Alcohol (drug)

Last updated

Ethanol-3D-balls.png Ethanol-3D-vdW.png
Clinical data
Pronunciation /ˈɛθənɒl/
Other namesAbsolute alcohol; Alcohol (USP); Cologne spirit; Drinking alcohol; Ethanol (JAN); Ethylic alcohol; EtOH; Ethyl alcohol; Ethyl hydrate; Ethyl hydroxide; Ethylol; Grain alcohol; Hydroxyethane; Methylcarbinol
Moderate [1]
Moderate (10–15%) [2]
Routes of
Common: by mouth
Uncommon: suppository, inhalation, ocular, insufflation, injection [3]
Drug class Analgesic; Depressants; Sedatives; Anxiolytics; Euphoriants; GABAA receptor positive modulators
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability 80%+ [4] [5]
Protein binding Weakly or not at all [4] [5]
Metabolism Liver (90%): [6] [7]
Alcohol dehydrogenase
Metabolites Acetaldehyde; Acetate; Acetyl-CoA; Carbon dioxide; Water; Ethyl glucuronide; Ethyl sulfate
Onset of action Peak concentrations: [6] [4]
• Range: 30–90 minutes
• Mean: 45–60 minutes
Fasting: 30 minutes
Elimination half-life Constant-rate elimination at typical concentrations: [8] [7] [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 action 6–16 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]
  • ethanol
CAS Number
PubChem CID
PDB ligand
Chemical and physical data
Formula C2H6O
Molar mass 46.069 g·mol−1
3D model (JSmol)
Density 0.7893 g/cm3 (at 20 °C) [10]
Melting point −114.14 ± 0.03 °C (−173.45 ± 0.05 °F) [10]
Boiling point 78.24 ± 0.09 °C (172.83 ± 0.16 °F) [10]
Solubility in water Miscible mg/mL (20 °C)
  • CCO
  • InChI=1S/C2H6O/c1-2-3/h3H,2H2,1H3

Alcohol, sometimes referred to by the chemical name ethanol , is a depressant drug that is the active ingredient in 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 function. Ethanol is only one of several types of alcohol, but it is the only type of alcohol that is found in alcoholic beverages or commonly used for recreational purposes; other alcohols such as methanol and isopropyl alcohol are significantly more toxic. [11] A mild, brief exposure to isopropanol, being only moderately more toxic than ethanol, is unlikely to cause any serious harm. Methanol, being profoundly more toxic than ethanol, is lethal in quantities as small as 10–15 milliliters (2–3 tsp).


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 damage [13] and brain damage, [14] [15] and its consumption is the fifth leading cause of cancer. [16] [ failed verification ] 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.

Alcohol works in the brain primarily by increasing the effects of a neurotransmitter called γ-aminobutyric acid, or GABA. [19] This is the major inhibitory neurotransmitter in the brain, and by facilitating its actions, alcohol suppresses the activity of the central nervous system. [19] The substance also directly affects a number of other neurotransmitter systems including those of glutamate, glycine, acetylcholine, and serotonin. [20] [21] The pleasurable effects of alcohol ingestion are the result of increased levels of dopamine and endogenous opioids in the reward pathways of the brain. [22] [23] Alcohol also has toxic and unpleasant actions in the body, many of which are mediated by its byproduct acetaldehyde. [24]

Alcohol has been produced and consumed by humans for its psychoactive effects for almost 10,000 years. [25] 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. [26] 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 unique in that it is the only drug that damages others more than the user. [27] It is related to various societal problems, including drunk driving, accidental injuries, sexual assaults, domestic abuse, and violent crime. [28] 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. [29] [30] [31]

Use and effects

Symptoms of varying BAC levels. Additional symptoms may occur. Symptoms of BAC, 0.02%25 to 0.50%25 concentration.svg
Symptoms of varying BAC levels. Additional symptoms may occur.

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.

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 [32] 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 g/L), ethanol acts as a central nervous system depressant, [32] 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.

Standard drink

There is no single standard, but a standard drink of 10g alcohol, which is used in the WHO AUDIT (Alcohol Use Disorders Identification Test)'s questionnaire form example, [33] have been adopted by more countries than any other amount. [34] 10 grams is equivalent to 12.7 millilitres.


