LACTNET Archives

Lactation Information and Discussion

LACTNET@COMMUNITY.LSOFT.COM

Options: Use Forum View

Use Monospaced Font
Show Text Part by Default
Show All Mail Headers

Message: [<< First] [< Prev] [Next >] [Last >>]
Topic: [<< First] [< Prev] [Next >] [Last >>]
Author: [<< First] [< Prev] [Next >] [Last >>]

Print Reply
Subject:
From:
"katherine a. dettwyler" <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Tue, 24 Oct 1995 14:14:38 -0500
Content-Type:
text/plain
Parts/Attachments:
text/plain (159 lines)
>
>>After all, how long has it been since you were offered a glass of "udder
>>milk" with your cookies?
>
>ROFL -- Really, you guys, the humor on LactNet keeps me going.  At my house
we do distinguish "udder milk" from Mommy milk by calling it "Cows' milk."
Alexander will ask for "Cold cows' milk, in a cup" when that is what he=
 wants.
>
>Here are the sources and references for my comments about immune system
development, and about bf protecting infants who get botulism (from whatever
source).
>
>Dr. Doren Fredrickson has an M.D. and a Ph.D. in Epidemiology, he wrote a
"Commentary" for the book, Breastfeeding: Biocultural Perspectives (1995)
>
>We have long known about the high concentrations of maternal white cells
and antibodies in human milk (Lawrence, 1994).  However, the function of
lymphocytes beyond passive immune protection was not well understood.  We
know that children do not achieve adult immune status until the age of 5 to
6 years.  That is, children--especially infants--are susceptible to numerous
viral and bacterial infections, and blood immunoglobulin levels do not
approximate adult levels until that age (Behrman, Kliegman, Vaughan and
Nelson, 1992).  Recent reports indicate that breastfeeding serves a powerful
immune-enhancing and modulating role during this period of relative immune
incompetence (Hahn-Zoric, Fulconis, Minoli, Moro, Carlsson, Bottiger, Raiha
and Hanson, 1990; Pabst and Spady, 1990).  These studies indicate that the
immune systems of the mother and child are linked by breastfeeding, with the
naivete and incompetence of the child's own immune system bolstered and
enhanced by direct stimulation induced by maternal breastmilk lymphocytes.
In short, the infant's immune system seems to be strengthened and taught
what to attack.  At the same time, the large number of studies reporting
reduced allergic and autoimmune disease among breastfed children (Hanson,
Carlsson, Ekre, Hahn-Zoric, Osterhaus and Roberton, 1989; Lawrence, 1994)
indicate that the infant's immune system is taught what not to attack as=
 well.
>
>Behrman, R.E., R.M. Kliegman, V.C. Vaughan, and W.E. Nelson, eds.
>       1992  Nelson Textbook of Pediatrics, 14th edition. Philadelphia: W.B.
Saunders.
>
>Hahn-Zoric, M., F. Fulconis, I. Minoli, G. Moro, B. Carlsson, M. Bottiger,
N. Raiha, and L.A. Hanson
>       1990 Antibody responses to parenteral and oral vaccines are impaired by
conventional and low protein formulas as compared to breast-feeding.  Acta
Paediatrica Scandinavica 79:1137-1142.
>
>Hanson, L.A., B. Carlsson, H.P. Ekre, M. Hahn-Zoric, A.D. Osterhaus, and D.
Roberton=20
>       1989  Immunoregulation mother-fetus/newborn, a role for anti-idiotype
antibodies. Acta Paediatrica Scandinavica Suppl. 351:38-41.
>
>Pabst, H.F., and D.W. Spady
>       1990  Effect of breast-feeding on antibody response to conjugate vaccine.
Lancet 336:269-270.
>
>
>BOTULISM INFO
>=0CFrom James McKenna and Nicole Bernshaw's chapter in Breastfeeding:
Biocultural Perspectives (1995)
>
>       Infant botulism is an infectious disease that, according to Arnon (1983)
can sometimes masquerade as SIDS.  It results when the ingested spores of
the bacterium Clostridium botulinum germinate, multiply, and produce their
toxin in the baby's intestine (see Arnon, 1983:539).  The toxin, one of the
most potent poisons known, can be carried anteriorly to motor nerve endings,
causing irreversible respiratory muscle paralysis and death, strikingly
resembling SIDS deaths.  The age distribution of infant botulism also
matches closely that of SIDS.  It is estimated that 5% of SIDS cases may be
attributed to infant botulism (Arnon, 1984).
>       With regard to the immunological benefits, it may be noted that SIDS rates
peak at between 2-4 months postpartum (90% of all SIDS deaths occur before
six months) supposedly when maternal antibodies, abundant in the first and
second months of life, are declining, "generally reaching the lowest level
at three months of age before the infant builds up its own immunoglobulin to
achieve immunological independence" (Huang, 1983:593; see also Arnon, 1983).
Such a statement can be misleading, however.  It has been shown, indeed over
