TRAINING AND DEVELOPMENT STRATEGY

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Running head: CHILD DEVELOPMENT
Child Development: Prenatal Drugs and Alcohol Usage by Mother in Infancy and Toddlers
Katherine Lin
Professor Fusaro
San Jose State University
1
CHILD DEVELOPMENT
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Child Development: Prenatal Drugs and Alcohol Usage by Mother in Infancy and Toddlers
Introduction
Substance abuse within society is a subject that has received significant attention
owing to the prevalence of the problem since early years. The intricacies associated with
addiction are not easily managed. These intricacies are even more distinct in instances of
drug and substance abuse by women who are pregnant, a mater that has been constantly
present in public discussion forums in the recent past. Behnke, Smith, and the Committee on
Substance Abuse (2013) define maternal prenatal drug and substance abuse as “chronic use
of alcohol and/or other drugs.” Scholars often use the acronym AOD to designate the
recurrent and general challenges of drugs and alcohol. Nevertheless, AOD is not only specific
to mothers and comprises both postnatal and prenatal use, in addition to use by men. Use of
drugs and alcohol by mothers during the prenatal stage of pregnancy results in many adverse
effects on the general development of the child, and the effects of such practices often result
in cognitive development challenges in later years.
Pradhan et al. (2014) note that chemical neurotransmitters carry out important
functions in the brain development processes, and in particular in the development of brain
circuits and neurons. Psychoactive medications control transporters, receptors, and other
constituents of the neurotransmission process, the majority of which are articulated in the
course of prenatal stages of brain development. Nevertheless, their functionality and pattern
expressions are at times diverse from their more usual functions later in life. Therefore, the
existence of these proteins within the confines of the developing brain triggers the wellresearched effects of exposure to prenatal medication on brain neurobehavioral function,
chemistry, and architecture in both animal models and clinical cohorts.
A number of authorized drugs, for instance, alcohol and nicotine can result in more
serious brain development deficits than many illegal drugs such as cocaine. Nevertheless,
CHILD DEVELOPMENT
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biased and erroneous interpretations of the medical research literature many times affect
learning programs, as well as legal proceedings. For instance, in late 2003, a pregnant woman
from Tennessee whose ER toxicology medical evaluations indicated heavy cocaine usage
was sentenced and incarcerated after being convicted of intentionally using a deadly weapon
against her yet to be born child. It is policy decisions such as the one outlined above that may
have unintentional negative effects: for instance, they may injure the fetus because of
pathophysiological triggering of the MSRS (Maternal Stress Response System) (Thorsell &
Nätt, 2016).
The policy pronouncements highlighted above might have inadvertent undesired
outcomes: for instance may cause harm to the fetus owing to pathophysiological stimulation
of the maternal stress reaction system and may lead pregnant women abusing drugs to elude
prenatal healthcare. Stein et al. (2014) note that research findings in animal and human
models should be applied to inform better program and policy development to lessen the
number of children who are at risk of being exposed to drugs during the prenatal stage of
their mothers’ pregnancy. A big part of the human statistics and data is being produced by the
NCS (National Children’s Study), whose main objective is to assess the outcomes of
environmental effects on the development and health of approximately 100,000 children
across the U.S. Nevertheless, issues regarding logistics and geographical placemen have
rendered it challenging to retain and coordinate participation of the children and their mothers
(Lipshultz, Miller, Wilkinson, & Mestre, 2013).
This research primarily addresses the main subject of child development and the case
of prenatal drugs and alcohol usage by mothers in infancy. In effect, the discussion will
encompass three primary categories of addictive drugs and substances used in the course of
pregnancy: alcohol, tobacco, and illegal drugs. MATID (Maternal Alcohol, Tobacco, as well
as Illegal Drugs) will be used in reference to the maternal use and abuse of these elements in
CHILD DEVELOPMENT
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the course of pregnancy, which puts at risk the general welfare of the child. This report
additionally reviews data concerning prevalence exposure rates, as well as both long term and
short term outcomes of exposed infants.
