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Med Hypotheses. 2012 Nov;79(5):642-8. doi: 10.1016/j.mehy.2012.07.043. Epub 2012 Sep 6.
High-level cadmium (Cd) exposure has long been known to induce nephropathy, severe osteoporosis, and fractures in humans. More recent epidemiology, however, reveals that, in populations not known to have important industrial exposure to this heavy metal, high-normal blood or urine Cd levels correlate with increased risk for vascular disorders, cancers, diabetes, and total mortality, as well as osteoporosis and nephropathy. Since these disorders appear unlikely to expedite Cd absorption, and since Cd has promoted these pathologies in rodent studies, it seems reasonable to conclude that Cd is an important mediating risk factor for these disorders in humans. Avoiding tobacco smoke or frequent ingestion of shellfish or organ meats can lessen humans exposure to Cd, but the chief dietary sources of Cd are plant-derived foods - green leafy vegetables, whole grains, tubers, and root vegetables - typically recommended for their health-supportive properties; indeed, among non-smokers, vegans tend to have the highest Cd body burden. Fortunately, iron sufficiency and ample dietary intakes of calcium, magnesium, and zinc can impede absorption of dietary Cd, both by down-regulating intestinal expression of mineral transporters, and by directly competing with Cd for access to these transporters. Correction of iron deficiency appears to be of particular importance for controlling Cd absorption. Moreover, zinc supplementation can counteract the toxicity of Cd already in the body via induction of metallothionein, which binds Cd avidly via its sulfhydryl groups; so long as it remains sequestered in this form, Cd is innocuous. Zinc supplementation may in any case be recommendable, as optimal zinc status exerts protective anti-inflammatory, antioxidant, and immunosupportive effects. Inasmuch as the toxicity of Cd appears to be mediated in large part by oxidative stress, ingestion of spirulina, lipoic acid, melatonin, and N-acetylcysteine may also have potential for mitigating the risk associated with Cd exposure, as suggested by rodent studies. Hence, although Cd may prove to be a major risk factor for morbidity and mortality in humans, practical strategies for limiting its absorption and pathogenic impact are at hand.
高水平的镉（Cd）暴露长期以来一直被认为会导致人类肾病、严重骨质疏松症和骨折。然而，最近的流行病学研究表明，在没有重要工业暴露于这种重金属的人群中，高正常的血液或尿液 Cd 水平与增加血管疾病、癌症、糖尿病和总死亡率以及骨质疏松症和肾病的风险相关。由于这些疾病似乎不太可能加速 Cd 的吸收，而且 Cd 已经在啮齿动物研究中促进了这些病理学，因此可以合理地得出结论，Cd 是人类这些疾病的重要中介风险因素。避免吸烟或经常摄入贝类或动物内脏可以减少人类对 Cd 的暴露，但 Cd 的主要饮食来源是植物性食物——绿叶蔬菜、全谷物、块茎和根茎类蔬菜——通常因其对健康的支持特性而被推荐；事实上，在不吸烟者中，素食者往往具有最高的 Cd 体负荷。幸运的是，铁充足和充足的膳食钙、镁和锌摄入可以通过下调肠道中矿物质转运体的表达，以及通过直接与 Cd 竞争进入这些转运体，来阻碍膳食 Cd 的吸收。纠正铁缺乏症似乎对控制 Cd 吸收尤为重要。此外，锌补充剂可以通过诱导金属硫蛋白来抵消体内已经存在的 Cd 的毒性，金属硫蛋白通过其巯基基团强烈结合 Cd；只要它以这种形式被隔离，Cd 就是无害的。无论如何，补充锌可能是值得推荐的，因为最佳的锌状态发挥着保护抗炎、抗氧化和免疫支持作用。由于 Cd 的毒性似乎在很大程度上是由氧化应激介导的，因此，根据啮齿动物研究，摄入螺旋藻、硫辛酸、褪黑素和 N-乙酰半胱氨酸也可能具有减轻与 Cd 暴露相关风险的潜力。因此，尽管 Cd 可能被证明是人类发病率和死亡率的主要危险因素，但限制其吸收和致病影响的实用策略已经存在。
