Womb to World: A Metabolic Perspective
Editor’s note: This article first appeared in Midwifery Today, Issue 61, Spring 2002.
Subscribe to Midwifery Today Magazine
Postnatal transition from fetus to neonate is characterised by discontinuity. Inevitably the neonate must change environment from the dark, warm, wet, sheltered place in the womb to the colder, dry, bright, loud conditions of the world; the umbilical cord is severed. Separation and rupture are the watchwords. Well-known changes require thermal, cardiovascular, pulmonary, vestibular, immune and metabolic adaptation.
Cardiopulmonary, immune and thermal adaptations are well documented in the medical and midwifery textbooks. Successful metabolic adaptation is just as critical to infant well-being. Yet, most midwifery and many pediatric texts fail to describe the normal physiology of metabolic transition from fetus to neonate. Instead, metabolic adaptation is discussed in chapters devoted to hypoglycemia or in relation to disorders of blood glucose homeostasis.
Just as neonatal heart rate, respirations and colour make cardiopulmonary transition tangible for midwifery assessment, neonatal nutrition offers a window into the assessment of metabolic adaptive processes. However, many current practices hinder an understanding of the normal physiology:
- Metabolic transition is not generally taught in midwifery and medical curricula as part of normal postnatal adaptation from fetus to neonate. Descriptions of metabolic changes are absent or sparse. When present, they are usually rooted in pathology.
- Research has shown that patterns of metabolic adaptation are different according to whether the baby is breastfed or has artificial feeds (Hawdon et al., 1992; Del Rooy et al.,1998; Hawdon et al., 2000). This is largely ignored in midwifery and pediatric assessment. Mixed feeding is common in the first three days postnatal even when the mother wants to breastfeed exclusively.
- Furthermore, in the early postnatal days, current breastfeeding definitions disregard dose. A baby is considered to be breastfed when receiving any amount of mother’s milk, however small. Not knowing whether the baby is exclusively breastfed blurs the understanding of those clinical characteristics associated with a baby who is wholly breastfed.
- Mothers are often encouraged to swaddle their babies from birth and to keep them in the cot unless they are actively feeding. This practice assumes that the continuity of maternal nutrition ends at birth as in bottle-feeding. Immediate swaddling also accentuates the discontinuity of postnatal transition, as mothers are physically separated from their babies even when they are in the same room. The early physical separation negates the continuity and postnatal effectiveness of the maternal body to maintain a homeostatic neutral/thermal environment from fetus to neonate. Keeping babies in the cot in between feeds instead of holding them during the first three days postpartum may have a negative effect upon early nurturing and breastfeeding (Colson and Hawdon, 2002).
- Maternal choice rather than physiology provides the framework that underpins midwifery assessment. When there are breastfeeding problems in the first three days postnatal, a bottle-feeding solution is often offered. For example, when the baby is being demand breastfed and is unsettled, it is often believed that mother’s early colostral milk is insufficient. Mothers are often told that they can give the baby a bottle if they want. The irony is that maternal choice then appears to motivate supplementation. One often sees written in the notes “baby unsettled, mother requested bottle.”
Research demonstrates the biological specificity and the benefits of exclusive breastfeeding from birth to six months postnatal (Inch, 1996; Lawrence, 1997; World Health Organization [WHO], 2001). Epidemiology reveals short- and long-term health benefits for mother and baby associated with breastfeeding (Inch, 1996; Lawrence, 1997). Many of these appear to be dose related. For example, research has demonstrated associations between increased respiratory and urinary tract infection, infantile gastrointestinal illness, obesity, asthma, early-onset insulin-dependent diabetes, and lower cognitive and acuitive functions with early introduction of artificial formula (Lawrence, 1997). In view of these dose-related benefits, it is surprising that more mothers do not wholly breastfeed during the first three days postpartum. Conflict has been identified between policies for breastfeeding and some of those to prevent neonatal hypoglycemia (Dodds, 1996; Colson, 1997). The first policies require that breastfed infants be given no food or drink other than mother’s milk. The latter policies stipulate supplementation, defined as pre-calculated amounts of infant formula, to be given to healthy tiny infants and healthy problem feeders even when breastfeeding is going well (Lucas, 1992; Dodds, 1996; Thureen et al.,1999). Supplementation in hospital is strongly associated with decreased maternal confidence and decreased rates of breastfeeding duration (Blomquist, et al., 1994; Dodds, 1996; Foster et al., 1997).
