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


Christmas food for thought: the gains and pains of laughter

As Christmas approaches like a freight train I, like many, scramble to buy last minute gifts and prepare myself to gorge on feasts and booze and laughter(?) – all part of a joyous(??) family gathering. In last effort to procrastinate until the very end, I present to you this short series of posts on various and totally random holiday-related themes. Enjoy!

Sings: Petri dish sterilizing near an open fire, lab rats nipping on my shoe, data woes cried by grad students, and PIs dressed like You-Know-Who! Ok, this might’ve gotten a laugh out of grad students. Anyone? I’ll show myself out.

Laughter permeates holiday gatherings. Dubbed “grooming at a distance”, laughter is thought to establish and maintain bonds between individual primates of all sorts. Like yawning, the mere sound of laughter often triggers giggling fits in others in a contagion-like manner. Within four-tenths of a second after exposure, electrical activity spreads out through areas involved in cognition, emotion, sensation and movement; this triggers facial contortions, spasmodic breathing and bodily convulsions as we involuntarily emit a series of curious vocalizations, ready to infect another.

Collapsing in a quivering heap, we are left under-the-influence of a deluge of a neuroendocrine cocktail. The amount of epinerphrine, a hormone in the fight-or-flight response plummets, while dopac, a major metabolite of dopamine, shoots up. Laughter also triggers the release of pain-relieving endorphins and growth- and metabolism-boosting growth hormone, which together with other chemicals form somewhat of a panacea for the mind and body. As Robert Burton once astutely wrote in 1621, “Mirth…prorogues life, whets the wit, makes the body young, lively and fit for any manner of employment.”

So where’s the evidence?

British Medical Journal produced a snicker-inducing, tongue-in-cheek report that synthesized findings from 785 papers on the health benefits of laughter. To round things up, they threw in harmful effects for good measure, while discarding papers written by authors with “Laugh” in their last name which where nonetheless “not particularly amusing”. Here’s what they found.

In terms of the psyche, laughter increased tolerance to pain in the lab, but hospital clowns did not reduce distress in children going through minor surgery to any observable extent. Humorous movies had minimal success on serious mental illnesses like schizophrenia, and group-based humor therapy did not particularly benefit late-onset depression in Alzheimer’s disease, though there was some improvement in patient morale and mood. Laughter was associated with life-long satisfaction, but there’s no evidence that one causes the other either way.

More mirthful news comes from laughter’s effect on the body. A 20min funny movie acutely reduced the stiffness of blood vessels and made them more limbre. A sense of humour lowers your risk of heart attack and improved lung function in those with chronic obstructive pulmonary disease, an illness that makes it difficult to breathe. In the latter case the credit goes to hospital clowns, whom apparently until the year of study (2008) were still regarded by some brave souls as non-terrifying entities.

Laughter had no consistent effects on immune functions such as natural killer cells, but sometimes aided the surgical removal of a pouch of pus by bursting it through laughter-generated muscle contractions. Laughter also benefits metabolism: compared to a monotonous lecture that drooled forever on, a comedy show helped control blood sugar levels after a meal. A 15min-bout of genuine laughter burns up to 40 calories, so battling the average 6000-calorie Christmas dinner would requires 37.5hrs of merriment to burn off. Better get those jokes ready.

Finally, if you’re trying to get pregnant through in vitro fertilization (test-tube baby), perhaps consider hiring a clown dressed like a chef de cuisine. In one study, such a clown entertained 110 would-be mothers after embryo transfer for 12-15 minutes with saucy jokes and magic tricks, “a recipe of success” that led to ~16% increase in pregnancy rate compared to the 109 non-clowned controls, adding another win for medicinal clowning.

Unfortunately laughter is not without its pains. Laughter weakens resolve and promotes your preference for certain brands, so keep a skeptic eye on that joke-cracking salesman. A hearty guffaw can cause temporary loss of consciousness, perhaps due to the sudden increase in pressure in the chest cavity that triggers a neural response. Laughing can screw up the electrical activity in the heart causing it to pump irregularly, to the point of cardiac arrest or rupture, giving “dying of laughter” a more sinister undertone.

Laughter can lead to abnormal collection of gas between the lung and chest wall or engorgement of air sacs of the lungs, resulting in labored breathing. The sharp intake of air to initiate laughter can promote inhaling foreign objects, causing you to choke on a small piece of turkey, while frequent exhaling disseminates infection. Laughter may also wreck havoc on your alimentary canal, dislocating the jaw or puncturing the esophagus (your “food-tube”), so maybe eat first and laugh later. You might also want a clear line to the wash(bath)room. Laughter can cause incontinence stemming from involuntary contractions of bladder muscles, which surprisingly may be counteracted by Ritalin.

