In the past, food allergy prevention strategies focused on the
avoidance of allergenic foods in infancy. The current paradigm,
however, is shifting from avoidance to controlled exposure. Recent
evidence from randomized controlled trials suggests that
the early introduction of allergenic foods such as peanuts may
reduce the prevalence of food allergies in high-risk infants. In
countries where peanut allergy is prevalent, healthcare professionals
should recommend the introduction of peanut-containing
products into the diets of “high-risk” infants early in life (between
4 and 11 months of age).
Worldwide, the most common food allergies in children are allergies
to cow’s milk, hen’s egg, soy, peanut, tree nuts, wheat,
fish, and seafood. Although a large proportion of those with
milk or egg allergies will develop tolerance as they age, certain
subgroups remain allergic and are at risk of developing other
disorders such as respiratory allergic disease. For instance, the
presence of both egg allergy and eczema in infants is a predictor
of later respiratory allergies. Those with high levels of IgE antibodies
to cow’s milk, egg white, wheat, and soy are also more
likely to have persistent food allergy.
Current international guidelines state that the introduction of
allergenic foods (including egg and peanut) does not need to
be postponed beyond 4–6 months of age, but they provide no
concrete guidance on whether these foods should be actively introduced
within this time frame. The LEAP (Learning Early About
Peanut Allergy) trial was the first prospective randomized study
regarding early peanut introduction. Results from the LEAP study
suggest that early introduction of peanut into the diets of highrisk
infants may be beneficial. However, safety and practicality remain
key issues when extrapolating the results of this study to the
general population. Open questions remain on the optimal timing
and doses that should be used, and whether such regimens
should be stratified according to the infant’s allergy risk.
du Toit G, Tsakok T, Lack S, Lack G: Prevention of food allergy.
J Allergy Clin Immunol 2016;137:998–1010.
There is level 1 evidence that early introduction of
peanuts (from 4 to 11 months of age) reduces the
prevalence of peanut allergy in infants at high risk of
allergic disease (infants with severe eczema and/or
The majority of current international guidelines
recommend that complementary foods, including
allergenic foods, can be introduced from 4 to 6
months of age irrespective of family history risk.
As delayed peanut introduction may increase the risk
of peanut allergy, interim guidelines state that
healthcare providers should recommend introducing
peanut-containing products into the diets of
“high-risk” infants early on in life (between 4 and 11
months of age) in countries where peanut allergy is
While earlier food allergy prevention strategies implemented
avoidance of allergenic foods in infancy, the current paradigm
is shifting from avoidance to controlled exposure. This
review focuses on the outcome of recent randomized controlled
trials, which have examined the early introduction of
allergenic foods for allergy prevention, and discusses the implementation
of results in clinical practice. In infants at high
risk of allergic disease, there is now direct evidence that regular
early peanut consumption will reduce the prevalence of
peanut allergy, compared to avoidance. Many international
infant feeding guidelines already recommend complementary
foods, including allergenic foods, to be introduced from
4 to 6 months of age irrespective of family history risk. Interim
guidelines from 10 International Pediatric Allergy Associations
state that healthcare providers should recommend
the introduction of peanut-containing products into
the diets of infants at high risk of allergic disease in countries
where peanut allergy is prevalent. Direct translation of the
results obtained from a cohort of high-risk infants to the
general population has proved difficult, and issues regarding
feasibility, safety, and cost-effectiveness have been
raised. Five randomized placebo-controlled trials have assessed
the effects of early egg exposure in infancy with varying
results. In a recent comprehensive meta-analysis, there
was moderate-certainty evidence that early versus late introduction
of egg was associated with a reduced egg allergy
risk. Although promising, optimal timing, doses, and if the
feeding regimen should be stratified according to infant allergy
risk remain to be determined. The single study that assessed
introduction of multiple foods from 3 months whilst
breastfeeding compared with exclusive breastfeeding until
6 months of age showed no reduction in food allergy prevalence.
Future research should aim at optimizing infant feeding
regimens and support a tolerogenic gastrointestinal microenvironment
during the period of food allergen introduction.
