Journal of Communication Disorders 57 (2015) 29–40

Contents lists available at ScienceDirect

Journal of Communication Disorders

Review

Breastfeeding and language outcomes:

A review of the literature
Jamie Mahurin Smith *
Illinois State University, Normal, IL 61790, United States

A R T I C L E I N F O A B S T R A C T

Article history: Many researchers have investigated the potential impact of breastfeeding in infancy on a
Received 18 September 2014 child’s subsequent development, but only a small subset of these studies considers
Received in revised form 10 April 2015 language development and impairment. This paper reviews that literature, discussing
Accepted 19 April 2015
postnatal neurodevelopment, potential mechanisms for dietary influences on communi-
Available online 7 May 2015
cation outcomes, studies of typically developing children, and studies of children with
communication concerns. For population based studies of language development, a
Keywords:
modest but statistically robust relationship is seen across large samples that account for
Feeding
Breastfeeding breastfeeding exclusivity. A similar protective relationship is seen in studies that evaluate
Child language the relationship between breastfeeding and language disorders; effect sizes are typically
Language delay larger in these papers. Implications for researchers and service providers are reviewed.
Language disorder Learning outcomes: Readers will be able to describe possible mechanisms by which
Neurodevelopment early diet might influence neurodevelopment. They will be able to describe the
relationships observed between diet in infancy and language outcomes in large
population-based studies, as well as the trends observed in studies of the relationship
between infant diet and communication impairment.
ß 2015 Elsevier Inc. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
2. Postnatal neurodevelopment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
3. Why would diet influence language development? Potential mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
4. The existing literature on typical development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
5. The existing literature on communication disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34
6. Human neurodevelopment and infant diet: highly publicized null findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
7. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
7.1. Review of findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
7.2. Assessment of the existing research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
7.3. Implications for professionals in communication sciences and disorders (CSD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
8. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

* Tel.: +1 309 438 5308.

E-mail address: j.m.smith@ilstu.edu

http://dx.doi.org/10.1016/j.jcomdis.2015.04.002
0021-9924/ß 2015 Elsevier Inc. All rights reserved.
30 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40

1. Introduction

Imagine that two communities in two different parts of the world are building a network of roads. As a cost-saving
measure, the planning teams opt to use lower-grade building materials for half of each community. One community’s
climate is mild: temperatures tend to stay in the 40–70 8F range. The second community experiences much more
temperature variability: winter temperatures might plummet to 20 8F or cycle rapidly from freeze to thaw and back again,
while summer temperatures might hover around 100 8F.
Drivers who have navigated pothole-ridden streets in spring might guess that the roads built with lower-grade materials
could show signs of wear more rapidly in Community #2. When the strains on the materials are greater, the breakdowns in
the network may be apparent more rapidly. Drivers in Community #1 might notice only minor signs of wear on the lower-
grade sections of their roadways, while drivers in Community #2 might find a conspicuous difference.
The neurological system can be envisioned as a vast network of roads, undergoing large-scale construction projects
during pregnancy, infancy, and toddlerhood. The ‘‘road-building’’ materials available to children can vary with their early
diet, leading to differences in brain structure (Farquharson, Jamieson, Logan, Cockburn, & Ainslie Patrick, 1992; Farquharson
et al., 1995; Jamieson et al., 1999; Makrides, Neumann, Byard, Simmer, & Gibson, 1994). These differences in brain structure
may be associated with differences in brain function (Greiner, Moriguchi, Hutton, Slotnick, & Salem, 1999; Salem et al., 2000).
For children whose network of genetic and other environmental effects does not predispose them to language difficulties –
similar to the roads in Community #1 – diet in infancy may be linked to modest differences in later life (Anderson, Johnstone,
& Remley, 1999). For children whose genotype renders them more vulnerable to language impairment, like the roads in
Community #2, early diet may make a more significant difference as they mature (Schultz et al., 2006).
Breastfeeding is widely recommended for infants, and the differences in morbidity between breastfed and formula-fed
children are well-documented (American Academy of Pediatrics, 2012; World Health Organization, 2003). Less familiar,
perhaps, are the differences in neurodevelopment that have also been observed in studies of breastfed versus formula-fed
children. Although a subset of this literature looks explicitly at the relationship between feeding mode in infancy
and subsequent speech-language development, these investigations are seldom referenced in communication sciences and
disorders (CSD) journals (Rogers et al., 2015). This paper will first describe the process of postnatal brain development
and the mechanisms through which diet might influence neurodevelopment, followed by a review of the existing literature
on associations between breastfeeding and subsequent language development and impairment. It will conclude with a
review of potential implications arising from these findings.

2. Postnatal neurodevelopment

Lawrence and Lawrence (2005) report that the average newborn will arrive with a brain weighing approximately 350 g; a
year later, that brain will have grown to approximately 1100 g. By age 3 the brain will have quadrupled relative to its size at
birth; the steepness of this early trajectory is particularly clear when one considers that the brain will require a further
15 years to approach the quintuple mark (Dekaban & Sadowsky, 1978). Neurons proliferate in regions including the dentate
gyrus of the hippocampus, a region associated with memory; during the first 2 weeks of life this process is especially
vulnerable to environmental influences such as the presence or absence of growth factors (Watson, DeSesso, Hurtt, &
Cappon, 2006). In addition to the rapid growth of the brain itself, other types of neural tissue proliferate during the early
years of life. The most rapid period of postnatal myelination occurs during the first 2 years of life; the major fiber tracts are
clearly visible in 3-year-old children (Matsuzawa et al., 2001). During the first 18 months of life neurons must migrate to
other parts of the brain, including the prefrontal cortex (Sanai et al., 2011). This is also a period of dramatic growth in synapse
formation, so much so that at the point of peak synaptic density there are 55 synapses per 100 mm3 in the human brain
(Watson et al., 2006).
The decline in synaptic density observed between toddlerhood and adulthood is the result of a form of programmed cell
death known as pruning. It is common to think of brain cell death as undesirable, but pruning is a critical part of normal
neurodevelopment, distinct from other causes of cell death such as injury or toxin exposure (Watson et al., 2006). Inadequate
pruning has been posited as a factor in autism (Hill & Frith, 2003), highlighting the potential importance of this
neurodevelopmental process.
During infancy the brain is also building its own protective mechanisms, a process that takes time to complete. In the first
6 months of life the blood-brain barrier is more permeable than it will be in later life, increasing the infant’s vulnerability to
neurotoxins (e.g., methylmercury) with the potential to affect future cognitive skills (see Watson et al., 2006; Dzwilewski
et al., in this issue). To sum up, then, infants not only must build brain cells, they must also establish connections between
them, re-sculpt brain architecture, and create a selectively permeable wall between the brain and the outside world. Their
diet provides the raw materials available for these tasks.

3. Why would diet influence language development? Potential mechanisms

The idea that breastfeeding or formula-feeding could influence language development immediately raises the question of
mechanism: why would children’s diets in infancy exert any long-term influence over their speech-language skills? Four
possibilities will be reviewed in the section that follows. The explanation most often proposed is that differences in the fatty
 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40 31

