Nutrition and the developing brain: nutrient priorities and
measurement1–3
Michael K Georgieff
ABSTRACT
Nutrients and growth factors regulate brain development during fetal
and early postnatal life. The rapidly developing brain is more vul-
nerable to nutrient insufficiency yet also demonstrates its greatest
degree of plasticity. Certain nutrients have greater effects on brain
development than do others. These include protein, energy, certain
fats, iron, zinc, copper, iodine, selenium, vitamin A, choline, and
folate. The effect of any nutrient deficiency or overabundance on
brain development will be governed by the principle of timing, dose,
and duration. The ability to detect the specific effects of nutrient
deficiencies is dependent on knowing which area of the brain is
preferentially affected and on having neurologic assessments that
tap into the functions of those specific areas. As examples, protein-
energy malnutrition causes both global deficits, which are testable
by general developmental testing, and area-specific effects on the
hippocampus and the cortex. Iron deficiency alters myelination,
monoamine neurotransmitter synthesis, and hippocampal energy
metabolism in the neonatal period. Assessments of these effects
could include tests for speed of processing (myelination), changes in
motor and affect (monoamines), and recognition memory (hip-
pocampus). Zinc deficiency alters autonomic nervous system regu-
lation and hippocampal and cerebellar development. Long-chain
polyunsaturated fatty acids are important for synaptogenesis, mem-
brane function, and, potentially, myelination. Overall, circuit-
specific behavioral and neuroimaging tests are being developed for
use in progressively younger infants to more accurately assess the
effect of nutrient deficits both while the subject is deficient and after
recovery from the deficiency. Am J Clin Nutr 2007;85(suppl):
614S–20S.
KEY WORDS Nutrition, brain, development, assessment, ne-
onate, fetus
GENERAL PRINCIPLES OF NUTRIENT EFFECTS ON
THE DEVELOPING BRAIN
Nutrients and growth factors regulate brain development dur-
ing fetal and early postnatal life. The developing brain between
24 and 42 wk of gestation is particularly vulnerable to nutritional
insults because of the rapid trajectory of several neurologic pro-
cesses, including synapse formation and myelination (for more
extensive reviews, see references 1–5). Conversely, the young
brain is remarkably plastic and therefore more amenable to repair
after nutrient repletion. On balance, the brain’s vulnerability to
nutritional insults likely outweighs its plasticity, which explains
why early nutritional insults result in brain dysfunction not only
while the nutrient is in deficit, but also after repletion.
614S Am J Clin Nutr 2007;85(suppl):614S–20S. Printed in USA. © 2007 American Society for Nutrition
All nutrients are important for neuronal cell growth and
development, but some appear to have greater effects during
the late fetal and neonatal time periods. These include protein,
iron, zinc, selenium, iodine, folate, vitamin A, choline, and
long-chain polyunsaturated fatty acids (1–3). The effect of
nutrient deficiency or supplementation on the developing
brain is a function of the brain’s requirement for a nutrient in
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specific metabolic pathways and structural components. The
effects are regionally distributed within the brain on the basis
of which areas are rapidly developing at any given time (4).
During late fetal and early neonatal life, regions such as the
hippocampus, the visual and auditory cortices, and the stria-
tum are undergoing rapid development characterized by the
morphogenesis and synaptogenesis that make them functional
(5, 6). The hippocampus that subserves recognition memory
behavior is one of the earliest areas to show cortical-cortical
connectivity and functionality. Furthermore, brain-wide pro-
cesses such as myelination accelerate during late fetal and
early neonatal life and are vulnerable to deficits of nutrients
that support them. A nutrient that promotes normal brain
development at one time may be toxic at another point in
development. Similarly, a nutrient that promotes normal brain
development at one concentration may be toxic at another.
Several nutrients, including iron, are regulated within a rela-
tively narrow range, where either an excess or a deficiency
induces abnormal brain development. Others have wider
ranges of tolerance.
Nutrients are necessary not only for neurons but also for sup-
porting glial cells. For any given region, early nutritional insults
have a greater effect on cell proliferation, thereby affecting cell
number (7, 8). Later nutritional insults affect differentiation,
including size, complexity, and in the case of neurons, synapto-
genesis and dendritic arborization. Microarray analysis of
genomic transcripts from various brain regions in the developing
rat shows an important breakpoint at approximately postnatal
day 7, before which proliferation genes are predominantly ex-
pressed (8). After this time point, genes that control differentia-
tion are preferentially expressed. Postnatal day 7 in the rat brain
is roughly equivalent to a late-gestation human fetal brain.
1
From the Department of Pediatrics and Child Development, University
of Minnesota School of Medicine, Minneapolis, MN.
2
Presented at the conference “Maternal Nutrition and Optimal Infant
Feeding Practices,” held in Houston, TX, February 23–24, 2006.
3
Address reprint requests to MK Georgieff, MMC 39, D-136 Mayo Build-
ing, 420 Delaware Street SE, Minneapolis, MN 55455. E-mail:
georg001@umn.edu.
 NUTRITION AND THE DEVELOPING BRAIN 615S
Nutrients can affect not only neuroanatomy, but also neuro- TABLE 1
chemistry and neurophysiology. Neurochemical alterations in- Important nutrients during late fetal and neonatal brain development1
clude changes in neurotransmitter synthesis, receptor synthesis, Predominant brain circuitry
and neurotransmitter reuptake mechanisms (9, 10). Neurophys- Brain requirement for the or process affected by
iologic changes reflect changes in metabolism and signal prop- Nutrient nutrient deficiency
agation. The changes across all 3 venues ultimately result in
Protein-energy Cell proliferation, cell Global
altered neuronal performance at the time that the nutrient status
differentiation
is altered. Long-term changes in form and function can occur if Synaptogenesis Cortex
the altered nutrient state changes the trajectory of brain devel- Growth factor synthesis Hippocampus
opment in a substantive anatomical or neurochemical way, be- Iron Myelin White matter
yond the period where repair can occur. Monoamine synthesis Striatal-frontal
Neuronal and glial energy Hippocampal-frontal
metabolism
BRAIN DEVELOPMENT BETWEEN 24 AND 44 WK Zinc DNA synthesis Autonomic nervous system
AFTER CONCEPTION Neurotransmitter release Hippocampus, cerebellum
Copper Neurotransmitter synthesis, Cerebellum
The human brain undergoes remarkable structural and func- neuronal and glial energy
tional changes between 24 and 44 wk after conception, progress- metabolism, antioxidant
ing at the beginning of the third trimester from a smooth bilobed activity
structure with few gyrations or sulcations to a complex one at LC-PUFAs Synaptogenesis Eye
term that morphologically resembles the adult brain (11). The Myelin Cortex

