Comorbidity, defined as the simultaneous occurrence of more than one disorder in a single patient, is commonplace in psychiatry and somatic medicine. In research, as well as in routine clinical settings.
In March 2016 the new H2020 collaborative project “CoCA” (Comorbidity in adult ADHD) was officially launched, with a 3-day kick-off meeting in Frankfurt, Germany. This ambitious project, which is coordinated by professor Andreas Reif and is co-maintaining this shared blog, will investigate multiple aspects of comorbidity in ADHD.
For instance, CoCA will “identify and validate mechanisms common to the most frequent psychiatric conditions, specifically ADHD, mood and anxiety disorders, and substance use disorders (SUD), as well as a highly prevalent somatic disorder, i.e. obesity”.
As reflected in this bold mission, most scientists trained in the biological sciences agree that studies of overlapping and concurrent phenomena may reveal some underlying common mechanisms, e.g. shared genetic or environmental risk factors.
However, particularly in psychiatry and psychology, the origins of comorbidity have been fiercely debated. Critics have argued that observed comorbidities are “artefacts” of the current diagnostic systems (Maj, Br J Psychiatry, 2005 186: 182–184).
This discussion relates to fundamental questions of how much of our scientific knowledge reflects an independent reality, or is merely a product of our own epistemological traditions. In psychiatry, the DSM and ICD classification systems have been accused of actively producing psychiatric phenomena, including artificial diagnoses and high comorbidity rates, rather than being “true” representations of underlying phenomena. Thus, the “constructivist” tradition argues that diagnostic systems are projected onto the phenomena of psychiatry, while “realists” acknowledge the presence of an independent reality of psychiatric disorders.
In an attempt to explain these concepts and their implications, psychiatric diagnoses and terminology have been termed “systems of convenience”, rather than phenomena that can be shown to be true or false per se (van Loo and Romeijn, Theor Med Bioeth. 2015, 41-60). It remains to be seen whether such philosophical clarifications will advance the ongoing debate related to the nature of medical diagnoses and their co-occurrence.
CoCA will not resolve these controversies. Neither can we expect that our new data will convince proponents of such opposing perspectives.
It is important to acknowledge the imperfections and limitations of concepts and instruments used in (psychiatric) research.
However, it may provide some comfort that similar fundamental discussions have a long tradition in other scientific disciplines, such as physics and mathematics. Rather than being portrayed as a weakness or peculiarity of psychiatric research, I consider that an active debate, with questioning and criticism is considered an essential part of a healthy scientific culture.
Hereby, you are invited to join this debate on this blog page!
2 thoughts on “How can we make sense of comorbidity?”
Dear Jan, thanks a lot for this thoughtful post! In my opinion, at least some of the controversies comes from the fact that we still do know only little about the biological causal chains leading to disorders. If, say, we find that gene X increases the risk towards e.g. both ADHD and bipolar disorder (watch this blog to find out more about gene X… 😉 ), this might help us in conceptualizing the comorbidity of both disorders. Still two possibilities might exist, a) both disorders are comorbid, and gene X contributes to this or b) there is a seperate disease mimicking the comorbid condition, caused (partially) by X. However both hypotheses can be tested, and this is what would be the next step. Likely both models are present in psychiatry, with a huge overlap.
Also I think that lots of our epistemiological debates come from the fact that it is often considered that disease definitions can be mapped 1:1 to biological mechanisms. Disease definitions are often man-made, not made by nature, even if we know the mechanisms (see e.g. hypertension – the border between normal and pathology is entirely epidemiological, not biology-made). Biology is just another level to classify diseases. One might lead to better understanding and therapies, the other might aid everyday clinical life. None is plainly right or wrong: you can classify cars by brand, color, or power, all of which are valid classification systems, but it depends on your aim which one you should aim for.
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I agree that all disease definitions and diagnoses are man-made. Still, classifying certain behaviors as “normal” or “disordered” may seem more provoking than defining hypertension or normotension. Some “professional” science philosophers have strong opinions about psychiatric practice and research. If scientists who are actually doing the research also engage in these fundamental discussions, we may correct some common misconceptions and perhaps increase mutual understanding and trust.
We should not only Mind these gaps, but also attempt to Close them!
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