>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.
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Katherine A. Dettwyler, Ph.D. email:=
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Anthropology Department phone: (409) 845-5256
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