Iron and folate supplementation during pregnancy is commonly practiced to prevent maternal anemia, which is often caused by iron deficiency. Part of the rationale for this practice is the high iron requirement during pregnancy, almost 3 times that required for nonpregnant women of childbearing years, which is difficult to meet from dietary sources (1). Another reason for supplementation is that anemia caused by iron deficiency alone or in combination with other factors, eg, folate deficiency, vitamin A deficiency, and malaria, has been implicated as having several negative effects on maternal and fetal health. Therefore, anemia prevention through iron supplementation may help to improve reproductive outcomes.
In this supplement, Rush (2) questions the benefit of routine iron supplementation in relation to the evidence of the harm or burden of anemia on reproductive outcomes. Specifically, he notes that a high hemoglobin value during pregnancy has been associated with adverse birth outcomes. He questions whether efforts to prevent anemia through iron supplementation can put some women at risk by placing their hemoglobin in a higher range that is associated with poor pregnancy outcomes.
The purpose of this review is to look at normal and abnormal hemoglobin values in terms of their causes and consequences. This review will also reassess the evidence for iron supplementation and the strength of the evidence that implicates either a low or a high hemoglobin concentration in morbidity and mortality during pregnancy and the perinatal period. In doing this, the evidence will be categorized with respect to deficiency, risk, benefit, and feasibility to increase the effectiveness of public health programs.
Evidence of deficiency is provided by a dietary nutrient intake that is inadequate to meet the requirement estimated to be necessary to avoid a deficient state. Often, the deficient state is a clearly defined disease or nutritional disorder with specific signs and symptoms, eg, beriberi for severe thiamin deficiency. A clearly defined pathophysiologic mechanism is required for classification of a nutritional disease or disorder, and an estimated nutrient requirement has been widely used for clinical and public health purposes.
Evidence of risk is based on finding associations between nutritional factors and adverse health outcomes, often by observational studies. For example, greater saturated fat intake increases the risk of coronary heart disease. This is regarded as indirect evidence because epidemiologic findings of an association cannot distinguish whether the relation is causal. Because health and nutritional problems may coexist in a population as a result of a common risk factor, evidence of risk alone may not be sufficient to justify program action without greater proof that the association is indeed causal.
Evidence of benefit is obtained when a specific risk factor is thought to contribute to adverse health outcomes, and intervention trials show that removing the risk factor results in improved outcomes. This is regarded as direct evidence to establish a causal relation between the risk factor and poor outcome. The process to prove such evidence often involves controlled trials with proper randomization. The measured beneficial effect under controlled research conditions is known as efficacy, which is the maximum achievable effect under ideal conditions. Often, this is a necessary condition but may not be sufficient for the consideration of large-scale program action.
After the indication for program action is clear on the basis of evidence of deficiency and benefit of the intervention, evidence of feasibility is needed for initiating large-scale programs based on resource and technical capacity. One requirement for a large-scale program is evidence of effectiveness, ie, sufficient benefit under the field conditions. Often, the feasibility of a public health program is based on its cost-effectiveness compared with other programs.---(Ray Yip, American Journal of Clinical Nutrition)---
