What Can We Learn About Antidepressants from Alcohol?

Why do we recognize its dangers, but not the dangers of other antidepressants such as SSRIs?


It’s a common enough idea: people who abuse alcohol are self-medicating. People drink to diminish feelings of intense physical or emotional pain. Now a new study, published in the journal Nature Communications, confirmed this hypothesis by examining the impact of alcohol on brain chemistry. Their findings indicate that alcohol has rapid antidepressant and antianxiety effects.

Photo credit: Flickr
Photo credit: Flickr

“Acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviors,” write the researchers, led by Dr. Kimberly Raab-Graham at the University of Texas, Austin. In their study on the brain chemistry of mice, the researchers found that the effects of alcohol were comparable to other rapid-acting antidepressants.

The authors first conducted a behavioral test with mice by injecting them with ethanol and observing their behavior. They found that the mice behaved in ways associated with rapid antidepressant and antianxiety effects. These effects are also observed in studies of ketamine, a tranquilizer popular as a recreational drug, which has been undergoing numerous tests as an antidepressant. Although rodent studies have limited validity in predicting human behavior, they are commonly used methods to determine initial theory validity.

The authors’ research into the neurophysiological action of alcohol identified GABABR2 as the main protein increased by use, with the RNA-binding protein FMRP regulating this action. The GABA neurological mechanism is associated with the effects of other psychopharmaceuticals, such as gabapentin (Neurontin), which strengthens this finding.

Of course, the researchers caution against self-medicating with alcohol. The side effects of alcohol range from short term effects like dizziness, nausea, and impaired cognition and judgment, to long-term impairment in cognition and social-emotional functioning. Tolerance becomes so high in alcohol addiction that withdrawal from chronic use of alcohol can be deadly.

The researchers also write that over time, “the initial antidepressant actions of alcohol are shifted to depressant allostatic states with chronic abuse,” meaning that in the short term, alcohol has an antidepressant effect, but in the long run, its effects create a new, perpetual state in the body which is actually more depressed. The same argument has been raised regarding the use of prescribed antidepressant medications (SSRIs such as Prozac, for instance).

Decades of accumulated evidence increasingly shows that use of antidepressant medications has altered the progression of depression. Once an episodic illness from which it was common to recover without treatment, now depression is considered a chronic illness that requires lifelong medication use to treat.  And that drug use itself is problematic: side effects of antidepressant medications include nausea, sexual dysfunction, impaired cognition, diabetes, increased depressive and anxious states, and suicidality. Severe withdrawal states have been noted by patients attempting to reduce their use of antidepressant medications and the benefits of antidepressant drugs have been questioned as well. Research indicates that they are far less effective than commonly believed.

Particularly since ketamine has been referred to as the “miracle cure” for depression, and as researchers continue to search for the next biochemical panacea, it is important to remember that even if a substance has antidepressant effects, it still may not be an appropriate treatment for depression. Just as alcohol appears to have far more risks than benefits, so too might ketamine—and so too might SSRIs.



Wolfe, S. A., Workman, E. R., Heaney, C. F., Niere, F., Namjoshi, S., Cacheaux, L. P., . . . Raab-Graham, K. (2016). FMRP regulates an ethanol-dependent shift in GABABR function and expression with rapid antidepressant properties. Nature Communications, 7. doi: 10.1038/ncomms12867 (Abstract)


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Peter Simons
Peter Simons was an academic researcher in psychology. Now, as a science writer, he tries to provide the layperson with a view into the sometimes inscrutable world of psychiatric research. As an editor for blogs and personal stories at Mad in America, he prizes the accounts of those with lived experience of the psychiatric system and shares alternatives to the biomedical model.


  1. Does withdrawal from SSRI’s resemble withdrawal from alcohol? I ask, because physical withdrawal from alcohol can be safely done using multiple gram quantities of niacin (and thiamine) over a period of days. I’m in no position to answer this myself, not being nor wishing to be on SSRI’s and not being crazy enough to induce someone else to try this method.

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    • I don’t know how much it resembles alcohol, considering I’ve never been addicted to it, but for me Zoloft withdrawal, from 50mgs, was fucking awful, and I honestly don’t think I’ve gotten over it, even after restarting drugs. It included severe insomnia, anxiety and intense irritability and emotional lability, disturbing dreams, mania etc. I even had some seizure like episodes, and what people call the brain zaps. This has lasted for about s year and half. I’ve tried to quit twice. The first time wasn’t as severe, but I became incredibly depressed, which wasn’t a “relapse” because I wasn’t depressed before. I took Zoloft for anxiety. I have now been diagnosed bipolar, which I’m certain wouldn’t have happened if it weren’t for the drugs. In my honest opinion I think ssris are way more dangerous than alcohol

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      • “In my honest opinion I think ssris are way more dangerous than alcohol”.

        Yes, I agree, as with alcohol we are all aware of its dangers, it is illegal to give it to people under a certain age, women are very strongly discouraged from consuming it in pregnancy, and if a doctor spots dodgy blood tests you are likely to be closely questioned and then, if necessary, given assistance to reduce your consumption.

