By: Alan H. Pressman, DC

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Alan H. Pressman, MS, DC, DACBN, CCSP, is past president of the Council on Nutrition of the American Chiropractic Association; former chairman, department of nutrition, New York Chiropractic College, and, associate professor of biology, University of Bridgeport, Conn. He is currently the director of research, Institute of Rehabilitative Nutrition, and maintains an active practice in New York City.

In a recent paper published in the journal Seminars in Arthritis and Rheumatism, rheumatologists Bland and Cooper reviewed the possible reversibility of degenerative joint disease.¹ In this article they propose that the degeneration of hyaline cartilage occurs as a consequence of activation of monocytes, macrophages and neutrophils which re­lease oxidants that in turn attack connective tissue and the joint lubricant substance hyaluronic acid. The activation of white cells that in turn release alarm substances and oxidants occurs as a consequence of an inflammatory cascade modulated through receptor sites on the surface of white cells which are stimulated by the presence of foreign molecules. These foreign molecules have been termed metabolic toxins and are from exogenous and endogenous sources.

The proposed mechanism that describes the degeneration of connective tissue resulting in degenerative joint disease also applies to other neuromuscular degenerative problems including fibromyalgia.² The accumulation of exogenous or endogenously produced substances that exceeds the threshold of activation is well acknowledged to produce an inflammatory cascade. This inflammatory cascade results in the production of alarm messenger substances called leucotrienes which in turn activate white cells such as the macrophages, monocytes and neutrophils to release oxidants, which include superoxide and its conversion products, hydrogen peroxide and hydroxyl radical. These very reactive non-specific oxidants in turn attack the localized tissue resulting in inflammation or irritation which in the long tern produces degeneration.³