Glucosamine in osteoarthritis

Sir—In my commentary I neither said nor implied that glucosamine should not be used. I urged informed consent (specifically) and that the patients be aware of the short duration of the studies of efficacy and safety, and I requested longer-term studies of its efficacy and safety, especially since osteoarthritis (OA) can often last for 20–30 years.

Alistair Cumming says I call into question advertising by criticising unrelated imagery versus text or tables in advertisements for health-related products; this is true, but his allegation that I treated glucosamine unfairly, with respect to conventional pharmaceuticals, is unfounded. I included antidepressants, which are clearly conventional pharmaceuticals. The list was not comprehensive. He says, “advertisers always [my emphasis] operate just within [my emphasis] the bounds allowed”? I think that some are conservative and some are outside the bounds. Certainly, glucosamine at 750 mg or 500 mg is being used pharmacologically. That is the reason why such products should be considered drugs. Lucio Rovati and colleagues seem to agree.

In my opinion NSAIDs are never first-line treatment of osteoarthritis. As Rovati et al point out they are quite toxic—almost certainly more than glucosamine, though the COX-2 specific inhibitors might change that. Furthermore, I cannot agree that unsatisfactory products are strictly a consumer issue, not a scientific issue, because it is the science that determines, in a large part, the efficacy and safety of health-related products.

Truly not all so-called conventional medical treatments are well proven, but most newer ones have had intense scientific scrutiny, much more so than many, if not most, of the nonconventional pharmaceuticals.

I think that all substances being used pharmacologically should have the same degree of scrutiny as do conventional pharmaceuticals. Although Australia and some other jurisdictions may have such control, not all jurisdictions do for all products—not only glucosamine—that are available for the intent of treating or preventing diseases. I am very pleased that recently longer-term studies have been presented.

We all look forward eagerly to Rovati and colleagues’ data and any other longterm clinical studies published in peerreviewed journals with sufficient detail to be interpretable.

With respect to Alan Russell and Mark McCarty, the issue I raised was a potential increase in insulin resistance, not glucose concentrations. The osteoarthritic population is often of advanced age and high body mass, so some probably already have insulin resistance. I am unaware of any published study of glucosamine that measures changes in insulin values, so we do not know that they are not raised. Insulin is increased in several conditions, including type II diabetes and polycystic ovary disease, in which the long-term insulin resistance may be part of the pathogenesis. Might not increased insulin resistance (by whatever degree, however induced) over a very long period be associated with adverse effects? There are no data, though probably millions of people are taking glucosamine in pharmacological doses. I think that it is appropriate to suggest in an editorial that this should be done. Some seemingly think it is alarmist. Why? rather than calling it speculation, I think it is valid concern raised by theoretical issues. Should we ignore it and be so practical that we throw away our ideals and do not think about such issues? I think not. I believe that such questions should be answered.

I was, responsibly I believe, calling for longer-term data for safety and efficacy (more than the 4–8 weeks follow-up that has been published in peer-reviewed publications), and clarification of that to patients, many of whom have long-term osteoarthritis.