Health Blog: Quell the Inflammation in Your Body

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Inflammation is at the core of heart disease

Excess body fat can lead to a host of heart diseases. Veins and arteries become more compromised, and blood vessels in legs and microcapillaries in eyes can wear out three times faster in overweight individuals. There is also an increased risk of high blood pressure with each additional pound of fat.[1]

Many of us know the effects of being overweight where the heart is concerned. Less well known, unfortunately, is the effect that excess inflammation can place on the heart. You may associate inflammation with the redness, swelling, or heat you see or feel when you get a cut, bite, or minor infection, or with the pain you feel in a swollen joint (as in arthritis). But uncontrolled inflammation is one of the major culprits behind the beginning of the end of that little fist-sized muscle that beats over 100 thousand times each day delivering oxygen-rich blood through 60 thousand miles of blood vessels to your 100 trillion cells.

Research published in a 2004 issue of the journal Circulation indicates that the immune cells of obese individuals seem to exist in a pro-inflammatory state, which places these individuals at an increased risk of developing heart disease and diabetes.[2] Increasingly, researchers are showing that fat cells are prime production sites for pro-inflammatory messengers like: IL-6, TNF-a and C-reactive protein (CRP levels are a well-known indicator of heart disease).[3]

Cholesterol is not the culprit

Because modern practitioners believe that high LDL cholesterol levels (the bad kind) are the main cause of heart disease (cardovascular), they prescribe cholesterol-lowering medications (statins) to people who are at risk for heart disease. However, ongoing studies have been revealing that more than half of the people who experience heart attacks have LDL cholesterol levels within normal range.[4] It turns out that uncontrolled inflammation has been linked to heart disease since 1985, yet we are only now beginning to accept this realization.[5]

It is important to understand that inflammation is normally a controlled reaction initiated by the immune system to help correct or repair a problem. As it pertains to heart disease, inflammation can begin with a small tear in an arterial wall, causing the immune system to send specialized cells and cholesterol to repair the damage by covering it with plaque. However, over time, the plaque builds up, causing a narrowing of the arterial space (atherosclerosis).

Excess inflammation can cause plaque to break free, which may result in the forming of a blood clot that can lead to a heart attack or stroke. Numerous researchers believe that excess inflammation may be the main cause of triggering a heart attack.[6]

Here are a few things you can do to control inflammation levels in your body:

• Ask your doctor to have your C-reactive protein (CRP) levels checked. If your test comes back at less than 1.0 mg/L you are at low risk for inflammation. Average risk is between 1.0 to 3.0 mg/L and high risk is above 3.0 mg/L.
• Consume omega-3 fatty acids, including flaxseed oil, hempseed oil, and especially high-quality fish oil or krill oil daily, and avoid excess inflammation-producing fats found primarily in meats, dairy, and egg yolks.
• Supplement with proven inflammation-reducing herbs such as turmeric, ginger, rosemary, thyme, and oregano.
• Get sufficient sleep and exercise regularly.

[1] King B. Fat Wars: 45 days to Transform Your Body. Wiley & Sons, Toronto. 2002.

[2] Ghanim H. Circulating mononuclear cells in the obese are in a proinflammatory state. Circulation. 2004 Sep 21;110(12):1564-71.

[3] C. Gorman, A. Park, “The Fires Within,” TIME, February 15, 2004.

[4] C. Gorman, A. Park, “The Fires Within,” www.TIME.com, posted February 15, 2004.

[5] Centre for Science in the Public Interest, “New Clue to an Old Killer,” Nutrition Action Health Letter, Canadian edition, Vol. 27, No. 7, September 2000, p. 3.

[6] King B. Conquer Inflammation. Transforming Health Inc. Kelowna, B.C. 2006.