Abstract
One of the most fundamental causes of excessive alcohol abuse is the pathological effects it causes to the body organs. Among these organs, the brain is the most susceptible to the detrimental effects that come with alcohol consumption. Alcoholism causes chronic pathogenesis in the brain of an individual irrespective of their age. The fetus in the womb is in a similar level of risk as the adolescents or the aged. Therefore, it is imperative to note that alcohol has negative impacts on not only the formation of the brain but also its development as a person grows into becoming an adult. The focus of the paper will be on highlighting the how alcohol as a toxic agent influences several life processes in the brain hence affecting its proper formation and development. The discussion will also traverse different life stages ranging from the prenatal state to the adolescent period and lastly the adulthood.
Introduction
Chronic consumption of alcohol is the number one cause of many central nervous system (CNS) degenerative symptoms. Brain damage symptoms can broadly be classified as physical, cognitive, or behavioral. Examples of brain damage effects that could arise from heavy alcoholism are dementia and motor impairments among others. Fetuses can easily be exposed to the dangerous effects of alcohol through the heavy drinking behavior of the mother. Alcohol has toxins that can interact with the various life processes causing inhibitory actions leading to the malformation or poor development of the brain cells. Alcoholism is one of the significant social problems facing many people in the society. With many people potentially risking the proper functionality of the brains through its consumption, it is critical to assess the effects of alcohol on brain formation and development.
Delegate your assignment to our experts and they will do the rest.
Effects of Alcohol on Brain Formation
Before assessing how the alcohol affects the formation of the brain, it is critical to understand the process of brain formation. The Central Nervous System (CNS) is made up of the brain and the spinal cord. The primary function of the CNS is to control the body function by interpreting and sending out signals. The formation of the brain is affected by genes and environment. Genes are hereditarily acquired from both parents while the environment includes the condition existing within the womb, the delivery process, and the events and conditions after the delivery of the baby. Alcohol forms part of the environmental factors affecting the formation of the brain. Due to the toxicity nature of alcohol, it has gross effects on the formation of the brain during the early stages of life. Alcohol has a great penetrative power and utilizes this strength to pass through the mother's placenta into the system of the fetus. Once it reaches the fetus, again, its penetrative power enabled it to cross the blood-brain barrier into the brain. Therefore, the prenatal exposure to alcohol has immense effects on the fetal development of the baby.
FIG.1 is a schematic representation of the rodent brain indicating examples of the effect of moderate developmental ethanol exposure in different brain regions.
Technological advancement has enabled the monitoring of brain formation and development. Some of the machines that could be used to assess brain formation and development include the magnetic resonance imaging machine and the Commuter Tomography scan. In this regard, it is also vital to note some of the indicators that scientist use in monitoring the proper formation, development, and functionality of the brain. Some of these tenets include the size of the cranium, the intelligence quotient, and most importantly, the cognitive and behavioral tendencies of a fetus. Therefore one of the major signs that alcoholism has affected the brain formation of a fetus includes problems with some of the problems of the neurobehavioral development experienced by the child. Studies conducted on humans and animals using alcohol led to the revelation of an alcohol syndrome that comes as a result of the fetus-alcohol exposure known as the fetal alcohol exposure (FAS). Alcohol is known to possess some teratogenic characteristics that can disrupt the complete formation of the brain and further influence its development. One way in which alcohol can affect the formation of the brain is through its interference with DNA synthesis, the process of cell division, and the migration and development of cells. Structural brain deformities will mainly occur during the first trimester after pregnancy. Some of the structurally related brain abnormalities that are caused by alcohol include CNS abnormalities that manifest by a decreased size of the cranium at birth, structural brain deformities such as microcephaly and cerebella hyperplasia. Poor brain formation can also be depicted via the neurological hard or soft signs. Examples include impaired motor skills, hearing loss, and poor hand/eye coordination.
