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Early Brain Development for Social Work Practice

Abstract and Keywords

Development of the brain in the first 3 years of life is genetically programmed but occurs in response to environmental stimuli. The brain is organized “from the bottom up,” that is, from simpler to more complex structures and functions, so the experiences and environment that shape early development have consequences that reach far into the future. This entry describes the ontogeny and processes of fetal and infant brain development, as well as major risks to early brain development (during pregnancy and after birth), with emphasis on the factors seen in social-work practice. Neuroscience research is changing social work practice, and understanding early brain development and the contributors to poor development is critical for social workers in medical, mental health, child welfare, and other practice settings.

Keywords: brain, brain development, early brain development, environment, fetal brain development, genes, infant brain development, pregnancy

Introduction

The period of life from conception to age 3 is extremely important (if not critical) to healthy life-long brain functioning (Fox, Levitt, & Nelson, 2010). Rapid growth of underlying brain structures during this time lays down the foundations for higher structures and functions, and because of this rapid growth, the brain is most plastic (subject to influence by the environment).

Brain development occurs from the bottom up, that is, sequentially from the spinal cord and simple, automatic functions up to the frontal cortex and higher-order thinking (Perry, 2009). Because the more complex functions rely on sound underlying structures, damage or non-optimal development of the lower parts of the brain can result in subtle or dramatic limitations in higher-order brain structures and functions. Social workers see the results of poor early brain development in child welfare agencies, hospitals, mental health centers, schools, and virtually every other practice arena. They also see the results of poor early brain development in national statistics about school achievement and drop-out rates, crime, and un- or under-employment. Understanding how the brain develops in the first 3 years can enhance social policy and the planning and delivery of prenatal and early childhood services that have the potential to prevent or remediate many problems.

Because of the importance of the first 3 years, this period has been called a critical period of development. Use of the term critical has largely been discontinued in the early twenty-first century, except in regard to specific sensory functions, such as vision and hearing, which require specific sensory input within narrow stages of development to develop (Kolb & Fantie, 2009; Sheridan & Nelson, 2009). Current use of the term sensitive period connotes more clearly the special vulnerability and potential for influence during periods of development of areas of the brain related to other, more neuro-plastic, functions. Sheridan and Nelson (2009) define a sensitive period as “a time during development when the environment can have maximal impact on brain development” (p. 46).

Early brain development is largely sequenced by genetics, but experience becomes increasingly important with each day, especially after birth (Tierney & Nelson, 2009). Imaging technology, used more frequently since the 1990s and advancing daily, demonstrates that experience influences not only brain functioning, but also architecture, including the sizes of some parts of the brain and the connections among the parts. It is this connection between genetics and experience (called epigenesis) that mandates that social workers understand the ontogeny of early brain development (see Combs-Orme, 2013), because we now understand that social work practice has the potential to influence the availability and quality of experiences that shape early brain development and thus later functioning.

This entry begins with a necessarily superficial discussion of the ontological processes of development of the human brain beginning at conception, followed by a section integrating brain anatomy and the development of infant skills. This is followed by a discussion of important risk factors for brain damage and poor development, set in the context of social work practice. The final section discusses the roles of the social work profession and practitioners in enhancing early brain development.

Processes of Brain Development

Within the first days after conception, the cells of the embryo begin to multiply, differentiating into the neural tube that will become the central nervous system and brain (Sheridan & Nelson, 2009). The neural tube begins to close at 22 days and is completely closed by 26 days, if all goes well. Notably, this important step has occurred before many women realize that they are pregnant. Indeed, Thompson, Levitt, and Stanwood (2009) suggest that the brain is most susceptible to physical harm during the gestational period and that a public health focus on this period could perhaps reap more benefit than current efforts to enhance parenting and interaction with infants after birth.

Neurogenesis, the production of the brain cells (including neurons and glial cells, which make pathways on which neurons travel) on which all the other processes depend, begins around the fifth prenatal week, peaking at 3–4 months prenatally. By the time the infant is born, he will have about 100 billion neurons and his brain will be about 25% of its adult weight. Remarkably, in the first 3 years of life his brain will grow to about 90% of its adult weight (DiPietro, 2000), largely through proliferation of connections among neurons.

Neurotransmitters, chemicals released from neurons that act on specific receptors (Herlenius & Lagercrantz, 2004), also begin to develop in the first few weeks of gestation. Neurotransmitters carry the signals between neurons and other cells in the body and so are essential to brain function. They are released at nerve terminals and travel across the synaptic cleft to bind with receptors on target cells. Neurotransmitters are critical for the formation and survival of synapses (Herlenius & Lagercrantz). Perry (2009) states, “Due to their wide distribution throughout the brain, and their role in mediating and modulating a huge array of functions, impairment in the organization and functioning of these monoamine neurotransmitter systems can result in a cascade of dysfunction from lower regions (where these system originate) up to all of the target areas higher in the brain” (p. 242). Thus, malfunctions of neurotransmitters are implicated in many physical and mental disorders (Society for Neuroscience, 2009).

Herlenius and Lagercrantz (2004) provide an overview of the major neurotransmitters (of the 100 or so identified so far), including catecholamine, dopamine, serotonin, noradrenaline and adrenaline, and acetylcholine. Their review provides a view of how the different neurotransmitters are particularly active during sensitive periods of brain development and how various factors (described below) can interrupt their functioning and lead to impairment. Social workers may be familiar with some major neurotransmitters and their connections to disorders commonly seen in practice, such as serotonin (depression) and dopamine (drug addiction) (see Farmer, 2008).

Neurons begin to migrate to their appropriate locations in the brain by the sixth prenatal week, traveling along paths made of glial cells (de Graaf-Peters & Hadders-Algra, 2006). Errors of migration can occur for many reasons (see below) during this time and threaten the foundation for the development of higher-order thinking. Cells migrate from the inside out; neurons in the cerebral cortex, the seat of executive functioning (planning and problem solving) and reasoning located in the outer layer of the brain, have greater distances to travel and more potential for error (de Graaf-Peters & Hadders-Algra).

As they migrate, neurons also begin differentiating to develop into the right types of cells for their locations (based on chemical signals there) and developing axons and dendrites (spines that connect with other neurons). Dendrites will continue to form and to expand until the infant is about a year old (de Graaf-Peters & Hadders-Algra, 2006).

