No matter if one is a DC, ND, MD, DO, or PT, one of the many things that we have in common is that we all learn about inflammation; and we all typically learn from similar texts, including Robbins Pathology and Guyton's Physiology. One major problem with these texts is that they do not address inflammation in a clinical context; that is, we are not told how to treat inflammation.
We do learn that acute inflammation is caused by many agents, such as microbial infection, and tissue injury via physical, chemical, and thermal mechanisms. However, no approach to treatment is discussed that applies to chiropractic practice. Concerning chronic inflammation, we learn from Robbins Pathology that the most common cause is infection or autoimmune disease - two agents about which natural treatment options, if any, are not discussed.
The primary passive applications include adjusting and therapeutic modalities, and while inflammation may be influenced by such interventions, we have little information about whether or not the resolution of inflammation occurs ... and this holds true for conventional interventions as well, such as drugs and surgery.
"We need to eat less inflammatory foods rich in n-6 fatty acids, and eat more n-3-rich foods"
Charles Serhan, from Harvard Medical School, has been studying the mediators of inflammation for many years, and notes that "inflammation resolution" is an area that has received little research attention. In fact, he states that, "Resolution is essentially uncharted terrain."
1 There is a seemingly endless list of chemical mediators that participate in the inflammatory process, such as eicosanoids, cytokines, kinins, and growth factors. In this regard, Serhan asks the following poignant questions:1
"Should we make each 'pro-inflammatory mediator' a drug target? Should we try to selectively inhibit each of the hundreds if not thousands of important molecules?"
He notes that selective COX-2 inhibitors, for example, can disturb resolution inflammation, and lead to a delay in the return to homeostasis, which is likely to be an unwanted side-effect.
In 2000, Serhan first published his research about omega-3 fatty acid-derived mediators that function to resolve inflammation, and he referred to them as "resolvins." Eicosapentaenoic acid (EPA) is the precursor for 18R-resolvin, and docosahexaenoic acid (DHA) is the precursor for 17S-resolvin.1 Resolvins create "stop signals" and thus dampen inflammation; they appear to reduce cytokine activity and the chemotactic recruitment of neutrophils and their pro-inflammatory activity,1 and also reduce NFkB activity.2
Serhan points out that chronic inflammation is known to be involved in the pathogenesis of many chronic diseases, such as arthritis, periodontal disease, cancer, heart disease and Alzheimer's disease, and notes that lay magazines, such as the Feb. 23, 2004 issue of Time Magazine, have picked up on this fact. Serhan's research suggests that nutrition is likely to become the premier candidate to drive the resolution of inflammation.
From a nutritional perspective, it is known that our consumption of omega-3 (n-3) fatty acids from green vegetables, fish, wild game, and pasture-fed animals is quite low, such that researchers estimate that our average dietary omega-6 to omega-3 fatty acid ratio is about 20-30:1. Omega-6 (n-6) fatty acids from grains, flour products, corn, safflower, sunflower, and soybean oils serve as the precursors for pro-inflammatory eicosanoids such as prostaglandin-E2 and leukotriene-B4, and also promote free-radical generation and pro-inflammatory cytokine release.3 We know that this imbalance of fatty acid intake is far from the 1:1 ratio of n-6 to n-3 to which we are genetically adapted, and the likely cause of the inflammation-driven diseases mentioned above, including type 2 diabetes.3
In the clinical setting, we should consider viewing this fatty acid imbalance as a possible cause of pain syndromes that do not resolve. A 20:1 n-6 to n-3 fatty acid ratio and our high intake of trans-fatty acids are likely to result in a negligible production of eicosanoids and resolvins derived from EPA and DHA. This is because the same enzymes are utilized in the biosynthesis of n-6 eicosanoids and n-3 eicosanoids and resolvins, such that our substantial n-6 intake serves to functionally inhibit the production of n-3-derived anti-inflammatory mediators.
Chronic inflammation is known to be involved in the pathogenesis of many chronic diseases, such as arthritis, periodontal disease, cancer, heart disease and Alzheimer's disease
Without resolvins, it is likely that inflammation will persist without resolution, leading to chronic inflammatory disease in the long term and persistent pain throughout life. For this reason, we need to eat less inflammatory foods rich in n-6 fatty acids, and eat moren-3-rich foods. Supplementation with n-3 fatty acids is also very important. Most individuals are not likely to achieve appropriate n-6:n-3 ratios with diet alone. Taking 1-3 grams of EPA/DHA is reasonable and without side-effects, and this is because such supplementation merely restores n-3 intake to an appropriate level.
Only patients taking coumadin need to be wary of EPA/DHA supplements and other anti-inflammatory supplements, such as ginger and turmeric. Blood-clotting activity must be closely monitored in any patient taking coumadin or anti-inflammatory supplements.
References
- Serhan CN. Novel omega-3 derived local mediators in anti-inflammation and resolution. Pharmacol Ther 2005;105:7-21.
- Arita M, Bianchini F, Aliberti J, et al. Stereochemical assignment, antiinflammatory properties, and receptor for the omega-3 lipid mediator resolvin E1. J Exp Med 2005;201(5):713-22.
- Simopoulos AP. Essential fatty acids in health and chronic disease. Am J Clin Nutr 1999;70(3 Suppl):560S-569S.
