Maternal iron deficiency

Risk factor due to maternal deficiency

Low birth weight is a risk factor for coronary heart disease, diabetes, stroke and hypertension. Depression is highly associated with these conditions.

Ten years ago studies in Britain showed for the first time that people who had low birth weight were at increased risk of coronary heart disease and the disorders related to it: stroke, non-insulin dependent diabetes, raised blood pressure, and the metabolic syndrome. In a study of 16 000 men and women born in Hertfordshire death rates from coronary heart disease fell twofold between those at the lower and upper ends of the birth weight distribution. In groups investigated clinically the prevalence of non-insulin dependent diabetes and impaired glucose tolerance fell threefold. Such findings led to the "fetal origins hypothesis", which states that cardiovascular disease and non-insulin dependent diabetes originate through adaptations that the fetus makes when it is undernourished. These adaptations, which include slowing of growth, permanently change the structure and function of the body.

Life-long effects

Low birthweight, thinness and short body length at birth are now known to be associated with increased rates of cardiovascular disease and non-insulin dependent diabetes in adult life. The fetal origins hypothesis proposes that these diseases originate through adaptations which the fetus makes when it is undernourished. These adaptations may be cardiovascular, metabolic or endocrine. They permanently change the structure and function of the body. Prevention of the diseases may depend on prevention of imbalances in fetal growth or imbalances between prenatal and postnatal growth, or imbalances in nutrient supply to the fetus.

Anaemia and iron deficiency during pregnancy are associated with large placental weight and a high ratio of placental weight to birthweight. This points to maternal nutritional deficiency as a cause for discordance between placental and fetal growth. This may have important implications for the prevention of adult hypertension, which appears to have its origin in fetal life.

If the growth of a female fetus is constrained by lack of nutrients, there are persisting changes in her physiology and metabolism which lead to reduced fetal growth and raised blood pressure in the next generation. Public health policies to improve fetal growth in one generation may therefore benefit succeeding generations as well.

Children who have iron-deficiency anemia in infancy are at risk for long-lasting developmental disadvantage as compared with their peers with better iron status.

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