EARLY DIETARY INTERVENTION AND PREVENTION OF ATOPIC DERMATITIS IN

CHILDREN

By
Julia Mason

A senior project submitted

In partial fulfillment of the requirements for the degree of
Bachelor of Science in Nutrition
Food Science and Nutrition Department
California Polytechnic State University
San Luis Obispo, CA
June 2016

ABSTRACT
Nutritional choices made during pregnancy and the first 1000 days of a childs life may
have a preventative effect on the outcome of atopic dermatitis (AD). To date, no
definitive recommendations about the effect of early dietary choices on AD have been
made because the exact mechanism of interaction is unclear. AD is widely known to
have a hereditary component, but exposure to many environmental and nutritional
factors in the early stages of life can either diminish or exacerbate symptoms. Thus, the
purpose of this review is to systematically explore whether early dietary choices can
protect against the development of AD in children. In examining the relationship of
these key nutritional choices, four main areas of dietary intervention were explored:
maternal diet, formula feeding, breastfeeding, and introduction of complementary foods.
Findings regarding maternal antigen avoidance during pregnancy were not associated
with a reduction of AD in the child. Formula feeding with cows milk formula was not
found to be protective and may actually exacerbate symptoms, while hydrolyzed
formula decreased risk of AD by up to 50% in high risk infants. Breastfeeding is
recommended in all pregnancies regardless of atopic susceptibility, but results regarding
its role in AD prevention are inconsistent. Some studies have shown that there is an
increased risk of AD development associated with an increased duration of
breastfeeding, but many confounders make causation difficult to conclude. Conversely,
other larger studies have found a significant protective effect of exclusive breastfeeding
for at least three months, so more research is needed in this area with new, innovative
precautions to minimize the confounding factors associated with breastfeeding studies.
Finally, research involving the introduction of complementary foods is varied. Findings
show that introduction of a variety of solids as early as three months old may protect
against the development of allergies. However, premature presentation of solid food
may result in aspiration, overfeeding and metabolic dysfunction. Overall, results show
promise that it may be possible to overcome some genetic predisposition to AD with
appropriate early dietary intervention, but studies in this area are ethically challenging
and more in depth research is needed.
Introduction
Atopic dermatitis (AD) is a skin condition characterized by unrelenting itchiness and affects
more than a quarter of children worldwide (Nutten, 2015). AD is clinically difficult to diagnose as it
lacks a definitive biomarker and diagnosis relies on critical evaluation of symptoms from a trained
clinician (Eichenfield et. al., 2013). Nonetheless, the number of cases of AD has been increasing
substantially in recent decades, prompting an urgency to determine if any preventative measures can
reduce its incidence (Eichenfield, 2013). Despite having a genetic component, several environmental
risk factors of AD are also recognized and can spike flare ups that trigger the itch-scratch cycle,
meaning the more you scratch, the more it itches. AD symptoms have an episodic pattern of flare ups

that nutrition may be able to regulate and possibly, through early intervention, prevent all together
(Greer et. al., 2008). Scientists have recognized that early dietary choices in formative childhood years
can affect the development of disease later in life (Greer et. al., 2008).
Early nutritional intervention can begin as early as pregnancy and it has been suggested that
antigen avoidance during pregnancy could prevent the sensitization of the babys immature immune
system (Kramer & Kakuma, 2014). After birth, breastfeeding is widely considered as the ideal source
of nutrition and is generally recommended that exclusive breastfeeding is beneficial in the prevention
of AD. However, new evidence suggests the protective effects may not be as definitive as previously
thought (Yang et. al., 2008). Finally, the timing of introduction of complementary foods may effect AD
symptoms and other diseases later in life, but the outcomes are controversial. The purpose of this
literature review is to evaluate the nutritional options during pregnancy and the first 1000 days of life to
explore the implications it may have on the prevention of atopic dermatitis.
Atopic Dermatitis
Definition and Pathogenesis
AD is a chronic inflammatory skin disease caused by a combination of genetic and
environmental factors. It is characterized by dry skin, intense pruritus, and eczematous lesions
(Weidinger & Novak, 2016; Simpson et. al., 2012). First manifestations of AD usually appear early in
life and often precede other allergic diseases such as asthma or allergic rhinitis (hay fever) (Simpson et.
al., 2012). AD is widely considered the first clinical display of atopy, although recent evidence suggests
the development of allergic disease may not be cemented into this pattern (Barberio et. al., 2008). It is
considered one of the most common skin conditions and over the past several decades, the incidence of
AD and its comorbidities such as asthma, allergic rhinitis, and food allergies has increased dramatically
(Greer, Sicherer, & Burks, 2008; Weidinger & Novak, 2016; Silverberg, 2016; Margolis et. al., 2012;
Dharmage et. al., 2013) AD poses a significant burden on health-care resources and patients quality of

life due to financial costs, sleep deprivation from itchiness, employment loss, and time required to treat
(Nutten, 2015).
Definition. Although atopic dermatitis is the proper name for the condition, AD may be referred
to in a few different ways. It may be called pediatric dermatitis because it so commonly affects
children, however, the disease can carry into adulthood as well (Kenner et. al., 2015). Commonly, AD
is referred to as eczema, however, the American Academy of Dermatology (AAD) differentiates
between them. Eczema is a nonspecific, broad term for several forms of inflammatory rash, whereas
atopic dermatitis is a specific kind of eczema that follows a relapsing course of exacerbation and
remission with a predisposition for certain areas of the body. AD lesions are usually symmetrical and
are located primarily on flexural surfaces of the body such as the creases of elbows or behind knees, as
well as the scalp, face, neck, hands, and feet. Acute outbreaks cause redness and scaling which can lead
to the lichenification, exaggeration of lines in the skin, and hyperpigmentation associated with chronic
AD. No clinical biomarker exists, but patients present with multiple immunological abnormalities
(Kenner, Friedlander, Hanifin, & Norton, 2015).
Pathogenesis. Though it is well known that the skin is important as a barrier against pathogens,
allergen exposure, and protects against sensitization, the exact etiology of AD is unknown (Silverberg,
2016). AD is a combined dysfunction of the epidermal barrier and inflammatory process and is often
considered the first sign of allergic disease, or atopy (Silverberg, 2016; Margolis et. al., 2012).
Recently, AD has drawn more focus from the medical community because of its associations with the
increased risk of developing these other atopic diseases, a progression often referred to as the atopic
march (Dharmage et. al., 2013). The atopic march suggests that atopy progresses sequentially from
eczema during infancy, to food allergy, to rhinitis, and finally to asthma in childhood (Figure 1) (Pinart
et. al., 2016). However, new evidence suggests that the atopic march might not be so linear and may
not always follow the classic sequence. One cohort study out of Genoa, Italy, followed 745 children

ages 6 to 9 years old who were diagnosed with asthma but had no symptoms of AD. At the end of the
nine-year study, 20% had developed AD, suggesting that the classic atopic march symptoms may only
be related, not sequential (Barberio et. al., 2008). It has been estimated that approximately 30% of
patients with AD develop asthma and 60% develop allergic rhinitis. It is also acknowledged that AD
and food allergy co-associate at similar rates (Barberio et. al., 2008).

