I recently came across a study comparing glucosamine versus acetaminophen. Researchers from Madrid, Spain, compared the benefit of glucosamine sulfate versus acetaminophen (Tylenol) on the symptoms of knee osteoarthritis during a 6-month treatment course. Patients were randomly assigned to receive oral glucosamine sulfate 1,500 mg once daily, acetaminophen 3 gm a day, or placebo. There were more responders to glucosamine sulfate (39%) and acetaminophen (33%) than to placebo (21%). Safety was good, and was comparable among groups. The findings of this study indicate that glucosamine sulfate is more effective than placebo and more or as effective as acetaminophen in treating knee osteoarthritis symptoms.

Dr. Sahelian Comments: Acetaminophen works quicker to relieve pain, but can cause harm to the liver, even at doses of one gram a day. I do not think it is a good drug to be taken long term for a chronic condition such as osteoarthritis. There is a possibility that if glucosamine is combined with chondroitin and other nutrients or herbs it may be more beneficial than by itself. I wonder how many years it will take for the American Board of Family Medicine to include natural supplements as options in their multiple choice questions and answers.

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Many of the latest disease-modifying anti-rheumatic drugs (DMARDS), such as methotrexate, are immunosuppressants; the latest, the monoclonal antibodies, started life as a last-ditch cancer drug.

Before being reinvented as a drug for arthritis, ulcerative colitis, Crohn’s disease and other autoimmune disorders, this class of drugs, also known as anti-tumour necrosis factor (anti-TNF) agents, were used to combat non-Hodgkin’s lymphoma, usually in those patients whose cancer returned after more traditional chemotherapy didn’t work.

Anti-TNF drugs (known as ‘biological DMARDS’) work by neutralizing TNF within the cell and its membranes. These proteins, believed to play a central role in the development of RA, are present in the blood and joints of RA sufferers in excessive amounts, causing inflammation. Anti-TNF agents block the action of TNF and consequently reduce inflammation.

TNF also plays some other major roles in the body, however. It’s well known, at least in animal models, that TNF helps to fight infection in the body. TNF also plays a central role in natural killer cell activity, although, paradoxically, it also has some tumour-promoting effects as well.

Nevertheless, a fairly obvious question remains: wouldn’t turning off the body’s response to infection and its control of tumour growth lead to serious infection or cancer?

A recent major review of all the drug trials of anti-TNF antibody conducted by a number of researchers at the Mayo Clinic in America recently answered with a resounding ‘yes’. The review concluded that anti-TNF therapy at least trebles the risk of malignancies (lymphomas, plus skin, gastrointestinal, breast and lung tumours) and doubles the risk of serious infections (i.e., those requiring antimicrobial therapy and/or hospitalization) in patients with RA. What’s more, the study found a ‘dose-dependent’ effect; the higher the dosage of the drug taken, the more likely the patient was to be adversely affected.

Patients on high doses of the drug were more than four times likely to develop cancer (JAMA, 2006; 295: 2275-85).

The review concerned two of the anti-TNF drugs licensed for clinical use: the unpronounceable infliximab (Remicade) and an even bigger mouthful, adalimumab (Humira).

A third product, etanercept (Enbrel) is also licensed, but has a different binding capability and so was not included in the Mayo study.

Nevertheless, a recent study of etanercept showed a significant increase in the incidence of solid malignancies in patients given the drug (six solid cancers in 89 patients treated with the drug plus cyclophosphamide), compared with no malignancies in the control patients (N Engl J Med, 2005; 352: 351-61)

For the ‘meta-analysis’, a team of researchers from the Mayo Clinic in Minnesota combined the results of all randomized, placebo-controlled trials of the two licensed drugs tested over 12 weeks or more.

This totalled nine such trials, with nearly 3493 patients given the active drug, and approximately 1512 given a placebo. The investigators also inter-viewed the manufacturers of the two licensed drugs.

The actual statistics show even higher risks that those reported in the meta-analysis. Of the 3493 patients given at least 1 dose of an anti-TNF drug, 24 developed malignancies, compared with two in the control group.

Furthermore, the safety data reported to the US Food and Drug Administration showed even larger figures: a total of 37 malignancies among those given the drug, compared with three among the controls.

Nevertheless, the Mayo Clinic investigators chose not to count seven cases of skin cancer, which developed during the study periods but were deemed unrelated to the drug, and six cases of malignant lymphomas, which developed after the study had actually finished. The eventual pooled analysis concluded that patients taking the drug had 3.3 times the risk of developing a malignancy, compared to those given a placebo.

