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ORIGINAL PAPER
The Association Between Breastfeeding Exposureand Duration, Neuropsychological Deficits,and Psychopathic Personality Traits in Offspring: TheModerating Role of 5HTTLPR
Dylan B. Jackson1 • Kevin M. Beaver1,2
Published online: 16 May 2015� Springer Science+Business Media New York 2015
Abstract A wealth of research has revealed that a shorter duration of breastfeeding
during infancy can increase the risk of various maladaptive traits, including neuropsy-
chological deficits. Despite the number of studies that have been conducted on the topic,
few studies have explored whether the effects of breastfeeding on neuropsychological
functioning and personality features persist into adulthood. Furthermore, very little re-
search to date has examined whether this relationship is moderated by specific indicators of
genetic risk. The current study examines the direct and interactive effects of breastfeeding
experiences and the serotonin transporter polymorphism (5HTTLPR) on neuropsycho-
logical deficits and psychopathic personality traits. Using data from the National Longi-
tudinal study of Adolescent Health, we find that no exposure to breastfeeding and a shorter
duration of breastfeeding significantly increase the risk of exhibiting neuropsychological
deficits during adolescence and early adulthood as well as psychopathic personality traits
during adulthood. The results also reveal a number of gene 9 environment interactions
between 5HTTLPR, breastfeeding exposure and breastfeeding duration in the prediction of
neuropsychological deficits, but not in the prediction of psychopathic personality traits.
Keywords Breastfeeding � Neuropsychological deficits � Psychopathic personality traits �Genetic risk � 5HTTLPR � Serotonin transporter � Moderating effects
& Dylan B. [email protected]
Kevin M. [email protected]
1 Florida State University, Tallahassee, FL, USA
2 King Abdulaziz University, Jeddah, Saudi Arabia
123
Psychiatr Q (2016) 87:107–127DOI 10.1007/s11126-015-9366-2
Introduction
Both the World Health Organization (WHO) and scholars across disciplines have touted
breastfeeding as a highly beneficial component of pediatric nutrition [37]. The association
between breastfeeding and offspring health outcomes, including infant mortality, has been
consistently documented by over 40 years of research [20, 37]. Breastfeeding has been
shown to reduce the risk of a wide range of negative health outcomes in offspring, in-
cluding obesity [27], high blood pressure [49], respiratory illness [5], coeliac disease [2]
and inflammatory bowel disease [45]. Consequently, the WHO currently recommends that
mothers breastfeed their children exclusively for 6 months and in conjunction with solid
foods for 2 years (see [16]).
A more recent line of research has indicated that breastfeeding can also protect against
abnormal development of offspring across cognitive, psychological, social, and behavioral
domains [11, 16, 33, 36, 51, 53]. For example, research suggests that children who were
breastfed for longer time periods tend to evince greater language ability [23], motor ability
[23], and overall intelligence [52] relative to children who were never breastfed or who
were breastfed for shorter durations. A shorter duration of breastfeeding also seems to
increase the risk of several psychological and behavioral problems, including ADHD
symptoms [51], internalizing and externalizing problems [33, 53] and schizophrenia [64].
A number of studies have shown that the association between breastfeeding and neu-
ropsychological outcomes is at least partially driven by the nutritional content of breast
milk, particularly through the supplement of long-chain polyunsaturated fatty acids such as
docosahexaenoic acid [31, 46].
Despite the growing number of studies examining the relationship between breast-
feeding and various neuropsychological outcomes, very little research has examined
whether the influence of breastfeeding on the neuropsychological health of offspring ex-
tends to later life stages, such as adolescence and adulthood (for exceptions, see [11, 53]).
Furthermore, only a small number of studies has explored whether breastfeeding is linked
to adult mental health outcomes (see [64]). The possibility that genetic factors might
moderate the effects of breastfeeding on neuropsychological and mental health outcomes
has also been almost entirely overlooked (for an exception, see [19]). Finally, to our
knowledge, scholars have yet to explore whether neuropsychological deficits mediates the
link between breastfeeding experiences and mental health outcomes in adult offspring.
In light of the shortcomings of the literature, the goal of the present study is threefold.
First, we seek to examine whether less exposure to breastfeeding significantly increases the
likelihood of exhibiting neuropsychological deficits during adolescence and adulthood and
psychopathic personality traits during adulthood. Because these outcomes have been found
to be significantly correlated [10, 15, 30], we explore the extent to which breastfeeding, as
a facilitator of healthy brain development [43, 44], may influence both neurological de-
ficiencies and psychopathic personality traits. Our second objective is to test whether the
link between breastfeeding, neuropsychological deficits, and psychopathic personality
traits is conditioned by genetic risk on a serotonin transporter polymorphism (5HTTLPR).
Finally, due to the empirical overlap between neuropsychological deficits and psychopathic
personality traits [10, 15, 30], we explore the potential intervening role of neuropsycho-
logical deficits in the relationship between breastfeeding experiences during infancy and
adult psychopathic personality traits.
108 Psychiatr Q (2016) 87:107–127
123
Breastfeeding, Neuropsychological Deficits, and Psychopathic PersonalityTraits
The line of research examining the role of breastfeeding experiences in predicting various
elements of neuropsychological functioning is continually growing [11, 23, 43, 44, 69].
Findings from this research tend to reveal that the duration of breastfeeding, net of various
demographic and socialization factors, has important implications for the neuropsycho-
logical well-being of offspring. To illustrate, a very recent study by Julvez et al. [43]
revealed that both the duration and exclusivity of infant breastfeeding were predictive of
neuropsychological functioning of offspring during early childhood, independent of ma-
ternal IQ and social class. Julvez et al. [44] conducted a similar study and found that being
breastfed for more than 20 weeks resulted in an average increase in executive functioning
by 4.9 points at the age of 4. Longer durations of breastfeeding also appear to significantly
reduce the likelihood of developing neuropsychological deficits at later life stages,
although little research has examined outcomes past late childhood (although, see [11]).
Despite numerous studies linking breastfeeding to neuropsychological health, a relatively
small number of studies have explored the association between breastfeeding and abnormal
psychological functioning during adulthood [3, 50, 64]. Among the limited number of studies
in this area of research, the link between breastfeeding and the development of schizophrenia
is the most commonly examined relationship. For instance, research has suggested that while
breastfeeding is equally common in individuals with and without a schizophrenia diagnosis,
exposure to breast milk may postpone the onset of the illness in patients with schizophrenia
[3]. A study by Sørensen et al. [64], moreover, found that an extremely short duration of
breastfeeding (i.e.,\2 weeks) increased the risk of schizophrenia in adult offspring.