Other than the physical abnormalities associated with the alcohol-related brain malformation in fetuses, another primary symptom could be the behavior and cognitive defects that deviate from what a healthy child should be. Examples of symptoms these symptoms that could also be used to explain an alcohol-related malformation of the brain include learning difficulties, poor school performance, a lack of proper impulse control, and language problems among many others. In assessing some of the causes of the poor brain formation, the first major factor was the interference of DNA synthesis and damage thereof. Alcohol has several toxins including ethanol that interfere with the DNA synthesis process while others are also having a direct effect on the damage hence leading to genomic instability and subsequent death of neurons. Kruman, Henderson and Bergeson (2012) explained that the genetic instability that arises from interferences with the DNA leads to several neurodegenerative problems. Alcohol, through its major compound, ethanol, is also known to interact with other metabolic pathways such as the one-carbon metabolism (OCM) which plays a significant role in the synthesis of DNA.
FIG.2 Schematic representation of ethanol exposure paradigms used in the studies reviewed here.
The second main reason identified for the botched formation as a result of alcohol consumption is lack of proper cell division. Alcohol is identified as a factor that can inhibit cell growth. It is of the essence to appreciate the fact that cell growth is a programmed and coordinated process that could easily be disrupted using alcohol or any other inappropriate drug or chemical. As the fetus that grows in the womb is exposed to alcohol, the chemical contents move quickly to the developing brain cells hence slowing down the cell cycle. The stage of cell growth that is mainly targeted by alcohol is the G1 stage ( Hermens et al . 2013). In this stage, alcohol primarily inhibits translation and transcription of genes which have an important role in the regulation of the other steps in the cell cycle. As the cell proliferation is reduced in the brain, the most likely effect is the loss of the neurons especially in the hippocampus region hence leading to massive problems in learning and keeping a memory.
The third reason implicated in an incomplete brain formation resulting from alcohol use is the migration and the development of neuron cells. As stated earlier, Valenzuela et al . (2012) pointed out that maternal consumption of alcohol can cause grave birth defects on the growing fetus. All these syndromes culminate into a disorder known as the fetal alcohol syndrome (FAS) that characterizes poor formation and development of the brain. The defects associated with the migration of the migration of the glial and neuronal cells is implicated as one of the major causes of the incomplete brain formation. The action of alcohol in a developing brain include via cyclic nucleotide and calcium ions signaling. Also, alcohol results in the migration of immature cells most notably the neurons by taking control of a pathway known as the second messenger. Furthermore, exposure to alcohol also affects the migration of the cerebellar granule cells which also play an important role in the development of the brain.
Alcohol Effects on the Development of the Brain
Alcohol has detrimental effects on the development of the brain and the nervous system in general. There is no single theory or study model that could be used to explain how alcohol affects the development of the brain. However, scientists and researchers have come up with valid explanations that can be used to explain this correlation. In understanding the toxic alcohol effects on the brain development, it is critical to appreciate three important terms that include neurogenesis, synaptogenesis, and apoptosis. Crews and Vetreno (2014) illustrated that neurogenesis is a process whereby new neurons are formed during the development of the brain. Synaptogenesis involves the formation of synapses in between the neurons found in the nervous system. Thirdly, apoptosis is the programmed cell death that naturally occurs as part of the growth of an organism. Investigators have asserted that one of the most common effects of alcohol in brain development is that it plays a critical role in inhibiting cell growth and inhibition that occurs during the process of neurogenesis (Tabakoff & Hoffman, 2013). Furthermore, alcohol can also induce apoptosis during the process of synaptogenesis leading to the development of Alcohol-Related Neurodevelopment Disorder (ARND). Various studies have also attested to the fact that alcohol can act as a potent inhibitor of cellular proliferation more precisely during the development of the brain.
Prenatal alcohol exposure is one of the factors that increase the risk of impairing the brain development of the fetus. Alcohol causes damage to the central nervous system resulting in impaired cognitive function and other behavioral challenges. Research has indicated that offspring of mothers who grossly abused alcohol were most likely to show neuroanatomical changes such as a marked reduction in the size of the brain amongst other cellular alterations. Recent technology, especially in the area of neuroimaging has provided a way in which the neurotoxic effects that come as a result of alcohol exposure could be assessed ( Squeglia et al . 2015). In assessing the effects of alcohol on brain development, it is critical to note that the development of the brain is a continuous process that does not stop. It begins in the intrauterine life and goes on until an individual dies. Alcohol which contains huge amounts of the chemical part, ethanol, has significant impacts on the development of the brain at any given point in life. The ethanol compound in alcohol has debilitating effects on the brain that could be classified as genetic, expression of various receptors, protein synthesis, toxic and inflammatory changes, and dysregulation of neurotransmitters among others (Silveri, 2012).
