Low-Birthweight Baby: Born Too Soon or Too Small

N. D. Embleton, J. Katz, E. E. Ziegler

• Publisher: S. Karger
• Year: 2015
• ISBN:
  9783318027693
• Topic: Medicine
• Subtopic: Nutrition, Dietics & Bariatrics

Low birthweight, caused by premature birth, poor intrauterine growth, or both, is known to be a strong predictor of morbidity and mortality risks in the first year of life and beyond. It has to be born in mind, though, that premature infants may need different clinical and nutritional interventions and are at risk for different morbidities than those small for gestational age. This publication focuses on three main subjects: Global epidemiology, catch-up growth, and feeding practices. These topics have been selected to provide a solid contextual basis for the nature and extent of the problem, highlighting changes in prevalence and risk across different healthcare settings: The available data strongly suggest that growth outcomes are dependent on a multitude of environmental factors that interact with nutrient intakes. Epidemiology, modern technology and the latest science are brought together to promote a better understanding of the short- and long-term needs and outcomes of low-birthweight babies, depending on whether they are born too small or too early.

Catch-Up Growth

Embleton ND, Katz J, Ziegler EE (eds): Low-Birthweight Baby: Born Too Soon or Too Small.
Nestlé Nutr Inst Workshop Ser, vol 81, pp 51-60, (DOI: 10.1159/000365803)
Nestec Ltd., Vevey/S. Karger AG., Basel, © 2015

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Should We Promote Catch-Up Growth or Growth Acceleration in Low-Birthweight Infants?

Atul Singhal

Childhood Nutrition Research Centre, Institute of Child Health, University College London, London, UK

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Abstract

The idea that catch-up growth or growth acceleration has adverse effects on long-term health has generated much debate. This pattern of growth is most commonly seen after birth in infants of low birthweight; a global problem affecting over 20 million newborns a year. Faster postnatal growth may have short-term benefits but increases the long-term risk of aging, obesity and metabolic disease. Consequently, the optimal pattern of postnatal growth is unclear and is likely to differ in different populations. In infants born prematurely, faster postnatal growth improves long-term cognitive function but is associated with later risk factors for cardiovascular disease. So, on balance, the current policy is to promote faster growth by increasing nutrient intake (e.g. using higher-nutrient preterm formulas). Whether the same policy should apply to larger preterm infants is not known. Similarly, in infants from impoverished environments, the short-term benefits of faster postnatal growth may outweigh long-term disadvantages. However, whether similar considerations apply to infants from countries in transition is uncertain. For term infants from developed countries, promoting catch-up growth by nutritional supplementation has few advantages for short- or long-term health. Overall therefore, a ‘one size fits all’ solution for the optimal pattern of postnatal growth is unlikely.

© 2015 Nestec Ltd., Vevey/S. Karger AG, Basel

Introduction

Normally, growth, defined at the simplest level as the quantitative increase in body mass or size, is closely regulated and follows a regular and predictable path. Consequently, monitoring the rate of growth is one of the best indices of a child's health, and is an essential part of pediatric care. The pattern of growth is not only a marker of the immediate physical and emotional well-being of the child, but has long-term implications for health. Therefore, historically, achieving adequate growth and the prevention of growth faltering has been the highest priority in clinical research and pediatric practice.

Faltering growth has numerous causes, recovery from which is usually followed by a rate of growth much greater than that expected. This recovery phase of growth, or ‘catch-up growth’, has been a focus of intense research and debate, particularly in light of recent evidence that ‘accelerated’ or too fast growth has detrimental effects on long-term risk of noncommunicable disease. Catch-up growth is most commonly seen immediately after birth in infants with low birthweight (LBW), a problem which affects over 20 million newborns a year globally [1]. However, the factors contributing to this pattern of growth and its consequences for long-term health are poorly understood. The risk-benefit of faster postnatal growth may differ in different populations (e.g. in infants born preterm versus those born at term, or in infants from developed or developing countries). As a result, whether postnatal catch-up growth should be actively promoted (e.g. by increasing nutrient intake) remains controversial. The present review considers the evidence for the effects of faster postnatal growth on long-term health, focusing on the biology and clinical impact in term infants from developed countries. It will not address the causes and consequences of postnatal malnutrition (e.g. stunting), a major global issue, known to have adverse effects on long-term adult health and human capital [2].

Terminology and History

The phenomenon of a child growing at a rate faster than expected was recognized in the 18th and 19th centuries as the growth pattern in response to recovery from illness [3]. However, this pattern of growth was confused with faster growth associated with the adolescent growth spurt leading to the belief that for the adolescent growth spurt to occur the child had to be first ill. The concept of ‘catch-up’ growth was first formally described in 1954 by Bauer who noted faster growth in 19 children recovering from the nephrotic syndrome [as reviewed, 3]. This work was extended by the demonstration of catch-up growth in several clinical conditions by Prader in 1963 [4]. Importantly, catch-up growth was defined as the acceleration in growth in response to recovery from illness or starvation[4]. Faster growth following recovery was also known by some as ‘compensatory growth’. However, as pointed out by Tanner [3], this term originally referred to the overgrowth of an organ when a part of the organ had been removed or to the excess growth of the remaining member of a pair of organs (e.g. kidneys) when one of the pair had been removed.

