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Nutrition
Journal of Parenteral and Enteral
http://pen.sagepub.com/content/36/1_suppl/49S
The online version of this article can be found at:
DOI: 10.1177/0148607111420155
2012 36: 49SJPEN J Parenter Enteral Nutr
Janice M. Joneja
Infant Food Allergy : Where Are We Now?
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49S
Journal of Parenteral and
Enteral Nutrition
Volume 36 Supplement 1
January 2012 49S-55S
© 2012 American Society for
Parenteral and Enteral Nutrition
10.1177/0148607111420155
http://jpen.sagepub.com
hosted at
http://online.sagepub.com
For many years, the prevailing maxim for prevention of food allergy
in at-risk infants was to reduce allergic sensitization by avoiding
exposure to highly allergenic foods until the baby’s immune and
digestive systems were sufficiently developed to cope with the aller-
gen. Current thinking is completely different: exposure to food in
the early stages of development may be the way to induce toler-
ance. Exclusive breastfeeding until 4–6 months, followed by intro-
duction of complementary foods individually, is recommended. Any
restrictions on mother’s diet, other than avoidance of her own
allergens during pregnancy and breastfeeding, are contraindicated.
If a baby at high risk for allergy (defined as having 1 first-degree
relative with diagnosed allergy) cannot be exclusively breastfed to
4–6 months of age, the preferred method of feeding for the preven-
tion of atopic disease is an extensively hydrolyzed formula. There
appears to be no value in delaying the introduction of any food
beyond 6 months of age. Most food allergy is outgrown in child-
hood, but allergy to some foods tends to persist. Induction of toler-
ance to foods to which a child is allergic may be achieved by
low-dose exposure in a process known as specific oral tolerance
induction (SOTI). Early results indicate that some probiotic strains
of bacteria, such as Lactobacillus rhamnosus GG or Lactobacillus
F19, may reduce allergic sensitization. (JPEN J Parenter Enteral
Nutr. 2012;36:49S-55S)
Keywords: food allergy prevention; pediatric food allergy
management; probiotics in food allergy prevention; allergy
nutrition; specific oral tolerance induction (SOTI)
Infant Food Allergy:
Where Are We Now?
Janice M. Joneja, PhD
Financial disclosure: The publication of the supplement in which this article appears is sponsored by Nestlé Nutrition Institute.
high-risk infants have been used; the prevailing definition,
published as a joint statement of the European Society of
Paediatric Allergology and Clinical Immunology (ESPACI)
and the European Society for Paediatric Gastroenterology,
Hepatology and Nutrition (ESPGHAN)1 and the American
Academy of Pediatrics,2 defines high-risk infants as those
with at least 1 first-degree relative (parent or sibling) with
documented allergic disease, and most authorities rely on
this definition as the basis of their assessment of the at-
risk-for-allergy pediatric population.
Sensitization to food allergens occurs mainly in the
first year of life, and cow’s milk allergy is often the first
food allergy to appear in susceptible infants. The inci-
dence of allergy in children of allergic parents is signifi-
cantly greater than in children of nonatopics; it is
estimated that genetic factors account for 50%–70% of
asthma and allergy.3 However, many children who develop
atopic diseases during the first years of life come from
families without any history of allergy.
The potential to develop allergy is thought to be
inheritance of the Th2 response to allergens, not inherit-
ance of allergy to a specific allergen. Allergic sensitization
One of the most significant changes in pediatric
food allergy management in recent years has
been in strategies to prevent food allergy in early
infancy. Previously, the idea prevailed that if the most
highly allergenic foods are withheld from the infant until
the immune and digestive systems were more mature,
allergic sensitization would be prevented or significantly
reduced. Frequently, the advice regarding introduction of
the most highly allergenic foods was “the later the better.”
It was hoped that this would in turn prevent allergy not
only to food but to inhalant and contact allergies in later
life. However, new research seems to indicate the very
opposite—that exposure to allergens in early life may
actually tolerize the infant’s immune system and prevent
allergic sensitization to food.*
Early Allergy Predictors
Allergic diseases result from a strong relationship between
genetic and environmental factors. Various definitions of
From Vickerstaff Health Services, Inc, Kamloops, Canada.
Received for publication May 24, 2011; accepted for publica-
tion July 13, 2011.
Address correspondence to: Janice M. Joneja, PhD, Vickerstaff
Health Services, Inc, 2016 High Canada Place, Kamloops, V2E
2E3, Canada; e-mail: jmjoneja@shaw.ca.