Figure 1. Onset of symptoms in the atopic march. (The Allergy March, 2012)
The exact cause of AD is unknown, but there are two well-known theories on the mechanism
behind the condition. Both theories have strengths and weaknesses, but most of the uncertainty
regarding etiology is due to that variation in presentation across affected individuals (Dharmage et. al.,
2013).
The first theory on the common mechanism linking the allergic disorders is the predisposition
for immunoglobulin E (IgE) mediated responses to environmental stimuli (Dharmage et. al., 2013). IgE
antibodies are formed when an antigen is introduced to the body, either through the lungs or through
the epithelium as seen in AD. The antigen is presented to the immune system where B-lymphocytes are
transformed into plasma cells that produce IgE antibodies. The antibodies are designed to bind to a

specific antigen, and once released into the systemic circulation, are available to mount a quick
response for future contact with that antigen. In this way, IgE antibodies play a key role as
gatekeeper, and are pivotal in the management and recognition of pathogens and foreign material
(Dharmage et. al., 2013). IgE initiated immune responses are usually beneficial, as the typical reaction
to an antigen triggers mucus secretion, sneezing, coughing, inflammation, and itching, which function
to try and expel the pathogen from the host (Portnoy, 2015). However, in the case of atopy, the over
sensitization of IgE antibodies causes an inappropriate response to innocuous substances and manifests
in chronic inflammatory conditions like atopic dermatitis, asthma, allergic rhinitis, and food allergy
(Dharmage et. al., 2015). Those with skin barrier dysfunction mutations, commonly found in AD
patients, are more likely to interact with these antigens through the malformed barrier in the skin,
causing the typical presentation of AD as the first clinical sign (Dharmage et. al., 2015).
While the theory of IgE-sensitization linking the atopic march is well known, new evidence
suggests this association with other allergic disease may be weaker than previously thought (Pinart et.
al., 2016) In a study of more than 27,000 children from 12 ongoing European birth cohort studies
involved with the Mechanisms of the Development of Allergy project, researchers showed that despite
IgE-sensitization being independently associated with all three atopic diseases, only 38% of cases
involving children with coexisting disorders are attributable to the presence of IgE-sensitization.
Excess comorbidities were seen in children both with and without IgE-sensitization, yet could not be
attributed to chance (Pinart et. al., 2016).
The second theory relating AD involves a mutation in the human filaggrin gene. The barrier
dysfunction caused by the mutation leaves cells exposed to antigens through the open wounds caused
by scratching (Silverberg, 2016). When exposed to allergens, Langerhans cells from the immune
system cause an inflammatory reaction in the lymph nodes. This surge of inflammatory activity
includes a cascade of cytokines that trigger the involvement of helper T cells, tumor necrosis factor,

and interferon gamma (IFN-). Each of these compounds is involved in the inappropriate response to
inflammation, and IFN- is specifically known to further downregulate the human filaggrin gene (FLG)
(Silverberg, 2016). Filaggrin is a major structural protein in the stratum corneum layer of the skin.
Carriers of the filaggrin loss-of-function mutation (FLG null) are estimated to have a three times
increased risk of developing AD, and children with FLG null mutations are more likely to have
persistent AD into adulthood (Margolis et. al., 2012). The dysfunction in the epidermal barrier allows
for sensitization to allergens found in the environment. This sensitization facilitates the atopic march,
causing an influx of symptoms of food allergies, allergic rhinitis, and asthma (Silverberg, 2016).
Diagnosis
Atopic dermatitis was first described in the early 1800s, but remains a challenge to diagnose
because a definitive laboratory biomarker has never been identified (Leung, Boguniewicz, Howell,
Nomura, & Hamid, 2004). The most closely related laboratory feature is elevated serum IgE, but
approximately 20% of diagnosed AD patients have normal IgE levels. Some of these affected
individuals with IgE within normal limits will develop elevated levels later, which may suggest that
elevated serum IgE presents secondary to the skin barrier defect (Eichenfield et. al., 2013).
Additionally, elevated IgE levels are allergen related and not specific to AD. Approximately 55% of
Americans may have elevated IgE levels, as it can present in a variety of non-atopy related conditions
such as other autoimmune disorders and some cancers (Eichenfield et. al., 2013). Evidence also shows
that even in AD patients with elevated levels, IgE has no correlation with severity (Eichenfield et. al.,
2013). For these reasons, AD diagnosis remains subjective and must be decided on the basis of medical
signs and patient-reported symptoms, rather than diagnostic tests.
Clinical evaluation of AD presents a further challenge due to the uneven progression and the
variability in the severity and location of the lesions (Samochocki & Dejewska, 2012). There are
several clinical diagnostic methods in use today because no one method has been named as the

standard. The most well-known set of standards for diagnostics is the Hanifin and Rajka criteria. The
Hanifin and Rajka criteria were proposed in the 1980s following a panel discussion from experts in
atopic dermatitis (Lee, 2016). Their criteria encompass symptoms, aggravating environmental factors,
abnormal laboratory findings, visual findings, relevant family history, and past medical history (Lee,
2016). This method proves difficult to use in daily practice because it requires analyzing twenty-seven
separate criteria, including four major and twenty-three minor criteria (Samochocki & Dejewska,
2012). In order for the diagnosis to be made, three of the four major criteria and three of the twentythree minor criteria must be met (Eichenfield et. al., 2013). Issues with this diagnostic method are well
documented. Several minor criteria conditions are said to lack specificity or are poorly defined, while
others, although specific, are rare for AD (Eichenfield et. al., 2013). Despite its sensitivity, the inherent
problems of the Hanifin and Rajka criteria have spurred the proposal of new and innovative diagnostic
criteria. The United Kingdom (UK) Working Party turned the Hanifin and Rajka criteria into a more
concise definition that can be used by non-dermatologists (Eichenfield et. al., 2013). Their one
mandatory and five major criteria do not require any laboratory testing, but are significantly less
sensitive in cases of unusual presentation (Eichenfield et. al., 2013). In 2003, the American Academy of
Dermatology (AAD) revised these criteria into an approach that was suitable for all ages and is well
suited for use in a clinical setting (Table 1). Despite the AADs pragmatic approach, their new criteria
have yet to be universally adopted and there remains no gold standard for AD diagnosis (Eichenfield et.
al., 2013).

