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Chemically Correct: Alcohol!

Warning! This is hardcore info. If you are offended by profanity, perversion, or anything like that then check out some other articles.

Ethanol, aka "alcohol", is perhaps the most widely consumed drug on Earth. With the exception of its effects on heart disease, few people would claim it is good for you. But, because of its legality, omnipresence, and just the fact that it is so much fun, most think very little of having a few beers or even a few six packs. This includes many bodybuilders.

However, it is far from being a harmless vice, even to non-alcoholics. It affects numerous neurotransmitters, metabolic processes, and hormones -- and many of these effects go beyond the time period of intoxication. These have ramifications, not only for general health, but as you will see, body composition as well.

This is the first of a 2-part series - We will first look at the basic science of ethanol, then we will turn to its effects on body composition in the second installment. We will not be looking at the effects of chronic ethanol consumption, addiction and withdrawal; they are not relevant to what I consider as my target audience. Suffice it to say, such a lifestyle is utterly incompatible with getting the most out of one's bodybuilding efforts.


Ethanol, in addition to being a drug, is also a nutrient (1). However, unlike the other nutrients such as carbs, fat and protein, the body lacks the ability to store ethanol (1) - It is also the only toxic macronutrient (1). These two characteristics lead to some important consequences -- namely, it must be metabolized, and this metabolism takes precedence over all other nutrients (2).

It is metabolized by one of two pathways, depending on blood levels. The primary is to aldehyde, via alcohol dehydrogenase (ADH) (3). However, at high levels, what is known as the microsomal ethanol oxidizing system (MEOS) becomes a significant pathway (4). Both result in conversion to acetate, then acetyl-CoA - where it can either a) enter the tricarboxylic acid cycle and be oxidized into CO2 and water, or b) be stored as fat (1).


Ethanol is readily bioavailable with oral administration, however, oral clearance rate and % absorption decrease in the post-prandial state (i.e. with food) (5), due to the presence of ADH activity in the stomach (6). The more food in the stomach, the longer the ethanol stays there to be metabolized before it reaches the bloodstream. The type of food will effect this; protein and fat have the greater effect. Fat, due to slowing transport into the small intestine, protein, probably through direct binding with the ethanol molecule (7).

The type of drink can also effect blood alcohol levels obtained - particularly in the fed state. For instance, after a meal, a less concentrated drink (such as a beer) will be absorbed more quickly than a more concentrated one (such as a shot) - and, in rats, this led to an 80% higher peak blood alcohol level and 95% higher overall absorption (8). However, on an empty stomach, the opposite was found, though the magnitude of the difference was not as strong.

It is also interesting to note that when large amounts are taken in, absorption can exceed systemic distribution, thus exceptionally high concentrations can occur in arterial blood, and, therefore, the brain (7). This is why bonging 6 beers right in a row hits you harder than drinking 8 drinks over 2 hours.

Despite popular opinion to the contrary, women do not metabolize ethanol more slowly than men - the opposite is in fact true. Failure to take into account differences in total body water (i.e. LBM) between men and women has accounted for much of this confusion (9). But, when normalized for total body water, women metabolize ethanol 33% faster than men, due to a proportionally larger liver (10).

Due to limitations of ADH, metabolism of ethanol follows zero-order, straight line kinetics - meaning it is broken down at a constant rate (about a drink per hour) rather than having a half-life as most drugs do (11).

DHT has been shown to decrease breakdown of ethanol by increasing the breakdown of ADH, thus a good testosterone cycle will increase susceptibility to intoxication (12). Aldehyde

Aldehyde, as mentioned, is a product of ethanol metabolism. In the literature, its presence has generally been found to produce an aversive response, thus the basis of treatment of alcoholics with disulfiram (13). It is responsible for the flushing seen in some drinkers, usually Asians -- this can be reduced with the use of antihistamines (14). However, a few studies have shown it to be involved in the reinforcement of ethanol intake (15).

Aldehyde is also implicated in ethanol's hepatotoxic effects (16). The amino acid taurine enhances the metabolism of aldehyde by activating the hepatic enzyme aldehyde dehydrogenase, thus lowering levels - though this was with the equivalent of 45 grams for a 200lb person (17), so who knows if supplementing with reasonable levels would be effective.