*Allergic sensitization involves an immunological response to
the allergen with the production of allergen-specific IgE;
Immunological tolerance indicates that consumption of the
allergenic food does not result in an allergic response.
Symposium Report
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50S Journal of Parenteral and Enteral Nutrition / Vol. 36, Suppl. 1, January 2012
depends on the baby’s exposure to the allergen and the
response of his or her immune system at the time of expo-
sure, although some foods are more likely than others to
lead to allergy.
Food Allergy and Other Allergic Diseases
For many years, it was assumed that if the early onset of
allergy could be prevented or delayed, the child might avoid
what allergists like to call the “allergic march”—the pro-
gression from food allergy to inhalant-triggered respiratory
allergy and asthma, which usually have their onset at a
later age. It was assumed that the early expression of
allergy in the form of allergic reaction to foods “primed”
the immune system to take the Th2 route, and once
started, like a train starting from a station along a track, the
Th2 response would progress to respiratory allergy and
asthma. However, newer research has demonstrated that
this is not necessarily the case. Prevention of food allergy
in early infancy prevents or reduces food allergy; the direct
effect of food allergy in the development of allergy to air-
borne and environmental allergens has yet to be identified
by scientific studies. Nevertheless, it is extremely impor-
tant to prevent, reduce, or relieve food allergy as early as
possible because of the central role of allergy to foods in
many allergic diseases (particularly eczema), its contribu-
tion to asthma and allergic rhinitis, and the real danger of
life-threatening anaphylactic reactions.
This leads to an extremely important question: how
can we implement strategies to promote tolerance and
avoid sensitization of the baby to allergens? Clearly, the
first difficulty is in determining exactly when allergic sen-
sitization is likely to occur.
Does Atopic Disease Start in Fetal Life?
During pregnancy, immune responses in the uterus are
skewed to the Th2 (allergic) rather than the Th1 (protec-
tive) response because the fetus must be protected from
rejection by the mother’s system.4 The fetus, having
inheritance from both father and mother, has a different
cellular composition from its mother. Therefore, the
developing baby might be at risk of rejection by the
mother’s immune system, which would be a Th1 response.
To avoid this rejection, the fetal environment is thought
to develop a predominantly Th2 milieu, which suppresses
the mother’s protection/rejection response. This effec-
tively bathes the fetus in Th2-type cytokines that keep it
safe in its environment.
Because the fetus is enveloped by Th2-type cytokines
in the womb, it is logical to question whether allergens
from the mother’s diet might gain access to the developing
baby’s system and thereby start allergic sensitization even
before birth. Allergens have been detected in amniotic
fluid, indicating that allergenic material to which the
mother has been exposed can cross the placenta.5 However,
there is no real evidence to suggest that the fetal immune
system is primed to respond to these allergens.6 In fact,
some authorities suggest that exposure to food antigens in
utero may promote fetal tolerance7—that is, the immune
system is “educated” to recognize the food as “foreign but
safe” and not to mount a defensive action against it when
the food is encountered at any time in the future. So, in
utero exposure to food molecules may mark the beginning
of the ability to consume food with impunity.
At birth, all neonates have low levels of interferon
(INF)–γ and produce the cytokines associated with the
Th2 response, especially interleukin (IL)–4, and new-
borns of both atopic and nonatopic inheritance have a
predominantly Th2 response to antigens. As the baby
matures, there is a switch from the Th2 to the “protec-
tive” Th1 response, except in atopic babies, where the
Th2 response continues to predominate and sets the
stage for allergen sensitization and allergy.8 So here the
important question is, why do all neonates not have
allergy? New research is indicating that the answer may
lie with the immune system of the mother, which plays a
significant role in the expression of allergy in her baby.9
The only antibody that crosses the placenta from
mother to fetus is IgG. There are 4 subtypes of IgG, des-
ignated IgG1, IgG2, IgG3, and IgG4. IgG4 is frequently
associated with IgE in allergy. The nonatopic mother pro-
duces abundant IgG1 and IgG3, which cross the placenta
to protect her fetus in utero. Because food proteins can
cross the placenta, it is thought that fetal exposure to
these antigens in the environment of the uterus protected
by the mother’s IgG1 and IgG3 may promote fetal toler-
ance to these foods, and this continues in the neonatal
period. In contrast, the allergic mother tends to produce
IgE and IgG4; IgG4 is very poor at crossing the placenta,
and it is thought that the IgE/IgG ratio of the mother has
the greatest consequences for the offspring.9 In allergic
mothers, there is likely to be insufficient IgG1 and IgG3
to downregulate fetal IgE, and thus at birth, her baby may
be primed to become sensitized to allergens and to
develop allergic symptoms very early.