In this article it is assumed that a diet composed exclusively of mother’s milk during the first three days postpartum is the fodder for the physiology of metabolic transition from fetus to neonate. Exclusive breastfeeding is defined as the suckling that both mother and baby do together. This means baby ingests nothing but mother’s milk. Recent research has suggested that active suckling (as opposed to the baby being the passive recipient of expressed breast milk) may be a factor that facilitates exclusive breastfeeding from birth (Colson and Hawdon, 2002). This differs slightly from current definitions of exclusive breastfeeding. For a healthy term infant during the first three days of life, active suckling and participation in feeding are deemed as essential as an exclusive diet of mother’s milk. There is a difference between actively sucking at the breast and being cup/bottle fed mother’s milk. That does not deny the benefits of expressing milk for very preterm infants, sick infants or any infant unable to breast-suckle. For healthy babies who have suckling reflexes, it is preferable and may make breastfeeding feel more natural when the baby is an active participant.
Physiology of Metabolic Transition
(A simplified version of complex processes)
Just after birth, as soon as the umbilical cord ceases to pulsate, placental circulation stops abruptly. This means that the constant supply of maternal nutrition, and in particular, glucose transferred via the placenta, ends. Neonatal blood glucose levels immediately fall in almost all healthy infants (Srinivasan et al., 1986). The newborn must adapt to intermittent feeding, digestion and intestinal absorption of nutrients. Fetal life is dominated by insulin. Glucagon is mainly switched off during fetal life. This results in insulin being used as a growth hormone rather than as a metabolic regulator. At birth, lipogenesis (formation and storage of fat in the form of adipose tissue) and glycogenesis (formation and storage of glucose in the form of glycogen in the liver, cardiac muscle and brain) are replaced by the metabolic pathways of neonatal life. These are glycogenolysis (breakdown of glycogen), lipolysis (breakdown of fats), gluconeogenesis (endogenous glucose production) and ketogenesis (formation of ketone bodies). These pathways imply a metabolic switch at birth from glucose to fat and therefore a diet initially lower in carbohydrate and high in fats.
During pregnancy, the changes in maternal metabolic activity are specifically designed to help maintain optimal fetal nutrition. The maternal body builds, saves and stores. This means that the mother sends a constant supply of sugar straight to her baby’s blood via the placenta. The baby therefore grows, saves and stores. Fetal life is characterised by anabolism; the healthy term infant comes into the world “well fed.” Healthy term babies are born with glycogen stores and chubby baby fat stores to meet their needs in the first days while they are finding and learning how to latch onto the source of their extra-uterine food supply—the breast.
During approximately the first three days of life, the healthy term baby learns how to organise sucking, swallowing and breathing. After birth, the mammary gland ensures a smooth transition and takes over from the placenta to maintain a diet specific to the needs of the human offspring. Early mother’s colostral milk is high in medium and long chain fatty acids and lower in carbohydrate. Research has shown that the mean volume of early mother’s colostral milk is 37 milliliters: range 7 to 123 milliliters (Hartmann and Prosser, 1984; Hartmann, 1987). This physiological design corresponds to the baby’s reduced needs (on average equivalent to a little over an ounce during the first 24 hours of life). A larger quantity forces the baby to glug and may overwhelm the baby during the time needed to coordinate sucking, swallowing and breathing. Early mother’s colostral milk arrives in drips and drops as the suckling finds the breast, latches on, organises needs, latches off, sleeps and is breast-nurtured. Small amounts of early mother’s colostral milk are frequently ingested. This nourishes the baby appropriately, maintains physiological blood glucose concentrations and has a laxative effect to promote early evacuation of meconium. Because a large amount of milk is not ejected, infants who are exclusively breastfed in the first three days usually do not vomit.
