•+Alcohol+and+the+Brain

**General** • “A recent study done in the UK that classifies drugs by their overall harm scores, shows alcohol as the most harmful drug to users and others” (Alfonso-Loeches & Guerri, 2011, p.20).

•  Alcohol has a biphasic effect: While the level of alcohol in the blood is rising, the effect is stimulating and the individual feels an increase in sociability and well-being (Davison, Neale, Blankstein, & Flett, 2005, p.369). After the level of alcohol in the blood has peaked and begins declining, the effect is depressive and the individual may experience negative emotions (Davison et al.). Balance, motor coordination, speech and vision are impaired at this stage, and the sensation of pain may be reduced (Davison et al.). Ultimately, because of the depressive nature of alcohol, if too much alcohol is consumed during a given time period, the human brain and body will progress through states of decreasing awareness and arousal, to the point of death; see Figure 1 (Pearson Education, Inc., 2011, as cited in Lomp, 2012).

Figure 1.

• According to Wong, Ovaska and Korpi (1996), the major inhibitory neurotransmitter in the mammalian central nervous system is gamma-Aminobutyric acid, or GABA, and that many of the anxiolytic and sedative effects of alcohol result from its interaction with GABA receptors (Deitrich et al., 1989; Ticku, 1990; & Korpi, 1994, as cited in Wong et al., 1996).

• Alcohol increases levels of serotonin and dopamine, which may explain how it produces pleasurable effects (Davison et al., 2005).

• Alcohol inhibits glutamate receptors, which may be the mechanism by which it causes cognitive impairments such as slurred speech and memory loss (U.S. Department of Health and Human Services, 1994, as cited in Davison et al., 2005).

• Although alcohol is thought to stimulate aggression and increase sexual responsiveness, Davison et al. (2005) suggest that these reactions are more related to the beliefs of the individual drinking the alcohol than to the effects of the alcohol itself.

• Long-term consumption of alcohol adversely affects almost every tissue and organ in the body (Davison et al., 2005). Effects on the body were documented on the “Alcohol” page of this wiki; effects on the brain are as follows:

**Fetus** • Alcohol is one of the most common preventable causes of birth defects and developmental disorders, and the consumption of alcohol by the mother during pregnancy lead to a continuum of effects on the fetus and newborn (Alfonso-Loeches & Guerri, 2011), of which many effects remain with the individual for life.

• In the most extreme cases, the result is Fetal Alcohol Syndrome, or FAS, which is "... characterized by pre- and postnatal growth deficiencies, craniofacial anomalies and evidence of CNS dysfunction" (Alfonso-Loeches & Guerri, 2011, p.21). Specific effects of FAS include impairments in intelligence (mean estimate of IQ in the low 70s, but with a range between 20 and 120), memory, language, attention, learning, visuospatial abilities, executive functioning, motor skills, and adaptive functioning (Alfonso-Loeches & Guerri).

• In less extreme cases, the result is Fetal Alcohol Spectrum Disorder, or FASD, which results in dysfunctions of the central nervous system, including changes in brain structure and behaviour, and may not include the external physical deformities associated with FAS (Alfonso-Loeches & Guerri, 2011, p.21). Children with FASD may experience motor dysfunction including tremors, weak grasp, and difficulties in balance (Alfonso-Loeches & Guerri). They may also experience deficits in non-verbal memory, visual processing, and attention; ADHD is the most frequent comorbid psychiatric disorder in children who were exposed to alcohol during gestation (Alfonso-Loeches & Guerri).

• Children with FAS may have various types of brain damage, including agenesis of the corpus callosum and anterior commissure, and abnormalities of the basal ganglia, optic nerve, olfactory bulb, hippocampus, diencephalon, pituitary and neural tube (Alfonso-Loeches & Guerri, 2011). Certain parts of the brain are more vulnerable to the effects of alcohol than other, such as the parietal lobe, parts of the frontal lobe, and parts of the cerebellum (Alfonso-Loeches & Guerri). In the case of the cerebellum, children with FAS and FASD have been noted to have reduced surface area and volume of this part of the brain (Alfonso-Loeches & Guerri).

<span style="font-family: Tahoma,Geneva,sans-serif;">• In a study of rats, Taira, Porkka-Heiskanen & Korpi (1992, as cited in Wong et al., 1996) demonstrated that neonatal administration of a GABA transaminase inhibitor led to an increase in "voluntary" alcohol consumption in adulthood. Such empirical research in humans would not likely pass the ethics review process, but in the event that this research is applicable to human fetuses or infants, it could provide a possible explanation for alcohol abuse among adults with FAS or FASD.

