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8 Articles in Volume 8, Issue #7
Class IV Therapy Lasers Maximize Primary Biostimulative Effects
Functional Restoration and Complex Regional Pain Syndrome
Hamular Process Bursitis
Longitudinal Study of Long-term Opioid Patients
Omega-3 Fatty Acids and Neuropathic Pain
Osteopathic Manipulative Medicine (OMM) for Lower Back Pain
Pain Care for a Global Community: Part 2
Practical Application of Neuropostural Evaluations

Omega-3 Fatty Acids and Neuropathic Pain

Case studies demonstrate that oral intake of omega-3 polyunsaturated fatty acids from pharmaceutical-grade fish oil supplements results in pain reduction and functional improvement in patients with neuropathic pain.
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The literature of the past twenty years contains numerous studies and clinical investigations that highlight the critical role played by omega-3 polyunsaturated fatty acids (PUFAs) in human health and disease. Omega-3 fatty 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 depression.1

In this paper we will review the etiology, symptoms, and treatment of neuropathic pain; review the literature on the reported benefits of omega-3 fatty acids; present case studies of patients suffering from neuropathic pain treated with omega-3 FA; and provide some practical application recommendations for a clinical practice.

Neuropathic Pain Etiology

Neuropathic pain (NeP) is defined as pain caused by a lesion of the peripheral or central nervous system (or both) manifesting with sensory symptoms and signs.2 Current estimates suggest that this devastating condition may affect up to 3% of the population.3 NeP is costly to the health care system. In the U.S. alone, the costs associated with this disorder are estimated at $40 billion annually.2

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.g., HIV-1) or by the toxic side effects of various drug regimens.2,4,5

In states of NeP, sensory (nociceptive) neurons damaged by disease, injury or drugs discharge spontaneously and leads to sustained levels of excitability.4 These abnormal discharges “cross-talk” with adjacent uninjured nerve 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 state of hyperexcitability termed central sensitization.2 This heightened activity is thought 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.5,6

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 appropriate stimulus and results in NeP.5

Neuropathic Pain Symptoms and Treatment

Patients suffering from NeP experience a wide variety of symptoms. Some examples include spontaneous paresthesias and dysesthesias manifesting as abnormal sensations including crawling, numbness, itching, and tingling.4 Pain resulting from this disorder can be divided into two categories: stimulus-evoked pain and stimulus-independent (spontaneous) pain.2 Stimulus-evoked pain is associated with different types of hypersensitive pain behavior, including allodynia and hyperalgesia. Spontaneous pain can be either constant (e.g., burning) or intermittent (shooting, electric shock-like) and most patients describe having both.2

From a therapeutic standpoint, NeP is a difficult disorder to treat. 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 not necessary for its maintenance.7 Therefore, nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen have limited efficacy in treating NeP. Furthermore, the use 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 use but they are associated with significant adverse effects.3

Omega-3 Fatty Acids Structure, Sources and Dietary Intake.

Omega-3 (or n-3; w-3) fatty acids are long-chain PUFAs of plant and animal origin, that are typically 18, 20, or 22 carbon atoms in chain length. The term “w-3” signifies that the first double bond in the molecule is located at the third carbon position counting from the w-end of the fatty acid chain.

Fish oil from oily fish is a rich source of long chain n-3 PUFAs, consisting mainly of eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3)9 (see Figure 1). Vegetable oils are not a source of EPA or DHA although certain types (e.g., flaxseed and walnut oil) do contain varying amounts of an alternate form of omega-3 fatty acid known as alpha-linolenic acid (ALA; 18:3n-3).10,11 ALA can be metabolized by the body into the longer chain EPA and DHA via a series of desaturation/elongation reactions11 (see Figure 2) but, unlike rats, humans can only convert a small amount (5%) of ALA into EPA.

Figures 1. Molecular structures of Omega-3 fatty acids.

Figures 2. Omega-3 fatty acid pathway.

Omega-6 (or n-6; w-6) fatty acids, such as linoleic acid (LA; 18:2n-6) can be found in abundance in many vegetable oils (e.g. safflower, sunflower, corn, cottonseed, soybean). LA can be converted by the body into the longer chain arachidonic acid (AA; 20:4n-6).11 Arachidonic acid is known to lead into pro-inflammatory eicosanoids.

Both n-3 and n-6 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, n-3 and n-6 PUFAs serve as precursors to eicosanoids which are key mediators and regulators of various physiological processes such as inflammation, vascular tone, and hemostasis.

Since the dawn of the industrial age, the dietary intake of n-6 fatty acids has steadily increased—particularly in Western diets—to the point where they currently represent the principal dietary source of PUFAs.1,12 By contrast, the dietary intake of omega-3 fatty acids has dramatically declined in Western countries over the last 100 years1 (see Figure 3).

Figures 3. Changes in fat consumption throughout human history: note the dramatic rise in trans-fats, omega-6, saturated fats. From The Omega Plan by Artemis P. Simopoulos MD and Jo Robinson13 (with permission).

This is due, in part, to the vast consumption of omega-6 rich vegetable oils and products from animals fed with grains containing n-6 PUFAs.10 It has been suggested that the ideal dietary ratio of n-6 to n-3 fatty acids be approximately 1-2:1.1 However, in the typical North American diet, the n-6:n-3 dietary ratio is about 8:1 and, in some instances, may be as high as 20-30:1.1,11 This great discrepancy between n-6 and n-3 PUFA intake is not without consequence. It is thought that the elevated n-6:n-3 ratio most likely contributes to an increased incidence of cardiovascular disease (CVD), inflammatory disorders, autoimmune diseases, major depression, and cancer.12

Last updated on: December 20, 2011