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increase in complexity largely reflects cortical neuronal growth,
differentiation, and synaptic connections. In particular, the
auditory and visual cortices begin to develop rapidly, as do
areas underlying receptive language and higher cognitive
function (5). Myelination begins before term birth as well. Most
importantly, experience-dependent synapse formation occurs be-
fore birth and provides a neuronal basis for the fetus to learn. The
hippocampus, which is central to recognition memory processing,
has established most of its connections from the entorhinal cortex
and has begun to send projections through thalamic nuclear struc-
tures to the developing frontal cortex (12). These structures and
processes are worth considering because they (and the functions
they serve) are the ones that will be vulnerable to nutritional insults
in this time period.
NUTRIENTS AND PERINATAL BRAIN CIRCUITRY
As mentioned above, all nutrients are important for brain de-
velopment, but some appear to have a particularly large effect on
developing brain circuits during the last trimester and early neo-
natal period (Table 1). The importance of these nutrients has
been established primarily through nutrient deficit studies and
through knowledge of their role in the specific biochemical path-
ways that underlie neuronal and glial growth and function. A
complete consideration of all nutrient effects on brain develop-
ment is beyond the scope of this article, but the subject has been
reviewed elsewhere (1– 4). Nevertheless, certain nutrients are
commonly deficient in preterm and growth-retarded infants, and
their effects on the developing brain in animals and humans are
presented below.
Protein-energy malnutrition
Protein-energy malnutrition in fetal and early neonatal animal
models reduces neuronal DNA and RNA content and alters the
fatty acid profile (7, 13). Neuropathologically, this results in
lower neuronal number, reduced protein synthesis, and hypomy-
elination. Brain size is reduced through all of these mechanisms
as the result of changes in structural proteins, growth factor
concentrations, and neurotransmitter production. Ultrastructural
changes include reductions in synapse number and dendritic
Choline Neurotransmitter synthesis Global
DNA methylation Hippocampus
Myelin synthesis White matter
1
LC-PUFAs, long-chain polyunsaturated fatty acids.
arbor complexity (14 –19). The cortex and hippocampus appear
to be particularly vulnerable to protein-energy malnutrition (20).
Protein-energy malnutrition in humans between 24 and 44 wk
postconception can occur either in utero or ex utero. Fetal
protein-energy malnutrition results in intrauterine growth retar-
dation and is usually due to maternal hypertension or severe
malnutrition during pregnancy (21). Postnatal malnutrition is
common in sick preterm infants who are fluid restricted or who
do not tolerate high rates of nutrient delivery. Severe or pro-
longed intrauterine growth retardation results in poor prenatal
head growth associated with poorer developmental outcome (22,
23). In the absence of overt microcephaly, infants with intrauter-
ine growth retardation nevertheless have a 15% rate of mild
neurodevelopmental abnormalities characterized by cognitive
(rather than motor) disabilities (24). Verbal and visual recogni-
tion memory systems appear particularly to be vulnerable, which
is consistent with structures that are rapidly developing in this
time period (25, 26).
Iron
Iron is accreted rapidly by the fetus during the last trimester
and is necessary for basic neuronal processes such as myelina-
tion, neurotransmitter production, and energy metabolism (9).
The effect of iron deficiency on the developing brain has been
assessed largely in the rat model, where variations in the timing
and severity of the deficiency have helped to elucidate the bio-
chemical, structural, and behavioral effects. Biochemically, fetal
and neonatal iron deficiency results in reduced oxidative metab-
olism in the hippocampus and frontal cortex (27), elevated in-
tracellular neuronal glutamate concentrations (10), reduced stri-
atal dopamine concentrations (9), and altered fatty acid and
myelin profiles throughout the brain (28). Structurally, dendritic
arbors are truncated in the hippocampus (29), and global and
regional brain masses are reduced while the animals are iron
deficient and after iron repletion (30). Behaviorally, rodents have
616S GEORGIEFF
long-term deficits in trace recognition memory (31), proce-
dural memory (32), and spatial navigation (33) that indicate
structural and functional abnormalities in the hippocampus
and striatum.
Newborn human infants can have altered iron status as the
result of severe maternal iron deficiency anemia, intrauterine
growth retardation due to maternal hypertension, increased fetal
iron demand for erythropoiesis due to maternal diabetes mellitus,
or lack of fetal iron accretion due to premature birth (34 –38). Far
fewer studies have been conducted on the neurologic conse-
quences of perinatal iron deficiency than on classic postnatal
dietary iron deficiency. Infants with cord ferritin concentrations
in the lowest quartile have poorer neurodevelopment at school
age (39). Iron-deficient infants of diabetic mothers have im-
paired auditory recognition memory processing at birth (40),
whereas iron-deficient premature infants have a higher rate of
abnormal neurologic reflexes at 36 wk postconception (41).
Zinc
Fetal and neonatal zinc biology has been assessed in rodent
and primate models. Zinc is a cofactor in enzymes that mediate
protein and nucleic acid biochemistry (42). Fetal zinc deficiency
results in decreased brain DNA, RNA, and protein content (43).
Importantly, insulin-like growth factor I and growth hormone
receptor gene expression are regulated by zinc (44). Neuronally,
presynaptic boutons are dependent on adequate zinc for delivery
of neurotransmitters to the synaptic cleft (45). Structural studies
have shown truncated dendritic arbors and reduced regional
brain mass in the cerebellum, limbic system, and cerebral cortex
(45). Zinc-deficient rats have abnormal cortical electrophysiol-
ogy (46). The orbitofrontal cortex appears to be particularly
vulnerable. Behaviorally, zinc-deficient rhesus monkeys have
poor short-term memory (47). These effects suggest that zinc is
particularly important for the medial temporal lobe, frontal lobe,
and cerebellar development.
