By David Seaman, DC, MS
I COINED THE TERM DEFLAME as an easy way to think about combating the inflame created by proinflammatory foods. In 2002, the article “The diet-induced proinflammatory state: a cause of chronic pain and other degenerative diseases?” was published in the Journal of Manipulative and Physiological Therapeutics.1 In the first attempt at publication, the reviewers mercilessly hammered it, which required me to rewrite the entire article. I could have blown off the idea altogether. I say “idea” because from a scientific perspective, diet-induction of inflammation and disease was theoretical. The problem in the early 2000s was that there was little research about the relationship among diet, inflammation, pain and chronic disease. Most of the research involved omega-6 and omega-3 fatty acids. I had to piece together what was developing in the emerging research and create a theory. What I wrote in both the rejected and accepted drafts was exactly what research demonstrated in the years that have followed.
To be sure, the topic of diet-induced inflammation would have emerged without me. I just happened to see this trend before the explosion of research that began in the mid-2000s and have focused
on this topic for almost 30 years. For many years, I was urged by doctors of chiropractic (DCs) to write a book for laymen about the anti-inflammatory diet, which is now finally complete.
What is in The DeFlame Diet?
The basic concept of The DeFlame Diet is to replace proinflammatory calories from sugar, flour and omega-6 oils with anti-inflammatory vegetables. The mental concept for patients to embrace is that they need to extinguish the disease-promoting flame created by sugar, flour, refined omega-6 oils and trans fats, which represents approximately 60 percent of all the calories consumed by the average American. Ironically, the simple activity of eating more vegetables is simultaneously the biggest deflaming challenge for some patients to overcome. People tend to struggle with the volume of vegetation that should be consumed to make up for the eliminated proinflammatory calories. However, after getting used to the idea of eating more vegetation, most can easily recalibrate their calorie intake and readily adapt.
Diet-Induced Low-Grade Inflammation
The reason for avoiding proinflammatory foods in favor of those that are anti-inflammatory is to prevent chronic, low-grade inflammation, which is very different from acute inflammation. Inflamma tion has been historically taught in the context of an acute injury, as in trauma or infection. Especially with an infection, immune cells acutely and robustly release inflammatory chemicals such as prostaglandins (PGE2), leukotrienes (LTB4) and cytokines (IL-1, IL-6 and TNF). The outcome is swelling, redness and heat, which are known as the cardinal signs of inflammation. Without these signs, we are led to believe that inflammation is not present, but nothing could be further from the truth.
We now know, without question, that chronic inflammation can rage on for years without swelling, redness and heat, and over time, lead to the development of chronic pain, diabetes, depression, heart disease, cancer, Alzheimer’s and most other chronic conditions.
Diabetes. Even just a single sugar-eating event that leads to postprandial hyperglycemia causes
a low-grade acute inflammatory event in the pancreas but no associated symptoms of any kind. This is not something we are taught in a physiology or pathology book, wherein we are told that the pancreas responds to blood sugar surges by releasing insulin, which is true, but something else much more insidious also happens.
When the beta cells are exposed to a blood sugar surge, they actually respond in a fashion that can be likened to immune cells responding to a low-grade infection event. It turns out that the beta cells release proinflammatory IL-1 whenever they are exposed to surges in blood glucose. This was initially discovered in 2002 and surprised researchers because they did not expect to identify this type of inflammatory response by our insulin-producing cells.2 As stated above, we have all been incorrectly conditioned to believe that only immune cells release inflammatory chemicals. By 2011, the topic of sugar-induced beta cell inflammation was well known.3
It was also discovered that hyperglycemic events, when chronically repeated, cause the sugared-up beta cells to release chemotactic agents that attract immune cells such as monocytes that transform into macrophages within the pancreas, which subsequently gobble up the dying beta cells.3-5 This beta cell inflammatory process is known as insulitis, and the outcome, if not reversed by an anti-inflammatory diet and exercise, is type 2 diabetes.6 The medical alternative can get a bit pricey. A medication called Kineret® is a specific IL-1 antagonist and is being considered as a treatment for type 2 diabetes.7 Biologics, such as Kineret®, Humira®, Enbrel® and Remicade®, commonly cost more than $1,000 per month when used to treat autoimmune diseases.
Atherosclerosis. Vascular endothelial cells have also been studied in detail, and just like beta cells, they release inflammatory chemicals when exposed to surges of blood sugar.8 The excessive influx of glucose ultimately leads to the production of adenosine triphosphate (ATP) by mitochondria. Often forgotten is that when mitochondria produce ATP, they also produce a superoxide free radical, which needs to be reduced or quenched so it does not propagate and lead to local cell and tissue degeneration and ultimately, disease.