A striking point of continuity from fetus to neonate is that a mother’s body is apt and specifically designed to nurture her infant. At birth, physiology suggests that the baby has a major change in fuel type. Glucose supplied via the placenta is replaced by fat from early mother’s colostral milk and chubby baby fat stores. Early neonatal life is characterised by catabolism. This catabolic state does not, as in adult metabolism, imply pathology, but rather indicates a normal progression of metabolic change. After birth, plasma insulin levels fall as the Hypothalamic-Pituitary-Adrenal (HPA) axis wakes up. There are rapid surges of the stress hormones and pancreatic glucagon release (Hawdon and Aynsley-Green, 1999). These hormonal changes trigger the release of the enzymes required for the formation of energy fuels to meet the particular needs of the neonate (i.e., to meet the initial requirement of a diet high in fat and lower in carbohydrates).
Although successful metabolic adaptation involves intricate biochemical processes, for a majority of healthy infants the transition from womb to world progresses smoothly. However, recent fears concerning hypoglycemia have resulted in early hospital practices that often require routine admission to special care and supplementation with artificial milk even when the mother wants to breastfeed exclusively. Along with supplementation, admission to special care is associated with decreased maternal confidence and decreased rates of breastfeeding duration (Hawdon, 1993).
What is Neonatal Hypoglycemia?
Ask 20 health professionals what is meant by neonatal hypoglycemia and you will probably get 20 different answers. Simply put, hypoglycemia means less than a “normal amount” of circulating blood glucose (blood sugar) below which harm will occur. Under “ordinary circumstances” the adult brain and central nervous system are obligate consumers of glucose. Like hypothermia, hemorrhage-induced hypovolemia and hypoxia, glucose deprivation, is a major stressor, a challenge to the homeostasis of any mammal. Just like any of the above stressors, prolonged acute hypoglycemia will result in brain damage or death.
What remains complex is how to define “ordinary conditions” and a “normal amount” of neonatal blood glucose concentration. The normo-glycemia range in adults is 3.9 to 6.1 mmol/l (70–110 milligrams per deciliter). These numbers have been calculated statistically using a blood glucose concentration of more than 2 standard deviations above and below the mean for populations of well adults. A similar glycemia index for neonates is problematic as regards definition, significance and clinical management.
There is no medical consensus concerning the normo- to hypoglycemia cut-off point. A review of 35 pediatric textbooks and a survey among 178 pediatricians revealed a combined range of normal from less than 1 to 4 mmols/l (Koh, 1988). More recent research has demonstrated normo-glycemia concentrations from less than 1.5 to 6.2 mmols/l for healthy term infants (Hawdon et al., 1992) and from 1.4 to 5.3 mmols/l (Hoseth et al., 2000). Healthy breastfed infants have lower blood glucose concentrations than infants who are fed artificial formula. (Hawdon et al., 1992; Hawdon et al., 1992; Del Rooy, 1998; Hawdon et al., 2000).
The research design of earlier studies often lacks scientific rigour. Researchers examining neonatal hypoglycemia often fail to control for feeding methods, and when they do, exclusive breastfeeding often remains undefined. Furthermore, preterm babies are often grouped together with healthy and/or sick infants regardless of gestational age (GA). The actual age of the baby in days postnatal is rarely taken into consideration. Recommendations for practice resulting from such studies often extrapolate results for sick infants or younger GA groups who are older in actual age to normal healthy term infants during the first three days postnatal.
A large retrospective observational study examined the effects of hypoglycemia in a convenience subset of 661 preterm infants who weighed less than 1850 grams at birth and survived the first 48 hours (Lucas et al., 1988). No baby was exclusively breastfed. The findings of this seminal study indicated that, in this group of sick, very low birth weight babies, those who had blood sugar concentrations lower than 2.6 mmols/l on five or more separate days had adverse neurological outcomes. Instead of suggesting that these sick grossly preterm infants be closely supervised, findings were extrapolated to healthy term infants during the first three days postnatal. Recommendations for practice suggested that neonatal blood glucose levels be routinely maintained at or greater than 2.6 mmols/l for all babies from birth regardless of GA and health.
