 
	How does alcohol make you drunk? - Judy Grisel
 Ethanol: this molecule, made of little 
 more than a few carbon atoms,
  is responsible for drunkenness.
  Often simply referred to as alcohol,
  ethanol is the active ingredient 
 in alcoholic beverages.
  Its simplicity helps it 
 sneak across membranes
  and nestle into a many different nooks,
  producing a wide range of effects 
 compared to other, clunkier molecules.
  So how exactly does it cause drunkenness,
  and why does it have dramatically 
 different effects on different people?
  To answer these questions,
  we’ll need to follow alcohol 
 on its journey through the body.
  Alcohol lands in the stomach 
 and is absorbed into the blood
  through the digestive tract,
 especially the small intestine.
  The contents of the stomach 
 impact alcohol’s ability
  to get into the blood because 
 after eating, the pyloric sphincter,
  which separates the stomach 
 from the small intestine, closes.
  So the level of alcohol that reaches 
 the blood after a big meal
  might only be a quarter that
 from the same drink on an empty stomach.
  From the blood, 
 alcohol goes to the organs,
  especially those that get 
 the most blood flow:
  the liver and the brain.
  It hits the liver first, 
 and enzymes in the liver
  break down the alcohol molecule 
 in two steps.
  First, an enzyme called ADH turns alcohol 
 into acetaldehyde, which is toxic.
  Then, an enzyme called ALDH converts the 
 toxic acetaldehyde to non-toxic acetate.
  As the blood circulates, the liver 
 eliminates alcohol continuously—
  but this first pass of elimination 
 determines how much alcohol
  reaches the brain and other organs.
  Brain sensitivity is responsible 
 for the emotional, cognitive,
  and behavioral effects of alcohol— 
 otherwise known as drunkenness.
  Alcohol turns up the brain’s 
 primary brake, the neurotransmitter GABA,
  and turns down its primary gas, 
 the neurotransmitter glutamate.
  This makes neurons 
 much less communicative,
  and users feel relaxed at moderate doses, 
 fall asleep at higher doses,
  and can impede the brain activity 
 necessary for survival at toxic doses.
  Alcohol also stimulates 
 a small group of neurons
  that extends from the midbrain 
 to the nucleus accumbens,
  a region important for motivation.
  Like all addictive drugs,
  it prompts a squirt of dopamine 
 in the nucleus accumbens
  which gives users a surge of pleasure.
  Alcohol also causes some neurons 
 to synthesize and release endorphins.
  Endorphins help us to calm down 
 in response to stress or danger.
  Elevated levels of endorphins 
 contribute to the euphoria
  and relaxation associated 
 with alcohol consumption.
  Finally,
  as the liver’s breakdown of alcohol 
 outpaces the brain’s absorption,
  drunkenness fades away.
  Individual differences 
 at any point in this journey
  can cause people 
 to act more or less drunk.
  For example, a man and a woman who weigh 
 the same and drink the same amount
  during an identical meal will still have 
 different blood alcohol concentrations,
  or BACs.
  This is because women 
 tend to have less blood—
  women generally have 
 a higher percentage of fat,
  which requires less blood than muscle.
  A smaller blood volume, 
 carrying the same amount of alcohol,
  means the concentration 
 will be higher for women.
  Genetic differences in the liver’s alcohol
 processing enzymes also influence BAC.
  And regular drinking can 
 increase production of these enzymes,
  contributing to tolerance.
  On the other hand, those who drink 
 excessively for a long time
  may develop liver damage,
 which has the opposite effect.
  Meanwhile, genetic differences 
 in dopamine, GABA,
  and endorphin transmission 
 may contribute to risk
  for developing an alcohol use disorder.
  Those with naturally low endorphin 
 or dopamine levels may self-medicate
  through drinking.
  Some people have a higher risk 
 for excessive drinking
  due to a sensitive endorphin response 
 that increases the pleasurable effects
  of alcohol.
  Others have a variation 
 in GABA transmission
  that makes them especially sensitive 
 to the sedative effects of alcohol,
  which decreases their risk of developing 
 disordered drinking.
  Meanwhile, the brain adapts to chronic 
 alcohol consumption by reducing GABA,
  dopamine, and endorphin transmission, 
 and enhancing glutamate activity.
  This means regular drinkers tend 
 to be anxious, have trouble sleeping,
  and experience less pleasure.
  These structural and functional changes 
 can lead to disordered use
  when drinking feels normal, 
 but not drinking is uncomfortable,
  establishing a vicious cycle.
  So both genetics and previous experience 
 impact how a person experiences alcohol—
  which means that some people 
 are more prone
  to certain patterns 
 of drinking than others,
  and a history of consumption leads 
 to neural and behavioral changes.