Alcohol has a variety of short-term and long-term adverse effects. It also has reinforcement-related adverse effects, including addiction, dependence, and withdrawal.

Social harm

A 2010 study ranking various illegal and legal drugs based on statements by drug-harm experts. Alcohol was found to be the overall most dangerous drug, and the only drug that mostly damaged others. HarmCausedByDrugsTable.svg
A 2010 study ranking various illegal and legal drugs based on statements by drug-harm experts. Alcohol was found to be the overall most dangerous drug, and the only drug that mostly damaged others.

Alcohol causes a plethora of detrimental effects in society. [28] It is highly associated with drinking in public, passive drinking, drunk dialing, drunk driving, sexual risk-taking or drug facilitated sexual assault (especially with caffeinated alcoholic drinks), [35] and both violent and non-violent crime. [28] About one-third of arrests in the United States involve alcohol misuse. [28] Many emergency room visits also involve alcohol use. [28] 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. [28] Heavy drinking is associated with vulnerability to injury, marital discord, and domestic violence. [28] Alcohol use is directly related to considerable morbidity and mortality, for instance due to overdose and alcohol-related health problems. [36]

Automobile accidents

A 2002 study found 41% of people fatally injured in traffic accidents were in alcohol-related crashes. [37] Misuse of alcohol is associated with more than 40% of deaths that occur in automobile accidents every year. [28] The risk of a fatal car accident increases exponentially with the level of alcohol in the driver's blood. [38] Most drunk driving laws in the United States governing the acceptable levels in the blood while driving or operating heavy machinery set typical upper limits of legal blood alcohol content (BAC) at 0.08%. [39]

Sexual assault

Alcohol is often used to facilitate sexual assault or rape. [40] [41] Over 50% of reported rapes involve alcohol.[ clarification needed ] [28] It is the most commonly used date rape drug. [42]

Violent crime

Over 40% of all assaults and 40 to 50% of all murders involve alcohol. [28] More than 43% of violent encounters with police involve alcohol. [28] Alcohol is implicated in more than two-thirds of cases of intimate partner violence. [28] In 2002, it was estimated that 1 million violent crimes in the United States were related to alcohol use. [28] Alcohol is more commonly associated with both violent and non-violent crime than are drugs like marijuana. [28]

Health consequences

Alcohol use disorder is a major problem and many health problems as well as death can result from excessive alcohol use. [28] [36] Alcohol dependence is linked to a lifespan that is reduced by about 12 years relative to the average person. [28] In 2004, it was estimated that 4% of deaths worldwide were attributable to alcohol use. [36] Deaths from alcohol are split about evenly between acute causes (e.g., overdose, accidents) and chronic conditions. [36] The leading chronic alcohol-related condition associated with death is alcoholic liver disease. [36] Alcohol dependence is also associated with cognitive impairment and organic brain damage. [28] Some researchers have found that even one alcoholic drink a day increases an individual's risk of health problems by 0.4%. [43]

Adverse effects

Short-term effects

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. Rational harm assessment of drugs radar plot.svg
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.

Central nervous system impairment

Alcohol causes generalized central nervous system depression, is a positive allosteric GABAA modulator and is associated and related with cognitive, memory or memory loss, 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 (PAN), respiratory depression, shock, coma and death can result due to profound suppression of central nervous system function alcohol overdose and can finish in consequent dysautonomia.

Gastrointestinal effects

Diagram of mucosal layer Stomach mucosal layer labeled.svg
Diagram of mucosal layer

Alcohol can cause nausea and vomiting in sufficiently high amounts (varies 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 H. pylori. H. pylori secrete a toxin that weakens the mucosal wall, which as a result lead to acid and protein enzymes penetrating the weakened barrier. Because alcohol stimulates a person's 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. [45] 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. [46] A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation. [46]

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 this (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 (ROS), leukotrienes, chemokines and cytokines. These factors promote tissue inflammation and contribute to organ pathology. [47]

Allergic-like reactions

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: [48]

  • 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.

