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Background: Nutrition programs frequently approach wasting and stunting as 2 separate conditions with distinct causes and effects. Although several cross-sectional studies have identified an association between the 2 conditions, longitudinal studies are useful to quantify the risk of acute malnutrition based on the trajectory of linear growth.Objective: We analyzed data from a longitudinal study to explore associations between linear growth and relapse to acute malnutrition in high-risk children during the year after recovery from moderate acute malnutrition (MAM).Methods: This was a secondary data analysis from a cluster randomized trial involving 1487 Malawian children 6-62 mo old treated for MAM and enrolled upon recovery. Children were followed for 1 y, during which data were collected on anthropometric progress, symptoms of illness, and household food security. Multivariate fixed-effects logistic regression was used to identify associations between linear growth and relapse to acute malnutrition.Results: Children who have recovered from MAM proved to be a high-risk population, with nearly half experiencing a decrease in height-for-age z score (HAZ) for 12 mo. Children whose HAZ was declining were more likely to relapse to MAM or SAM than were those whose linear growth rate maintained or increased their HAZ (P < 0.001). Mean changes of +0.15, -0.03, -0.17, and -0.53 in HAZ were observed for those who sustained recovery, relapsed to MAM once, relapsed to MAM multiple times, and developed SAM, respectively.Conclusion: Our results add to the body of evidence suggesting that acute wasting is a harbinger of subsequent stunting. Children who experience poor linear growth after MAM are more likely to experience relapse. Given this bidirectional relation between wasting and stunting, supplementary feeding programs should consider both when designing protocols, aiming to optimize linear growth and achieve acute weight gain, as a means of reducing relapse. This trial was registered at clinicaltrials.gov as NCT02351687. [ABSTRACT FROM AUTHOR]

Background: The temporal relationship between length (linear) and weight (ponderal) growth in early life is important to support optimal nutrition program design. Studies based on measures of attained size have established that wasting often precedes stunting, but such studies do not capture responsiveness of growth to previous compared with current conditions. As a result, the temporality of linear and ponderal growth relationships remain unclear.Objectives: We used growth velocity indicators to assess the temporal bidirectional relationships between linear and ponderal growth in children.Methods: Using monthly anthropometric measurements from 5039 Burkinabè children enrolled at 6 months of age and followed until 28 months from August 2014 to December 2016, we employed multilevel mixed-effects models to investigate concurrent and lagged associations between linear and ponderal growth velocity, controlling for time trends, seasonality, and morbidity.Results: Faster ponderal growth is associated with faster concurrent and subsequent linear growth (0.21-0.72 increase in length velocity z-score per unit increase in weight velocity z-score), while faster linear growth is associated with slower future weight gain (0.009-0.02 decrease in weight velocity z-score per unit increase in length velocity z-score), especially among children 9-14 months. Ponderal growth slows around the same time as peaks in morbidity, followed roughly a month later by slower linear growth.Conclusions: Use of velocity measures to assess temporal dependencies between linear and ponderal growth demonstrate that the same growth-limiting conditions likely affect both length and weight velocity, that slow ponderal growth likely limits subsequent linear growth, and that linear growth spurts may not be accompanied by sufficient increases in dietary intake to avoid slowdowns in weight gain. [ABSTRACT FROM AUTHOR]

Background: Measures that better describe "healthy" and sustainable recovery during nutritional treatment of children with moderate acute malnutrition (MAM) are needed.Objectives: We compared changes to body composition among children receiving 1 of 4 specialized nutritious food (SNFs) during treatment of MAM and by recovery and relapse outcomes.Methods: The study was nested within a prospective, cluster-randomized, community-based, cost-effectiveness trial assessing 4 SNFs to treat children aged 6-59 mo with MAM [midupper arm circumference (MUAC) ≥11.5 cm and <12.5 cm without bipedal edema] in Sierra Leone. Biweekly SNF rations (1 of 3 fortified-blended foods or a lipid-based nutrient supplement) were given until children recovered (MUAC ≥12.5 cm), or up to 7 rations (∼12 wk). Deuterium dilution was used to estimate fat-free mass (FFM) and fat mass (FM) at enrollment and after 4 wk of treatment to ensure similar treatment exposure among the participants. Another MUAC measurement was performed among recovered children 4 wk after program exit to determine whether recovery was sustained. ANOVA, paired t tests, and linear regression models were used to determine significant differences in changes from baseline to 4 wk.Results: Among 312 analyzed participants, mean baseline weight comprised ∼80% FFM; mean weight gained after 4 wk comprised ∼82% FFM. Changes in FM and FFM among 4 SNFs were similar. Children who recovered gained more weight (241%), FFM (179%), and weight-for-height z score (0.44 compared with 0) compared with those who did not recover; sustainers gained 150% more weight. FM gains were positive among recovered children and sustainers, as well as negative among those who did not recover or sustain recovery, but not significantly different.Conclusions: Four SNFs had similar effects on body composition in children after 4 wk of treatment for MAM, showing a healthy pattern of weight gain, the majority being FFM. Differential responses to treatment underscore a need for further research to provide targets for healthy, sustainable recovery. This trial was registered at clinicaltrials.gov as NCT03146897. [ABSTRACT FROM AUTHOR]

Background: Exposure to aflatoxin has garnered increased attention as a possible contributor to adverse birth outcomes.Objective: The objective of this study was to investigate the relation of maternal aflatoxin exposure with adverse birth outcomes such as birth weight, birth length, anthropometric z scores, low birth weight (LBW), small-for-gestational-age (SGA), stunting, and preterm birth (PTB).Methods: This study used maternal and newborn data from the AflaCohort Study, an ongoing birth cohort study in Banke, Nepal (n = 1621). Data on aflatoxin B1 (AFB1)-lysine adducts in maternal serum were collected once during pregnancy (at mean ± SD: 136 ± 43 d of gestation). Maternal serum AFB1-lysine adduct concentration was measured via HPLC. Linear and logistic regression analyses were used to determine if maternal aflatoxin exposure was associated with 1) birth weight and length (primary outcomes) and 2) anthropometric z scores, LBW (weight <2.5 kg), SGA (weight <10th percentile for gestational age and sex), stunting at birth (length-for-age z score less than -2), or PTB (born <37 weeks of gestation) (secondary outcomes).Results: The geometric mean of maternal serum AFB1-lysine adduct concentration was 1.37 pg/mg albumin (95% CI: 1.30, 1.44 pg/mg albumin). Twenty percent of infants were of LBW and 32% were SGA. Sixteen percent of infants were stunted at birth. In addition, 13% of infants were born preterm. In logistic multivariate regression models, mean maternal serum AFB1-lysine adduct concentrations were significantly associated with SGA (OR: 1.13; 95% CI: 1.00, 1.27; P < 0.05).Conclusions: Findings from this study suggest a small but significant association between serum AFB1-lysine adduct concentrations in pregnant women and SGA. Maternal aflatoxin exposure was not associated with other birth outcomes. These results highlight the need for future research on a threshold level of aflatoxin exposure needed to produce detectable adverse birth outcomes. This trial was registered at clinicaltrials.gov as NCT03312049. [ABSTRACT FROM AUTHOR]