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Alcohol is one of the world’s favorite intoxicants. It is frequently found at social gatherings because it provides an anxiety-reducing effect. Consuming too much alcohol will result in alcohol poisoning, which can be fatal.

Our evidence-based analysis on alcohol features 134 unique references to scientific papers.

Research analysis led by Kamal Patel .
Reviewed by
Examine.com Team
Last Updated:

Summary of Alcohol

Primary Information, Benefits, Effects, and Important Facts

Alcohol, otherwise known as Drinking alcohol or ethanol, is the main ingredient in a wide range of social drinks and the reason for the differentiation between 'Alcoholic' and 'Non-alcoholic' drinks.

It is a neuroactive chemical that is able to change one's perception, and has a unique metabolic pattern relative to other sources of calories (the macronutrients; carbohydrates, proteins, and dietary fats). It contributes 7 calories per gram energy-wise, but this does not always correlate well with bodyweight like the other macronutrients do.

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Things To Know & Note

Also Known As

Ethanol, Drinking alcohol, Beer, Gin, Vodka, Wine, Jager

Do Not Confuse With

Alcohol (The chemistry definition)

Goes Well With

  • N-AcetylCysteine and related anti-oxidants (increases conjugation and safe metabolism via glutathione)

  • Ashwagandha, for social anxiety reduction

  • Agmatine (may help alcohol withdrawal)

  • Ethanol is slightly soluble in lipid, but completely miscible with water

  • The Danish myth of being able to get drunk through one's feet is false.[1]

How to Take Alcohol

Recommended dosage, active amounts, other details

Abstinence from drinking is defined as having no ethanol intake whatsoever.

"Moderate" drinking in the literature is dependent on gender and not ultimately defined, but an upper limit can be placed at 9 units per week for women and 12-14 units a week for men, with no single event exceeding 4 units.

A unit is typically 12 oz (355 mL) of 5% beer, 5 oz (150 mL) 12.5% wine, or 1.5 oz (45 mL) of drinks with a higher (40%) alcohol content.

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Frequently Asked Questions about Alcohol

A compound from beer may help fat loss
A recent study shows that a compound in beer may help with fat loss.
Can drinking wine really replace exercise?
Why do hangovers happen and what can you do about them?
We’re not quite sure how hangovers happen, and the evidence on cures and prophylactics isn’t too convincing, but following some basic guidelines may help prevent and relieve hangovers.

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Human Effect Matrix

The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects alcohol has on your body, and how strong these effects are.
Grade Level of Evidence
Robust research conducted with repeated double-blind clinical trials
Multiple studies where at least two are double-blind and placebo controlled
Single double-blind study or multiple cohort studies
Uncontrolled or observational studies only
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Outcome Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
- See all 9 studies
There appears to be a time-dependent influence on testosterone, with acute doses of alcohol increasing testosterone secondary to creating energy influx in the liver (small enough of an increase to be 'somewhat' effective but may contribute to libido) whereas abuse is known to reduce testosterone levels more notably. The acute increase in testosterone is thought to be related to spikes in libido
grade-c Minor - See study
Acute ingestion of alcohol may be able to reduce subsequent power output
grade-c - - See study
Serum adrenaline appears unaltered following alcohol ingestion
grade-c - Very High See 2 studies
No significant alterations in cortisol levels seen with alcohol ingestion in moderate levels
grade-c - Very High See all 3 studies
No significant influence on fasting estrogen levels in males
grade-c - Very High See all 5 studies
No significant influence of alcohol on luteinizing hormone levels when consumed moderately
grade-d Minor Moderate See 2 studies
Mixed effects on FSH, but although null effects have been reported an increase may be possible
grade-d Minor - See study
An acute suppression of growth hormone is noted with alcohol ingestion
grade-d Minor - See study
An increase in prolactin has been noted following acute ingestion of alcohol

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Research Breakdown on Alcohol

Click on any below to expand the corresponding section. Click on to collapse it.

Click here to fully expand all sections or here to fully collapse them.

Drinking alcohol after meals will reduce the peak blood values of ethanol regardless of nutrient composition,[2] the delay is due to gastric absorption of alcohol being slower than duodenal absorption rates, and food delaying gastric emptying.[3]

There also appears to be less Area-Under-Curve (AUC) and bioavailability with alcohol in the fed state[4][5][2] which may be due to increased First Pass Metabolism in the intestines and liver.[3][4]

The difference between the fasted and the fed state, quantitatively, varies between person to person but is typically in the range of complete absorption in the fasted state and around 65-70% bioavailability in the fed state.[6]

The average hourly decrease of breath alcohol levels is 0.082mg/L/hour[7] with females having a faster decline than males (0.087 versus 0.078).[7]

Ethanol reliably induces dopamine release in the nuclear accumbens (nAc) of animals[8][9][10][11] including humans,[12] an area of the brain associated with drugs of abuse when dopamine is spiked;[13] serum ethanol levels correlate with nuclear accumbens ethanol level and restore dopamine deficits seen in alcohol withdrawal in rats.[14][15][16]

This release of dopamine in the nAc appears to be dependent on an increase in extracellular taurine levels[17] (which ethanol does itself[18] and reducing taurine levels 40% in vivo using beta-alanine fails to abolish the dopamine spike[17]) with both taurine and ethanol acting vicariously through glycine receptors.[17][19][20] Actions of alcohol in increasing nAc dopamine is actually not localized either, and mediated in the Ventral Striatum (VTA) where ethanol acts as a co-agonist of nicotinic acetylcholine receptors (nAChRs) where it fails to act on these receptors in isolation but enhances other agonists,[21] which plays a role in ethanol augmenting nicotine addiction (prototypical nAChR agonist). This is further evidenced by the nAc increase in dopamine being blocked by the nAChR antagonist mecamylamine.[10] Futher studies noted that this effect is more localized to the anterior VTA rather than posterior[22] and that ethanol in this area may cause an increase in acetylcholine which then induces activation of nAChR alongside ethanol acting as co-agonist, as depletion of acetylcholine also abolishes the nAc increase in dopamine and the increase in acetylcholine has been observed in vivo.[23][24]

