Iron deficiency, pregnancy, and neonatal development

Abstract

Anemia affects 36% of pregnant women worldwide. Of those affected, around 40% is due to iron deficiency (ID). Iron is an essential micronutrient involved in vital processes such as erythropoiesis, immune responses, and importantly—during pregnancy—placental and fetal development. Although menstrual bleeding can impact the incidence of ID even before the onset of pregnancy, this narrative review is pregnancy focused and will explore the impact of ID on placental development and iron uptake, fetal development and immunity, and maternal and infant susceptibility to infection. Although there have been advances in this area of research, much is needed to understand the regulation of iron and the effects of ID during pregnancy. Notably, more human studies are essential to generate the best evidence to advance strategies to reduce the incidence of ID during pregnancy to improve maternal, neonatal, and infant health.

Assessment of cooking methods and freezing on the nutritional value and health risks of heavy metals in four fish species consumed in Douala, Cameroon

“…Iron deficiency is the cause of cognitive problems, anaemia, muscle fatigue, paleness and shortness of breath. Excessive iron intake leads to liver dysfunction, hypogonadism, hypothyroidism, fatigue, heart failure, diarrhoea, hair loss and grey pigmentation of the skin [ 64 ]. P. quadrifilis is the species with the highest zinc content.…”

Comparative efficacy and safety of Chinese patent medicines of iron deficiency anemia during pregnancy: A network meta-analysis

“…RBC, which reflects the body's capacity to transport oxygen, saw the greatest improvement with SXN + OI. Hb, crucial for the oxygen transport function of erythrocytes[ 68 ], also improved most notably with SXN + OI. SF, a sensitive marker of iron storage[ 64 ], showed the greatest improvement with YQWX + OI.…”

Physiologically based trimester-specific serum ferritin thresholds for iron deficiency in US pregnant women

“…[7][8][9] With the development of ID in otherwise healthy, nonpregnant women, as the supply of iron becomes insufficient for Hb synthesis, the onset of iron restricted erythropoiesis is accompanied by a correspondence between (1) a decrease in the Hb concentration, resulting from a reduction in red blood cell production, and (2) an increase in plasma sTfR1, indicating an inadequate supply of iron for red blood cell production and tissue iron requirements. [10][11][12][13][14] The concurrent increase in sTfR1 provides evidence that the decrease in Hb results from declining body iron stores, as indicated by SF concentrations-and not by the many other conditions that can diminish red blood cell production. Accordingly, correspondence between the SF concentration at which the Hb concentration begins to decline and the sTfR1 concentration begins to rise provides a physiological basis for identifying a SF concentration that clinically identifies the onset of ID without anemia.…”