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Excess
weight
Carrying extra pounds contributes to chronic inflammation because
fat encourages the production of pro-inflammatory cytokines.
According to a University of Vermont study, obese women who lost an
average of 39 pounds also reduced their inflammation levels by 32
percent (Circulation, 2002, vol. 105, no. 5).
High-glycemic
foods
Research by Simin Liu, MD, PhD, at Harvard Medical School found
that women who ate large quantities of high-glycemic carbohydrates
(such as sugar, white potatoes, white rice, processed cereals, and
muffins) had significantly increased CRP levels (American
Journal of Clinical Nutrition, 2002, vol. 75, no. 3). Elevated
CRP has been linked to increased risk of heart attack (New
England Journal of Medicine, 2002, vol. 347, no. 20).
Protein cooked
at high temps
Cooking meat at high temperatures, such as when grilling, creates
"advanced glycosylation end products," or AGEs, which crank up
inflammation. According to research conducted at Mount Sinai School
of Medicine in New York City, inflammation rose 35 percent in
diabetics who ate large quantities of AGEs, but it fell 20 percent
in those who ate low levels of AGEs (Proceedings of the National
Academy of Sciences, 2002, vol. 99, no. 24). High levels of AGEs
are also found in some cheeses, soy sauces, pretzels, and diet
sodas.
Saturated
fats
In 2004, researchers at the University of New York at Buffalo found
that people who ate a high-fat, high-calorie, fast-food breakfast
had significantly elevated levels of inflammatory markers in their
blood for three hours after the meal (American Journal of
Clinical Nutrition, 2004, vol. 79, no. 4). Eating such meals
on a frequent basis can create a chronic state of inflammation in
the blood vessels and lead to the development of
atherosclerosis.
Gum
disease
Chronic bacterial infection of the gums, also known as periodontal
disease, has been found to trigger the production of CRP and other
proteins that inflame and promote the formation of blood clots in
the arteries (Journal of Peridontology, 2001, vol. 72, no.
9).
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