Starting with the genetic influence of alcohol in brain development, it is critical to understand that it is not only massive drinking of the alcohol-independent individuals that can result in their impaired brain development but also the genetic factors to do with their parent's alcoholic consumption. Paulus (2014) illustrated that a study conducted by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) postulated that the reduced brain growth was more among people consuming excessive alcohol with a family history of alcohol abuse than those without.
The study conducted by the NIAAA further revealed that alcoholic children who also had alcoholic parents had an ICV of 4% less than those of alcoholics whose parents did not have a history of alcoholism. The research also utilized intelligence quotient (IQ) as an indicator of the development of brain among adult alcoholics who had a family history of alcoholism and those who did not have any family background of heavy drinking. The result was that the former had approximately 5.7 points less than the former in as their IQ score. It could, therefore, be concluded that alcohol alters the genes responsible for the brain development which are then transferred to the future generations (Luciana et al . 2013).
As earlier intimated, alcohol has a compound called ethanol that has toxic effects on the brain and its development. The compound ethanol has not only negative effects on the brain but also the entire nervous system. It is majorly known for its effects especially in the synaptic transmission through altering the proteins responsible for these actions. Some of the target proteins altered through the action of ethanol include neurotransmitter receptors, ion channels, and intracellular signaling proteins. Experiments conducted on animals such as the rats have shown that ethanol plays a negative role in inhibiting the process of protein synthesis in the brain. As such, the brain becomes deficient of important proteins that can act as enzymes and neurotransmitters hence setting a center stage for lack of development and the development of mental retardation seen among many alcoholics. Brain tissue damage is another factor that comes as a result of the toxicity of ethanol. The white matter is an important component that enhances the relaying of information between the brain cells. Therefore, Sudheendran et al . (2013) asserted that such destruction of white matter on the brain is dangerous because it would affect coordination among the brain cells leading to cognitive problems in an individual.
It is now common knowledge among many researchers and medical practitioners that excessive and long-term abuse of alcohol can result in serious neurological problems such as cognitive deficiencies and dementia. All these results from the inappropriate or lack of development of the brain that comes about as a result of extensive consumption of alcohol. One rationale that could be used to explain this is that chronic alcoholism can lead to the increased amounts of inflammatory lipids especially in the brains of adults. Silver, (2012) illustrated that research conducted by the National Institute on Drug abuse postulated that adult mice, which consumed alcohol for two months, had an immense amount of lipids in its brain compared to the others which did not consume alcohol. However, one vital aspect that is of the essence to take note of is that the brain is largely composed of fats and lipids.
In comparison to many other organs of the body, the brain is the most sensitive part of alcohol especially in the course of pregnancy. Ungerer, Knezovich, and Ramsay (2013) noted that during the developmental process in the uterus, alcohol exposure to the fetus would likely determine various factors that include structural abnormalities, neuropsychological, and behavioral dysfunction among others (Alfonso-Loeches, & Guerri, 2011). Critical to appreciate is that although the entire brain of the fetus is exposed to alcohol once the mother drinks, what remains apparent is that not all parts are affected. The regions are affected differently by a determinant being the developmental processes in these particular regions. Ron and Barak (2016) explained that Permanent brain damage among children would lead to learning disabilities, memory deficits, behavior problems, and mental retardation among others.
Fig 3 Prenatal exposure to moderate ethanol levels impairs hippocampus-dependent memory and plasticity.
