I'm Dr. Bob Arnot, a physician, a journalist who has covered
osteoarthritis for 20 years for three different networks, an author who
has written a book on OA called BEATING WEAR AND TEAR (Simon and
Schuster 2003) and a patient who suffers from severe OA of the right hip
and moderate of both knees. I'm a traditional physician and take only a
small handful of supplements...fish oil, SamE and a
Glucosamine/Chondroiton formula. In researching a book last year on OA,
I took a careful look at Glucosamine/Chondroiton and the idea of
prevention. In the news media we look not just at the shear volume of
data but at the one landmark study which changes the way medicine is
practiced.\
\
One of the most prominent studies was released in 2001. (Lourdes,
Belgium):* * I'd like to review this study in brief, the citation:
*Lancet 2001; 357: 251-56.\
\
***Methods:** 212 patients with knee osteoarthritis were randomly
assigned 1500 mg sulphate oral glucosamine or placebo once daily for 3
years. Weightbearing, anteroposterior radiographs of each knee in full
extension were taken at enrollment and after 1 and 3 years. Mean
joint-space width of the medial compartment of the tibiofemoral joint
was assessed by digital image analysis, whereas minimum joint-space
width was measured by visual inspection with a magnifying lens. Symptoms
were scored by the Western Ontario and McMaster Universities (WOMAC)
osteoarthritis index.\
\
**Findings:** [The 106 patients on placebo had a progressive joint-space
narrowing, with a mean joint-space loss after 3 years of -0·31 mm (95%
CI -0·48 to -0·13). There was no significant joint-space loss in the 106
patients on glucosamine sulphate: -0·06 mm]{.underline} (-0·22 to 0·09).
Similar results were reported with minimum joint-space narrowing. As
assessed by WOMAC scores, symptoms worsened slightly in patients on
placebo compared with the improvement observed after treatment with
glucosamine sulphate. There were no differences in safety or reasons for
early withdrawal between the treatment and placebo groups.  \
\
On the basis of this study, physicians I have canvassed at Johns
Hopkins, Harvard and Stanford regularly recommend this to their patients
as do I. As part of a regular program of strength and flexibility
training, I began taking a Glucosamine/Chondroiton combination. I went
from taking 16 Advil a day to none. I had not been able to ski, play
tennis, run or hike. I have returned to all of those activities. I
selected this product from a website that rated the quality of these
products.\
\
The biggest question before this panel today, is whether there is a
biological marker for OA. I would argue strongly that the loss of
cartilage is as good a biological marker as the gold standard markers of
cholesterol or bone density.. The FDA in its tentative conclusions
states Biomarkers are parameters from which the precense or risk of a
disease can be inferred rather than being a measure of the disease
itself. In conducting a health claim review, FDA does not rely on a
change in a biomarker as a measurement of the effect of a dietary factor
on a disease [unless]{.underline} there is evidence that altering the
parameter can affect the risk of developing that diseases or health
related condition. This is the case with serum cholesterol in that high
levels are generally accepted as a predictor of risk for coronary heart
disease. I'd argue strongly that preventing a bad event is prevention.
In fact I can't think of a more obvious one than slowing or stopping the
loss of articular cartilage. Decreased numbers of Heart attacks, the
necessity for bypass surgery or PCTA serve as the events which measure
the effectiveness of cholesterol lowering drugs. The key point is that
bone on bone pain and the need for joint replacement that comes with the
inexorable loss of cartilage is about as good as it gets when it comes
to clinical events. I was supposed to have a hip replacement four years
ago and have avoided that to date. I no longer take NSAIDS for pain.\
\
[The biggest problem area]{.underline} here appears to be at what point
the patient is diagnosed with OA, since the FDA would argue that the
Lancet study involves patients with disease rather than healthy
individuals whose disease was prevented. Yet patients with high
cholesterol can have dozens of hot, vulnerable plaques in their coronary
arteries and yet have no symptoms and carry no diagnosis of Coronary
Artery Disease. Still if their cholesterol is lowered because they are
guaged to be at risk, and they do not suffer a bad event, the
cholesterol lowering medication is judged to have prevented disease...