Following oral, intravenous, or intraperitoneal administration, ethanol produces central nervous system (CNS) effects of a biphasic nature. Lower concentrations (3-to-8 drinks) tend to produce stimulant effects (euphoria) while higher doses result in CNS depression (anti-anxiety, sedation) (18).

It was thought for quite some time that ethanol produces its effects through nonspecific means, by acting as a solvent, or interfering with lipid membranes (19, 20). In fact, as late as a 1997 drug education class I took in college, we were informed that it worked by coating the cells rather than interacting with specific receptors like all other drugs. This view has recently fallen out of favor for several reasons that I won't go into detail on, and it is now considered to exert its effects through binding to proteins on specific receptors (21). It is widely held that no specific ethanol receptor exists, though one prominent researcher suggests that the evidence suggests we should be moving toward the concept of a specific ethanol receptor (22).

The exact mechanism behind its subjective effects are still not completely understood, and involve multiple neurotransmitter systems and ion channels with many studies reporting effects that completely contradict other ones, and all of this is further complicated by the fact that ethanol seems to preferentially affect certain subtypes of the various receptors. An exhaustive presentation is best suited for a 500-page book, thus I have weeded through and analyzed the research in order to give what I consider the best overall generalization about its effects on the various systems.


Levels of the central neurotransmitter dopamine have been consistently shown to be increased by ethanol (23,24), and it is considered as the primary mediator of the reinforcing effects of all drugs of abuse (25). It is also involved in behavioral reinforcement in general. Of particular importance is the mesolimbic dopamine system, which is regulated by neurons in the Ventral Tagamental Area (VTA) and Nucleus Accumbens (NAC) (26).

Alcohol-preferring rats have been shown to have lower basal mesolimbic dopaminergic activation and innervation than non-preffering rats (27) - as well as altered serotonin, GABA, and opioid activity, all of which are major modulators of the mesolimbic dopamine system and likely contribute to the hypofunctioning of this area (27, 28). Acute administration of ethanol increases extracellular dopamine levels in the NAC as a result of increased firing of dopamine neurons in the VTA, thus bringing mesolimbic activity toward normal (29). Thus, ethanol intake is merely representing self-medication - bringing about behavioral activation (thought analogous to euphoria in humans) and decreased anxiety in alcohol-preffering rats, while non-preferring rats, whose dopamine system is not faulty, tend to just become sedated (27).


Ethanol has been found to increase brain levels of the endogenous opioid beta-endorphin (31), and it is likely that the opioid system mediates a large part of its effects on dopamine levels, by removing GABA mediated inhibition of dopamine neuron firing (32).

It has been found that alcoholics have lower basal levels of endogenous opioids than non-alcoholics, and when ethanol is consumed these levels increase to a level higher than those reached by non-alcoholics with ethanol consumption (33). Opiod receptor antagonists have been found to inhibit the reinforcing effects of ethanol in animals and the euphoric effect in humans (34). One of these, nalaxone, is considered a very promising drug in the fight against ethanol addiction.

However, if I may opine for a moment, I would like to point out that opioids are the brain's happy hormones, so alcoholics are self medicating to bring themselves happiness that the biochemistry of their brain withholds from them, so a drug that keeps someone from drinking by making it ineffective at making them happy seems a piss-poor approach to me. But, of course, they would never allow a long-acting morphine for such purposes, because, heaven forbid, someone might want a little more happiness than The Man deems appropriate and thus might "abuse" it.


The NMDA receptor is one of three types of glutamate receptors - the body's primary excitatory neurotransmitter. It is named for n-Methyl-d-Aspartate, its synthetic, high-affinity ligand (35). Ethanol has been found to block the action of this receptor (36). The likely mechanism is by preventing glutamate's removal of a magnesium ion which blocks calcium influx into the cell (37). This decreases the excitation of the cell, which, along with increased inhibition via GABA, results in the sedative-depressant effects of ethanol, particularly at higher doses.

This blockade leads to upregulation of glutamate receptors (38), which leads to hyperexcitability of the cell when ethanol is no longer present. This is one of the mechanisms responsible for ethanol-induced neurotoxicity seen with withdrawal (39). It has also been postulated that the end of each drinking episode represents a mini-withdrawal complete with the aforementioned excitotoxicity (40). Because magnesium is the natural antagonist for the receptor (41), it would probably not be a bad idea to take 400-800 mg before bed after a night of drinking. Zinc, and the amino acid taurine may be as well (42,43).

