Alcohol

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There is a high incidence of death due to respiratory depression when alcohol is combined with depressants such as opiates, benzodiazepines or other GABAergic substances.[1]

Alcohol
The skeletal formula of Alcohol (Ethanol).
Ethanol.png
Interesting alcoholic beverages.jpg
Chemical Nomenclature
Common names Alcohol
Systematic name Ethanol
Class Membership
Psychoactive class Depressant
Chemical class GABAergic
Routes of Administration



Oral
Dosage
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity.
  • Differs between its varying forms
Duration
Total 1.5 - 3 hours
Onset 15 - 30 minutes
Peak 30 - 90 minutes
Offset 45 - 60 minutes
Afterglow 1 - 36 hours









Summary sheet: Alcohol

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.[2]

Alcoholic beverages have been produced and consumed by humans since the Neolithic Era, from hunter-gatherer communities to nation-states.[3]

Chemistry

Ethanol is the second simplest alcohol compound. Ethanol is comprised of a chain of two carbon atoms, known as ethane, with a hydroxyl (-OH) functional group attached to form an alcohol.

Pharmacology

In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain.[4] However, molecular pharmacology studies have shown that alcohol has only a few primary targets. These effects are facilitatory in some systems and inhibitory in others.

Among the neurotransmitter systems with enhanced functions are:

  • GABA:[5] In a fashion similar to benzodiazepines, an enhancement of the inhibitory system known as GABA 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[6]
  • Nicotinic acetylcholine receptors[7]

Among those that are inhibited are:

  • Glutamate:[8] 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[9]

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.[10] 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 which progressively intensify proportional to dosage. These are described below and generally include:

Cognitive effects

The cognitive effects of alcohol can be broken down into several components which progressively intensify proportional to dosage.

Visual effects

The visual effects of alcohol can be broken down into several components which progressively intensify proportional to dosage.

Auditory effects

Toxicity and harm potential

Most significant of the possible long-term effects of ethanol
Radar plot showing relative physical harm, social harm, and dependence of alcohol[11]
Results of a 2010 study ranking the levels of damage caused by drugs, in the opinion of drug-harm experts. When harm to self and others is summed, alcohol was the most harmful of all drugs considered (scoring 72%).

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[12][13] to severe detrimental effects in cases of chronic alcohol abuse.[14]

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.[15][16] The long-term use of alcohol is capable of damaging nearly every organ and system in the body.[17] The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol.[18] 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 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%.[19]

Tolerance and addiction potential

The 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, gait and balance) and brain damage. Alcohol dependence is associated with hypertension, coronary heart disease, ischemic stroke, and also cancers of the respiratory system, the digestive system, liver, breast and ovaries. Heavy drinking is associated with liver disease, such as cirrhosis.[20]

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.[21] It can last for up to one week.[22] To be classified as alcohol withdrawal syndrome, patients must exhibit at least two of the following symptoms: increased hand tremors, insomnia, nausea or vomiting, transient hallucinations (auditory, visual or tactile), psychomotor agitation, anxiety, tonic-clonic seizures, and autonomic instability.[23]

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.[24] Symptoms are also grouped together and classified:

  • Alcohol hallucinosis: Patients have transient visual, auditory, or tactile hallucinations but are otherwise clear.[25]
  • Withdrawal seizures: Seizures occur within 48 hours of alcohol cessation and occur either as a single generalized tonic-clonic seizure or as a brief episode of multiple seizures.[26]
  • Delirium tremens: Hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations[27] 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.[28]

