Exploring Psychiatry and the Human Condition: Joanna Moncrieff, MD

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CONVERSATIONS IN CRITICAL PSYCHIATRY

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo.

Joanna Moncrieff, MD, is professor of critical and social psychiatry at University College London and works as a consultant in community psychiatry in London. She has researched and written about theories of drug action, drug efficacy, the subjective experience of taking psychiatric drugs; decision-making; the history of drug treatment; and the history, politics, and philosophy of psychiatry more generally. She is currently leading a United Kingdom (UK) government-funded study of antipsychotic reduction and discontinuation, called the RADAR study (Research into Antipsychotic Discontinuation and Reduction). She is one of the founders and the co-chairperson of the Critical Psychiatry Network. She has authored numerous papers and several books including The Myth of the Chemical Cure (Palgrave Macmillan, 2008); The Bitterest Pills: The Troubling Story of Antipsychotic Drugs (Palgrave Macmillan, 2013); and A Straight-Talking Introduction to Psychiatric Drugs (PCCS Publishers, 2013).

Moncrieff’s views on psychopharmacological mechanisms of action, although controversial, have been influential within the critical psychiatry community. We have discussed some implications of the drug-centered model in an earlier interview with Sandra Steingard, MD. Moncrieff’s ongoing randomized controlled trial investigating the long-term impact of gradual antipsychotic dose reduction and discontinuation in schizophrenia on outcomes such as psychotic relapse and social functioning (versus maintenance treatment) could alter how the field approaches management of chronic psychotic disorders.

Awais Aftab, MD

Joanna Moncrieff, MD

This interview, however, largely focuses on conceptual concerns, exploring her views on the nature of psychiatric suffering. My first conscious exposure to Moncrieff was at the 2017 annual meeting of the Association for the Advancement of Philosophy and Psychiatry, where Moncrieff gave the keynote lecture titled “Many Ways of Being Human,” in which she challenged the medical view of mental disorders and argued that medical and psychiatric conditions have a different relationship to agency, responsibility, and selfhood.

Moncrieff's ideas carry on the legacy of Thomas Szasz, MD, and given my own disagreements with how Szasz conceptualizes the notion of disease, this interview also represents an attempt on my part to understand how deep our philosophical disagreements go.

The article in Philosophy, Psychiatry, & Psychology referred to by Moncrieff was in press at the time this interview was conducted but has since been published online. I would also like to add that there is a large body of literature critically engaging with the ideas of Thomas Szasz, such as the 2019 book Thomas Szasz: An Appraisal of his Legacy (International Perspectives in Philosophy and Psychiatry; 2019), which I would encourage readers to explore.

AFTAB: Can you briefly tell us about the Critical Psychiatry Network? Its mission and how it has impacted British psychiatry over the years?

MONCRIEFF: When I was a trainee in psychiatry, I felt the way psychiatry was portrayed in the mainstream—in textbooks and medical journals—did not match my ideas about the nature of mental health problems or my experience of individuals who were deemed to have such problems. I was aware that other trainees felt like this too, so I started a club while I was at the Institute of Psychiatry in 1997. Initially we had discussions about interesting books and articles, and then we organized meetings, in conjunction with the Maudsley Hospital service-users group, with outside speakers, including the likes of Szasz, Nikolas Rose, PhD, and Andrew Scull, PhD. Around this time, we were contacted by some psychiatrists from another part of the UK, who were concerned about the upcoming review of the Mental Health Act. We got together to submit evidence to this review, and that was the start of the Critical Psychiatry Network. Since that time, it has functioned as a forum for mutual support, and as a mechanism for contributing a critical view of psychiatric practice to various parliamentary and governmental reviews, the media, and other organizations. Have we had any impact? I think the fact that members of the psychiatric profession are challenging mainstream views, particularly the dominance of the biological paradigm in psychiatry, is important, and helps to support broader movements that are trying to imagine and establish alternative approaches.