Table 1. Features to be considered in the diagnosis of patients with atopic dermatitis. AAD adaptation
of Eichenfield et. al. (2003).
Prevalence
Atopic dermatitis is one of the 50 most prevalent diseases in the world (Madhok et. al., 2015). It
affects up to 25% of children and 1-3% of adults (Eichenfield, 2013; Nutten, 2015). Its prevalence has
increased two- to threefold during the past three decades in developed countries but remains much
lower in agriculturally dominated countries (Leung, 2004). AD onset is most common between three
and six months of age and most affected children will grow out of the disease by adulthood, but 10% to
30% do not (Nutten, 2015). The most well-known global trend data for AD comes from the
International Study of Asthma and Allergies in Children (ISAAC) which covers nearly two million
children in one hundred countries and shows that prevalence of AD is changing throughout the world,
with the largest increase in newly developing countries (Nutten, 2015). The highest racial prevalence
has been seen among black children (Yaghmaie, et. al., 2013).
Comorbidities and Patient Burden

Atopic dermatitis comes with several well-documented comorbidities, including food allergy,
allergic rhinitis (hay fever), asthma, and an increased risk for cutaneous infection (Yaghmaie,
Koudelka, & Simpson, 2013). As previously discussed, AD is widely considered the first in a series of
allergic diseases known as the atopic march. These comorbidities - food allergy, allergic rhinitis, and
asthma - are well known in children and less frequently, can continue into adulthood (Hong et. al.,
2012). The condition of multiple allergic diseases is common among atopy sufferers, as patients with
one allergic condition have an increased risk of developing another (Hong et. al., 2012).
Patients with AD also experience mental health issues as a comorbidity, but the connection is
less well understood (Yaghmaie, et. al., 2013). Children with AD experience increased psychological
stress compared to their peers. Unrelenting itchiness, even in relatively mild cases, can negatively
influence quality of life, and severe cases have been compared to type 1 diabetes in terms of burden on
the child and family (Yaghmaie, et. al., 2013; Filanovsky et. al., 2016). Excoriation,orscratchingtothe
pointofdrawingbloodandproducinglesions,exacerbatethiscycle.Symptoms of AD and its
comorbidities can cause increased irritability, fussiness, and behavioral issues in children, especially
during intense itching episodes (Yaghmaie, et. al., 2013). Children can also suffer low self-esteem,
social embarrassment, and socialization difficulties stemming from visible lesions (Filanovsky et. al.,
2016). This may cause the heightened anxiety and fearfulness often seen in young AD patients
(Yaghmaie, et. al., 2013). However, sleep deprivation usually caused by nighttime itching seems to
have the most substantial effect on the patients wellbeing. Loss of sleep is proposed to be the primary
mechanism causing children with AD to be at 1.5 fold increased risk for developing attention deficit
hyperactivity disorder (ADHD) (Carroll et. al., 2005). Atopic dermatitis and sleep loss have also been
associated with depression, anxiety, conduct disorder, and autism (Weidinger & Novack, 2016). In a
survey of 100 AD patients, 84% reported difficulty falling asleep and 79% reported being awakened by
itchiness (Carroll et. al., 2005). In a recent study using wrist actigraphy to measure sleep quality in AD

patients, researchers found children with AD lose an average of two hours of sleep per night. This is
often followed by daytime drowsiness that can be compounded with drowsiness caused by
antihistamine use. Drowsiness during school can cause behavior problems and inhibit performance
(Carroll et. al., 2005). Additionally, stress often triggers itchiness, causing a cycle of scratching and
psychological burden that is difficult to break (Carroll et. al., 2005).
Cost. The financial burden of AD includes direct cost and indirect costs. Direct costs include
health care visits, prescription medications, over the counter treatments, special moisturizers, foods,
detergents, textiles, and treatments not covered by insurance (Filanovsky et. al., 2016). However, most
of the burden to families is felt through indirect costs. In a 2015 study, researchers found the average
personal cost per month totaled $274 ($75 on direct costs, $199 on indirect costs). The most significant
part of the direct costs came from medications and treatment products including moisturizers, topical
steroids, bath products, oral prescriptions, and antihistamines (Filanovsky et. al., 2016). Indirect costs,
the largest portion of total cost, resulted mostly from lost workdays by the caregiver, which averaged
20.5 hours missed in the month surveyed (Filanovsky et. al., 2016). Difficult to calculate costs that
were not surveyed in this study include travel costs, home changes such as carpeting changes or
removal of pets, insurance deductible costs, and caregiver career choice. Other non-financial burdens of
AD include missed sleep by both child and caregiver, lost school days, behavioral problems, and stress.
Some caregivers even reported being accused of neglect or abuse due to misconceptions about their
childs condition (Filanovsky et. al., 2016).
Treatment
Current medical interventions. There is no cure for atopic dermatitis so treatments focus on
managing symptoms and achieving long term control (Weidinger & Novak, 2016). Treatment centers
on continuous emollient protection to repair the epidermis, anti-inflammatory therapy with topical

corticosteroids, and avoidance of individual triggers. Severe or unresponsive cases may require
phototherapy or immunosuppressant medications (Weidinger & Novak, 2016).
The first and most frequent treatment is generous use of emollients. Emollients soften the skin
by providing lipids to reduce water loss and forming a protective barrier with humectants such as urea,
glycerine, and lactic acid (Weidinger & Novak, 2016). Emollients with fragrances, perfumes, or
excessive ingredients should be avoided as they can be irritating and may induce allergic reactions
(Weidinger & Novak, 2016). Specialized topical treatments like corticosteroids are prescribed
medications used to control acute flares. May misconceptions surround the use of topical
corticosteroids and fears about their perceived adverse effects often cause a lapse in treatment due to
poor adherence, but a 2012 systematic review showed there is little risk in appropriate use during
exacerbations (Weidinger & Novak, 2016).
Avoidance of personal triggers can help prevent flares and break the itch-scratch cycle that fuels
the disease. That is, the more you scratch, the more it itches, so breaking the cycle and avoiding
irritants is crucial. AD is exacerbated by physical and chemical irritants, exposure to food allergens,
stress, dust, detergents, fragranced soaps, some cosmetic products, and harsh materials (Kessel &
Goldenberg, 2016). Patients are advised to use mild detergents and fragrance free soaps. Cosmetic
products are not always required to list all ingredients so its best to purchase products specially
formulated for sensitive skin (Kessel & Goldenberg, 2016).
Risk Factors
Four major risk factors have been hypothesized to be most influential in the development of
AD. The first risk factor is genetic, although the connection is poorly understood. The other three risk
factors -- excessive cleanliness, antibiotic use early in life, and timing of the introduction of
complementary foods are all environmental.

