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From:
"Catherine Watson Genna, IBCLC" <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Sat, 27 Jan 1996 01:13:42 -0500
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Lisa,
Hope this isn't too late to be helpful, have had family illness and not much
time for Lactnet :(
        There are several interacting physiological mechanisms responsible for
milk supply at different times in lactation.  Not all are fully understood or
studied, but here is the picture I have as of this moment:
First 3 days- milk stim by deliv of the placenta, which removes it's prolactin
inhibiting factor (PIF) and allows prolactin to act on the alveoli,
stimulating them to rapidly increase milk production.
First 6 weeks or so- prolactin receptor formation (theory)- the degree of
breast stimulation and milk removal influences the number of prolactin
receptors that proliferate on the milk gland cells.  Receptors are neccessary
for many things to enter cells, the more receptors, the more prolactin can
enter the cell at once to stimulate milk production.  This seems to be a
critical phase, moms who begin to relactate in the first 6 weeks can be more
successful than moms who start later, barring pressure induced atrophy from
unrelieved engorgement.
Degree of Milk Removal- this seems to work hand in hand with prolactin
receptors to provide fine control of milk production from feeding to feeding.
 The more milk is removed from the breast, the less there is to cause feedback
reduction of milk production rates.  The theory is there is something in the
milk itself that feeds back into the stimulation cycle, dampening it.  This is
active throughout lactation.  This is the "autocrine control" theory.  There
is good experimental evidence that residual milk in the breast causes a
reduction in the RATE of milk synthesis between feeds.
Then there's the pressure induced atrophy, I suspect this is the emergency
exit, the ejector seat- when a catastrophe prevents milk from being needed
(fetal demise), the body digests the milk glands in response to unrelieved
engorgement.  Whether alveolar cells die from lack of blood supply (ischemia)
and are then phagocytized (Jay- eaten up by white blood cells, specifically
macrophages or "big mouths") or whether there is some other mechanism is not
well studied, to my knowlege.
        My own feeling here is that all these control mechanisms work together
to allow real fine tuning of milk supply.  If the mom nurses early and often,
and baby sucks well, she will develop good prolactin levels, higher calorie
milk, more prolactin receptors, and keep all her alveoli by avoiding
engorgement.  I personally think that early engorgement is the most damaging
of insults to supply, with lack of stim in the first few weeks being second.
Milk supply seems to be more forgiving later in the process - witness all the
weaning toddlers who go days in between nursings without mom losing supply.
        I usually tell moms that there is usually a better response to efforts
to increase milk supply in the first 6 weeks, but that it is not hopeless
thereafter.  It's sometimes hard to walk that fence between encouraging
someone to try and painting the picture either too rosy or too grey...
        In my practice, moms have regained full milk supplies if they began
relactation efforts in the first 7 weeks postpartum.  One mom with a 3 m.o.
baby was nursing 3x/day and giving formula all other feeds, it took her a
month to work up to exclusive bf, but there were suck issues involved as well.
 Another mom of a 4.5 mo old child had low supply secondary to suck problems,
improving positioning and giving some specific oral support led to increase in
milk supply/above avg weight gain, baby still nursing at 16 mos of age.  These
are the outer limits of my experience with developing and rebuilding milk
supplies.
        There, now I've made up for being scarce for the past few weeks!
Catherine Watson Genna, IBCLC  NYC  [log in to unmask]

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