These connections among parts of the brain are critical for efficient functioning of the brain. Myelination is the process of insulating the glial connections with a fatty or lipid sheath that improves and speeds conduction of signals from neuron to neuron, which begins around 10 weeks after conception in the brain stem and spinal cord, proceeding outward to the cortex (Craik & Bialystok, 2006). Myelination is not completed in the frontal cortex until the third decade of life (Craik & Bialystok). Maternal and infant diets are crucial to proper myelination (see below). For example, research has shown that deficiencies in protein, iron, and possibly long-chain polyunsaturated fatty acids can alter myelination in ways that undermine proper functioning (see discussion in Georgieff, 2007).

Synaptogenesis, the formation of connections among neurons, begins at different times and proceeds for different periods in different parts of the brain, beginning in fetal life, occurring most rapidly in infancy, and continuing throughout life. However, synapses must be used repeatedly to be maintained and strengthened or they will fade, through a natural process that allows human infants to develop the skills they need for the specific environment in which they live (Lenroot & Giedd, 2011). Synaptogenesis is the origin of the phrase “Neurons that fire together, wire together,” describing how experiences shape and strengthen the neural connections in the brain. This process is frequently categorized as experience-expectant or experience-dependent (discussed below).

Neurons die in a programmed process called apoptosis, beginning in the second trimester. Apoptosis is genetically programmed, occurring in several molecular steps. Although cell death is normal, it also has been shown that animals placed in a diverse, enriched environment during apoptosis have more neurons in adulthood (de Graaf-Peters & Hadders-Algra, 2006). Images of 3-year-old brains show much denser connections than those of adult brains because the pruning of unused (and thus presumably unneeded) synapses is more intense in early childhood than it will ever be again, although another period of intense pruning occurs in adolescence, allowing those remaining (because of use) to be more efficient (Blakemore, 2010).

Neuroarchitecture and Infant Skills Development

Birth is often called the fourth trimester because development of the central nervous system still has a long way to go. Although the lower parts of the brain such as the brain stem and the limbic system are fully developed, the higher, more complex systems develop in response to the environment that the infant encounters following birth. The hippocampus, critical to learning and memory, in particular experiences its most rapid period of growth in the first year of life and will reach its full volume by about 10 months of age (Herschkowitz, 2000).

Newborn Senses and Learning

The newborn infant is amazingly ready to learn from the moment he emerges, his senses on high alert. His senses provide the information about the world that will encourage further brain development. During the first 5 weeks of rapid development, glucose uptake, the brain’s energy metabolism, is highest in the sensorimotor cortex, thalamus, brain stem, and cerebellar vermis (Johnson, 2001). These areas together form a section of the basic motor pathway of the primary motor cortex (Hatsopoulos & Suminski, 2011), which is responsible for generating neural impulses controlling the execution of movement. The cerebellum (which integrates sensory information from all sources) is also growing rapidly in the first year, laying down the foundation for cognition (Choe et al., 2012).

The infant is learning to track objects and then to reach for them, for example, by repeatedly practicing and building synapses in the parts of the brain that process and connect visual and motor behavior, and over time the infant’s movements will go from automatic and jerky to smooth and intentional. Piaget described the first 2 years of life as the sensorimotor stage because infants’ interactions with the world through their senses serve as the basis for their expanding knowledge (Piaget, 1973).

Touch is the earliest and most fully developed sense at birth, and the skin is the largest organ (Muir, 2002). Skin contact engages the infant easily, helping to calm her when she is tense or upset by moderating her stress response (discussed more fully below). Touch is also believed to be important in the infant’s growing attachment to her caregiver, as well as development of the social brain (Parsons, Young, Murray, Stein, & Kringelbach, 2010).

Hearing is also well developed, permitting the infant to receive the stimuli necessary to learn language from the first day (Vouloumanos & Werker, 2007). The infant also recognizes her mother’s voice from birth (albeit coming now through the air rather than the amniotic fluid) and responds to that voice. Beauchemin et al. (2011) also showed that the mother’s voice activates language centers in the infant’s brain, whereas a stranger’s voice did not.

Indeed, from moments after birth, the infant’s brain is hearing and sorting the sounds of his native language, learning what sounds combine to form words, as well as the grammar of the language. This type of learning, referred to as statistical or computational learning, occurs at the most basic level of language (phonemes, the vowels and consonants that are combined in varying combinations to construct words), as well as with the learning of grammar and syntax. Kuhl’s (2010) research suggests that it is social interaction that triggers the critical period for learning language in the first year of life and hypothesizes that the social brain (structures in the right side of the brain stimulated by social interaction) “gates” the computational processes that underlie early learning of language. She and her colleagues have shown in several studies that infants learn both their native languages and second languages only through social interaction; television and audio recordings do not produce learning, although adults are better able to learn second languages using these means.

The newborn’s vision, on the other hand, is not well developed (a fact almost universally acknowledged as new parents hold their newborns close to their faces to establish eye contact), but the visual cortex and synaptogenesis in that area develop rapidly between the second and fourth postnatal months (Huttenlocher & de Courten, 1987). Fox et al. (2010) described the process through which the newborn’s immature visual cortex goes from being able to perceive color, form, and movement to being able to recognize faces based on visual stimuli in the first few weeks of life. Moreover, as her vision improves, her interest in faces and motion will help her attend to language (Kuhl, 2010). Improved competence in each of the senses promotes further learning in all of the senses.

Recently, the discovery of a type of neurons in the brain called mirror neurons has shown that the same systems of the brain that are activated during performance of a motor activity such as running or throwing a ball are also activated during observation of the motor activity (see discussion in Diamond & Amso, 2008). These neurons promote motor learning and are also apparently an important part of emotional empathy (Gallesse, Keysers, & Rizzolatti, 2004; Del Giudice, Manera, & Keysers, 2008).

Also, about this time the infant’s cerebellum, which is involved in motor coordination and balance, has more than doubled in size (Knickmeyer et al., 2008). This remarkable growth supports rapid motor development during infancy.

In the second year of life, the infant begins producing language (Herschkowitz, 2000), although she has understood much of what she has heard for some time. Language learning is enhanced by better connections between the two brain hemispheres through the corpus callosum and growing connections (dendrites and synapses) among the higher areas of the brain (Herschkowitz). Executive functioning also greatly improves because of denser networks among the higher parts of the brain, including the hippocampus and frontal cortex.