Although early breastfeeding experiences have been linked to schizophrenia, researchers
have yet to examine whether indicators of psychopathy are more likely to emerge in adults
who had minimal exposure to breastfeeding. Still, several studies have indicated that neu-
ropsychological deficits are significantly predictive of psychopathy [10, 15, 76, 77]. To be
precise, psychopaths have been found to evince significant structural and functional abnor-
malities in the prefrontal cortex, including reductions in prefrontal gray matter volume [76,
77]. Given the body of research linking breastfeeding to neuropsychological deficits [43, 44,
69], it is reasonable to extend this line of research by exploring whether the development of
psychopathic personality traits is similarly influenced by breastfeeding experiences during
infancy. The hypothesized association between breastfeeding and psychopathic personality
traits is also buttressed by research showing that individuals who were not breastfed during
infancy are more likely to develop an aggressive, hostile temperament by adulthood [50]. In
light of these findings, it is reasonable to suggest that breastfeeding experiences may be
associatedwith the development of psychopathic personality traits during adulthood, and that
such a relationship may be explained by the greater likelihood of neuropsychological deficits
among individuals with less exposure to breastfeeding.
5HTTLPR Genotype, Impaired Executive Functioning, and PsychopathicPersonality Traits
In addition to perinatal environments, such as breastfeeding, research suggests that genetic
factors likely play a role in the development of neuropsychological deficits and psycho-
pathic personality traits [25, 35, 54]. Allelic variation in a functional polymorphism in the
Psychiatr Q (2016) 87:107–127 109
123
promoter region of the SLC6a4 serotonin transporter gene (i.e., 5HTTLPR) has been
associated with differences in cognition, temperament, and behavior [1, 17, 28, 29].
Although the results can vary depending on whether other genetic and environmental
factors are simultaneously considered, this body of research broadly suggest that indi-
viduals possessing one or more short (s) alleles are at greater risk of a variety of mal-
adaptive outcomes [60, 72], including impairments in executive functioning [35, 54].
For example, Canli et al. [18] conducted a whole-brain analysis using functional
magnetic resonance imaging (fMRI) and found that carriers of the 5HTTLPR s allele
consistently showed less brain activation relative to non-carriers. The study also revealed
that s allele carriers are more likely to exhibit a reduction in the volume, neuronal density
and gray matter density of the middle frontal gyrus, a sub-region of the prefrontal cortex
which plays an important role in several neuropsychological functions, such as non-spatial
working memory and attentional set-shifting [67].
A number of other studies have also linked 5HTTLPR to poorer performance on a
number of executive functioning tasks [35, 54]. To illustrate, a study by He et al. [35]
revealed that s allele homozygotes on 5HTTLPR scored relatively low on two decision-
making tasks, resulting in more disadvantageous choices. This may be explained in part by
the tendency of s allele carriers to score higher on performance measures of impulsivity
and delay aversion relative to long (l) allele homozygotes [54, 63]. As research has re-
vealed, poor concentration, impaired decision-making and the inability to delay immediate
reward are all key indicators of deficits in neuropsychological functioning [58]. Roiser
et al. [61] also note that individuals who are homozygous on the s allele are particularly
vulnerable to 5-HT (serotonin) depletion, which may decrease inhibition and cognitive
flexibility.
Although several studies have explored the relationship between 5HTTLPR and indi-
cators of neuropsychological functioning, comparatively little research has examined the
link between 5HTTLPR and psychopathic personality traits [28, 48]. The results of the
research to date, however, suggest that the s allele is associated with greater psychopathy
scores (see [28]). The findings are consistent with the results of several studies linking
5HTTLPR genetic risk with other important correlates of psychopathy, such as aggression/
violence [29], risk seeking [17], and criminal justice involvement [71].
Are the Effects of Breastfeeding on Neuropsychological Deficitsand Psychopathic Personality Traits Conditional?
The vast majority of studies have not considered whether environmental or genetic
factors moderate the effects of breastfeeding duration on neuropsychological and mental
health outcomes. Nevertheless, research to date suggests that the benefits of breast-
feeding might be conditional [19, 47, 66, 68]. A number of studies have indicated, for
instance, that breastfeeding may be especially beneficial for children who experience
premature birth or whose weight is particularly low at birth [68]. Maternal engagement
and positive socialization also appears to work jointly with longer breastfeeding dura-
tions to minimize internalizing problems during childhood [47]. Some evidence for
genetic moderation has also been found [19]. A genetic variant in FADS2 has been
proposed as a potentially important moderator of the link between breastfeeding and
neuropsychological outcomes, primarily because both breastfeeding and FADS2 are
implicated in modulation of long-chain fatty acids that are essential to
110 Psychiatr Q (2016) 87:107–127
123
neuropsychological health (See [19]). This research suggests that allelic variation in the
FADS2 gene might condition the effect of breastfeeding on specific indicators of in-
telligence during childhood (for an exception, see [66]).
To date, no research has specifically examined whether allelic differences on the
serotonin transporter polymorphism (5HTTLPR) moderate the associations between
breastfeeding experiences and neuropsychological functioning as well as breastfeeding
experiences and psychopathic personality traits. Nevertheless, research on 5HTTLPR has
generally suggested that individuals who possess one or more risk alleles have high sen-
sitivity to particularly stressful and/or noxious environments [1, 25, 73]. For example, Way
and Taylor [73] found that stressful environments are particularly taxing on the verbal and
arithmetic capabilities of s allele carriers relative to l allele homozygotes. Similar gene–
environment interactions also appear to increase the likelihood of undesirable personality
features, such as borderline and antisocial traits (see [48]). Given that the absence of
breastfeeding can be considered a noxious environment that impedes the developing brain,
it may very well be the case that variation on 5HTTLPR conditions the relationship
between breastfeeding experiences and neuropsychological deficits as well as breastfeed-
ing experiences and psychopathic personality traits.
Methods
Sample
The present study uses data from the National Longitudinal Study of Adolescent Health
(Add Health). The study is a prospective, longitudinal study of a nationally representative
sample of adolescents who were in grades 7–12 at the first wave of data collection [32, 70].
The main objective of the Add Health study was to examine the traits, behaviors, rela-
tionships, and social life of teenagers as they move towards adulthood. Although over
90,000 students were assessed using in-school self-report surveys at the first wave of data
collection, a subsample of more than 20,000 youth and 17,000 caregivers was randomly
chosen to participate in in-home interviews covering more nuanced and sensitive topics
[32]. Since the first wave of data collection, which occurred during the 1994–1995 school
year, three additional waves of data have been collected, with the most recent wave of data
collection taking place in the years 2008 and 2009, when most subjects were between the
ages of 24 and 32.
