Physiological adaption to maternal malaria and other adverse exposure: low birth weight, functional capacity, and possible metabolic disease in adult life.

The concept of developmental origins of health and disease and the epidemic of noncommunicable diseases in low- and middle-income countries has increased the focus on low birth weight (LBW). Most studies linking LBW to future risk of metabolic diseases have focused on maternal nutrition and anemia. Several studies have shown that LBWis linked to skeletal muscle insulin resistance and future risk of type 2 diabetes, possibly caused by permanent modifications in skeletal muscle morphology and biochemistry leading to lowered functional capacity and physical activity in adult life. In some parts of the world, malaria infection during pregnancy is the most common cause of anemia and LBW. By causing disruption to nutrient supply, as well as hypoxia, placental malaria and anemia negatively impact intrauterine fetal development. Thus, in utero exposure to placental malaria and consequent LBW may impart a higher risk of developing type 2 diabetes in early adult life. This has not been investigated systematically. Worldwide, an estimated 125 million pregnancies occur annually in malarial areas with a vast potential for intrauterine growth restriction, LBW, and subsequent risk of metabolic dysfunction, including type 2 diabetes; this potential link also opens an opportunity for early prevention of future metabolic diseases by paying greater attention to malaria during pregnancy.