Is Alcohol Both a Stimulant and a Depressant?

 

The other day I was drinking with a bunch of friends and discussing the effects of alcohol, and one such friend tried to convince me that hard alcohol differs from wine and beer  not only in alcohol content but also in that it acts as a stimulant rather than a depressant.  This rang slightly off, but I have also definitely felt what one might consider “stimulant” effects from beer and wine on occasion.  I’ve always wondered why we learned that alcohol is a depressant back in health class, when tequila clearly doesn’t immediately increase fatigue and decrease motor functions as a tranquilizer would.  How can alcohol act as both a stimulant and a depressant? Why am I suddenly getting sleepy when I was so energetic before?

The Answer Lies with Metabolism

The answer begins to unravel (along with your inhibitions) when that shot is poured down your esophagus.  Almost immediately your body makes metabolizing the alcohol in your system a priority.  Most people believe that alcohol is metabolized as sugar, as that’s what it’s made from, but that’s wrong.  Because of the fermentation process, alcohol is a completely different “nutrient.”  Unlike protein, fat, and carbohydrates, alcohol can’t be stored in our body.  It is therefore metabolized first.

Alcohol in your Brain and Blood Stream

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In your stomach, approximately 20% of the alcohol can be absorbed directly into your blood stream.  From there it travels into your brain, where it’s able to penetrate the blood brain barrier.  The rest of the alcohol travels to the small intestines, where it is absorbed along with other “nutrients”.  The liver is the primary site for alcohol oxidation, which is why excessive drinking can lead to liver problems.

For more information on alcohol metabolism, check out: A Brief Guide to Alcohol Metabolism and Blood Glucose.

A Stimulant and a Depressant?

Drugs are typically classified by their chemical targets in the brain.  By definition, stimulants often influence the neurotransmitters dopamine and norepinephrine.  Depressants often stimulate GABA, an inhibitory neurotransmitter, which works to reduce neuronal excitability throughout the central nervous system, which is why depressants typically increase fatigue, cause dizziness, and tend to lower blood pressure.  Although the mechanism of alcohol’s stimulatory and depressant effects is not well understood, there are a number of studies that suggest that alcohol actually works on multiple systems.

Much of the research suggests that alcohol use affects multiple neurotransmitter systems in the brain.  Some research actually suggests that alcohol can act as either a stimulant or a depressant depending on whether your BAC is rising or falling.  Drinking both increases norepinephrine as well as acts at GABA receptors.  Research has suggested that drinking may increase norepinephrine as BAC is rising.  This could explain how alcohol acts as a stimulant.

According to one study, a less common type of GABA receptor contains a delta subunit, which responds only to low levels of alcohol, such as a beer or a glass of wine.  This suggests that we may feel depressant effects at certain low BAC levels, such as after savoring a glass of wine with dinner or at the end of a long night.

In conclusion, there may be some truth to what my friend argued.  Your body may react differently to different types of alcohol, but it may have more to do with the amount of alcohol in your blood stream than anything else.  We also know that alcohol targets the prefrontal cortex, but again we still don’t really know the exact mechanism.  What is clear, is that we have a lot to learn when it comes to alcohol.

Edited May 18th, 2017

Olsen RW, Hanchar HJ, Meera P, Wallner M. GABAA receptor subtypes: the “one glass of wine” receptors. Alcohol. 2007 May;41(3):201-9.

C. FERNANDO VALENZUELA, M.D., PH.D.  Alcohol and Neurotransmitter Interactions.

McDougle CJ, Krystal JH, Price LH, Heninger GR, Charney DS. Noradrenergic response to acute ethanol administration in healthy subjects: comparison with intravenous yohimbine. Psychopharmacology (Berl). 1995 Mar;118(2):127-35.

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