The learning of language simply through exposure is extraordinary, a feat that not even computers can accomplish (Kuhl, 2010). Kuhl (2010) explains that the infant brain tracks the language it hears from birth, statistically sorting and computing to recognize first the phonemes (distinct sounds) in her native language and then the words. This learning results from and causes intense growth of dendrites and synapses in the language centers of the brain.

It appears that the first 2 years of life constitute a critical period for aural stimulation and, furthermore, that it is necessary that the language come from a live person. Kuhl’s (2007) work showed no learning by infants using videos or television.

Experience-Expectant versus Experience-Dependent Development

As stated previously, the sequence of development is largely genetically programmed, but the stages occur in relationship to the environment. Experience-expectant development occurs in response to experiences (including metabolic ones) that are universal for a species, such as light and language and movement. Neural plasticity for this type of development occurs in a fairly narrow time frame (thus the term critical period). For example, development of vision and hearing requires visual and aural stimuli during a limited phase in development early in life. Infants who are born with congenital cataracts, for example, will not develop the synapses for proper vision unless the condition is corrected very early after birth because specific types of visual stimuli are needed at a specific time to properly wire the brain (see discussion in Fox et al., 2010).

Experience-dependent development is more specific to individuals and cultures rather than universal, and it allows human beings to develop abilities and characteristics for success in specific environments that not all species members will experience (DiPietro, 2000). For example, musical training early in life appears to change the brain in specific ways that may be termed experience-dependent (Hyde et al., 2009). Plasticity for this kind of development is open for a longer period of time. For example, it is often observed that young children find it much easier to learn music and second languages, although this kind of experience-dependent learning is possible throughout life.

Because neuroplasticity is highest during rapid or intense cell growth, migration, myelination, and synaptogenesis, the fetal brain is most susceptible to both good influences (nurturing, good nutrition, exposure to language) and bad influences (toxic environmental chemicals and drugs, poor nutrition), but the entire first 3 years of life are marked by high neuroplasticity and thus the potential for environment to influence both positive and negative. The next section describes these important influences on early brain development with a focus on issues pertinent to social work practice.

Influences on Healthy Brain Development

Major risks to infant brain development begin at conception and include poor nutrition; maternal exposure to toxic environmental chemicals; use of alcohol, tobacco, and other drugs; viruses and other infections; and high levels of stress. These risks also have detrimental effects on brain development after birth, when experiences expand to include parenting and contact with the child’s community.

Diet and Nutrition

Although the social work profession has not explicitly recognized the importance of fetal and infant nutrition with regard to brain development, the profession has advocated for and provided services designed to improve the nutrition of women, infants, and children for many years (Combs-Orme, 1988), and many social workers practice in health and public-assistance settings that offer opportunities to provide important information about nutrition and brain development (Jaffee & Perloff, 2003).

All social workers are obligated to advocate for social policies and programs that may influence maternal and child nutrition in ways that influence brain development (Juby & Meyer, 2011). This is particularly true given the connection between poverty and inadequate diet: in 2005, 25 million Americans lived in homes deemed food-insecure, and half of those individuals were children under age 18 (Cook & Frank, 2008). This section describes the importance of nutrition during pregnancy and infancy for healthy brain development and the neurological risks posed by various types of malnutrition.

Prenatal Diet.

A pregnant mother’s diet must provide all the critical nutrients used to develop fetal tissues and organs, as well as formation of the placenta and increased blood volume required to support the fetus, while also supporting the mother’s health (Shapira, 2008). In developing nations, serious under-nutrition contributes to millions of poor pregnancy outcomes annually, causing untold human misery as well as limitations in achievement and productivity.

In addition to insufficient food, poor nutrition during pregnancy and deficiencies in essential vitamins and trace minerals also pose serious risks to the developing fetal brain (Guerrini, Thomson, & Gurling, 2007) and have effects that last a lifetime. Such deficiencies are far more common among the poor (Blumfield, Hure, Macdonald-Wicks, Smith, & Collins, 2012). Food insecurity (limited or uncertain availability of adequate nutritious food) does exist in the United States, however, and may be played out in chronic disease and persistent under-achievement that perpetuate poverty (Biggerstaff, Morris, & Nichols-Casebolt, 2002). Malnutrition poses multiple risks to the growth and development of the fetus and infant, but this discussion focuses on brain development. Over-nutrition and obesity, although believed to contribute to poor health and chronic disease, are believed to play less of a role in poor brain development and will not be discussed here.

The Institute of Medicine (2005) and the American College of Obstetricians and Gynecologists (2012) have published recommendations for weight gain and recommended daily allowances of specific nutrients during pregnancy. All micro-nutrients probably influence fetal brain development, although some have been studied more extensively and are more understood than others. Theoretically, all women in developed countries should be able to meet all their nutritional needs through diet alone (Jones, Housman, & McAleese, 2010), but because the standard American diet is often deficient in nutrients, supplementation is believed to be helpful (Shapira, 2008). Research shows that pregnant women understand the importance of nutrition during pregnancy, but do not know how to achieve the best nutrition. Disadvantaged women and pregnant adolescents are particularly likely to be poorly nourished (Haggarty et al., 2009).

One of the most thoroughly researched risks to the developing fetal central nervous system is posed by a diet lacking folate, found mostly in vegetables and fruits (Copp & Greene, 2010). Failure of the spinal cord to close properly early in pregnancy, resulting in spina bifida, anencephaly, and other neural tube defects, was linked to inadequate folate in pregnant mothers in the 1980s. Widespread publicity and advice to women to take supplements were not successful, probably in part because formation of the spinal cord occurs so early in pregnancy, before many women realize they are pregnant and certainly before they begin prenatal care. Campaigns in a number of nations, including the United States, led to requirements that widely-consumed flour products such as bread be enriched with folic acid (the synthetic supplement for folate), and this supplementation was related to large reductions in the incidence of these disorders of the neural tube (Običan, Finnell, Mills, Shaw, & Scialli, 2010). Indeed, dietary intake in the United States rarely meets pregnant women’s need for folate, which is especially critical to neurogenesis, described above (Massaro, Rothbaum, & Aly, 2006).

Research also has elaborated on the effects of deficiencies in choline, vitamin C, iron, vitamin D, vitamins B6 and B12, essential fatty acids, and a number of minerals on fetal brain development. Massaro et al. (2006) demonstrated in their review that these nutrients play key roles in DNA expression, neurogenesis, cell migration and differentiation, and synaptogenesis. Depending upon the severity of the deficiency and the presence of other risk factors that may interact with nutritional deficiencies (such as alcohol and tobacco), the long-lasting effects may be dramatic or subtle.

