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Subject:
From:
Cathy Fetherston <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Wed, 8 May 2002 19:32:27 +0800
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I have to say I feel very strongly in support of Patricia's views about one
sided/two sided feeding. I think wherever prescriptive advise is given that
attempts to "manage" the normal breastfeeding experience, mothers are not
encouraged to accept the huge variation that exists in feeding patterns
between women or to learn what is right for them and their baby.

But what I really wanted to comment on was the true and tried, old topic of
prolactin. I did want to reinforce Denise's comment about serum prolactin
not being a regulator of milk production once lactation is established.
However , prior to this, ie at initiation it is probable that the very high
peaks in serum prolactin (seen 45 mins after suckling occurs) do play an
important part in the initiation or establishment of lactogenesis II. Once
however lactogenesis II is established, it appears that serum prolactin has
a permissive role only. My erstwhile colleague Mark Cregan who does a lot of
prolactin research bears the opinion that once lactation is established it
wouldn't matter what the serum prolactin level was, so long as it wasn't
zero - I actually do disagree and feel there is probably a minimum threshold
at which prolactin levels should be maintained, although we donšt know what
this might be.

However milk prolactin at the breast level is a different matter. Prolactin
is actively taken up into the lactocyte from the circulation and it has been
found that prolactin uptake from the blood by the lactocyte is dependent on
the fullness of the breast. For those interested see:

Cregan, Mitoulas & Hartmann. 2002. Milk prolactin, feed volume & duration
between feeds in women breastfeeding their full term infants over a 24 hour
period. Experimental Physiology. 87(2): 207-214.

So milk prolactin perhaps plays a part in the autocrine control of milk
production along with FIL (feedback inhibitor of lactation) and the change
in the milk fatty acids and the change in the morphology of the cell.
Obviously no one has yet elucidated a mechanism that combines all of these
factors, although we think they all probably "do something"

A very quick mention of switch nursing. I donšt think we actually KNOW milk
synthesis does decrease with the length of the feed but using thermography
we have been able to show that breast temperature decreases substantially as
the length of the feed increases (this has been shown over as little as a 15
minute period and has not been published). Because of this we assume that
perhaps milk synthesis is inhibited because of the likely associated decease
in perfusion of the breast.  We recommend switch nursing in low supply for
this reason and it also enables the infant to optimise milk intake.

Cathy Fetherston
Perth, Western Australia

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