Additionally, in order to determine the long-term effects of substance abuse on children, one must include the study of other environmental issues.
The development of children impacted by maternal substance use does "not stem from prenatal exposure alone, but rather are the result of a constellation of biological, psychosocial, and environmental circumstances" Poulsen, While the child has most likely incurred damage due to the intake of substances by the mother, the proper support and assistance will help to further the development of the child to maximize his abilities within the limitations of his condition.
This paper seeks to describe the possible effects of substance abuse in gestation, the environmental effects from typical substance-abusive households, and the implications in the field of education. It also seeks to outline curricular adaptations, which can be made to appropriately educate children affected by these issues. Substance Abuse and Pregnancy While the specific effects of substances taken during pregnancy are unclear, much recent research has shed light on a number of physical and cognitive abnormalities mainly found in connection with exposure to substances in utero.
The most commonly researched substances are: alcohol, cigarettes, cocaine in various forms , and heroin. The fact that there is more information available about the effects of these substances does not mean that they are the only substances that will cause damage to a fetus. Alcohol is a "teratogenic substance" which, in connection with pregnancy, causes a fetus to be born with a condition termed, Fetal Alcohol Syndrome FAS Hess, Due to the commonalities between signs and symptoms of children affected by FAS, this has received a tremendous amount of attention by researchers because it is more easily detectable than the effects of other drugs on the fetus.
Currently, alcohol abuse during pregnancy hails as "the third leading cause of birth defects The physical signs of FAS are as follows: "short palpebral fissures, flat midface, indistinct philtrum, thin upper lip, epicanthal folds, low nasal bridge, minor ear anomalies, micrognathia strabismus, ptosis of the upper eyelid, narrow receding forehead, and a short upturned nose" Hess, These physical deficiencies make it difficult to overlook the damage from alcohol on children displaying these characteristics. While the physical effects of FAS are quite recognizable, it is more difficult to ascertain whether a child has sustained any of the cognitive effects.
It is believed that many children with FAS might also display "hyperactivity, fine and gross motor developmental delays or incoordination, impaired language development, impulsivity, problems with memory, poor judgment, learning problems, distractibility, seizures, and structural abnormalities of the brain or indications of deficient brain growth" Hess, Because there are over chemicals found in a single cigarette, it is difficult to analyze the effects of each specific chemical and easier to analyze the effects of cigarettes in general on a growing fetus.
However, researchers have established that "the majority of the adverse effects are attributable to two main ingredients; nicotine and carbon monoxide". One reason for concern regarding the effects of cigarette smoking on pregnancy is that "it is estimated that over 22 million women in this country smoke, and among women of reproductive age, almost one-third are smokers". It is believed that the problems associated with smoking during pregnancy might affect children later in life.
Cocaine and Crack the freebase form of Cocaine use in the United States has increased in recent years Askin, While the long-term effects of Cocaine exposure in utero have not been conclusively established, many researchers agree that children who were exposed to Cocaine in utero most likely sustained some degree of damage. The effects of prenatal ethanol on the dopaminergic system in these brain regions are also significant, with the VTA having an increased response to dopaminergic agonists and the NA having increased sensitivity to the stimulatory effects of alcohol in offspring , , Although ghrelin has been found to be involved in the rewarding feeling of alcohol , there are currently no studies on how low ethanol levels during the prenatal period affects this peptide and other neurochemical systems in these brain regions of offspring.
While there exists plenty of research describing the effects of high gestational ethanol exposure on the developing brain, there are only a few studies measuring the effects of low ethanol exposure on other brain areas not discussed above. Some of the findings include an ethanol-induced increase in progenitor cell proliferation in the basal ganglia and a decrease in neural activity in the infralimbic cortex They also include increased neurogenesis in regions of the hippocampus The amygdala has been suggested to be affected by low levels of ethanol during the prenatal period.
Offspring exposed to low ethanol display anxiety-like behavior when exposed to stressful conditions, and this behavior has been related to both an increase in synaptic connectivity in the basolateral amygdala and a decrease in GABA inhibition , both of which stimulate the excitability of the amygdala , There are several studies that reveal high ethanol exposure during the prenatal period to induce dramatic epigenetic changes in offspring.
The adult liver provides a clear example, with high levels of ethanol exposure found to alter DNA methylation related to alcoholic liver disease — Also, chronic maternal ethanol exposure is shown to decrease methylation at a gene called agouti viable yellow, which affects the color of their coat, that is passed down to offspring , while acute prenatal exposure to high levels of ethanol globally causes hypomethylation of DNA in embryos Long-term prenatal exposure to high ethanol levels also induces changes in methylation and microRNA in hippocampal neurons In light of these studies of high ethanol exposure, further investigations of epigenetic effects are clearly needed involving low concentrations of ethanol, which as described above have strong, stimulatory effects on neuronal development in the brain.
Although only a few studies exist, ethanol intake has also been linked to inflammatory systems. The most commonly studied peripheral organ is the liver, with excessive drinking linked to alcoholic liver disease that increases inflammatory mediators , More recent studies in adult animals have also shown ethanol exposure to stimulate inflammatory systems in the central nervous system.