AFTAB: Models of drug action have been an important focus of your work—in particular, the distinction between the disease-centered model and drug-centered model. In the disease-centered model, drugs help correct an abnormal brain state and the therapeutic effects of drugs are derived from their effects on an underlying disease process. In the drug-centered model, drugs are psychoactive agents that create an abnormal brain state, and therapeutic effects are derived from the impact of drug-induced states on behavioral and emotional problems. Can you elaborate for us how ignoring this has distorted our understanding of the treatment of psychiatric conditions and has biased our assessments of risks and benefits?

MONCRIEFF: The assumption that drugs work by acting on the underlying biological mechanisms of mental symptoms, the disease-centered model, has obscured the fact that the drugs we use in psychiatry are psychoactive drugs—that is, drugs change the brain in ways we do not fully understand and, by doing so, produce more or less subtle alterations to normal mental experiences and behavior—what I have called the drug-centered model of drug action. Because we have ignored the fact that psychiatric drugs are psychoactive substances, we have not bothered to properly research or even describe the physical and mental physical alterations they produce and all the short- and long-term consequences of these. Therefore, we are not making fully informed assessments of the benefits and harms of drug treatment, and because we assume we are rectifying an underlying abnormality, we tend to over-estimate the benefits of treatment and understate its harms.

Although I think there are some situations in which some drugs can be useful—eg, antipsychotics in acute psychosis, benzodiazepines in acute agitation—this has led to millions of individuals who are taking drugs that are doing them little or no good, but are causing them harm; both harm that we know about and harm that we have not properly researched yet.

AFTAB: I wonder if the disease-centered model conflates instances of disease processes with biological mechanisms. Let us consider a thought experiment. Assume that in patient A, biological mechanism X mediates the subjective experience of anhedonia. We are not qualifying mechanism X as an abnormality or disease, we are simply saying that it is a mechanism, among others, of generating anhedonia. Patient A takes a medication M, which has a direct action on X that leads to an improvement in anhedonia. Again, we are not saying that M is fixing an abnormality in X, just that it has a direct action on mechanism X. In this thought experiment, M is neither correcting a disease process nor is it producing a therapeutic effect indirectly from a drug-induced state; it is producing a therapeutic effect by a direct action on a mechanism that is not necessarily abnormal but is nonetheless directly involved in the experience being targeted. How would your framework incorporate such hypotheticals?

MONCRIEFF: I think I make it clear in my writings that the disease-centered model I have outlined is not restricted to what we think of as diseases, especially as the use of this term in psychiatry is not clear-cut. The disease-centered model consists of the idea that drugs work by targeting underlying biological mechanisms that produce what we call the symptoms of mental disorders. Hence, your thought experiment is an example of the disease-centered model as I have noted.

My response to your example is this: First of all, we have no idea what biological mechanism mediates anhedonia or almost any other subjective experience. The idea that we can pin down the biological mechanisms of complex human thoughts, feelings, and behaviors is part of the problem with our thinking. We cannot do this now, and we have no indication that we will be able to do so in the future—a view put forward in critical neuroscience too, by the way.^1-3

Second, if you give a drug that affects mechanisms P, Q, R, S and some others, and through its action produces an altered mental state in anyone who takes it regardless of diagnosis, allowing for individual variation, you will get some impact on emotions, including feelings of anhedonia. This may involve mechanisms related to anhedonia, including your hypothetical mechanism X, but it may not, since any significant alteration of mental state and activity will affect emotions in some way. Now this is a drug-centered action, and this is what I propose is happening when we use psychiatric drugs.

We recognize the fact that psychoactive substances such as alcohol and heroin change our mental states and can therefore interact with unwanted mental states and feelings. We talk of using alcohol to drown our sorrows, but we do not consider alcohol to be targeting the biological basis of misery in any specific way. When we recognize that psychiatric drugs have psychoactive properties, then we can start to understand what they are doing in individuals who suffer from mental health problems, and we can start to make a thorough and informed judgement about the pros and cons of using them.

AFTAB: When you say, “The idea that we can pin down the biological mechanisms of complex human thoughts, feelings, and behaviors is part of the problem with our thinking in my view. We cannot do this now, and we have no indication that we will be able to do so in the future,” do you say that in an epistemological sense, that is, reflective of the limits of human knowledge and understanding, or do you say that in an ontological sense, that is, you do not think that complex human thoughts, feelings, and behaviors are mediated by biological mechanisms? By mediate I mean that biological mechanisms are part of the causal chain that eventually generates human thoughts and behaviors; I am not implying that human thoughts and behaviors can be reduced to or entirely explained by biological mechanisms.

