marți, 21 decembrie 2010

“Just One Bottle Won’t Hurt” -- or Will It?

“Just One Bottle Won’t
Hurt” -- or Will It?
Supplementation of the Breastfed Baby
an article by
Marsha Walker
From Health e-Learning
This and many more articles available at of the Breastfed Baby
“Just One Bottle Won’t Hurt”---or Will It?
Marsha Walker, RN, IBCLC (
· The gastrointestinal (GI) tract of a normal fetus is sterile
· the type of delivery has an effect on the development of the intestinal microbiota
o vaginally born infants are colonized with their mother’s bacteria
o 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
· breastfed and formula-fed infants have different gut flora
o 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
o 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
o 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
o 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
o Infants have a functionally immature and immunonaive gut at birth
o Tight junctions of the GI mucosa take many weeks to mature and close the
gut to whole proteins and pathogens
o Open junctions and immaturity play a role in the acquisition of NEC,
diarrheal disease, and allergy
o sIgA from colostrum and breast milk coats the gut, passively providing
immunity during the time of reduced neonatal gut immune function
o mothers’ sIgA is antigen specific. The antibodies are targeted against
pathogens in the baby’s immediate surroundings
o the mother synthesizes antibodies when she ingests, inhales, or otherwise
comes in contact with a disease-causing microbe
o 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
o 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)
o 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)
o 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)
o 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)
o 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)
· 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)
o 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)
o 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)
o 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)
o sensitization and development of immune memory to cow’s milk protein
is the initial step in the etiology of IDDM (Kostraba, et al, 1993)
ß sensitization can occur with very early exposure to cow’s milk
before gut cellular tight junction closure
ß 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
ß 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;
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