Inflammation and Diet: A growing concern
Nutrition
Written by David Seaman, D.C., M.S., D.A.B.C.N., F.A.C.C.   
Saturday, 03 April 2004 16:13 Read : 913 times

The January 1st issue of the New England Journal of Medicine (NEJM) contained an editorial entitled, “From asthma to atherosclerosis–5-lipoxygenase, leukotrienes, and inflammation.”  Inflammation is something we are all aware of, and I have written about in most of my TAC articles this past year.  What about 5-lipoxygenas and leukotrienes; what are they?

Our cell membranes are made up of fat; they are made up of cholesterol and phospholipids, which are sort of like triglycerides.  There are two fatty acids in a phospholipid, and one is reserved for dietary fatty acids.  In other words, our body is programmed to place a dietary fatty acid in every cell membrane phospholipid, and we have multiple 100’s of trillions of phospholipids; so we literally “are what we eat.”

If you eat inflammatory fats, you make inflammatory cells that drive chronic pain and other chronic inflammatory diseases, such as cancer, heart disease, and Alzheimer’s disease.  The reason fatty acids can be inflammatory has to do with what the body does to them after cell injury.  The fatty acids from our diet are released from phosopholipids when cells are injured.  The most common fatty acid found in cell membranes is arachidonic acid, which we get indirectly from grains, seeds, seed oils (corn, safflower, sunflower, and soybeans), margarine, most salad dressings, and from nearly all packaged foods.  We also get arachidonic acid preformed from the animal products we eat, assuming they were fed grains.  Arachidonic acid and its precursor, linoleic acid, are both known as omega-6 fatty acids.

When arachidonic acid (AA) is released from injured cell membranes, the AA is acted upon by certain enzymes that create inflammatory eicosanoids.  If AA is acted on by cyclooxygenase, or COX2, we get prostaglandin E2, which goes on to drive inflammation and nociception.  If AA is acted on by lipoxygenase, or LOX, we get leukotrienes, which also go on to drive inflammation and nociception.  There are many leukotrienes, including leukotriene A4, B4, C4, D4, and E4, and they all have inflammatory properties.  The difference between COX and LOX is that LOX is mostly expressed in immune cells such as neutrophils, monocytes, macrophages, dendritic cells and mast cells.
The recent editorial in NEJM focuses on lipoxygenase and leukotrienes.  Leukotrienes are involved in the promotion of rheumatoid arthritis, inflammatory bowel disease, psoriasis, allergic rhinitis, asthma, and atherosclerosis.  These are very different diseases, yet they have a common etiology…chronic subclinical inflammation, which is driven by leukotrienes that are produced by diet-derived arachidonic acid.

As it turns out, omega-3 fatty acids, from green vegetables, flaxseeds, fish, and grass-fed beef and chickens, are anti-inflammatory.  They produce prostaglandins and leukotrienes that do not promote inflammation.  We should have a 1:1 ratio of omega-6 to omega-3 fatty acids in our diet; however, we currently tip the scales with a 20:1 or greater ratio.  This is exceedingly pro-inflammatory and likely a major cause of most chronic diseases.

What do Americans currently do to defend against the inflammatory barrage created by our 20:1 ratio?  We literally live on aspirin and nonsteroidal anti-inflammatory drugs (NSAID’s).  The problem with these drugs is that they only act on the COX enzyme, which allows all the arachidonic acid to be potentially acted upon by LOX, which results in excessive production of leukotrienes.  A clinical example of this problem is aspirin-induced asthma.  More recently, and yet to be published, was a long term study with nurses who took aspirin or NSAID’s.  It turns out that those taking the meds had a significantly greater chance of developing pancreatic cancer.  I contacted the author who told me that this outcome was likely due because the meds blocked COX and diverted the AA to LOX, which resulted in leukotriene production.

The key to this problem is avoiding the abovementioned omega-6 foods and eating more omega-3 foods.  Taking fish and flaxseed oil supplements is also wise.  Natural inhibitors of COX and LOX include ginger, turmeric, and bioflavonoids, which can also be taken as supplements.  These are simple dietary and supplement modifications we all can make, and represent what I have longtime referred to as “a nutritional adjustment.”  Make sure to give your patients chiropractic and nutritional adjustments.

Dr. Seaman is the Clinical Chiropractic Consultant for Anabolic Laboratories, one of the first supplement manufacturers to service the chiropractic profession.  He is on the faculty of Palmer College of Chiropractic Florida and on the postgraduate faculties of several other chiropractic colleges, providing nutrition seminars that focus on the needs of the chiropractic patient.  Dr. Seaman believes that chiropractors should be thinking like chiropractors, while providing nutritional recommendations.  Doctors and patients who follow his programs report improved feelings of well-being, weight loss, dramatic increases in energy, and significant pain reduction.  Dr. Seaman can  be reached by e-mail at This e-mail address is being protected from spambots. You need JavaScript enabled to view it .


 
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