Supplementation mitigates some of the effects of nutritional deficiencies, and so antenatal vitamins are a standard part of modern prenatal care (American College of Obstetricians and Gynecologists, 2012). Supplementation is not always effective, however, and in any case cannot be helpful unless and until it is used. It is unknown how cost may deter disadvantaged women from compliance with recommendations for prenatal vitamins, but research has shown that depression and anxiety reduce compliance (Newport et al., 2012).

Breast-feeding.

After birth, breast milk is the ideal food for infants, containing the perfect combination of macro- and micro-nutrients needed by infants in the first year of life (American Academy of Pediatrics, 2005). Unless a mother’s diet is extremely deficient, breast milk can meet all the infant’s needs and is the preferred method of feeding infants in the first year of life (American Academy of Pediatrics). Despite extensive research and “tinkering” with supplemental nutrients, manufacturers will never be able to make an infant formula that contains all of the nutrients of breast milk (Petherick, 2010). Social workers practice in hospital and public health settings that provide many opportunities for advocating, educating about, and supporting breast-feeding, and there are clear social inequalities in barriers to breast-feeding for poor women (Hurst, 2007).

Human breast milk contains long-chain polyunsaturated fatty acids such as docosahexaenoic acid and arachidonic acid, which are important for brain development, particularly myelination (Herba et al., 2012). This fact is probably related to the many studies demonstrating that breast-fed infants develop better and achieve more in school (Herba et al.; Kafouri et al., 2013; Quigley et al., 2012), but breast-feeding mothers differ from non-breast-feeding mothers in many ways (such as education and socioeconomic status) that confound the interpretation of these data (Michaelsen & Mortensen, 2009). Research explaining the mechanisms through which these accomplishments occur is more difficult and comes mostly from animal research.

Two studies show evidence of breast-feeding effects on brain structure. Consistent with animal evidence, Isaacs et al. (2010) demonstrated a dose-response relationship between breast-feeding and IQ and the size and white matter (synapses) in adolescents’ brains, especially in boys. They suggest that long-chain polyunsaturated fatty acids, notably docosahexaenoic acid, may be the mechanism behind this effect, although they caution that breast milk contains many other, possibly related ingredients. (They also note that the process of breast-feeding itself, involving frequent close contact between mother and baby, may play a role in brain structure.)

Kafouri et al. (2013) examined the brains of another sample of adolescents and found that duration of exclusive breast-feeding was associated with cortical thickness in the parietal lobes, as well as with performance and total IQ. These authors also suggest that the docosahexaenoic acid in breast milk may be a primary mechanism that promotes neural and glial cell growth.

Early child nutrition.

The infant’s brain continues rapid development through the first 3 years of life, particularly through myelination and synaptogenesis, so nutrition remains critical for optimal development. Although extreme malnutrition is rare in the United States and other developed countries, food insecurity threatens early brain development. In 2007, nearly 16% of American households with children were food-insecure during some part of the year (Nord, 2009). Young children in these households run the risk of inadequate calories, protein, and essential fatty acids, as well as specific micro-nutrients.

Moreover, the usual American diet, which includes high levels of fast food, sugar, and processed food, is frequently deficient in important micro-nutrients that are critical to early brain development, including iron and zinc, which are both important to the production of neurotransmitters and myelination, as well as the late-developing hippocampus (Georgieff, 2007).

Two major social programs provide supplementation to infants and children with inadequate nutrition resulting from economic deprivation: the Supplemental Nutrition Assistance Program, a means-tested program for poor families, and the Supplemental Nutrition Program for Women, Infants, and Children (WIC) program (Juby & Meyer, 2011). The WIC program provides vouchers (averaging about $38 monthly for young children) for specific nutritious food items for pregnant, lactating, and non-lactating mothers and for infants and children up to age 5 (U.S. Department of Agriculture, 2012). Recent years have seen improvements in the WIC program, including the addition of specific vouchers for fruits and vegetables, reductions in the availability of sugary cereals, and limited eligibility for produce from farmers’ markets (Juby & Meyer).

Prenatal Substance Use

Social workers may encounter prenatal substance abuse in medical, public health, and addiction treatment settings (Carter, 2002). Sun (2004) has described important practice roles for social- work practice with substance-abusing pregnant women.

Although little is known about how particular substances influence specific parts of the fetal brain in humans, it is clear that the nature of the damage is dependent on the dose of the substance and the gestational stage at which it occurs (Azmitia, 2001). During early pregnancy, drug exposure is most likely to affect production of neurons and dendrites, migration of cells to their proper locations, and differentiation of neurons (early processes described above). The earlier forming parts of the brain (lower structures) such as the brain stem and the neurotransmitter systems are most susceptible to errors resulting from drug use in early pregnancy (often before a mother is aware of the pregnancy) and provide a poor foundation for further brain development (Thompson et al., 2009).

Drug use in later pregnancy is most likely to influence growth, including both overall growth and growth of later-forming brain structures, for example, the hippocampus, frontal cortex, and other higher structures that are critical to learning, memory, and executive functioning. Most significantly, growth of dendrites, glial cells (the cells through which glucose is delivered to neurons), and synapses may be compromised by substance use in late pregnancy (Azmitia, 2001).

The mature human brain is protected from toxicants in the blood system by a tight barrier called the blood–brain barrier. The blood–brain barrier is formed in the walls of the capillaries by epithelial cells that form tight junctions that most substances cannot cross (Abbott, Patabendige, Dolman, Yusof, & Begley, 2010), but which permit needed nutrients to cross. Although the blood–brain barrier begins to form during gestation, at least by the start of the second trimester, it is not mature until birth (Abbott et al.). Therefore, and especially because of the small size of the fetus, the developing brain is vulnerable to damage from exposure levels that might pose no or little risk to the adult brain.

Human research on the effects of specific drugs on the developing fetal brain is difficult to conduct because drug abuse usually involves multiple drugs and is also usually accompanied by a number of other important risk factors for poor brain development, such as poverty, malnutrition, and high levels of stress (Jansson & Velez, 2011). However, although hampered by differences in the timing of brain maturation (Thompson, et al., 2009), animal research has provided some important information.

Alcohol.

