter of science, there is, just as before, little to nothing to support that intuition.

Conclusion: Protecting the Potential of Neuroscience to the Law

The importance of carefully policing the use of the term neuroscience is augmented by the potential for actual neuroscience to materially improve the just and efficient application of the law. As noted in the introduction, a huge appeal for the field of neuroscience to the law is the possibility that it can provide answers to questions long presumed out of reach. Tens of millions of dollars have been invested in developing the neuroscientific research necessary to begin providing answers with the confidence the scientific process provides. These efforts have produced meaningful results. As an example, recent work has begun to establish neural markers of subjective pain, deception, recognition, and even conscious awareness. Other work is beginning to inform how development changes the way young adults process and react to their environment. Still, more research is evaluating the brain mechanisms that support punishment decision-making in order to better understand what drives these decisions and how they can be influenced by spurious information. Each of these lines of research promises to potentially provide legal decision-makers and legislators with useful information that can improve the accuracy and effectiveness of our laws.

While most of this research is still far from providing the answers of interest to the law, it is moving in that direction. Two recent cases demonstrate what using good neuroscience in the courts might look like. In Miller v Alabama, the US Supreme Court referenced a large body of peer-reviewed neuroscience on adolescent development in support of its holding that mandatory sentences of life without the possibility of parole are unconstitutional for juvenile offenders.13 In U.S. v Semrau, a federal appeals court reviewed the scientific merit of testimony based on fMRI lie detection and found that it did not meet the standards of the Federal Rules of Evidence. However, in making this determination the court laid a clear framework for its possible future admission as evidence.14 And, perhaps most importantly, researchers have started to scientifically address some of the shortcomings raised by the court. While both examples are incremental, they can be lauded for their fidelity to the science.

In 1988, David Faust and Jay Ziskin wrote of the unfortunate irony behind the revelation that the forensic psychology being used in the courts was without scientific merit. Though written three decades ago, the rapid advancement of neuroscience makes their words truer now than ever. They wrote: ‘research should eventually yield more certain knowledge and methods that provide meaningful assistance to the trier of fact’ but that ‘the courts, having learned to distrust clinicians’ claims, may refuse to admit testimony based on truly useful knowledge and methods despite more than adequate supportive studies.’15 Thirty years later, psychology's reputation in the law still has not recovered despite marked improvements in the field. The only question now is whether in 30 years’ time neuroscience will have the same fate. By being casual with the use of the term neuroscience we are asking for just that.

Footnotes

Francis X. Shen, The Law and Neuroscience Bibliography: Navigating the Emerging Field of Neurolaw, 38 INT'L J. LEGAL INFO. 352 (2010).

Owen D. Jones & Matthew Ginther, Law and Neuroscience, in INTERNATIONAL ENCYCLOPEDIA OF THE SOCIAL & BEHAVIORAL SCIENCES 489, 490 (Neil J. Smelser and Paul B. Baltes ed., 2d ed. 2015).

Nita A. Farahany, Neuroscience and Behavioral Genetics in Us Criminal Law: An Empirical Analysis, 2 J. L. BIOSCI. 485 (2015).

Jennifer A. Chandler, The Use of Neuroscientific Evidence in Canadian Criminal Proceedings, 2 J. L. BIOSCI. 550 (2015).

C.H. de Kogel & E.J.M.C. Westgeest, Neuroscientific and Behavioral Genetic Information in Criminal Cases in the Netherlands, 2 J. L. BIOSCI.580 (2015).

Paul Catley & Lisa Claydon, The Use of Neuroscientific Evidence in the Courtroom By Those Accused Of Criminal Offenses in England and Wales, 2 J. L. BIOSCI. 510 (2015).

See Edward Vul et al., Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition, 4 PERSP. ON PSYCHOL. SCI.274 (2009); Nikolaus Kriegeskorte et al., Circular Analysis in Systems Neuroscience: The Dangers of Double Dipping, 12 NATURE 535, 540 (2009).

Catley & Claydon supra note 6, at 514.

RON ROSENBAUM, TRAVELS WITH DR. DEATH 210 (1991).

Paul C. Giannelli, ‘Junk Science’: The Criminal Cases, 84 J. CRIM. L. & CRIMINOLOGY 105, 115 (1993).

David Faust & Jay Ziskin, The Expert Witness in Psychology and Psychiatry, 241 SCIENCE 31, 31 (1988).

Id. at 32, 34.

132 S. Ct. 2455 (2012).

693 F.3d 510 (2012).

A Brief Aside: The State of the Science

Recent advances in neuroscience make it compelling to apply such knowledge in a forensic context. As early as 1981, computed tomographic (CT) scan evidence was admitted in the John Hinckley, Jr. case to illustrate that Hinckley had widened sulci, a cardinal marker for schizophrenia, despite the fact that it was unknown whether this had anything to do with his mental state at the time of the crime, which was the forensic question at hand.1 As the field has advanced over the past several decades, neuroimaging has been introduced as evidence in other forensic contexts as well, including culpability, aggravating or mitigating circumstances, and risk management in the criminal arena, and tort claims or functional decisional capacities in the civil arena.4

Despite these advancements and the temptation to apply our growing knowledge, many would consider the state of the field of neuroscience to be still in its infancy. Critics contend that there is a dearth of findings that pin a specific brain scan pattern to a specific psychiatric disorder, much less with the more complex cognitive and behavioral functions underlying many legal debates.4 In other words, it is one thing to say that a scan shows reduced blood flow to the anterior cingulate area or structural differences in the orbitofrontal region. It is another to say that those differences mean that someone lacked the capacity to appreciate the wrongfulness of his conduct. Problems with defining what is normal, with creating predictive models, and even with the technology itself preclude our ability to state with a reasonable degree of medical certainty that specific brain pathology even correlates with, much less causes, specific behaviors or mental states.4 However, it is distinctly possible (perhaps even likely) that continued advancements in neuroimaging and neuroscientific research will someday yield greater sophistication in our understanding of just how specific brain abnormalities contribute to certain behaviors and to mental states such as intentionality, appreciation, and moral judgment. So, again, what do we do with this information?

Previous Section

Next Section

Science and the Law: A Cultural Divide

Scientists and philosophers have long wrestled with what is known as mind/body dualism (what some have called the Cartesian impasse), which is essentially, where the boundary lies between free will and determinism. This debate (which is not even settled within disciplines) takes on an entirely new dimension when applied to the law, where fundamental assumptions about human behavior widen even further. According to the law, human behavior is the product of free will or rational choice, whereas neuroscience reduces cognition, emotion, and behavior to cold, mechanistic brain functioning. Morse asserts, “brains do not commit crimes, people commit crimes” (Ref. 5, p 397), noting that brain-based causation does not absolve one of criminal responsibility. Humans are viewed as intentional agents, and it is our behavior (not our brains) that determines responsibility. Yet, neuroscientists fire back that behavior is determined by the brain, making it (and therefore, us) the true agent. These fundamental assumptions about the nature of human behavior collide when mental health experts are summoned to the courtroom to shed light on some forensic question.

Different priorities across these disparate disciplines also mean that the gaze is sometimes focused in different directions: in psychology and psychiatry, causality often is the cardinal interest, and usually it is seen as a complex interplay of biological and environmental factors, whereas for law it is the effect of a particular behavior that is most important.1 Although the philosophical “clash of cultures” often pulls us to think of things in terms of polar opposites, both sides of the debate likely can agree that the answer lies somewhere in the middle. We are likely no more devoid of the myriad external influences in our lives (and hence, not entirely free) than we are mechanistically reduced to a complex weaving of neural circuitry (and hence, not entirely determined). To ask the question one more time, against this philosophically different backdrop of law, what do we do with our scientific knowledge?

Returning to Im's theory, the juxtaposition of ASD and violence elicits many questions. What are the forensic implications of such a theory? Might this mean that we should not hold individuals with ASD criminally responsible for violent acts, because their complex brain dysfunction prevents them from appreciating right from wrong or from controlling their behavior once triggered? Should they be deemed ineligible for certain punishments, like the death penalty, as other groups of developmentally immature individuals (for instance, the intellectually disabled, and adolescents) have been so excluded? If a specific brain dysfunction is said to exculpate one's behavior, is this true for all individuals with a similar affliction? If not, why not? Should the data stand alone, or should they be interpreted in a moral and sociopolitical context that considers the impact on society's standards of decency? A closer look at how certain neuroscientific research has been applied in the forensic context may help to illustrate the complexities (and the potential pitfalls if we do not exercise caution in how we do it).

The Prefrontal Cortex and Its Influence on Behavior

In Roper v. Simmons,6 the United States Supreme Court held that juveniles (that is, offenders under the age of 18 when they committed their crime) were ineligible for the death penalty under the Eighth and Fourteenth Amendments. The Court reasoned that adolescents' vulnerability to negative influences, poor impulse control, and overall developmental immaturity make them less culpable than their adult counterparts; thus, inflicting this most extreme form of punishment on them does not serve the fundamental elements of justice. This decision relied in part on an amicus brief, filed by the American Psychological Association (APA), citing neuroscientific research that showed incomplete maturation of the frontal lobes, and particularly the prefrontal cortex, in adolescents.7

The prefrontal cortex, the most anterior of the frontal lobe divisions, is considered to be “the most complex, selectively derived neurological feature” of the brain (Ref. 2, p 220). It has long been known to be central to numerous higher order cognitive (or executive) functions, including: behavioral motivation, impulse control, emotional processing and intelligence, recognition of conventional behavior, goal-setting and -directed behavior, analysis of reward and punishment (and avoidance of the latter), complex problem solving, and task-relevant attention and persistence. Damage to this area (or, failure to develop in the first place) thus leads to amotivation and apathy, lack of empathy, poor social judgment, impulsivity, failure to benefit from operant conditioning, and inability to organize and execute a set of behaviors aimed toward task completion. According to the APA brief, the adolescent brain is more prone to risk-taking, less capable of weighing the advantages and disadvantages of a particular course of action (especially one that involves proximal advantages and distal disadvantages), and more vulnerable to social influence than is the adult brain. One “hallmark of frontal lobe dysfunction is difficulty in making decisions that are in the long-term best interests of the individual” (Ref. 7, p 10). Thus, citing the Court's own reasoning in Atkins v. Virginia, the brief argued that, given their less developmentally mature brains, the imposition of the death penalty on adolescents “does not serve the judicially recognized purposes of the sanction … [and thus amounts to] purposeless and needless imposition of pain and suffering” (Ref. 8, p 319).

That analysis seems reasonable. The prefrontal cortex is one of the core structures Im3 refers to in his analysis of how trauma relates to violence, as well as in his theory of how individuals with ASD are particularly vulnerable to the impact of trauma. Both groups show dysfunction in this region that impairs their social–emotional capacities and narrows their range of appropriate behavioral responses; but what about other conditions, with brain dysfunction and resulting behaviors that can be (and has been) demonstrated through neuroscience? Numerous studies suggest that psychopaths show dysfunction in the prefrontal cortex similar to that of adolescents (or individuals with ASD, or trauma survivors). Would (or should) these same proscriptions extend to that condition?

The Neurobiology of Psychopathy

Psychopathy is a personality and behavioral disorder characterized by shallow affect and reduced autonomic reactivity; a lack of empathy or concern for others; a conning, manipulative interpersonal style; and impulsive, antisocial, and often criminal, behavior. Although most criminals are not psychopathic, psychopaths make up about 20 percent of the prison population and commit an inordinate number of violent acts compared with their nonaffected counterparts.9 Research suggests that the core features of this disorder (the affective and interpersonal traits) are to various degrees biological in nature, tied to specific abnormalities in the brain.10

Specifically, psychopaths are said to have damage to areas of the prefrontal cortex (contributing to impulsivity, irresponsibility, poor decision-making, and deficient emotional information processing); deficits in the orbitofrontal/ventromedial area of the prefrontal cortex (contributing to disinhibition, impaired moral decision-making, and failure to process adequately reward and punishment); deficits in the dorsolateral prefrontal cortex (contributing to response perseveration in the face of punishing consequences, and failure to direct attention to relevant emotional cues); damage to the superior temporal cortex and the amygdala–hippocampus complex (contributing to rule-breaking behavior, moral judgment deficiency, and failure to avoid punishment); damage to the superior temporal gyrus (contributing to a lack of empathy for others or concern for one's actions and noncompliance with prosocial rules); reduced volume in the amygdala and in the amygdala–hippocampus complex (contributing to deficits in perspective taking or empathy, emotional intelligence, and fear conditioning); and damage to the anterior cingulate cortex (contributing to disinhibition, perseveration, and poor emotion regulation10,–,17). In short, neuroimaging studies have provided support for the theory that psychopaths have deficits in various areas of the prefrontal cortex, temporal structures, and the amygdala and other areas of the limbic system that contribute to their deficits in emotional intelligence (aligning with others', as well as regulating their own), impulse control, fear-based conditioning, and moral decision-making. These deficits in turn make them more likely to harm or exploit others, to engage in behavior that most others would avoid because of its consequences, and to feel no remorse or shame for behavior that repeatedly violates the rights of others. So, do these brain-based deficits make them less responsible for their actions, and less deserving of punishment, in the same way that adolescents' yet-to-develop prefrontal cortex makes them less responsible for their conduct?

Of course, this is not to say that adolescent and psychopathic brains are exactly alike, any more than the brains of individuals with ASD are exactly like those of trauma survivors. Clearly, numerous factors play a role in the execution of any behavior or mental state. However, given the similarity in brain structure and function among different behavioral expressions, it raises the question: if policymakers at the nexus of psychology and law are going to argue that specific brain dysfunction can absolve one of (or at least, soften one's) culpability, why is that true of one group (adolescents) and not of another (psychopaths)? What causes us to recoil at the very notion of suggesting that these individuals would be anything other than wholly responsible for the violence and damage that they perpetrate?

These comparisons are not meant to suggest that this author believes that psychopathy is a disorder akin to ASD, or that it should be the basis for a diminished capacity defense, or that such individuals should not be punished for their wrongdoings on account of their “bad brains.” Indeed, some might argue that individuals with ASD are not responsible for their crimes because of deficits A, B, and C, yet those same deficits may make us perceive a psychopath to be more responsible, more at risk, or more deserving of punishment. Perhaps it is not just those specific deficits, but the presence of capacities X, Y, and Z (present in psychopaths but not ASDs) that make us hold them more reprehensible and thus more legally culpable. Nor are they meant to imply that even individuals who share the same constellation of symptoms or behaviors (that is, diagnostic categories) should be treated similarly. Every case is different, and we cannot make such sweeping generalizations that all individuals with ASD should not be held culpable for crimes, the same way that we do not make the claim that all individuals with intellectual disabilities, or dementia, or other brain dysfunctions are similarly inculpable. Rather, the questions and points raised herein are meant to stimulate thought and discussion, to encourage others to think through how our science is used, before we have the capacity to use it. If we are going to rely on neuroscience to back up our arguments as to why certain individuals are less culpable or less deserving of punishment, we ought to be prepared to explain why other individuals with similar deficits are not; else we should not pretend that it is because of the brain dysfunction itself. More broadly, if we embark on a path of using neuroscience, not just to inform the state of reality (for instances, one's capacities with respect to various decision-making contexts or in comparison to their functioning preinjury), but also to integrate it with our principles of fairness and justice to make psycholegal judgments about people's accountability, liberties, and in some cases, lives, we must give thoughtful consideration to just how those judgments are made.

Conclusion

Im3 adds to our understanding of violence by summarizing the neuroscientific findings and theoretical underpinnings regarding specific brain dysfunctions and ASD and by hypothesizing a mechanism for the link between trauma and violence in individuals with ASD. We, as a science, will continue to wrestle with complex questions regarding the relationship between neural circuitry and behavior. As our science advances, we, as psycholegal scholars, are going to be forced to bring this knowledge into the forensic arena, whether by defense attorneys arguing that their clients are not responsible for their criminal actions, or by parole boards attempting to make determinations regarding risk management, or by probate courts wrestling with questions regarding an individual's basic freedoms or decisional capacities. We will be confronted with complex questions involving mental states, intentionality, free will, culpability, and risk of recidivism. We must resist the temptation to apply these findings prematurely, before we have a more nuanced understanding of the complex network of factors that weave together to influence behavior in each unique case.

