Infectious and parasitic diseases cause about

Infectious and parasitic diseases cause about half the anaemia burden. Stevens and colleagues estimate that iron-amenable anaemia was about 50% in non-pregnant and pregnant women, and 42% in children in 2011. In addition to the contributions of malaria, schistosomiasis, hookworm infection, and HIV, which Stevens and colleagues list as causes of low haemoglobin concentrations, presence of species should perhaps be added as an emerging issue. Improved sanitation and disease control can be expected to make a substantial contribution to anaemia reduction, again especially in transition countries in which diet and disease control are likely to improve in parallel. Direct interventions are needed, especially for the poorest populations, and these can improve health and nutrition even when underlying causes remain important. Moreover, these improvements enhance human capital, and can contribute to a virtuous ABT-199 cost by fostering economic development, which in turn enhances the health and nutrition of women and children. A step in the right direction is the specific attention to maternal anaemia as a problem of importance in the US Global Health Initiative\'s Feed the Future programme. Now that the World Health Assembly has proposed a target of 50% reduction in anaemia in women by 2025, the necessary resources and policy priority will hopefully be directed towards this pervasive but under-recognised problem.
In , Anne Lee and colleagues from the Child Health Epidemiology Reference Group (CHERG) make an important contribution to our understanding of the global burden of intrauterine growth restriction. What is new in this work is the evidence that the majority of growth-restricted neonates (assessed with the proxy of small-for-gestational-age birth) weigh 2500 g or more at birth, even in low-income and middle-income countries. In high-income countries, most preterm infants—particularly those born at 34–36 completed weeks of gestation—also weigh at least 2500 g. Lee and colleagues show that nearly half of preterm infants from countries of low and middle income also are born above this birthweight threshold. Thus, globally, the traditional maternal and child health indicator of low birthweight (defined as <2500 g) fails to identify most newborn babies who are born either too small or too soon. This fact alone undermines Lee and colleagues\' claim that “low birthweight is an important population indicator for tracking neonatal health”. Not only does the definition of low birthweight exclude most preterm and small-for-gestational-age neonates, it also conflates two problems. First, difficulties arise when distinguishing countries and regions where most low-birthweight infants are born small for gestational age (eg, south Asia) from those where most such babies are preterm (eg, sub-Saharan Africa). Second, understanding temporal trends within countries or regions is tricky. In Canada, for example, rates of low birthweight fell steadily during the 1980s and 1990s, hiding opposite trends in small-for-gestational-age births (decline) and preterm births (rise). For this reason, Canada and some other high-income countries no longer include low birthweight as a perinatal health surveillance indicator. Of course, in settings in which either a large proportion of pregnant women do not have access to antenatal care or many births occur in the home, valid estimates for gestational age might be more difficult to obtain than birthweight. In those settings, low birthweight might indicate the need for extra clinical surveillance and intervention in the postnatal period. If the 2500 g cutoff for low birthweight is arbitrary, what about the cutoffs used by Lee and colleagues to define preterm birth (<37 completed weeks of gestation) and small for gestational age (<10th centile birthweight for gestational age)? These cutoffs are the conventional accepted ones recommended by WHO yet they are no less arbitrary than that for low birthweight. Study findings show that infants born at 37–38 completed weeks of gestation, compared with those born at 39–41 weeks, are at increased risk of neonatal mortality and morbidity and later neurocognitive difficulties. The same is true for fetal growth. In fact, the optimum birthweight for gestational age, at least from the viewpoint of minimising risk of neonatal death, is not the 10th or even the 50th centile but is close to the 90th centile, the conventional cutoff for defining large-for-gestational-age births. Why has evolution selected for birthweights that are so far below the weight that minimises the risk for the newborn baby? Probably because of competition from the mother. Without the option of caesarean or forceps delivery, a large fetus was a major risk to the mother\'s own survival and, thus, her ability to have other babies. When considering birthweight-for-gestational-age as an indicator of newborn health, perhaps we should seek a more functionally defined cutoff—eg, based on the relative risk of neonatal death or serious morbidity.