Fetuses of zinc-deficient mothers show decreased fetal move-
ment and heart rate variability, which is suggestive of altered
autonomic nervous system stability (48). Although intelligence
quotient does not seem to be affected, infants born to zinc-
deficient mothers have decreased preferential looking behavior,
which is indicative of altered hippocampal function.
Copper
Copper is an essential divalent cation for proteins involved in
brain-energy metabolism, dopamine metabolism, antioxidant
activity, and iron accretion in the fetal and neonatal brain (49 –
52). Although nutritional copper deficiency does not appear to be
a common clinical problem in the human fetus and neonate, the
neurodevelopmental effects in the developing rodent are strik-
ing, both while the animals are copper deficient as pups and after
copper repletion. In particular, the developing cerebellum ap-
pears to be particularly at risk in models of gestational copper
deficiency with long-term effects on motor function, balance,
and coordination (53).
Long-chain polyunsaturated fatty acids
Extensive reviews of the effects of long-chain polyunsaturated
fatty acids on the developing brain have been published and will
not be reviewed here (3, 54, 55). Nevertheless, it is important to
note that these fats, particularly docosahexaenoic acid (DHA),
are potent neurobiological agents that affect neuronal membrane
structure, synaptogenesis, and myelination. Studies in preterm hu-
mans indicate important benefits for retinal and cognitive develop-
ment, as indexed by improved electroretinogram activity, visual
acuity, and short-term global developmental outcome after DHA
supplementation of preterm infant formula (56, 57). The effects in
term infants are far less convincing and are substantially underpow-
ered to draw any conclusions (58). DHA supplementation trials
should be considered “formula repletion of deficit state” studies,
because the fetus normally receives adequate DHA transplacentally,
and breastfed neonates receive DHA in human milk.
Other nutrients
Additional nutrients that affect brain and behavior develop-
ment include iodine and selenium, which mediate their effects
through thyroid hormone metabolism (59, 60); folate and cho-
line, which mediate their effects through one-carbon metabo-
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lism, DNA methylation, and neurotransmitter synthesis (61– 63);
and vitamins A and B-6. A review of their effects can be found in
reference 1.
CIRCUIT-SPECIFIC ASSESSMENT OF NUTRIENT
EFFECTS ON THE DEVELOPING BRAIN
Ideally, specific nutrient deficiencies would result in a recogniz-
able, characteristic spectrum of neuroanatomical, neurochemical,
and neurophysiologic dysfunction in perinatal humans. Each nutri-
ent would thus have a “signature” neurodevelopmental effect. Un-
fortunately, limitations exist that preclude the use of this concept to
generate accurate developmental outcome predictions for preterm
infants, based on neurologic assessment in the newborn period.
Preterm and term infants have limited behavioral expression of the
higher-function cortical activities that are the basis for behaviors
later assessed as intelligence. For example, they are preverbal,
which distinctly limits intellectual reasoning. Furthermore, ongoing
illness can depress brain activity and behavior. Finally, later
catch-up brain growth and the capacity for repair make predictive
assessments difficult.
Nevertheless, neurobehavioral assessments can be per-
formed in infants at or near term that can give insight into
structure and function. Brain size can be estimated either by
occipitofrontal head circumference (assuming no hydroceph-
alus), computerized axial tomography (CAT), or magnetic
resonance imaging (MRI) scans. Moreover, regional brain
volumes or track size can be measured by structural MRI and
diffusion tensor imaging (DTI) (64, 65). Objective metrics of
brain electrical function can be obtained by electroencepha-
logram (EEG), auditory brainstem evoked response (ABR), or
event-related potentials (ERPs) (66). The advantage of ERPs
is that activity in response to cognitive stimuli and events,
such as auditory recognition memory, can be assessed (66,
67). Functioning of the hypothalamic-pituitary-adrenal axis
and the autonomic nervous system in response to stressors can
also be measured at this age (68). Finally, limited information
can be obtained from neurologic examination of the infant,
including assessment of neurologic reflexes (41).
Although these measurements are not specifically designed to
assess nutritional effects in the perinatal period, they can be used
 NUTRITION AND THE DEVELOPING BRAIN 617S
TABLE 2 nutrient. The repertoire of assessments expands rapidly after the
The repertoire of neurodevelopmental assessments that can be used in neonatal period, particularly at 4 mo of age, when infant behavior
infants between 36 and 44 wk after conception and the relation to specific
becomes more cortically dominant. By 4 – 6 mo of age adjusted
nutritional deficits1
for prematurity, the recognition memory system can be assessed
Assessment Brain region or process Risk nutrients behaviorally by the preferential looking task (69), and both the
OFC Whole brain Protein-energy explicit and implicit memory systems can be assessed electro-
Neurologic reflexes Whole brain, nervous system Protein-energy physiologically by using ERPs (70). Speed of processing,
Myelination Iron which indexes myelination and synaptic efficacy, can be es-
Neurologic examination Whole brain, nervous system Protein-energy timated from ABR and ERPs. Affect and distractiblility,
Copper
which at this age index striatal integrity and monoamine neu-
EEG maturity Cortex Protein-energy
(LC-PUFAs) rotransmitter function, can be assessed through direct obser-
Stimulated heart rate, Autonomic nervous system Zinc (Protein- vation and scoring (71). By the end of the first postnatal year,
blood pressure, energy) more complex reasoning skills can be inferred from the sub-
salivary cortisol scales of the Bayley Scales of Infant Development (BSID) and
responses from specific testing of memory encoding, storage, and re-
HPA axis
trieval using elicited imitation (72, 73). The recent develop-
ABR, ERG Myelination Iron
Synaptic efficacy LC-PUFAs ment of these region- and process-specific assessments for
Auditory ERP Hippocampal function Iron (Zinc) at-risk newborns and young infants are welcome additions to
(Choline) the repertoire that has depended on global assessments in the

