Background
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Vaginally born
infants are colonized with their mother’s bacteria.
*
Cesarean born
infants’ initial exposure is more likely to environmental
microbes from the air, other infants, and the nursing staff
which serves as vectors for transfer.
-
Babies at highest risk of colonization
by undesirable microbes or when transfer from maternal sources
cannot occur are cesarean-delivered babies, preterm infants,
full term infants requiring intensive care, or infants separated
from their mother.
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Breastfed and formula-fed infants
have different gut flora.
*
Breastfed babies
have a lower gut pH (acidic environment) of approximately
5.1-5.4 throughout the first six weeks that is dominated by
bifidobacteria with reduced pathogenic (disease-causing) microbes
such as E coli, bacteroides, clostridia, and streptococci
o
babies fed formula
have a high gut pH of approximately 5.9-7.3 with a
variety of putrefactive bacterial
species.
*
In infants fed breast milk
and formula supplements the mean pH is approximately 5.7-6.0
during the first four weeks, falling to 5.45 by the sixth
week.
*
When formula supplements
are given to breastfed babies during the first seven days
of life, the production of a strongly acidic environment is
delayed and its full potential may never be reached.
*
Breastfed infants
who receive supplements develop gut flora and behavior like
formula-fed infants.
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Infants have a functionally
immature and immuno-naive gut at birth.
*
Tight junctions of the GI
mucosa take many weeks to mature and close the gut to whole
proteins and pathogens.
*
Open junctions and immaturity
play a role in the acquisition of NEC, diarrheal disease,
and allergy.
*
sIgA from colostrum and breast
milk coats the gut, passively providing immunity during the
time of reduced neonatal gut immune function.
*
Mothers’ sIgA is antigen
specific. The antibodies are targeted against pathogens in
the baby’s immediate surroundings.
*
The mother synthesizes antibodies
when she ingests, inhales, or otherwise comes in contact with
a disease-causing microbe.
*
These antibodies ignore
useful bacteria normally found in the gut and ward off disease
without causing inflammation.
*
Once dietary supplementation
begins, the bacterial profile of breastfed infants resembles
that of formula-fed infants in which bifidobacteria are no
longer dominant and the development of obligate anaerobic
bacterial populations occurs. (Mackie, Sghir, Gaskins, 1999)
*
Relatively small amounts
of formula supplementation of breastfed infants (one supplement
per 24 hours) will result in shifts from a breastfed to a
formula-fed gut flora pattern. (Bullen, Tearle, Stewart, 1977)
*
The introduction of solid
food to the breastfed infant causes a major perturbation in
the gut ecosystem, with a rapid rise in the number of enterobacteria
and enterococci, followed by a progressive colonization by
bacteroides, clostridia, and anaerobic streptococci. (Stark
& Lee, 1982)
*
With the introduction of
supplementary formula, the gut flora in a breastfed baby becomes
almost indistinguishable from normal adult flora within 24
hours. (Gerstley, Howell, Nagel, 1932)
*
If breast milk were again given
exclusively, it would take 2-4 weeks for the intestinal environment
to return again to a state favoring the grampositive flora.
(Brown & Bosworth, 1922; Gerstley, Howell, Nagel, 1932)
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In susceptible families, breastfed
babies can be sensitized to cow’s milk protein by the giving
of just one bottle, (inadvertent supplementation, unnecessary
supplementation, or planned
supplements), in the newborn nursery during the first
three days of life. (Host, Husby,
Osterballe, 1988; Host, 1991)
*
Infants at high risk of
developing atopic disease has been calculated at 37% if one
parent has atopic disease, 62-85% if both parents are affected
and dependant on whether the parents have similar or dissimilar
clinical disease, and those infants showing elevated levels
of IgE in cord blood irrespective of family history. (Chandra,
2000)
*
In breastfed infants at risk,
hypoallergenic formulas can be used to supplement
breastfeeding; solid foods should not be introduced until
6 months of age, dairy products delayed until 1 year of age,
and the mother should consider eliminating peanuts, tree nuts,
cow’s milk, eggs, and fish from her diet. (AAP, 2000)
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In susceptible families, early
exposure to cow’s milk proteins can increase the risk
of the infant or child developing
insulin dependent diabetes mellitus. (IDDM) (Mayer et al,
1988; Karjalainen, et al, 1992)
*
The avoidance of cow’s milk
protein for the first several months of life may reduce the
later development of IDDM or delay its onset in susceptible
individuals. (AAP, 1994)
*
Sensitization and development
of immune memory to cow’s milk protein is the initial step
in the etiology of IDDM. (Kostraba, et al, 1993)
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Sensitization can occur
with very early exposure to cow’s milk before
gut cellular tight junction closure.
-
Sensitization can occur
with exposure to cow’s milk during an infection-caused
gastrointestinal alteration when the mucosal barrier is
compromised allowing antigens to cross and initiate immune
reactions.
-
Sensitization can occur
if the presence of cow’s milk protein in the gut damages
the mucosal barrier, inflames the gut, destroys binding
components of cellular junctions, or other early insult
with cow’s milk protein leads to sensitization. (Savilahti,
et al, 1993)
References
American Academy of Pediatrics,
Work Group on Cow’s Milk Protein and Diabetes Mellitus. Infant
feeding practices and their possible relationship to the etiology
of diabetes mellitus. Pediatrics 1994; 94:752-754
American Academy of Pediatrics,
Committee on Nutrition. Hypoallergenic infant formulas. Pediatrics
2000; 106:346-349
Brown EW, Bosworth AW. Studies of
infant feeding VI. A bacteriological study of the feces and the
food of normal babies receiving breast milk. Am J Dis Child 1922;
23:243
Bullen CL, Tearle PV, Stewart MG.
The effect of humanized milks and supplemented breast feeding
on the faecal flora of infants. J Med Microbiol 1977; 10:403-413
Chandra RK. Food allergy and nutrition
in early life: implications for later health. Proc Nutr Soc 2000;
59:273-277
Gerstley JR, Howell KM, Nagel BR.
Some factors influencing the fecal flora of infants. Am J Dis
Child 1932; 43:555
Host A, Husby S, Osterballe O. A
prospective study of cow’s milk allergy in exclusively breastfed
infants. Acta Paediatr Scand 1988; 77:663-670
Host A. Importance of the first
meal on the development of cow’s milk allergy and intolerance.
Allergy Proc 1991; 10:227-232
Karjalainen J, Martin JM, Knip M,
et al. A bovine albumin peptide as a possible trigger of
insulin-dependent diabetes mellitus.
N Engl J Med 1992; 327:302-307
Kostraba JN, Cruickshanks KJ, Lawler-Heavner
J, et al. Early exposure to cow’s milk and solid foods in infancy,
genetic predisposition, and risk of IDDM. Diabetes 1993; 42:288-295
Mackie RI, Sghir A, Gaskins HR.
Developmental microbial ecology of the neonatal
gastrointestinal tract. Am J Clin
Nutr 1999; 69(Suppl):1035S-1045S
Mayer EJ, Hamman RF, Gay EC, et
al. Reduced risk of IDDM among breastfed children. The Colorado
IDDM Registry. Diabetes 1988; 37:1625-1632
Savilahti E, Tuomilehto J, Saukkonen
TT, et al. Increased levels of cow’s milk and blactoglobulin antibodies
in young children with newly diagnosed IDDM. Diabetes Care 1993;
16:984-989
Stark PL, Lee A. The microbial ecology
of the large bowel of breastfed and formula-fed infants during
the first year of life. J Med Microbiol 1982; 15:189-203
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