Strengthening NICU Healthcare Professionals’ Knowledge...

Strengthening NICU Healthcare Professionals’ Knowledge

NICUCurrentsOctober 2011 • Volume 2, Issue 2

The Barker Hypothesis: The Developmental Origins of Adult Disease 8Nutrition and the Late Preterm Infant

Earn free CE credits by reading the article and taking the online post test - see page 4 for details.1

HeadlineBy Author

Nutrition and the Late Preterm Infant By Jackie Wessel, MEd, RD, CSP, CNSD, CLE

LEarnIng ObjECtIVEsUpon completion of this article the reader will be able to:1. Explain the physiologic reasons that a late preterm infant may breastfeed poorly;2. Identify the late preterm infant as at-risk for re-hospitalization within the first 2 weeks of life

for feeding difficulties, dehydration and jaundice;3. Identify three nutritional interventions for the late preterm infant.

Since the 2006 National Institutes of Child Health and Human De-velopment meeting, Optimizing

care and outcomes for late preterm infants, there has been a plethora of research and articles about the late preterm infant: born at 34 0/7 to 36 6/7 weeks of gesta-tion.1 Beginning in the 1990s, this group of infants was called “near-term,” placed in normal newborn nurseries and treated as if they were full-term infants. The inci-dence of late preterm births has increased by 25% from 1990 to 2006, far outstrip-ping the 7.2% increase in early preterm births in the same time frame.2 Today, the majority of preterm infants, 8.7% of the 12.3% preterm births in the U.S., are late preterm infants.3

Late preterm infants are at higher risk for complications such as transient tachypnea of the newborn, respiratory distress syndrome, persistent pulmonary hypertension, respira-tory failure, temperature instability, jaun-dice, feeding problems, metabolic stressors and prolonged NICU stays.4,5

Late preterm infants are also at greater risk for hospital readmission6 within their first two weeks of life than infants of all other gestational ages.7 The most frequent reasons for re-hospitalization are jaundice (34%) and feeding difficulties (26%).7 The latest re-search on late preterm infants finds long-term

2 | October 2011 NICU Currents

Feature: Nutrition and the Late Preterm Infant

neurodevelopmental consequences of be-ing born too soon.4,8,9 Since 1995 there has been a gradual increase in mortality rates for the late preterm infant, with rates 4.6 times higher than that of term infants.10,11

Nutritional ConcernsPostnatal HypoglycemiaNeonatal hypoglycemia is more common in late preterm infants because of their higher metabolic rate and limited stores.10,12 Term-appropriate for gestational age infants have greater stores of fat and glycogen, which they are able to convert to calories.12 With tem-perature instability, brown fat and other en-ergy reserves of the late preterm can be easily depleted.12 The resulting hypoglycemia may lead to permanent neurological damage. The American Academy of Pediatrics (AAP) has published a clinical practice guideline for postnatal glucose screening and monitoring of late preterm and term infants.13

Developmental ImmaturityLate preterm infants are at particular risk for poor feeding because of their developmental immaturity.6 Cardiorespiratory instability contributes to lack of stamina necessary for feeding. Immaturity of state regulation also leads to fatigue during feeding. These infants often tire quickly and fall asleep before a feeding is complete. Immaturity of the suck/ swallow/ breathe pattern, as well as decreased oral motor tone, contribute to sucking diffi-culty.6 The immature infant is unable to gen-erate enough negative pressure in sucking for efficient and successful breastfeeding.14

Breastfeeding DifficultyMothers of late preterm infants are at risk for delayed lactogenesis.14 Because late preterm infants are unable to stimulate the breast with adequate negative pressure and spend less time nursing, their mothers have difficulty creating a full milk supply.

The infants receive insufficient breast milk intake and, over time, the mothers pro-duce less breast milk. Because this cascade of events often occurs after the late pre-term infant is discharged home, readmis-sion may be necessary.

The pattern of poor feeding leading to breastfeeding failure in the late preterm in-fant is well described in papers by Meier14

and Wight,15 which also include strategies for management. The Supporting Preterm Infants Nutrition program also has thought-ful policies and procedures to screen and support breastfeeding in the late preterm in-fant.16 Interestingly, the late preterm infant may be less likely to be breastfed than his term or even preterm counterparts.4

Re-hospitalizationRe-hospitalizations for jaundice, dehydra-tion, and poor feeding occur almost twice as often for breastfed late preterm infants as for

breastfed term or formula-fed late preterm infants.4 Poor feeding resulting in insuffi-cient human milk intake leads to jaundice and dehydration.17-19 Peak readmission times are at 4 to 5 days of life, and nearly all these infants present with suboptimal intake in ad-dition to severe jaundice.20 In a 2003 study kernicterus –bilirubin encephalopathys was significantly more frequent in late preterm infants, especially those who were large for gestational age.21 There is little data about whether mothers continue to breastfeed after the trauma of a hospital readmission for lac-tation problems, but anecdotal reports indi-cate that many discontinue breastfeeding.14

Since human milk is the optimal nutrition for term infants and, when fortified, is the optimal choice for early preterm infants, it is unfortunate that breastfeeding may be dis-continued for the late preterm infant.

