Department of Medicine, New York Methodist Hospital, Brooklyn, NY, 11215, USA.
J Inherit Metab Dis. 2011 Feb;34(1):67-73. doi: 10.1007/s10545-010-9150-2. Epub 2010 Jun 25.
The success of folic acid fortification has generated consideration of similar fortification with cobalamin for its own sake but more so to mitigate possible neurologic risks from increased folate intake by cobalamin-deficient persons. However, the folate model itself, the success of which was predicted by successful clinical trials and the known favorable facts of high folic acid bioavailability and the infrequency of folate malabsorption, may not apply to cobalamin fortification. Cobalamin bioavailability is more restricted than folic acid and is unfortunately poorest in persons deficient in cobalamin. Moreover, clinical trials to demonstrate actual health benefits of relevant oral doses have not yet been done in persons with mild subclinical deficiency, who are the only practical targets of cobalamin fortification because >94% of persons with clinically overt cobalamin deficiency have severe malabsorption and therefore cannot respond to normal fortification doses. However, it is only in the severely malabsorptive disorders, such as pernicious anemia, not subclinical deficiency, that neurologic deterioration following folic acid therapy has been described to date. It is still unknown whether mild deficiency states, which usually arise from normal absorption or only food-bound cobalamin malabsorption, have real health consequences or how often they progress to overt clinical cobalamin deficiency. Reports of cognitive or other risks in the common subclinical deficiency state, although worrisome, have been inconsistent. Moreover, their observational nature proved neither causative connections nor documented health benefits. Extensive work, especially randomized clinical trials, must be done before mandatory dietary intervention on a national scale can be justified.
叶酸强化的成功引发了人们对钴胺素类似强化的考虑,不仅是为了自身,更是为了减轻钴胺素缺乏人群叶酸摄入增加可能带来的神经风险。然而,叶酸模式本身,其成功已被成功的临床试验所预测,并且已知高叶酸生物利用度和叶酸吸收不良的罕见性这两个有利事实,可能不适用于钴胺素强化。钴胺素生物利用度比叶酸更受限制,而且在钴胺素缺乏的人中最差。此外,尚未在轻度亚临床缺乏症患者中进行证明相关口服剂量实际健康益处的临床试验,而这些患者是钴胺素强化的唯一实际目标,因为 >94%的临床明显钴胺素缺乏症患者有严重的吸收不良,因此无法对正常强化剂量做出反应。然而,只有在严重的吸收不良疾病中,如恶性贫血,迄今为止才描述了叶酸治疗后神经恶化的情况。目前仍不清楚轻度缺乏状态是否有实际的健康后果,这些状态通常是由正常吸收或仅食物结合的钴胺素吸收不良引起的,以及它们进展为明显临床钴胺素缺乏的频率如何。虽然令人担忧,但关于常见亚临床缺乏症状态的认知或其他风险的报告一直不一致。此外,它们的观察性质既没有证明因果关系,也没有证明健康益处。在全国范围内进行强制性饮食干预之前,必须进行广泛的工作,特别是随机临床试验。