Endotoxin treatment after ethanol exposure has been found to induce a long-term inflammatory state in the brain and increase nitric oxide synthase and cyclooxygenase, which lead to inflammation This increase in inflammation has also been detected in offspring after prenatal exposure. Similar to prenatal HFD exposure, our lab recently found prenatal ethanol to induce several changes in the CCL2 chemokine system. We found low levels of ethanol during gestation to increase in the offspring the genesis of neurons that co-express CCR2 and melanin-concentrating hormone in the lateral hypothalamus 17 , a neuropeptide implicated in excessive ethanol drinking With current research showing low levels of ethanol exposure to increase drinking in offspring and produce changes in the immune system that ultimately affects neuronal function, future research on inflammatory systems could be very informative and important.
The effects of prenatal nicotine exposure are broad in nature, affecting both behavioral and neuronal development in several regions of offspring brain. Human studies show that children exposed to tobacco during gestation exhibit an increased risk for tobacco use, craving, and withdrawal , as well as dependence Animal studies similarly reveal increased nicotine self-administration and consumption in adolescent and adult offspring — , along with increased ingestion of other substances including fat and ethanol Additional behavioral problems include an increased risk of hyperactivity , impulsivity , and anxiety 34 , High levels of nicotine exposure are also associated with detrimental effects, such as growth retardation While these nicotine studies lead one to question whether these changes are attributed to certain chemicals from the tobacco , rather than to nicotine itself and result from social smoking as well as chronic smoking, the overall evidence clearly demonstrates that prenatal nicotine exposure negatively affects offspring.
Similar to prenatal HFD and ethanol exposure, these changes in physiology and behavior induced by nicotine or smoking may be attributed to neuronal changes in the offspring brain Figure 5. Figure 5. Effects of prenatal nicotine exposure on offspring brain. A schematic summarizing some of the changes that occur in the brains of offspring after being exposed to nicotine during gestation.
Similar to dietary fat and ethanol, prenatal nicotine exposure has been found to affect the neuronal architecture and function of the hypothalamus. Several neuropeptides have been found to be altered in offspring during exposure to both low and high levels of nicotine. Some of the findings include a decrease in CRF and an increase in glucocorticoid receptors in the hypothalamus They also show an increase in several orexigenic peptides, including neuropeptide Y, agouti-related peptide, and proopiomelanocortin in the arcuate nucleus , enkephalin in the medial hypothalamic paraventricular nucleus, and orexin and melanin-concentrating hormone in the perifornical lateral hypothalamus 18 , One of the more important findings from our lab shows that exposure to nicotine actually stimulates the genesis of neurons that express enkephalin, orexin, and melanin-concentrating hormone in the offspring hypothalamus 18 , with these peptides positively related to the intake of nicotine A small number of epigenetic studies also show changes in DNA methylation of the gene encoding brain-derived neurotrophic factor in human studies , , revealing the need for further epigenetic studies of specific cell types.
Prenatal nicotine exposure has been found to varying degrees to change neurons in the VTA and NA in offspring. With regards to the mesolimbic dopamine system, prenatal nicotine exposure decreases the number of dopaminergic neurons in the VTA , dopamine release from the NA , , and the number of dopamine binding sites in the striatum , altering the rewarding effects of nicotine in offspring.
Neuronal connections to the VTA are also affected, with orexin innervation from the lateral hypothalamus to the VTA found to be increased Additionally, prenatal nicotine reduces the number of nicotinic cholinergic receptor expression in both the VTA and NA core Similar to the neurogenesis effect in the hypothalamus, prenatal nicotine increases cell survival in the NA and inhibits cell death related pathways , with this increase in cell survival consistent with the finding that prenatal nicotine exposure increases the nerve growth factor, BDNF Further studies on this reward region in offspring will shed more light on how prenatal exposure reprograms offspring to become more prone to abusing nicotine.
Prenatal nicotine exposure has been found to affect several other brain regions in offspring. In the hippocampus, this exposure decreases the number of neurons while increasing the number of astrocytes , and it also decreases the neuronal area and cell size , , suggesting decreased hippocampal function. Similar effects are also found in the cortex of early postnatal rats , pre-weaned rats , and embryos , with studies revealing fewer glutamatergic neurons These changes in the cortex induced by prenatal exposure have been linked to cognitive deficits and impaired executive control, causing rats to be more impulsive Similar to the VTA and NA, dopamine levels are also decreased in the cortex of postnatal offspring In the amygdala, one study found nicotine exposure to reduce the size of the amygdala in adolescent offspring , while a recent study from our lab has described an increase in neurogenesis and expression of enkephalin neurons in the central amygdala With nicotine intake shown to generally reduce anxiety, future studies with prenatal exposure that relate behavior to amygdaloid function in offspring, as well as to other brain regions involved in decision making, would be interesting.
