Christmas food for thought: which booze causes the worst hangover?

What’s Christmas without a bottle of good wine, a snifter (or two) of peaty Ardburg and a few raunchy family tales that, upon awakening the next morning with a pulsing head and stone-cold sober realization, constitute as Too Much Information that you wish had never graced your ears?

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Pick your poison. Here’s mine. Source: living room

If you’re like me, however, you’re probably in too much misery to care about what your 65-year-old-aunt-did-in-that-summer-30-years-ago. Despite its long history and frequent occurrence, hangovers remain enigmatic monsters that haunt those reckless enough to seek the dew of the gods with no reservation. The symptoms appear AFTER the alcohol is eliminated from the body, and (against popular belief) may not be a direct result of dehydration.

Physiological causes aside, perhaps it’s more useful to figure out what type of booze precipitates the worst hangovers all else equal. One common rumour is that dark-coloured alcohols – think bourbons, dark rum and scotch – give more of a punch than their paler counterparts.

Alcohol by itself is colorless. The colour of unadulterated alcoholic beverages comes from congeners – chemicals other than ethanol that seep into the final product due to the fermentation and aging process. They are complex organic molecules with toxic effects, including acetaldehyde (metabolite of ethanol that gives the “Asian glow”), tannins (astringent-tasting molecules found in red wines) and even methanol. That’s not the say they’re BAD – bourbon contains 37 times more of these flavorful molecules than vodka, which gives them their distinctive taste. Nevertheless, congeners are thought to make hangovers worse. A study in 2009 put this theory to the test, pitting Wild Turkey bourbon against Absolute vodka.

Researchers recruited 95 college-aged, non-alcoholic participants and invited them for two wine-and-dine sessions in the lab. One of the nights they got either bourbon or vodka mixed with coke to mask the taste, the other night they got coke-mixed tonic water as a non-alcoholic control bevarage. After ensuring the participants were indeed intoxicated, researchers put them to bed. Since alcohol negatively affects the quality and duration of sleep, researchers monitored the participants’ sleep architecture. The next morning, the team measured the intensity of the participant’s hangovers with a symptom-based scale and tested the subject’s cognitive function with 2 tasks that required sustained attention and reaction time.

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Full protocol for each session. Polysomnograph monitors sleep.

Sure enough, bourbon caused a worse self-reported hangover than vodka in both men and women. Alcohol consumption also made it more difficult to fall asleep for women and decreased sleep efficacy in both sexes, which led to poorer performance on the cognitive tasks. However, although bourbon made the subjects FEEL crappier, its effects on sleep and next-day brain function were no worse than that of vodka.

These results seem to suggest that alcohol is alcohol, regardless of what type you drink. Bourbons may make you suffer more the next morning, but as coke can hardly mask the spicy bite of Wild Turkey, placebo effects could have skewed the participant’s subjective hangover ratings. But the data is hard to extrapolate. Most of the participants were caucasian (79%); since many asians lack the aldehyde dehydrogenase enzyme that helps break down acetylaldehyde – a toxic metabolite of ethanol and a common congener – it’s likely that asians may find bourbon more intolerable than vodka. Furthermore, the amount of alcohol consumed in this study was just enough to reliably induce a hangover – it’s hard to say how well results hold if you drink more. After all, even for congeners the dose makes the poison.

In line with this, a survey in 2006 among Dutch college students after drinking beer, wine or liquors showed that it takes fewer high-congener drinks to get a hangover and a worse one at that (see graph below). Unfortunately as surveys are hardly strictly controlled and rely on self-reporting, so take these “naturalistic” results as you will. Personally, I think I’ll keep embracing the dark side.


“Ethanol diluted in OJ” is a very unsatisfying alternative to a good Screwdriver. Source doi:10.1093/alcalc/agm163. 

Finally, one special case in hangovers is the notorious red wine headache. Although red wine is lower in alcohol content than spirits, it’s especially high in histamines, tannins, flavonoids and sugar (especially the cheaper reds), all of which along with alcohol makes a perfect hangover stew. Add to the fact that wine glasses are much larger in size than shot or tall glasses, and that people tend to pour more into wider glasses and when they’re holding the glass, it’s perhaps not so surprising that a classy family night with wine can still feel like a night out clubbing the morning after.

Ultimately, you’re probably going to keep drinking your drink-of-choice no matter what science says. But maybe stick to lighter quality booze at family gatherings just in case. It just might make your boxing day shopping a little easier.
Rohsenow DJ, Howland J, Arnedt JT, Almeida AB, Greece J, Minsky S, Kempler CS, & Sales S (2010). Intoxication with bourbon versus vodka: effects on hangover, sleep, and next-day neurocognitive performance in young adults. Alcoholism, clinical and experimental research, 34 (3), 509-18 PMID: 20028364


Is the taste of beer dangerously intoxicating?