Since 1988, 2.6 mmols/l has been a widely used definition of neonatal hypoglycemia. This means that extrapolated data informs policy and practice in many maternity units both in the UK and the United States. Because of these recommendations, healthy babies are often screened (drawing blood through heel or finger pricks) and supplemented with artificial feeds accordingly. It would be as if the rationale supporting postnatal maternal feeding policies were underpinned by research demonstrating that some mothers who developed gestational diabetes had neurological sequelae following successive episodes of postnatal hypoglycemia. Suppose all mothers who declined to eat after birth were screened for hypoglycemia and fed an artificial energy drink via naso-gastric tube in the early postnatal period!
Even though these views have been recently challenged by a number of experts in the field (Cornblath et al., 2000), most hospital policies continue to use 2.6 mmol/l as the cut-off point to define neonatal hypoglycemia.
Neonatal hypoglycemia is often not associated with clinical signs. Any suspicious clinical signs are usually non-specific; that is, they could be related to many different conditions. The non-specificity of clinical signs has led to routine management criteria for those babies considered at risk of neonatal hypoglycemia. These fall into three broad categories:
- Very large (greater than 4 kg) or very small (less than 2.5kg) and growth restricted infants
- All infants born before 37 completed weeks of gestation
- Any infant on postnatal ward who is not feeding well
The first recommendation for treatment is always to “feed the baby.” Again misunderstanding of the physiological design behind the relatively small amounts of early mother’s colostral milk prompts supplementation with artificial milk. However, giving bottles of artificial formula does not always raise blood glucose concentrations. Recent research has demonstrated that giving artificial formula feeds to supplement or complement breastfeeds suppresses ketogenesis, in an inverse relationship to the amount of artificial formula given (Hawdon et al., 2000). This routine practice often disturbs breastfeeding. For the metabolically compromised infant, exclusive bottle feeding may exacerbate the very condition it sets out to treat. In the eyes of the physiologist, early mother’s colostral milk and artificial formula milk are not interchangeable!
There is no research concerning the length of time that mild hypoglycemia is harmful for the healthy term neonate during the first three days postnatal (Hawdon, 1999; Cornblath et al., 2000). However, a couple of hours of low blood glucose concentrations appear to be physiological following birth (Srinivasan et al., 1986).
Neonatal hypoglycemia has been called “an ill-characterised clinical entity” (Williams, 1999). Williams points out that unreliable bedside screening techniques aggravate the problem. Taken together the findings highlight the futility of defining neonatal hypoglycemia using numbers. Consultant neonatalogists such as Hawdon, Williams and DeRooy and Cornblath et al., in the U.S., avoid rigid numerical cut-off levels (Cornblath et al. 2000). Instead, they look at neonatal glycemia on a continuum. The definition of neonatal hypoglycemia should be “the lowest concentration of glucose which in combination with other metabolic fuels allows normal brain function” (Aynsley-Green and Hawdon, 1997). This will vary in a range of normal patterns during postnatal transition and from one individual baby to another. During the first three days, postnatal threats to the normo-glycaemia continuum are cold stress (in particular), infant crying and any hospital practices that interrupt frequent ingestion of the drips and drops of mother’s early colostral milk. Healthy infants for whom there are concerns require a full clinical assessment of feeding and neonatal well-being to rule out a wide range of pathologies, e.g., infection. A blood glucose concentration in isolation offers very little diagnostic information. Knowledge of the normal neurology and range of feeding patterns of babies is essential.
An operational definition of hypoglycemia is not a midwifery remit but midwives are involved. As the guardians of the normal, they are responsible for detecting any deviation from neonatal well-being as early as possible. This requires advanced clinical assessment skills, an awareness of the individuality of the neonatal metabolic profile and a basic understanding of some elegant protective physiological mechanisms during the first three days of neonatal life.