acid profiles of human milk and infant formula might make a difference in subsequent brain structure and function; a closely
related possibility is that the fatty acid content of cell membranes could influence gene expression within those cells. The
second idea is that human milk might contain a variety of constituents that promote optimal neurodevelopment, perhaps
with synergistic effects seen across multiple nutrients. A third consideration is that the well-documented relationship
between breastfeeding and immune system function/regulation of inflammation might exert a moderating influence on
learning and memory. A fourth potential mechanism involves the impact of lactation on mothers, who in turn shape their
children’s learning and language. These mechanisms are not mutually exclusive, and the reader is reminded that a single
causal mechanism is unlikely to provide an adequate explanation for a phenomenon as complex as neurodevelopment.
Analysis of the brain tissue acquired during infancy indicates that more than half of its solid weight is lipid (Lawrence &
Lawrence, 2005), and that the fatty acid profile of an infant’s diet plays a significant role in the composition of brain tissue
(Farquharson et al., 1992, 1995; Jamieson et al., 1999; Makrides et al., 1994). Of particular importance are two long-chain
polyunsaturated fatty acids: an omega-3 (or n-3) fatty acid known as docosahexaenoic acid (DHA) and an omega-6 (n-6)
fatty acid called arachidonic acid (AA). Across mammal species, DHA is the most abundant fatty acid found in the brain, but
the amounts of DHA in brain tissue are directly related to an individual’s diet (Innis, 2007). Not all of the infant formulas for
sale in the US contain DHA and AA; those that do are consistently more expensive than formulations with supplemental
LC-PUFA. For this reason, formula-fed infants in the US may lack a dietary source of DHA and AA.
Much of the evidence supporting the relationships among dietary fatty acid intake, brain composition, and learning/
behavioral outcomes comes from animal studies, in which diet can be manipulated to a degree that would be gravely
unethical in studies of human infants. It has long been documented that rat pups fed a diet free of n-3 fatty acids build brain
tissue with much less DHA and a corresponding increase in n-6 fatty acids (Bourre et al., 1984). These differences in n-3
intake are associated with poorer learning and memory impairment in adult rats (Greiner et al., 1999), as well as worse
scores on measures of depression and aggression (DeMar et al., 2006).
Studies of human children also suggest that the fatty acid content of the diet influences the structure of neural tissue, both
gray matter and white matter. Kafouri et al. (2012) investigated cortical thickness in 571 adolescents and found that
increased duration of exclusive breastfeeding was strongly correlated with both increased thickness of the parietal cortex
and with higher cognitive scores; the authors posited that the DHA in human milk may explain these findings. Another
recent study (Deoni et al., 2013) found slower myelination in formula-fed children as compared to their breastfed
counterparts. These authors state, ‘‘While the exact mechanism(s) that underlie these. . .differences remain unclear, our
results lend support to the hypothesis that the docosahexaenoic and arachidonic acids present in breast milk promote
preferential neural growth and white matter development’’ (Deoni et al., 2013, p. 83).
Gross quantitative measures of neural tissue offer only a rough index of brain maturation. At a microscopic level, LC-PUFA
intake influences the growth of dendritic spines and the creation of synaptic membranes, thus shaping neurotransmission
and cell-to-cell signaling (Nyaradi, Li, Hickling, Foster, & Oddy, 2013). For scholars of genetically mediated phenomena such
as speech and language, it is perhaps even more important to know that the fatty acid content of cell membranes can shape
gene transcription and expression (Innis, 2007). Animal studies have indicated that dietary intake is well-documented as an
agent of DNA methylation, a process in which a gene is kept inactive by addition of methyl groups to a DNA strand. The coats
of agouti mice, for instance, can be either brown or a striking bright yellow, depending on the nutrient content of the
maternal prenatal diet (Gilbert & Epel, 2009). The process by which the same genotypes can be expressed as strikingly
different phenotypes as a result of environmental influences is known as epigenesis, and across species it can offer a
powerful explanatory tool for the wide variations seen in genetically mediated conditions. In other words, it is not simply
that children with a diet low in DHA/AA may have less brain tissue; it may also be true that their brains function less
efficiently in certain contexts, and that the genes directing their future development may manifest their influence in very
different ways.
Many other human milk constituents may play a role in brain development, and they may work synergistically to
optimize neurodevelopmental outcomes. The results of studies investigating LC-PUFA supplementation in formula-fed
children lend support to this point of view. A meta-analysis by Simmer, Schulzke, and Patole (2008) reported that LC-PUFA-
supplemented formula was not associated with neurodevelopmental benefit, indicating that DHA is unlikely to be the sole
explanation for the differences observed between breastfed and formula-fed children. A related Cochrane review asserted
that providing supplemental LC-PUFA to breastfeeding mothers did not result in improved cognition or language skills for
their children (Delgado-Noguera, Calvache, & Bonfill Cosp, 2010). Clearly, then, it is prudent to consider other possible
reasons why human milk might be associated with neurodevelopmental differences. One example of a nutrient that may
play a role in neurodevelopment is choline, a substance sometimes known as Vitamin B4. In a 2006 review, Zeisel stated that
choline is important for neural tube closure in human fetuses; animal research indicates that choline supplementation can
have long-lasting effects on memory. Human milk is rich in choline. In infant formula, on the other hand, although the Food
and Drug Administration (FDA) has established a minimum for choline content (FDA Infant Formula Nutrient Requirements,
2014), levels of this nutrient vary from one formulation to another (Zeisel & da Costa, 2009).
In addition to choline, other human milk constituents have been identified as potentially important in neurodevelop-
ment. In a 2010 investigation of brain volume in 50 adolescents, Isaacs and colleagues reported significant correlations
between the percentage of breastmilk in the diet of infant boys, total brain volume, white matter volume, and verbal IQ. In
other words, boys who received more human milk in infancy grew into adolescents with larger brains, more white matter,
and stronger performance on tests of verbal IQ. (No significant effects were observed among the girls in the sample.) The
32 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40

authors propose that multiple human milk constituents could promote brain growth, including nutrients such as cholesterol
(which is absent from infant formula but potentially important for production of glial cells and myelin), hormones such as
thyroxin, and additional elements such as nerve growth factor. Other compounds of interest could include carnitine, which
plays a role in LC-PUFA metabolism; lactose, which is important for generating compounds called galactolipids thought to be
crucial to CNS development (Lawrence & Lawrence, 2005); cytokines such as transforming growth factor-beta, which may
influence regulation of inflammation (Oddy & Rosales, 2010); and sialic acid, which may influence memory formation
(Wang, 2009). The large array of substances found in human milk makes it difficult to investigate the differential effects of
individual constituents. Furthermore, regulatory standards allow manufacturers some latitude in determining the levels of
selected constituents; lactose, for instance, is absent from soy formula but abundant in formula based on cow’s milk.
In addition to directly influencing brain structure and function through its nutrient profile, breastfeeding may exert more
indirect effects as well. It is well established that early diet plays a role in long-term immune function (Wilson et al., 1998); it
is less widely known that early diet affects the body’s ability to regulate inflammation (McDade, 2012). Shorter breastfeeding
duration has been identified as a predictor for elevated levels of C-reactive protein (CRP), a widely recognized marker for
inflammation (McDade et al., 2014). Wärnberg, Gomez-Martinez, Romeo, Dı́az, and Marcos (2009) report that CRP has
directly neurotoxic effects. Exploration of the relationship between inflammation and neurodevelopment is in its infancy,
but dysregulation of immune function and inflammation has been reported in children with autism (Ashwood, Wils, & van de
Water, 2006).
Breastfeeding affects mothers as well as their infants, altering the maternal hormonal milieu (Lawrence & Lawrence,
2005), and these influences have the potential to inform speech-language outcomes as well. With every feeding, or 10–12
times per day for a fully breastfeeding or exclusively pumping mother, the pituitary repeatedly secretes prolactin and
oxytocin to elicit milk production and ejection.
Much of the available data on lactation and the maternal brain comes from animal studies. Although caution is essential
in extrapolating from rodent dams to human mothers, rodent studies may have ramifications for human studies of
breastfeeding outcomes. It has been known since the 1980s that oxytocin, the hormone that drives milk ejection, induces
changes in maternal behavior in rats (see Pedersen, Ascher, Monroe, & Prange, 1982). More recent investigations have
indicated that motherhood is associated with significant cognitive changes across many rodent studies: learning and
memory are improved and related changes in brain function and/or morphology have been reported. Oxytocin has been
suggested as a mediator of these changes (Darnaudéry et al., 2007; Tomizawa et al., 2003), which may be long-lasting (Love
et al., 2005).
Human studies lend some support to the idea that lactation influences mothers’ brains and behavior, potentially shaping
(1) maternal affect, (2) maternal brain structure and activation, and (3) mother–child interactions. On the topic of maternal
affect, Mezzacappa and Katkin (2002) reported that breastfeeding can buffer maternal stress levels and negative maternal
mood, even with control for demographic confounds. Regarding the maternal brain, anatomical changes have also been
observed in the brains of lactating mothers, with postpartum gray matter growth in multiple regions including the prefrontal
cortex (Kim et al., 2010). Kim et al. (2011) found that lactating mothers showed greater brain activation than formula-
feeding mothers in the first month postpartum. In both groups, greater brain activation in the regions of interest was
associated with improved maternal sensitivity when babies were 3–4 months old. This finding, together with reports that
oxytocin may influence caregiver–infant relations (Feldman, 2007; Feldman, Weller, Zagoory-Sharon, & Levine, 2007;
Gordon, Zagoory-Sharon, Leckman, & Feldman, 2010), suggests that breastfeeding might have long-lasting effects on
mother–child interactions (see further discussion of this issue in Strathearn, Mamun, Najman, & O’Callaghan, 2009).
Longitudinal studies of mother–infant dyads have reported positive correlations between maternal sensitivity during the
infant period and later language development (Baumwell, Tamis-LeMonda, & Bornstein, 1997), with stronger effects
observed for children at higher risk of developmental delay (Landry, Smith, Miller-Loncar, & Swank, 1997). While these
relationships between lactation and maternal brain/behavior changes require further investigation, they may offer another
lens through which to view the potential effects of infant feeding decisions.
The next three sections of this paper will consider the existing literature on infant feeding as a predictor for language
outcomes, first in population-based studies emphasizing typical development, and then in studies that focus on specific
forms of communicative impairment, with a brief review of two well-publicized studies that reported null findings based on
a single large dataset. Given the focus of this paper, no distinction is made between direct breastfeeding and feeding
expressed milk. In both cases, the mother lactates and the child receives human milk.

