Soothing the Burning Heart

[Guest guest]

Soothing the Burning Heart

Doctors increasingly consider inflammation as the cause of heart

disease. Here's why – and what you can do about it…

http://www.willner.com/article.aspx?artid=33

©2004 By Jack Challem

 

Over just the past several years, researchers and physicians have

been redefining the cause of coronary artery (heart) disease. The

old view was that high-fat diets led to cholesterol deposits in

arteries, choking off the blood supply and eventually causing a

heart attack. The new view is that heart disease begins as an

inflammatory disorder of the blood vessels, with cholesterol-laden

lesions forming after the initial damage to arteries.

This is a fundamentally different way of explaining the leading

cause of death among Americans. Some 60 million people have coronary

heart disease, resulting in approximately 725,000 deaths each year.

As you might imagine, new thinking on the cause heart disease leads

to different strategies for prevention.

Inflammation

About 15 years ago, researchers began piecing together exactly how

the " bad " low-density lipoprotein (LDL) form of cholesterol was

related to inflammation and heart disease.

 

In a series of human and cell studies, Ishwarlal " Kenny " Jialal,

M.D., then with the University of Texas Southwestern Medical Center,

Dallas, discovered that normal LDL did not promote heart disease.

LDL caused heart disease only when it became " oxidized, " or damaged

by harmful molecules known as free radicals.

Jialal's studies found that the immune system responded to oxidized

LDL much the way it did to bacteria. White blood cells would attack

and engulf globules of oxidized LDL, but they would ignore normal

LDL. After capturing oxidized LDL, the white blood cells would then

become lodged in the walls of arteries, creating the initial lesions

that most people call " cholesterol deposits. " Jialal also found that

vitamin E, an antioxidant, prevented LDL oxidation and reduced the

activity of white blood cells against LDL.

 

C-Reactive Protein and Inflammation

Still, it was not until 2000 that the role of inflammation in heart

disease gained momentum. Paul Ridker, M.D., of the Harvard Medical

School, developed a new blood test, known as high-sensitivity C-

reactive protein (CRP), to measure inflammation. He reported in the

New England Journal of Medicine that people with elevated blood

levels of CRP were four times more likely to suffer a heart attack,

compared with people who had normal CRP levels.1

 

CRP is both an indicator and a promoter of inflammation. It is part

of a family of molecules called cytokines, which cells use to

communicate with each other. CRP, interleukin-6 (IL-6), and many

other cytokines tell immune cells to mount an inflammatory response.

Other types of cytokines let cells know when it is time to reduce

inflammation.

 

Some researchers believe that inflammation, stimulated in part by

CRP and white blood cells, directly damages blood vessel walls.

Another view is that inflammation destabilizes cholesterol deposits,

prompting them to break apart and block a blood vessel.2

 

A Pro-Inflammatory Diet

 

Although the research points to a strong cause-and-effect

relationship between inflammation and heart disease, a crucial

question remains: What causes this chronic inflammation? The answer

may lie in our eating habits.

 

Two of the body's principal arbiters of inflammation are the omega-6

and omega-3 families of fats, and the building blocks of these fats

are found in foods. The omega-6 family of fats generally promotes

inflammation, whereas the omega-3 family reduces inflammation.

Ancient human diets contained relatively equal portions of these

fats. However, modern processed foods—convenience foods and fast

foods—have tilted this ratio to about 30:1 in favor of pro-

inflammatory omega-6 fats. These fats are found in common cooking

oils (such as corn, safflower, peanut, and soybean oils), as well as

in mayonnaise,salad dressings, potato chips, fries, and baked goods.

 

Many of these foods also contain trans fats, which interfere with

the body's processing of anti-inflammatory omega-3 fats.

Furthermore, research by Simin Liu, M.D., Sc.D., of the Harvard

Medical School, has shown that simple sugars, refined carbohydrates

and other high-glycemic foods increase CRP levels. Diets high in

sugars also displace more nutritious antioxidant-rich vegetables,

which can reduce LDL oxidation and CRP levels.

 

Adopting an Anti-Inflammatory Diet

To restore a balance between pro- and anti-inflammatory fats, it is

important to emphasize coldwater fish (such as salmon and herring),

which contain substantial amounts of anti-inflammatory omega-3 fats.

