Nielsen Forrest H, Milne David B, Gallagher Sandra, Johnson LuAnn, Hoverson Bonita
US Department of Agriculture, Grand Forks, ND, 58202-9034, USA.
Magnes Res. 2007 Mar;20(1):19-31.
Enzyme and or hormone actions have not been shown to be consistently changed by consuming a low-magnesium diet similar to one that may occur in the general population. Thus, a human metabolic study was performed to determine whether deficient intakes of magnesium similar to those that occur naturally have pathophysiological effects through altering calcium retention and the metabolism of other minerals (sodium, potassium, phosphorus) involved in cellular ionic balance. Fifteen postmenopausal Caucasian women were recruited by advertisement throughout the United States. Eleven women (ages 49 to 71 years) completed the study as designed. The women resided in a metabolic research unit and consumed a basal Western-type diet that resulted in a mean intake of 4.40 mmol (107 mg) magnesium/d. The women were fed the basal diet supplemented with 9.05 mmol (220 mg) magnesium/d for 18 d (equilibration) before being assigned to one of two groups in an experiment with a double blind, crossover design. One group was fed the basal diet and supplemented with a lactose placebo while the other group continued consuming the basal diet supplemented with 9.05 mmol magnesium/d for 72 d, then each group switched to the other's diet, which they consumed for 72 d. Magnesium was supplemented as magnesium gluconate. Magnesium deprivation resulted in a non-positive magnesium balance (-0.21 mmol or -5 mg/d) that was highly positive during magnesium supplementation (+2.22 mmol or +54 mg/d). Magnesium deprivation decreased red blood cell membrane magnesium (2.5 versus 2.7 nmol or 0.061 versus 0.065 microg/mg protein; p < or = 0.05). Magnesium deprivation increased calcium balance (+0.82 mmol or +35 mg/d versus -0.02 or -1 mg/d; p < or = 0.009); decreased the fecal excretion of phosphorus (28.9% versus 32.3% of intake; p < or =0.0001); increased the urinary excretion of phosphorus (73.4% versus 71.0%; p < 0.003); and decreased the urinary excretion of potassium (40.4 mmol or 1.58 g/d versus 41.9 mmol or 1.64 g/d; p < 0.04). Non-positive magnesium balance and decreased red blood cell membrane magnesium concentration apparently are indicators of magnesium deprivation. Moderate magnesium deprivation achieved through diet alone results in increased calcium retention. Magnesium deprivation also alters phosphorus and potassium excretion. The changes indicate that an intake of 4.40 mmol (107 mg) magnesium/d is inadequate for postmenopausal women because of changes in cellular ionic balance that may lead to pathophysiological conditions.
与普通人群可能出现的低镁饮食相比，酶和/或激素的作用并未表现出持续的变化。因此，进行了一项人体代谢研究，以确定与自然发生的镁摄入量不足类似的情况是否会通过改变钙潴留以及参与细胞离子平衡的其他矿物质（钠、钾、磷）的代谢而产生病理生理效应。通过在美国各地发布广告招募了15名绝经后白人女性。11名女性（年龄49至71岁）按设计完成了研究。这些女性居住在一个代谢研究单元，食用基础西式饮食，平均镁摄入量为4.40 mmol（107 mg）/天。在采用双盲交叉设计的实验中，这些女性在被分配到两组之一之前，先食用添加了9.05 mmol（220 mg）镁/天的基础饮食18天（平衡期）。一组食用基础饮食并补充乳糖安慰剂，而另一组继续食用添加了9.05 mmol镁/天的基础饮食72天，然后两组交换饮食，再食用72天。镁以葡萄糖酸镁的形式补充。缺镁导致镁平衡为非正值（-0.21 mmol或-5 mg/天），而在补充镁期间则为高度正值（+2.22 mmol或+54 mg/天）。缺镁降低了红细胞膜镁含量（2.5对2.7 nmol或0.061对0.065 μg/mg蛋白质；p≤0.05）。缺镁增加了钙平衡（+0.82 mmol或+35 mg/天对-0.02或-1 mg/天；p≤0.009）；降低了磷的粪便排泄量（占摄入量的28.9%对32.3%；p≤0.0001）；增加了磷的尿排泄量（73.4%对71.0%；p＜0.003）；并降低了钾的尿排泄量（40.4 mmol或1.58 g/天对41.9 mmol或1.64 g/天；p＜0.04）。非正值的镁平衡和红细胞膜镁浓度降低显然是缺镁的指标。仅通过饮食实现的中度缺镁会导致钙潴留增加。缺镁还会改变磷和钾的排泄。这些变化表明，由于细胞离子平衡的改变可能导致病理生理状况，绝经后女性每天摄入4.40 mmol（107 mg）镁是不足的。