Although there is no evidence that the fetus of the aller-
gic mother can mount an IgE-mediated response to specific
allergens in utero, the potential to produce allergen-specific
IgE predominates at birth. The only defence against this at
present is to reduce the allergic mother’s exposure to her
own allergens throughout pregnancy in an attempt to
decrease her production of IgE and IgG4 and, it is hoped,
enhance production of the protective IgG1 and IgG3. The
mother should avoid foods to which she is allergic at all
times and obtain complete balanced nutrition from alternate
sources. There is no evidence to suggest that maternal avoid-
ance of any foods other than her own allergens (and not
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Infant Food Allergy / Joneja 51S
those of the baby’s father) during pregnancy will improve the
allergic status of her baby. A 1988 report10 indicated that
excluding highly allergenic foods from the mother’s diet
from week 28 to the end of pregnancy did not affect the
atopic status of the infant in any way.
Breastfeeding and Allergy
Breast milk provides the ideal nutritional, immunologic,
and physiologic nourishment for all newborns.
Components of human milk enhance the baby’s natural
defences and promote maturation of the immune sys-
tem.11 Ninety percent of antibodies in human colostrum
and milk are secretory IgA, which provide the baby with
protection at mucosal surfaces until the infant is produc-
ing adequate quantities of its own sIgA at about 6 months
of age.12 However, the effect of breastfeeding on the
development of allergic diseases in the breastfed infant
remains controversial.
Several studies report that breastfeeding is protective
against allergy, with a definite improvement in infant
eczema and associated gastrointestinal complaints, as
well as a reduced risk of asthma in the first 24 months,
when the baby is exclusively breastfed and the mother
eliminates highly allergenic foods from her diet.13 A
recent (2010) report indicates that IgG immune com-
plexes found in breast milk are potent inducers of toler-
ance to aerosolized antigens to which the mother was
sensitized, providing antigen-specific protection from
asthma in their babies.14
However, other studies seem to indicate that breast-
feeding has no effect on the infant’s symptoms of allergy
or, worse, may be associated with an increased prevalence
of atopic eczema.15,16 One of the reasons for this apparent
contradiction may be explained by data that indicate that
the breast milk of atopic mothers differs immunologically
from that of the nonallergic.17-19
Atopic mothers tend to have a higher level of the
cytokines and chemokines associated with allergy in their
breast milk and also have a lower level of the cytokine
known as transforming growth factor (TGF)–β1 that pro-
motes tolerance to food components in the intestinal
immune response. A normal level of TGF-β1 in the moth-
er’s colostrum and breast milk is likely to facilitate toler-
ance to food encountered by the infant in the mother’s
breast milk and later to formulas and solids.20 Evidence
seems to suggest that breastfeeding is protective against
allergies when the mother is nonatopic21 but that babies
of allergic mothers may be at risk of developing allergies,
especially to foods, during breastfeeding.
In view of the large amount of evidence regarding the
role of breast milk in promoting the well-being of all
babies, on the basis of careful analysis of all research data
on the topic, ESPACI and ESPGHAN strongly recom-
mend exclusive breastfeeding for 4–6 months, and the
American Academy of Pediatrics (AAP)2,22 recommends at
least 4 months, with introduction of complementary
foods no earlier than 4–6 months as the hallmark for
allergy prevention.2,23
Prevention of Food Allergic Sensitization
During the First 6 Months
From the results of epidemiological studies, it is thought
that initial sensitization to food allergens in the exclu-
sively breastfed baby occurs predominantly from external
sources, such as a single feeding of infant formula or
perhaps by accident. In an important study of 1749 new-
borns in Odense, Denmark, 39 (2.2%) were identified as
being sensitized to cow’s milk proteins soon after birth. Of
these, 9 developed symptoms of cow’s milk allergy before
3 months of age, despite being exclusively breastfed.
Review of records from the newborn nursery revealed that
all 9 infants had been exposed to cow’s milk formula in
amounts corresponding to approximately 0.4–3.0 g of
β-lactoglobulin (BLG) during the first 3 days of life.
