Does Omega 3 Repair Repair Nerve Damage
Case studies demonstrate that oral intake of omega-iii polyunsaturated fat acids from pharmaceutical-course fish oil supplements results in pain reduction and functional improvement in patients with neuropathic pain.
The literature of the past twenty years contains numerous studies and clinical investigations that highlight the disquisitional part played past omega-iii polyunsaturated fatty acids (PUFAs) in human being health and disease. Omega-iii fat acids are essential for growth and development and play a vital role in the prevention and treatment of cardiovascular disease, inflammatory and autoimmune disorders, cancer, diabetes, and low.i
In this newspaper we volition review the etiology, symptoms, and treatment of neuropathic pain; review the literature on the reported benefits of omega-3 fat acids; present example studies of patients suffering from neuropathic pain treated with omega-3 FA; and provide some practical application recommendations for a clinical practice.
Neuropathic Hurting Etiology
Neuropathic hurting (NeP) is divers as hurting caused by a lesion of the peripheral or central nervous system (or both) manifesting with sensory symptoms and signs.2 Electric current estimates suggest that this devastating status may affect upwardly to 3% of the population.3 NeP is costly to the health intendance system. In the U.South. alone, the costs associated with this disorder are estimated at $40 billion annually.ii
NeP can be caused by trauma, inflammation, transection, nerve compression, ischemia or metabolic injury to neuronal cell bodies. NeP can also be caused by cancer, diabetes, multiple sclerosis (MS), Parkinson disease, infectious agents (e.chiliad., HIV-1) or by the toxic side effects of various drug regimens.2,4,five
In states of NeP, sensory (nociceptive) neurons damaged by disease, injury or drugs discharge spontaneously and leads to sustained levels of excitability.four These abnormal discharges "cross-talk" with adjacent uninjured nervus fibers, resulting in amplification of pain impulses which causes peripheral sensitization. In turn, central neurons innervated by such nociceptors undergo dramatic functional changes including a land of hyperexcitability termed primal sensitization.2 This heightened activity is idea to result from increased neuronal expression and activation of ion channels, such as voltage-gated sodium channels (VGSCs), and receptors that initiate and mediate the abnormal generation of action potentials and synaptic transmission in pain pathways.five,6
To summarize, following injury to sensory nerves, nociceptor-driven activity in the spinal cord becomes divorced from normal physiology, so that pain is produced in the absence of any advisable stimulus and results in NeP.5
Neuropathic Hurting Symptoms and Treatment
Patients suffering from NeP feel a wide variety of symptoms. Some examples include spontaneous paresthesias and dysesthesias manifesting every bit abnormal sensations including itch, numbness, itching, and tingling.4 Pain resulting from this disorder can be divided into two categories: stimulus-evoked hurting and stimulus-contained (spontaneous) pain.2 Stimulus-evoked hurting is associated with different types of hypersensitive pain behavior, including allodynia and hyperalgesia. Spontaneous pain can be either constant (e.g., called-for) or intermittent (shooting, electrical stupor-similar) and most patients describe having both.two
From a therapeutic standpoint, NeP is a difficult disorder to care for. Animal models of chronic NeP induced by spinal root ligation or sciatic nerve constriction show that prostaglandins are required to initiate the NeP process, but are non necessary for its maintenance.7 Therefore, nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen have limited efficacy in treating NeP. Furthermore, the apply of opiates to alleviate NeP is challenging because of the high doses that are often required which effectively narrow the therapeutic index.8 Other drugs, such as anticonvulsants and tricyclic antidepressants, may have some limited apply but they are associated with significant adverse effects.3
Omega-iii Fatty Acids Construction, Sources and Dietary Intake.
Omega-iii (or due north-3; w-3) fatty acids are long-chain PUFAs of institute and creature origin, that are typically eighteen, 20, or 22 carbon atoms in chain length. The term "w-3" signifies that the get-go double bond in the molecule is located at the third carbon position counting from the west-finish of the fatty acrid chain.