In endothelial cells, the sugar-induced overproduction of superoxide, or the lack of its adequate reduction, will lead to the activation of a proinflammatory signaling molecule called nuclear factor-kappaB (NF-kB).8 The nuclear factor is then transported from the cytoplasm to the nucleus, which leads to the synthesis of proinflammatory enzymes, growth factors and cytokines, which then drive the atherosclerotic process. Such inflammatory activity can go on for years without symptoms; the worst-case scenario is sudden death due to a myocardial infarction. For many people, death from such a heart attack can be their first symptom of heart disease.
In addition to the beta cells and endothelial cells, hyperglycemia can also influence the immune system. When I was in chiropractic college in the 1980s, I went to a seminar where we were told that sugar consumption inhibits the immune system. The image presented was that sugar essentially made immune cells sleepy and could not properly fight infections. This rumor is apparently still making
the rounds as I often get asked about this. It turns out that the opposite occurs; immune cells more robustly release inflammatory cytokines to promote inflammation when exposed to sugar.
A hyperglycemic event or state will activate toll-like receptors (TLR) on immune cells, which leads to the release of inflammatory cytokines. Here is a description of TLR function in monocytes9:
“Toll-like receptors (TLRs) recognize conserved pathogen-associated molecular patterns and induce innate immune responses that are essential for host defenses. TLRs are activated by both endogenous and exogenous agonists of microbial and nonmicrobial origin. TLR activation by their agonists triggers a signaling cascade, leading to cytokine production and initiation of an adaptive immune response.”
This means that the same receptors on monocytes that respond to microbes also respond to hyperglycemia; in other words, refined sugar behaves like a pathogen. So as a consequence of being exposed to a hyperglycemic event, monocytes produce both IL-1 and TNF.10,11 Clearly, the immune system is not inhibited by sugar. In contrast, immune cells are activated by sugar, which suggests that sugar will exaggerate an inflammatory response created by microbes and make an infection worse.
Based on the information presented in this section, it should be obvious that beta cells, endothelial cells and immune cells require The DeFlame Diet in order to function optimally. When these cells are fed inflammatory foods, the outcome is inflammatory disorders that create unnecessary suffering. As you will see in the following section, even cartilaginous cells flame up when fed a proinflammatory diet.
The Musculoskeletal System. I am often told by DCs that they are mechanical or structural in their approach to patient care rather than nutritional or biochemical. When this mindset is maintained, it is not difficult to steer oneself away from considering nutrition in the treatment of patients with musculoskeletal pain. The reasoning behind this mindset is that biomechanics is considered to be separate and distinct from biochemistry, and most of us have been taught this in school; however, the facts tell a different story.
Simply stated, human beings are made of chemistry. This means that our structure is chemistry, and so biomechanics and postural correction are really about the movement and repositioning of our chemistry. Not surprisingly, whenever we move our musculoskeletal tissues, we create chemistry.12 Despite this unavoidable fact, it does not mean that I believe all patients need nutritional modifications to handle their musculoskeletal complaints. Quite to the contrary, many patients respond rapidly to manual, postural and rehabilitative treatments. And, of course, it is much easier on the DC if the patient is a responder rather than one who needs to be counseled about nutritional and lifestyle changes.
My impression is that The DeFlame Diet should be applied to any patient wishing to avoid any of the chronic inflammatory conditions mentioned earlier and also for musculoskeletal pain patients who do not respond to manual, postural or rehabilitative methods. Very often, these non-responders regularly use over-the-counter or prescription anti-inflammatory drugs to control their pain, and this is an indication that they could benefit from an anti-inflammatory diet. The reason is because these medications inhibit the conversion of proinflammatory dietary omega-6 arachidonic acid into painful prostaglandins.
Additional diet-induced drivers of chronic musculoskeletal pain syndromes are obesity, metabolic syndrome and type 2 diabetes. Commonly expressed painful conditions include tension-type and migraine headaches, fibromyalgia, local and widespread pain, neck pain, low-back pain, cervical and lumbar disc herniation and tendinopathies.13 Additionally, patients with type 2 diabetes have reduced mobility across all joints tested compared with age- and weight-matched controls, and are more likely to develop lumbar stenosis compared with non-diabetics.13
We DCs should not underestimate the impact that the metabolic syndrome may have on our patient population. The prevalence of metabolic syndrome is shockingly high, ranging from 11 percent to almost 35 percent of adults who range in age from 30 to 59. This jumps to about 43 percent of individuals 60 to 69 years of age.14 Studies have shown that The DeFlame Diet can reverse metabolic syndrome and associated fatty liver in as little as 12 weeks.15,16
In general, the evidence that a proinflammatory diet can promote pain is becoming more accepted. The dietary recommendations that researchers are coming up with to reduce pain actually mirror what I have been describing for years and now outline here.17-19
The Diet Concept
When it comes to diet, the waters always seem somewhat muddied. The oftentimes, seemingly contradictory information about diet can be confusing. The utility of The DeFlame Diet is its simplicity and lack of contradictions. You need to consider only one question when it comes to eating: “Will this food inflame me or DeFlame me?”
