Chronic pain is an insidious disease that impacts all aspects of life- physically, emotionally and economically. More and more evidence suggests that inflammation in the peripheral and central nervous systems is the major factor in creating and perpetuating chronic pain states. After an injury, activation of glial and immune cells in the peripheral nervous system releases pro-inflammatory mediators which sensitize nociceptors and cause neuroinflammation in the central nervous system. When macrophages and glial cells in both systems don’t ultimately kick in once the injury is healed to release anti- inflammatory mediators and specialized pro- resolving mediators, chronic pain ensues.
Nociceptors, literally meaning “pain receptors” in Latin, are activated by any potentially damaging stimuli. They are critical in activating the physiological processes necessary to protect our bodies from harm. Our nociceptor sensory neurons do this by eliciting pain and encouraging avoidance behaviors. When a threat is perceived signals pass through the spinal cord to the brain where the sensation of pain is generated in order to direct attention to the body part involved. In this way the threat can be mitigated or stopped. Without it we’d never withdraw our hand from the hot stove or stop walking when we step on a nail. It’s increasingly clear that these neurons actively interact with the immune system to regulate inflammatory diseases, pain and our defense strategies. This dialogue is a fundamental aspect of the acute and ultimate chronic inflammation that leads to chronic pain states.
Pain is a hallmark of tissue injury, inflammatory diseases, pathogen invasion and neuropathy. They are all mediated by nociceptor sensory neurons within our, skin, joints, bones, muscles, and mucosal tissues.
They protect us from noxious stimuli when activated by inflammatory mediators released through the immune system. This then causes the release of neuropeptides from their terminals. Ultimately, this shapes how we respond to the initial injury and whether it stops or persists long after the event is resolved.
The word inflammation means, “to set on fire”, in Latin. Celsus, a Roman who lived in the first century A.D. documented four cardinal signs of inflammation:
- redness
- swelling
- heat
- pain
It’s a critical acute defense mechanism that prevents damage and future injury. When pain becomes chronic it’s progressed to a maladaptive and pathological state. Stopping that process before, or the very least, after it’s happened, is the goal.
Pain is often categorized into two types:
Neuropathic. This is caused by direct nerve damage, disease or lesions in the neural circuitry within the somatosensory system that mediates pain. It can be continuous or intermittent abnormal sensations (dysesthesia) or pain from normally non-painful stimuli (allodynia).
Or
Inflammatory. This is driven by immune associated stimuli. But research has shown immune cells significantly contribute to both neuropathic and inflammatory pain by causing the release of mediators that act on the terminals of nociceptors to drive increased sensitization. When this happens, we feel heightened pain in response to a normally painless or minimally painful stimuli. In acute inflammatory states, pain follows the immune response and diminishes as the inflammation resolves e.g. a twisted ankle, laceration, or bruised muscle. In chronic states such as rheumatoid arthritis or colitis, persistent immune triggers such as cytokines mediate long lasting pain.
The interaction between nociceptors and immune cells is like a beautifully orchestrated tango. The initial response is required to save the organism, but their persistence becomes damaging. They allow the immune system to integrate pain with inflammation and infectious signals in a finely tuned dance. Just like everything in our bodies maintaining an equilibrium, or homeostasis, is imperative. When the scales tip significant consequences ensue.
Because immunity is a system not a specific entity, it requires balance and harmony to function smoothly. There’s still so much we need to learn and so many possibilities for helping chronic diseases and pain. Our bodily functions improve when they are protected from environmental assaults and bolstered by heathy living. Here are a few ways to improve overall health, well- being, your immune system and ultimately decrease pain, on your own:
- Don’t smoke.
- Eat a well-rounded diet filled with fruits, vegetables, whole plants, healthy fats, fermented foods.
- Stay hydrated.
- Limit sugars.
- Exercise. Exercise. Exercise.
- Maintain a healthy weight. New studies show it’s not just the body mass index that’s important, it’s our waist measurement. Men should be less than 40 and women less than 35.
- Decrease alcohol consumption.
- Sleep 7-9 hours every night.
- Minimize stress.
- Keep current with physical exams, routine testing, vaccines that can prime and/ or boost your immune system to fight or prevent infections before they take hold.
- Wash hands frequently and properly.
- Cook meats thoroughly and refrigerate food quickly after meals.
- Do not rely on supplements. They are not monitored and too often contain dangerous substances. The immune system is filled with millions of different cells each working in unison to protect us. Taking pills won’t replace a healthy diet and is too many cases they may cause harm. Studies have shown all we really need is a multivitamin daily. Just remember, if it doesn’t dissolve in a glass of water over night it won’t dissolve in your GI tract. It’ll just pass through as waste. I use a gummy vitamin.
There’s no question keeping our immune system healthy will decrease pain, improve activity and help us enjoy a better life.
-https://pubmed.ncbi.nlm.nih.gov/37220667/
-https://www.cdc.gov/nccdphp/dnpao/features/enhance-immunity/index.html
https://www.health.harvard.edu/staying-healthy/how-to-boost-your-immune-system
-https://pubmed.ncbi.nlm.nih.gov/27793571/
-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700742/
-https://pubmed.ncbi.nlm.nih.gov/30874629/
-https://www.science.org/doi/10.1126/science.abm5658