One feature of the Add Health that distinguishes it from many other studies is that a
subset of about 2500 subjects was ultimately genotyped. Respondents who had a sibling or
a cotwin who was also participating in the study were determined to be eligible for DNA
analysis. These subjects were asked to provide swabs of their buccal cells for genetic
typing. Through this process, paternal and maternal alleles on a number of candidate genes
were identified (e.g., DRD2, DRD4). For the purposes of our study, the genetically in-
formed subsample permits us to effectively carry out our research agenda to examine
whether an indicator of genetic risk (i.e., possession of the s allele on the serotonin
transporter 5HTTLPR) interacts with breastfeeding duration to predict neuropsychological
deficits and psychopathic personality traits in adolescence and adulthood. Consequently,
the present analysis is limited to an examination of data collected from the genotyped
subsample of the Add Health.
Psychiatr Q (2016) 87:107–127 111
123
Measures
Outcome Measures
Neuropsychological Deficits
Prior research using the Add Health data has typically relied on the abbreviated version of
the Peabody Picture Vocabulary Test (PPVT) as an indicator of neuropsychological
functioning (see [11, 71]). A number of researchers have investigated the validity and
reliability of the PPVT [22, 26]. This research has shown that the instrument is indeed a
valid and reliable indicator of receptive vocabulary and verbal ability [22]. Importantly,
scores on these indicators are highly correlated with other measures of neurocognitive
ability [56], making the PPVT a useful tool for detecting the presence of neuropsycho-
logical deficits. Participants were administered the PPVT during the in-home interviews
conducted at waves 1 and 3. PPVT percentile scores, in which higher scores reflect greater
relative verbal ability, were provided in the ADD Health data. For the purposes of our
study and to facilitate interpretation, these original PPVT percentile scores were recoded so
that a higher score reflects poorer neuropsychological functioning of the subject relative to
the other participants in the study.
Three different neuropsychological deficits measures were ultimately used in the pre-
sent study as dependent variables. First, PPVT percentile scores at wave 1 were reverse-
coded and subsequently standardized in order to assess neuropsychological deficits during
adolescence. Second, PPVT percentile scores at wave 3 were reverse-coded and subse-
quently standardized in order to assess neuropsychological deficits during early adulthood
(i.e., ages 18–26). Finally, a composite measure of neuropsychological deficits was created
by standardizing wave 1 and wave 3 deficits scores and summing them together (a = 0.81;
correlation = 0.68). Table 1 includes the descriptive statistics of the neuropsychological
deficits measures as well as all other variables and scales included in the analysis.
Table 1 Descriptive statistics for the ADD health genotyped subsample
Variable Mean SD Range
Neuropsychological deficits (wave 1) 0.00 1 -1.83 to 1.65
Neuropsychological deficits (wave 3) 0.00 1 -1.84 to 1.66
Neuropsychological deficits (composite) 0.00 0.92 -1.84 to 1.64
Psychopathic personality traits (wave 4) 0.00 0.44 -1.58 to 1.49
Never breastfed 0.57 0.50 0 to 1
Short duration of breastfeeding 4.91 1.59 0 to 6
5HTTLPR 0.87 0.72 0 to 2
Sex (male = 1) 0.47 0.50 0 to 1
Race (non-white = 1) 0.34 0.47 0 to 1
Age wave 1 16.01 1.67 12.12 to 20.86
Low SES 0.21 0.41 0 to 1
Neighborhood disadvantage 0.00 0.61 -1.14 to 2.30
Low maternal attachment 0.00 0.87 -0.44 to 6.35
Maternal disengagement 0.00 0.76 -0.92 to 3.72
Low maternal involvement 0.03 0.16 0–1
112 Psychiatr Q (2016) 87:107–127
123
Psychopathic Personality Traits
In addition to our threemeasures of neuropsychological deficits, we also employed ameasure
of psychopathic personality traits as a dependent variable in the current study. At the final
wave of data collection (i.e., wave 4), respondents were asked 41 questions concerning their
general disposition and character. Initially, these items were designed to tap a five-factor
model of personality as well as respondent self-regulation. However, a number of researchers
have conducted factor analyses and internal reliability tests and have identified a subset of
these items as indicative of psychopathic personality traits (see [8]). Following the lead of
research on this topic [8, 24], we created a scale of psychopathic personality traits by stan-
dardizing and summing 23 items from the personality inventory at wave four of data col-
lection (a = 0.82). The items measured several dimensions of a psychopathic personality,
including lack of sociability, narcissism, callous/unemotional traits, and low self-control. For
example, participants were asked about the extent to which they have little empathy/sym-
pathy for others, lose their temper, have frequent mood swings, get angry easily, rely on their
impulses, enjoy taking risks, and have little concern for other people. Scores on these items
ranged from 1 (strongly agree) to 5 (strongly disagree). All items were coded so that higher
scores reflected a greater propensity towards psychopathic personality traits.
Early Childhood and Genetic Measures
Breastfeeding Measures
Studies examining the relationship between the duration of breastfeeding and various child
outcomes are not completely uniform in their measurement of breastfeeding (see [4, 11, 20,
23]). Still, research has suggested that measures using slightly different criteria tend to be
highly correlated [38] and the results are relatively consistent across studies [4]. In order to
capture potential differences in the effects of no exposure versus relatively short duration, we
employed twodistinct breastfeedingmeasures in the present study: (1) never breastfed and (2)
short duration of breastfeeding.During thewave 1 interview, caregiverswere asked questions
about their child’s health and events shortly after the time of their birth, including a question
regarding the child’s duration of breastfeeding. Response options included never (7),
\3 months (1), 3 to \6 months (2), 6 to \9 months (3), 9 to \12 months (4), 12 to
\24 months (5), and 24 months or more (6).
For our first measure (i.e., never breastfed), we created a binary variable inwhichwe assigned
participants who had never been breastfed a score of 1, and all other participants who had been
breastfed for any amount of time a score of 0, in order to capture the absence of any exposure to
breastfeeding. For our secondmeasure (i.e., short duration of breastfeeding), we created a seven-
category item in which the original response options were recoded so that subjects who were
breastfed for less time received higher scores. Importantly, this secondmeasure was also utilized
in a subset of analyses (see Table 4) which tested whether a decrease in the length of time
breastfed is associated with neuropsychological deficits and psychopathic personality traits
among breastfed subjects only [i.e., never breastfed subjects (6) were excluded].
5HTTLPR
During wave 3 of data collection, genetic information on a number of polymorphisms was
obtained for approximately 2500 subjects. Fortunately, the vast majority of caregivers of
Psychiatr Q (2016) 87:107–127 113
123
the genotyped subjects were interviewed at wave 1, making the study of genetic mod-
erators of breastfeeding possible. A serotonin transporter gene known as 5HTTLPR was
one of the polymorphisms examined in the genotyped subsample of the Add Health study.