By the way, magnesium and zinc's antagonism of the NMDA receptor may account for ZMA's positive effects on sleep. Unfortunately, it is disruption of the NMDA receptor that leads to the decrease in REM sleep caused by alcohol (43b).

The NMDA receptor complex is also implicated in memory loss and blackouts from ethanol (35). This is due to its effects on long-term potentiation (LTP). We will address this in more detail later.


Another very important system is the gamma-aminobutyric acid (GABA) system -- the body's primary inhibitory pathway (44). Ethanol potentiates GABA's activity at its receptor (45). It likely has a biphasic effect on behavior, with lower doses inhibiting inhibitory GABA interneurons on dopamine receptors in the VTA, thus causing dopamine-induced stimulation and euphoria, and higher doses producing widespread inhibition of CNS activity, thus overriding the stimulant effects (46, 47). This is likely one of the major mechanisms through which it produces its sedative-hypnotic and anxiolytic actions.


Ethanol also has significant effects on serotonin (5-HT), though it is not as well characterized as the afore-mentioned ones. Ethanol has a biphasic effect on serotonin, first raising levels, then lowering them (48).

5-HT2 agonists, as well as serotonin reuptake inhibitors, have been found to substitute for ethanol in drug discrimination tests (49, 50). 5HT3 activity is probably responsible for the nausea with excessive consumption (51). It is also likely to partially account for increased dopamine release as antagonists have been shown to block ethanol induced dopamine release (52).

Ethanol administration eventually results in depressed 5-HT levels, and thus activity, due to increased peripheral metabolism of its precursor, l-tryptophan (53). Low levels of 5-HT are associated with increased aggression (53), and it is also quite likely that subsequent drinking episodes (and their accompanying initial increase in 5-HT levels) represent self-medication, to be followed by a fall in levels and repeat of the cycle. It seems possible that lowered 5-HT levels could contribute to the malaise of a next-day hangover, so the use of 50mg of 5-HTP upon waking might not be a bad idea.


The cholinergic system is yet another target for the actions of ethanol (54). It has been found to act as a co-agonist with acetylcholine at the nicotinic acetylcholine receptors, as well as to potentiate the effect of nicotine at this receptor, both of which ultimately result in an increase in mesolimbic dopamine (55). This interaction accounts quite nicely for the fact that 90% of ethanol addicts are also nicotine addicts (56).


There is also likely some interaction by ethanol with the endocannabinoid system. They are somewhat similar in their effects in that both produce euphoria and stimulation at low doses and CNS depression at high doses (57). Cross-tolerance between the effects of THC and ethanol have been shown in rats (58), and down regulation of the CB1 subtype of cannabinoid receptors has been reported in rats chronically exposed to ethanol (59).

N-arichidonyl-ethanolamide (AnNH) is a naturally occurring derivative of the long-chain fatty acid, arachidonic acid, which has been found to bind to the CB1 cannabinoid receptor and to mimic the effects of THC (60). Ethanol increases the formation of AnNH from arachidonic acid.

The administration of a CB1 antagonist has been shown to limit ethanol consumption, suggesting that it might be involved in ethanol's reinforcement (62).


Ethanol consumption increases central and peripheral levels of epinephrine (E) and norepinephrine (NE), which contributes to the stimulatory affects of ethanol, particularly in the ascending arm of the blood alcohol curve (63, 64). Brain levels of norepinephrine have been shown to increase up to three-fold (64). These elevations occur primarily due to increased release and decreased clearance, rather than increases in synthesis (65). A consequence of this is eventual depletion of E and NE stores - to as low as 8% and 20% in the adrenals after 4 days of ethanol intoxication (66). This fall likely contributes to the CNS depression that occurs with prolonged drinking.


There exists a real and significant relationship between ethanol and aggression (67), which might be of particular importance to bodybuilders who are supplementing with exogenous androgens or an EC stack, reading T-Mag on a regular basis, or any other things which could already be facilitating aggressive behavior.

The possible mechanisms by which it does this are several. As an anxiolytic, it can reduce fear of retaliation and consequences of behaviors, as a psychomotor stimulant, it can increase sensation-seeking behavior, and as an analgesic, it can reduce the perception of consequences of painful stimuli (68).