At the same time, we must not allow our science to advance faster than we can harness it; we must think through the ways in which we use it in combination with our principles of fairness and justice to shape a better society, one that continues to embrace evolving standards of decency. In other words, the state of the science is but one part of the equation. We should not dismiss these hard-to-answer questions simply because the data remain uncertain. Equally important is the way in which we integrate the data to make judgments in the forensic context, especially when it comes to what should and should not happen with people's lives. At some point, the science will catch up, and we will be forced to decide how it should be applied in alliance with our principles of justice and morality.

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Knabb JJ, Welsh RK, Ziebell JG, et al: Neuroscience, moral reasoning, and the law. Behav Sci & L 27:219 –36, 2009

Im, DS: Trauma as a contributor to violence in autism spectrum disorder. J Am Acad Psychiatry Law 44:184 –92, 2016

Martell DA: Neuroscience and the law: philosophical differences and practical constraints. Behav Sci & Law 27:123–36, 2009

Morse SJ: Brain overclaim syndrome and criminal responsibility: a diagnostic note. Ohio State J Crim L 3:397– 412, 2006

Roper v. Simmons, 543 U.S. 551 (2005)

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Introduction

We propose that romantic love is a natural addiction (Frascella et al., 2010) that evolved from mammalian antecedents (Fisher et al., 2006). Brain scanning studies show that feelings of intense romantic love engage regions of the brain’s “reward system,” specifically dopamine pathways associated with energy, focus, learning, motivation, ecstasy, and craving, including primary regions associated with substance addiction, such as the ventral tegmental area (VTA), caudate and accumbens (Breiter et al., 1997; Bartels and Zeki, 2000, 2004; Fisher et al., 2003, 2005, 2006, 2010; Aron et al., 2005; Ortigue et al., 2007; Acevedo et al., 2011; Xu et al., 2011). Several of these reward regions of the mesolimbic system associated with romantic love and substance addiction are also activated during non-substance or behavioral addiction, including viewing images of appealing food (Wang et al., 2004), shopping (Knutson et al., 2007), playing video games (Hoeft et al., 2008), and gambling (Breiter et al., 2001). Indeed, several researchers have taken the position that “addiction is a disease of the reward system” (Rosenberg and Feder, 2014). Moreover, men and women who are passionately in love and/or rejected in love show the basic symptoms of substance-related and gambling addiction listed in the Diagnostic and Statistical Manual of Mental Disorders-5, including craving, mood modification, tolerance, emotional and physical dependence and withdrawal. Relapse is also a common problem for those suffering with a substance and/or behavioral addiction, as well as among rejected lovers.

Because passionate romantic love is regularly associated with a suite of traits linked with all addictions, several psychologists have come to believe that romantic love can potentially become an addiction (Peele, 1975; Tennov, 1979; Hunter et al., 1981; Halpern, 1982; Schaef, 1989; Griffin-Shelley, 1991; Mellody et al., 1992). However, many define addiction as a pathological, problematic disorder (Reynaud et al., 2010); and because romantic love is a positive experience under many circumstances (i.e., not harmful), researchers remain hesitant to officially categorize romantic love as an addiction. But even when romantic love can’t be regarded as harmful, it is associated with intense craving and can impel the lover to believe, say and do dangerous and inappropriate things.

All forms of substance abuse, including alcohol, opioids, cocaine, amphetamines, cannabis, and tobacco activate reward pathways (Breiter et al., 1997; Melis et al., 2005; Volkow et al., 2007; Frascella et al., 2010; Koob and Volkow, 2010; Diana, 2013), as do several of the behavioral addictions (see Cuzen and Stein, 2014); and several of these same reward pathways are also found to be activated among men and women who are happily in love, as well as those rejected in love (Bartels and Zeki, 2000, 2004; Fisher et al., 2003, 2010; Aron et al., 2005; Ortigue et al., 2007; Acevedo et al., 2011; Xu et al., 2011). So regardless of its official diagnostic classification, we propose that romantic love should be considered as an addiction (Fisher, 2004, 2016): a positive addiction when one’s love is reciprocated, non-toxic and appropriate, and a negative addiction when one’s feelings of romantic love are socially inappropriate, toxic, not reciprocated and/or formally rejected (Fisher, 2004; Frascella et al., 2010).

Romantic love may have evolved at the basal radiation of the hominin clade some 4.4 million years ago in conjunction with the evolution of serial social monogamy and clandestine adultery–hallmarks of the human reproductive strategy (Fisher, 1998, 2004, 2011, 2016). Its purpose may have been to motivate our forebears to focus their mating time and energy on a single partner at a time, thus initiating the formation of a pair-bond to rear their young together as a team (Fisher, 1992, 1998, 2004, 2011, 2016; Fisher et al., 2006; Fletcher et al., 2015). Thus, as products of human evolution, the neural systems for romantic love and mate attachment could be considered as survival systems among humans.

Addiction-Like Behaviors in Early Stage, Passionate Lovers: Euphoria, Obsession, Risky Behavior

Men and women in the early stage of intense passionate romantic love express many of the basic traits associated with all addiction (Tennov, 1979; Liebowitz, 1983; Hatfield and Sprecher, 1986; Harris, 1995;Lewis et al., 2000; Meloy and Fisher, 2005; American Psychiatric Association, 2013). Like all addicts, they focus on their beloved (salience); and they yearn for the beloved (craving). They feel a “rush” of exhilaration when seeing or thinking about him or her (euphoria/intoxication). As their relationship builds, the lover seeks to interact with the beloved more and more frequently (tolerance). If the beloved breaks off the relationship, the lover experiences the common signs of drug withdrawal, too, including protest, crying spells, lethargy, anxiety, insomnia, or hypersomnia, loss of appetite or binge eating, irritability and chronic loneliness. Like most addicts, rejected lovers also often go to extremes, even sometimes doing degrading or physically dangerous things to win back the beloved (Meloy, 1998; Lewis et al., 2000; Meloy and Fisher, 2005). Romantic partners are willing to sacrifice, even die for the other. Romantic jealousy is particularly dangerous and can lead to major crimes including homicide, and/or suicide. Lovers also relapse the way drug addicts do: long after the relationship is over, events, people, places, songs, and/or other external cues associated with their abandoning sweetheart can trigger memories and initiate renewed craving, obsessive thinking and/or compulsive calling, writing or showing up in hopes of rekindling the romance–despite what they suspect may lead to adverse consequences.

Passionate lovers also express strong sexual desire for the beloved; yet their yearning for emotional union tends to overshadow their craving for sexual union with him or her (Tennov, 1979). Most characteristic, the lover thinks obsessively about the beloved (intrusive thinking). Besotted lovers may also compulsively follow, incessantly call, write or unexpectedly appear, all in an effort to be with their beloved day and night (Tennov, 1979; Lewis et al., 2000; Meloy and Fisher, 2005). Paramount to this experience is intense motivation to win him or her. All these behaviors are common to those with substance addictions. However, not everyone exhibits these types of behaviors after a breakup, just as not everyone who uses a substance exhibits dependency and withdrawal effects (e.g., Shiffman, 1989; Shiffman et al., 1995;Shiffman and Paty, 2006; Haney, 2009).

The Brain Systems Associated with Romantic Love

Neuroimaging studies of intense, passionate romantic love reveal the physiological underpinnings of this universal or near-universal human experience, and they all show activation of the VTA (Fisher et al., 2003,2010; Bartels and Zeki, 2004; Aron et al., 2005; Ortigue et al., 2007; Zeki and Romaya, 2010; Acevedo et al., 2011; Xu et al., 2011). In our first experiment (Fisher et al., 2003; Aron et al., 2005), we used functional magnetic resonance imaging (fMRI) to study 10 women and 7 men who had recently fallen intensely and happily in love. All scored high on the Passionate Love Scale (Hatfield and Sprecher, 1986), a self-report questionnaire that measures the intensity of romantic feelings; all participants also reported that they spent more than 85% of their waking hours thinking of their beloved.

Participants alternately viewed a photograph of their sweetheart and a photograph of a familiar individual, interspersed with a distraction-attention task. Group activation occurred in several regions of the brain’s reward system, including the VTA and caudate nucleus (Fisher et al., 2003; Aron et al., 2005), regions associated with pleasure, general arousal, focused attention and motivation to pursue and acquire rewards and mediated primarily by dopamine system activity (Delgado et al., 2000; Schultz, 2000; Elliott et al., 2003). These regions of the reward system are directly associated with addiction in many studies of drugs of abuse (Breiter et al., 1997; Panksepp et al., 2002; Melis et al., 2005; Volkow et al., 2007; Frascella et al., 2010; Koob and Volkow, 2010; Diana, 2013) and behavioral addictions (see Cuzen and Stein, 2014).

These data from several studies indicate that individuals who are happily in the early stages of passionate love express activity in neural regions associated with drug and some behavioral addictions.

There is also a difference between “wanting” and “liking/pleasure” suggested by Berridge et al. (2009). As in substance addiction, “wanting” the romantic partner is different from “liking” a pretty face and finding pleasure in a beautiful sight. We found that brain activation to an attractive face (“liking”) was different from activation to the beloved partner (“wanting”): the former activated the left VTA, while the latter activated the right VTA (Aron et al., 2005). The result suggests the addictive aspects of romantic love are mediated through the right VTA, and that pleasure, or “liking” is different.

Addiction-Like Behaviors Associated with Romantic Rejection: Craving, Relapse and Destructive Behavior

Cross-culturally, few men or women avoid suffering from romantic rejection at some point across their lives. In one American college community, 93% of both sexes queried reported that they had been spurned by someone whom they passionately loved; 95% reported they had rejected someone who was deeply in love with them (Baumeister et al., 1993). Romantic rejection can cause a profound sense of loss and negative affect (although this is not always the case e.g., Lewandowski and Bizzoco, 2007). Like many addictions, romantic rejection can also jeopardize one’s health, because abandonment rage stresses the heart, raises blood pressure and suppresses the immune system (Dozier, 2002). It can also induce clinical depression, and in extreme cases lead to suicide and/or homicide. Some broken-hearted lovers even die from heart attacks or strokes caused by their depression (Rosenthal, 2002). The suite of negative phenomena associated with rejection in love, including protest, the stress response, frustration attraction, abandonment rage, and jealousy, in conjunction with craving and withdrawal symptoms, most likely also contribute to the high worldwide incidence of crimes of passion (see Meloy, 1998; Meloy and Fisher, 2005).

One pathology is also regularly associated with romantic love, stalking. There are two common types of stalkers: those who sustain pursuit of a former sexual/romantic intimate who has rejected them; and those who pursue a stranger or acquaintance who has failed to return the stalker’s romantic overtures (Meloy and Fisher, 2005). In both cases, the stalker exhibits several of the characteristic components of all addictions, including focused attention on the love object, increased energy, following behaviors, and obsessive thinking about and impulsivity directed toward the victim, suggesting that stalking also activates aspects of the reward system in the brain (Meloy and Fisher, 2005) and may be akin to addiction. Another pathology, de Clerambault’s syndrome, also known as erotomania, has not been associated with addiction. This syndrome is characterized by the patient’s delusional notion that another person is madly in love with him or her; generally it is a young woman who believes that she is the love object of a man of higher social or professional standing. But because this syndrome has no direct association with reward system activity and may be a form of paranoid schizophrenia or other delusional disorder (Jordan and Howe, 1980; Kopelman et al., 2008) rather than addiction, discussion of this syndrome is beyond the scope of this paper.

It appears, however, as if evolution has overdone the negative response to romantic abandonment. But romantically rejected individuals have wasted precious courtship time and metabolic energy; they have lost essential economic and financial resources; their social alliances have been jeopardized; their daily rituals and habits have been altered; they may have lost property; and they have most likely experienced damage to their personal happiness, self-esteem and reputation (see Leary, 2001; Fisher, 2004). Most important, rejected lovers of reproductive age are likely to have lost breeding opportunities or a parenting partner for the offspring they have already produced—forms of reduced future genetic viability (Fisher, 2004). Thus, romantic rejection can have severe social, psychological, economic, and reproductive consequences.

Romantic Rejection Also Activates Brain Regions Associated with Drug Craving

To identify some of the neural systems associated with this natural craving state elicited by romantic rejection, we used fMRI to study 10 women and 5 men who had recently been rejected by a partner, but reported that they were still intensely “in love” (Fisher et al., 2010). The average length of time since the initial rejection and the participants’ enrollment in the study was 63 days. All scored high on the Passionate Love Scale (Hatfield and Sprecher, 1986); all reported that they spent most of their waking hours thinking about the person who rejected them; and all yearned for their abandoning partner to return to the relationship.

Participants alternately viewed a photograph of their rejecting partner and a photograph of a familiar, emotionally neutral individual, interspersed with a distraction-attention task. Their responses while looking at their rejecter in the scanner included feelings of romantic passion, despair, joyous, and painful memories, rumination about why this had happened, and mental assessments of their gains and losses from the experience. Brain activations coupled with viewing the rejecter occurred in several regions of the brain’s reward system. Included were: the VTA associated with feelings of intense romantic love; the ventral pallidum associated with feelings of attachment; the insular cortex and the anterior cingulate associated with physical pain and the distress associated with physical pain; and the nucleus accumbens and orbitofrontal/prefrontal cortex associated with assessing one’s gains and losses, as well as craving and addiction (Fisher et al., 2010). Activity in several of these brain regions has been correlated with craving for cocaine and other drugs of abuse (Melis et al., 2005; Frascella et al., 2010; Koob and Volkow, 2010;Diana, 2013).

To understand the impact of right VTA activations associated with happy early stage relationships and romantic rejection, it is important to consider both “liking” (hedonic impact) and “wanting” (e.g., incentive salience) aspects of reward. That is, approach behavior and desired interaction with a person or a substance may or may not involve actual pleasurable experiences. In the context of addiction, it is often the case that a strong desire for the substance or a behavioral addiction, approach motivation and use, occurs even when the stimuli no longer provides a “high” and the reward-seeking behavior is associated with negative outcomes (e.g., the addiction is detrimental to the individual’s health, career, social relationships etc.). Those who are rejected in love still “want” the ex-partner and experience approach motivation (e.g., desiring to contact the ex-partner) even when contact with the ex may be accompanied by negative outcomes and not pleasurable (e.g., experiences of sadness and pain). A distinction between hedonic impact and incentive salience has been explored in animal studies (Berridge et al., 2009). We also found that looking at the partners face activated the right VTA while left VTA activation correlated with the attractiveness of faces in the study (Aron et al., 2005).

Attachment

For those who stay in a relationship beyond the early stage, intense romantic phase, an important second constellation of feelings sets in, associated with attachment (Acevedo et al., 2011). In our studies of individuals who are happily in love (Fisher et al., 2003; Aron et al., 2005), we found that those in longer partnerships (8–17 months as opposed to 1–8 months) began to show activity in the ventral pallidum, associated with attachment in animal studies (Insel and Young, 2001), while continuing to show activity in the VTA and caudate nucleus associated with passionate romantic love. Thus, with time, feelings of attachment begin to accompany feelings of passionate romantic love (Fisher, 2004; Acevedo et al., 2011). Working in conjunction, these two basic neural systems for romantic love and attachment may constitute the biological foundation of human pair-bonding—and provide the context for the evolution of love addictions (Insel, 2003; Burkett and Young, 2012; Fisher, 2016).

Evolution of Romantic Love and Attachment

It has been proposed that the neural systems associated with feelings of intense romantic love and partner attachment evolved in conjunction with the evolution of the human predisposition for pair-bonding, serving as mechanisms to stimulate mate choice and motivating individuals to remain with a mate long enough to breed and rear their offspring through infancy as a team (Fisher, 2004, 2011, 2016; Fisher et al., 2006). This hypothesis suggests that the neural systems for romantic love and attachment are survival systems with evolutionary roots (Frascella et al., 2010).

Pair-bonding is a hallmark of humanity. Data from the Demographic Yearbooks of the United Nations on 97 societies canvassed in the 1980s indicate that approximately 93.1% of women and 91.8% of men in that decade married by age 49 (Fisher, 1989, 1992). Worldwide, marriage rates have declined since then; but today 85 to 90% of men and women in the United States are projected to marry (Cherlin, 2009). Cross-culturally, most individuals are monogamous; they form a sexual and socially sanctioned partnership with one person at a time. Polygyny (many females) is permitted in 84% of human societies; but in the vast majority of these cultures, only 5 to 10% of men actually have several wives simultaneously (Van den Berghe, 1979; Frayser, 1985). Moreover, because polygyny in humans is regularly associated with rank and wealth, monogamy (i.e., pair-bonding) may have been even more prevalent in the pre-horticultural, unstratified societies of our long human hunting-gathering past (Daly and Wilson, 1983), when the neural systems for intense early stage romantic love and partner attachment most likely evolved.

