Dietary, Nutritional and Botanical Interventions to Reduce Pain and Inflammation
By Alex Vasquez, DC, ND
Generally speaking, the allopathic/pharmaceutical paradigm of anti-inflammatory intervention is forced to be ineffective and dangerous by the very nature of the pharmaceutical agents that are relied upon.
Since the vast majority of drugs are single molecules that intervene at a specific part of a complex inflammatory phenomena, the end result often is similar to throwing a monkey wrench into a machine that is malfunctioning - a single aspect of inflammation might be stopped, but the system continues to malfunction and might become even more imbalanced as a result of the so-called "intervention."
Of course, the most recent - and most tragic - example of this iatrogenesis is the Cox-2-inhibitor (coxib) and Vioxx catastrophe, which injured or killed more than 139,000 Americans.1 Any student of nutritional biochemistry could have anticipated the problems years before these drugs caused their first deaths and injuries.2 Indeed, the alarms were sounded within the first few years after the first coxibs were unleashed onto the "health care" market,3 but these alarms were ignored in favor of the most aggressive and successful drug-marketing campaign that the world had ever seen - one that made celecoxib/Celebrex the most successful drug launch in U.S. history, with more than 7.4 million prescriptions written within its first six months.4 The obvious problem with these drugs is that by targeting the Cox-2 enzyme, they block formation of prostacyclin, long considered "the good prostaglandin" due to its vasodilatory and antithrombotic actions, which are cardioprotective. Furthermore, any inhibition of cyclooxygenase tends to shunt arachidonic acid into the formation of leukotrienes, which promote painless inflammation and the acceleration of cardiovascular disease.5
The failure of the coxibs exemplifies a major failure of the drug paradigm; namely that excessive focus on the inhibition of isolated pathways creates additional imbalance due to its failure to appreciate the multifaceted and interconnected nature of physiologic systems and biochemical pathways. On the contrary, our holistic perspective holds that inflammation is most effectively treated by focusing not on isolated pathways per se, but on the patient's overall health. Using an effective overall approach allows specific pathways to be nutritionally supported and modulated, rather than pharmacologically inhibited. In other words, whereas anti-inflammatory drugs are specific and inhibitory of normal function, the natural approach is more general and supportive of optimal function.
How can clinicians orchestrate a practical nutritional wellness protocol that specifically alleviates pain and inflammation? In essence, we start by getting the pro-inflammatory junk out of the diet, because we realize that high-fat and high-carb meals are pro-inflammatory.
Once we've created some space for healthy foods, we encourage consumption of anti-inflammatory foods such as low-carb, phytonutrient-rich fruits, vegetables, nuts, seeds and berries. We correct general vitamin and mineral insufficiencies with a multivitamin and multi-mineral supplement (which provides an anti-inflammatory benefit6), and we ensure that the daily vitamin D requirement of 3,000-5,000 IU is met by ensuring daily full-body sun exposure or by using a supplement that provides the appropriate amount.7 We replace the health-promoting fatty acids that are missing from the American diet by supplementing with ALA, GLA, EPA and DHA, and we recommend probiotics to counteract the barrage of antibiotics that most patients have had to endure during the course of their viral infections, allergies, and other non-bacterial ailments. Weight loss and the attainment of optimal weight are the natural results of proper diet and frequent exercise; adipose tissue is inherently pro-inflammatory,8 and its "replacement" by lean muscle tissue (which is anti-inflammatory9) helps shift the balance away from inflammation and toward homeostasis and healing. Up to this point, we merely have turned off the gas lines that were fueling the inflammatory fire; we have not yet done anything specifically anti-inflammatory per se. By the time we've re-established the foundation for health, a large percentage of patients already are healed of their primary ailments, and inflammation and pain might be reduced significantly.10