Despite parental concerns about difficult feeding, excessive sleeping, and increased jaundice,20 they often receive reassuring tele-phone comments from primary care provid-ers, This pattern, along with constipation in breastfed infants, has been seen in our hospital. Investigation of some of these calls found that not all advice was given by edu-cated healthcare providers. To remedy this situation, in-service education was offered to the local office nurses’ association about the potential disastrous effects of giving the wrong information to parents of breastfed, late preterm infants.

Nutritional InterventionsAlthough late preterm infants have unique nutrition needs, there is no document that delineates what these needs are. All too often these infants are cared for and treat-ed like term infants who are “just a little slower” to feed. They are discharged with unresolved feeding issues. The late preterm infant is in a critical period of brain growth. At 34 weeks gestational age (GA) the late

Mothers of late preterm infants are at risk for delayed lactogenesis.14 Because late preterm infants are unable to stimulate the breast with adequate negative pressure and spend less time nursing, their mothers have difficulty creating a full milk supply.

NICU Currents October 2011 | 3

preterm’s brain weighs only 65% of that of a term infant’s brain22 and at 36 weeks GA the brain weighs 80% of the term infant’s brain.14 The late preterm infant’s brain is in a dynamic growth period, with 50% of the increase in cortical volume occurring between 34 and 40 weeks gestation.5,23,24 How do we best support this very impor-tant growth? Have earlier nutrition plans been adequate or are they lacking and con-tributing to the less–than-optimal neuro-developmental outcomes of this group of vulnerable infants?

In the flurry of new papers, few ad-dress the nutrition of the late preterm infant other than to discuss the feeding difficulties.4 What kind of nutrition will best support these vulnerable infants? If there are golden hours in the immediate time after birth to establish nutrition for early preterm infants, is there also a crucial window of time for late preterm infants?

Data from researchers exploring the link between improved immediate nutrition and growth,25 growth and developmental outcomes,26 and all three27 in extremely low birth weight (ELBW) infants, show that early, aggressive nutrition improves outcome. Lucas showed improved neu-rodevelopment in larger preterm infants fed a post-discharge premature formula as compared to those being fed a term infant formula.28,29 Can we draw any conclusions from these early-preterm studies for the care of the late preterm infant?

As a late preterm infant is evaluated and treated for common morbidities, he is often

maintained nutritionally on IV dextrose solutions without the benefits of protein, vitamins, minerals, amino acids and suf-ficient calories for growth. In the ability of term breastfed infants to sustain them-selves without supplemental nutrition, we often assume that the same experience ap-plies to the late preterm. If lactation pro-ceeds normally, term breastfed infants typi-cally obtain 30 ml of milk in the first 24 hours, 100 ml at 48 hours, and 700 ml by the end of their first week of life.14,30 How-ever, since lactation for the late preterm infant does not proceed normally, these in-fants are often underfed and less vigorous.

Despite parental concerns about difficult feeding, excessive sleeping, and increased jaundice,20 they often receive reassuring telephone comments from primary care providers…



Without supplemental stimulation from breast pumping, the mother-infant dyad has difficulty establishing and maintaining lactation. Is a lower quantity of nutritional intake sufficient for late preterm infants with incomplete brain growth? Should late preterm infants receive formula supplemen-tation while breastfeeding?

Until further research provides evidence-based answers, we are left with unanswered questions. However, clinically we are still chal-lenged with caring for the nutritional needs of this population of at-risk infants. Adequate birth weights (see weight ranges in Table 1) may fool healthcare providers into thinking that the late preterm infant is mature. Provid-ers may nutritionally support smaller babies but give average- or larger-weight neonates

“standard fare” nutrition for term babies. This results in periods of low nutritional intake in these infants. In the absence of

guidance from the literature, the following are my recommendations for how to care for the late preterm infant:

Complete the quiz on line at www.anhi.org at no charge. Please note online questions or answers are randomized and may not appear in the same sequence below. Do not assume that the “letter” preceding the correct response will be identical to the online version.

Post-Test: Nutrition and the Late Preterm Infant

abbott nutrition Health Institute, is an approved provider of continuing nursing education by the California board of registered nursing Provider #CEP 11213.

