Every drink spiked

This post is written anonymously (see Petra’s story).

I outlined how my daughter Petra came to take Cymbalta on this blog a few months ago (see Petra’s story; also see Symbolta of Sorts). This post tells of events that led to her coming off.

Petra is an enthusiast for motor sport events. She has been on track days, hill climbs and driver training events. She is a member of an Italian car club. She is a safe, smooth and confident driver, who has held a driver’s license since age 17 – for over six years now. She has had no disqualifications or accidents.

Cymbalta and alcohol affected her judgment

Shortly after starting Cymbalta, she noticed that alcohol seemed to affect her judgment while driving. So she stopped driving if she had had any drink. This was easy because at the time she would tend to drink quite heavily or not at all.

One afternoon she had two glasses of beer (8 oz each) while listening to music at a city venue. The event ran for most of the afternoon. She felt happy to drive home. On the way home she was stopped for a random breath test and to her horror recorded a 0.05 Blood Alcohol level on the police breathalyzer. Fortunately, the police officer decided that since the reading was exactly 0.05 and probably falling, she could wait in her car for a while and then continue home.

Close to disaster

This was very close to a disaster. In Australia a reading of 0.05 or higher means that your driver’s license may be suspended pending a court hearing, which is likely to result in a fine plus automatic license disqualification for a minimum of 3 months. The loss of independence and convenience and the loss of something that she takes pride in would have been a real blow.

I purchased an alcometer. A standard drink for Australian purposes is one that contains 10 gm (about 12.5 ml) of alcohol. One such standard drink can be expected to raise Blood Alcohol Content (BAC) by about 0.025 grams per 100ml of blood. BAC levels are commonly thought to fall at the rate of about 0.02 per hour.

We confirmed on several tests that Petra would return a reading of 0.04 per 375 ml of beer (this was 1.4 standard drinks). This was the first problem. The second was that the reading didn’t fall at the expected 0.02 per hour and her BAC would consistently show 0.08 for 2 beers and 0.12 for 3 beers consumed over 2-3 hours.

Her blood alcohol levels were a shock

Petra’s friends, brother and myself all had much lower readings. The consistency of the tests was good. I also tested our device against a police roadside check and obtained the same result as the police device. Finding that Petra returned readings in excess of 0.2 after the consumption of several alcoholic beverages over quite long periods of time was a shock and a big concern. Clearly alcohol was going to be a serious problem for her under these circumstances.

Just Girls!

Petra raised this with her doctor, whose response was dismissive – your device was ‘probably inaccurate’. A local pharmacist observed that some young women return much higher readings than expected and that this was probably ‘normal for them’. Our solicitor said that ‘Magistrates are not interested in young women who claim to have only had 2 drinks’.

Petra has now stopped Cymbalta. She says that alcohol does not now seem to affect her anywhere near as much.

So we ran the test again, with the same device as before. This time she returned a reading of 0.03 soon after the consumption of 2 x 375 mls beers, where the figure was 0.08 for the same drinks while taking Cymbalta. This is almost the same as her brother’s reading of 0.02 for the same consumption.

She then had one 375 ml drink with lunch and we checked how quickly her levels fell. She returned a reading of 0.00 1 hour and 35 mins after the start of lunch.

This has probably led to loss of life…..

Conclusion: Cymbalta more than doubles the effect of alcohol for some people at least. This could lead to and probably has led to regrettable consequences including harm to self and others, loss of driving licenses, fines, and other losses.

Eli Lilly’s prescribing information for Cymbalta is as follows:

7.16 Alcohol

When Cymbalta and ethanol were administered several hours apart so that peak concentrations of each would coincide, Cymbalta did not increase the impairment of mental and motor skills caused by alcohol.

17.10 Alcohol

Although Cymbalta does not increase the impairment of mental and motor skills caused by alcohol, use of Cymbalta concomitantly with heavy alcohol intake may be associated with severe liver injury. For this reason, Cymbalta should not be prescribed for patients with substantial alcohol use

There is no mention of the risks Petra ran and others seem likely to be running.

DH Comment:

It is difficult to explain this finding but if valid there is no reason to think these risks are confined to Cymbalta. The testing that drugs undergo does not test for this possibility. There are routine drug and alcohol driving simulation tests which an hour after alcohol often show better performance on the combination of drug and alcohol than on alcohol alone – but no-one tests what might be happening several hours later.