The most well documented and strongest risk factor for the development of AD is a family
history of allergic disease, especially AD itself (Weidinger & Novak, 2016). Currently, scientists have
used gene mapping to distinguish 32 susceptibility loci, but these only explain 20% of the genetic
inheritance (Weidinger & Novak, 2016). As mentioned, the most influential of these is the FLG protein.
Epidemiological studies have suggested up to 10% of people with European ancestry carry a single
copy of the FLG null mutation. Carriers hold an increased risk for development of the disease, but
nearly 60% of carriers will never develop AD. Additionally, many individuals with AD do not carry this
mutation, suggesting FLG mutations are neither essential nor sufficient to develop the disease without
other influence (Weidinger & Novak, 2016).
The first hypothesized environmental risk factor regarding risk for atopy proposes that the
significant increase in cleanliness in the past several decades has contributed to the risk of AD around
the world. Prevalence of AD is higher in urban communities, industrialized nations, smaller families,
and in families of higher socioeconomic status (Flohr, Pascoe, & Williams, 2005). Some studies have
suggested the development of AD may be related to the increase in hygienic practices such as frequent
washing of the hands and body, as well as frequent cleaning of living spaces (Flohr et. al., 2005).
Explanations range from the simple abrasive nature of soap and water wearing down already dry,
sensitive skin, to the more complicated mechanism related to the introduction of bacteria early in life
(Flohr et. al., 2005). The latter theory, known as the hygiene hypothesis, was developed by David
Strachan in 1989 when he noticed the significant rise in allergic disease in developed countries post
industrial revolution and the relative stability of AD rates among less developed nations (Strachan,
1989). He noticed an inverse relationship between children with older siblings and children with AD.
The first child in a family is kept cleaner and more sterile than subsequent children, weakening their
immune system and increasing their risk of developing symptoms. He also compared children living on
farms with rural controls and found that AD symptoms were significantly reduced in the children raised

on farms (Strachan, 1989). Since then, this phenomenon has been documented several times. The
higher bacterial load associated with growing up on a farm seems to have an immune boosting effect
that may be protective against allergic disease (Kilpelainen, Terho, Helenius, & Koskenvuo, 2000).
However, though exposures may be protective at moderate levels, exposure to bacterial can be
dangerous, especially for those with open sores as are common for AD sufferers (Flohr et. al., 2005)
Early use of antibiotics has been suggested as a second possible environmental risk factor for
the development of AD. In a meta-analysis of 20 observational studies involving nearly 290,000
children, researchers found that a positive association between early antibiotic use and AD
development that increased risk by up to 40% (Madhok, Futamura, Thomas, & Barbarot, 2015). Risk
increased by 7% for each addition course of antibiotics used under one year of age and seemed to be
highest for broad spectrum antibiotic use. However, causation cannot be determined in the case of a
skin barrier defect because children with atopy may be at higher risk for infection and thus, have
increased antibiotic use (Madhok et. al., 2015).
The final environmental hypothesis involves the introduction of complementary foods and
subsequent exposure to new potential allergens in the diet (Niinivirta, Isolauri, Nermes, & Laitinen,
2013). When breastfeeding is no longer enough to feed a growing infant, solid foods need to be
introduced to complement breastmilk. Hypotheses regarding the introduction of solid foods, especially
those with common antigens like cows milk, remain controversial. These will be discussed at length
later on.
Early Dietary Strategies for Health
Early Nutrition and Health
Early nutrition has a key formative effect on health outcomes later in life (Koletzko, Brands,
Poston, Godfrey, & Demmelmair, 2012). Poor dietary choices starting in early postnatal life seem to
create a profound risk of non-communicable diseases like obesity, cardiovascular disease, and type 2
diabetes (Koletzko et. al., 2012; Wrottesley, Lamper, & Pisa, 2015). Short term changes in the

environment during the first year of life influence the infant during a time of extraordinary plasticity,
which can permanently affect organ development. Evidence shows that the first 1000 days of an
infants life -- from conception to around age 2 -- encompass a delicate window in the prevention of
non-communicable diseases through epigenetic programming (Wrottesley et. al., 2015). During this
window, nutrition is essential in the development of the child. The first 1000 days of life are a period of
critical plasticity that put the child at risk for poor environmental exposures, but also provides an
opportunity for intervention. Adequate nutrition during this time has been linked to decreased mortality
and morbidity, increased cognitive, motor, and socioemotional development, increased social
performance and learning capacity, increased adult height, decreased obesity and chronic degenerative
diseases, and increased work capacity and productivity (Cunha et. al., 2015).
Adequate nutrition in the 1000 days of an infants life begins with maternal nutrition.
Inadequate maternal nutrition has long been linked to adverse outcomes for both mother and child.
Mothers who are underweight, overweight, or have micronutrient deficiencies are associated with many
conditions including preeclampsia, premature delivery, birth trauma, small for gestational age infants,
suboptimal growth, and perinatal morbidity and mortality (Wrottesley et. al., 2015). Calorie monitoring
is important to ensure proper weight gain, along with supplementation of micronutrients like iron and
folate (Cunha et. al., 2015).
Breastfeeding
After birth, the ideal source of nutrition is breast milk. The protective effect of breastfeeding
works in two main ways, by promoting development of the newborns intestinal immunity and by
providing bioactive immune factors (Cunha, Leite, & Almeida, 2015).
Mechanism of action. It is widely accepted that postnatal nutrition is best supported by breast
milk. Breastmilk contains all the essential nutrients for growth and development and changes
composition with the needs of the growing infant. This is especially helpful in stimulating the

maturation of the infants intestinal mucosa and host defenses (Walker, 2010). Colostrum in particular
has been shown to protect against immune mediated infections while the infants immune system is still
immature. Because of this, the longer breastfeeding is delayed, the greater the risk of infant mortality
by infection. In fact, evidence shows breastfeeding within the first hour of life is associated with a 22%
reduced risk of newborn mortality (Cunha et. al., 2015). Several studies have found that breastfed
infants have a decreased risk for infections than formula fed infants, including a decreased risk of
diarrhea in the first 6 months of life. This can be life-saving in low income countries where diarrhea is
a major cause of death (Walker, 2015). During this early period of life while the intestinal immune
defenses are still developing, mothers milk provides the missing immune components to protect the
infant during this vulnerable time (Walker, 2015). In one example, infants are born deficient in
secretory immunoglobulin A (sIgA), and they cannot develop this component of immunity until the
intestine is populated by Bifidobacteria and Lactobacilli. It can take 30 days or more to develop
significant sIgA levels. During this time, levels of sIgA in breast milk are at their highest and specific to
the mother and babys environment. Additionally, the fermentation of oligosaccharides in breast milk
stimulate the population of these gut flora, helping the baby to develop their own immune defenses
(Walker, 2015).
Researchers have suggested a protective effect of breast milk is compounded by its ability to
decrease the immature and overactive inflammatory response in the infant gut. Several antiinflammatory components of breastmilk such as transforming growth factor (TGF)-, interleukin (IL)10, erythropoietin, and lactoferrin have been shown to contain this response, which may reduce the
incidence of autoimmune diseases like celiac disease (Walker, 2015). The decrease in inflammation
may also be the mechanism that deceases risk of necrotizing enterocolitis in breastfed infants compared
to formula fed infants (Walker, 2015).

