Mental disorder is a cause of crime: what is meant by "cause"?

In psychiatric terminology, behaviour is considered an aspect of the mental. The easiest way to deal with the relationship between mental disorder and crime would therefore be just to consider criminal acts to be a form of mental disorder. This stance has never been met with much enthusiasm, however, neither in clinical psychiatry, nor in science or jurisprudence.

Thought of as two distinct phenomena, the connection has been postulated as leading from mental disorder to crime and to be, at least in some respect, causal. At the same time, it is evident that causation in this context cannot mean that mental disorder is a necessary or sufficient cause of crimes.

Modern medicine has increasingly come to work with probabilistic models. Probabilistic theory defines the relation between “risk” factors and effects as an increased probability of the effect in the presence of the risk factor (cf. Reichenbach, 1956; Cartwright, 1979). In our context, probabilism would mean that particular forms of mental disorders are likely to be associated with particular forms of criminal acts. The risk factor may then be assumed to be a (full or partial, see below) cause of the event (meaning that causation is “attributed” to the factor) if there is a temporal relation so that the risk factor can be shown to generally precede the effect, if covariation with other factors (referred to as “confounders”) can be accounted for by logistic or other multivariate statistical models, and if reasonable models are at hand for understanding how the causation operates. 

In other cases, risk factors can be judged to be coincidental to or reflections of common causes. By using probabilism in this way, scientific exploration has been made possible beyond experimental models testing causation. The terms “risk” and “risk factors” are assigned to the cardiologist Dawber (Kannel, Dawber, Kagan, Revotskie & Stokes, 1961) as a model to identify background factors, such as elevated blood pressure, cholesterol, and smoking, behind coronary heart disease. They have become central to medical research and have even come to represent a paradigmatic feature of today's society (Beck, 1992). The concept of risk is therefore a means of avoiding statements of causation, and “explanatory value” in this context will mean “proportion of the variation statistically related to the variation in the risk factor”, which does not necessarily “explain” it in the common, causal meaning of the word.

In the vast majority of those afflicted, mental disorder does not lead to crime. A possible definition of causation in this context would therefore be that a mental factor is a cause of a crime if the mental factor is an insufficient but necessary part of a set of conditions that together are unnecessary but sufficient for the crime (a so-called INUS condition, Mackie, 1965, 1974). Suppose, for example, that a lit match causes a forest fire. The lighting of the match is not by itself sufficient; many matches are lit without bringing about forest fires. But the lit match is in this case a part of a constellation of conditions that together are sufficient for the fire. The match was dropped on a pile of dry leaves, and a gust of wind contributed to the lighting of the fire. Each of the components, the match, the pile of leaves, and the wind, is an INUS condition, each was insufficient, each was necessary, and all together were sufficient for the forest fire, even if other sets of conditions also could have led up to the same effect.

Counter-factuality is thus a prerequisite for a factor to be an INUS condition under the given set of conditions (it should be possible to conclude that “if the mental factor had not occurred or been present, then the crime would not have occurred”, cf. Lewis, 1973; Mackie, 1965, 1974). From this follows manipulability, that it is possible to change the effect or the probability of the effect by changing the cause.

Mackie’s model provides a useful framework to deal with causation behind complex human behaviours such as violent crime. The way we attribute causation even in the sense of INUS conditions in complex chains of events has to be considered. Singling out one of the INUS conditions as the cause of a certain event is often a matter of choice and not based on rigorous scientific investigations. Since each factor, by definition, forms a necessary part of the overall condition, we do not really have any grounds for pinpointing one of them as contributing to the effect to a higher degree than the others. 

Human minds, however, strive to attribute causes in order to be able to predict what will happen in the future. Only in very rare instances are such attributions of causation based on experiments or strict, logical deductions. As the factors that may be shown to cause human actions in the INUS sense are invariably numerous and interact in complex constellations, the way we identify causes and assign importance to them is in itself the object of psychological research (Cheng, 1997).

As for crime and punishment, there is every reason to believe that mental disorders attract undue attention among possible explanatory factors. Generally, we have a strong tendency to assign causation of undesired events to factors that are strange or exotic in relation to ourselves, classically to other ethnic groups or to people with features that in one way or the other make them different from us. This powerful force directs our attention towards mental disorders among all the possible INUS conditions that may be discerned in the background to a crime. 