Cymbalta and many other drugs can have an effect on liver function. At present this seems the likeliest way to explain this effect.

In the meantime, anyone on any medication who thinks they might have been affected should check themselves out. Anyone who has ever had a driving conviction may have a case to have their conviction overturned on the basis of company negligence. The same may apply to anyone who has ever lost a job or had an accident at work.

Anyone paying increased premiums on their insurance as a result of a drink driving accident or offence may have a case to reclaim their insurance payments.

There is an urgent need to establish the genetic bases behind effects like this. It is likely that not just Petra but others in her family would be similarly affected, and so it is not just the affected person who needs checking.

The implications for employers of possible accidents at work apparently linked to alcohol but not primarily caused by alcohol are immense.

The already high risks of birth defects and miscarriages in women of child-bearing years stemming from antidepressants, and possible mental handicap in their children, would be compounded in this case by additional increased risks from alcohol. A woman taking a single glass of wine, of which several a week should be harmless, might be exposing her child to riskier concentrations than she thought.

There are clearly issues here for health and other insurance companies covering occupational hazards at large corporations such as General Motors.

We are interested in every report we can get of people having problems that might be attributed to intoxication by alcohol and drugs as well as all possible reports of drug induced cravings for alcohol – See Out of my Mind: Driven to Drink. Please add your accounts to these posts to help get recognition for these issues

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  1. Some years ago I did research on a genetic disorder that included, at onset, a craving for nicotine (even in non-smokers), caffeine and carbohydrates. In light of the craving for alcohol (which is metabolized as a carbohydrate) in some people on certain antidepressants, I wonder if anyone has had or knows of the development of carbohydrate craving in a like manner? Cakes, cookies, pasta, potatoes, soft drinks seem to be the most common.

    • I was tapering off of mirtazapine, had reached about 8 mg/day (started at 30 about a year before), and developed a strong sweet craving, but only late at night. Peior to this I’d been losing weight, 25 lbs. I finished with the mirt about 2 weeks ago and haven’t had the craving at all. It stopped within 48 hours of finishing the taper. A little taste of something tastes good, but there’s a big difference in the strength of the urge. And it’s easy to stop once I start. Previously I stopped only when I reached the bottom of the ice cream container.

  2. This may not be isolated to genetic subtypes, antidepressants in general may affect metabolism of alcohol. Yet another overlooked adverse effect would not be a surprise.

    Irene, I have many anecdotal reports that antidepressants induce carb craving.

    Clearly, they’re hormonal disruptors and have widespread effects throughout the body.

  3. Anne-Marie says:

    There are lots of people reporting cravings for carbohydrates on antidepressants on many websites as well as cravings for alcohol, I agree that these drugs effect lots of things. When I was on citalapram my weight went from 8.4 st to 7.4 st, my blood pressure also fell from approx 110/60 to approx 70/50 and at my worst reading it was 60/40 which really worried me, I was at this time in hospital and they had to tilt the bed up and were querying if I had any stomach problems, (my stomach was always churning like a washing machine on ssris) but I didnt have any pain so they left it. I also had intense cravings for alcohol and found that my blood sugar reading was also very low often at 2.0 but this was after drinking. On Mirtazapine Ive gone the other way I dont crave alcohol anymore but do get hungry more often especially an hour after taking it then I have to eat something, my weight can you believe is now 9.3 st which Im getting a bit worried about as I dont want to put on any more weight, but my blood pressure and blood sugar is back to normal thankgod.

  4. I came across this article this morning and I was wondering if this poor man was another victim of ‘every drink spiked’? It seems to have all the trademarks. http://www.camdennewjournal.com/news/2012/may/man-49-found-dead-mother-living-room-floor-had-taken-anti-depressants-and-alcohol-cock

    • This seems to me a particularly important comment. In the sense here there have been several deaths by misadventure reported in individuals who have had combinations of antidepressants and alcohol on board at the time. A high alcohol reading might inappropriately suggest suicide. Drinking in a safe setting might well be safe but if unexpected drunkenness occurs in another setting the effects might be serious

  5. In 2002, California’s Stanford University published a study where it claimed that Citalopram/Celexa was effective in treating compulsive shoppers. Lundbeck was then targeting compulsive shoppers by marketing Citalopram as the new ‘anti-shopping drug’.
    An article in the Daily Mail described 3 compulsive shopper’s experience on Celexa:

    Luke, 21 was on the drug for 3 months and did ok.