Fish oil from oily fish is a rich source of long chain n-3 PUFAs, consisting mainly of eicosapentaenoic acrid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3)ix (encounter Figure 1). Vegetable oils are not a source of EPA or DHA although sure types (due east.g., flaxseed and walnut oil) do contain varying amounts of an alternate form of omega-3 fatty acid known as alpha-linolenic acrid (ALA; xviii:3n-iii).10,eleven ALA tin can be metabolized past the trunk into the longer concatenation EPA and DHA via a series of desaturation/elongation reactions11 (see Effigy 2) but, unlike rats, humans can only catechumen a small amount (5%) of ALA into EPA.
Omega-6 (or n-half dozen; w-half dozen) fatty acids, such as linoleic acid (LA; 18:2n-half-dozen) tin can exist constitute in abundance in many vegetable oils (east.g. safflower, sunflower, corn, cottonseed, soybean). LA can exist converted by the body into the longer concatenation arachidonic acid (AA; 20:4n-half dozen).eleven Arachidonic acid is known to lead into pro-inflammatory eicosanoids.
Both due north-3 and n-vi PUFAs are used for phospholipid production and are thus components of cell membranes throughout the body, contributing to the physical and functional properties of those membranes. In addition, northward-3 and due north-6 PUFAs serve as precursors to eicosanoids which are fundamental mediators and regulators of diverse physiological processes such as inflammation, vascular tone, and hemostasis.
Since the dawn of the industrial historic period, the dietary intake of n-half dozen fatty acids has steadily increased—particularly in Western diets—to the point where they currently represent the chief dietary source of PUFAs.one,12 By contrast, the dietary intake of omega-3 fatty acids has dramatically declined in Western countries over the last 100 yearsi (see Effigy 3).
This is due, in office, to the vast consumption of omega-6 rich vegetable oils and products from animals fed with grains containing n-6 PUFAs.10 Information technology has been suggested that the ideal dietary ratio of n-six to n-3 fatty acids be approximately 1-2:1.1 However, in the typical North American diet, the n-half dozen:n-iii dietary ratio is about eight:1 and, in some instances, may be as high equally 20-30:i.1,11 This great discrepancy betwixt due north-6 and n-3 PUFA intake is not without consequence. It is idea that the elevated n-6:n-three ratio almost likely contributes to an increased incidence of cardiovascular disease (CVD), inflammatory disorders, autoimmune diseases, major low, and cancer.12
PUFAs and Eicosanoid Metabolism
The n-iii and n-vi fat acids are chemically and metabolically distinct and have contrasting physiological functions12 (see Figure 4). The eicosanoid metabolic products synthesized from AA, namely prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), hydroxy fatty acids and lipoxins are formed in larger quantities than those formed from north-iii PUFAs—such equally EPA—because of the increased amounts of n-6 PUFAs in the Western diet.1 Eicosanoids derived from AA are biologically active in small quantities and, if they are formed in inordinate amounts, they contribute to the germination of atheromas and thrombi.ane In addition, they lead to the development of allergic and inflammatory disorders and to cell proliferation.