Credit: 1 contact

hour

True/False:1. Late preterm infants have no more feeding

problems than any term infant. a. True b. False

2. Late preterm infants are at increased risk for rehospitalization for feeding difficulties, dehydration and jaundice within their first 2 weeks of life.

a. True b. False

3. Late preterm infants are at particular risk for poor feeding because of their developmental immaturity.

a. True b. False

4. Mothers of late preterm infants do not need to pump their breasts.

a. True b. False

5. Postnatal hypoglycemia is common in the late preterm infant.

a. True b. False

6. The late preterm infant has a mature suck/swallow/breathe reflex.

a. True b. False

7. Nutritional support for the late preterm in-fant has been well researched.

a. True b. False

8. Late preterm infants do not need to be sup-ported with TPN and lipids if they remain NPO for > 24 hours.

a. True b. False

9. Late preterm infants do not have to be awakened to be fed during the night.

a. True b. False

10. Feeding a neonate cereal is a recommended practice.

a. True b. False

Table 1: Weight Ranges for Gestational Ages

gestational age 10th% 50th% 90th%

34 weeks 1500 2100 2800

35 weeks 1700 2300 3000

36 weeks 1900 2600 3200

37 weeks 2100 2800 3400

Compiled from visual inspection of the Fenton Growth Curve: Fenton TR: A new growth chart for preterm babies: Babson and Benda’s chart updated with recent data and a new format BMC Pediatrics 2003; 3:13. http://www.biomedcentral.com/1471-2431/3/13


A nutrition care plan should be devel-oped for each late preterm infant, utiliz-ing the interdisciplinary expertise of a neonatal registered dietician, a lactation consultant, medical/nursing-care provid-ers and parents:

• If the late preterm infant requires nothing by mouth (NPO) status, consider beginning amino acids in the IV fluids (similar to early initiation of amino acids in the ELBW preterm). If NPO is projected to be necessary for > 24 hours start:

- Total parenteral nutrition (TPN) with 2.5-3 grams/kg of protein;

- Glucose infusion rate (GIR) of 6-8 mg/kg/minute;

- Lipids of 1gram/kg.• If the infant is too tachypneic to eat

by mouth, consider establishing en-teral nutrition temporarily through a nasogastric tube.

• If the mother has delayed lactogen-esis, consider use of donor human milk or formula to provide nutrition to the infant. If donor milk is not available or practical, consider us-ing nutritionally supplemented pre-term formula for increased protein and minerals.

• Encourage mothers of late preterm in-fants to breastfeed. Initially this may be more work for the mother because she may need to pump her breasts in addition to nursing the infant to es-tablish and maintain a milk supply. As the late preterm infant approaches 40 weeks GA, matures his nutritive suck-ling, and develops more stamina for feeding, the use of a breast pump will no longer be necessary to maintain the milk supply.

• Late preterm infants need to be awak-ened during the night for feedings. These infants are unable to add more volume to daytime feedings to make up for the loss of nocturnal intake. Sleeping through the night results in lost intake of needed fluids and calo-ries. (Do not feed any neonate cereal, the only nutrition they need is breast milk or formula.)



• Follow the AAP recommendations for infant feeding and introduce solids at 6 months of age (Use corrected age for pre-terms). Do not give juice or water; neo-nates need the nutrition from human milk or formula.

• Consult a feeding therapist if the introduc-tion of solids or table food at the appropri-ate time becomes a problem.

ConclusionResearch has shown that nutritional support of the ELBW infant influences outcome, but whether changing nutritional support for the late preterm infant results in better neurodevel-opmental outcomes is currently unknown. Our concern for the growing brain and altered neu-rodevelopment potential in late preterm infants should guide us to pursue further research. New evidence may result in altering current nutrition standards for this group of vulnerable infants to improve their outcomes.

About the Author Jacqueline J. Wessel, MEd, RD, CNSD, CSP, CLE is a Neonatal Nutritionist in the Regional Center for Neonatal Intensive Care at Cincin-nati Children’s Hospital. The author was com-pensated by Abbott Nutrition l

ReFeRenCes 1. Raju TnK, Higgins RD, stark AR, et al: Optimiz-

ing care and outcome for late preterm infants: A summary of the workshop sponsored by the national Institute of Child Health and Human Development Pediatrics 2006; 118:1207.

2. Martin JA, Kirmeyer s, Osterman M, shepherd RA: Born a bit too early: Recent trends in late pre-term births. nCHs data brief, no 24. Hyattsville, MD: national Center for Health statistic, 2009.

3. Martin JA, Hamilton Be, sutton PD, et al: Births: Final Data for 2008 National Vital Statistics Re-ports 59:1 Dec 8, 2010. www.cdc.gov/nchs/data/nvsr/nvsr59/nvsr59_01.pdf

4. Ramachandrappa A, Jain L: Health issues of the late preterm infant Pediatr Clin N Am 2009; 56:565.

5. Mally PV, Bailey s, Hendricks-Munoz KD: Clinical issues in the management of late preterm infants Curr Probl Pediatr Adolesc Health Care 2010; 40:218.

6. Radtke JV: The paradox of breastfeeding-associated morbidity among late preterm infants JOGNN 2011; 40:9.

7. escobar GJ, Gonzales VM, Armstrong M, et al: Rehospitalization after birth: Hospitaliza-tion patterns among infants of all gestational ages Arch Dis Child 2005; 90:125.

8. Woythaler MA, McCormick MC, smith VC: Late preterm infants have worse 24-month neurodevelopmental outcomes than term infants Pediatrics 2011; 127:e622.