Another interesting possibility, is that ethanol disrupts executive cognitive functioning (ECF) (68). ECF encompasses higher order mental abilities such as abstract reasoning, attention, planning, self-monitoring, and the ability to adapt future behavior based on feedback from the outside world. Basically, ECF is the ability to use the above to consciously self-regulate goal-directed behavior (69).

ECF is governed by the prefrontal cortex (70), and patients with lesions in this area have been noted to have decreased regulation of social behavior, including a "disinhibition syndrome" characterized by impulsivity, socially inappropriate behavior, and aggression (71, 72) - sound at all familiar? :) Lower scores on tests of ECF processes, such as the ability to inhibit aggression to obtain a monetary reward, have been reported for both prefrontal cortex lesioned patients and those intoxicated with ethanol (73). It should also be noted that it is on the ascending limb of the blood ethanol curve - i.e. when blood ethanol levels are increasing - when effects on ECF are particularly apparent (68).

The neurotransmitter, serotonin, has been implicated in this ethanol-induced aggression as well. Decreases in serotonin levels, as well as 5-HT receptors, have been correlated with aggressive behavior (53). Acute ethanol consumption decreases the availability of the 5-HT precursor l-tryptophan to the brain (53). So, it might not be a bad idea to take 25-50mg of 5-HTP if you are prone to aggressive behavior when drinking.


Alcohol is neuorotoxic, and this toxicity is likely mediated by several factors. Fatty acid ethyl esters are a toxic byproduct of fatty acids and ethanol (74) which increase mitochondrial uncoupling and disrupt lipids of cell membranes (75) - both l-carnitine and acetyl-l-carnitine in doses of 50mg/kg have been shown to decrease formation of FAEE by 3-to-6 fold, with ALC being particularly effective (75).

There is also strong evidence that ethanol induces oxidative damage - in the form of increased free-radicals and indirect markers of oxidative damage such as lipid peroxides and protein carbonyl (76), thus the use of antioxidants is recommended - Grape seed extract, resveratrol, SAMe, ALC, vitamin E and selenium have all been shown effective (77, 78, 79, 80). As mentioned previously, NMDA modulated excitotoxicity is another mechanism.

Hepatotoxicity will not be reviewed as it is not a real concern for non-alcoholics, and alcoholics are not the intended audience of this article. Though, I will note that the notion that a single episode of concomitant Tylenol and ethanol use causing permanent liver damage has no basis in fact (81).


The NMDA receptor complex is implicated in memory loss and blackouts from ethanol. This is due to its suppression of long-term potentiation (LTP) in the hippocampus (35). LTP is a sustained increase in synaptic efficacy following brief intense stimulation of presynaptic inputs (82) - basically, it is a physiological change by which memories are formed.

NMDA activation is required for the induction, but not sustaining of LTP (83), and as mentioned, ethanol results in the blockade of NMDA receptor transmission. Indeed, ethanol has been directly shown to inhibit LTP in concentrations as low as 5mM (equivalent to 1-2 drinks) (84).

This effect is very much dose-dependent (as well as exhibiting interindividual differences and tending to be related to rapidly rising blood ethanol levels) and exists as a continuum, with lower concentrations producing minor loss and concentrations between 50-100mM (20+ drinks) producing so-called "blackouts" (85).

Contrary to popular notion, the occurrence of more frequent blackouts is not a predictor of subsequent alcoholism (86). Blackouts and short-term memory deficits have been found to be related (87), so if you want to test whether your drunken friend will experience a blackout the next day, ask him about a conversation 5 minutes earlier, and if he does not remember it at all, you will know that he will.

GABA (88), dopamine (89), and serotonin (90)are also likely to be involved in ethanol induced memory disruption, though the data for both is scarce at present. With serotonin, this is likely due to decreased availability of tryptophan and has been shown to be reversible with an SSRI. Thus, 25-50mg of 5-HTP is again recommended.

