The associations found in the general populations of a number of different countries are suggestive and warrant an integrated program of laboratory and epidemiologic research to reject or confirm the magnesium-IHD hypothesis. Singling out this particular risk factor has two justifications. First, as would be the case with any epidemiologic risk factor for IHD whose attributable risk was large enough to be detectable through epidemiology, applying that attributable risk to the vast annual morbidity and mortality from IHD would translate into tens of thousands of lives benefited and millions of dollars in hospital costs avoided per year. Second, this particular risk factor could conceivably be eliminated by an inexpensive supplementation program. For example, a low-sodium, higher-magnesium and -potassium table salt has been recommended and used in Finland for many years, during a period when the prevalence of hypertension in population surveys was said to decrease (117). Interventions which do not require behavioral change have always been the most cost-effective in public health. We therefore urge funding agencies to give priority to studies determining whether there are unforeseen adverse effects of magnesium for some population subgroups and whether the apparent benefit derived from low doses of magnesium in the development of IHD or IHD death is real. Furthermore, researchers should determine which chemical form of magnesium is best absorbed and most effective. We need to better understand the interrelation of various water and food constituents, as well as individual risk factors, in the pathogenesis of IHD. Susceptible individuals who are at higher risk of being depleted of magnesium need to be identified, and potential untoward effects of magnesium should be studied. Future research must provide better answers about low level waterborne magnesium before recommendations to the public can be made.