4. The existing literature on typical development

Very little of the research literature in communication sciences and disorders has evaluated infant diet as a possible
environmental variable influencing speech-language development. There are, however, a number of studies from pediatrics,
epidemiology, and related disciplines that have investigated this relationship. The question of whether breastfeeding might
influence speech-language outcomes was first raised by Broad and colleagues in a series of 3 studies (Broad, 1972, 1975;
Broad & Duganzich, 1983). All three studies reported that formula-fed children, particularly boys, were more likely to
experience slower communicative development even with covariate control. These findings are mentioned here primarily
for their historical interest, as recent advances in infant formula limit the extent to which extrapolation from Broad’s
research is advisable.
 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40 33

More recent studies span the range of ages from infancy to adolescence. In a 1999 study of 1656 8-month-old Danish
infants, Vestergaard and colleagues reported that 73.4% of the infants exclusively breastfed for 6 months were engaging in
variegated babbling, versus 34.0% of the formula-fed infants. The overall odds ratio for emergence of variegated babbling was
1.5 (95% CI = 1.3–1.8). The relationship persisted with covariate control for factors including social class, maternal education,
prenatal smoking, birthweight, gestational age, and number of prior illnesses. The authors reported that they purposefully
chose to investigate differences in infancy, to reduce the period of time in which potential confounding variables such as
maternal education could exert an influence.
In a related study of 2302 Danish infants, Obel, Henriksen, Hedegaard, Secher, & Østergaard (1998) investigated the
relationship between babbling in babyhood and prenatal smoking among mothers. They reported a dose-response
relationship between prenatal exposure to cigarette smoke and decreased odds that babbling would emerge by 8 months,
with an odds ratio (OR) of 2.0 (95% CI = 1.1–3.6) for maternal use of 10 cigarettes per day. They reported, however, that
breastfeeding appeared to confer a measure of protection against the effects of prenatal cigarette smoke exposure on pre-
linguistic development. The infants who did not receive at least 4 months of exclusive breastfeeding were even less likely to
be babbling at 8 months, OR = 2.7 (CI = 1.3–5.8).
These two studies of pre-linguistic development appear to be unique in the breastfeeding literature; many authors, in
contrast, have looked at neurodevelopment in older children through IQ scores. Since many cognitive assessment tools rely
heavily on verbal skills, these studies can be very relevant to discussions of language ability. These findings, which generally
show a modest but statistically robust difference in favor of breastfed children, have been summarized in other sources (see
Anderson et al., 1999; Drane & Logemann, 2000). The remainder of this section will emphasize studies that have assessed
language development with instruments developed by and for speech-language pathologists, with one exception at the end
for an important 2008 study that used novel methodology to measure differences in verbal IQ.
Thorpe, Rutter, and Greenwood (2003) studied 96 twin pairs in an attempt to find factors that predicted at 20 months how
a child would perform on measures of language skill at 36 months. The twins were contrasted with 98 pairs of singleton
siblings, because twins are known to develop language skills more slowly than singletons. The investigators collected data on
breastfeeding duration, but not breastfeeding exclusivity. To evaluate language development, the investigators used the
Preschool Language Scale–Third Edition (PLS-3; Zimmerman, Steiner, & Pond, 1992). The language skills of breastfed
singletons were significantly stronger at both 20 and 36 months than those of the formula-fed singletons, but the effect
ceased to be significant when the investigators controlled for maternal vocabulary. No association between breastfeeding
and language was observed in the twin pairs.
Gibson-Davis and Brooks-Gunn (2006) studied the children of 1645 American-born mothers, a subset of the Fragile
Families and Child Wellbeing Survey cohort, to examine the impact of breastfeeding on the language skills of 3-year-old
children. Raw PPVT-R scores were 6.2 points lower among bottle-fed children, a significant finding that remained so after
adjustment for demographic factors, home environment, and health-related variables. When maternal PPVT-R scores were
factored in, however, the difference was only marginally significant (p = .06). The authors described an interaction between
breastfeeding and education as predictor variables, with a clearer effect of breastfeeding observed among more educated
mothers. Gibson-Davis and Brooks-Gunn point out that their findings cannot be extrapolated to the general population, as
the Fragile Families cohort includes a large proportion of disadvantaged children and differences are evident in the
descriptive statistics for both the independent and dependent variables (IV and DV). Specifically, breastfeeding initiation and
duration rates in this sample (the IV) were much lower than those in the population as a whole, leading the authors to use a
bivariate classification for breastfeeding: breastfed <1 month, or 1 month. No measures of breastfeeding exclusivity were
available. Mean PPVT-R scores for both mothers and children in this sample were also significantly lower than the population
means (89.9 and 86.8, respectively, versus a population mean of 100), illustrating clear differences in the DV as well.
A prospective longitudinal study of breastfeeding-related outcomes among children in Western Australia has generated a
number of publications, summarized in Oddy, Li, Robinson, and Whitehouse (2012). Among the observational studies
described here, it deserves particular attention for its large n (2860 children), its methodological strengths, its thorough
assessment of breastfeeding exclusivity, and its attention to covariate control. Oddy and colleagues evaluated multiple
domains, including language, in children at ages 1, 2, and 3 years. In an effect that remained significant after control for
multiple confounding variables, they reported that communication and adaptability were the domains most sensitive to the
effects of breastfeeding duration, with lower scores in children breastfed <4 months (Oddy et al., 2011b). This observed
effect persisted across the follow-up assessments of the cohort. Lower scores on the Peabody Picture Vocabulary Test –
Revised (Dunn & Dunn, 1981) were associated with shorter breastfeeding duration among 6-year-olds (Oddy et al., 2003)
and 10-year-olds (Whitehouse, Robinson, Li, & Oddy, 2011) in the sample. The investigators have also reported duration-
related effects for school performance on reading and spelling tasks among boys in the cohort (Oddy, Li, Whitehouse,
Zubrick, & Malacova, 2011a). Four noteworthy trends are evident from a review of the results seen in this cohort: the first is a
consistent dose-related effect of breastfeeding, with more potent effects seen with increasing exclusivity and duration; the
second is a modest effect size when covariates are considered; the third is an interaction between breastfeeding and gender,
with clearer effects observed in boys; and the fourth is an interaction between maternal education and breastfeeding, with
the effect that the offspring of more educated mothers seem to reap more of an advantage from breastfeeding.
In the most recent of the studies reviewed here, Belfort et al. (2013) looked prospectively at PPVT-3 scores (Dunn & Dunn,
1997) in 3-year-olds and Kaufman Brief Intelligence Test – Second Edition (Kaufman & Kaufman, 2004) results for 7-year-
olds. For this sample of 1312 children, the researchers controlled for a number of covariates, including maternal intelligence
34 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40

