How Inflammation Affects Your Mental Health

Biomarkers

“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. 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. 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.”

In other words an inflammation of brain brain cells is activated by genetic makeup via the blood cells and results in various mental states identified as: ” melancholic depression, bipolar disorder, and postpartum depression”.  

The author continues and presents more causes:

Pharmacology

One of the most predictable side effects of interferon therapy for Hepatitis C is depression. In fact, 45 percent of patients develop depression  with interferon treatment, which appears to be related to elevated levels of inflammatory cytokines IL-6 and TNF. 

A number of trials have examined the role of anti-inflammatory agents in the treatment of depression. In one recent trial,  a subset of patients resistant to antidepressant treatment and identified by serum markers of inflammation, most notably C-reactive protein >3mg/L, were responsive to treatment with the TNF-alpha antagonist (anti-inflammatory) infliximab (Remicade).

The pain-killer celecoxib (Celebrex) has been found in randomized, placebo-controlled trials  to be superior to placebo in antidepressant augmentation. In the setting of psoriasis treatment with etanercept (Enbrel), mood was improved independent of psoriatic relief.

 The Gut

“The communication between our gut,  which houses at least 10 times as many human cells as there are in our bodies 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.

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.

The stage is set  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.

Continued on next page.

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