Maternal nutrition and pregnancy outcome. (Leading Article).

(See paper by A. Begley, page 175-180)(Leading Article)

A successful pregnancy has been defined by Jackson and Robinson (1) as one in which maternal heath is maintained, a healthy baby is delivered and the mother is able to nurture her newborn adequately. More recently attention has focussed not only on the immediate health of the newborn but also on his or her long-term health through childhood and into adulthood.

Barker and colleagues were the first to hypothesise that the major chronic diseases may have their origins in the womb and that a mother's nutritional intake may have a subsequent long-term impact on the health of her offspring (2). Early epidemiological studies showed a relationship between infant birth weight and cardiovascular disease. Based on this evidence Barker proposed that the pathogenesis of cardiovascular disease is programmed during the period of rapid growth in early life. The Barker's hypothesis, also called the foetal origins hypothesis, contends that undernutrition during critical periods of foetal development may permanently alter the body's structure, physiology and metabolism, and thereby increase the susceptibility to disease in adult life (2). Subsequent epidemiological studies have shown a relationship between infant birth size and stroke, blood pressure, type 2 diabetes, renal failure and metabolic syndrome (2).

In most instances however, epidemiological studies have not actually measured nutritional intake of mothers, maternal under-nutrition being inferred only indirectly from measurements of birth weight. Data from studies of European populations that experienced food restriction during the second world war provide more direct evidence of the influence of maternal nutrition on reproductive outcome (3). The foetal origins hypothesis is further supported by evidence from animal studies (4). While it is now generally accepted that foetal programming is related to undernutrition, the mechanism of the relationship has not been fully explained.

The major influence regulating foetal growth is the supply of nutrients to the foetus (5). During pregnancy foetal supply is affected by what the mother eats during pregnancy, the transfer of nutrients to the placenta and transfer across it. The story does not however, begin and end with the gestational period as foetal supply depends also on the mother's body composition and size and her nutrient stores, which in turn are influenced and established during her own foetal life and by her nutrition experiences in childhood and adolescence.

Typically infant birth weight has been used as a primary indicator of a successful pregnancy. Low birth weight (LBW), defined as <2.5 kg, is considered a poor outcome and can be due to preterm delivery and to intrauterine growth retardation (6). Poor maternal nutrition during pregnancy however, is not the only factor which influences birth weight. Maternal size, age, smoking habits and level of social deprivation have all been reported as being independently related to birth weight. While some researchers have shown, in epidemiological studies, a relationship between aspects of maternal diet and birth weight, there is limited evidence from intervention studies that manipulation of the maternal diet can prevent or ameliorate intrauterine growth retardation (7).

Adverse pregnancy outcomes for which there is strong evidence of a direct link to maternal diet include birth defects such as neural tube defects (folate) and mental retardation (iodine) (1). While achievements have been made in increasing women's awareness of the need for periconceptual folate supplements (8), iodine is a nutrient that may deserve renewed and increased attention when counselling pregnant women. A recent study of pregnant women in Scotland, where the majority of salt is not iodised, revealed that 40% were consuming less than half the recommended intake of iodine (unpublished data, Professor R. Hurne, University of Dundee, August 2002). In light of the reported re-emergence of iodine deficiency in Tasmania (9) this finding may have some bearing for pregnant women, in this state at least.

Not only are we challenged by our lack of understanding of the relationship between maternal nutrient intake and either the birth weight of offspring or their subsequent long-term health, we are challenged also by the problems that women have in changing their diets in order to meet current nutritional recommendations for pregnancy. It is clear that while women are generally aware of the importance of healthy eating while pregnant, they are confused about what constitutes a healthy diet. The paper by Begley (10) in this issue provides some insight into this confusion and the barriers that women face in consuming a healthy diet prior to and during pregnancy.

The current Recommended Dietary Intakes for adults in general, are based on the requirements to prevent malnutrition and deficiencies and do not take into account requirements for optimal health (11). Similarly, current dietary recommendations for pregnancy are based on estimates of the cost of supporting the increased maternal tissue mass associated with pregnancy and the delivery of an infant weighing approximately 3.5 kg. The specific aspects of the maternal diet which serve as foetal programming stimuli remain unclear and we know little about the level, and timing of intake, of individual nutrients required during pregnancy for optimal health of offspring in later childhood and adulthood.

We are only just beginning to understand the effects of maternal malnutrition on foetal development and later health outcomes. Jackson and Robinson (1) contend that while studies have failed to describe clear links between maternal diet and foetal growth, it is unlikely that the quality of the maternal diet has no impact on foetal nutrient supply, and the importance of maternal diet cannot be discounted. In the meantime, it is the general consensus that in the absence of good scientific evidence women entering pregnancy should consume an adequate diet, based upon our normal understanding of requirements (12).

References

(1.) Jackson A, Robinson S. Dietary guidelines for pregnancy: a review of current evidence. Pub Health Nutr 2001;4:625-30.

(2.) Barker D. Mothers, babies and health in later life. Edinburgh: Churchill Livingston; 1998.

(3.) Susser M, Stein Z. Timing in prenatal nutrition: A reprise of the Dutch Famine Study. Nutr Rev 1994;52:84-94.

(4.) Ozanne S. Metabolic programming in animals. Brit Med Bull 2001;60:143-52.

(5.) Barker D. The malnourished baby and infant. Brit Med Bull 2001;60:69-88.

(6.) Ramakrishnan U, Manjrekar R, Rivera J, Gonzales-Cossio T, Martorell R. Micronutrients and pregnancy outcome: a review of the literature. Nutr Res 1999;19:103-59.

(7.) de Onis M, Villar J, Gulmezoglu M. Nutritional interventions to prevent intrauterine growth retardation: evidence from randomised controlled trials. Eur J Clin Nutr 1998;52:S83-593.

(8.) Williams P, McHenry J, McMahon A, Anderson H. Impact evaluation of a folate education campaign with and without the use of a health claim. Aust N Z J Public Health 2001;25:396-404.

(9.) Guttikonda K, Burgess J, Hynes K, Boyages S, Byth K, Parameswaran V. Recurrent iodine deficiency in Tasmania, Australia: a salutary lesson in sustainable iodine prophylaxis and its monitoring. J Clin Endocrinol Metab 2002;87:2809-15.

(10.) Begley A. Barriers to good nutrition during pregnancy: A qualitative analysis. Nutr Diet 2002;59:175-80.

(11.) Cobiac L, Dreosti I, Baghurst K. Recommended dietary intakes--is it time for a change? Canberra: Commonwealth Department of Health and Family Services; 1998.

(12.) National Health and Medical Research Council. Recommended dietary intakes for use in Australia. Canberra: Australian Government Publishing Service; 1991.