Long-term effects

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

Brain damage

Alcohol can cause brain damage, Wernicke's encephalopathy and Alcoholic Korsakoff syndrome (AKS) which frequently occur simultaneously, known as Wernicke–Korsakoff syndrome (WKS). [49] Lesions, or brain abnormalities, are typically located in the diencephalon which result in anterograde and retrograde amnesia, or memory loss. [49]

Liver damage

During the metabolism of alcohol via the respective dehydrogenases, NAD (nicotinamide adenine dinucleotide) 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

Ethanol is classified as a teratogen.[ medical citation needed ] According to the U.S. Centers for Disease Control (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. [50]


IARC list ethanol in alcoholic beverages are classified as a Group 1 carcinogens in human beings 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." [51]

Other effects

Frequent drinking of alcoholic beverages is a major contributing factor in cases of elevated blood levels of triglycerides. [52]

Reinforcement disorders


Alcohol addiction is termed alcohol use disorder.

Two or more consecutive alcohol-free days a week have been recommended to improve health and break dependence. [53] [54] [55]

Dependence and withdrawal

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.


Death from ethanol consumption is possible when blood alcohol levels reach 0.4%. A blood level of 0.5% or more is commonly fatal. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3–0.4%. [56]

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. Symptoms of ethanol overdose may include nausea, vomiting, central nervous system depression, coma, acute respiratory failure, or death


Alcohol can intensify the sedation caused by other central nervous system depressants such as barbiturates, benzodiazepines, opioids, nonbenzodiazepines/Z-drugs (such as zolpidem and zopiclone), antipsychotics, sedative antihistamines, and certain antidepressants. [56] It interacts with cocaine in vivo to produce cocaethylene, another psychoactive substance. [57] Ethanol enhances the bioavailability of methylphenidate (elevated plasma dexmethylphenidate). [58] [ irrelevant citation ] In combination with cannabis, ethanol increases plasma tetrahydrocannabinol levels, which suggests that ethanol may increase the absorption of tetrahydrocannabinol. [59]

Disulfiram-like drugs


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.


One of the most important drug/food interactions is between alcohol and metronidazole.

Metronidazole is an antibacterial agent that kills bacteria by damaging cellular DNA and hence cellular function. [60] Metronidazole is usually given to people who have diarrhea caused by Clostridium difficile bacteria. C. difficile is one of the most common microorganisms that cause diarrhea and can lead to complications such as colon inflammation and even more severely, death.

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.

Methanol and ethylene glycol

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. [61] Ethylene glycol poisoning can be treated in the same way.



The precise mechanism of action of ethanol has proven elusive and remains not fully understood. [19] [62] Identifying molecular targets for ethanol has proven unusually difficult, in large part due to its unique biochemical properties. [62] 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. [62] [63] 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. [62] [63] Instead, researchers have had to rely on functional studies to elucidate the actions of ethanol. [62] Moreover, although it has been established that ethanol modulates ion channels to mediate its effects, [21] 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). [19] [62]

Much progress has been made in understanding the pharmacodynamics of ethanol over the last few decades. [20] [62] 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 central nervous system. [19] [20] [21] [62] 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, [64] the nicotinic acetylcholine receptors, [65] the serotonin 5-HT3 receptor, voltage-gated calcium channels, and BK channels, among others. [19] [20] [21] [66] [67] 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. [62] 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. [19] [62] Indeed, ethanol has been found to enhance GABAA receptor-mediated currents in functional assays. [19] [62] In accordance, it is theorized and widely believed that the primary mechanism of action is as a GABAA receptor positive allosteric modulator. [19] [62] However, the diverse actions of ethanol on other ion channels may be and indeed likely are involved in its effects as well. [20] [62]

Recently, a study showed the accumulation of an unnatural lipid phosphatidylethanol (PEth) competes with PIP2 agonists sites on lipid-gated ion channels. [68] This presents a novel indirect mechanism and suggests that a metabolite, not the ethanol itself, can effect the primary targets of ethanol intoxication. Many of the primary targets of ethanol are known to bind PIP2 including GABAA receptors, [69] but the role of PEth will need to be investigated for each of the primary targets.