In forensic psychiatric research and expert opinion, the attribution of causation has no doubt been influenced by ideas developed within the professional psychiatric paradigm. And for the causation that is to be judged by the lawyer, counter-faction will be non-informative. How could any mental condition (i.e. inner experiences, cognitions, and/or behaviour patterns) be ruled out as a contributing factor in the very complex sets of factors influencing human action?

This blog post is to a large extent excerpted from the paper "Mental disorder is a cause of crime" I co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. 

The mind and the body in (forensic) psychiatry

Throughout the history of human thought, few other distinctions have evoked so much controversy as the one between the mind and the body. In the DSM-IV-TR, it was regretted that the term “mental disorder” emphasizes mental as something distinct from physical, which is regarded as an “anachronism of mind/body dualism” (APA, 2000, p. xxx).

Causation is key to understand the relation between the mind and the body. The body influences the mind (most clearly shown by drug effects), but the jury is still out on whether the mind can influence the body. 

Material determinists deny that it can, mainly based on the lack of a reasonable mechanistic explanation. 

Bi-, or rather multi-directional causation body>mind>body>mind etc, is, however, indicated by e.g. real-life experiences of acts of will, the placebo effect and the influence of expectations on health.

This conflict partly stems from epistemology. The mind is considered in terms of “experience”, “knowledge”, and “being” that are distinct from how the brain and its physiological processes are conceived of. Different types of knowledge are difficult to join in a common model, even if the clinical psychiatrist approaches a person who happens to have a body and a mind.

And different ways of aquiring knowledge do not exclude that information refer to the same underlying phenomenon. 

Just as a notion of beauty may be applied to the same body that is scientifically examined as an organism, and perhaps to some extent even be causally determined by it (correlations between notions of beauty and physiological processes may be assumed), it is obvious that notions of beauty and of physiology operate according to different epistemological premises. The means by which we decide upon aesthetical matters are not the same as those we use in the natural sciences, nor are the concepts used in the different contexts inter-translatable in a straight-forward sense. The use of a plurality of concepts and methods does not in itself imply a plurality of real world items.

In order to meet medical or legal definitions, mental disorder are thought to refer to the form (processes, abilities) rather than the content (subjective experiences, as defined by Jaspers). The form is intuitively thought of as being more "brain-based" than the content. 

This remains an attractive idea. It is a common assumption in psychiatry that there are "real" mental disorders rooted in cerebral malfunctioning, and other, less severe conditions, which are more related to the person and her choices, life-style and experiences. 

But from the perspective of neuroscience, it makes little reason to think that one mental problem should be less "brain-related" than another. The body and the mind are intrinsically linked, mysteriously even.

The epistemological framework of psychiatry does not produce the concepts or the data that can give an answer to what is freely willed, morally good or bad. Science studies regularities, and acts of free will are unpredictable. Therefore, notions that presuppose freedom (such as evil) escape scientific explanations. Needless to say, this does not prevent the consequences of mental processes, e.g. behaviours, to be objectively good or bad.

As long as we do not know how the body and the mind interact to create a human person, nor whether determinism is true or there is a causal effect of free choices, scientific expertise for courts should be carefully worded to express what we know and what we don't know, and to refer to the findings of assessments rather than to legal or moral definitions that presume free will.

Medical conditions can preclude free choice and insight, but medicine cannot say that a specific act was done freely. This does not mean that a judge can't.  

This blog post is partly excerpted from the paper "Mental disorder is a cause of crime" co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. 

Mental disorder is a cause of crime

The next couple of entries in the Forensic Friday series will continue the series on causation by addressing the notion that “mental disorder is a cause of crime”. This statement is really the foundation of forensic psychiatry. 

If mental disorders do not cause crimes, why should we have forensic psychiatry at all? After all, we don't have forensic internal medicine for diabetics who commit crimes, even if they may have done so during hypoglycaemia and need treatment while serving prison.

