For years, the scientific community focused almost exclusively on brain chemistry as the likely cause of depression; but new research upends this longheld premise, suggesting inflammation sparked by an immune system in overdrive — a root, physical origin — is instead responsible for associated feelings of despair, distress, and hopelessness.
Chemicals such as serotonin and dopamine, and their balance and imbalance, long comprised the locus around which research into depression and its treatment to varying degrees of clinical and anecdotal success — but mounting evidence places the blame for unshakable despondence on an immune system refusing to shut down after serious illness or trauma.
“It’s pretty clear that inflammation can cause depression,” asserted Professor Ed Bullmore, Head of the Department of Psychiatry at the University of Cambridge, to a London audience, in no uncertain terms.
So convincing is the physical link between inflammation and the abject doldrums commonly experienced with depression, Bullmore imagines it won’t be long until the advent of a new field: “immuno-neurology.”
“In relation to mood, beyond a reasonable doubt, there is a very robust association between inflammation and depressive symptoms,” Bullmore continued, quoted by The Telegraph.
“We give people a vaccination and they will become depressed. Vaccine clinics could always predict it, but they could never explain it.
“The question is does the inflammation drive the depression or vice versa or is it just a coincidence?
“In experimental medicine studies, if you treat a healthy individual with an inflammatory drug, like interferon, a substantial percentage of those people will become depressed. So we think there is good enough evidence for a causal effect.”
Indeed, a 20-year study, concluded in June — which noted similar results — described the necessity for and promise of the same focus of study championed by Bullmore, stating,
“The field has burgeoned in the last few years, and we have now clear translational opportunities for psychoneuroimmunology and immunopsychiatry to help patients, delivering both predictive biomarkers to implement precision psychiatry and novel pharmacological agents that improves depression through an anti-inflammatory action.”
According to the Telegraph, scientists from Cambridge University and Wellcome Trust plan to investigate anti-inflammatory medication as a means to halt depression, since, the professor notes, “There is evidence to suggest it should work.”
Evincing further correlation, 30 percent of those experiencing chronic inflammatory diseases like rheumatoid arthritis also suffer from depression — a rate four times that of the normal population.
Baneful though the symptoms, depression actually served a purpose. Scientists surmise the reflex to withdraw, rest, and cordon oneself from regular activity during an illness or recovery from injury would have prevented contagions from spreading to the healthy population.
Scientists clung to the idea of a blood-brain barrier — a distinct separation in function between the brain and immune system — but have been forced to relegate that to the dustbin as evidence mounts of their inextricable connection.
“All psychiatric and neurological disorders are based in brain and brain is not static but structurally and functionally responsive to a range of biological, psychological and social issues,” explained Dr. Alan Carson, Reader in Neuropsychiatry at the University of Edinburgh. “Yet institutionally we use an outmoded code which separates brain disorders into psychiatric ‘f’ codes and neurological ‘g’ codes which holds back both scientific and clinical progress.”
Revealing evidence inflammation can drive depression was the first step; now, scientists hope for more meticulous research to use that information for treating the ailment efficaciously.
It should be noted the connection now prominently featured in a growing body of research does not preclude or supplant additional causes of depression, nor current treatment models.