On a final practical note, asking patients about their diets can be annoying and make the doctor feel like a nag. Compared with asking patients about how their dieting is going, asking about their DeFlaming progress is much more fun for the doctor and patient. The DeFlame Diet is easy to implement and will make the nutrition part of chiropractic practice much easier and stress-free.
1) Seaman DR. The diet-induced proinflammatory state: a cause of chronic pain and degenerative diseases? J Manipulative Physiol Ther. 2002 Mar-Apr;25(3):168-79.
2) Maedler K, Sergeev P, Ris F, Oberholzer J, et al. Glucose-induced beta cell production of IL-1 contributes to glucotoxicity in human pancreatic islets. J Clin Invest. 2002;110:851-60.
3) Donath MY, Shoelson SE. Type 2 diabetes as an inflammatory disease. Nat Rev Immunol. 2011;11(2):98-117.
4) Böni-Schnetzler M, Ehses JA, Faulenbach M, Donath MY. Insulitis in type 2 diabetes. Diabetes Obes Metab. 2008;10(Suppl 4):201–4.
5) Donath MY, Schumann DM, Faulenbach M, Ellingsgaard H, Perren A, Ehses JA. Islet inflammation in type 2 diabetes: from metabolic stress to therapy. Diabetes Care. 2008 Feb;31 Suppl 2:S161-4.
6) Seaman DR, Palombo AD. An overview of the identification and management of the metabolic syndrome in chiropractic practice. J Chiropr Med. 2014;13(3):210.
7) Böni-Schnetzler M, Donath MY. How biologics targeting the IL-1 system are being considered for the treatment of type 2 diabetes. Br J Clin Pharmacol. 2013;76(2):263-8.
8) Ceriello A. New insights on oxidative stress and diabetic complications may lead to a ‘causal’ antioxidant therapy. Diabetes Care. 2003;26(5):1589-96.
9) Dasu MR, Devaraj S, Zhao L, Hwang DH, Jialal I. High glucose induces Toll-like receptor expression in human monocytes: mechanism of activation. Diabetes. 2008;57:3090-98.
10) Dasu MR, Devaraj S, Jialal I. High glucose induces IL-1 beta expression in human monocytes: mechanistic insights. Am J Physiol Endocrinol Metab. 2007;293: E337–E346.
11) Gonzalez Y, Herrera MT, Soldevila G, et al. High glucose concentrations induce TNF-a production through the down-regulation of CD33 in primary human monocytes. BMC Immunol. 2012 Apr 14;13:19.
12) Langberg H, Boushel R, Skovgaard D, Risum N, Kjaer M. Cyclo-oxygenase-2 mediated prostaglandin release regulates blood flow in connective tissue during mechanical loading in humans. J Physiol. 2003;551(Pt 2):683-9.
13) Seaman DR. Body mass index and musculoskeletal pain: is there a connection? Chiropr Man Ther. 2013;21(1):15.
14) Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002;287(3):356-9.
15) Pérez-Guisado J. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
16) Pérez-Guisado J, Muñoz-Serrano A. The effect of the Spanish Ketogenic Mediterranean Diet on nonalcoholic fatty liver disease: a pilot study. J Med Food. 2011;14(7-8):677-80.
17) Tick H. Nutrition and pain. Phys Med Rehabil Clin N Am. 2015;26(2):309-20.
18) Totsch SK, Waite ME, Sorge RE. Dietary influence on pain via the immune system. Prog Mol Biol Transl Sci. 2015;131:435-69.
19) Masino SA, Ruskin DN. Ketogenic diets and pain. J Child Neurol. 2013;28(8):993-1001.
Other Anti-Inflammatory Topics
Another deflaming challenge is learning about the healthy anti-inflammatory nature of both saturated fatty acids and cholesterol, which have perhaps been the most maligned lipids found in food. Patients and many doctors are terrified of these two lipids due to the antilipid propaganda that has flourished for decades. Detailed chapters in The DeFlame Diet are devoted to both saturated fatty acids and cholesterol to thoroughly dismantle the propaganda and reduce the lipid fear that is so pervasive.
Multiple other dietary inflammation topics are discussed, including gluten sensitivity, endotoxemia, small intestine bacterial overgrowth, nightshades, trans fats, potassium, alkaline foods, polyphenols, carotenoids, omega-3 fatty acids, magnesium, vitamin D, probiotics and nutritional supplements. The general topic of inflammation is also described in a fashion that patients can understand, especially in the context of low-grade, chronic inflammation that must be actively combated throughout life. Chiropractic physicians may also find this information useful since we are typically taught about inflammation in the context of traumatic injury and infection rather than diet induced inflammation.