Nielsen Forrest H
Research Nutritionist Consultant, Grand Forks, ND, USA.
J Inflamm Res. 2018 Jan 18;11:25-34. doi: 10.2147/JIR.S136742. eCollection 2018.
Animal studies have shown that magnesium deficiency induces an inflammatory response that results in leukocyte and macrophage activation, release of inflammatory cytokines and acute-phase proteins, and excessive production of free radicals. Animal and in vitro studies indicate that the primary mechanism through which magnesium deficiency has this effect is through increasing cellular Ca, which is the signal that results in the priming of cells to give the inflammatory response. Primary pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-1; the messenger cytokine IL-6; cytokine responders E-selectin, intracellular adhesion molecule-1 and vascular cell adhesion molecule-1; and acute-phase reactants C-reactive protein and fibrinogen have been determined to associate magnesium deficiency with chronic low-grade inflammation (inflammatory stress). When magnesium dietary intake, supplementation, and/or serum concentration suggest/s the presence of magnesium deficiency, it often is associated with low-grade inflammation and/or with pathological conditions for which inflammatory stress is considered a risk factor. When magnesium intake, supplementation, and/or serum concentration suggest/s an adequate status, magnesium generally has not been found to significantly affect markers of chronic low-grade inflammation or chronic disease. The consistency of these findings can be modified by other nutritional and metabolic factors that affect inflammatory and oxidative stress. In spite of this, findings to date provide convincing evidence that magnesium deficiency is a significant contributor to chronic low-grade inflammation that is a risk factor for a variety of pathological conditions such as cardiovascular disease, hypertension, and diabetes. Because magnesium deficiency commonly occurs in countries where foods rich in magnesium are not consumed in recommended amounts, magnesium should be considered an element of significant nutritional concern for health and well-being in these countries.
动物研究表明，镁缺乏会引发炎症反应，导致白细胞和巨噬细胞活化、炎症细胞因子和急性期蛋白释放，以及自由基过度产生。动物研究和体外研究表明，镁缺乏产生这种效应的主要机制是通过增加细胞内钙，而钙是引发细胞产生炎症反应的信号。已确定主要促炎细胞因子如肿瘤坏死因子-α和白细胞介素（IL）-1；信使细胞因子IL-6；细胞因子反应蛋白E-选择素、细胞间黏附分子-1和血管细胞黏附分子-1；以及急性期反应物C反应蛋白和纤维蛋白原与镁缺乏和慢性低度炎症（炎症应激）相关。当膳食镁摄入量、补充量和/或血清浓度提示存在镁缺乏时，它通常与低度炎症和/或与炎症应激被视为危险因素的病理状况相关。当镁摄入量、补充量和/或血清浓度提示状态充足时，通常未发现镁会显著影响慢性低度炎症或慢性病的标志物。这些发现的一致性可能会受到影响炎症和氧化应激的其他营养和代谢因素的改变。尽管如此，迄今为止的研究结果提供了令人信服的证据，表明镁缺乏是慢性低度炎症的重要促成因素，而慢性低度炎症是心血管疾病、高血压和糖尿病等多种病理状况的危险因素。由于镁缺乏在那些未按推荐量食用富含镁食物的国家普遍存在，在这些国家，镁应被视为对健康和幸福具有重要营养意义的元素。
