Quinlivan Eoin P, Gregory Jesse F
Biomedical Mass Spectrometry Laboratory, General Clinical Research Center, University of Florida, Gainesville, FL 32611-0370, USA.
Am J Clin Nutr. 2007 Dec;86(6):1773-9. doi: 10.1093/ajcn/86.5.1773.
In the United States, folic acid fortification of cereal- grain foods has significantly increased folate status. However, blood folate concentrations have decreased from their postfortification high as a result, in part, of decreasing food fortification concentrations and the popularity of low-carbohydrate weight-loss diets.
The objectives of the study were to quantify changes in folate intake after folic acid fortification and to estimate the effect on neural tube defect (NTD) occurrence.
Expanding on an earlier model, we used data from 11 intervention studies to determine the relation between chronic folate intervention and changes in steady state serum folate concentrations. With serum folate data from the National Health and Nutrition Examination Survey (NHANES), we used reverse prediction to calculate postfortification changes in daily folate equivalents (DFEs). With the use of NHANES red blood cell folate data and a published equation that related NTD risk to maternal red cell folate concentrations, we calculated NTD risk.
Folate intake decreased by approximately 130 microg DFE/d from its postfortification high, primarily as a result of changes seen in women with the highest folate status. This decrease in folate intake was predicted to increase the incidence of NTD by 4-7%, relative to a predicted 43% postfortification decrease. In addition, the number of women consuming >1 mg bioavailable folate/d decreased.
Folate consumption by women of childbearing age in the United States has decreased. However, the decrease in those women with the lowest folate status was disproportionately small. Consequently, the effect on NTD risk should be less than would be seen if a uniform decrease in folate concentrations had occurred. These results reinforce the need to maintain monitoring of the way fortification is implemented.
在美国,谷物食品强化叶酸显著提高了叶酸水平。然而,血液叶酸浓度已从强化后的高位下降,部分原因是食品强化浓度降低以及低碳水化合物减肥饮食的流行。
本研究的目的是量化叶酸强化后叶酸摄入量的变化,并估计对神经管缺陷(NTD)发生情况的影响。
在早期模型的基础上进行扩展,我们使用了11项干预研究的数据来确定慢性叶酸干预与稳态血清叶酸浓度变化之间的关系。利用国家健康和营养检查调查(NHANES)的血清叶酸数据,我们采用反向预测来计算强化后每日叶酸当量(DFE)的变化。利用NHANES的红细胞叶酸数据以及一个将NTD风险与孕妇红细胞叶酸浓度相关联的已发表公式,我们计算了NTD风险。
叶酸摄入量从强化后的高位下降了约130微克DFE/天,主要是由于叶酸水平最高的女性出现了变化。预计叶酸摄入量的这种下降将使NTD的发生率增加4 - 7%,而强化后预计下降43%。此外,每天摄入>1毫克生物可利用叶酸的女性数量减少。
美国育龄妇女的叶酸摄入量有所下降。然而,叶酸水平最低的那些女性的下降幅度相对较小。因此,对NTD风险的影响应小于叶酸浓度均匀下降时的情况。这些结果强化了持续监测强化实施方式的必要性。