The effect of zinc-biofortified rice on zinc status of Bangladeshi preschool children: a randomized, double-masked, household-based, controlled trial.
The effect of zinc-biofortified rice on zinc status of Bangladeshi preschool children: a randomized, double-masked, household-based, controlled trial.
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DOI：
10.1093/ajcn/nqab379
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发表时间：
2022-03-04
期刊：
影响因子：
--
通讯作者：
Wegmueller R
中科院分区：
文献类型：
--
作者：
Jongstra R;Hossain MM;Galetti V;Hall AG;Holt RR;Cercamondi CI;Rashid SF;Zimmermann MB;Mridha MK;Wegmueller R
在普遍缺锌且以大米为主食的国家，水稻生物强化锌可以持续改善锌状况，但其功效尚未得到检验。脂肪酸去饱和酶（FADS）被认为是新的锌状态生物标志物。我们的目的是测试锌生物强化大米（BFR）对学龄前缺锌儿童的疗效。我们的假设是食用BFR会增加血浆锌浓度（PZC）。我们在12 - 36岁的孟加拉国农村儿童中进行了一项为期9个月的双盲干预试验，其中大多数儿童缺锌（PZC <70µg/dL）和发育不良（n = 520）。这些儿童被随机分配，每天在其家庭中获得煮熟的对照米饭（CR）或BFR，并进行依从性监测。主要结局为PZC。次要结果为缺锌、线性生长、感染相关发病率、FADS活性指数、肠道脂肪酸结合蛋白（I-FABP）和粪便钙保护蛋白。我们采用稀疏串行抽样进行中点测量，并使用混合效应模型通过意向治疗分析数据。基线时，中位（IQR） PZC为60.4（56.3-64.3）µg/dL， 78.1%的儿童缺锌，59.7%的儿童发育不良。试验期间CR和BFR的日均锌摄入量分别为1.20±0.34和2.22±0.47 mg/d （P < 0.001）。在PZC、缺锌率、FADS活性、I-FABP或粪便钙保护蛋白方面，治疗时间无显著影响（均P < 0.05）。身高-年龄比值z分数存在时间-治疗交互作用（P < 0.001），有利于BFR组。由于BFR组有更多的上呼吸道疾病，与CR组相比，BFR组和CR组的发病率纵向患病率为1.08 （95% CI: 1.05, 1.12）。食用BFR 9个月，每天为孟加拉国儿童额外提供~ 1mg锌，对PZC、缺锌率或FADS活性没有显著影响。该试验已在clinicaltrials.gov注册为NCT03079583。
Zinc biofortification of rice could sustainably improve zinc status in countries where zinc deficiency is common and rice is a staple, but its efficacy has not been tested. Fatty acid desaturases (FADS) are putative new zinc status biomarkers. Our objective was to test the efficacy of zinc-biofortified rice (BFR) in preschool-aged children with zinc deficiency. Our hypothesis was that consumption of BFR would increase plasma zinc concentration (PZC). We conducted a 9-mo, double-masked intervention trial in 12–36-mo-old rural Bangladeshi children, most of whom were zinc-deficient (PZC <70 µg/dL) and stunted (n = 520). The children were randomly assigned to receive either control rice (CR) or BFR provided in cooked portions to their households daily, with compliance monitoring. The primary outcome was PZC. Secondary outcomes were zinc deficiency, linear growth, infection-related morbidity, FADS activity indices, intestinal fatty acid binding protein (I-FABP) and fecal calprotectin. We applied sparse serial sampling for midpoint measures and analyzed data by intention-to-treat using mixed-effects models. At baseline, median (IQR) PZC was 60.4 (56.3–64.3) µg/dL, 78.1% of children were zinc deficient, and 59.7% were stunted. Mean ± SD daily zinc intakes from the CR and BFR during the trial were 1.20 ± 0.34 and 2.22 ± 0.47 mg/d, respectively (P < 0.001). There were no significant time-by-treatment effects on PZC, zinc deficiency prevalence, FADS activity, I-FABP, or fecal calprotectin (all P > 0.05). There was a time–treatment interaction for height-for-age z-scores (P < 0.001) favoring the BFR group. The morbidity longitudinal prevalence ratio was 1.08 (95% CI: 1.05, 1.12) comparing the BFR and CR groups, due to more upper respiratory tract illness in the BFR group. Consumption of BFR for 9 mo providing ∼1 mg of additional zinc daily to Bangladeshi children did not significantly affect PZC, prevalence of zinc deficiency, or FADS activity. The trial was registered at clinicaltrials.gov as NCT03079583.
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