fbpx
Wikipedia

Alcohol (drug)

January 07, 2024

This article is about ethanol as a psychoactive or recreational substance. For the class of chemical compounds, see Alcohol (chemistry). For types and characteristics of alcoholic beverages from a cultural perspective, see Alcoholic drink. For medical uses of alcohols, see Alcohols (medicine). For the substance in general, see Ethanol.

Alcohol, sometimes referred to by the chemical name ethanol, is a depressant drug that is the active ingredient in fermented drinks such as beer, wine, and distilled spirits (hard liquor).[11] It is one of the oldest and most commonly consumed recreational drugs, causing the characteristic effects of alcohol intoxication ("drunkenness").[12] Among other effects, alcohol produces happiness and euphoria, decreased anxiety, increased sociability, sedation, impairment of cognitive, memory, motor, and sensory function, and generalized depression of central nervous system (CNS) function.

Ethanol
Clinical data
Pronunciation/ˈɛθənɒl/
Other namesAbsolute alcohol; Alcohol (USPTooltip United States Pharmacopeia); Cologne spirit; Drinking alcohol; Ethanol (JANTooltip Japanese Accepted Name); Ethylic alcohol; EtOH; Ethyl alcohol; Ethyl hydrate; Ethyl hydroxide; Ethylol; Grain alcohol; Hydroxyethane; Methylcarbinol
Dependence
liability		Moderate[1]
Addiction
liability		Moderate (10–15%)[2]
Routes of
administration		Common: Oral
Uncommon: suppository, inhalation, ocular, insufflation, injection[3]
Drug classAnalgesic; Depressants; Sedatives; Anxiolytics; Euphoriants; GABAA receptor positive modulators Neurotoxins;
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability80%+[4][5]
Protein bindingWeakly or not at all[4][5]
MetabolismLiver (90%):[6][8]
• Alcohol dehydrogenase
• MEOS (CYP2E1)
MetabolitesAcetaldehyde; Acetic acid; Acetyl-CoA; Carbon dioxide; Water; Ethyl glucuronide; Ethyl sulfate
Onset of actionPeak concentrations:[6][4]
• Range: 30–90 minutes
• Mean: 45–60 minutes
• Fasting: 30 minutes
Elimination half-lifeConstant-rate elimination at typical concentrations:[7][8][6]
• Range: 10–34 mg/dL/hour
• Mean (men): 15 mg/dL/hour
• Mean (women): 18 mg/dL/hr
At very high concentrations (t1/2): 4.0–4.5 hours[5][4]
Duration of action6–16 hours (amount of time that levels are detectable)[9]
Excretion• Major: metabolism (into carbon dioxide and water)[4]
• Minor: urine, breath, sweat (5–10%)[6][4]
Identifiers
  • ethanol
CAS Number
  • 64-17-5
PubChem CID
  • 702
IUPHAR/BPS
  • 2299
DrugBank
  • DB00898 Y
ChemSpider
  • 682 Y
UNII
  • 3K9958V90M
KEGG
  • D00068
ChEBI
  • CHEBI:16236 Y
ChEMBL
  • ChEMBL545 Y
PDB ligand
  • EOH (PDBe, RCSB PDB)
Chemical and physical data
FormulaC2H6O
Molar mass46.069 g·mol−1
3D model (JSmol)
  • Interactive image
Density0.7893 g/cm3 (at 20 °C)[10]
Melting point−114.14 ± 0.03 °C (−173.45 ± 0.05 °F) [10]
Boiling point78.24 ± 0.09 °C (172.83 ± 0.16 °F) [10]
Solubility in waterMiscible mg/mL (20 °C)
  • CCO
  • InChI=1S/C2H6O/c1-2-3/h3H,2H2,1H3
  • Key:LFQSCWFLJHTTHZ-UHFFFAOYSA-N

Ethanol is only one of several types of alcohol; other alcohols such as methanol and isopropyl alcohol are significantly more toxic.[11] A mild, brief exposure to isopropyl alcohol (which is only moderately more toxic than ethanol) is unlikely to cause any serious harm, but methanol is lethal even in small quantities, as little as 10–15 milliliters (2–3 teaspoons).[citation needed] However, several analogues that naturally occur as psychoactive alcohols in alcoholic drinks are less toxic than ethanol. Unlike primary alcohols like ethanol, tertiary alcohols cannot be oxidized into aldehyde or carboxylic acid metabolites, which are often toxic. For example, the tertiary alcohol 2M2B is 20 times more potent than ethanol, and has been used recreationally.

Alcohol has a variety of short-term and long-term adverse effects. Short-term adverse effects include generalized impairment of neurocognitive function, dizziness, nausea, vomiting, and hangover-like symptoms. Alcohol is addictive to humans, and can result in alcohol use disorder, dependence and withdrawal. It can have a variety of long-term adverse effects on health, such as liver and brain damage,[13][14][15] and its consumption can cause cancer.[16] The adverse effects of alcohol on health are most important when it is used in excessive quantities or with heavy frequency. However, some of them, such as increased risk of certain cancers, may occur even with light or moderate alcohol consumption.[17][18] In high amounts, alcohol may cause loss of consciousness or, in severe cases, death. In 2021, there were 2,627 deaths in the US due to alcohol poisoning.[19]

Alcohol works in the brain primarily by increasing the effects of γ-Aminobutyric acid (GABA),[20] the major inhibitory neurotransmitter in the brain; by facilitating GABA's actions, alcohol suppresses the activity of the CNS.[20] The substance also directly affects a number of other neurotransmitter systems including those of glutamate, glycine, acetylcholine, and serotonin.[21][22] The pleasurable effects of alcohol ingestion are the result of increased levels of dopamine and endogenous opioids in the reward pathways of the brain.[23][24] Alcohol also has toxic and unpleasant actions in the body, many of which are mediated by its byproduct acetaldehyde.[25]

Alcohol consumption recommendations edit

Main article: Alcohol consumption recommendations

The recommended maximum intake (or safe limits) of alcohol varies from no intake, to daily, weekly, or daily/weekly guidelines provided by health agencies of governments. The World Health Organization published a statement in The Lancet Public Health in April 2023 that "there is no safe amount that does not affect health".[26]

Social effects edit

 
Table from the 2010 DrugScience study ranking various drugs (legal and illegal) based on statements by drug-harm experts. This study rated alcohol the most harmful drug overall, and the only drug more harmful to others than to users.[27]
 
Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and legal services engaged in delphic analysis regarding 20 popular recreational substances. Alcohol was ranked 6th in dependence, 11th in physical harm, and 2nd in social harm.[28]

Alcohol causes a plethora of detrimental effects in society.[29] Many emergency room visits involve alcohol use.[29] As many as 15% of employees show problematic alcohol-related behaviors in the workplace, such as drinking before going to work or even drinking on the job.[29] Drunk dialing refers to an intoxicated person making phone calls that they would not likely make if sober. Alcohol availability and consumption rates and alcohol rates are positively associated with nuisance, loitering, panhandling, and disorderly conduct in open spaces.[30]

Alcohol use is stereotypically associated with crime,[30] both violent and non-violent.[29] Some crimes are uniquely tied to alcohol, such as public intoxication or underage drinking, while others are simply more likely to occur together with alcohol consumption. Crime perpetrators are much more likely to be intoxicated than crime victims. Many alcohol laws have been passed to criminalize various alcohol-related activities.[30][31] Underage drinking and drunk driving are the most prevalent alcohol‐specific offenses in the United States[30] and a major problem in many, if not most, countries worldwide.[32][33][34] About one-third of arrests in the United States involve alcohol misuse,[29] and arrests for alcohol-related crimes constitute a high proportion of all arrests made by police in the U.S. and elsewhere.[35] In general, programs aimed at reducing society's consumption of alcohol, including education in schools, are seen as an effective long-term solution. Strategies aiming to reduce alcohol consumption among adult offenders have various estimates of effectiveness.[36] Policing alcohol‐related street disorder and enforcing compliance checks of alcohol‐dispensing businesses has proven successful in reducing public perception of and fear of criminal activities.[30]

In the early 2000s, the monetary cost of alcohol-related crime in the United States alone has been estimated at over $205 billion, twice the economic cost of all other drug-related crimes.[37] In a similar period in the United Kingdom, the cost of crime and its antisocial effects was estimated at £7.3 billion.[36] Another estimate for the UK for yearly cost of alcohol-related crime suggested double that estimate, at between £8 and 13 billion.[38] Risky patterns of drinking are particularly problematic in and around Russia, Mexico and some parts of Africa.[39] Alcohol is more commonly associated with both violent and non-violent crime than are drugs like marijuana.[29]

Alcohol-related crimes edit

Main article: Alcohol-related crime

Violent crime edit

Main article: Violent crime

The World Health Organization has noted that out of social problems created by the harmful use of alcohol, "crime and violence related to alcohol consumption" are likely the most significant issue.[39] In the United States, 15% of robberies, 63% of intimate partner violence incidents, 37% of sexual assaults, 45–46% of physical assaults and 40–45% of homicides (murders) involved use of alcohol.[40][37] A 1983 study for the United States found that 54% of violent crime perpetrators, arrested in that country, had been consuming alcohol before their offenses.[35] In 2002, it was estimated that 1 million violent crimes in the U.S. were related to alcohol use.[29] More than 43% of violent encounters with police involve alcohol.[29] Alcohol is implicated in more than two-thirds of cases of intimate partner violence.[29] Studies also suggest there may be links between alcohol abuse and child abuse.[30] In the United Kingdom, in 2015/2016, 39% of those involved in violent crimes were under alcohol influence.[41] International studies are similar, with an estimate that 63% of violent crimes worldwide involves the use of alcohol.[37]

The relation between alcohol and violence is not yet fully understood, as its impact on different individuals varies.[citation needed] Studies and theories of alcohol abuse suggest, among others, that use of alcohol likely reduces the offender's perception and awareness of consequences of their actions.[42][30][35][43] Heavy drinking is associated with vulnerability to injury, marital discord, and domestic violence.[29] Moderate drinkers are more frequently engaged in intimate violence than are light drinkers and abstainers, however generally it is heavy and/or binge drinkers who are involved in the most chronic and serious forms of aggression. Research found that factors that increase the likelihood of alcohol‐related violence include difficult temperament, hyperactivity, hostile beliefs, history of family violence, poor school performance, delinquent peers, criminogenic beliefs about alcohol's effects, impulsivity, and antisocial personality disorder. The odds, frequency, and severity of physical attacks are all positively correlated with alcohol use. In turn, violence decreases after behavioral marital alcoholism treatment.[30]

Automobile accidents edit

Main articles: Drunk driving and Driving under influence
 
An Estonian billboard warning against drunk driving

A 2002 study found 41% of people fatally injured in traffic accidents were in alcohol-related crashes.[44] Misuse of alcohol is associated with more than 40% of deaths that occur in automobile accidents every year.[29] The risk of a fatal car accident increases exponentially with the level of alcohol in the driver's blood.[45]

Most countries have passed laws prohibiting driving a motor vehicle while impaired by alcohol. In the U.S., these crimes are generally referred to as Driving under the influence (DUI), although there are many naming variations among jurisdictions, such as driving while intoxicated (DWI).[46] With alcohol consumption, a drunk driver's level of intoxication is typically determined by a measurement of blood alcohol content or BAC; but this can also be expressed as a breath test measurement, often referred to as a BrAC. A BAC or BrAC measurement in excess of the specific threshold level, such as 0.08% in the U.S.,[47] defines the criminal offense with no need to prove impairment.[48] In some jurisdictions, there is an aggravated category of the offense at a higher BAC level, such as 0.12%, 0.15% or 0.25%. In many jurisdictions, police officers can conduct field tests of suspects to look for signs of intoxication.

Criminologist Hung‐En Sung has concluded in 2016 that with regards to reducing drunk driving, law enforcement has not generally proven to be effective. Worldwide, the majority of those driving under the influence do not end up arrested. At least two thirds of alcohol‐involved fatalities involve repeat drinking drivers. Sung, commenting on measures for controlling drunk driving and alcohol‐related accidents, noted that the ones that have proven effective include "lowering legal blood alcohol concentrations, controlling liquor outlets, nighttime driving curfews for minors, educational treatment programs combined with license suspension for offenders, and court monitoring of high‐risk offenders."[30]

Sexual assault edit

Main article: Alcohol and sex

Alcohol abuse increases the risk of individuals either experiencing or perpetrating sexual violence and risky, casual sex.[49] Caffeinated alcoholic drinks are particularly implicated.[50]

Often, a victim becomes incapacitated due to having consumed alcohol, which then facilitates sexual assault or rape, a crime known as drug-facilitated sexual assault.[51][52] Over 50% of reported rapes involve alcohol.[clarification needed][29] Alcohol remains the most commonly used predator drug,[53][54] and is said to be used in the majority of sexual assaults.[42] Many assailants use alcohol because their victims often willingly imbibe it, and can be encouraged to drink enough to lose inhibitions or consciousness. Sex with an unconscious victim is considered rape in most if not all jurisdictions, and some assailants have committed "rapes of convenience" whereby they have assaulted a victim after he or she had become unconscious from drinking too much.[55]

Public drunkenness edit

Main article: Public intoxication
 
Drunkard passed out on a bench

Public drunkenness or intoxication is a common problem in many jurisdictions. Public intoxication laws vary widely by jurisdiction, but include public nuisance laws, open-container laws, and prohibitions on drinking alcohol in public or certain areas. The offenders are often lower class individuals and this crime has a very high recidivism rate, with numerous instances of repeated instances of the arrest, jail, release without treatment cycle. The high number of arrests for public drunkenness often reflects rearrests of the same offenders.[35]

Methanol-laced alcohol edit

Main article: Methanol poisoning outbreaks

Methanol is not produced in toxic amounts by fermentation of sugars from grain starches. However, outbreaks of methanol poisoning have occurred when methanol is used to lace moonshine (bootleg liquor).[56] This is commonly done to bulk up the original product to gain profit. Because of its similarities in both appearance and odor to ethanol (the alcohol in beverages), it is difficult to differentiate between the two.

Methanol has a high toxicity in humans. If as little as 10 mL of pure methanol is ingested, for example, it can break down into formic acid, which can cause permanent blindness by destruction of the optic nerve, and 30 mL is potentially fatal,[57] although the median lethal dose is typically 100 mL (3.4 fl oz) (i.e. 1–2 mL/kg body weight of pure methanol[58]). Reference dose for methanol is 0.5 mg/kg/day.[59] Toxic effects take hours to start, and effective antidotes can often prevent permanent damage.[57]

Social benefits edit

Research on the societal benefits of alcohol is rare, but studies suggests there are benefits.[60] Alcohol consumption while socializing increases occurrences of Duchenne smiling, talking, and social bonding, even when participants are unaware of their alcohol consumption or lack thereof.[61] In a study of the UK, regular drinking was correlated with happiness, feeling that life was worthwhile, and satisfaction with life. According to a causal path analysis, alcohol consumption was not the cause, but rather satisfaction with life resulted in greater happiness and an inclination to visit pubs and develop a regular drinking venue. City centre bars were distinguished by their focus on maximizing alcohol sales. Community pubs had less variation in visible group sizes and longer, more focused conversations than those in city centre bars. Drinking regularly at a community pub led to higher trust in others and better networking with the local community, compared to non-drinkers and city centre bar drinkers.[60]

Health effects edit

Main articles: Alcohol and health and Alcoholism § Moderate drinking
See also: Health effects of wine

Alcohol has a variety of short-term and long-term adverse effects. It also has reinforcement-related adverse effects, including addiction, dependence, and withdrawal. Alcohol use is directly related to considerable morbidity and mortality, for instance due to overdose and alcohol-related health problems.[62] The World Health Organization advises that there is no safe level of alcohol consumption.[63]

Short-term effects edit

Main article: Short-term effects of alcohol consumption
 
Symptoms of varying BAC levels. Additional symptoms may occur.

The amount of ethanol in the body is typically quantified by blood alcohol content (BAC); weight of ethanol per unit volume of blood. Small doses of ethanol, in general, are stimulant-like[64] and produce euphoria and relaxation; people experiencing these symptoms tend to become talkative and less inhibited, and may exhibit poor judgement. At higher dosages (BAC > 1 gram/liter), ethanol acts as a central nervous system (CNS) depressant,[64] producing at progressively higher dosages, impaired sensory and motor function, slowed cognition, stupefaction, unconsciousness, and possible death. Ethanol is commonly consumed as a recreational substance, especially while socializing, due to its psychoactive effects.

Central nervous system impairment edit

Alcohol causes generalized CNS depression, is a positive allosteric GABAA modulator and is associated and related with cognitive, memory, motor, and sensory impairment. It slows and impairs cognition and reaction time and the cognitive skills, impairs judgement, interferes with motor function resulting in motor incoordination, loss of balance, confusion, sedation, numbness and slurred speech, impairs memory formation, and causes sensory impairment. At high concentrations, it can induce amnesia, analgesia, spins, stupor, and unconsciousness as result of high levels of ethanol in blood.

At very high concentrations, alcohol can cause anterograde amnesia, markedly decreased heart rate, pulmonary aspiration, positional alcohol nystagmus, respiratory depression, shock, coma and death can result due to profound suppression of CNS function alcohol overdose and can finish in consequent dysautonomia.

Gastrointestinal effects edit

 
Diagram of mucosal layer

Alcohol can cause nausea and vomiting in sufficiently high amounts (varying by person).

Alcohol stimulates gastric juice production, even when food is not present, and as a result, its consumption stimulates acidic secretions normally intended to digest protein molecules. Consequently, the excess acidity may harm the inner lining of the stomach. The stomach lining is normally protected by a mucosal layer that prevents the stomach from, essentially, digesting itself. However, in patients who have a peptic ulcer disease (PUD), this mucosal layer is broken down. PUD is commonly associated with the bacteria Helicobacter pylori, which secretes a toxin that weakens the mucosal wall, allowing acid and protein enzymes to penetrate the weakened barrier. Because alcohol stimulates the stomach to secrete acid, a person with PUD should avoid drinking alcohol on an empty stomach. Drinking alcohol causes more acid release, which further damages the already-weakened stomach wall.[65] Complications of this disease could include a burning pain in the abdomen, bloating and in severe cases, the presence of dark black stools indicate internal bleeding.[66] A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation.[66]

Ingestion of alcohol can initiate systemic pro-inflammatory changes through two intestinal routes: (1) altering intestinal microbiota composition (dysbiosis), which increases lipopolysaccharide (LPS) release, and (2) degrading intestinal mucosal barrier integrity – thus allowing LPS to enter the circulatory system. The major portion of the blood supply to the liver is provided by the portal vein. Therefore, while the liver is continuously fed nutrients from the intestine, it is also exposed to any bacteria and/or bacterial derivatives that breach the intestinal mucosal barrier. Consequently, LPS levels increase in the portal vein, liver and systemic circulation after alcohol intake. Immune cells in the liver respond to LPS with the production of reactive oxygen species, leukotrienes, chemokines and cytokines. These factors promote tissue inflammation and contribute to organ pathology.[67]

Allergic-like reactions edit

Main articles: Alcohol-induced respiratory reactions and Alcohol flush reaction
See also: Short-term effects of alcohol consumption § Allergic reaction-like symptoms

Ethanol-containing beverages can cause alcohol flush reactions, exacerbations of rhinitis and, more seriously and commonly, bronchoconstriction in patients with a history of asthma, and in some cases, urticarial skin eruptions, and systemic dermatitis. Such reactions can occur within 1–60 minutes of ethanol ingestion, and may be caused by:[68]

  • genetic abnormalities in the metabolism of ethanol, which can cause the ethanol metabolite, acetaldehyde, to accumulate in tissues and trigger the release of histamine, or
  • true allergy reactions to allergens occurring naturally in, or contaminating, alcoholic beverages (particularly wine and beer), and
  • other unknown causes.