and home environment. At both time points, a significant dose-response relationship was observed between breastfeeding
duration and the children’s test scores; this relationship was markedly attenuated by covariate control but remained
statistically meaningful. The authors estimated that each month of breastfeeding duration was associated with an increment
of 0.21 points on the PPVT-3, and 0.35 points on the verbal element of the KBIT-2.
Across these studies, the reader will have observed a trend: differences between breastfed and formula-fed children are
attenuated when maternal IQ or vocabulary skills are taken into account. While the observed effect remained statistically
significant in studies with a larger n, a longer breastfeeding duration, and information on breastfeeding exclusivity (Belfort
et al., 2013; Obel et al., 1998; Oddy et al., 2012; Vestergaard et al., 1999), statistical significance evaporated in studies with a
smaller sample (as in Thorpe et al., 2003), a shorter duration of breastfeeding (as in Gibson-Davis & Brooks-Gunn, 2006), and
no assessment of breastfeeding exclusivity (seen in both of these examples). These changes in effect size and their associated
p values raise a vexing methodological issue. If, as discussed in the mechanism section, the hormonal milieu associated with
breastfeeding can improve the long-term capacity of the maternal brain for learning and memory, it is statistically dubious to
control for maternal variables that may be affected by breastfeeding. In other words, it is impossible to measure accurately
the potential effects of breastfeeding (on a child) while also partialing out the potential effects of breastfeeding (on a
mother). At the same time, it is undeniable that well-educated women are more likely to breastfeed their babies (Coates &
Riordan, 2005), and that it would be naı̈ve and inadvisable to assume that differences between breastfed and formula-fed
children arise solely from their diets. The final study reviewed in this section, however, neatly sidesteps this conundrum.
For a study known as PROBIT (Promotion of Breastfeeding Intervention Trial), Kramer et al. (2008) recruited more than
17,000 Belorussian women who planned to breastfeed their babies and randomized them to hospitals and clinics. The
experimental group delivered their babies and received follow-up treatment under the care of healthcare providers (HCP)
with special training in breastfeeding support; the control group used hospitals and clinics where providers did not receive
this training. Although all of the mothers planned to initiate breastfeeding, the differences in HCP training were associated
with highly significant differences in breastfeeding exclusivity and duration (Kramer et al., 2001). This element of
randomization has allowed the investigators to consider differences between the two groups with considerably less
interference from the confounding variables that plague observational studies. In their 2008 report on cognitive outcomes at
age 6 for the 13,889 children still enrolled in the study, the investigators stated that the experimental group outscored the
control group by 7.5 points on the Wechsler Abbreviated Scales of Intelligence (Wechsler, 1999) verbal IQ subscale. This
difference is, for reference, on the same order as the cognitive differences observed between children with and without
elevated blood lead levels (Canfield et al., 2003). The control group was also rated significantly lower on teacher evaluations
of reading and writing skills. While it would be unwise to assign too much weight to the findings of a single study, the unique
methodological strengths and the large size of this study together suggest that these results will have significant
ramifications for researchers and service providers with an interest in child language development.

5. The existing literature on communication disorders

For most children, speech-language development proceeds uneventfully with no need for parental concern or outside
assistance. For some children, however, this is not the case. This section will describe the results of studies that have
examined the relationship between breastfeeding and communicative impairment within the last 20 years. Studies that
have evaluated the potential moderating influence of breastfeeding on a different IV–DV relationship related to
communicative impairment (otitis media in Zumach, Gerrits, Chenault, & Anteunis, 2010; prematurity in Mahurin Smith,
DeThorne, Logan, Channell, & Petrill, 2014) are excluded.
One critical index of delayed speech-language development is parental concern. Dee, Li, Lee, & Grummer-Strawn, (2007)
evaluated data from the 2003 National Survey of Children’s Health, looking at relationships between breastfeeding and the
development of language and motor skills in a cohort of 22,399 children. Participating mothers rated their level of concern
regarding expressive language development, receptive language development, fine motor skill, and gross motor skill. For
each domain assessed, Dee et al. reported an inverse relationship between the duration of breastfeeding and maternal
concern about development; in other words, the longer a mother breastfed her child, the less likely she was to describe
concern about his or her development. The relationship persisted after control for multiple confounding variables. For all
domains, the authors described a threshold effect: this effect of breastfeeding on maternal concern was observed only among
children breastfed 3 months.
Harrison and McLeod (2010) reported on data from 4983 participants in the Longitudinal Study of Australian Children.
Like Dee et al. (2007), they considered parent concern as an outcome variable, looking separately at concerns about receptive
and expressive language skills. These authors also assessed use of SLP services and scores on the adapted PPVT-3 (Rothman,
2003). For all 4 of these outcomes, breastfeeding >9 months was associated with a significant protective effect. Odds ratios
for the effect ranged from 0.49 to 0.79, indicating that children who were not breastfed for >9 months faced an increased
risk of parental concern about their language skills, need for SLP services, and scores >1 SD below the mean on the adapted
PPVT-3.
For children diagnosed with specific language impairment (SLI), breastfeeding appears to be a statistically robust
predictor variable. Tomblin, Smith, & Zhang (1997) considered prenatal and perinatal risk factors for SLI in a case-control
study with 1102 children, 177 of whom had an SLI diagnosis. These researchers evaluated children during kindergarten and
interviewed their parents to assess factors potentially associated with SLI. Breastfeeding incidence and duration were lower
 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40 35

among children with SLI, even after differences in maternal education were accounted for. Children breastfed for less than
nine months faced a significant increase in their risk of SLI, with an odds ratio of 2.5. In an unpublished dissertation, Drane
(2003) re-analyzed the data from Tomblin et al.’s 1997 study while employing improved covariate control. She found that
the odds ratio for SLI in formula-fed children declined only slightly, from 2.5 to approximately 2.4. Drane concluded that
breastfeeding does appear to protect against SLI.
Several studies have investigated the hypothesis that breastfeeding might protect against autism. Although they fall
outside the scope of the present review, which is focused on language outcomes, interested readers are referred to a
1989 paper by Tanoue and Oda, replicated in 2006 by Schultz et al. Two other recent papers (Al-Farsi et al., 2012; Dodds et al.,
2011) have reported on this relationship as well. In addition to effects on language and interaction, investigators have also
described significant relationships between infant feeding and protection against speech impairment. These papers are not
reviewed in full here, but interested readers are referred to Mahurin-Smith and Ambrose (2013), Barbosa et al. (2009), and
Fox, Dodd, and Howard (2002).