Ethanol can increase dopamine release in the Nuclear Accumbens (nAc) which is most likely due to acetylcholine acting on nAChR (its receptors) in the Ventral Striatum, where ethanol enhances signalling here and said signalling enhances dopamine release in the nAc

In humans, an increase in dopamine has also been observed in the Ventral Striatal (VTA) which correlates with subjective estimates of euphoria and stimulation.[12]

There is a strong correlation between chronic ethanol consumption and cancers of the intestinal tract, although ethanol itself is not carcinogenic;[25] causation may lie with the metabolite acetaldehyde.[26] This includes oral cancers[27] and has been hypothesized to be related to 25-68% of Upper gastrointesinal tract cancers.[27] The risk appears to be dose dependent[28][25] in both smokers and non-smokers[29][30]

The link between stomach cancer is slightly more controversial[25] as the risk ratios are much smaller.[31] That being said, there seems to be a stronger correlation in those with genetically less active alcohol dehydrogenase activities (Asian populations).[32][33] Colon cancer shares much of the same pathology, with there being a positive but minor increase in cancer rates that become more significant in those with less active alcohol dehydrogenase enzymes.[34][35][36]

Alcohol appears to work synergistically with tobacco smoke in increasing the risk of various oral and oesophageal cancers/[37][25] Individuals who both drink (greater than 1.5 bottles of wine) and smoke (greater than 10 cigarettes daily) have approximately a 150-fold increased risk of oesophageal cancers.[25] More moderate consumption of either parameter has negligible risk, but the combination increases risk by 12-19 fold, with women at higher risk.[38]

In regards to cancers that may be furthered by mTOR[39] and Phospholipase D signalling,[40] alcohol has been hypothesized to reduce these cancer risks via suppression of phospholipase D induced mTOR activation[41] and this mechanism has been demonstrated via Rapamycin (a selective mTOR antagonist).[42]

There is substantial evidence that light to moderate alcohol consumption is associated increased longevity in large-scale surveys.[43][44][45]

A proposed mechanism of action for alcohol on longevity is via indirect inhibition of mTOR by replacing an agonist,[41] mTOR is sometimes referred to as a metabolic 'lever' that determines aging.[46]

mTOR is the nutrient sensing protein (senses and is activated during surplus) that is one of the targets of study for longevity secondary to caloric restriction.[47][48]

Alcohol consumption may suppress protein synthesis slightly via inhibition of exercise-induced mTOR, which is partially dependent on phosphatidic acid (PA) from the cell membrane for complex stabilization.[49] Ethanol is used as preferential substrate by the enzyme Phospholipase D and phosphatidylethanol is produced in lieu of phosphatidic acid, which causes an indirect suppression of mTOR.[41] It appears to act more on the mTORc1 subcomponent, as higher concentrations are needed to inhibit the mTORc2 component.[49][41] This mechanism of action has been demonstrated acutely with mouse myocytes[50] and chronic alcoholism adversely affects mTOR and S6K1 phosphorylation.[51][52]

In studies measuring liver protein kinetics, one study in humans pairing a meal of 632kcal with alcohol (71g) alcohol reduced the protein synthesis rate (assessed by fibrinogen and albumin) by about 30% over the 4 hours measured afterwards; this study also noted that leucine oxidation (a marker of muscle protein breakdown) was reduced by 24%;[53] and later it was found that lower doses of alcohol (28g) found smaller hindering of protein synthesis (albumin) but not fibrinogen and also noted a blunting of leucine oxidation.[54] A later study confirmed that alcohol, relative to saline, was able to suppress leucine oxidation at two varying doses and was more effective this apparent anti-catabolic action when no circulating nutrients were present.[55]

Although these studies measuring liver protein synthesis may not be too valid for talking about muscle protein synthesis, the apparent reduction in leucine oxidation suggests that alcohol may have an anti-catabolic effect

In rats, injections of ethanol suppress muscle protein synthesis rates and this is mediated by both ethanol itself as well as acetylaldehyde.[56]

When measured acutely, moderate doses of alcohol (0.83g/kg) in resistance trained men when consumed immediately after exercise (where nothing was eaten 3.5 hours before, food given during drinking ab libitum) failed to note any significant differences in testosterone levels for up to 300 minutes after exercise[57] and another sports related study using 1g/kg after a simulated rugby match failed to note a decrease in testosterone despite noting a reduction in power output.[58] A third study using that did not pair ethanol with exercise but used a low dose of 0.45g/kg on three separate pulses 90 minutes apart noted that although there was a trend (via the circadian rhythm) for testosterone to increase in this study that it did not differ between ethanol and water intake.[59]