Overdose edit

Main article: Alcohol intoxication

Symptoms of ethanol overdose may include nausea, vomiting, CNS depression, coma, acute respiratory failure, or death. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3–0.4%.[69] Death from ethanol consumption is possible when blood alcohol levels reach 0.4%. A blood level of 0.5% or more is commonly fatal. The oral median lethal dose (LD50) of ethanol in rats is 5,628 mg/kg. Directly translated to human beings, this would mean that if a person who weighs 70 kg (150 lb) drank a 500 mL (17 US fl oz) glass of pure ethanol, they would theoretically have a 50% risk of dying.

Long-term effects edit

Main article: Long-term effects of alcohol

Prolonged heavy consumption of alcohol can cause significant permanent damage to the brain and other organs, resulting in dysfunction or death.

Brain damage edit

Main articles: Alcohol-related brain damage, Long-term impact of alcohol on the brain, and Neurotoxin

Alcohol can cause brain damage, Wernicke's encephalopathy and Alcoholic Korsakoff syndrome which frequently occur simultaneously, known as Wernicke–Korsakoff syndrome.[70] Lesions, or brain abnormalities, are typically located in the diencephalon which result in anterograde and retrograde amnesia, or memory loss.[70]

Liver damage edit

Main articles: Alcoholic liver disease, Cirrhosis, Hepatotoxin, Alcoholic hepatitis, and Fatty liver disease

During the metabolism of alcohol via the respective dehydrogenases, nicotinamide adenine dinucleotide (NAD) is converted into reduced NAD. Normally, NAD is used to metabolize fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in alcohol use disorder) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called cirrhosis.

Birth defects edit

Main article: Fetal alcohol spectrum disorder

Ethanol is classified as a teratogen.[medical citation needed] According to the U.S. Centers for Disease Control and Prevention (CDC), alcohol consumption by women who are not using birth control increases the risk of fetal alcohol syndrome. The CDC currently recommends complete abstinence from alcoholic beverages for women of child-bearing age who are pregnant, trying to become pregnant, or are sexually active and not using birth control.[71]

Cancer edit

Main article: Alcohol and cancer

The International Agency for Research on Cancer lists ethanol in alcoholic beverages as a Group 1 carcinogen in humans and argues that "There is sufficient evidence and research showing the carcinogenicity of acetaldehyde (the major metabolite of ethanol) which is excreted by the liver enzyme when one drinks alcohol."[72] In 2020, alcohol was estimated to cause 750,000 cases of cancer worldwide, particularly esophagus, liver, and breast cancer.[73]

Other effects edit

Frequent drinking of alcoholic beverages is a major contributing factor in cases of elevated blood levels of triglycerides.[74]

Alcoholism edit

Main article: Alcoholism
 
Early 20th century Dutch poster about the dangers of alcoholism

Alcoholism or its medical diagnosis alcohol use disorder refers to alcohol addiction, alcohol dependence, dipsomania, and/or alcohol abuse. It is a major problem and many health problems as well as death can result from excessive alcohol use.[29][62] Alcohol dependence is linked to a lifespan that is reduced by about 12 years relative to the average person.[29] In 2004, it was estimated that 4% of deaths worldwide were attributable to alcohol use.[62] Deaths from alcohol are split about evenly between acute causes (e.g., overdose, accidents) and chronic conditions.[62] The leading chronic alcohol-related condition associated with death is alcoholic liver disease.[62] Alcohol dependence is also associated with cognitive impairment and organic brain damage.[29] Some researchers have found that even one alcoholic drink a day increases an individual's risk of health problems by 0.4%.[75]

Two or more consecutive alcohol-free days a week have been recommended to improve health and break dependence.[76][77]

Alcohol withdrawal syndrome edit
Main articles: Alcohol withdrawal syndrome and Delirium tremens

Discontinuation of alcohol after extended heavy use and associated tolerance development (resulting in dependence) can result in withdrawal. Alcohol withdrawal can cause confusion, paranoia, anxiety, insomnia, agitation, tremors, fever, nausea, vomiting, autonomic dysfunction, seizures, and hallucinations. In severe cases, death can result. Delirium tremens is a condition that requires people with a long history of heavy drinking to undertake an alcohol detoxification regimen.

Interactions edit

See also: Caffeinated alcoholic drink and Nicotini

Alcohol can intensify the sedation caused by other CNS depressants such as barbiturates, benzodiazepines, opioids, nonbenzodiazepines/Z-drugs (such as zolpidem and zopiclone), antipsychotics, sedative antihistamines, and certain antidepressants.[69] It interacts with cocaine in vivo to produce cocaethylene, another psychoactive substance which may be substantially more cardiotoxic than either cocaine or alcohol by themselves.[78][additional citation(s) needed] Ethanol enhances the bioavailability of methylphenidate (elevated plasma dexmethylphenidate).[79][irrelevant citation] In combination with cannabis, ethanol increases plasma tetrahydrocannabinol levels, which suggests that ethanol may increase the absorption of tetrahydrocannabinol.[80]

Disulfiram-like drugs edit

Main article: Disulfiram-like drug

Disulfiram edit

Disulfiram inhibits the enzyme acetaldehyde dehydrogenase, which in turn results in buildup of acetaldehyde, a toxic metabolite of ethanol with unpleasant effects. The medication or drug is commonly used to treat alcohol use disorder, and results in immediate hangover-like symptoms upon consumption of alcohol, this effect is widely known as disulfiram effect.

Metronidazole edit

Metronidazole is an antibacterial agent that kills bacteria by damaging cellular DNA and hence cellular function.[81] Metronidazole is usually given to people who have diarrhea caused by Clostridium difficile bacteria. Patients who are taking metronidazole are sometimes advised to avoid alcohol, even after 1 hour following the last dose. Although older data suggested a possible disulfiram-like effect of metronidazole, newer data has challenged this and suggests it does not actually have this effect.

Alcohol induced dose dumping (AIDD) edit

Main article: Dose dumping

This dose dumping effect is an unintended rapid release of large amounts of a given drug, when administered through a modified-release dosage while co-ingesting ethanol.[82] This is considered a pharmaceutical disadvantage due to the high risk of causing drug-induced toxicity by increasing the absorption and serum concentration above the therapeutic window of the drug. The best way to prevent this interaction is by avoiding the co-ingestion of both substances or using specific controlled-release formulations that are resistant to AIDD.

Methanol and ethylene glycol edit

Main articles: Methanol, Ethylene glycol, and Methanol toxicity

The rate-limiting steps for the elimination of ethanol are in common with certain other substances. As a result, the blood alcohol concentration can be used to modify the rate of metabolism of methanol and ethylene glycol. Methanol itself is not highly toxic, but its metabolites formaldehyde and formic acid are; therefore, to reduce the rate of production and concentration of these harmful metabolites, ethanol can be ingested.[83] Ethylene glycol poisoning can be treated in the same way.

Pharmacology edit

Dynamics edit

See also: Alcohol intoxication § GABAA receptors, and Calcium channel blocker § Ethanol

The principal mechanism of action for ethanol has proven elusive and remains not fully understood.[20][84] Identifying molecular targets for ethanol has proven unusually difficult, in large part due to its unique biochemical properties.[84] Specifically, ethanol is a very low molecular weight compound and is of exceptionally low potency in its actions, causing effects only at very high (millimolar mM) concentrations.[84][85] For these reasons, unlike with most drugs, it has not yet been possible to employ traditional biochemical techniques to directly assess the binding of ethanol to receptors or ion channels.[84][85] Instead, researchers have had to rely on functional studies to elucidate the actions of ethanol.[84] Moreover, although it has been established that ethanol modulates ion channels to mediate its effects,[22] ion channels are complex proteins, and their interactions and functions are complicated by diverse subunit compositions and regulation by conserved cellular signals (e.g. signaling lipids).[20][84]

Much progress has been made in understanding the pharmacodynamics of ethanol over the last few decades.[21][84] While no binding sites have been identified and established unambiguously for ethanol at present, it appears that it affects ion channels, in particular ligand-gated ion channels, to mediate its effects in the CNS.[20][21][22][84] Ethanol has specifically been found in functional assays to enhance or inhibit the activity of a variety of ion channels, including the GABAA receptor, the ionotropic glutamate AMPA, kainate, and NMDA receptors, the glycine receptor,[86] the nicotinic acetylcholine receptors,[87] the serotonin 5-HT3 receptor, voltage-gated calcium channels, and BK channels, among others.[20][21][22][88][89] However, many of these actions have been found to occur only at very high concentrations that may not be pharmacologically significant at recreational doses of ethanol, and it is unclear how or to what extent each of the individual actions is involved in the effects of ethanol.[84] In any case, ethanol has long shown a similarity in its effects to positive allosteric modulators of the GABAA receptor like benzodiazepines, barbiturates, and various general anesthetics.[20][84] Indeed, ethanol has been found to enhance GABAA receptor-mediated currents in functional assays.[20][84] In accordance, it is theorized and widely believed that the primary mechanism of action is as a GABAA receptor positive allosteric modulator.[20][84] However, the diverse actions of ethanol on other ion channels may be and indeed likely are involved in its effects as well.[21][84]

In 2007, it was discovered that ethanol potentiates extrasynaptic δ subunit-containing GABAA receptors at behaviorally relevant (as low as 3 mM) concentrations.[20][84][90] This is in contrast to previous functional assays of ethanol on γ subunit-containing GABAA receptors, which it enhances only at far higher concentrations (> 100 mM) that are in excess of recreational concentrations (up to 50 mM).[20][84][91] Ro15-4513, a close analogue of the benzodiazepine antagonist flumazenil (Ro15-1788), has been found to bind to the same site as ethanol and to competitively displace it in a saturable manner.[84][90] In addition, Ro15-4513 blocked the enhancement of δ subunit-containing GABAA receptor currents by ethanol in vitro.[84] In accordance, the drug has been found to reverse many of the behavioral effects of low-to-moderate doses of ethanol in rodents, including its effects on anxiety, memory, motor behavior, and self-administration.[84][90] Taken together, these findings suggest a binding site for ethanol on subpopulations of the GABAA receptor with specific subunit compositions via which it interacts with and potentiates the receptor.[20][84][90][92]

A 2019 study showed the accumulation of an unnatural lipid phosphatidylethanol (PEth) competes with PIP2 agonist sites on lipid-gated ion channels.[93] This presents a novel indirect mechanism and suggests that a metabolite, not the ethanol itself, can affect the primary targets of ethanol intoxication. Many of the primary targets of ethanol are known to bind PIP2 including GABAA receptors,[94] but the role of PEth will need to be investigated for each of the primary targets.

Rewarding and reinforcing actions edit

The reinforcing effects of alcohol consumption are mediated by acetaldehyde generated by catalase and other oxidizing enzymes such as cytochrome P-4502E1 in the brain.[95] Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the mesolimbic dopamine system.[96]

Ethanol's rewarding and reinforcing (i.e., addictive) properties are mediated through its effects on dopamine neurons in the mesolimbic reward pathway, which connects the ventral tegmental area to the nucleus accumbens (NAcc).[97][98] One of ethanol's primary effects is the allosteric inhibition of NMDA receptors and facilitation of GABAA receptors (e.g., enhanced GABAA receptor-mediated chloride flux through allosteric regulation of the receptor).[99] At high doses, ethanol inhibits most ligand-gated ion channels and voltage-gated ion channels in neurons as well.[99]

With acute alcohol consumption, dopamine is released in the synapses of the mesolimbic pathway, in turn heightening activation of postsynaptic D1 receptors.[97][98] The activation of these receptors triggers postsynaptic internal signaling events through protein kinase A, which ultimately phosphorylate cAMP response element binding protein (CREB), inducing CREB-mediated changes in gene expression.[97][98]

With chronic alcohol intake, consumption of ethanol similarly induces CREB phosphorylation through the D1 receptor pathway, but it also alters NMDA receptor function through phosphorylation mechanisms;[97][98] an adaptive downregulation of the D1 receptor pathway and CREB function occurs as well.[97][98] Chronic consumption is also associated with an effect on CREB phosphorylation and function via postsynaptic NMDA receptor signaling cascades through a MAPK/ERK pathway and CAMK-mediated pathway.[98] These modifications to CREB function in the mesolimbic pathway induce expression (i.e., increase gene expression) of ΔFosB in the NAcc,[98] where ΔFosB is the "master control protein" that, when overexpressed in the NAcc, is necessary and sufficient for the development and maintenance of an addictive state (i.e., its overexpression in the nucleus accumbens produces and then directly modulates compulsive alcohol consumption).[98][100][101][102]

Relationship between concentrations and effects edit

Blood alcohol levels and effects[103]
mg/dL mM % v/v Effects
50 11 0.05% Euphoria, talkativeness, relaxation, happiness, gladness, pleasure, joyfulness.
100 22 0.1% Central nervous system depression, anxiety suppression, stress suppression, sedation, nausea, possible vomiting, impaired motor and sensory function,impaired memory impaired cognition
>140 30 >0.14% Decreased blood flow to brain, slurred speech, double or blurry vision.
300 65 0.3% Stupefaction, confusion, numbness, dizziness, loss of consciousness.
400 87 0.4% Ethylic intoxication, drunkenness, inebriation, alcohol poisoning or possible death.
500 109 >0.55% Unconsciousness, coma and death.

Recreational concentrations of ethanol are typically in the range of 1 to 50 mM.[91][20] Very low concentrations of 1 to 2 mM ethanol produce zero or undetectable effects except in alcohol-naive individuals.[91] Slightly higher levels of 5 to 10 mM, which are associated with light social drinking, produce measurable effects including changes in visual acuity, decreased anxiety, and modest behavioral disinhibition.[91] Further higher levels of 15 to 20 mM result in a degree of sedation and motor incoordination that is contraindicated with the operation of motor vehicles.[91] In jurisdictions in the U.S., maximum blood alcohol levels for legal driving are about 17 to 22 mM.[104][105] In the upper range of recreational ethanol concentrations of 20 to 50 mM, depression of the central nervous system is more marked, with effects including complete drunkenness, profound sedation, amnesia, emesis, hypnosis, and eventually unconsciousness.[91][104] Levels of ethanol above 50 mM are not typically experienced by normal individuals and hence are not usually physiologically relevant; however, such levels – ranging from 50 to 100 mM – may be experienced by alcoholics with high tolerance to ethanol.[91] Concentrations above this range, specifically in the range of 100 to 200 mM, would cause death in all people except alcoholics.[91]

List of known actions in the central nervous system edit

Ethanol has been reported to possess the following actions in functional assays at varying concentrations:[85]

Some of the actions of ethanol on ligand-gated ion channels, specifically the nicotinic acetylcholine receptors and the glycine receptor, are dose-dependent, with potentiation or inhibition occurring dependent on ethanol concentration.[85] This seems to be because the effects of ethanol on these channels are a summation of positive and negative allosteric modulatory actions.[85]

Kinetics edit

Absorption edit

Ethanol can be taken orally, by inhalation, rectally, or by injection (e.g., intravenous),[6][110] though it is typically ingested simply via oral administration.[4] The oral bioavailability of ethanol is around 80% or more.[4][5] In fasting volunteers, blood levels of ethanol increase proportionally with the dose of ethanol administered.[110] Blood alcohol concentrations may be estimated by dividing the amount of ethanol ingested by the body weight of the individual and correcting for water dilution.[6]

Onset edit

Peak circulating levels of ethanol are usually reached within a range of 30 to 90 minutes of ingestion, with an average of 45 to 60 minutes.[6][4] People who have fasted overnight have been found to reach peak ethanol concentrations more rapidly, at within 30 minutes of ingestion.[6]

The onset varies depends on the type of alcoholic drink:[111]

  • Vodka/tonic: 36 ± 10 minutes
  • Wine: 54 ± 14 minutes
  • Beer: 62 ± 23 minutes

Also, carbonated alcoholic drinks seem to have a shorter onset compare to flat drinks in the same volume. One theory is that carbon dioxide in the bubbles somehow speeds the flow of alcohol into the intestines.[112]

Food in the gastrointestinal system and hence gastric emptying is the most important factor that influences the absorption of orally ingested ethanol.[6][110] The absorption of ethanol is much more rapid on an empty stomach than with a full one.[6] The delay in ethanol absorption caused by food is similar regardless of whether food is consumed just before, at the same time, or just after ingestion of ethanol.[6] The type of food, whether fat, carbohydrates, or protein, also is of little importance.[110] Not only does food slow the absorption of ethanol, but it also reduces the bioavailability of ethanol, resulting in lower circulating concentrations.[6]

Distribution edit

Upon ingestion, ethanol is rapidly distributed throughout the body.[4] It is distributed most rapidly to tissues with the greatest blood supply.[6] As such, ethanol primarily affects the brain, liver, and kidneys.[4] Other tissues with lower circulation, such as bone, require more time for ethanol to distribute into.[6] Ethanol crosses biological membranes and the blood–brain barrier easily, through a simple process of passive diffusion.[4][110] The volume of distribution of ethanol is around .55 L/kg (0.53 US pt/lb).[4] It is only weakly or not at all plasma protein bound.[4][5]

Metabolism edit

See also: Ethanol metabolism, Alcohol dehydrogenase, and Aldehyde dehydrogenase

Approximately 90% of the metabolism of ethanol occurs in the liver.[6][8] This occurs predominantly via the enzyme alcohol dehydrogenase, which transforms ethanol into its metabolite acetaldehyde (ethanal).[6][8] Acetaldehyde is subsequently metabolized by the enzyme aldehyde dehydrogenase into acetate (ethanoate), which in turn is broken down into carbon dioxide and water.[6] Acetate also combines with coenzyme A to form acetyl-CoA, and hence may participate in metabolic pathways.[4] Alcohol dehydrogenase and aldehyde dehydrogenase are present at their highest concentrations in the liver, but are widely expressed throughout the body, and alcohol dehydrogenase may also be present in the stomach and small intestine.[4] Aside from alcohol dehydrogenase, the microsomal ethanol-oxidizing system (MEOS), specifically mediated by the cytochrome P450 enzyme CYP2E1, is the other major route of ethanol metabolism.[6][8] CYP2E1 is inducible by ethanol, so while alcohol dehydrogenase handles acute or low concentrations of ethanol, MEOS is predominant with higher concentrations or with repeated/chronic use.[6][8] A small amount of ethanol undergoes conjugation to form ethyl glucuronide and ethyl sulfate.[4] There may also be another metabolic pathway that metabolizes as much as 25 to 35% of ethanol at typical concentrations.[5]

At even low physiological concentrations, ethanol completely saturates alcohol dehydrogenase.[6] This is because ethanol has high affinity for the enzyme and very high concentrations of ethanol occur when it is used as a recreational substance.[6] For this reason, the metabolism of ethanol follows zero-order kinetics at typical physiological concentrations.[8] That is, ethanol does not have an elimination half-life (i.e., is not metabolized at an exponential rate), and instead, is eliminated from the circulation at a constant rate.[8][7] The mean elimination rates for ethanol are 15 mg/dL per hour for men and 18 mg/dL per hour for women, with a range of 10 to 34 mg/dL per hour.[8][6] At very high concentrations, such as in overdose, it has been found that the rate of elimination of ethanol is increased.[5] In addition, ethanol metabolism follows first-order kinetics at very high concentrations, with an elimination half-life of about 4 or 4.5 hours (which implies a clearance rate of approximately 6 L/hour/70 kg).[5][4] This seems to be because other processes, such as the MEOS/CYP2E1, also become involved in the metabolism of ethanol at higher concentrations.[4] However, the MEOS/CYP2E1 alone does not appear sufficient to fully explain the increase in ethanol metabolism rate.[5]

Some individuals have less effective forms of one or both of the metabolizing enzymes of ethanol, and can experience more marked symptoms from ethanol consumption than others.[113] However, those having acquired alcohol tolerance have a greater quantity of these enzymes, and metabolize ethanol more rapidly.[113]

Elimination edit

Ethanol is mainly eliminated from the body via metabolism into carbon dioxide and water.[6] Around 5 to 10% of ethanol that is ingested is eliminated unchanged in urine, breath, and sweat.[4] Transdermal alcohol that diffuses through the skin as insensible perspiration or is exuded as sweat (sensible perspiration) can be detected using wearable sensor technology[114] such as SCRAM ankle bracelet[115] or the more discreet ION Wearable.[116] Ethanol or its metabolites may be detectable in urine for up to 96 hours (3–5 days) after ingestion.[4]

Chemistry edit

Main articles: Ethanol and Ethanol (data page)
See also: Alcohols (medicine), Alcohol powder, Ethanol fermentation, and Yeast in winemaking

Ethanol is also known chemically as alcohol, ethyl alcohol, or drinking alcohol. It is a simple alcohol with a molecular formula of C2H6O and a molecular weight of 46.0684 g/mol. The molecular formula of ethanol may also be written as CH3−CH2−OH or as C2H5−OH. The latter can also be thought of as an ethyl group linked to a hydroxyl (alcohol) group and can be abbreviated as EtOH. Ethanol is a volatile, flammable, colorless liquid with a slight characteristic odor. Aside from its use as a psychoactive and recreational substance, ethanol is also commonly used as an antiseptic and disinfectant, a chemical and medicinal solvent, and a fuel.

