[ozmidwifery] Re: feeds in 24 hours....

[TinaPettigrew]

Hello everyone,

A fantastic resource that provides a wealth of evidence and information on nutrition in the newborn infant is the WHO (1997) literature review  of 'Hypoglycemia in the newborn'.

http://www.who.int/reproductive-health/docs/hypoglycaemia_newborn.htm

In particular, the following paragraphs just demonstrates how wonderful mother nature is at providing for the healthy newborn in the first few days post birth with 'suckling hypoglycemia'

Great to be back on the list!!!
Tina Pettigrew
Midwife (registration pending)
B. Mid.
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Metabolic substrates. Data on metabolic substrate concentrations during early postnatal adaptation in the human newborn are relatively few and many date from the era in which early starvation was fashionable and feeding (usually with formula) was postponed for hours or days after birth (Beard et al, 1966; Melichar et al, 1967; Persson & Gentz, 1966; Stanley et al, 1979; Anday et al, 1981). Principal findings of these studies were, first, that blood glucose concentration falls with the duration of starvation and, second, that the concentrations of other metabolic substrates (free fatty acids, ketone bodies and glycerol) rise as blood glucose concentration falls. For example, Beard et al (1966) alternately allocated term and preterm infants to an "early feeding" group (fed with formula from 6 hours of age) and a group fasted for 72 hours. Mean blood glucose concentration at 72 hours was 40 mg dl-1 (2.2 mmol l-1) in the fasted term infants, as compared to 68 mg dl-1 (3.8 mmol l-1) in the "early-fed" group. 58% of the fasted premature infants had a blood glucose concentration of <25 mg dl-1 (1.4 mmol l-1) by 72 hours of age, as compared to only 4% (1 infant) among the early-fed group; though no complications were noted. The fasted group also showed a reduced increment in blood glucose concentration on injection of glucagon and adrenaline, suggesting a relative reduction in their glycogen stores. Free fatty acid concentrations nevertheless rose in the fasted infants and over 50% of the fasted healthy premature infants showed ketonuria by 48-72 hours of age. Persson & Gentz (1966) similarly noted increases in free fatty acid, glycerol and ketone body levels among fasted term infants. The highest values were noted in babies with the lowest blood glucose concentrations. Increases in the concentration of glucogenic precursors (alanine and lactate) and ketone body concentrations with starvation at this time of life are nevertheless smaller than those in older children with similarly low glucose levels (Stanley et al, 1979; Anday et al, 1981). Moreover it is important to emphasise that the "premature" babies of thirty years ago were probably more mature as a group than preterm infants of today whose adaptive capacity may be even less well developed.

More recently Hawdon et al (1992) conducted a cross-sectional study of whole blood glucose concentration among 156 healthy term babies. This work is of importance for many reasons. Firstly, infants were demand-fed. Secondly, breastfed babies were studied (46% of the sample). Thirdly, metabolic substrates other than glucose (glycerol, lactate, pyruvate, alanine, non-esterified fatty acids, ketone bodies) were measured. Finally, infants were studied throughout the first week and not only in the first eight hours (Stanley et al, 1979) to three days (Beard et al, 1966; Anday et al, 1981). It was shown convincingly that although healthy term breastfed babies had significantly lower blood glucose concentrations than those who were bottle-fed (breastfed: mean 3.6 mmol l-1, range 1.5-5.3 mmol l-1; bottle-fed: mean 4.0 mmol l-1, range 2.5-6.2 mmol l-1), their ketone body concentrations were elevated in response. A statistically significant negative correlation between [log] ketone body and blood glucose concentration was measured at 2-3 days of age, but not within the first 24 hours or after 3 days. Lucas et al (1981) also found breastfed babies to have significantly higher ketone body concentrations than formula-fed babies studied on the sixth day of life. In summary, blood glucose concentration falls in babies who are not fed. But healthy term babies of appropriate weight for gestation (AGA) mobilise alternative metabolic substrates (free fatty acids and ketone bodies) in response. Breastfed babies as a group have lower blood glucose concentrations (referred to later as "suckling hypoglycaemia") and higher ketone body levels than those who are bottle-fed. It is not clear whether this reflects specific promotion of ketogenesis (e.g. by breastmilk fat or another milk component), or whether it is simply the result of differences in blood glucose concentrations and postprandial increments in plasma insulin concentration.

AND

The newborn's capacity to promote ketogenesis in the face of "suckling hypoglycaemia" has been described previously (Section 2.3). Newborn term infants rapidly increase ketone body flux to rates observed in adults, but only after several days of fasting, flux (i.e. rate of ketone body turnover) being correlated with plasma ketone body concentration (Bougneres et al, 1986). Furthermore, free fatty acid, glycerol (Persson & Gentz, 1966) and ketone body concentrations (Hawdon et al, 1992) are inversely related to blood glucose concentration. Extensive evidence from animal species (Dombrowski et al, 1989; Nehlig et al, 1993), including primates (Levitsky et al, 1977), demonstrates that ketone bodies are important cerebral energy substrates. Owen et al (1967) first demonstrated that the human brain consumes ketones. They catheterised the cerebral vessels of three adults and found that ketone bodies became the predominant cerebral fuel with prolonged (5-6 weeks) starvation.