Conversely, a slightly lesser intake (0.5g/kg) has been shown to actually increase circulating testosterone from 13.6nmol/L to 16nmol/L (+17%) 2 hours after ingestion (which normalized by 4 hours), and inhibiting ethanol metabolism with 4-methylpyrazole (alcohol dehydrogenase inhibitor) by 37+/-3% and thus increasing the time ethanol could act abolished the increase in testosterone.[60] This increase in testosterone after 0.5g/kg has also been noted in premenopausal women,[61] and suggested to be act vicariously through the increased NADH/NAD+ ratio in the liver after these doses. Steroid metabolism and REDOX couplets interact in the liver,[62] where an increased rate of 17β-HSD type 2 enzyme and its conversion of androstenedione to testosterone is observed due to the increased NADH relative to NAD+ observed after ethanol intake, and this also explains the reduction in androstenedione observed in studies where testosterone is increased[61][62] and may help explain the increased levels of androstenedione in studies where testosterone is suppressed, where androstenedione may be increased by up to 54% (and dehydroepiandrosterone by 174%) 12 hours after large intakes of alcohol.[63]

That being said, another study using 0.675g/kg noted that testosterone increased and was more sensitive to being increased by gonadotropin releasing hormone, suggesting multiple pathways may be at play.[64] Red Wine may also confer additional benefits through its phenolic content, as Quercetin appears to be glucuronidated by the enzyme UGT2B17 in place of testosterone (sacrificial substrate) and may indirectly increase testosterone.[65] This study was in vitro, however, and Quercetin has low bioavailability.

Low to moderate doses timed around exercise have twice failed to demonstrate an increase or decrease in testosterone levels, with the increase being from a favorable change in the testosterone:androstenedione ratio in the liver (mimicking the NADH:NAD+ ratio, which is increased during alcohol consumption). Not all studies not this increase though, and some just note no significant changes at all

One study lasting 3 weeks with daily consumption of 30-40g alcohol in non-smoking and social drinkers noted a 6.8% decrease in circulating testosterone levels in men (n=10), with no significant effect in women.[66] At the end of the study, control had circulating testosterone measured at 16.4nmol/L while the alcohol group was measured at 15.3nmol/L.[66]

These low doses, when taken over a prolonged period of time, might decrease testosterone; the degree of suppression is not likely to be practically relevant, however

Higher doses of alcohol, 1.5g/kg (average dose of 120g), have been demonstrated to suppress testosterone by 23% when measured between 10-16 hours after acute ingestion with no statistically significant difference between 3 and 9 hours of measurement.[67] It appeared, in this study, that alcohol suppressed a rise of testosterone that occurred in the control group which may have been based on the circadian rhythm.[67] Anothers study using an even higher dose (1.75g/kg over 3 hours) noted that over the next 48 hours that a small short-lived dip occurred at 4 hours, but a more statistically significant drop was seen at 12 hours which was mostly corrected by 24 hours (still significantly less than control) and completely normalized at 36 hours.[63] By 12 hours, the overall reduction in testosterone was measured at 27% while the overall decrease in testosterone at 24 hours was 16%.[63] Finally, a third study using 100-proof vodka at a dose of 2.4ml/kg bodyweight in 15 minutes (to spike blood alcohol concentration (BAC) up to 109+/-4.5mg/100mL, similar to the aforementioned 1.75g/kg study) noted suppressed testosterone levels correlating with the peak BAC, observed 84 minutes after ingestion.[68] This time delay seen in some studies, when put in social context, correlate with the observed lower serum testosterone levels seen with hangovers.[69] This study also noted that the changes in hormones were further from baseline in persons self-reporting a hangover, and less significant in persons without hangovers.[69]

Finally, an intervention in which alcohol was supplied intravenously (via catheter) to keep a breath alcohol level of 50mg% noted that free testosterone was suppressed at this level of intake in young (23+/-1) men only, with young women experiencing an increase in testosterone and older (59+/-1) men and women having no significant influences.[70] This correlates to a moderate dose of oral ethanol.

The mechanism of alcohol suppressing testosterone levels sub-chronically is via its actions as a testicular toxin, where it can reduce testosterone synthesis rates with no negative influence on the hypothalamus signals to the testes (if anything, a stimulatory effect occurs on the hypothalamus).[71][72]

Around the 1.5g/kg or higher ethanol intake, it appears that a subsequent dose-dependent decreasing of testosterone occurs and appears to occur with some degree of time delay up to 10 hours after consumption. One study using shots of vodka did note this suppression of testosterone occurring within 90 minutes though

In alcohol abusers, the chronic high intake of alcohol appears to be negatively correlated with circulating testosterone at rest; with longer duration and higher intakes of alcohol leading to less testosterone.[73]

Overall, alcohol can increase testosterone acutely through increasing a REDOX ratio in the liver (NADH:NAD+) but this spike is short lived; a reverse trend is seen at a later point when alcohol probably reaches the testicles to suppress testosterone synthesis, this is also short-lived for the most part. Chronic alcohol consumption at low doses is associated with a decrease in testosterone, but to a degree where it may not be practically relevant; alcoholism is associated with a larger and significant reduction in testosterone levels

A three week intervention in middle aged men and post-menopausal women drinking 30-40g of alcohol daily noted that in both genders there was no significant influence of this dose of alcohol on circulating estrogen levels.[66]

Another study measuring serum levels during hangover (induced by 1.5g/kg ethanol the night prior) noted less circulating estrogen levels associated with hangover[69] yet another study using similarily high levels of 1.75g/kg ethanol noted no significant influence of ethanol on estrogens for the next 48 hours measured, if anything a slight trend to decrease estrogens was noted.[63]

Luteinizing Hormone, as well as follicle-stimulating hormone (FSH), do not appear to have neither their wave amplitude nor frequency affected when healthy male subjects ingest a large dose (1.5g/kg) of alcohol and are measured for the subsequent 20 hours,[67] although one study using a slightly higher dose (1.75g/kg over 3 hours) noted that, at 24 hours post-ingestion, that a small but statistically significant increase occurred and somewhat normalized over the next 24 hours (was no longer significant, but still trended to being higher).[63]