Production edit

Ethanol is produced naturally as a byproduct of the metabolic processes of yeast and hence is present in any yeast habitat, including even endogenously in humans, but it does not cause raised blood alcohol content as seen in the rare medical condition auto-brewery syndrome (ABS). It is manufactured through hydration of ethylene or by brewing via fermentation of sugars with yeast (most commonly Saccharomyces cerevisiae). The sugars are commonly obtained from sources like steeped cereal grains (e.g., barley), grape juice, and sugarcane products (e.g., molasses, sugarcane juice). Ethanol–water mixture which can be further purified via distillation.

Analogues edit

See also: Comparison of psychoactive alcohols in alcoholic drinks

Ethanol has a variety of analogues, many of which have similar actions and effects. Methanol (methyl alcohol) and isopropyl alcohol (also called rubbing alcohol) are both toxic, and thus unsafe for human consumption.[11] Methanol is the most toxic alcohol; the toxicity of isopropyl alcohol lies between that of ethanol and methanol, and is about twice that of ethanol.[117] In general, higher alcohols are less toxic.[117] n-Butanol is reported to produce similar effects to those of ethanol and relatively low toxicity (one-sixth of that of ethanol in one rat study).[118][119] However, its vapors can produce eye irritation and inhalation can cause pulmonary edema.[117] Acetone (propanone) is a ketone rather than an alcohol, and is reported to produce similar toxic effects; it can be extremely damaging to the cornea.[117]

The tertiary alcohol tert-amyl alcohol (TAA), also known as 2-methylbutan-2-ol (2M2B), has a history of use as a hypnotic and anesthetic, as do other tertiary alcohols such as methylpentynol, ethchlorvynol, and chloralodol. Unlike primary alcohols like ethanol, these tertiary alcohols cannot be oxidized into aldehyde or carboxylic acid metabolites, which are often toxic, and for this reason, these compounds are safer in comparison.[120] Other relatives of ethanol with similar effects include chloral hydrate, paraldehyde, and many volatile and inhalational anesthetics (e.g., chloroform, diethyl ether, and isoflurane).

History edit

Main articles: Alcoholic drink § History, and History of alcoholic drinks

Alcohol was brewed as early as 7,000 to 6,650 BCE in northern China.[121] The earliest evidence of winemaking was dated at 6,000 to 5,800 BCE in Georgia in the South Caucasus.[122] Beer was likely brewed from barley as early as the 13,000 years ago in the Middle East.[123] Pliny the Elder wrote about the golden age of winemaking in Rome, the 2nd century BCE (200–100 BCE), when vineyards were planted.[124]

Society and culture edit

See also: Drinking culture

Ethanol is typically consumed as a recreational substance by mouth in the form of alcoholic beverages such as beer, wine, and spirits. It is commonly used in social settings due to its capacity to enhance sociability.

Drinking alcohol is generally socially acceptable and is legal in most countries, unlike with many other recreational substances. However, there are often restrictions on alcohol sale and use, for instance a minimum age for drinking and laws against public drinking and drinking and driving.[125] Alcohol has considerable societal and cultural significance and has important social roles in much of the world. Drinking establishments, such as bars and nightclubs, revolve primarily around the sale and consumption of alcoholic beverages, and parties, festivals, and social gatherings commonly involve alcohol consumption. Alcohol is related to various societal problems, including drunk driving, accidental injuries, sexual assaults, domestic abuse, and violent crime.[29] Alcohol remains illegal for sale and consumption in a number of countries, mainly in the Middle East. While some religions, including Islam, prohibit alcohol consumption, other religions, such as Christianity and Shinto, utilize alcohol in sacrament and libation.[126][127][128]

Legal status edit

Main articles: Alcohol law, Prohibition, and Legal drinking age

Alcohol consumption is fully legal and available in most countries of the world.[129] Home made alcoholic beverages with low alcohol content like wine, and beer is also legal in most countries, but distilling moonshine outside of a registered distillery remains illegal in most of them.

Some majority-Muslim countries, such as Saudi Arabia, Kuwait, Pakistan, Iran and Libya prohibit the production, sale, and consumption of alcoholic beverages because they are forbidden by Islam.[130][131][132] Also, laws banning alcohol consumption are found in some Indian states as well as some Native American reservations in the U.S.[129]

In addition, there are regulations on alcohol sales and use in many countries throughout the world.[129] For instance, the majority of countries have a minimum legal drinking age to purchase or consume alcoholic beverages, although there are often exceptions such as underage consumption of small amounts of alcohol with parental supervision. Also, some countries have bans on public intoxication.[129] Drinking while driving or intoxicated driving is frequently outlawed and it may be illegal to have an open container of alcohol or liquor bottle in an automobile, bus or aircraft.[129]

Standard drink edit

Main article: Standard drink

A standard drink is a measure of alcohol consumption representing a fixed amount of pure ethanol, used in relation to recommendations about alcohol consumption and its relative risks to health. The size of a standard drink varies from 8g to 20g across countries, but 10g alcohol (12.7 millilitres) is used in the World Health Organization (WHO) Alcohol Use Disorders Identification Test (AUDIT)'s questionnaire form example,[133] and has been adopted by more countries than any other amount.[134]

