Inflammation can be described as an immune response to a stimulus, particularly something that the body thinks could be harmful.[i] A typical inflammation response results in symptoms of redness, heat, swelling, loss of function, and/or pain. Most may associate inflammation with a sprained ankle, infection, or a skin wound, but even certain foods we consume may lead to inflammatory responses (see Inflammation Nation). Chronic inflammation is associated with diseases such as Rheumatoid Arthritis, Irritable Bowel Disease, and Psoriasis.
What is this thing called pain? Pain is a sensation of discomfort and may be described as sharp, burning, aching, dull, tight, or throbbing, and can result in unwanted symptoms such as poor sleep and irritability. In the absence of inflammation, noxious stimuli are detected by nociceptors that cause pain when a certain threshold is reached (the hot-stove response). When an area is inflamed, pain receptors can become hypersensitive, thus, lowering the pain threshold. Because inflammation is typically the result of homeostasis being compromised, the pain associated with inflammation is considered to be “protective,” to avoid further harm to that area. However, ongoing inflammation can sensitize pain receptors in the periphery and cause plastic changes in the brain. This central sensitization can produce pathological pain syndromes such as in fibromyalgia, interstitial cystitis, TMJ, etc., where pain is experienced without noxious stimuli or inflammation.
The sending of pain messages to the central nervous system is mediated by ion channel activity and amino acids. Molecules such as prostaglandins (PGs) lower the threshold for the initiation of ion channel conduction during the early stages of inflammation. Prostaglandins are released by cytokines. Over time, inflammation may lead to increased production of receptors, ion channels, and transmitters. Intervention here could be the addition of anti-inflammatories such as omega 3 fish oil and herbals such as turmeric and boswellia, which modulate prostaglandin synthesis away from inflammatory pathways.
Glutamate, an excitatory amino acid that dominates communication between the peripheral system and central nervous system, acts as a mediator in this pain pathway. Glutamate’s NMDA receptor is activated during inflammation, which results in increased sensitivity to pain and the central sensitization mentioned above. When this happens, Substance P (a neuropeptide) and other neurotrophic factors are released from a type of pain fiber called C fibres. This enhances NMDA receptor activity and increases responsiveness to successive stimuli. This change in NMDA activity is what can eventually establish the sensation of “chronic pain and hypersensitivity pain syndromes.”[2]
The first step to dealing with chronic inflammation may be to see where your body stands. Measuring glutamate levels, along with neurotransmitters that have inhibitory influences on pain, including dopamine, serotonin, and norepinephrine, could give you helpful insight to what is going on. In the case of excess glutamate, consider assessing diet for exogenous sources of glutamate (MSG, aspartame, glutamine, and/or processed foods) to reduce glutamate levels, which may potentially minimize inflammation. For some other helpful tips on reducing inflammation without the use of anti-inflammatory medication, check out our “Inflammation Nation” blog.
References
[1] Woolf, CJ. What is this thing called pain? J Clin Invest. (2010) 120 (11):3742-3744.
[2] Kidd, BL and Urban, LA. Mechanisms of inflammatory pain. Br. J. Anaesth. (2001) 87 (1): 3-11.
Clinical Contributor
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