Inflammation and oxidation contribute to many, if not most, diseases.Based on this observation one would suspect that anti-inflammatories and antioxidants should prevent many diseases. Indeed, there is excellent data that anti-inflammatories can help prevent many diseases. However, support for antioxidants is more limited.
First, antioxidants.
There are a number of antioxidants that one must consume (e.g., vitamin E, vitamin C, zinc, and selenium). There is a lot of mileage in making sure that one is not deficient in any of these antioxidants. However, there is decent evidence that, in general, after sufficiency is attained, more is not better.
The body also has a number of in-house antioxidants, known as endogenous antioxidants (e.g., superoxide dismutase, glutathione peroxidase, alpha lipoic acid, catalase and coenzyme Q10). Many external, or exogenous, antioxidants (like the vitamins and minerals mentioned above) are necessary to maintain proper levels of these all-important endogenous antioxidants. Moreover, many exogenous antioxidants also happen to have other biological effects aside from reducing oxidation (e.g., some have anti-inflammatory effects and some are polyphenols with diverse effects)
And, that might very well be all there is to exogenous antioxidants -- they're important, but perhaps not because of their (direct) capacity to reduce oxidation...
And now, inflammation.
Inflammation generally starts with injury (e.g., acid or bile injury in the case of esophagitis). The body responds to an injury by sending lots of blood to the area to address the underlying problem. The body's response is modulated by a cascade of signaling molecules designed to cause the inflammatory reaction.
On a molecular level, the signaling cascade starts with omega 3 and omega 6 fatty-acids. These fatty-acids, made from dietary polyunsaturated fat, are turned into signaling molecules called eicosanoids. Two families of enzymes catalyze fatty acid oxygenation to produce the eicosanoids: (1) cyclooxygenase, or COX, which generates the prostanoids (Cox-2 generates PGE2) and (2) lipoxygensase, or LOX ( 5-LOX generates the leukotrienes).
It turns out (and this is a bit of a simplification) that there are two broad types of prostanoids and leukotrienes: (1) inflammatory prostanoids and leukotrienes and (2) anti-inflammatory prostanoids and leukotrienes. Significantly, omega 6 fatty acids are the precursors to the inflammatory prostanoids and leukotrines while omega 3 fatty acids are the precursors to the anti-inflammatory prostanoids and leukotrines.
Almost all modern people eat way more omega 6 than omega 3 fatty acid (some eating 50 times more). Unfortunately for us, most people for the last 2 million years ate a fairly even ratio. Sounds like trouble...
With such an over-abundance of omega 6 in our tissue, there generally aren't enough omega 3 precursors present to be made into anti-inflammatory signaling molecules. Chronic inflammation, inflammation that outlives its biological purpose, seems to be the result.
Tissue highly unsaturated fat (omega 3 and omega 6) has a two-year half-life on average. That means that it takes two years for your body to replace half this fat in your body. In addition, omega 6 oil is ubiquitous in our food supply (vegetable oils, corn/soy fed animal, nuts & seeds). Thus, replacing all that tissue omega 6 with tissue omega 3s takes a long time and is hard to do. That said, I am currently in the process of doing it because it is the actual cure rather than the band aid.
In the meantime, NSAIDs can help to stop chronic inflammation by inhibiting the Cox-2 enzyme and/or by inhibiting the 5-Lox enzyme (by the way, it might be ideal to inhibit both Cox-2 and 5-Lox at the same time). Turmeric, ginger, green tea, french pine bark, and numerous other natural compounds inhibit both enzymes. In addition, aspirin is a potent inhibitor Cox enzymes and boswellia is a potent inhibitor of 5-Lox.
In the context of the chemoprevention of esophageal cancer in people with Barrett's esophagus, there is very good epidemiological data for aspirin. Indeed, aspirin is currently the subject of a placebo-controlled trial in England, which should produce some preliminary data in 2011. However, aspirin's effect on cancer progression, if any, might be due to mechanisms other than Cox-2 inhibition (as suggested by a trial, albeit a small & short one, in which selective a Cox-2 inhibitor didn't perform so well). For instance, aspirin also promotes cellular adhesion. (I believe that the authors of the U.K. trial also share my suspicions about aspirin as the dose they are using, 300mg, is well in excess of the dose required to effectively inhibit Cox-2, suggesting they are interested in exploring some of the other benefits of aspirin.)
I know this sounds like a broken record, but vitamin D also promotes cellular adhesion, probably better than does aspirin.