MONCRIEFF: It depends what you mean by mediate. The Wittgenstein scholar, Peter Hacker, PhD, puts this issue well. For Hacker, the mind is a set of capacities of the human organism, like Aristotle’s psuche or psyche. The human brain working as a whole is necessary to generate these capacities, but individual mental processes cannot necessarily be pinned down to specific brain mechanisms. Think of emotional states like anger, elation, anxiety, and fear. They are all associated with increased adrenaline and other arousal mechanisms, but they have their own character, and this character derives from how the individual appraises their worldly situation, not from the nature of the biochemical or physiological reactions.

AFTAB: You give the example of opioid medications as having disease-centered effects as well as drug-centered effects. Given that our understanding of causal mechanisms of serious mental illness as well as mechanisms of drug action is less than comprehensive, how do we know that such dual effects are not the case in at least some individuals with serious mental illness? Because that is an empirical matter, I do not think we can rule this possibility out on an a priori basis.

MONCRIEFF: There are many things we cannot rule out, but that does not mean they are useful ideas. The drug-centered model provides an adequate explanation of drug action in mental disorders. There is no need to postulate a hypothetical disease-centered action alongside it.

AFTAB: What is your view of the philosophy of psychiatry literature that has emerged, in great part thanks to British academics such as Bill Fulford, PhD, and Tim Thornton, PhD? I am particularly thinking of the body of work that is devoted to questions of whether the boundary between supposedly normal and pathological can be drawn on the basis of objective, scientific facts, and what is the relationship between meaning and disease, ie, Derek Bolton, PhD; and how to best understand and explain causal mechanisms in psychiatric conditions, ie, Ken Kendler, MD, and Peter Zachar, PhD. This body of work seems to have great relevance to your interests; have you engaged with it in your writings?

MONCRIEFF: I have followed the work of Fulford and, to a lesser extent, the others you mention in detail over the past few decades and I am about to have a paper published in the journal Philosophy, Psychiatry, & Psychology that responds to their work.⁴ However, I think it was Szasz, who I met a couple of times in my life, who identified the main problem with psychiatry, and few modern philosophers seem prepared to engage with his core arguments, with the exception of Fulford.

For Szasz, there is a key distinction between a condition of the body and a situation that is characterized by self-directed, human behavior, as opposed to involuntary behavior caused by a biological process or event. In this, he follows antipositivist philosophers, including the later work of Ludwig Wittgenstein, PhD, who stress the differences between the natural world and the human world, and how these entail different forms of knowledge. Szasz argues that psychiatry mostly deals with self-directed behavior and is therefore different from other parts of medicine that deal with bodily conditions.

Much of the psychiatric establishment clearly agrees with Szasz’s distinction, because it wants to demonstrate that psychiatry too deals with bodies—or more specifically brains—and that psychiatric disorders are, in fact, brain diseases. I agree with both Szasz and the biological psychiatrists that it is important to know whether behavior is the direct result of a specific biological mechanism or not. However, I do not think research that finds a slightly higher rate of this or that biological feature in the brains of individuals with a psychiatric diagnosis compared to allegedly healthy controls demonstrates that mental disorders originate in the brain, as opposed to in the individual’s agency or character.

But I also do not think that the behavior that characterizes some mental disorders is quite the same as fully volitional behavior as Szasz suggests. The thinking and behavior characteristic of psychosis, for example, is not rational in a clear-cut way. Individuals with psychosis do not respond to environmental cues and evidence in the usual way, and their purposes are not easily and immediately discernible to others. They may not have as much control over their behavior as individuals ordinarily do, either.

Although the behavior we associate with mental disorder is not simply the same as everyday behavior, I do not think it is distinct either. It is not a biological reflex, and therefore it can be viewed as part of the self or character, just as other, more clearly voluntary behavior is. This is why I refer to mental disorder as “part of the range of ways in which human beings live within, and interact with, their world.”⁴

AFTAB: What about psychological experiences that are involuntary, unwanted, and distressing, such as auditory hallucinations and obsessions? At least in some instances, they are perceived to be intrusive and threatening to their sense of selves and lead to help-seeking behaviors. Do you think of those experiences as parts of the self or reflective of the individual’s values, desires, and intentions?