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(Protein- past. The BSID administered at 12 mo corrected age remains
energy) the most commonly used general assessment in many nutrient
MRI (structural) Global and regional volume Protein-energy
and structure (Iron) (Zinc)
outcome studies because it is widely available, requires little
(Copper) special equipment, and is easily performed in multicenter
MR-DTI Myelin and tract integrity Protein-energy trials. Nevertheless, significant specific neurobehavioral
(Iron) morbidities can be embedded with a normal Bayley-derived
(Copper) Developmental Quotient, which can mask potentially impor-
MR-proton Neurochemistry (Iron)
tant neurologic processing deficits.
spectroscopy
More detailed and region-specific interrogation of the in-
1
Nutrients with unproven but likely effects based on animal models are fant’s neurobehavioral repertoire can be conducted as post-
marked in parentheses. EEG; electroencephalogram; LC-PUFAs, long-chain natal age increases. The frontal lobes become more testable
polyunsaturated fatty acids; HPA, hypothalamic-pituitary-adrenal; ABR, audi-
by 5 y of age with use of the Cambridge Neuropsychological
tory brainstem evoked response; ERG, electroretinogram; ERP, event-related
potential; MRI, magnetic resonance imaging; DTI, diffusion tensor imaging; Test automated battery (CANTAB), which assesses behaviors
OFC, occipitofrontal head circumference. such as strategy switching, executive function, planning,
and working memory (74). The integrity of these behaviors
may ultimately determine success in school performance (75).
in such a manner (Table 2). It is important to note that many of By 6 y of age, children can be imaged by MRI scanning
the nutrient deficits will affect similar regions and processes, without sedation. Functional MRI becomes a useful tool
making it difficult to obtain a signature effect of any single for assessing attention, structure-function relations on