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Me adhering to Asian stereotypes after pouring my first pint of beer bartending.
It looks pretty pathetic, I know 😛

Last Friday around lunch break, sweating profusely on the way back to lab, I was suddenly struck by an irresistible urge to chug a cold fizzy beer. Crisp! Grassy! Bubbly! The punchline? Due to a genetic inability to metabolize alcohol, I stick to the extra lights (I know, I know). To me, beer is intoxicating even without apparent alcohol intoxication.

And the culprit that triggers this lust for a sip –or keg- of beer? A new study points to dopamine, a neurotransmitter involved in reward prediction and motivation. In the early stages of drug use, cocaine, meth and amphetamines all trigger a dopamine rush in the brain’s reward system, which induces a sense of high-flying pleasure, power and jazzed-up ENERGY. But the “feel good” molecule has a dangerous side: it also encodes for triggers that lead to the expectation for reward. Hence the theory goes, with each increased pint of beer, the sight, smell and taste of it starts becoming sufficient to trigger a dopamine rush, signalling to us that reward is coming long before the beverage touches our lips. One camp of thought stipulates that these beer-related cues may eventually trigger feelings of wanting and craving, leading to alcoholism in the vulnerable.

Is it possible that the taste of beer, instead of the alcohol it carries, can act as a cue and kick-start the cycle of use, reuse and abuse?

Brandon G Oberlin et al (2013). Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism. Neuropsychopharmacology 38: 1617-1624

To answer this question, researchers recruited 49 male beer lovers, ranging from the occasional social drinker to the potentially problematic binger. The volunteers were separated into three groups: those with or without a family history of alcoholism, and those who don’t know. Researchers then teased their taste buds (and brain) with a tiny squirt of either their favourite beer or Gatorade – an amount way too small to cause intoxication – while monitoring their brains’ responses to the flavours with Positron Emission Topography (PET) and the radioactive tracer RAC. RAC competes with dopamine released in the brain for binding spots on the dopamine receptor – hence low RAC binding tells us that there’s MORE dopamine around, and vice-versa.

The findings were remarkable straightforward: a taste of beer, but not Gatorade, elicited a desire to drink more beer in all volunteers, regardless of family history. Pooling all of the volunteer’s data together, RAC binding dropped significantly in the right ventral striatum during beer tasting compared to Gatorade tasting, indicating more dopamine release. Unfortunately, the magnitude of dopamine release was NOT related to subjective feelings of wanting to drink beer, how much beer the volunteers drank previously or how much more they preferred beer to Gatorade.

However, as you can see below, the taste of beer did induce larger dopamine release in those with a family history of alcoholism (black bar) compared to those who didn’t (white) or those who didn’t know (grey). The authors hence concluded that the taste of beer (“intraoral sensory properties”, gotta love jargon sometimes), in cahoots with its alcohol properties, might together induce dopamine responses that in turn promote and maintain booze-craving and seeking behaviour.

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Yellow spots indicate areas where dopamine levels changes.

My first non-scientific reaction: has anyone ever become an alcoholic from drinking light beers? How much, if any, does the taste of alcohol contribute to addiction, even in those with bad/vulnerable genetics? Based on this study, I’d say very little. If you look closely at the graph above, the effect size is incredibly small. So small that, when researchers looked at each group separately (not pooled like described above), only people with a history of alcoholism (Family History Positive) showed significant dopamine release after tasting beer.

Next, even though FHP volunteers had larger dopamine release in response to beer, it did not correlate with how much pleasure they felt nor how much they wanted beer afterwards; the neurobiological response did not translate to behaviour. The magnitude of dopamine response also didn’t correlate with how much the volunteers drank on average. Together, the results show that dopamine release in response to a taste of beer CANNOT predict a person’s potential of alcoholism, regardless of family history.

The one solid conclusion from the study is that beer-related cues make you want more beer if you already like beer. (Do we really need science to tell us that?) In some people this is paralleled in time to dopamine release – which we already know from previous studies that used pictures of alcoholic beverages. In fact, the same dopamine response is seen for most rewarding things, such as food and drugs (and maybe even Gatorade!).

Maybe someone should study whether reading about beer-related studies triggers dopamine release in the beer-lovers’ brains.
Oberlin BG, Dzemidzic M, Tran SM, Soeurt CM, Albrecht DS, Yoder KK, & Kareken DA (2013). Beer flavor provokes striatal dopamine release in male drinkers: mediation by family history of alcoholism. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 38 (9), 1617-24 PMID: 23588036

Drinking doesn’t sooth the soul

Bolder, Colorado

You’re in the theater, completely engrossed. You wipe away a tear at Albert’s departure, at Bruce Wayne’s broken body, at the demise of Gotham. Then you smell the smoke. See the panic. Hear the scream.

