Department of Child Health, School of Medicine, Nursing and Dentistry, University of Glasgow, Glasgow, United Kingdom.
Institute of Health and Wellbeing, University of Glasgow, Glasgow, United Kingdom.
J Nutr. 2021 Jul 1;151(7):2022-2028. doi: 10.1093/jn/nxab054.
Few studies have had sufficient longitudinal data to track how different malnourished states relate to mortality at different ages and interrelate over time.
This study aims to describe the RRs and proportions of mortality associated with wasting and stunting and the pathways into and out of these nutritional states.
Longitudinal growth data sets collected for children ages 0-24 months from Malawi, South Africa, and Pakistan were combined (n = 5088). Children were classified as deceased, wasted (weight for height < -2 SD; 1-4%), stunted (length < -2SD; 20-47%), or wasted and stunted (WaSt; 2-5%) at ages 3, 6, 9, 12, 18, and 24 months. Mixed-effects Cox models were used to study the association between nutritional status and mortality.
By age 3 months, 20% of children were already stunted, rising to 49% by 24 months, while wasting (4.2% and 2.2% at 3 months, respectively) and WaSt (0.9% and 3.7% at 24 months, respectively) were less common. The HR for mortality in WaSt was 9.5 (95% CI, 5.9-15), but 60% of WaSt-associated mortality occurred at 3-6 months. Wasting or WaSt was associated with 10-23% of deaths beyond 6 months, but in the second year over half of deaths occurred in stunted, nonwasted children. Stunting persisted in 82% of children and wasting persisted in 44%. Wasted children were more likely than nonwasted, nonstunted children to become stunted (RR, 1.93; 95% CI, 1.7-2.2), but 94% of children who progressed to stunting had not been wasted in the prior period.
WaSt greatly increased the risk of death, particularly in very young infants, but more deaths overall were associated with stunting. Most stunting appeared to be either intrauterine in origin or arose in children without prior wasting. Either stunting and wasting represent alternative responses to restricted nutrition, or stunting also has other, nonnutritional causes.
很少有研究有足够的纵向数据来跟踪不同的营养不良状态与不同年龄的死亡率之间的关系，并随着时间的推移相互关联。
本研究旨在描述消瘦和发育迟缓与死亡率的相关风险比（RR）和比例，并描述进入和离开这些营养状态的途径。
合并了来自马拉维、南非和巴基斯坦的 0-24 个月儿童的纵向生长数据集（n=5088）。在 3、6、9、12、18 和 24 个月时，将儿童分为死亡、消瘦（身高体重指数 < -2SD；1-4%）、发育迟缓（长度 < -2SD；20-47%）或消瘦和发育迟缓（WaSt；2-5%）。使用混合效应 Cox 模型研究营养状况与死亡率之间的关系。
在 3 个月时，20%的儿童已经发育迟缓，到 24 个月时上升至 49%，而消瘦（分别为 3 个月时的 4.2%和 2.2%）和 WaSt（分别为 24 个月时的 0.9%和 3.7%）则较为少见。WaSt 相关死亡率的 HR 为 9.5（95%CI，5.9-15），但 60%的 WaSt 相关死亡率发生在 3-6 个月。消瘦或 WaSt 与 6 个月后 10-23%的死亡有关，但在第二年，超过一半的死亡发生在未消瘦、未发育迟缓的儿童中。82%的儿童持续发育迟缓，44%的儿童持续消瘦。消瘦儿童比非消瘦、非发育迟缓儿童更有可能发育迟缓（RR，1.93；95%CI，1.7-2.2），但在之前时期没有消瘦的儿童中，有 94%进展为发育迟缓。
WaSt 极大地增加了死亡风险，尤其是在非常年幼的婴儿中，但总体而言，更多的死亡与发育迟缓有关。大多数发育迟缓似乎是宫内起源的，或者发生在没有先前消瘦的儿童中。消瘦和发育迟缓都代表了对限制营养的不同反应，或者发育迟缓也有其他非营养原因。