Data suggest that the human predisposition for pair-bonding (often preceded by romantic attraction) also has a biological basis. The investigation of human attachment began with Bowlby (1969, 1973) andAinsworth et al. (1978) who proposed that, to promote the survival of the young, primates have evolved an innate attachment system designed to motivate infants to seek comfort and safety from their primary caregiver, generally the mother. Since these early studies, extensive research has been done on the behaviors, feelings and neural mechanisms associated with this attachment system in adult humans and other animals (Fraley and Shaver, 2000; Eisenberger et al., 2003; Panksepp, 2003a,b; Bartels and Zeki, 2004; MacDonald and Leary, 2005; Tucker et al., 2005; Noriuchi et al., 2008). Currently, researchers believe that this biologically based attachment system remains active throughout the human life course, serving as the foundation for attachment between pair-bonded partners for the purpose of raising offspring (Hazan and Shaver, 1987; Hazan and Diamond, 2000).

Pair-bonding could have evolved at any point in hominin evolution; and with it, various love addictions (Fisher, 2016). However, two lines of data suggest that the neural circuitry for human pair-bonding may have evolved at the basal radiation of the hominin stock (Fisher, 1992, 2011, 2016), in tandem with the hominin adaptation to the woodland/savannah eco-niche some time prior to 4 million years B.P.Ardipithecus ramidus, currently dated at 4.4 million years B.P., displays several physical traits that have been linked with pair-bonding in many species (Lovejoy, 2009); so Lovejoy (2009) proposes that human monogamy had evolved by this time. Anthropologists have also re-measured Australopithecus afarensisfossils for skeletal variations; and they report that by 3.5 million years B.P. hominins exhibited roughly the same degree of sexual dimorphism in several physical traits that the sexes exhibit today. Thus, some have proposed that these hominins were “principally monogamous” (Reno et al., 2003).

The emergence of bipedalism may have been a primary factor in the evolution of the neural circuitry for hominin pair-bonding (Fisher, 1992, 2011, 2016) and the concomitant evolution of romantic love (and possibly attachment) addiction. While foraging and scavenging in the woodland/savannah eco-niche, bipedal Ardipithecine females were most likely obliged to carry infants in their arms instead of on their backs, thus needing the protection and provisioning of a mate while they transported nursing young. Meanwhile, Ardipithecine males may have had considerable difficulty protecting and providing for a harem of females in this open woodland/savannah eco-niche. But a male could defend and provision a single female with her infant as they walked near one another, within the vicinity of the larger community.

So the exigencies of bipedalism in conjunction with hominin expansion into the woodland/savannah eco-niche may have pushed Ardipithecines over the “monogamy threshold,” selecting for the neural system for attachment to a pair-bonded partner. And along with the evolution of pair-bonding and the neural system for attachment may have emerged the brain system for intense positive romantic addiction—serving to motivate males and females to focus their mating energy on a single partner and remain together long enough to trigger feelings of attachment necessary to initiate and complete their co-parenting duties of highly altricial young (Fisher, 1992, 2004, 2011, 2016).

Human Romantic Love as a Developed Form of a Mammalian Courtship Mechanism

Considerable data suggest that the human brain system for romantic love arose from mammalian antecedents. Like humans, all birds and mammals exhibit mate preferences; they focus their courtship energy on favored potential mates and disregard or avoid others (Fisher, 2004; Fisher et al., 2006). Moreover, most of the basic traits associated with human romantic love are also characteristic of mammalian courtship attraction, including increased energy, focused attention, obsessive following, affiliative gestures, possessive mate guarding, goal-oriented behaviors and motivation to win and keep a preferred mating partner for the duration of one’s species-specific reproductive and parenting needs (Fisher et al., 2002, 2006; Fisher, 2004).

The brain system for human romantic love shows biological similarities with mammalian neural systems for courtship attraction. When a female laboratory–maintained prairie vole is mated with a male, she forms a distinct preference for him, associated with a 50% increase of dopamine in the nucleus accumbens (Gingrich et al., 2000). When a dopamine antagonist is injected into the nucleus accumbens, the female no longer prefers this partner; and when a female is injected with a dopamine agonist, she begins to prefer the conspecific who is present at the time of the infusion, even if she has not mated with this male (Wang et al., 1999; Gingrich et al., 2000). An increase in the activities of central dopamine is also associated with courtship attraction in female sheep (Fabre-Nys et al., 1997). In male rats, increased striatal dopamine release has also been shown in response to the presence of a receptive female rat (Robinson et al., 2002;Montague et al., 2004).

Because human romantic love shares many behavioral and biological characteristics with mammalian courtship attraction, it is likely that human romantic love is a developed form of this mammalian neural courtship mechanism (Fisher, 1998, 2004, 2011, 2016; Fisher et al., 2006). However, in most species courtship attraction is brief, lasting only minutes, hours, days, or weeks; while in humans, intense, early stage romantic love can last 12–18 months (Marazziti et al., 1999) or much longer (Acevedo et al., 2011). So in early hominin prehistory, activity in this mammalian neural system for courtship attraction may have become intensified and prolonged as pair-bonding evolved, eventually becoming the positive (or negative) romantic addictions experienced by men and women cross-culturally today.

Romantic Love May Act As A Reward Replacement for Other Addictions

High quality social relationships (including romantic relationships) can be extremely beneficial to those recovering from an addiction (e.g., Hänninen and Koski-Jännes, 1999). One potential mechanism for this benefit comes from the therapeutic approach to drug addiction of reward replacement. That is, when quitting one addictive substance or behavior, the addicted individual replaces this addiction with another form of rewarding behavior, often without prompting from an outside source, such as a clinician (Donovan, 1988; Marks, 1990; DiNardo and Lemieux, 2001; Haylett et al., 2004; Alter et al., 2006). Because of this, clinicians who treat addictions are known to effectively engage patients in new reinforcers (see Bickel et al., 2014), specifically healthy replacement reinforcers such as sports activities, new hobbies and more or new social interactions (e.g., Vaillant, 1983; Salvy et al., 2009; Liu et al., 2011).

Could early stage romance provide a replacement reward for those engaged in substance abuse (or a behavioral addiction)? To explore this question, Xu et al. (2012) put 18 Chinese overnight nicotine-deprived smokers who had just fallen madly in love into a brain scanner, using fMRI. These men and women looked at side-by-side photos, one of a hand holding either a lighted cigarette (cue) or a pencil (control) and one of their newly beloved or a familiar acquaintance (non-smokers so they were not cigarette-cues). Among those who were moderately addicted to nicotine, when the cigarette cue was presented next to the image of the beloved (compared to the acquaintance), less activation was observed in regions associated with cigarette cue-reactivity. Additionally, more activation in the caudate was observed during trials that included the beloved’s pictures (compared to the acquaintance’s).

These preliminary data provide more evidence that romantic love could be considered a powerful and primordial natural addiction because it can, under some circumstances, modify brain activations associated with a more contemporary addiction, nicotine.

“Self-expansion” and “incorporation of others into one’s sense of self” may also act as reward substitutes for addictions, including love addiction.

First proposed by Aron and Aron (1986), the self-expansion model proposes that a basic human motivation is the desire to increase one’s self-concept by engaging in novel, interesting, challenging and/or other exciting pursuits in order to gain resources and perspectives that can enhance one’s self concept and capabilities (for review see Aron et al., 2013), as well as garner positive emotions and reward feelings (Aron et al., 1995, 2000; Strong and Aron, 2006). They propose that rapid self-expansion occurs during early stage romance.

This self-expansion, which is rooted in approach motivation (see Mattingly et al., 2012), may be beneficial when attempting to quit or reduce use of a substance or behavioral addiction because it offers a replacement and distracting rewarding experience. Self-expansion in the context of romantic love has been shown to attenuate perceptions of physical pain (Younger et al., 2010) via a reward mechanism (rather than distraction), which suggests that it might assist with the painful process of withdrawal after romantic rejection. Further, self-expansion may also be beneficial in the context of quitting any addiction because it facilitates self-concept change (e.g., starting to think of oneself as a writer, musician, bird watcher or whatever the self-expanding experience may be) into a new and healthier direction, and away from one’s identity as a “user” (Kellogg and Kreek, 2005). In addition to providing distraction, replacement and redirection, engaging in self-expanding (i.e., novel, interesting, and/or challenging) activities may be biologically beneficial, because any form of novelty activates the dopamine system in the brain to facilitate energy and optimism, thereby potentially providing a replacement reward.

Indeed, three studies have directly investigating self-expansion in the context of nicotine addiction, each finding quite positive results. Ex-smokers reported that significantly more self-expanding experiences had occurred directly before they successfully quit smoking than did current smokers who reported on their unsuccessful attempts to quit (Xu et al., 2010). Even among the current smokers who relapsed, the number of self-expanding experiences occurring directly before their quit attempt was significantly positively correlated with how long they were able to abstain from smoking (Xu et al., 2010). Two fMRI studies of overnight abstinent smokers suggest that self-expansion via activities with a romantic partner attenuates cigarette cue-reactivity in the brain (Xu et al., 2012, 2014). These data suggest that when smokers engage in self-expansion, they are less responsive to smoking cues.

Another cognitive phenomenon that may play a role in attenuating romantic addiction is “inclusion of the other in the self” (IOS). This occurs when representations of the self change to incorporate aspects of a romantic partner. A scale has been developed to measure this cognitive process (Aron et al., 1992). Over time the partner’s perspectives, identities, and resources become incorporated into the person’s own sense of self and the distinction between self and partner blur. For example, people transition to more use of plural pronouns like “we” and “us”(Agnew et al., 1998), and become slower at distinguishing a partner’s belongings or traits from one’s own (Aron et al., 1991; for a review, see Aron et al., 2004). This growth of the self-concept can provide positive outcomes (e.g., additional resources, positive feelings), which may be effective in a therapeutic situation. Indeed, activation of the reward system through the VTA was correlated with a lover’s IOS scores (Acevedo et al., 2011), which suggests that a moderate amount of positive identification with another person or group could be therapeutic–by boosting a positive self-image and providing a reward substitute for a substance or behavioral addiction that a person has given up.

Implications for Treatment of Romantic Rejection and Addiction

Clinicians have a host of strategies for helping lovers and drug addicts. However, when data on romantic love and substance abuse are considered together, some approaches have a particularly strong rationale.

Perhaps most important, like giving up a drug, rejected lovers should remove all reasonable evidence of their abandoning sweetheart, such as cards, letters, songs, photos, and memorabilia, as well as avoid contact with their rejecting partner, because reminders and partner contact can act as cues that induce craving and are likely to sustain the activity of brain circuits associated with romantic passion and thus interfere with the healing process. Self-expansion research also finds that positive outcomes such as personal growth and positive emotions are possible (even likely) following a break-up if the relationship had offered few self-expanding opportunities and if the newly single person engages in rediscovery of the self (Lewandowski and Bizzoco, 2007).

Close, positive contact with a friend or friends is rewarding and may also help to replace the craving for substances or a rejecting partner, because looking at a photo of a close friend activates the nucleus accumbens, associated with reward (Acevedo et al., 2011). Looking at a photo of a close friend also activates the periaqueductal gray, associated with oxytocin receptors and the calm of attachment. This suggests that group therapies, such as Alcoholics Anonymous and other 12 step programs, are successful because these group dynamics engage the brain’s reward and attachment systems. Participating in group programs may be important for rejected lovers as well as for those addicted to substances like alcohol or those with a behavioral addiction, such as gambling.

Data suggest that rejected lovers should also stay busy to distract themselves (Thayer, 1996; Rosenthal, 2002). Physical exertion may be especially helpful as it elevates mood (Rosenthal, 2002), triggering dopamine activity in the nucleus accumbens to bestow pleasure (Kolata, 2002). Exercise also increases levels of β-Endorphin and endocannabinoids which reduces pain and increases feelings of calm and well-being (Goldfarb and Jamurtas, 1997; Dietrich and McDaniel, 2004). Also, engaging in a new form of exercise can be a self-expanding experience (see Xu et al., 2010). Because of these benefits of exercise, some psychiatrists believe that exercise (aerobic or anaerobic) can be as effective in healing depression as psychotherapy or antidepressant drugs (Rosenthal, 2002).

Self-expanding activities (e.g., hobbies, sports, spiritual experiences) can be helpful both in the context of addiction and heartbreak as they offer reward, benefits to the self-concept, and distraction. It is recommended that a person has more than one source of self-expansion in their life, thus should one no longer become available (e.g., a partner leaves), the other sources can help buffer the impact of that loss. It would also be helpful to have multiple and diverse sources of self-expansion in various domains of life (e.g., hobby, workplace, friends, family, volunteer organization, spiritual group, and academic interest etc.) and to have strong social networks to which one can turn for support in times of need (e.g., breakup, attempting to quit). It is important, however, to note that self-expansion should be pursued in a healthy manner with caution about potentially risky behaviors (e.g., seeking to fall in love with a new person immediately after the loss of a partner, picking up unhealthy habits or becoming an addict of another substance when quitting).

Similarly, it is important to remember that relationships and addictions can co-exist and influence each other and it may be especially difficult to have a strong and positive romantic relationship when issues of addiction need to be dealt with. As addiction often leads to less desire for and response to alternative rewards, it may be especially difficult for those dealing with addiction to engage in pro-relationship behaviors, and thus increase the risk of rejection. In addition, romantic rejection increases the risk of relapse, so close attention to romantic relationships during substance abuse withdrawal may be important.

Furthermore, smiling utilizes facial muscles that activate nerve pathways in the brain that can stimulate feelings of pleasure (Carter, 1998). Focusing on the positive may be effective too. A study byLewandowski (2009) found that writing for 20 min on three consecutive days about a recent relationship break-up was beneficial when people wrote about positive feelings as opposed to when they wrote about negative feelings or wrote without expressing any feelings. Perhaps most important, time attenuates the attachment system. In our study of rejected men and women, the greater the number of days since rejection, the less the activity in a brain region (the ventral pallidum) associated with feelings of attachment (Fisher et al., 2010).

As disappointed lovers use strategies originally developed to quit a substance addiction, their love addiction is likely to eventually subside.

Conclusion

Researchers have long discussed whether the compulsive pursuit of non-substance rewards, such as uncontrolled gambling, eating, sex, exercise, Internet use, compulsive buying disorder and other obsessive behavioral syndromes can be classified as addictions (Frascella et al., 2010; Rosenberg and Feder, 2014). All can lead to salience, obsession, tolerance, emotional, and physical dependence, withdrawals, relapse and other traits common to substance abuse. Moreover, several of these non-substance rewards have been shown to produce specific activity in dopamine pathways of the reward system similar to drugs of abuse (see Frascella et al., 2010; see Rosenberg and Feder, 2014). This suggests that uncontrolled use of these non-substances can be considered addictions. Romantic love is likely to be a similar addiction, with one exception. Unlike other addictions (that afflict only a percentage of the population), some form of love addiction is likely to occur to almost every human being that lives now and in our human past; few avoid the pain of romantic rejection either.

Romantic love appears to be a natural addiction, “a normal altered state” experienced by almost all humans (Frascella et al., 2010, p. 295) that evolved during human evolution to motivate our ancestors to focus their mating energy on a specific partner, thereby conserving mating time and energy, initiating reproduction, triggering feelings of attachment and subsequent mutual parenting, and assuring the future of their mutual DNA (Fisher, 2004, 2011, 2016; Fisher et al., 2006). Romantic love may be a positive addiction when the relationship is reciprocated, non-toxic and appropriate; but a harmful, negative addiction when unreciprocated, toxic, inappropriate and/or formally rejected.

To alleviate the negative symptoms of love addiction, addicted lovers are advised to remove the cues that fan their ardor, follow some advisories of a 12-step program, build new daily habits, meet new people, take up new interests, find the appropriate medication and/or therapist, and wait out the days and nights of intrusive thinking and craving, because feelings of attachment to a former romantic partner decrease over time (Fisher et al., 2010). Moreover, therapies that increase self expansion and incorporate new individuals into one’s sense of self may also be useful in alleviated love addiction. Self expansion approaches may help drug and other negative addiction therapies, also.