  1. Prentice AM. Alcohol and obesity. Int J Obes Relat Metab Disord 1995 Nov;19 Suppl 5:S44-50
  2. Shelmet JJ, Reichard GA, Skutches CL, Hoeldtke RD, Owen OE, Boden G. Ethanol causes acute inhibition of carbohydrate, fat, and protein oxidation and insulin resistance. J Clin Invest 1988 Apr;81(4):1137-45
  3. Carpenter TM. The metabolism of alcohol: A review. Quart j Stud alcohol 1940 1:201-226
  4. Pirola RC, Lieber CS. Hypothesis: energy wastage in alcoholism and drug abuse: possible role of hepatic microsomal enzymes.Am J Clin Nutr 1976 Jan;29(1):90-3
  5. Jones AW, Jonsson KA. Food-induced lowering of blood-ethanol profiles and increased rate of elimination immediately after a meal. J Forensic Sci 1994 Jul;39(4):1084-93
  6. Hernandez-Munoz R, Caballeria J, Baraona E, Uppal R, Greenstein R, Lieber CS. Human gastric alcohol dehydrogenase: its inhibition by H2-receptor antagonists, and its effect on the bioavailability of ethanol. Alcohol Clin Exp Res 1990 Dec;14(6):946-50
  7. Gentry RT. Effect of food on the pharmacokinetics of alcohol absorption. Alcohol Clin Exp Res 2000 Apr;24(4):403-4
  8. Roine R. Interaction of prandial state and beverage concentration on alcohol absorption. Alcohol Clin Exp Res 2000 Apr;24(4):411-2
  9. Kalant H. Effects of food and body composition on blood alcohol curves. Alcohol Clin Exp Res 2000 Apr;24(4):413-4
  10. Thomasson H. Alcohol elimination: faster in women? Alcohol Clin Exp Res 2000 Apr;24(4):419-20
  11. Lundquist F, Wolthers H. The kinetics of alcohol elimination in man. Acta Pharmacol Toxicol 1958; 14:265-289
  12. Vaubourdolle M, Guechot J, Chazouilleres O, Poupon RE, Giboudeau J. Effect of dihydrotestosterone on the rate of ethanol elimination in healthy men. Alcohol Clin Exp Res 1991 Mar;15(2):238-40
  13. Johnsen J, Stowell A, Morland J. Clinical responses in relation to blood acetaldehyde levels. Pharmacol Toxicol 1992 Jan;70(1):41-5
  14. Alcohol-histamine interactions. Zimatkin SM, Anichtchik OV. Alcohol Alcohol 1999 Mar-Apr;34(2):141-7
  15. Takayama S, Uyeno ET. Intravenous self-administration of ethanol and acetaldehyde by rats.Yakubutsu Seishin Kodo 1985 Dec;5(4):329-34
  16. Lieber CS. Hepatic, metabolic and toxic effects of ethanol: 1991 update. Alcohol Clin Exp Res 1991 Aug;15(4):573-92
  17. Alcohol Alcohol 2001 Jan-Feb;36(1):39-43 Taurine modulates catalase, aldehyde dehydrogenase, and ethanol elimination rates in rat brain. Ward RJ, Kest W, Bruyeer P, Lallemand F, De Witte P.
  18. Little HJ. The contribution of electrophysiology to knowledge of the acute and chronic effects of ethanol. Pharmacol Ther 1999 Dec;84(3):333-53
  19. Goldstein DB. The effects of drugs on membrane fluidity.Annu Rev Pharmacol Toxicol 1984;24:43-64
  20. Seeman P.Pharmacol Rev The membrane actions of anesthetics and tranquilizers. 1972 Dec;24(4):583-655
  21. Peoples RW, Li C, Weight FF. Lipid vs protein theories of alcohol action in the nervous system. Annu Rev Pharmacol Toxicol 1996;36:185-201
  22. Harris RA. Ethanol actions on multiple ion channels: which are important? Alcohol Clin Exp Res 1999 Oct;23(10):1563-70
  23. Little HJ. Mechanisms that may underlie the behavioural effects of ethanol. Prog Neurobiol 1991;36(3):171-94
  24. Samson HH, Tolliver GA, Haraguchi M, Hodge CW. Alcohol self-administration: role of mesolimbic dopamine. Ann N Y Acad Sci 1992 Jun 28;654:242-53
  25. Manley LD, Kuczenski R, Segal DS, Young SJ, Groves PM. Effects of frequency and pattern of medial forebrain bundle stimulation on caudate dialysate dopamine and serotonin. J Neurochem 1992 Apr;58(4):1491-8
