From: "Richard Padilla" 
Newsgroups: alt.invest.real-estate.methods
Subject: Mona Vie helps to alleviate your 
Date: Tue, 14 Mar 2006 04:33:06 GMT

Symptom Alleviations



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.

Goto http://GotMonavie.net