Since the precise etiology of most back pain is unknown, we must conclude that the term "mechanical low back" is flawed. Other terms, such as biochemical low back pain, are also flawed. The best term to date is "nonspecific low back pain," and it should be understood that mechanical, biochemical, psychological, lifestyle and genetic factors are likely to be involved in its generation.1
The nature of the biochemical side of the spine pain equation remains elusive for most chiropractors, orthopedists, and other practitioners who were largely trained from a mechanical perspective.
Back in 1969, Alf Nachemson reported that an acidic pH was correlated with inflammatory changes around painful nerve roots. The lower the pH, the more inflammation and fibrosis, and the greater the degree of pain.2
In 1977, Marshall, et al., put forward the term "chemical radiculitis," describing it as "an inflammatory condition of the nerve root due to rupture of the annulus fibrosus and dissemination of disk fluid along the nerve root sheath." They even told us to avoid prolonged rest because it increases the risk of developing radicular adhesions.3
Jumping to 1990, Saal, et al., stated:4 "Inflammation of neural elements is frequently mentioned clinically in association with lumbar radiculopathy. Mechanical embarrassment of neural elements by definable structural abnormalities is inadequate as a sole explanation of nerve injury in this condition."
Their study suggested that the inflammatory power of the enzyme phospholipase A2 in herniated disc tissue was 20 to 100,000 times stronger than normal. Phospholipase A2 is responsible for generating pro-inflammatory eicosaonoids, such as prostaglandin E2 and leukotriene B4.
Then, in 1995, Saal wrote the following in a review article:5
"The clinical features of many cases of low back pain [are] inadequately explained by anatomic abnormalities alone. A pathophysiologic mechanism that includes a combination of mechanical and biochemical factors is an alternative explanation that is accompanied by less paradox than a purely structural paradigm. A potential unifying feature includes inflammation of neural elements caused by the chemical components of the intervertebral disc."
In response to a letter to the editor, Saal re-emphasized his position that disc herniation and discogenic pain are not solely mechanical phenomena:6
"The emphasis of the Role of Inflammation in Lumbar Pain paper is that the structural paradigm for painful lumbar disc disorders is flawed. The effect of mechanical factors alone cannot fully explain the range of clinical observations as outlined in the paper, and the disc has been shown to generate an in situ chronic inflammatory response and to contain inflammogenic substances, among them phospholipase A2. These facts are used to support the hypothesis that the combination of inflammation and mechanical factors are necessary to explain the clinical entity of lumbar radiculopathy caused by disc herniation and discogenic low back pain."
In 1997, researchers reported that inflammation-causing phospholipase A2 was more active in sequestrated herniations compared with other disc abnormalities. These same researchers reviewed the literature and concluded that degenerated facet joints and discs produce numerous inflammatory enzymes and mediators, including phoslpholipase A2, metalloproteinases, prostaglandins, nitric oxide, and various cytokines.7
In the Oct. 1, 2004 issue of Spine, a study reported that pro-inflammatory cytokines were found in joint cartilage and synovium of facet joint tissue harvested from patients suffering with disc herniation and lumbar spinal canal stenosis. Intriguingly, a higher concentration of cytokines was found in patients suffering with canal stenosis, compared to disc herniation.8
In short, many continue to believe that spinal dysfunction is a mechanical problem, which is incorrect. Spinal dysfunction is both a mechanical and a biochemical problem, among other factors, and the biochemical aspect requires a biochemical intervention.
Fortunately, we as chiropractors can offer an anti-inflammatory biochemical approach that is safe. As it turns out, dietary factors and nutritional supplements can dramatically influence the biochemistry of inflammation.
The diet to reduce inflammation is straightforward: Humans should consume vegetation (fruits and vegetables) and animals that eat vegetation (grass-fed cattle, etc., or wild game). The supplements that support an anti-inflammatory state include a multivitamin, magnesium (400-1,000 mg/day), EPA/DHA (1-2 g/day), and coenzyme Q10 (100 mg/day).9-10 Anti-inflammatory proteolytic enzymes should also be considered in the acute state.10
- Adams M, Bogduk N, Burton K, Dolan P. The Biomechanics of Back Pain. New York: Churchill Livingstone; 2002: p.80.
- Nachemson A. Intradiscal measurements of pH in patients with lumbar rhizopathies. Acta Ortho Scand 1969;40:23-42.
- Marshall LL, Trethewie ER, Curtain CC. Chemical radiculitis: a clinical, physiological, and immunological study. Clin Ortho Rel Res 1977;129:61-67.
- Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990;15:674-78.
- Saal JS. The role of inflammation in lumbar pain. Spine, Aug. 15, 1995;20(16):1821-27.
- Saal JS. Letter to editor in response to Dr. Timothy Floyd. Spine 1996;21:898.
- Piperno M, le Graverand MP, Reboul P, et al. Phospholipase A2 activity in herniated lumbar discs. Clinical correlations and inhibition with piroxicam. Spine 1997;22:2061-65.
- Igarashi AI, Kickuchi S, Konno S, Olmarker K. Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders. Spine 2004;29:2091-95.
- Seaman DR. Clinical Nutrition for Pain, Inflammation, and Tissue Healing. Wilmington (NC): NutrAnalysis; 1998.
- Seaman DR. The diet-induced proinflammatory state: a cause of chronic pain and other degenerative diseases? J Manipulative Physiol Ther 2002;25(3):168-79.
David Seaman, DC, MS, DABCN
Port Orange, Florida
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