In people with fibromyalgia, higher levels of a specific inflammatory protein in the blood are linked to less severe autonomic nervous system symptoms.
Mechanism
Synthesis from 1 study
When the gut lining gets damaged, bacterial parts leak into the blood and trigger inflammation. In fibromyalgia, this inflammation seems to quiet down the overactive nerves that control heart rate and digestion, making symptoms feel less intense. This is the opposite of what happens in similar...
Most probable mechanism
When the lining of the gut becomes leaky, bacteria and their parts escape into the bloodstream, which wakes up immune cells. These immune cells release inflammatory signals that affect the nerves controlling heart rate, digestion, and blood pressure. In fibromyalgia, this inflammation seems to calm down the overactive stress response, making autonomic symptoms feel less severe.
Intestinal epithelial tight junctions are disrupted, increasing permeability of the gut barrier
Bacterial lipopolysaccharide translocates from the gut lumen into systemic circulation
Circulating lipopolysaccharide binds to soluble CD14, activating monocytes and macrophages via TLR4 signaling
Activated monocytes and macrophages produce interleukin-1-beta and other inflammatory mediators
Systemic interleukin-1-beta signaling modulates central and peripheral autonomic nervous system activity, reducing symptom severity
Evidence from Studies
Supporting (1)
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Contradicting (0)
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