In 2007, it was discovered that ethanol potentiates extrasynaptic δ subunit-containing GABAA receptors at behaviorally relevant (as low as 3 mM) concentrations. [19] [62] [70] 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). [19] [62] [71] 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. [62] [70] In addition, Ro15-4513 blocked the enhancement of δ subunit-containing GABAA receptor currents by ethanol in vitro. [62] 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. [62] [70] 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. [19] [62] [70] [72]

Rewarding and reinforcing actions

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. [73] 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. [74]

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). [75] [76] 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). [77] At high doses, ethanol inhibits most ligand-gated ion channels and voltage-gated ion channels in neurons as well. [77]

With acute alcohol consumption, dopamine is released in the synapses of the mesolimbic pathway, in turn heightening activation of postsynaptic D1 receptors. [75] [76] 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. [75] [76]

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; [75] [76] an adaptive downregulation of the D1 receptor pathway and CREB function occurs as well. [75] [76] 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. [76] These modifications to CREB function in the mesolimbic pathway induce expression (i.e., increase gene expression) of ΔFosB in the NAcc, [76] 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). [76] [78] [79] [80]

Relationship between concentrations and effects

Blood alcohol levels and effects [81]
mg/dLmM % v/vEffects
50110.05%Euphoria, talkativeness, relaxation, happiness, gladness, pleasure, joyfulness.
100220.1%Central nervous system depression, anxiety suppression, stress suppression, sedation, nausea, possible vomiting, impaired motor and sensory function,impaired memory impaired cognition
>14030>0.14%Decreased blood flow to brain, slurred speech, double or blurry vision.
300650.3%Stupefaction, confusion, numbness, dizziness, loss of consciousness.
400870.4%Ethylic intoxication, drunkeness, inebriation, alcohol poisoning or possible death.
500109>0.55%Unconsciousness, coma and death.

Recreational concentrations of ethanol are typically in the range of 1 to 50 mM. [71] [19] Very low concentrations of 1 to 2 mM ethanol produce zero or undetectable effects except in alcohol-naive individuals. [71] 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. [71] 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. [71] In jurisdictions in the United States, maximum blood alcohol levels for legal driving are about 17 to 22 mM. [82] [83] 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. [71] [82] 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. [71] Concentrations above this range, specifically in the range of 100 to 200 mM, would cause death in all people except alcoholics. [71]

List of known actions in the central nervous system

Ethanol has been reported to possess the following actions in functional assays at varying concentrations: [63]

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. [63] This seems to be because the effects of ethanol on these channels are a summation of positive and negative allosteric modulatory actions. [63]



Ethanol can be taken orally, by inhalation, rectally, or by injection (e.g., intravenous), [6] [88] 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. [88] 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]


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: [89]

  • 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. [90]

Food in the gastrointestinal system and hence gastric emptying is the most important factor that influences the absorption of orally ingested ethanol. [6] [88] 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. [88] Not only does food slow the absorption of ethanol, but it also reduces the bioavailability of ethanol, resulting in lower circulating concentrations. [6]


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] [88] 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]


Approximately 90% of the metabolism of ethanol occurs in the liver. [6] [7] This occurs predominantly via the enzyme alcohol dehydrogenase, which transforms ethanol into its metabolite acetaldehyde (ethanal). [6] [7] 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] [7] 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] [7] 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. [7] 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. [7] [8] 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. [7] [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. [91] However, those having acquired alcohol tolerance have a greater quantity of these enzymes, and metabolize ethanol more rapidly. [91]


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 [92] such as SCRAM ankle bracelet [93] or the more discreet ION Wearable. [94] Ethanol or its metabolites may be detectable in urine for up to 96 hours (3–5 days) after ingestion. [4]


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.


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.


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. [95] In general, higher alcohols are less toxic. [95] 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). [96] [97] However, its vapors can produce eye irritation and inhalation can cause pulmonary edema. [95] 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. [95]

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. [98] Other relatives of ethanol with similar effects include chloral hydrate, paraldehyde, and many volatile and inhalational anesthetics (e.g., chloroform, diethyl ether, and isoflurane).


