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Maternal nutrition as a determinant of birth weight
  1. T Stephenson,
  2. M E Symonds
  1. Academic Division of Child Health, School of Human Development, University Hospital, Nottingham NG7 2UH, UK
  1. Correspondence to:
    Professor Stephenson;

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Maternal nutrition, encompassing maternal dietary intake, circulating concentrations, uteroplacental blood flow, and nutrient transfer across the placenta, influences birth weight


Birth weight is correlated between half siblings of the same mother but not of the same father1 because of the greater contribution of the maternal genotype and environment.2 As summarised in table 1, the latter includes maternal nutrition.

Table 1

Genetic and environmental contributions (%) to birth weight variation (adapted from James & Stephenson3)


In the narrow sense, “maternal nutrition” describes the pregnant woman's diet. The effects of severe macronutrient deficiency depend on the stage of gestation. During the Dutch famine of 1944–1945, a 50% reduction in energy intake during the first trimester was associated with increased placental weight but no change in birth weight.4 Maternal undernutrition in late gestation was associated with reduced placental and fetal weights.

“The effects of severe macronutrient deficiency depend on the stage of gestation.”

Embryo transfer and litter reduction experiments similarly show that maternal environment predominantly influences later fetal growth.5 Although macronutrient deficits in later pregnancy would be expected to exert greatest impact on birth weight (the human fetus weighs only 20% of term weight at 24 weeks3), catch up growth often occurs.6,7 In contrast, the earlier in postnatal life that undernutrition occurs, the more likely it is to have permanent—that is, programming—effects.8 In normal pregnancies of malnourished women, dietary supplementation during late pregnancy increases birth weight.9


In developed countries, dietary macronutrient or micronutrient deficiency are rarely thought to be responsible for clinically significant impaired fetal growth.10 Lower birth weight is associated with lower social class, but although it is often assumed that this is nutritional, there are many confounders such as smoking and genetic factors. Recent human pregnancy studies do not confirm the dietary hypothesis,11,12 but these studies have been criticised.13 Contemporary studies in Australia, however, indicate that nearly 30% of women who deliver babies with a low birth weight (< 2500 g) suffer from eating disorders.14 Experimentally increasing maternal nutrition in sheep enhances birth weight.13

Epidemiological studies have shown that size at birth and/or placental weight predict adult disease.15,16 The hypothesis that variations in maternal diet within the normal range can lead to concomitant variations in birth weight and hence to later disease remains the subject of intense debate. These studies are criticised because of possible confounding factors. However, later blood pressure is independent of maternal blood pressure and smoking,17 social class at birth, adult social class, later cigarette smoking, and obesity.15 In the Hertfordshire cohort,18 birth weight is unrelated to social class either at birth or currently.15 Moreover, birth weight was not associated with lung cancer or deaths from non-cardiovascular causes, which may also be expected to be influenced by social class and lifestyle.


So far, this review has focused on the mother's dietary intake. In the wider sense, maternal “nutrition” encompasses the complete supply line of maternal intake, circulating concentrations, uteroplacental blood flow, and nutrient transfer across the placenta.3 Experimental reduction of the number of placentomes in sheep results in a smaller fetus,19 as does reduction in uterine artery blood flow.20 Maternal smoking21 and pre-eclampsia are associated with lower birth weight.22 Nutritional or vascular factors probably account for the association between lower birth weight and placental anomalies, twin-twin transfusion syndrome, and maternal diseases (respiratory, cardiac, renal, and collagen).23 Nutrition is a dominant influence on insulin-like growth factor-I concentrations prenatally,24 and the correlation between birth weight and insulin-like growth factor-I25 is further evidence that nutrition, in this broader sense, is a determinant of birth weight.

However, most fetuses with clinical intrauterine growth restriction have a reduced placental to birth weight ratio, suggesting that the fetus adapts to improve placental transfer when the placenta is pathologically small. In contrast, in Barker's studies of predominantly healthy (and surviving) infants from 50 years ago, it was men with a high placental to birth weight ratio who had highest death rates from cardiovascular disease,15 suggesting different mechanisms. The association between maternal anaemia and increased placental weight26,27 could be linked by nutrition or oxygen delivery.

In the Dutch famine, dietary restriction during early gestation increased the placental to birth weight ratio and resulted in a much greater risk of adult coronary heart disease and obesity.28 In a sheep model, maternal nutrient restriction between early to mid gestation resulted in increased placental weight but not fetal weight at term.29


Small for gestational age does not necessarily equate with intrauterine growth restriction. Even if birth weight remains within the normal range, this may conceal a birth weight significantly below genetic potential because of suboptimal maternal or fetal nutrition.30 Nutritional deprivation redistributes maternal cardiac output away from the uterine vasculature,31 and a chronic fetal “stress response” to this could permanently reprogramme steroid sensitivity. Fetal overexposure to maternal glucocorticoids may programme hypertension32,33 In sheep, dexamethasone treatment during early pregnancy results in persistent hypertension in the offspring.34

Sensitivity to glucocorticoids is regulated by expression of the glucocorticoid receptor and 11β-hydroxysteroid dehydrogenase (11β-HSD). 11β-HSD1 catalyses the conversion of cortisone to the more potent cortisol,35,36 and 11β-HSD2 does the opposite, “protecting” the fetus from adverse glucocorticoid exposure.32,37 The renin-angiotensin system is also regulated by glucocorticoids38 and is critical to the control of blood pressure during fetal and postnatal life.39,40 Increased tissue exposure to cortisol could explain how early reduction in maternal nutrition affects fetal cardiovascular development while birth weight remains within the normal range.

In the sheep model with maternal nutrient restriction in early gestation and increased placental to fetal weight ratio at term,29 both glucocorticoid and type 1 angiotensin II receptor mRNA expression are increased in the offsprings' adrenal and kidney.41 Conversely, placental 11β-HSD2 mRNA expression is decreased, which could increase cortisol transfer across the placenta in the absence of any apparent change in maternal cortisol.42,43


In developing countries, maternal dietary intake can affect birth weight, and intervention helps. In developed countries, epidemiological studies and experiments using animals indicate that modest reductions in maternal food intake could affect survival at birth and longevity, in the absence of pathological changes in birth weight.44,45 It appears to be earlier maternal nutrient restriction that increases placental size29 and alters the expression of genes regulating the glucocorticoid and renin-angiotensin systems.41

Maternal nutrition, encompassing maternal dietary intake, circulating concentrations, uteroplacental blood flow, and nutrient transfer across the placenta, influences birth weight


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