When humans increase their consumption of EPA and DHA, from oily fish or from fish oil supplements (liquids or capsules), an increased proportion of these fatty acids are found in the cell membranes of inflammatory cells in particular.xiv EPA and DHA incorporation into these membranes occurs in a dose-response fashion and is partly at the expense of AA.xv Hence, since at that place is less AA available for eicosanoid biosynthesis by the cyclooxygenase (COX) and lipoxygenase (LOX) enzymes, fish oil supplementation of the diet results in a decreased production of the proinflammatory prostaglandin E2 (PGE2), thromboxane A2 (TXA2), TXB2, leukotriene B4 (LTB4), LTE4 and 5-hydroxyeicosatetraenoic acid, but not of prostacyclin I2 (PGI2).12,fourteen
EPA can also act equally a substrate for both COX and LOX enzymes and thereby compete with AA for prostaglandin and leukotriene synthesis.12 EPA gives ascension to the 3-series PGs and TXs (such every bit TXA3, PGE3, PGI3) and to the 5-series LTs (LTB5, LTE5) and 5-hydroxyeicosapentaenoic acid.14 The eicosanoids formed from EPA are frequently less biologically strong than those formed from AA.15 For example, LTB5 is 10- to 100- fold less stiff as a neutrophil chemotactic agent than LTB4 and PGE3 is a less potent inducer of COX-2 cistron expression in fibroblasts than PGE2.15 Furthermore, TXA3 is a weaker platelet aggregator and vasoconstrictor than TXA2.12 Recent studies have shown that EPA and DHA also give rise to resolvins (from EPA and DHA) and docosanoids (from DHA) through pathways involving COX and LOX enzymes.xvi In jail cell culture and animal-feeding studies, these novel mediators were demonstrated to exist anti-inflammatory, inflammation resolving, and immu-nomodulatory.16
Some of the furnishings of n-3 PUFAs are elicited by eicosanoid-independent mechanisms. Studies take shown, for instance, that the intake of dietary fish oil results in decreased leukocyte chemotaxis, decreased expression of adhesion molecules and decreased generation of reactive oxygen species.15 n-3 PUFAs have also been shown to inhibit the product of proinflammatory cytokines such equally tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6 and IL-8, in both cell culture studies and in human trials.14,xv Additionally, northward-three PUFAs might exert their effects on inflammatory factor expression through direct action on intracellular signaling pathways which lead to activation of 1 or more transcription factors such every bit nuclear factor kappa B (NF-kb).14
north-3 PUFAs and Chronic Affliction
The benefits of n-iii PUFA supplementation are well documented in the literature for the prevention and direction of a wide diverseness of health atmospheric condition including inflammatory and autoimmune diseases, cardiovascular disease, and depression. Less is known, all the same, nearly the use and efficacy of these fatty acids in the treatment of other disorders such equally fibromyalgia syndrome and neuropathic pain.
n-3 PUFAs and Inflammatory/ Autoimmune Diseases
A number of clinical trials have been conducted assessing the benefits of dietary supplementation with n-three PUFAs in inflammatory and autoimmune disease in humans, including RA, Crohn'southward diseases, ulcerative colitis, psoriasis, lupus erythematosus, MS, and migraine headaches.12
A recent meta-analysis of 17 randomized controlled trials (RCTs) was conducted by Goldberg et al. to assess the pain relieving furnishings of n-3 PUFAs in patients with rheumatoid arthritis (RA) or joint pain secondary to inflammatory bowel disease and dysmenorrhea.17 Results from the analysis showed that supplementation with n-3 PUFAs for iii-4 months reduces patient-reported articulation pain intensity, minutes of morning stiffness, number of painful and/or tender joints, and NSAID consumption.