Since ancient times it has been known that prenatal alcohol exposure (PAE) can have negative effects on the developing fetus (http://www.humanillnesses.com/original/E-Ga/Fetal-Alcohol-Syndrome.html). In fact, the advice to abstain from alcohol during pregnancy is a classic part of prenatal care (Bailey & Sokol, 2008). Alcohol passes through the placenta and into the amniotic fluid (Jansson & Velez, 2011), where, because of its smaller size, the fetus experiences a much more potent dose than the mother.

Generally, PAE affects the white matter (synapses and dendrites, which connect parts of the brain) in the frontal and occipital lobes most seriously (Fryer et al., 2008). Riley et al. (1995) demonstrated PAE to result in smaller regions of the corpus callosum, the part of the brain that connects the two hemispheres so that information can be integrated efficiently. As with other teratogens, the effects of PAE depend upon the amount and timing of the dose, interactions with other risk factors, and possibly genetic susceptibility (Guerrini et al., 2007).

Based on the sequence of brain development and both animal and human research, it appears that high consumption of alcohol in the first trimester may result in damage related to neurogenesis, the production of dendrites, and migration of the neural cells to their appropriate locations in the brain (although apparently some repair is possible) (Guerrini et al., 2007). Damage during these most basic phases of brain development provides a less optimal foundation for the more complex processes, of course. It has been noted that before implantation in the uterus in the first few days after conception (and notably before the mother is aware of her pregnancy), the blastocyst has full access to all substances consumed by the mother (Pollard, 2007). First-trimester alcohol exposure is probably common, because most women are likely to continue their usual patterns of use for weeks or months before recognizing they are pregnant (Kotrla & Martin, 2009).

In the last trimester, concern focuses on the parietal lobes, cerebellum, hippocampus, and frontal cortex, which continue maturation late in pregnancy and are particularly vulnerable to damage from alcohol (Riley & McGee, 2005). These particular structures, which are key to learning, memory, and higher-order thinking, have been shown to be smaller in the offspring of severe alcoholics (Guerrini et al., 2007).

Fetal alcohol syndrome is the most common and preventable type of mental retardation, and has been a concern of the social work profession (Kotrla & Martin, 2009). It is diagnosed by the presence of anomalies in growth, facial characteristics, and central nervous system dysfunctions. Subsets of these sequelae are often referred to as fetal alcohol effects or fetal alcohol spectrum disorders and appear to exist on a continuum (Riley & McGee, 2005). Children with these conditions are usually smaller than their peers, have distinctive facial features, and show behavioral problems associated with damage to the brain. It is believed that many of the common difficulties children experience in school, such as attention deficit–hyperactivity disorder, impulsivity, and learning disorders, may also be the results of PAE (Riley & McGee). Lebel et al. (2012) also have demonstrated in longitudinal research that PAE restricts the plasticity of the brain, thus reducing later chances of recovery and repair of damage.

Smoking.

Smoking during pregnancy causes the most developmental damage of any of the recognized teratogens, depositing thousands of chemicals in the mother’s and the fetus’s bodies (Rogers, 2008). Centers for Disease Control statistics demonstrated that 22.0% of women smoked cigarettes in 1998, and recent estimates are that between 12.9 and 22% of women continue to smoke during pregnancy (Centers for Disease Control, 2012); however, rates are higher for poor women, and only about a quarter of female smokers stop when they learn they are pregnant, with less educated women less likely to quit (Martin et al., 2007). Epidemiological research has established that maternal smoking is associated with a host of childhood mental and behavioral problems that are believed to result from effects on the brain, including attention deficit–hyperactivity disorder, behavioral problems, hyperactivity, and learning disabilities (see review in Bublitz & Stroud, 2012); however, little human research has connected these conditions with brain morphology and the mechanisms responsible for the damage. In this regard, animal research is quite informative.

Although tobacco contains many harmful chemicals that may affect the fetus, most of the available research concerns nicotine, and so nicotine is the focus of this review. Damage occurs both directly through affecting developing brain structures and indirectly through effects on the placenta and the mother’s health. Moreover, emerging knowledge suggests that drugs can alter gene expression in the developing brain and that some of that epigenetic damage may be passed on to the progeny of the fetus (Jansson & Velez, 2011).

Nicotine is rapidly absorbed into the bloodstream (Shea & Steiner, 2008) and has numerous detrimental effects on fetal development, including growth retardation through both direct smoking and second-hand smoke exposure by pregnant women (Rogers, 2008). The small size of the fetus results in its experiencing larger concentrations of tobacco components compared with the mother. Shea and Steiner suggest that it is probably the effects of tobacco exposure on the brain, and particularly the brain stem, that leads to the increase in risk of sudden infant death syndrome in children with PAE.

Nicotine causes a decrease in blood flow and increased vascular constriction and resistance (Shea & Steiner, 2008) because it binds to hemoglobin receptors and deprives the fetus of both essential nutrients and oxygen. Animal research demonstrates that the resulting malnutrition and hypoxia affect brain development processes all the way from neurogenesis through migration and cell differentiation, myelination, synaptogenesis, and even pruning (Ekblad et al., 2010; Roza et al., 2007). Moreover, Shea and Steiner also demonstrated that nicotine disrupts the formation of neurotransmitters, including serotonin, catecholamine, and dopamine, suggesting that neurotransmitter damage is probably related to well-documented difficulties in attention, ability to handle stress, learning, memory, behavior control, and depression among individuals exposed to nicotine in utero.

Specific effects of nicotine on the fetal brain are dependent on the timing of the dose. Bublitz and Stroud’s (2012) review of the research suggested that nicotine exposure in the first trimester is most likely to result in premature development and subsequently altered neuronal activity in the brain stem, the lowest part of the brain that is responsible for autonomic functions such as heartbeat and breathing, and the midbrain structures, which relay visual and aural signals to higher regions of the brain. Ekblad et al.’s (2010) research with premature infants also is informative on the effects of the timing of early exposure to nicotine, because it was possible to use imaging to view specific parts of the brain and to factor in gestational age. This research showed reduced size in the frontal lobe and cerebellum. These structures play important roles in emotion, impulse control, and attention.

Bublitz and Stroud’s (2012) review suggests that second- and third-trimester exposure to nicotine is linked to persistent abnormalities in neuronal maturation and decreased cell size in the higher-order cerebral cortex, hippocampus, and cerebellum. Huang, Abbott, and Winzer-Serhan’s (2007) research with rats during the period that equates to the third trimester in humans also indicates that late-pregnancy exposure to nicotine particularly affects the structure of the hippocampus because that structure, so critical to memory and learning, is relatively late in developing. That research also suggests that nicotine may impair the long-term survival of neurons; this connection may be the mechanism for decreased cognitive functioning in tobacco-exposed individuals.