Protective effect of breastfeeding. In 2011, the U.S. Department of Health and Human Services
(DHHS) released the U.S. Surgeon Generals Call to Action to Support Breastfeeding public statement.
According to the Surgeon General, breast milk is ideal for the nutritional needs of a growing infant and
protects against disease thanks to its immunological and anti-inflammatory properties (U.S.
Department of Health and Human Services [DHHS], 2011). The report goes on to affirm the health

risks of formula feeding and early weaning, including everything from common ailments like diarrhea
and ear infections to more serious conditions like leukemia and sudden infant death syndrome (SIDS).
The health benefits appear to extend to the mother as well, as the DHHS cites increased risk of breast
and ovarian cancer in women who have never breastfed. The DHHS findings of the increased risk of
various diseases found in non-breastfed infant are summarized in table 2 (DHHS, 2011).

Table 2. Excess risk of disease among non-breastfed babies (U.S. DHHS, 2011).

In 2012, the American Academy of Pediatrics (AAP) released a policy statement reinforcing
their current view on breastfeeding (American Academy of Pediatrics, 2012). The AAP statement
continues to support its recommendation of exclusive breastfeeding for 6 months, followed by
continued breastfeeding while complementary foods are introduced. Breastfeeding should continue for
a year or longer as long as it suits the needs of both infant and mom. Similar to the health benefits cited
by DHHS, evidence presented by the American Academy of Pediatrics (2012) shows that breastfeeding
is associated with the reduction in the risk of acute otitis media, atopic dermatitis, asthma, severe lower
respiratory tract infections, gastroenteritis, obesity, type 1 and type 2 diabetes, necrotizing enterocolitis,
childhood leukemia, and SIDS (American Academy of Pediatrics, 2012). Further, the statement
addresses that while medical contraindication for breastfeeding are rare, hospitals and medical facilities
are encouraged to monitor and promote healthful breastfeeding practices as outlined by the Surgeon
Generals Call to Action, the CDC, and the Joint Commission (American Academy of Pediatrics, 2012).
Breastfeeding rates. Rates of breastfeeding are improving in the U.S. In 2014, the
Division of Nutrition, Physical Activity, and Obesity within the Centers for Disease Control and
Prevention (CDC) released its biennial report Breastfeeding: Report Card showing only a marginal
increase in breastfeeding (Center for Disease Control and Prevention [CDC], 2014). The CDCs goal is
to improve the health of Americans and promotes breastfeeding as an important strategy in
accomplishing that goal. Despite slow improvement, the U.S. still falls short when compared to other
developed countries. For example, exclusive breastfeeding at 6 months reaches 40% in the Netherlands
compared with just 16% in the U.S (Donnan et. al., 2013). The CDC hopes to improve the duration of
breastfeeding in the U.S. in coming years and supports this with objectives in Healthy People 2020
(table 3). These objectives aim to increase the prevalence and duration of breastfeeding and considers
them a significant part of the nations health priorities (CDC, 2014).

Table 3. Healthy People 2020 objectives relating to breastfeeding goals for Americans. (CDC, 2014).
Barriers to breastfeeding. Despite the innumerable benefits breastfeeding provides, it may not
come easy to some mothers and challenges do exist. Researchers Dunn, Kalich, Henning, & Fedrizzi
(2014) examined common barriers to breastfeeding in a 2014 study. They found some barriers may be
medical, such as mastitis, pain or fear of pain, prescription drug use, or substance abuse (Dunn, Kalich,
Henning, & Fedrizzi 2014). Further, barriers may also come from the environment around the mother,
including modesty issues or embarrassment when feeding in front of others, negative reactions from
family members or significant others, and availability of free formula samples. Personal barriers may
also prevent breastfeeding, including ethnic or cultural perceptions, lack of knowledge of the benefits
of breastfeeding, sexual abuse, or worry she will not produce enough milk (Dunn et. al., 2014). Of the
mothers Dunn questioned, the biggest reported barrier to breastfeeding at the individual level was
modesty or discomfort at breastfeeding in front of others. At the interpersonal level, many mothers
expressed it was the desire from family members to feed the baby that prompted them to turn to
formula feeding. At the community level, the most common barrier was the lack of knowledge
surrounding breastfeeding laws. Many mothers believed breastfeeding in public might be considered
indecent exposure and would not feed in public (Dunn et. al., 2014).

Formula Feeding

Despite the known benefits of breastfeeding, some mothers choose to formula feed. Cows milk
formulas are the most basic and the most common. These formulas try to recreate breast milk by
altering cows milk protein to resemble human ones. They usually contain 20 kcals per ounce compared
to the approximate 22 kcals per ounce in human milk (OConnor, 2009). Most formulas are fortified
with iron, which is important in preventing iron deficiency anemia in infants. Low iron formulas are
available and some parents speculate that they reduce colic, but there is little medical evidence of this
and low iron formulas should be avoided unless indicated by medical necessity (OConnor, 2009).
Some formulas are enriched with docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA), two
omega 3 fatty acids found in breastmilk but not basic formula. These compounds are important in the
development of the nervous system, but there is controversial evidence on their effectiveness in
formulas. Most infants handle cows milk formula well, although some evidence suggests it may
provoke the early development of allergies (Bhanegaonkar et. al., 2015). For infants who are born at
high risk for allergies, breastfeeding may be the best option for reducing risk, although this remains
controversial. Other types of formula like protein hydrolysate may help to reduce the childs risk of
allergies (Lee et. al., 2015). Cows milk allergy is the most common allergy in children. It affects 2-3%
of infants, and these children are often co-sensitized to whey and and casein. In cases of infants with
cows milk or other allergies that cannot be breastfed, a hydrolysed, amino acid based, or soy based
formula is indicated (Lee et. al., 2015). These formulas can be more expensive, so breastfeeding has
traditionally been the first recommendation. However, some evidence suggests that hydrolyzed
formulas may be beneficial in the prevention of some forms of allergic disease, such as atopic
dermatitis (Berg et. al. 2010).
Early dietary intervention and prevention of AD
Although atopic dermatitis and other allergic diseases have a clear genetic component,
environmental aspects involving early infant nutrition may prevent or delay the onset of AD (Greer et.