    Christelle, 26, “It had a very strange effect on me. I don’t know if this was due to all the other drugs I was on, but it knocked me out, and I could hardly move. So I suppose it did cure me of shopping, I couldn’t get out of the house.”

    The interesting one was Anya, assuming the doctor reported the side-effects it seems that Lundbeck could have been aware of the dangers of ‘every drink spiked’ for at least a decade…

    Anya, 32, “However, I made a mistake when I didn’t cut down on my alcohol. One evening I was enjoying my favourite drink – an alcopop – when suddenly I felt very sick, and very drunk. Worse than this, my libido vanished.”


  6. Most, if not all of the evidence we have about eating and serotonin comes from rat experiments. I’ve never found these particularly persuasive but am willing to give them a chance to shed some light on human behaviour. Serotonin has many receptors throughout the body, not just in the brain. These receptors are substances that, basically, allow the neurotransmitter to travel. There are at least 14 established serotonin receptors. Each of these will produce different effects, explaining to some degree, the varying reactions to SSRIs. Pratt and colleagues concentrated on five specific receptors and showed that rats will go to great lengths to gain access to sugar pellets i.e. pure carbohydrate, just like alcohol, as well as being what they define as “palatable.” Palatability in humans is most often associated with sweetness. This is the last taste sensation to remain normal in the elderly and the reason that sweet food is ingested to a greater degree than salt, sour or bitter. It may well be an adaptive mechanism in that early humans could, for the most part, recognize ripeness by the sweetness of fruit and berries. Babies show this preference very early.
    The area of the brain Pratt and colleagues experimented on by increasing serotonin was the nucleus accumbens that has been repeatedly identified as one of our main “hedonic” or pleasure centres. Stimulation of receptors other than those identified above, causes appetite suppression in rats and, it is believed, in humans.
    The rat experiments show that some specific serotonin receptors in the nucleus accumbens influence how motivated rats are to get that sugar pellet, often pushing the pellet-releasing lever until exhaustion. It may be that different SSRIs have varying effects on different serotonin receptors or the influence depends on dosage in relationship to gender, weight and other factors. We are far from an explanation of this effect and, indeed, still far from an understanding of the brain’s mysteries but there are clues that anecdotal information may very well play an important role in pointing the way to appropriate treatments and the reasons for dangerous ones. Reports of effects such as these are, in my view, as important as reports of more frequently described adverse events.

  7. This is human nature, shopping, eating, drinking, smoking, taking drugs, having sexual relationships, playing computer games, gambling, but when is one person’s excess, another’s norm.

    If we all do the above to excess, then the straitlaced professionals enter our lives by invitation and we are then invited to take medication to cure us of our ills and ails.

    Those shopping persons mentioned were, once again, hijacked into thinking that a pill could cure their habit. The professionals, once again, got the wrong end of the stick thinking ‘the pill’ would stop the habit.

    It fails every time.

    The habit will go on despite, perhaps, a brief interlude when a brain numbing pill enters the equation for a short while and renders the person immobile.

    On it goes, the gift to the socially inadequate to give them some relief.

    Until it all goes very, very wrong.

    When I was coming off an ssri, cold turkey, I could down a bottle of wine in the time it took to drink a bottle of Perrier on a hot day.
    Total craving.

    I always enjoyed a glass of wine; we always had a drink before dinner. But, I was, at this time, swallowing glasses of wine as if it was water.

    I don’t remeber getting drunk on it. It was like a self-medication. I still walked the dog; I still played with my daughter; I still functioned.
    I did not get drunk.

    I think all the drugs I was given during cold turkey from Seroxat = Lorazapam, Diazapam, Beta blockers, Valium, Ativan, etc. etc. made me immune from drunkeness from alcohol. I was so away with the fairies with all these drugs that alcohol actually gave me a form of awareness and brought me back.

    Anyway, all these drugs and alcohol was not a good idea.

    Prescription drugs and alcohol do not mix at all well.

