Inflammation seems to be the new suspected cause for a number of common (and distressingly, becoming more common every day) diseases and disorders. Inflammation, from the Latin word inflammo, meaning to ignite or set afire, describes the human body’s complex biological reaction to a number of different stimuli. In many cases, similar to the phenomenon which causes some people to die from a bee sting while others barely notice it, it doesn’t seem to be the toxins or the irritants or the pathogens themselves that cause the disease reaction, but the body’s overreaction to these things. Inflammation has been strongly linked as a suspected cause or risk factor for heart disease, diabetes, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (gallbladder carcinoma).
Now a new study conducted in Sweden and due to be published in an upcoming issue of the journal Neuropsychopharmacology suggests that a compound called quinolinic acid, known to be generated by inflammation, is linked to suicide.
Trying to find the roots of suicidal urges
In the study, led by Lena Brundin, a professor of translational science and molecular medicine at Michigan State University, the researchers tested 100 Swedish adults for the presence of quinolinic acid. The testing itself was not trivial, because quinolinic acid can’t be detected in blood samples, and requires that the drawing of samples of cerebrospinal fluid, the liquid that surrounds and cushions the brain and spinal cord.
Approximately two-thirds of the study subjects were tested immediately after their hospitalization following an unsuccessful suicide attempt; the remaining third were healthy. What the researchers found was that the higher the level of quinolinic acid in the subjects’ spinal fluid, the stronger their desire to commit suicide was. As Brundin put it in the study, “The sicker the patient, the higher the quinolinic acid.”
The researchers theorize that quinolinic acid may be the “missing link” between inflammation and mental illness. Inflammation had been strongly linked to suicidal feelings in the past, but the assumption always was that the inflammation itself occurred as a result of illness and stress, not as a direct cause in itself. They now suspect that quinolinic acid may have the effect that it does because of its chemical similarity to the neurotransmitter glutamate, which plays a key role in the excitation of nerve cells, and in the control of the brain’s memory and learning abilities. They suspect that the increased levels of quinolinic acid “mimic” or “play copycat” to glutamate, and over-stimulate the brain, causing an inflammation reaction that in turn causes depression and/or suicidal thoughts.
Why this research is important
Suicide is one of the most prevalent but least understood conditions facing the medical and psychological communities today. There are nearly 40,000 deaths per year in the United States due to suicide, and nearly 700,000 emergency room visits necessitated by suicide attempts. Between the years of 2000 and 2009, according to the Centers for Disease Control and Prevention, suicide actually surpassed automobile accidents as the number one cause of injury-related deaths in the U.S.
Studies in mice have indicated that the immune system and inflammation are strongly linked to depression, but the “missing link” indicating how inflammation affects the brain was still missing. This study may provide important clues that can help researchers and doctors find new ways to treat depressed patients, and prevent their depression from escalating to thoughts of suicide.
Previous studies have already indicated that the drug ketamine, injected directly into the bloodstream, can eliminate suicidal thoughts and symptoms within a number of hours. Ketamine suppresses glutamate, so the researchers hope that similar pharmaceutical agents can be found to treat mental illness. As study leader Brundin says, “If the pharmaceutical industry can continue developing anti-glutamate medication, I think that might be a great hope for suicidal and depressive patients.”