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How alcohol work

Ethanol is an organic chemical that belongs to the chemical class of alcohols; it is also called ethyl alcohol, grain alcohol, methyl carbinol, and ethyl hydrate. The molecular formula of ethanol is C2H6O. Ethanol is used as a food, a drug, and in the manufacture of industrial and consumer products. The use of alcohol as a beverage at social events and festivals dates back to the ancient Egyptian, Mesopotamian, Greek, and Roman civilizations. Moderate alcohol use, up to two drinks per day for men and one drink per day for non-pregnant women and older people, is not harmful for most adults.

Pharmacokinetics of Ethanol

Ethanol is rapidly absorbed on ingestion; approximately 80–90% of ethanol is absorbed within 30–60 min, although food may delay the absorption for a longer period of time (4–6 h). Ethanol is both water- and lipid-soluble, easily penetrates the blood– brain barrier, and distributes into the brain and total body fluid. Approximately 90–98% of any consumed ethanol is oxidized by the liver, and 5–10% is excreted by the kidneys and lungs.
Ethanol can be a central nervous system (CNS) depressant. Mild ethanol intoxication (blood alcohol concentration, BAC, 0.05–0.15%) leads to the impairment of visual acuity, changes in mood and personality, decreased reaction time, and muscular incoordination. Severe ethanol intoxication (BAC 0.3–0.5%) exacerbates these problems and in addition brings about hypothermia, vomiting, nausea, hypoglycemia and convulsions, depressed reflexes, and death from respiratory or circulatory failure. Alcohol consumption during pregnancy can lead to a congenital malformation of the offspring, which is known as fetal alcohol syndrome. Affected infants often show mental deficiency, microcephaly, and irritability.

Alcohol Reinforcement
Alcohol's basic action on the CNS causes pleasant subjective effects or a high feeling. This mild euphoria produced by alcohol often reinforces alcohol drinking. Alcohol also relieves anxiety from stressful life situations by reducing the aversive physiological stimuli associated with anxiety and stress. The reinforcing effects of alcohol involve chemical communication between various neuronal systems, including opioidergic neurons in the CNS.

Alcoholism
Alcoholism, or alcohol dependence, normally refers to when a person loses control over his or her alcohol drinking and develops a tolerance to and dependence on alcohol. Whereas moderate alcohol consumption may relieve stress and improve psychological wellbeing, alcohol dependence and depression are a prevalent combination of psychiatric disorders among patients seeking treatment. The highest psychiatric comorbidity for people with alcohol dependence appears to be affective anxiety and antisocial personality disorders.

Behavioral Aspects
The stress-relieving action of alcohol has been well documented in human subjects. This anxiolytic action of alcohol led to the belief that the motivation for abusing this substance may be prompted by individuals' needs to cope with (relieve) stress. Stress is often defined as a process involving the perception of, interpretation of, and response to harmful, threatening, and challenging events. Psychosocially, it is defined as tensions or challenges that an organism faces; physiologically, it is the biological responses upregulated by exposure to stressors. People often use drugs to enhance mood and alleviate emotional distress, and the motivation to enhance mood is great in acute and chronic stress states. There is a link between the maladaptive stress response and drug addiction in vulnerable individuals who are exposed to stress. The maladaptive stress response includes high or low reactivity and sensitivity to stress stimuli, a slow biological recovery after the initiation of stress, and poor cognitive and behavioral coping. Individuals at high risk for alcoholism show a heightened physiological and subjective sensitivity to the stress-reducing effects of ethanol. In addition, genetic and individual vulnerability factors may influence the maladaptive stress response to increase the use of abusive substances. Clinical studies have suggested a link between genetically related risks for alcoholism and an alteration in the hypothalamic-pituitary-adrenal (HPA) axis. It has been shown that the capacity of the HPA axis to respond to stress ismore labile in family-historypositive individuals, and this may promote their use of ethanol to relieve stress.

