Person:

Andersen, Christopher

Background: Effects of early-life stunting on adiposity development later in childhood are not well understood, specifically with respect to age in the onset of overweight and obesity. Objectives: We analyzed associations of infant stunting with prevalence of, incidence of, and reversion from high body mass index–for-age z score (BMIZ) later in life. We then estimated whether associations of infant stunting with BMIZ varied by sex, indigenous status, and rural or urban residence. Methods: Data were collected from 1942 Peruvian children in the Young Lives cohort study at ages 1, 5, 8, and 12 y. Multivariable generalized linear models estimated associations of stunting (height-for-age z score <−2) at age 1 y with risk of BMIZ > 1 and BMIZ > 2 prevalence, incidence (moving above a BMIZ threshold between ages), and reversion (moving below a BMIZ threshold between ages) at later ages. Results: After adjustment for covariates, stunting at age 1 y was associated with a lower prevalence of BMIZ > 1 at age 8 y (RR: 0.81; 95% CI: 0.66, 1.00; P = 0.049) and 12 y (RR: 0.75; 95% CI: 0.61, 0.91; P = 0.004), as well as a lower prevalence of BMIZ > 2 at age 8 y. Stunting was not associated with incident risk of BMIZ > 1 or BMIZ > 2. Stunting was positively associated at age 5 y with risk of reversion from BMIZ > 1 (RR: 1.22; 95% CI: 1.05, 1.42; P = 0.008) and BMIZ > 2. We found evidence that the association of stunting with prevalent and incident BMIZ > 1 was stronger for urban children at ages 5 and 8 y, and for nonindigenous children at age 8 y. Conclusions: Stunting predicted a lower risk of prevalent BMIZ > 1 and BMIZ > 2, even after controlling for potential confounders. This finding may be driven in part by a higher risk of reversion from BMIZ > 1 by age 5 y. Our results contribute to an understanding of how nutritional stunting in infancy is associated with BMIZ later in life.

Abstract Background Anaemia is common among HIV-infected children and iron supplementation is prescribed routinely for the prevention and management of anaemia among children. Limited evidence suggests iron supplementation may have adverse effects among HIV-infected populations. We aimed to estimate the effect of iron supplement use on mortality, disease progression and haematological outcomes among HIV-infected children in Dar es Salaam, Tanzania.

Methods A prospective cohort study was conducted among HIV-infected children (aged 0–14 years) receiving antiretroviral treatment or supportive care between October 2004 and September 2014. Clinical data were recorded on morbidity and vital status, haematological status and prescriptions at each clinical visit. Cox proportional hazards models adjusted for time-varying covariates were used to estimate the association of time-varying iron supplementation on the hazard rate of mortality, HIV disease stage progression, tuberculosis incidence and anaemia and microcytosis persistence.

Results In all, 4229 children were observed during 149 260 clinic visits for a mean follow-up of 2.9 years. After adjustment for time-varying clinical covariates, time-varying iron supplementation was associated with a 2.87 times higher hazard rate of mortality (95% CI: 1.70, 4.87) and a 1.48 times higher hazard rate of HIV disease stage progression (95% CI: 1.10, 1.98). Iron supplementation was also associated with a lower rate of anaemia persistence (HR = 0.47; 95% CI: 0.37, 0.61). No differences in the association between iron supplementation and clinical outcomes were observed by antiretroviral therapy or anaemia status.

Conclusions Iron supplementation may increase the risk of HIV disease stage progression and mortality among HIV-infected children, while reducing the risk of anaemia.

Background: While the causes of anemia at an individual level (such as certain nutritional deficiencies, infections, and genetic disorders) are well defined, there is limited understanding of the relative burden of anemia attributable to each cause within populations. Objective: To estimate the proportion of anemia cases attributable to nutritional, infectious disease, and other risk factors among women, men, and children in six regions of Ethiopia. Methods: A population-based cross-sectional study was conducted. Data were obtained from 2520 women of reproductive age (15–49 years), 1,044 adult men (15–49 years), and 1,528 children (6–59 months). Participants provided venous blood samples for assessment of hemoglobin concentration, ferritin, folate, vitamin B12, C-reactive protein, and malaria infection. Stool samples were collected to ascertain helminth infection status. Sociodemographic questionnaires and a 24-hour diet recall were administered. Population-weighted prevalences of anemia and risk factors were calculated. Multivariable-adjusted associations of risk factors with anemia and partial population attributable risk percentages (pPAR%) were estimated using generalized linear models. Results: Anemia prevalence was 17% (95% CI: 13%, 21%) among women, 8% (6%, 12%) among men, and 22% (19%, 26%) among children. Low serum ferritin contributed to 11% (-1%, 23%) of anemia cases among women, 9% (0%, 17%) among men, and 21% (4%, 34%) among children. The proportion of anemia attributable to low serum folate was estimated at 25% (5%, 41%) among women and 29% (11%, 43%) among men. Dietary iron intake was adequate for nearly all participants, while inadequacy was common for folate and vitamin B12. Inflammation and malaria were responsible for less than one in ten anemia cases. Conclusions: Folate deficiency, iron deficiency, and inflammation appear to be important contributors to anemia in Ethiopia. Folic acid food fortification, targeted iron interventions, and strategies to reduce infections may be considered as potential public health interventions to reduce anemia in Ethiopia.