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Quieting a Body's Defenses
Researchers are linking inflammation to an ever-wider array of chronic 
illnesses. But treatments that block the inflammatory response can backfire.

By Anne Underwood
Newsweek

Summer 2005 - A decade ago, the cause of meta Kiss's heart attack might have 
been written off as a medical mystery. The 59-year-old homemaker had never 
smoked, weighed in at a slender 119 pounds and had fabulous cholesterol 
readings, with her good cholesterol actually surpassing the bad. And there 
was no history of heart disease in her family. So what put her at risk for 
the heart attack she suffered in 2000? To Eric Matteson, one of her doctors 
at the Mayo Clinic, the answer leapt right out. "She had rheumatoid 
arthritis," he says.


If the two conditions sound unrelated, that's because most of us are just 
now awakening to the risks of chronic inflammation. A decade ago, 
researchers were blaming oxidative damage for everything from cancer to 
heart disease. Now chronic, low-grade inflammation is seizing the spotlight. 
"Inflammation is the evil twin of oxidation," says neuroscientist James 
Joseph of Tufts University. "Where you find one, you find the other." That 
would include not only such obvious inflammatory conditions as asthma and 
rheumatoid arthritis, but also ailments never previously associated with 
inflammation-such as atherosclerosis, Alzheimer's disease, colon cancer and 
diabetes. Suddenly medical puzzles seem to be fitting together, such as why 
hypertension puts patients at increased risk of Alzheimer's, or why 
rheumatoid-arthritis sufferers have higher rates of sudden cardiac death. 
They're all connected on some fundamental level-which raises a tantalizing 
question. If there are common threads in the development of all these 
diseases, are there common treatments? Drug companies are eager to find out. 
But it's not as simple as it seems.


If you can't live with inflammation, you can't live without it, either. 
Inflammation is a key component of the immune system's defenses. If you cut 
yourself, the body sends in a barrage of microbe-fighting molecules 
(including oxidants), and the wound becomes red, hot and swollen. When the 
threat of infection recedes, so does the inflammation. But persistent 
insults like cigarette smoke, excess cholesterol and lingering infections 
can produce a low-grade, chronic inflammation that simmers on, like the low 
flame on the back burner that we're unaware of until the pot burns.


DIABETES-

Diabetes has emerged as a recent example. The correlation between type 2 
diabetes and obesity is so well established that some researchers refer to 
the two collectively as "diabesity." Now we're starting to understand why 
they're linked. When you gain weight, fat cells grow more biochemically 
active, churning out inflammatory compounds. As obesity ratchets up 
inflammation, inflammation in turn promotes insulin resistance, a central 
feature of diabetes and the so-called metabolic syndrome that precedes it. 
Just why inflammation leads to insulin resistance is unclear. But Dr. Steven 
Shoelson, associate director of research at Joslin Diabetes Center, has bred 
a strain of mice whose fat cells produce exceptional levels of inflammatory 
compounds like TNF-alpha, IL-1 and resistin (as in insulin resistance). "We 
reproduced the whole constellation of metabolic syndrome in these mice," he 
says, "just by inciting inflammation."


HEART DESEASE-

In addition to diabetes, heart disease is a risk for people who are 
overweight. Inflammation may be the common denominator. "Inflammation is the 
alpha and omega of atherosclerosis," says Dr. Peter Libby, chief of 
cardiovascular medicine at Brigham and Women's Hospital in Boston. "It's 
there at every step of the process." Plaque formation begins when 
cholesterol gets stuck in arterial walls and oxidizes, prompting the immune 
system to attempt a cleanup. Although inflammation is the body's attempt to 
heal, it only encourages the formation of bigger, more complicated plaques. 
With luck, plaques will remain stable for decades and cause no trouble. But 
inflammatory chemicals can weaken the fibrous cap that holds a plaque in 
place. If it ruptures, fat spills into the blood, where it collides with 
clotting factors, producing a clot that can block an artery and cause a 
heart attack or stroke.


CANCER-

Even certain cancers are being linked to inflammation. "People with chronic 
inflammatory bowel diseases have tremendously enhanced risk of colon 
cancer," says Lisa Coussens, a cancer biologist at the University of 
California, San Francisco. Other triggers of tumor-inducing inflammation 
include cigarette smoke in the lungs, persistent infections like hepatitis C 
in the liver and chronic heartburn, which repeatedly irritates the lining of 
the esophagus with gastric acid. Whatever the cause, says Coussens, the 
result is a series of changes that can set a cell on the road to malignancy. 
These include oxidative damage to DNA, the disabling of suicide mechanisms 
that should cause an abnormal cell to self-destruct, and the release of 
growth factors that can make the abnormal cell grow and divide.


INFLAMATION-

This knowledge is beginning to change clinical approaches to treatment. For 
example, doctors used to use bare wire-mesh frames called stents to hold 
open clogged arteries, but the blood vessels routinely formed scar tissue 
over the stents and often narrowed again. Now doctors are achieving much 
better success rates with stents that are coated with anti-inflammatory 
drugs. And they're starting to look beyond cholesterol alone for the keys to 
reducing heart attacks. Several large trials suggest that those patients who 
do best reduce both cholesterol and inflammation. Statin drugs help many 
patients reduce both, but future treatments may target inflammation more 
directly. Millennium Pharmaceuticals in Cambridge, Mass., is working with an 
experimental drug that blocks macrophages, a type of inflammatory immune 
cell, from moving out of the bloodstream and into vessel walls and other 
tissues.