Alcohol was brewed as early as 7,000 to 6,650 BCE in northern China. [25] The earliest evidence of winemaking was dated at 6,000 to 5,800 BCE in Georgia in the South Caucasus. [99] Beer was likely brewed from barley as early as the 6th century BCE (600–500 BCE) in Egypt. [100] Pliny the Elder wrote about the golden age of winemaking in Rome, the 2nd century BCE (200–100 BCE), when vineyards were planted. [101]

Society and culture

Alcohol consumption is fully legal and available in most countries of the world. [102] Home made alcoholic beverages with low alcohol content like wine, and beer is also legal in most countries, but distilling moonshine outside 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. [103] [104] [105] Also, laws banning alcohol consumption are found in some Indian states as well as some Native American reservations in the United States. [102]

In addition, there are regulations on alcohol sales and use in many countries throughout the world. [102] For instance, some countries have a minimum legal age to purchase or consume alcoholic beverages. Also, some countries have bans on public intoxication. [102] 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. [102]

See also

Related Research Articles

<span class="mw-page-title-main">Alcohol intoxication</span> Negative effects due to ethanol (alcohol)

Alcohol intoxication, also known as alcohol poisoning, commonly described as drunkenness or inebriation, is the negative behavior and physical effects caused by a recent consumption of alcohol. In addition to the toxicity of ethanol, the main psychoactive component of alcoholic beverages, other physiological symptoms may arise from the activity of acetaldehyde, a metabolite of alcohol. These effects may not arise until hours after ingestion and may contribute to the condition colloquially known as a hangover.

<span class="mw-page-title-main">Disulfiram</span> Chemical compound

Disulfiram is a medication used to support the treatment of chronic alcoholism by producing an acute sensitivity to ethanol. Disulfiram works by inhibiting the enzyme acetaldehyde dehydrogenase, causing many of the effects of a hangover to be felt immediately following alcohol consumption. Disulfiram plus alcohol, even small amounts, produces flushing, throbbing in the head and neck, a throbbing headache, respiratory difficulty, nausea, copious vomiting, sweating, thirst, chest pain, palpitation, dyspnea, hyperventilation, fast heart rate, low blood pressure, fainting, marked uneasiness, weakness, vertigo, blurred vision, and confusion. In severe reactions there may be respiratory depression, cardiovascular collapse, abnormal heart rhythms, heart attack, acute congestive heart failure, unconsciousness, convulsions, and death.

<span class="mw-page-title-main">Acetaldehyde dehydrogenase</span> Class of enzymes

Acetaldehyde dehydrogenases are dehydrogenase enzymes which catalyze the conversion of acetaldehyde into acetic acid. The oxidation of acetaldehyde to acetate can be summarized as follows:

<span class="mw-page-title-main">Alcoholic polyneuropathy</span> Medical condition

Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously. It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.

GABA<sub>A</sub> receptor Ionotropic receptor and ligand-gated ion channel

The GABAA receptor (GABAAR) is an ionotropic receptor and ligand-gated ion channel. Its endogenous ligand is γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Upon opening, the GABAA receptor on the postsynaptic cell is selectively permeable to chloride ions (Cl) and, to a lesser extent, bicarbonate ions (HCO3). Depending on the membrane potential and the ionic concentration difference, this can result in ionic fluxes across the pore. If the membrane potential is higher than the equilibrium potential (also known as the reversal potential) for chloride ions, when the receptor is activated Cl will flow into the cell. This causes an inhibitory effect on neurotransmission by diminishing the chance of a successful action potential occurring at the postsynaptic cell. The reversal potential of the GABAA-mediated inhibitory postsynaptic potential (IPSP) in normal solution is −70 mV, contrasting the GABAB IPSP (-100 mV).

Neuropharmacology is the study of how drugs affect function in the nervous system, and the neural mechanisms through which they influence behavior. There are two main branches of neuropharmacology: behavioral and molecular. Behavioral neuropharmacology focuses on the study of how drugs affect human behavior (neuropsychopharmacology), including the study of how drug dependence and addiction affect the human brain. Molecular neuropharmacology involves the study of neurons and their neurochemical interactions, with the overall goal of developing drugs that have beneficial effects on neurological function. Both of these fields are closely connected, since both are concerned with the interactions of neurotransmitters, neuropeptides, neurohormones, neuromodulators, enzymes, second messengers, co-transporters, ion channels, and receptor proteins in the central and peripheral nervous systems. Studying these interactions, researchers are developing drugs to treat many different neurological disorders, including pain, neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease, psychological disorders, addiction, and many others.