two decades ago, that the concentration of IgA decreases rapidly after birth
(17 mg/ml in initial colostrum, 4.1 mg/ml in 2-to 4-day colostrum, 1.8 mg/ml
in milk from 2 to 20 weeks) (Mata and Wyatt, 1971).  These figures take an
entirely different meaning when we take into account the volume of milk that
exclusively breastfed babies ingest daily (between 7 and 137 mls colostrum
on day 1, 500 mls on day 5, 750 mls at 3 to 5 months) (Riordan and Auerbach,
1993).  Multiplying the IgA concentration by the volume of ingested milk per
day yields a relatively constant intake of 1500 to 2000 mg IgA/day,
reinforcing the concept of protective role of breastfeeding through
immunity.  The same concentration/volume phenomenon has been shown recently
in the investigation of gliadin-specific and cow's milk-specific IgA in
human milk (Juto and Holm, 1992).=20
>       A more plausible explanation for the protective role of breastfeeding in
infant botulism may depend in part on "the presence, the specificity, and
the titer of the antibodies in human milk" (see Arnon, 1984).  Human milk
contains secretory A (S-IgA) antibody that can specifically agglutinate
vegetative cells of C. botulinum.  However, "not every woman's milk
contained S-IgA against all strains of C. botulinum tested, and among those
whose milk had agglutinating antibody, substantial variations in titers of
antibody against a given strain was found."  These variations in titers (or
concentrations) of S-IgA would be due to the "mucosal immune system" (Arnon,
1984), also called the "enteromammary immune system" (Arnon, 1983).
Briefly, lymphocytes in maternal gut-associated lymphoid tissue become
sensitized to indigenous antigens, and migrate to the breast where they
produce antigen-specific S-IgA as early as three days after the mother's
ingestion of the antigen.  Therefore, the mother's sensitization to a
specific strain is only one component of the protection.  Assuming the
specific sensitization has occurred, the level of protection conferred to
her infant is then a matter of degree: the higher the titer of S-IgA in her
milk, the greater the protection, and vice versa.
>       The toxicity of the botulism toxin is so great that it is estimated that
as few as 10 to 100 spores may be sufficient to infect an infant (Arnon,
1986).  This, together with variable IgA titers in milk, make it conceivable
that a single exposure to a foreign antigen (e.g., a drop of
Clostridium-containing honey) could seriously compromise the health of
infants breastfed to various degrees.  The relative protective property of
human milk against sudden death from infant botulism is illustrated by the
fact that "all 10 SIDS positive at autopsy for C. botulinum occurred in
infants who had been formula-fed, whereas 50 hospitalized patients were
primarily (but not exclusively=96-author's emphasis) breast-fed" (Arnon,
1984).  This deserves emphasis: all dead infants were artificially fed; all
surviving infants were breastfed.  It follows that if "botulism can be
prevented by proper handling of food and utensils and avoidance of foods
implicated in harboring spores," breastfeeding is the easiest, cheapest and
most effective way to do so (Bernshaw, 1991b).  It also emphasizes the
importance of exclusive breastfeeding that precludes exposure of the infant
to any food potentially containing the botulism toxin.
>
>Arnon, S.S.
>       1983  Breast-feeding and toxigenic intestinal infections: Missing links in
SIDS.  In Sudden Infant Death Syndrome, edited by J.T. Tildon, L.M. Roeder,
and A. Steinschneider, pp. 539-556.  New York: Academic Press.
>       1984  Breast feeding and toxigenic intestinal infections: Missing links in
crib death. Reviews of Infectious Diseases 6(Suppl. 1):S193-S201.
>       1986  Infant botulism: Anticipating the second decade.  J. Infect. Dis.
154:201-206.
>
>Bernshaw, N.B.
>       1991a  Does breastfeeding protect against Sudden Infant Death Syndrome?
J. Human Lactation 7(2):73-79.
>       1991b  Breastfeeding and SIDS=96Reply to Bruen (letter).  J. Human=
 Lactation
7(4):176.
>
>Huang, S.
>       1983  Infectious diseases, immunology, and SIDS: An overview.  In Sudden
Infant Death Syndrome, edited by J.T. Tildon, L.M. Roeder, and A.
Steinschneider, pp. 593-606.  New York: Academic Press.
>
>Mata, L.J., and R.G. Wyatt
>       1971  Host resistance to infection.  American Journal of Clinical
Nutrition 24:976-986.
>
>
----------------------------------------------------------------------------
-------
Katherine A. Dettwyler, Ph.D.                         email:=
 [log in to unmask]
Anthropology Department                               phone: (409) 845-5256
Texas A&M University                                    fax: (409) 845-4070
College Station, TX  77843-4352

ATOM RSS1 RSS2