Connecting Inflammation and Depression
The well-known behavioral response called “fight-or-flight” has been around since the early evolution of humans. It is how our body reacts to threats or stress. Today, we know this reaction to drive heart rate, make us sweat, and raise blood pressure in situations like public speaking or walking alone at night. A unique element of this sympathetic response is its activation of pathways throughout the body that produces inflammatory symptoms mimicking depression.
Unfortunately, depression remains a leading cause of death in adults worldwide. As the severity of this disease progresses, research is being conducted on its underlying causes in order to navigate new pathways for treatment. A major component in this research has been the effects of inflammation on the body related to the presentation of depressive symptoms .
Inflammation is a biological response to infections that can present in different ways. When someone experiences a localized injury, that body part may become red and inflamed as an infection-fighting mechanism. But, when inflammation is spread throughout the body, people experience what is called “sickness behavior” . This response consists of changes physically, behaviorally, and mentally. Symptoms can include fatigue, slow reaction time, loss of appetite, sleep disruption, anhedonia (loss of enjoyment), and cognitive problems . The similarity of these inflammatory response symptoms to depressive symptoms has suggested a possible link between the two conditions.
When the immune system encounters parasites, bacteria, viruses, and other toxins, it utilizes proteins, cells, and tissues to combat intruders. As inflammation occurs, certain cytokine molecules are released that impact the monoamines serotonin, noradrenaline, and dopamine. This trio of monoamines is also a huge determinant of depressive disorders. The pro-inflammatory cytokines alter brain circuits when they cross the blood-brain barrier leading to behavior change .
Certain biological markers (IL-6 and C-reactive Protein) have been identified as possible predictors of depressive development. Current treatment using SSRI medication only relieves a handful of patients with Major Depressive Disorder . These antidepressants increase monoamine availability (rises in serotonin), but inflammation appears to be a large barrier to the treatment’s effects. The blockage of these neurocircuits impacts pathways that control motivation, motor activity, arousal, anxiety, and alarm . Current research is underway to determine a way to block specific cytokines in order to reduce depressive symptoms.
An interesting factor in the link between depression and inflammation remains under close investigation. This is the resulting behavior from stress and trauma. People experiencing depression typically show many psychosocial risk factors for inflammation as well. These can stem from traumatic experiences or medical comorbidities that activate fight-or-flight responses. As the understanding of the relationship between these two conditions increases, researchers are getting closer to finding anti-inflammatory agents that may have antidepressant effects .