9. Morse sB, Tang Y, Roth J: school age out-comes and healthy late preterm neonates Pediatr Res Suppl 2006; 158: Abstract 4355.

10. Khashu M, narayanan M, shargave s, et al: Perinatal outcomes associated with preterm birth at 33 to 36 weeks gestation: A popu-lation based cohort study Pediatrics 2009; 123:100.

11. Committee on Obstetric Practice, ACOG committee opinion: Late preterm infants Ob-stet & Gynecol 2008; 111:1029.

12. Garg M, Devaskar sU: Glucose metabolism in the late preterm infant Semin Perinatol 2000; 24:136.

13. Adamkin DH and the Committee on Fetus and newborn: Postnatal glucose homeosta-sis in late preterm and term infants Pediatrics 2011; 127:55.

14. Meier P, Furman LM, Degenhardt M: In-creased lactation risk for the late preterm infants and mothers: evidence and manage-ment strategies to protect breastfeeding J Midwife & Womens Health 2007; 52:579.

15. Wight ne: Breastfeeding the borderline (near-term) preterm infant Pediatr Ann 2003; 32(5):329. supporting Preterm Infants nutri-tion Program. Available at: www. [email protected]. Accessed 6/10/2011.

16. esobar GJ, Gonzales VM, Armstrong M, et al: Rehospitalization for neonatal dehydra-tion: A nested case control study Arch Pedi-atr Adol Med 2002; 156:155.

17. Tomashek KM, shapiro-Mendoza CK, Weiss J, et al: early discharge among late preterm and term newborns and risk of neonatal morbidity Sem Perinatol 2006; 30:61.

18. shapiro-Mendoza CK, Tomashek KM, Kotel-chuck M, et al: Risk factors for neonatal morbid-ity and mortality among “healthy” late preterm newborns Sem Perinatol 2006; 30:54.

19. Watchko JF, Maisels MJ: Jaundice in low birth-weight infants: Pathophysiology and outcome Arch Dis Child Fetal Neonatal Ed 2003; 88: F455

20. sarici sU, serdar MA, Korkmaz A, et al: Inci-dence, course, and prediction of hyperbili-rubinemia in near- term and term newborns Pediatrics 2004; 113:775.

21. Huppi Ps, Warfield s, Kikinis R, et al: Quantita-tive MRI of brain development in premature and mature brain Ann Neurol 1998; 43:224.

22. Guthard-Costa AM, Larrosche JC: Differential growth between the fetal brain and its infraten-torial part Early Hum Dev 1990; 23:27.

23. Kinney HC: The near term (late preterm) human brain and risk for periventricular leukomalacia Semin Perinatol 2006; 30:81.

24. Valentine CJ, Fernandez s, Rogers JK, et al: early amino acid administration improves pre-term weight J Perinatol 2009; 29:428.

25. ehrenkranz RA, Dusick AM, Vohr BR, et al: Growth in the neonatal intensive care unit in-fluences neurodevelopmental and growth out-comes of extremely low birthweight infants Pediatrics 2006; 117:1253.

26. stephens Be, Walden RV, Gargus RA, et al: First week protein and energy intakes are associated with 18 month developmental outcomes in ex-tremely low birthweight infants Pediatrics 2009; 123:1337.

27. Lucas A, Morley R, Cole TJ: Randomised trial of early diet in preterm babies and later in-telligence quotient BMJ 1998, 31:1481.

28. Lucas A, Morley R, Cole TJ, et al: early diet in preterm babies and developmental status at 18 months Lancet 1990; 335:1477.

29. neville MC, Keller R, seacat J, et al: studies in human lactation: Milk volumes in lactat-ing women at the onset of lactation and full lactation Am J Clin Nutr 1988; 48:1375.

A nutrition care plan should be developed for each late preterm infant, utilizing the interdisciplinary expertise of a neonatal registered dietician, a lactation consultant, medical/ nursing-care providers and parents:

Accessed online continuing education courses.

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Feature: The Barker Hypothesis

In the late 1980s, David Barker, MD, PhD, a clinical epidemiologist, and his colleagues, published research about the relationship

between birth weight and later adult cardiovas-cular disease.1,2 The initial study, at the Medi-cal Research Council Unit of the University of Southampton, found that regions in England with the highest rates of infant mortality, also decades later, had the highest rates of mortality from coronary artery disease.1 Because infant mortality at the beginning of the 20th century was most commonly due to low birth weight, the researchers hypothesized that surviving low-birth-weight babies might be at increased risk for coronary heart disease as adults.