See also edit

References edit

  1. ^ WHO Expert Committee on Problems Related to Alcohol Consumption : second report. Geneva, Switzerland: World Health Organization. 2007. p. 23. ISBN 9789241209441. Retrieved 3 March 2015. ...alcohol dependence (is) a substantial risk of regular heavy drinking...
  2. ^ Vengeliene V, Bilbao A, Molander A, Spanagel R (May 2008). "Neuropharmacology of alcohol addiction". British Journal of Pharmacology. 154 (2): 299–315. doi:10.1038/bjp.2008.30. PMC 2442440. PMID 18311194. (Compulsive alcohol use) occurs only in a limited proportion of about 10–15% of alcohol users....
  3. ^ Gilman JM, Ramchandani VA, Crouss T, Hommer DW (January 2012). "Subjective and neural responses to intravenous alcohol in young adults with light and heavy drinking patterns". Neuropsychopharmacology. 37 (2): 467–77. doi:10.1038/npp.2011.206. PMC 3242308. PMID 21956438.
  4. ^ a b c d e f g h i j k l m n o p q r s t u Principles of Addiction: Comprehensive Addictive Behaviors and Disorders. Academic Press. 17 May 2013. pp. 162–. ISBN 978-0-12-398361-9.
  5. ^ a b c d e f g h i Holford NH (November 1987). "Clinical pharmacokinetics of ethanol". Clinical Pharmacokinetics. 13 (5): 273–92. doi:10.2165/00003088-198713050-00001. PMID 3319346. S2CID 19723995.
  6. ^ a b c d e f g h i j k l m n o p q r s t u v w Pohorecky LA, Brick J (1988). "Pharmacology of ethanol". Pharmacology & Therapeutics. 36 (2–3): 335–427. doi:10.1016/0163-7258(88)90109-x. PMID 3279433.
  7. ^ a b Becker CE (September 1970). "The clinical pharmacology of alcohol". California Medicine. 113 (3): 37–45. PMC 1501558. PMID 5457514.
  8. ^ a b c d e f g h i Levine B (2003). Principles of Forensic Toxicology. Amer. Assoc. for Clinical Chemistry. pp. 161–. ISBN 978-1-890883-87-4.
  9. ^ Iber FL (26 November 1990). Alcohol and Drug Abuse as Encountered in Office Practice. CRC Press. pp. 74–. ISBN 978-0-8493-0166-7.
  10. ^ a b c Haynes WM, ed. (2011). CRC Handbook of Chemistry and Physics (92nd ed.). Boca Raton, FL: CRC Press. p. 3.246. ISBN 1-4398-5511-0.
  11. ^ a b c Collins SE, Kirouac M (2013). "Alcohol Consumption". Encyclopedia of Behavioral Medicine. pp. 61–65. doi:10.1007/978-1-4419-1005-9_626. ISBN 978-1-4419-1004-2.
  12. ^ "10th Special Report to the U.S. Congress on Alcohol and Health: Highlights from Current Research" (PDF). National Institute of Health. National Institute on Alcohol Abuse and Alcoholism. June 2000. p. 134. Retrieved 21 October 2014. The brain is a major target for the actions of alcohol, and heavy alcohol consumption has long been associated with brain damage. Studies clearly indicate that alcohol is neurotoxic, with direct effects on nerve cells. Chronic alcohol abusers are at additional risk for brain injury from related causes, such as poor nutrition, liver disease, and head trauma.
  13. ^ Bruha R, Dvorak K, Petrtyl J (March 2012). "Alcoholic liver disease". World Journal of Hepatology. 4 (3): 81–90. doi:10.4254/wjh.v4.i3.81. PMC 3321494. PMID 22489260.
  14. ^ Brust JC (April 2010). "Ethanol and cognition: indirect effects, neurotoxicity and neuroprotection: a review". International Journal of Environmental Research and Public Health. 7 (4): 1540–57. doi:10.3390/ijerph7041540. PMC 2872345. PMID 20617045.
  15. ^ Venkataraman A, Kalk N, Sewell G, Ritchie CW, Lingford-Hughes A (March 2017). "Alcohol and Alzheimer's Disease-Does Alcohol Dependence Contribute to Beta-Amyloid Deposition, Neuroinflammation and Neurodegeneration in Alzheimer's Disease?". Alcohol and Alcoholism. 52 (2): 151–158. doi:10.1093/alcalc/agw092. hdl:10044/1/42603. PMID 27915236.
  16. ^ de Menezes RF, Bergmann A, Thuler LC (2013). "Alcohol consumption and risk of cancer: a systematic literature review". Asian Pacific Journal of Cancer Prevention. 14 (9): 4965–72. doi:10.7314/apjcp.2013.14.9.4965. PMID 24175760.
  17. ^ Bagnardi V, Rota M, Botteri E, Tramacere I, Islami F, Fedirko V, Scotti L, Jenab M, Turati F, Pasquali E, Pelucchi C, Bellocco R, Negri E, Corrao G, Rehm J, Boffetta P, La Vecchia C (February 2013). "Light alcohol drinking and cancer: a meta-analysis". Annals of Oncology. 24 (2): 301–8. doi:10.1093/annonc/mds337. PMID 22910838.
  18. ^ Yasinski, Emma, Even If You Don't Drink Daily, Alcohol Can Mess With Your Brain, Discover (magazine), January 12, 2021
  19. ^ Centers for Disease Control and Prevention. "Multiple Cause of Death, 2018-2021". National Vital Statistics System. National Center for Health Statistics. Retrieved 29 November 2023.
  20. ^ a b c d e f g h i j k l m Lobo IA, Harris RA (July 2008). "GABA(A) receptors and alcohol". Pharmacology Biochemistry and Behavior. 90 (1): 90–4. doi:10.1016/j.pbb.2008.03.006. PMC 2574824. PMID 18423561.
  21. ^ a b c d e Narahashi T, Kuriyama K, Illes P, Wirkner K, Fischer W, Mühlberg K, Scheibler P, Allgaier C, Minami K, Lovinger D, Lallemand F, Ward RJ, DeWitte P, Itatsu T, Takei Y, Oide H, Hirose M, Wang XE, Watanabe S, Tateyama M, Ochi R, Sato N (May 2001). "Neuroreceptors and ion channels as targets of alcohol". Alcoholism: Clinical and Experimental Research. 25 (5 Suppl ISBRA): 182S–188S. doi:10.1097/00000374-200105051-00030. PMID 11391069.
  22. ^ a b c d Olsen RW, Li GD, Wallner M, Trudell JR, Bertaccini EJ, Lindahl E, Miller KW, Alkana RL, Davies DL (March 2014). "Structural models of ligand-gated ion channels: sites of action for anesthetics and ethanol". Alcoholism: Clinical and Experimental Research. 38 (3): 595–603. doi:10.1111/acer.12283. PMC 3959612. PMID 24164436.
  23. ^ Charlet K, Beck A, Heinz A (2013). "The dopamine system in mediating alcohol effects in humans". Current Topics in Behavioral Neurosciences. 13: 461–88. doi:10.1007/7854_2011_130. ISBN 978-3-642-28719-0. PMID 21533679.
  24. ^ Méndez M, Morales-Mulia M (June 2008). "Role of mu and delta opioid receptors in alcohol drinking behaviour". Current Drug Abuse Reviews. 1 (2): 239–52. doi:10.2174/1874473710801020239. PMID 19630722.
  25. ^ Burcham PC (19 November 2013). An Introduction to Toxicology. Springer Science & Business Media. pp. 42–. ISBN 978-1-4471-5553-9.
  26. ^ "No level of alcohol consumption is safe for our health". World Health Organization. 4 January 2023.
  27. ^ Nutt DJ, King LA, Phillips LD (November 2010). "Drug harms in the UK: a multicriteria decision analysis". Lancet. 376 (9752): 1558–65. CiteSeerX 10.1.1.690.1283. doi:10.1016/S0140-6736(10)61462-6. PMID 21036393. S2CID 5667719.
  28. ^ Nutt D, King LA, Saulsbury W, Blakemore C (March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Lancet. 369 (9566): 1047–53. doi:10.1016/s0140-6736(07)60464-4. PMID 17382831. S2CID 5903121.
  29. ^ a b c d e f g h i j k l m n o p Butcher JN, Hooley JM, Mineka SM (25 June 2013). Abnormal Psychology. Pearson Education. p. 370. ISBN 978-0-205-97175-6.
  30. ^ a b c d e f g h i Sunga HE (2016). "Alcohol and Crime". The Blackwell Encyclopedia of Sociology. American Cancer Society. pp. 1–2. doi:10.1002/9781405165518.wbeosa039.pub2. ISBN 9781405165518.
  31. ^ Trevor B, Katy H (1 April 2005). Understanding Drugs, Alcohol And Crime. McGraw-Hill Education (UK). p. 6. ISBN 9780335212576.
  32. ^ . Law Office of Douglas Herring. 13 November 2017. Archived from the original on 22 September 2019. Retrieved 22 September 2019.
  33. ^ "Drunk Driving Increasing Concern Worldwide". Voice of America. Retrieved 22 September 2019.
  34. ^ Sweedler BM, Stewart K (2009). "Worldwide trends in alcohol and drug impaired driving". In Verster JC, Pandi-Perumal SR, Ramaekers JG, de Gier JJ (eds.). Drugs, Driving and Traffic Safety. Birkhäuser Basel. pp. 23–41. doi:10.1007/978-3-7643-9923-8_2. ISBN 9783764399238.
  35. ^ a b c d Clinard M, Meier R (14 February 2007). Sociology of Deviant Behavior. Cengage Learning. p. 273. ISBN 9780495093350.
  36. ^ a b McMurran M (3 October 2012). Alcohol-Related Violence: Prevention and Treatment. John Wiley & Sons. pp. 337–338. ISBN 9781118411063.
  37. ^ a b c McMurran M (3 October 2012). Alcohol-Related Violence: Prevention and Treatment. John Wiley & Sons. p. 37. ISBN 9781118411063.
  38. ^ . WHO. Archived from the original on 4 May 2014. Retrieved 22 September 2019.
  39. ^ a b "Global status report on alcohol and health" (PDF). World Health Organization. 2011.
  40. ^ "Alcohol-Related Crimes: Statistics and Facts". Alcohol Rehab Guide. Retrieved 3 September 2019.
  41. ^ "Alcohol statistics". Alcohol Change UK. Retrieved 22 September 2019.
  42. ^ a b Christopher P. Holstege, et al., eds. (25 October 2010). Criminal poisoning: clinical and forensic perspectives. Sudbury, Mass.: Jones and Bartlett Publishers. pp. 232. ISBN 978-0763744632.
  43. ^ Dingwall G (23 July 2013). Alcohol and Crime. Routledge. pp. 160–161. ISBN 9781134029709.
  44. ^ Hingson R, Winter M (2003). "Epidemiology and consequences of drinking and driving". Alcohol Research & Health. 27 (1): 63–78. PMC 6676697. PMID 15301401.
  45. ^ Naranjo CA, Bremner KE (January 1993). "Behavioural correlates of alcohol intoxication". Addiction. 88 (1): 25–35. doi:10.1111/j.1360-0443.1993.tb02761.x. PMID 8448514.
  46. ^ Driving Under the Influence: A Report to Congress on Alcohol Limits. U.S. Department of Transportation, National Highway Traffic Safety Administration. 1992. pp. 1–.
  47. ^ "Legislative History of .08 per se Laws – NHTSA". NHTSA. National Highway Traffic Safety Administration. July 2001. Retrieved 21 July 2017.
  48. ^ Nelson B. . NVPAC. Advisory Council for Prosecuting Attorneys. Archived from the original on 22 April 2017. Retrieved 3 July 2017.
  49. ^ Chersich MF, Rees HV (January 2010). "Causal links between binge drinking patterns, unsafe sex and HIV in South Africa: its time to intervene". International Journal of STD & AIDS. 21 (1): 2–7. doi:10.1258/ijsa.2000.009432. PMID 20029060. S2CID 3100905.
  50. ^ Ball NJ, Miller KE, Quigley BM, Eliseo-Arras RK (April 2021). "Alcohol Mixed With Energy Drinks and Sexually Related Causes of Conflict in the Barroom". Journal of Interpersonal Violence. 36 (7–8): 3353–3373. doi:10.1177/0886260518774298. PMID 29779427. S2CID 29150434.
  51. ^ Hall JA, Moore CB (July 2008). "Drug facilitated sexual assault—a review". Journal of Forensic and Legal Medicine. 15 (5): 291–7. doi:10.1016/j.jflm.2007.12.005. PMID 18511003.
  52. ^ Beynon CM, McVeigh C, McVeigh J, Leavey C, Bellis MA (July 2008). "The involvement of drugs and alcohol in drug-facilitated sexual assault: a systematic review of the evidence". Trauma, Violence & Abuse. 9 (3): 178–88. doi:10.1177/1524838008320221. PMID 18541699. S2CID 27520472.
  53. ^ Alcohol Is Most Common 'Date Rape' Drug 17 October 2007 at the Wayback Machine. Medicalnewstoday.com. Retrieved on 1 June 2011.
  54. ^ Schwartz RH, Milteer R, LeBeau MA (June 2000). "Drug-facilitated sexual assault ('date rape')". Southern Medical Journal. 93 (6): 558–61. doi:10.1097/00007611-200093060-00002. PMID 10881768.
  55. ^ Date Rape. Survive.org.uk (20 March 2000). Retrieved on 1 June 2011.
  56. ^ "Application to Include Fomepizole on the WHO Model List of Essential Medicines" (PDF). November 2012. p. 10.
  57. ^ a b Vale A (2007). "Methanol". Medicine. 35 (12): 633–4. doi:10.1016/j.mpmed.2007.09.014.
  58. ^ . Antizol. Archived from the original on 5 October 2011. Retrieved 11 October 2011. dead link
  59. ^ Methanol (CASRN 67–56–1)
  60. ^ a b Dunbar RI, Launay J, Wlodarski R, Robertson C, Pearce E, Carney J, MacCarron P (June 2017). "Functional Benefits of (Modest) Alcohol Consumption". Adaptive Human Behavior and Physiology. 3 (2): 118–133. doi:10.1007/s40750-016-0058-4. PMC 7010365. PMID 32104646.
  61. ^ Sayette MA, Creswell KG, Dimoff JD, Fairbairn CE, Cohn JF, Heckman BW, et al. (August 2012). "Alcohol and group formation: a multimodal investigation of the effects of alcohol on emotion and social bonding". Psychological Science. 23 (8): 869–878. doi:10.1177/0956797611435134. PMC 5462438. PMID 22760882.
  62. ^ a b c d e Friedman HS (26 August 2011). The Oxford Handbook of Health Psychology. Oxford University Press, USA. pp. 699–. ISBN 978-0-19-534281-9.
  63. ^ "No level of alcohol consumption is safe for our health". www.who.int. Retrieved 13 October 2023.
  64. ^ a b Hendler RA, Ramchandani VA, Gilman J, Hommer DW (2013). "Stimulant and sedative effects of alcohol". Current Topics in Behavioral Neurosciences. 13: 489–509. doi:10.1007/7854_2011_135. ISBN 978-3-642-28719-0. PMID 21560041.
  65. ^ Overview of Peptic Ulcer Disease: Etiology and Pathophysiology. Medscape.com. Retrieved 27 April 2013.
  66. ^ a b Peptic Ulcer Disease (Stomach Ulcers) Cause, Symptoms, Treatments. Webmd.com. Retrieved 27 April 2013.
  67. ^ Patel S, Behara R, Swanson GR, Forsyth CB, Voigt RM, Keshavarzian A (October 2015). "Alcohol and the Intestine". Biomolecules. 5 (4): 2573–88. doi:10.3390/biom5042573. PMC 4693248. PMID 26501334.
  68. ^ Adams KE, Rans TS (December 2013). "Adverse reactions to alcohol and alcoholic beverages". Annals of Allergy, Asthma & Immunology. 111 (6): 439–45. doi:10.1016/j.anai.2013.09.016. PMID 24267355.
  69. ^ a b Yost DA (2002). (PDF). Postgraduate Medicine Online. 112 (6). Archived from the original (PDF) on 14 December 2010. Retrieved 29 September 2007.
  70. ^ a b Arts NJ, Walvoort SJ, Kessels RP (27 November 2017). "Korsakoff's syndrome: a critical review". Neuropsychiatric Disease and Treatment. 13: 2875–2890. doi:10.2147/NDT.S130078. PMC 5708199. PMID 29225466.
  71. ^ "More than 3 million US women at risk for alcohol-exposed pregnancy". Centers for Disease Control and Prevention. 2 February 2016. Retrieved 3 March 2016. 'drinking any alcohol at any stage of pregnancy can cause a range of disabilities for their child,' said Coleen Boyle, Ph.D., director of CDC's National Center on Birth Defects and Developmental Disabilities.
  72. ^ Agents Classified by the IARC Monographs, Volumes 1–111 25 October 2011 at the Wayback Machine. monographs.iarc.fr
  73. ^ "Report Details Alcohol's Global Cancer Burden - NCI". www.cancer.gov. 12 August 2021. Retrieved 13 October 2023.
  74. ^ . American Heart Association. Archived from the original on 27 August 2007. Retrieved 4 September 2007.
  75. ^ Bakalar N (27 August 2018). "How Much Alcohol Is Safe to Drink? None, Say These Researchers". The New York Times. Retrieved 17 September 2018.
  76. ^ Tomlinson A (26 June 2018). "Tips and Tricks on How to Cut Down on the Booze". The West Australian. Seven West Media (WA). Retrieved 22 March 2019.
  77. ^ . British Liver Trust. Archived from the original on 11 July 2019. Retrieved 22 March 2019.
  78. ^ Laizure SC, Mandrell T, Gades NM, Parker RB (January 2003). "Cocaethylene metabolism and interaction with cocaine and ethanol: role of carboxylesterases". Drug Metabolism and Disposition. 31 (1): 16–20. doi:10.1124/dmd.31.1.16. PMID 12485948.
  79. ^ Sakalo VS, Romanenko AM, Klimenko IA, Persidskiĭ I (1988). "Effects of chemotherapy on regional metastases of non-seminomatous tumors of the testis". Voprosy Onkologii. 34 (10): 1219–24. PMID 3188424.
  80. ^ Lukas SE, Orozco S (October 2001). "Ethanol increases plasma Delta(9)-tetrahydrocannabinol (THC) levels and subjective effects after marihuana smoking in human volunteers". Drug and Alcohol Dependence. 64 (2): 143–9. doi:10.1016/S0376-8716(01)00118-1. PMID 11543984.
  81. ^ Repchinsky C (ed.) (2012). Compendium of pharmaceuticals and specialties, Ottawa: Canadian Pharmacists Association.[full citation needed]
  82. ^ D'Souza S, Mayock S, Salt A (December 2017). "A review of in vivo and in vitro aspects of alcohol-induced dose dumping". AAPS Open. 3 (1). doi:10.1186/s41120-017-0014-9. ISSN 2364-9534.
  83. ^ McCoy HG, Cipolle RJ, Ehlers SM, Sawchuk RJ, Zaske DE (November 1979). "Severe methanol poisoning. Application of a pharmacokinetic model for ethanol therapy and hemodialysis". The American Journal of Medicine. 67 (5): 804–7. doi:10.1016/0002-9343(79)90766-6. PMID 507092.
  84. ^ a b c d e f g h i j k l m n o p q r s Santhakumar V, Wallner M, Otis TS (May 2007). "Ethanol acts directly on extrasynaptic subtypes of GABAA receptors to increase tonic inhibition". Alcohol. 41 (3): 211–21. doi:10.1016/j.alcohol.2007.04.011. PMC 2040048. PMID 17591544.
  85. ^ a b c d e Spanagel R (April 2009). "Alcoholism: a systems approach from molecular physiology to addictive behavior". Physiological Reviews. 89 (2): 649–705. doi:10.1152/physrev.00013.2008. PMID 19342616.
  86. ^ a b c Söderpalm B, Lidö HH, Ericson M (November 2017). "The Glycine Receptor-A Functionally Important Primary Brain Target of Ethanol". Alcoholism: Clinical and Experimental Research. 41 (11): 1816–1830. doi:10.1111/acer.13483. PMID 28833225.
  87. ^ a b Wu J, Gao M, Taylor DH (March 2014). "Neuronal nicotinic acetylcholine receptors are important targets for alcohol reward and dependence". Acta Pharmacologica Sinica. 35 (3): 311–5. doi:10.1038/aps.2013.181. PMC 4647894. PMID 24464050.
  88. ^ Dopico AM, Bukiya AN, Kuntamallappanavar G, Liu J (2016). "Modulation of BK Channels by Ethanol". International Review of Neurobiology. 128: 239–79. doi:10.1016/bs.irn.2016.03.019. ISBN 978-0-12-803619-8. PMC 5257281. PMID 27238266.
  89. ^ a b c d e Möykkynen T, Korpi ER (July 2012). "Acute effects of ethanol on glutamate receptors". Basic & Clinical Pharmacology & Toxicology. 111 (1): 4–13. doi:10.1111/j.1742-7843.2012.00879.x. PMID 22429661.
  90. ^ a b c d Wallner M, Olsen RW (May 2008). "Physiology and pharmacology of alcohol: the imidazobenzodiazepine alcohol antagonist site on subtypes of GABAA receptors as an opportunity for drug development?". British Journal of Pharmacology. 154 (2): 288–98. doi:10.1038/bjp.2008.32. PMC 2442438. PMID 18278063.
  91. ^ a b c d e f g h Harrison NL, Skelly MJ, Grosserode EK, Lowes DC, Zeric T, Phister S, Salling MC (August 2017). "Effects of acute alcohol on excitability in the CNS". Neuropharmacology. 122: 36–45. doi:10.1016/j.neuropharm.2017.04.007. PMC 5657304. PMID 28479395.
  92. ^ Förstera B, Castro PA, Moraga-Cid G, Aguayo LG (2016). "Potentiation of Gamma Aminobutyric Acid Receptors (GABAAR) by Ethanol: How Are Inhibitory Receptors Affected?". Frontiers in Cellular Neuroscience. 10: 114. doi:10.3389/fncel.2016.00114. PMC 4858537. PMID 27199667.
  93. ^ Chung HW, Petersen EN, Cabanos C, Murphy KR, Pavel MA, Hansen AS, et al. (January 2019). "A Molecular Target for an Alcohol Chain-Length Cutoff". Journal of Molecular Biology. 431 (2): 196–209. doi:10.1016/j.jmb.2018.11.028. PMC 6360937. PMID 30529033.
  94. ^ Laverty D, Desai R, Uchański T, Masiulis S, Stec WJ, Malinauskas T, et al. (January 2019). "Cryo-EM structure of the human α1β3γ2 GABAA receptor in a lipid bilayer". Nature. 565 (7740): 516–520. Bibcode:2019Natur.565..516L. doi:10.1038/s41586-018-0833-4. PMC 6364807. PMID 30602789.
  95. ^ Karahanian E, Quintanilla ME, Tampier L, Rivera-Meza M, Bustamante D, Gonzalez-Lira V, Morales P, Herrera-Marschitz M, Israel Y (April 2011). "Ethanol as a prodrug: brain metabolism of ethanol mediates its reinforcing effects". Alcoholism: Clinical and Experimental Research. 35 (4): 606–12. doi:10.1111/j.1530-0277.2011.01439.x. PMC 3142559. PMID 21332529.
  96. ^ a b Melis M, Enrico P, Peana AT, Diana M (November 2007). "Acetaldehyde mediates alcohol activation of the mesolimbic dopamine system". The European Journal of Neuroscience. 26 (10): 2824–33. doi:10.1111/j.1460-9568.2007.05887.x. PMID 18001279. S2CID 25110014.
  97. ^ a b c d e "Alcoholism – Homo sapiens (human) Database entry". KEGG Pathway. 29 October 2014. Retrieved 9 February 2015.
  98. ^ a b c d e f g h Kanehisa Laboratories (29 October 2014). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014.
  99. ^ a b c d e Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 372. ISBN 978-0-07-148127-4.
  100. ^ Ruffle JK (November 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". The American Journal of Drug and Alcohol Abuse. 40 (6): 428–37. doi:10.3109/00952990.2014.933840. PMID 25083822. S2CID 19157711.
  101. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 15 (4): 431–43. doi:10.31887/DCNS.2013.15.4/enestler. PMC 3898681. PMID 24459410. Despite the Importance of Numerous Psychosocial Factors, at its Core, Drug Addiction Involves a Biological Process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement
  102. ^ Robison AJ, Nestler EJ (October 2011). "Transcriptional and epigenetic mechanisms of addiction". Nature Reviews. Neuroscience. 12 (11): 623–37. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194.
  103. ^ Pohorecky LA, Brick J (1988). "Pharmacology of ethanol". Pharmacology & Therapeutics. 36 (2–3): 335–427. doi:10.1016/0163-7258(88)90109-X. PMID 3279433.
  104. ^ a b Liu Y, Hunt WA (6 December 2012). The "Drunken" Synapse: Studies of Alcohol-Related Disorders. Springer Science & Business Media. pp. 40–. ISBN 978-1-4615-4739-6.
  105. ^ Rubin R, Strayer DS, Rubin E, McDonald JM (2008). Rubin's Pathology: Clinicopathologic Foundations of Medicine. Lippincott Williams & Wilkins. pp. 257–. ISBN 978-0-7817-9516-6.
  106. ^ Situmorang JH, Lin HH, Lo H, Lai CC (January 2018). "Role of neuronal nitric oxide synthase (nNOS) at medulla in tachycardia induced by repeated administration of ethanol in conscious rats". Journal of Biomedical Science. 25 (1): 8. doi:10.1186/s12929-018-0409-5. PMC 5791364. PMID 29382335.
  107. ^ Steffensen SC, Shin SI, Nelson AC, Pistorius SS, Williams SB, Woodward TJ, Park HJ, Friend L, Gao M, Gao F, Taylor DH, Foster Olive M, Edwards JG, Sudweeks SN, Buhlman LM, Michael McIntosh J, Wu J (September 2017). "α6 subunit-containing nicotinic receptors mediate low-dose ethanol effects on ventral tegmental area neurons and ethanol reward". Addiction Biology. 23 (5): 1079–1093. doi:10.1111/adb.12559. PMC 5849490. PMID 28901722.
  108. ^ Sitte H, Freissmuth M (2 August 2006). Neurotransmitter Transporters. Springer Science & Business Media. pp. 472–. ISBN 978-3-540-29784-0.
  109. ^ Allen-Gipson DS, Jarrell JC, Bailey KL, Robinson JE, Kharbanda KK, Sisson JH, Wyatt TA (May 2009). "Ethanol blocks adenosine uptake via inhibiting the nucleoside transport system in bronchial epithelial cells". Alcoholism: Clinical and Experimental Research. 33 (5): 791–8. doi:10.1111/j.1530-0277.2009.00897.x. PMC 2940831. PMID 19298329.
  110. ^ a b c d e Henri B, Kissin B (1996). The Pharmacology of Alcohol and Alcohol Dependence. Oxford University Press. pp. 18–. ISBN 978-0-19-510094-5.
  111. ^ Mitchell MC, Teigen EL, Ramchandani VA (May 2014). "Absorption and peak blood alcohol concentration after drinking beer, wine, or spirits". Alcoholism: Clinical and Experimental Research. 38 (5): 1200–1204. doi:10.1111/acer.12355. PMC 4112772. PMID 24655007.
  112. ^ "Champagne does get you drunk faster". New Scientist.
  113. ^ a b Agarwal DP, Goedde HW (April 1992). "Pharmacogenetics of alcohol metabolism and alcoholism". Pharmacogenetics. 2 (2): 48–62. doi:10.1097/00008571-199204000-00002. PMID 1302043.
  114. ^ Lansdorp B, Ramsay W, Hamidand R, Strenk E (May 2019). "Wearable Enzymatic Alcohol Biosensor". Sensors. 19 (10): 2380. Bibcode:2019Senso..19.2380L. doi:10.3390/s19102380. PMC 6566815. PMID 31137611.
  115. ^ "SCRAM CAM® Bracelet Alcohol Ankle Monitor". SCRAM Systems. Retrieved 19 March 2022.
  116. ^ "ION Wearable". ION Wearable. Retrieved 19 March 2022.
  117. ^ a b c d Philp RB (15 September 2015). Ecosystems and Human Health: Toxicology and Environmental Hazards, Third Edition. CRC Press. pp. 216–. ISBN 978-1-4987-6008-9.
  118. ^ n-Butanol (PDF), SIDS Initial Assessment Report, Geneva: United Nations Environment Programme, April 2005.
  119. ^ McCreery MJ, Hunt WA (July 1978). "Physico-chemical correlates of alcohol intoxication". Neuropharmacology. 17 (7): 451–61. doi:10.1016/0028-3908(78)90050-3. PMID 567755. S2CID 19914287.
  120. ^ Carey F (2000). Organic Chemistry (4 ed.). McGraw-Hill. ISBN 0-07-290501-8. Retrieved 5 February 2013.
  121. ^ McGovern PE, Zhang J, Tang J, Zhang Z, Hall GR, Moreau RA, Nuñez A, Butrym ED, Richards MP, Wang CS, Cheng G, Zhao Z, Wang C (December 2004). "Fermented beverages of pre- and proto-historic China". Proceedings of the National Academy of Sciences of the United States of America. 101 (51): 17593–8. Bibcode:2004PNAS..10117593M. doi:10.1073/pnas.0407921102. PMC 539767. PMID 15590771.
  122. ^ McGovern P, Jalabadze M, Batiuk S, Callahan MP, Smith KE, Hall GR, Kvavadze E, Maghradze D, Rusishvili N, Bouby L, Failla O, Cola G, Mariani L, Boaretto E, Bacilieri R, This P, Wales N, Lordkipanidze D (November 2017). "Early Neolithic wine of Georgia in the South Caucasus". Proceedings of the National Academy of Sciences of the United States of America. 114 (48): E10309–E10318. Bibcode:2017PNAS..11410309M. doi:10.1073/pnas.1714728114. PMC 5715782. PMID 29133421.
  123. ^ Rosso AM (2012). "Beer and wine in antiquity: beneficial remedy or punishment imposed by the Gods?". Acta medico-historica Adriatica. 10 (2): 237–62. PMID 23560753.
  124. ^ Brostrom GG, Brostrom JJ (30 December 2008). The Business of Wine: An Encyclopedia: An Encyclopedia. ABC-CLIO. pp. 6–. ISBN 978-0-313-35401-4.
  125. ^ Babor T, Caetano R, Casswell S, Edwards G, Giesbrecht N, Graham K, et al. (2010). Alcohol: No Ordinary Commodity: Research and Public Policy (2nd ed.). Oxford: Oxford University Press. ISBN 978-0-19-955114-9. OCLC 656362316.
  126. ^ Ruthven M (1997). Islam : a very short introduction. New York: Oxford University Press. ISBN 978-0-19-154011-0. OCLC 43476241.
  127. ^ "Eucharist | Definition, Symbols, Meaning, Significance, & Facts". Encyclopedia Britannica. Retrieved 3 August 2021.
  128. ^ Bocking B (1997). A popular dictionary of Shintō (Rev. ed.). Richmond, Surrey [U.K.]: Curzon Press. ISBN 0-7007-1051-5. OCLC 264474222.
  129. ^ a b c d e Boyle P (7 March 2013). Alcohol: Science, Policy and Public Health. OUP Oxford. pp. 363–. ISBN 978-0-19-965578-6.
  130. ^ "Getting a drink in Saudi Arabia". BBC News. BBC. 8 February 2001. Retrieved 7 July 2015.
  131. ^ "Can you drink alcohol in Saudi Arabia?". 1 August 2012. Retrieved 7 July 2015.
  132. ^ . Swifty.com. Archived from the original on 2 July 2015. Retrieved 7 July 2015.
  133. ^ "AUDIT The Alcohol Use Disorders Identification Test (Second Edition)" (pdf). WHO. 2001. Retrieved 2 January 2020.
  134. ^ Kalinowski A, Humphreys K (July 2016). "Governmental standard drink definitions and low-risk alcohol consumption guidelines in 37 countries". Addiction. 111 (7): 1293–1298. doi:10.1111/add.13341. PMID 27073140.