Over the past few decades, we have experienced a rising
prevalence of Immunoglobulin E (IgE)-mediated
food allergies in the pediatric setting, particularly in developed
countries, although the prevalence also appears
to be rising in developing countries . Most reports are
based on self-reported food allergy, however, and it has
been repeatedly shown that
self-reported data will overestimate
the prevalence as compared
with evaluation by an
oral food challenge [2–4]. It is
estimated that IgE-mediated
food allergy affects approximately
6–8% of children in
developed countries [1, 3, 4],
thereby posing a significant burden on the afflicted children,
their families, and the healthcare system. Globally,
the by far most common IgE-mediated food allergies in
childhood are allergies to cow’s milk, hen’s egg, soy, peanut,
tree nuts, wheat, fish, and seafood [3–5]. Tolerance
development is prevalent in milk and egg allergy; and the
majority of milk-allergic children [6, 7] and about a half
to two-thirds of egg-allergic children [8, 9] will outgrow
their food allergy before school age. The rate of peanut
allergy resolution is worse; when assessed by oral food
challenges both at diagnosis and at follow-up in the Australian
HealthNuts cohort study, only 22% of the children
outgrew their peanut allergy by 4 years of age . Collectively,
a significant proportion of children will remain
food allergic and are at risk of developing other comorbidities
such as respiratory allergic disease. For instance,
infant egg allergy, particularly when coexisting with eczema,
has been reported to be a predictor of later respiratory
allergies , and high levels of IgE antibodies to
cow’s milk, egg white, wheat, and soy are predictors of
persistent food allergy .
Avoidance remains the only available treatment in established
food allergy. Oral immune therapy, which includes
a stepwise dose increase of the food allergen followed
by a maintenance phase, is an emerging treatment
option. Oral immune therapy has been demonstrated to
induce desensitization, i.e., an increase in the amount of
offending food that can be ingested as long as it is consumed
regularly . It is still undecided if permanent
tolerance will develop, and oral immune therapy is not
generally recommended unless within a clinical trials
protocol. Adherence to an elimination diet is difficult,
and there is still risk of accidental exposure and allergic
reactions, including anaphylaxis . Allergic children
on elimination diets are also at risk of nutritional deficiencies
[15, 16], impaired growth [16–18], and reduced
quality of life . Collectively, there is urgent need to
develop effective strategies to promote tolerance development
and prevent food allergy.
While earlier food allergy prevention
strategies implemented food
avoidance in early infancy, the current
paradigm is shifting from avoidance
to controlled exposure
While earlier food allergy prevention strategies implemented
food avoidance in early infancy, the current paradigm
is shifting from avoidance
to controlled exposure.
The collective evidence from
epidemiological studies reporting
an association between
delayed introduction of
complementary foods and allergy
risk, and animal models
demonstrating that oral tolerance
induction is driven by exposure to antigens and allergens
[reviewed in 20 , 21], led to the first randomized
controlled trials (RCTs) to examine the role of early, regular
exposure to “allergenic” foods for food allergy prevention.
This review focuses on the outcome of these recently
published RCTs and discusses the implementation
of the results in clinical practice.
Risk Factors for Food Allergy
Both genetic and environmental factors will influence
the risk of developing food allergy, and multifaceted
changes in our modern environment are a likely driver.
The hypotheses proposed to explain the epidemic rise in
allergic disease include (a) the biodiversity hypothesis,
which theorizes that reduced diversity and intensity of
microbial exposures will impair normal development of
immunoregulatory networks and increase allergy risk
, (b) the vitamin D hypothesis that builds on epidemiological
evidence that vitamin D deficiency is associated
with an increased risk of allergic disease, and (c) the
dual-barrier hypothesis [23, 24], which is discussed below.
There are also data to suggest that food allergens,
specific nutrients, lifestyle factors, and microbial exposures
may influence the development of allergic disease
through epigenetic mechanisms .