For patients who need additional anti-inflammatory interventions and relief from pain, now we can begin the implementation of treatment, which is customized to the needs of the patient. For osteoarthritis, we can use the tried-and-true glucosamine and purified chondroitin sulfates (note that purified chondroitin sulfate is cardioprotective11), and now that a study has finally been published on the use of MSM12 we can be confident that it works, even though we've been using it successfully for years! For pain associated with inflammation and edema (i.e., recent injury), proteolytic and pancreatic enzymes work well and work quickly.13 If we are only treating pain (rather than that which is marked by significant inflammation) we can use a combination of analgesic botanicals, namely devil's claw (Harpagophytum procumbens),14 Willow bark (Salix spp)15 and Boswellia serrata.16 If inflammation predominates over pain, then we might choose to temporarily inhibit NF-kappaB with nutrients and botanicals such as curcumin17 (requires piperine for absorption in humans18), lipoic acid,19 green tea,20 rosemary,21 propolis22 and resveratrol.23,24
Somewhere along the way, when pain and inflammation particularly are severe or recalcitrant, we need to consider that the inflammation might be being triggered by an occult or "silent" infection,25,26 and so we will need to assess and treat the various foci of dysbiosis.27 Antimicrobial interventions can include time-released oregano,28,29 berberine,30 artemisinin31,32 hyperforin33 myrrh (Commiphora molmol),34 bismuth,35 peppermint, uva ursi,36 thyme,37 clove,38 anise,39 buchu,40 caprylic acid, dill,41 Brucea javanica,42 and Acacia catechu.43 The attainment of anti-rheumatic benefits via the use of antimicrobial treatments, immunosupportive interventions (rather than immuno-suppressive drugs), xenobiotic detoxification, and the correction of hormonal imbalances is the leading edge of anti-inflammatory treatments for autoimmune diseases and other disorders characterized by severe "idiopathic" inflammation.44
Different health care professions are empowered and disabled by their respective paradigms, and the merits of each can be contrasted by the results they obtain. Here in America, drug-centered allopathic medicine, (which mislabels itself "traditional medicine" even though it has existed for only 60 of the 2.5 million years of human history) is the third or fourth leading cause of death, responsible for more than 1 million iatrogenic injuries and approximately 180,000 unnecessary deaths per year.45-47 The American medical system also is the most expensive and inefficient "health care" system in the world, and it burdens and bankrupts our families, businesses, and communities48-52 while drug companies enjoy record-breaking multi-billion dollar profits.53-55 Summarizing the situation in 2000, the Director of World Health Organization's Global Program on Evidence for Health Policy, Christopher Murray, MD, PhD,56 concluded, "Basically, you die earlier and spend more time disabled if you're an American rather than a member of most other advanced countries." In contrast, a lifestyle of healthy living that includes meditation, yoga, herbal dietary supplements, and a whole foods diet can reduce total medical expenses by 59% over four years and by 63% over 11 years compared to patients under "conventional" medical care; hospital admission rates are reduced 11.4-fold for cardiovascular disease, 3.3-fold for cancer, and 6.7-fold for mental health and substance abuse.57 Thankfully, as the naturopathic profession continues to increase its scope of practice, more and more Americans will be able to experience true health without lifelong medicalization - with the use of proper diets, nutritional supplements, and treatments that focus on the cause of the problem, not merely the symptoms.
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- Mukherjee D, Nissen SE, Topol EJ. Risk of cardiovascular events associated with selective COX-2 inhibitors. JAMA 2001;286(8):954-9.
- Topol EJ. Arthritis medicines and cardiovascular events - "house of coxibs." JAMA, Jan. 19, 2005;293(3):366-8.
- Monsanto, Pfizer celebrate Celebrex. St. Louis Business Journal, July 20, 1999. Click to view it online. Accessed on Jan. 5, 2006.
- Dwyer JH, Allayee H, Dwyer KM, et al. Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic acid, and atherosclerosis. N Engl J Med, Jan. 1, 2004;350(1):29-37.
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- Fain JN, Madan AK, Hiler ML, et al. Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissues of obese humans. Endocrinology May 2004;145(5):2273-82. Click to view it online.
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- Morrison LM, Enrick N. Coronary heart disease: reduction of death rate by chondroitin sulfate A. Angiology May 1973;24(5):269-87.
- Kim LS, Axelrod LJ, Howard P, Buratovich N, Waters RF. Efficacy of methylsulfonylmethane (MSM) in osteoarthritis pain of the knee: a pilot clinical trial. Osteoarthritis Cartilage, Nov. 22, 2005.
- Vasquez A. Reducing pain and inflammation naturally - Part 3: Improving overall health while safely and effectively treating musculoskeletal pain. Nutritional Perspectives 2005;28:34-38, 40-42. Available at Click to view it online.