Among those given the drugs, an additional 126 patients developed serious infections, compared with 26 in the control groups.

The main infection risk from this class of drugs has been assumed to be granulomatous infections (like pneumonia or tuberculosis). Nevertheless, only 10 per cent of serious infections were of this variety.

Indeed, a recent Dutch study shows that up to one-quarter of patients taking these drugs develop skin infections, rashes or eczema (Arthritis Research and Therapy, 2005; 7: R666-R676).

The results of the Mayo Clinic meta-analysis are similar to the findings of the German Biologics Register, which showed that patients given infliximab trebled their risk of serious infection (Arthritis Rheum, 2005; 52: 3403-12).

Up until now, the drug companies claimed that malignancies caused by anti-TNF therapy for RA were rare. Only a single drug study of 18,000-plus patients, comparing those receiving methotrexate or anti-TNF agents, found an increased risk of malignancies of the blood in the patients given the monoclonal antibodies (Arthri Rheum, 1994; 50: 1740-51). The results of this meta-analysis put paid to that optimistic view.

The National Institute for Clinical Evidence (NICE), an organization that advises the National Health Service in Britain, is now re-evaluating how widely these drugs should be prescribed. The researchers of the Mayo Clinic suggest that infliximab doses above 3 mg/kg every eight weeks can cause problems. In fact the research shows no additional benefit in taking higher doses.

Lynne McTaggart

Conventional NSAIDs work by decreasing the production of prostaglandins; they do this by inhibiting the enzyme cyclooxygenase (COX). Prostaglandins are responsible for inflammatory changes in the body.

But, despite being ‘demonised’ by modern medicine, prostaglandins also have important parts to play in everyday health. They are, for instance, involved in the normal functioning of blood platelets, the kidneys and lining of the gastrointestinal tract. Because of this, sweeping inhibition of prostaglandin synthesis can produce a variety of unwanted effects in addition to the desired helpful anti-inflammatory effect.

There are two distinct forms of COX enzymes in the body. The one known as COX-1 is released primarily in the gastrointestinal tract, kidneys and platelets. The other, COX-2, is released primarily in response to inflammation.

At least two COX-2 inhibitors, celecoxib (Celebrex, approved in December 1998) and rofecoxib (Vioxx, approved in May 1999) are available in the marketplace. In 2001, a third – valdecoxib (Bextra) – was added to the list. At their launches, the COX-2 inhibitors were considered a major advance in pain management.

But problems began to surface almost immediately. The first was calling these drugs ‘COX-2 inhibitors’, on the basis of a blood assay done in a lab, not in the body, despite the fact that the US Food and Drug Administration (FDA) has never approved the designation of any drug as ‘COX-2 specific’- that is, specifically designed to block only the actions of COX-2.

Currently available NSAIDs block both COX-1 and COX-2 to some degree (see box p 2), and it’s likely that inhibiting COX-1 causes the well-known toxic side-effects of NSAIDs – peptic ulcer, bleeding and perforation, and kidney damage. So, in theory, a drug that selectively blocks COX-2 will have anti-inflammatory effects, but without the toxic side-effects.

But, in reality, the actions of the two enzymes are not so well delineated. COX-1 and COX-2 serve identical functions in the body, and the involvement of the one more than the other depends on the other enzymes present – however specific they may act in the test-tube.

The FDA classes celecoxib, rofecoxib and valdecoxib as traditional NSAIDs. If the FDA approves a drug as a ‘COX-2 inhibitor’, it will probably have to demonstrate that it produces fewer serious gastrointestinal complications, such as bleeding, perforation and obstruction, than ordinary NSAIDs. But given the complex interactions of these and other enzymes in the body, none of the current so-called COX-2 inhibitors has yet been able to prove their specificity for COX-2 to the FDA’s satisfaction.

First, the good news
Human studies have found benefit with COX-2 inhibitors. When celecoxib and rofecoxib were compared with traditional NSAIDs (such as ibuprofen, naproxen and diclofenac) for osteoarthritis (OA) and/or rheumatoid arthritis (RA), results after six weeks showed pain relief that was significantly better than placebo in OA patients and comparable to that with traditional NSAIDs (J Rheumatol, 1999; 26: 2438-47). Similarly, patients with RA had significantly less pain, and joint swelling and tenderness with either rofecoxib or celecoxib than with a placebo (Lancet, 1999; 354: 2106-11; Clin Ther, 1999; 21: 1688-702).

