You wrote
<It's my understanding that the MER is what "brings down" the hind milk.  Is
that correct or have I misunderstood?
<Thanks!
<Cynthia

Yes, I think you could say that the "MER brings down" the hind milk.  But to
be more precise, the way I understand it from the Woolridge and Fisher
article* in Lancet, the fat content of the milk rises throughout the feed.  So
it's not like the bottle of unhomogenized milk that sits in your fridge and
separates into skim on the bottom and cream on the top; it's not like...the
baby drinks up the foremilk and then, POW!  he gets to the hind milk.  It's a
gradual change in fat content, and the longer the baby stays on the
breast---or better, the emptier the baby gets the breast---the creamier the
milk he gets.

It's been described to me as being similar to a sponge.  When the sponge is
sopping wet, water drips out freely.  That's like the foremilk running down
the ducts to collect in the sinuses.  But as you wring the sponge, you get
more water that wouldn't have come out by itself.  The basket cells
contracting are like you wringing the sponge.  Increasing pressure "upstream"
in the alveoli pushes the milk "downstream" toward the nipple.  And what I've
been told---I have no way of knowing whether the physics of this is
correct---is that the fat tends to stick to the walls of the alveolus, so
that's why it doesn't run as freely down the ducts and has to be squeezed out.

But now your question has sent me to the textbook.  Lawrence, 4th edition, pp
79-83.  Milk fat is packaged in globules that look (in the diagrams) as if
they are protruding from the apical side of the cell, just hanging there
waiting to be pinched off and float away into the milk.  So maybe we're not
talking about STICKING to the inside of the alveolus.  Maybe we'rebout being
hitched to the apical surface.  Maybe there's a mechanical effect on the
pinching off process.  Maybe the more the alveolus gets squeezed---which puts
pressure on the cells, with the lumen of the alveolus being the area of least
pressure---the more those little globules get pinched off and float away.

Gee, does the increased pressure inside the cell actually push more fat INTO
the globule?  Hmmm.

And here's another thought.  On page 81 it says "Hormonal control of the
glycerol precursors and the enzymatic release of fatty acids, leading to the
formation of triglycerides, have been associated not only with prolactin but
also with insulin, which stimulates the uptake of glucose into the mammary
cells."  Do you suppose that this means fat is synthesized at a faster rate
when the prolactin level rises in response to suckling?  That would give
another reason for post-prolactin-rise milk to be fattier than pre-prolactin-
rise milk.  It's my understanding that the rate of milk systhesis is pretty
constant, but are the components all synthesized at constant rates?  Where are
our lactation physiology experts? dairy scientists? Anne Magliaro, are you
here on Lactnet?

So would this explain why "drip milk" collected from the non-suckled breast
during a feed on the other breast is fairly low in fat?  (And that's why
premies in those early studies of donor-milk-fed premies didn't gain well.)
The MER is happening in both breasts, yes, but in the non-suckled breast
there's higher pressure in the lumen, because it's full of milk that not being
taken out by the baby.  That higher pressure would push back on the apical
side of the cell, and keep as much bulging out and pinching off from happening
as is happening on the suckled breast.  Is it harder to blow up a balloon if
it's under water with the water pressing on it than it is in the air?  I don't
know.  I'll have to try it.

One more thought.  Fat is lighter than the rest of the milk, so it rises.  So
would a baby nursing prone get higher fat/higher calorie milk than a baby
nursing supine?  Maybe that's one reason the prone positions help babies cope
with oversupply!

Enough speculation for one night.

Peace.  Chris

*(Woolridge MW and C Fisher (1988). Colic, "overfeeding," and symptoms of
lactose malabsorption in the breast-fed baby: a possible artifact of feed
management?  Lancet, 382-384.)