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Supplementation of the Breastfed Baby
“Just One Bottle Won’t Hurt”---or Will It?
Marsha Walker, RN, IBCLC ([log in to unmask])
Background
The gastrointestinal (GI) tract of a normal fetus is sterile
the type of delivery has an effect on the development of the intestinal
microbiota
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
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
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
The neonatal GI tract undergoes rapid growth and maturational change
following birth
Infants have a functionally immature and immunonaive 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
infant formula should not be given to a breastfed baby before gut closure
occurs
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 gram-positive
flora (Brown & Bosworth, 1922; Gerstley, Howell, Nagel, 1932)
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)
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)
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 b-lactoglobulin 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
postamble();
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