TABLE 3
Neurobehavioral and neuroimaging assessments that can be performed to evaluate the effects of neonatal nutrients on general brain development during
the first 6 y of postnatal life1
Risk nutrients for Age of
Neurologic domain domain Behavioral reliability Neuroimaging technique Age of reliability

Global function Protein-energy, iron, Bayley Scales 12–36 mo OFC Any age
zinc, LC-PUFAs
WPPSI 쏜4 y MR regional volumetrics Newborn and 쏜6 y
Myelination Iron Speed of 4 mo ABR, VEP Any age
processing
LC-PUFAs ERP After term
DTI Newborn and 쏜6 y
Motor function Protein-energy Bayley Scales 12–36 mo Regional MR Newborn and 쏜6 y
(PDI)
Iron Activity Any age Actigraph Any age
Copper Coordination Any age
1
LC-PUFAs, long-chain polyunsaturated fatty acids; WPPSI, Wechsler Preschool and Primary Scale of Intelligence; MR, magnetic resonance; ABR,
auditory brainstem evoked response; VEP, visual evoked potential; ERP, event-related potential; DTI, diffusion tensor imaging; OFC, occipitofrontal head
circumference.
618S GEORGIEFF

TABLE 4
Neurobehavioral and neuroimaging assessments that can be performed to evaluate the effects of neonatal nutrients on cognitive development during the
first 6 y of postnatal life1