Catch-up growth was recognized to occur as a natural phenomenon in infancy in the 1950s [3]. Children who were small at birth grew more quickly postnatally than those who were larger (and vice versa). It was assumed that this pattern of growth was the same as catch-up growth and that the infants were recovering from undernutrition in utero. However, early postnatal growth is strongly influenced by genes, and infants with genes for large size but born to small mothers show faster postnatal growth (and vice versa). This reassortment of size occurs soon after birth, and had been described many years previously in animal models. In the classic experiments of Walton and Hammond, foals born to small (Shetland) horses crossed with large (Shire) horses showed faster growth after birth (and vice versa) [as reviewed, 3]. The same phenomenon is seen in humans (see ‘mechanisms’ below). Therefore, faster growth after birth is a natural pattern of growth and is not necessarily the same as catch-up growth (i.e. a consequence of recovery from a period of undernutrition in utero).

A growth rate much faster than expected can also be seen after birth as a consequence of changes in the plane of nutrition. This was first demonstrated in the 1960s by McCance who showed that overfeeding rats during a critical window in early postnatal life permanently increased later body size [5]. Similar effects of a higher plane of early postnatal nutrition occur in humans. Infants born preterm and randomly assigned to a higher-nutrient diet (nutrient-enriched infant formula) compared to a lower-nutrient diet (human milk or standard formula) were found to have greater propensity to obesity, dyslipidemia, raised blood pressure, and insulin resistance in adolescence [6]. Faster growth in infancy was also associated with insulin resistance, markers of inflammation, higher blood pressure and endothelial dysfunction (an early stage in the atherosclerotic process) [6]. Based on these data, and previous epidemiological studies linking faster postnatal weight gain with greater risk of later obesity, we proposed the postnatal ‘growth acceleration’ hypothesis [6]. This concept suggests that upward centile crossing (for weight or length) could explain, in part, the adverse long-term effects on health seen in infants born small for gestation (SGA; who show ‘catch-up’ growth immediately after birth) and long-term cardiovascular benefits in babies breastfed (who are relatively undernourished and have slower growth compared to those given formula) [6]. The term ‘growth acceleration’ was specifically chosen because it makes no assumption about the causes of faster postnatal growth, and it encompasses several potential causes such as faster growth arising from recovery from illness or starvation (i.e. ‘catch-up’ growth), genetic factors or accelerated growth as a consequence of a higher plane of postnatal nutrition.

The Impact of Growth Acceleration on Long-Term Health

The fact that ‘catch-up’ occurs in animal species as diverse as mammals, birds, fish as well as humans suggests that this pattern of growth must be an evolutionary conserved adaptive response [7, 8]. These beneficial effects may include faster maturity and hence greater reproductive success, and greater likelihood of survival as a result of a larger size in early life (e.g. protection from predators, infectious disease or starvation) [7, 8]. However, the fact that humans and animals do not grow as fast as they are capable of (e.g. as seen during catch-up growth) suggests that faster growth in early life must also have a biological cost. Therefore, there is a trade-off in order to optimize growth trajectories between short-term benefits and long-term costs, the concept of ‘grow now pay later’ [7]. The short-term advantages of faster growth in infancy either in those born LBW or SGA is well recognized and include, for example, a lower risk of hospitalization in poorer environments [9]. The long-term cost of this faster growth, however, is an increased risk of noncommunicable disease. Importantly, because the effects of faster postnatal growth on risk of diabetes, CVD, and even, more rapid aging, are usually manifest later in life, after reproduction, these ‘diseases’ are not greatly affected by selective pressures.

The concept that growth acceleration has adverse consequences for long-term health is now strongly supported by a wealth of evidence. The association is biologically plausible and experimentally reproducible in several animal models [10-12]. In humans, faster weight gain in infancy (upward centile crossing for weight) is associated with a greater risk of later obesity in more than 30 studies (summarized in 5 systematic reviews [13-17]). The evidence is consistent across studies [15, 16] and includes an individual-level meta-analysis in 47,661 participants from 10 cohorts [16]. The association between postnatal growth acceleration is consistent for cohorts during the last 80 years [13-15], is seen in breastfed and formula-fed populations, and has been shown to influence the main components of the metabolic syndrome [6, 18]. For instance, in infants born SGA, faster weight gain in the first 3 months of life is associated with lower insulin sensitivity and HDL cholesterol concentrations, and higher triglyceride concentrations, obesity and markers of atherosclerosis at age 18-24 years [18]. Long-term effects of postnatal growth acceleration are evident in both infants born preterm or at term, infants born small or appropriate weight for gestation, in adults as well as children, and in developed and developing countries [19]. For example, in a cohort study from Delhi, rapid gain in BMI in the first year was associated with development of the metabolic syndrome in adulthood [as reviewed, 19]...

Table of contents

• Cover Page
• Front Matter
• Global Epidemiology
• Catch-Up Growth
• Feeding Practices - Current and Improved?
• Concluding Remarks
• Subject Index