It is difficult to separate the neurological effects of exposure to tobacco smoke before and after birth, although there is significant research linking postpartum secondhand smoke exposure to other types of health problems (Rosenthal, 2011). Infants are exposed to tobacco through breast milk and skin, in addition to inhalation (Bruin, Gerstein, & Holloway, 2010). Moreover, Rosenthal’s review shows mixed results with regard to whether exposure to second-hand smoke in early childhood is related to the typical behavior problems related to neurological damage, such as conduct disorder and attention deficit–hyperactivity disorder because of failure to control for relevant related variables. Research has demonstrated that both prenatal and postnatal maternal smoking increase the risk of childhood asthma through modification of gene expression (Breton et al., 2009), so this is a line for further research.

Illegal drugs.

Different illegal drugs affect fetal brain development through different mechanisms, and space does not permit a comprehensive discussion of the effects on neurodevelopment related to all illegal drugs. Generally, however, prenatal exposure to the most commonly used illegal drugs (such as cocaine, opioids, and amphetamines) is damaging to brain development. Research has demonstrated changes in both morphology and functioning. Because of the tendency of drug abusers to use multiple substances (and to smoke and drink alcohol as well), the evidence is not always clear of the specific effects of isolated substances in humans, but animal research provides some such information (Thompson et al., 2009).

Opioids, including heroin, methadone, codeine, and morphine, influence reuptake of the monoaminergic neurotransmitters dopamine, norepinephrine, and serotonin and result in excess dopamine in the synaptic cleft and excess stimulation of dopamine receptors, which are located throughout the brain (Salisbury, Ponder, Padbury, & Lester, 2009; Thompson, et al., 2009). Research shows long-term behavioral effects that resemble attention deficit–hyperactivity resulting from fetal exposure to cocaine, although those changes appear to be mild. Exposure in the second trimester is believed to be the most harmful to cognition and executive functioning (Thompson et al.).

A recent review of the long-term effects of prenatal exposure to cocaine (Lambert & Bauer, 2012) notes attention, impulsivity, and emotional reactivity problems in children who were prenatally exposed to cocaine, in keeping with the drug’s influence on the developing dopaminergic system. In addition, mental health, juvenile delinquency, high rates of risky behavior, and possibly higher rates of addiction have been observed in adolescents who were prenatally exposed to cocaine. These authors emphasize that long-term effects appeared to be significantly moderated by quality of parenting, the home environment, and socioeconomic status. Longer follow-ups are needed to determine further effects, especially with larger samples that permit control for the important moderating variables, but it appears that behavioral effects are mild (Thompson et al., 2009).

According to Thompson et al. (2009), amphetamines and methamphetamine also enhance the release of dopamine, as well as noradrenaline and serotonin in the synaptic cleft, thus damaging the neurotransmitter (signaling) system in the brain, although the process through which this occurs is a bit different than with cocaine. Recent increases in the use of amphetamines and especially methamphetamine in the United States are alarming in view of the demonstrated behavioral effects of prenatal exposure reviewed by Thompson et al., which are similar to those for prenatal exposure to cocaine.

Prescription drugs.

Research related to the effects of fetal exposure to prescription drugs has focused on anti-depressants (particularly selective serotonin reuptake inhibitors) and anti-seizure medications. Selective serotonin reuptake inhibitors are of particular concern because they are so commonly prescribed. Selective serotonin reuptake inhibitors target serotonin receptors, reducing reuptake and increasing levels in the brain. Animal research has shown that prenatal exposure to selective serotonin reuptake inhibitors can cause a paradoxical effect in rats, increasing exposed individuals’ responses to stress and symptoms of depression and anxiety (Homberg, Schubert, & Gaspar, 2010). Homberg et al. found evidence of effects on the sensorimotor cortex, with subtle changes in sensory responses and fine motor skills. Thompson et al.’s (2009) recent review of research demonstrates mixed evidence of damage to the developing human fetal brain with exposure to these drugs. Effects appear to be subtle, however, and must be weighed against the risks imposed on the developing fetal brain by untreated depression, anxiety, and seizures.

Environmental Contaminants

Social justice is the frame for social work’s concern with environmental contaminants because minorities and the disadvantaged are exposed to these toxic chemicals in much greater amounts (Rogge & Combs-Orme, 2003). Moreover, concern about risks posed to infants and children are consistent with the profession’s traditional special attention to this constituency.

Toxic environmental chemicals pose greater risks to children than to adults, in part because of children’s smaller body size and rapid growth (Landrigan & Goldman, 2011). Research has linked exposure to environmental chemicals during gestation to birth defects, intrauterine growth retardation, chronic illness, and reduced intelligence. Other effects are being discovered daily because new untested chemicals are constantly being introduced to the environment.

The special risk posed to children, infants, and fetuses by environmental chemicals was only recognized in 1993 (National Research Council, 1993). This report was the first to call attention to the fact that not only are young children more sensitive to environmental toxicants than adults because of their smaller bodies, but also there are qualitative differences in the effects because of the developmental process. Moreover, children have more time to develop some of the chronic diseases associated with exposure to some chemicals, such as cancer and asthma (Landrigan & Goldman, 2011). Nevertheless, U.S. environmental policy continues to regulate environment toxins using a standard of safety for the “average adult” (Landrigan & Carlson, 1995).

It is not possible to discuss all of the environmental chemicals known to affect fetal and infant brain development in this entry (and there are probably many that remain unknown), but they include chemicals found in pesticides, building materials, food products and packaging, household products, cosmetics, fabrics, and toys.

Lead is a toxic heavy metal found in the earth’s crust that causes serious brain damage. The removal of lead from gasoline in the 1970s led to a dramatic reduction in childhood lead levels in this country and has been hailed as a major “public health victory” (Bridbord & Hanson, 2009). Nevertheless, lead exposure continues to be a risk to the developing fetal brain, even at very low levels (Jedrychowski et al., 2009). Lead easily crosses the placenta, and maternal and fetal blood lead levels are highly correlated (Jedrychowski et al.).

Prenatal lead exposure is believed to cause neurocognitive damage through modification of apoptosis, effects on neurotransmitter development, and other mechanisms, and animal research shows specific damage to the hippocampus and cerebellum, as well as the neurotransmitter system (Sanders, Liu, Buchner & Tchounwou, 2009).