6. Human neurodevelopment and infant diet: highly publicized null findings

While the studies described in the preceding sections have generally reported statistically significant positive
relationships between breastfeeding duration and neurodevelopmental outcomes, results in the literature on cognition have
been more mixed and contentious. Two large studies from the past decade (Colen & Ramey, 2014; Der, Batty, & Deary, 2006)
claimed that the purported influence of breastfeeding on cognition was in fact attributable to confounding variables,
particularly maternal IQ. Because of the many similarities between measures of verbal IQ and measures of language
development/impairment, the methodological issues raised by these studies are germane to the present review. These
results have public health and policy implications, since it would be unhelpful to instruct mothers to breastfeed in hopes of
improving neurodevelopmental outcomes if there is not in fact a relationship between the predictor and the outcome. For
this reason the following section will briefly discuss the issues raised by Der et al. (2006) and Colen and Ramey (2014), both
of which utilized data from the National Longitudinal Survey of Youth (NLSY) to evaluate the relationship between
breastfeeding and cognition. The NLSY includes information on both maternal and child cognition, as well as information on
feeding history for multiple siblings within participating families, and thus could be viewed as a natural way to evaluate the
relationships among these variables in a large cohort.
In their 2006 paper, Der and colleagues found substantial differences in maternal IQ for mothers who breastfed their
children and children who formula-fed their children. When the researchers controlled for this difference, breastfeeding
ceased to be a significant predictor of cognitive outcomes for their children. This study, along with the 2014 Colen and Ramey
investigation, also considered the question of discordant sibling outcomes. If one sibling is breastfed and another is bottle-
fed, are there differences in IQ between the two children? Both studies reported that no significant differences were observed
between discordant sibling pairs, and concluded from this finding that the importance of breastfeeding in long-term
outcomes has been overstated.
These studies raise three important issues. First is the need for definition of terms and for recognition of the impact of
exclusivity and duration. No definition of breastfeeding is given in either of the two papers discussed in this section. If a
mother breastfeeds her child once and decides to formula-feed thereafter, did she breastfeed or bottle-feed? As discussed
previously, more consistent effects have been described in studies that accounted for breastfeeding exclusivity. A related
question is the importance of breastfeeding duration. Some authors have reported a threshold effect with 3 months of
breastfeeding (Barone et al., 2006; Dee et al., 2007), and it is thus noteworthy that the median duration of breastfeeding in
the NLYS cohort was 3 months. If a study of acetaminophen users announced that the medication had proven ineffective for
headache treatment, it would make a difference in the generalizability of the findings if half of the participants had only
taken a fraction of a pill. Similarly, the conclusions that can be drawn from a sample in which half of the participants received
less than the hypothesized threshold ‘‘dose’’ of human milk are necessarily limited.
The second issue, mentioned above, is the issue of appropriate covariate control. It is well known that feeding decisions
are influenced by extended family norms. Mothers who were themselves breastfed in infancy are significantly more likely to
breastfeed their own children as adults (Meyerink & Marquis, 2002). If the 2008 PROBIT report from Kramer et al. is accurate,
and breastfeeding is indeed associated with a boost of 0.5 SD in IQ, much of the 0.6 SD difference between groups in the Der,
Batty, and Deary study would be explained. In a similar way, if the maternal capacity for learning and remembering is
influenced by lactation, as discussed in the mechanism section, the question of how to control for differences in maternal
ability becomes particularly thorny. While some form of covariate control is important, it may be imprudent to treat
maternal IQ as a simple predictor to be partialed out. Further PROBIT reports or other randomized controlled trials may shed
additional light on this question; observational studies from parts of the world in which breastfeeding is not associated with
socioeconomic advantage (e.g., Daniels & Adair, 2005) may also be helpful in resolving these unanswered questions.
A third issue raised by these two studies is the complexity of sibling comparisons. Although Colen and Ramey described
discordant siblings as ‘‘a natural experiment,’’ the reality is that older and younger siblings differ from each other in both
predictable and unpredictable ways. Comparisons of discordant sibling data must consider the context of maternal feeding
decisions, as well as the constrained variability in outcomes inherent in a comparison of children who share, on average, 50%
of their genetic material. Sibling comparisons may contribute something to the discussion of neurodevelopmental outcomes,
but it would be premature to extrapolate too much from studies such as these.
36 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40

7. Discussion

7.1. Review of findings

The key points of this paper can be summarized as follows: first, it is reasonable to consider the influence of diet on
language outcomes, as both human and animal studies have supported the idea of neurodevelopmental differences related
to breastfeeding. Second, large population-based studies that consider language outcomes in relation to breastfeeding
exclusivity have generally reported modest but statistically significant differences in favor of breastfed children. Third,
studies of language impairment have consistently reported a protective effect of breastfeeding, with larger effect sizes noted
in these populations. Finally, while null findings make occasional appearances in the headlines, caution is called for in
interpreting studies of populations where breastfeeding exclusivity and duration are low and/or poorly documented.
Across all of the studies described here, there is a trend for stronger associations to be observed in studies with a wider
range of breastfeeding duration and a higher degree of breastfeeding exclusivity. Gibson-Davis and Brooks-Gunn (2006),
with their <1 month/1 month classification scheme, reported that their results lost statistical significance after covariates
were included in their models; this was not the case for investigators such as Belfort et al. (2013), where longer breastfeeding
durations were described. In a similar vein, Dodds et al. (2011) described a significant but very small association between
autism and breastfeeding at hospital discharge, while Schultz et al. (2006) found a much stronger link when they considered
longer periods of breastfeeding.
Perhaps the most striking contrast between the population-based studies of typical development and the studies focused
on disorders is the difference in effect sizes. A 3- to 5-point between-groups difference on a measure with a 15-point standard
deviation represents a small effect size; the 7.5-point difference reported by Kramer et al. (2008) is a medium-sized effect.
Effect sizes for the odds ratios reported in the studies of communication impairment, however, range from medium for the
effect observed in Tomblin et al. (1997) to large for the restricted sample described in the 2006 study by Schultz et al. (see
Chinn, 2000, on effect sizes for odds ratios). The idea that the protective effect of an environmental variable might be observed
more easily in an at-risk population is supported by the existing literature on language development (Landry et al., 1997) and
by the existing literature on breastfeeding, as in the seminal study by Lucas, Morley, Cole, Lister, and Leeson-Payne (1992)
showing substantial differences for preterm infants who received human milk via tube-feedings. On a related note, boys seem
to suffer a disproportionate disadvantage from formula-feeding (Broad, 1972; Mahurin-Smith & Ambrose, 2013; Oddy et al.,
2011a). SLPs are well aware that boys are disproportionately vulnerable to autism, persistent stuttering, and ADD/ADHD, so it
is perhaps unsurprising that a protective effect might be more apparent among boys than in a sample of girls.

7.2. Assessment of the existing research

The difficulty with studying any environmental variable is that environments are inherently complex systems; this
reality creates interesting questions and untidy statistics. Infant feeding decisions are not made in isolation. Instead, they
are influenced by many other factors within the dyad’s environment: culture, maternal age and education, maternal
history of sexual abuse, maternal employment, a spouse’s and/or extended family members’ views on breastfeeding,
healthcare provider support or lack thereof, perinatal events, and others too numerous to list. Women who breastfeed
tend to differ from women who formula-feed (see Der et al., 2006 for a partial assessment of this question), and these
differences pose problems for any observational study. Longer maternity leave, for instance, is associated with longer
breastfeeding duration; at the same time, a family that can afford a longer maternity leave may also have greater financial
stability, improved access to health care, and the ability to pay for higher quality childcare. All of these factors confer
advantages that may be more significant than optimal choline levels. Observational studies must therefore be interpreted
with caution, and randomization is difficult to incorporate into studies of infant feeding. An additional consideration with
any observational study is the question of reverse causality. Is it possible, for instance, that a newborn predisposed to
develop autism might be less interactive or more temperamentally difficult from an early age, so that the predisposition
drives the feeding choices and not the reverse? While some studies offer evidence to controvert concerns about reverse
causality (cf. Mahurin-Smith & Ambrose, 2013; Schultz et al., 2006), clear confirmation of a causal link is notoriously
difficult to establish.
Despite these intrinsic limitations, the preponderance of the evidence reviewed here, including studies designed to
mitigate the influence of other environmental variables (Kramer et al., 2008; Vestergaard et al., 1999), supports the
hypothesis that breastfeeding in infancy promotes healthy neurodevelopment and protects against communication
impairment in childhood. The American Academy of Pediatrics (AAP) concludes that ‘‘infant feeding should not be
considered as a lifestyle choice but rather as a basic health issue’’ (2012, p. 837). Breastfeeding is recommended over
formula-feeding in the vast majority of circumstances, even for mothers who are concerned that they may have been
exposed to environmental toxins (Ribas-Fitó, Júlvez, Torrent, Grimalt, & Sunyer, 2007).