Barker’s group studied two large sets of Brit-ish men born in the first quarter of the 20th century and found a strong relationship be-tween growth-restricted neonates (who had de-creased birth weight, head circumference and/or ponderal index) and death from coronary heart disease.2,3 Multiple studies have replicated the results found by the UK researchers, includ-ing studies of adult women who were growth-restricted at birth.4-7 Even after correcting for known risk factors for heart disease, such as

The Barker Hypothesis: The Developmental Origins of Adult DiseaseBy Sandra L. Gardner, RN, MS, CNS, PNP

diet, exercise and smoking, the correlation be-tween birth size and heart disease remains.4,5,8

Growth restriction was also shown to be re-lated to diseases such as type 2 diabetes mel-litus, hypertension and hyperlipidemia, known risk factors for cardiovascular disease. If an adult was growth-restricted at birth, altered glucose and insulin metabolism (i.e. insulin resistance,

higher fasting insulin concentrations and type 2 diabetes) are more likely to occur.9 A system-atic review of more than 80 studies of adults and children demonstrated an inverse relation-ship between birth weight and blood pressure: a 2mmHg decrease in systolic blood pressure for every kilogram increase in birth weight.10 Small neonatal abdominal circumference has been shown to predict higher cholesterol and fibrino-gen levels, both risk factors for heart disease in later life for men.11,12

Other systemic diseases are strongly associ-ated with size at birth. In replicated studies, dis-eases such as stroke,13,14 non-insulin dependent diabetes,9 elevated clotting factors,15 aging, os-teoporosis, and impaired neurodevelopment16-20 are linked with low birth weight. Large size at birth is associated with polycystic ovary dis-ease,21 breast/ovarian,22 prostate23 and testicu-lar24 cancers, childhood leukemia,25 and type 2 diabetes mellitus.26-29

EtiologyDespite increased genetic risk for specific dis-eases, clearly not everyone with an increased risk develops those diseases. Environment has

Multiple studies have rep-licated the results found by the UK researchers… Even after correcting for known risk factors for heart disease, such as diet, exercise and smoking, the correlation be-tween birth size and heart disease remains.4,5,8


a major impact on genetic expression. Although heredity can not be changed, humans, from the moment of conception, are influenced by intra-uterine, as well as extra-uterine, environment. Reduced placental weight and surface area have been associated with hypertension in both males and females in later life.30-32 Research shows that under-nutrition during fetal life, poor growth in the first year of life and rapid weight gain in later childhood, have cumulative effects on the risk of developing diabetes, cardiac disease and hypertension in adulthood.30,33-35

Fetal programming, insult during a sensi-tive or critical period of development and other stimuli lead to long-term effects, including the development of adult disease. In both animals and humans, alterations in fetal nutrition—both under- and over-nutrition—are primary programmers of postnatal anatomy and physi-ology.36 Imbalance of maternal macronutrients such as protein and carbohydrates, as well as mi-cronutrients, like calcium and antioxidants, is associated with low birth weight, hypertension, and glucose intolerance.36 Infants of diabetic mothers, classic examples of over-nutrition, are at increased risk in later life of developing glu-cose intolerance and type 2 diabetes.37-39 Table 1 lists the mechanisms of fetal programming in response to altered maternal nutrition in devel-oping adult diseases.

Fetal programming for adult diseases may also be due to exposure of the fetus to excess glucocorticoids, which leads to fewer gluco-corticoid receptors in the hypothalamus. This results in impaired negative feedback and long-term up-regulation of the hypothalamic-pitu-itary-adrenal axis after birth, which contribute, in turn, to hypertension and glucose intoler-ance.36,40 As adults, low birth-weight newborns have higher basal plasma cortisol levels.41

Because reduction in somatic growth is as-sociated with repeated administration of glu-cocorticoids during pregnancy, only a single course of antenatal steroids should be admin-istered to women at risk for preterm birth.42 Single courses of antenatal steroids have no ef-fect on birth weight, blood pressure, or plasma cortisol levels in childhood or at 30 years of age.43-45 The first direct evidence of a program-ming effect of antenatal steroids was found at a 30-year follow-up study of preterm infants who developed mild insulin resistance.45

Unanswered Questions and Ongoing ResearchSpecial populations, such as twins and preterm infants, are also being studied. The relationship of gestational age, rather than birth weight, to the development of adult diseases is unclear. In some studies increased incidence of hyperten-sion appears in young adults who were born pre-

term.46,47 Large population-based studies have shown incidence of adult hypertension to be inversely related to gestational age.48,49 Studies also show that young adults born preterm tend to have elevated plasma cortisol levels,50 elevated fasting insulin levels46 and insulin resistance.51

Twin studies were once considered the definitive answer to the difference between

Table 1: etiologic Mechanisms of Adult Disease

adult Disease Mechanism of Fetal Programming in response to altered nutrition

Coronary Heart Disease Accelerated or diminished maturation of cardiac muscle, resulting in fewer cardiac muscle cells and diminished reserve for repair in later life. Small abdominal circumference of the newborn reflects poor liver growth in utero and higher cholesterol levels in later life.

Hypertension Small placentas with narrower vessels may require higher blood pressure to maintain adequate delivery of oxygen and nutrition to the fetus. With aging, blood pressure rises sharply (instead of a slow rise with age), becomes hypertensive, increases risk for stroke, coronary heart disease and renal damage. Kidneys of low-birth-weight newborns have three times fewer nephrons, which must process more blood. They wear, age and die sooner, causing a vicious cycle of increasing blood pressure, more nephron death and kidney failure.