<span class="mw-page-title-main">Fomepizole</span> Medication

Fomepizole, also known as 4-methylpyrazole, is a medication used to treat methanol and ethylene glycol poisoning. It may be used alone or together with hemodialysis. It is given by injection into a vein.

<span class="mw-page-title-main">Alcohol tolerance</span> Bodily responses to the functional effects of ethanol in alcoholic beverages

Alcohol tolerance refers to the bodily responses to the functional effects of ethanol in alcoholic beverages. This includes direct tolerance, speed of recovery from insobriety and resistance to the development of alcohol use disorder.

<span class="mw-page-title-main">Acamprosate</span> Medication

Acamprosate, sold under the brand name Campral, is a medication used along with counselling to treat alcohol use disorder.

Ethanol, an alcohol found in nature and in alcoholic drinks, is metabolized through a complex catabolic metabolic pathway. In humans, several enzymes are involved in processing ethanol first into acetaldehyde and further into acetic acid and acetyl-CoA. Once acetyl-CoA is formed, it becomes a substrate for the citric acid cycle ultimately producing cellular energy and releasing water and carbon dioxide. Due to differences in enzyme presence and availability, human adults and fetuses process ethanol through different pathways. Gene variation in these enzymes can lead to variation in catalytic efficiency between individuals. The liver is the major organ that metabolizes ethanol due to its high concentration of these enzymes.

<span class="mw-page-title-main">Ro15-4513</span> Chemical compound

Ro15-4513(IUPAC: Ethyl-8-azido-5,6-dihydro-5-methyl-6-oxo-4H-imidazo-1,4-benzodiazepine-3-carboxylate) is a weak partial inverse agonist of the benzodiazepine class of drugs, developed by Hoffmann–La Roche in the 1980s. It acts as a inverse agonist, and can therefore be an antidote to the acute impairment caused by alcohols, including ethanol, isopropanol, tert-butyl alcohol, tert-amyl alcohol, 3-methyl-3-pentanol, methylpentynol and ethchlorvynol.

<span class="mw-page-title-main">Hangover</span> Effects following consumption of alcohol

A hangover is the experience of various unpleasant physiological and psychological effects usually following the consumption of alcohol, such as wine, beer, and liquor. Hangovers can last for several hours or for more than 24 hours. Typical symptoms of a hangover may include headache, drowsiness, concentration problems, dry mouth, dizziness, fatigue, gastrointestinal distress, absence of hunger, light sensitivity, depression, sweating, nausea, hyper-excitability, irritability, and anxiety.

<i>tert</i>-Amyl alcohol Chemical compound

tert-Amyl alcohol (TAA) or 2-methylbutan-2-ol (2M2B), is a branched pentanol.

<span class="mw-page-title-main">Alcohol withdrawal syndrome</span> Symptoms that can occur following a reduction in alcohol use after a period of excessive use

Alcohol withdrawal syndrome (AWS) is a set of symptoms that can occur following a reduction in alcohol use after a period of excessive use. Symptoms typically include anxiety, shakiness, sweating, vomiting, fast heart rate, and a mild fever. More severe symptoms may include seizures,and delirium tremens (DTs). Symptoms typically begin around six hours following the last drink, are worst at 24 to 72 hours, and improve by seven days.

<span class="mw-page-title-main">Short-term effects of alcohol consumption</span> Overview of the short-term effects of the consumption of alcoholic beverages

The short-term effects of alcohol consumption range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), to stupor, unconsciousness, anterograde amnesia, and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream, it can diffuse into nearly every cell in the body.

In pharmacology and biochemistry, allosteric modulators are a group of substances that bind to a receptor to change that receptor's response to stimulus. Some of them, like benzodiazepines, are drugs. The site that an allosteric modulator binds to is not the same one to which an endogenous agonist of the receptor would bind. Modulators and agonists can both be called receptor ligands.