If the public and the therapeutic, medical and legal communities come to understand that passionate early stage romantic love is an evolved drive (Fisher, 2004) and a natural addiction (Frascella et al., 2010) that can have profound social, economic, psychological, and genetic consequences (both beneficial and adverse), clinicians and researchers might develop more effective procedures for dealing with this powerful and primordial neural mechanism for mate preference and initial partner attachment, romantic love.

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I. Introduction

Brains do not commit crimes; people commit crimes. This conclusion should be self-evident, but, infected and inflamed by stunning advances in our understanding of the brain, advocates all too often make moral and legal claims that the new neuroscience does not entail and cannot sustain. Particular brain findings are thought to lead inevitably to moral or legal conclusions. Brains are blamed for offenses; agency and responsibility disappear from the legal landscape. For example, in Roper v. Simmons,1 advocates for abolition of the death penalty for adolescents who committed murder when they were sixteen or seventeen years old argued that the demonstrated lack of complete myelination of the cortical neurons of the adolescent brain was reason to believe that sixteen and seventeen year old murderers were insufficiently responsible to deserve capital punishment. These types of responses, I claim, are the signs of a disorder that I have preliminarily entitled Brain Overclaim Syndrome [BOS].

This brief diagnostic note first lays the contextual foundation for how one should think about the relation of neuroscience to criminal responsibility. Then it attempts to identify the nature of the pathology, to offer the criteria for the diagnosis, to evaluate the disorder in the Roper arguments, and to suggest the route to total cure. Footnotes will be scarce. Most of this note is an extended conceptual argument or based on this investigator’s first-hand clinical observations. Where it depends on assertions about the state of the science, it takes positions, albeit sometimes controversial, that have strong support. Trust me: I’m a doctor (of psychology).

II. Declaration of Interest

Many journals in psychiatry and medicine now ask authors to include a “declaration of interest” to indicate possible conflicts of interests or other influences on the author’s conclusions. For example, sources of support for the research should be disclosed. As a diagnostic investigator and in the spirit of disclosure, please permit me to list the most important philosophical, moral and legal commitments with which I approach this investigation. First, I am a thorough-going, matter-up materialist who believes that all mental and behavioral activity is the causal product of lawful physical events in the brain. Second, I am a non-reductive materialist who believes, roughly, with John Searle and many others, that conscious mental states are real, that they are caused by lower level biological processes in the brain, that conscious states are realized in the brain— the mind-brain—but not at the level of neurons, and that conscious states can be causally efficacious.2 Third, I am a compatibilist who believes that moral and criminal responsibility are compatible with determinism or universal causation. Fourth, I believe that desert is a necessary condition of just punishment under current law and that it should be at least a partial justification for the fair imposition of punishment under any proposed criminal law. Last, I oppose the death penalty.

III. Thinking About Neuroscience and Criminal Responsibility

This section considers the logical and conceptual space in which claims about the relation of neuroscience to responsibility can arise.

To think sensibly about the relation of any other variable—whether that variable is biological, psychological, sociological, or astrological—to criminal responsibility first requires that one have an account of criminal responsibility. After all, one cannot relate two variables to one another unless one has a definition of both. Assuming that one has a definition of criminal responsibility, then the argument based on the other variable may be either internal or external. An internal argument accepts that criminal responsibility is a coherent concept and uses the other variable to explain the positive rules and practices we have or to criticize those rules and practices normatively for the purpose of improving them.

An external argument uses the other variable to demonstrate that the concept of criminal responsibility is incoherent or unjustifiable and therefore it should be abandoned. Thus, any commentator who accepts that at least some people who commit crimes are responsible and may justifiably be punished are necessarily making an internal argument, at least implicitly, because the justifiability of responsibility is assumed.

A. A Positive Account of Criminal Responsibility

As a matter of current, positive common law, an agent will be prima facie criminally responsible if the agent acts intentionally and with the appropriate mental state, the mens rea, required by the definition of the offense, such as purpose, knowledge, recklessness, or negligence. Criminal law typically defines an act as an intentional bodily movement performed by an agent whose consciousness is reasonably intact. Mental states have their ordinary language, common-sense meanings. If the agent does not act at all because the bodily movement was not intentional or the agent’s consciousness was substantially compromised, the agent is not prima facie responsible. Similarly, if the agent lacks a requisite mental state, the agent is also not prima facie criminally responsible. Even if the agent is fully prima facie responsible, however, the agent ultimately may still not be criminally responsible if an excusing condition, an affirmative defense, such as legal insanity (essentially a rationality defect) or duress (a compelling “hard choice” situation, such as a “do-it-or-else” threat at gunpoint) was present when the agent committed the offense. A defendant who wants to avoid imputation of criminal responsibility must create reasonable doubt about whether he or she acted intentionally, consciously and with the required mens rea, or the defendant must establish an affirmative defense. Although one might quibble about details, I believe that this account accurately reflects the law’s current conception of criminal responsibility.

The concept of the responsible legal person implicit in this account is an intentional, reasonably fully conscious and potentially rational agent who is not exposed to an unreasonably hard choice about whether to offend. The specific criteria for prima facie responsibility and excuse are all behavioral, broadly conceived as conduct and mental states. The causes for the behavioral criteria are not part of the criteria themselves. For example, an agent’s capacity for rationality might be diminished by faulty neurotransmitters, psychological stress, trauma, or a host of other causes. The excusing condition is the lack of rational capacity.

The underlying biological, psychological, sociological, and astrological causes for any of the criteria for criminal responsibility, including mental states, can be nothing more than evidentiary support for the assertion that the criterion in question was in fact satisfied at the time of the crime. Causation cannot be an excuse per se for an internalist, who accepts responsibility, because all behavior is caused and thus all behavior would have to be excused. I have termed the erroneous belief to the contrary the “fundamental psycholegal error.” It is as erroneous when the postulated cause of behavior is neurological as when it is psychological, sociological, or astrological. Once one has assumed that responsibility is possible, causation cannot excuse per se.

All the criteria for criminal responsibility are normative. The meaning of rationality and how much rational capacity must be present for responsibility, for example, are legal issues that the law must decide. Other disciplines might provide potentially relevant knowledge about human behavioral capacities, but the other, empirical disciplines must fall silent about the ultimate criteria the law adopts. No general finding from any other discipline entails any general legal conclusion about legal responsibility unless it conclusively undermines the possibility of responsibility at all, in which case it is the basis for an external rather than an internal critique. Moreover, demonstrable differences among people or groups of people concerning the criteria do not mean that the law must treat them differently. For example, one person may be more rational than another, but they both may be rational enough to deserve the same punishment for the same crime committed under similar circumstances. No normative differences are logically entailed by behavioral differences unless, counter-factually to reality, the behavioral differences precisely track the normative differences.

Finally, we assess all the criminal law’s behavioral criteria for responsibility primarily by considering evidence of the defendant’s conduct, including speech acts, and drawing inferences from that conduct. Based on the behavioral evidence, it seems patently obvious, and few commentators disagree, that most agents who appear to violate criminal prohibitions act intentionally, consciously, with the requisite mens rea, possess the capacity for rationality (by any sensible standard), and do not act under a hard choice threat.

B. Internal Arguments: Neuroscience and the Assessment of Criminal Responsibility

The new neuroscience might logically assist assessment of criminal responsibility in specific cases and in general. In specific cases, we will virtually never have direct neuroscientific evidence contemporaneous with the time of the crime. At most, we will have ex ante or ex post evidence that can produce inferences of varying validity about brain structure and function at the time of the crime. Moreover, at present, neuroscience is insufficiently advanced to offer precise data that will be genuinely legally relevant. Thus, even if the science is good enough to pass muster for admission as expert scientific evidence under federal and state evidentiary rules, it may still be inadmissible because it will not be probative. As neuroscience advances, it may become probative in a wider class of cases, but we have not yet reached this stage.

Despite the foregoing qualifications, neuroscience evidence may be relevant in two classes of specific cases. First, in cases in which the behavioral evidence concerning prima facie liability or an affirmative defense seems clear, neuroscientific evidence may demonstrate that appearances are deceptive. For example, neuroscience might indicate that a defendant who appeared to have been acting consciously was in fact acting in an unconscious or automatic state, such as sleepwalking or in the wake of physical trauma. Or, neuroscience might indicate that an apparently entirely rational defendant lacked the capacity for rationality. I speculate that such cases will be rare. Further, when the behavioral evidence is clear and the potentially conflicting neuroscience will be inevitably speculative to a greater or lesser degree, common sense dictates that we should believe the behavioral evidence rather than the neuroscience evidence because the criteria for responsibility are behavioral. Still, this is a logical possibility.

A second class of specific cases involves those in which the behavioral evidence is in doubt. For example, suppose the defendant had received a blow to the head not long before committing an offense and whether the defendant acted consciously is unclear. Neuroscience will rarely be dispositive in such cases because the relation of the brain to complex behavior is itself immensely complex and beyond all but the most general current understanding. Nonetheless, in some cases valid neuroscience will help the finder of fact resolve the legal issue, although caution must always be exercised because the neuroscientific evidence often will not be sufficiently contemporaneous to permit valid inferences about the time of the crime. Such cases may arise relatively frequently, especially as advances in neuroscience allow more precise specification of how the brain affects behavior. I do not know how large this class of cases is, but it is surely considerably larger than the first class.

Neuroscience might be relevant in general if its findings demonstrate that the current criteria for criminal responsibility are unjust because they do not comport with our biologically-based understanding of behavior. For example, some claim that the number of defendants who do not meet the criminal law’s current criteria for conscious action is much larger than we believe. This type of claim goes far beyond the argument that neuroscience will be relevant in large numbers of specific cases. It may suggest that the law’s criteria are too narrow generally and must be normatively reformed to be just. Such claims would of course be hard to support if the behavioral evidence were clearly to the contrary. What kind of neuroscience evidence would it take to convince us that when we act, most of the time most of us are not conscious (according to any sensible standard of consciousness)?

C. External Arguments: Criminal Responsibility Rejected

At the extreme, claims about the general implications of neuroscience may cease to be the basis of a normative critique of criminal responsibility conceptions and may become an external critique of the coherence or justice of the possibility of responsibility tout court. Two types of external criticism are possible. First, the externalist might claim that responsibility is impossible because its criteria are based on a conception of human action that is simply wrong. We are not the type of creatures we take ourselves to be. For example, suppose, despite all common-sense first-person and third-person evidence to the contrary, neuroscience could show that all human conduct is done in a state indistinguishable from spasm or sleepwalking, or, more extravagantly, that we do not have mental states at all. In a word, suppose neuroscience could demonstrate conclusively that all of us all the time are automatons or without any mental life whatsoever and that thinking otherwise is simply an illusion. In the philosophy of mind, such arguments are associated with various forms of reductive or eliminative materialism.

No current conception of responsibility that would support imposing deserved blame and punishment can accept blaming and punishing those who act automatically or creatures that have no mental life. If this were really the case, rationality would demand that the criminal law would have to abandon any robust notion of responsibility and seek alternative means of ordering human affairs and protecting society. (One might ask whether automatons or creatures without minds can rationally decide how to respond to their own status as automatons, but let us leave this question for another day.)

The second type of external critique accepts that we are the types of intentional, conscious, potentially rational creatures that we take ourselves to be, a position associated with various forms of non-reductive materialism in the philosophy of mind. But the second external critique denies that anyone can be genuinely responsible because neuroscience and other disciplines conclusively demonstrate that all our actions are mechanistically determined and determinism (or universal causation or some such) is incompatible with ultimate responsibility. In the philosophy of responsibility, this position is termed “incompatibilism.” This is a perfectly respectable conceptual position, but it cannot be proven metaphysically or normatively to be right. Many thorough-going naturalists, such as myself, who believe that all the phenomena of the universe are causally explicable by natural physical laws, believe that responsibility is compatible with determinism, a position termed “compatibilism.” Indeed, compatibilism is probably the dominant position among philosophers of responsibility. It is surely the position that best explains our responsibility practices, which hold some people accountable but excuse others. Science cannot resolve the dispute because the issue is metaphysical and normative and it is unlikely ever to be resolved by logic. Finally, proponents of deterministic type arguments cannot have it both ways. They must either accept jettisoning any responsibility for anyone or they must recognize that determinism, which is not selective or partial, is not a criterion that bears on responsibility.

In conclusion, the first type of external critique fundamentally denies our ordinary understanding of ourselves and is conceivably demonstrable by scientific findings. Until it does so, however, it is unlikely to undermine the powerful sense we all have of the efficacy and importance of mental states and reason. The second external critique is also unlikely to be successful because many people, the compatibilists, believe already that it is just to hold others responsible despite the belief that determinism or universal causation is true. Some day, an external critique may convince us to abandon criminal responsibility, but for now such arguments are academic in the most literal sense. Only internal critiques have a chance on the ground.

Now that we have explored generally the logical relation between brain explanations and criminal responsibility, let us turn to the errors that are the signs and symptoms of Brain Overclaim Syndrome.

IV. Brain Overclaim Syndrome: The Signs and Symptoms 

New, powerful scientific findings about the correlates and causes of behavior often have a potent and, alas, rationality-unhinging effect on the thinking of Potential Commentators [PCs]. Most flow from misunderstanding the relation between brains and responsibility that the last section considered. This section attempts to catalogue those effects that I have identified to date, many of which are related to each other, but the list has no pretensions to being complete. After all, this is a preliminary diagnostic investigation and future investigators may discover hitherto unidentified signs and symptoms. The final pathway in all cases, however, is that more legal implications are claimed for the brain science than can be justified.

A. Confusion About the Relation Between Brain and Complex, Intentional Action

For a materialist, the brain always plays a causal role in behavior. Despite all the astonishing recent advances in neuroscience, however, we still know woefully little about how the brain enables the mind, and especially about how consciousness and intentionality can arise from the complicated hunk of matter that is the brain. At a recent conference on the abnormal brain, the eminent philosopher of mind and action, John Searle, opened his keynote speech by telling the following anecdote.3 Some years ago, Searle said, he decided to learn what the new neuroscience had to teach about the relation of brain to mind and action. He devoured the most important texts only to be dismayed that these texts did not all begin with a disclaimer that we do not know much about this relation yet. Just so.

Brain imaging studies have been the most potent pathogen causing BOS, so it is useful to say a few words about such studies. Imaging is at present very expensive and requires carefully chosen and cooperative subjects. Consequently, the number of experimental subjects and controls in any study tends to be small and precise replications are infrequent. The problem of small samples will probably be remedied by advances in the efficiency of the technology of imaging—indeed, this is already happening for readings of activity at the surface of the brain—but for now it is a dominant feature of imaging studies.

Statistically valid findings are based on mean differences and do not imply that there is an absolutely clear distinction between the experimental and control groups. Usually there is substantial overlap, meaning that some individual experimental brains look like individual control brains and vice versa. For example, suppose the experimental hypothesis is that task X will cause brain region Y to be activated. After controlling for other variables that might cause Y to be activated in both the experimental and control conditions (the “subtraction” method), the investigators discover that there is still a difference: Y is activated statistically significantly more in the experimental subjects. Nonetheless, some experimental subjects will not have Y activated by X and some control subjects will. Therefore, one could not predict perfectly from the brain image whether the subject was an experimental or a control. The question would always be how much overlap there was between the two groups. The greater the overlap, the more difficult it would be to predict that subject’s experimental or control status from the image.4

Discovering the neural correlates of mental phenomena does not tell us how these phenomena are possible. For example, we may be able to identify the neural correlates of consciousness, but we do not have a clue about how those parts of the brain make subjective experience possible. Moreover, the causation of virtually any complex behavior is affected by psychological and sociological variables, even when brain causation has been identified. For example, the brains of late adolescents are almost certainly the same around the globe—holding nutrition and the like constant—but the rates of behaviors associated with immature adolescent brains, such as impulsive criminality, vary widely from place to place and from time to time. Monolithic brain explanation of complex behavior is almost always radically incomplete.

Certain lesions can of course disable various human capacities, but few criminal responsibility cases in which the result is not already obvious based on behavioral evidence will involve a precise, identifiable neurological mechanism that will demonstrate that criminal responsibility was not present. Further, current neuroscience cannot begin to demonstrate that our view of ourselves as generally conscious, intentional, and potentially rational agents is false.

Until we know vastly more than we do now, in most cases we will not be in a position to add much to assessing responsibility behaviorally in individual cases, and even less do we have the resources to mount a potentially convincing external critique of responsibility vel non. In individual cases in which neuroscientific findings could be demonstrated to be genuinely relevant and probative, they should of course be admissible consistent with the usual evidentiary standards for scientific evidence.