Further reading edit

External links edit

Pathophysiology of ethanol
Pharmacology of ethanol

January 07, 2024
alcohol, drug, this, article, about, ethanol, psychoactive, recreational, substance, class, chemical, compounds, alcohol, chemistry, types, characteristics, alcoholic, beverages, from, cultural, perspective, alcoholic, drink, medical, uses, alcohols, alcohols,. This article is about ethanol as a psychoactive or recreational substance For the class of chemical compounds see Alcohol chemistry For types and characteristics of alcoholic beverages from a cultural perspective see Alcoholic drink For medical uses of alcohols see Alcohols medicine For the substance in general see Ethanol Alcohol sometimes referred to by the chemical name ethanol is a depressant drug that is the active ingredient in fermented drinks such as beer wine and distilled spirits hard liquor 11 It is one of the oldest and most commonly consumed recreational drugs causing the characteristic effects of alcohol intoxication drunkenness 12 Among other effects alcohol produces happiness and euphoria decreased anxiety increased sociability sedation impairment of cognitive memory motor and sensory function and generalized depression of central nervous system CNS function EthanolClinical dataPronunciation ˈ ɛ 8 e n ɒ l Other namesAbsolute alcohol Alcohol USPTooltip United States Pharmacopeia Cologne spirit Drinking alcohol Ethanol JANTooltip Japanese Accepted Name Ethylic alcohol EtOH Ethyl alcohol Ethyl hydrate Ethyl hydroxide Ethylol Grain alcohol Hydroxyethane MethylcarbinolDependenceliabilityModerate 1 AddictionliabilityModerate 10 15 2 Routes ofadministrationCommon Oral Uncommon suppository inhalation ocular insufflation injection 3 Drug classAnalgesic Depressants Sedatives Anxiolytics Euphoriants GABAA receptor positive modulators Neurotoxins ATC codeV03AZ01 WHO Legal statusLegal statusAU Unscheduled BR Unscheduled CA Unscheduled DE Unscheduled NZ Unscheduled UK General sales list GSL OTC US Unscheduled UN Unscheduled EU Unscheduled In general Legal for recreational use except in Muslim countries of Middle East and parts of North Africa and South AsiaPharmacokinetic dataBioavailability80 4 5 Protein bindingWeakly or not at all 4 5 MetabolismLiver 90 6 8 Alcohol dehydrogenase MEOS CYP2E1 MetabolitesAcetaldehyde Acetic acid Acetyl CoA Carbon dioxide Water Ethyl glucuronide Ethyl sulfateOnset of actionPeak concentrations 6 4 Range 30 90 minutes Mean 45 60 minutes Fasting 30 minutesElimination half lifeConstant rate elimination at typical concentrations 7 8 6 Range 10 34 mg dL hour Mean men 15 mg dL hour Mean women 18 mg dL hrAt very high concentrations t1 2 4 0 4 5 hours 5 4 Duration of action6 16 hours amount of time that levels are detectable 9 Excretion Major metabolism into carbon dioxide and water 4 Minor urine breath sweat 5 10 6 4 IdentifiersIUPAC name ethanolCAS Number64 17 5PubChem CID702IUPHAR BPS2299DrugBankDB00898 YChemSpider682 YUNII3K9958V90MKEGGD00068ChEBICHEBI 16236 YChEMBLChEMBL545 YPDB ligandEOH PDBe RCSB PDB Chemical and physical dataFormulaC 2H 6OMolar mass46 069 g mol 13D model JSmol Interactive imageDensity0 7893 g cm3 at 20 C 10 Melting point 114 14 0 03 C 173 45 0 05 F 10 Boiling point78 24 0 09 C 172 83 0 16 F 10 Solubility in waterMiscible mg mL 20 C SMILES CCOInChI InChI 1S C2H6O c1 2 3 h3H 2H2 1H3Key LFQSCWFLJHTTHZ UHFFFAOYSA NEthanol is only one of several types of alcohol other alcohols such as methanol and isopropyl alcohol are significantly more toxic 11 A mild brief exposure to isopropyl alcohol which is only moderately more toxic than ethanol is unlikely to cause any serious harm but methanol is lethal even in small quantities as little as 10 15 milliliters 2 3 teaspoons citation needed However several analogues that naturally occur as psychoactive alcohols in alcoholic drinks are less toxic than ethanol Unlike primary alcohols like ethanol tertiary alcohols cannot be oxidized into aldehyde or carboxylic acid metabolites which are often toxic For example the tertiary alcohol 2M2B is 20 times more potent than ethanol and has been used recreationally Alcohol has a variety of short term and long term adverse effects Short term adverse effects include generalized impairment of neurocognitive function dizziness nausea vomiting and hangover like symptoms Alcohol is addictive to humans and can result in alcohol use disorder dependence and withdrawal It can have a variety of long term adverse effects on health such as liver and brain damage 13 14 15 and its consumption can cause cancer 16 The adverse effects of alcohol on health are most important when it is used in excessive quantities or with heavy frequency However some of them such as increased risk of certain cancers may occur even with light or moderate alcohol consumption 17 18 In high amounts alcohol may cause loss of consciousness or in severe cases death In 2021 there were 2 627 deaths in the US due to alcohol poisoning 19 Alcohol works in the brain primarily by increasing the effects of g Aminobutyric acid GABA 20 the major inhibitory neurotransmitter in the brain by facilitating GABA s actions alcohol suppresses the activity of the CNS 20 The substance also directly affects a number of other neurotransmitter systems including those of glutamate glycine acetylcholine and serotonin 21 22 The pleasurable effects of alcohol ingestion are the result of increased levels of dopamine and endogenous opioids in the reward pathways of the brain 23 24 Alcohol also has toxic and unpleasant actions in the body many of which are mediated by its byproduct acetaldehyde 25 Contents 1 Alcohol consumption recommendations 2 Social effects 2 1 Alcohol related crimes 2 1 1 Violent crime 2 1 2 Automobile accidents 2 1 3 Sexual assault 2 1 4 Public drunkenness 2 1 5 Methanol laced alcohol 2 2 Social benefits 3 Health effects 3 1 Short term effects 3 1 1 Central nervous system impairment 3 1 2 Gastrointestinal effects 3 1 3 Allergic like reactions 3 1 4 Overdose 3 2 Long term effects 3 2 1 Brain damage 3 2 2 Liver damage 3 2 3 Birth defects 3 2 4 Cancer 3 2 5 Other effects 3 2 6 Alcoholism 3 2 6 1 Alcohol withdrawal syndrome 4 Interactions 4 1 Disulfiram like drugs 4 1 1 Disulfiram 4 1 2 Metronidazole 4 2 Alcohol induced dose dumping AIDD 4 3 Methanol and ethylene glycol 5 Pharmacology 5 1 Dynamics 5 1 1 Rewarding and reinforcing actions 5 1 2 Relationship between concentrations and effects 5 1 3 List of known actions in the central nervous system 5 2 Kinetics 5 2 1 Absorption 5 2 1 1 Onset 5 2 2 Distribution 5 2 3 Metabolism 5 2 4 Elimination 6 Chemistry 6 1 Production 6 2 Analogues 7 History 8 Society and culture 8 1 Legal status 8 2 Standard drink 9 See also 10 References 11 Further reading 12 External linksAlcohol consumption recommendations editMain article Alcohol consumption recommendations The recommended maximum intake or safe limits of alcohol varies from no intake to daily weekly or daily weekly guidelines provided by health agencies of governments The World Health Organization published a statement in The Lancet Public Health in April 2023 that there is no safe amount that does not affect health 26 Social effects edit nbsp Table from the 2010 DrugScience study ranking various drugs legal and illegal based on statements by drug harm experts This study rated alcohol the most harmful drug overall and the only drug more harmful to others than to users 27 nbsp Addiction experts in psychiatry chemistry pharmacology forensic science epidemiology and the police and legal services engaged in delphic analysis regarding 20 popular recreational substances Alcohol was ranked 6th in dependence 11th in physical harm and 2nd in social harm 28 Alcohol causes a plethora of detrimental effects in society 29 Many emergency room visits involve alcohol use 29 As many as 15 of employees show problematic alcohol related behaviors in the workplace such as drinking before going to work or even drinking on the job 29 Drunk dialing refers to an intoxicated person making phone calls that they would not likely make if sober Alcohol availability and consumption rates and alcohol rates are positively associated with nuisance loitering panhandling and disorderly conduct in open spaces 30 Alcohol use is stereotypically associated with crime 30 both violent and non violent 29 Some crimes are uniquely tied to alcohol such as public intoxication or underage drinking while others are simply more likely to occur together with alcohol consumption Crime perpetrators are much more likely to be intoxicated than crime victims Many alcohol laws have been passed to criminalize various alcohol related activities 30 31 Underage drinking and drunk driving are the most prevalent alcohol specific offenses in the United States 30 and a major problem in many if not most countries worldwide 32 33 34 About one third of arrests in the United States involve alcohol misuse 29 and arrests for alcohol related crimes constitute a high proportion of all arrests made by police in the U S and elsewhere 35 In general programs aimed at reducing society s consumption of alcohol including education in schools are seen as an effective long term solution Strategies aiming to reduce alcohol consumption among adult offenders have various estimates of effectiveness 36 Policing alcohol related street disorder and enforcing compliance checks of alcohol dispensing businesses has proven successful in reducing public perception of and fear of criminal activities 30 In the early 2000s the monetary cost of alcohol related crime in the United States alone has been estimated at over 205 billion twice the economic cost of all other drug related crimes 37 In a similar period in the United Kingdom the cost of crime and its antisocial effects was estimated at 7 3 billion 36 Another estimate for the UK for yearly cost of alcohol related crime suggested double that estimate at between 8 and 13 billion 38 Risky patterns of drinking are particularly problematic in and around Russia Mexico and some parts of Africa 39 Alcohol is more commonly associated with both violent and non violent crime than are drugs like marijuana 29 Alcohol related crimes edit Main article Alcohol related crime Violent crime edit Main article Violent crime The World Health Organization has noted that out of social problems created by the harmful use of alcohol crime and violence related to alcohol consumption are likely the most significant issue 39 In the United States 15 of robberies 63 of intimate partner violence incidents 37 of sexual assaults 45 46 of physical assaults and 40 45 of homicides murders involved use of alcohol 40 37 A 1983 study for the United States found that 54 of violent crime perpetrators arrested in that country had been consuming alcohol before their offenses 35 In 2002 it was estimated that 1 million violent crimes in the U S were related to alcohol use 29 More than 43 of violent encounters with police involve alcohol 29 Alcohol is implicated in more than two thirds of cases of intimate partner violence 29 Studies also suggest there may be links between alcohol abuse and child abuse 30 In the United Kingdom in 2015 2016 39 of those involved in violent crimes were under alcohol influence 41 International studies are similar with an estimate that 63 of violent crimes worldwide involves the use of alcohol 37 The relation between alcohol and violence is not yet fully understood as its impact on different individuals varies citation needed Studies and theories of alcohol abuse suggest among others that use of alcohol likely reduces the offender s perception and awareness of consequences of their actions 42 30 35 43 Heavy drinking is associated with vulnerability to injury marital discord and domestic violence 29 Moderate drinkers are more frequently engaged in intimate violence than are light drinkers and abstainers however generally it is heavy and or binge drinkers who are involved in the most chronic and serious forms of aggression Research found that factors that increase the likelihood of alcohol related violence include difficult temperament hyperactivity hostile beliefs history of family violence poor school performance delinquent peers criminogenic beliefs about alcohol s effects impulsivity and antisocial personality disorder The odds frequency and severity of physical attacks are all positively correlated with alcohol use In turn violence decreases after behavioral marital alcoholism treatment 30 Automobile accidents edit Main articles Drunk driving and Driving under influence nbsp An Estonian billboard warning against drunk drivingA 2002 study found 41 of people fatally injured in traffic accidents were in alcohol related crashes 44 Misuse of alcohol is associated with more than 40 of deaths that occur in automobile accidents every year 29 The risk of a fatal car accident increases exponentially with the level of alcohol in the driver s blood 45 Most countries have passed laws prohibiting driving a motor vehicle while impaired by alcohol In the U S these crimes are generally referred to as Driving under the influence DUI although there are many naming variations among jurisdictions such as driving while intoxicated DWI 46 With alcohol consumption a drunk driver s level of intoxication is typically determined by a measurement of blood alcohol content or BAC but this can also be expressed as a breath test measurement often referred to as a BrAC A BAC or BrAC measurement in excess of the specific threshold level such as 0 08 in the U S 47 defines the criminal offense with no need to prove impairment 48 In some jurisdictions there is an aggravated category of the offense at a higher BAC level such as 0 12 0 15 or 0 25 In many jurisdictions police officers can conduct field tests of suspects to look for signs of intoxication Criminologist Hung En Sung has concluded in 2016 that with regards to reducing drunk driving law enforcement has not generally proven to be effective Worldwide the majority of those driving under the influence do not end up arrested At least two thirds of alcohol involved fatalities involve repeat drinking drivers Sung commenting on measures for controlling drunk driving and alcohol related accidents noted that the ones that have proven effective include lowering legal blood alcohol concentrations controlling liquor outlets nighttime driving curfews for minors educational treatment programs combined with license suspension for offenders and court monitoring of high risk offenders 30 Sexual assault edit Main article Alcohol and sex Alcohol abuse increases the risk of individuals either experiencing or perpetrating sexual violence and risky casual sex 49 Caffeinated alcoholic drinks are particularly implicated 50 Often a victim becomes incapacitated due to having consumed alcohol which then facilitates sexual assault or rape a crime known as drug facilitated sexual assault 51 52 Over 50 of reported rapes involve alcohol clarification needed 29 Alcohol remains the most commonly used predator drug 53 54 and is said to be used in the majority of sexual assaults 42 Many assailants use alcohol because their victims often willingly imbibe it and can be encouraged to drink enough to lose inhibitions or consciousness Sex with an unconscious victim is considered rape in most if not all jurisdictions and some assailants have committed rapes of convenience whereby they have assaulted a victim after he or she had become unconscious from drinking too much 55 Public drunkenness edit Main article Public intoxication nbsp Drunkard passed out on a benchPublic drunkenness or intoxication is a common problem in many jurisdictions Public intoxication laws vary widely by jurisdiction but include public nuisance laws open container laws and prohibitions on drinking alcohol in public or certain areas The offenders are often lower class individuals and this crime has a very high recidivism rate with numerous instances of repeated instances of the arrest jail release without treatment cycle The high number of arrests for public drunkenness often reflects rearrests of the same offenders 35 Methanol laced alcohol edit Main article Methanol poisoning outbreaks Methanol is not produced in toxic amounts by fermentation of sugars from grain starches However outbreaks of methanol poisoning have occurred when methanol is used to lace moonshine bootleg liquor 56 This is commonly done to bulk up the original product to gain profit Because of its similarities in both appearance and odor to ethanol the alcohol in beverages it is difficult to differentiate between the two Methanol has a high toxicity in humans If as little as 10 mL of pure methanol is ingested for example it can break down into formic acid which can cause permanent blindness by destruction of the optic nerve and 30 mL is potentially fatal 57 although the median lethal dose is typically 100 mL 3 4 fl oz i e 1 2 mL kg body weight of pure methanol 58 Reference dose for methanol is 0 5 mg kg day 59 Toxic effects take hours to start and effective antidotes can often prevent permanent damage 57 Social benefits edit Research on the societal benefits of alcohol is rare but studies suggests there are benefits 60 Alcohol consumption while socializing increases occurrences of Duchenne smiling talking and social bonding even when participants are unaware of their alcohol consumption or lack thereof 61 In a study of the UK regular drinking was correlated with happiness feeling that life was worthwhile and satisfaction with life According to a causal path analysis alcohol consumption was not the cause but rather satisfaction with life resulted in greater happiness and an inclination to visit pubs and develop a regular drinking venue City centre bars were distinguished by their focus on maximizing alcohol sales Community pubs had less variation in visible group sizes and longer more focused conversations than those in city centre bars Drinking regularly at a community pub led to higher trust in others and better networking with the local community compared to non drinkers and city centre bar drinkers 60 Health effects editMain articles Alcohol and health and Alcoholism Moderate drinking See also Health effects of wine Alcohol has a variety of short term and long term adverse effects It also has reinforcement related adverse effects including addiction dependence and withdrawal Alcohol use is directly related to considerable morbidity and mortality for instance due to overdose and alcohol related health problems 62 The World Health Organization advises that there is no safe level of alcohol consumption 63 Short term effects edit Main article Short term effects of alcohol consumption nbsp Symptoms of varying BAC levels Additional symptoms may occur The amount of ethanol in the body is typically quantified by blood alcohol content BAC weight of ethanol per unit volume of blood Small doses of ethanol in general are stimulant like 64 and produce euphoria and relaxation people experiencing these symptoms tend to become talkative and less inhibited and may exhibit poor judgement At higher dosages BAC gt 1 gram liter ethanol acts as a central nervous system CNS depressant 64 producing at progressively higher dosages impaired sensory and motor function slowed cognition stupefaction unconsciousness and possible death Ethanol is commonly consumed as a recreational substance especially while socializing due to its psychoactive effects Central nervous system impairment edit Alcohol causes generalized CNS depression is a positive allosteric GABAA modulator and is associated and related with cognitive memory motor and sensory impairment It slows and impairs cognition and reaction time and the cognitive skills