More than 50 million Americans suffer with chronic pain, accounting for more than 25 million physician visits per year for low back pain alone.1 The outcome is a nation of people who rely on nonsteroidal anti-inflammatory drugs (NSAIDs) for relief.Unfortunately, this is associated with various side effects that can be life-threatening for some. The second leading cause of peptic ulcers is the use of NSAIDs. Concerning ulcer-induced mortality, one third of NSAID / aspirin deaths are associated with low-dose aspirin use, presumably to prevent cardiovascular disease.2
NSAID use is also associated with cardiovascular mortality, particularly in the elderly. Associations exist for both selective COX-2 inhibitors, such as Celebrex, and non-selective NSAIDs, such as ibuprofen and naproxen.1
Diet Is Connected to NSAID Use
It is well-known that dietary omega-6 fatty acids (linoleic and arachidonic acid) become a painful prostaglandin (PGE2) and a cardiovascular-promoting thromboxane (TXA2).3-4 Also well-known is that we in America consume excessive levels of omega-6-rich foods.5 Over time, excess omega-6 fatty acids become incorporated in human tissues, an example being joints. Studies have identified an excess concentration of arachidonic acid in arthritic joints.6-9 In 1991, it was determined that the histological severity of osteoarthritis was associated with increasing levels of arachidonic acid.7
In short, this means we need to stop eating plates full of "pain" – the best examples of which include fast food, bags of potato chips, and omega-6-oiled packaged foods. It is difficult to modulate pain unless the excessive consumption of "painful" foods is slowed.
Chronic NSAID Use Is No Surprise
Based on the fact that we consume arachidonic acid / PGE2 excessively, it is no surprise that we have become reliant on drugs that inhibit the COX enzyme that converts arachidonic acid into painful PGE2. Consider comments from a recent Cochrane review:10 "Non-steroidal anti-inflammatory drugs (NSAIDs) are the most frequently prescribed medications worldwide and are commonly used for treating low-back pain."
Dietary Changes to Reduce Pain
Making behavioral changes to reduce dietary inflammation is not easy for most people, so the likelihood that a substantial reduction in NSAID intake will occur in the near future is not high. Motivating patients to consider that food choices can influence painful body chemistry is very important – urging people to eat more vegetables, fruit, nuts, omega-3 seeds, and lean animal protein is known to substantially reduce the inflammation chemistry associated with pain.3-4,11-14
An added benefit to making such dietary changes is that fruits and vegetables contain salicylates. Vegetable and fruit intake at a level consumed by vegetarians provides a level of dietary salicylates that appears to be equivalent to 75 mg of aspirin.15-16
Basic supplementation should also be considered. No matter what level of dietary change is made, supplementation with magnesium, vitamin D and omega-3 fatty acids seems reasonable, as low levels of each have been linked to the expression of inflammation.3,17-18 Magnesium deficiency in animal models is known to increase nociceptive activity,19 and vitamin D deficiency has been linked to musculoskeletal pain expression in general20-21 and with low back pain in particular.22 These supplements may be beneficial no matter what level of dietary change is initiated.
White Willow Bark
An additional supplement to consider is white willow bark, which may be an effective alternative to NSAID use. Bogduk23 provides the following commentary on its efficacy:
"Studies of natural therapies have provided a challenging alternative to conventional drugs for the management of acute low back pain, at least in the context of exacerbation. Controlled trials have shown that willow (Salix) bark extracts are more effective than placebo, and no less effective than a COX-2 inhibitor or NSAID; yet they are considerably less expensive."
In 2007, the American Pain Society and the American College of Physicians developed a joint clinical practice guideline for the treatment of acute low back pain that was published in the Annals of Internal Medicine.24 The level of evidence supporting the use of white willow was fair and the net benefit was moderate, which is the same benefit as acetaminophen, NSAIDs and muscle relaxants.
The dose of salicin that was used to offer analgesic benefits, 240 mg, is found in 1,000 mg of white willow bark extract. Side effects with white willow are less than with NSAIDs and the same as placebo.25-26 Salicin is converted to salicylic acid after absorption, which is thought to be a reason why there are minimal side effects compared to aspirin and traditional NSAIDs.27
Additionally, 240 mg of salicin produces salicylate concentrations equivalent to those after consumption of 100 mg acetylsalicylate, which is a more cardioprotective rather than an analgesic dose. Other co-active compounds such flavonoids provide the additional the anti-inflammatory and analgesic effects and are not harmful to the gastrointestinal mucosa, in contrast to acetylsalicyclic acid (aspirin).28
Dietary change appears to be a key to creating body chemistry that is anti-inflammatory / analgesic. Supplemental magnesium, vitamin D, and omega-3 fatty acids are important additions. White willow bark extract can be used as a natural analgesic as needed.