Most molecular genetic research has suggested that the short (s) allele (484 base pairs) is
the risk allele [60, 72], despite some contradictory research (see [13]).
Following the lead of prior research using the Add Health (see [71, 72]), both the maternal
and paternal alleleswere used to formourmeasure of genetic risk on 5HTTLPR. s alleleswere
assigned a value of 1, whereas l alleles were assigned a value of 0. Consequently, individuals
with 2 s alleles were assigned a value of 2, individuals with 1 s allele were assigned a value of
1, and individuals with no s alleles were assigned a value of 0.
Neighborhood and Parent Socialization Measures
Neighborhood Disadvantage
Several items concerning the participants’ family and neighborhood contexts were also
provided in the data. We utilized six items to construct a measure of neighborhood dis-
advantage that assessed the safety and overall appeal of each respondent’s neighborhood
(for a similar measure, see [12]). At the first wave of data collection, youth were asked a
number of questions including whether they felt safe in their neighborhood, whether they
knew most of their neighbors, whether they were happy in their neighborhood, and whether
they wanted to move. Higher scores reflected greater problems and dissatisfaction with the
neighborhood. Subsequently, items were standardized and summed to create an index of
neighborhood disadvantage (a = 0.62).
Low Maternal Attachment
In addition to our measure of neighborhood disadvantage, we followed the lead of prior
research [34] and created an index of maternal attachment. At wave 1, subjects were asked
two questions about their bond with their mother, including how much they felt their mother
cared about them. Response options ranged from 1 (not very much) to 5 (very much). For the
present study, we created our index of maternal attachment by first reverse-coding these
items, and then subsequently standardizing and summing them together (a = 0.68).
Maternal Disengagement
Following the lead of prior research [9], we created an index of maternal disengagement. At
wave 1, adolescents indicated whether they were satisfied with their relationship with their
mother and with the way she communicates with them, whether their mother was warm
toward them, and whether she calmly corrected them when necessary. The five possible
responses ranged from strongly agree (1) to strongly disagree (5). An index of maternal
disengagement was created by standardizing and summing the items (a = 0.82).
Low Maternal Involvement
An item assessing low maternal involvement was also developed in order to examine the
extent to which the mothers of adolescent subjects were not involved in their lives. At
wave 1, adolescents were asked if they had gone shopping, played a sport, attended church,
114 Psychiatr Q (2016) 87:107–127
123
gone to a movie or special event, talked about a personal problem, or talked about school
with their mother during the 4 weeks preceding the interview. Adolescents who did not
report engaging in any of the activities were assigned a 1, whereas adolescents who
reported engaging in one or more of the activities were assigned a 0 (see [21, 34] for
similar measures).
Control Variables
Age
Because the respondents began the study at different ages (ranging from 12 to 20), we
opted to include a continuous measure of each respondent’s age in our analysis.
Sex
A dichotomous measure of the respondents’ sex (1 = male; 0 = female) was also included
as a control variable in the current study.
Race
A number of studies have revealed that both breastfeeding and neuropsychological deficits
have been found to vary by race [14, 62]. Consequently, we controlled for race
(1 = nonwhite; 0 = white) in each of our analyses.
Low SES
Finally, we included a measure of low SES as a control variable in our study. Our measure
employs four items that asked caregiver respondents about their economic stability at wave
1 (see [40]). Specifically, respondents were asked to indicate whether they had received
unemployment compensation, Aid to Families with Dependent Children, public hous-
ing/housing subsidy, or food stamps during the month prior to data collection. Participants
who reported receiving any of these forms of financial assistance were assigned a 1 on this
variable, whereas participants who reported receiving no such assistance were assigned a 0.
Plan of Analysis
For the current study, the associations between breastfeeding exposure and duration,
5HTTLPR,neuropsychological deficits, and psychopathic personality traitswere estimated in a
number of ordinary least squares (OLS) regression models. Due to the presence of siblings in
our sample, the potential for the artificial deflation of standard errors exists. In order to correct
for this bias, we followed the lead of other researchers (e.g., [41] and estimated Huber/White
standard errors [75]). The first set of models examines whether individuals who were never
breastfed as infants are significantly more likely to evince neuropsychological deficits during
adolescence and early adulthood as well as psychopathic personality traits during adulthood.
The second set of models examines whether shorter durations of breastfeeding (ranging from
never to more than 24 months) are significantly predictive of neuropsychological deficits
during adolescence and early adulthood as well as psychopathic personality traits during
Psychiatr Q (2016) 87:107–127 115
123
adulthood. In conjunction with this second set of models, we test whether shorter durations of
breastfeeding significantly increase the risk of neuropsychological deficits and psychopathic
personality traits among breastfed subjects only (i.e., excluding those with no exposure to
breastfeeding). Finally, we test whether our measures of neuropsychological deficits during
adolescence and early adulthood significantly mediate the relationship between no exposure to
breastfeeding and psychopathic personality traits.
We also estimate a series of models examining gene–environment interactions for both
the full genotyped sample and the breastfed only subsample. Specifically, we created
multiplicative interaction terms between our breastfeeding measures and the serotonin
transporter polymorphism (5HTTLPR) in order to explore whether these gene–environ-
ment interactions are significantly predictive of neuropsychological deficits and psycho-
pathic personality traits later in life. We also mean-centered the covariates prior to creating
the interaction terms in an effort to reduce collinearity [39].
Results
We begin our analysis by estimating whether the absence of breastfeeding significantly
increases the risk of neuropsychological deficits and psychopathic personality traits during
later life stages using multivariate regression. The results of these regression equations are
displayed in Table 2. Specifically, Models 1, 3, and 5 display the findings for the main
effects models predicting measures of neuropsychological deficits, whereas model 7 dis-
plays the findings for the main effects models predicting psychopathic personality traits.
Models 2, 4, 6, and 8 display the findings for the models containing interaction terms
between no exposure to breastfeeding and 5HTTLPR. The results reveal that subjects who
did not experience any breastfeeding as an infant are significantly more likely to exhibit
(a) neuropsychological deficits during adolescence (b) neuropsychological deficits during
early adulthood and (c) psychopathic personality traits during adulthood, net of family,
neighborhood, and demographic factors. Conversely, neuropsychological deficits and
psychopathic personality traits were inconsistently related to measures of family and
neighborhood context. The interactive models also reveal that 5HTTLPR significantly
moderated the association between no exposure to breastfeeding and neuropsychological
deficits in both adolescence and early adulthood. The coefficient is negative, indicating that
the positive association between never having been breastfed and developing neuropsy-
chological deficits is significantly diminished for individuals with a riskier genotype on
5HTTLPR (i.e., more short alleles). Model 8, however, reveals that 5HTTLPR does not
significantly condition the relationship between no exposure to breastfeeding as an infant
and the development of psychopathic personality traits as an adult.