impairs judgement interferes with motor function resulting in motor incoordination loss of balance confusion sedation numbness and slurred speech impairs memory formation and causes sensory impairment At high concentrations it can induce amnesia analgesia spins stupor and unconsciousness as result of high levels of ethanol in blood At very high concentrations alcohol can cause anterograde amnesia markedly decreased heart rate pulmonary aspiration positional alcohol nystagmus respiratory depression shock coma and death can result due to profound suppression of CNS function alcohol overdose and can finish in consequent dysautonomia Gastrointestinal effects edit nbsp Diagram of mucosal layerAlcohol can cause nausea and vomiting in sufficiently high amounts varying by person Alcohol stimulates gastric juice production even when food is not present and as a result its consumption stimulates acidic secretions normally intended to digest protein molecules Consequently the excess acidity may harm the inner lining of the stomach The stomach lining is normally protected by a mucosal layer that prevents the stomach from essentially digesting itself However in patients who have a peptic ulcer disease PUD this mucosal layer is broken down PUD is commonly associated with the bacteria Helicobacter pylori which secretes a toxin that weakens the mucosal wall allowing acid and protein enzymes to penetrate the weakened barrier Because alcohol stimulates the stomach to secrete acid a person with PUD should avoid drinking alcohol on an empty stomach Drinking alcohol causes more acid release which further damages the already weakened stomach wall 65 Complications of this disease could include a burning pain in the abdomen bloating and in severe cases the presence of dark black stools indicate internal bleeding 66 A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation 66 Ingestion of alcohol can initiate systemic pro inflammatory changes through two intestinal routes 1 altering intestinal microbiota composition dysbiosis which increases lipopolysaccharide LPS release and 2 degrading intestinal mucosal barrier integrity thus allowing LPS to enter the circulatory system The major portion of the blood supply to the liver is provided by the portal vein Therefore while the liver is continuously fed nutrients from the intestine it is also exposed to any bacteria and or bacterial derivatives that breach the intestinal mucosal barrier Consequently LPS levels increase in the portal vein liver and systemic circulation after alcohol intake Immune cells in the liver respond to LPS with the production of reactive oxygen species leukotrienes chemokines and cytokines These factors promote tissue inflammation and contribute to organ pathology 67 Allergic like reactions edit Main articles Alcohol induced respiratory reactions and Alcohol flush reaction See also Short term effects of alcohol consumption Allergic reaction like symptoms Ethanol containing beverages can cause alcohol flush reactions exacerbations of rhinitis and more seriously and commonly bronchoconstriction in patients with a history of asthma and in some cases urticarial skin eruptions and systemic dermatitis Such reactions can occur within 1 60 minutes of ethanol ingestion and may be caused by 68 genetic abnormalities in the metabolism of ethanol which can cause the ethanol metabolite acetaldehyde to accumulate in tissues and trigger the release of histamine or true allergy reactions to allergens occurring naturally in or contaminating alcoholic beverages particularly wine and beer and other unknown causes Overdose edit Main article Alcohol intoxication Symptoms of ethanol overdose may include nausea vomiting CNS depression coma acute respiratory failure or death Levels of even less than 0 1 can cause intoxication with unconsciousness often occurring at 0 3 0 4 69 Death from ethanol consumption is possible when blood alcohol levels reach 0 4 A blood level of 0 5 or more is commonly fatal The oral median lethal dose LD50 of ethanol in rats is 5 628 mg kg Directly translated to human beings this would mean that if a person who weighs 70 kg 150 lb drank a 500 mL 17 US fl oz glass of pure ethanol they would theoretically have a 50 risk of dying Long term effects edit Main article Long term effects of alcohol Prolonged heavy consumption of alcohol can cause significant permanent damage to the brain and other organs resulting in dysfunction or death Brain damage edit Main articles Alcohol related brain damage Long term impact of alcohol on the brain and Neurotoxin Alcohol can cause brain damage Wernicke s encephalopathy and Alcoholic Korsakoff syndrome which frequently occur simultaneously known as Wernicke Korsakoff syndrome 70 Lesions or brain abnormalities are typically located in the diencephalon which result in anterograde and retrograde amnesia or memory loss 70 Liver damage edit Main articles Alcoholic liver disease Cirrhosis Hepatotoxin Alcoholic hepatitis and Fatty liver disease During the metabolism of alcohol via the respective dehydrogenases nicotinamide adenine dinucleotide NAD is converted into reduced NAD Normally NAD is used to metabolize fats in the liver and as such alcohol competes with these fats for the use of NAD Prolonged exposure to alcohol means that fats accumulate in the liver leading to the term fatty liver Continued consumption such as in alcohol use disorder then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death These cells are then replaced with scar tissue leading to the condition called cirrhosis Birth defects edit Main article Fetal alcohol spectrum disorder Ethanol is classified as a teratogen medical citation needed According to the U S Centers for Disease Control and Prevention CDC alcohol consumption by women who are not using birth control increases the risk of fetal alcohol syndrome The CDC currently recommends complete abstinence from alcoholic beverages for women of child bearing age who are pregnant trying to become pregnant or are sexually active and not using birth control 71 Cancer edit Main article Alcohol and cancer The International Agency for Research on Cancer lists ethanol in alcoholic beverages as a Group 1 carcinogen in humans and argues that There is sufficient evidence and research showing the carcinogenicity of acetaldehyde the major metabolite of ethanol which is excreted by the liver enzyme when one drinks alcohol 72 In 2020 alcohol was estimated to cause 750 000 cases of cancer worldwide particularly esophagus liver and breast cancer 73 Other effects edit Frequent drinking of alcoholic beverages is a major contributing factor in cases of elevated blood levels of triglycerides 74 Alcoholism edit Main article Alcoholism nbsp Early 20th century Dutch poster about the dangers of alcoholismAlcoholism or its medical diagnosis alcohol use disorder refers to alcohol addiction alcohol dependence dipsomania and or alcohol abuse It is a major problem and many health problems as well as death can result from excessive alcohol use 29 62 Alcohol dependence is linked to a lifespan that is reduced by about 12 years relative to the average person 29 In 2004 it was estimated that 4 of deaths worldwide were attributable to alcohol use 62 Deaths from alcohol are split about evenly between acute causes e g overdose accidents and chronic conditions 62 The leading chronic alcohol related condition associated with death is alcoholic liver disease 62 Alcohol dependence is also associated with cognitive impairment and organic brain damage 29 Some researchers have found that even one alcoholic drink a day increases an individual s risk of health problems by 0 4 75 Two or more consecutive alcohol free days a week have been recommended to improve health and break dependence 76 77 Alcohol withdrawal syndrome edit Main articles Alcohol withdrawal syndrome and Delirium tremens Discontinuation of alcohol after extended heavy use and associated tolerance development resulting in dependence can result in withdrawal Alcohol withdrawal can cause confusion paranoia anxiety insomnia agitation tremors fever nausea vomiting autonomic dysfunction seizures and hallucinations In severe cases death can result Delirium tremens is a condition that requires people with a long history of heavy drinking to undertake an alcohol detoxification regimen Interactions editSee also Caffeinated alcoholic drink and Nicotini Alcohol can intensify the sedation caused by other CNS depressants such as barbiturates benzodiazepines opioids nonbenzodiazepines Z drugs such as zolpidem and zopiclone antipsychotics sedative antihistamines and certain antidepressants 69 It interacts with cocaine in vivo to produce cocaethylene another psychoactive substance which may be substantially more cardiotoxic than either cocaine or alcohol by themselves 78 additional citation s needed Ethanol enhances the bioavailability of methylphenidate elevated plasma dexmethylphenidate 79 irrelevant citation In combination with cannabis ethanol increases plasma tetrahydrocannabinol levels which suggests that ethanol may increase the absorption of tetrahydrocannabinol 80 Disulfiram like drugs edit Main article Disulfiram like drug Disulfiram edit Disulfiram inhibits the enzyme acetaldehyde dehydrogenase which in turn results in buildup of acetaldehyde a toxic metabolite of ethanol with unpleasant effects The medication or drug is commonly used to treat alcohol use disorder and results in immediate hangover like symptoms upon consumption of alcohol this effect is widely known as disulfiram effect Metronidazole edit Metronidazole is an antibacterial agent that kills bacteria by damaging cellular DNA and hence cellular function 81 Metronidazole is usually given to people who have diarrhea caused by Clostridium difficile bacteria Patients who are taking metronidazole are sometimes advised to avoid alcohol even after 1 hour following the last dose Although older data suggested a possible disulfiram like effect of metronidazole newer data has challenged this and suggests it does not actually have this effect Alcohol induced dose dumping AIDD edit Main article Dose dumping This dose dumping effect is an unintended rapid release of large amounts of a given drug when administered through a modified release dosage while co ingesting ethanol 82 This is considered a pharmaceutical disadvantage due to the high risk of causing drug induced toxicity by increasing the absorption and serum concentration above the therapeutic window of the drug The best way to prevent this interaction is by avoiding the co ingestion of both substances or using specific controlled release formulations that are resistant to AIDD Methanol and ethylene glycol edit Main articles Methanol Ethylene glycol and Methanol toxicity The rate limiting steps for the elimination of ethanol are in common with certain other substances As a result the blood alcohol concentration can be used to modify the rate of metabolism of methanol and ethylene glycol Methanol itself is not highly toxic but its metabolites formaldehyde and formic acid are therefore to reduce the rate of production and concentration of these harmful metabolites ethanol can be ingested 83 Ethylene glycol poisoning can be treated in the same way Pharmacology editDynamics edit See also Alcohol intoxication GABAA receptors and Calcium channel blocker Ethanol The principal mechanism of action for ethanol has proven elusive and remains not fully understood 20 84 Identifying molecular targets for ethanol has proven unusually difficult in large part due to its unique biochemical properties 84 Specifically ethanol is a very low molecular weight compound and is of exceptionally low potency in its actions causing effects only at very high millimolar mM concentrations 84 85 For these reasons unlike with most drugs it has not yet been possible to employ traditional biochemical techniques to directly assess the binding of ethanol to receptors or ion channels 84 85 Instead researchers have had to rely on functional studies to elucidate the actions of ethanol 84 Moreover although it has been established that ethanol modulates ion channels to mediate its effects 22 ion channels are complex proteins and their interactions and functions are complicated by diverse subunit compositions and regulation by conserved cellular signals e g signaling lipids 20 84 Much progress has been made in understanding the pharmacodynamics of ethanol over the last few decades 21 84 While no binding sites have been identified and established unambiguously for ethanol at present it appears that it affects ion channels in particular ligand gated ion channels to mediate its effects in the CNS 20 21 22 84 Ethanol has specifically been found in functional assays to enhance or inhibit the activity of a variety of ion channels including the GABAA receptor the ionotropic glutamate AMPA kainate and NMDA receptors the glycine receptor 86 the nicotinic acetylcholine receptors 87 the serotonin 5 HT3 receptor voltage gated calcium channels and BK channels among others 20 21 22 88 89 However many of these actions have been found to occur only at very high concentrations that may not be pharmacologically significant at recreational doses of ethanol and it is unclear how or to what extent each of the individual actions is involved in the effects of ethanol 84 In any case ethanol has long shown a similarity in its effects to positive allosteric modulators of the GABAA receptor like benzodiazepines barbiturates and various general anesthetics 20 84 Indeed ethanol has been found to enhance GABAA receptor mediated currents in functional assays 20 84 In accordance it is theorized and widely believed that the primary mechanism of action is as a GABAA receptor positive allosteric modulator 20 84 However the diverse actions of ethanol on other ion channels may be and indeed likely are involved in its effects as well 21 84 In 2007 it was discovered that ethanol potentiates extrasynaptic d subunit containing GABAA receptors at behaviorally relevant as low as 3 mM concentrations 20 84 90 This is in contrast to previous functional assays of ethanol on g subunit containing GABAA receptors which it enhances only at far higher concentrations gt 100 mM that are in excess of recreational concentrations up to 50 mM 20 84 91 Ro15 4513 a close analogue of the benzodiazepine antagonist flumazenil Ro15 1788 has been found to bind to the same site as ethanol and to competitively displace it in a saturable manner 84 90 In addition Ro15 4513 blocked the enhancement of d subunit containing GABAA receptor currents by ethanol in vitro 84 In accordance the drug has been found to reverse many of the behavioral effects of low to moderate doses of ethanol in rodents including its effects on anxiety memory motor behavior and self administration 84 90 Taken together these findings suggest a binding site for ethanol on subpopulations of the GABAA receptor with specific subunit compositions via which it interacts with and potentiates the receptor 20 84 90 92 A 2019 study showed the accumulation of an unnatural lipid phosphatidylethanol PEth competes with PIP2 agonist sites on lipid gated ion channels 93 This presents a novel indirect mechanism and suggests that a metabolite not the ethanol itself can affect the primary targets of ethanol intoxication Many of the primary targets of ethanol are known to bind PIP2 including GABAA receptors 94 but the role of PEth will need to be investigated for each of the primary targets Rewarding and reinforcing actions edit The reinforcing effects of alcohol consumption are mediated by acetaldehyde generated by catalase and other oxidizing enzymes such as cytochrome P 4502E1 in the brain 95 Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol it appears to play a central role in the activation of the mesolimbic dopamine system 96 Ethanol s rewarding and reinforcing i e addictive properties are mediated through its effects on dopamine neurons in the mesolimbic reward pathway which connects the ventral tegmental area to the nucleus accumbens NAcc 97 98 One of ethanol s primary effects is the allosteric inhibition of NMDA receptors and facilitation of GABAA receptors e g enhanced GABAA receptor mediated chloride flux through allosteric regulation of the receptor 99 At high doses ethanol inhibits most ligand gated ion channels and voltage gated ion channels in neurons as well 99 With acute alcohol consumption dopamine is released in the synapses of the mesolimbic pathway in turn heightening activation of postsynaptic D1 receptors 97 98 The activation of these receptors triggers postsynaptic internal signaling events through protein kinase A which ultimately phosphorylate cAMP response element binding protein CREB inducing CREB mediated changes in gene expression 97 98 With chronic alcohol intake consumption of ethanol similarly induces CREB phosphorylation through the D1 receptor pathway but it also alters NMDA receptor function through phosphorylation mechanisms 97 98 an adaptive downregulation of the D1 receptor pathway and CREB function occurs as well 97 98 Chronic consumption is also associated with an effect on CREB phosphorylation and function via postsynaptic NMDA receptor signaling cascades through a MAPK ERK pathway and CAMK mediated pathway 98 These modifications to CREB function in the mesolimbic pathway induce expression i e increase gene expression of DFosB in the NAcc 98 where DFosB is the master control protein that when overexpressed in the NAcc is necessary and sufficient for the development and maintenance of an addictive state i e its overexpression in the nucleus accumbens produces and then directly modulates compulsive alcohol consumption 98 100 101 102 Relationship between concentrations and effects edit Blood alcohol levels and effects 103 mg dL mM v v Effects50 11 0 05 Euphoria talkativeness relaxation happiness gladness pleasure joyfulness 100 22 0 1 Central nervous system depression anxiety suppression stress suppression sedation nausea possible vomiting impaired motor and sensory function impaired memory impaired cognition gt 140 30 gt 0 14 Decreased blood flow to brain slurred speech double or blurry vision 300 65 0 3 Stupefaction confusion numbness dizziness loss of consciousness 400 87 0 4 Ethylic intoxication drunkenness inebriation alcohol poisoning or possible death 500 109 gt 0 55 Unconsciousness coma and death Recreational concentrations of ethanol are typically in the range of 1 to 50 mM 91 20 Very low concentrations of 1 to 2 mM ethanol produce zero or undetectable effects except in alcohol naive individuals 91 Slightly higher levels of 5 to 10 mM which are associated with light social drinking produce measurable effects including changes in visual acuity decreased anxiety and modest behavioral disinhibition 91 Further higher levels of 15 to 20 mM result in a degree of sedation and motor incoordination that is contraindicated with the operation of motor vehicles 91 In jurisdictions in the U S maximum blood alcohol levels for legal driving are about 17 to 22 mM 104 105 In the upper range of recreational ethanol concentrations of 20 to 50 mM depression of the central nervous system is more marked with effects including complete drunkenness profound sedation amnesia emesis hypnosis and eventually unconsciousness 91 104 Levels of ethanol above 50 mM are not typically experienced by normal individuals and hence are not usually physiologically relevant however such levels ranging from 50 to 100 mM may be experienced by alcoholics with high tolerance to ethanol 91 Concentrations above this range specifically in the range of 100 to 200 mM would cause death in all people except alcoholics 91 List