Your patients can benefit from an anti-inflammatory diet.
Inflammation is the new holistic buzzword. It stands at the forefront of health concerns. Because research has indicated that subclinical inflammation is at the core of many health problems,1 Time magazine has called inflammation a “secret killer.”2
Inflammation appears to be associated with many chronic conditions such as cardiovascular disease, cancer, diabetes, obesity, and musculoskeletal degeneration.3-5 Diet can be a major contributor to subclinical inflammation, which is not readily detectable.6,7
What is inflammation?
Inflammation is part of the body’s natural defense system. Typical inflammation is expressed by pain, swelling, redress, and heat.8 Subclinical inflammation, while difficult to diagnose through routine bloodwork and physical examination, can be present at low levels like a smoldering fire within the body. When your immune system shifts out of balance, your body senses foreign invaders and sets off a cascade of events that slowly contribute to disease and weight gain.9,10
Causes of inflammation
The body responds with systemic or chronic inflammation to a number of well-known causes:
- Poor diet: e.g., consumption of trans fats; overconsumption of sugars, white flour, processed foods, and saturated fats
- Lack of exercise
- Hidden food allergens
- Bacterial or viral infections11-13
- Environmental toxins: e.g, BPA, phthalates, acrylamide, mold14,15
- Faulty movement patterns
Inflammation leads to aging and chronic diseases. It is also by far the leading contributor to obesity.16 Being overweight is being inflamed.
Since food is a potentiator for inflammation, hidden sensitivities and allergies to common and popular foods are making your patients sick and overweight. While individuals who are extremely allergic to certain foods have a hypersensitivity reaction, others may have a delayed response that can take up to 72 hours to manifest as subclinical inflammation.
Why patients become sensitive to foods
A number of things can change gut bacteria populations and damage the gut lining, which is a critical barrier for a healthy immune system. You can become sensitive to foods through a faulty diet, sedentary lifestyle, consumption of NSAIDs, and antibiotic medication without collateral probiotic therapy.
Increased permeability of your intestinal tract leads to leaky gut syndrome. Undigested food particles and toxins that should be blocked make their way into the blood stream in a leaky gut scenario. This ignites the immune system and raises levels of subclinical inflammation.18-21
The 5R protocol
A properly functioning digestive system is critical to good health. Furthermore, research has confirmed the effectiveness of a regimen called the 5R program:22
- Remove the offending substances from a patient’s diet including grain containing gluten and dairy products.
- Replace digestive enzymes. Add betaine HCL and bile acids required for proper digestion.23
- Re-inoculate the gut tract with probiotics. These well-researched probiotics are specific strains of acidophilus and bifidus bacteria to help promote an optimal balance of GI microflora. Probiotics should be taken along with a prebiotic such as inulin or fructooligosaccherides. Prebiotics are specific fibers that are a food source for friendly probiotic organisms.24,25
- Regenerate the GI mucosa lining by adding such nutrients as antioxidants, selenium, zinc, L-glutamine, turmeric, ginger, pantothenic acid, omega-3 fish oil, vitamin E, glycines, humulus lupulus, and a rice protein.26-29
- Retain the health and function of your GI tract with a proper lifestyle.
Chronic and degenerative conditions can be prevented and controlled by adhering to an anti-inflammatory protocol. Proper diet and nutritional supplements remain the cornerstone for reducing subclinical inflammation and promoting optimal health.
Implementing the 5R program has been shown in research to be an effective way to treat subclinical inflammation. After all, true health begins from within.
Robert Silverman, DC, CNS, CCN, CSCS, CKTP, CES, CIISN, DACBN, DCBCN, HKC, SASTM, teaches seminars nationwide and in Canada and has a successful sports injury and performance private practice in Westchester County, New York. He can be reached at drrobertsilverman.com, firstname.lastname@example.org, or through erchonia.com.
1 Egger G, Dixon J. Obesity and chronic disease: always offender or often just accomplice? Br J Nutr. 2009;102(8):1238-42.
2 Gorman C. Inflammation: The Secret Killer. Time. Feb. 23, 2004.
3 Reuter S, Gupta SC, Chaturvedi MM, Aggarwal BB. Oxidative stress, inflammation, and cancer: how are they linked? Free Radic Biol Med. 2010;49(11):1603-16.
4 Desai A, et al. META060 inhibits multiple kinases in the NF-κB pathway and suppressed LPS-mediated inflammation in vitro and ex vivo. Inflamm Res. 2009;58(5):229-34.
5 Konda VR, Desai A, Darland G, Bland JS, Tripp ML. META060 inhibits osteoclastogenesis and matrix metalloproteinases in vitro and reduces bone and cartilage degradation in a mouse model of rheumatoid arthritis. Arthritis Rheum. 2010;62(6):1683-92.
