The key to treating difficult cases of bipolar depression may be a drug commonly used to treat inflammation and arthritis, suggests preliminary research.

Researchers recruited 55 adults with bipolar depression who had earlier proven resistant to antidepressants for an 8-week randomized controlled trial. While all the volunteers were given the antidepressant Lexapro, half were also given the nonsteroidal anti-inflammatory drug (NSAID) celecoxib and the other half a placebo. The combination drug group not only had a greater reduction of depressive symptoms compared to the control group, they found, but they also responded to the treatment at a faster rate, taking an average of one week as opposed to the typical 4 to 6 weeks.

The findings were presented at the International Congress on Psychiatry and the Neurosciences held in Greece earlier this October.

Seventy-eight percent of the combination group experienced a 50 percent or more reduction in their symptoms and 63 percent reported a complete recovery, according to a news release issued by the Loyola University Health System in Illinois, home of the study’s lead researcher and psychiatrist, Dr. Angelos Halaris. Meanwhile, 45 percent of the Lexapro-only group reported a 50 percent or more reduction, and 10 percent a complete recovery. The combination group also had noticeably lower levels of stress and anxiety compared to before the trial, while the Lexapro group experienced little to no changes.

The findings reaffirmed the researchers’ theory on the role inflammation plays in depression. Halaris and his colleagues have published extensive research on the connection between inflammation, particularly the kind associated with cardiovascular disease, and depression. And they’ve speculated that certain types of proinflammatory molecules could serve as an important marker of clinical major depression, since they’re higher in these patients.

Elsewhere, other researchers have used the same type of drug used in the current study, a COX-2 inhibitor, to treat severe depression in combination with standard antidepressants — with some impressive, if small-scale, success. The current study, however, is seemingly the first to use the combination strategy on patients with bipolar depression, defined as having periods of extremely high and low emotion.

Scientists like Halaris theorize that inflammation interferes with the normal regulation of neurotransmitters like serotonin, already thought to be a key aspect of causing depression. This inflammation mucks with the ability of antidepressants like Lexapro, called selective serotonin reuptake inhibitors (SSRIs), to help fine-tune serotonin back into balance. By reducing inflammation early on, the researchers said, we might be able to stop the progression of bipolar depression dead in its tracks as well as punch through cases of treatment-resistant depression.

Encouraging as the findings are, though, much of the work involved in proving this connection, including the current study, remains in the earliest stages of research. Halaris’s team hopes that future studies can pinpoint the exact inflammatory and anti-inflammatory molecules associated with depression in order to someday craft personalized treatments for previously hard to help patients.

Source: Halaris A. Modulation Of Immune System Activation May Arrest Neuroprogression In Affective Disorders. International Congress on Psychiatry and the Neurosciences. 2016.