A commonly used definition of allergy risk is based on
a history of allergic disease in a first-degree relative 
and is frequently used in both epidemiological studies
and clinical trials. In some of the recently conducted
RCTs, however, only infants with an already established
allergic phenotype (eczema and/or manifest egg allergy)
were included as they are at an even heightened risk [27,
28] (Table 1). For instance, it has been demonstrated that
infant eczema is associated with an increased risk of percutaneous
sensitization to environmental food allergens,
facilitated by an impaired skin barrier . Normally, a
food allergen is introduced to and handled by the immune
system in the gut to induce a tolerogenic response
to the food protein [20, 30]. Accordingly, the dual-barrier
hypothesis theorizes that avoidance of a specific food
(such as egg or peanut) can increase the risk of developing
food allergy if the infant is still exposed to the food allergen
in the environment and is percutaneously sensitized
The “Optimal” Window of Introduction of
Complementary Foods for Allergy Prevention
Almost 2 decades ago, the American Academy of Pediatrics
Committee on Nutrition launched guidelines
suggesting a delayed introduction of dairy products in the
first year of life in infants with a family history of allergic
disease: egg until 2 years, peanuts, nuts, and fish until 2–3
years of age . This recommendation also became integrated
in infant feeding guidelines in many other countries
at the time. Following the publication of more recent
epidemiological studies across the globe, the guidelines
were revised to reflect the lack of solid scientific evidence
that delayed introduction of complementary foods beyond
4–6 months of age, or avoidance of “allergenic”
foods such as cow’s milk, egg, peanuts, tree nuts, fish, and
seafood, reduce allergy risk [32–36]. Still, the “optimal”
time for introduction of complementary food for allergy
prevention is not known. There are data to suggest that
starting complementary foods before 3–4 months of age
may increase the risk of allergic disease [37, 38]. At that
age, the gut is more permeable and gastrointestinal colonization
is not yet well established, which might contribute
to the observed risk increase [39, 40]. Consequently,
many international infant feeding guidelines for allergy
prevention recommend introduction of any solid food
after 4 months of age [32–36].
RCTs for Food Allergy Prevention
In a cross-sectional study, du Toit et al.  found that
the prevalence of peanut allergy was 10-fold higher in
Jewish children in the UK compared with children in Israel.
Interestingly, peanut consumption was initiated earlier
and in larger quantities in Israel than in the UK. Based
on these findings, the Learning Early About Peanut Allergy
(LEAP) study was designed to examine if early, regular,
controlled peanut consumption, compared with
avoidance, could prevent peanut allergy in high-risk infants
with severe eczema, egg allergy, or both  (Table
1). As part of the screening, a skin prick test (SPT) to
peanut was performed, and infants with a wheal size ≥ 5
mm were excluded. The intervention was initiated between
4 and 11 months and continued until 5 years of age.
The study results were pronounced; in the early-introduction
group, peanut allergy was reduced with 86% in
the group with a negative SPT to peanut at baseline, and
with 70% in the group with SPT peanut 1–4 mm at baseline,
compared with the avoidance group. Reassuringly,
the investigators recently reported that 12-month peanut
avoidance in the early-introduction group did not increase
the prevalence of peanut allergy at the age of 6 years
, suggesting that avoidance for a prolonged period
will not break tolerance. Still, the long-term consequences
of peanut avoidance beyond 12 months are unknown.
There is also epidemiological evidence to support that
delayed introduction of egg to the infant diet increases
allergy risk. In the HealthNuts cohort study, delayed introduction
of egg at 10–12 months or after 12 months of
age was associated with an increased risk of egg allergy
compared with egg introduction at 4–6 months of age
. To date, 5 RCTs have examined if early versus late
introduction of egg can reduce the risk of egg allergy [45–
49] (Table 1). In the Solids Timing for Allergy Reduction
(STAR) study, high-risk infants with moderate-to-severe
eczema were randomized to intake of pasteurized raw
whole egg powder or rice powder (placebo) from 4 to 8
months of age . At 12 months of age, 33% in the active
group versus 51% in the placebo group had developed egg
allergy (relative risk 0.65, 95% CI 0.38–1.11, p = 0.11). In
the Starting Time of Egg Protein (STEP) study, high-risk
infants (based on maternal atopy but no allergic manifestation
in the infant at baseline) were randomized to intake
of pasteurized raw whole egg powder or rice powder (placebo)
from 4 to 10 months of age . At 12 months of
age, 7% in the active group versus 10.3% in the placebo
group had egg allergy (adjusted relative risk 0.75, 95% CI
0.48–1.17, p = 0.20). The Beating Egg Allergy Trial (BEAT)
also included high-risk infants (based on allergic disease
in any or both parents) . Infants were randomized to
pasteurized raw whole egg or rice powder (placebo) from
4 to 8 months of age. The primary outcome was egg sensitization
at 12 months of age, and 11% in the active group
versus 20% in the placebo group were sensitized (odds
ratio 0.46, 95% CI 0.22–0.95, p = 0.03). Twenty-one infants
were classified as having probable egg allergy. Of
these, 6.2% were in the active group and 10.5% were in
the placebo group ( p = 0.20).