Nevertheless, neither celecoxib nor rofecoxib has been taken for long enough periods of treatment in a large enough population to conclusively prove their safety.

Data from small trials do suggest a small reduction in GI events (JAMA, 1999; 282: 1919-33). Ulcers were far less frequent with celecoxib and rofecoxib in RA and OA patients compared with traditional NSAIDs. In OA, ulcers larger than 3 mm in diameter (which can develop into serious problems) were seen four to seven times less frequently with rofecoxib (depending on the dosage) than with ibuprofen (Gastroenterology, 1999; 117: 776-83).

In RA patients, the incidence of GI ulcers at 12 weeks with celecoxib was four to six times less frequent than with naproxen (Arthritis Rheum, 1998; 41: 1591-1602). However, with non-ulcer GI symptoms such as dyspepsia, rofecoxib and celecoxib have not convincingly proved able to reduce these symptoms compared with traditional NSAIDs.

The same study also found that neither of these COX-2 inhibitors interfered with blood clotting or bleeding time. However, both can slightly slow blood clotting in warfarin (Coumadin)-treated patients. Consequently, caution is now urged if patients taking anticoagulants are treated with selective COX-2 agents.

In the US, where drug companies are allowed to advertise directly to the public, ads on national television and in popular magazines regularly accentuate the positive side of the COX-2 inhibitors. Most reassure the public that these new anti-inflammatory drugs will safely reduce pain without the risks of adverse effects associated with older anti-inflammatories such as aspirin.

Unfortunately, the truth is that postmarketing medical research is rapidly proving that COX-2 inhibitors can be associated with severe and sometimes life-threatening toxic effects.

A price to pay
As with all ‘miracle cures’, the relief brought about by COX-2 inhibitors comes with a price. Much of the hoopla over these drugs has been based on the ‘fact’ that they cause fewer GI problems than conventional NSAIDs.

But, four years to the day after Celebrex was approved, a study suggests that the drug is no more effective in preventing a recurrent bleeding ulcer in arthritis patients than a traditional NSAID plus a proton-pump inhibitor such as Prilosec (N Engl J Med, 2002; 347: 2104-10). A popular treatment for heartburn that can help prevent stomach ulcers, Prilosec is often given to arthritis patients with a history of bleeding ulcer to counteract the high risk of NSAID aggravation of the problem.

In this study, nearly 5 per cent of patients taking Celebrex had recurrent bleeding – a potentially life-threatening condition – compared with 6 per cent of those taking a traditional NSAID plus Prilosec.

To medical news observers, this result was no surprise. In 1999, the findings of controlled clinical trials were already showing problems. In one of over 1000 patients with RA given celecoxib and compared with those given naproxen or a placebo, a similar rate of GI symptoms occurred with celecoxib and naproxen – 26 and 31 per cent, respectively.

The only real difference was with ulcers: naproxen resulted in five times more ulcers than celecoxib. Although the ulcers were usually less than 3 mm in diameter (and thus not clinically important), nevertheless, they can lead to serious ulcer complications such as perforation or bleeding (JAMA, 1999; 282: 1921-8).

In the same year, a review pooled the results of eight similar randomised controlled studies comparing rofecoxib, traditional NSAIDs and placebo in more than 5000 OA patients. The analysis focused on complications of GI ulcers (perforation, pain and bleeding). In a 12-month period, twice as many bleeding peptic ulcers were seen with NSAIDs than with rofecoxib. Rates for dyspepsia were similar in both groups – somewhere around 25 per cent (JAMA, 1999; 282: 1929-33).

An editorial accompanying the review suggested that to prevent one ulcer complication among low-risk patients in one year, some 500 patients would need to be treated with COX-2 inhibitors – at a cost of nearly $400,000 (JAMA, 1999; 282: 1961-3).

Taking heart
In the last couple of years, more disturbing adverse effects have come to light. An analysis by the World Health Organization of the side-effects of COX-2 inhibitors that have emerged since their release onto the marketplace suggests that the risks of kidney and cardiovascular problems (hypertension and cardiac failure) associated with the use of rofecoxib may be significantly greater than those associated with celecoxib or NSAIDs such as diclofenac and ibuprofen (Clin Ther, 2001; 23: 1478-91).