Studies conducted on the adolescents have shown that excessive alcohol consumption is likely to result in a 10% reduction in the size of the hippocampus. The research has also intimated that the hippocampus is among the parts of the brain that is uniquely sensitive to alcohol at this particular time in development. As a result, the poisonous ethanol compound in alcohol can result in the destruction of the nerve cells in the hippocampus hence jeopardizing their functionality. The second part is known as the prefrontal lobe. Petersen (2017) intimated that the functions of this part include judgment, planning, impulse control, decision making, and language. Research conducted with adolescents engaging in heavy drinking revealed that this is one of the most sensitive parts of the brain with alcohol.
In conclusion, alcohol is a dangerous toxin in the formation and the development of the brain. The formation of the brain mainly occurs as the child develops in the mother's womb. When the mother engaged in risky behaviors such as heavy drinking, then the chances are high that the child will have poor formation and development of the brain that will subsequently culminate to a host of physical, cognitive, and behavioral problems collectively known as a fetal alcohol syndrome. Also, it is vital to appreciate that the brain development does not complete when the child is born. It is a continuous process that goes on through an individual's entire life. Use of alcohol, therefore, influences several factors including exposing the brain to toxins, altering the biological processes of the brain, and influencing the genes among others hence leading to both physical and behavioral problems such as a decreased cranium, memory loss, and difficulty in learning among others.
References
Alfonso-Loeches, S., & Guerri, C. (2011). Molecular and behavioral aspects of the actions of alcohol on the adult and developing brain. Critical Reviews In Clinical Laboratory Sciences , 48 (1), 19-47. doi:10.3109/10408363.2011.580567
Crews, F. T., & Vetreno, R. P. (2014). The neuroimmune basis of alcoholic brain damage. In an International review of neurobiology (Vol. 118, pp. 315-357). Academic Press.
Hermens, D. F., Lagopoulos, J., Tobias-Webb, J., De Regt, T., Dore, G., Juckes, L. ... & Hickie, I. B. (2013). Pathways to alcohol-induced brain impairment in young people: a review. Cortex , 49 (1), 3-17.
Kruman, I. I., Henderson, G. I., & Bergeson, S. E. (2012). DNA damage and neurotoxicity of chronic alcohol abuse. Experimental biology and medicine , 237 (7), 740-747.
Luciana, M., Collins, P. F., Muetzel, R. L., & Lim, K. O. (2013). Effects of alcohol use initiation on brain structure in typically developing adolescents. American Journal of Drug & Alcohol Abuse , 39 (6), 345-355. doi:10.3109/00952990.2013.837057
Paulus, W. (2014). Lifestyle neuropathology: how our behavior harms our brains and what we can do about it.
Petersen, A. (2017). Brain maturation and cognitive development: Comparative and cross-cultural perspectives . Routledge.
Ron, D., & Barak, S. (2016). Molecular mechanisms underlying alcohol-drinking behaviors. Nature Reviews Neuroscience , 17 (9), 576.
Silveri, M. M. (2012). Adolescent Brain Development and Underage Drinking in the United States: Identifying Risks of Alcohol Use in College Populations. Harvard Review Of Psychiatry (Taylor & Francis Ltd) , 20 (4), 189-200. doi:10.3109/10673229.2012.714642
Squeglia, L. M., Tapert, S. F., Sullivan, E. V., Jacobus, J., Meloy, M. J., Rohlfing, T., & Pfefferbaum, A. (2015). Brain development in heavy-drinking adolescents. American journal of psychiatry , 172 (6), 531-542.
Sudheendran, N., Bake, S., Miranda, R. C., & Larin, K. V. (2013). Comparative assessments of the effects of alcohol exposure on fetal brain development using optical coherence tomography and ultrasound imaging. Journal of Biomedical Optics , 18 (2), 020506.
Tabakoff, B., & Hoffman, P. L. (2013). The neurobiology of alcohol consumption and alcoholism: an integrative history. Pharmacology Biochemistry and Behavior , 113 , 20-37.
Ungerer, M., Knezovich, J., & Ramsay, M. (2013). In Utero Alcohol Exposure, Epigenetic Changes, and Their Consequences. Alcohol Research: Current Reviews , 4 (1), 37-46.
