Durlach J, Durlach V, Bac P, Rayssiguier Y, Bara M, Guiet-Bara A
SDRM, Hôpital St Vincent-de-Paul, Paris, France.
Magnes Res. 1993 Dec;6(4):379-94.
Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.
衰老构成镁缺乏的一个风险因素。原发性镁缺乏源于两种病因机制：缺乏和耗竭。原发性镁缺乏是由于镁摄入不足。无论年龄大小，整个人群的膳食镁含量都处于边缘水平。与自由生活的老年群体相比，机构养老群体的营养缺乏更为明显。原发性镁耗竭是由于控制镁状态的因素失调所致：肠道镁吸收减少、骨骼对镁的摄取和动员减少、有时尿液流失、对应激适应性降低导致的肾上腺糖皮质激素过多、胰岛素抵抗和肾上腺素能低反应性。衰老过程中的继发性镁缺乏主要源于老年人常见的各种疾病和治疗，即非胰岛素依赖型糖尿病和使用高镁尿性利尿剂。镁缺乏可能参与衰老的临床症状，特别是在神经肌肉、心血管和肾脏症状方面。肾上腺糖皮质激素过多的后果——其最简单的指标是对地塞米松抑制试验无反应——可能包括免疫抑制、肌肉萎缩、脂肪堆积集中、骨质疏松、高血糖、高血脂、动脉粥样硬化，以及特别是通过加速海马体衰老导致的情绪和心理表现紊乱。需要指出的是，镁缺乏和应激在一个真正的“致病恶性循环”中相互加剧，特别是在衰老的应激状态下。镁缺乏在胰岛素抵抗病因以及衰老过程中的肾上腺素能、骨骼、致癌、免疫和氧化应激紊乱中的重要性仍不确定。口服生理性镁补充剂（5毫克镁/千克/天）是确定镁缺乏重要性的最佳诊断工具。关于老年人群中镁缺乏和镁耗竭治疗效果的开放和双盲研究做得太少。有必要进一步研究以评估镁缺乏在衰老病理生理学中的真正地位。