  8. @secuti says:

    It’s easy to appreciate that antidepressants might interfere with driving performance given the need for sustained vigilance and attention, indeed recently researchers have examined the effects of antidepressants and other prescription drugs driving accidents using a primary care database in the UK (Gibson et al., 2009). Using the year prior to drug exposure as a baseline risk, after 4 weeks of use the risk of driving accidents increased and remained increased for the duration of SSRI treatment (IRR = 1.16, 95% CI =1.06–1.28). The risk returned to the baseline level on stopping the SSRI. (IRR = 1.03, 95% CI = 0.92–1.16). While much of this effect may be from the direct adverse effect of the drugs eg sedation, it is conceivable that some of the increased risk might be attributable to a SSRI induced change in alcohol pharmacokinetics.

    o changes in alcohol pharmacokinetics

  9. Here’s another tragic story from 2010 involving antidepressants and alcohol: http://www.herald.ie/news/booze-and-pills-alert-after-bertie-tragedy-2139007.html

    This incident involves a nephew of Ireland’s ex-taoiseach (prime minister) Bertie Ahern who was head of Irish Government from 1997 till 2008. His nephew died after a night out, from a mixture of Alcohol and Antidepressants. I’m sure this was big news in Ireland at the time but I don’t remember hearing about it, as it happened shortly after Shane died.

    In the article Dr Chris Luke warned of the “lethal” consequences of combining alcohol and prescription medication.


  10. No alcohol craving but I have always suffered with hypoglyceamia (low blood sugar) and it feels like it controls my life and eating patterns, I manage to stay within correct BMI through exercise and watching what I eat, but it’s a constant battle, and I was interested to read in Ann Blake Tracy’s book Prozac: Pandora or Panacea that this was linked to SSRI use. It seems like whatever I eat doesn’t even touch the sides for long and I’m hungry very quickly, mid morning start getting the shakes and have to eat something to keep me going, and I do crave sweet things as well.

  11. alexejice says:

    I developed a drinking problem while on Lexapro and klonopin. I had no history of alcohol abuse as a teen. I started on Lexapro at 18, klonopin shortly after. On turning 21 I found myself drinking. And drinking. I attempted to stop and also discontinue my psychiatric medication at age 24.

    I experienced a horrific withdrawal episode and I escalated alcohol consumption. Was referred to rehab where my psych meds were stabilized and new ones added. I became convinced I was an alcoholic. I spent the next 4 years drinking alcoholically and, for a brief period while also on neuroleptics and wellbutrin, abusing street stimulants.

    I have spent a total of 14 months living in sober living homes, halfway houses, inpatient treatment centers due to addiction. I have attended hundreds of AA meetings.

    In late 2009 I resolved to get off my medications. This went very poorly and has compromised my health in a variety of ways. However, one big surprise …. Cravings for drugs and alcohol have dissipated. During my terrible withdrawal period in 2010, I tried to use alcohol to cope but had no interest.

    I’d reverted to my preferences of my teens. In the last 20 months I have consumed alcohol on two occasions, each time I failed to even finish one drink due to lack of appreciation of the effects.

    For almost a decade, I believed I was a hopeless alcoholic. I couldn’t abstain. I went bankrupt due to my addictive behavior.

    I find it vastly more likely that my addictive drinking and drugging which defined and ruined my 20s were merely an unwanted effect from psychiatric medications.


  12. I was started on Prozac in May 2012. I felt great initially. I have taken almost every other SSRI, & feel great for 1-2 months, then, I get even more depressed, & wean myself off of them. I have gone for long periods without any antidepressants. I have been a Registered Nurse for 30+ years, with a very strong background in critical care. I know medications have side effects, & every patient is different. I started craving alcohol about 1-2 months after I started on Prozac. I consider myself a social drinker, & have gone for prolonged periods where I didn’t drink @ all. I started drinking Tequila straight out of the bottle @ 8 am. I had never in my life drank any alcohol out of the bottle, nor had I ever drank anything stronger than a mimosa in the morning. I also started sweating profusely (hyperhidrosis). I asked 2 MD’s (my psychiatrist & my gynecologist) about this excessive sweating, & was told it was not the Prozac, even though this is a common side effect of SSRI’s. I go to Zumba classes 3 x week, & I had to stop because I was sweating profusely before I started class, & my heart rate would get up to 200. My 25 y/o son caught me drinking in the morning, & told me he would not have anything to do with me, unless I completed 30 days in rehab. I also had suicidal thoughts while on Prozac. I weaned myself off the Prozac, & the profuse sweating stopped 2 days after I quit. I went to rehab for 30 days in November 2012, & was discharged December 2012. I have not had any cravings for alcohol, & have been to a few AA meetings since I was discharged. I don’t think AA meetings or working a 12 step program is the solution for me. (I know AA truly helps those who are addicted) I drank 2 glasses of wine with dinner a few evenings ago, & had a glass of champagne New Year’s Eve. Neither time did I feel like I couldn’t stop or had any further cravings since. I will always believe that the Prozac caused me to start drinking, the excessive sweating, & made me have suicidal thoughts.