Prenatal Exposure to Drugs: Effects on Brain Development
Chemical neurotransmitters play important roles in the organization and
synchronization of the development of brain circuits and neurons. Psychoactive drugs control
the neurotransmission components such as transporters and brain receptors, the majority of
which are pronounced in the course of prenatal phases of the brain development process,
even though their expression functions and patterns are at times diverse from their more usual
functions later in life. Research findings in animal and human models need to be applied to
apprise and inform better program and policy development to lessen the number of children
who are at risk of being exposed to drugs during the prenatal stage of their mothers’
pregnancy.
Cocaine
Cocaine is a drug categorized as a psychostimulant, which binds to monoaminergic
blood transporters. It has characteristics that inhibit the uptake of extracellular monamines, a
process that leads to the existence of more than normal neurotransmitters in the synaptic cleft,
as well as stimulating the production of more dopamine receptors in the body. Rocchetti et al.
(2015) note that there are five widely known dopamine receptors: D1, D2, D3, D4 and D5. Of
these, D1 and D2-like receptors are the main categories. Scientists have shown the role of the
receptors and dopamine in reward channels in both animal and human models. Dopamine
receptors are additionally found in the brainstem, hypothalamus, prefrontal cortex, as well as
outside the Central Nervous System.
Beaulieu, Espinoza, and Gainetdinov (2015) note that the dopamine system forms
early during the gestation period in all vertebrate species. The authors note that this may thus
CHILD DEVELOPMENT
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be sensitive to external influence and manipulation during the early periods of gestation. A
number of researchers have proposed a very stringent phenotype in children that are exposed
to the cocaine drug in a woman’s uterus; before birth (Johnson, Womble, Jackson, &
Goodman, 2014). From their analysis, they note that children were thought to be less likely to
interact socially, cognitively impaired, emotionally disrupted, and had a higher chance of
dying from SIDS (Sudden Infant Death Syndrome). It is for this and many other related
factors that the term “crack-baby” was fashioned to denote children pre-exposed to cocaine
before birth.
It is known that, devoid of the type or category of species, the level to which preexposure to cocaine before birth affects the development and functionality of the brain
fluctuates considerably. The suppositions and assumptions that the public makes regarding
the biological effect of exposing a child to cocaine prenatally might be founded on the level
of symptom severity related with addiction to cocaine, as well as the unlawful characteristic
of the element. In the case of humans, multiple research studies have demonstrated that there
are protracted effects of prenatal exposure to cocaine; nevertheless, the interactive
dysfunction effects seem to be minor. The social use of cocaine in the course of one’s
pregnancy leads to subtle, but leading developmental phenotype, which bears a close
semblance to ADHD (Attention Deficit Disorder) (Koob & Volkow, 2016).
It has also been shown that exposure to cocaine use prenatally can result in long term
negative outcomes on attention and cognitive systems, facilitated through higher-order areas,
which get projections that have high contents of dopamine and dopamine receptors from the
midbrain (Richardson, Goldschmidt, Larkby, & Day, 2015). The authors further argue that
there is a high probability that prenatal exposure of children to cocaine will necessitate
special needs attention, which, when assessed from the societal and individual perspective, is
costly.
CHILD DEVELOPMENT
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Research conducted on animal test subjects indicates that prenatal exposure to cocaine
leads to permanent molecular, cellular, and behavioral changes (Riley, Maymi, Pawlyszyn,
Lili, & Zhdanova, 2017). A circulatory simulation of prenatal exposure to cocaine in the
rabbit models bears a close semblance to the complex human model. These rabbit models
have been applied to explain some of the highly particular changes, which include
transformed aminobutyric acid content in the cortex, decreased levels of D1 receptors,
morphological changes in pyramidal cells, and changed calcium binding protein expression.
Animal models indicate that exposure to cocaine prenatally changes the primary processes of
neocortical growth and development, including cell migration and production. The research
results highlighted above are in line with research by Hedlund et al. (2016) that has shown
that dopamine can control the proliferation of progenitor cells, as well as controlling neural
migration in the course of prenatal development. Researchers have reported changes in
numerous animal models, including reduced concentration, emotional reactivity as well as the
reinforcement of the properties of drugs. All these studies relate positively with studies that
acknowledge some level of disturbances in both emotional regulation and attention in
children that have a known history of prenatal exposure to cocaine.