Documented long-term effects of prenatal lead exposure include delayed cognitive development in infants and lower intelligence in school-age children and adolescents; behavioral problems in adolescents; mood disorders; and possibly psychiatric disorders (see review by Sanders et al., 2009).

After birth, infants are exposed to environmental chemicals through breast milk, other food, air and water pollution, and dirt. Because of their small size, exposures are greater to these contaminants than they are for adults. Social workers are concerned because low-income and minority neighborhoods suffer the greatest exposures (Rogge & Combs-Orme, 2003).

Stress and Trauma

Since the 1970s, science has provided dramatic evidence of the harmful effects of chronic stress and trauma on multiple systems in the human body, leading to heart disease, diabetes, mental health problems, and many other disorders (Thoits, 2010). Social workers are actively involved in the delivery of services to the victims of stress and trauma (Smyth, 2012), especially because disadvantaged populations are most likely to experience trauma and chronic stress (Moore, Redd, Burkhauser, Mbwana, & Collins, 2009). However, although there are a few references to prenatal stress in the social work literature, the profession is just beginning to recognize its influence on early brain development (Egan, Neely-Barnes, & Combs-Orme, 2011; see Lefmann, 2012). This discussion focuses on the effects of trauma and chronic stress on brain development in early life.

Stress and trauma experienced by the mother are directly experienced by the developing fetus through the maternal hypothalamic–pituitary–adrenal axis, the system in the brain that mediates the human stress response. The human stress response consists of a set of functions mediated by the brain to promote survival in the face of threat. When a human feels threatened (or under conditions of chronic stress), whatever the source, the hypothalamus in the brain signals to the pituitary gland to release corticotrophin-releasing factor, which then binds to receptors in the anterior pituitary gland, in turn producing adrenocorticotropic hormone, which stimulates the production of glucocorticoids and cortisol. These hormones cause the body’s autonomic nervous system to prime the body for the fight-or-flight response (Latendresse, 2009).

In this phase, the sympathetic branch of the autonomic nervous system increases arousal, blood pressure, heart rate, respiratory rate, and physical activity through the release of norepinephrine and epinephrine (or adrenaline, the American term for epinephrine) (McEwen & Wingfield, 2003). All systems needed to run or fight the threat are activated. At the same time, the parasympathetic branch shuts down systems that are not needed so that all energy can be placed on survival, inhibiting muscular activity, digestion, reproduction, etc. Adrenocorticotropic hormone or corticotrophin is then transported to the adrenal glands, causing the release of other hormones, such as cortisol and adrenaline. The release of cortisol acts as a feedback mechanism and moves to bring the body back to homeostasis and all systems back to normal.

In the short run, the human stress response is an elegant design that has enabled survival of the species, but constant or high levels of stress disrupt normal functions and are correlated with poor health and a number of chronic diseases, such as high blood pressure, heart disease, and mental illness (Thoits, 2010).

Because a pregnant woman and her fetus share a common blood supply, maternal stress is communicated directly to the developing fetus (the placenta protects against some cortisol, but cannot handle excessive levels), causing the same physiological reactions in the fetus, who is receiving a higher dose for its size. Moreover, because the fetus’s hypothalamic–pituitary–adrenal axis is still developing, the high levels of stress hormones described above appear to lead to heightened sensitivity and over-expression of the stress reaction (Davis, Glynn, Waffarn, & Sandman, 2011).

The neurotransmitter cortisol is critical for the development of most regions of the brain, and receptors for cortisol expression are highly expressed in the fetal brain, with specific effects determined by the timing of exposure during gestation. Monk, Georgieff, and Osterholm (2012) reviewed the available evidence and concluded that there is ample human and animal evidence for neurocognitive deficits and behavior problems in infants exposed to in utero stress, especially in the hippocampus and in connections among brain regions. They note that many of these outcomes (as well as the mechanisms) are similar to those of infants whose mothers suffered malnutrition during pregnancy.

There is a tendency to discount the stress experienced by young infants. Infants experience stress and trauma, just as their parents do. They can experience it directly, such as occurs with child abuse and neglect (see Perry, 2009), or indirectly, such as through their parents’ stress; indeed, children are traumatized by their parents’ terror (Masten & Narayan, 2012) because they are sensitive to the emotions of their caregivers.

Although much of the infant’s stress response is programmed in utero, development in these systems continues in the first few months of life. For example, Meaney’s (2001) research has demonstrated with rats that licking and grooming (the equivalent of nurturing for humans) are correlated with offspring’s brain development and behavior. Across a normal distribution, rats whose mothers provided the most licking and grooming developed more glucocorticoid receptors (which take up the glucocorticoid in the brain) and demonstrated healthier responses to stress throughout life. These same offspring mimicked their mothers’ nurturing behavior when they became mothers.

Meaney’s subsequent research (for example, Meaney, 2010) has clarified the mechanism through which nurturing influences the brain. Licking and grooming lead to greater expression of the genes that drive development of glucocorticoid receptors in the early days of brain development, so that well-nurtured offspring have more receptors to take up the stress hormones. Cross-fostering the newborns of poorly nurturing mothers (and vice versa) demonstrated that these effects were not caused simply by genetic differences in these mice, but rather were specifically caused by parental care.

Poverty

Social work has a long history of recognizing and attempting to ameliorate the enormous risks posed to infants and children in poverty (see discussion of the history in social work in Combs-Orme, 1988). It has been abundantly clear that children who grow up in poverty are disadvantaged in virtually every way, as measured for many years (Brooks-Gunn & Duncan, 1997; McLoyd, 1998; Yeung, Linver, & Brooks-Gunn, 2002). Only recently has the profession recognized the role played by poverty in poor brain development and the connections between poor brain development and poor life outcomes (for example, Farmer, 2008; Egan et al., 2011).

Both before and after birth, poverty operates through poor nutrition, poor health care, drug abuse, and exposure to toxins, stress, and other damaging factors to influence brain development and handicap a child long before she starts kindergarten (see discussion in Hackman, Farah, & Meaney, 2010). Although it is possible that these differences between poor and non-poor children are the causes of poverty rather than vice versa, Hackman et al.’s careful exploration of the literature concludes that this is not the case. Moreover, gaps in achievement and mental health between poor and non-poor children expand over time, with poverty influencing development every day through multiple mechanisms, as discussed above (Combs-Orme & Cain, 2006).

