A recent research study performed in Thailand has been reported in the American Journal of Veterinary Research (AJVR) which addresses the possibility that oral glucosamine might be useful for treating Feline Interstitial Cystitis (FIC).
Panchaphanpong J, Asawakarn T, Pusoonthornthum R. Effects of oral administration of N-acetyl-d-glucosamine on plasma and urine concentrations of glycosaminoglycans in cats with idiopathic cystitis. Am J Vet Res. 2011 Jun;72(6):843-50.
FIC is a poorly understood condition in which cats experience many of the symptoms of a bladder infection, including blood in their urine and straining to urinate, and which can even lead to urinary tract obstruction in males. For years, such cats were assumed to have bacterial urinary tract infections (UTIs) and treated with antibiotics. Since most were given a 7-10 days course of antibiotics and most got better within that period, it was long believed that the treatment was working and was confirmation of the diagnosis of UTI. This is a classic example of how misleading clinical experience and the post hoc ergo propter hoc fallacy can be. Eventually, controlled scientific research revealed that the condition is usually inflammatory, not infectious, and typically resolves on its own. Antibiotics don’t help, and since they can cause vomiting, diarrhea, loss of appetite, or wounds on the hands of the person trying to give them to a cat, they are actually more likely to do harm than to help these patients.
Because glycosoaminoglycans (GAGs), like glucosamine, are a normal part of the protective lining of the bladder wall, it has been hypothesized that supplementing with GAGs might be useful in preventing or treating this condition. This paper, however, doesn’t provide much support for that hypothesis.
The study was double-blinded and placebo controlled w/ randomization. There were only 19 cats with FIC (7 in the placebo group and 12 in the glucosamine group), and 10 normal cats were used as controls. The authors gave the treatment group glucosamine (and the placebo group an identical placebo) for 28 days. Blood and urine samples were obtained (though not always from every subject) on the first day before treatment and then at 7, 14, 21, 28, and 56 days after the start of the study. Treatment was discontinued at 28 days.
There were no bloodwork abnormalities in any of the normal or FIC cats. The only difference in urine test results was in the presence of blood in the urine. Before treatment, 6/12 (50%) of the treatment group had no blood in their urine, and at the end of treatment 10/12 (83%) cats in the treatment group were without blood in their urine. In the placebo group, 1/7 (14%) were free of blood before treatment and 5/7 (70%) had no blood in the urine at the end of the 28 days. The authors suggest that because a higher percentage of the treatment group were free of blood in the urine at the end, this suggests the treatment reduced this symptom of FIC. However, no statistical analysis was done to determine if the difference between 83% and 70% is significant, which it may well not be in so small a sample. And a much higher percentage of the placebo group had blood in their urine to begin with, so if anything this group seemed to have a greater improvement over the course of the study than the cats receiving glucosamine.\
Another variable measured was the concentration of GAG in the blood and urine. If GAGs are going to be useful as an oral medication, they have to be absorbed and reached therapeutic levels in the tissue where the problem is. In this study, blood levels of GAG did increase significantly in the treatment group at Days 21 and 28. GAG levels were greater in the treatment group than the placebo group at Day 21, but not at Day 28. And the starting GAG levels in the blood were the same for the normal control cats and for those with FIC. So while it seems the oral glucosamine did increase the blood level of GAG somewhat, it is not clear that blood levels are related to the presence of FIC or that the increase was meaningful since it was not consistently present but only seen at one out of four measurement times.
Another variable measured in the study was the level of GAGs in the urine. Urine GAG levels at the start of the study were higher in cats with FIC than in normal cats. The authors suggest this may be the result of GAG leakage from the inflamed bladder wall in cats with FIC. Urine GAG levels in cats treated with glucosamine were significantly higher than that of cats in the placebo group at only one of the four measurement times, Day 14. The authors imply that this might be a sign of the oral glucosamine reaching the bladder, a necessary prerequisite for the glucosamine having any potential medicinal use for this condition. However, as mentioned the difference only existed at one time point. And if it is true that the FIC cats had higher urine GAG levels than the normal cats at the start of the study because this was a symptom of their diseases, then why are higher levels later interpreted as a potentially positive sign rather than as an indication of greater inflammation and leakage from the bladder wall?
This was a well-designed and conducted study which, as so often happens, was interpreted in a more positive way than really justified by the data reported. Overall, it is consistent with previous studies which suggest that oral glucosamine is probably absorbed to some extent, though it may or may not reach physiologically meaningful concentrations in blood or other tissues. However, there is little indication that the supplement had any significant impact on the FIC affected cats. No clear, consistent effect on clinical symptoms or laboratory measures was observed. The study is useful in investigating in a systematic and generally objective way the potential for oral glucosamine as a therapy for FIC, and by and large it does not suggest there is much value in glucosamine as an FIC therapy.