Valenzuela, C. F., Morton, R. A., Diaz, M. R., & Topper, L. (2012). Does moderate drinking harm the fetal brain? Insights from animal models. Trends in Neurosciences , 35 (5), 284-292.
Appendix
Appendix A
Valenzuela, C. F., Morton, R. A., Diaz, M. R., & Topper, L. (2012). Does moderate drinking harm the fetal brain? Insights from animal models. Trends in neurosciences , 35 (5), 284-292. Retrieved from https://www.cell.com/trends/neurosciences/pdf/S0166-2236(12)00018-5.pdf
Fig 1 is a schematic representation of the rodent brain indicating examples of the effect of moderate developmental ethanol exposure in different brain regions.
Appendix B
Valenzuela, C. F., Morton, R. A., Diaz, M. R., & Topper, L. (2012). Does moderate drinking harm the fetal brain? Insights from animal models. Trends in neurosciences , 35 (5), 284-292. Retrieved from https://www.cell.com/trends/neurosciences/pdf/S0166-2236(12)00018-5.pdf
FIG.2 Schematic representation of ethanol exposure paradigms used in the studies reviewed here. To model first and second trimester ethanol exposure, pregnant rodents were exposed to moderate doses of ethanol using: (a) forced (i.e. ethanol-containing solutions were the only source of water and/or food or continuous or limited voluntary drinking paradigms. Voluntary drinking has also been used to expose monkeys to ethanol at different stages of pregnancy. (b) To model human exposure during the third trimester, rat pups and dams were exposed via ethanol vapor inhalation chambers or (c) pups were exposed via intraperitoneal or subcutaneous ethanol injections.
Appendix C
Valenzuela, C. F., Morton, R. A., Diaz, M. R., & Topper, L. (2012). Does moderate drinking harm the fetal brain? Insights from animal models. Trends in neurosciences , 35 (5), 284-292. Retrieved from https://www.cell.com/trends/neurosciences/pdf/S0166-2236(12)00018-5.pdf
Fig 3 Prenatal exposure to moderate ethanol levels impairs hippocampus-dependent memory and plasticity. (a) Left panel: schematic representation of the Morris Water Task, which measures training-induced changes in the time required to find a hidden platform (escape latency) in a tub full of opaque water. Animals typically use environmental cues to locate the platform. MPAE animals typically need longer time to find the escape platform. Right panel: escape latency was significantly increased in MPAE adult rat offspring [voluntary drinking paradigm during pregnancy; 5% ethanol (v/v) plus 0.066% saccharin (v/v) in water] and this effect was reversed by the H3 receptor inhibitor, ABT-239 [ 26 ]. (b) Left panel: schematic representation of the contextual fear conditioning test, which measures the duration of immobility (i.e. freezing time) in rodents re-exposed to the environmental context in which they had received a foot shock. MPAE animals typically freeze less (i.e. fail to link the context with the shock received previously) than control animals. Right panel: freezing in a contextual fear conditioning test was reduced in MPAE adult offspring and this effect was reversed by ABT-239. (c) Left panel: shown in the top panel is a schematic representation of a coronal section of the hippocampal formation showing the CA1 and CA3 hippocampal subfields, as well as the dentate gyrus (DG). A granule cell (GC) in the DG is shown in green. GCs receive glutamatergic input from the entorhinal cortex via the perforant path (PP). The lower panel illustrates a PP–GC synapse, including presynaptic H3 receptors and postsynaptic NMDA and AMPA receptors. Prenatal ethanol exposure may result in a long-lasting increase in the activity of H3 receptors, decreasing glutamate release and synaptic plasticity. Right panel: LTP recorded in the DG from urethane-anesthetized rats was impaired in MPAE adult offspring (grey circles) with respect to saccharin control group offspring (red circles) and this effect was reversed by the H3 receptor blocker ABT-239 (white circles). The graph shows the change in field excitatory postsynaptic potential (fEPSP) amplitude over a 1 h period. Reprinted with permission from Panels (a,b), © Wiley-Blackwell] and Panel (c), American Society for Pharmacology and Experimental Therapeutics.