A Neonatal Perspective
It is common to regard infants as miniature carbon copies of adults. Whereas, in fact, the opposite is probably true. From an evolutionary perspective, what an animal is or does is governed by events that have happened, not by events that are going to happen (Morgan, 1994). The adult brain is an avid consumer of glucose. Findings from studies on rats and human neonates where early diet was composed of exclusive colostrum suggest that neonatal body economy may be regulated differently from that of the adult (Widmaier,1990). Widmaier highlights that the HPA axis of mammals is not fully functional throughout the mammalian life cycle. During pregnancy and the first weeks of postnatal life, the relatively dormant state of the HPA axis “raises questions of whether glucoprivation is a true neonatal stressor as the term applies to the adult” (Widmaier, 1990). For Widmaier, it is clear that an understanding of the regulation of neonatal glucose homeostasis in the first days postpartum goes hand in hand with an understanding of the development of the HPA axis at the same period. Widmaier compares the stress of hypoglycemia to hypoxia. In adult mammals hypoxia results in a rapid predictable increase in the activity of the HPA axis. However, hypoxia fails to elicit much of an increase in plasma ACTH or glucocorticoids in neonatal rats. Although hypoxia is one of the most common and potentially damaging stresses for the neonatal mammal, there is a relative neonatal resistance to the effects of oxygen deprivation at least in the short term. Faced with an hypoxic episode, Widmaier describes a unique neonatal compensatory ability that is subsequently “lost in the adult.”
Research concerning human neonates demonstrates that the newborn infant relies upon a number of mechanisms that may offer protection from the effects of the physiological systemic glucopenia that commonly occurs during the first days postnatal. These include intracerebral glycogen stores, low glucose requirements, modulating cerebral blood flow and utilisation of alternative fuels, such as lactate and ketone bodies (Hawdon, 1999).
Ketosis, although usually pathological for adults, may reflect appropriate and counter-regulatory neonatal physiological responses. The neonatal rat is well equipped to utilise ketone bodies for energy even in the fed state and ketone bodies begin to rise dramatically in neonatal plasma within the first 24 hours after birth (Widmaier, 1990). Like mother’s colostrum, rat colostrum has a high fat content. Widmaier asserts that it is not surprising that the neonatal brain would be biochemically competent to make efficient use of this fuel source. Hawdon et al. (1992) have characterised similar patterns of metabolic adaptation in healthy term breastfed human neonates of appropriate birthweight for gestational age. Their findings indicate that when blood glucose concentrations are low, ketone body concentrations are high. Ketone bodies result from the beta oxidation of fatty acids utilising either body fat stores or fat from milk. Hawdon’s research on human neonates shows that ketone body concentrations peak on the third day postnatal. This has been called suckling ketosis, and probably provides an alternative cerebral fuel particularly well adapted to the needs of the neonatal brain. Hawdon highlights that there is no doubt that hypoglycaemic brain damage does occur, but the severity and duration of low blood glucose levels required to cause harm varies between subjects and is related to the ability of each baby to mount a protective response (Hawdon et al., 1992).
More recent research evidence suggests that healthy but moderately preterm infants (34 to 36 completed weeks’ gestation) and healthy small/large for gestational age infants generate ketone bodies like healthy term infants when they are wholly breastfed (Hawdon et al., 1992; DeRooy, 1998; Hawdon et al., 2000). We found that the ability of these healthy but vulnerable infants to generate ketone bodies was largely related to breastfeeding/supplementation strategy.
A strategy to facilitate breastfeeding and therefore postnatal adaptation consists of encouraging mothers to hold their babies from birth in close body contact as often as they want in an undisturbed environment. Regardless of feeding intention, mothers are encouraged to enjoy frequent cuddling during the first hour following birth and during the first three days postpartum. The strategy is called biological nurturing and is based upon the strategy used during the research mentioned above, examining breastfeeding and metabolic adaptation for moderately preterm infants (Colson, 2000; Colson and Hawdon, 2002).
What Is Biological Nurturing?