Other study results have only served to strengthen the WHO’s position. Indeed, the bad news has been uncovered almost by accident.

For instance, a recent review of smaller studies pooled the findings from 23,407 patients with data submitted to the US FDA by pharmaceutical companies (JAMA, 2001; 286: 954-9). Among these studies were two major randomised trials that originally investigated the gastrointestinal safety of rofecoxib and celecoxib: the Vioxx Gastrointestinal Outcomes Research Study (VIGOR), which involved 8076 patients, and the Celecoxib Long-term Arthritis Safety Study (CLASS), involving 7968 patients.

In the VIGOR, RA patients taking rofecoxib had a 238 per cent higher risk of having a cardiovascular event such as a heart attack, unstable angina, cardiac thrombus (blood clot), cardiac arrest, sudden or unexplained death, ischaemic stroke (due to narrowed or blocked blood vessels) and transient ischaemic attacks (mini-strokes in the brain) compared with those taking naproxen.

In the CLASS, there were no significant differences in cardiovascular event rates (myocardial infarction, stroke and death) between celecoxib and conventional NSAIDs (ibuprofen and diclofenac).

However, participants in the CLASS were allowed to take aspirin while those in the VIGOR were not – a twist that was significant for the gastrointestinal safety of celecoxib.

Although both studies were able to show an overall twofold reduction in serious GI complications, in the CLASS, this benefit with celecoxib was cancelled out if the patient also took low-dose aspirin. This finding is particularly relevant given the large number of elderly adults who regularly take low-dose aspirin to protect against heart attack.

Taken altogether, the yearly heart attack rates for COX-2 inhibitors, according to the findings in both the VIGOR and CLASS, were significantly higher than usual: 0.74 per cent with rofecoxib and 0.80 per cent with celecoxib compared with 0.52 per cent among those taking a placebo.

Not surprisingly, the results of this meta-analysis caused some outrage among COX-2 enthusiasts. They noted – and correctly – that neither CLASS nor VIGOR had been originally designed to look at cardiovascular events. Furthermore, they claim that the analysis of these data was done on a post-hoc basis – concluding a causal relationship between events solely because they took place one after the other in time.

Similarly, others have questioned the tactic of using ‘historical’ controls – comparing the findings with results from earlier studies in the medical literature.

Nevertheless, these disturbing findings raise a cautionary flag that should not be ignored.

Smaller studies have also thrown up problems with cardiovascular risk. In one study, blood pressure was increased significantly in 17 per cent of patients taking rofecoxib and in 11 per cent of those taking celecoxib (Am J Ther, 2001; 8: 85- 95). Indeed, no study so far has proven that taking COX-2 inhibitors is safe for the heart.

A kidney punch
High blood pressure increases the risk for heart attack and stroke, and also increases the risk of kidney failure. And case reports are now emerging that describe kidney problems in association with taking COX-2 inhibitors. What’s more, these kinds of side-effects are often reported as mere footnotes to studies – as if they are of no major importance at all.

In one report, it was concluded that Celebrex was effective for pain relief. Yet, the data also showed that celecoxib resulted in kidney problems such as hypertension, peripheral oedema and kidney failure in one-quarter of all patients receiving the COX-2 drug (N Engl J Med, 2002; 347: 2104-10).

In a recent case study reported in The Lancet, doctors describe a patient whose kidneys started to fail after taking Vioxx. The patient’s condition improved following discontinuation of the drug, an indication that the drug was the cause of the kidney dysfunction (Lancet, 2001; 357: 1946-7).

In another study comparing the effects of rofecoxib with the conventional NSAID indomethacin during regular long-term use, both drugs hampered the kidney’s ability to filter waste. However, the authors also suggest that the problem is likely to apply to the entire class of medications. This means that people on sodium-restricted diets and diuretic therapy, and those with impaired kidney function, hypertension, congestive heart failure or liver disease should avoid NSAID therapy, including COX-2 inhibitors (Ann Intern Med, 2000; 133: 1-9).

As sodium excretion by the kidneys is at least partly assisted by the COX-2 enzymes, the use of COX-2 inhibitors can slow the elimination of sodium from the body, thereby leading to fluid retention and raising high blood pressure even further (Curr Opin Rheumatol, 1997; 9: 178-82).

The decision to prescribe COX-2 inhibitors should take into account more than just the degree of pain.