B. The Confusion of Internal and External Critiques

Causation is not per se an excusing condition and partial causation does not exist. If this is a causal world, as neuroscientists and I believe, then all phenomena are fully caused by their necessary and sufficient causal conditions. Partial knowledge about causation does not mean that there is partial causation. Causation is also not the equivalent of being subjected to compulsion, which exists when the agent is non-culpably faced with a normative hard choice. All behavior is caused, but not all behavior results from a threat at gunpoint or the equivalent. And to think that causation per se excuses is an external critique. If causation excuses per se or is the equivalent of compulsion, responsibility as we know it is impossible. As an argument from within our responsibility practices, it is the fundamental psycholegal error to argue that causation excuses. The discovery that the brain, including a brain abnormality, played some causal role in the production of what is undeniably human action does not lead to any legal conclusions about responsibility. The proper internal question is whether the neuroscience evidence helps to establish the presence or absence of action, mental states or a genuine affirmative defense, such as lack of rational capacity.

C. Misunderstanding the Criteria for Responsibility

The criteria for responsibility are behavioral and normative, not empirically demonstrable states of the brain. Even if there were a perfect correlation between brain states and the behavioral criteria for responsibility, the brain states would be nothing more than evidence of the behavioral states. Such a correlation is a fantasy based on present knowledge and probably always will be when we are considering complex human actions. If the person meets the behavioral criteria for responsibility, the person should be held responsible, whatever the brain evidence may indicate, such as the presence of an abnormality. If the person does not meet the behavioral criteria, the person should be held not responsible, however normal the brain may look. Brains are not held responsible. Acting people are. To believe that brain evidence has more than simple evidentiary value for assessing responsibility is to misconceive the criteria for responsibility.

One could claim, of course, that normatively the law should adopt brain-based criteria for responsibility, but this would be a category mistake. Even if it is not, it amounts to an external critique. In the alternative, one could argue that the positive account of responsibility that I have presented is fundamentally incorrect and that the brain science is more relevant to the properly understood criteria of responsibility. Perhaps so, but this requires an argument to demonstrate that the account is wrong. Finally, one could argue that the behavioral and normative criteria should be different as a result of what we have learned from brain science and other disciplines. This would be an internal critique that would depend on a normative argument about the relevance of brain science to responsibility. If this argument went through, however, it would not undermine this diagnostic note’s claims about the relevance of brain science to current, positive responsibility criteria, and, even then, the brain science would still be relevant only as evidence concerning the new, improved behavioral responsibility criteria.

D. The Confusion of the Normative and the Positive

Factual behavioral differences between people do not entail the necessity of differential legal treatment unless one is operating under a normative theory that indicates why the factual difference should make a legal difference. I am not suggesting that it is impossible to derive an “ought” from an “is,” a contentious issue most famously addressed by David Hume. I am agnostic about this. I am claiming, however, that one cannot assume an “ought” from an “is.” This requires an argument.

Suppose that we can reliably identify valid group differences, say, between men and women on measures of upper body strength, a capacity useful in some occupations, such as fighting fires. Should the ranks of firefighters be limited to men? Of course not, because we might decide that values of equality trump those of efficiency or because we think that we can individualize decisions about an applicant’s ability to do the job. Even if proportionately fewer women might qualify, some surely will, and we would not be able to predict whether an applicant could do the job based solely on sex. Virtually no finding, no practice, however hoary, necessarily entails any normative outcome without an argument about why it should. This is as true of neuroscience evidence as of any other kind of scientific evidence. Neuroscience evidence may provide premises in normative arguments, but it does not alone entail conclusions. To think otherwise is to confuse the positive with the normative.

In conclusion, based on the foregoing confusions and others that may be identified, the final pathway, the final expression of BOS is to make claims about the relation of the brain to responsibility that cannot be sustained logically or empirically.

V. Evaluating Roper

Few if any responsible commentators who accept the coherence and validity of criminal responsibility ascriptions—the internalists—claim that most adolescent offenders commit their crimes in automatic states or without mens rea. Crimes committed impulsively, for example, are still committed consciously and intentionally. Nor do most commentators claim that late adolescent offenders do not know the nature and quality of their acts, do not know their acts are wrong, or act in response to duress. No evidence from the behavioral or neurosciences even hints that the contrary might be true. Rather, the claim is that culpable adolescents, whose behavior meets the prima facie case for guilt and who do not have an affirmative defense, are nonetheless less criminally responsible because they have insufficiently developed rationality. Thus, to be relevant, any evidence must be addressed to the sixteen and seventeen year olds’ capacity for rationality, broadly speaking.

In Thompson v. Oklahoma,5 the Supreme Court barred capital punishment of murderers who killed when they were fifteen years old or younger, and in Atkins v. Virginia,6 the high Court categorically prohibited capital punishment of convicted killers with mental retardation. Although the Court provided many reasons for its Thompson and Atkins holdings, crucial to both was the conclusion that younger adolescents and persons with retardation are categorically less culpable, less responsible, and therefore do not deserve capital punishment. The operative language in Atkins concerning culpability and responsibility is instructive. The Court wrote:

Mentally retarded persons frequently know the difference between right and wrong . . . . Because of their impairments, however, by definition they have diminished capacities to understand and process information, to communicate, to abstract from mistakes and learn from experience, to engage in logical reasoning, to control impulses, and to understand the reactions of others . . . . Their deficiencies do not warrant an exemption from criminal sanctions, but they do diminish their personal culpability.

....

With respect to retribution—the interest in seeing that the offender gets his “just deserts”—the severity of the appropriate punishment necessarily depends on the culpability of the offender.7

All the criteria the Court mentions are behavioral (broadly understood to refer to cognitive and “control” functioning8) and their relevance to criminal responsibility is based on the relation to desert.

Advocates of abolition in Roper seized on this language to make similar arguments concerning sixteen and seventeen year old murderers. Although apparently normal adolescents do not suffer from abnormal impairments, lack of full developmental maturation allegedly distinguishes them from adults on behavioral dimensions, such as the capacity for judgment, that are relevant to rationality and therefore to responsibility and desert.

What was striking and new about the argument in Roper, however, was that advocates of abolition used newly discovered neuroscientific evidence concerning the adolescent brain to bolster their argument that sixteen and seventeen year old killers do not deserve to die. Editorial pages encouraged the High Court to consider the neuroscientific evidence to help it reach its decision. Although neuroscience evidence had been adduced in earlier, high profile cases, such as the 1982 prosecution of John Hinckley, Jr. for the attempted assassination of President Reagan and others, Roper has been the most important case to propose use of the new neuroscience to affect responsibility questions generally. Indeed, the American Medical Association, the American Bar Association, the American Psychiatric Association, and the American Psychological Association, among others, all filed or subscribed to amicus briefs urging abolition based in part on the neuroscience findings. The real question was whether and how the new neuroscience was relevant to responsibility ascriptions and just punishment for adolescent offenders (or anyone else).

Here is the opening of the summary of the amicus brief filed by, inter alia, the American Medical Association, the American Psychiatric Association, the American Academy of Child and Adolescent Psychiatry, and the American Academy of Psychiatry and the Law: “The adolescent’s mind works differently from ours. Parents know it. This Court [the United States Supreme Court] has said it. Legislatures have presumed it for decades or more.”9

Precisely. The brief points to evidence concerning impulsivity, poor short term risk and long term benefit estimations, emotional volatility, and susceptibility to stress among adolescents compared to adults. These are common sense, “fireside” conclusions that parents and others have drawn in one form or another since time immemorial. In recent years, common sense has been bolstered by methodologically rigorous behavioral investigations that have confirmed ordinary wisdom. Most important, all these behavioral characteristics are clearly relevant to responsibility because they all bear on the adolescent’s capacity for rationality. Without any further scientific evidence, advocates of abolition would have an entirely ample factual basis to support the types of moral and constitutional claims they made.

The Roper briefs were filled with discussion of new neuroscientific evidence that confirms that adolescent brains are different from adult brains in ways consistent with the observed behavioral differences that alone bear on culpability and responsibility. Assuming the validity of the neuroscientific evidence, what does it add? The rigorous behavioral studies already confirm the behavioral differences. No one thinks that these data are invalid because adolescent subjects are faking or for some other reason. The moral and constitutional implications of the data may be controversial, but the data are not. At most, the neuroscientific evidence provides a partial causal explanation of why the observed behavioral differences exist and thus some further evidence of the validity of the behavioral differences. It is only of limited and indirect relevance to responsibility assessment, which is based on behavioral criteria.

Advocates claimed, however, that the neuroscience confirmed that adolescents are insufficiently responsible to be executed, thus confusing the positive and the normative. The neuroscience evidence in no way independently confirms that adolescents are less responsible. If the behavioral differences between adolescents and adults were slight, it would not matter if their brains are quite different. Similarly, if the behavioral differences were sufficient for moral and constitutional differential treatment, then it would not matter if the brains were essentially indistinguishable.

Decisions regarding whether the mean differences are large enough and whether the overlap between the two populations is small enough to warrant treating adolescents differently categorically as a class rather than trying to individuate responsibility are normative, moral, political, social, and ultimately legal constitutional questions about which behavioral and neuroscience must finally fall silent. Even if there were virtually no behavioral or brain overlaps between, say, sixteen and seventeen year olds on the one hand and eighteen and nineteen year olds on the other, it would still not entail that we must categorize rather than individuate. After all, because there is overlap—indeed, substantial overlap in the groups just mentioned—we know that some sixteen and seventeen years olds will be behaviorally and neurologically indistinguishable from many eighteen and nineteen year olds. Finally, even if there were no behavioral or brain overlap whatsoever, it would still not entail that abolition was constitutionally mandated. As a normative matter, the Court could decide that sixteen and seventeen year olds are responsible enough to be executed despite all of them being less responsible than older murderers. Assuming the validity of the findings of behavioral and biological difference, the size of that difference entails no necessary moral or constitutional conclusions.

In the event, the Roper majority cited many reasons for its decision, including the abundant common sense and behavioral science evidence that adolescents differ from adults. This evidence demonstrates, said the Court, “that juvenile offenders cannot with reliability be classified among the worst offenders,” for whom capital punishment is reserved. The Court cited three differences: adolescents have “[a] lack of maturity and an underdeveloped sense of responsibility;”10 adolescents are more “vulnerable or susceptible to negative influences and outside pressures, including peer pressure,” a difference in part explained by the adolescent’s weaker control or experience of control over his or her own environment; adolescents do not have fully formed characters.11 As a result of these factors—all of which, we may note, are behavioral and all of which can be confirmed with behavioral evidence alone—juvenile culpability is diminished and the penological justifications for capital punishment apply to adolescents with “lesser force.”12 The Court’s opinion thus reflects two conclusions: the group difference between the rationality of late adolescents and of adults is constitutionally significant for Eighth Amendment purposes and it is large enough to justify abandoning individualized decision-making concerning responsibility for the former.

Characteristically, the Court did not cite much evidence for the empirical propositions that supported its diminished culpability argument. What is notable, however, is that the Court did not cite any of the neuroscience evidence concerning myelination and pruning that the amici and others had urged them to rely on. It did cite six behavioral sources, five of which were high quality behavioral science. Perhaps the neuroscience evidence actually played a role in the decision, as many advocates for the use of neuroscience would like to believe, but there is no evidence in the opinion to support this speculation.

As this note has argued, the behavioral science was crucial to proper resolution of the case and furnished completely adequate resources to decide the issue. The neuroscience was largely irrelevant. The reasoning of the case is consistent with this argument and the opinion showed no signs of Brain Overclaim Syndrome. In my view, Roper properly disregarded the neuroscience evidence and thus did not provide unwarranted legitimation for the use of such evidence to decide culpability questions generally.

VI. The Royal Road to Complete Recovery: Cognitive-Jurotherapy [CJ] for BOS

The signs and symptoms of BOS are all cognitive. I therefore propose that CJ is likely to be the best treatment. The therapeutic techniques, all of which require motivation, effort and practice, follow directly from the signs and symptoms of BOS.

First, the Potential Commentator [PC] must have a good understanding of the relevance of the new neuroscience to complex behavior generally, including an understanding of the relevant literature in philosophy of mind. Reasonable minds can differ about the basic neuroscience and the philosophy of mind, of course, and disagreement is not a sign of BOS. But naive neuroscience and philosophy of mind and question-begging about these subjects are signs, although they are completely curable.

Second, the PC must understand whether his or her contribution is an internal or external criticism, and what type it is within the two broad domains. Confusion between and within the critical domains must at all costs be avoided. This is also simple enough if one understands the distinctions.

Third, the PC must be very clear about precisely what criteria for criminal responsibility he or she is using and about whether it is a positive account of the current state of the law or a proposed account of what the law should be. There may of course be disagreement about the current state of the law, and, once again, disagreement is not a sign or symptom of BOS. But using naive criteria and question-begging about the criteria, without argument, are signs. If the PC is offering a proposed account, the PC should set forth the argument for why the legal system should accept this account. In either case, the criteria should be clear enough to permit reasonably apparent conclusions about the relevance of brain evidence to those criteria.

Fourth, the PC must understand the positive/normative distinction, and if he or she wishes to use brain findings as premises in an argument for legal change, the normative reasons for preferring the change should be crisply identified.

All of the above is really just a “high falutin,” partially tongue-in-cheek way of suggesting that people need to think more clearly and make more transparent, logical arguments about the relationship of anything to criminal responsibility. The question is why more PCs do not do this. I do not know the answer, but I suspect that two primary culprits are at work: intellectual naiveté and ideological blinders. Sophisticated, non-hand waving treatment of these issues requires a lot of capital investment by lawyers in disciplines outside the law and by non-lawyers in the law. Many PCs do not have the capital, but this is easily remedied by appropriate investment.

Ideological blinders are harder to fix, and sometimes it is not clear what role ideology is playing. Is the PC making an argument he or she knows is not the best argument because it supports his or her position and it does (barely) pass the “smell test”? I suppose that this is less objectionable for a practitioner than for a scholar, although it is less objectionable even for scholars if they are openly engaging in advocacy. Or, is the desire to achieve a certain result so important that the PC does not even recognize that the argument deployed is weak? This is a problem for anyone.

My impression is that most people who wish to inject neuroscience into criminal responsibility assessments believe that the neuroscience must necessarily be exculpatory. We have seen that this does not follow, and, indeed, even if neuroscience could be demonstrated to be routinely relevant, it is a knife that cuts both ways. Unless one makes the fundamental psycholegal error of believing that causation per se excuses, it is clear that neuroscience might also be a means to inculpate. One is reminded of the analogy to DNA evidence. For the moment it is being used extensively to exculpate alleged murderers on death row, but as many have pointed out, if inaccuracy is the primary criticism of application of the death penalty, DNA could erode that critique and give new impetus to capital punishment.

VII. Conclusion

As the biological and behavioral sciences offer ever more sophisticated understandings of normal and abnormal behavior alike, there will be constant pressure to use their findings to affect assessment of criminal responsibility and other legal doctrines. A lot will be at stake morally, politically and legally, and much will be debatable. I hope, however, that this modest contribution will help identify and ameliorate a pathological entity that can deleteriously affect the debate.

Endnotes

543 U.S. 551 (2005).

JOHN R. SEARLE, MIND: A BRIEF INTRODUCTION 113–14 (2004) (terming his position about consciousness “biological naturalism”).

John Searle, Keynote Address at the Arizona State University College of Law Conference: The Abnormal Brain and Criminal Responsibility (Apr. 29, 2005).

At the conference at which this diagnostic note was first presented, I asked with what accuracy, based only on the images of myelination, one could accurately distinguish the individual brains of sixteen and seventeen year olds on the one hand and eighteen and nineteen year olds on the other. One neuroscientist claimed that the scientist could do this with great accuracy if the scientist were furnished with the sex and handedness of the subject. This claim would have been quite believable if the comparison groups were thirteen and fourteen year olds versus twenty-five and twenty-six year olds, but it seemed doubtful to me because development is continuous and the groups were so close in age. After the conference, I therefore asked the question of other equally credentialed and experienced neuroscientists and neuroanatomists. My informants uniformly agreed that they could not very accurately distinguish sixteen and seventeen year old brains from eighteen and nineteen year old brains. I do not know who is right. To the best of my knowledge, a study to determine accuracy of this type has not been performed, but the outcome would be very interesting.