Similar proteins were detected in their mother’s breast
milk, to which the allergic infants reacted with the devel-
opment of symptoms. The authors conclude that early
inadvertent and occasional exposure to cow’s milk pro-
teins may initiate sensitization in predisposed neonates;
subsequent exposure to minute amounts of bovine milk
proteins in human milk may then act as booster doses
eliciting allergic reactions.24
The current directives from position papers and con-
sensus documents from many countries now recognize that
restriction of the maternal diet during pregnancy and lacta-
tion is probably contraindicated in allergy prevention.
•The AAP2 suggests that antigen avoidance dur-
ing lactation does not prevent atopic disease,
with the caveat that more data are needed to
substantiate this conclusion.
•The European Academy of Allergology and
Clinical Immunology states that “no conclusive
evidence for protective effect of maternal exclu-
sion diet during pregnancy or lactation has been
documented.”1
•The Australasian Society of Clinical Immunology
and Allergy states, “Dietary restrictions in preg-
nancy are not recommended,” and “Maternal
dietary restrictions during breast feeding are
not recommended.”25
In summary, professional groups do not recommend the
elimination of any specific foods from the maternal diet
during breastfeeding, except for the mother’s own aller-
gens, unless the baby has been diagnosed with allergy
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52S Journal of Parenteral and Enteral Nutrition / Vol. 36, Suppl. 1, January 2012
to 1 or more foods, in which case the baby’s allergenic
food should be avoided by its mother as long as she is
breastfeeding.
Formula Feeding
It is not always possible for a baby to be breastfed, and
when the infant is at risk for or has developed allergies,
making the best choice of formula is extremely important.
Most authorities suggest that if a baby has no signs or
symptoms of cow’s milk allergy, a conventional cow’s
milk–based formula is safe for infant feeding.
However, in high-risk-for-allergy babies, there is
emerging evidence that hydrolyzed infant formulas pro-
vide a measure of protection against the development of
atopic disease26 compared to conventional milk-based
formulas. Hydrolysis of cow’s milk breaks the protein into
smaller, potentially less allergenic proteins.
On the basis of evidence from a variety of studies,27-29
the AAP, in its position paper published in 2008,2 states
that “in studies of infants at high risk of developing atopic
disease who are not breast-fed exclusively for 4 to 6
months or are formula fed, there is modest evidence that
atopic dermatitis may be delayed or prevented by the use
of extensively hydrolyzed or partially hydrolyzed formulas,
compared with cow’s milk formula, in early childhood.”
The AAP further stated that “extensively hydrolyzed for-
mulas may be more effective than partially hydrolyzed in
the prevention of atopic disease.” However, the authors of
a more recent research study (2011) stated that, “Despite
current dietary guidelines, we found no evidence to sup-
port recommending the use of pHWF (partially hydro-
lysed whey formula) at weaning for the prevention of
allergic disease in high-risk infants.”30
There is good consensus among pediatric groups
worldwide that no evidence exists for the use of soy-based
infant formula for the purpose of allergy prevention.2,25,31
So in summary, it is fair to state that if a baby at high
risk for allergy cannot be exclusively breastfed to 4–6
months of age, the preferred method of feeding in the
prevention of atopic disease is an extensively hydrolyzed
formula.
Introducing Solid Foods
The first consensus document on the introduction of
solid foods for the food-allergic infant was published in
July 2006 by the Adverse Reactions to Foods Committee
of the American College of Allergy, Asthma and
Immunology.32 It recommended that introduction of the
multiple allergens in solid foods to the allergic infant is
preferably delayed until after 6 months of age. Until this
age, the authors suggest that the infant’s immature diges-
tive tract and immune system may increase the risk of
sensitization and development of allergy. Furthermore, it
was recommended that the most highly allergenic foods
should not be introduced until after 1 year of age or later.
Specific times of introduction were suggested as follows:
cow’s milk at 12 months; egg at 24 months; and peanut,
tree nut, and fish at 3 years.
However, more recent research has demonstrated
that these recommendations were neither supported by
evidence-based research nor were effective in practice.
Newer position papers reflect this change in approach.
The AAP paper, published in 2008,2 states, “The evidence
. . . does not allow one to conclude that there is a strong
relationship between the timing of the introduction of
complementary foods and development of atopic disease.”