MONCRIEFF: This is a good question, and it highlights the complexity of our human nature, which I cannot do justice here. Certainly, some mental processes are not straightforwardly voluntary. Our moods and emotions, for example, are not brought on at our demand. Yet, although feelings are usually unbidden, we can nevertheless usually exercise some control over how we behave in response to them, and, often, with time and experience, over the feelings themselves. In the normal course of things, we see our moods and emotions as being part of ourselves or our character. As I put it in my recent paper “the way we express our emotions is part of what is characteristic about us as individuals.”⁴

Many symptoms of mental disorders, including extreme or prolonged moods, but also obsessional thoughts and hallucinations, are of the same nature. Individuals who end up in services may find their experiences difficult to resist and control, but that is true to some degree of many mental states and does not mean they are simply the meaningless byproducts of biological events.

AFTAB: We know that psychosis can occur in conditions such as Parkinson disease and Alzheimer disease, and there are phenomenological similarities between psychosis in these instances and the psychosis experienced in schizophrenia. I assume you consider the former pair to be diseases but the not the latter. If we restrict ourselves to examining the psychotic experiences only, without considering the concomitant presence of motor or cognitive symptoms, is there anything in the nature of these psychotic experiences that tells you whether they should be considered a disease or not?

MONCRIEFF: Physical states can occasionally mimic psychological ones. Thyroid hormone deficiency is famously said to cause depression. Often there are some phenomenological differences, but probably not always. Amphetamine abuse can cause psychosis. Again, there are some phenomenological differences if you were to look at a group level, but you cannot necessarily distinguish amphetamine-induced psychosis from an idiopathic psychotic episode on the basis of symptoms alone. However, this does not mean that the majority of instances of psychosis and depression are of the same nature.

As I have said before, many philosophers have pointed to how human emotions and mental states cannot be understood in a mechanical sense as isolated phenomena or events. They are intrinsically connected to the whole life history and experience of the individual, and the society in which that individual has grown up. Whereas thyroid deficiency may provide an adequate explanation of an episode of depression brought on by hypothyroidism, and thyroid hormone will usually provide an adequate treatment, an episode of depression has to be understood and treated in quite a different way, as a human reaction that requires a human-level response.

AFTAB: You seem to suggest that if a behavior or experience can be seen as a meaningful response to experiences, environment trauma, social alienation, and so on, then it should not be considered the product of a brain disease. Two questions: One, human minds are great at conjuring explanations where none may exist. How can we ensure that our attributions of meaning are not simply instances of creative storytelling? Second, there is no philosophical reason why meaning and biological abnormalities should be considered mutually exclusive. Someone who is experiencing paranoia as a result of cocaine use can still find that paranoia as imbued with meaning and distorted reason, but there is no denying that it was the result of a brain aberration. Your thoughts?

MONCRIEFF: We can never be sure about meaning. It is not a categorical thing—this is one of the many aspects in which the activity of human beings differs from the natural world and the form of our understanding needs to reflect this difference. Psychotherapy is premised on the idea that meaning is opaque and contested. The therapist’s interpretation of feelings and events may be quite different from the subject’s and this is not an arena where we can ever know the truth as we know it in a physical science.

I take issue with your statement that “there is no philosophical reason why meaning and biological abnormalities should be considered mutually exclusive,” and I argue this point in my recent paper.⁴ We are biological beings, and our behavior and activity is reflected in our biology, so of course “meaning and biological abnormalities” coexist. Yet, when we think of behavior, biological causation trumps meaning and agency. If an action—a twitch or a seizure, for example—is caused by a biological process, this removes it from the realm of agency. It does not make sense to think of an action as both caused by a biological reflex and initiated by the self in an intentional fashion. They are mutually incompatible situations.