487 U.S. 815 (1988).

536 U.S. 304 (2002).

Id. at 318–19; see also Thompson, 487 U.S. at 834−35.

I put “control” in scare quotes because I am highly skeptical about claims concerning lack of control as an independent mitigating or excusing condition. I argue that lack of control can always be reduced to a cognitive deficiency. Stephen J. Morse, Uncontrollable Urges and Irrational People, 88 VA. L. REV. 1025, 1054−63 (2002).

Brief of the American Medical Association et al. as Amici Curiae in Support of Respondent at 2, Roper v. Simmons, 543 U.S. 551 (2005) (No. 03-633).

Roper, 543 U.S. at 569 (quoting Johnson v. Texas, 509 U.S. 350, 367 (1993)).

Id.

During the 1982 trial of John W. Hinckley Jr. for the attempted assassination of President Reagan and others, Hinckley introduced evidence of a brain abnormality to buttress his claim that he was legally insane. An expert witness used a computerized axial tomography (CAT) scan to demonstrate that Hinckley’s sulci (the grooves in the folds of the brain’s top layer) were wider than normal, a finding the expert then believed was linked to schizophrenia. None of the experts or commentators was sure of the legal significance of this finding, however, and we do not know whether that evidence influenced the jury’s verdict that Hinckley was legally insane.

Today, as the Supreme Court considers whether it is unconstitutional to execute killers who were 16 or 17 years old when they committed homicide—a practice approved by a substantial minority of the states—opponents of executing juvenile killers are using more sophisticated brain imaging techniques to demonstrate that the brains of late adolescents are not fully developed. The opponents claim such findings indicate that the death penalty would be unfair for teenagers who commit capital crimes.

Although the brain science of today is vastly advanced compared with its 1982 precursors, the legal implications are still not clear. No necessary connection exists between the findings of neuroscience and legal or moral policies or decisions. The law’s concept of the person and the nature of law itself are both so fundamental to our understanding of ourselves and society that the new neuroscience may have fewer implications for law and society than popular imagination and even many scientists believe.

The Law’s Concept of the Person

The legal concept of the person is that of an agent who is capable of acting intentionally and for reasons. We are social creatures whose interactions are not governed primarily by innate repertoires; we are able to guide our behavior in light of reasons we may have for acting and do not solely and blindly follow instinct.

Law is a practical system of rules and institutions that evaluate, guide and govern human action. It gives people good reason to behave one way or another, by making the consequences of noncompliance clear or through peoples’ understanding of the reasons that support a particular rule. Law shares many characteristics with other sources of guidance, such as morality and custom, but is different because its rules and institutions are created and enforced by the state.

Physical causes explain the structure and mechanisms of the brain and nervous system (and all the other moving parts of the physical universe), but only human action—intentional bodily movements and other intentionally-produced states—can also be explained by reasons. Law views human action as reason-governed and treats people as intentional agents, not simply as part of the biophysical flotsam and jetsam of the causal universe. It could not be otherwise. It makes no sense to ask a bull that gores a matador, “Why did you do that?” But this question makes sense and is vitally important when it is addressed to a person who sticks a knife into the chest of another human being. It makes a great difference to us if the knife-wielder is a surgeon who is cutting with the patient’s consent or a person who is enraged at the victim and intends to kill him.

Only human beings are fully intentional creatures. To ask why a person acted a certain way is to ask for reasons, not for reductionist biophysical, psychological, or sociological explanations. I am not positing the existence of nonnatural properties, such as a soul; I assume that a perfectly naturalistic set of causes can explain intentionality and consciousness. But only persons can deliberate about what action to perform and can determine their conduct by practical reason.

Today we have no idea how the brain enables the mind (and scant information about precisely how it disables it), but when we solve this problem—if we ever do—the solution will revolutionize our understanding of biological processes. Our view of ourselves and all our moral and political arrangements are likely to be as profoundly altered as our understanding of biological processes. For now, however, despite the impressive gains in neuroscience and related disciplines, we still do not know mechanistically how action happens even if we are convinced, as I am, that a physicalist account of some sort must be correct.

For the law, then, a person is a practical reasoner. It assumes simply that people are capable of acting for reasons and are generally capable of minimal rationality according to mostly conventional, socially-constructed standards of rationality.

The Touchstones of Responsibility and Excuse

Rationality is the touchstone of responsibility. Only agents capable of rationality can use legal and moral rules as potential reasons for action. Only by its influence on practical reason can law directly and indirectly affect the world we inhabit. In order to maximize liberty and autonomy, the law presumes that adults are capable of minimal rationality and responsibility and that the same rules may be applied to all, but this presumption can be rebutted in appropriate cases.

No uncontroversial definition of rationality exists in the disciplines that study it, such as philosophy, economics, and psychology. In various legal contexts, how much and what type of rationality is required for responsibility is a social, moral, and political issue that divides people. For example, the United States Supreme Court was asked to decide if the criteria for competence to stand trial should be different from the criteria for competence to plead guilty. In a closely split decision, the Court ruled that the same criteria should apply. Science could not answer this question because it is not a scientific issue; the debate is about human action. But the rationality criterion for responsibility is perfectly consistent with the facts—most adults are capable of minimal rationality virtually all the time—and with moral theories concerning fairness and justice that we have good reason to accept.

Conversely, lack of the capacity for rationality is the touchstone of excuse. Unless people were reasonably capable of understanding and using legal rules as premises in deliberation, law would be powerless to affect human behavior and it would be unfair to hold them responsible. What rationality and consequent responsibility demands will differ across contexts. For example, a person is incompetent to contract if he or she is incapable of understanding the nature of the bargain; a person is criminally nonresponsible if the agent did not know the nature of his or her conduct or the applicable law.

The law contains coercion or compulsion criteria for nonresponsibility, but these criteria are demanding and only infrequently provide an excusing condition. Properly understood, coercion occurs when the person is placed through no fault of her own in a threatening “hard choice” situation from which she cannot readily escape and in which she yields to the threat. The classic example in criminal law is the excuse of duress. This requires that the person must be threatened with death or serious bodily harm unless she commits the crime and that a person of “reasonable firmness” would have yielded to the threat. The agent thus has acted intentionally and rationally to avoid death or grievous bodily harm. The crime is excused, because requiring human beings not to yield to some threats is simply too much to ask of creatures such as ourselves. How hard the choice must be can vary across contexts; a compulsion excuse for crime might require a greater threat than a compulsion excuse for a contract.

A persistent, vexing question is how to assess the responsibility of people who seem to be acting in response to some inner compulsion, or, in more ordinary language, seem to have trouble controlling themselves. What does it mean to say that an agent who is acting cannot control himself? I have explored this puzzle in my professional writing, and have arrived at the conclusion that defects in rationality best explain these cases and that the law does not need an independent compulsion excuse in these “one party cases.”1 People who act in response to such inner states are intentional agents. Simply that an abnormal biological condition played a causal role—and neuroscientific evidence frequently confirms this—does not mean the person was compelled. In some cases, however, the persistence or intensity of the desire or craving makes it supremely difficult for the person to access reason. They still might not be excused, however, if they recognize, as many do, that they are subject to such desires frequently and behave badly when this happens. In such cases, they may have an obligation when they are more rational to take steps to prevent themselves from being in a position to harm themselves or others when they are in the throes of their intense desires.

Neuroscience will surely discover much more about conditions that can compromise rationality and may broaden current legal excusing doctrines or widen the class of people who can raise a plausible claim under current law. Neuroscience may help to adjudicate excusing and mitigating claims more accurately. But unless neuroscience demonstrates that no one is capable of minimal rationality (or that everyone is always responding to supremely intense and persistent cravings)—an implausible scenario discussed below—fundamental criteria for responsibility will be intact.

Confusions About Responsibility and Excuse

Responsibility has nothing to do with “free will” even though legal cases and commentary concerning responsibility are replete with talk about it. Nor is the truth of a fully physically-caused universe (sometimes referred to as “determinism”) part of the criteria for any legal doctrine that holds some people nonresponsible. Thinking that causation itself excuses, including causation by abnormal variables, is an analytic error that I have termed the fundamental psycho-legal error. All behavior may be caused in a physical universe, but not all behavior is excused, because causation per se has nothing to do with responsibility. For example, many variables caused you to be reading this article now, but you are perfectly responsible for intentionally reading it. Reading it is presumably not evidence of incapacity for rationality and presumably no one is forcing you to read it. Causation is not the equivalent of either lack of capacity for rationality or compulsion. If causation negated responsibility, no one would be morally responsible and holding people legally responsible would be extremely difficult.

The fundamental psycholegal error wrongly leads people to try to create a new excuse every time an allegedly valid new “syndrome” or any other cause is discovered that plays a role in behavior. But syndromes and other causes, including those of brain structure and function, do not have excusing force unless they sufficiently diminish rationality in the context in question. In that case, it is diminished rationality that is the excusing condition, not the presence of any particular type of cause. An assertion about “free will” based on causation is simply a conclusion about responsibility that must have been reached based on criteria such as the presence of rationality or absence of coercion.

Assessing Responsibility and Excuse

The criteria for excuse—lack of capacity for rationality and the presence of coercion— concern components of human action, such as desires and beliefs, that must in the first instance be assessed behaviorally, including by the use of behavioral tests devised for this purpose. It is human action that is at issue, not the state of the brain. If the person’s rational capacities, which we infer from her behavior, seem unimpaired, she will be held responsible, whatever the neuroscience might show, and vice versa. We knew that young children were not fully responsible long before we understood the neuroscience.

Although neuroscientific evidence may surely provide assistance in performing responsibility evaluations, neuroscience could never tell us how much rationality is required for responsibility. The question is social, moral, political, and, ultimately, legal. Moreover, it is unlikely, except in extreme cases in which we wouldn’t need brain evidence, that brain states will map legal criteria precisely. For the foreseeable future, neuroscience as a tool cannot replace behavioral investigation and commonsense when we assess responsibility.

The issue in deciding if teen killers should be executed, for example, is whether they suffer from sufficiently less rationality than adults, and that must be evaluated by examining adolescents’ reasoning and judgment. Brains do not have defective judgment; conscious, intentional agents— people—do. I am an opponent of capital punishment, but if our society decides morally and legally that the capacity for rationality in normal late adolescents is sufficient for capital punishment, even if their brains are less developed than those of adults, then the brain science alone cannot demonstrate that capital punishment is unjustified.

The Neuroscience Challenge to Personhood and Responsibility

Advances in neuroscience and related fields have revealed hitherto unimagined biological causes of behavior, including abnormal neurotransmitters, that may increase the risk of antisocial or otherwise undesirable behavior, 2 but we have no convincing conceptual or empirical reason to abandon our view of ourselves as creatures whose desires, beliefs, and intentions cause and explain our behavior.

Scientific discoveries might indicate that mental causation does not exist as we think it does, but a brain correlate or cause does not mean that the action is not an action. If actions exist, they have causes, including those arising in the brain. The real question is whether studies have shown that intentional behavior is rare or nonexistent. Despite our intuition and experience that action is ubiquitous and genuinely explainable, increasing numbers of scientists and philosophers claim that intention is an illusion. They cite two kinds of empirical evidence: first, demonstrations that most of our behavior is caused by variables we are unaware of and, second, studies indicating that much behavior occurs when our consciousness is diminished.

A person may not be aware of all the causes of forming and acting on an intention, but this is not to say she did not form an intention and was not a fully conscious agent. Even if we were never aware of the causes of our actions, it would not mean that we do not act intentionally and consciously.

Knowledge that a variety of causes can diminish human consciousness long predates contemporary neuroscience. Demonstrating that partial consciousness is more common than it seems extends the range of cases in which people are not responsible or have diminished responsibility. Nevertheless, such studies do not demonstrate that most apparently intentional human actions occur in states of unintegrated consciousness. One cannot generalize from abnormal cases. No scientific study has produced a general demonstration that causal intentionality is an illusion, and I suspect that none ever will. As the eminent philosopher of mind Jerry Fodor has written, the only thing we can be as sure of as the existence of “mid-sized” objects is that we are creatures who act for reasons.3

Let us suppose, however, you were convinced by the mechanistic view of persons that you were not an intentional, rational agent after all. (Of course, the notion of being “convinced” would be an illusion. Being convinced means that you were persuaded by evidence or argument, but a mechanism is not persuaded by anything. It is simply neurophysically transformed or some such.) What should you do now? You know it’s an illusion to believe that your deliberation and intention have any causal efficacy in the world. (Again, what does it mean mechanistically to “know” something? But enough.) Nonetheless, you also know that you care about what happens to you and to the world. You cannot just sit quietly and wait for your neurotransmitters to fire. You will deliberate and act. Even if pure mechanism is true, human beings will find it impossible not to treat themselves as rational, intentional agents.

People think that the discovery of causes of behavior over which people have no control, including brain states, suggests that determinism is true and undermines “free will.” This concept is what terrifies people about scientific understanding of human behavior, which relentlessly exposes the numerous causal variables that seem to toss us about like small boats in a raging sea. They fear that scientific explanations, biological or otherwise, will demonstrate that we are only mechanisms. But the new neuroscience casts little doubt on responsibility generally; there is no reason to doubt that we are conscious, intentional, and rational creatures. Causation alone does not undermine that knowledge or provide an excusing condition. Western theories of morality and the law properly hold some people responsible and excuse others, and when we do excuse, it is not because a little local determinism has been at work. Determinism cannot tell us which goals we should pursue and it cannot explain or justify our present practices.

Neuroscience and Legal Reform

Under what conditions will the new neuroscience suggest reform of existing legal rules? The law is in many respects a conservative enterprise and will always resist supposed reforms other disciplines suggest. For example, despite the extraordinary advances in the understanding of mental disorder in the past half century and consistent calls for reform based on such understanding, the dominant version of the insanity defense—which excuses if the defendant with a disorder did not know what he was doing or did not know that it was wrong—is scarcely changed from the form adopted in 1843 by the English, the M’Naghten rule. This is unsurprising. Mental health science can teach us much about why some people lack rationality and can help identify and treat those people, but it cannot tell society which rationality defects are sufficient to excuse a wrongdoer. Deciding who is blameworthy and deserves to be punished depends on established social norms and practices about which mental health science must fall silent.

Legal rules do, of course, change in response to evolving principles and new scientific discoveries. Racial discrimination was banned by civil rights legislation simply because it was wrong. It is now unlawful to dump toxic waste, in large part because science demonstrated the health hazards. But before legislators and judges will be rationally justified in changing existing legal rules in response to the discoveries of any scientific discipline, at the least they should be convinced, first, that the data are valid; second, that the data are genuinely relevant to particular rules; third, that the data convincingly imply that specific changes to those rules would have desirable effects; and, fourth, that those changes will not infringe upon other values that may be more important. All this is a tall order.

I predict that neuroscience will not have widespread, profound influence on doctrine in most areas unless its discoveries radically alter our conception of ourselves. On the other hand, one can easily imagine substantial changes in discrete doctrines. For example, neuroscience may teach us much about cognitive processing under stress that would influence our doctrines of informed consent to medical care. For another example, neuroscience may be able to identify when people are consciously lying or consciously or unconsciously discriminating on the basis of objectionable factors such as race. Such discoveries could have profound effects on evidentiary practices. But even an exceptionally sensitive technique to detect lying or discrimination might not be used, because we fear state invasion of our innermost thoughts, even for purposes such as discovering truth or uncovering conscious or unconscious discrimination. In cases involving discrete doctrinal change, we already have the tools to weigh the desirability of the change.

Potential Threats to Civil Liberties

Neuroscientific discoveries might well raise profound challenges to civil liberties. Other sciences, too, might make discoveries that would do likewise, so the following discussion surely generalizes. The potential of neuroscience to invade our privacy by revealing various aspects of our private, subjective experience may produce the strongest reaction against its use and lead to substantial regulation. Still, the techniques that permit valuable ends such as accurate lie detection may be so alluring that the temptation to use them will be great.