Maroon et al. conducted a non-placebo controlled report to make up one's mind if patients could effectively substitute fish oil as an anti-inflammatory for NSAIDs.xviii The written report included 250 participants who had been seen by a neurosurgeon and were found to have chronic, nonsurgical, neck or back pain. After taking north-3 PUFAs for an average of 75 days, 59% discontinued their use of prescription NSAIDs and 60% stated that their overall pain was improved. Moreover, 88% stated they would continue to take the n-3 PUFAs. No pregnant agin furnishings were reported. These results corroborate other controlled studies that compared ibuprofen and n-3 PUFAs demonstrating equivalent furnishings in reducing arthritic hurting.eighteen Furthermore, such findings suggest that n-3 PUFAs may exist a safe alternative to NSAIDs, particularly the COX-ii inhibitors which have been associated with extreme complications such equally gastric ulcers, bleeding, blood force per unit area increase, myocardial infarction, and even death.19
n-3 PUFAs and Cardiovascular Disease
Numerous intervention and clinical trials support the use of n-3 PUFAs in the reduction of diverse run a risk factors for CVD, myocardial infarction, and sudden cardiac death.11 Some of the cardiovascular benefits that accept been associated with n-3 PUFA supplementation include reduction in ventricular arrhythmias, increase in eye rate variability, antithrombotic and other effects on the hemostatic system (moderately longer haemorrhage times, reduced plasma viscosity), lipid lowering, improved endothelial relaxation, inhibitory effect on arthero-sclerosis and inflammation, and sup-pressed product of inflammatory cytokines (interleukins and TNF) and mitogens.11
The anti-arrhythmic event of n-3 PUFAs is thought to be the primary benefit associated with their use. However, this effect has not been conspicuously demonstrated in clinical trials.20 A meta-analysis of iii RCTs was conducted by Jenkins et al. to decide the effects of fish oil supplementation in patients with implantable cardioverter defibrillators who were at risk of ventricular arrhythmia.twenty They too wanted to determine if at that place was meaning heterogeneity between trials. Meta-analysis of information nerveless at one year showed no overall consequence of fish oil on the relative take chances of implantable cardioverter defibrillator discharge. Results also showed meaning heterogeneity between trials. Furthermore, patient response to fish oil supplementation was heterogeneous with one report showing a significant do good of fish oil and some other an adverse tendency.
n-3 PUFAs and Depression
Mounting evidence from laboratory, epidemiological, and clinical studies suggests that n-3 PUFAs may play a function in the prevention and management of depression. For the fourth dimension being, the bulk of clinical testify indicates that EPA may be most important in mood stability and that relatively low levels are required for successful outcomes.ten
The beneficial effects of n-iii PUFA supplementation in depression may be due in part to the modulation of brain-derived neurotrophic cistron (BDNF). cAMP response element binding protein (CREB) upregulation, via n-iii PUFA mediated inhibition of PGE2 and IL-1b, may activate the downstream target BDNF. BDNF is known to be lower in depressed patients and thus may play an important role in major low.10
n-three PUFAs and Fibromyalgia Syndrome
Some clinical show suggests n-three PUFAs may be of use in the management of fibromyalgia. Ozgocmen et al. investigated the effect of northward-3 PUFAs in the management of fibromyalgia syndrome in an open, non-controlled unmarried-blind study involving 12 female patients.21 The patients were treated for a flow of 4 weeks with high doses of due north-iii PUFAs. Results from the study showed statistically significant beneficial changes from baseline for tender indicate counts, chest expansion measurements and hurting severity, fatigue, and depression scales that were evaluated using the Fibromyalgia Impact Questionnaire.21
n-3 PUFAs and Neuropathic Pain
To date, in that location are no clinical trials that have examined the effects of n-iii PUFA supplementation in the treatment of NeP patients. Moreover, very few studies have investigated the mechanism(due south) whereby n-3 PUFAs may modulate NeP mechanisms. In that location are considerable differences between chronic NeP and chronic inflammatory hurting. The eicosanoid-dependent anti-inflammatory furnishings of north-3 PUFAs may not be relevant to NeP weather. A meaning gene in NeP is the activation in the spinal string of non-neural glial cells, macroglia, and astrocytes.5 Activated glia are characterized by proliferation, hypertrophy and increased production of inflammatory cytokines such every bit IL-1b, IL-6 and TNF-a. EPA and DHA could possibly reduce the production of these cytokines merely this remains to be determined.17 Specifically, DHA has recently been shown to play a larger function in neurogenic inflammation which was non previously predictable.22,23
It has been suggested that n-three PUFAs may block pain neuron voltage-gated sodium channels (VGSCs) which underlie NeP.,six The cistron encoding ane of the nociceptor specific VGSCs, SNS/PN3, shares a very similar genomic construction with the human cardiac VGSC factor. n-3 PUFAs are known to potently and reversibly bind to and block current through this cardiac VGSC.6 Outside of their neurological influences, some testify suggests a role in modulation of the stress response through influence of plasma cortisol. Low plasma cortisol, which is required to blunt the inflammatory process and therefore influence the inflammatory component of NeP, is associated with EFA deficiencies.24
Case Studies
We at present present a case serial of neuropathic pain patients who improved with the use of omega-3 fat acid supplements. This instance series is the first ever published on using omega-iii fatty acids supplements in the handling of neuropathic pain (and using updated criteria in diagnosis such as the DN4 and Pain Discover Questionnaires).
