| Alcohol |
| Alcohol | |||||||||||||||||||
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| The skeletal formula of Alcohol (Ethanol). | |||||||||||||||||||
| Chemical Nomenclature | |||||||||||||||||||
| Common names | Alcohol | ||||||||||||||||||
| Systematic name | Ethanol | ||||||||||||||||||
| Routes of Administration | |||||||||||||||||||
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Alcohol (also known as Ethyl Alcohol or Ethanol) is one of the oldest and most widely used psychoactive drugs in history and continues to be the most widely used recreational substance. Based on its subjective effects, this substance can be classed as a depressant.
An alcoholic beverage is a drink that typically contains 3%–60% ethanol, commonly known as alcohol. Alcoholic beverages are divided into three classes: beers, wines, and spirits (distilled beverages). They are legally consumed in most countries around the world. More than 100 countries have laws regulating their production, sale, and consumption.[1]
Alcoholic beverages have been produced and consumed by humans since the Neolithic Era, from hunter-gatherer peoples to nation-states.[2]
Contents
Chemistry
Ethanol is an extremely simplistic molecule and is comprised of a chain of two carbon atoms with a hydroxyl (-OH) functional group attached.
Pharmacology
In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain.[3] However, molecular pharmacology studies have shown that alcohol has only a few primary targets. In some systems, these effects are facilitatory and in others inhibitory.
Among the neurotransmitter systems with enhanced functions are:
- GABA[4] : In a fashion similar to benzodiazepines, an enhancement of the inhibitory system known as GABA and effectively induces neurological inhibition. This depresses the behavioral inhibitory centers, slows down the processing of information from the senses, Inhibits thought processes and generally induces a suppression of both normal physical and cognitive functioning.
- 5-HT3 receptor agonism[5]
- Nicotinic acetylcholine receptors[6]
Among those that are inhibited are:
- Glutamate[7]: By making this excitatory neurotransmitter less effective, neurological functioning is further inhibited. Alcohol does this by interacting with the receptors on the receiving cells in these pathways and blocking glutamate from allowing the passing of electrical signals between NDMA receptors.
- Dihydropyridine[8]
The result of these direct effects is a wave of further indirect effects involving a variety of other neurotransmitter and neuropeptide systems, leading finally to the behavioural or symptomatic effects of alcohol intoxication.[9] It's worth noting however that in terms of how these processes directly result in the subjective experience of ethanol intoxication, the exact mechanisms are still largely unknown beyond speculation.
Subjective effects
The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects will rarely if ever occur all at once but heavier dosages will increase the chances and are more likely to induce a full range of effects.
Physical effects
The physical effects of alcohol can be broken down into several components all of which progressively intensify proportional to dosage. These are described below and generally include:
- Nausea
- Pain relief
- Motor control loss
- Dizziness
- Sedation
- Frequent urination
- Dehydration
- Tactile suppression
- Temporary erectile dysfunction
- Headaches
- Respiratory depression
- Salivation
Cognitive effects
The cognitive effects of alcohol can be broken down into several components all of which progressively intensify proportional to dosage. It contains a large number of typical depressant cognitive effects which generally include:
- Disinhibition
- Information processing suppression
- Thought deceleration
- Empathy, love and sociability enhancement
- Amnesia
- Euphoria
- Depression
- Compulsive redosing
Visual effects
Toxicity and harm potential
Although the sensible use of alcohol in the short term is extremely unlikely to have any positive or detrimental effects on one's physical health. The long-term effects of alcohol consumption range from cardioprotective health benefits for low to moderate alcohol consumption in industrialized societies with higher rates of cardiovascular disease[11][12] to severe detrimental effects in cases of chronic alcohol abuse.[13] High levels of alcohol consumption are associated with an increased risk of alcoholism, malnutrition, chronic pancreatitis, alcoholic liver disease, and cancer. In addition, damage to the central nervous system and peripheral nervous system can occur from chronic alcohol abuse.[14][15] The long-term use of alcohol is capable of damaging nearly every organ and system in the body.[16] The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol.[17] In addition, the developing fetal brain is also vulnerable, and fetal alcohol syndrome (FAS) may result if pregnant mothers consume alcohol.
Lethal dosage
Death from ethanol consumption is possible when blood alcohol level reaches 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%.[18]
Tolerance and addiction potential
Frequent use of alcohol can be considered as extremely addictive and is capable of causing both physical and psychological dependence.
Tolerance to many of the effects of alcohol develops with prolonged use. This results in users having to consume increasingly large doses to achieve the same effects.
Chronic excess alcohol intake, or alcohol dependence, can lead to a wide range of neuropsychiatric or neurological impairment, cardiovascular disease, liver disease, and malignant neoplasms. The psychiatric disorders which are associated with alcoholism include major depression, dysthymia, mania, hypomania, panic disorder, phobias, generalized anxiety disorder, personality disorders, schizophrenia, suicide, neurologic deficits (e.g. impairments of working memory, emotions, executive functions, visuospatial abilities and gait and balance) and brain damage. Alcohol dependence is associated with hypertension, coronary heart disease, and ischemic stroke, cancer of the respiratory system, and also cancers of the digestive system, liver, breast and ovaries. Heavy drinking is associated with liver disease, such as cirrhosis.[19]
Withdrawals
When physical dependence has developed, withdrawal symptoms may occur if a person suddenly stops their usage. The severity of withdrawal can vary from mild symptoms such as sleep disturbances and anxiety to severe and life-threatening symptoms such as delirium, hallucinations, and autonomic instability.