Biochemical Aspects
Endogenous opioid peptide mediation of ethanol action Opioid deficiency may be partly responsible for the maladaptive stress response that may promote alcohol abuse in vulnerable humans following stress. A slow biological recovery of the HPA axis after the initiation of stress may be explained by the opioid deficiency hypothesis. After the perception of stress, the neuronal input converges on the corticotropin releasing hormone (CRH) neurons. These neurons secrete CRH into hypophysial portal circulation.
CRH then enters the pituitary and acts primarily on corticotrophs (and melanotrophs) to stimulate the release of adrenocorticotropic hormone (ACTH) and ¥â-endorphin from the pituitary gland. ACTH acts on the adrenal gland to release glucocorticoids. When the glucocorticoids reach threshold levels, it prevents CRH secretion and brings about homeostasis. The CRH-producing neurons receive signals through three major neurotransmitter systems: stimulatory input from serotonergic-producing neurons and inhibitory inputs from gamma-aminobutyric acid (GABA) neurons and ¥â-endorphin neurons. Because of the powerful inhibitory input of ¥â-endorphin neurons on CRH release, an acquired or inborn abnormality in ¥â-endorphin activity can be an important determinant of the magnitude of the stress response. More ¥â-endorphin activity allows the constrained stress response, whereas less ¥â-endorphin activity allows for a more labile stress response. If individuals at high risk for alcoholism have reduced functional ¥â-endorphin neurons, these opioid differences may explain why these individuals show slow biological recovery after the initiation of stress.
Three major groups of endogenous opioid peptides have been isolated and characterized: the endorphins from the ¥â-endorphin/ACTH precursor known as proopiomelanocortin, the enkephalin from the proenkephalin precursor, and the dynorphins and neoendorphins from the prodynorphin precursor. The 31-amino-acid peptide ¥â-endorphin, with a reasonably high affinity for the mu and delta forms of the opiate receptors, is present in high concentrations in the hypothalamus. The ¥â-endorphin-producing perikarya are located mainly in the ventromedial arcuate nucleus region, which projects to widespread brain structures, including many areas of the hypothalamus and the limbic system, where this opioid peptide has been proposed to function as a neurotransmitter or neuromodulator regulating a variety of brain functions.
These brain functions include psychomotor stimulation; positive reinforcement; adaptive processes; drinking, eating, and sexual behaviors; pituitary function; thermoregulation; nociception; and mood. It is generally believed that the endogenous opioid system mediates some of the reinforcing properties of ethanol. Neurobiological studies indicate that alcohol alters opioid peptide systems. Acute alcohol administration increases endorphin and enkephalin gene expression in discrete brain regions and increases the release of these peptides from the brain and pituitary in rodents. Chronic or binge alcohol administration decreases proopiomelanocortin gene expression and alters the diurnal rhythm of proopiomelanocortin gene expression, ¥â-endorphin release, hypothalamic levels of ¥â-endorphin, and opioid receptor affinity and binding. Opioid-receptor antagonists have been shown to decrease ethanol consumption. The extended amygdala is considered to be a site of the opioid action because a high proportion of cells in the medial nucleus of the amygdala and the bed nucleus of the stria terminalis express ¥ì- and ¥ä-opioid receptors. The extended amygdala is also a major brain area involved in excessive ethanol consumption.
The abnormal expression of opioid receptors in the brain is connected with the volitional ethanol consumption. ¥ì-Opioid receptor densities have been shown to be higher in the extended amygdala in alcohol-preferring rat and mouse strains. Selective ¥ì-opioidn receptor antagonists reduced ethanol drinking in selectively bred alcohol-preferring rats and normal rats. Targeted gene mutation (knockout) strategies have produced mice that lack either ¥ì- or ¥ä-opioid receptors. ¥ì-Opioid receptor knockout mice avoid alcohol, but d-opioid receptor knockout mice self-administer more alcohol. The excess alcohol administration in d-opioid receptor knockout mice is considered to be due to increased ¥ì-opioid receptor activity, because ¥ì- andd-opioid receptor systems may oppose one another.

Cellular action of ethanol on hypothalamic opioid peptides Using primary cultures of hypothalamic neurons, it has been shown that low concentrations of ethanol acutely stimulate ¥â-endorphin release from cultured hypothalamic neurons. Similarly, a single administration of ethanol acutely stimulated the plasma levels of ¥â-endorphin in male rats. However, an inhibitory effect of chronic ethanol on ¥â-endorphin secretion has been demonstrated in both in vivo and in vitro studies. Hypothalamic proopiomelanocortin gene expression also increases following acute ethanol, but it decreases following chronic ethanol in both in vivo and in vitro systems. These functional changes in ¥â-endorphin neurons following ethanol treatments parallel many behavioral changes observed following ethanol use in humans. It is proposed that by enhancing opioid activity, ethanol could compensate for constitutive deficiencies of endogenous opioids that may contribute to ethanol self-administration. In increasing the sensitivity of the opioid peptide as well as other neurotransmissions, ethanol could increase the rate of ethanol self-administration. Ethanol may produce tolerance and physical dependence, in part, by altering opioid neurotransmissions.
Studies using hypothalamic cells in primary cultures have elucidated primary transduction pathways for the ethanol action on ¥â-endorphin release. These studies suggest that acute ethanol stimulates ¥â-endorphin secretion, possibly by activating the cAMP cascade, protein kinase C (PKC), and Ca2+-dependent mechanisms (Figure 1). The ethanol action on the cAMP system appears to involve the inhibition of adenosine uptake, leading to increasing extracellular levels of adenosine and the activation of membrane adenosine receptors and, consequently, to an increase in cAMP production and ¥â-endorphin secretion. Acute ethanol action on ¥â-endorphin release also involves calcium entry via the activation of voltage-dependent calcium channels. Furthermore, acute ethanol stimulates the expression and translocation of ¥ä- and є-PKC isoforms to activate ¥â-endorphin release. In contrast to this, chronic ethanol causes the development of tolerance and desensitization of ¥â-endorphin neurons due to reduction in the production and translocation of ¥ä- and є-PKC isoforms and the production of intracellular levels of cAMP. The inhibitory effect of chronic ethanol on cAMP is a result of the development of heterologous desensitization of adenosine, prostaglandins, and adrenergic receptors on these neurons. Hence, the changes in signal transduction could be critical for the adaptation of ¥â-endorphin neurons to chronic ethanol exposure (Figure 1).