Biological nurturing is explicitly defined as any mother/baby behaviour at the breast where the baby is in close chest contact with the mother’s body contours. For the baby, biological nurturing means:
- Mouthing, licking, smelling, nuzzling, and nesting at the breast
- Sleeping at the breast
- Groping and rooting at the breast
- Latching onto the breast
- Sucking, swallowing, glugging breast milk through active feeding
For the mother, biological nurturing means:
- Holding the baby so that baby’s chest is in close contact with a maternal body contour
- Offering unrestricted access to the breast with as much skin-to-skin contact as mother desires
Under physiological conditions, maternal and neonatal oxytocin is released simultaneously stimulating metabolic and behavioural effects that promote further maternal-neonatal contact (Uvnas-Moberg, 1996; Uvnas-Moberg et al., 1998). When physical contact between mother and infant is unrestricted following birth, peripheral concentrations of oxytocin in the maternal circulation seem to be higher in the first hour than immediately before birth (Nissen et al., 1996). At the same time, in a protected and unhurried atmosphere, physiological beacons of smell (Varendi et al., 1994; Righard, 1995) may light the way to the breast. During the first days of extrauterine life, the newborn demonstrates a few instinctive actions for finding and latching onto the breast (Pryor, 1963; Odent , 1977; Widstrom et al., 1987). Mothers demonstrate natural preference for holding their infants (DeChateau, 1987). Even though certain labour ward practices may mask instinctive competence (Righard, 1990), biologically it is the suckling baby who takes the initiative in feeding. The baby’s body on or closely wrapped around the mother’s body seems to trigger breastfeeding reflexes, while the infant cues elicit maternal responses in a reciprocal manner (Colson 2000; Colson and Hawdon, 2002). The above is part of the theoretical framework that underpins the concept of biological nurturing. Taken together with some early evidence from the 1960s and 1970s (Winnicott, 1964; Brazelton 1973; Klaus and Kennell, 1976), the wealth of research about Kangaroo Mothering Care (Anderson , 1989; Luddington-Hoe, 1993; Anderson, 1999), and the physiology of metabolic transition, it becomes clear that breastfeeding is a complex nurturing relationship.
The research evidence illustrates two examples of continuity during postnatal transition: continuity of maternal oxytocin and the maternal body as a thermal and nurturing support for feeding. Research has demonstrated an association between longer intervals between feeds and lower blood glucose concentrations (Lucas et al., 1981; Hawdon et al., 1992). Biological nurturing reduces these intervals. The frequency of active feeding is usually increased with a decreased duration during the first three days postnatal.
Of course, it is impossible for mothers to hold their babies constantly. When they take a break, father’s arms provide warmth and security. Many fathers say that biological nurturing is sheer joy and a lovely way to get to know their baby.
In practical as well as biological terms the nutritional, developmental and emotional needs of the newborn infant are met through suckling (McNabb and Colson, 2000). As early as 1954, Grantly Dick-Reed summarised maternal biological capacity to meet neonatal need. He claimed that breastfeeding satisfies neonatal needs for warmth, security and food. These claims have always made good common sense. Research findings now support common sense. Grounded in the continuity inherent in the transition from fetus to neonate, biological nurturing is a “back to the future” strategy that builds upon previous observations (Reed, 1954; Winnicott, 1964; Montagu, 1971; Pryor, 1973). Biological nurturing can help parents explore more traditional nurturing styles and experience the joys of exclusive breastfeeding from birth.
This paper highlights gaps in knowledge both for mothers and midwives. Mothers should be better informed how the biological specificity of their early milk meets the changing needs of their babies. Midwives should have a formal programme of education concerning the physiology of normal metabolic changes from womb to world as well as the theoretical framework that underpins biological strategy. It is urgent for educators to address these gaps in knowledge.
This article summarises the content of a practice development project called CATCHTM. Funded by the UK Department of Health, South Bank University and E. Kent Hospitals NHS Trust, CATCHTM aims to catch in a breastfeeding safety net those mothers who stop breastfeeding during the first two postnatal weeks. Hospital documentation and materials for health professionals are being developed to include:
- the booklet Mother-Baby Experiences of Nurturing
- a mother-baby suckling diary
- a hypoglycaemia hospital policy
- a Nurturing Action Plan (NAP) for healthy but vulnerable (moderately preterm 34–36 weeks gestation and term small for gestational age) infants
- a hospital flow chart to guide health professionals in the support of breastfeeding during the first three days postnatal
- midwifery feeding competencies from a metabolic perspective
- Anderson, G.C. (1989). Skin to skin: kangaroo care in western Europe American Journal of Nursing 89:662–666.
- Anderson, G.C. (1999). Kangaroo care of the premature infant, in E. Goldson (Ed) Nurturing the premature infant: Developmental interventions in the neonatal intensive care nursery. New York: Oxford University Press, pp.131–160.