Several studies show prenatal nicotine exposure to have epigenetic effects on peripheral organs in offspring. Prenatal nicotine has been found to decrease methylation on the promoter-expressing angiotensin receptor type 1a and increase histone acetylation of the protein and fatty acid synthase in liver Human studies have also reveal global changes in DNA methylation in offspring , Evidence of a generational effect has also been shown in rat models, with maternal nicotine use and exposure during the prenatal period found to induce asthma and epigenetic changes in lungs of offspring that are two generations past the original exposure This evidence suggests that the changes induced by prenatal nicotine exposure on brain neurochemical systems may be related to epigenetic changes occurring during development.
While reports of pure nicotine on adult systems generally reveal a reduction in inflammation , , several studies in humans show cigarette smoking to cause an increase in inflammation Also, in a rat model, exposure to pure nicotine during the gestational period is found to increase the inflammatory mediators, IL-6 and TNF-alpha, in newborn blood serum While this evidence is limited, it suggests the possibility that prenatal nicotine may have similar effects to HFD and ethanol exposure on inflammatory mediators, including CCL2.
The current knowledge of the neural control of ingestive behavior in offspring that are prenatally exposed to substances of abuse has come a long way from observational human studies. We are now only beginning to piece together how these changes in specific brain regions affect the overall neuronal communication within the brain. In addition, other systems of the central nervous system, such as glial cells, astrocytes, and oligodendrocytes, may also play a major role in this disturbed communication.
Newborn Drug Dependency: Signs & Symptoms
More importantly is the emerging function of the immune system in the development of these neuronal systems in offspring and how substances of abuse disturb its actions. Future studies using these prenatal animal models will provide much insight in both the molecular and neuronal network changes as well as the mechanisms leading to these changes.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Pattern of malformation in offspring of chronic alcoholic mothers. Lancet 1 — Children of alcoholic parents — observed anomalies: discussion of cases. Ther Drug Monit 25 —6. Chernoff GF. The fetal alcohol syndrome in mice: an animal model. Teratology 15 —9. Ethanol-induced malformations in mice. Alcohol Clin Exp Res 1 — Effects of prenatal alcohol exposure on growth and development in rats. J Pharmacol Exp Ther — PubMed Abstract Google Scholar. Simpson WJ. A preliminary report on cigarette smoking and the incidence of prematurity.
Am J Obstet Gynecol 73 — Google Scholar. Cigarette smoking in pregnancy: its influence on birth weight and perinatal mortality. Br Med J 2 — Maternal smoking and behavior problems of children. Pediatrics 90 —9. Maternal smoking during pregnancy and attention deficit hyperactivity disorder symptoms in offspring. Am J Psychiatry —9. Maternal smoking during pregnancy and smoking by adolescent daughters.
Am J Public Health 84 — Effects of prenatal cigarette and marijuana exposure on drug use among offspring. Neurotoxicol Teratol 27 — Pregnancy in the massively obese: course, outcome, and obesity prognosis of the infant.
Am J Obstet Gynecol — Obesity in pregnancy: risks and outcome. Obstet Gynecol 56 — Birth weight and adult hypertension and obesity in women. Circulation 94 —5. Maternal high-fat diet and fetal programming: increased proliferation of hypothalamic peptide-producing neurons that increase risk for overeating and obesity.
J Neurosci 28 — Prenatal ethanol exposure stimulates neurogenesis in hypothalamic and limbic peptide systems: possible mechanism for offspring ethanol overconsumption. Neuroscience — Prenatal exposure to ethanol stimulates hypothalamic CCR2 chemokine receptor system: possible relation to increased density of orexigenic peptide neurons and ethanol drinking in adolescent offspring. Prenatal exposure to nicotine stimulates neurogenesis of orexigenic peptide-expressing neurons in hypothalamus and amygdala.
J Neurosci 33 — Common effects of fat, ethanol, and nicotine on enkephalin in discrete areas of the brain. J Neurochem — How cytokines can influence the brain: a role for chemokines? J Neuroimmunol — Eur J Neurosci 28 — Chemokines released from astrocytes promote chemokine receptor 5-mediated neuronal cell differentiation. Exp Cell Res — J Neuroinflammation 8 Dev Biol — Saito S. J Reprod Immunol 52 — Changes in melanocortin expression and inflammatory pathways in fetal offspring of nonhuman primates fed a high-fat diet.
Endocrinology — Prenatal alcohol exposure alters steady-state and activated gene expression in the adult rat brain. Alcohol Clin Exp Res 39 — Autism spectrum disorder in children born preterm-role of exposure to perinatal inflammation.
Front Neurosci 7 Maternal inflammation contributes to brain overgrowth and autism-associated behaviors through altered redox signaling in stem and progenitor cells. Stem Cell Reports 3 — Priming the brain for psychosis: maternal inflammation during fetal development and the risk of later psychiatric disorder.
Am J Psychiatry —5. Relation between intrauterine growth and subsequent intellectual disability in a ten-year population cohort of children in Western Australia. Am J Epidemiol — Schendel D, Bhasin TK.nobulutoring.tk
Newborn Drug Dependency: Signs & Symptoms
Birth weight and gestational age characteristics of children with autism, including a comparison with other developmental disabilities. Pediatrics — Late emerging effects of prenatal and early postnatal nicotine exposure on the cholinergic system and anxiety-like behavior. Neurotoxicol Teratol 32 — Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus.