对那些发生过一次心肌梗塞的患者来说，如果用叶酸和维生素B12补充剂来降低他们的同型半胱氨酸的血浓度并不会出现相关的心肌梗塞、冠心病死亡或中风风险的降低。 然而，研究人员也发现，叶酸补充剂没有像人们所猜测的会增加罹患癌症的风险。
根据文章的背景资料，同型半胱氨酸的血浓度与心血管疾病具有正相关性，但人们不确定的是，这一相关性是否具有因果关系。 文章的作者写道：“每日服用叶酸补充剂通常可将同型半胱氨酸血浓度降低约25%，而增添维生素B12还会进一步地降低7个百分点的同型半胱氨酸血浓度。”
University of Oxford, United Kingdom的Jane M. Armitage, F.R.C.P.及其在Study of the Effectiveness of Additional Reductions In Cholesterol and Homocysteine (SEARCH)试验中的同僚评估了在1万2064名心肌梗塞幸存者中用叶酸加上维生素B12来降低血液同型半胱氨酸浓度的效果。该研究是在1998-2008年期间在英国的二级医院中开展的。 这些患者被随机分配接受或是每日2毫克的叶酸加上1毫克的维生素B12或是接受与之匹配的安慰剂。
文章的作者得出结论：“将本次的研究结果与从前的降低同型半胱氨酸浓度的试验进行综合，SEARCH的结果表明，叶酸补充剂即使对心血管疾病没有产生什么裨益性功效，但它对癌症或其它重大的健康问题也没有显着的不良反应。另外，这些结果凸显了在预防心血管疾病时应该将重点放在药物（如：阿斯匹林、他汀类药物和降压药治疗）治疗和被证明有好处的生活方式的变更（尤其是戒烟和避免体重过度增加）上的重要性，而不是用基于叶酸的维生素补充疗法来降低同型半胱氨酸。”
推荐原文出处：
JAMA. 2010;303(24):2486-2494.
Effects of Homocysteine-Lowering With Folic Acid Plus Vitamin B12 vs Placebo on Mortality and Major Morbidity in Myocardial Infarction Survivors
Jane M. Armitage, FRCP; Louise Bowman, MRCP; Robert J. Clarke, FRCP; Karl Wallendszus, BA, MSc; Richard Bulbulia, FRCS; Kazem Rahimi, MRCP; Richard Haynes, MRCP; and Sarah Parish, PhD, Clinical Trial Service Unit, University of Oxford, Oxford, United Kingdom; Peter Sleight, FRCP, Department of Cardiovascular Medicine, University of Oxford; and Richard Peto, FRS,and Rory Collins, FRCP, Clinical Trial Service Unit, University of Oxford.
Context Blood homocysteine levels are positively associated with cardiovascular disease, but it is uncertain whether the association is causal.
Objective To assess the effects of reducing homocysteine levels with folic acid and vitamin B12 on vascular and nonvascular outcomes.
Design, Setting, and Patients Double-blind randomized controlled trial of 12 064 survivors of myocardial infarction in secondary care hospitals in the United Kingdom between 1998 and 2008.
Interventions 2 mg folic acid plus 1 mg vitamin B12 daily vs matching placebo.
Main Outcome Measures First major vascular event, defined as major coronary event (coronary death, myocardial infarction, or coronary revascularization), fatal or nonfatal stroke, or noncoronary revascularization.
Results Allocation to the study vitamins reduced homocysteine by a mean of 3.8 μmol/L (28%). During 6.7 years of follow-up, major vascular events occurred in 1537 of 6033 participants (25.5%) allocated folic acid plus vitamin B12 vs 1493 of 6031 participants (24.8%) allocated placebo (risk ratio [RR], 1.04; 95% confidence interval [CI], 0.97-1.12; P = .28). There were no apparent effects on major coronary events (vitamins, 1229 [20.4%], vs placebo, 1185 [19.6%]; RR, 1.05; 95% CI, 0.97-1.13), stroke (vitamins, 269 [4.5%], vs placebo, 265 [4.4%]; RR, 1.02; 95% CI, 0.86-1.21), or noncoronary revascularizations (vitamins, 178 [3.0%], vs placebo, 152 [2.5%]; RR, 1.18; 95% CI, 0.95-1.46). Nor were there significant differences in the numbers of deaths attributed to vascular causes (vitamins, 578 [9.6%], vs placebo, 559 [9.3%]) or nonvascular causes (vitamins, 405 [6.7%], vs placebo, 392 [6.5%]) or in the incidence of any cancer (vitamins, 678 [11.2%], vs placebo, 639 [10.6%]).
Conclusion Substantial long-term reductions in blood homocysteine levels with folic acid and vitamin B12 supplementation did not have beneficial effects on vascular outcomes but were also not associated with adverse effects on cancer incidence.
