There has been a lot of talk lately about some recent research out of Chicago that suggests that depression can be detected using a blood test. More specifically, researchers have published their findings that suggest that certain genetic markers differ between individuals that meet the researchers’ criteria for major depressive disorder and those that do not. Furthermore, they concluded that markers could also help to delineate whether cognitive behavioural therapy would be helpful for a given person, and could potentially be used to help determine whether treatment is working throughout the treatment process.
These findings have been met with mixed reactions. Many point out that this new finding may result in earlier diagnosis (and thus treatment) and suggest that a blood test diagnosis will help to ‘legitimize’ the diagnosis and will have far reaching benefits in reducing stigma. Others wonder what it will mean for people who identify themselves as depressed but whose genetic markers do not fit the ‘depression’ profile (or vice versa: those who do not identify themselves as depressed but whose markers do fit the depression profile). Some people who have come across articles about this research might take issue with the way in which the complex nature of depression tends to be reduced to a very simple and straightforward issue. I wonder how these new ideas about diagnosis will impact antidepressant prescribing behaviour, particularly given the research that is starting to pile up that suggests that antidepressants may not be more effective than placebos for mild and moderate depression.
We know that people that experience major depressive episodes are more likely to experience future episodes. If depression can be detected earlier, intervention can in turn start sooner, which could reduce the number of lifetime episodes of depression and reduce the overall number of disability-adjusted life years lost to depression. The question remains whether this new approach to diagnosis will really result in earlier detection for people with depression. For example, it will obviously fail to benefit those that do not attend a family physician or otherwise seek help, and I suspect that it is these individuals that make up a large percentage of those considered ‘underdiagnosed.’
The study suggests that particular genetic biomarkers may be helpful in identifying those who are likely to benefit from cognitive behavioural therapy and those who are not. This is an important finding, however, there are important ethical implications of determining a patient’s appropriateness for a treatment on the basis of such a test alone. Countless variables must surely impact upon an individual’s ability to benefit from a given treatment, and particularly a psychotherapeutic one such as CBT. For example, research suggests that the process of psychotherapy (and mindfulness, and addictive behaviours, and countless other activities) changes the brain, which should not be surprising, because of course our brains are constantly changing and rewiring on the basis of our thoughts, behaviour, and experience. The relationship between the biomarkers and the efficacy of CBT is interpreted in one direction in this research, but it is entirely possible that those same biomarkers that identify a person as unlikely to benefit from CBT could actually be changed through the course of therapy.
More effectively gauging the progress of therapy is another possibility alluded to in this research. Presumably, this would involve periodic assessment of genetic biomarkers – as the profile shifted over time this would provide evidence of improvement in, well in what exactly? Severity of depression? Number of symptoms? In my experience, clients who are benefitting from treatment are quite able to recognize it and communicate it in a straightforward way to their treatment providers. I do see the potential for benefit for those patients that are unaware of their difficulties or less willing to see their problems in the context of their mental health, or for physicians to be able to quickly get a sense of whether their treatment approach can broadly be considered 'working' or 'not working'.
With regard to stigma, it is sad to say that a blood test approach to diagnosis probably will afford some legitimacy to depression. It may also create a sort of dualism, whereby one person's experience of depression is judged to be 'real' while another's is not.
One thing that must be kept in mind is that the findings of Redei and associates can largely be considered preliminary, in part due to the very low number of participants involved in the research. Their effect must be validated with many more patients with varying presentations and differing circumstances before we can expect it to see it in our healthcare provider’s office. The other thing that must be considered is that depression, despite its prevalence and broad recognition, is not a simple thing. The experience of depression is made up of a very complex combination and interaction of biological, physical, emotional, and social factors. This is evident when brain chemistry is considered. For example, even though it is well known that a low level of serotonin is implicated in depression, this is not the end of the story. If it was, then the efficacy of typical antidepressants would be much better than it is, and discontinuation rates much lower than they are. Similarly, while this latest advance in the understanding of biomarkers implicated in depression are interesting, they too are probably not the end of the story either.
There is little doubt that there are many people that experience symptoms of depression for a whole variety of complicated reasons. Research on genetic markers will certainly advance our understanding of depression and may provide assistance in diagnosing depression for some patients that are less psychologically minded. However, we must be careful to recognize the limitations of the discovery and the risks associated with the possible simplification of what is ultimately a very personal and complicated issue.