al., 2005). It is unclear exactly what dietary recommendations change the outcome of AD, so families
have many strategies to choose from to try to prevent, delay onset, and reduce severity of AD
symptoms. Maternal antigen avoidance is the earliest dietary intervention possible. Once the child is
born, choices in breastfeeding and formula feeding must be made, with special consideration given for
high risk infants versus low risk infants. Finally, the timing of introduction of complementary foods
may affect the onset of atopic dermatitis (Greer et. al., 2008).
Maternal Diet and AD outcomes
The earliest available dietary intervention for a child is during pregnancy. Maternal dietary
antigens are known to cross the placenta and it has been suggested that antigen avoidance during
pregnancy could reduce the risk of development of allergic disease in the infant (Kramer & Kakuma,
2014). The main focus of this intervention is on high risk infants, as defined as a family history of
atopic disease in the mother, father, or older sibling.
In the late 1980s, several studies evaluated the usefulness of elimination diets in pregnancy. One
study by Flth-Magnusson, man, & Kjellman, (1987) asked 334 pregnant women to eliminate (or
reduce as much as possible) their consumption of common antigenic foods such as cows milk, egg,
peanut, and fish (Flth-Magnusson, man, & Kjellman 1987). The evidence from the trial suggests that
antigen avoidance during pregnancy does not have a positive effect on the development of AD in the
infants first 18 months (RR 1.01; 95% CI: 0.57-1.79). In fact, cord blood IgE levels were higher in the
antigen avoidance group. Additionally, antigen avoidance was associated with potential increased risk
of preterm birth and low birthweight (Flth-Magnusson et. al., 1987). Because of the adverse effects
found in this trial and similar trials of its time, intervention studies that require avoidance have not been
repeated and most data comes from retrospective observational studies (Kramer & Kakuma, 2014).
In general, maternal avoidance diets during high atopy-risk pregnancies have showed no
protective effects on the development of atopy in the child. It is widely recommended that antigen

avoidance should not be used as a primary intervention for allergic disease and may be potentially
harmful (Kramer & Kakuma, 2014). In fact, a 2014 prospective prenatal cohort study of high atopicrisk pregnancies found that higher maternal intakes of antigenic foods during early pregnancy were
associated with lower risk of allergy in childhood (Bunyavanich et. al., 2014). Peanuts, cows milk, and
wheat were associated with decreased atopic response in the child, while egg and soy consumption had
no effect. In particular, wheat consumption during the second trimester had a direct effect on AD
outcome in the child (Bunyavanich et. al., 2014). A Cochrane review involving 952 participants
concluded that antigen avoidance during pregnancy probably does not have a protective effect against
AD on the baby during the first 18 months of life (Kramer & Kakuma, 2014). Because of the lack of
significant beneficial evidence, there are no recommendations for avoiding intake of antigens during
pregnancy at this time (Kramer & Kakuma, 2014).
Breastfeeding and atopic dermatitis
Breastfeeding is widely recommended for all infants, regardless of allergic propensity, due to
the extensive list of benefits discussed earlier. In mothers with a high risk of an atopic infant, exclusive
breastfeeding is generally recommended for its potentially protective effect regarding allergic disease.
However, the evidence for effect of breastfeeding on AD is still controversial and difficult to study. For
one, it would be unethical to run a randomized clinical trial with a non-breastfeeding group (Gamboni,
Allen, & Nixon, 2012). Similarly, double blinding is impossible. Further, there are many ways to feed a
growing infant, and ultimately, it is a familys decision. This can lead to a reverse causation bias, in
which choices made by families are influenced by current guidelines, which are then recycled into new
studies where parents choose their method of feeding (Gamboni et. al., 2012). Despite these issues,
studies do exist but their findings are far from undisputed.
Traditionally, infants with a high risk for atopy are recommended to breastfeed for 4 to 6
months (AAP, 2012; CDC, 2014). In a 2001 meta-review of 18 prospective studies, Gdalevich et. al.

(2001) examined the incidence of AD in breastfed infants and in infants fed with cows milk formula
(Gdalevich, Mimouni, David, & Mimouni, 2001). The authors gathered MEDLINE data from January
1966 to 2000. Overall, there was a 42% decreased risk of the development of AD in high risk infants
who had been exclusively breastfed for 3 months (OR: 0.58, 95% CI: 0.4-0.92). However, there was no
protective effect in infants without a history of allergic disease (OR: 1.43, 95% CI: 0.72-2.86)
(Gdalevich et. al. 2001). Kramer and Kakuma (2014) also found no benefit of exclusive breastfeeding
for more than 3 months on the risk of AD in low risk infants (Kramer & Kakuma, 2014). An
observational study of healthy infants from the German Infant Nutritional Intervention (GINI) cohort
found exclusive breastfeeding provided a significant protective effect in high risk infants compared
with cows milk formula (Laubereau et. al., 2004). The European Academy of Allergology and Clinical
Immunology concluded that 4 to 6 months of breastfeeding was associated with a decreased risk of AD
up to 3 years old (Gamboni et. al., 2012).
However, other studies indicate the association between breastfeeding and AD may not be so
protective. A 2009 meta-review found no protective effect of exclusive breastfeeding for 3 months on
the risk of AD (Yang, Tsai, & Lu, 2009). A 2010 study of a high risk birth cohort in Copenhagen found
that increased duration of breastfeeding increased the risk of AD but decreased the risk of asthma
(Giwercman et al., 2010). In a Japanese study, Ito and Fujiwara (2014) studied 38,757 infants born in
Japan in 2001. In this study, questionnaires were mailed to participants when the infant was 6, 18, 30
and 42 months old. Mothers were asked about their feeding patterns and were categorized into
exclusive breastfeeding (22.4%), partial breastfeeding (71.9%), and exclusive formula feeding (5.7%).
They were also surveyed on their childs symptoms or diagnosis of AD. Overall, 3.6% of children had
persistent AD and 22.7% had episodic AD. The infants who had persistent AD were more likely to also
be the infants who had exclusively breastfeed and who had breastfed at all for more than 6 months
(exclusive breastfeeding and AD: 26%, >6 months: 62.3%). Exclusive breastfeeding and breastfeeding

at all for more than 6 months were 21.7% and 55% respectively for those without family history of AD
(Ito and Fujiwara, 2014). The results of the statistical analysis showed that breastfeeding was positively
associated and dose-response associated with risk of AD. Exclusively breastfed infants were 26% more
likely to have AD (OR: 1.26; 95% CI: 1.12-1.41). Further, infants who had breastfed longer were also
more likely to develop AD (OR: 1.24; 95% CI: 1.11-1.38). Ito and Fujiwara (2014) concluded
breastfeeding was associated with increased risk of AD. The authors hypothesized the mechanism of
action, but conceded more research would need to be done in this area. They proposed the hygiene
hypothesis may explain the association between AD and breastfeeding, as breastfeeding reduces the
effect of exposure to bacteria or endotoxins on the immune system. This means that the protective
effect breastfeeding has on other diseases may actually increase the risk of AD development. Because
the hygiene hypothesis involves an inverse relationship with the number of older siblings a child has,
Ito and Fujiwara controlled for older siblings as a proxy for the hygiene hypothesis. Once this
confounder was adjusted for, the association became weak but remained significant. The authors still
described it as a possible mechanism but agreed it was unlikely (Ito and Fujiwara, 2014).
The association found in Ito and Fujiwara has been found in several smaller studies as well.
This association in high risk infants could be related to the IgE levels in the mother (Wright, Sherrill,
Holberg, Halonen, & Martinez, 1999). Wright et. al., (1999) found mothers with IgE concentrations in
the lower two tertiles were associated with reduced serum IgE levels in the infant. However, mothers
with IgE levels in the highest tertile were associated with increased IgE in the child. This dependency
on the degree of atopy in the mother could explain the inconsistencies in breastfeeding research and its
association with AD (Wright et. al., 1999). Additionally, mothers who notice early symptoms of atopy
may be more likely to continue breastfeeding longer to try and reduce the severity of their childs
symptoms. This could help explain the association between increased length of breastfeeding and
increased risk of AD (Sears et. al., 2002).

