Marx A, Neutra R R
Division of Environmental and Occupational Disease Control, California Department of Health Services, Emeryville, USA.
Epidemiol Rev. 1997;19(2):258-72. doi: 10.1093/oxfordjournals.epirev.a017957.
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.
在一些不同国家的普通人群中发现的关联具有启发性,需要开展一项综合的实验室和流行病学研究计划,以否定或证实镁与缺血性心脏病的假说。挑出这一特定风险因素有两个理由。首先,就缺血性心脏病的任何流行病学风险因素而言,如果其归因风险大到足以通过流行病学检测到,那么将该归因风险应用于每年因缺血性心脏病导致的大量发病和死亡情况,每年将挽救数万人的生命,并避免数百万美元的医院费用。其次,可以想象通过一个低成本的补充计划就能消除这一特定风险因素。例如,一种低钠、高镁和高钾的食盐在芬兰已被推荐并使用多年,在此期间,据报道人群调查中的高血压患病率有所下降(117)。在公共卫生领域,不需要行为改变的干预措施一直是最具成本效益的。因此,我们敦促资助机构优先开展研究,以确定镁对某些人群亚组是否存在不可预见的不良影响,以及在缺血性心脏病或缺血性心脏病死亡的发生过程中,低剂量镁所带来的明显益处是否真实。此外,研究人员应确定哪种镁的化学形式吸收最好且最有效。我们需要更好地了解各种水和食物成分以及个体风险因素在缺血性心脏病发病机制中的相互关系。需要识别出镁缺乏风险较高的易感个体,并研究镁可能产生的不良影响。在向公众提出建议之前,未来的研究必须就低水平的水中镁给出更好的答案。