<span class="mw-page-title-main">Effects of alcohol on memory</span> Health effect of alcohol consumption

Ethanol is the type of alcohol found in alcoholic beverages. It is a volatile, flammable, colorless liquid that acts as a central nervous system depressant. Ethanol can impair different types of memory.

Kindling due to substance withdrawal refers to the neurological condition which results from repeated withdrawal episodes from sedative–hypnotic drugs such as alcohol and benzodiazepines.

GABA<sub>A</sub> receptor positive allosteric modulator

In pharmacology, GABAA receptor positive allosteric modulators are positive allosteric modulator (PAM) molecules that increase the activity of the GABAA receptor protein in the vertebrate central nervous system.

A GABAA receptor negative allosteric modulator is a negative allosteric modulator (NAM), or inhibitor, of the GABAA receptor, a ligand-gated ion channel of the major inhibitory neurotransmitter γ-aminobutyric acid (GABA). They are closely related and similar to GABAA receptor antagonists. The effects of GABAA receptor NAMs are functionally the opposite of those of GABAA receptor positive allosteric modulators (PAMs) like the benzodiazepines, barbiturates, and ethanol (alcohol). Non-selective GABAA receptor NAMs can produce a variety of effects including convulsions, neurotoxicity, and anxiety, among others.


  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. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 Principles of Addiction: Comprehensive Addictive Behaviors and Disorders. Academic Press. 17 May 2013. pp. 162–. ISBN   978-0-12-398361-9.
  5. 1 2 3 4 5 6 7 8 9 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. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 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. 1 2 3 4 5 6 7 8 9 Levine B (2003). Principles of Forensic Toxicology. Amer. Assoc. for Clinical Chemistry. pp. 161–. ISBN   978-1-890883-87-4.
  8. 1 2 Becker CE (September 1970). "The clinical pharmacology of alcohol". California Medicine. 113 (3): 37–45. PMC   1501558 . PMID   5457514.
  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. 1 2 3 Haynes, William M., ed. (2011). CRC Handbook of Chemistry and Physics (92nd ed.). Boca Raton, FL: CRC Press. p. 3.246. ISBN   1-4398-5511-0.
  11. 1 2 3 Collins SE, Kirouac M (2013). "Alcohol Consumption". Encyclopedia of Behavioral Medicine: 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. 1 2 3 4 5 6 7 8 9 10 11 12 13 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.
  20. 1 2 3 4 5 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.
  21. 1 2 3 4 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.
  22. 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.
  23. 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.
  24. Burcham PC (19 November 2013). An Introduction to Toxicology. Springer Science & Business Media. pp. 42–. ISBN   978-1-4471-5553-9.
  25. 1 2 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.
  26. 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.
  27. 1 2 Nutt DJ, King LA, Phillips LD (November 2010). "Drug harms in the UK: a multicriteria decision analysis". Lancet. 376 (9752): 1558–65. CiteSeerX . doi:10.1016/S0140-6736(10)61462-6. PMID   21036393. S2CID   5667719.
  28. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Butcher JN, Hooley JM, Mineka SM (25 June 2013). Abnormal Psychology. Pearson Education. p. 370. ISBN   978-0-205-97175-6.
  29. Ruthven M (1997). Islam : a very short introduction. New York. ISBN   978-0-19-154011-0. OCLC   43476241.
  30. "Eucharist | Definition, Symbols, Meaning, Significance, & Facts". Encyclopedia Britannica. Retrieved 3 August 2021.
  31. Bocking B (1997). A popular dictionary of Shintō (Rev. ed.). Richmond, Surrey [U.K.]: Curzon Press. ISBN   0-7007-1051-5. OCLC   264474222.
  32. 1 2 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.
  33. "AUDIT The Alcohol Use Disorders Identification Test (Second Edition)" (pdf). WHO. 2001. Retrieved 2 January 2020.
  34. 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.
  35. 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.
  36. 1 2 3 4 5 Friedman HS (26 August 2011). The Oxford Handbook of Health Psychology. Oxford University Press, USA. pp. 699–. ISBN   978-0-19-534281-9.
  37. Hingson R, Winter M (2003). "Epidemiology and consequences of drinking and driving". Alcohol Research & Health. 27 (1): 63–78. PMC   6676697 . PMID   15301401.
  38. 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.
  39. "Legislative History of .08 per se Laws – NHTSA". NHTSA. National Highway Traffic Safety Administration. July 2001. Retrieved 21 July 2017.
  40. 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.
  41. 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.
  42. 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.
  43. Bakalar N (27 August 2018). "How Much Alcohol Is Safe to Drink? None, Say These Researchers". The New York Times. Retrieved 17 September 2018.