In coming posts, we will look at the historical roots of forensic psychiatry and adress each of the definitions “mental”, “disorder”, "cause" and “crime” conceptually, epistemologically, and empirically. The blog posts will be based on the paper "Mental disorder is a cause of crime" I co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. Without the collaborative work behind that paper, I wouldn't have been able to write any of the following texts. Many of them will be expanded and up-dated versions of paragraphs from the paper.  Of course, my version of philosphical analysis is over-simplified and not up to the level of my colleagues from philosophy, but I write this from the perspective of a clinician. On the other hand, I will go deeper into empirical data and try to sum up the considerable developments we have seen since 2009. 

Neither “mental”, “disorder” or “crime”, nor the “causation” implied, are clear-cut concepts. “Mental” denotes heterogeneous aspects of a person, such as inner experiences, cognitive abilities, and behaviour patterns, described in a non-physical vocabulary. In psychology and psychiatry, “mental” describes law-bound, caused aspects of human functioning that in some respect are predictable and generalizable. A corner-stone in these sciences is behaviour, as it is the easiest aspect to observe and quantify, and in itself contains a better-than-chance prediction of future behaviour. Indeed, even interviews and other more clearly “mental” assessments focus on reporting behaviours rather than “inner” mental processes.

Problems defined as “disorders” seem to be end-points of dimensional inter-individual differences rather than natural categories.

Deficits in cognitive faculties, such as attention, verbal understanding, and reality assessment, may be susceptibility factors that relate to behaviours, such as crimes, as risk factors in the sense of increasing the probability for a specific negative behaviour, and/or as causes in the sense of INUS conditions (insufficient but non-redundant parts of unnecessary but sufficient conditions).

Neurobiological measures (e.g. regional brain activity, neurotransmitters, genetics) may be related to crimes in a similar way as assessments of mental health problems or cognitive faculties.

Attributing causation to behaviours is not unbiased, and factors we feel estranged from, such as mental disorders, tend to attract disproportionate attention in explaining abject behaviours, such as crimes. 

When a forensic psychiatrist testifies in court, (s)he may describe mental health assessments, effects on accountability and ability, but the court and laypersons will understand what is said in terms of “causation”. Sometimes we are either lead to or volunteering to proffer an opinion on causation per se. I hope that this blog series will clarify what we can know and what we can’t know about whether mental disorders cause crimes based on psychiatry and psychology. To be continued.

Genetic causation in mental health and behaviour /cont./

Let’s take another look at heritability and genetic causation. I go on ranting on this topic as we so often hear that this or that is “highly heritable” or “mostly caused by genes”. For complex conditions, these claims are made based on estimates of heritability (see last week’s post).

Heritability is generally calculated as the difference in concordance (i.e. that both twins share a feature) between monozygotic pairs (who share 100% of their genes or almost) and dizygotic pairs (who are no more alike than any pair of siblings, sharing on average 50% of genetic variation). Tripartiate models assign percents of the population variance to genetic, shared environment or unique environment effects. Shared environment is non-genetic effects that make the twins more similar, unique that which makes the individuals more different.

But let’s focus on one aspect of twin research: monozygotic pairs who are concordant or discordant for a feature. They share almost all their genetic information, even if each individual may have unique de novo-mutations. If one of the twins has a certain feature, what is then the probability that his/her sibling also has it? This is answered by the pairwise or proband-wise concordance rates. Pairwise looks at each pair just once, while proband-wise counts concordant pairs twice (as both individuals with the feature are counted once as proband and once as sibling). The latter is often preferred for statistical reasons, but the former gives us a more accurate view to understand causation.

Pairwise concordance looks at pairs in which at least one of the twins is affected. Given that the co-twin will have the same genes and, to a fair extent, the same environment, his/her probability of having the phenomenon under study will be an easy-to-grasp measure of its overall predictability, the degree to which it is caused by shared factors.

