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Dispelling Myths About Chondroitin

by Dr. Jason Theodosakis, M.D.

Here's the real evidence...

Chondroitin was the first supplement shown to reduce the cartilage loss in osteoarthritis, not glucosamine.

Two studies showed this in 1998, over a year before the Lancet glucosamine study was presented and two years before its publication.

Hre are the two chondroitin studies:

Chondroitin Sulfate: S/DMOAD (Structure/Disease Modifying Anti-Osteoarthritis Drug) in the Treatment of Finger Joint OA

Gust Verbruggen, Stefan Goemaere and Eric M. Veys Department of Rheumatology, Ghent University Hospital, Ghent, Belgium

Summary:

A total of 119 patients were included in a randomized, double-blind, placebo-controlled trial in order to assess the S/DMOAD properties in OA of chondroitin sulfate (CS 4&6, 3 x 400 mg/day, Condrosulfr IBSA, Lugano, CH).

Posteranterior roentgenographies of the interphalangeal (IP) joints were carried out at the start of the study and at yearly intervals. This enabled the investigators to document the radiological progression of the anatomical lesions in the pathological finger joints over a 3-year period. It was shown that the progression of OA in the IP finger joints in an individual can be determined by the evolution of his finger joints through previously described anatomical phases: INƒ (not affected), 'S' (classical OA), IJƒ (loss of joint space), IEƒ (erosive OA) and IRƒ (remodeled joint).

Structure/disease-modifying anti-OA drug (S/DMOAD) properties were searched for by assaying the number of patients developing OA in previously normal IP joints ('N' > 'S'), or progressing through the described anatomical phases of the disease ('S' > IJƒ, 'S' > IEƒ, IJƒ > IEƒ, 'S' > IRƒ, IJƒ > IRƒ, IEƒ > IRƒ). In the CS 4&6 group we observed a significant decrease in the number of patients with new 'erosive' OA finger joints. This result is particularly important since OA of the finger joints becomes a clinical problem (pain, functional loss) when 'S' joints progress to IJƒ and especially 'E' phases. During and after these IEƒ phases, joints will remodel and show the nodular deformities characteristic of Heberden's and Bouchard's nodes.

Treated patients were protected against erosive evolution.

SOURCE: Osteoarthritis and Cartilage (1998) 6, (Supplement A), 37-38 Osteoarthritis Research Society

Effects of Oral Chondroitin Sulfate on the Progression of Knee Osteoarthritis: A Pilot Study

Daniel Uebelhart, Eugene J-M. A. Thonar, Pierre D. Delmas, Alex Chantraine and Eric Vignon Division of Physical Medicine & Rehabilitation, Department Neuclid, University Hospital of Geneva, Switzerland; Department of Biochemistry and WHO Collaborating Center for the Field of Osteoarthritis, Rush Presbyterian-St. Luke's Medical Center, Chicago, IL, USA; INSERM 403 Unit and Division of Rheumatology, E. Herriot Hospital, Lyon, France; and Division of Rheumatology, Lyon-Sud Hospital, France

Summary:

The aim of this study was to assess the clinical, radiological and biological efficacy and tolerability of the SYSADOA, chondroitin 4- and 6-sulfate (CS, CondrosulM, IBSA, Lugano, Switzerland), in patients suffering from knee osteoarthritis.

This was a 1-year, randomized, double-blind, controlled pilot study which included 42 patients of both sexes, aged 35-78 years with symptomatic knee OA. Patients were treated orally with 800 mg chondroitin sulfate (CS) per day or with a placebo (PBO) administred in identical sachets. The main outcome criteria were the degree of spontaneous joint pain and the overall mobility capacity. Secondary outcome criteria included the actual joint space measurement and the levels of biochemical markers of bone and joint metabolism.

This limited study confirmed that chondroitin sulfate was well-tolerated and both significantly reduced pain and increased overall mobility capacity. Treatment with CS was also associated in a limited group of patients with a stabilization of the medial femoro-tibial joint width, measured with a digitized automatic image analyzer, whereas joint space narrowing did occur in placebo-treated patients. In addition, the metabolism of bone and joint assessed by various biochemical markers also stabilized in the CS patients whereas it was still abnormal in the PBO patients.

These results confirm that oral chondroitin 4- and 6-sulfate is an effective and safe symptomatic slow-acting drug for the treatment of knee OA. In addition, CS might be able to stabilize the joint space width and to modulate bone and joint metabolism. This is the first preliminary demonstration that a SYSADOA might influence the natural course of OA in humans.

SOURCE: Osteoarthritis and Cartilage (1998) 6, (Supplement A), 39-46 1998 Osteoarthritis Research Society

Chondroitin alone was shown to be more effective than glucosamine alone.

In the same study, chondroitin alone was more effective than glucosamine alone when cartilage was examined microscopically.

Furthermore, a major article, published in 2000 in the Journal of the American Medical Association, reviewed all of the glucosamine and chondroitin studies performed before July, 1999. Of the 37 studies reviewed, 15 were double-blinded and placebo-controlled. Nine of these studies were human, clinical studies using chondroitin and six used glucosamine. The summary revealed that the overall treatment effect for chondroitin, 0.78 (high effect) was almost double that for glucosamine, 0.44 (moderate effect). Reference: JAMA. 2000;283:1469-1475

Don't be fooled by products that skimp on the chondroitin dose. Most of the evidence supports the use of 800 - 1,200 mg of chondroitin per day.

Chondroitin dosages of 800 mg have substantial evidence. 800 mg has beaten 1,200 mg head-to-head but the results was a trend and not statistically different (therefore 800 mg = 1,200 mg). A 200 mg dose of chondroitin was not shown to be effective.

Beware of products that try to deceive you or hide the chondroitin dose by using the words "glucosamine or chondroitin complex", contain gelatin, hydrolyzed collagen, or microlactin. None of these latter substances are chondroitin and none have evidence they can replace chondroitin.

Shark cartilage is only about 13 - 20% chondroitin, so this is to be avoided as well. 1,200 mg of shark cartilage is only 156 - 240 mg of chondroitin, well below the 800 mg that is needed.

More on these issues to follow...

Dr. Theo

SOURCE: Dr. Jason Theodosakis, M.D. (Drtheo.com)

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Dispelling Myths About Chondroitin