Patient 1: C7 Radiculopath
A 53-year-onetime left-handed police officeholder, married father of two, was diagnosed with correct-sided cervical radiculopathy. He had developed cervix symptoms in 2004. His symptoms worsened to the betoken where by Dec of 2005 he could no longer play hockey and had sleeping problems. MRI results showed evidence of a C6/C7 right lateral disc herniation compressing the correct C7 nerve root with spinal stenosis and muti-level degenerative disc disease. Past medical history included feet/panic attacks, depression, gout, and vasectomy.
Previous treatments included: physiotherapy, which was passive and did not focus on core stability grooming; prescribed pain-killers (Naproxen), and other NSAIDs such as Advil. His other medications included Diltiazam, Losec, ECASA (enteric coated acetylsalicylic acrid) and Tylenol-3.
Physical test (July 2006) revealed a height of 6'1" with a weight of 230 lbs. Blood pressure level (BP) was 106/77 mmHg. Biomechanical examination revealed a marked head-forward posture with tight pectorals and poor core stability. Neurological examination revealed a possible right rotator cuff damage besides as vasculogenic thoracic outlet compression which also would perpetuate symptoms. Additionally, he had a positive Allen'due south examination and weakness in the C6/C7 myotomes. Prior to taking n-3 PUFAs his SF-MPQ (curt class McGill pain questionnaire) rating was 30/45.
"He was started on a treatment of loftier doses of n-3 PUFAs (8 capsules/day with EPA-DHA full dose of 4800mg/day). After two and a half weeks his pain started to subside. Strength measurements were done and there was noticeable comeback in his C7 innervated muscles in the correct arm."
He was started on a handling of loftier doses of n-iii PUFAs (8 capsules/twenty-four hours with EPA-DHA total dose of 4800mg/day). After two and a half weeks his pain started to subside. Strength measurements were done and in that location was noticeable comeback in his C7 innervated muscles in the right arm. In fact, his triceps strength now on the right side was greater than the left side, measured at 125lbs and 123lbs respectively, with the Lafayette transmission muscle tester. Jamar grip forcefulness was also improved: Rt 39.ix lbs and Lt 42 lbs. After taking northward-3 PUFAs for a little over eight months, his SF-MPQ decreased to 0/45 and he started playing hockey and working out again.
He returned back on Feb 21 2008. He was nonetheless benefiting from the n-three PUFAs (his NRS pain score was 0/10 and SFMcGill 4/45). Weight and blood pressure were unchanged. He cited a time when he forgot to bring his n-iii PUFAs to a hockey tournament and noted recurrence of neck pain afterward 4 days. Otherwise, he continues to be hurting free and able to play total equipment ice hockey.
Patient 2: Thoracic Outlet Syndrome
A 48-year-quondam right-handed registered nurse, married mother of 2, was diagnosed with left lateral epicondylalgia. Her work, in the standing care department of the hospital, involves the transfer of heavy patients. She injured her left arm while transferring a 245lb patient. Following the injury, she was not able to cut the grass or shovel snow. With assistance, she could perform some household chores including vacuuming. Symptoms were aggravated by activity and alleviated by rest. Past medical history includes a piece of work-related injury to the low back in August of 2005 and neck pain due to a whiplash injury.
Previous treatments included physiotherapy, which ameliorated symptoms, equally well as Mobicox. She took daily calcium carbonate and vitamin D supplements.