First, we will see that the overall prevalence of the phenomenon in the population will influence the results. Naomi Wray and Robert Maier put it like this in a recent review:

“For example, for a disease with lifetime prevalence of 1% and heritability of 80%, less than half of cases are expected to report family history when considering all first, second, and third generation relatives (Yang and co-workers, 2010). Likewise, for the same disease more than 60% of monozygotic twins are expected to be discordant for disease status (Smith, 1970).“

Sebastian Lundström recently mapped all twin pairs with an autism spectrum disorder in the Child and Adolescent Twin Study in Sweden (CATSS). Autism is often cited as one of the most heritable conditions in psychiatry, and indeed among all complex conditions in medicine, with a heritability of 80%. How many affected monozygotic siblings of a proband with autism did we find? Thirty-nine percent. This means that the causation from genes to mental disorder is not straight-forward. It is wrong to assume that genetic causes of autism will add up to explain 80% of all autism, or that a person with autism is doomed by his/her genes to go on having autism in 80% of cases, or to 80% of the present degree.

But genes do matter. Not only did they rise the risk of autism 30 times or more, they also predicted other types of early-onset mental health problem in nine out of ten siblings. If you share your gene set-up and early environment with someone who has autism, you have a small chance of being completely healthy.

One possible explanation to this finding is that genes interact on a “final common pathway”, which can give rise to many different forms of health problems. I will go into this possibility at length later in the series.

Take-home message: genes matter, but genetic causation is much less clear-cut than assumed in statements such as “autism is 80% genetic”. The enigma of the “missing heritability” is not so enigmatic after all, but results from a simplified translation of heritability estimates to causal pathways.

Heritability estimates: do they equal degree of genetic causation?

This is the first entry in a series on causation, mental problems and criminality that will run on the blog for the next month or so as Forensic Fridays. This first entry will deal with genetics and what can be inferred from heritability estimates. The series will start broadly with causation in neuroscience and behavioural sciences and later focus on forensic psychiatry and the use of mental health expertise in courts of law, where sometimes diverging understandings of causation come to the fore.

Almost every type of behaviour, personality trait or liability for mental health problem that has been subjected to family studies (esp twin studies), has been shown to be to some extent under genetic influence. The proportion of the population variance ascribable to genetic effects is usually between 40 and 80%, with the higher end of the range reserved for narrow phenotypes such as autism, schizophrenia or bipolar disorder. Personality traits typically come in around 50%, while some behaviour patterns are higher, like persistent aggressive antisocial behaviours at 65% (Burt and coworkers, 2009). The great value of this research is that it has proved beyond any reasonable doubt that life is unjust (as if we hadn't guessed before, but the blank-slate model was actually commonly defended not that long ago ). Humans indeed come into the world differently equipped and have different possibilities of abstaining from substance abuse, violence and other destructive behaviours. Let this inspire some humility in all of us.

But then things get less clear-cut. Very few gene variants that account for more than a percent of the variance have been identified, and, even when combined, such effects amount to far less than the heritability calculated in family studies. This is referred to as the “missing heritability”. But why has it been so hard to identify the responsible gene variants? There is a high degree of complexity in the integrations between genes (meaning that each carries a small effect size on the group level but may exert large effects in specific families or individuals), there are epigenetic modifications, gene x environment interactions and many other possible explanations.

But did a heritability of, say, 65%, ever mean that 65% of the causation behind the phenomenon under study was genetic? No, it didn’t, it just said that 65% of the difference in liability across a given population at a  given time could statistically be referred to genetic effects. Consider this: over history, sociocultural changes have had very large effects on, for example, violence. The introduction of a strong state in the 15-17th centuries reduced violence by factors of 10 to 100. During such a time frame, very little genetic change happened. Yet the spectrum of violence in society changed dramatically.

Or take the example of height. If nutrition is lacking, people will be of short stature. Then, genetic effects will be smaller, as the general growth is hampered by an environmental factor and the overall variance is constrained. But when nutrition is adequate, the role of genes in the total variance will be larger. Children of tall parents will be much taller than children of shorter parents. But wouldn’t this also mean that nutrition is the main cause of someone attaining his/her adult height? 

So, for this week, heritability means that the variation of something in a population is under genetic influence - but it does not measure the degree of genetic causation for the phenomenon per se. Therefore, the missing heritability may not be such an enigma after all. There was never any reason to believe that it would be easy to identify the genes behind non-Mendelian, partly heritable behaviours or health problems.