  26. Erickson CK. Review of neurotransmitters and their role in alcoholism treatment.Alcohol Alcohol Suppl 1996 Mar;1:5-11
  27. McBride WJ, Murphy JM, Ikemoto S. Localization of brain reinforcement mechanisms: intracranial self-administration and intracranial place-conditioning studies. Behav Brain Res 1999 Jun;101(2):129-52
  28. McBride WJ, Li TK. Animal models of alcoholism: neurobiology of high alcohol-drinking behavior in rodents. Crit Rev Neurobiol 1998;12(4):339-69
  29. Zhou FC, Pu CF, Murphy J, Lumeng L, Li TK. Serotonergic neurons in the alcohol preferring rats. Alcohol 1994 Sep-Oct;11(5):397-403
  30. Li TK. Pharmacogenetics of responses to alcohol and genes that influence alcohol drinking. J Stud Alcohol 2000 Jan;61(1):5-12
  31. de Waele JP, Kiianmaa K, Gianoulakis C. Spontaneous and ethanol-stimulated in vitro release of beta-endorphin by the hypothalamus of AA and ANA rats. Alcohol Clin Exp Res 1994 Dec;18(6):1468-73
  32. Gianoulakis C. Implications of endogenous opioids and dopamine in alcoholism: human and basic science studies. Alcohol Alcohol Suppl 1996 Mar;1:33-42
  33. Johnson SW, North RA. Opioids excite dopamine neurons by hyperpolarization of local interneurons. J Neurosci 1992 Feb;12(2):483-8
  34. Altshuler HL, Phillips PE, Feinhandler DA. Alteration of ethanol self-administration by naltrexone. Life Sci 1980 Mar 3;26(9):679-88
  35. Woodward JJ. Ethanol and NMDA receptor signaling. Crit Rev Neurobiol 2000;14(1):69-89
  36. Dildy JE, Leslie SW. Ethanol inhibits NMDA-induced increases in free intracellular Ca2+ in dissociated brain cells. Brain Res 1989 Oct 16;499(2):383-7
  37. Collingridge GL, Bliss TV. Memories of NMDA receptors and LTP.Trends Neurosci 1995 Feb;18(2):54-6
  38. Gulya K, Grant KA, Valverius P, Hoffman PL, Tabakoff B. Brain regional specificity and time-course of changes in the NMDA receptor-ionophore complex during ethanol withdrawal. Brain Res 1991 Apr 26;547(1):129-34
  39. Iorio KR, Tabakoff B, Hoffman PL. Glutamate-induced neurotoxicity is increased in cerebellar granule cells exposed chronically to ethanol. Eur J Pharmacol 1993 Aug 2;248(2):209-12
  40. Nutt D. Alcohol and the brain. Pharmacological insights for psychiatrists. Br J Psychiatry 1999 Aug;175:114-9
  41. Chandler LJ, Guzman NJ, Sumners C, Crews FT. J Pharmacol Exp Ther 1994 Oct;271(1):67-75 Magnesium and zinc potentiate ethanol inhibition of N-methyl-D-aspartate-stimulated nitric oxide synthase in cortical neurons.
  42. Westbrook GL, Mayer ML. Micromolar concentrations of Zn2+ antagonize NMDA and GABA responses of hippocampal neurons. Nature 1987 Aug 13-19;328(6131):640-3
  43. Kurachi M, Yoshihara K, Aihara H. Effect of taurine on depolarizations induced by L-glutamate and other excitatory amino acids in the isolated spinal cord of the frog. Jpn J Pharmacol 1983 Dec;33(6):1247-54
  44. b. Prospero-Garcia O, Criado JR, Henriksen SJ. Pharmacology of ethanol and glutamate antagonists on rodent sleep: a comparative study.Pharmacol Biochem Behav 1994 Oct;49(2):413-6
  45. Meldrum B. Pharmacology of GABA. Clin Neuropharmacol 1982;5(3):293-316
  46. Suzdak PD, Schwartz RD, Skolnick P, Paul SM. Ethanol stimulates gamma-aminobutyric acid receptor-mediated chloride transport in rat brain synaptoneurosomes. Proc Natl Acad Sci U S A 1986 Jun;83(11):4071-5
  47. Kalivas PW, Duffy P, Eberhardt H. Modulation of A10 dopamine neurons by gamma-aminobutyric acid agonists. J Pharmacol Exp Ther 1990 May;253(2):858-66
  48. Grobin AC, Matthews DB, Devaud LL, Morrow AL. The role of GABA(A) receptors in the acute and chronic effects of ethanol. Psychopharmacology (Berl) 1998 Sep;139(1-2):2-19
