Lisa,

I feel "qualified" to answer some of your questions about Peter Hartmann's
research, as I have heard him speak about all this on more occasions than I
can recall, over a period of many years, and as his findings have unfolded.
I live in the same city (Perth) as Peter and he generously give much time
to NMAA (and NMAA generously gives lots of time to him, ie the mothers he
uses are NMAA Counsellors and members).

Thus, a
>possible explanation for why some babies are "snackers" while others are
>"feasters"! I see a great application for this re: Prep for
>Parenting/Babywise: could it be that the mothers who "fail" on the prescribed
>schedule do so because they physiologically *cannot* provide enough milk at
>his intervals, though they can do so over 24 hours? And are the "success
>stories" of those women who have large storage capacities?

I would say undoubtedly YES!!!

>Of course, by embracing this aspect of Peter's research and applying it this
>way, I am excluding other research that has noted minimum #'s of breastfeeds
>per day as apparent necessity for guaranteeing milk supply. Or are they
>really an average of all of Peter's women? I'm wondering.

Again, I would say "Yes". I assume Peter showed the graphs of his two
mothers that are each end of the spectrum (he uses these 2 a lot as they
show the point so clearly). The large storage capacity mum who needed to
feed only a few times a day is a bit exceptional, I think. The majority of
mothers would be in between, so I think as a guideline for practical
purposes, we do need to keep talking about minimum numbers of feeds to
maintain supply.


 How does this apply to the transfer of drugs into
>milk? I have operated under the belief that much of the milk is made at the
>time of nursing/pumping, and that the blood levels at that time are important
>for determining transfer. Do we not tell mothers to time their doses
>accordingly to minimize transfer? And yet, Peter Hartmann's research suggests
>to me that milk is synthesized continuously at more constant, though
>changing, rates, depending upon current milk volume!

This used to puzzle me also, but I have since heard pharmacists talk about
this and it does fit in. My understanding of what is happening is that the
milk is synthesised and is there, but there is a dynamic process of
exchange going on, so that drugs pass back and forth between milk and blood
according to relative levels and the drug's dynamics (protein-binding,
etc). So as plasma levels fall, more drug is drawn back from the milk that
is there. So when serum levels are low, baby drinks the milk with low
levels of the drug.


>Now, what is there to say about multiple MER's?  Are they more frequent in
>women with smaller storage capacities not only because they don't store as
>much at one time, but because perhaps the rate of sythesis remains higher for
>them because complete emptying occurs sooner and more frequently? Do they
>actually have more milk to "let down" because they are producing it more
>quickly than mothers with large capacities?  Does this explain the varying
>MER patterns that we see with women?

I am not sure if this relates to multiple MER's at all. I understood that
all have multiple MER's and that it just a difference in perception of
them. I assume that baby gets less or equal to what's available at any one
feeding (according to what he wants), and if the storage capacity is small,
he just asks for more frequent feeds.

>-Human milk not just a food; also complements immaturity of organs in
> infants

Peter, being a biochemist, is very convincing on this one. All those
wonderful growth factors, etc that artificially fed babies miss out on. You
wonder how this affects their whole makeup.


>-Lactogenesis occurs between 30-40 hrs from withdrawal of progesterone,
> which is removal of placenta

Peter points out that this does not correlate (ie it is usually earlier)
than when mothers notice milk "coming in". And in his studies, he has found
no such sudden change - interesting compared to what *seems* to be
happening.

>-It is the large protein of casein that makes cow's milk look "thicker" and
> more substantial than human milk (there's that normalizing the  abnormal
>again!)

This is the basis of the old wives' tale about human milk being "watery"
and thin. (I avoid using these terms - they sound so negative.) Peter
suggests we tell mothers that the concentration of nutrients in human milk
is the same or greater than in cow's milk - it is just the casein that
makes the cow's milk look whiter.


>-"Quiescent" cells---> reserve cells that may not always be in use for milk
> production, but may be recruited later on down the line. (Does this  perhaps
>explain the dilemma of relactation? Do some women have  these extra cells,
>and others not, to call on after involution of primary cells?)

I'm not sure if this is related. I would assume at the beginning of
lactation all mothers have these reserve cells. I think with relactation,
one factor might be how the initial breastfeeding went - was there extreme
engorgement that might have caused rapid involution? etc that would tend to
more permanently shut down lactation. From a thread on Lactnet some time
ago, it was decided that rate of involution in general was *very* variable
- some still having milk years after weaning, so perhaps this would explain
the variability for relactation to a great extent. Could it be to do with
hormones? I don't really know.

Any other comments from others?

Joy Anderson IBCLC, NMAA Breastfeeding Counsellor,
Perth, Western Australia
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