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Glucosamin im BB

 
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ramrot




Anmeldedatum: 05.08.2005
Beiträge: 77
Wohnort: Yuma-City

BeitragVerfasst am: 27.09.05 | 14:49    Titel: Glucosamin im BB

Glucosamin ist ein Aminozucker, der natürlich in unserem menschlichen Organismus zu finden ist, speziell in Knochen und Knorpeln. Wir nehmen einen Teil Glucosamin aus der natürlichen Nahrung auf, da es hier in geringem Umfang enthalten ist. Manches deutet jedoch darauf hin, dass viele Menschen für die Aufrechterhaltung oder den Aufbau des körperlichen Vorrats an Glucosamin einen zusätzlichen Bedarf dafür haben - gerade im fortgeschrittenen Alter und unter hoher Belastung ist der Organismus nicht mehr in der Lage ausreichend Glucosamin über die Nahrung aufzunehmen.

Verschiedene wissenschaftliche Studien haben gezeigt, dass Glucosamin eine nützliche Wirkung auf Gelenke und Gelenkfunktionen hat. Am bekanntesten ist die so genannte "Lancet Studie" Es ist dokumentiert, dass die Zuführung von Glucosamin den Abbau von Knorpel, der häufig im Alter stattfindet, stoppen kann.

In den wissenschaftlichen Studien werden keine nennenswerten Nebenwirkungen erwähnt. Es wird jedoch beschrieben, dass einzelne Personen Magenbeschwerden gemeldet haben; dies ist jedoch nur äußerst selten vorkommende Nebenwirkung. Da Glucosamin aus Schalentieren gewonnen wird, wird Personen mit einer Schalentierallergie davon abgeraten, das Produkt zu verwenden. Das gleiche gilt für Schwangere oder Stillende. Diabetiker müssen bei der Einnahme von Glucosamin den Blutzuckergehalt aufmerksam beobachten. Da Glucosamin wie erwähnt bereits in größeren Mengen im Organismus und in unserer täglichen Nahrung zu finden ist, handelt es sich nicht um einen Fremdstoff, sondern um ein Nahrungsergänzungsmittel.

Glucosamin wird hauptsächlich in zwei Varianten, Glucosaminulfat und Glucosamin Hydrochlorid (HCl), auf dem Markt gebracht. Das Erstgenannte ist das am besten getestete, und im Großen und Ganzen basieren alle wissenschaftlichen Untersuchungen auf dieser Variante.

Woher stammt das Glucosamin?

Glucosamin kann aus Schalentieren und auch aus Knochen von z. B. Rindern gewonnen werden. Aufgrund des Risikos des Creutzfeld-Jacob-Syndroms, verwenden heute alle seriösen Anbieter ausschließlich GS das aus Schalentieren gewonnen wurde. Somit können Sie sicher sein, dass das Produkt kein Fleisch- oder Knochenmehl enthält.


Hier Auzüge aus der Studie:

Background

Treatment of osteoarthritis is usually limited to short-term symptom control. We assessed the effects of the specific drug glucosamine sulphate on the long-term progression of osteoarthritis joint structure changes and symptoms.

Methods

We did a randomised, double-blind placebo controlled trial, in which 212 patients with knee steoarthritis 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 enrolment 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—ie, at the narrowest point—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 (−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.

Interpretation

The long-term combined structure-modifying and symptom-modifying effects of gluosamine sulphate suggest that it could be a disease modifying agent in osteoarthritis.

Introduction

Osteoarthritis is a major cause of disability and is among the most frequent forms of musculoskeletal disorders.1 The goal of pharmacological treatment is usually to control symptoms of the disease, pain, and limitation of function, which is traditionally accomplished by the use of analgesic agents or non-steroidal anti-inflammatory drugs (NSAIDs).2 Drugs for the treatment of osteoarthritis have been classified as symptom-modifying drugs and also as structure-modifying drugs if they are able to alter the joint structure favourably and thus actually interfere with the progression of the disease.3,4 Although no drug can be included in the second category as yet, compounds are being searched for that may exert more specific effects than those of NSAIDs, directly interfering with some of the possible disease processes. Thus, these compounds might also favourably affect joint structure changes during long-term treatment, contrary to what has been observed with some NSAIDs that could even worsen progression.5
Glucosamine sulphate is the sulphate derivative of the natural aminomonosaccharide glucosamine. Glucosamine, a normal constituent of glycosaminoglycans in cartilage matrix and synovial fluid,6 could have various pharmacological actions in articular cartilage and joint tissues. Several short-term to medium-term clinical trials in osteoarthritis have shown the significant symptom-modifying effect of glucosamine sulphate and its good safety profile.7–10 The need for long-term clinical trials with this compound has been emphasised.11,12 We did a randomised double-blind placebo-controlled trial to establish whether glucosamine sulphate can affect progression of symptoms and joint structure changes in osteoarthritis.