Stroke Poorly-developed blood vessels in the brain of low-birth-weight individuals weaken with aging, and are either blocked with a clot or hemorrhage.

Type 2 Diabetes and Obesity

Pancreatic beta cells develop and function improperly, resulting in reduced production of insulin. Obesity results in an increased demand for insulin and less responsiveness to insulin. This combination results in an inability to maintain blood sugar in the normal range. It rises and diabetes develops. Low birth weight also predisposes to increased insulin resistance in newborns and with aging. Thrifty use of sugar (prioritizing maintenance of adequate blood sugar rather than storing sugar in muscles) leads to rising blood sugar levels.

Osteoporosis Lower bone and muscle mass in low-birth-weight neonates persists throughout life. Life-long alterations in growth hormone and cortisol result in lower peak bone mass and more rapid bone loss with age.

Aging More fragile maintenance of biologic, psychological and physiologic homeostasis in those born with low birth weight results in disease.

Breast and Ovarian Cancer

Above average birth weight is associated with higher rates of breast cancer. Daughters of mothers with broad hips (a marker for good nutrition and estrogen in puberty) are at increased risk for breast and ovarian cancer. Exposure to estrogen of fetal stem cells for breast and ovarian tissue may create genetic instability of these tissues and make them more prone to becoming cancerous in later life.

Adapted from: The Barker Theory at www.barkertheory.org



genetic and environmental influences. How-ever, even for twins, the uterine environment may not be the same. An example is the twin-to-twin transfusion syndrome, where unequal circulation leads to disparate fetal growth and development, resulting in both short- and long-term effects.52 Studies on the incidence of hy-pertension in twins are conflicting, with some showing greater incidence of low birth weight in twins,53-56 while other studies find no such relationship.57,58 Glucose intolerance and type 2 diabetes have been shown to be associated with being a twin,59-61 but some studies found that the affected twins were of lower birth weight than the unaffected twins. Even so, this was not found in all studies.59,60,62

SummaryIt has been long understood that under-nutri-tion in fetal life results in alterations of anat-omy, physiology and metabolism. In 2004, Dr. Barker came to the Heart Research Center at Oregon Health and Science University to continue work on placental growth, maternal nutrition and their role in fetal programming. International partnerships with the United

Kingdom, Finland, France, the Netherlands, India, China, Thailand and Saudi Arabia have resulted in ongoing studies of maternal malnu-trition, low-birth-weight infants and lifelong al-terations in health in a wide variety of cultures. Dr. Mary Barker (Dr. David Barker’s daughter), has established an international network, the Food Choice Group, to study the diets of young women and how these can be improved.63 To read more about the group see the list of books in Box 1 and visit the website www.barkertheo-ry.org. and www.nutritioninthewomb.org.

About the AuthorSandra Gardner, RN, MS, CNS, PNP has worked in perinatal, neonatal, and pediatric care for the past 44 years as a clinician, prac-titioner, educator, author and consultant. She is the Director of Professional Outreach Consultation, a national and international consulting firm established in 1980. She is also senior editor of Handbook of Neonatal Intensive Care, ed 7, 2011. The author was compensated by Abbott Nutrition. l

ReFeRenCes1. Barker DJ, Osmond C: Infant mortality, childhood nu-

trition, and ischaemic heart disease in england and Wales. Lancet 1986; 1:1077.

2. Barker DJ, Winter PD, Osmond C, et al: Weight in in-fancy and death from ischaemic heart disease. Lancet 1989; 2:577.

3. Barker DJ, Osmond C, simmonds sJ, et al: The rela-tion of small head circumference and thinness at birth to death from cardiovascular disease in adult life. Br Med J 1993; 306:422.

4. Rich-edwards JW, stampfer MJ, Manson Je, et al: Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. Br Med J 1997; 315:396.

5. Frankel s, elwood P, sweetman P, et al: Birthweight, body mass index in middle age, and incident coronary heart disease. Lancet 1996; 348:1478.

6. stein Ce, Fall CH, Kumaran K, et al: Foetal growth and coronary heart disease in south India. Lancet 1996; 348:1269.

7. Osmond C, Barker DJ, Winter PD, et al: early growth and death from cardiovascular disease in women. Br Med J 1993; 307:1519.

8. Leon DA, Lithell HO, Vagero D, et al: Reduced foetal growth rate and increased risk for death from ischaemic heart disease: Cohort study of 15,000 swedish men and women born 1915-29. Br Med J 1998; 317:241.

9. newsome CA, shiell AW, Fall CH, et al: Is birth weight related to later glucose and insulin metabolism?—A systematic review. Diabet Med 2003; 20:339.

10. Huxley RR, shiell AW, Law CM: The role of size at birth and postnatal catch-up growth in determining systolic blood pressure: A systematic review of the literature. J Hypertens 2000; 18:815.

