Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
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I am a long-term myeloma survivor and myeloma cancer coach. Have you heard the Groucho Marx joke that he wouldn’t want to join a club that would have him as a member? Well, you don’t want MM and you don’t want pain from MM. And I am sad to say that I have a lot of both.
Most of the pain experienced by Multiple Myeloma patients and survivors (MMers) is from either bone damage from the disease itself (a symptom of MM), or from the damage done by chemotherapy or radiation (a side-effect). The main problem with pain caused by MM is that it is often ignored. I ignored my neck pain for months before I got an x-ray.
Like most MM symptoms and side effects the sooner you identify and address the source of the pain the more likely you are to resolve your pain. Knowledge, as the saying goes, is power. Especially with multiple myeloma.
“Multiple myeloma can cause soft spots in the bone called osteolytic lesions, which appear as holes on an X-ray. These osteolytic lesions are painful and can increase the risk of painful breaks or fractures.
Myeloma can also cause nerve damage or pain when a tumor presses up against a nerve. Tumors can also compress the spinal cord, which can cause back pain and muscle weakness.
According to the Multiple Myeloma Research Foundation, approximately 85 percent of patients diagnosed with multiple myeloma experience some degree of bone loss and the pain associated with it…”
“Recommendations: On the basis of the paucity of high-quality, consistent evidence, there are no agents recommended for the prevention of CIPN. With regard to the treatment of existing CIPN, the best available data support a moderate recommendation for treatment with duloxetine. Although the CIPN trials are inconclusive regarding tricyclic antidepressants (such as nortriptyline), gabapentin, and a compounded topical gel containing baclofen, amitriptyline HCL, and ketamine, these agents may be offered on the basis of data supporting their utility in other neuropathic pain conditions given the limited other CIPN treatment options. Further research on these agents is warranted…”
“Treatment options for neuropathic pain have limited efficacy and use is fraught with dose-limiting adverse effects. The endocannabinoid system has been elucidated over the last several years, demonstrating a significant interface with pain homeostasis. Exogenous cannabinoids have been demonstrated to be effective in a range of experimental neuropathic pain models, and there is mounting evidence for therapeutic use in human neuropathic pain conditions. This article reviews the history, pharmacologic development, clinical trials results, and the future potential of nonsmoked, orally bioavailable, nonpsychoactive cannabinoids in the management of neuropathic pain.”
“Cannabidiol, the major psycho-inactive component of cannabis, has substantial anti-inflammatory and immunomodulatory effects. This study investigated its therapeutic potential on neuropathic (sciatic nerve chronic constriction) and inflammatory pain (complete Freund’s adjuvant intraplantar injection) in rats. In both models, daily oral treatment with cannabidiol (2.5-20 mg/kg to neuropathic and 20 mg/kg to adjuvant-injected rats) from day 7 to day 14 after the injury, or intraplantar injection, reduced hyperalgesia to thermal and mechanical stimuli. In the neuropathic animals, the anti-hyperalgesic effect of cannabidiol (20 mg/kg) was prevented by the vanilloid antagonist capsazepine (10 mg/kg, i.p.), but not by cannabinoid receptor antagonists.
Cannabidiol’s activity was associated with a reduction in the content of several mediators, such as prostaglandin E(2) (PGE(2)), lipid peroxide and nitric oxide (NO), and in the over-activity of glutathione-related enzymes. Cannabidiol only reduced the over-expression of constitutive endothelial NO synthase (NOS), without significantly affecting the inducible form (iNOS) in inflamed paw tissues. Cannabidiol had no effect on neuronal and iNOS isoforms in injured sciatic nerve. The compound’s efficacy on neuropathic pain was not accompanied by any reduction in nuclear factor-kappaB (NF-kappaB) activation and tumor necrosis factor alpha (TNFalpha) content. The results indicate a potential for therapeutic use of cannabidiol in chronic painful states.”