7.3. Implications for professionals in communication sciences and disorders (CSD)

The AAP’s recommendation may sound straightforward, but for some women breastfeeding is a daunting undertaking.
The purpose of this paper is not to heap any additional guilt upon mothers who may already blame themselves for their
 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40 37

children’s communicative challenges; rather, it is to share the available findings in hopes of mobilizing better support for
women who want to breastfeed. If breastfeeding can mitigate language difficulties, it is critical to provide accessible and
competent help to mothers who encounter breastfeeding difficulties. For practicing SLPs, this may take multiple forms.
For SLPs providing pediatric feeding assessment and intervention, it may mean acquiring new skills to assist
breastfeeding infants. For other SLPs, it may mean giving accurate information about the recommended duration of
breastfeeding to families of toddlers (American Academy of Pediatrics, 2012; World Health Organization, 2003), or
sharing the research summarized here with families interested in information on potential prevention strategies for
future children. For CSD professionals in higher education, it is recommended that curricula for SLP students include
information on feeding-related outcomes and on best practices for feeding assessment and intervention with
breastfeeding dyads. It is further recommended that research within the discipline continue to address the unanswered
questions raised in this paper.

8. Conclusion

This paper began with a comparison of breastfeeding to road-building, but the topic of breastfeeding frequently elicits
more complex emotional reactions than highway construction proposals. Breastfeeding can spark responses ranging from
delight to disgust, and reader comments on media coverage of research into breastfeeding-related outcomes often reflect
sharply divergent points of view. These responses can cloud careful consideration of the evidence base. In this paper I have
reviewed potential mechanisms by which breastfeeding might influence neurodevelopmental outcomes, identified
variables influencing study findings, and described reports of small-to-medium effect sizes in large population-based studies
and medium-to-large effect sizes in studies of children with language disorders. To return to the road-building analogy from
the introduction, the literature suggests that materials used by a long-ago road-building crew may shape the flow of traffic
along the roadway for years into the future.

Acknowledgments

The author would like to thank Nicoline Ambrose, Laura DeThorne, and Cynthia Johnson for their thoughtful comments
on the research project that prompted an investigation of this literature, as well as Maddie Mangieri, Angela Steffen, and
Ellyn Virden for their assistance with preparing this manuscript.

Appendix A. Continuing education

CEU Questions

1. Which of the following is the most accurate statement about docosahexaenoic acid (DHA)?
a. Its inclusion in infant formula is federally mandated in the US
b. Most varieties of infant formula contain higher concentrations of DHA than human milk
c. Studies of fortified formula have shown an unmistakable advantage for infants who receive DHA-fortified formula
d. It is a particularly important fatty acid for the process of neurodevelopment
2. Which of the following mechanisms is least likely to explain the differences observed in breastfed children?
a. Gene transcription may be influenced by the fatty acid content of a cell membrane
b. An absence of DHA in the diet may contribute to differences in brain structure for formula-fed children
c. Clear behavioral differences have been observed in studies of breastfeeding and formula-feeding mothers
d. Substances such as choline and nerve growth factor may be absent from infant formula
3. Which of the following best describes the differences observed in population-based studies of the relationship between
breastfeeding and language outcomes
a. Clear differences on the order of a 1 SD advantage for breastfed children have been observed
b. Modest differences in favor of breastfed children, representing a small-to-medium effect size, have been observed
c. Modest differences in favor of formula-fed children, representing a small-to-medium effect size, have been observed
d. No differences have been observed
4. Which of the following is true of the relationship between breastfeeding and autism?
a. Studies suggest that breastfeeding may protect against autism
b. Studies suggest that breastfed children may be more vulnerable to autism
c. Studies suggest that there is no relationship between breastfeeding and autism
d. Studies suggest that breastfeeding only makes a difference with regard to autism for mothers older than 40 at the time
of the child’s birth
5. Which of the following may be an important covariate in studies of breastfeeding-related outcomes?
a. Maternal IQ
b. Maternal education
38 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40

