>>141196
I was considering making a much longer and more informative post about chronic pain and its causes, because the topic was interesting enough for me to do a lot of searching for studies, but I've been a bit busy. I hope you will list more of your health problems and any other symptoms you have, as it can help narrow down the potential remedies for your condition. For now I have one bit of advice. If you've been lurking, you may have seen some of my posts that keep repeating the same things:
• Everyone needs total intake of polyunsaturated fat to be low.
• Everyone needs to avoid eating omega-6 fatty acids (a type of polyunsaturated fat) like the plague.
• In practice, avoiding omega-6 fatty acids and polyunsaturated fat in general often means avoiding consumption of vegetable oils, most tree nuts, most seeds, and fatty fish.
Other than switching to a high carbohydrate diet (which I understand some of you don't agree with) those three points are more or less the most important parts of the solution to nearly every major health problem modern Western society encounters. Depending on your situation, you may need to do more than merely remove those things from your diet, but for now I just wanted to mention that I repeatedly see polyunsaturated fat—especially omega-6 fatty acids—involved in countless medical issues whenever I look for scientific studies. Everybody gets better when their intake is low. Here are examples potentially pertinent to you and relevant to what I just said:
Prostaglandin E2 is a derivative of arachidonic acid which comes from linoleic acid (an omega-6 fatty acid).
• Ma, Weiya, and James C. Eisenach. Morphological and pharmacological evidence for the role of peripheral prostaglandins in the pathogenesis of neuropathic pain. European Journal of Neuroscience 15.6 (2002): 1037-1047.
☞ https://doi.org/10.1046/j.1460-9568.2002.01940.x
>Inflammatory mediators produced in the injured nerve have been proposed as contributing factors in the development of neuropathic pain. Prostaglandins (PGs) are probably included in these important inflammatory mediators.
• Kawabata, Atsufumi. Prostaglandin E2 and pain—an update. Biological and Pharmaceutical Bulletin 34.8 (2011): 1170-1173.
☞ https://doi.org/10.1248/bpb.34.1170
>Prostaglandin E(2) (PGE(2)), a cyclooxygenase (COX) product, is the best known lipid mediator that contributes to inflammatory pain. Nonsteroidal anti-inflammatory drugs (NSAIDs), inhibitors of COX-1 and/or COX-2, suppress inflammatory pain by reducing generation of prostanoids, mainly PGE(2),
• Park, Jean Y., Michael H. Pillinger, and Steven B. Abramson. Prostaglandin E2 synthesis and secretion: the role of PGE2 synthases. Clinical immunology 119.3 (2006): 229-240.
☞ https://doi.org/10.1016/j.clim.2006.01.016
>Prostaglandin E2 (PGE2) is a principal mediator of inflammation in diseases such as rheumatoid arthritis and osteoarthritis. Nonsteroidal anti-inflammatory medications (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors reduce PGE2 production to diminish the inflammation seen in these diseases,
• Willis, A. L., and Mary Cornelsen. Repeated injection of prostaglandin E2 in rat paws induces chronic swelling and a marked decrease in pain threshold. Prostaglandins 3.3 (1973): 353.
☞ https://doi.org/10.1016/0090-6980(73)90073-7
• Kim, Hee Kee, et al. Analgesic effect of vitamin E is mediated by reducing central sensitization in neuropathic pain. Pain 122.1-2 (2006): 53-62.
☞ https://doi.org/10.1016/j.pain.2006.01.013
>Recent studies suggest that reactive oxygen species (ROS) are critically involved in neuropathic pain. Although vitamin E is a well-known antioxidant, its efficacy on chronic pain is not known. This study investigated the efficacy and mechanisms of vitamin E analgesia in a rat model of neuropathic pain produced by spinal nerve ligation. […] Results showed that a systemic single injection of a high dose or repetitive daily injections of low doses of vitamin E significantly reduced neuropathic pain behaviors.