According to Dr Joan M. Bathon in a discussion of COX-2 inhibitors in OA (www.hopkins-arthritis.som.jhmi. edu), there have been clinical trials showing that both rofecoxib and celecoxib can cause serious swelling of the feet even in patients who have normal kidney function.

Disturbingly, though, none of the current COX-2 inhibitors has yet been tested for safety in patients with compromised kidney function

Pain as a result of arthritis can be both debilitating and discouraging. Given that medical science has so little to offer sufferers of either rheumatoid arthritis or osteoarthritis in the way of a cure, simply relieving the pain of arthritis has become the major focus of treatment.

There are many alternative approaches that can help not only to reduce pain, but also to improve mobility and quality of life. A look at the ‘bigger picture’ of the problems of arthritic pain needs to be part of the conventional medical thinking if doctors are ever to offer sufferers more than a trade-off of debilitating symptoms.
Pat Thomas

This was the finding of a three year randomised placebo controlled European trial, involving 212 patients with osteoarthritis of the knee. Patients were randomly assigned to receive either 1500 mg of oral glucosamine sulphate or placebo, once daily, for three years. Benefit was assessed by weightbearing X-rays of each knee, taken after one year and at the end of the study. All patients in the placebo group showed joint deterioration whereas those taking glucosamine did not. Placebo patients also reported a worsening of symptoms while those taking the supplement reported improvement (Lancet, 2001; 357: 251-6).

This study is something of a breakthrough for pundits of nutritional supplements. An accompanying commentary suggests that glucosamine could represent a new era not just in the treatment of osteoarthritis, but also when doctors must begin to “accommodate the possibility that many nutritional products may have valuable therapeutic effects” (Lancet, 2001; 357: 247).

* Think twice if you are under 60. It’s likely that you’ll need a revision in your lifetime.

* Use the cementless variety if your bones are strong.

* Insist on a hospital and a surgeon with a long and successful track record in performing this particular operation.

* Opt for tried-and-tested materials. At the last count, there were more than 60 brands of artificial hips. In one study, two-thirds of Charnley prostheses, among the oldest and best-tested models, were still operational after 25 years (J Bone Joint Surg, 1997; 79: 1599-617).

In a 1998 health-technology assessment of all research on the various hip brands, the lowest revision rates were seen with the Exeter, Lubinus and Charnley prostheses. Another good performer is the Stanmore (J Bone Joint Surg, 1995; 77-B: 520-7).

Among the cementless varieties, the AML Total Hip Replacement is the most widely used model in the world. The lowest wear rate is with metal-on-metal (alumina-on-alumina) (Clin Orthop, 1996; 329 Suppl: S78-88; Clin Orthop, 2000; 379: 123-33).

* Avoid these products: hip prostheses made from zirconia ceramic, hydroxyapatite (HA)-coated total hip replacements with a thin polyethylene inlay, and the W Hex Loc cementless hip socket (J Bone Joint Surg, 1999; 81 [B]: 835-42; Acta Orthop Scand, 1998; 69: 253-8; Clin Orthop, 2001; 393: 112-20).

The study, conducted by the University of Oslo, enlisted 53 patients with classic rheumatoid arthritis, then allocated27 of them to a four week stay at a health farm. The study group were then put on a near total fast using only herbal teas, garlic, vegetable broth and juice extracts from carrots, beets and celery. The fast did not allow fruit juices.

After the fast, the patients were allowed to reintroduce a new food every other day. If they reported an increase in pain or joint swelling up to two days after ingesting the new item, they omitted it again for another week.

For three and a half months, they were asked to avoid gluten, meat, fish, eggs, dairy products, refined sugar, citrus fruits, alcoholic beverages, tea, coffee, salt strong spices and preservatives.

After three and a half months, the patients were allowed to reintroduce dairy products and gluten so long as they did not react to them.

A control group spent four weeks at a home eating an unrestricted diet.

After four weeks, those on the restricted diet showed significant improvements in joint tenderness and swelling, pain, morning stiffness and grip strength. These benefits carried on for a year, leading the researchers to concludes that “a substantial reduction in disease activity can be obtained by fasting followed by an individually adjusted vegetarian diet”.

These results caused the ordinarily conservative Lancet to begrudgingly admit:”It is already clear . . . that every rheumatology department needs a dietitian, if not a health farm.”

These days, glucosamine is hailed as a cure for osteoarthritis. Most supplements consist of the compound glucosamine sulphate as the sulphate form appears to strengthen glucosamine’s effect (Pharmatherapeutica, 1981; 2: 504-8).