Methods

Study design and selection of patients

We recruited patients from the outpatient clinic of the Bone and Cartilage Metabolism Research Unit of the University Hospital Centre in Liege, Belgium. Inclusion criteria were age over 50 years and primary knee osteoarthritis of the medial femorotibial compartment, diagnosed according to the clinical and radiological criteria of the American College of Rheumatology.13 Disease severity was graded on the basis of the Kellgren and Lawrence radiographic system.4 Major exclusion criteria were: history or active presence of other rheumatic diseases that could be responsible for secondary osteoarthritis;3,4 severe articular inflammation as confirmed by physical examination (excluded also by erythrocyte sedimentation rate <40 mm/h and serum rheumatoid factor titre < 1:40); traumatic knee lesions; overweight defined as a body mass index >30; substantial abnormalities in haematological, hepatic, renal, or metabolic functions; and intra-articular or systemic corticosteroids in the 3 months preceding enrolment. The study was approved by the ethics commitee of the University of Liege and all patients gave their oral and written informed consent to participate.

Results

Of 355 patients screened, 212 were enrolled in the study and randomly assigned to receive glucosamine sulphate or placebo (figure 1). A similar number of patients in the two groups did not complete the 3-year treatment course:38 of 106 (36%) in the glucosamine sulphate group and 35 of 106 (33%) in the placebo group (p=0·77), without significant differences in reasons for withdrawal. Patients in the two groups had similar demographic and baseline characteristics (table 1). Patients had similar mild to moderate osteoarthritis radiographic grading and joint-space widths at enrolment, with a degree of symptoms expressed by the WOMAC index that was also similar and of mild to moderate average severity. During the 6 months before enrolment, 51% of patients in both groups did not report any pharmacological treatment for osteoarthritis, whereas within the remaining patients 24% had received NSAIDs, 15% simple analgesics, 8% both NSAIDs and simple analgesics, 2% corticosteroids, without differences between groups. Compliance with study treatment was good: the proportion of patients who reported over 70% drug intake ranged between 81% and 91%, without significant differences between groups Table 2 shows the final joint-space narrowing in the medial compartment of the tibiofemoral joint for the patients assessed for 3 years and the intention-to-treat worst-scenario analysis. With both approaches there was no average loss of joint-space width in the patients receiving glucosamine sulphate. Conversely, patients on placebo had a significant mean and minimum joint-space narrowing after 3 years. Final differences between groups were significant in all instances. A similar effect was recorded when the intention-to-treat analysis was done by the last observation carried-forward approach (data not shown) and especially by the random sampling approach, in which the median of significant differences was p=0·044 for the mean and p=0·013 for the minimum joint-space narrowing. After the first year of treatment, the intention-to-treat change in mean joint-space width with placebo was only &#8722;0·05 mm (95% CI &#8722;0·23 to 0·14), compared with the 0·12 mm (-0·06 to 0·29) change with glucosamine sulphate (ie, only a non significant favourable trend in the difference: 0·17 mm [95% CI &#8722;0·09 to 0·42]; p=0·21).After 3 years, 32 of 106 patients (30%) randomised to placebo had a severe mean joint-space narrowing of more than 0·5 mm, compared with only 16 (15%) with glucosamine sulphate (p=0·013).
There were similar mean joint-space narrowing trends after 3 years in the contralateral medial compartments of patients assessed for 3 years with bilateral involvement—ie, a significant loss with placebo and a non-significant change with glucosamine sulphate (final difference between groups: 0·46 mm [95% CI 0·04 to 0·88]; p=0·033; n=66 and n=54, respectively). Changes in the same direction occurred also in the joint lateral compartments, but they were smaller and not significant.



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