Risk nutrients Behavioral Age of

Cognitive domain for domain assessment reliability Neuroimaging technique Age of reliability

Explicit-recognition Protein-energy, VPC 쏜4 mo ERP (auditory) Newborn

memory iron, zinc
DNMS 쏜6 mo ERP (visual) 쏜4 mo
Elicited imitation 쏜12 mo MR volume Newborn and 쏜6 y
(hippocampus)
Working memory Protein-energy Elicited imitation 쏜12 mo MR volume (prefrontal Newborn and 쏜6 y
cortex)
Iron CANTAB 쏜4 y
fMRI 쏜6 y
Implicit-procedural Iron Priming 쏜4 mo MR volume (striatum) Newborn and 쏜6 y
memory
fMRI Newborn and 쏜6 y
1
VPC, Visual Paired Comparison (test); ERP, event-related potential; DNMS, Delay Non-Match to Sample (test); MR, magnetic resonance; CANTAB,
Cambridge Neuropsychological Test Automated Battery; fMRI, functional magnetic resonance imaging.

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working memory, and implicit memory tasks (76). The be-
havioral and neuroimaging assessments for general, cogni-
tive, and affective neurobehavioral domains and the corre-
sponding ages of utilization in this population between the
neonatal period and 6 y of age are summarized in Tables 3, 4
and 5.
Unfortunately, the longer the time period between the nutri-
tional deficiency and the subsequent neurobehavioral assess-
ment, the greater the risk that intervening confounding variables
such as postdischarge nutrition, illness, and home environment
will influence the outcome measure (77). Thus, there is a high
premium on further development of neurobehavioral assess-
ments in close temporal proximity to the time of nutritional insult
in the neonatal period. Potential new methods that may be useful
include near infrared spectroscopy (NIRS) and magnetoen-
cephalography (MEG) (78, 79).
SUMMARY
Fetal and neonatal malnutrition can have global or circuit-
specific effects on the developing brain. These effects are based
on the timing and magnitude of the nutrient deficit and on the
brain’s need for the particular nutrient at the time of the deficit.
It is important to recognize that nutritional effects on the devel-
oping brain include not only the provision of specific substrates,
but also the synthesis and activation of growth factors.
Although it would be attractive for each nutrient deficit to have
a signature effect on the brain that could be assessed behaviorally
or through neuroimaging, this is unlikely to occur with the cur-
rently available neuroimaging and behavioral techniques, in part
because common nutrient deficiencies in the neonate occur to-
gether and affect the same developing brain region. For example,
protein-energy, iron, and zinc malnutrition all affect the devel-
oping hippocampus. Ultimately, the attribution of short- and
long-term neurodevelopmental dysfunction to perinatal nutri-
tional status will need to follow specific rules of developmental
neuroscience. The nutrient deficit must be present during the
developmental window when the brain requires that nutrient for
growth and function. Furthermore, the abnormal behavioral
function should be subserved by a brain region or process that is
affected by the nutrient. Usually, a multitier approach from hu-
man epidemiology to animal and cellular models will be neces-
sary to provide reasonable scientific evidence of a cause-and-
effect association.

TABLE 5
Neurobehavioral and neuroimaging assessments that can be performed to evaluate the effects of neonatal nutrients on affective development during the
first 6 y of postnatal life1

Risk nutrients Age of

Affective domain for domain Behavioral assessment reliability Neuroimaging technique Age of reliability

Attention Iron, zinc Bayley Scales rating 쏜12 mo MR volume (prefrontal cortex) Newborn and 쏜6 y
CANTAB 쏜4 y
Flanker task 쏜5 y fMRI 쏜6 y
Reactivity (HPA/ Iron, zinc Response to: 쏜Newborn
ANS)
Restraint Salivary cortisol Any age
Separation HR response Any age
Immunization Vagal tone Any age
Social interaction Iron, zinc Spontaneous movement Any age fMRI 쏜6 y
Bayley Scales rating 쏜12 mo
1
MR, magnetic resonance; CANTAB, Cambridge Neuropsychological Test Automated Battery; fMRI, functional magnetic resonance imaging; HPA/
ANS, hypothalamic pituitary adrenal/autonomic nervous system; HR, heart rate.
 NUTRITION AND THE DEVELOPING BRAIN
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