One hard-drinking study (2.4mL/kg 100-proof vodka in 15 minutes) noted that at peak BAC that the suppression of testosterone also existed alongside an increase in luteinizing hormone above baseline.[68]

Growth hormone does not appear to have its pulse amplitude influenced by alcohol for up to 20 hours after ingestion of a large dose (1.5g/kg) of alcohol acutely in otherwise healthy men.[67] However, pulse frequency during these 20 hours was slightly but significantly reduced (from 4.7+/-0.2 to 3.8+/-0.3).[67]

After consumption of 1.75g/kg ethanol, a spike in cortisol is seen at 4 hours and persists for up to 24 hours after consumption, normalizing at 36 hours.[63] At 4 hours, the largest spike of cortisol seen, it was measured to be 152% higher than control and this increaes in cortisol does not appear to correlate to the decrease in testosterone.[63]

After administration of a large bolus of ethanol (1.75g/kg) a significant spike in prolactin to 412% of control value (586+/-185mU/l relative to 142+/-40mU/l) is seen by 4 hours, which according to this study is abolished by 12 hours and a slight suppression may occur at 24 hours (not seen at 36 nor 48 hours).[63]

In a study where 14 healthy persons were given multiple pulses of 0.45g/kg ethanol (low dose, but numerous) either in the morning (7:30am, measured for 6 hours) or evening (5:30, measured for 14 hours) was able to decrease circulating leptin to variable degrees (measured at both 11.7% and 25.7% on different days)[59]

Alcohol can adversely interact with acetaminophen (paracetamol) and potentially cause acute liver failure,[74][75][76] although only high doses of acetaminophen have been associated with acute failure, any dose can theoretically cause a degree of damage.[75]

The mechanism of action if via the enzyme CYP2E1, one of the two enzymes responsible for degradation of ethanol. After consumption of ethanol, CYP2E1 levels rise in order to accommodate more ethanol metabolism. When this occurs, acetaminophen can diverge from normal routes of metabolism and be metabolized through CYP2E1 to a greater extent. Only via CYP2E1 will acetaminophen form the metabolite NAPQI, which is highly hepatotoxic.[77][78] Although acetominophen will always metabolize into some amount of NAPQI, the overall percentage of orally ingested acetominophen devoted to this pathway increases after CYP2E1 induction.[79]

Taking Acetominophen (Tylenol) after heavy drinking is an absolutely horrible decision for your liver

Another inducer of CYP2E1 include the ketone body acetone[80][81] whereas the other two ketone bodies (Acetoacetate and Beta-hydroxybutyrate) induce translation of CYP2E1 mRNA.[82] This potentially means that alcohol in the state of ketosis or otherwise during starvation may be more hepatotoxic than during a fed state.[83][82]

Taking Acetominophen after a night of drinking while on a ketosis diet (little to no dietary carbohydrates) or after spurious vomiting (can increase ketone bodies) is even worse than just taking acetominophen after drinking. Ketosis, ethanol, and acetominophen may be the trifecta of cirrhosis
Note that the enhanced liver damage from alcohol under ketosis may be related to 'getting smashed faster' than is commonly reported with ketosis, and the combination of keto and alcohol may not be as problematic if alcohol consumption is limited

Aspirin, when taken alongside alcohol, can increase blood alcohol levels by inhibiting gastric alcohol dehydrogenase.[84] It does not seem to do this to hepatic alcohol dehydrogenase.[85] These results, however, have been contested. Aspirin may also delay gastric emptying[86] which would increase the time that ethanol is exposed to the remaining alcohol dehydrogenase enzymes and thus make partial inhibition a less critical point.[87]

Conversely, ethanol can benefit Aspirin by increasing intestinal uptake of aspirin.[88] This would result in more circulating levels of Aspirin at the same oral dose.

N-Acetylcysteine is a compound that is able to increase levels of the endogenous anti-oxidant Glutathione.[89] Co-ingestion of NAC with alcohol can reduce some of the unwanted oxidant-mediated side-effects of alcohol[90] and alcohol-potentiated acetaminophen toxicity can be attenuated with N-AcetylCysteine, although not completely.[91]

There are a class of herbs that can accelerate regeneration of liver cells and reduce fatty liver deposits induced by a night of drinking, but have a critical catch to their benefits. These compounds must be consumed after drinking, either the next morning or prior to sleep; pre-loading these 'Night After' herbs can exacerbate (increase) damage from alcohol.

These herbs and molecules include Milk Thistle and its active silybins (most notably), and can also extend to molecules like Tauroursodeoxycholic acid; known as TUDCA.

It is critical to consume these herbs after drinking, as consuming them before drinking confers the opposite effect and can be damaging

Withania Somnifera, more commonly known as Ashwagandha, appears to be able to be more effective at decreasing social anxiety when paired with alcohol; doses too low of either to be seen as effective appear to be highly effective when combined.[92]

The anxiolytic (anxiety reducing) effects of Ashwagandha have also been shown to, in rats, reduce spikes in anxiety that are a result of cessation of chronic alcohol consumption; basically, possibly able to prevent anxiety from increasing as a result of quitting alcohol.[92]

Agmatine is a neurotransmitter derived from L-Arginine that is currently thought to be highly involved in helping neuropathic pain and drug addiction, and appears to interact with a wide variety of drugs. It has both positive and negative interactions with alcohol dependent on context.

