Extinguishing Inflammation: A Practical Guide
Part 1 of a 2-Part Series
Part 1: Why inflammation is important in health
Inflammation spurs plaque growth, cancer, arthritis, and diabetes. Up to 70% of people
have unsuspected, asymptomatic inflammation smoldering within. Turning off
inflammation can be an important part of your program.
Conventional notions of inflammation make us think of a red-hot scraped knee, gastritis from stomach acid, or an arthritic joint. But the modern conception of inflammation is not so visible. It's imperceptible to you. There's no wound, no redness, no pain. It can fester beneath the surface for years without your awareness, building until more obvious evidence surfaces, like elevated blood sugar, rupture of a plaque in the coronary arteries, or a tumor growth in the colon. Inflammation can be detected and measured before it gets to this obvious stage.
Scores of clinical studies have confirmed that sedentary lifestyles, diets loaded with saturated and hydrogenated fats, processed foods, and refined starches magnify the likelihood of disease. It was previously unclear how obesity causes cancer. Or why inactivity magnifies the risk of heart attack. Inflammation provides the crucial missing links between unhealthy lifestyle and disease.
How is inflammation measured?
The blood test, C-reactive protein (CRP), has emerged as a practical measure of low-grade, hidden inflammation. The new "high-sensitivity" method of measure permits detection of inflammation at levels below the threshold of perception and is available from most laboratories in the U.S.
Studies have shown that the higher your CRP, the brighter the flame of inflammation is burning in your body, and the greater your risk of various illnesses.
We estimate that 70% of people beginning the Track Your Plaque program have elevated CRP as a contributor to plaque growth.
CRP is produced by the liver and released into the blood. Active inflammatory blood cells anywhere in the body generate increased levels of the signaling protein, IL-6. Excess fat cells also cause increased IL-6. IL-6, in turn, activates liver production of CRP.
If there's an obvious source of inflammation like pneumonia, flu, or a healing wound, then CRP can be dramatically elevated, often 100 g/l or higher. We don't need CRP to tell us this.
It's the inconspicuous levels of inflammation we're interested in. You feel fine—no fever, no wound, no aches—yet CRP can be elevated at levels from 0.5 to 10 mg/l. This indicates that inflammation is smoldering somewhere in the body.
Cancer, diabetes, glaucoma, macular degeneration, carotid disease, depression, and dementia are all more likely when inflammation is increased. Risk of heart attack doubles or triples, regardless of LDL cholesterol levels. This finding shook the cholesterol world but has held up repeatedly to scrutiny. CRP is a useful measure of inflammation in atherosclerotic plaque and gauges heart attack risk. Inflamed plaque is more rupture-prone, triggering heart attack. When high CRP occurs in the company of small LDL particle size, heart attack risk is 7-fold greater.
Body fat is a potent activator of inflammation. CRP is increased so predictably with excessive weight that some authorities have argued that CRP is only a reflection of obesity and the resistance to the body's insulin that accompanies excess weight. Recent data suggest that high CRP can occur independently of obesity. Obesity, however, does stand out as a powerful—and modifiable—factor in the equation.
Dowse the fire!
We aim to inactivate inflammation as completely as possible. For this we target a CRP of 0.5 mg or less. This is achievable and translates into improved outcomes.
It's no surprise that drug manufacturers are trying to make inflammation a mandate for drug therapy. Several trials are ongoing to "prove" that high CRP is reduced by statin cholesterol-reducing drugs and that lives will be saved. Preliminary experience suggests that CRP is reduced 30% by statin agents, most notably Lipitor®. However, considerable data have proven that the most potent influences over inflammation are lifestyle and nutrition based, not drugs.
The most powerful influence of all is body weight. Fat cells produce IL-6 and thereby activate CRP. Overweight and obese people suffer far more diabetes, cancer, and heart disease driven by inflammation. Excess weight leads to the metabolic syndrome, the collection of low HDL cholesterol, increased triglycerides, high blood pressure, resistance to insulin, and high CRP, a syndrome now affecting 47 million U.S. adults.
Weight reduction to ideal weight can yield dramatic drops in CRP. If you're overweight (BMI>25), losing excess weight should be the main thrust of your inflammation-reducing efforts. Interestingly, the variety of diet you choose—low-fat, low-carbohydrate, calorie-restricted, Mediterranean—seems to not play a substantial role from the viewpoint of inflammation. The principal determinant is the amount of weight lost, not the means by which you achieve it.
It is clear, however, that without weight loss, food choices do play a vital role in suppressing inflammation. Reducing saturated fats, replacing them with healthy oils like olive and canola (for anti-inflammatory linolenic acid), selecting low glycemic index foods such as lean proteins, oat products, and vegetables; avoiding high glycemic index foods like cookies, crackers, breakfast cereals, candies, cakes, and breads, all subdue inflammation.
The Mediterranean diet is a particularly powerful inflammation-suppressing tool. The ATTICA Study of 3000 men and women in Athens, Greece yielded 20% lower CRP in participants who most closely adhered to a dietary approach of plentiful olive oil (monounsaturated fat and linolenic acid), vegetables and fruits, nuts, and fish. Another study conducted in Italy at the University of Napoli showed that the Mediterranean diet reduced CRP by an astounding 60%. (We will detail how to apply principles of the Mediterranean diet to your Track Your Plaque program in future.)
A fascinating dietary experiment was conducted by Dr. David Jenkins at the Clinical Nutrition & Risk Factor Modification Center in Toronto. Forty-six participants followed a "dietary portfolio" providing 1.0 g of phytosterols (a soy bean derivative available as Benecol or Take Control butter substitutes) per 1000 kcal; 9.8 g viscous fibers (as oat bran and oat products, barley, and psyllium seed) per 1000 kcal; and 21.4 g soy protein per 1000 kcal, and almonds. (A 2400 kcal diet would therefore provide 2.4 g phytosterols, 24 g viscous fiber, 51 g soy protein, and 34 g almonds.) Average fiber intake for participants was an impressive 78 g/day (compared to the average American intake of a meager 14 g/day.) Another group followed a control diet based on the American Heart Association (AHA) recommendations, containing whole wheat products lacking viscous fibers.
The dietary portfolio achieved a 28% reduction in LDL cholesterol and a 30% reduction in CRP. The control AHA diet achieved a paltry 8% reduction in LDL and 10% reduction in CRP. Another treatment group on the AHA diet along with the cholesterol drug, lovastatin, achieved virtually identical drops in LDL and CRP as Jenkins' dietary portfolio.
Exercise can be another important aspect of lifestyle that scales down inflammation. Exercise by itself, even without weight loss, reduces inflammation. An Israeli experience in 28 people showed that 12 weeks of aerobic exercise at 70–80% of maximum heart rate reduced CRP 19% in non-diabetics, 40% in diabetics. However, weight loss is probably a more important factor than exercise itself. The greatest inflammation reducing benefits develop from a combination of the two.
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