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Subject:
From:
Kermaline Cotterman <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Tue, 2 May 2006 10:10:20 -0400
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Jan writes:

<If some women can have insufficient mammary tissue, wouldn't it stand to
reason that some women can have an overabundant amount of functional mammary
tissue producing an amazing amount of milk???>

As Diane says, "Watch our language!" My way of explaining it to a mom in
order that she feels "blessed" instead of "abnormal" has been to explain in
the simplest possible terms that when she was forming inside her own mother,
the development of the breast in its earliest stages involves the growth of
tiny "sprouts", just like roots start to develop from a seed or a bulb in
the garden. Apparently, she received the full normal complement of
"sprouts", whereas some other women get fewer sprouts than others.


And I continue to refer to this as "being blessed with the full potential",
and that since she didn't have twins or triplets this time, that a different
pattern from the one advised for other mothers may be a wiser way to manage
to avoid problems. They have a smile on their faces the whole time we're
solving any problems.



That's usually all the further I go with moms themselves, but for our
purposes here, I think it merits a little more discussion.  About halfway
along in the her mother's own pregnancy, the "sprouts" of the fetus
undergo a process called "canalization" which forms the hollow center.
Apparently, not all "sprouts" undergo this. Surgeons report that many
breasts they see under the microscope have some "blind ducts", so maybe they
remain "blind" as a partial failure of the canalization process. (I'm not
certain if the testosterone of developing male fetuses ever lets them get as
far as canalization, but maybe it does, since boys, too, can have "witches
milk".)


In early puberty in females, when each of these sprouts develops into a
separate lobe, some women (who were gifted with fewer initial secondary
buds) have fewer lobes than others. This enlargement and change period
apparently happens in response to the early start up of the girl's pubertal
ovarian activity. Ovarian cycling (reflected in menstrual patterns)
changes the type I cells of the "TDLU" (terminal ductal lobular units) into
Type II cells. Each lobe develops the TDLU into "lobules" with milk-making
tissue developing like tiny bunches of grapes (alveoli). This gets
complicated and I don't have my references at hand. Apparently, if she never
becomes pregnant, the development of the cell type in the TDLU never
progresses beyond type I and type II. Pregnancy stimulates the development
into type III and type IV cells. (I just attended a fascinating conference
In Toledo on Breastfeeding and Natural Family Planning in which a breast
surgeon explained this non-reversible change in these cells in early
pregnancy in relation to the future risks for development of breast cancer.)



Here is how my reading of some embryological and histological references has
formed the image in my mind.  For purely hypothetical purposes, lets choose
some easy numbers to illustrate the possibilities. The ectodermal layer of
the embryo first forms the primary bud, which soon sprouts secondary buds.
Let's say one female infant was born with what some textbooks say about
eventual # of lobes: 15-20 "sprouts" in each breast bud. I envision these as
7-10 sprouts, most of them branching immediately into two, outward from the
primary bud. This would explain the fact that there are not 15-20 holes in
the nipple, (and the branching place the site of future lactiferous sinuses,
but that's another post;-).


Each of these secondary buds grows inward into the fat pad which is part of
the mesenchyme (connective tissue layer). This fatty tissue is essential to
the inward growth of the ectodermal layer which seems to "invite" inward
growth along into patterned pathways. In laboratory experiments, if the
fatty layer is absent, there is no inward growth. Perhaps we could translate
that into "slight congenital defects" in some areas of the embryonic fat pad
to explain the embryonic growth in those moms who end up with insufficient
glandular tissue. (I have one such mom, who was greatly comforted by the
idea when I presented it that way. I told her she was probably getting the
"full dose" of breastfeeding hormones for bonding and stimulating the tissue
she had, and she was then very happy nursing directly, doing lots of pumping
and using a supplementer for EBM and/or necessary formula calories, always
feeding at the breast. She weaned at 18 months, and is now expecting again.)


I digress (often;-) Purely hypothetically, let's say we have 3 women. #1
received secondary buds to make 15-20 lobes in each breast. #2 received
enough to make 10-15 lobes in each breast. #3 received enough to make 5-10
lobes in each breast. Let's say that every lobe develops 10 lobules, and
every lobule has say-100 alveoli. ( I am totally unaware of actual numbers
under a microscope, but I'm just imagining.) (Generally speaking I believe
this might be more likely in women with larger breasts, but actual bra cup
size probably has very little to do with it, as some women have more
connective tissue than others. Some women could have lots of glandular
tissue and less connective tissue, and have smaller breasts, and still a
large complement of milk making  tissue. Fat is considered part of
connective tissue.) That means that


Woman #1 would have 15-20 lobes, adding up to 150-200 lobules in each
breast, and 15,000 to 20,000 alveoli.


Woman #2 would have 10-15 lobes, adding up to 100-150 lobules in each
breast, and 10,000 to 15,000 alveoli.


Woman #3 would have 5-10 lobes, adding up to 50-100 lobules in each breast,
and 5000-10,000 alveoli.

Or perhaps, or more likely, each breast was a little different from her
other breast. But using the examples above, it seems logical to me that,
receiving the same amount of hormonal stimulation in the blood stream,  the
lactation course of the woman with 20,000 alveoli and 20 main ducts would
have more binding sites for prolactin, more alveolar contents and ductal
storage to respond to oxytocin, etc. etc. than the woman with 5,000 or
10,000 alveoli exposed to the same blood levels of those hormones. So, I
think it would be necessary, in the case of a singleton birth, to make wiser
use of feedback inhibition from the start, perhaps using one side for any
and all feedings in a 2-3 hour period, switching to the other breast for any
and all feedings in the next 2-3 hour block, and eventually, after the
height of engorgement has passed, increasing the length of the time block
gradually. And absolutely no pumping "for comfort" unless a slight bit were
absolutely necessary, because it would remove the ductal contents and the
feedback inhibition the milk could provide. Essentially, more or less the
"first breast first pattern", but switching breasts less often.


Again-no flames-this is purely as I have imagined it, and I don't have time
to access my references for the complicated processes I mentioned.


But again-we must take Diane's advice and watch our language. Such women
were "blessed" with a full complement of potential mammary cells "from their
mother's womb". Perhaps we need to manage them differently. I am not aware
that the technology currently exists to identify just how many lobes the
living breast has, even for research purposes, although it would be very
interesting to check with those in the pathology field what they find on
breast dissection in the laboratory.  BTW, I just learned that Russo and
Russo, very well-known researchers on the breast, are based now in
Philadelphia. Where the ILCA conference is this year! It sure would be nice
to be able to make contact.

Jean
****************
K. Jean Cotterman RNC, IBCLC
Dayton, OH, USA

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