11. Barker DJ, Martyn Cn, Osmond C, Wield GA: Ab-normal liver growth in utero and death from coronary heart disease. Br Med J 1995; 310:703.

12. Barker DJ, Meade TW, Fall CH, et al; Relation of foe-tal and infant growth to plasma fibrinogen and fac-tor VII concentrations in adult life. Br Med J 1992; 304:148.

13. Rich-edwards JW, Kleinman K, Michels KB, et al: Lon-gitudinal study of birth weight and adult body mass index in predicting risk of coronary heart disease and stroke in women. Br Med J 2005; 330:1115.

14. Hypponen e, Leon DA, Kenward MG, Lithell H: Pre-natal growth and risk of occlusive and haemorrhagic stroke in swedish men and women born 1915-29: Historical cohort study. Br Med J 2001; 323:1033.

15. Henry JA, Bolla M, Osmond C, et al: The effects of genotype and infant weight on adult plasma levels of fibrinogen, factor VII, and LDL cholesterol are addi-tive. J Med Genet 1997; 34:553.

16. McCarton CM, Wallace IF, Divon M, Vaughan HG: Cognitive and neurologic development of the pre-mature, small for gestational age infant through age 6: Comparison by birth weight and gestational age. Pediatrics 1996; 98:1167.

17. Low JA, Handley-Derry MH, Burke sO, et al: Asso-ciation of intrauterine foetal growth retardation and learning deficits at age 9-11 years. Am J Obstet Gy-necol 1992; 167:1499.

18. Robertson CM, etches PC, Kyle JM: eight-year school performance and growth of preterm, small for gestational age infants: Comparative study with subjects matched for birth weight or gestational age. J Pediatr 1990; 116:19.

19. smedler AC, Faxelius G, Bremme K, Lagerstrom M: Psychological development in children born

Box 1: Books about The Barker Hypothesis


with very low birth weight after severe intrauterine growth retardation: A 10-year follow-up study. Acta Paediatr 1992; 81:197.

20. sung IK, Vohr B, Oh W: Growth and neurodevelop-mental outcome of very low birth weight infants with intrauterine growth retardation: Comparison with control subjects matched by birth weight and gesta-tional age. J Pediatr 1993; 123:618.

21. Cresswell JL, Barker DJ, Osmond C, et al: Foetal growth, length of gestation, and polycystic ovaries in adult life. Lancet 1997; 350:1131.

22. Michel KB, Trichopoulos D, Robins JM, et al: Birthweight as a risk factor for breast cancer. Lancet 1996; 348:1542.

23. nilsen TI, Romundstad PR, Troisi R, Vattan LJ: Birth size and subsequent risk for prostate cancer: A pro-spective population-based study in norway. Int J Cancer 2005; 113:1002.

24. Richardi L, Askling J, Granath F, Akre O: body size at birth and adulthood and the risk for germ-cell testicular cancer. Cancer Epidemiol Biomarkers Prev 2003;12:669.

25. Hjalgrim LL, Rostgaard K, Hjalgim H, et al: Birth weight and risk for childhood leukemia in Denmark, sweden. norway, and Iceland. J Natl Cancer Inst 2004; 96:1549.

26. Pettit DJ, Aleck KA, Baird HR, et al: Congenital sus-ceptibility to nIDDM: Role of intrauterine environ-ment. Diabetes 1988; 37:622.

27. silverman BL, Metzger Be, Cho nH, Loeb CA: Im-paired glucose tolerance in adolescent offspring of diabetic mothers: Relationship to fetal hyperinsulin-ism. Diabetes Care 1995; 18:611.

28. Pettit DJ, Baird HR, Aleck KA, et al: excessive obe-sity in offspring of Pima Indian women with diabetes during pregnancy. N Engl J Med 1983; 308:242.

29. silverman BL, Landsberg L, Metzger Be: Fetal hy-perinsulinism in offspring of diabetic mothers: Asso-ciation with subsequent development of childhood obesity. Ann NY Acad Sci 1993; 699:36.

30. eriksson J, Forsen T, Tuomilehto J, et al: Foetal and childhood growth and hypertension in adult life. Hy-pertension 2000; 36:790.

31. Barker DJ, Bull AR, Osmond C, simmonds sJ: Foetal and placental size and risk of hypertension in adult life. Br Med J 1990; 301:259.

32. Barker DJ, Thornburg KL, Osmond C, et al: The sur-face area of the placenta and hypertension in the offspring in later life. The International J Develop-mental Biol 2010; 54:525.

33. Forsen T, Osmond C, eriksson JG, Barker DJ: Growth of girls who later develop coronary heart disease. Heart 2004; 90:20.

34. eriksson JG, Forsen T, Tuomilehto J, et al: early growth and coronary heart disease in later life: Lon-gitudinal study. Br Med J 2001; 322:949.

35. eriksson JG, Forsen T, Tuomilehto J,et al: early adi-posity rebound in childhood and risk of Type 2 dia-betes in adult life. Diabetologia 2003; 46:190.