Her physical exam revealed a pinnacle of 5'4" with a weight of 125 lbs. BP was 123/76 mmHg. She had regional myofascial hurting which spread interest proximally into the shoulder girdle and down into the hand. Some caste of thoracic outlet pinch was also noted with positive Allen's test often brought on with caput forward posture and tight scalene and pectoral muscles. Prior to taking northward-iii PUFAs, her SF-MPQ rating was vii/45 with mild use of emotional descriptors. Pain at its worst was rated eight/x. Her Pain Discover Questionnaire score was 20/35 and her DN4 (Neuropathic Hurting 4 Questionnaire) score was 5/10.
She was started on a handling of loftier doses of n-iii PUFAs (4 capsules/24-hour interval). Her epicondylitis pain was much improved although she still reported called-for pain when she would exert her elbow. She did not require cortisone injections. Her jamar grip was: Rt 55lbs and Lt 40lbs. Overall pain was reported lower at 2/x with a best of 0/10 and worst 4/10. Afterward taking n-3 PUFAs for vii months her SF-MPQ rating was 4/45. After thirteen months, her Pain Discover score dropped to half-dozen/35 and her DN4 score dropped to one/x.
Patient 3: Neuropathic Leg Hurting and Knee Osteoarthritis
A l-year-old right handed teacher, married father of ii, was diagnosed with severe osteoarthritis of the knee. He had left knee pain for the past 30 years due to a lacrosse injury where he sustained an ACL and meniscus tear. At the time he had surgery to remove the medial meniscus in his left genu. Pain was mostly related to activities such equally jogging, twisting, pivoting, going up—and specially, downward—the stairs. MRI results revealed degenerative changes with marked loss of joint infinite in medial compartment.
He had physiotherapy to treat his genu hurting which incorporated acupuncture, transmission therapy, and exercise. He also had 3 injections of synvisc into the left knee but experienced severe post-injection swelling.
Physical exam revealed a height of five'8" with a weight of 240lbs. BP was 138/88 mmHg. Biomechanical examination revealed left articulatio genus pain in both medial and lateral compartments of the knee, slightly more than severe in lateral parts. Human knee range of motion was 150° bilaterally with end range pain and flexion of the knee. Range of motion was adequate with mild effusion noted in the left knee and mild signs of synovial thickening. Neurological testing revealed motor strength at v/5 and a DN4 score of 5/10 (burning pain, cold worse, numbness, balmy brush allodynia, pinprick hypoesthesia) His average pain was reported at seven-8/10 with a all-time of 5/x and worst 8/10. His SF-MPQ was 11/45.
He was started on a treatment of high doses of n-3 PUFAs (eight capsules/day) and began supplementing with vitamin D and glucosamine. He reported dramatic improvement in range of move, tolerance for physical activeness, and reduced swelling afterwards aggravating activities following taking n-three PUFAs for six months.
Patient 4: Cervical Radiculopathy and Carpal Tunnel Syndrome
A 50-yr-old right-handed Holter Monitor Company representative, married father of two, was diagnosed with chronic right C7 radiculopathy/carpal tunnel syndrome. In 2003, he was involved in a motor vehicle accident. MRI results revealed evidence of right central disc protrusion at C6/C7. There was also evidence of astringent spinal stenosis at C5/C6 and moderate stenosis at C4/C5 and C6/C7. He reported limitations in such areas as, self-care, household responsibilities, social activity, recreation, sports, grip, lifting from floor to waist, and lifting overhead.
By treatments included physiotherapy, chiropractic treatment, massage therapy and occasional NSAIDs. He also supplemented with B-vitamins and coenzyme-Q10.
Concrete exam revealed a height of 5'ix½" with a weight of 240 lbs. BP was 142/95 mmHg. His jamar grip was: Lt 145lbs and Rt 130lbs. He showed evidence, both electrodiagnostically (moderately prolonged median sensory and motor latencies, 2+ denervation in C7 myotomes) and on clinical exam, of weakness in the right arm. His SF-MPQ prior to north-3 PUFA supplementation was 17/45. His average pain was reported at half-dozen/10 with a best of 0/ten and worst 9/10. His Pain Detect and DN4 scores were 10/35 and 4/10 respectively.