- Hochman JS, Shah NR. What price pain relief? Circulation, 2006;113:2868-70.
- Lanas A, Perez-Aisa MA, Feu F, et al. A nationwide study of mortality associated with hospital admission due to severe gastrointestinal events and those associated with nonsteroidal anti-inflammatory drug use. Am J Gastroenterol, 2005;100:1685-93.
- Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ration in cardiovascular disease and other chronic diseases. Exp Biol Med, 2008;233:674-88.
- Seaman DR. The diet-induced proinflammatory state: a cause of chronic pain and other degenerative diseases? J Manipulative Physiol Ther, 2002;25:168-79.
- Cordain L, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr, 2005;81(2):341-54.
- Bonner WM, Jonsson H, Malanos C, Bryant M. Changes in the lipids of human articular cartilage with age. Arthritis Rheum, 1975;18(5):461-73.
- Lippiello L, Walsh T, Fienhold M. The association of lipid abnormalities with tissue pathology in human osteoarthritic articular cartilage. Metabolism, 1991;40(6):571-76.
- Adkisson HD, et al. Unique fatty acid composition of normal cartilage: discovery of high levels of n-9 eicosatrienoic acid and low levels of n-6 polyunsaturated fatty acids. FASEB J, 1991;5(3):344-53.
- Plumb MS, Aspden RM. High levels of fat and (n-6) fatty acids in cancellous bone in osteoarthritis. Lipids Health Dis, 2004;3:12.
- Roelofs PDDM, Deyo RA, Koes BW, Scholten RJPM, van Tulder MW. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database of Systematic Reviews, 2008;1.
- Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: emphasis on the betabolic syndrome. J Am Coll Cardiol, 2006;48;677-85.
- Basu A, Sridevi Devaraj S, Jialal I. Dietary factors that promote or retard inflammation. Arterioscler Thromb Vasc Biol, 2006;26;995-1001.
- O'Keefe JH, Gheewala NM, O'Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol, 2008;51;249-255
- Galland L. Diet and inflammation. Nutr Clin Pract, 2010;25:634-40.
- Hare LG, Woodside JV, Young IS. Dietary salicylates. Another benefit of fruit and vegetable consumption? J Clin Pathol, 2003;56:649–50.
- Lawrence JR, Peter R, Baxter GJ, Robson J, Graham AB, Paterson JR. Urinary excretion of salicyluric and salicylic acids by non-vegetarians, vegetarians, and patients taking low dose aspirin. J Clin Pathol, 2003;56:651–53.
- Kim DJ, Xun P, Liu K, Loria C, Yokota K, Jacobs DR Jr, He K. Magnesium intake in relation to systemic inflammation, insulin resistance, and the incidence of diabetes. Diabetes Care, 2010;33(12):2604-10.
- Ngo DT, Sverdlov AL, McNeil JJ, Horowitz JD. Does vitamin D modulate asymmetric dimethylarginine and C-reactive protein concentrations? Am J Med, 2010 Apr;123(4):335-41.
- Soave PM, Conti G, Costa R, Arcangeli A. Magnesium and anaesthesia. Curr Drug Targets, 2009;10(8):734-43.
- Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc, 2003;78:1463-1470.
- Holick MF. Vitamin D deficiency: what a pain it is. Mayo Clin Proc, 2003;78:1457-59.
- Schwalfenberg G. Improvement of chronic back pain or failed back surgery with vitamin D repletion: a case series. J Am Board Fam Med, 2009;22:69-74.
- Bogduk N. Pharmacological alternatives for the alleviation of back pain. Expert Opin Pharmacother, 2004;5(10):2091-98.
- Chou R, Qaseem A, Snow V et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med, 2007;147:478-91.
- Chrubasik S, Eisenberg E, Balan E, Weinberger T, Luzati R, Conradt C. Treatment of low back pain exacerbations with willow bark extract: a randomized double-blind study. Am J Med, 2000;109:9-14.
- Chrubasik S, Kunzel O, Model A, Conradt C, Black A. Treatment of low back pain with a herbal or synthetic anti-rheumatic: a randomized controlled study. Willow bark extract for low back pain. Rheumatology, 2001;40(12):1388-93.
- Akao T, et al. Evaluation of salicin as an antipyretic prodrug that does not cause gastric injury. Planta Med, 2002;68(8);714-18.
- Vlachojannis JE, Cameron M, Chrubasik S. A systematic review on the effectiveness of willow bark for musculoskeletal pain. Phytother Res, 2009;23:897-900.
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