Depression has been long understood to involve changes in function within pathways in the brain’s prefrontal cortex. These brain systems require monoamine neurotransmitters to adequately function, including serotonin, dopamine, and norepinephrine. Most psychiatric medications used to treat depression target these neurotransmitter systems in one manner or another. However, it is fundamentally inappropriate to reduce depression to a simple neurotransmitter deficit. There are other neurological and physiological processes involved in depressive disorders, and medicine is still in the early stages of understanding the myriad factors that lead to a depressive condition.
A great deal of recent scientific investigation has focused on the role of inflammation in the pathophysiology of depression. An article in Psychiatric Times by Dr. Andrew Miller addresses the current state of knowledge regarding the influence of inflammation in depressive disorders. While we know that depression is not an inflammatory disorder in and of itself, there are often increased markers of inflammation in depressed patients compared with controls. Inflammation has been shown to affect subcortical and cortical brain circuits associated with motivation and motor activity as well as cortical brain regions associated with arousal, anxiety, and alarm. Inflammatory markers have been shown to be associated with suicidal ideation and suicide attempts.
Inflammation has been shown to also decrease the precursors for monoamine neurotransmitters. It can decrease Brain Derived Neurotrophic Factor (BDNF), a primary signaling molecule that allows neurons to form new connections. Inflammatory markers can predict treatment response to medications, in that patients with higher inflammatory loads are less likely to have a positive response to serotonin reuptake inhibitor antidepressants.
All of this strongly implies that strategies to reduce inflammation are an essential component of a healthy emotional framework.
The full article can be found here: