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Raising false hopes

MagazineJuly 1994 (Vol. 5 Issue 4)Raising false hopes

If you've been reading the papers on either side of the Atlantic, you've probably think there is "new hope" for victims of Alzheimer's disease

If you've been reading the papers on either side of the Atlantic, you've probably think there is "new hope" for victims of Alzheimer's disease.

These headlines appeared after the publication of a study of the drug tacrine in the Journal of the American Medical Association (6 April 1994), claiming that 42 per cent of patients given the new drug were considered significantly approved. Tacrine, released in the US in September 1993, has not yet been approved for use in Britain.

The JAMA study, led, incidentally, by the manufacturer of the drug, was published four days after the appearance of another study in the British Medical Journal, which found that tacrine produced no benefits. Not surprisingly, the only appearance of the negative study was in the medical literature, not the general press.

Editorial writers in both JAMA and the BMJ were quick to write off the discrepancy as dose related; patients in the JAMA study were given 160 mg a day, whereas in the BMJ study, they received, at most, 100 mg. The JAMA study was also much bigger more than 200 patients, compared with 32 in the second. Therefore, the writers concluded, the contradictory results didn't mean that more work needs to be done on the drug so much as more of the drug needs to be taken to have any effect.

What also didn't make it into any news stories was that more than half the original participants in the large JAMA study dropped out, most because they could not tolerate tacrine's side effects: liver toxicity, nausea and vomiting. A similar number in the BMJ study quit for the same reason.

Another study published in the same issue of JAMA analyzed liver function in some 2500 patients taking tacrine. About half had abnormal blood alanine aminotransferase levels (an enzyme essential to the formation of alanine, an amino acid found in components of proteins). One fourth had levels more than three times the upper limit of normal. Although there were no deaths, what this means in the long term is anyone's guess.

It's also wise to remember that tacrine only increases the concentration of a chemical neurotransmitter; it doesn't in any way actually treat the disease. As Dr Margaret Winker pointed out in a JAMA editorial, tacrine only improved cognitive function in the studies by the amount equivalent to the deterioration that occurs over six months of the disease. But mental deterioration moves apace, even on the drug; if the patient stops taking tacrine, his cognition will return to the level it would have been had he never taken it. Dr Barry Reisberg of New York University School of Medicine pointed out that the effects of tacrine are, at best, "modest and temporary".

As with AIDS, in the rush to seen to be doing something against this other modern scourge of the 20th century, medicine and the government agencies have served up another phony magic bullet. The media and medicine help no one in pushing forward as a miracle cure a drug with modest benefits and potential for enormous harm.

!ALynne McTaggart


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