CNS regulation of peripheral inflammation, implications in fibromyalgia?
The central nervous system (CNS = brain and spinal cord) can regulate peripheral inflammation, but the pathways and mechanisms by which it does so remain unclear.
The study summarized below investigates the possibility that the neurotransmitter acetylcholine (ACh) exerts an anti-inflammatory effect via binding to a specific receptor found primarily on the synovial lining of rheumatoid arthritis and osteoarthritis joints.
That possibility is confirmed by observations of reduced pro-inflammatory cytokine activity as a result of such binding.
While the authors suggest that the receptor identified in rheumatoid arthritis and osteoarthritis joints might be a potential target for drug development, I am curious if a similar mechanism might explain the connection between observed neurotransmitter abnormalities seen in fibromyalgia and the persistence of peripheral inflammation.
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In a nutshell 
those suffering with fibromyalgia or rheumatoid arthritis experienced a substantial improvement in their conditions when they switched to a raw, vegan diet. Specifically, they experienced a decrease in pain and stiffness and self-perception of their health was improved.
The problem, of course, is that this diet represents a substantial and some would say extreme departure from our ‘normal’ diet. A vegan diet includes no animal products whatsoever – no milk, eggs, butter. The “living food” diet studied here included only raw foods – no cooking whatsoever.
The obvious reality is that very few people will ever attempt such an extreme dietary modification, and fewer still will adhere to it. Nonetheless, it is one option, and might result in general improvement in conditions related to inflammation other than those specifically studied.
As an alternative, one might want to add more fruits and vegetables to the diet, especially fresh, raw fruits and vegetables. Supplements might be considered as well.
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Two studies are consistent with the theory that excess inflammation often results from the body’s inability to shut down NF-kB – the Master Switch of inflammation.
Turning on NF-kB results in inflammation. If NF-kB cannot be turned off, chronic inflammation results.
One of many ways the body turns off NF-kB is with a protein messenger known as “CARD8.” Normally, CARD8 is made when NF-kB is activated. The negative feedback loop (the result of turning on NF-kB is a product that feeds back and turns off NF-kB) is one reason inflammation does not normally get out of hand.
A genetic defect has been identified that results in less effective CARD8. Less effective CARD8 means the normal, negative feedback loop that helps keep inflammation in check is missing – so inflammation continues.
This defect in CARD8 has been identified as a contributor to Alzheimer’s and rheumatoid arthritis. Some studies have suggested that defective CARD8 might also be associated with Crohn’s disease.
What seems clear is that CARD8 is only one of many ways the body keeps inflammation in control. To the extent that this and other defects result in deficient NF-kB inhibitors, supplementing NF-kB inhibitors, as suggested on this site, might be helpful.
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Osteoclasts (OCs) are involved in several pathologies associated with bone loss, including rheumatoid arthritis, osteoporosis, bone metastasis of myeloma, osteosarcoma, and breast cancer.
In this review we determined the effects of natural compounds, including extracts from medicinal plants, on differentiation and survival of human primary osteoclasts.
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Postmenopausal osteoporosis and rheumatoid joint destruction result from increased osteoclast formation and bone resorption that is under the control of NF-kB.
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