Northern Ireland Centre for Food and Health, University of Ulster, Coleraine, Northern Ireland, United Kingdom.
Am J Clin Nutr. 2012 Mar;95(3):766-72. doi: 10.3945/ajcn.111.026245. Epub 2012 Jan 25.
We recently reported that the elevated blood pressure (BP) observed in patients with cardiovascular disease who are homozygous for the 677C→T polymorphism (TT genotype) in the gene encoding methylenetetrahydrofolate reductase (MTHFR) was responsive to supplementation with riboflavin-the cofactor for MTHFR.
The objective was to investigate the effect of riboflavin on BP targeted at patients with the TT genotype 4 y after initial investigation, during which time major changes in the clinical guidelines for antihypertensive therapy were introduced.
A total of 83 patients (representing all 3 genotypes) who participated in a placebo-controlled riboflavin intervention for 16 wk in 2004 agreed to take part. Nested within this follow-up, those with the TT genotype (n = 31) proceeded to intervention with riboflavin (1.6 mg/d for 16 wk) or placebo, conducted in a crossover style whereby the 2004 treatment groups were reversed.
At follow-up in 2008, as in 2004, patients with the TT genotype had higher systolic BP (P < 0.01), with a nonsignificant trend noted for higher diastolic BP (P = 0.051). Despite the marked changes in antihypertensive therapy that had occurred, BP remained unchanged in patients with the TT genotype at the time of follow-up. Riboflavin supplementation (administered in 2004 and 2008) produced an overall decrease in systolic (-9.2 ± 12.8 mm Hg; P = 0.001) and diastolic (-6.0 ± 9.9 mm Hg; P = 0.003) BP.
Optimizing riboflavin status offers a low-cost targeted strategy for managing elevated BP in this genetically at-risk group. These findings, if confirmed in the general population, could have important implications for the prevention of hypertension.
我们最近报道称,患有心血管疾病且亚甲基四氢叶酸还原酶(MTHFR)基因编码 677C→T 多态性(TT 基因型)纯合子的患者血压升高,对补充核黄素(MTHFR 的辅助因子)有反应。
目的是在最初研究后的 4 年,调查核黄素对血压的影响,在此期间,抗高血压治疗的临床指南发生了重大变化。
共有 83 名(代表所有 3 种基因型)患者参加了 2004 年为期 16 周的安慰剂对照核黄素干预研究,同意参加后续研究。在这种随访中,TT 基因型(n=31)患者以交叉方式进行核黄素(1.6mg/d,持续 16 周)或安慰剂干预,2004 年的治疗组进行了反转。
在 2008 年的随访中,与 2004 年一样,TT 基因型患者的收缩压更高(P<0.01),舒张压也有升高的趋势(P=0.051)。尽管降压治疗发生了明显变化,但在随访时 TT 基因型患者的血压仍未改变。核黄素补充剂(2004 年和 2008 年给药)使收缩压(-9.2±12.8mmHg;P=0.001)和舒张压(-6.0±9.9mmHg;P=0.003)整体下降。
优化核黄素状态为管理该遗传高危人群的高血压提供了一种低成本的靶向策略。如果在一般人群中得到证实,这些发现可能对预防高血压具有重要意义。