Iron deficiency and reduced work capacity: A critical review of the research to determine a causal relationship
Iron deficiency and reduced work capacity: A critical review of the research to determine a causal relationship
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DOI：
10.1093/jn/131.2.676s
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发表时间：
2001-02-01
影响因子：
4.2
通讯作者：
Brownlie, T
中科院分区：
文献类型：
--
作者：
Haas, JD;Brownlie, T
通过对研究文献（包括动物和人类研究）的系统回顾，评估了缺铁和体力劳动能力之间的因果关系。沿着从重度缺铁性贫血（SIDA）到中度缺铁性贫血（MIDA）再到缺铁性贫血不伴贫血（IDNA）的连续体检查铁缺乏。工作能力评估有氧能力，耐力，精力效率，自愿活动和工作生产力。所审查的29份研究报告表明，SIDA和MIDA对动物和人类的有氧能力有很强的因果关系。这种效应的推测机制是与贫血相关的氧转运减少;组织缺铁也可能通过降低细胞氧化能力发挥作用。SIDA和MIDA的耐力也受到损害，但在动物中观察到的细胞氧化能力差的强烈介导作用尚未在人类中得到证实。在实验室和现场，能量效率在人类缺铁的所有水平上都受到影响。在田间研究中观察到的工作效率降低可能是由于贫血和氧运输减少。缺铁性贫血（IDA）和IDNA的社会和经济后果尚未阐明。IDA对工作能力影响的生物学机制足够强大，足以证明改善铁状况的干预措施是增强人力资本的一种手段。这种情况也可能延伸到经历国际药物缺乏症的那部分人口，他们的工作能力可能受到的影响比较微妙，但因此受到影响的人数可能比经历国际药物缺乏症的人数多得多。
The causal relationship between iron deficiency and physical work capacity is evaluated through a systematic review of the research literature, including animal and human studies. Iron deficiency was examined along a continuum from severe iron-deficiency anemia (SIDA) to moderate iron-deficiency anemia (MIDA) to iron deficiency without anemia (IDNA). Work capacity was assessed by aerobic capacity, endurance, energetic efficiency, voluntary activity and work productivity. The 29 research reports examined demonstrated a strong causal effect of SIDA and MIDA on aerobic capacity in animals and humans. The presumed mechanism for this effect is the reduced oxygen transport associated with anemia; tissue iron deficiency may also play a role through reduced cellular oxidative capacity. Endurance capacity was also compromised in SIDA and MIDA, but the strong mediating effects of poor cellular oxidative capacity observed in animals have not been demonstrated in humans. Energetic efficiency was affected at all levels of iron deficiency in humans, in the laboratory and the field. The reduced work productivity observed in field studies is likely due to anemia and reduced oxygen transport. The social and economic consequences of iron-deficiency anemia (IDA) and IDNA have yet to be elucidated. The biological mechanisms for the effect of IDA on work capacity are sufficiently strong to justify interventions to improve iron status as a means of enhancing human capital. This may also extend to the segment of the population experiencing IDNA in whom the effects on work capacity may be more subtle, but the number of individuals thus affected may be considerably more than those experiencing IDA.