Whether or not breastfeeding helps in the prevention of AD, the benefits far outweigh the risks.
It reduces the risk for other disorders and helps forge a bond between mother and baby (Yang et. al.,
2009). Although a strong association between breastfeeding and the prevention of AD is not clear at
this time, exclusive breastfeeding is still recommended due to its numerous other benefits. Studies
involving breastfeeding are logistically and ethically challenging, so results should be interpreted with
caution (Yang et. al., 2008).

Formula Feeding and Atopic Dermatitis

For children with a family history of allergic disease, nutritional prevention of atopic dermatitis
has focused on avoiding early exposure antigens in cows milk by hydrolyzing intact milk proteins
(Berg et. al., 2010). In a double blind, prospective intervention trial from the German Infant Nutritional
Intervention (GINI) cohort, researchers gathered 5,991 heathy term infants. Of these, 2,252 infants with
a family history of allergic disease were randomized to a category of hydrolyzed formula: partially
hydrolyzed whey (pHF-W), extensively hydrolyzed whey (eHF-W), extensively hydrolyzed casein
(eHF-C), or a conventional cows milk formula (CMF). Researchers recommended exclusive
breastfeeding for 4 months, and formulas were only provided to families who could not or did not want
to breastfeed. In addition to formula, the intervention group received recommendations for
complementary feeding and regular physical exams. One group remained fully breastfed and also
received these additional interventions but did not receive the formula. Regular physical exams and
evaluations for atopic dermatitis were performed on the children in all groups until age 6. The course of
atopic dermatitis was nearly identical for the fully breastfed children in the intervention and the nonintervention groups. Follow up evaluation results are summarized in table 4. Children with a
predisposition had a two times increased risk for developing the condition. Infants with a positive
family history of AD had an increased risk of developing the disease when fed with a cows milk

formula. However, even children with a susceptibility for AD had a reduced risk of up to 50% when fed
with the hydrolysate formulas (Berg et. al., 2010).

Table 4. Onset of atopic dermatitis in formula fed children. Non-compliant: participants did not follow
recommendations from the intervention group. Not applicable: formula was parents own decision, no
recommendations were made (Berg et. al., 2010).
Comparison between results from a randomized trial and an observational trial is difficult, but
Berg et. al. (2010) has good randomization and high validity of results. However, the authors did not
adjust for other dietary confounders such as timing of introduction of complementary food, duration of
exclusive breastfeeding before supplementation with formula of the parents choice, and diet variation
in children. Additionally, while they did not adjust duration of breastfeeding before adding
supplementary formula, they did specify that timing of formula introduction and breastfeeding duration
was equally distributed across the groups. Further, randomization is somewhat restricted in a maternal
and child study. Ethically, breastfeeding cannot be randomized and ultimately, the choice lies with the
parents. Families who chose to breastfeed and not participate in the intervention group differed in
lifestyle factors from the formula feeders, including increased parental education and decreased

smoking. Because of this, Berg et. al (2010) compared the breastfed children and non-breastfed
children separately. Ultimately, although comparability is limited in this type of study, the researchers
demonstrated that it may be possible to overcome genetic predisposition with appropriate early dietary
intervention (Berg et. al., 2010).
Introduction of complementary foods
Evidence for the timing of the introduction of solid foods as a supplement to breastfeeding and
its association with the development of allergic disease is inconclusive. In general, the AAP, the
American College of Obstetrics and Gynecology, and the American Academy of Family Physicians
recommend that infants should not be introduced solid foods before approximately 6 months of age
(Clayton, Li, Perrine, & Scanlon, 2013). There are several reasons for delaying the introduction of solid
food until this age or later. First, children may not be developmentally ready. Offering solid food to an
infant who cannot sit up and does not have good head control increases the risk of aspiration,
particularly those under 4 months of age. Second, evidence suggests that premature introduction of
solid food increases the babys risk of some chronic diseases like diabetes, obesity, eczema, and celiac
disease. Third, early introduction of solids has been connected to a decrease in continued breastfeeding.
The health benefits of breast milk explored earlier in this paper demonstrate how detrimental the early
cessation of breastfeeding can be (Clayton et. al., 2013). Despite these recommendations, recent
evidence suggests that early introduction may be beneficial regarding atopic sensitization (Nwaru et.
al., 2013).
Effects of early introduction of food. The timing and amount of early feeding influences the
development of metabolic problems in adulthood (Kuo, Inkelas, Slusser, Maidenberg, & Halfon, 2010).
The mechanism is poorly understood because ethical dilemmas limit the potential for solid studies in
this area. Some research suggests that premature introduction of solids exceeds the functional capacity
of the gastrointestinal tract and the kidneys in infants under 4 months. These early stressors can upset
development and set the child up for metabolic issues later in life (Kuo et. al., 2010). Alternatively, the

dysfunction associated with early introduction of solids may be associate with overfeeding (Doub,
Moding, & Stifter, 2015). Doub et. al. (2015) demonstrates that mothers who introduce solids before 4
months of age are most likely to do so because they believed their infant was not getting enough food
on milk feeding alone. These beliefs correlated with a low responsiveness to baby hunger and fullness
cues, indicating the supplementary solid foods often result in overfeeding (Doub et. al, 2015).
Overfeeding strains developing organ systems and primes the body for metabolic dysfunction. It also
leads to excess calorie consumption, rapid weight gain, and contributes to the childhood obesity
epidemic (Doub et. al., 2015). However, despite documented risk for metabolic disease, evidence
associating early introduction of solids to allergic disease is weak. Back when the first research into the
immunology of allergic disease was new, some research suggested exposure to common food allergens
like milk, eggs, peanuts, and wheat during infancy would lead to atopy. This has resulted in most
preventative strategies focusing on avoidance of these proteins until later in childhood. Despite little
epidemiological data to support this theory, the fact that so many expert groups have recommended it
has given it self-fulfilling credibility (Nwaru et. al., 2013).
Benefits of early introduction. New evidence suggests that recommendations about the delay of
solid food may be unfounded. The Committee on Nutrition and Section on Allergy and Immunology
division of the AAP found little support for the delay of complementary foods as a measure to prevent
development of allergic disease (Greer et. al., 2008). In a 2013 observational cohort study in Finland,
data on the timing of infant feeding was collected in 3,781 children from infancy to 2 years. At age 5,
serum IgE levels were tested toward common antigenic proteins to compare infant feeding and atopic
sensitization (Nwaru et. al., 2013). Researchers found that the early introduction of complementary
foods may protect against atopic sensitization in childhood, especially among high risk infants.
Additionally, the authors discovered that less food diversity as early as 3 months was associated with
an increase in atopic sensitization. At 3 months of age, infants who had been offered less than 3 types