Methamphetamine/Amphetamine
Methamphetamine and amphetamine are also categorized as psychostimulants;
nevertheless, they target the monoaminergic framework in an automatously different
mechanism from cocaine. Both methamphetamine and amphetamine counter monoamine
transporters actions and precipitate the release of serotonin, norepinephrine, and dopamine
into the synaptic cleft, which improves their capacity to act upon the post-synaptic receptors.
Consequently, both methamphetamine and amphetamine drugs can restrict the degradation
and uptake of the highlighted neurotransmitters, which further increases their numbers in the
synaptic cleft. The methyl group addition enables methamphetamine to be carried with ease
CHILD DEVELOPMENT
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through the lipid permeable membranes. Both methamphetamine and amphetamine are
regularly smoked, snorted, and ingested. The frequency of abuse or use of methamphetamine
and amphetamine has consistently gone up in the human populaces in the recent past; the use
of these two drugs rival that of cocaine in many different parts in the U.S (Wurita et al.,
2016).
Since people have recently increased the rates of abuse of methamphetamine and
amphetamine during pregnancies, there are some researches that have outlined the long-term
effects of continued use. Abar et al. (2014) note that children exposed to methamphetamine
or amphetamine prenatally exhibit low birth weight, movement disturbances, reduced school
achievements, increased stress, and reduced arousal. Diaz et al. (2014) showed that children
exposed prenatally to methamphetamine or amphetamine score lower on visual motor
integration, long term verbal and spatial memory, as well as sustained attention. Digital
neuroimaging has given reports of smaller hippocampus and striatum volumes, as well as
lessened aggregate numbers of D2 receptors, as well as the reduced density of dopamine
transporters. Psychosocial risks including the use of polydrugs introduce extra challenges,
which make it more challenging to outline the clinical effects on every individual drug.
Scientists have studied the neurobiological effects of prenatal exposure to
methamphetamine and amphetamine in rats and mice test subjects. Kiblawi et al. (2014) note
that the effects of exposure of methamphetamine and amphetamine in animals are that there
is manifest deficits in visual system development, increased incidence of microgyria, as well
as lower weights of children a birth. Animals further exposed to methamphetamine and
amphetamine display impaired motor postural movements, decreased pre-pulse inhibition,
and increased startle reflexes. In addition, the researchers noted alterations in the activity and
level of the serotonergic and noradrenergic systems in animals that have been exposed to
methamphetamine or amphetamine. A number of the functional outcomes of prenatal
CHILD DEVELOPMENT
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exposure to methamphetamine and amphetamine are transferred biologically through
inheritance. These research results show that prenatal exposure to methamphetamine or
amphetamine results in an intricate behavioral phenotype that has the same complicated
cellular and molecular foundations.
Effects of Legal Drugs of Abuse
Nicotine
Nicotine, commonly found in tobacco products binds to nAChRs (nicotine
acetylcholine receptors). These nAChRs belong to a category of ligand-gated ion channels,
which are extensively articulated all through the nervous system of the fetus. Nicotine is
normally presented to the fetus by way of environmental exposure to 2nd hand smoke or
maternal smoking. Studies have availed proof that show passive exposure to cigarette smoke,
as well as active smoking can increase the risk of SIDs and preterm births, can result in
reduced birth weight, and can be teratogenic (Cho, Frijters, Zhang, Miller, & Gruen (2013).
All these are factors that lead to behavioral impairment.
Medical research scientists have also established a positive relationship between
exposure to developmental tobacco smoke and ADD, learning disabilities, antisocial
behavior, and hyperactivity. Nevertheless, variations in the amount of nicotine contained in
different cigarette strokes, as well as other chemicals in various tobacco-related products
render it a challenge to contrast research results across age or ethnic groups. In addition, the
existence of biomodulators and neurotoxicants in tobacco smoke make it a challenge to
assess and come to a scientific conclusion of the exact effects of being exposed to nicotine.
Relying on animal studies, being exposed to nicotine may likely cause protracted interference
of brain chemistry and architecture.