c. Parental socioeconomic status

d. Maternal employment
e. All of the above

References

Al-Farsi, Y. M., Al-Sharbati, M. M., Waly, M. I., Al-Farsi, O. A., Al-Shafaee, M. A., Al-Khaduri, M. M., et al. (2012). Effect of suboptimal breast-feeding on occurrence of
autism: A case–control study. Nutrition, 28(7), e27–e32.
American Academy of Pediatrics (2012). Breastfeeding and the use of human milk. Pediatrics, 129, e827–e841.
Anderson, J. W., Johnstone, B. M., & Remley, D. T. (1999). Breast-feeding and cognitive development: A meta-analysis. The American Journal of Clinical Nutrition,
70(4), 525–535.
Ashwood, P., Wils, S., & van de Water, J. (2006). The immune response in autism: A new frontier for autism research. Journal of Leukocyte Biology, 80, 1–15.
Barbosa, C., Vasquez, S., Parada, M. A., Gonzalez, J. C. V., Jackson, C., Yanez, N. D., et al. (2009). The relationship of bottle feeding and other sucking behaviors with
speech disorder in Patagonian preschoolers. BMC Pediatrics, 9, 66.
Barone, J. G., Ramasamy, R., Farkas, A., Lerner, E., Creenan, E., Salmon, D., et al. (2006). Breastfeeding during infancy may protect against bed-wetting during
childhood. Pediatrics, 118(1), 254–259.
Baumwell, L., Tamis-LeMonda, C. S., & Bornstein, M. H. (1997). Maternal verbal sensitivity and child language comprehension. Infant Behavior and Development,
20(2), 247–258.
Belfort, M. B., Rifas-Shiman, S. L., Kleinman, K. P., Guthrie, L. B., Bellinger, D. C., Taveras, E. M., et al. (2013). Infant feeding and childhood cognition at ages 3 and
7 years: Effects of breastfeeding duration and exclusivity. JAMA Pediatrics, 167(9), 836–844.
Bourre, J., Pascal, G., Durand, G., Masson, M., Dumont, O., & Piciotti, M. (1984). Alterations in the fatty acid composition of rat brain cells (neurons, astrocytes,
and oligodendrocytes) and of subcellular fractions (myelin and synaptosomes) induced by a diet devoid of n-3 fatty acids. Journal of Neurochemistry, 43(2),
342–348.
Broad, D. J. (1972). Formants in automatic speech recognition. International Journal of Man-Machine Studies, 4(4), 411–424.
Broad, F. E. (1975). Further studies on the effects of infant feeding on speech quality. The New Zealand Medical Journal, 82(553), 373–376.
Broad, F. E., & Duganzich, D. M. (1983). The effects of infant feeding, birth order, occupation and socio-economic status on speech in six-year-old children. The New
Zealand Medical Journal, 96(734), 483–486.
Canfield, R. L., Henderson, C. R., Jr., Cory-Slechta, D. A., Cox, C., Jusko, T. A., & Lanphear, B. P. (2003). Intellectual impairment in children with blood lead
concentrations below 10 mg per deciliter. New England Journal of Medicine, 348(16), 1517–1526.
Chinn, S. (2000). A simple method for converting an odds ratio to effect size for use in meta-analysis. Statistics in Medicine, 19(22), 3127–3131.
Coates, M. M., & Riordan, J. (2005). Tides in breastfeeding practice. In J. Riordan (Ed.), Breastfeeding and human lactation (3rd edition, pp. 3–29). Sudbury, MA: Jones
and Bartlett.
Colen, C. G., & Ramey, D. M. (2014). Is breast truly best? Estimating the effects of breastfeeding on long-term child health and wellbeing in the United States using
sibling comparisons. Social Science & Medicine, 109, 55–65.
Daniels, M. C., & Adair, L. S. (2005). Breast-feeding influences cognitive development in Filipino children. The Journal of Nutrition, 135(11), 2589–2595.
Darnaudéry, M., Perez-Martin, M., Del Favero, F., Gomez-Roldan, C., Garcia-Segura, L. M., & Maccari, S. (2007). Early motherhood in rats is associated with a
modification of hippocampal function. Psychoneuroendocrinology, 32(7), 803–812.
Dee, D. L., Li, R., Lee, L. C., & Grummer-Strawn, L. M. (2007). Associations between breastfeeding practices and young children’s language and motor skill
development. Pediatrics, 119(Suppl. 1), S92–S98.
Dekaban, A. S., & Sadowsky, D. (1978). Changes in brain weights during the span of human life: Relation of brain weights to body heights and body weights. Annals
of Neurology, 4(4), 345–356.
Delgado-Noguera, M. F., Calvache, J. A., & Bonfill Cosp, X. (2010). Supplementation with long chain polyunsaturated fatty acids (LCPUFA) to breastfeeding mothers
for improving child growth and development. Cochrane Database of Systematic Reviews, 12.
DeMar, J. C., Ma, K., Bell, J. M., Igarashi, M., Greenstein, D., & Rapoport, S. I. (2006). One generation of n-3 polyunsaturated fatty acid deprivation increases
depression and aggression test scores in rats. Journal of Lipid Research, 47(1), 172–180.
Deoni, S. C., Dean, D. C., III, Piryatinsky, I., O’Muircheartaigh, J., Waskiewicz, N., Lehman, K., et al. (2013). Breastfeeding and early white matter development: A
cross-sectional study. NeuroImage, 82, 77–86.
Der, G., Batty, G. D., & Deary, I. J. (2006). Effect of breast feeding on intelligence in children: Prospective study, sibling pairs analysis, and meta-analysis. British
Medical Journal, 333(7575), 945.
Dodds, L., Fell, D. B., Shea, S., Armson, B. A., Allen, A. C., & Bryson, S. (2011). The role of prenatal, obstetric and neonatal factors in the development of autism. Journal
of Autism and Developmental Disorders, 41(7), 891–902.
Drane, D. L. (2003). Breastfeeding and specific language impairment. Dissertation Abstracts International, 65(01).. (UMI No. 3118535).
Drane, D. L., & Logemann, J. A. (2000). A critical evaluation of the evidence on the association between type of infant feeding and cognitive development. Paediatric
and Perinatal Epidemiology, 14, 349–356.
Dunn, L. M., & Dunn, L. M. (1981). Peabody picture vocabulary test: Forms L and M. Circle Pines, MN: American Guidance Service.
Dunn, L. M., & Dunn, L. M. (1997). PPVT-III: Peabody picture vocabulary test. Circle Pines, MN: American Guidance Service.
Farquharson, J., Jamieson, E. C., Abbasi, K. A., Ainslie Patrick, W. J., Logan, R. W., & Cockburn, F. (1995). Effect of diet on the fatty acid composition of the major
phospholipids of infant cerebral cortex. Archives of Disease in Childhood, 72, 198–203.
Farquharson, J., Jamieson, E. C., Logan, R. W., Cockburn, F., & Ainslie Patrick, W. (1992). Infant cerebral cortex phospholipid fatty-acid composition and diet. The
Lancet, 340(8823), 810–813.
FDA Infant Formula Nutrient Requirements, 21C.F.R. § 107. 100 (2014).
Feldman, R. (2007). Parent-infant synchrony and the construction of shared timing: Physiological precursors, developmental outcomes, and risk conditions.
Journal of Child Psychology and Psychiatry, 48, 329–354.
Feldman, R., Weller, A., Zagoory-Sharon, O., & Levine, A. (2007). Evidence for a neuroendocrinological foundation of human affiliation: Plasma oxytocin levels
across pregnancy and the postpartum period predict mother-infant bonding. Psychological Science, 18, 965–970.
Fox, A. V., Dodd, B., & Howard, D. (2002). Risk factors for speech disorders in children. International Journal of Language & Communication Disorders, 37(2), 117–131.
Gibson-Davis, C. M., & Brooks-Gunn, J. (2006). Breastfeeding and verbal ability of 3-year-olds in a multicity sample. Pediatrics, 118, 1444–1451.
Gilbert, S. F., & Epel, D. (2009). Ecological developmental biology: Integrating epigenetics, medicine, and evolution. Sunderland, MA: Sinauer Associates.
Gordon, I., Zagoory-Sharon, O., Leckman, J. F., & Feldman, R. (2010). Oxytocin and the development of parenting in humans. Biological Psychiatry, 68, 377–382.
Greiner, R. S., Moriguchi, T., Hutton, A., Slotnick, B. M., & Salem, N., Jr. (1999). Rats with low levels of brain docosahexaenoic acid show impaired performance in
olfactory-based and spatial learning tasks. Lipids, 34(1), S239–S243.
Harrison, L. J., & McLeod, S. (2010). Risk and protective factors associated with speech and language impairment in a nationally representative sample of 4- to 5-
year-old children. Journal of Speech, Language, and Hearing Research, 53(2), 508–529.
Hill, E. L., & Frith, U. (2003). Understanding autism: Insights from mind and brain. Philosophical Transactions of the Royal Society of London Series B: Biological
Sciences, 358(1430), 281–289.
Innis, S. M. (2007). Dietary (n-3) fatty acids and brain development. Journal of Nutrition, 137, 855–859.
 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40 39

