Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid
Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid
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DOI：
10.1093/qjmed/90.8.519
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发表时间：
1997-08-01
期刊：
影响因子：
--
通讯作者：
Scott, JM
中科院分区：
文献类型：
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作者：
Ward, M;McNulty, H;Scott, JM
升高的血浆同型半胱氨酸是心血管疾病（CVD）的一个独立危险因素，可以通过给予药理剂量的叶酸来降低。目前尚不清楚低剂量对明显正常受试者的影响，但与食品强化问题高度相关。健康男性志愿者（n=30）参加了一项长期干预研究（26周）。每天给予叶酸补充剂，剂量从100 μ g（6周）增加到200 μ g（6周），再增加到400 μ g（14周）。在干预前、干预期间和干预后10周收集的东血样本分析血浆同型半胱氨酸、血清和红细胞叶酸水平。结果表示为基线血浆同型半胱氨酸浓度的三分位数，显示仅在顶部（10.90+/-0.83 μ mol/l）和中间（9.11 +/- 0.49 μ mol/l）三分位数中同型半胱氨酸显著降低（p小于或等于0.001）。在低三分位数中，平均基线同型半胱氨酸水平为7.07 +/- 0.84 μ mol/l，未观察到显著反应。在三种叶酸剂量中，200 μ g似乎与400 μ g一样有效，而100 μ g显然不是最佳剂量。因此，血浆同型半胱氨酸有一个最低水平，低于这个水平，叶酸就没有进一步的降低作用，这可能是因为叶酸已经达到了最佳状态。低至200 μ g/天的叶酸剂量可有效降低明显正常受试者的血浆同型半胱氨酸浓度。任何旨在降低心血管疾病风险的降低同型半胱氨酸水平的公共卫生计划都不应基于不必要的高剂量叶酸。
Elevated plasma homocysteine, an independent risk factor for cardiovascular disease (CVD) can be lowered by administration of pharmacological doses of folic acid. The effect of lower doses in apparently normal subjects is currently unknown but is highly relevant to the question of food fortification. Healthy male volunteers (n=30) participated in a chronic intervention study (26 weeks). Folic acid supplements were administered daily at doses increasing from 100 mu g (6 weeks), to 200 mu g (6 weeks), to 400 mu g (14 weeks). Easting blood samples collected before, during and 10 weeks post intervention were analysed for plasma homocysteine, serum and red-cell folate levels. Results, expressed as tertiles of baseline plasma homocysteine concentration, showed significant (p less than or equal to 0.001) homocysteine lowering in the top (10.90+/-0.83 mu mol/l) and middle (9.11 +/- 0.49 mu mol/l) tertiles only. In the low tertile, where the mean baseline homocysteine level was 7.07 +/- 0.84 mu mol/l, no significant response was observed. Of the three folic acid doses, 200 mu g appeared to be as effective as 400 mu g, while 100 mu g was clearly not optimal. There is thus a minimal level of plasma homocysteine below which folic acid has no further lowering effect, probably because an optimal folate status has been reached. A dose as low as 200 mu g/day of folic acid is effective in lowering plasma homocysteine concentrations in apparently normal subjects. Any public health programme for lowering homocysteine levels, with the goal of diminishing CVD risk, should not be based on unnecessarily high doses of folic acid.