Alcohol's reduction of anxiety (anxiolysis) is prevented by inhibition of the arginine decarboxylase enzyme, suggesting that it works via agmatine.[93] The increase in anxiety seen during alcohol withdrawal is also normalized with agmatine.[93]

Additionally, the analgesic (pain killing) effects of alcohol appear to be augmented with agmatine injections in rats thought to be due to imidazoline receptor signalling[94] and agmatine has been noted to block the alcohol induced hyperactivity seen in rats (male only) at 5-20mg/kg without affecting locomotion inherently.[95] There does not appear to be any interaction between agmatine and conditioned place preference (CPP), thought to be indicative of no alterations on motivation/addiction.[96] 

On a negative side, agmatine is known to be a gastroprotective agent (aids in protecting parietal cells from stomach acid[97]) but has counterintuitively enhanced ulcer formation from alcohol consumption in rats.[98]

At this moment in time, agmatine appears to be useful for alcohol withdrawal. The usage of agmatine alongside alcohol might not be prudent as one study noted an enhancement of stomach ulceration, so timing of agmatine and alcohol consumption would be prudent


  1. ^ Hansen CS, Faerch LH, Kristensen PL. Testing the validity of the Danish urban myth that alcohol can be absorbed through feet: open labelled self experimental study. BMJ. (2010)
  2. ^ a b Jones AW, Jönsson KA, Kechagias S. Effect of high-fat, high-protein, and high-carbohydrate meals on the pharmacokinetics of a small dose of ethanol. Br J Clin Pharmacol. (1997)
  3. ^ a b Gentry RT. Effect of food on the pharmacokinetics of alcohol absorption. Alcohol Clin Exp Res. (2000)
  4. ^ a b Ramchandani VA, Kwo PY, Li TK. Effect of food and food composition on alcohol elimination rates in healthy men and women. J Clin Pharmacol. (2001)
  5. ^ Roine R. Interaction of prandial state and beverage concentration on alcohol absorption. Alcohol Clin Exp Res. (2000)
  6. ^ Sadler DW, Fox J. Intra-individual and inter-individual variation in breath alcohol pharmacokinetics: The effect of food on absorption. Sci Justice. (2011)
  7. ^ a b Pavlic M, et al. Elimination rates of breath alcohol. Forensic Sci Int. (2007)
  8. ^ Di Chiara G, Imperato A. Ethanol preferentially stimulates dopamine release in the nucleus accumbens of freely moving rats. Eur J Pharmacol. (1985)
  9. ^ Profound decrement of mesolimbic dopaminergic neuronal activity during ethanol withdrawal syndrome in rats: electrophysiological and biochemical evidence.
  10. ^ a b Blomqvist O, et al. Accumbal dopamine overflow after ethanol: localization of the antagonizing effect of mecamylamine. Eur J Pharmacol. (1997)
  11. ^ Blomqvist O, et al. The mesolimbic dopamine-activating properties of ethanol are antagonized by mecamylamine. Eur J Pharmacol. (1993)
  12. ^ a b Boileau I, et al. Alcohol promotes dopamine release in the human nucleus accumbens. Synapse. (2003)
  13. ^ Wise RA, Rompre PP. Brain dopamine and reward. Annu Rev Psychol. (1989)
  14. ^ Weiss F, et al. Oral alcohol self-administration stimulates dopamine release in the rat nucleus accumbens: genetic and motivational determinants. J Pharmacol Exp Ther. (1993)
  15. ^ Molander A, et al. Involvement of accumbal glycine receptors in the regulation of voluntary ethanol intake in the rat. Alcohol Clin Exp Res. (2005)
  16. ^ Ethanol Self-Administration Restores Withdrawal-Associated Deficiencies in Accumbal Dopamine and 5-Hydroxytryptamine Release in Dependent Rats.
  17. ^ a b c Ericson M, et al. Rising taurine and ethanol concentrations in nucleus accumbens interact to produce dopamine release after ethanol administration. Addict Biol. (2011)
  18. ^ Olive MF. Interactions between taurine and ethanol in the central nervous system. Amino Acids. (2002)
  19. ^ Molander A, Söderpalm B. Accumbal strychnine-sensitive glycine receptors: an access point for ethanol to the brain reward system. Alcohol Clin Exp Res. (2005)
  20. ^ Molander A, Söderpalm B. Glycine receptors regulate dopamine release in the rat nucleus accumbens. Alcohol Clin Exp Res. (2005)
  21. ^ Marszalec W, Aistrup GL, Narahashi T. Ethanol-nicotine interactions at alpha-bungarotoxin-insensitive nicotinic acetylcholine receptors in rat cortical neurons. Alcohol Clin Exp Res. (1999)
  22. ^ Ericson M, et al. Nicotinic acetylcholine receptors in the anterior, but not posterior, ventral tegmental area mediate ethanol-induced elevation of accumbal dopamine levels. J Pharmacol Exp Ther. (2008)
  23. ^ Larsson A, et al. Voluntary ethanol intake increases extracellular acetylcholine levels in the ventral tegmental area in the rat. Alcohol Alcohol. (2005)
  24. ^ Ericson M, et al. Ethanol elevates accumbal dopamine levels via indirect activation of ventral tegmental nicotinic acetylcholine receptors. Eur J Pharmacol. (2003)
  25. ^ a b c d e Salaspuro MP. Alcohol consumption and cancer of the gastrointestinal tract. Best Pract Res Clin Gastroenterol. (2003)