Farah’s work shows that the reduced opportunity for exposure to stimulating experiences and the stress associated with poverty are measureable in the neurostructure of poor children’s brains (Farah, 2010; Farah et al., 2006), particularly in areas of the brain related to executive functioning, especially working memory and cognitive control (prenatal cortex); and language, which is highly correlated with reading ability (left perisylvian).

Parenting and Nurturing

Parenting is of major concern to social work and is critical in most settings in which social workers practice, from mental health to school social work to child welfare agencies (Combs-Orme, 2008). As with other topics in this entry, however, the profession has only recently begun to integrate the importance of parenting for healthy brain architecture (for example, Shapiro & Applegate, 2000).

Arguably, parenting makes the most important contribution to infant brain development (Landry, Smith, & Swank, 2003; Lugo-Gil & Tamis-LeMonda, 2008). In part because of limited time outside the home, particularly for a newborn, parents provide the environment and most of the stimulating daily experiences that influence how the genetically programmed process of brain development unfolds in the early weeks of life. These experiences include the meeting of basic needs (such as nutrition), exposure to necessary sensory experiences (such as visual and aural stimulation), and social nurturing and interaction; indeed, these are the basics of parenting infants (Combs-Orme, Wilson, Cain, Page, & Kirby, 2003).

It is important for social workers to educate parents to understand that the very plastic brain of a newborn is primed to make connections, positive or negative, from the first moment of birth. If every time baby cries she is picked up and soothed and her need for food or a clean diaper is met, she learns that she can influence the world, that she is safe, and that her caregivers value her (and, not coincidentally, she develops more glucocorticoid receptors to deal with future stress in her life). If when she cries her caregivers ignore her or yell at her, she learns a different kind of message and does not develop healthy systems to handle future stress. It is probably for this reason that nurturant parenting can serve as a buffer against poverty, stress, and other events and circumstances that can hinder healthy brain development (Shapiro & Applegate, 2000). The stress diathesis model has emphasized parenting as an important buffer against stress for children (Meaney, 2010).

Infant learning occurs in relationship with caregivers, literally changing the architecture of the brain by promoting the dense wiring among parts of the brain that drives response to stimuli and allows information from both the right and the left sides of the brain to be integrated (Miehls, 2010). The right side of the brain, which processes emotional information, usually outside of awareness, is most active in the first year of life (Schore, 2001) and is stimulated by interaction, affection, and eye contact. In particular, the right orbitofrontal cortex, which is related to facial recognition, recognition of social cues, and empathy, may also appropriate specific neural circuits for language in the left side of the brain because an infant’s hearing is believed to be biased for the sounds of language, and an infant is especially attuned to her mother’s voice (Kuhl, 2010).

At the motor level, this is how an infant learns to walk: once she has developed the muscles and previous skills such as crawling, she keeps trying to walk until the right neurons fire together and she is able to do it, if clumsily. Synapses form. She keeps practicing, firing those neurons and strengthening the synapses, and she gets better and better. Other systems develop in the same way.

As discussed above, the higher regions of the brain, including the frontal cortex and the hippocampus, are not mature at birth and continue to organize and grow in response to stimuli from the infant’s world. Organization of the limbic system (the seat of emotional memory), the cerebellum and motor cortex, and other lower structures described here provides the basis for those higher systems. Language also provides important stimulation to the infant’s developing abilities to solve problems, reason, and plan and execute her actions.

Language Development

Parenting is especially critical to the development of language. The more words young children hear, the better the computational aspects of language learning described above can work. Kuhl (2010) hypothesizes that the right side of the brain that is stimulated by nurturing also gates the learning of language by appropriating space in the brain for language. One of the major differences between low-income and middle-class children when they begin school is the much larger vocabularies of middle-class children. Hart and Risley (1995) observed infants in families over a 2-year period to document and explain vocabulary differences among children of welfare, working-class, and professional families. They reported that over 4 years, children of public-assistance recipients experienced about 13 million words, whereas working-class children experienced 26 million and children of professionals 45 million words. Children’s vocabularies at kindergarten entry paralleled these findings about word experiences. Better language skills, of course, correlate with better reading ability, facilitating the acquisition of knowledge in every area. Thus, low-income children begin school with a disadvantage and only continue to fall behind as time passes.

Early Maltreatment

Abusive or neglectful parenting causes a range of physical and mental health problems in later life (see Wells, 2008). Recently it has become clear that these poor outcomes are mediated by structural brain damage wrought during sensitive early development when “adverse experiences interfere with normal patterns of experience-guided neurodevelopment by creating extreme and abnormal patterns of neural and neurohormonal activity” (Perry, 2009, p. 241).

When a very young child is abused or his needs are severely neglected, his human stress response (described above) activates in the interest of his survival, releasing the hormones and neurotransmitters described above, at a time when the system is still organizing. Maltreatment during the early months of life thus creates patterns of neural and hormonal activity that provide a poor basis for organization and development of the higher parts of the brain, such as those used in cognition and executive functioning. Although some of these patterns can be repaired with later therapeutic intervention, it becomes more and more difficult as a child gets older and his brain is less plastic.

Infants do not remember specific events during these early months (because the parts of the brain that manage episodic memory are not yet developed), but because the emotional parts of their brains, especially the limbic system, are very well developed, these patterns of neuronal and hormonal activity create associations referred to as implicit memories (Perry, 2009). Thus, a child who was abused as an infant may not remember those occasions, but has learned not to complain or express his needs, or to be fearful of his caregivers (and possibly anyone more powerful than he), and those implicit memories do influence his behavior (Perry). The hyper-vigilance or social withdrawal exhibited by maltreated children is based on a malorganized stress response system.

Implications for the Future of Social Work Practice

Neuroscience is already changing social work practice, informing clinical practice in mental health (for example, see Shapiro & Applegate, 2000; Farmer, 2008; Matto & Strolin-Goltzman, 2010) and the addictions (Littrell, 2011). Perry’s work (for example, Perry, 2009) with maltreated children is providing insights for more effective practice in child welfare. Neuroscience also is providing information that is critical for designing policy and programs to enhance the lives of children (for example, Dawson, Ashman, & Carver, 2000; Juby & Meyer, 2011).

It is likely that research will continue to offer new insights and understanding for social work practice, both for clinical work and for policy and program development. Better understanding of early brain development is essential as the social work profession seeks to enhance evidence-based practice.

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