People deal with traumatic experiences differently. Some are able to work through painful memories, eventually returning to their daily lives. Others drown in feelings of pervasive fear and hopelessness, persistently re-experiencing the trauma in dreams or in flashbacks, impairing any attempt at a normal life. People with anxiety disorders may drown in alcohol, wishing to drink their fears away.

Unfortunately, alcohol may be one of the things impairing critical brain mechanisms for recover from trauma.

Holmes et al., 2012. Chronic alcohol remodels prefrontal neurons and disrupts NMDAR-mediated fear extinction encoding. Nat Neurosci. 2012 Oct;15(10):1359-61. doi: 10.1038/nn.3204. Epub 2012 Sep 2.

From a neurobiological point of view, conditioned fear is a memory, linking an event or object to the biological fear response. As such, it can be encoded, strengthened, retrieved, and extinguished.  Extinction of a memory is not really “forgetting” it – it doesn’t erase the fear memory trace in the brain. Instead, the brain learns a new association, that whatever you were afraid of (worms!!!) is actually harmless – this new memory trace, thought to be encoded by the medial prefrontal cortex (mPFC), competes with the conditioned fear memory when you’re re-exposed to the source of terror. If it wins, the fear memory is not expressed – that is, you wouldn’t experience the terror associated with the trigger.

Chronic alcohol use is known to affect the mPFC, changing its size, neuron number and activation, leading to deficits in attention and higher cognitive function. Given mPFC’s critical role in fear memory extinction, would heavy drinkers be more vulnerable to anxiety disorders following a traumatic event?

Researchers doused mice with vaporized alcohol with a schedule mimicking cycles of “heavy drinking” as seen in alcoholism, with a total amount roughly equivalent to twice the legal driving limit in humans. The mice were allowed to rest for two days to nurse their hangovers, and then were trained to fear a tone by pairing the tone with an electric foot shock.  As it turns out, these alcoholic mice learned to fear the tone as fast as normal mice, showing no problem with memory encoding.

To extinguish the memory, the researchers played the tone again and again without the foot shock. Compared to normal mice, the alcoholic ones lacked behind in learning this new memory, although they eventually caught up. However, when both groups were shocked again with the tone (reinstatement), the alcoholics clearly showed greater freezing – meaning that the newly encoded extinction memory was not as strong or as easily recalled as the original fear memory . On the other hand, these alcoholic mice didn’t differ from their normal littermates in tests for general (non-tone related) anxiety, fear or motor performance, meaning that fear retention is specific to the tone.

So what mediates this behavior? Turning to the mPFC, researchers found that chronic alcohol remolded the shape of neurons, so that their dendrites were longer on the non-terminal branches on one side of the neurons. Since dendrites are the basic units of neuronal computation, and form dictates function, researchers went on to measure directly brain activity in the alcoholic mouse with electrodes. Chronic alcohol breathing decreased neuronal activity both during later periods of extinction and extinction retrieval, hinting that mPFC activity is greatly suppressed.  The authors went on to show that a type of receptor generally thought to be involved in learning and memory, the NMDA receptor, was also malfunctioning, giving lower currents than usual. In fact, by inhibiting just the NMDA receptor with a drug in normal mice, the researchers were able to mimic the extinction deficiency as seen in alcoholic mice.

This study suggests that chronic alcohol users if subjected to traumatic experiences, may be unable to efficiently deal with the associated fear and may be more at risk for developing anxiety disorders. While the study makes a good case for the dysfunction of mPFC in extinction deficits, it also begs the question: what about the hippocampus? Buried deep inside the brain, the hippocampus is long known to be the center of memory processing. Previous studies in brain slices (not animals) have also shown that alcohol exposure can inhibit NMDAR currents, so it’s conceivable that hippocampus is also playing a role. Another question that comes to mind is whether the perceived deficit in extinction is actually a deficit in “updating” the existing memory – that is, a decreased ability to flexibly learn and retain an opposite association when there is a similar memory present.

Regardless, this study adds to the pool of data that we currently have on the factors that predispose people to anxiety problems following traumatic experiences. While the study won’t make me give up on weekend happy hours, it might make me pause and think twice before I reach for that second bottle of weekday beer.
Holmes A, Fitzgerald PJ, Macpherson KP, Debrouse L, Colacicco G, Flynn SM, Masneuf S, Pleil KE, Li C, Marcinkiewcz CA, Kash TL, Gunduz-Cinar O, & Camp M (2012). Chronic alcohol remodels prefrontal neurons and disrupts NMDAR-mediated fear extinction encoding. Nature neuroscience, 15 (10), 1359-61 PMID: 22941108