  44. 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.
  45. Overview of Peptic Ulcer Disease: Etiology and Pathophysiology. Retrieved 27 April 2013.
  46. 1 2 Peptic Ulcer Disease (Stomach Ulcers) Cause, Symptoms, Treatments. Retrieved 27 April 2013.
  47. 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.
  48. 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.
  49. 1 2 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.
  50. "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.
  51. Agents Classified by the IARC Monographs, Volumes 1–111 Archived 25 October 2011 at the Wayback Machine .
  52. "Triglycerides". American Heart Association. Archived from the original on 27 August 2007. Retrieved 4 September 2007.
  53. 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.
  54. 5 Ways Your Body Changes When you Have Alcohol Mountainside Treatment Center access-date=22 March 2019
  55. "Alcohol". British Liver Trust. Archived from the original on 11 July 2019. Retrieved 22 March 2019.
  56. 1 2 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.
  57. 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.
  58. 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.
  59. 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.
  60. Repchinsky C (ed.) (2012). Compendium of pharmaceuticals and specialties, Ottawa: Canadian Pharmacists Association.[ full citation needed ]
  61. 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.
  62. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 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.
  63. 1 2 3 4 5 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.
  64. 1 2 3 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.
  65. 1 2 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.
  66. 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.
  67. 1 2 3 4 5 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.
  68. 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.
  69. 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.
  70. 1 2 3 4 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.
  71. 1 2 3 4 5 6 7 8 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.
  72. 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.
  73. 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.
  74. 1 2 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.
  75. 1 2 3 4 5 "Alcoholism – Homo sapiens (human) Database entry". KEGG Pathway. 29 October 2014. Retrieved 9 February 2015.
  76. 1 2 3 4 5 6 7 8 Kanehisa Laboratories (29 October 2014). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014.
  77. 1 2 3 4 5 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.
  78. 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.
  79. 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
  80. 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.
  81. 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.
  82. 1 2 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.
  83. 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.
  84. 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.
  85. 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.
  86. Sitte H, Freissmuth M (2 August 2006). Neurotransmitter Transporters. Springer Science & Business Media. pp. 472–. ISBN   978-3-540-29784-0.
  87. 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.
  88. 1 2 3 4 5 Henri B, Kissin B (1996). The Pharmacology of Alcohol and Alcohol Dependence . Oxford University Press. pp.  18–. ISBN   978-0-19-510094-5.
  89. 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.
  90. "Champagne does get you drunk faster". New Scientist.
  91. 1 2 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.
  92. 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.
  93. "SCRAM CAM® Bracelet Alcohol Ankle Monitor". SCRAM Systems. Retrieved 19 March 2022.
  94. "ION Wearable". ION Wearable. Retrieved 19 March 2022.
  95. 1 2 3 4 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.
  96. n-Butanol (PDF), SIDS Initial Assessment Report, Geneva: United Nations Environment Programme, April 2005.
  97. 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.
  98. Carey F (2000). Organic Chemistry (4 ed.). ISBN   0-07-290501-8 . Retrieved 5 February 2013.
  99. 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.
  100. 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.
  101. 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.
  102. 1 2 3 4 5 Boyle P (7 March 2013). Alcohol: Science, Policy and Public Health. OUP Oxford. pp. 363–. ISBN   978-0-19-965578-6.
  103. "Getting a drink in Saudi Arabia". BBC News. BBC. 8 February 2001. Retrieved 7 July 2015.
  104. "Can you drink alcohol in Saudi Arabia?". 1 August 2012. Retrieved 7 July 2015.
  105. "13 Countries With Booze Bans". Archived from the original on 2 July 2015. Retrieved 7 July 2015.

Further reading

Pathophysiology of ethanol
Pharmacology of ethanol