even though they have not been diagnosed as heart disease patients. The
same logic should apply here. Here's why.\
\
The key with OA (osteoarthritis) is that x-ray changes PRECEED the
clinical diagnosis and precede the onset of symptoms. Most people over
60 have disease on X-ray, and about one-third have actual symptoms. That
means that the majority of individuals with x-ray changes and proven
cartilage loss are not formally diagnosed with Osteoarthritis. So any
treatment in this group would appear to prevent events. The great
difficulty has been that the Millions of Americans are loosing cartilage
year in year out... yet are not diagnosed with osteoarthritis. This is a
steady progressive loss that will result in many bad events...  There
are beneficial changes in the surrogate endpoints for the disease...
less loss of cartilage, without dispute, delays the onset of a bad
event...and the need for joint replacement surgery.\
\
The biggest difficulty is the point at which a diagnosis can actually be
made. Presumably, any events which are avoided before the patient has
diagnosed disease, would constitute real prevention. To be clear, there
is first a period of pure mechanical destruction of cartilage. I call
this wear and tear. The British call this Arthrosis.\
Eric L Raidin MD... Prof Emeritus Tufts University says\
"Arthritis is a joint problem primarily from metabolic or inflammatory
cause." That means that there is a transformation from a mechanical
process to a chemical process..\
Were is the dividing line between mechanical damage and chemical
destruction? Simply stated, no clinician can measure that point. So,
since x-ray changes are evident in the vast majority of older Americans
well in advance of symptoms, this group would be an enormous population
in which true prevention could be undertaken.\
\
RISK BENEFIT: In any analysis of evidence based medicine, the risk
benefit ratio is absolutely key. Let's first look at what happens with
standard pain relievers.  In a study by Rush Presbyterian St Luke's
Medical Center, 53 subjects with symptomatic radiographic evidence of
wear and tear arthritis of the knee were studied. They took
acetominophen relieving their pain. When gait was analyzed, those with
decreased knee pain tended to increase the load on the degenerated
portion of their knee... loading the worn and torn cartilage with forces
high enough to do further damage to the joint. Bottom line, traditional
pain relievers may accelerate the destruction of cartilage.\
**\
\
**Glucosamine/Chondroiton are called "**Incredibly safe compared to
NSAIDS" by** Tim McAldindo of the BU Arthritis Center.\
How safe? There are over 16500 deaths per year from NSAIDS. Many of
those individuals who are taking NSAIDS, such as ibuprofen or aspirin,
for arthritis. There have been none attributed to GC products that I am
aware of.\
\
AS you consider what the worst is that can happen with the use of
Glucosamine/Chondroiton for the prevention of OA... it is that fewer
patients will die from the catastrophic effects off NSAIDS. There are no
reported deaths from Glucosamine/Chondroiton. The best is that the loss
of cartilage is prevented. What physician wants to bet against GC, given
the risk of developing OA and the complications of its treatment.\
\
**Who should take preventive GC?:** The field of osteoarthritis
prevention is virtually nonexistent. Knee OA can be as disabling as any
cardiovascular disease except stroke yet there is noting being offer in
terms of prevention. GC is a great first step at the point of sale to
educate consumers about what they can do. Who is at risk?\
-Osteoarthritis affects an estimated 20.7 million Americans, mostly
after age 45\
-Women are more commonly affected than men\
-Those with Joint injuries due to sports, work related activity or
accidents.\
-Those with faulty biomechanics due to a Pistol Grip Hip, knock need
condition, bow leggedness, cavus foot, hypermobile foot, past ACL
injuries.\
\
OA is a disease that every American will get if they live long enough,
yet there is no prevention of any kind at present. This results in
billions of dollars in disability and the loss of thousands of lives.