• How Inflammation Affects The Body And May Cause Depression

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  • Psychoneuroimmunology is the study of the interaction between psychological processes and the nervous and immune systems of the human body.

    By Dr. Kelly Brogan

    Psychoneuroimmunology. This is what I aim to practice. Medical terms of this length command our respect for the interconnectedness of different subspecialties, for the futile segmentation and compartmentalization of the body into different organ systems.

    As discussed in this previous article I wrote for Dr. Mercola, deconstructing the serotonin model of depression, psychiatry is in a crisis. It can no longer stand on its own, throwing more and more medications at its perceived target.

    It seems, therefore, fitting that psychiatry would follow the investigative path of other lifestyle-triggered chronic diseases such as cancer, autoimmunity, and heart disease. There already exists a bidirectional relationship between all of the major chronic diseases and psychiatric diagnoses (patients who struggle with chronic diseases are more likely to be depressed and vice versa).

    The role of inflammation, across these disease states, is better elucidated each day. Let's deconstruct what is known as it applies to mental health.

    Inflammation and Depression

    In this model, depression is a non-specific fever that tells us little about what is actually causing the body to react and protect itself in this way. The body is “hot” and we need to understand why. Depressive symptoms are the manifestation of many downstream effects on horminflamationones and neurotransmitters, but if we swim up to the source, we will find a river of inflammatory markers coursing by.

    The source itself may be singularly or multiply-focused as stress, dietary, and toxic exposures, and infection, as we will discuss here. As explored in the medical literature, inflammation appears to be a highly relevant determinant of depressive symptoms such as flat mood, slowed thinking, avoidance, alterations in perception, and metabolic changes. We understand this relationship based on:

    Biomarkers  

    Psychiatrists have longed to be legitimized in their role as science-based physicians. Despite this, there are no diagnostic tests that are validated for the assessment of psychiatric pathology. In the practice of functional medicine, however, the diagnosis becomes secondary to the individual's personalized interplay of factors and the “biomarkers” that can light the way toward healing.

    Cytokines in the blood, or inflammatory messengers, such as CRP, IL-1, IL-6, and TNF-alpha have taken the stage as predictive and linearly correlative with depression.

    Researchers have validated that, in melancholic depression, bipolar disorder, and postpartum depression, white blood cells called monocytes express pro-inflammatory genes leading to secretion of cytokines, while simultaneously leading to decreased cortisol sensitivity, the body's stress hormone and inflammatory buffer – a feedforward cycle.

    Once triggered in the body, these inflammatory agents transfer information to the nervous system, typically through stimulation of major nerves such as the vagus, which connects the gut and brain. Specialized cells called microglia in the brain represent the brain's immune hubs and are activated in inflammatory states.

    In activated microglia, an enzyme called IDO (indoleamine 2 3-dioxygenase) has been shown to direct tryptophan away from the production of serotonin and melatonin and towards the production of an NMDA agonist called quinolinic acid that may be responsible for symptoms of anxiety and agitation.

    These are just some of the changes that may conspire to let your brain in on what your body may know is wrong.

    The Gut-Brain Dance

    What is driving this inflammation? How does it get kicked off? And how does it induce depression? With the limited clinical applications and revelations that came with the completion of the Human Genome Project in 2002, we have begun to focus on where we have outsourced our physiologic functions.

    The microbiome has become an important consideration, and particularly, the gut, which houses at least 10 times as many human cells as there are in our bodies, and 150 times as many genes as are in our genome. These microbes control many vital operations and are responsible for synthesis of neuroactive and nutritional compounds, for immune modulation, and for inflammatory signaling.

    Our greatest interface with the environment is the 70+ percent of your immune system housed in your gut wall. Disturbances in gut microbiota, autoimmunity, head injury, childbirth, and infection can all trigger systemic inflammation. This immune activity takes the form of a TH1 dominant cellular response in which macrophages produce ILI, IL6, and TNFalpha, all of which have been shown to be elevated in the setting of depression.

    The communication between our guts and brains appears to rely, in part, on the vagus nerve, and is bidirectional in nature as reported in this 12-year prospective study that looked at relationships between gut problems like irritable bowel disease, anxiety, and depression.

    The stage is set for the microbiome when we descend the vaginal canal and are breastfed. Unfortunately, the rate of cesarean sections doubled from 1990-2008, comprising one-third of US births. Maternal inflammatory states and diseases such as type 1 diabetes can increase risk of surgical birth, as can interventions such as ultrasound, monitoring, and the epidural. Without vaginal transfer of mom's flora, the baby misses out on the most important inoculation.

    A study of 24 Canadian babies at four months demonstrated that elective section resulted in the most diminished bacterial diversity. Surgically born babies had significantly less Bacteroides and EscherichiaShigella species. In this cohort, formula-fed babies had overrepresentation of Clostridiumdifficile, Peptostreptococcaceae, and Verrucomicrobiaceae. Excitingly, research is being done on “vaginal swabs” for inoculation in the setting of C-section.

     

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