Alcohol

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This page has not been approved by the PsychonautWiki administrators.

It may potentially contain incorrect information, particularly regarding that of dosage, duration, subjective effects, toxicity and other risks.

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Death may occur when alcohol is combined with other depressants such as opiates, benzodiazepines, barbiturates, thienodiazepines or other GABAergic substances.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

Summary sheet: Alcohol
Alcohol
Molecular structure of Ethanol
Ethanol.svg
Chemical Nomenclature
Common names Alcohol, Booze
Substitutive name Ethanol
Systematic name Ethyl alcohol
Class Membership
Psychoactive class Depressant
Chemical class Alcohol
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.



Oral
Dosage
Threshold 1 unit
Light 1 - 2 units
Common 2 - 4 units
Strong 4 - 6 units
Heavy 6 units +
Duration
Total 1.5 - 3 hours
Onset 15 - 30 minutes
Peak 30 - 90 minutes
Offset 45 - 60 minutes
After effects 6 - 48 hours









DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Ethanol (also known as Ethyl alcohol, Drinking alcohol or simply Alcohol) is a naturally occurring depressant substance of the alcohol chemical class. It is historically one of the oldest and most widely used psychoactive substances and continues to be the most widely used recreational substance to this day.

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]

Alcoholic beverages have a different taste depending on their contents and brewing ingredients.

Chemistry

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

Other alcohols in alcoholic beverages

Alcohols other than ethyl alcohol, such as 2-methyl-2-butanol, can also contribute flavor and aroma notes to beverages, causing a product to taste sweet, spicy, hot, or as a burning, "rubbing alcohol-like" mouthfeel. Products like wine may smell of a specific, usually pleasant scent because of their grape ingredients.

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 binding to NMDA receptors and triggering electrochemical signals.
  • 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.

The diagram above shows the average amount of units within common alcoholic beverages. This can be used in accordance with the chart below to determine one's desired dosage.

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include injury or death.

Physical effects
Child.svg

Visual effects
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Cognitive effects
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Auditory effects
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After effects
Aftereffects (3).svg

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

The most significant of the possible long-term effects of ethanol
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%).
Radar plot showing relative physical harm, social harm, and dependence of alcohol[12]

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[13][14] to severe detrimental effects in cases of chronic alcohol abuse.[15]

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.[16][17] The long-term use of alcohol is capable of damaging nearly every organ and system in the body.[18] The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol.[19] In addition, the developing fetal brain is also vulnerable, and fetal alcohol syndrome (FAS) may result if pregnant mothers consume alcohol.

Alcoholism

Alcoholism, also known as alcohol use disorder (AUD), is a broad term for any drinking of alcohol that results in mental or physical health problems. It was previously divided into two types: alcohol abuse and alcohol dependence

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%.[20]

It is strongly recommended that one use harm reduction practices when using this drug.

Tolerance and addiction potential

The chronic use of this compound can be considered extremely addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to many of the effects of alcohol develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Alcohol presents cross-tolerance with all GABAgenic depressants, meaning that after the consumption of alcohol all depressants will have a reduced effect.

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.[21]

Withdrawals

Lolol.pngMain article: Alcohol withdrawal

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.[22] It can last for up to one week.[23] 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.[24]

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

  • Alcohol hallucinosis: Patients have transient visual, auditory, or tactile hallucinations but are otherwise clear.[26]
  • 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.[27]
  • Delirium tremens: Hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations[28] 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.[29]

Dangerous interactions

Although many psychoactive substances 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.

  • Stimulants - It can be dangerous to combine depressants with stimulants due to the risk of accidental excessive intoxication. Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
  • Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
  • 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.
  • Hepatoxic drugs - Combining alcohol with hepatoxic (liver-damaging) drugs such as acetaminophen (paracetamol) may result in liver damage, liver failure, and death in extreme cases.[citation needed]

Legal status

Handcuffs-300px.png

This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

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

External links

References

  1. Risks of Combining Depressants (Tripsit) | https://tripsit.me/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 (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0197018699000546
  7. Neuronal nicotinic acetylcholine receptors: a new target site of ethanol (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0197018699000558
  8. 5-HT3 receptors and the neural actions of alcohols: an increasingly exciting topic (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0197018699000546
  9. Ethanol directly modulates gating of a dihydropyridine-sensitive Ca2+ channel in neurohypophysial terminals (PubMed.gov / NCBI) | 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. Application of an Electronic Nose to Diagnose Liver Cirrhosis from the Skin Surface | https://books.google.fr/books?id=jf3otMX1KsoC&pg=PA150&lpg=PA150#v=onepage&q&f=false
  12. Development of a rational scale to assess the harm of drugs of potential misuse (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0140673607604644
  13. 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
  14. 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.
  15. 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.
  16. Neurophysiologic findings in chronic alcohol abuse (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/2988001
  17. Alcoholic diseases in hepato-gastroenterology: a point of view (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/18613369
  18. http://books.google.co.uk/books?id=nPvbDUw4w5QC&hl=en
  19. Mechanisms involved in the neurotoxic, cognitive, and neurobehavioral effects of alcohol consumption during adolescence (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/20113871?dopt=Abstract
  20. https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf
  21. Understanding the health impact of alcohol dependence | http://www.ajhp.org/content/64/5_Supplement_3/S5
  22. Outpatient management of alcohol withdrawal syndrome (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/24364635
  23. The alcohol withdrawal syndrome (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17986499
  24. Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
  25. Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
  26. Alcohol Withdrawal Syndrome | http://www.webcitation.org/5uFSqlAGz
  27. Alcohol withdrawal (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/23128805
  28. Alcohol Withdrawal Syndrome | http://www.aafp.org/afp/2004/0315/p1443.html
  29. Alcohol withdrawal (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/23128805
  30. "Minimum Age Limits Worldwide" - International Center for Alcohol Policies | http://icap.org/table/Worldwide
  31. Minimum age limits worldwide | http://icap.org/Table/MinimumAgeLimitsWorldwide