In the Prevention of Egg Allergy with Tiny Amount
Intake (PETIT) study, high-risk infants with established
eczema were randomized to intake of either heated egg
powder or squash powder (placebo) from 6 to 12 months
of age, with an increased dose of egg protein from 9
months . There was a marked effect of the intervention
with egg allergy diagnosed at 12 months in 9% in the
active group versus 38% in the placebo group (risk ratio
0.221, 95% CI 0.09–0.543, p = 0.0001). In fact, the striking
effect of the intervention in the preplanned interim analyses
led the investigators to terminate the trial prematurely.
As discussed by the investigators  the difference
might be biased, leading to a bigger difference between
the active and placebo groups than if the study had
not been closed.
In contrast to the above-mentioned studies that included
high-risk infants, the Hen’s Egg Allergy Prevention
(HEAP) study, randomized infants with normal risk
(from the general population) to intake of pasteurized egg
white powder or rice powder from 4 to 6 months until 12
months of age . Infants were screened for egg sensitization,
and all included infants had specific IgE to egg
<0.35 kU/L at baseline. As in the BEAT study , the
primary outcome was egg sensitization at 12 months.
5.6% in the active group were sensitized to egg versus
2.6% in the placebo group (relative risk 2.20, 95% CI 0.68–
7.14, p = 0.24). At that age, 2.1% in the active group had
egg allergy versus 0.6% in the placebo group (relative risk
3.30, 95% CI 0.35–31.32, p = 0.35).
Collectively, 4 out of 5 conducted RCTs designed for
egg allergy prevention were negative (Table 1), although
3 of these studies [45–47] had nonsignificant results that
might suggest a benefit of early egg introduction.
Multiple Foods Approach
Observational studies have also reported an association
between low food diversity in early life and both
sensitization  and allergic manifestations . In the
Enquiring About Tolerance (EAT) study  (Table 1),
3-month-old breastfed infants from the general population
were randomized to continued breastfeeding with
introduction of cow’s milk, peanut, hard-boiled egg, sesame,
white fish, and wheat in a sequential order from 3
months of age or to continued exclusive breastfeeding
for the first 6 months of life . In the intention-totreat
analysis, 5.6% of the children in the early-introduction
group had developed food allergy at 3 years of age
compared to 7.1% in the group that introduced solid
foods from the age of 6 months (relative risk 0.80, 95%
CI 0.51–1.25, p = 0.32). Of note, only 42% in the earlyintroduction
group were able to adhere to the food introduction
regimen, demonstrating that it can be difficult
to introduce multiple foods as compared to a single
food item. In the per protocol analysis, however, the
prevalence of “any” food allergy was 2.4% in the earlyintroduction
group compared with 7.3% in the standard-
introduction group ( p = 0.01). The prevalence of
peanut and egg allergy was also reduced in the earlyintroduction
group (0 vs. 2.5%, p = 0.003, and 1.4 vs.
5.5%, p = 0.009, respectively). There was no difference
between the 2 groups in the prevalence of allergy to milk,
sesame, fish, or wheat.