According to the published guidelines of all pediatric
societies and consensus committees, solid foods should
be introduced individually and gradually, starting at about
4–6 months of age. Each food should be introduced, ide-
ally over a 4-day period, with careful monitoring of the
baby for the development of signs of allergy. No mixed
foods should be given until each food in the mixture has
been given to the baby and is tolerated.
Prognosis for Infant Food Allergy
Many children outgrow their early allergies to foods spon-
taneously. A few examples are as follows.
Cow’s Milk Allergy
Most children with early cow’s milk allergy outgrow their
allergy by 3 years of age. A 1990 study reported that 56%
of the infants with cow’s milk allergy outgrew their allergy
at 1 year, 77% at 2 years, and 87% at 3 years.33 However, a
2007 study34 reported that 19% of their patients with cow’s
milk allergy developed tolerance by age 4 years, 42% by age
8 years, 64% by age 12 years, and 79% by age 16 years.
Those children with the highest level of cow’s milk–spe-
cific IgE were least likely to outgrow their cow’s milk
allergy. Furthermore, children with asthma, atopic rhino-
conjunctivitis (hay fever), and atopic dermatitis (eczema)
are reported to be less likely to outgrow their early cow’s
milk allergy, suggesting that the most highly allergic indi-
viduals are most at risk for persistent food allergies.35
Egg Allergy
It has been reported that 80% of infants with egg allergy
are able to consume egg by 5 years of age.36 Other more
recent reports using predicted resolution of egg allergy
are more pessimistic: 4% of egg-allergic children were
predicted to outgrow their allergy by 4 years, 12% by 6
years, 37% by 10 years, and 68% by 16 years of age.37 The
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Infant Food Allergy / Joneja 53S
persistence of egg allergy was related to the presence of
asthma and allergic rhinitis and higher levels of egg-
specific IgE. Nevertheless, the consensus from published
studies concludes that most patients with egg allergy are
likely to develop tolerance to egg by late childhood, with
the exception of patients with an egg IgE >50 kUA/L, in
whom egg allergy is likely to persist into adulthood.
Peanut Allergy
Recent reports suggest that at least 21% of peanut-allergic
children will outgrow their peanut allergy over time38
(median age 6 years). Traditionally, allergy to peanut was
considered to be lifelong and unlikely to be outgrown. Those
children with lower peanut-specific IgE (<5 kUA/L at time of
challenge) and lower rates of asthma and allergic rhinitis
were reported to be more likely than those with high levels
to outgrow their peanut allergy. An earlier report from the
United Kingdom indicated that 9.8% of their peanut-allergic
patients outgrew their peanut allergy39 in childhood.
Tree Nut Allergy
Allergy to tree nuts is another condition that traditionally
has been considered to be rarely outgrown. However, a
study of 278 tree nut allergic patients reported that 9%
outgrew their tree nut allergy, including some who had
previous severe reactions.40 The authors suggested that
patients aged 4 years or older with tree nut–specific IgE
levels of 5 kUA/L or less should be considered for chal-
lenge of tree nuts under medical supervision to determine
whether they remain allergic to tree nuts.
It is important that children who have outgrown their
early allergy to foods should be identified so that the pre-
viously allergenic food can be included in their diet. This
is important for several reasons:
•The diet becomes easier to formulate and
maintain.
•The vigilance previously exerted to avoid the
culprit food can be relaxed, which reduces the
stress associated with maintaining restricted
diets, especially those that contain foods that
may be considered “life-threatening.”
•Including the now-tolerated food in the diet on
a regular basis reduces the likelihood of recur-
rence of the allergy because maintenance of
tolerance reduces this risk.41
Oral Tolerance in the Management of
Established Food Allergy
In some cases, desensitization or tolerance to a food
allergy can be achieved even if the child has not sponta-
neously outgrown the allergy. This is a relatively new
concept as previous directives for food allergy manage-
ment emphasized strict avoidance of the culprit allergen.
Now specific desensitization protocols are being devel-
oped that expose the allergic child to the offending aller-
gen by the oral route in a safe environment in order to
induce tolerance to it.
