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OUR GUARANTEE:
Flexicose is backed by a no questions asked, 90 day complete
refund policy, even if you use the entire bottle. You
really have nothing to lose but your symptoms. |
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What Are COX2 (COX-2) Inhibitors And How Do They Work?
Bear with us because this may get a little technical but it is important to understand why alternatives to Flexicose can be so harmful. COX-2 inhibitors are drugs such as Vioxx, Celebrex and Bextra. To
understand COX-2 (COX2) Inhibitors, you first have to understand
COX-1 (COX1) and what its role in the body is. Regular NSAIDS
(mostly COX-1 and a bit of COX-2 Inhibitors) work by inhibiting
the production of prostaglandins (PGs). Prostaglandins are
fatty-acid derivatives located all over your body that are
well known for their inflammation and immune response effects.
However, they also have many different functions in the body.
A scientific list would read as such: PG’s are involved
in as diverse normal processes as ovulation, blood clotting,
renal function, wound healing, vasomotor tone, platelet aggregation,
differentiation of immune cells, nerve growth, bone metabolism,
and initiation of labor. Pretty essential to your body, wouldn’t
you say? The key point here is that shutting down PG's does more than just shut down your pain - it impacts your entire body too!
If
you are familiar with the fact that when you are using drugs
such as aspirin, your blood thins and you bruise easier,
that is a “side effect” of the COX-1 inhibitor.
In the above list, that would fall under the blood clotting
category. Remember, COX-1 inhibitors work by inhibiting PG’s.
Due to the acidity of the stomach, the cells of your stomach
are normally replaced very quickly, within a few days. One of the
major roles of PG’s is to keep the lining of the stomach
intact, and when your PG system is disrupted (say by taking
COX-1 drugs like many NSAIDS) stomach irritation, digestive
tract problems and even intestinal or stomach bleeding and
ultimately death could occur. In fact, according to The New England
Journal of Medicine,
over 103,000 hospitalizations and 16,500 deaths annually are caused by complications from NSAID drugs. Remember, NSAIDS are common pain relievers such as aspirin! Aspirin makes your stomach bleed! Surely COX-2 drugs, being designed to be more specific would not have these side effects? That was the original thinking, anyway...
COX-2
inhibitors were discovered later, and were presumed to be
a “healthier, more targeted” way of treating
the soreness – without the side effects. This makes
sense as COX-2 is found more commonly in inflammatory and
immune cells than COX-1 drugs, which exist throughout the
body. Unfortunately, this would prove to be far, far from
the truth. While COX-2 is more specific to soreness, the
side effects can be far worse than COX-1 drugs. Vioxx, Bextra and Celebrex are all COX-2 drugs.
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The
side effects of COX-1 drugs are pretty terrible. It is
estimated that 25% experience some kind of side effect
and 5% develop SERIOUS health consequences such as GI (stomach)
bleeding, acute renal failure, or worse. The New England
Journal of Medicine reports that “anti-inflammatory
drugs (prescription and over-the-counter, which include
Advil®, Motrin®, Aleve®, Ordus®, Aspirin,
and over 20 others) alone cause over 16,500 deaths and
over 103,000 hospitalizations per year in the US”,
according to a review article published in the New England
Journal of Medicine1.
You
can see why researchers would believe there was a clear
cut and dry line between COX-1 and COX-2. The message was
clear: research (and get patents for) drugs that actually
inhibited only COX-2 and you would have a blockbuster drug
on your hands. The sad part was that the people who took COX-2 drugs were the ones to suffer. Over the counter drugs
such as Ibuprofen and Naproxen work to inhibit COX-1 and
COX-2. Aspirin works more on COX-1. Some others such as
diclofenac work primarily on COX-2 but also affect COX-1.
However, even “selective” COX-2 inhibitors
are not that selective. At therapeutic dosages, they
inhibit enough COX-1 to potentially cause the same stomach
toxicity and other associated problems as regular COX-1
drugs. Not to the exact same extent but more than enough
to do damage. Remember, 16,500 people are KILLED by “harmless” and “common” NSAIDS
such as aspirin or ibuprofen every year. In development
are other “newer aspirins” that may prove to
ACTUALLY be more selective for COX-2 than COX-1, but in
the mean time – despite claims of being “selective” – the
current COX-2’s such as Vioxx® (rofecoxib) or
Celebrex® (celecoxib) are simply not selective enough,
not to mention some of their potentially horrible side
effects and the associated lawsuits that have been filed
(and won) due to side effects such as heart attacks, stroke and blood
clots. Our advice is to explore (for osteoarthritis) other
alternative, cheaper and far more effective treatments
for your pain. Glucosamine is a natural (and as such not
patentable by large drug companies) substance that has
been shown in many, well designed studies to be at least as effective
as Ibuprofen, and other related drugs - even Celebrex! Plus, it works to
improve flexibility and mobility by helping your body heal from within - not just covering up the pain and making your stomach bleed. Not even an as yet nonexistent "second generation"
COX-2 drug will be able to do that.
Unlike some other products with white willow bark, Flexicose
contains absolutely no artificial or natural COX-2 or COX-1 drugs, only
superior-quality Liquid Glucosamine, Chondroitin, MSM and 10 other synergistic
ingredients, designed to knockout your joint discomfort
while improving flexibility from within. Stop simply covering
up your discomfort while things get worse and worse. You have to take action today. Flexicose
has little to no side effects and is far less expensive
than prescription drugs - under 90 cents a day! Give Flexicose a try now, you have
90 days risk free and we even include free U.S.
shipping. Order
Flexicose now. Still not convinced? Get more information on the benefits
of Flexicose.
References
1. Wolfe MM, et. al. NEJM 1999;340(24):1888-99
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