One of the most challenging aspects of mental health treatment is establishing causation. Taking an Advil for a headache may relieve symptoms, but if the underlying cause of the headache happens to be a brain tumor, the effect is likened to that of attempting to climb Mt. Everest blindfolded. Of late, the mainstream medical community has been wrestling with the root causes of Bipolar Disorder. While ibuprofen is far from a cure, studies are showing that the role of inflammation in this condition bears close examination.
Bipolar Disorder affects approximately 2.6% (5.7 million people) of adult population in the United States (National Institutes of Mental Health). It’s a chronic brain illness that causes extreme shifts in mood & energy and often interferes with daily life function. Emotional swings range from elevated ‘highs’ (manic) to debilitating ‘lows’ (depressive) and can severely impair quality of life. The cause? A wide range of components appear to be at work including genetics, chemical imbalances, and environmental factors. While there is no particular gender or cultural bias, recent studies reveal that more than two-thirds of individuals with the disorder have at least one close relative who is also affected.
Treatment modalities can be frustrating as many of the current preferred medications are mired in negative side-effects. However, research on the implications of inflammation are proving vital to developing more effective treatment modalities.
One pertinent question may be how we first arrived at considering inflammation in the mental health equation. Inflammatory conditions like periodontal disease, autoimmune disorders and cardiovascular disease can overstimulate the immune system - leading to warranted stress response. Sujecting our brain chemistry to that type of neurological chaos over extended periods is a major contributor to mental illness.
Numerous studies have long revealed the link between Bipolar Disorder and the presence of inflammatory disease. A 2015 JAMA study confirms that brain inflammation is 30% higher in patients that present with clinical depression. Even further back, a study published by the Journal of Clinical Psychiatry screened more than 14,000 individuals for depression between 2007 and 2012. Researchers found that 46% of those who had depression also had higher levels of C-reactive protein - an essential marker for inflammation. Armed with this insight, the attack on Bipolar Disorder has grown to include the addition of nonsteroidal anti-inflammatory drugs (NSAIDs) to treatment protocols.
Targeting inflammation appears to have shown some progress. A 2016 meta-analysis and systematic review focused on a series of randomly controlled trials assessing the effects of utilizing NSAIDs concurrently with accepted bipolar disorder treatments. Researchers found that the NSAIDs resulted in a statistically significant antidepressant effect. Cracking the inflammation code may prove to be extremely beneficial in aiding overall treatment effectiveness. A 2016 study by Maya Amitai in the Journal of Child and Adolescent Psychopharmacology followed 41 patients ages 9 to 18 diagnosed with major depression. Those with high levels of inflammatory markers were less likely to respond favorably to treatment with antidepressants.
Isolating this one piece of the puzzle is indicative of progress, but has not necessarily identified a smoking gun. Most psychiatric conditions exist on basic scale ranging from deterioration to some degree of recovery. Bipolar Disorder involves of extreme swings and complex variations in neurology that can manifest in a myriad of ways. These complexities make it difficult to effectively identify inflammation as a reliable biomarker for Bipolar Disorder - leading to the necessity of further investigation. However, on the whole, a growing body of research that shows the benefit of NSAIDs as an effective adjunctive treatment.