6 Dalla Pellegrina C, Perbellini O, Scupoli MT, et al. Effects of wheat germ agglutinin on human gastrointestinal epithelium: insights from an experimental model of immune/epithelial cell interaction. Toxicol Appl Pharmacol. 2009;237(2):146-53.
7 Rubio-Tapia A, Kyle RA, Kaplan EL, et al. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology. 2009;137(1):88-93.
8 Abbas AK, Lichtman AHH, Pillai S. (2012). Basic immunology: Functions and disorders of the immune system. Chap 2 Innate immunity. Philadelphia: Saunders.
9 Ludvigsson JF, Montgomery SM, Ekbom A, Brandt L, Granath F. Small-intestinal histopathology and mortality risk in celiac disease. JAMA. 2009;302(11):1171-1178.
10 Farrell RJ, and CP Kelly. Celiac sprue. N Engl J Med. 2002;346(3):180-88. Review.
11 Wyatt J, Vogelsang H, Hübl W, Waldhöer T, Lochs H. Intestinal permeability and the prediction of relapse in Crohn’s disease. Lancet. 1993;341(8858):1437-9.
12 Asfaha S, MacNaughton WK, Appleyard CB, Chadee K, Wallace JL. Persistent epithelial dysfunction and bacterial translocation after resolution of intestinal inflammation. Am J Physiol Gastrointest Liver Physiol. 2001;281(3):G635-44.
13 Pagnelii R, et al. Intestinal Permeability in irritable bowel syndrome. Annals of Allergy. 1990;64:377-380.
14 vom Saal FS, Myers JP. Bisphenol A and risk of metabolic disorders. JAMA. 2008;300(11):1353-54.
15 Trasande L, Attina TM, Blustein J. Association between urinary bisphenol A concentration and obesity prevalence in children and adolescents. JAMA. 2012;308(11):1113-21.
16 Kantartzis K, Machann J, Schick F, et al. The impact of liver fat vs visceral fat in determining categories of prediabetes. Diabetologia. 2010;53(5):882-89.
17 Metagenics. “5R GI Restoration Program Guide.” http://www.metagenics.com/sites/default/files/resources/met1935_5r_gi_program_guide_ipad.pdf. Published 2013.
18 Kiefer D, Ali-Akbarian L. A brief evidence- based review of two gastrointestinal illnesses: irritable bowel and leaky gut syndromes. Altern Ther Health Med. 2004;10(3):22-30.
19 Bjarnason I, So A, Levi AJ, et al. Intestinal permeability and inflammation in rheumatoid arthritis: effects of non-steroidal anti-inflammatory drugs. Lancet. 1984;324(8413):1171-1228.
20 G Sigthorsson, J Tibble, J Hayllar, et al. Intestinal permeability and inflammation in patients on NSAIDs. Gut. 1998;43(4):506–511.
21 Galdeano CM, de Moreno de LeBlanc A, Vinderola G, Bonet ME, Perdigón G. Proposed model: mechanisms of immunomodulation induced by probiotic bacteria. Clin Vaccine Immunol. 2007;14(5):485-492.
22 Bland S, Hyman M. (2014). The Disease Delusion: Conquering the Causes of Chronic Illness for a Healthier, Longer, and Happier Life. (p. 115-118). South Brunswick, NJ: HarperWave.
23 Jockers D. “The destructive nature of leaky gut syndrome.” Natural News. http://www.naturalnews.com/037033_leaky_gut_syndrome_flora_microorganisms.html. Published Aug. 7, 2012. Accessed Feb 2, 2015.
24 Liu Q, Nobaek S, Adawi D, et al. Administration of Lactobacillus plantarum 299v reduces side-effects of external radiation on colon anastomotic healing in an experimental model. Colorectal Dis. 2001;3(4):245-52.
25 Naruszewicz M, Johansson ML, Zapolska-Downar D, Bukowska H. Effect of Lactobacillus plantarum 299v on cardiovascular disease risk factors in smokers. Am J Clin Nutr. 2002;76(6):1249-55.
26 Hong JA, Carroll KS. Deciphering the role of histidine 252 in mycobacterial adenosine 5′-phosphosulfate (APS) reductase catalysis. J Biol Chem. 2011;286(32):28567-73.
27 Safayhi H, Sailer ER, Ammon HPT. 5-lipoxygenase inhibition by acetyl-11-keto-ß-boswellic acid (AKBA) by a novel mechanism. Phytomed. 1996;3:71-72.
28 Plummer SM, Holloway KA, Manson MM, et al. Inhibition of cyclo-oxygenase 2 expression in colon cells by the chemopreventive agent curcumin involves inhibition of NF-kappaB activation via the NIK/IKK signalling complex. Oncogene. 1999;18(44):6013-20.
29 Kuhn KS, Muscaritoli M, Wischmeyer P, Stehle P. Glutamine as indispensable nutrient in oncology: experimental and clinical evidence. Eur J Nutr. 2010;49(4):197-210.