I wrote here on the basic theory of what inflammation is. Briefly: in initial stages, inflammation is part of non-specific immunity. It just means something hurts and your immune system calls all hands on deck to deal with it.
In later stages, inflammation becomes specific: this means your immune system is carefully targeting a specific invader, and trying to avoid collateral damage. This article goes into the details of the specific immune system more deeply. Inflammatory markers are also called acute phase reactants, meaning they tend to go up when your body is in the acute stage of an illness.
But if you’re measuring inflammation on a lab test, it’s usually not when you’re acutely ill—in those cases, you know there’s inflammation. No need to test for it. Instead, they tend to be used as markers of chronic immune overactivity. CRP, ESR, and hsCRP are indirect ways to measure the activity of cytokines, or chemical signals sent by the immune system’s T-helper cells to coordinate activity of the rest of the immune system. (It is possible to test cytokines directly, but they’re harder to detect on lab work, so most commercial labs generally test their surrogates instead.)
Inflammatory Marker: CRP (and hsCRP)
CRP (C-Reactive Protein) is released from the liver in response to the inflammatory cytokine IL-6 (interleukin-6), which is released by Th2 cells. (For more on Th2 versus Th1, check out this article). The reference ranges from 10 to 1000 mg/L.
High sensitivity CRP (hsCRP), as you might expect from the name, is just a more sensitive measurement of inflammation. Its reference range is more narrow, from 0.5 to 10 mg/L (so CRP picks up where hsCRP leaves off). This is most useful for detecting cardiovascular inflammation, though it may be elevated due to lower level inflammation in other systems as well.
Inflammatory Marker: ESR (and Fibrinogen)
Much like CRP and hsCRP, ESR (Erythrocyte Sedimentation Rate) is released from the liver, and also in response to the Th2 cytokine IL-6 as well as the Th1 cytokine TNF-a (Tumor Necrosis Factor alpha).
Fibrinogen is a protein in the bloodstream that gets activated and turned into fibrin in the presence of injury, and forms the foundation of a blood clot. ESR is determined by the amount of fibrinogen present in the bloodstream, plus some other proteins. In the presence of injury (and inflammation), fibrinogen goes up, and therefore ESR goes up.
How to Lower Inflammatory Markers:
If you have chronically elevated CRP, hsCRP, fibrinogen, and/or ESR, the real treatment of course is to identify the cause. If there is an underlying obstacle to cure, you’ll need to find and correct it.
However, it’s possible that your issue is functional, meaning that the inflammatory markers are simply an early warning system that you’re not giving your body the building blocks it needs to heal. Here’s a quick check-list of interventions that can help, in this case:
- Exercise. Mild to moderate exercise is one of the best ways to lower elevated CRP and hsCRP (and their corresponding cytokines), according to this study.
- Eat real food. This study also shows that a Mediterranean diet (plenty of veggies and good oils) lowers CRP and hsCRP. This study also establishes that sugar increases hsCRP, while adequate vitamin and mineral status decreases it.
- Take your fish oil. This study is one of many that shows that supplementation of essential fatty acids (fish oil, flax oil — high in the Mediterranean diet, incidentally) also lowers CRP.
- Get enough sleep. This study shows that sleep deprivation increases CRP; therefore, getting enough sleep should lower it as well.
- Try taking curcumin. One effective way to lower fibrinogen (and thereby ESR) is with curcumin, the active ingredient in turmeric. (Side note: not all curcumin is created equal. My favorites are curcumin in a phospholipid delivery system—usually called Meriva—but curcumin is also better absorbed when combined with black pepper if you can’t find this.)