of known actions in the central nervous system edit Ethanol has been reported to possess the following actions in functional assays at varying concentrations 85 GABAA receptor positive allosteric modulator primarily of d subunit containing receptors 99 NMDA receptor negative allosteric modulator 89 99 Decreased levels of nitric oxide in brain medulla 106 Increased levels of dopamine and endogenous opioids in the mesolimbic pathway secondary to other actions 96 99 AMPA receptor negative allosteric modulator 89 Kainate receptor negative allosteric modulator 89 Glycine receptor positive allosteric modulator 86 Serotonin receptor positive allosteric modulator 86 Opioid receptor endogenous positive allosteric modulator 89 Muscarinic acetylcholine receptor positive allosteric modulator Nicotinic acetylcholine receptor positive allosteric modulator 87 107 5 HT3 receptor positive allosteric modulator Glycine reuptake inhibitor 108 Adenosine reuptake inhibitor 109 L type calcium channel blocker GIRK channel openerSome of the actions of ethanol on ligand gated ion channels specifically the nicotinic acetylcholine receptors and the glycine receptor are dose dependent with potentiation or inhibition occurring dependent on ethanol concentration 85 This seems to be because the effects of ethanol on these channels are a summation of positive and negative allosteric modulatory actions 85 Kinetics edit Absorption edit Ethanol can be taken orally by inhalation rectally or by injection e g intravenous 6 110 though it is typically ingested simply via oral administration 4 The oral bioavailability of ethanol is around 80 or more 4 5 In fasting volunteers blood levels of ethanol increase proportionally with the dose of ethanol administered 110 Blood alcohol concentrations may be estimated by dividing the amount of ethanol ingested by the body weight of the individual and correcting for water dilution 6 Onset edit Peak circulating levels of ethanol are usually reached within a range of 30 to 90 minutes of ingestion with an average of 45 to 60 minutes 6 4 People who have fasted overnight have been found to reach peak ethanol concentrations more rapidly at within 30 minutes of ingestion 6 The onset varies depends on the type of alcoholic drink 111 Vodka tonic 36 10 minutes Wine 54 14 minutes Beer 62 23 minutesAlso carbonated alcoholic drinks seem to have a shorter onset compare to flat drinks in the same volume One theory is that carbon dioxide in the bubbles somehow speeds the flow of alcohol into the intestines 112 Food in the gastrointestinal system and hence gastric emptying is the most important factor that influences the absorption of orally ingested ethanol 6 110 The absorption of ethanol is much more rapid on an empty stomach than with a full one 6 The delay in ethanol absorption caused by food is similar regardless of whether food is consumed just before at the same time or just after ingestion of ethanol 6 The type of food whether fat carbohydrates or protein also is of little importance 110 Not only does food slow the absorption of ethanol but it also reduces the bioavailability of ethanol resulting in lower circulating concentrations 6 Distribution edit Upon ingestion ethanol is rapidly distributed throughout the body 4 It is distributed most rapidly to tissues with the greatest blood supply 6 As such ethanol primarily affects the brain liver and kidneys 4 Other tissues with lower circulation such as bone require more time for ethanol to distribute into 6 Ethanol crosses biological membranes and the blood brain barrier easily through a simple process of passive diffusion 4 110 The volume of distribution of ethanol is around 55 L kg 0 53 US pt lb 4 It is only weakly or not at all plasma protein bound 4 5 Metabolism edit See also Ethanol metabolism Alcohol dehydrogenase and Aldehyde dehydrogenase Approximately 90 of the metabolism of ethanol occurs in the liver 6 8 This occurs predominantly via the enzyme alcohol dehydrogenase which transforms ethanol into its metabolite acetaldehyde ethanal 6 8 Acetaldehyde is subsequently metabolized by the enzyme aldehyde dehydrogenase into acetate ethanoate which in turn is broken down into carbon dioxide and water 6 Acetate also combines with coenzyme A to form acetyl CoA and hence may participate in metabolic pathways 4 Alcohol dehydrogenase and aldehyde dehydrogenase are present at their highest concentrations in the liver but are widely expressed throughout the body and alcohol dehydrogenase may also be present in the stomach and small intestine 4 Aside from alcohol dehydrogenase the microsomal ethanol oxidizing system MEOS specifically mediated by the cytochrome P450 enzyme CYP2E1 is the other major route of ethanol metabolism 6 8 CYP2E1 is inducible by ethanol so while alcohol dehydrogenase handles acute or low concentrations of ethanol MEOS is predominant with higher concentrations or with repeated chronic use 6 8 A small amount of ethanol undergoes conjugation to form ethyl glucuronide and ethyl sulfate 4 There may also be another metabolic pathway that metabolizes as much as 25 to 35 of ethanol at typical concentrations 5 At even low physiological concentrations ethanol completely saturates alcohol dehydrogenase 6 This is because ethanol has high affinity for the enzyme and very high concentrations of ethanol occur when it is used as a recreational substance 6 For this reason the metabolism of ethanol follows zero order kinetics at typical physiological concentrations 8 That is ethanol does not have an elimination half life i e is not metabolized at an exponential rate and instead is eliminated from the circulation at a constant rate 8 7 The mean elimination rates for ethanol are 15 mg dL per hour for men and 18 mg dL per hour for women with a range of 10 to 34 mg dL per hour 8 6 At very high concentrations such as in overdose it has been found that the rate of elimination of ethanol is increased 5 In addition ethanol metabolism follows first order kinetics at very high concentrations with an elimination half life of about 4 or 4 5 hours which implies a clearance rate of approximately 6 L hour 70 kg 5 4 This seems to be because other processes such as the MEOS CYP2E1 also become involved in the metabolism of ethanol at higher concentrations 4 However the MEOS CYP2E1 alone does not appear sufficient to fully explain the increase in ethanol metabolism rate 5 Some individuals have less effective forms of one or both of the metabolizing enzymes of ethanol and can experience more marked symptoms from ethanol consumption than others 113 However those having acquired alcohol tolerance have a greater quantity of these enzymes and metabolize ethanol more rapidly 113 Elimination edit Ethanol is mainly eliminated from the body via metabolism into carbon dioxide and water 6 Around 5 to 10 of ethanol that is ingested is eliminated unchanged in urine breath and sweat 4 Transdermal alcohol that diffuses through the skin as insensible perspiration or is exuded as sweat sensible perspiration can be detected using wearable sensor technology 114 such as SCRAM ankle bracelet 115 or the more discreet ION Wearable 116 Ethanol or its metabolites may be detectable in urine for up to 96 hours 3 5 days after ingestion 4 Chemistry editMain articles Ethanol and Ethanol data page See also Alcohols medicine Alcohol powder Ethanol fermentation and Yeast in winemaking Ethanol is also known chemically as alcohol ethyl alcohol or drinking alcohol It is a simple alcohol with a molecular formula of C2H6O and a molecular weight of 46 0684 g mol The molecular formula of ethanol may also be written as CH3 CH2 OH or as C2H5 OH The latter can also be thought of as an ethyl group linked to a hydroxyl alcohol group and can be abbreviated as EtOH Ethanol is a volatile flammable colorless liquid with a slight characteristic odor Aside from its use as a psychoactive and recreational substance ethanol is also commonly used as an antiseptic and disinfectant a chemical and medicinal solvent and a fuel Production edit Ethanol is produced naturally as a byproduct of the metabolic processes of yeast and hence is present in any yeast habitat including even endogenously in humans but it does not cause raised blood alcohol content as seen in the rare medical condition auto brewery syndrome ABS It is manufactured through hydration of ethylene or by brewing via fermentation of sugars with yeast most commonly Saccharomyces cerevisiae The sugars are commonly obtained from sources like steeped cereal grains e g barley grape juice and sugarcane products e g molasses sugarcane juice Ethanol water mixture which can be further purified via distillation Analogues edit See also Comparison of psychoactive alcohols in alcoholic drinks This article may require cleanup to meet Wikipedia s quality standards The specific problem is Puncuation in complex sounding sentences Please help improve this article if you can February 2021 Learn how and when to remove this template message Ethanol has a variety of analogues many of which have similar actions and effects Methanol methyl alcohol and isopropyl alcohol also called rubbing alcohol are both toxic and thus unsafe for human consumption 11 Methanol is the most toxic alcohol the toxicity of isopropyl alcohol lies between that of ethanol and methanol and is about twice that of ethanol 117 In general higher alcohols are less toxic 117 n Butanol is reported to produce similar effects to those of ethanol and relatively low toxicity one sixth of that of ethanol in one rat study 118 119 However its vapors can produce eye irritation and inhalation can cause pulmonary edema 117 Acetone propanone is a ketone rather than an alcohol and is reported to produce similar toxic effects it can be extremely damaging to the cornea 117 The tertiary alcohol tert amyl alcohol TAA also known as 2 methylbutan 2 ol 2M2B has a history of use as a hypnotic and anesthetic as do other tertiary alcohols such as methylpentynol ethchlorvynol and chloralodol Unlike primary alcohols like ethanol these tertiary alcohols cannot be oxidized into aldehyde or carboxylic acid metabolites which are often toxic and for this reason these compounds are safer in comparison 120 Other relatives of ethanol with similar effects include chloral hydrate paraldehyde and many volatile and inhalational anesthetics e g chloroform diethyl ether and isoflurane History editMain articles Alcoholic drink History and History of alcoholic drinks Alcohol was brewed as early as 7 000 to 6 650 BCE in northern China 121 The earliest evidence of winemaking was dated at 6 000 to 5 800 BCE in Georgia in the South Caucasus 122 Beer was likely brewed from barley as early as the 13 000 years ago in the Middle East 123 Pliny the Elder wrote about the golden age of winemaking in Rome the 2nd century BCE 200 100 BCE when vineyards were planted 124 Society and culture editSee also Drinking culture Ethanol is typically consumed as a recreational substance by mouth in the form of alcoholic beverages such as beer wine and spirits It is commonly used in social settings due to its capacity to enhance sociability Drinking alcohol is generally socially acceptable and is legal in most countries unlike with many other recreational substances However there are often restrictions on alcohol sale and use for instance a minimum age for drinking and laws against public drinking and drinking and driving 125 Alcohol has considerable societal and cultural significance and has important social roles in much of the world Drinking establishments such as bars and nightclubs revolve primarily around the sale and consumption of alcoholic beverages and parties festivals and social gatherings commonly involve alcohol consumption Alcohol is related to various societal problems including drunk driving accidental injuries sexual assaults domestic abuse and violent crime 29 Alcohol remains illegal for sale and consumption in a number of countries mainly in the Middle East While some religions including Islam prohibit alcohol consumption other religions such as Christianity and Shinto utilize alcohol in sacrament and libation 126 127 128 Legal status edit Main articles Alcohol law Prohibition and Legal drinking age Alcohol consumption is fully legal and available in most countries of the world 129 Home made alcoholic beverages with low alcohol content like wine and beer is also legal in most countries but distilling moonshine outside of a registered distillery remains illegal in most of them Some majority Muslim countries such as Saudi Arabia Kuwait Pakistan Iran and Libya prohibit the production sale and consumption of alcoholic beverages because they are forbidden by Islam 130 131 132 Also laws banning alcohol consumption are found in some Indian states as well as some Native American reservations in the U S 129 In addition there are regulations on alcohol sales and use in many countries throughout the world 129 For instance the majority of countries have a minimum legal drinking age to purchase or consume alcoholic beverages although there are often exceptions such as underage consumption of small amounts of alcohol with parental supervision Also some countries have bans on public intoxication 129 Drinking while driving or intoxicated driving is frequently outlawed and it may be illegal to have an open container of alcohol or liquor bottle in an automobile bus or aircraft 129 Standard drink edit Main article Standard drink A standard drink is a measure of alcohol consumption representing a fixed amount of pure ethanol used in relation to recommendations about alcohol consumption and its relative risks to health The size of a standard drink varies from 8g to 20g across countries but 10g alcohol 12 7 millilitres is used in the World Health Organization WHO Alcohol Use Disorders Identification Test AUDIT s questionnaire form example 133 and has been adopted by more countries than any other amount 134 See also editBinge drinking Holiday heart syndrome Alcohol myopia Rum running GABAergics GABRD d subunit containing receptors List of countries by alcohol consumption per capita Pigovian taxes which are to pay for the damage to society caused by these goods Sin taxes are used to increase the price in an effort to lower their use or failing that to increase and find new sources of revenue References edit WHO Expert Committee on Problems Related to Alcohol Consumption second report Geneva Switzerland World Health Organization 2007 p 23 ISBN 9789241209441 Retrieved 3 March 2015 alcohol dependence is a substantial risk of regular heavy drinking Vengeliene V Bilbao A Molander A Spanagel R May 2008 Neuropharmacology of alcohol addiction British Journal of Pharmacology 154 2 299 315 doi 10 1038 bjp 2008 30 PMC 2442440 PMID 18311194 Compulsive alcohol use occurs only in a limited proportion of about 10 15 of alcohol users Gilman JM Ramchandani VA Crouss T Hommer DW January 2012 Subjective and neural responses to intravenous alcohol in young adults with light and heavy drinking patterns Neuropsychopharmacology 37 2 467 77 doi 10 1038 npp 2011 206 PMC 3242308 PMID 21956438 a b c d e f g h i j k l m n o p q r s t u Principles of Addiction Comprehensive Addictive Behaviors and Disorders Academic Press 17 May 2013 pp 162 ISBN 978 0 12 398361 9 a b c d e f g h i Holford NH November 1987 Clinical pharmacokinetics of ethanol Clinical Pharmacokinetics 13 5 273 92 doi 10 2165 00003088 198713050 00001 PMID 3319346 S2CID 19723995 a b c d e f g h i j k l m n o p q r s t u v w Pohorecky LA Brick J 1988 Pharmacology of ethanol Pharmacology amp Therapeutics 36 2 3 335 427 doi 10 1016 0163 7258 88 90109 x PMID 3279433 a b Becker CE September 1970 The clinical pharmacology of alcohol California Medicine 113 3 37 45 PMC 1501558 PMID 5457514 a b c d e f g h i Levine B 2003 Principles of Forensic Toxicology Amer Assoc for Clinical Chemistry pp 161 ISBN 978 1 890883 87 4 Iber FL 26 November 1990 Alcohol and Drug Abuse as Encountered in Office Practice CRC Press pp 74 ISBN 978 0 8493 0166 7 a b c Haynes WM ed 2011 CRC Handbook of Chemistry and Physics 92nd ed Boca Raton FL CRC Press p 3 246 ISBN 1 4398 5511 0 a b c Collins SE Kirouac M 2013 Alcohol Consumption Encyclopedia of Behavioral Medicine pp 61 65 doi 10 1007 978 1 4419 1005 9 626 ISBN 978 1 4419 1004 2 10th Special Report to the U S Congress on Alcohol and Health Highlights from Current Research PDF National Institute of Health National Institute on Alcohol Abuse and Alcoholism June 2000 p 134 Retrieved 21 October 2014 The brain is a major target for the actions of alcohol and heavy alcohol consumption has long been associated with brain damage Studies clearly indicate that alcohol is neurotoxic with direct effects on nerve cells Chronic alcohol abusers are at additional risk for brain injury from related causes such as poor nutrition liver disease and head trauma Bruha R Dvorak K Petrtyl J March 2012 Alcoholic liver disease World Journal of Hepatology 4 3 81 90 doi 10 4254 wjh v4 i3 81 PMC 3321494 PMID 22489260 Brust JC April 2010 Ethanol and cognition indirect effects neurotoxicity and neuroprotection a review International Journal of Environmental Research and Public Health 7 4 1540 57 doi 10 3390 ijerph7041540 PMC 2872345 PMID 20617045 Venkataraman A Kalk N Sewell G Ritchie CW Lingford Hughes A March 2017 Alcohol and Alzheimer s Disease Does Alcohol Dependence Contribute to Beta Amyloid Deposition Neuroinflammation and Neurodegeneration in Alzheimer s Disease Alcohol and Alcoholism 52 2 151 158 doi 10 1093 alcalc agw092 hdl 10044 1 42603 PMID 27915236 de Menezes RF Bergmann A Thuler LC 2013 Alcohol consumption and risk of cancer a systematic literature review Asian Pacific Journal of Cancer Prevention 14 9 4965 72 doi 10 7314 apjcp 2013 14 9 4965 PMID 24175760 Bagnardi V Rota M Botteri E Tramacere I Islami F Fedirko V Scotti L Jenab M Turati F Pasquali E Pelucchi C Bellocco R Negri E Corrao G Rehm J Boffetta P La Vecchia C February 2013 Light alcohol drinking and cancer a meta analysis Annals of Oncology 24 2 301 8 doi 10 1093 annonc mds337 PMID 22910838 Yasinski Emma Even If You Don t Drink Daily Alcohol Can Mess With Your Brain Discover magazine January 12 2021 Centers for Disease Control and Prevention Multiple Cause of Death 2018 2021 National Vital Statistics System National Center for Health Statistics Retrieved 29 November 2023 a b c d e f g h i j k l m Lobo IA Harris RA July 2008 GABA A receptors and alcohol Pharmacology Biochemistry and Behavior 90 1 90 4 doi 10 1016 j pbb 2008 03 006 PMC 2574824 PMID 18423561 a b c d e Narahashi T Kuriyama K Illes P Wirkner K Fischer W Muhlberg K Scheibler P Allgaier C Minami K Lovinger D Lallemand F Ward RJ DeWitte P Itatsu T Takei Y Oide H Hirose M Wang XE Watanabe S Tateyama M Ochi R Sato N May 2001 Neuroreceptors and ion channels as targets of alcohol Alcoholism Clinical and Experimental Research 25 5 Suppl ISBRA 182S 188S doi 10 1097 00000374 200105051 00030 PMID 11391069 a b c d Olsen RW Li GD Wallner M Trudell JR Bertaccini EJ Lindahl E Miller KW Alkana RL Davies DL March 2014 Structural models of ligand gated ion channels sites of action for anesthetics and ethanol Alcoholism Clinical and Experimental Research 38 3 595 603 doi 10 1111 acer 12283 PMC 3959612 PMID 24164436 Charlet K Beck A Heinz A 2013 The dopamine system in mediating alcohol effects in humans Current Topics in Behavioral Neurosciences 13 461 88 doi 10 1007 7854 2011 130 ISBN 978 3 642 28719 0 PMID 21533679 Mendez M Morales Mulia M June 2008 Role of mu and delta opioid receptors in alcohol drinking behaviour Current Drug Abuse Reviews 1 2 239 52 doi 10 2174 1874473710801020239 PMID 19630722 Burcham PC 19 November 2013 An Introduction to