Several studies have reported achievement of toler-
ance to cow’s milk by starting with minute quantities of
milk and increasing the dosage over time, a process
termed specific oral tolerance induction (SOTI). Examples
include the following:
•One study reported that starting with 1 drop of
milk and increasing to 120 mL over a period of
136 days, 13 of 16 children achieved tolerance
to 120 mL milk in 3–12 months.42
•Starting with an initial dose of 0.05 mL cow’s
milk, reaching 1 mL on the first day, and
increasing the dosage weekly until a dose of
200–250 mL of milk taken once a day was toler-
ated, 16 of 18 patients 4 years and older
achieved tolerance after a median length of 14
weeks (range, 11–17 weeks). Thirteen children
continued to tolerate 200–250 mL per day of
milk after more than a year.43
•Another study44 reported achievement of toler-
ance to cow’s milk in 7 of 10 children with
established milk allergy, starting with 1 drop of
milk and increasing weekly over a period of 4
months until a dose of 200 mL was tolerated.
A similar tolerance to foods other than milk have
been achieved, for example, to egg45,46 and peanut.47,48
Undoubtedly, successful SOTI to other allergenic foods
will be achieved over time.
Probiotics and Allergy
Studies in the past decade have indicated that the intes-
tinal microflora might be the major source of microbial
stimulation that promotes maturation of the immune
system in early childhood.49 The appropriate microbial
stimulus soon after birth may be extremely important in
balancing the Th1/Th2 response of the immune system,
which is skewed to the Th2 (allergy) type at birth.50
Lactic acid bacteria and bifidobacteria are found more
commonly in the intestinal flora of nonallergic children,
and atopic children appear to have a different microflora
composition than nonatopics, with higher levels of
clostridia and lower levels of bifidobacteria.51 These obser-
vations may pave the way for selecting probiotic strains
that might promote the intestinal environment most ben-
eficial in developing tolerance rather than sensitization to
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54S Journal of Parenteral and Enteral Nutrition / Vol. 36, Suppl. 1, January 2012
allergens in the immature infant. A number of studies sug-
gest that the appropriate selection of the bacterial strains
used in probiotics may help in certain allergic conditions,
but at the present time, we have insufficient evidence to
recommend probiotics as a therapy for allergy prevention
in regular clinical practice.52,53
The use of probiotic therapy to prevent allergic dis-
ease has been demonstrated in a few studies using the
probiotic strain Lactobacillus rhamnosus GG in neonates.
This seemed to be particularly effective in reducing the
incidence and severity of atopic eczema.54
In a Finnish study, infants with milk allergy and
atopic dermatitis had milder symptoms and fewer inci-
dences of intestinal infections if their milk formula was
fortified with lactobacilli.55 However, a similar study from
Singapore reported that administration of a cow’s milk
formula supplemented with probiotics (Bifidobacterium
longum and L rhamnosus) for the first 6 months showed
no effect on prevention of eczema or allergen sensitiza-
tion in the first year of life in Asian infants at risk of
allergic disease.56 Another study using the probiotics L
rhamnosus or Lactobacillus GG in infant formula for 3
months in children younger than 5 months as prevention
or management of atopic dermatitis (AD) concluded that
the results “indicate that oral supplementation with these
probiotic bacterial strains will not have a significant
impact on the symptoms of infantile AD.”57
A positive effect of probiotics on symptoms of allergy
was reported in a study from Sweden that evaluated the
effects of feeding Lactobacillus F19 in cereals during wean-
ing on the incidence of eczema in children aged between 4
and 13 months (89 in the study group; 90 in the control
group). At 13 months of age, the incidence of eczema was
reported as 11% in the study group and 22% in the placebo
group. The authors conclude that “feeding Lactobacillus
F19 during weaning could be an effective tool in the preven-
tion of early manifestations of allergy, e.g. eczema.”58
The problem with comparing such studies at the pre-
sent time is that there are so many variables to consider
before any conclusions can be made as to the effective-
ness of probiotics, prebiotics, and synbiotics on childhood
allergy—for example:
•The specific species and strains of the micro-
organisms
•The number of micro-organisms required to be
delivered orally (dosage) as colony-forming
units (CFU)
•The number of micro-organisms surviving in
their movement through the digestive tract
•The number colonizing (implantation and mul-
tiplication in) the bowel, usually measured as
live organisms in the feces
•The age at which the probiotic is administered,
whether prenatally or postnatally
•The duration of consumption of the probiotic
•The means of administering the probiotic (in
milk, formula, cereal, or other)
•The selection of an appropriate prebiotic (milk,
oligosaccharides [eg, fructo-oligosaccharide],
inulin) or other appropriate substrates
It is hoped that evidence-based studies will begin to answer
these questions, possibly offering an additional method for
managing pediatric food allergies in the future.
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2. Greer FR, Sicherer SH, Burks AW, and the Committee on
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