Research on animals has availed the most convincing proof that nicotine has
significant unfavorable neurodevelopment effects. Activation of nicotine acetylcholine
CHILD DEVELOPMENT
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receptors affects neural survival, spontaneous neural activity, and morphogenesis in rodents
(Ton, Biet, Delabre, Morin, & Dumaine, 2017). Ton et al. (2017); and Holz et al. (2014) note
that from their research, plasma nicotine levels lead to strong neurobehavioral effects, which
include alterations in cognition, anxiety, reward systems, as well as locomotor activity in
offspring. Higher dosages lead to substantial retardation in growth as well as fetal hypoxia.
Cortical cholinergic frameworks control the how senses work and exposure to nicotine
prenatally weakens cognitive functionality in both children and animals. Surprisingly,
nicotine has been proven to be an inhibitor factor to aromatase, an enzyme, which is involved
in the breakdown of estrogen in the human placenta. This breakdown may impede the process
of sexual differentiation in the human brain particularly in males and researchers have
observed changes in the timing of the beginning of puberty in male adolescents exposed
gestationally.
Alcohol
The use of alcohol spans all cultural groups, education, race, gender, and
socioeconomic classes. Alcohol is a pharmacological sedative, which increases GABAergic
activity while consequently restricting NMDA receptor activity, thus lessening sub-cortical
and cortical activity. Alcohol can additionally destabilize growth factor receptor signaling by
violating the integrity of the plasma membrane. The GABA receptors are usually present
during the early stages of neurological development. These receptors have the capacity to
control the proliferation of progenitor cells, neurite growth, and cell migration. During
pregnancy, alcohol crosses the placenta barrier with ease, and therefore might negatively
affect various histogenic processes (Han et al., 2015).
There is a litany of both clinical and basic proof that relates to the negative
neurodevelopmental effects of exposure to alcohol prenatally. These constitute FAS (Fetal
Alcohol Syndrome), typified by damage to the central nervous system, craniofacial
CHILD DEVELOPMENT
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dysmorphologies, and growth deficiencies. Exposure to alcohol prenatally can result in
hyperactivity, motor and attention development, deficits in learning, and intellectual
disability (Olson et al., 2016). Even though simultaneous use of alcohol with other drugs is
common, alcohol is many times used alone. Many animal specimens and research models of
exposure to ethanol prenatally have established an increased rate at which birth defects are
recorded. These birth defects also include neurological dysfunctions. Other research
outcomes note there are decreases in cranial and spinal motor neuron size and production.
Others include hippocampal and neocortical dysgenesis, reduced myelination, delayed or
reduced neuronal migration, and increased neuronal cell death. Prenatal exposure to ethanol
additionally disrupts the plasma membrane receptors integrity.
Effects of Prescription Neurotherapeutics
Antidepressant Medications
Past animal research analyses have long connected serotonin, the target of the
majority of numerous antidepressants, in the course of growth and the development of
peripheral organs, as well as the brain. Serotonin, together with its receptors is articulated in
the brain during the early prenatal phases of growth and development, and can change axonal
and dendritic diversity. Even though the biological processes under it is done is not known,
initial serotonin signaling disruptions in the animal test subjects can disrupt learning and
increase the likelihood of suffering from anxiety-related challenges.
Hedlund et al. (2016) note that the animal tests conducted in the years past are
convincing, although they further note that epidemiological researches to date give no proof
of heightened risk of birth defects attributable to the use neurotherapeutics in the course of
one’s pregnancy. It is of paramount importance to note that although the frequency of birth
defects contrasted to the general populace has no effect at normal doze quantities levels,
CHILD DEVELOPMENT
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small but important behavioral lack of functionality in children is the same as for the
observed effects of cocaine discussed above.
Other Prescription Medications
Numerous prescription medicines are needed for treating maternal, neurological, and
psychiatric pregnancy disorders. There is insufficient research that has investigated the
functional implications of drug treatment in the long run. There are apprehensions in regard
to the consequences of antipsychotic medicines in the course of pregnancy. Animal
researches indicate there are serious neurodevelopmental dangers. Nevertheless, there have
not been sufficient medical researches, which make it hard to make informed conclusions in
regard to long term effects of fetal development.
Valproate is a commonly prescribed drug, which is categorized as an anti-mania and
anti-convulsant therapeutic that restricts T-type calcium and voltage-gated sodium channels
and restricts the transfer of GABA. Valproate can additionally be used in regulating the gene
transcription epigenetic modulation. Kiblawi et al. (2014) note that data shows the risk is …
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