        With SSRIs, the doctor will tell you they are safe and that any difficulties you might encounter are because of YOU, not the drug. They will dismiss any side effects you report and/or INCREASE the dose and/or throw another drug into the mix to counter the effects of the first.

        They will absolutely INSIST you keep using, sometimes to the point of locking you up in a “hospital” that will force the drugs upon you on the basis that you must be mad because you don’t recognise that the drugs are helping….even if you become violent and/or suicidal while taking them.

        So yes….the drugs ARE far more dangerous than alcohol, and yes, I too know from experience that coming off them is hell and it can take years for your brain to recover from the assault it has suffered. Some brains never do recover.

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    • It’s actually central nervous system excitation that makes alcohol withdrawals dangerous and produces the symptoms of acute alcohol withdrawal syndrome that can lead to delirium tremens. Nutrition has absolutely nothing to do with it (“wet brain” is another issue and thiamine is used to treat it). It’s because alcohol is a powerful CNS depressant, and of course the brain makes compensatory adaptations to changes in its normal functioning (decrease CNS, brain works to increase it; this is how tolerance develops in the first place)

      But I’m really only replying because I think your recommendation of niacin is dangerous. Niacin in high doses is very toxic to the liver and a chronic alcohol user likely already has fatty liver and increased liver enzymes (impaired liver function)

      The only tried-and-true treatment for alcohol withdrawal are substituting the CNS depressant effects of alcohol with a drug (benzos or barbituates) that also depresses the CNS and then tapering them off of that.

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      • No, it’s actually used by those much more educated and practiced than I. It’s been used in multigram quantities by practitioners since the mid 1950’s. I’ve supervised withdrawals for individuals who were going to keel over in the street without intervention (something I wouldn’t recommend doing casually). The question was concerning a class of antidepressant.

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        • I’ve detoxed in several ER’s and rehab centers, not one of them used Niacin. It’s because I’m so skeptical about doctors and medicine that I learned so much about this topic in the first place (alcohol withdrawals and the do’s and don’ts of managing them)

          It’s also common knowledge that Niacin in high doses causes liver damage. It’s even been in the news over the years and with discussions about legally restricting it as a dietary supplement because of it.

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  2. Again, did we really need a study to find out that alcohol has short-term antidepressant and anti-anxiety effects? I think the more important aspect of this to highlight is that taking pills to reduce depression is not substantively different than drinking to reduce depression. It’s not a “treatment,” it’s a temporary way to feel better that has unpredictable long-term consequences, including a good shot at making the depressed and anxious feelings worse. Why should we pretend we’re doing anything else? Just because it makes people feel less bad about being dependent on a substance to make it through the day if a doctor prescribed it? If so, why not just prescribe controlled doses of alcohol as “treatment?”

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  3. I do not understand the chemical effects of withdrawal. I admit to being a Chemistry 101 dropout. However, I do understand the effects of the suffering from withdrawal. Several years after college and after several years of heavy drinking, I got horribly ill after a night of drinking at the local “bar” with friends. For one night, I was terribly ill. I had chills, insomnia, shook all over. I can not remember everything, but memory is that it was one of the sickest nights of my life. I now register an allergy of alcohol that if I drink 4oz, I would be hospitalized, 8oz would most likely kill me. I can even cook with it. Now to add to this story, I have also been years and years (way to many years) taking way to many psychiatric drugs including the above mentioned SSRIs. The withdrawal of all is more treacherous in that instead of awful night, I have had to suffer for about two to three years. I say two to three years, because, despite being hospitalized when to any ethical physician, it would have been obvious that my body was rejecting the drugs finally after about twenty years, they kept using me as a drug guinea pig. Finally, it got to the point, I could no longer swallow a pill without getting sick. At that time, I said “no more!.” I told the psychiatrist that was it and that I feel “clean inside” like I did after stopping the alcohol. She then wrote me a prescription for an atypical antipsychotic at she said a “lower dose” because she did not want me to have a “relapse.” That was a year and a half ago. I have suffered physically (the withdrawal) but isn’t so funny, absolutely no relapse! It seems that the “relapses” were “caused” by the drugs. It seems now I have more allergies to to other types of “drugs” and I wonder, perhaps the SSRIS and the atypical antipsychotics might be “chemically related.” Of course, I could never know, but ,it is a question. I question, if we might not be “lied” to as to the “chemical composition” of any and all of these drugs. There is a great deal of suffering going on that I am sure is related to these “drugs.” I now know I was never sick at all. I now know most all drugs and alcohol would probably at least make me very sick, if not kill me. Thank you.

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    • Hard to say. I’ve seen olanzapine prescribed more as an antidepressant than as an antipsychotic. I was even at a kind of lecture, where the lecturer asked if anyone in the audience knew what antidepressant sometimes caused patients to gain more than 50 pounds when they were on it. She gave me a public thumbs up when I answered correctly.

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