Isaacs, E. B., Fischl, B. R., Quinn, B. T., Chong, W. K., Gadian, D. G., & Lucas, A. (2010). Impact of breast milk on intelligence quotient, brain size, and white matter
development. Pediatric Research, 67(4), 357–362.
Jamieson, E. C., Farquharson, J., Logan, R. W., Howatson, A. G., Patrick, W. J. A., Weaver, L. T., et al. (1999). Infant cerebellar gray and white matter fatty acids in
relation to age and diet. Lipids, 34, 1065–1071.
Kafouri, S., Kramer, M., Leonard, G., Perron, M., Pike, B., Richer, L., et al. (2012). Breastfeeding and brain structure in adolescence. International Journal of
Epidemiology (dys172).
Kaufman, A. S., & Kaufman, N. L. (2004). Kaufman brief intelligence test (2nd edition). Bloomington, MN: Pearson Inc.
Kim, P., Feldman, R., Mayes, L. C., Eicher, V., Thompson, N., Leckman, J. F., et al. (2011). Breastfeeding, brain activation to own infant cry, and maternal sensitivity.
Journal of Child Psychology and Psychiatry, 52(8), 907–915.
Kim, P., Leckman, J. F., Mayes, L. C., Feldman, R., Wang, X., & Swain, J. E. (2010). The plasticity of human maternal brain: Longitudinal changes in brain anatomy
during the early postpartum period. Behavioral Neuroscience, 124(5), 695.
Kramer, M. S., Aboud, F., Mironova, E., Vanilovich, I., Platt, R. W., Matush, L., et al. (2008). Breastfeeding and child cognitive development: New evidence from a
large randomized trial. Archives of General Psychiatry, 65(5), 578–584.
Kramer, M. S., Chalmers, B., Hodnett, E. D., Sevkovskaya, Z., Dzikovich, I., Shapiro, S., et al. (2001). Promotion of breastfeeding intervention trial (PROBIT):
A randomized trial in the Republic of Belarus. Journal of the American Medical Association, 285(4), 413–420.
Landry, S. H., Smith, K. E., Miller-Loncar, C. L., & Swank, P. R. (1997). Predicting cognitive-language and social growth curves from early maternal behaviors in
children at varying degrees of biological risk. Developmental Psychology, 33(6), 1040.
Lawrence, R. A., & Lawrence, R. M. (2005). Breastfeeding: A guide for the medical profession (6th edition). Philadelphia: Elsevier, Mosby.
Love, G., Torrey, N., McNamara, I., Morgan, M., Banks, M., Hester, N. W., et al. (2005). Maternal experience produces long-lasting behavioral modifications in the
rat. Behavioral Neuroscience, 119(4), 1084.
Lucas, A., Morley, R., Cole, T. J., Lister, G., & Leeson-Payne, C. (1992). Breast milk and subsequent intelligence quotient in children born preterm. The Lancet, 339,
261–264.
Makrides, M., Neumann, M. A., Byard, R. W., Simmer, K., & Gibson, R. A. (1994). Fatty acid composition of brain, retina, and erythrocytes in breast- and formula-fed
infants. American Journal of Clinical Nutrition, 60, 189–194.
Matsuzawa, J., Matsui, M., Konishi, T., Noguchi, K., Gur, R. C., Bilker, W., et al. (2001). Age-related volumetric changes of brain gray and white matter in healthy
infants and children. Cerebral Cortex, 11(4), 335–342.
Mahurin-Smith, J., & Ambrose, N. G. (2013). Breastfeeding may protect against persistent stuttering. Journal of Communication Disorders, 46(4), 351–360.
Mahurin Smith, J., DeThorne, L. S., Logan, J. A., Channell, R. W., & Petrill, S. A. (2014). The impact of prematurity on language skills at school age. Journal of Speech,
Language & Hearing Research, 57(3), 901–916.
McDade, T. W. (2012). Early environments and the ecology of inflammation. Proceedings of the National Academy of Sciences, 109, 17281–17288.
McDade, T. W., Metzger, M. W., Chyu, L., Duncan, G. J., Garfield, C., & Adam, E. K. (2014). Long-term effects of birth weight and breastfeeding duration on
inflammation in early adulthood. Proceedings of the Royal Society B: Biological Sciences, 281(1784), 20133116.
Meyerink, R. O., & Marquis, G. S. (2002). Breastfeeding initiation and duration among low-income women in Alabama: The importance of personal and familial
experiences in making infant-feeding choices. Journal of Human Lactation, 18(1), 38–45.
Mezzacappa, E. S., & Katkin, E. S. (2002). Breast-feeding is associated with reduced perceived stress and negative mood in mothers. Health Psychology, 21(2), 187.
Nyaradi, A., Li, J., Hickling, S., Foster, J., & Oddy, W. H. (2013). The role of nutrition in children’s neurocognitive development, from pregnancy through childhood.
Frontiers in Human Neuroscience, 7.
Obel, C., Henriksen, T. B., Hedegaard, M., Secher, N. J., & Østergaard, J. (1998). Smoking during pregnancy and babbling abilities of the 8-month-old infant.
Paediatric and Perinatal Epidemiology, 12, 37–48.
Oddy, W. H., Kendall, G. E., Blair, E., De Klerk, N. H., Stanley, F. J., Landau, L. I., et al. (2003). Breast feeding and cognitive development in childhood: A prospective
birth cohort study. Paediatric and Perinatal Epidemiology, 17(1), 81–90.
Oddy, W., Li, J., Robinson, M., & Whitehouse, A. (2012). The long-term effects of breastfeeding on development. In Contemporary pediatrics. Rijeka: Intek.
Oddy, W. H., Li, J., Whitehouse, A. J., Zubrick, S. R., & Malacova, E. (2011). Breastfeeding duration and academic achievement at 10 years. Pediatrics, 127(1),
e137–e145.
Oddy, W. H., Robinson, M., Kendall, G. E., Li, J., Zubrick, S. R., & Stanley, F. J. (2011). Breastfeeding and early child development: A prospective cohort study. Acta
Paediatrica, 100(7), 992–999.
Oddy, W. H., & Rosales, F. (2010). A systematic review of the importance of milk TGF-b on immunological outcomes in the infant and young child. Pediatric Allergy
and Immunology, 21, 47–59.
Pedersen, C. A., Ascher, J. A., Monroe, Y. L., & Prange, A. J. (1982). Oxytocin induces maternal behavior in virgin female rats. Science, 216(4546), 648–650.
Ribas-Fitó, N., Júlvez, J., Torrent, M., Grimalt, J. O., & Sunyer, J. (2007). Beneficial effects of breastfeeding on cognition regardless of DDT concentrations at birth.
American Journal of Epidemiology, 166(10), 1198–1202.
Rothman, S. (2003). An Australian version of the Adapted PPVT-III for use in research (Unpublished manuscript) Australian Council for Educational Research.
Salem, N., Moriguchi, T., Greiner, R. S., McBride, K., Ahmad, A., Catalan, J. N., et al. (2000). Alterations in brain function after loss of docosahexaenoate due to dietary
restriction of n-3 fatty acids. Journal of Molecular Neuroscience, 16, 299–307.
Sanai, N., Nguyen, T., Ihrie, R. A., Mirzadeh, Z., Tsai, H. H., Wong, M., et al. (2011). Corridors of migrating neurons in the human brain and their decline during
infancy. Nature, 478(7369), 382–386.
Schultz, S. T., Klonoff-Cohen, H. S., Wingard, D. L., Akshoomoff, N. A., Macera, C. A., Ji, M., et al. (2006). Breastfeeding, infant formula supplementation, and Autistic
Disorder: The results of a parent survey. International Breastfeeding Journal, 1(16.).
Simmer, K., Schulzke, S. M., & Patole, S. (2008). Longchain polyunsaturated fatty acid supplementation in preterm infants. Cochrane Database of Systematic Reviews,
1, 1–27.
Strathearn, L., Mamun, A. A., Najman, J. M., & O’Callaghan, M. J. (2009). Does breastfeeding protect against substantiated child abuse and neglect? A 15-year cohort
study. Pediatrics, 123, 483–493.
Tanoue, Y., & Oda, S. (1989). Weaning time of children with infantile autism. Journal of Autism and Developmental Disorders, 19(3), 425–434.
Thorpe, K., Rutter, M., & Greenwood, R. (2003). Twins as a natural experiment to study the causes of mild language delay: II: Family interaction risk factors. Journal
of Child Psychology and Psychiatry, 44(3), 342–355.
Tomblin, J. B., Smith, E., & Zhang, X. (1997). Epidemiology of specific language impairment: Prenatal and perinatal risk factors. Journal of Communication Disorders,
30(4), 325–344.
Tomizawa, K., Iga, N., Lu, Y.-F., Moriwaki, A., Matsushita, M., Li, S.-T., et al. (2003). Oxytocin improves long-lasting spatial memory during motherhood through
MAP kinase cascade. Nature Neuroscience, 6(4), 384–390.
Vestergaard, M., Obel, C., Henriksen, T. B., Sørensen, H. T., Skajaa, E., & Østergaard, J. (1999). Duration of breastfeeding and developmental milestones during the
latter half of infancy. Acta Paediatrica, 88(12), 1327–1332.
Wang, B. (2009). Sialic acid is an essential nutrient for brain development and cognition. Annual Review of Nutrition, 29, 177–222.
Wärnberg, J., Gomez-Martinez, S., Romeo, J., Dı́az, L. E., & Marcos, A. (2009). Nutrition, inflammation, and cognitive function. Annals of the New York Academy of
Sciences, 1153(1), 164–175.
Watson, R. E., DeSesso, J. M., Hurtt, M. E., & Cappon, G. D. (2006). Postnatal growth and morphological development of the brain: A species comparison. Birth
Defects Research Part B: Developmental and Reproductive Toxicology, 77(5), 471–484.
Wechsler, D. (1999). Wechsler abbreviated scales of intelligence. San Antonio, TX: Psychological Corporation.
Whitehouse, A. J., Robinson, M., Li, J., & Oddy, W. H. (2011). Duration of breast feeding and language ability in middle childhood. Paediatric and Perinatal
Epidemiology, 25(1), 44–52.
40 J. Mahurin Smith / Journal of Communication Disorders 57 (2015) 29–40

Wilson, A. C., Forsyth, J. S., Greene, S. A., Irvine, L., Hau, C., & Howie, P. W. (1998). Relation of infant diet to childhood health: Seven year follow up of cohort of
children in Dundee infant feeding study. British Medical Journal, 316(7124), 21–25.
World Health Organization (2003). Global strategy for infant and young child feeding. Geneva: World Health Organization.
Zeisel, S. H. (2006). Choline: Critical role during fetal development and dietary requirements in adults. Annual Review of Nutrition, 26, 229.
Zeisel, S. H., & da Costa, K.-A. (2009). Choline: An essential nutrient for public health. Nutrition Reviews, 67, 615–623.
Zimmerman, I. L., Steiner, V. G., & Pond, R. E. (1992). PLS-3: Preschool language scale (3rd edition). San Antonio, TX: Psychological Corporation.
Zumach, A., Gerrits, E., Chenault, M., & Anteunis, L. (2010). Long-term effects of early-life otitis media on language development. Journal of Speech, Language, and
Hearing Research, 53(1), 34–43.