The effects of single or moderate ethanol administration (acute ethanol) and binge or long-term ethanol administration (chronic ethanol) on the ¥â-endorphin system.



Figure 1 The effects of single or moderate ethanol administration (acute ethanol) and binge or long-term ethanol administration (chronic ethanol) on the ¥â-endorphin system. Acute ethanol enhances and chronic ethanol suppresses ¥â-endorphin synthesis or release by altering the activity of key intracellular transducers (cAMP, Ca2+, and PKC). Up arrows symbolize upregulation; down arrows symbolize downregulation; IP3, inositol triphosphate; PI cycle, phosphatidylinositol cycle; PPi, inorganic pyrophosphate.


Genetic Aspects
Findings from twin, adoption, and cross-fostering studies and pedigree analyses have indicated that genetic and environmental factors plays an important role in determining an individual's vulnerability to alcoholism. Although a multitude of biological differences have been found as a function of a family history of alcoholism, a number of studies suggest that diminished endogenous hypothalamic opioid activity and opioid receptor polymorphisms may increase an individual's vulnerability to becoming an alcoholic.
Genetic studies have shown that a genetic predisposition toward alcohol drinking is accompanied by an altered plasma ¥â-endorphin response to alcohol. These studies have shown an altered opioid regulation of the HPA axis in family-history-alcoholism-positive individuals. Polymorphisms in opioid receptor genes and other opioid-regulated neurotransmitters has shown to be partly involved in the altered opioid regulation of the HPA axis in family-history-positive individuals. A common A118G nucleotide exchange in exon 1 of the ¥ì-opioid receptor has been shown to cause an Asn40Asp substitution polymorphism in the extracellular N-terminal domain of the ¥ì-opioid receptor. It is believed that opioid receptor polymorphisms decrease dopamine secretion, which contributes to the altered capacity of the HPA axis to respond to stress, and that this may promote the use of ethanol to relieve stress.


Alcohol Effects on the Developing Brain
Alcohol abuse during pregnancy has been shown to be deleterious to the normal structural development of the fetal brain. Animal studies have also shown that alcohol alters the number and the shape of neurons in the developing brain. The alcohol effects on the developing brain are believed to cause the behavioral abnormalities seen in alcohol-exposed offspring. Animal models have proven useful in determining how alcohol exposure during development affects behavior. Using rat as an animal model, research has shown that the neurotransmitter system that regulates neuroendocrine and autonomic responses to stress is especially vulnerable to ethanol during the developmental period. Behavioral and neurochemical studies indicate that defects in the ability of these rats to respond appropriately to stress appears to be due to alterations in the function of hypothalamic neurons, including ¥â-endorphin neurons and CRH neurons. The biological basis for the abnormalities in ¥â-endorphin neuronal functions in animals exposed to ethanol during the fetal period is unknown, but it presumably involves an alteration in ¥â-endorphin neuron growth and differentiation.
How ethanol affects ¥â-endorphin neuron growth, differentiation, and neuronal connection in theCNS is not well understood. Some recent studies suggested the possibility that ethanol may reduce the production of a neurotrophic factor necessary for ¥â-endorphin neuron growth and differentiation. One of the neurotrophic agents that affects ¥â-endorphin neuronal growth in cultures is cAMP. Using cells from the rat fetal hypothalamic tissues, it has been shown that cAMP increases ¥â-endorphin cell numbers and neurite growth by preventing programmed cell death. Ethanol reduces the production of cellular levels of cAMP and increases the secretion of transforming growth factor b1 and consequently upregulates the expression of proapoptotic genes and induces programmed cell death of these neurons. The loss of ¥â-endorphin neurons during the developmental period can lead to permanent opioid deficiency in the hypothalamus and abnormality in stress axis function.
G-proteins are membrane-bound proteins that regulate cellular adenylyl cyclase activity and maintain the production of intracellular cAMP. Recently, abnormalities in G-protein expression and adenylyl cyclase activity have been observed in lymphocytes and erythrocytes derived from alcohol-dependent individuals. Similar abnormalities in the cAMP-signaling system have been documented in high-drinking lines of rats. In nonalcoholic children of alcoholics, an enhanced expression of the stimulatory Gsa protein was observed in erythrocyte and lymphocyte membranes. It has been postulated that adenylyl cyclase and G-protein expression may be markers for vulnerability to alcoholism.



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