- Aynsley-Green, A., Hawdon, J.M. (April 1997) Hypoglycaemia in the neonate : current controversies. Acta Paediatr 39(suppl 1): pp. S12–S16.
- Blomquist, H.K., Jonsbo, F., Serebuys F., Persson L.A. (1994). Supplementary feeding in the maternity ward shortens the duration of breastfeeding. Acta Paediatr 83:1122–6.
- Brazelton, T.B. (1973). Effect of maternal expectations on early infant behavior. Early Child Development and Care 2: pp. 259–273.
- Colson, S. (1997). A Cry for Neonatal Research, Midwives 110(1314): p. 174.
- Colson, S.D. (2000). Biological suckling facilitates exclusive breastfeeding from birth a pilot study of 12 vulnerable infants, Dissertation submitted as Course requirement of MSc in Midwifery Studies South Bank University.
- Colson, S.D., Hawdon, J.M. (2002). Biological nurturing increases duration of breastfeeding for a vulnerable cohort. Book of Conference Proceedings, International Confederation of Midwives Conference Vienna, Austria.
- Cornblath,M., Hawdon, J.M., Williams, A.F., Aynsley-Green, A., Ward-Platt, M.P., Schwartz, R., Kalhan, S.C. (2000). Controversies regarding definition of neonatal hypoglycemia: suggested operational thresholds. Pediatrics 105(5).
- DeChateau, P. (1987). Left-side preference in holding and carrying newborn infants: A three-year follow-up study. Acta Psychiatr Scand (75): pp. 283–86.
- DeRooy, L., Williams, A.F., Lawrence, S.M., Thurston, J.G., Colson, S. (1998). Breastfeeding augments metabolic adaptation in small for gestational age and preterm neonates. European Society for Paediatric Research Conference, Belfas.
- Dodds R. (1996). When policies collide: breastfeeding and hypoglycaemia. MIDIRS Midwifery Digest 6(4): 382–386.
- Foster, K., Lader, D., Cheesbrough, S. (1997). Infant Feeding 1995 Office for National Statistics London: The Stationery Office
- Hartmann P.E., (1987) Lactation and reproduction in western Australian women. J Reprod Med (32):543–47.
- Hartmann, P.E., Prosser, C.G. (1984). Physiological basis of longitudinal changes in human milk yield and composition. Fed Proc (43):2448–53.
- Hawdon, J.M., Ward Platt, M.P., Aynsley-Green, A. (1992) Patterns of metabolic adaptation in term and preterm infants in the first postnatal week. Arch Dis Child (67):357–365.
- Hawdon, J.M. (February 1993). Diabetes Neonatal hypoglycaemia: the consequences of admission to the special care nursery. Maternal and Child Health pp. 48–51.
- Hawdon, J.M., Aynsley-Green, A. (1999). Metabolic Disease, Disorders of blood glucose homeostasis in the neonate, in Rennie J.M. and Roberton, N.R.C. Textbook of Neonatalogy. London: Churchill.
- Livingstone (3rd edition).
- Hawdon, J.M. (December 1999). Hypoglycaemia and the neonatal brain. European Journal of Peadiatrics 158(1): pp. S9–S12.
- Hawdon, J.M., Williams, A.F., Lawrence, S.M., Colson, S., Thurston, J.G. (April 2000). Formula supplements given to healthy breastfed preterm babies inhibit postnatal metabolic adaptation: results of a randomised controlled trial. Arch Dis Child (82)suppl 1.
- Hoseth, E., Joergensen, A., Ebbesen, F., Moeller, M. (2000). Blood glucose levels in a population of healthy, breast fed, term infants of appropriate size for gestational age. Arch Dis Child Fetal Neonatal Ed (83): F117–F119.
- Inch, S. (1996). The importance of breastfeeding. MIDIRS Midwifery Digest (6)1: 79–83 and (6)2: 208–212.
- Klaus, M.H., Kennell, J.H. (1976). Maternal-Infant Bonding. St Louis: Mosby Company.
Lawrence, R. (1997). A Review of the Medical Benefits and Contraindications to Breastfeeding in the United States. Maternal and Child Health Technical Information Bulletin. HRSA.