- Chrubasik S, Junck H, Breitschwerdt H, Conradt C, Zappe H. Effectiveness of Harpagophytum extract WS 1531 in the treatment of exacerbation of low-back pain: a randomized, placebo-controlled, double-blind study. Eur J Anaesthesiol Feb. 1999;16(2):118-29.
- Chrubasik S, Eisenberg E, Balan E, et al. Treatment of low-back pain exacerbations with willow bark extract: a randomized double-blind study. Am J Med 2000;109:9-14.
- Kimmatkar N, Thawani V, Hingorani L, Khiyani R. Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee - a randomized double blind placebo controlled trial. Phytomedicine January 2003;10(1):3-7.
- Curcumin, EGCG and resveratrol have been shown to suppress activation of NF-kappa B; Surh YJ, Chun KS, Cha HH, et al. Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: down-regulation of COX-2 and iNOS through suppression of NF-kappa B activation. Mutat Res, Sept. 1, 2001;480-481:243-68.
- Shoba G, Joy D, Joseph T, et al. Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers. Planta Med May 1998;64(4):353-6.
- Lee HA, Hughes DA. Alpha-lipoic acid modulates NF-kappaB activity in human monocytic cells by direct interaction with DNA. Exp Gerontol, Jan-Mar 2002;37(2-3):401-10.
- Yang F, Oz HS, Barve S, et al. The green tea polyphenols epigallocatechin-3-gallate blocks nuclear factor-kappa B activation by inhibiting I kappa B kinase activity in the intestinal epithelial cell line IEC-6. Mol Pharmacol Sept. 2001;60(3):528-33.
- Lo AH, Liang YC, Lin-Shiau SY, Ho CT, Lin JK. Carnosol, an antioxidant in rosemary, suppresses inducible nitric oxide synthase through down-regulating nuclear factor-kappaB in mouse macrophages. Carcinogenesis 2002;23(6):983-91.
- Caffeic acid phenethyl ester (CAPE) is an anti-inflammatory component of propolis (honeybee resin). CAPE is reportedly a specific inhibitor of nuclear factor-kappaB (NF-kappaB); Fitzpatrick LR, Wang J, Le T. Caffeic acid phenethyl ester, an inhibitor of nuclear factor-kappaB, attenuates bacterial peptidoglycan polysaccharide-induced colitis in rats. J Pharmacol Exp Ther, December 2001;299(3):915-20.
- Resveratrol's anticarcinogenic, anti-inflammatory, and growth-modulatory effects may thus be partially ascribed to the inhibition of activation of NF-kappaB and AP-1 and the associated kinases; Manna SK, Mukhopadhyay A, Aggarwal BB. Resveratrol suppresses TNF-induced activation of nuclear transcription factors NF-kappa B, activator protein-1, and apoptosis: potential role of reactive oxygen intermediates and lipid peroxidation. J Immunol, June 15, 2000;164(12):6509-19.
- Both resveratrol and quercetin inhibited NF-kappaB-, AP-1- and CREB-dependent transcription to a greater extent than the glucocorticosteroid, dexamethasone; Donnelly LE, Newton R, Kennedy GE, et al. Anti-inflammatory effects of resveratrol in lung epithelial cells: molecular mechanisms. Am J Physiol Lung Cell Mol Physiol, June 4, 2004 [Epub ahead of print].
- "At the time of initial evaluation, 57 (69%) of the patients with oligoarthritis and 4/20 (20%) of the control subjects were carriers of clinically silent infections." Weyand CM, Goronzy JJ. Clinically silent infections in patients with oligoarthritis: results of a prospective study. Ann Rheum Dis February 1992;51(2):253-8.
- Fendler C, Laitko S, Sorensen H, et al. Frequency of triggering bacteria in patients with reactive arthritis and undifferentiated oligoarthritis and the relative importance of the tests used for diagnosis. Ann Rheum Dis April 2001;60(4):337-43. Click to view it online.
- Vasquez A. Reducing pain and inflammation naturally. Part 6: Nutritional and botanical treatments against "silent infections" and gastrointestinal dysbiosis, commonly overlooked causes of neuromusculoskeletal inflammation and chronic health problems. Nutritional Perspectives January 2006; in press. Click to view it online.
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