by David Seaman, DC, MS, DABCN

NFkB is a cell-signaling molecule that promotes the expression of inflammation.

We know that COX-2 inhibitors can promote heart attacks in susceptible individuals, and research also suggests that COX-2 inhibitors can slow the healing process.¹ Although NFkB-specific inhibitors have yet to be developed, research has demonstrated that NFkB activity is reduced by aspirin, NSAIDs, acetaminophen, and corticosteroids.²

Exactly how does NFkB work, and why is this important to know? And moreover, what can we do about it? These questions are easily answered in the remainder of this article.

Cells related to the spinal tissues we treat include fibroblasts, chondrocytes, mast cells, macrophages, and others. All cells are surrounded by a plasma membrane that contains receptors for the numerous chemicals found in the human body, which allows for cells to respond to the needs of the environment. Accordingly, all cells contain receptors for inflammatory molecules, such as cytokines and free radicals, which damage tissues directly and also drive the production of additional pro-inflammatory mediators.

NFkB is the cell-signaling molecule that must be activated to induce the expression of enzymes and other proteins that participate in the inflammatory process. NFkB is found in the cytoplasm and is bound to its inhibitor, known as IkB. When cytokines, free radicals and other inflammatory molecules stimulate cell membrane receptors, a sequence of cytoplasmic events occurs that lead to the separation of IkB from NFkB. The freed NFkB now moves from the cytoplasm into the nucleus, where it induces the expression of enzymes involved in the inflammatory process, such as phospholipase A2, COX-2, LOX, and inducible nitric oxide synthase, in addition to various pro-inflammatory proteins such as cytokines, growth factors, and cell adhesion molecules.³

Numerous diseases are associated with NFkB. Via the expression of the various chemicals of inflammation, NFkB has been found to mediate arthritis, osteoporosis, cancer, atherosclerosis, myocardial infarction, diabetes, allergy, Crohn's disease, multiple sclerosis, septic shock, AIDS and other inflammatory diseases.⁴ Chronic pain syndromes are also likely to be mediated by NFkB.⁵ This information should lead us to reconsider how we view various diseases.

Because NFkB is the driver of atherosclerosis, pain, multiple sclerosis, osteoporosis, and many other conditions, this suggests that these conditions are "biochemically" the same; the difference is in the location of the body in which inflammatory biochemistry is being expressed. This view is a bit contrary to how all doctors are trained to view disease. We memorize symptoms and certain specific disease markers, and so we focus on the differences among diseases for diagnostic purposes; however, with this approach, we never learn the commonalities of the "disease process."

Consider that syndrome X, also called metabolic syndrome and insulin resistance syndrome, is known to be a driver of many diseases, including cancer, hypertension, atherosclerosis, diabetes, stroke, and likely many other conditions.⁶ And as it turns out, NFkB activation is part of the mechanism by which syndrome X drives disease. Specific activators of NFkB, which are components of syndrome X, include hyperglycemia and increased free-radical activity.³ This information should lead you to immediately think of an important nutritional intervention that should be applied to all patients ­ maintaining proper blood sugar control, which can be accomplished by eating low glycemic index/load foods. Foods made of sugar and refined carbohydrates constitute the majority of high glycemic index/load foods, so these foods need to be avoided. We should live on fruits, vegetables, and healthy animal products, and add healthy lipids in moderation, such as coconut oil, olive oil, and butter.

My experience is that most people are tempted to eat refined carbohydrates because their meals are not very tasty. In fact, many Americans are terrible when it comes to properly spicing their foods, and this includes everything from scrambled eggs and omelets to salads and steak. Most tend to default to salt and pepper a fairly boring way to eat. It is time to spice up our lives; and this is because our food will taste better, and because numerous spices are known to reduce the activity of NFkB.⁴

Research has demonstrated that numerous spices reduce NFkB activity, including ginger, turmeric, garlic, red chili, basil, rosemary, fennel, anise, coriander, and cloves.⁴ It is important to sample all of these spices and regularly use the ones you like. I personally use all of the above, with the exception of cloves. My favorite is ginger, and I use a combination of the others in a pre-made mixture that can be purchased in most supermarkets. If you do not regularly spice your foods with anti-inflammatory herbs, make sure to take ginger, turmeric, and garlic in supplement form.

The easiest way to pursue an anti-inflammatory state is by eating an anti-inflammatory diet, supplementing with anti-inflammatory herbs/spices, and taking basic supplements such as a multiple, magnesium, EPA/DHA, and coenzyme Q₁₀. Try this with your patients; they will be quite gratified. Only those taking powerful anti-coagulants need to be wary.