The question is, what constitutional or legislative limits may be placed on such techniques. The government will not be able to use neuroscientific investigative techniques to go on “mental fishing expeditions” generally, but various state interests may permit infringing hitherto protected interests. For example, the Supreme Court recently held that under limited conditions the State has the right to force psychotropic medication on a psychotic criminal defendant solely for the purpose of restoring the defendant’s competence to stand trial.4

Neuroscientific techniques might also increase the ability to make accurate predictions about various forms of future behavior. If socially troublesome behaviors can be accurately predicted, use of such techniques for screening and intervention will be tempting. For example, neuroscientific techniques may well enhance the ability to predict antisocial conduct. It would be less difficult to justify screening prisoners and others under criminal justice control, but widespread screening of others, such as apparently at-risk children—even if the risk status were identified by objective, valid measures—would be legally and politically fraught with civil-liberties implications. The widespread use of psychotropic medications such as methylphenidate (Ritalin) among school children suggests, however, that a screening/intervention scenario would not be unthinkable under some conditions. It is difficult to envision how society would respond to techniques that identified risk-creating abnormalities highly accurately and to effective interventions that would prevent undoubtedly serious social and personal harms. Traditional attitudes towards privacy and liberty might change considerably.

Many consider the potential for direct, biological intervention in the working of the brain and nervous system to change thoughts, feelings, and actions—often polemically characterized as “mind control”—a greater threat to liberty than genetic intervention. The government already has the constitutional authority to compel the use of psychotropic medications under limited circumstances, but the potential for widespread intervention to change behavior is apparent. The biological and behavioral definitions of abnormality and disorder can be controversial. At the extremes, little problem exists, but the criteria for abnormal brain structure or function are not self-defining. The criteria for behavioral abnormality are even more fluid, and there is a tendency to pathologize troubling behaviors. Thus, a relatively value-neutral criterion of abnormality cannot impose strict limits on the ability of the state to compel behavior-altering interventions.

The current science and political will to accomplish effective, widespread behavior control are lacking. Nonetheless, as screening and intervention methods become more precise and effective, pressure will build to use them, and proponents will defend their constitutional legitimacy. If neuroscience or other sciences ever reach the levels of understanding and efficacy necessary to make the civil liberties concerns a realistic possibility, it is difficult to predict what legislatures and courts will do. If pressing social problems seem amenable to a technological fix, current political and constitutional constraints may weaken.

New Neuroscience, Old Problems

The new neuroscience poses familiar moral, social, political, and legal challenges that can be addressed using equally familiar conceptual and theoretical tools. Discoveries that increase our understanding and control of human behavior may raise the stakes, but they don’t change the game. Future discoveries may so radically alter the way we think about ourselves as persons and about the nature of human existence that massive shifts in all our societal practices and institutions may ensue. For now, however, neuroscience poses no threat to ordinary notions of personhood and responsibility that undergird our civic life and the law.

References

Morse, SJ. “Uncontrollable Urges and Irrational People,” 88 Virginia Law Review 1025 (2002).

See, e.g., Caspi, A, et al, “Role of Genotype in the Cycle of Violence in Maltreated Children,” 297 Science851 (2002); Goldstein, RZ and Volkow, ND, “Drug Addiction and Its Underlying Neurobiological Basis: Neuroimaging Evidence for the Involvement of the Frontal Cortex,” 159 American Journal of Psychiatry1542 (2002); Potenza, MN, et al., “Gambling Urges in Pathological Gambling: A Functional Magnetic Resonance Imaging Study,” 60 Archives of General Psychiatry 828 (2003); Stein, MB, et al., “Genetic and Environmental Influences on Trauma Exposure and Posttraumatic Stress Disorder Symptoms: A Twin Study,” 159 American Journal of Psychiatry 1675 (2002).

Fodor, J. Psychosemantics: The Problem of Meaning in the Philosophy of Mind xii (1987 MIT Press).

Hedonic Reasons

According to rational egoists, we only have reasons to promote our own well-being. According to utilitarians, we have reasons to promote well-being of everyone equally. According to commonsense morality, however, we have reasons of both kinds— prudential reasons to promote our own well-being, as well as moral ones to promote the well-being of others. What it is exactly we have reason to promote on any of these views depends on our understanding of well-being. On hedonic theories of well-being, a person’s well-being consists of the balance of pleasure over pain. On this view, our reasons to promote well-being are reasons to make people feel as good as possible, and to feel least bad. I will call these hedonic reasons. On such theories, these are the only reasons given by well-being. But even on most competing theories of well-being—desire- satisfaction and objective theories—we would still have such hedonic reasons, although well-being would also generate other kinds of reasons (e.g. to fulfil desires that do not have hedonic content, or, on some objective theories, to obtain important knowledge, or nurture personal relations, independently of whether these will give us pleasures.)

Our hedonic reasons instruct us to generate as much pleasure as we can, and diminish pain to the minimum possible. They instruct us, for example, to take pain-killers whenever possible, and to do things we will enjoy. Few would deny that we should follow such reasons to prevent or minimize physical pain. And, to a somewhat lesser extent, it is uncontroversial that we should also follow them with respect to physical pleasure (so long as we leave enough space for the pursuit and appreciation of other kinds of goods).

To the extent, then, that positive mood enhancers make us feel better, our hedonic reasons deliver a clear verdict: take the pill.2 Many supporters of the biomedical enhancement of mood explicitly or implicitly base their case on such appeal to hedonic reasons.

Affective Reasons

But things are more complicated. For, besides hedonic reasons, we also have what I will call affective reasons, reasons to feel.

Let me quickly clarify the key notions of feeling, emotion, and mood. Feelings are episodes of consciousness. There is something it feels like to feel angry or sad. Emotions are broader behavioural dispositions which include dispositions to have certain feelings, as well as dispositions to behave, think and attend in certain ways. Importantly, although to be angry at someone is, among other things, to be disposed to feel angry at the person, one can be angry even when one isn’t literally feeling angry. Moods are even broader dispositions, dispositions that govern one’s entire emotional orientation for a certain period. To be bored or elated is not to have some particular emotion but to have a general orientation to things that shapes one’s various more specific emotions.

Having distinguished feelings and emotions, I will from now on, for reasons of simplicity, use these terms more or less interchangeably. The distinction between mood and emotion will, however, have some further role to play later on.

Do affective reasons really exist? Some people would find the idea surprising. After all, reason and emotion are often presented as contraries. We sometimes speak as if to be emotional is to be unreasonable, and to be reasonable is to be unemotional. But this of course can’t be quite right. Emotions are not just things that happen, like headaches or itches. Some situations call for certain feelings, some emotions are in order, others inappropriate. As someone is struck by disease or good news arrive, as disasters unfold or a war ends, we cannot remain impassive observers. The world around us is laden with value, and reason calls upon us to respond to it, with feeling.3

Why then are reason and feeling sometimes seen as contraries? This might be because strong emotions can disturb the operation of reason. They can make it hard for us to properly respond to our reasons. However, even strong emotions are within the scope of reason. Sometimes we have reasons to feel strong emotions—to feel very sad or angry—even though such feelings also increase the risk that we would act, feel or believe irrationally.

There are reasons for feelings: reasons to feel sad, or pleased or indignant. The existence of such affective reasons is often overlooked, and sometimes denied. Some worry, for example, that feelings are involuntary, and thus cannot be subject to reasons. But our beliefs are also involuntary, and if this worry were valid, we could not have reasons for belief either, an absurd claim.

Others admit that, in one sense, there are affective reasons, but think that these are merely pragmatic or instrumental. What matters, they think, is not how we feel but what gets done—what happens in the world. They hold that emotions are merely means to promoting certain forms of appropriate behaviour. Thus, for example, moral indignation is useful because it disposes us to treat wrongdoers in certain appropriate ways. But they also think that if we could behave in those ways without feeling indignation, what we feel would not matter.

I reject this view. We often have intrinsic affective reasons. Think of someone who is about to die. A person in such a situation might have reasons to feel regret or satisfaction with her life, or to feel affection for or disappointment in others. She would have these reasons even if there was no way in which they could shape her behaviour.4

Value and Affective Reasons

If we have various feelings to feel, what, then, ought we to feel? Unfortunately, ethics has not yet provided a systematic answer to this question. It has largely focused on how we ought to act—or at most, on what motives should guide our acts. But one source of affective reasons is widely recognised: value often generates reasons to feel. We have reasons to respond positively to the good, and negatively to the bad. These reasons often call for certain actions—for example to take acts that would bring good things into existence. They also often call for certain emotions. We should feel good about the good, and feel bad about the bad, though what it is exactly we should feel (elation, joy, content, satisfaction, etc.) will depend on the different respects in which different things are valuable.5

This is just a rough statement of the relation between value and reasons for feeling. For obviously, although the world around us is teeming with value, with both good and evil, our capacity to feel is limited. We couldn’t possibly feel for all the world. Thus, although value generates various pro tanto affective reasons, it is a separate question what, overall, we ought to feel at some point in time.

The Priority of Affective Over Hedonic Reasons

We have hedonic reasons to make ourselves feel good, and to avoid feeling bad. These reasons have sovereignty when it comes to physical pleasure and pain. They do not directly govern physical pleasure and pain, because such hedonic states do not directly respond to reason. Nobody can be sensibly criticized for not enjoying his meal. So hedonic reasons are reasons for action; for doing what it takes to cause ourselves to feel better.

Like physical pleasure and pain, emotions also have a hedonic dimension. Negative emotions typically feel bad, positive ones typically feel good.6 So here our hedonic reasons come into direct competition with our affective reasons. For, at least in the case of negative emotions, the two types of reasons will often point in opposite directions. A loss gives us affective reasons to feel grief. But grief can be excruciating. So it seems we should have hedonic reasons to alleviate it.

I think it clear enough that in such cases we give priority to our affective reasons.7 Few of us think that if a nice vacation could prevent grief at the loss of a loved on, it would be right for us to take it. To do so might make us feel better, but it would also corrupt our emotional lives. It would be to focus on how things feel like inside at the expense of a full appreciation of how things are around us—it would distort our relation to what matters in the same way that a person entering Robert Nozick’s ‘experience machine’ has lost touch with reality.

This is not to say that even in such cases we just ignore hedonic considerations. We do try to comfort others who are in deep grief—not just because of their loss, but also because of their pain. And to the extent that people feel grief for longer, or more intensely, than is reasonable, we do try to alleviate it, not just because such grief is in itself unreasonable, but because it involves needless suffering.8

Depression, Mood Enhancement, and What We Ought to Feel

Turn now to positive mood enhancers. Suppose someone is doing very badly. He is going through an acrimonious breakup, or has been fired from his job. He becomes increasingly unhappy and desperate. Some would think that it would be in order for such a person to start taking positive mood enhancers. This recommendation is clearly driven by what I called hedonic and pragmatic reasons. This person is suffering, and that is bad in itself. And his suffering might also prevent him from dealing with his problems, making him sink even further into despair. But what about his affective reasons? What happened to their alleged priority?

It might be replied that this complaint overlooks the point that such a person might be not just sad but depressed. But I have deliberately avoided referring to depression. I think that it is better if we first think of such situations in terms of affective reasons. People often tend to feel bad when they have no affective reasons to do so. Or even when they do have such reasons, they feel worse, and for longer, than they should—their emotions are disproportionate. As I noted above, in such situations we would indeed have strong hedonic and pragmatic reasons to alleviate their mental suffering. This is something we can say without referring to depression or disorder. To be sure, one common explanation of why people respond in such unreasonable ways might be some abnormality in the biochemistry of their brain. But, in principle such an abnormality might have made them better respond to their affective reasons. When we judge that such a person is depressed, and should therefore be treated, we are not making some biological or medical judgement. We are firstly making a substantive normative judgment about how their emotions measure against their affective reasons.

Suppose we judged differently. Suppose that, after reflection, we judged that this person’s unhappiness is not disproportionate—that it is broadly the right affective response to the difficult situation he is in. If that person went and took a positive mood enhancer that would greatly reduce his unhappiness, he would no longer be responding to his affective reasons. He might be feeling better, which would in itself be good, but he would no longer be giving his affective reasons the priority they deserve compared to hedonic reasons. In this case, it seems wrong for him to take the pill.9

Two Objections to Positive Mood Enhancers

This, then, is the kind of worry about biomedical mood enhancement that I wish to consider here. My discussion of this worry will make some assumptions about the nature of positive mood enhancers. I will assume that when taken regularly they have a continuous effect on mood;10 that this effect is fairly general, not focussed on this or that particular emotion; and that positive mood enhancers tend to generally reduce negative emotion and also (though perhaps to a lesser extent) to increase positive emotion. I take it that this is a broadly accurate characterisation of common antidepressants. But given the nature of the questions I want to consider, I will remain at this rather abstract level of description, and set the empirical details to one side.11

Now given these assumptions, two objections can be raised against the use of positive mood enhancers. First, positive mood enhancers make us feel contrary to reason, by making us feel good (or even just ‘neutral’) when we should feel bad. Second, even when mood enhancers make us feel good when we should feel good, they prevent us from genuinely responding to our reasons. When we take positive mood enhancers—so the objection goes—we merely conform to our reasons. We feel good when we ought to, but not because we ought to. In these two ways, positive mood enhancers might be said to corrupt our emotional lives. They prevent us from properly responding to our affective reasons.

Threats to Authenticity and Spontaneity

These two objections, I believe, capture at least an aspect of the more familiar worry that biomedical enhancement of mood can compromise our authenticity.12 If authenticity involves being true to oneself, or to one’s values, then there is a sense in which, if these objections are correct, when one uses mood enhancers, one is at most conforming to one’s values. Even if the exterior seems right, there is still a sense of falsity or artificiality. Similarly for the worry that the use of enhancement expresses a calculating as opposed to spontaneous attitude to one’s life.13 Again, one aspect of spontaneity seems to be the immediate and unmediated responsiveness to one’s affective reasons—feeling sad when things go bad, feeling thrilled at a victory, and so forth. Spontaneity is lost if one needs to work at feeling sad.

I just wanted to highlight these apparent connections. But there may well be more to these other objections to biomedical enhancement of mood than the worry I am considering here—and vice versa. Indeed, it’s an advantage of the worry about affective reasons that it makes no appeal to the controversial and perhaps obscure notions of authenticity and the true self, or to what is ‘natural’ or ‘given’.14

Conforming vs. Responding to Reasons

The example of using positive mood enhancers to overcome grief is an example of feeling contrary to one’s affective reasons. I now want to say some more about what I mean by mere conformity to such reasons.

It might be useful to briefly consider a parallel problem about belief. Think of how reasons for belief work. If you have good evidence that p, then you ought to believe that p. If the question whether p is an important matter, then you have reasons to seek out relevant evidence. It is valuable to know important truths.

Suppose, however, that I form a belief about some important matter not through some normal process of gathering evidence and responding to epistemic reasons (including, importantly, testimonial reasons to believe things you were told by authoritative others), but by taking a pill. A belief formed in such a way might be true, but, it seems, it would not be justified. Such a belief would merely conform to one’s epistemic reasons, but not be based on them.

The same goes for affective reasons. Even if I should feel happy, because things are going so well, and a mood enhancer makes me feel happy, this happiness merely conforms to my affective reasons. For it seems that I feel happy because of the pill, not because I am responding to the fact that things are good.

Second Best is Still Better than Nothing

I now turn to consider possible replies to this objection. Consider again the example of belief. Suppose that, although you have been provided with an overwhelming amount of evidence supporting the theory of evolution, your traditional upbringing makes it psychologically impossible for you to genuinely believe it. You are suffering from epistemic weakness of the will. Since you can’t believe in evolution on the basis of your epistemic reasons, it might still be better if you believe in it by taking the pill, compared to not believing it at all. True beliefs merely in conformity with reasons might still be better than having false beliefs on the matter.

Again, the same goes for our affective reasons. If we cannot directly respond to our affective reasons, it might still be better to conform to them than not to even feel what we ought to feel. It might be best to directly feel grief in response to a loss, but if some emotional inhibition prevents this, it would still be better to feel grief by artificial means, than not to feel grief at all.

In such cases, we still are responding to our epistemic and affective reasons, just not directly. We are responding to them by taking actions that are likely to cause us to enter the right mental state.

Mere Causal Manipulation or Increased Responsiveness?

I have so far granted that positive mood enhancers can merely cause us to feel better. But this is by no means obvious. Recall the earlier distinction between emotion and mood. Mood enhancers change our mood, our general affective orientation. And it is possible that what they do is help us better appreciate the good things in life—they might just make it easier for us to recognize and respond to our positive affective reasons. Now whether this is really the case is, in part, an empirical question. If it can be answered it in the affirmative, then the worry about mere conformity would be misplaced.15

Whether We Even Know What We Ought to Feel

These two replies address the mere conformity objection. But positive mood enhancers can’t be plausibly said to make us better conform—let alone be more responsive—to our negative affective reasons. So the first objection, that positive mood enhancers make us feel contrary to reason, still stands.