Biological processes are not meaningful, but biology is the context in which human agency takes place, and it sets the limits of possibility. Individuals with intellectual disability, Alzheimer disease, or other brain diseases may make meaningful choices, but their agency is circumscribed, as it is for all of us, by the nature of their brains. And so it is for those under the influence of substances. The biological limitations are not meaningful in themselves, but within these limits, individuals may still be able to make choices and act in an intentional fashion. However, the extent to which behavior is driven, changed, or limited by a brain disease is not meaningful.

As I show in my recent philosophical paper, Szasz was trying to highlight how this distinction plays out in the difference between disease and behavior. Only when behavior is the product of a specific physical process, such as a brain tumor, can it be thought of as the symptom of a disease, and in this case, it is not meaningful. Otherwise it is part and parcel of the individual’s character; it reflects the individual’s values, desires and intentions—in other words it has meaning.

AFTAB: When it comes to schizophrenia, a large body of research literature shows that there is a robust genetic component, that there are well-replicated associations with obstetrical complications, infections, inflammatory processes, cannabis use, and as a group, individuals with schizophrenia show differences in brain volume and cognitive functioning. I agree, there is no specific abnormality of brain structure or function, but there is a range of non-specific neurobiological factors that have been implicated as risk factors on a consistent basis. If schizophrenia was merely a problem in living or a different way of being human, why would we observe this risk factor profile in research studies?

MONCRIEFF: I would put it another way. Despite decades of extremely well-funded research, we have yet to identify any specific biological factor associated with any type of mental disorder, including schizophrenia. There is a genetic component to many things, and it is likely this includes some aspects of character or temperament that are associated with developing schizophrenia. As far as other research goes, despite what you and others say, findings are not well replicated, and the research has failed to control for crucial confounding factors such as drug treatment, social class, stress, and IQ.

There are myriad reasons why individuals who show unusual behavior that is classified as schizophrenia are likely to have higher rates of obstetric complications, inflammatory markers, dopamine abnormalities, drug use, etc, when compared with stable, employed, middle class individuals that become the normal controls in biological studies. The most consistent and well-replicated finding in individuals with schizophrenia is the evidence of smaller brain size and larger brain ventricles, yet after years of talk about “schizophrenic brains,” it transpires that this is, at least in large part, caused by antipsychotic drug treatment.

AFTAB: Thank you!

Conversations in Critical Psychiatry’s aim is to engage prominent experts within and outside the profession who have made meaningful criticisms of psychiatry and have offered constructive alternative perspectives to the current status quo. The opinions expressed in the interviews are those of the participants and do not necessarily reflect the opinions of Psychiatric TimesTM.

Dr Aftab is a psychiatrist in Cleveland, Ohio, and clinical assistant professor of Psychiatry at Case Western Reserve University. He is a member of the executive council of Association for the Advancement of Philosophy and Psychiatry and has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry. He is also a member of the Psychiatric Times^TM Advisory Board. He can be reached at awaisaftab@gmail.com or on twitter @awaisaftab.

Drs Aftab and Moncrieff have no relevant financial disclosures or conflicts of interest. Dr Moncrieff discloses that she is the cochairperson of the Critical Psychiatry Network, a board member of the Council for Evidence-Based Psychiatry, chief investigator on the RADAR study of antipsychotic reduction funded by the UK government’s National Institute of Health Research (NIHR) and co-investigator on the REDUCE study of antidepressant discontinuation also funded by the NIHR.

An extended version of this article was posted online ahead of print as Psychiatry and the Human Condition: Joanna Moncrieff, MD. -Ed

References

1. Bennett MR, Hacker PMS. Philosophical Foundations of Neuroscience. Blackwell Publishing; 2003.

2. Nachev P, Hacker P. The neural antecedents to voluntary action: a conceptual analysis. Cogn Neurosci. 2014;5(3-4):193-208.

3. Tallis R. Aping Mankind: Neuromania, Darwinitis and the Misrepresentation of Humanity. Acumen Publishing; 2011.

4. Moncrieff J. “It Was the Brain Tumor That Done It!” Szasz and Wittgenstein on the Importance of Distinguishing Disease from Behavior and Implications for the Nature of Mental Disorder. Philosophy, Psychiatry, & Psychology. 2020;27(2):169-181. ❒