He was started on a treatment of high doses of n-iii PUFAs at 8 capsules/day and afterwards increased his dosage to ten-12 capsules per day. He later reported no pain during action and was able to actively work out at the gym. He besides reported sharper brain role and feeling articulate-headed. After taking n-3 PUFAs for 17 months, his Pain Detect and DN4 scores were downwards to 1/35 and 0/ten respectively.
Patient 5: Worker Compensation Fire Injury
A 54 year old rt-handed restaurant worker barbarous downwardly stairs with a vat of hot oil and sustained thirty% full body surface area burns (2nd and third caste; encounter Figure 5). He was stabilized in the local hospital and then transferred to Sunnybrook Wellness Sciences Eye (trauma burn unit). He was hospitalized in the burn unit of measurement for forty days and underwent extensive skin grafting and debridement procedures. When he was transferred to the rehabilitation hospital in March 2006, he was taking morphine 10mg up to 9/day. Despite extensive multidisciplinary management (physiotherapy, occupational therapy, nursing, psychological counseling, massage therapy), he still had astringent called-for hurting (DN4 criteria was seven/x with burning, electric shocks, tingling, pins and needles, numbness, pinprick and lite impact hypoesthesia). Numeric Ratings Scale (NRS) pain 8/10. Neuropathy Pain calibration (NPS): 85/100.
He was transitioned to long-acting morphine (MS Contin). Pregabalin (Lyrica) was added at 25mg qam and 75mg qhs. Wellbutrin was introduced and helped with mood. NRS pain improved to 6/10. Neuropathy Hurting Scale: 68/100. In May 2006, omega-3 fatty acids were added and titrated up to 2 capsules for every fifty lbs of trunk weight. When reassessed on September 29, 2006, there were objective improvements in goniometric range of motion of the shoulder and cervix. The NRS hurting was 4.5/10 and the Neuropathy Pain Calibration farther improved to 32/100.
The patient transitioned successfully to outpatient intendance and subsequent voca-tional retraining. He was able to wean down the morphine and found that the high dose omega-3 fat acids to be nigh beneficial.
Applied Awarding Recommendations for Omega-3 FA
Prior to prescribing omega-3 or any other nutraceutical, information technology is important to do a full medical work-up to dominion out more serious pathology such as cancer, infection, aneurysm, etc. One must become a total list of medications and over-the-counter products used by patients. Important interactions with the employ of omega-three include effects on coagulation. For example, if patients are on coumadin, then a more gradual titration of omega-3 and frequent checking of the INR would be advisable. If patients are diabetic, then the add-on of omega-iii will increase calories and patients are advised to adjust their diet and insulin accordingly (long-term apply of omega-three, yet, does reduce insulin resistance and improves diabetic command).
Because of the "blood-thinning" effects of omega-3, we ordinarily advise patients to stop such supplements, likewise as herbal products such as ginkgo, curcumin, ginger, ii weeks prior to whatsoever surgery, dental work, and invasive procedures such as a colonoscopy.
