Thanks Tina: you've actually posted that before
'cause I had copied it and pasted it into my breastfeeding research file!! Found
it when I went to copy it again!! I have read the whole thing a few times now
and am somewhat reassured that the baby I referred to with a BSL of 0.6 mmol/L
may have had a good counterregulatory response going on since he only had "soft"
signs of hypoglycemia: some jitteryness and slightly increased irritability.
Still unsure of why his BSL would be so low (even supposing mum had zero
colostrum) as his intrapartum stress could not be interpreted as
intrapartum asphyxia in any way. I now have a high index of suspicion that
mum may have actually been gestationally diabetic despite her
reassuring/non-glucose impaired GTT. In which case it would be a transient
hypoglycemia and the lab results should show hyperinsulinemia right? I
hope so. I have been off since so i don't know if the hypoglycemia recurred
which would be the case if baby had some rare metabolic disorder right? Sorry,
thinking zebras now (instead of horses, when I hear galloping).
regards
marilyn
----- Original Message -----
Sent: Thursday, December 16, 2004 2:35
AM
Subject: [ozmidwifery] Re: feeds in 24
hours....
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. ----------------------------------------------------------------------- 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.
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