Dangerous interactions

Although many drugs are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

  • Depressants (1,4-Butanediol, 2-methyl-2-butanol, barbiturates, benzodiazepines, GHB/GBL, methaqualone, opioids, phenothiazines[29]) - This combination can result in dangerous or even fatal levels of respiratory depression. These substances also potentiate the muscle relaxation, sedation and amnesia caused by one another and can lead to unexpected loss of consciousness at high doses. There is also an increased risk of vomiting during unconsciousness and death from the resulting suffocation. If this occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.
  • Dissociatives - This combination can result in an increased risk of vomiting during unconsciousness and death from the resulting suffocation. If this occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.
  • Stimulants - It is dangerous to combine alcohol, a depressant, with stimulants due to the risk of excessive intoxication. Stimulants decrease the sedative effect of alcohol, which is the main factor most people consider when determining their level of intoxication. Once the stimulant wears off, the effects of alcohol will be significantly increased, leading to intensified disinhibition as well as other effects. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour. This combination can also potentially result in severe dehydration if hydration is not monitored. It also interacts with cocaine in vivo to produce cocaethylene, another psychoactive substance.[30]
  • MAOIs - This combination can result in dangerous reactions through the way in which tyramine, a chemical commonly found in alcoholic beverages, causes increased blood pressure.

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.[31] 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.[32]

See also

References

  1. https://tripsit.me/combining-depressants/ | Tripsit - Risks of Combining Depressants
  2. http://icap.org/table/Worldwide
  3. 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.
  4. Neuropharmacology of alcohol addiction | http://onlinelibrary.wiley.com/doi/10.1038/bjp.2008.30/abstract
  5. Sites of alcohol and volatile anaesthetic action on GABAA and glycine receptors | http://www.nature.com/nature/journal/v389/n6649/full/389385a0.html
  6. 5-HT3 receptors and the neural actions of alcohols: an increasingly exciting topic | http://www.sciencedirect.com/science/article/pii/S0197018699000546
  7. Neuronal nicotinic acetylcholine receptors: a new target site of ethanol | http://www.sciencedirect.com/science/article/pii/S0197018699000558
  8. 5-HT3 receptors and the neural actions of alcohols: an increasingly exciting topic | http://www.sciencedirect.com/science/article/pii/S0197018699000546
  9. Ethanol directly modulates gating of a dihydropyridine-sensitive Ca2+ channel in neurohypophysial terminals | http://www.ncbi.nlm.nih.gov/pubmed/7521910
  10. Neuropharmacology of alcohol addiction | http://onlinelibrary.wiley.com/doi/10.1038/bjp.2008.30/abstract
  11. Development of a rational scale to assess the harm of drugs of potential misuse | http://www.sciencedirect.com/science/article/pii/S0140673607604644
  12. 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
  13. 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.
  14. 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.
  15. Neurophysiologic findings in chronic alcohol abuse | http://www.ncbi.nlm.nih.gov/pubmed/2988001
  16. Alcoholic diseases in hepato-gastroenterology: a point of view | http://www.ncbi.nlm.nih.gov/pubmed/18613369
  17. http://books.google.co.uk/books?id=nPvbDUw4w5QC&hl=en
  18. Mechanisms involved in the neurotoxic, cognitive, and neurobehavioral effects of alcohol consumption during adolescence | http://www.ncbi.nlm.nih.gov/pubmed/20113871?dopt=Abstract
  19. https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf
  20. Understanding the health impact of alcohol dependence | http://www.ajhp.org/content/64/5_Supplement_3/S5
  21. Outpatient management of alcohol withdrawal syndrome | http://www.ncbi.nlm.nih.gov/pubmed/24364635
  22. The alcohol withdrawal syndrome | http://www.ncbi.nlm.nih.gov/pubmed/17986499
  23. Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
  24. Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
  25. Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
  26. Alcohol withdrawal | http://www.ncbi.nlm.nih.gov/pubmed/23128805
  27. Alcohol Withdrawal Syndrome | http://www.aafp.org/afp/2004/0315/p1443.html
  28. Alcohol withdrawal | http://www.ncbi.nlm.nih.gov/pubmed/23128805
  29. https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf
  30. Cocaethylene Metabolism and Interaction with Cocaine and Ethanol: Role of Carboxylesterases | http://dmd.aspetjournals.org/content/31/1/16
  31. "Minimum Age Limits Worldwide" - International Center for Alcohol Policies | http://icap.org/table/Worldwide
  32. Minimum age limits worldwide | http://icap.org/Table/MinimumAgeLimitsWorldwide