But taming the immune system isn't as simple as it sounds. As Libby 
explains, there are three ways to go about it. You can reduce the triggers 
that cause inflammation. You can hamper the cellular "master switches" that 
orchestrate the body's inflammatory response. Or you can knock out the 
inflammatory chemicals-the "foot soldiers," as Libby dubs them-that actually 
produce the inflammation. Here's the catch. If you turn down the central 
switches too much, "you run the untoward risk of secondary infections," says 
Dr. Mark Fishman, president of the Novartis Institutes for BioMedical 
Research. Tysabri, an immune-modulating drug for multiple sclerosis, was 
voluntarily withdrawn from the market earlier this year after two patients 
taking it with another medication called Avonex developed an additional 
neurodegenerative disease, this one caused by a latent virus most of us 
harbor. Scientists need a much more detailed knowledge of how the various 
parts of the immune system interact and overlap, so they can develop key 
blood tests to tell them just how much they're turning down the system.


As for the foot soldiers, it turns out that many of the body's inflammatory 
chemicals also have beneficial functions, like protecting the stomach or 
guarding the lining of blood vessels against clots. If you knock out 
something that causes harm in one part of the body, you may eliminate 
positive effects elsewhere. Drugs like Vioxx and Bextra are a case in point. 
By inhibiting inflammatory Cox-2 enzymes, they relieved pain, but also 
hampered a compound that helps prevent dangerous blood clots from forming in 
arteries. A second problem with the foot soldiers is that there are so many 
with overlapping functions that eliminating a single one doesn't necessarily 
help you. The drugs Enbrel and Remicade fight rheumatoid arthritis by 
targeting the inflammatory compound TNF-alpha, but they do nothing for 
congestive heart failure, which many cardiologists believe is also an 
inflammatory condition.


Instead of aiming at narrower and narrower targets, some scientists are 
doing the opposite and striving for broader "immune modulation." One such 
treatment, called Celecade, is now in advanced testing for congestive heart 
failure. Doctors withdraw a test tube of the patient's blood and place it in 
a machine that delivers bursts of UV radiation for 10 to 15 minutes. The 
radiation kills immune-system white cells by triggering mechanisms of 
self-destruction. The blood is then reinjected into the patient's hip. As 
the procedure is repeated during the following weeks and months, the immune 
system interprets the self- destruction of white cells as a signal that the 
danger is reduced and responds by turning down systemic inflammation across 
the board. "When I first saw this data, I was intrigued but highly 
skeptical," says cardiologist James Young of the Cleveland Clinic 
Foundation. Now that he has taken part in trials, he's cautiously optimistic 
that it will become a useful treatment. W. R. Woofter, 59, of Berea, Ohio, 
is one patient who's tried it. He's had five heart attacks since 1968 and 
severe congestive heart failure since 2002. Since last August, he's been 
going for monthly treatments. "I haven't deteriorated any more," he says. 
"I've been able to cut back on diuretic drugs by a third and cut another 
medicine for cardiac dysrhythmia by half." And he's back to golfing. "I'm 
still taking people's money," he says.


Medicine doesn't provide the only way to beat inflammation. Exercise and 
weight loss work to reduce inflammation in the fat cells and liver. And a 
diet rich in fruits, vegetables, whole grains and omega-3 fatty acids tones 
down inflammation overall.


The omega-3s are particularly important. Found in coldwater fish like 
salmon, sardines and mackerel, as well as walnuts, flaxseed and dark leafy 
greens, they form the building blocks of a number of anti-inflammatory 
compounds in the body. Dozens of studies have shown that the omega-3s can 
help prevent heart attacks and sudden cardiac death by preventing 
arrhythmias, making blood less likely to clot in arteries, improving the 
balance of good and bad cholesterol and limiting inflammation. But the 
modern diet is generally deficient in them. That's why a growing number of 
doctors are recommending fish-oil capsules.


A diet rich in fruits and vegetables also helps. One anti-inflammatory 
compound in food that has been studied extensively is curcumin, the yellow 
pigment in the curry spice turmeric. Greg Cole, professor of medicine and 
neurology at UCLA, has found that small doses reduce TNF-alpha and IL-1. 
Larger doses lead to a decrease in Cox-2 enzymes. But Cole considers 
curcumin a far safer Cox-2 inhibitor than, say, Vioxx. While drugs usually 
block a single target molecule and reduce its activity dramatically, he 
says, natural anti-inflammatories, such as Monavie, gently tweak a broader 
range of inflammatory compounds. "You'll get greater safety and efficacy 
reducing five inflammatory mediators by 30 percent than reducing one by 100 
percent," he notes.


The beauty of these lifestyle changes is that they're so low tech, 
affordable and effective. When patients with a sedentary lifestyle and 
miserable diets come into the office of cardiologist Herbert Insel at New 
York University, they invariably ask if he can help them. "Sure," he 
replies. "But you can help yourself better." We may all have it within our 
grasp to reduce inflammation-if we can just muster the willpower.

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