by Elmer M. Cranton, M.D.

The American Medical Association published a deceptively worded and blatantly unscientific study that alleged to disprove benefit from EDTA chelation as a treatment for heart disease—the so-called Calgary PATCH study.(1) Nowhere do they actually claim to have disproven chelation, although that is implied and that is the way many readers will interpret it. They merely state that they found, “no evidence to support a beneficial effect.” In their final sentence they reiterate that conclusion: “Larger trials with a broader range of patients will be needed to assess the safety and impact of EDTA chelation therapy on clinical event rates.” That conclusion is not surprising, since a careful reading of the published report clearly shows that this study was too small, too flawed, and too poorly designed in many ways to produce anything of significance, beneficial or otherwise. It is puzzling that the American Medical Association, with its reputation for scientific integrity to uphold, would publish such pseudoscience in its flagship journal.

Careful analysis shows that the study seems designed to disprove chelation from the outset. Only one-fourth the number of patients needed for statistical significance was included. Patients most likely to benefit were selectively excluded. Most patients in the study had only minor symptoms, and 30% had no symptoms at all. It is not possible to study a treatment for angina in patients who do not have angina.

Twice as many patients were placed in the EDTA-treated group who had previously experienced myocardial infarctions.

The exercise protocol was bizarre. They failed to screen for reproducibility as a condition for entry. Accepted scientific guidelines were ignored. The primary endpoint was not clearly defined. The type of electrocardiographic ST-depression used as an endpoint is now considered non-specific and is no longer accepted as diagnostic for coronary disease.

Approximately twice as many patients in the misrepresented “placebo” group were given potent anti-anginal drugs. That would obscure comparative improvement in EDTA-treated patients, who received only half as much anti-anginal drug therapy.  There was therefore no true “placebo” group. The F.D.A. in the United States. has never approved a new drug to treat angina without first requiring trials wherein all other anti-anginal medications had been discontinued.

Four patients in the placebo group and none in the EDTA-treated group underwent angioplasty during the one-year follow-up after chelation, suggesting that EDTA chelation reduces the need for invasive procedures. EDTA-treated patients also showed more improvement in maximal oxygen consumption. If the study had only included more subjects for statistical analysis, and produced these same results, it would have been a very favorable study showing a greatly reduced need for angioplasty or bypass following chelation therapy.