36. DeBoo HA, Harding Je: The developmental origins of adult disease (Barker) hypothesis Australian and New Zealand. J of Obstet Gynecol 2006; 46:4.

37. Van Assche FA, Holemans K, Aerts L: Long-term con-sequences for offspring of diabetes during pregnan-cy. Br Med Bull 2001; 60:173.

38. Dabelea D, Pettitt DJ: Intrauterine diabetic envi-ronment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. J Pediatr Endocrinol Metab 2001; 14:1085.

39. sobngwi e, Boudou P, Mauvais-Jarvis F. et al: ef-fect of a diabetic environment in utero on pre-disposition to type 2 diabetes. Lancet 2003; 361:1861.

40. seckl JR: Prenatal glucocorticoids and long-term programming. Eur J Endocrinol 2004; 151:U49.

41. Phillips DI: Insulin resistance as a programmed re-sponse to foetal undernutrition. Diabetologia 1996; 39:1119.

42. national Institutes of Health; Antenatal cortico-steroids revisited: Repeat courses, nIH Consensus Statement. 2000; 17:1.

43. Liggins GC, Howie Rn: A controlled trial of antepar-tum glucocorticoid treatment for prevention of the respiratory distress syndrome in premature infants. Pediatrics 1972; 50:515.

44. Dalziel sR, Liang A, Parag V, et al: Blood pressure at 6 years of age after prenatal exposure to betametha-sone: Follow-up results of a randomized, controlled trial. Pediatrics 2004; 114:e373.

45. Dalziel sR, Walker nK, Parag V et al: Cardiovascular risk factors after antenatal exposure to betametha-sone: 30-year follow-up of a randomized controlled trial. Lancet 2005; 365:1856.

46. Irving RJ, Belton nR, elton RA, Walker BR: Adult car-diovascular risk factors in premature babies. Lancet 2000; 355:2135.

47. Keijzer-Veen MG, Finken MJ, nauta J, et al: Is blood pressure increased 19 years after intrauterine growth restriction and preterm birth? A prospective follow-up study in the netherlands. Pediatrics 2005; 116:725

48. Leon DA, Johansson M, Rasmussen F: Gestational age and growth rate of foetal mass are inversely associated with systolic blood pressure in young

adults: An epidemiologic study of 165,136 swedish men aged 18 years. Am J Epidemiol 2000; 152:597.

49. siewert-Delle A, Ljungman s: The impact of birth weight and gestational age on blood pressure in adult life: A population-based study of 49-year old men. Am J Hypertens 1998; 11:946.

50. szathmari M, Vasarhelyi B, Reusz G, Tulassay T: Adult cardiovascular risk factors in premature ba-bies. Lancet 2000; 356:939.

51. Hofman PL, Refan F, Jackson We, et al: Premature birth and later insulin resistance. N Engl J Med 2004; 351:2179.

52. Cheung YF, Taylor MJ, Fisk nM, et al: Foetal ori-gins of reduced arterial distensibility in the do-nor twin-twin transfusion syndrome. Lancet 2000; 355:1157.

53. Dwyer T, Blizzard L, Morley R, Ponsonby AL: Within pair association between birth weight and blood pressure at age 8 in twins from a cohort study. Br Med J 1999; 319:1325.

54. Levine Rs, Hennekens CH, Jesse MJ: Blood pres-sure in prospective population–based cohort of newborn and infant twins. Br Med J 1994; 308:298.

55. Loos RJ, Fagard R, Beunen G, et al: Birth weight and blood pressure in young adults: A prospective twin study. Circulation 2001; 104:1633.

56. Poulter nR, Chang CL, MacGregor AJ, et al: As-sociation between birth weight and adult blood pressure in twins: Historical cohort study. Br Med J 1999; 319:1330.

57. Williams s, Poulton R: Twins and maternal smok-ing: Ordeals for the foetal origins hypothesis? A cohort study. Br Med J 1999; 318:897.

58. Zhang J, Brenner RA, Klebanoff MA: Differences in birth weight and blood pressure at age 7 years among twins. Am J Epidemiol 2001; 153:779.

59. Bo s, Cavallo-Perin P, scaglione L, et al: Low birth-weight and metabolic abnormalities in twins with susceptibility to type 2 diabetes mellitus. Diabetic Med 2000; 17:365.

60. Poulsen P, Vang AA, Kyvik KO, et al: Low birth weight is associated with nIDDM in discordant monozygotic and dizygotic twin pairs. Diabetolo-gia 1997; 40:439.

61. Iliadou A, Cnattingius s, Lichtenstein P: Low birth-weight and type 2 diabetes: A study on 11,162 swedish twins. Int J Epidemiol 2004; 33:948.

62. Kyvik KO, Bache I, Green A, et al: no association between birth weight and type1 diabetes mellitus-a twin-control study. Diabetic Med 2000; 17:158.

63. The Barker Theory at www.thebarkertheory.org. Accessed 2/14/2011.



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