Dr. Turhan Canli poses for a photo during Tedx SBU on November 14, 2014, where he presented his lecture titled "Is Depression an Infectious Disease?" (SYLWIA TUZINOWSKA / THE STATESMAN)
Dr. Turhan Canli poses for a photo during Tedx SBU on November 14, 2014, where he presented his lecture titled “Is Depression an Infectious Disease?” (SYLWIA TUZINOWSKA / THE STATESMAN)

Stony Brook psychology professor Turhan Canli has a radical idea on the cause of depression, a condition that is estimated by the CDC to affect one in 10 Americans.

In a paper published in “Biology of Mood and Anxiety Disorders,” Canli proposed that depression might actually be caused by a traditional infectious agent, whether it be a bacteria, virus or parasite.

For something that has been traditionally seen as a psychological issue or even a genetic issue, the thought of depression as an infectious disease is very unorthodox.

“Its a very unexplored way of thinking about it,” Canli said.

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Canli’s proposal comes from the discovery of inflammatory biomarkers in depressed patients. Inflammation is a major facet of the body’s immune system—the stuffy nose one feels during a cold, the red nose of allergies and the fever of the flu are all examples of inflammation.

“We currently don’t have a well-defined problem to solve,” Canli said. “We’re not really treating depression, we’re just messing with the symptoms. If you’re lucky, if you have major depression, you get something prescribed, and it might work. It might not work, in which case they up the dose or switch you to some other medication until they find something works. That’s not a very satisfying way to treat illness. It’s very much trial and error.”

Eighty percent of sufferers of clinical depression receive no treatment for their condition, according to the CDC.

There are several hallmarks of the brain in depressed patients. Sufferers of depression have low levels of certain chemicals called neurotransmitters. Canli said. Neurotransmitters are a type of messenger chemical and when the make their way to the cells of the brain, they cause the brain to react in a specific way.

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The neurotransmitters depressed patients lack include serotonin, epinephrine and dopamine, and the message those neurotransmitters carry is related to moods such as anxiety, pleasure and energy. Common antidepressants increase the levels of
these neurotransmitters.

But there is more to depression than lowered neurotransmitters.

Depression has also been linked to changes in brain structure. Patients have been found to have a smaller hippocampus, a brain region associated with mood, Canli said. There are also differences in neuroplasticity, or the ability of the brain to physically change its connections, in depressed patients.

There are previous examples of infectious agents causing behavior changes, too. Canli cites Toxoplasmosis in his paper, a condition caused by a parasite that has been known to cause behavior changes in rats and possibly humans.

Furthermore, up to a third of the world is affected by it, without any visible symptoms, Canli said. The infectious disease hypothesis also explains the high rate of recurrence of depression.

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“Once you have one episode of depression, there’s a 50-percent chance you will have another, and if you do there is an 80-percent chance of a third,” Canli said.

Such high rates of recurrence could be due to an infectious agent never leaving the body, instead going dormant and re-appearing later.

There is a distinction between an infectious disease and a contagious disease. It would impossible to “catch” depression from a depressed patient. There is no increase in the rate of depression of mental health workers, and depression does not match the spreading patterns of a contagious disease, Canli said.

Canli said he hopes to eventually perform a study on this subject. However, he admitted that “it’s hard to do science without funding.” Canli has to consult existing data available to him to find clues to this idea in order to create a proposal for this study. Eventually, he hopes to be able to dig through gathered patient data to try and find evidence of an infectious agent, and, if so, what type of agent it would be.

“If you think about it in terms of ‘could it be some sort of infectious disease, some kind of infection’, then there are ways to systematically search for such infectious agents,” Canli said, adding, “and if you were to discover one or more than one, then you could study what they do and how they work, and then you get the actual mechanism.”

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