Table 3 displays the results from the next set of models, which estimate whether a
shorter duration of breastfeeding significantly increases the risk of exhibiting neuropsy-
chological deficits during adolescence and early adulthood and psychopathic personality
traits during adulthood. Again, models 1, 3, 5 and 7 show the findings for the main effects
models, whereas models 2, 4, 6 and 8 display the findings for the models containing
interaction terms. The results closely parallel those from Table 2, as the main effects of
short duration of breastfeeding on neuropsychological deficits and psychopathic person-
ality traits are consistently positive and significant. The results suggest that shorter periods
of breastfeeding increase the likelihood of neuropsychological deficits and psychopathic
personality traits in a dose–response fashion. The interactive models also suggest that the
116 Psychiatr Q (2016) 87:107–127
123
Table
2Thedirectandinteractiveeffectsofnoexposure
tobreastfeedingand5HTTLPRonneuropsychological
deficits
andpsychopathic
personalitytraits
Neuropsychological
deficits
(wave1)
Neuropsychological
deficits
(wave3)
Neuropsychological
deficits
(composite)
Psychopathic
personalitytraits
(wave4)
Model
1b/Beta
Model
2b/Beta
Model
3b/Beta
Model
4b/Beta
Model
5b/Beta
Model
6b/Beta
Model
7b/Beta
Model
8b/Beta
Never
breastfed
0.14*
0.14(0.02)
0.14*
0.14(0.02)
0.14*
0.14(0.02)
0.14*
0.14(0.02)
0.14*
0.15(0.02)
0.14*
0.15(0.02)
0.03*
0.06(0.01)
0.03*
0.06(0.01)
5HTTLPR
0.00
0.00(0.02)
-0.01
-0.01(0.02)
0.00
0.00(0.02)
0.00
0.00(0.02)
0.00
0.00(0.02)
0.00
0.00(0.02)
0.01
0.03(0.01)
0.01
0.03(0.01)
Age
0.01
0.02(0.01)
0.01
0.01(0.01)
-0.06*
-0.11(0.01)
-0.06*
-0.11(0.01)
-0.03*
-0.05(0.01)
-0.03*
-0.05(0.01)
-0.01
-0.04(0.01)
-0.01
-0.04(0.01)
Sex
-0.15*
-0.08(0.04)
-0.15*
-0.07(0.04)
-0.10*
-0.05(0.04)
-0.10*
-0.05(0.04)
-0.13*
-0.07(0.04)
-0.13*
-0.07(0.04)
-0.02
-0.02(0.02)
-0.02
-0.02(0.02)
Race(non-w
hite)
0.59*
0.27(0.04)
0.57*
0.27(0.04)
0.50*
0.23(0.04)
0.48*
0.23(0.04)
0.54*
0.27(0.04)
0.53*
0.27(0.04)
0.01
0.01(0.02)
0.01
0.01(0.02)
Low
SES
0.43*
0.18(0.05)
0.43*
0.18(0.05)
0.47*
0.19(0.05)
0.46*
0.19(0.05)
0.45*
0.20(0.04)
0.44*
0.20(0.04)
0.08*
0.08(0.02)
0.08*
0.08(0.02)
Neighborhooddisadvantage
0.08*
0.05(0.03)
0.08*
0.05(0.03)
0.03
0.02(0.03)
0.02
0.01(0.03)
0.05
\0.03(0.03)
0.04
0.03(0.03)
0.07*
0.10(0.02)
0.07*
0.10(0.02)
Low
maternal
attachment
-0.05
-0.04(0.03)
-0.05
-0.04(0.03)
0.00
0.00(0.03)
0.00
0.00(0.03)
-0.03
-0.02(0.03)
-0.02
-0.02(0.03)
0.03*
0.06(0.01)
0.03*
0.06(0.01)
Maternal
disengagem
ent
0.00
0.00(0.03)
0.00
0.00(0.03)
-0.05
-0.04(0.03)
-0.05
-0.04(0.03)
-0.03
-0.02(0.03)
-0.03
-0.02(0.03)
0.03
0.05(0.02)
0.03
0.05(0.02)
Low
maternal
involvem
ent
0.29
0.04(0.17)
0.30
0.04(0.17)
0.52*
0.07(0.15)
0.53*
0.07(0.16)
0.42*
0.06(0.14)
0.43*
0.06(0.14)
0.02
0.00(0.10)
0.02
0.00(0.10)
Never
breastfed
95HTTLPR
NA
-0.06*
-0.06(0.02)
NA
-0.08*
-0.08(0.02)
NA
-0.06*
-0.07(0.02)
NA
-0.01
-0.02(0.01)
N2193
2193
2219
2219
2268
2268
2056
2056
R2
0.18
0.18
0.17
0.18
0.20
0.20
0.04
0.04
*Analphalevel
of.05was
usedto
determinestatisticalsignificance
inthisstudy(p\
0.05)
Psychiatr Q (2016) 87:107–127 117
123
Table
3Thedirectandinteractiveeffectsofshortdurationofbreastfeedingand5HTTLPRonneuropsychological
deficitsandpsychopathic
personalitytraits
Neuropsychological
deficits
(wave1)
Neuropsychological
deficits
(wave3)
Neuropsychological
deficits
(composite)
Psychopathic
personalitytraits
(wave4)
Model
1b/Beta
Model
2b/Beta
Model
3b/Beta
Model
4b/Beta
Model
5b/Beta
Model
6b/Beta
Model
7b/Beta
Model
8b/Beta
Shortdurationofbreastfeeding
0.15*
0.15(0.02)
0.14*
0.15(0.02)
0.15*
0.15(0.02)
0.15*
0.15(0.02)
0.15*
0.16(0.02)
0.14*
0.16(0.02)
0.03*
0.07(0.01)
0.03*
0.07(0.01)
5HTTLPR
-0.01
-0.01(0.02)
-0.01
-0.01(0.02)
0.00
0.00(0.02)
0.00
0.00(0.02)
0.00
0.00(0.02)
0.00
0.00(0.02)
0.01
0.03(0.01)
0.01
0.03(0.01)
Age
0.01
0.02(0.01)
0.01
0.02(0.01)
-0.06*
-0.10(0.01)
-0.06*
-0.10(0.01)
-0.03*
-0.05(0.01)
-0.03*
-0.05(0.01)
-0.01
-0.04(0.01)
-0.01
-0.04(0.01)
Sex
-0.15*
-0.08(0.04)
-0.15*
-0.08(0.04)
-0.10*
-0.05(0.04)
-0.10*
-0.05(0.04)
-0.13*
-0.07(0.04)
-0.13*
-0.07(0.03)
-0.02
-0.02(0.02)
-0.02
-0.02(0.02)
Race(non-w
hite)
0.59*
0.27(0.04)
0.58*
0.27(0.04)
0.50*
0.23(0.04)
0.49*
0.23(0.04)
0.53*
0.27(0.04)
0.53*
0.27(0.04)
0.01
0.01(0.02)
0.010.01(0.02)
Low
SES
0.43*
0.18(0.05)
0.43*
0.18(0.05)
0.47*
0.20(0.05)
0.47*
0.19(0.05)
0.44*
0.20(0.04)
0.44*
0.20(0.04)
0.08*
0.08(0.02)
0.08*
0.08(0.02)
NeighborhoodDisadvantage
0.08*
0.05(0.03)
0.07*
0.04(0.03)
0.02*
0.01(0.03)
0.02*
0.01(0.03)
0.05
0.03(0.03)
0.04
0.03(0.03)
0.07*
0.10(0.02)
0.07*
0.10(0.02)
Low
maternal
attachment
-0.05
-0.04(0.03)
-0.05
-0.04(0.03)
0.00
0.00(0.03)
0.00
0.00(0.03)
-0.02
-0.02(0.03)
-0.02
-0.02(0.03)
0.03*
0.06(0.01)
0.03*
0.06(0.01)
Maternal
disengagem
ent
0.00
0.00(0.03)
0.00
0.00(0.03)
-0.05
-0.04(0.03)
-0.05
-0.04(0.03)
-0.03
-0.02(0.03)