<span style="font-family: Tahoma,Geneva,sans-serif;">**Adolescents** <span style="font-family: Tahoma,Geneva,sans-serif;">• Adolescence is marked by another phase of brain development, and consequently, "...adolescents are more vulnerable [than adults] to the deleterious effects that alcohol has on brain functions and behaviour" (Alfonso-Loeches & Guerri, 2011, p.28).

<span style="font-family: Tahoma,Geneva,sans-serif;">• MRI studies have demonstrated abnormalities of the prefrontal cortex in adolescent binge drinkers, including a reduction in the integrity of white matter (<span style="font-family: Tahoma,Geneva,sans-serif;">Alfonso-Loeches & Guerri, 2011).

<span style="font-family: Tahoma,Geneva,sans-serif;">• The volume of the hippocampus, which is associated with learning and memory, has been demonstrated to be smaller in adolescents who began drinking at younger ages than those who began drinking later (Alfonso-Loeches & Guerri, 2011).

<span style="font-family: Tahoma,Geneva,sans-serif;">• Visual-spatial functioning and verbal and non-verbal information have shown alterations "...in adolescents who report alcohol episodes, or in adolescents with AUD [alcohol use disorders] during abstinence" (Alfonso-Loeches & Guerri, 2011, p. 28).

<span style="font-family: Tahoma,Geneva,sans-serif;">• Female adolescents are more sensitive to the adverse effects of alcohol than male adolescents; alcohol induces greater impairments in both brain functioning and gray matter volume for female adolescents than male adolescents (Alfonso-Loeches & Guerri, 2011).

<span style="font-family: Tahoma,Geneva,sans-serif;">**Adults** <span style="font-family: Tahoma,Geneva,sans-serif;">• Because alcohol is high in calories, heavy drinkers often eat less food. However, these calories provide no essential nutrients, and malnutrition often follows (Davison et al., 2005). Alcohol also impairs absorption and vitamins, and “in older chronic alcohol abusers, a deficiency of B-complex vitamins can cause amnestic syndrome” (Davison et al., 2005, p.370), which manifests itself as a drastic loss of long-term and short-term memory (Davison et al.).

<span style="font-family: Tahoma,Geneva,sans-serif;">• According to Pfefferman et al. (1998, as cited in Davison et al., 2005), a five-year longitudinal study found significant loss of grey matter from the temporal lobes. In addition, long-term alcohol abuse can lead to a reduction in gray matter in the frontal lobes, and women appear to be more susceptible to this than are men (Alfonso-Loeches & Guerri, 2011). Shorter-term alcohol abuse can also produce cognitive impairment, as was demonstrated by Sher et al. (1997, as cited in Davison et al., 2005) in alcohol-abusing college students who showed impairment on neuropsychological tests.

<span style="font-family: Tahoma,Geneva,sans-serif;">• Chronic, heavy drinkers may experience delirium tremens when the level of alcohol in their blood drops suddenly (Davison et al., 2005). Del<span style="font-family: Tahoma,Geneva,sans-serif;">irium tremens is characterized by delirium, tremors, and hallucinations, both visual and tactile (Davison et al.).

<span style="font-family: Tahoma,Geneva,sans-serif;">• Long-term alcohol consumption leads to adaptive changes in neurotransmitter systems involving glutamate, GABA, dopamine, and serotonin, as well as endogenous opioids and "the corticotrophin-releasing factor (CRF)" (Alfonso-Loeches & Guerri, 2011, p. 32). Changes in reinforcement, increased sensitivity to stress, and enhanced anxiety have all been linked to the adaptation of these systems to the chronic presence of alcohol, and are suspected to play a role in relapses among alcoholics who had been abstinent (Alfonso-Loeches & Guerri).

<span style="font-family: Tahoma,Geneva,sans-serif;">• In post-mortem studies of human alcoholic brains, alcoholics had reduced brain weight than non-drinking controls, and this loss of brain weight and volume was associated with loss of white matter, primarily in the frontal lobe (Alfonso-Loeches & Guerri, 2011). However, these studies were not always able to discern whether the structural changes in the examined brains were caused by alcohol abuse, or by exposure to alcohol in stages of early development (either prenatally, or during adolescence) (Alfonso-Loeches & Guerri).

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