  26. ^ Salaspuro M. Interrelationship between alcohol, smoking, acetaldehyde and cancer. Novartis Found Symp. (2007)
  27. ^ a b Epidemiology and Prevention of Oral Cancer.
  28. ^ Tavani A, et al. Risk factors for esophageal cancer in lifelong nonsmokers. Cancer Epidemiol Biomarkers Prev. (1994)
  29. ^ Oesophageal Cancer in non-smoking drinkers and non-drinking smokers.
  30. ^ Oral Cavity Cancer in Non-Users of Tobacco.
  31. ^ Franceschi S, La Vecchia C. Alcohol and the risk of cancers of the stomach and colon-rectum. Dig Dis. (1994)
  32. ^ Goedde HW, et al. Distribution of ADH2 and ALDH2 genotypes in different populations. Hum Genet. (1992)
  33. ^ Alcohol-related cancers and aldehyde dehydrogenase-2 in Japanese alcoholics.
  34. ^ Murata M, et al. Genotype difference of aldehyde dehydrogenase 2 gene in alcohol drinkers influences the incidence of Japanese colorectal cancer patients. Jpn J Cancer Res. (1999)
  35. ^ Scheppach W, et al. WHO consensus statement on the role of nutrition in colorectal cancer. Eur J Cancer Prev. (1999)
  36. ^ Kune GA, Vitetta L. Alcohol consumption and the etiology of colorectal cancer: a review of the scientific evidence from 1957 to 1991. Nutr Cancer. (1992)
  37. ^ The effect of joint exposure to alcohol and tobacco on risk of cancer of the mouth and pharynx.
  38. ^ Castellsagué X, et al. Independent and joint effects of tobacco smoking and alcohol drinking on the risk of esophageal cancer in men and women. Int J Cancer. (1999)
  39. ^ Guertin DA, Sabatini DM. Defining the role of mTOR in cancer. Cancer Cell. (2007)
  40. ^ Foster DA. Phosphatidic acid signaling to mTOR: signals for the survival of human cancer cells. Biochim Biophys Acta. (2009)
  41. ^ a b c d Reduced mortality and moderate alcohol consumption The phospholipase D-mTOR connection.
  42. ^ Harrison DE, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. (2009)
  43. ^ de Groot LC, Zock PL. Moderate alcohol intake and mortality. Nutr Rev. (1998)
  44. ^ Doll R, et al. Mortality in relation to alcohol consumption: a prospective study among male British doctors. Int J Epidemiol. (2005)
  45. ^ Ronksley PE, et al. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ. (2011)
  46. ^ Blagosklonny MV. An anti-aging drug today: from senescence-promoting genes to anti-aging pill. Drug Discov Today. (2007)
  47. ^ Martin DE, Hall MN. The expanding TOR signaling network. Curr Opin Cell Biol. (2005)
  48. ^ Colman RJ, et al. Caloric restriction delays disease onset and mortality in rhesus monkeys. Science. (2009)
  49. ^ a b Toschi A, et al. Regulation of mTORC1 and mTORC2 complex assembly by phosphatidic acid: competition with rapamycin. Mol Cell Biol. (2009)
  50. ^ Hong-Brown LQ, et al. Alcohol and indinavir adversely affect protein synthesis and phosphorylation of MAPK and mTOR signaling pathways in C2C12 myocytes. Alcohol Clin Exp Res. (2006)
  51. ^ Acute alcohol intoxication enhances myocardial eIF4G phosphorylation despite reducing mTOR signaling.
  52. ^ Vary TC, Deiter G, Lantry R. Chronic alcohol feeding impairs mTOR(Ser 2448) phosphorylation in rat hearts. Alcohol Clin Exp Res. (2008)
  53. ^ De Feo P, et al. Ethanol impairs post-prandial hepatic protein metabolism. J Clin Invest. (1995)
  54. ^ Volpi E, et al. Moderate and large doses of ethanol differentially affect hepatic protein metabolism in humans. J Nutr. (1998)
  55. ^ Berneis K, Ninnis R, Keller U. Ethanol exerts acute protein-sparing effects during postabsorptive but not during anabolic conditions in man. Metabolism. (1997)
  56. ^ Preedy VR, Keating JW, Peters TJ. The acute effects of ethanol and acetaldehyde on rates of protein synthesis in type I and type II fibre-rich skeletal muscles of the rat. Alcohol Alcohol. (1992)
  57. ^ Koziris LP, et al. Effect of acute postexercise ethanol intoxication on the neuroendocrine response to resistance exercise. J Appl Physiol. (2000)
  58. ^ Barnes MJ, Mundel T, Stannard SR. The effects of acute alcohol consumption on recovery from a simulated rugby match. J Sports Sci. (2012)
  59. ^ a b Röjdmark S, Calissendorff J, Brismar K. Alcohol ingestion decreases both diurnal and nocturnal secretion of leptin in healthy individuals. Clin Endocrinol (Oxf). (2001)
  60. ^ Sarkola T, Eriksson CJ. Testosterone increases in men after a low dose of alcohol. Alcohol Clin Exp Res. (2003)
  61. ^ a b Sarkola T, et al. Acute effect of alcohol on androgens in premenopausal women. Alcohol Alcohol. (2000)
  62. ^ a b Redox Effects of Ethanol on Steroid Metabolism.
  63. ^ a b c d e f g h Välimäki MJ, et al. Sex hormones and adrenocortical steroids in men acutely intoxicated with ethanol. Alcohol. (1984)
  64. ^ Phipps WR, et al. Acute ethanol administration enhances plasma testosterone levels following gonadotropin stimulation in men. Psychoneuroendocrinology. (1987)
  65. ^ Jenkinson C, Petroczi A, Naughton DP. Red wine and components flavonoids inhibit UGT2B17 in vitro. Nutr J. (2012)