-0.03
-0.02(0.03)
0.03
0.05(0.02)
0.03
0.05(0.02)
Low
maternal
involvem
ent
0.30
0.04(0.17)
0.30
0.04(0.17)
0.52*
0.07(0.16)
0.52*
0.06(0.16)
0.42*
0.06(0.14)
0.42*
0.06(0.14)
0.02
0.00(0.10)
0.01
0.00(0.10)
Shortdurationofbreastfeeding9
5HTTLPR
NA
-0.05*
-0.05(0.02)
NA
-0.07*
-0.07(0.02)
NA
-0.05*
-0.06(0.02)
NA
-0.01
-0.02(0.01)
N2193
2193
2219
2219
2268
2268
2056
2056
R2
0.18
0.19
0.17
0.18
0.20
0.20
0.04
0.04
*Analphalevel
of.05was
usedto
determinestatisticalsignificance
inthisstudy(p\
0.05)
118 Psychiatr Q (2016) 87:107–127
123
effects of short breastfeeding duration on neuropsychological deficits are weaker for in-
dividuals with a greater number of risk alleles on 5HTTLPR. Again, a significant inter-
action did not emerge in the case of psychopathic personality traits.
In order to check the robustness of the results displayed in Table 3, we limited our analysis
to subjects who had any exposure to breastfeeding, which was roughly 43 % of the genetic
subsample. The results of these analyses are displayed in Table 4. The purpose of these
models is to test whether the significant direct and interactive relationships that were detected
in previous models between short duration of breastfeeding, 5HTTLPR, neuropsychological
deficits, and psychopathic personality traits persist when the most at-risk group (i.e., the
‘‘never breastfed’’ group) is excluded from the sample. The main effects models reveal that
breastfeeding for a shorter amount of time as an infant still significantly increases the like-
lihood of developing neuropsychological deficits in adolescence and early adulthood, even
when ‘‘never breastfed’’ subjects are excluded. However, such is not the case with psycho-
pathic personality traits. For breastfed children, the age at which they stopped breastfeeding
was not significantly associated with their risk of developing psychopathic personality traits.
This finding suggests that while the positive effect of breastfeeding on adult psychopathic
personality traits emerges for individuals with no exposure to breastfeeding, it does not
emerge for individuals who began breastfeeding, but were weaned relatively early.
Table 4 also contains the results frommodels testingwhether or not 5HTTLPR continues to
significantly moderate the relationship between short breastfeeding duration and neuropsy-
chological deficits once the sample is limited to subjects with some exposure to breastfeeding.
Models 2, 4 and 6 reveal that, regardless of the outcome measure used, interactions between
5HTTLPR and a shorter duration of breastfeeding are no longer significant. Thus, when indi-
viduals with no exposure to breastfeeding are excluded from the sample, interactions between
short duration of breastfeeding and 5HTTLPR are consistently null. Interestingly, the null
results in this case reveal that the significant interaction between 5HTTLPR and breastfeeding
emerges when examining breastfeeding exposure, but not when examining breastfeeding du-
ration independent of exposure. This is corroborated by the positive, significant coefficients for
the direct effects of 5HTTLPR in models 1, 3, and 5 of Table 4. The results indicate that the
genetic risk of neuropsychological deficits incurred by 5HTTLPR only emerges for subjects
who have been exposed to some degree of breastfeeding (also see Figs. 1, 2). For example, after
fixing covariates to their means, predicted percentile scores on neuropsychological deficits of
breastfed and never breastfed participants are quite similar to each other for those possessing 2
risk alleles (i.e.,withina fewpercentile points).On theother hand, predictedpercentile scoresof
breastfed and never breastfed participants are significantly different from each other among
those with no risk alleles (i.e., approximately an 18-point difference at wave 3), suggesting that
breastfeeding experiences are particularly relevant for the neuropsychological health of indi-
viduals with the lowest genetic risk on 5HTTLPR.
Finally, the results displayed in Table 5 indicate whether the relationship between no
exposure to breastfeeding and psychopathic personality traits in adulthood is mediated by
neuropsychological deficits. The findings suggest that neuropsychological deficits may
partially explain why subjects who were never breastfed as infants are significantly more
likely to develop psychopathic personality traits during adulthood. Specifically, in two of
the three mediating models, the coefficients for the breastfeeding measure became non-
significant once the composite measure of neuropsychological deficits was included in the
model. Sobel tests also reveal significant mediation in all three of the models (coefficients:
4.77; 4.84; 5.37; p\ 0.00000). The reduction in the size of the breastfeeding coefficients,
moreover, ranges from 28 to 43 % when the measure of neuropsychological deficits is
included in each model.