Chicken and beef from free-range (not grain fed) animals also have

large amounts of omega-3 fats with relatively small amounts of

saturated fat.

 

In addition, opt for cooking oils that contain large amounts of anti-

inflammatory omega-9 fats. These oils include extra-virgin olive oil

and macadamia nut oil.

 

Also, eat nonstarchy vegetables (such as salads, broccoli,

cauliflower, and green beans) and nonstarchy fruits (such as

blueberries, raspberries, and kiwi). These foods are rich in

antioxidants, which curtail inflammation. Meanwhile, reduce your

consumption of foods with sugars and refined starches, and avoid all

foods with trans fats (found in partially hydrogenated vegetable

oils).

 

Taking Anti-Inflammatory Supplements

Several supplements have a pronounced anti-inflammatory effect and,

not surprisingly, have been found to reduce the risk of heart

disease.

• Vitamin E. Vitamin E has been used since the 1940s to prevent and

treat heart disease. Several clinical studies have found that

natural-source vitamin E can lower CRP levels by 30 to 50

percent.4,5 Its anti-inflammatory effect has also been corroborated

in two studies of patients with rheumatoid arthritis.6,7 Try 400 IU

daily.

• Fish oil supplements. Fish oil supplements provide a concentrated

source of anti-inflammatory omega-3 fats. These fats reduce the risk

of blood clots and heart-rhythm abnormalities.8,9 Try 1,000 to 3,000

mg daily.

• Other antioxidants. Vitamin C, alpha-lipoic acid, mixed

carotenoids (beta-carotene, lutein, and lycopene), and flavonoids

(such as Pycnogenol and grape-seed extract) may also reduce

inflammation and CRP levels.

Finally, you can reduce CRP levels by losing weight. Fat cells,

particularly those that form around the belly, produce their own CRP—

which may be why obesity is a risk factor for heart disease.

 

Jack Challem is the author of The Inflammation Syndrome (John Wiley

& Sons, 2003). This article was originally published in GreatLife

magazine and is reprinted with permission of the author. © Jack

Challem. For additional information, visit

www.inflammationsyndrome.com

 

 

References:

1. Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and

other markers of inflammation in the prediction of cardiovascular

disease in women. New England Journal of Medicine, 2000;342: 836-

843.

2. Buffon A, Biasucci LM, Liuzzo G, et al. Widespread coronary

inflammation in unstable angina. New England Journal of Medicine,

2002;347:5-12.

2. Liu S, Manson JE, Buring HE, et al. Relation between a diet with

a high glycemic load and plasma concentrations of high-sensitivity C-

reactive protein in middle-aged women. American Journal of Clinical

Nutrition, 2002;75:492-498.

4. Upritchard JE, Sutherland WHF, Mann JI. Effect of supplementation

with tomato juice, vitamin E, and vitamin C on LDL oxidation and

products of inflammatory activity in type 2 diabetes. Diabetes Care,

2000, 23:733-738.

5. Devaraj S, Jialal I. Alpha tocopherol supplementation decreases

serum C-reactive protein and monocyte interleukin-6 levels in normal

volunteers and type 2 diabetic patients. Free Radical Biology &

Medicine, 2000; 29:790-792.

6. Edmonds SE, Yinyard PG, Guo R, et al. Putative analgesic activity

of repeated oral doses of vitamin E in the treatment of rheumatoid

arthritis. Results of a prospective placebo controlled double blind

trial. Annals of the Rheumatic Diseases, 1997;56:649-655.

7. Helmy M, Shohayeb M, Helmy MH, et al. Antioxidants as adjuvant

therapy in rheumatoid disease—a preliminary study. Arzneimittel-

Forschung/Drug Research, 2001;51:293-298.

8. Dwyer JH, Allayee H, Dwyer KM, et al. Arachidonate 5-lipoxygenase

promoter genotype, dietary arachidonic acid, and atherosclerosis.

New England Journal of Medicine, 2004;350:29-37.

9. Ernst E, Saradeth T, Achhammer G. n-3 fatty acids and acute-phase

proteins. European Journal of Clinical Investigation

 

 

 

 

 

 

 

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