Toxicology Springer Science amp Business Media pp 42 ISBN 978 1 4471 5553 9 No level of alcohol consumption is safe for our health World Health Organization 4 January 2023 Nutt DJ King LA Phillips LD November 2010 Drug harms in the UK a multicriteria decision analysis Lancet 376 9752 1558 65 CiteSeerX 10 1 1 690 1283 doi 10 1016 S0140 6736 10 61462 6 PMID 21036393 S2CID 5667719 Nutt D King LA Saulsbury W Blakemore C March 2007 Development of a rational scale to assess the harm of drugs of potential misuse Lancet 369 9566 1047 53 doi 10 1016 s0140 6736 07 60464 4 PMID 17382831 S2CID 5903121 a b c d e f g h i j k l m n o p Butcher JN Hooley JM Mineka SM 25 June 2013 Abnormal Psychology Pearson Education p 370 ISBN 978 0 205 97175 6 a b c d e f g h i Sunga HE 2016 Alcohol and Crime The Blackwell Encyclopedia of Sociology American Cancer Society pp 1 2 doi 10 1002 9781405165518 wbeosa039 pub2 ISBN 9781405165518 Trevor B Katy H 1 April 2005 Understanding Drugs Alcohol And Crime McGraw Hill Education UK p 6 ISBN 9780335212576 Drunk Driving Statistics in the US and Across the World Law Office of Douglas Herring 13 November 2017 Archived from the original on 22 September 2019 Retrieved 22 September 2019 Drunk Driving Increasing Concern Worldwide Voice of America Retrieved 22 September 2019 Sweedler BM Stewart K 2009 Worldwide trends in alcohol and drug impaired driving In Verster JC Pandi Perumal SR Ramaekers JG de Gier JJ eds Drugs Driving and Traffic Safety Birkhauser Basel pp 23 41 doi 10 1007 978 3 7643 9923 8 2 ISBN 9783764399238 a b c d Clinard M Meier R 14 February 2007 Sociology of Deviant Behavior Cengage Learning p 273 ISBN 9780495093350 a b McMurran M 3 October 2012 Alcohol Related Violence Prevention and Treatment John Wiley amp Sons pp 337 338 ISBN 9781118411063 a b c McMurran M 3 October 2012 Alcohol Related Violence Prevention and Treatment John Wiley amp Sons p 37 ISBN 9781118411063 WHO Governments confront drunken violence WHO Archived from the original on 4 May 2014 Retrieved 22 September 2019 a b Global status report on alcohol and health PDF World Health Organization 2011 Alcohol Related Crimes Statistics and Facts Alcohol Rehab Guide Retrieved 3 September 2019 Alcohol statistics Alcohol Change UK Retrieved 22 September 2019 a b Christopher P Holstege et al eds 25 October 2010 Criminal poisoning clinical and forensic perspectives Sudbury Mass Jones and Bartlett Publishers pp 232 ISBN 978 0763744632 Dingwall G 23 July 2013 Alcohol and Crime Routledge pp 160 161 ISBN 9781134029709 Hingson R Winter M 2003 Epidemiology and consequences of drinking and driving Alcohol Research amp Health 27 1 63 78 PMC 6676697 PMID 15301401 Naranjo CA Bremner KE January 1993 Behavioural correlates of alcohol intoxication Addiction 88 1 25 35 doi 10 1111 j 1360 0443 1993 tb02761 x PMID 8448514 Driving Under the Influence A Report to Congress on Alcohol Limits U S Department of Transportation National Highway Traffic Safety Administration 1992 pp 1 Legislative History of 08 per se Laws NHTSA NHTSA National Highway Traffic Safety Administration July 2001 Retrieved 21 July 2017 Nelson B Nevada s Driving Under the Influence DUI laws NVPAC Advisory Council for Prosecuting Attorneys Archived from the original on 22 April 2017 Retrieved 3 July 2017 Chersich MF Rees HV January 2010 Causal links between binge drinking patterns unsafe sex and HIV in South Africa its time to intervene International Journal of STD amp AIDS 21 1 2 7 doi 10 1258 ijsa 2000 009432 PMID 20029060 S2CID 3100905 Ball NJ Miller KE Quigley BM Eliseo Arras RK April 2021 Alcohol Mixed With Energy Drinks and Sexually Related Causes of Conflict in the Barroom Journal of Interpersonal Violence 36 7 8 3353 3373 doi 10 1177 0886260518774298 PMID 29779427 S2CID 29150434 Hall JA Moore CB July 2008 Drug facilitated sexual assault a review Journal of Forensic and Legal Medicine 15 5 291 7 doi 10 1016 j jflm 2007 12 005 PMID 18511003 Beynon CM McVeigh C McVeigh J Leavey C Bellis MA July 2008 The involvement of drugs and alcohol in drug facilitated sexual assault a systematic review of the evidence Trauma Violence amp Abuse 9 3 178 88 doi 10 1177 1524838008320221 PMID 18541699 S2CID 27520472 Alcohol Is Most Common Date Rape Drug Archived 17 October 2007 at the Wayback Machine Medicalnewstoday com Retrieved on 1 June 2011 Schwartz RH Milteer R LeBeau MA June 2000 Drug facilitated sexual assault date rape Southern Medical Journal 93 6 558 61 doi 10 1097 00007611 200093060 00002 PMID 10881768 Date Rape Survive org uk 20 March 2000 Retrieved on 1 June 2011 Application to Include Fomepizole on the WHO Model List of Essential Medicines PDF November 2012 p 10 a b Vale A 2007 Methanol Medicine 35 12 633 4 doi 10 1016 j mpmed 2007 09 014 Methanol Poisoning Overview Antizol Archived from the original on 5 October 2011 Retrieved 11 October 2011 dead link Methanol CASRN 67 56 1 a b Dunbar RI Launay J Wlodarski R Robertson C Pearce E Carney J MacCarron P June 2017 Functional Benefits of Modest Alcohol Consumption Adaptive Human Behavior and Physiology 3 2 118 133 doi 10 1007 s40750 016 0058 4 PMC 7010365 PMID 32104646 Sayette MA Creswell KG Dimoff JD Fairbairn CE Cohn JF Heckman BW et al August 2012 Alcohol and group formation a multimodal investigation of the effects of alcohol on emotion and social bonding Psychological Science 23 8 869 878 doi 10 1177 0956797611435134 PMC 5462438 PMID 22760882 a b c d e Friedman HS 26 August 2011 The Oxford Handbook of Health Psychology Oxford University Press USA pp 699 ISBN 978 0 19 534281 9 No level of alcohol consumption is safe for our health www who int Retrieved 13 October 2023 a b Hendler RA Ramchandani VA Gilman J Hommer DW 2013 Stimulant and sedative effects of alcohol Current Topics in Behavioral Neurosciences 13 489 509 doi 10 1007 7854 2011 135 ISBN 978 3 642 28719 0 PMID 21560041 Overview of Peptic Ulcer Disease Etiology and Pathophysiology Medscape com Retrieved 27 April 2013 a b Peptic Ulcer Disease Stomach Ulcers Cause Symptoms Treatments Webmd com Retrieved 27 April 2013 Patel S Behara R Swanson GR Forsyth CB Voigt RM Keshavarzian A October 2015 Alcohol and the Intestine Biomolecules 5 4 2573 88 doi 10 3390 biom5042573 PMC 4693248 PMID 26501334 Adams KE Rans TS December 2013 Adverse reactions to alcohol and alcoholic beverages Annals of Allergy Asthma amp Immunology 111 6 439 45 doi 10 1016 j anai 2013 09 016 PMID 24267355 a b Yost DA 2002 Acute care for alcohol intoxication PDF Postgraduate Medicine Online 112 6 Archived from the original PDF on 14 December 2010 Retrieved 29 September 2007 a b Arts NJ Walvoort SJ Kessels RP 27 November 2017 Korsakoff s syndrome a critical review Neuropsychiatric Disease and Treatment 13 2875 2890 doi 10 2147 NDT S130078 PMC 5708199 PMID 29225466 More than 3 million US women at risk for alcohol exposed pregnancy Centers for Disease Control and Prevention 2 February 2016 Retrieved 3 March 2016 drinking any alcohol at any stage of pregnancy can cause a range of disabilities for their child said Coleen Boyle Ph D director of CDC s National Center on Birth Defects and Developmental Disabilities Agents Classified by the IARC Monographs Volumes 1 111 Archived 25 October 2011 at the Wayback Machine monographs iarc fr Report Details Alcohol s Global Cancer Burden NCI www cancer gov 12 August 2021 Retrieved 13 October 2023 Triglycerides American Heart Association Archived from the original on 27 August 2007 Retrieved 4 September 2007 Bakalar N 27 August 2018 How Much Alcohol Is Safe to Drink None Say These Researchers The New York Times Retrieved 17 September 2018 Tomlinson A 26 June 2018 Tips and Tricks on How to Cut Down on the Booze The West Australian Seven West Media WA Retrieved 22 March 2019 Alcohol British Liver Trust Archived from the original on 11 July 2019 Retrieved 22 March 2019 Laizure SC Mandrell T Gades NM Parker RB January 2003 Cocaethylene metabolism and interaction with cocaine and ethanol role of carboxylesterases Drug Metabolism and Disposition 31 1 16 20 doi 10 1124 dmd 31 1 16 PMID 12485948 Sakalo VS Romanenko AM Klimenko IA Persidskiĭ I 1988 Effects of chemotherapy on regional metastases of non seminomatous tumors of the testis Voprosy Onkologii 34 10 1219 24 PMID 3188424 Lukas SE Orozco S October 2001 Ethanol increases plasma Delta 9 tetrahydrocannabinol THC levels and subjective effects after marihuana smoking in human volunteers Drug and Alcohol Dependence 64 2 143 9 doi 10 1016 S0376 8716 01 00118 1 PMID 11543984 Repchinsky C ed 2012 Compendium of pharmaceuticals and specialties Ottawa Canadian Pharmacists Association full citation needed D Souza S Mayock S Salt A December 2017 A review of in vivo and in vitro aspects of alcohol induced dose dumping AAPS Open 3 1 doi 10 1186 s41120 017 0014 9 ISSN 2364 9534 McCoy HG Cipolle RJ Ehlers SM Sawchuk RJ Zaske DE November 1979 Severe methanol poisoning Application of a pharmacokinetic model for ethanol therapy and hemodialysis The American Journal of Medicine 67 5 804 7 doi 10 1016 0002 9343 79 90766 6 PMID 507092 a b c d e f g h i j k l m n o p q r s Santhakumar V Wallner M Otis TS May 2007 Ethanol acts directly on extrasynaptic subtypes of GABAA receptors to increase tonic inhibition Alcohol 41 3 211 21 doi 10 1016 j alcohol 2007 04 011 PMC 2040048 PMID 17591544 a b c d e Spanagel R April 2009 Alcoholism a systems approach from molecular physiology to addictive behavior Physiological Reviews 89 2 649 705 doi 10 1152 physrev 00013 2008 PMID 19342616 a b c Soderpalm B Lido HH Ericson M November 2017 The Glycine Receptor A Functionally Important Primary Brain Target of Ethanol Alcoholism Clinical and Experimental Research 41 11 1816 1830 doi 10 1111 acer 13483 PMID 28833225 a b Wu J Gao M Taylor DH March 2014 Neuronal nicotinic acetylcholine receptors are important targets for alcohol reward and dependence Acta Pharmacologica Sinica 35 3 311 5 doi 10 1038 aps 2013 181 PMC 4647894 PMID 24464050 Dopico AM Bukiya AN Kuntamallappanavar G Liu J 2016 Modulation of BK Channels by Ethanol International Review of Neurobiology 128 239 79 doi 10 1016 bs irn 2016 03 019 ISBN 978 0 12 803619 8 PMC 5257281 PMID 27238266 a b c d e Moykkynen T Korpi ER July 2012 Acute effects of ethanol on glutamate receptors Basic amp Clinical Pharmacology amp Toxicology 111 1 4 13 doi 10 1111 j 1742 7843 2012 00879 x PMID 22429661 a b c d Wallner M Olsen RW May 2008 Physiology and pharmacology of alcohol the imidazobenzodiazepine alcohol antagonist site on subtypes of GABAA receptors as an opportunity for drug development British Journal of Pharmacology 154 2 288 98 doi 10 1038 bjp 2008 32 PMC 2442438 PMID 18278063 a b c d e f g h Harrison NL Skelly MJ Grosserode EK Lowes DC Zeric T Phister S Salling MC August 2017 Effects of acute alcohol on excitability in the CNS Neuropharmacology 122 36 45 doi 10 1016 j neuropharm 2017 04 007 PMC 5657304 PMID 28479395 Forstera B Castro PA Moraga Cid G Aguayo LG 2016 Potentiation of Gamma Aminobutyric Acid Receptors GABAAR by Ethanol How Are Inhibitory Receptors Affected Frontiers in Cellular Neuroscience 10 114 doi 10 3389 fncel 2016 00114 PMC 4858537 PMID 27199667 Chung HW Petersen EN Cabanos C Murphy KR Pavel MA Hansen AS et al January 2019 A Molecular Target for an Alcohol Chain Length Cutoff Journal of Molecular Biology 431 2 196 209 doi 10 1016 j jmb 2018 11 028 PMC 6360937 PMID 30529033 Laverty D Desai R Uchanski T Masiulis S Stec WJ Malinauskas T et al January 2019 Cryo EM structure of the human a1b3g2 GABAA receptor in a lipid bilayer Nature 565 7740 516 520 Bibcode 2019Natur 565 516L doi 10 1038 s41586 018 0833 4 PMC 6364807 PMID 30602789 Karahanian E Quintanilla ME Tampier L Rivera Meza M Bustamante D Gonzalez Lira V Morales P Herrera Marschitz M Israel Y April 2011 Ethanol as a prodrug brain metabolism of ethanol mediates its reinforcing effects Alcoholism Clinical and Experimental Research 35 4 606 12 doi 10 1111 j 1530 0277 2011 01439 x PMC 3142559 PMID 21332529 a b Melis M Enrico P Peana AT Diana M November 2007 Acetaldehyde mediates alcohol activation of the mesolimbic dopamine system The European Journal of Neuroscience 26 10 2824 33 doi 10 1111 j 1460 9568 2007 05887 x PMID 18001279 S2CID 25110014 a b c d e Alcoholism Homo sapiens human Database entry KEGG Pathway 29 October 2014 Retrieved 9 February 2015 a b c d e f g h Kanehisa Laboratories 29 October 2014 Alcoholism Homo sapiens human KEGG Pathway Retrieved 31 October 2014 a b c d e Malenka RC Nestler EJ Hyman SE 2009 Chapter 15 Reinforcement and Addictive Disorders In Sydor A Brown RY eds Molecular Neuropharmacology A Foundation for Clinical Neuroscience 2nd ed New York McGraw Hill Medical p 372 ISBN 978 0 07 148127 4 Ruffle JK November 2014 Molecular neurobiology of addiction what s all the D FosB about The American Journal of Drug and Alcohol Abuse 40 6 428 37 doi 10 3109 00952990 2014 933840 PMID 25083822 S2CID 19157711 Nestler EJ December 2013 Cellular basis of memory for addiction Dialogues in Clinical Neuroscience 15 4 431 43 doi 10 31887 DCNS 2013 15 4 enestler PMC 3898681 PMID 24459410 Despite the Importance of Numerous Psychosocial Factors at its Core Drug Addiction Involves a Biological Process the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs and loss of control over drug use that define a state of addiction A large body of literature has demonstrated that such DFosB induction in D1 type NAc neurons increases an animal s sensitivity to drug as well as natural rewards and promotes drug self administration presumably through a process of positive reinforcement Robison AJ Nestler EJ October 2011 Transcriptional and epigenetic mechanisms of addiction Nature Reviews Neuroscience 12 11 623 37 doi 10 1038 nrn3111 PMC 3272277 PMID 21989194 Pohorecky LA Brick J 1988 Pharmacology of ethanol Pharmacology amp Therapeutics 36 2 3 335 427 doi 10 1016 0163 7258 88 90109 X PMID 3279433 a b Liu Y Hunt WA 6 December 2012 The Drunken Synapse Studies of Alcohol Related Disorders Springer Science amp Business Media pp 40 ISBN 978 1 4615 4739 6 Rubin R Strayer DS Rubin E McDonald JM 2008 Rubin s Pathology Clinicopathologic Foundations of Medicine Lippincott Williams amp Wilkins pp 257 ISBN 978 0 7817 9516 6 Situmorang JH Lin HH Lo H Lai CC January 2018 Role of neuronal nitric oxide synthase nNOS at medulla in tachycardia induced by repeated administration of ethanol in conscious rats Journal of Biomedical Science 25 1 8 doi 10 1186 s12929 018 0409 5 PMC 5791364 PMID 29382335 Steffensen SC Shin SI Nelson AC Pistorius SS Williams SB Woodward TJ Park HJ Friend L Gao M Gao F Taylor DH Foster Olive M Edwards JG Sudweeks SN Buhlman LM Michael McIntosh J Wu J September 2017 a6 subunit containing nicotinic receptors mediate low dose ethanol effects on ventral tegmental area neurons and ethanol reward Addiction Biology 23 5 1079 1093 doi 10 1111 adb 12559 PMC 5849490 PMID 28901722 Sitte H Freissmuth M 2 August 2006 Neurotransmitter Transporters Springer Science amp Business Media pp 472 ISBN 978 3 540 29784 0 Allen Gipson DS Jarrell JC Bailey KL Robinson JE Kharbanda KK Sisson JH Wyatt TA May 2009 Ethanol blocks adenosine uptake via inhibiting the nucleoside transport system in bronchial epithelial cells Alcoholism Clinical and Experimental Research 33 5 791 8 doi 10 1111 j 1530 0277 2009 00897 x PMC 2940831 PMID 19298329 a b c d e Henri B Kissin B 1996 The Pharmacology of Alcohol and Alcohol Dependence Oxford University Press pp 18 ISBN 978 0 19 510094 5 Mitchell MC Teigen EL Ramchandani VA May 2014 Absorption and peak blood alcohol concentration after drinking beer wine or spirits Alcoholism Clinical and Experimental Research 38 5 1200 1204 doi 10 1111 acer 12355 PMC 4112772 PMID 24655007 Champagne does get you drunk faster New Scientist a b Agarwal DP Goedde HW April 1992 Pharmacogenetics of alcohol metabolism and alcoholism Pharmacogenetics 2 2 48 62 doi 10 1097 00008571 199204000 00002 PMID 1302043 Lansdorp B Ramsay W Hamidand R Strenk E May 2019 Wearable Enzymatic Alcohol Biosensor Sensors 19 10 2380 Bibcode 2019Senso 19 2380L doi 10 3390 s19102380 PMC 6566815 PMID 31137611 SCRAM CAM Bracelet Alcohol Ankle Monitor SCRAM Systems Retrieved 19 March 2022 ION Wearable ION Wearable Retrieved 19 March 2022 a b c d Philp RB 15 September 2015 Ecosystems and Human Health Toxicology and Environmental Hazards Third Edition CRC Press pp 216 ISBN 978 1 4987 6008 9 n Butanol PDF SIDS Initial Assessment Report Geneva United Nations Environment Programme April 2005 McCreery MJ Hunt WA July 1978 Physico chemical correlates of alcohol intoxication Neuropharmacology 17 7 451 61 doi 10 1016 0028 3908 78 90050 3 PMID 567755 S2CID 19914287 Carey F 2000 Organic Chemistry 4 ed McGraw Hill ISBN 0 07 290501 8 Retrieved 5 February 2013 McGovern PE Zhang J Tang J Zhang Z Hall GR Moreau RA Nunez A Butrym ED Richards MP Wang CS Cheng G Zhao Z Wang C December 2004 Fermented beverages of pre and proto historic China Proceedings of the National Academy of Sciences of the United States of America 101 51 17593 8 Bibcode 2004PNAS 10117593M doi 10 1073 pnas 0407921102 PMC 539767 PMID 15590771 McGovern P Jalabadze M Batiuk S Callahan MP Smith KE Hall GR Kvavadze E Maghradze D Rusishvili N Bouby L Failla O Cola G Mariani L Boaretto E Bacilieri R This P Wales N Lordkipanidze D November 2017 Early Neolithic wine of Georgia in the South Caucasus Proceedings of the National Academy of Sciences of the United States of America 114 48 E10309 E10318 Bibcode 2017PNAS 11410309M doi 10 1073 pnas 1714728114 PMC 5715782 PMID 29133421 Rosso AM 2012 Beer and wine in antiquity beneficial remedy or punishment imposed by the Gods Acta medico historica Adriatica 10 2 237 62 PMID 23560753 Brostrom GG Brostrom JJ 30 December 2008 The Business of Wine An Encyclopedia An Encyclopedia ABC CLIO pp 6 ISBN 978 0 313 35401 4 Babor T Caetano R Casswell S Edwards G Giesbrecht N Graham K et al 2010 Alcohol No Ordinary Commodity Research and Public Policy 2nd ed Oxford Oxford University Press ISBN 978 0 19 955114 9 OCLC 656362316 Ruthven M 1997 Islam a very short introduction New York Oxford University Press ISBN 978 0 19 154011 0 OCLC 43476241 Eucharist Definition Symbols Meaning Significance amp Facts Encyclopedia Britannica Retrieved 3 August 2021 Bocking B 1997 A popular dictionary of Shintō Rev ed Richmond Surrey U K Curzon Press ISBN 0 7007 1051 5 OCLC 264474222 a b c d e Boyle P 7 March 2013 Alcohol Science Policy and Public Health OUP Oxford pp 363 ISBN 978 0 19 965578 6 Getting a drink in Saudi Arabia BBC News BBC 8 February 2001 Retrieved 7 July 2015 Can you drink alcohol in Saudi Arabia 1 August 2012 Retrieved 7 July 2015 13 Countries With Booze Bans Swifty com Archived from the original on 2 July 2015 Retrieved 7 July 2015 AUDIT The Alcohol Use Disorders Identification Test Second Edition pdf WHO 2001 Retrieved 2 January 2020 Kalinowski A Humphreys K July 2016 Governmental standard drink definitions and low risk alcohol consumption guidelines in 37 countries Addiction 111 7 1293 1298 doi 10 1111 add 13341 PMID 27073140 Further reading editThe National Institute on Alcohol Abuse and Alcoholism maintains a database of alcohol related health effects ETOH Archival Database 1972 2003 Alcohol and Alcohol Problems Science Database External links editWHO fact sheet on alcohol ChEBI biology related Kyoto Encyclopedia of Genes and Genomes signal transduction pathway KEGG human alcohol addiction Pathophysiology of ethanol Pharmacology of ethanol Retrieved from https en wikipedia org w index php title Alcohol drug amp oldid 1193708742, wikipedia, wiki, book, books, library,

article

, read, download, free, free download, mp3, video, mp4, 3gp, jpg, jpeg, gif, png, picture, music, song, movie, book, game, games.