How Normal Inflammation Becomes Chronic

Want to feel better than you’ve ever felt?

Here’s another excerpt from my 10th book, The Secret of Vigor – How to Overcome Burnout, Restore Biochemical Balance and Reclaim Your Natural Energy

Some of the most popular New Year’s resolutions every year are:
*Lose Weight
*Get in Shape
*Reduce Stress
*Get Healthier
*Win the Lottery

The Secret of Vigor can help you with 4 out of 5 of the most popular resolution goals, so I’ll be posting excerpts from the book for the next several weeks – so please stay tuned for each installment.

If you simply can’t wait, then you can certainly get a copy at or at your favorite library or bookstore.

How Normal Inflammation Becomes Chronic
When a tissue is damaged—whether from infection, trauma, or unbalanced turnover—it releases signaling chemicals called “cytokines.” These cytokines are like flare guns, sending up a call for help that signals surrounding cells to jump into action to stop (wall off) and repair the damage. The cytokines also call immune-system cells (white blood cells) into the area to help clean up the damaged tissue. You have no doubt experienced the blood rush that leads to the recognizable redness, warmth, and swelling common to many injuries. As the white blood cells rush in to the damaged area, they release more and more of their own inflammatory chemicals. This blast of inflammation is intended to cause even more tissue destruction as a way to either kill bacteria and viruses or to take away damaged tissue and set the stage for repair efforts to begin. As you can imagine, this part of the inflammatory process is supposed to be short term. If it were to continue without shutting down, you’d simply destroy your own tissue without ever rebuilding healthy tissue in its place. Unfortunately, this “never-shut-down” scenario precisely describes the chronic inflammation and constant state of tissue destruction with which millions of Americans live their lives every day.

A number of mechanisms are in place to shut down the process of inflammation, including the naturally short half-life of cytokines and other inflammatory molecules and the production of anti-inflammatory cytokines (with such names as TGF-beta and IL-10). Unfortunately, immune-system cells can remain in a state of chronic inflammation if the “cell-damage” signals keep coming to them as a result of free-radical damage (as discussed in Chapter 3) and from cortisol-induced tissue breakdown (covered in Chapter 6); or if signals to “shut down” the inflammatory process are not “heard” by target cells (as in the case of cells damaged by problems with glucose [blood-sugar] levels, a subject covered in the next chapter).

Unfortunately, chronic inflammation is not confined to the tissue in which it starts. Cytokines—such as those labeled IL-6, IL-8, and TNF-alpha—are able to leave the original site of inflammation. They can then travel in the blood to spread inflammatory signals through the blood vessels and into every tissue in the body (leading to metabolic diseases, such as obesity, diabetes, and depression, and to structural/damage diseases, such as Alzheimer’s, Parkinson’s, and arthritis).

Because most of the cytokine molecules are produced by immune-system cells (specifically by macrophages, neutrophils, and NK cells of the innate immune system), numerous drug companies attempt to control chronic inflammation by suppressing immune function. The problem, of course, is that wholesale suppression of immune function also limits your body’s ability to protect you from actual pathogens—so you’re “protected” from chronic inflammation, but you may become more susceptible to infections and certain cancers. Not a great trade-off!

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