Several studies suggest that glucosamine sulphate relieves pain better than NSAIDs like ibuprofen (Curr Med Res Opin, 1982; 8: 145-9; Pharmatherapeutica, 1981; 2: 504-8; Curr Med Res Opin, 1980; 7: 104-9). Also, instead of making the condition worse – like NSAIDs do (Am J Med, 1987; 83 [Suppl 5A]: 29-34) – it seems to reverse the disease by stimulating the production of more cartilage.

In one study, 80 patients with osteoarthritis were given either 500 mg of glucosamine sulphate three times a day or a placebo. While symptoms decreased in both groups, those receiving glucosamine had a significantly greater reduction in symptoms compared with placebo – 73 vs 41 per cent. Furthermore, a sample of cartilage from the placebo group, looked at under electron microscopy, showed definite evidence of osteoarthritis whereas samples from the treated patients showed what appeared to be healthy cartilage (Clin Ther, 1980; 3: 260-72).

The effects of glucosamine sulphate improve over time, so if you wish to try it, give it time – at least three months.

The researchers measured knee joint rotation in 20 women who alternatively walked barefoot or in one of two pairs of their own shoes of comparable heel heights.

The average heel height was 7.0 cm. The narrow base shoes were an average of 1.2 cm wide while the wide base shoes averaged 4.5 cm wide.

It was found that increasing the width of a shoe’s heel did nothing to improve the abnormal gait caused by wearing high heels, and that wearing wide heeled shoes had a 30 per cent greater adverse effect on knee rotation than walking barefoot.

The doctors also noted that women who opt for wide heels are putting increased pressure on the surrounding tendons and joints. Even more than thin heeled shoes, wide heels raised the risk of such degenerative changes in the knee as osteoarthritis (Lancet, 2001; 357: 1097-8).

* Investigate food allergies. NSAIDs can make you more food-sensitive. Remove nightshades (potato, tomato, bell peppers, aubergine) from your diet.

* Increase your levels of antioxidants, particularly vitamin C, which is necessary for collagen synthesis. High levels can reduce the rate of cartilage loss by 70 per cent (Arthritis Rheum, 1996; 39: 648-56). Vitamin E (600 IU) can also help collagen breakdown in OA (J Am Geriatr Soc, 1978; 26: 328-30). Take both vitamins together.

* Take high doses of B vitamins, particularly niacinamide, or vitamin B3 (from 900 mg to 4 g, in divided doses), to increase movement in OA (J Am Geriatr Soc, 1955; 3: 927) – but only under medical supervision, as high levels can cause glucose intolerance and liver damage. Vitamin B12 and folic acid can help control pain (J Am Coll Nutr, 1994; 13: 351-6).

* Increase your levels of omega-3 fatty acids through fish, fish oils, omega-3 supplements and zinc.

* Supplement with Devil’s claw (Harpagophytum procumbens), which can increase mobility (J Appl Nutr, 1987; 27: 45-50).

* Take boron, also shown to help with bone and OA (J Nutr Med, 1990; 1: 127-32). Dr Melvyn Werbach suggests that, as the minimum daily allowance for boron is still not established, patients should increase their consumption of boron-rich foods (vegetables such as soya, cabbage, lettuce and peas; fruits such as apples, dates, raisins and prunes; nuts, especially almonds, hazelnuts and peanuts).

* Try supplementing with glucosamine, the chief component of proteoglycans, a major building-block of cartilage, to rebuild damaged cartilage (Orthop Praxis, 1970; 9: 225). Research shows that it helps reverse the disease (Int J Tissue React, 1992; 14: 243-51; Clin Ther, 1980; 3: 260-72).

Glucosamine is often taken with chondroitin sulphate, one of the main glycosaminoglycans found in cartilage,as the two often work in synergy. However, when using intermuscular chondroitin, be wary of kidney/liver toxicity (Lancet, 1989; i: 1275).

* New Zealand green-lipped mussel extract may help (Lancet, 1981; i: 439).

The pet dogs of 15 patients diagnosed with SLE were examined by the Department of Immunology at the University Hospital at Nottingham. Dogs, like humans, can suffer from the illness.

All the patients’ dogs were found to have abnormal antibody and blood levels corresponding to canine SLE.

The researchers concluded that SLE may be transmissible and cross the species barrier, or be due to some common environmental factor.