- Lucas, A., Boyes, S., Bloom, S.R., Aynsley-Green, A. (1981). Metabolic and endocrine responses to a milk feed in 6 day old term infants: differences between breast and cow’s milk formula feeding. Acta Paediatr Scand, 70: pp. 195–200.
- Lucas, A., Morley, R, and Cole T.J. (1988). Adverse neurodevelopmental outcome of moderate neonatal hypoglycaemia. BMJ 297: pp. 1304–08.
- Lucas, A. (1992). Infant Feeding Nutritional Physiology Part I: Dietary requirements of term and preterm infants, Part II: Feeding the fullterm infant in Roberton N.R.C. Textbook of Neonatology Edinburgh: Churchill Livingstone.
- Luddington-Hoe, S.M. with Golant, S.K. (1993). Kangaroo Care. New York: Bantam Books.
- McNabb, M., Colson S. (2000). From pregnancy to lactation: changing relations between mother and baby—a biological perspective. Midwifery Practice Core Topics 3.
- Montagu, A. (1971). Touching: The Human Significance of the Skin. New York: Harper & Row.
- Morgan, E. (1994). The Descent of the Child: Human Evolution from a New Perspective. London: Penguin Books Ltd.
- Nissen, E., Uvnas-Moberg, K., Svensson, K., Stock, S., Widstrom, A.M., Winberg, J. (1996). Different patterns of oxytocin, prolactin but not cortisol release during breastfeeding in women delivered by Caesarean section or by the vaginal route. Early Hum Dev (45):103–118.
- Odent, M. (1977). The early expression of the rooting reflex. Proceedings of the 5th international congress of psychosomatics, obstetrics and gynaecology. London: Academic Press.
Pryor, K. (1963). Nursing Your Baby. New York: Harper & Row.
- Reed, G.D. (1954). Childbirth Without Fear. London: Willliam Heinemann.
- Righard, L., Alade, O.M. (1990). Effects of delivery room routines on success of first feed. Lancet (336):1105–07.
- Righard, L. (1995). How do newborns find their mother’s breast? Birth (22) 3: pp. 174–5.
- Srinivasan, G., Voora, S., Lilien, L.D. (July 1986). Clinical and laboratory observations Plasma glucose values in normal neonates: a new look. The Journal of Paediatrics, pp. 114–22.
- Thureen, P.J., Deacon, J., O’Neill, P., Hernandez, J. (1999). Assessment and care of the well newborn. Philadelphia:W.B. Saunders Company.
- Uvnas-Moberg, K. (1996). Neuroendocrinology of the Mother-Child Interaction. Trends in Endocrinology and Metabolism (7)4: pp. 126–31.
- Uvnas-Moberg, K., Alster, P., Petersson, M., et al. (1998). Postnatal oxytocin injections cause sustained weight gain and increased nociceptive thresholds in male and female rats. Pediatric Research 43(3): pp. 344–44.
- Varendi, H., Porter, R.H., Windberg, J. (1994). Does the newborn baby find the nipple by smell? Lancet (344): pp. 989–90.
- WHO (2001). The optimal duration of exclusive breastfeeding—A systematic review online. www.who.int+/inf-pr-2001/en/note2001-07.html
- Widmaier, E.P. (1990). Changes in responsiveness of the hypothalamic-pituitary-adrenocortinal axis to 2-deoxy-D-Glucose in developing rats. Endocrinology 126(6): pp. 3116–23.
- Widstrom, A.M., Ransjo-Arvidson, A.B., Christensson, K., Mathiesen, A.S., Winberg, J., & Uvnas-Moberg, K. (1987). Gastric suction in healthy newborn infants. Effects on circulation and developing feeding behaviour. Acta Paediatr Scand (76): pp. 566–72.
- Williams, A. (1997). Hypoglycaemia of the Newborn: Review of the Literature, World Health Organisation, Geneva, online at www.who.int/chd/publications/imci/bf/hypoglyc/hypoglyc.htm.
- Winnicott, D.W. (1964). The Child, the Family and the Outside World. Harmondsworth, Middlesex, England: Penguin Books Ltd.