of food items had increased atopic reactions to wheat, timothy grass, and birch allergens. Those
exposed to 1-2 foods at 4 months old and less than 4 foods at 6 months old had increased risk for
sensitization toward cows milk, wheat, egg, timothy grass, birch, and cat allergens compared with
children who were offered more variation. Cereals, fish, and egg are some of the more typical food
allergens, but Nwaru et. al. (2013) found them to be the most important and indicated that their early
exposure to a childs diet may be beneficial (Nwaru et. al., 2013). The strengths of this study are the
well-defined study population and the prospective design that allowed for the comparison of
consecutively introduced foods while limiting recall bias. However, the cohort used for this study was
assembled from a type 1 diabetes study of children born with human leukocyte antigen, also known as
HLA-conferred increased risk of type 1 diabetes. Researchers believe that HLA does not have an effect
on the development of allergies, but the commonality of it among all children in the study reduce its
external validity.
In the 2013 Infant Feeding Practices Study II (IFPSII), 1,334 mothers were enrolled in a
longitudinal mail-based study to assess the adherence to infant feeding recommendations in the U.S.
(Clayton et. al., 2013). Mothers were asked to complete 6 food frequency questionnaires once per
month describing their childs eating habits during the previous week. Researchers defined early
introduction of solid foods as less than 4 months old (17 weeks). Over 40% of mothers introduced
solids before 4 months old (Clayton et. al., 2013; Doub et. al., 2015). Prevalence of the introduction of
solids before 4 months of age varied by the method the child was milk fed. The group with the highest
rates of the early introduction of solids was formula fed babies at 52.7%. Mixed fed infants were a
close second at 50.2%, followed by breastfed infants at 24.3% having solid food introduced before 4
months old (Clayton et. al., 2013). This correlation makes it difficult to distinguish whether the
association of increased risk of disease actually corresponds to the act of introducing solid food or to

the previous method of milk feeding. Because of this, delay of introduction of solid foods remains
controversial (Joeseph et. al., 2011).
Conclusion and future research needs
Evidence now shows that early nutrition impacts long term health and wellbeing into adulthood.
Dietary choices made in the first 1000 days can alter the trajectory of atopic dermatitis, which can help
foster the wellbeing of the individual as well as improve the allocation of resources in the healthcare
system. The itch-scratch cycle of AD can be miserable and the cost can be high both financially and
personally. The physical lesions can lead to behavior problems, self-consciousness, and social
ostracism that can leave unseen scars on AD sufferers. Additionally, AD leaves the skin, the first line of
immunological defense, vulnerable and increases exposure to pathogens, increasing risk of infection
and complications in these patients. Managing these symptoms can reduce the burden felt by patients
and by the health care system by reducing doctors visits, complications, and improving quality of life.
Simply making educated choices in early dietary decisions can help to prevent, delay onset, or reduce
the severity of AD symptoms, especially in those hereditarily predisposed to the condition.
It is evident that there are problems with the ethics and execution of studies which prevent firm
conclusions from being drawn about AD prevention through nutrition. Despite the lack of satisfactory
studies regarding pregnancy diet, breastfeeding, and introduction on complementary foods, the lack of
definitive proof does not disprove the potential for altering the course of the disease through dietary
means. In fact, every strategy discussed in this paper, excluding antigen avoidance during pregnancy,
confers other documented benefits even if its use for AD prevention remains unverified.
In the context of these limitations, the following is a summary of the current evidence as
presented in this paper. At the present time, there is no convincing evidence that antigen avoidance
during pregnancy plays a substantial role in the prevention of AD. In fact, some evidence points to the
fact that increased exposure to allergens during pregnancy helps strengthen the babys growing immune
system. Exclusive breastfeeding is recommended for all infants with or without atopic family history as
the ideal source of nutrition. Some evidence suggests that breastfeeding can increase the risk for

allergic disease, but there are too many confounders that cannot be adjusted for to determine causation
vs correlation. Its possible that mothers who are aware of the genetic probability of AD or notice
atopic symptoms in their children breastfeed longer to combat its onset. It is also possible that there is a
threshold in which mothers with allergic disease (measured through IgE serum levels) may pass on
portions of their overactive immune system through breastmilk. In situations where mothers are unable
or unwilling to breastfeed, there are options for formula feeding that may help prevent the onset or
reduce the severity of symptoms. Cows milk formulas seem to increase the risk of AD while
hydrolyzed formulas may reduce it, but the effect is only seen in high risk infants with a genetic
predisposition. Even here, not all hydrolyzed formulas have the same benefits, and extensively
hydrolyzed formulas might be more protective than partially hydrolyzed. Finally, the research
regarding introduction of complementary foods and its relationship to AD is inconclusive. There are
several good reasons for delaying the introduction of solids until the baby is developmentally ready and
that age varies child to child. Its possible that early variation in food helps to desensitize the infant, but
introduction of food too early can prime for metabolic dysfunction, obesity, and increase the risk for
aspiration.
While evidence about the benefits of breastfeeding and the delay of complementary foods
remain controversial in their effectiveness on AD prevention, their benefits in other ways are more
clear. Breastfeeding confers numerous benefits to the baby apart from potential allergy prevention.
However, barriers to breastfeeding are common. The timing of the introduction of food also depends on
the individual child and where they are developmentally. This means that families have to weigh the
choice individually to decide whats best for their baby, given their needs and family history.
Further research is needed in this field before official recommendations regarding dietary
interventions to prevent AD can be made. The ethical challenges prevent studies from making more
definite statements regarding diet and atopy, resulting in weak and unsatisfying conclusions. Currently,
it appears that interventions past the age of 4 to 6 months have no effect on AD regardless, so new

research should focus on that critical young age. Other questions regarding highly allergic mothers and
the benefits of breastfeeding on children need to be address in greater detail. It seems there is a bell
shaped curve of atopy that reaches a point where breastfeeding begins to increase risk in the child, but
more research will be needed to discover just where that is.
Research in this area is important for several reasons. Costs are high for AD sufferers and for
healthcare. While AD typically doesnt result in hospitalizations or major surgeries, it is one of the most
common skin disorders and it lasts a lifetime. Over time, costs of treatments, lost employment, and
secondary infections multiplied by the sheer number of sufferers add up and stress the health care
system. It also impacts social relationships, academic performance, and ultimately, can damper a
childs potential. More research into identifying triggers to keep symptoms manageable can help reduce
this strain on sufferers as well as allocate medical resources to other, more life threatening diseases.
While atopic dermatitis is a genetic disease fraught with unrelenting itching and lesions, early dietary
intervention can help to prevent, delay the onset, or reduce the severity of symptoms. Choices on
nutritional therapy strategies are highly individualized and vary by family need. At this time, very few
official recommendations for the nutritional prevention of AD exist, but future research focusing on
unique perspectives and new interventions can increase the evidence base for novel recommendations
and ultimately, relief from atopic dermatitis.
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