  66. ^ a b c Sierksma A, et al. Effect of moderate alcohol consumption on plasma dehydroepiandrosterone sulfate, testosterone, and estradiol levels in middle-aged men and postmenopausal women: a diet-controlled intervention study. Alcohol Clin Exp Res. (2004)
  67. ^ a b c d e Välimäki M, et al. The pulsatile secretion of gonadotropins and growth hormone, and the biological activity of luteinizing hormone in men acutely intoxicated with ethanol. Alcohol Clin Exp Res. (1990)
  68. ^ a b Mendelson JH, Mello NK, Ellingboe J. Effects of acute alcohol intake on pituitary-gonadal hormones in normal human males. J Pharmacol Exp Ther. (1977)
  69. ^ a b c Low plasma testosterone values in men during hangover.
  70. ^ Vatsalya V, et al. Pharmacodynamic effects of intravenous alcohol on hepatic and gonadal hormones: influence of age and sex. Alcohol Clin Exp Res. (2012)
  71. ^ Cicero TJ, et al. Ethanol and acetaldehyde directly inhibit testicular steroidogenesis. J Pharmacol Exp Ther. (1980)
  72. ^ Orpana AK, et al. Role of ethanol metabolism in the inhibition of testosterone biosynthesis in rats in vivo: importance of gonadotropin stimulation. J Steroid Biochem Mol Biol. (1990)
  73. ^ Maneesh M, et al. Alcohol abuse-duration dependent decrease in plasma testosterone and antioxidants in males. Indian J Physiol Pharmacol. (2006)
  74. ^ Krähenbuhl S, et al. Acute liver failure in two patients with regular alcohol consumption ingesting paracetamol at therapeutic dosage. Digestion. (2007)
  75. ^ a b Prescott LF. Paracetamol, alcohol and the liver. Br J Clin Pharmacol. (2000)
  76. ^ Riordan SM, Williams R. Alcohol exposure and paracetamol-induced hepatotoxicity. Addict Biol. (2002)
  77. ^ Rumack BH. Acetaminophen misconceptions. Hepatology. (2004)
  78. ^ James LP, Mayeux PR, Hinson JA. Acetaminophen-induced hepatotoxicity. Drug Metab Dispos. (2003)
  79. ^ Hinson JA, et al. Acetaminophen-induced hepatotoxicity: role of metabolic activation, reactive oxygen/nitrogen species, and mitochondrial permeability transition. Drug Metab Rev. (2004)
  80. ^ Sánchez-Catalán MJ, et al. Distribution and differential induction of CYP2E1 by ethanol and acetone in the mesocorticolimbic system of rat. Alcohol Alcohol. (2008)
  81. ^ Forkert PG, et al. Induction and regulation of CYP2E1 in murine liver after acute and chronic acetone administration. Drug Metab Dispos. (1994)
  82. ^ a b Yun YP, et al. Pretranslational activation of cytochrome P450IIE during ketosis induced by a high fat diet. Mol Pharmacol. (1992)
  83. ^ Hu Y, Ingelman-Sundberg M, Lindros KO. Induction mechanisms of cytochrome P450 2E1 in liver: interplay between ethanol treatment and starvation. Biochem Pharmacol. (1995)
  84. ^ Gentry RT, et al. Mechanism of the aspirin-induced rise in blood alcohol levels. Life Sci. (1999)
  85. ^ Roine R, et al. Aspirin increases blood alcohol concentrations in humans after ingestion of ethanol. JAMA. (1990)
  86. ^ Kechagias S, et al. Low-dose aspirin decreases blood alcohol concentrations by delaying gastric emptying. Eur J Clin Pharmacol. (1997)
  87. ^ Oneta CM, et al. First pass metabolism of ethanol is strikingly influenced by the speed of gastric emptying. Gut. (1998)
  88. ^ Kato H, et al. Oral administration of ethanol with aspirin increases the concentration of salicylic acid in plasma and organs, especially the brain, in mice. Eur J Pharmacol. (2010)
  89. ^ Varma PS, et al. Alcohol and thermally oxidized pufa induced oxidative stress: role of N-acetyl cysteine. Ital J Biochem. (2004)
  90. ^ Volkmer DL, et al. Antioxidant therapy attenuates deficient bone fracture repair associated with binge alcohol exposure. J Orthop Trauma. (2011)
  91. ^ Alhelail MA, et al. Clinical course of repeated supratherapeutic ingestion of acetaminophen. Clin Toxicol (Phila). (2011)
  92. ^ a b Gupta GL, Rana AC. Effect of Withania somnifera Dunal in ethanol-induced anxiolysis and withdrawal anxiety in rats. Indian J Exp Biol. (2008)
  93. ^ a b Taksande BG, et al. Agmatine, an endogenous imidazoline receptor ligand modulates ethanol anxiolysis and withdrawal anxiety in rats. Eur J Pharmacol. (2010)
  94. ^ Aglawe MM, et al. Participation of central imidazoline binding sites in antinociceptive effect of ethanol and nicotine in rats. Fundam Clin Pharmacol. (2013)
  95. ^ Ozden O, et al. Agmatine blocks ethanol-induced locomotor hyperactivity in male mice. Eur J Pharmacol. (2011)
  96. ^ Sameer SM, Chakraborty SS, Ugale RR. Agmatine attenuates acquisition but not the expression of ethanol conditioned place preference in mice: a role for imidazoline receptors. Behav Pharmacol. (2013)
  97. ^ Steer H. The source of carbon dioxide for gastric acid production. Anat Rec (Hoboken). (2009)
  98. ^ Utkan T, et al. Investigation on the mechanism involved in the effects of agmatine on ethanol-induced gastric mucosal injury in rats. Life Sci. (2000)