Withdrawal usually begins 6 to 24 hours after the last drink.[20] It can last for up to one week.[21] To be classified as alcohol withdrawal syndrome, patients must exhibit at least two of the following symptoms: increased hand tremor, insomnia, nausea or vomiting, transient hallucinations (auditory, visual or tactile), psychomotor agitation, anxiety, tonic-clonic seizures, and autonomic instability.[22]
The severity of symptoms is dictated by a number of factors, the most important of which is degree of alcohol intake, length of time the individual has been using alcohol, and previous history of alcohol withdrawal.[23] Symptoms are also grouped together and classified:
- Alcohol hallucinosis: Patients have transient visual, auditory, or tactile hallucinations, but are otherwise clear.[24]
- Withdrawal seizures: Seizures occur within 48 hours of alcohol cessations and occur either as a single generalized tonic-clonic seizure or as a brief episode of multiple seizures.[25]
- Delirium tremens: Hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations[26] usually occur 24 to 72 hours after alcohol cessation. Delirium tremens is the most severe form of withdrawal and occurs in 5 to 20% of patients experiencing detoxification and 1/3 of patients experiencing withdrawal seizures.[27]
Interactions
Alcohol can intensify the sedation caused by other central nervous system depressant drugs such as barbiturates, benzodiazepines, opioids, phenothiazines, and anti-depressants.[28] At sufficiently high dosages, these combinations can result in fatal respiratory depression. It also interacts with cocaine in vivo to produce cocaethylene, another psychoactive substance.[29]
Legal issues
Alcoholic beverages are legally consumed in most countries around the world. More than 100 countries have laws regulating their production, sale, and consumption.[30] In particular, such laws often specify the legal drinking age which usually varies between 16 and 25 years, sometimes depending on the type of drink. Some countries do not have a legal drinking or purchasing age, but most set the age at 18 years.[31]
See also
References
- ↑ http://icap.org/table/Worldwide
- ↑ Arnold, John P (2005). Origin and History of Beer and Brewing: From Prehistoric Times to the Beginning of Brewing Science and Technology. Cleveland, Ohio: Reprint Edition by BeerBooks. ISBN 0-9662084-1-2.
- ↑ Neuropharmacology of alcohol addiction | http://onlinelibrary.wiley.com/doi/10.1038/bjp.2008.30/abstract
- ↑ Sites of alcohol and volatile anaesthetic action on GABAA and glycine receptors | http://www.nature.com/nature/journal/v389/n6649/full/389385a0.html
- ↑ 5-HT3 receptors and the neural actions of alcohols: an increasingly exciting topic | http://www.sciencedirect.com/science/article/pii/S0197018699000546
- ↑ Neuronal nicotinic acetylcholine receptors: a new target site of ethanol | http://www.sciencedirect.com/science/article/pii/S0197018699000558
- ↑ 5-HT3 receptors and the neural actions of alcohols: an increasingly exciting topic | http://www.sciencedirect.com/science/article/pii/S0197018699000546
- ↑ Ethanol directly modulates gating of a dihydropyridine-sensitive Ca2+ channel in neurohypophysial terminals | http://www.ncbi.nlm.nih.gov/pubmed/7521910
- ↑ Neuropharmacology of alcohol addiction | http://onlinelibrary.wiley.com/doi/10.1038/bjp.2008.30/abstract
- ↑ Development of a rational scale to assess the harm of drugs of potential misuse | http://www.sciencedirect.com/science/article/pii/S0140673607604644
- ↑ Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. Paul E Ronksley, Susan E Brien, Barbara J Turner, Kenneth J Mukamal, William A Ghali BMJ 2011;342:d671
- ↑ Prospective study of alcohol drinking patterns and coronary heart disease in women and men. Janne Tolstrup, Majken K Jensen, Tjønneland Anne, Kim Overvad, Kenneth J Mukamal, and Morten Grønbæk. BMJ 2006;332:1244.
- ↑ No authors listed (2000). "Health Risks and Benefits of Alcohol Consumption Health Risks and Benefits of Alcohol Consumption". Alcohol Res Health 24 (1) 5–11.
- ↑ Neurophysiologic findings in chronic alcohol abuse | http://www.ncbi.nlm.nih.gov/pubmed/2988001
- ↑ Alcoholic diseases in hepato-gastroenterology: a point of view | http://www.ncbi.nlm.nih.gov/pubmed/18613369
- ↑ http://books.google.co.uk/books?id=nPvbDUw4w5QC&hl=en
- ↑ Mechanisms involved in the neurotoxic, cognitive, and neurobehavioral effects of alcohol consumption during adolescence | http://www.ncbi.nlm.nih.gov/pubmed/20113871?dopt=Abstract
- ↑ https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf
- ↑ Understanding the health impact of alcohol dependence | http://www.ajhp.org/content/64/5_Supplement_3/S5
- ↑ Outpatient management of alcohol withdrawal syndrome | http://www.ncbi.nlm.nih.gov/pubmed/24364635
- ↑ The alcohol withdrawal syndrome | http://www.ncbi.nlm.nih.gov/pubmed/17986499
- ↑ Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
- ↑ Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
- ↑ Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
- ↑ Alcohol withdrawal | http://www.ncbi.nlm.nih.gov/pubmed/23128805
- ↑ Alcohol Withdrawal Syndrome | http://www.aafp.org/afp/2004/0315/p1443.html
- ↑ Alcohol withdrawal | http://www.ncbi.nlm.nih.gov/pubmed/23128805
- ↑ https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf
- ↑ Cocaethylene Metabolism and Interaction with Cocaine and Ethanol: Role of Carboxylesterases | http://dmd.aspetjournals.org/content/31/1/16
- ↑ "Minimum Age Limits Worldwide" - International Center for Alcohol Policies | http://icap.org/table/Worldwide
- ↑ Minimum age limits worldwide | http://icap.org/Table/MinimumAgeLimitsWorldwide