This objection might have force only if taken literally. For positive mood enhancers can also prevent us from responding to merely illusory negative affective reasons—from feeling bad when there is no reason to. And they might also reduce our response to negative affective reasons in ways that make our response more proportionate. But I’ll concede here that positive mood enhancers might in some cases prevent us from responding to genuine negative affective reasons.

It might be replied that the force of this objection is limited by the fact that we do not yet have a good enough understanding of our affective reasons. That is, although we often agree on what pro tanto affective reasons are given by particular things, we have a far weaker grasp on how all of these different affective reasons fit together. We have a fear weaker grasp on the question, What ought we to feel overall? Is it better to feel strongly or intensely, or should we feel only moderate and measured emotions? Should our feelings change rapidly as things around us change, or should they be lasting and stable? Should we respond at once both to the positive and to the negative—feeling bitter sweet contentment, or sadness mixed with joy—or should our feelings alternate, responding once to the bad, once to the good? But until we have answers to these and similar questions, how can we be confident that positive mood enhancers would corrupt our emotional lives?

This seems too quick. For we clearly do accept the priority of negative affective reasons over hedonic ones in many specific contexts, and if so, there should be at least a prima facie presumption that the use of positive mood enhancers prevents us from responding to these reasons. We do not need a systematic theory of affective reasons to know that.

The Affective Priority of Good over Bad

There is a better way to block this objection to positive mood enhancers. I now want to argue that once we reflect what we ought to feel overall, the tentative answer that emerges doesn’t only defuse the objection, but actually turns out to support the use of positive mood enhancers.

Think of the sheer scale of evil and misfortune in our world. When we reflect on all the suffering and wickedness around us, it can seem depraved, or a kind of moral blindness, that anyone feels happy. But if so, should we live our lives in grim, sober sadness? Many of us, however, think that this would not be the right response. We think that we should rather maintain cheer in the face of adversity. That we should appreciate the glimmers of goodness in what is otherwise a dark landscape.

There seems to be an interesting asymmetry in our normative thinking. When it comes to action, we tend to give the prevention of evil clear priority over the promotion of good. We think that it’s more important to relieve misery than to increase happiness. But when it comes to feeling, we seem to take the opposite view. We think that people should, overall, look on the bright side of things.

What explains this priority? It is certainly supported by the hedonic and pragmatic reasons we have already discussed. If we add up all our hedonic reasons (which all point in the positive directions) with our affective reasons (which point in both), perhaps the result is something skewed upwards. And there are pragmatic reasons not to feel too bad (though perhaps also not to feel too good either), for that would make us less able to fight evil and adversity. However, given the priority we earlier noted of affective over hedonic (and pragmatic) reasons, these suggestion couldn’t be the whole story.

Indeed, it seems to me that there are intrinsic affective reasons in favour of orienting our lives around the good. The existence of good somehow matters more than that of evil—goodness is the primary notion, and evil is merely an obstacle to its full realization.16 The idea is not that we should ignore evil, but that we should refuse to grant it equal standing.

In other words, although affective reasons have general priority over hedonic ones, there is within the affective realm priority to positive affective reasons over negative ones.17

To the extent that such a normative priority really holds, then positive mood enhancers, on the whole, are something to favour—something that directs our affective orientation in exactly the right direction.18 This would apply most strongly if, as I suggested above, mood enhancers actually allow us to better respond to our positive affective reasons. It would apply more weakly if positive mood enhancers merely made it easier for us to conform to such reasons.19

Now this argument has even greater force in the case of those whose affective orientation naturally points in the opposite, negative direction. And as we shall now see, consideration of this fact—the fact that our present affective dispositions are hardly purely responsive to reason—offers even further support to the use of positive mood enhancers.

Affective Adaptation: Why Our Affective Lives are already Defective

Questions about the ethics of biomedical enhancement often require us to answer many empirical questions, questions about the possible future effects, good or ill, of various forms of enhancement. We often have little evidence to answer such questions, and can only crudely speculate. The final consideration I wish to raise also revolves around empirical claims. But these are empirical claims, not about the possible future effects of biomedical enhancement, but about how people actually happen to be, prior to such enhancement.

What I have in mind are two broad findings of decades of scientific research into subjective well-being. First, there is strong evidence that people’s subjective well- being—a notion that is meant to be at least a rough measure of both positive feeling and subjective satisfaction—is to a significant extent rooted in innate factors that vary widely between individuals.20 Second, there is extensive evidence that people’s basic level of subjective well-being (their ‘hedonic set point’) is largely unaffected by even the most dramatic life events. Those who are typically cheerful or grim would remain so whether or not they win the lottery, witness the death of their lifelong spouse, or lose both legs in a car accident. Although such events produce some immediate (positive or negative) effect on one’s mood, it fairly quickly returns to its initial level. Our subjective well- being almost always ‘adapts’ to changing circumstances.21

What does all of this mean? First, it means that to a large extent our feelings seem to be shaped by non-rational factors. If I tend to see things more pessimistically than you do, this needn’t be because I am more accurately registering what really matters, but rather because of some arbitrary fact about my genes. The ‘state of nature’ is already not one of pure responsiveness to affective reasons.

Second, the surprising fact that even, for example, bereavement or severe disability might not, in the long term, have much affect on our mood, shows that we already often fail to respond to what we take to be strong affective reasons. Most people not only expect to feel prolonged grief after the death of a loved one but also think they ought to feel such grief.22 But, when they do in fact suffer such a loss, the evidence shows they are not likely to feel nearly as much grief as they expect.23

Third, because of their natural endowment, at least some people are naturally disposed to negative mood and find it generally difficult to appropriately respond to their positive affective reasons. The evidence about hedonic adaptation suggests that external factors will not significantly change this fact—indeed, most of the goods that many people spend their lives seeking would in fact have little effect on how they feel. Here there seem to be both strong hedonic reasons and indirect affective reasons to use mood enhancers.24

To summarize, this large body of empirical evidence strongly suggests that in our current state we are very far from being perfectly responsive to our affective reasons. And this means that our emotional lives were never in some pristine natural state that mood enhancers might corrupt. Many of us fail to appropriately respond to our affective reasons, and our emotions are at least partly shaped by clearly irrational factors. Thus in many (though certainly not all) cases, mood enhancement might significantly improve our responsiveness to our affective reasons, or at least help us better conform to them.

Alternative Forms of Mood Enhancement?

When people talk about biomedical enhancement of mood, they typically have in mind positive mood enhancement, and I have so far focused on this form of mood enhancement. Now if we only had hedonic reasons, then positive mood enhancement would have been the only form of enhancement worth having. However, once we consider the full range of affective reasons, other possible forms of mood enhancement come into view. I would like to end with a brief discussion of these.

Consider first negative mood enhancement. This may sound like an oxymoron, or some perverted invention for masochists. But to think in this way is to assume that we only have hedonic reasons. We do, however, often have strong reasons to feel bad, and we may be bad in responding to these reasons. When we say that someone has finally managed to grieve some childhood loss only after years of therapy, and treat this as an achievement, we implicitly recognize the value of such negative mood enhancement. Indeed some people might be endowed with a strong cheerful disposition that is inappropriate to their life circumstances. These points hold even if we take into account the overall priority of positive over negative affective reasons.

Consider next the possibility of mood enhancers that generally increase our responsiveness to affective reasons, both positive and negative. I said that it is unclear whether positive mood enhancers cause us to feel better, or rather make us more responsive to positive affective reasons we genuinely have. But such enhancers clearly work only in one direction. Might it be possible to generally increase our responsiveness to our affective reasons—both positive and negative? This is an empirical question that depends on how our cognition, valuation and emotion are neurally wired.25

Furthermore, it might be possible to enhance our responsiveness to certain kinds of affective reasons. Take the affective reasons given by past life events. There is now some discussion of memory erasing drugs which could be used to treat or prevent post-traumatic stress disorder. Here we are preventing people from being over-responsive to what are usually genuine and important affective reasons. Such treatment would be broadly motivated by hedonic reasons: these people needlessly suffer. One effect, however, might be that they would also be prevented from responding at all to these affective reasons. All I want to point out here is that we can also conceive of biomedical treatment that would improve autobiographical memory, and thus increase our capacity to respond to the affective reasons given by past events. Similarly, treatments that increase our foresight and awareness of the long term consequences of our actions might also increase our responsiveness to affective reasons given by possible future events.

I do not expect that such enhancers would arrive anytime soon. People are generally more easily motivated by their hedonic reasons than by negative affective ones, and the focus of biomedical research reflects this psychological asymmetry. And, as I suggested, there might be an affective priority of good over bad. But when we discuss biomedical mood enhancement, it would nevertheless be a mistake to assume it can only take only a positive form.

Conclusion

I started by noting the numerous familiar ways in which all of us try to control our feelings. When the use of biomedical enhancement is criticized, it is common to respond by pointing out its continuity with these more mundane forms of enhancement. This strategy is appropriate in the context of a dialectic—it exposes an apparent inconsistent on the part of the critic. But it often sheds little light on the underlying normative issues. For it may be that reflection on biomedical enhancement would lead us to realise that even our current ways need mending. Critique of enhancement need not be conservative in a literal sense.

In this chapter, I have tried to argue that ethical questions about the biomedical enhancement of mood are often really questions about our affective reasons, as well as about their relation to other kinds of reasons. These are difficult and, unfortunately, largely neglected questions. Those who entirely dismiss affective reasons, or at least think that negative affective reasons are extremely weak, are likely to see little problem with positive mood enhancers. Those who give great weight to negative affective reasons would see things rather differently. This is not really a debate about the use of biomedical enhancement. It is a substantive normative debate about the form that our emotional lives should take.

Notes

Elliott (2003).

What about the so-called ‘paradox of hedonism’? This is the claim that if we directly tried to maximize our pleasure, this would be self-defeating, because if we were so calculating in the pursuit of pleasure, we would enjoy life far less. But this is an empirical claim. And although it might have some truth when it comes to the active pursuit of pleasant activities, it simply has no hold when it comes to biomedical intervention. If a pill makes you feel better then, by definition, by taking it you will succeed in making yourself feel better. There is nothing self-defeating here.

Isn’t this an over-intellectualized picture of the emotions? You might get this impression if you failed to distinguish reasons and reasoning. We of course do not usually need to engage in any kind of reasoning or inference in order to respond to our affective reasons. Which is not to say that there aren’t difficult situations where finding out what we ought to feel requires careful imaginative deliberation.

Affective reasons can be both moral and non-moral. In what follows I will simply assume that they have intrinsic normative force. It is another question, which I will not consider, whether responding appropriately to our affective reasons also directly contributes to our well-being.

The tie between values and reasons for emotion is closest in the case of so-called ‘thick’ evaluative properties such as cruelty. But it is widely agreed that value generally generates reasons to hold appropriate attitude, including feelings, towards it.

There are exceptions: for example, people sometimes enjoy being angry. Note also that it is of course not emotions per se but feelings—episodes of consciousness—that have such an hedonic dimension.

This is of course in the first instance a priority to our negative affective reasons—to our reasons for feeling negatively-toned affect. But we can also conceive of cases where one’s hedonic reasons give reasons not to feel some positive feeling, because such a feeling would lead to lesser overall pleasure later on. I think that even in such cases we will often see no overall reason to suppress the feeling.

Moreover, there might be a threshold of mental suffering beyond which we might stop giving priority to affective reasons. Think, for example, of cases where we think

Wasserman and Liao (2008) discuss somewhat different issues in connection with what they call ‘duties to have emotions’.

I thus won’t be considering mood enhancers that induce short-lived ecstatic effect—though the extension of the arguments of this chapter to that type of case is fairly straightforward.

There appears to be stronger evidence that existing antidepressants reduce negative emotion rather than directly increase positive emotion, and even this evidence is strong only with respect to more severe forms of depression. But my interest here is in substantive normative questions, not with these empirical issues—including important issues about possible harmful side effects. Notice also that for my purposes, it does not matter at all to what extent the effect of some positive mood enhancers is due to the placebo effect. This is merely a point about the mechanism that produces the affective change. What really matters to us is that there is such an effect, however it is produced.

There is no agreed definition of authenticity, and I do not intend to offer one. For discussion of the problem of authenticity in the context of biomedical enhancement, see Parens (2005).

I first heard this worry raised by Allan Buchanan in his 2008 Uehiro Lectures at Oxford.

Although the President’s Council on Bioethics (2003) is often interpreted as expressing a concern about authenticity, there are many passages in it that are better read as expressing the worry I am discussing here, for example, when they write that we ‘desire not simply to be satisfied with ourselves and the world, but to have this satisfaction as a result of deeds and loves and lives worthy of such self-satisfaction,’ (p. 251) or when they discuss the ‘danger that our new pharmacological remedies will keep us ‘bright’ or impassive in the face of things that ought to trouble, sadden, outrage, or inspire us—that our medicated souls will stay flat no matter what happens to us or around us.’ (p. 255). See also their discussion of grief on pp. 255-257.

Positive mood enhancers are often presented in an unfavourable light compared to psychotherapy. Perhaps it is assumed it is only through psychotherapy that people really develop a genuine appreciation of their positive affective reasons. My response to the ‘mere conformity’ objection should also cast some doubt on this assumption. Indeed, it might even be the case that it is rather some forms of psychotherapy that merely cause people to feel better without improving their responsiveness to genuine positive affective reasons (for example, certain forms of cognitive therapy that focus on reducing negative thoughts might be based on repressing our capacity to respond to our negative affective reasons).

This idea echoes (but is not the same as) the view that evil is merely the privation of good.

This claim should not be understood too strongly. A permanently cheerful demeanour, smiling brightly even when one’s loved ones are suffering or dying, is something we don’t appreciate even in the saintly. The overall balance of positive vs. negative affective reasons ultimately depends on the circumstances we find ourselves in, and these might sometimes be just too bleak. But it seems to me that even in grief, there is reason to give space to the good—say, to fond remembrance of the good in the life of the deceased, and that exclusive focus on the badness of the loss is often mistaken.

Note that I am not claiming that positive mood enhancers are likely to make us perfectly respond (or conform) to what we ought to feel. It might indeed be that, as claimed by the objection, they would cause us to sometimes fail to respond to genuine negative affective reasons. The claim is only that, on balance, positive mood enhancers are likely to make many of us better respond (or conform) to our affective reasons, compared to not taking them.

Indeed, even if such enhancers merely reduced our responsiveness to negative affective reasons (whether genuine and illusory), and did not directly increase positive affect, this would still shift our overall affective orientation upwards, and leave more space for positive emotions.

Goldsmith (1983); Tellegen et al. (1988).

Brickman, Coates, & Janoff-Bulman (1978); Fujita & Diener (2005).

Note I am not claiming here that, for example, people ought to feel deeply unhappy if they become severely disabled. I am only claiming that most people believe that such a condition is a grave misfortune that merits such a response. The empirical findings on adaptation at the very least show that we are not responsive to what most people take to be very strong affective reasons.

For discussion of the implications of this particular finding, see Moller (2007).

Although the phenomenon of adaptation is extensive, I don’t want to give the impression that it is all encompassing or insurmountable. There are negative things to which people do not adapt to—these include physical pain and continuous noise. And although people’s subjective well-being does largely adapt even to severe disability, they do not always completely regain their prior levels of subjective well-being. Finally, close personal relationships and other factors do seem to have a positive long term effect on subjective well-being. For discussion, see Diener, Lucas & Scollon (2006).

Some people are made more emotional by alcohol—but being generally more emotional is not the same things as being more accurately responsive to one’s affective reasons.

Bibliography

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Diener, E., Lucas, R. E., Scollon, N. C. (2006), ‘Beyond the Hedonic Treadmill: Revising the Adaptation Theory of Well-Being’, American Psychologist, 61 (4), 305-314.

Elliott, C. (2003), Better Than Well: American Medicine Meets the American Dream, Norton, New York. 

Fujita, F., & Diener, E. (2005), ‘Life satisfaction set point: Stability and change’, Journal of Personality and Social Psychology, 88, 158-164.

Goldsmith, H. H. (1983), ‘Genetic influences on personality from infancy to adulthood. Child Development, 54, 331-355.

Moller, D. (2007), ‘Love and death’, The Journal of Philosophy, 104, 301-316.

Parens, E. (2005), ‘Authenticity and Ambivalence: Toward Understanding the Enhancement Debate,’ The Hastings Center Report, 35 (3) 34-41.

President’s Council on Bioethics (2003). Beyond Therapy, Regan Books, New York.

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