  99. Obad A, et al. Alcohol-Mediated Organ Damages: Heart and Brain. Front Pharmacol. (2018)
  100. Maxwell CR, et al. Acetate causes alcohol hangover headache in rats. PLoS One. (2010)
  101. Tipple CT, Benson S, Scholey A. A Review of the Physiological Factors Associated with Alcohol Hangover. Curr Drug Abuse Rev. (2017)
  102. Mackus M, et al. Proceeding of the 8th Alcohol Hangover Research Group Meeting. Curr Drug Abuse Rev. (2017)
  103. Penning R, et al. The pathology of alcohol hangover. Curr Drug Abuse Rev. (2010)
  104. Rohsenow DJ, Howland J. The role of beverage congeners in hangover and other residual effects of alcohol intoxication: a review. Curr Drug Abuse Rev. (2010)
  105. Rohsenow DJ, et al. Intoxication with bourbon versus vodka: effects on hangover, sleep, and next-day neurocognitive performance in young adults. Alcohol Clin Exp Res. (2010)
  106. Schroeder DJ, Collins WE. Effects of congener and noncongener alcoholic beverages on a clinical ataxia test battery. Aviat Space Environ Med. (1979)
  107. Thompson T, et al. Analgesic Effects of Alcohol: A Systematic Review and Meta-Analysis of Controlled Experimental Studies in Healthy Participants. J Pain. (2017)
  108. Armstrong LE, et al. Mild dehydration affects mood in healthy young women. J Nutr. (2012)
  109. Ganio MS, et al. Mild dehydration impairs cognitive performance and mood of men. Br J Nutr. (2011)
  110. van Schrojenstein Lantman M, et al. Total sleep time, alcohol consumption, and the duration and severity of alcohol hangover. Nat Sci Sleep. (2017)
  111. Ebrahim IO, et al. Alcohol and sleep I: effects on normal sleep. Alcohol Clin Exp Res. (2013)
  112. Jayawardena R, et al. Interventions for treatment and/or prevention of alcohol hangover: Systematic review. Hum Psychopharmacol. (2017)
  113. Wang F, et al. Natural Products for the Prevention and Treatment of Hangover and Alcohol Use Disorder. Molecules. (2016)
  114. Verster JC, Penning R. Treatment and prevention of alcohol hangover. Curr Drug Abuse Rev. (2010)
  115. Pittler MH, Verster JC, Ernst E. Interventions for preventing or treating alcohol hangover: systematic review of randomised controlled trials. BMJ. (2005)
  116. Howland J, et al. The incidence and severity of hangover the morning after moderate alcohol intoxication. Addiction. (2008)
  117. Cederbaum AI. Alcohol metabolism. Clin Liver Dis. (2012)
  118. Mitchell MC Jr, Teigen EL, Ramchandani VA. Absorption and peak blood alcohol concentration after drinking beer, wine, or spirits. Alcohol Clin Exp Res. (2014)
  119. Lee HS, et al. Effect of Korean pear (Pyruspyrifolia cv. Shingo) juice on hangover severity following alcohol consumption. Food Chem Toxicol. (2013)
  120. Kim MJ, et al. Effect of Mixed Fruit and Vegetable Juice on Alcohol Hangovers in Healthy Adults. Prev Nutr Food Sci. (2018)
  121. Wiese J, et al. Effect of Opuntia ficus indica on symptoms of the alcohol hangover. Arch Intern Med. (2004)
  122. Kim H, et al. A standardized extract of the fruit of Hovenia dulcis alleviated alcohol-induced hangover in healthy subjects with heterozygous ALDH2: A randomized, controlled, crossover trial. J Ethnopharmacol. (2017)
  123. Lee MH, et al. Red ginseng relieves the effects of alcohol consumption and hangover symptoms in healthy men: a randomized crossover study. Food Funct. (2014)
  124. Baek KS, et al. In vitro and in vivo anti-inflammatory activities of Korean Red Ginseng-derived components. J Ginseng Res. (2016)
  125. Hong M, et al. Anti-inflammatory and antifatigue effect of Korean Red Ginseng in patients with nonalcoholic fatty liver disease. J Ginseng Res. (2016)
  126. Bang JS, et al. Clinical effect of a polysaccharide-rich extract of Acanthopanax senticosus on alcohol hangover. Pharmazie. (2015)
  127. Takahashi M, et al. Clinical effectiveness of KSS formula, a traditional folk remedy for alcohol hangover symptoms. J Nat Med. (2010)
  128. Tiwari V, Chopra K. Protective effect of curcumin against chronic alcohol-induced cognitive deficits and neuroinflammation in the adult rat brain. Neuroscience. (2013)
  129. Kasperczyk S, et al. The administration of N-acetylcysteine reduces oxidative stress and regulates glutathione metabolism in the blood cells of workers exposed to lead. Clin Toxicol (Phila). (2013)
  130. Alidoost F, et al. Effects of silymarin on the proliferation and glutathione levels of peripheral blood mononuclear cells from beta-thalassemia major patients. Int Immunopharmacol. (2006)
  131. Ozaras R, et al. N-acetylcysteine attenuates alcohol-induced oxidative stress in the rat. World J Gastroenterol. (2003)
  132. Verster J and Berthélemy O. Consumer Satisfaction and Efficacy of the Hangover Cure After-Effect©. Adv Prev Med. (2012)
  133. Kaivola S, et al. Hangover headache and prostaglandins: prophylactic treatment with tolfenamic acid. Cephalalgia. (1983)
  134. Verster JC. The "hair of the dog": a useful hangover remedy or a predictor of future problem drinking?. Curr Drug Abuse Rev. (2009)