Psychiatr Q (2016) 87:107–127 119
123
Table
4Thedirectandinteractiveeffectsofshort
durationofbreastfeedingand5HTTLPR
onneuropsychological
deficits
andpsychopathic
personalitytraits
among
breastfed
subjectsonly
Neuropsychological
deficits
(wave1)
Neuropsychological
deficits
(wave3)
Neuropsychological
deficits
(composite)
Psychopathic
personality
traits(w
ave4)
Model
1b/Beta
Model
2b/Beta
Model
3b/Beta
Model
4b/Beta
Model
5b/Beta
Model
6b/Beta
Model
7b/Beta
Model
8b/Beta
Shortdurationofbreastfeeding
0.08*
0.09(0.03)
0.08*
0.08(0.03)
0.10*
0.11(0.03)
0.10*
0.11(0.03)
0.09*
0.11(0.03)
0.09*
0.10(0.03)
0.02
0.04(0.01)
0.02
0.04(0.01)
5HTTLPR
0.06*
0.06(0.03)
0.06*
0.06(0.03)
0.09*
0.09(0.03)
0.09*
0.09(0.03)
0.07*
0.08(0.03)
0.07*
0.08(0.03)
0.02
0.06(0.01)
0.02
0.06(0.01)
Age
-0.01
-0.02(0.02)
-0.01
-0.02(0.02)
-0.07*
-0.12(0.02)
-0.07*
-0.12(0.02)
-0.04*
-0.08(0.02)
-0.04*
-0.08(0.02)
-0.01
-0.05(0.01)
-0.01
-0.05(0.01)
Sex
-0.17*
0.09(0.06)
-0.17*
-0.09(0.06)
-0.10
-0.05(0.06)
-0.10
-0.05(0.06)
-0.13*
-0.08(0.05)
-0.13*
-0.08(0.05)
-0.06*
-0.06(0.03)
-0.06*
-0.06(0.03)
Race(non-w
hite)
0.67*
0.30(0.07)
0.68*
0.30(0.07)
0.49*
0.21(0.08)
0.49*
0.21(0.08)
0.60*
0.28(0.07)
0.60*
0.28(0.07)
0.06
0.05(0.04)
0.06
0.05(0.04)
Low
SES
0.60*
0.21(0.09)
0.61*
0.22(0.09)
0.64*
0.23(0.09)
0.64*
0.23(0.09)
0.63*
0.24(0.08)
0.63*
0.25(0.08)
0.06
0.05(0.04)
0.06
0.05(0.04)
Neighborhooddisadvantage
0.03
0.02(0.05)
0.03
0.02(0.05)
0.02
0.01(0.05)
0.02
0.01(0.05)
0.02
0.01(0.05)
0.02
0.01(0.05)
0.05*
0.07(0.03)
0.05*
0.07(0.03)
Low
maternal
attachment
-0.05
-0.04(0.04)
-0.05
-0.04(0.04)
0.06
0.04(0.04)
0.06
0.04(0.04)
0.01
0.01(0.04)
0.01
0.01(0.04)
0.05*
0.09(0.03)
0.05*
0.09(0.03)
Maternal
disengagem
ent
0.03
0.02(0.05)
0.03
0.02(0.05)
-0.11*
-0.08(0.05)
-0.11*
-0.08(0.05)
-0.04
-0.03(0.04)
-0.04
-0.03(0.04)
0.02
0.04(0.03)
0.02
0.04(0.03)
Low
maternal
involvem
ent
-0.18
-0.02(0.35)
-0.20
-0.02(0.34)
0.57
0.05(0.38)
0.56
0.05(0.37)
0.29
0.03(0.34)
0.28
0.03(0.33)
0.01
0.00(0.13)
0.01
0.00(0.13)
Shortdurationofbreastfeeding9
5HTTLPR
NA
-0.02
-0.02(0.03)
NA
-0.02
-0.02(0.03)
NA
-0.02
-0.03(0.03)
NA
0.00
0.00(0.01)
N972
972
973
973
994
994
923
923
R2
0.18
0.18
0.16
0.16
0.20
0.20
0.05
0.05
*Analphalevel
of.05was
usedto
determinestatisticalsignificance
inthisstudy(p\
0.05)
120 Psychiatr Q (2016) 87:107–127
123
Discussion
The literature to date has revealed that breastfeeding exposure and duration can have
important implications for the neuropsychological and behavioral well-being of offspring
[11, 16, 33, 36, 51, 53]. Despite the increased attention given to the contribution of
breastfeeding experiences during infancy to the subsequent functioning of offspring, most
research focuses on child outcomes, with few studies exploring the effects of breastfeeding
exposure and duration on neuropsychological and mental health outcomes during later life
30
35
40
45
50
55
60
No Short Alleles 1 Short Allele 2 Short Alleles
Neu
rops
ycho
logi
cal D
efic
its P
erce
ntile
(W1)
5HTTLPR Genetic Risk
Never BreastfedBreastfed
Fig. 1 The predicted neuropsychological deficits percentile score (wave 1). By level of 5HTTLPR geneticrisk and exposure to breastfeeding when covariates are at their mean
30
35
40
45
50
55
60
65
No Short Alleles 1 Short Allele 2 Short Alleles
Neu
rops
ycho
logi
cal D
efic
its P
erce
ntile
(W3)
5HTTLPR Genetic Risk
Never BreastfedBreastfed
Fig. 2 The predicted neuropsychological deficits percentile score (wave 3). By level of 5HTTLPR geneticrisk and exposure to breastfeeding when covariates are at their mean
Psychiatr Q (2016) 87:107–127 121
123
stages (for exceptions, see [11, 53]). The potential for gene–environment interactions be-
tween breastfeeding and indicators of genetic risk has also been largely neglected (for an
exception, see [19]). Finally, the possibility that neuropsychological deficits might mediate
the relationship between breastfeeding indicators and adult psychopathic personality traits
has not yet been tested. In the present study, we sought to address these important voids in the
literature by exploring (a) whether breastfeeding experiences and a serotonin transporter
polymorphism known as 5HTTLPR interact to predict neuropsychological deficits in ado-
lescence and early adulthood as well as psychopathic personality traits during adulthood and
(b) whether neuropsychological deficits explain the relationship between breastfeeding ex-
periences and adult psychopathy. Our OLS models revealed three key findings.
First, we found that subjects who experienced shorter breastfeeding durations were at an
increased risk of neuropsychological deficits during adolescence and adulthood, whereas
subject who were never breastfed incurred the additional risk of psychopathic personality
Table 5 Is the link between no exposure to breastfeeding and psychopathic personality traits mediated byneuropsychological deficits?