  49. LeMarquand D, Pihl RO, Benkelfat C. Serotonin and alcohol intake, abuse, and dependence: clinical evidence. Biol Psychiatry 1994 Sep 1;36(5):326-37
  50. Maurel S, Schreiber R, De Vry J. Substitution of the selective serotonin reuptake inhibitors fluoxetine and paroxetine for the discriminative stimulus effects of ethanol in rats. Psychopharmacology (Berl) 1997 Apr;130(4):404-6
  51. Signs SA, Schechter MD. The role of dopamine and serotonin receptors in the mediation of the ethanol interoceptive cue. Pharmacol Biochem Behav 1988 May;30(1):55-64
  52. Wilde MI, Markham A. Ondansetron. A review of its pharmacology and preliminary clinical findings in novel applications. Drugs 1996 Nov;52(5):773-94
  53. Carboni E, Acquas E, Frau R, Di Chiara G. Differential inhibitory effects of a 5-HT3 antagonist on drug-induced stimulation of dopamine release. Eur J Pharmacol 1989 May 30;164(3):515-9
  54. Badawy AA, Morgan CJ, Lovett JW, Bradley DM, Thomas R. Decrease in circulating tryptophan availability to the brain after acute ethanol consumption by normal volunteers: implications for alcohol-induced aggressive behaviour and depression. Pharmacopsychiatry 1995 Oct;28 Suppl 2:93-7
  55. Narahashi T, Aistrup GL, Marszalec W, Nagata K. Neuronal nicotinic acetylcholine receptors: a new target site of ethanol. Neurochem Int 1999 Aug;35(2):131-41
  56. Soderpalm B, Ericson M, Olausson P, Blomqvist O, Engel JA. Nicotinic mechanisms involved in the dopamine activating and reinforcing properties of ethanol. Behav Brain Res 2000 Aug;113(1-2):85-96
  57. Batel P, Pessione F, Maitre C, Rueff B. Addiction 1995 Jul;90(7):977-80 Relationship between alcohol and tobacco dependencies among alcoholics who smoke.
  58. Hollister LE, Gillespie HK. Mood and mental function alterations. Marihuana, ethanol, and dextroamphetamine. Arch Gen Psychiatry 1970 Sep;23(3):199-203
  59. Newman LM, Lutz MP, Gould MH, Domino EF. 9 -Tetrahydrocannabinol and ethyl alcohol: evidence for cross-tolerance in the rat. Science 1972 Mar 3;175(25):1022-3
  60. Basavarajappa BS, Cooper TB, Hungund BL. Chronic ethanol administration down-regulates cannabinoid receptors in mouse brain synaptic plasma membrane. Brain Res 1998 May 18;793(1-2):212-8
  61. Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, Gibson D, Mandelbaum A, Etinger A, Mechoulam R. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 1992 Dec 18;258(5090):1946-9
  62. Basavarajappa BS, Hungund BL. Chronic ethanol increases the cannabinoid receptor agonist anandamide and its precursor N-arachidonoylphosphatidylethanolamine in SK-N-SH cells. J Neurochem 1999 Feb;72(2):522-8
  63. Arnone M, Maruani J, Chaperon F, Thiebot MH, Poncelet M, Soubrie P, Le Fur G. Selective inhibition of sucrose and ethanol intake by SR 141716, an antagonist of central cannabinoid (CB1) receptors. Psychopharmacology (Berl) 1997 Jul;132(1):104-6
  64. Pohorecky LA. Influence of alcohol on peripheral neurotransmitter function. Fed Proc 1982 Jun;41(8):2452-5
  65. Wang YL, Wei JW, Sun AY. Effects of ethanol on brain monoamine content of spontaneously hypertensive rats (SHR). Neurochem Res 1993 Dec;18(12):1293-7
  66. Howes LG, MacGilchrist A, Hawksby C, Sumner D, Reid JL. Plasma [3H]-noradrenaline kinetics and blood pressure following regular, moderate ethanol consumption. Br J Clin Pharmacol 1986 Nov;22(5):521-6
  67. Adams MA, Hirst M. Adrenal and urinary catecholamines during and after severe ethanol intoxication in rats: a profile of changes. Pharmacol Biochem Behav 1984 Jul;21(1):125-31