  13. I was unknowingly given an antidepressant called Imipramine 26 years ago for the treatment of migraine. The doctor told me it was a migraine preventative. I was 21, trusting and had no idea. What followed was 16 years of trying to find out what was wrong with me.
    I was diagnosed with depression about 2 years later. I had stopped the imipramine only 2-3 months earlier because I was still getting migraines and didn’t see the point of taking it if it didn’t stop them. I was given Prozac to start but suddenly found myself increasingly aggressive within 2 months and I was never violent. The doctor at the time did blame the drug, so changed it to Zoloft.
    I didn’t link stopping imipramine with the onset of depression because I didn’t know imipramine was an antidepressant.
    About 6 months after starting Zoloft, because it seemed to be not working, the diagnosis was changed to Bipolar and I was given Lithium. No link was made to Zoloft causing the mania. No link was made to the mood swings being caused by a recent trauma. I was told I had a chemical imbalance and may have been born with it.
    The reaction to Lithium was so horrendous I was swapped to Epilim. My brain was seriously in a zone that was ugly and I couldn’t think like I used to be able to. I had memory and concentration issues. I blamed the drugs for this plateau zone and I stopped taking them. The doctor didn’t warn me about gradual removal. I went into meltdown and ended up in a psychiatric hospital twice in a year. What I now know as discontinuation syndrome. Still no link to the drugs, no link to the trauma.
    I refused medication because of the way my brain felt but the wild mood swings were still happening and I finally believed a year or so later that perhaps the doctors were right and was started on Effexor. This lovely gem caused damage to my glycaemic control systems. While I was on it I experienced intense cravings for alcohol, an inability to control my drinking if I started, disinhibition and increased aggression again. I was even arrested at one point. It was the increasing aggression that triggered my memory of Prozac. They then tried Lexapro and it reminded me of Zoloft with the bipolar. I happened to meet someone who was imipramine and so I sympathised about migraines only to be told she didn’t have them but was diagnosed with depression. This was like a light bulb going off and I started my own research project to find out more.
    I found a psychologist who treated the trauma with CBT and hypnosis, the mood swings disappeared.
    I was never depressed, never bipolar, never an alcoholic, never an aggressive person.
    I still get migraines and treat these with stress management and diet. I have gained a problem with alcohol control, permanent damage with reactive hypoglycaemia and a nervous system that is still delicate over stress due to the increased cortisol over the years meaning IBS, hand trembles etc. All of this because I had migraines and trauma. And you cannot sue anyone because they can say it was all me. It’s been about 8 years no drugs and my brain is finally starting to feel like it’s recovering and I still think those drugs damaged my brain.

  14. I have a mysterious problem that may be related to being on a cocktail of psych meds for years. After finishing a slow taper of 4 psych meds, 4 years ago, I started feeling very drugged after dinner to the point where I had to lay down immediately which persisted repeatedly.

    At the end of 2011, I was diagnosed with sleep apnea but have been unable to stay asleep on the machine for more than 4 hours. Of course, conventional sleep doctors blame it on insomnia and offer more drugs which simply have not helped.

    The carb intolerance comes into play because out of concern I may have metabolic issues, I started testing my blood glucose and found out that eating high carb foods caused severe spikes. But even foods not known for spiking blood sugar such as blueberries, caused me to feel drugged last night after eating dinner in combination with chicken. I have gotten to the point where I feel I need to eliminate all carbs in an attempt solve this problem.

    If anyone has experienced similar difficulties, I would love to hear from you. Mentioning this problem to sleep doctors simply got me one of those looks. Primary care doctor was alot more sympathetic but I sensed she was quite puzzled also.


    • David_Healy says:

      It is normal to feel “drugged” or drowsy after a meal. This is called a post-prandial dip. Perhaps what’s involved here is an exaggeration of the normal post-prandial dip, maybe linked to prior drug intake, maybe for other reasons.



  1. […] None of these peoples experiences are very convincing, Anya in particular seemed to be suffering from a side-effect which is only coming to light lately; see Prof. Healy’s “Every Drink Spiked“. […]

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