A fascinating theory has been put forward by Turhan Canli PhD, Associate Professor of Psychology and Radiology at Stony Brook University, which could change the future direction for research and treatments of depression.
According to Dr Canli, depression should be re-conceptualised as an infectious disease. His argument is a compelling one.
In a paper published in Biology of Mood & Anxiety Disorders, Dr Canli suggests that depression could be the result of a parasitic, bacterial or viral infection.
Depression is a pervasive illness, with around 16% of people experiencing an episode at some point in their lives.
There has been little change in treatments over the last few decades and although antidepressants are effective in reducing symptoms in patients with severe symptoms, in patients with mild to moderate symptoms they are no more clinically effective than placebos.
Recurrence of depression is common. Those who have experienced one episode have a 50% chance of recurrence. Those who have experienced depression twice have an 80% chance of experiencing it a third time.
Dr Canli explains, ‘Given this track record, I argue that it is time for an entirely different approach. Instead of conceptualising depression as an emotional disorder, I suggest to reconceptualise it as some form of an infectious disease.’
Dr Canli is also a member of the Program in Neuroscience, and a Senior Fellow in the Center for Medical Humanities, Compassionate Care, and Bioethics. ‘I propose that future research should conduct a concerted search for parasites, bacteria, or viruses that may play a causal role in the etiology of depression.
Dr Canli presents three arguments for reconceptualising depression as an infectious disease:
‘Patients with depression experience sickness behaviour’.
The main criteria for a diagnosis of depression are affective symptoms, specifically a loss of energy and diminished interest in the world and previously enjoyable activities. However inflammatory biomarkers of depression strongly suggest the origin of depression to be illness related. Dr Canli suggests that the inflammatory markers may indicate the stimulation of the immune system in response to a pathogen such as a parasite, bacterium or virus. He acknowledges that there is currently no direct evidence that depression is caused by a micro-organism, however the process is a plausible one and warrants further research.
There is clear evidence that parasites, bacteria and viruses can affect emotional behavior.
Parasites: There is evidence that infection by the parasite, T. gondii is associated with elevated inflammatory biomarkers similar to that observed in depressed patients;
Bacteria: Research has begun to investigating the causal links between emotional behaviour and bacteria in the gut.
Viruses: A meta-analysis of 28 studies looked at the link between depression and infectious agents. Borna disease virus (BDV) has been found to be 3.25 times more likely to be found in depressed patients than in normal controls. Further research is necessary to understand the link.
The genetics of the illness.
Genetic studies to date have looked at human genes within the human genome (complete set of DNA). However, the human body is host to other micro-organisms, with their own genetic makeup, that can be passed across generations. As a result, ‘the opportunity for genetic discoveries is vastly amplified’.
Based on these three arguments, Dr Canli suggests the future research in the area involve large-scale studies with depressed patients, controls, and infectious-disease related protocols. He explains, ‘Such efforts, if successful, would represent the ‘end of the beginning’, as any such discovery would represent the first step toward developing a vaccination for major depression.’
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