  68. Bushman BJ, Cooper HM. Effects of alcohol on human aggression: an integrative research review. Psychol Bull 1990 May;107(3):341-54
  69. Hoaken PN, Giancola PR, Pihl RO. Executive cognitive functions as mediators of alcohol-related aggression. Alcohol Alcohol 1998 Jan-Feb;33(1):47-54
  70. Stuss DT, Benson DF. Neuropsychological studies of the frontal lobes. Psychol Bull 1984 Jan;95(1):3-28
  71. Peterson JB, Rothfleisch J, Zelazo PD, Pihl RO. Acute alcohol intoxication and cognitive functioning. J Stud Alcohol 1990 Mar;51(2):114-22
  72. Alcohol Clin Exp Res 1995 Feb;19(1):130-4 Related Articles, Books, LinkOut Alcohol-related aggression in males and females: effects of blood alcohol concentration, subjective intoxication, personality, and provocation. Giancola PR, Zeichner A.
  73. Heinrichs RW. Frontal cerebral lesions and violent incidents in chronic neuropsychiatric patients. Biol Psychiatry 1989 Jan 15;25(2):174-8
  74. Hoaken PN, Assaad JM, Pihl RO. Cognitive functioning and the inhibition of alcohol-induced aggression. J Stud Alcohol 1998 Sep;59(5):599-607
  75. Saghir M, Werner J, Laposata M. Rapid in vivo hydrolysis of fatty acid ethyl esters, toxic nonoxidative ethanol metabolites. Am J Physiol 1997 Jul;273(1 Pt 1):G184-90
  76. Calabrese V, Scapagnini G, Catalano C, Dinotta F, Bates TE, Calvani M, Stella AM. Effects of acetyl-L-carnitine on the formation of fatty acid ethyl esters in brain and peripheral organs after short-term ethanol administration in rat. Neurochem Res 2001 Feb;26(2):167-74
  77. Mantle D, Preedy VR. Free radicals as mediators of alcohol toxicity. Adverse Drug React Toxicol Rev 1999 Nov;18(4):235-52
  78. J Nutr 1973 Apr;103(4):536-42 Related Articles, Books Nutritional interrelationships among vitamin E, selenium, antioxidants and ethyl alcohol in the rat. Levander OA, Morris VC, Higgs DJ, Varma RN.
  79. Sun AY, Sun GY. Ethanol and oxidative mechanisms in the brain. J Biomed Sci 2001 Jan-Feb;8(1):37-43
  80. Lieber CS. ALCOHOL: its metabolism and interaction with nutrients. Annu Rev Nutr 2000;20:395-430
  81. Cha YS, Sachan DS. Acetylcarnitine-mediated inhibition of ethanol oxidation in hepatocytes. Alcohol 1995 May-Jun;12(3):289-94
  82. Prescott LF. Paracetamol, alcohol and the liver. Br J Clin Pharmacol 2000 Apr;49(4):291-301
  83. Givens B, McMahon K. Ethanol suppresses the induction of long-term potentiation in vivo Brain Res 1995 Aug 7;688(1-2):27-33
  84. Woodward JJ. Ethanol and NMDA receptor signaling. Crit Rev Neurobiol 2000;14(1):69-89
  85. Blitzer RD, Gil O, Landau EM. Long-term potentiation in rat hippocampus is inhibited by low concentrations of ethanol. Brain Res 1990 Dec 24;537(1-2):203-8
  86. Melia KR, Ryabinin AE, Corodimas KP, Wilson MC, Ledoux JE. Hippocampal-dependent learning and experience-dependent activation of the hippocampus are preferentially disrupted by ethanol. Neuroscience 1996 Sep;74(2):313-22
  87. Melchior CL, Ritzmann RF. Neurosteroids block the memory-impairing effects of ethanol in mice. Pharmacol Biochem Behav 1996 Jan;53(1):51-6
  88. Goodwin DW, Hill SY Short-term memory and the alcoholic blackout.Ann N Y Acad Sci 1973 Apr 30;215:195-9
  89. Goodwin DW. Alcoholic blackout and state-dependent learning. Fed Proc 1974 Jul;33(7):1833-5
  90. White AM, Matthews DB, Best PJ. Ethanol, memory, and hippocampal function: a review of recent findings. Hippocampus 2000;10(1):88-93
  91. Lau AH, Frye GD. Acute and chronic actions of ethanol on CA1 hippocampal responses to serotonin. Brain Res 1996 Aug 26;731(1-2):12-20

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