Lab work should be washed to follow patients on high dose omega-3. This includes markers of "silent inflammation" and include the Arachidonic acid to Eicosapentaenoic acid ratio (AA:EPA ratio). The average Northward American ratio is 12:1. An optimal ratio for cardiovascular health is one.5-3:1. Excess intake of omega-3 with a ratio of 0.5:1 is associated with an increased adventure for hemorrhagic stroke. Unfortunately, such lab testing is expensive (nigh $130 ) and most of our patients did not undergo such testing unless they were taking extremely high doses—seven.5 gm EPA/DHA or more per solar day. Testing is available at a lab such equally Nutrasource Diagnostics, Inc., Ontario, Canada. This lab measures the serum phospholipid levels which is more authentic, and more studied, than red blood cell (RBC) levels. Other useful lab tests to detect silent inflammation include the HS-CRP (optimal levels are <1.0), fasting insulin (optimal is <10 uIU/ml) and TG:HDL ratio (optimal is <ii). The references and research for this are summarized nicely in chapters iv and 7 in the "Anti-inflammation Zone" book by Barry Sears, PhD.25
Information technology is important to recommend a high quality make of omega-3. Patients are taught to read labels and ensure that products take good authorization—i gets more than for the money in a capsule or teaspoon that has a higher concentration of EPA/DHA—and has been tested for impurities. Websites such every bit the www.ifosprogram.com will list omega-three products that have been independently lab tested for contaminants such as heavy metals—including mercury—PCBs, and dioxin. The standards set by IFOS for ultra-refined EPA/DHA concentrate are very rigorous with upper limits fix as follows: mercury <ten parts per billion (ppb), pcbs <45 ppb, dioxins <1 part per trillion, total oxidation <xiii meq/L.
Our preferred products, based on purity and patient compliance (sense of taste), are the SuperEFA liquid (Seroyal Inc) and the Run across Yourself Well capsules (Nutratec). A recommended bourgeois dose is 2700mg of EPA + DHA, based on the Goldberg meta-assay. Nevertheless, a more aggressive arroyo for more severe pain can exist upwardly to 7500mg EPA+DHA. The latter arroyo volition require serum lab tests to monitor the AA:EPA ratio.
For patients who experience tummy difficulties or nausea from the employ of omega-3, we usually advise them to attempt freezing the capsules. A better response occurs with enteric coated capsules for which we recommend the Metagenics' EPA-DHA extra strength product. Digestion is improve when omega-3 are taken with nutrient. It is besides useful to split the dosage through several meals instead of all at once.
Instruct patients clearly to take only omega-3 and not omega-iii-half dozen-9. Equally noted earlier, the omega-6's are pro-inflammatory and the use of such products will non help in ameliorating pain. Omega half-dozen'south are essential just, in the typical Due north American nutrition, an excess of this is already ingested.
Remember that omega-iii FA are just 1 component of an overall integrative medical arroyo in treating hurting and optimizing wellness. Patients must learn to improve their diets and reduce arachidonic acid sources such as too much red meat and fried foods. Diets that are deficient in vitamin B6, magnesium, zinc and take excessive trans-fat acids, caffeine will have impaired delta-6 desaturase action (needed to convert alpha-linolenic acrid in the pathway towards EPA). We ofttimes combine omega-3 FA and other nutraceuticals with judicious courses of anti-inflammatory drugs (celecoxib)26 for post-surgical and postal service-musculoskeletal trauma. For astringent neuropathic pain (NRS pain >6/ten), we combine omega-3 FA with pregabalin. For opioid-resistant neuropathic pain, pharmaceutical cannabinoids are also helpful (nabilone, sativex spray).
Long-lasting lifestyle changes need to be adopted to ensure long-term relief of pain. This includes appropriate exercise, both cardio and core strengthening, weight-loss, stress reduction (prayer, meditation, humor), and good sleep hygiene. Efforts to detoxify the trunk of unhealthy "toxic" substances, such every bit trans-fats, and unhealthy "talk-sick" attitudes and behaviour are all important.
Determination
Case studies using omega-iii FA supplementation for neuropathic pain—in a variety of patient presentations—has demonstrated the efficacy of this modality. While pain questionnaires were utilized in documenting upshot measures, further research in the way of randomized double-blind controlled trials would exist needed to validate the utilise of omega-iii fatty acids for neuropathic hurting. We promise this article will stimulate such research and pb to greater pain-free health in our patients. n
Last updated on: December 20, 2011
Source: https://www.practicalpainmanagement.com/treatments/nutraceutical/omega-3-fatty-acids-neuropathic-pain
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