Meta-Analysis of Egg and Peanut Prevention
In a recent comprehensive systematic review and
meta-analysis, Ierodiakonou et al.  included the trials
discussed above that had assessed early versus late egg introduction
for egg allergy prevention (5 trials, 1,915 participants)
[45–49] (Table 1). They found with moderate
certainty evidence that early versus late introduction of egg
was associated with a reduced egg allergy risk (risk ratio
0.56, 95% CI 0.36–0.87, p = 0.009). They also identified the
LEAP  and EAT  studies (Table 1) (2 trials, 1,550
participants) to be included in a meta-analysis of early versus
late introduction of peanuts and reported that early
introduction was associated with a reduced peanut allergy
risk (risk ratio 0.29, 95% CI 0.11–0.74, p = 0.009). The authors
underscored that the studies were few and that the
certainty of the evidence was reduced due to imprecision,
indirectness, and heterogeneity in interventions and study
populations . An interesting finding, however, was
that there was no distinct difference among infants at
“normal” versus high risk of allergy in their analyses.
Allergic Reactions and Safety Issues
A shared feature of the studies that included high-risk
infants and used pasteurized raw egg powder is that a
varying proportion (4.7–31%) of the participants in the
early egg intake groups discontinued egg ingestion due to
allergic reactions to the egg powder [45–47]. This has
raised the question if screening for sensitization would be
necessary before introducing egg to the infant diet. Reassuringly,
in the STEP trial that included infants with familial
predisposition but no eczema, there were no anaphylactic
reactions to the egg powder . The authors
underscored that assessment of egg sensitization before
the introduction of egg and egg-containing products to
the infant diet is not necessary in the community setting
. In the PETIT trial , which included high-risk
infants with eczema, a few participants reported mild to
moderate allergic manifestations following ingestion of
the study powder, but at a similar frequency in the active
and placebo groups. No participant discontinued the intervention
because of allergic reactions to the egg powder,
and it has been argued that this could be a matter of reduced
allergenicity of heated versus pasteurized (raw) egg
powder . The risk of adverse reactions to peanut was
low in the LEAP study; 5% of infants randomized to early
peanut intake reacted at the baseline peanut challenge.
However, infants at a presumably higher risk (peanut
wheal size ≥ 5 mm) were excluded.
Current international guidelines already state that introduction
of allergenic foods, including egg and peanut,
does not need to be postponed beyond 4–6 months of age
[32–36]. With a few exceptions, these guidelines do not,
however, advocate that allergenic foods should be actively
introduced to the infant diet between 4–6 months of
age. Based on level 1 evidence from the LEAP study ,
interim guidelines on peanut introduction for allergy prevention
in high-risk infants were launched in 2015 ( Table
2 ) . In an opinion paper, Allen and Koplin 
identified and discussed the challenges in translating the
findings from the LEAP study to the general population
level. Safety remains one issue, particularly in very highrisk
infants, as the LEAP study excluded infants with an
SPT to peanut ≥ 5 mm, cost-effectiveness another .
Very recently, addendum guidelines for penaut allergy
prevention in the United States were launched . In
brief, the guideline panel suggests introducing peanuts at
home to the majority of infants in the first year of life. Infants
with severe eczema, egg allergy, or both should undergo
medical assessment including assessment of sensitization
to peanut before peanut introduction at 4–6
months of age . If other allergenic foods, such as egg,
should also be actively introduced to the infant diet from
4 to 6 months of age remains undetermined. Recent allergy
prevention guidelines in Australia now suggest introducing
cooked (but not raw) egg from 4 to 6 months
of age irrespective of allergic heredity . As underlined
by Ierodiakonou et al. , the findings from their systematic
review on early versus late introduction of complementary
foods for allergy prevention cannot be directly
translated to new guidelines. Collectively, the optimal
timing, doses and form of egg, and if these regimens
should be stratified according to the infant’s allergy risk
remain to be determined.
The level 1 evidence form the LEAP study  has resulted
in interim guidelines recommending early introduction
of peanut into the diets of “high-risk” infants
. Further studies should aim at optimizing infant
feeding regimens. Supporting the most favorable “tolerogenic”
microenvironment in the gut during the period of
food allergen introduction is also likely to involve “optimal”
colonization of the gastrointestinal tract, breastfeeding,
and other dietary factors with immunomodulatory
capacity [39, 40].
The author reports no conflict of interest in relation the topic. The writing of this article
was supported by Nestlé Nutrition Institute.
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