Psychopathic personality traits (wave 4)
Model 1b/Beta
Model 2b/Beta
Model 3b/Beta
Model 4b/Beta
Never breastfed 0.03*0.06 (0.01)
0.02*0.05 (0.01)
0.020.04 (0.01)
0.020.04 (0.01)
Neuropsychological deficits (wave 1) NA 0.07*0.16 (0.01)
NA NA
Neuropsychological deficits (wave 3) NA NA 0.07*0.17 (0.01)
NA
Neuropsychological deficits (composite) NA NA NA 0.09*0.19 (0.01)
5HTTLPR 0.010.03 (0.01)
0.010.03 (0.01)
0.010.03 (0.01)
0.010.03 (0.01)
Age -0.01-0.04 (0.01)
-0.01*-0.05 (0.01)
-0.01-0.02 (0.01)
-0.01-0.03 (0.01)
Sex -0.02-0.02 (0.02)
-0.01-0.01 (0.02)
-0.01-0.01 (0.02)
-0.01-0.01 (0.02)
Race (non-white) 0.010.01 (0.02)
-0.04-0.04 (0.02)
-0.030.04 (0.02)
-0.040.04 (0.02)
Low SES 0.08*0.08 (0.02)
0.05*0.05 (0.03)
0.05*0.05 (0.02)
0.040.04 (0.02)
Neighborhood disadvantage 0.07*0.10 (0.02)
0.07*0.10 (0.02)
0.08*0.10 (0.02)
0.07*0.10 (0.02)
Low maternal attachment 0.03*0.06 (0.01)
0.04*0.07 (0.01)
0.03*0.06 (0.01)
0.03*0.06 (0.01)
Maternal disengagement 0.030.05 (0.02)
0.03*0.05 (0.02)
0.04*0.07 (0.02)
0.04*0.05 (0.02)
Low maternal involvement 0.020.00 (0.10)
-0.01-0.01 (0.11)
-0.12-0.03 (0.10)
-0.02-0.01 (0.10)
N 2056 1983 2005 2051
R2 0.04 0.06 0.07 0.07
* An alpha level of .05 was used to determine statistical significance in this study (p\ 0.05)
122 Psychiatr Q (2016) 87:107–127
123
traits during adulthood. Our results build upon prior research showing greater neuropsy-
chological deficiencies in children with little to no exposure to breastfeeding [43, 44] as
well as research indicating a greater risk of abnormal psychological functioning during
adulthood (e.g., schizophrenia) among children with minimal exposure to breastfeeding [3,
50, 64]. Second, our results indicate that 5HTTLPR significantly moderated the association
between the absence of breastfeeding and neuropsychological deficits in adolescence and
early adulthood, although the gene–environment interaction did not significantly predict
psychopathic personality traits. Specifically, the link between breastfeeding experiences
and neuropsychological deficits during adolescence and early adulthood was significantly
attenuated for individuals who possess a greater number of risk alleles on 5HTTLPR.
Importantly, this gene–environment interaction only emerged in the case of breastfeeding
exposure, not duration independent of exposure. Third, our results revealed that neu-
ropsychological deficits significantly mediated the relationship between exposure to
breastfeeding and psychopathic personality traits during adulthood, explaining, at least in
part, the neuropsychological mechanism through which subjects who were never breastfed
incur a greater risk of exhibiting psychopathic personality traits during adulthood.
The gene–environment interplay detected in the present study builds upon research that
has provided evidence for the role of biosocial processes in various maladaptive outcomes
[57, 59, 74]. Raine [57] offered a compelling explanation of negative gene–environment
interactions, suggesting that the influence of genes on neurological and behavioral out-
comes is most pronounced among individuals in a socially advantageous context. Raine’s
hypothesis is known as the social push perspective [57], as genetic risk factors are expected
to have the strongest effect on maladaptive outcomes under conditions in which social
‘‘pushes’’ toward such outcomes are minimal. According to this perspective, the accu-
mulation of various social risks can camouflage biological contributions to cognition and
behavior [57, p. 314]. The results of the present study are consistent with this perspective,
since the genetic risk incurred by 5HTTLPR only emerged among individuals who were
breastfed as infants (i.e., individuals who repeatedly experienced an important environ-
mental advantage shortly after birth). Put differently, although both shorter breastfeeding
durations and no breastfeeding exposure significantly increased neuropsychological defi-
cits, these effects were most relevant to the neuropsychological functioning of individuals
with low genetic risk on 5HTTLPR, providing support for the social push perspective.
The present study is the first to provide some initial evidence that breastfeeding ex-
periences may be differentially relevant to neuropsychological outcomes, depending on the
level of genetic risk on 5HTTLPR. Even so, our research is not without its limitations.
First, our measure of neuropsychological deficits was comprised of one dimension of
neuropsychological functioning: verbal skills. Although prior research has employed
verbal deficits as a proxy for executive functioning (see [7, 55, 65]), it would have been
preferable to directly detect neurological deficiencies in specific cortical regions of the
brain using neuroimaging procedures such as fMRI. Nevertheless, our study likely pro-
vides a conservative test of the influence of breastfeeding on executive functioning, due to
the influence of other brain regions on verbal deficits (e.g. the temporal lobe). Second, it
would have been useful to have additional information concerning the frequency of
breastfeeding sessions, the average duration of breastfeeding sessions, as well as the timing
of the incorporation of solid foods, since such details appear to be relevant for various
offspring outcomes (see [42]). Finally, since the genotyped subsample included siblings,
we are unable to definitively determine if our results are generalizable to the broader
population of non-siblings (however, see [6]).
Psychiatr Q (2016) 87:107–127 123
123
In sum, breastfeeding experiences during infancy appear to have a lasting impact on the
neuropsychological and mental health of offspring though adulthood. Moreover, in the case of
neuropsychological outcomes, the impact of breastfeeding seems to be conditioned by the level
of genetic risk possessed on the 5HTTLPR polymorphism. Neuropsychological deficits also
appear to be an important mediating mechanism through which individuals who were never
breastfed incur a significant risk of adult psychopathy. Future research should continue to
explore the genetic and social conditions under which short breastfeeding durations, or the
absence of breastfeeding altogether, result in an increased likelihood of maladaptive outcomes
in offspring. Moving forward, scholars exploring the role of breastfeeding in neuropsycho-
logical health should consider the stability of effects into adulthood, since the current literature
has been almost entirely limited to child outcomes (for an exception, see [11]). Since the current
study only focused on a single dimensionofmental health (i.e., psychopathic personality traits),
future research should explore the relevance of breastfeeding in the formation of a broader array
of psychopathologies. Doing so will hopefully contribute to a better understanding of how to
identify childrenwho are at risk for impaired neuropsychological andmental health, so that the
appropriate interventions can take place at the earliest stages of the life course.
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Dylan B. Jackson, MS is a PhD candidate in the College of Criminology and Criminal Justice at FloridaState University. His research explores the biosocial underpinnings of antisocial behaviors. His recent workhas examined the influence of neuropsychological deficits on low self-control and misconduct as well as theimpact of perinatal and early childhood risk factors on criminogenic outcomes.
Kevin M. Beaver, PhD is a professor in the College of Criminology and Criminal Justice at Florida StateUniversity and a visiting distinguished professor in the Center of Social and Humanities Research at KingAbdulaziz University. His research examines the development of antisocial behaviors from a biosocialperspective.
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