Reprinted with the kind permission of Cort Johnson and Health Rising.
From opioids to anticonvulsants to antidepressants, etc. doctors throw a wide variety of drugs at nerve pain, yet the prognosis is generally poor, with 40-60% of patients receiving only partial relief. (Some studies indicate alpha lipoic acid and benfotiamine (thiamine) can be helpful for some, as well.)
Nerve pain comes in many shades and can produce burning, tingling, numbness, shooting, stabbing, allodynia, etc. Usually associated with central sensitization (increased pain sensitivity), inflammation in the brain/spinal column appears to play a significant role but few drugs are effective at reducing inflammation there.
Lyrica’s incredible success, in spite of issues with side effects and efficacy, highlights the great need for better means of dealing with neuropathic pain. Increasing restrictions on opioid use makes the development of more effective means of pain relief imperative.
Probably the most intriguing [new development] is a compound called neuroprotectin D1 (NPD1) – the subject of increasingly intense investigation. NPD1 has been mostly investigated as a protective agent in central nervous system, eye and kidney disorders but a recent study suggested it may be effective against the hardest to treat pain of all – nerve pain.
Enter a potentially cheap drug derived from a fatty acid often used in chronic fatigue syndrome and fibromyalgia.
A ‘Good’ Fatty Acid Derivative
“These compounds are derived from omega-3 fatty acids found in fish oil, but are 1,000 times more potent than their precursors in reducing inflammation,” Ru Rong Ji
Derived from DHA, an omega-3 fatty acid found in fish oils, NPD1 has neuroprotective properties.
In contrast to omega-6 fatty acids, which have pro-inflammatory effects, omega-3 fatty acids have anti-inflammatory effects. Studies have not generally borne out their efficacy in ME/CFS but they are commonly recommended and used. With NPD1 clocking in at about 1,000 times the potency of its precursor, DHA, NPDI – if it ever gets to market – will be like fish oil on speed.
NPD1 is potentially much more than a pain reliever; indeed, pain is only the latest symptom NPD1 is being thrown at. An aptly named drug, neuroprotectin D1 is produced in response to a variety of conditions, some of which occur in chronic fatigue syndrome and fibromyalgia, including oxidative stress (high in ME/CFS/FM), protein misfolding (perhaps occurring in ME/CFS), seizures and brain ischemia-reperfusion (conjectured to occur in ME/CFS/FM).
Reduced NPD1 levels may be a factor in Alzheimer’s, and just last month the Michael J. Fox Foundation awarded a NPD1 grant in hopes the compound will slow neuron loss in rodent models of Parkinson’s.
Just this month, NPD1’s effectiveness in reducing pain in mice was assessed.
Mouse Study Produces Results
”Notably…. treatment, started a few hours after the nerve trauma, eliminated neuropathic pain.”
What they did to these mice was not pretty and some people may want to skip this part. First they induced long-lasting allodynia in the mice by surgically damaging their sciatic nerve. They found that applying NPD1 prevented the allodynia from occurring. Far fewer of the mice given NPD1 chewed their toes (sometimes off) as they usually do when suffering from neuropathic pain, and the mice that did chew their paws, chewed them less.
Dorsal Horn of the Spinal Cord
A key neuropathic pain-regulating area, the dorsal horn of the spinal cord, was examined less. The dorsal horn refers to a horn of the spinal cord that received sensory information from the body via the dorsal ganglia.
Long-term potentiation and microglial activation sets the stage for increased pain signal production in the dorsal horn but neither were found in the NPD1 treated mice (while both were found in the untreated mice.) Levels of a key cytokine involved in invoking neuropathic pain, IL-1B, was reduced in the NPD1 treated mice, as well. Finally, the macrophage infiltration that is a trademark of neuroinflammation did not occur.
NPD1, then, was very effective at reducing or eliminating three important aspects of neuropathic pain and central sensitization.
DHA Not Enough – The Pure Stuff Needed
Even large doses of the precursor to NPD1 – DHA – failed to elicit significant pain reduction. A common neuropathic pain reliever, gabapentin, did reduce some of the allodynia but only at very high doses.
NPD1 appears to be able to stop the production of immune factors that attract the proinflammatory macrophages that tweak the nerves more. NPD1 also reduces neuron firing – a important factor in an over-active system.
Keep Your Eyes on NPD1
Duke researchers said they hoped to start a clinical trial to measure NPD1’s effects on pain.
NPD1 is also being studied in animal models in Parkinson’s and Alzheimer’s. It will take time, but given the amount of research NPD1’s received in the last nine years (seven studies in this year alone), it’s a good bet that NPD1 will show up in drug form at some point, possibly bringing a new and, according to these researchers, a quite safe approach to neuropathic pain and neuroinflammation.
About the Author: Cort Johnson has had ME/CFS for over 30 years. The founder of Phoenix Rising and Health Rising, Cort has contributed hundreds of blogs on chronic fatigue syndrome, fibromyalgia and their allied disorders over the past 10 years. Find more of Cort’s and other bloggers’ work at Health Rising
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