And finally, uproarious laughter may not be so funny to your brain. Cataplexy, a condition where a person suddenly looses muscle tone, can be triggered by laughter and other salient stimuli, leaving you unceremoniously collapsed under the Christmas tree. That is, unless only one side of you is affected. In one documented case, laughter triggered cataplexy only on the right side of a patient’s body, leaving her presumably capable of continuing laughing on the left side of her face.

Laughter and other pleasurable things may precipitate headaches in the unfortunate, sometimes due to sacs of jello-like material in the third ventricle, a fluid-filled compartment in the brain. Laughter may also be no laughing matter to people with patent foramen ovale (PFO), whom have a hole in the heart that should’ve closed after birth but didn’t. Take this case for example: after 3 minutes of roaring laughter, a PFO patient lost her words (literally) and had a stroke.

This report from BJM obviously shows that laughter is not all beneficial, but it overall carries a low risk of harm in the general population. In terms of cost-benefit analysis a good laugh is still beneficial. Yet, as always, more research calls. As the authors put it:

“It remains to be seen whether, for example, sick jokes make you ill, if dry wit causes dehydration, or jokes in bad taste cause dysgeusia (note: distortion of the sense of taste), and whether our views on comedians stand up to further scrutiny.”
R E Ferner, & J K Aronson (2013). Laughter and MIRTH (Methodical Investigation of Risibility, Therapeutic and Harmful): narrative synthesis BJM DOI: 10.1136/bmj.f7274

Physiological responses to chew & spit – ghrelin and obestatin

This is my second guest post for Science of Eating Disorders blog. Tetyana has a lovely piece up looking at Deep Brain Stimulation as a potential therapy for intractable AN. If you haven’t seen it yet, please go check it out and join the discussion!

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Google “Yummy food”. Oh god salivating!!!

Your body responds to food long before it reaches your stomach. The taste, smell, even the mere sight of food all act to trigger a physiological response, “priming” the gut by stimulating various enzymes required for proper digestion and absorption of nutrients. This is called the “cephalic response”, and it is mediated by a part of the nervous system that’s generally not under conscious control (the autonomous nervous system). Keep in mind, the actual consumption of food is NOT necessary to trigger this reflex.

As you may have already guessed, the act of chewing and spitting out food activates this response, increasing the secretion of stomach acid, digestive enzymes and insulin as well as changing one’s metabolic rate. Which leads me to wonder – what are the changes that occur in the body during the cephalic response? Are these responses altered in patients with eating disorders who also chew and spit? If so, how? And are there any long-term consequences for engaging in chew and spit?

These are obviously very broad questions. To narrow it down, in this post I’d like to look specifically at two hormones involved in appetite control: ghrelin and obestatin. A little background first. Ghrelin and obestatin are both gut-brain hormones that are secreted (mainly) from the stomach and act on the brain. While ghrelin has many neurological functions (such as buffering against stress-induced depression), it was first identified as a hunger-promoting hormone. Ghrelin is secreted during the cephalic phase, and can promote feeding in multiple ways.

First, ghrelin travels through the bloodstream to areas of the brain involved in appetite regulation.  There it acts directly on specific receptors designed to trigger hunger and drive food-seeking behaviors. In fact, injecting humans with synthetic ghrelin was enough to produce feelings of intense hunger. Ghrelin can also make food seem more desirable. It does this by activating the reward system, causing dopamine release at the sight, taste and smell of yummy foods.  Hence, it may play a central role in conveying the pleasure and reinforcing aspects of high-calorie “rewarding” foods. Finally, ghrelin can directly act on the GI tract, blunting the stomach’s “fullness” signal and promoting overeating.

There is much less research on the recently discovered obestatin. However, it seems to directly oppose ghrelin’s effect on food intake, acting as a “brake” for the desire to feed (note, this is a MASSIVE oversimplification).

In the current paper, researchers wanted to know if patients with anorexia nervosa (AN) secret ghrelin and/or obestatin differently than control subjects when allowed to chew, taste and spit out food. To test this, they recruited 8 women with AN (both binge-purging and restrictiving) and 8 age-matched healthy female subjects. Following an overnight fast and a standardized breakfast, researchers served the women a lunch made up of 67% carbohydrates, 13%protein and 20%fat. To chew and spit in a controlled setting (in this case, called “modified sham feeding”), the women were allowed to see and smell the food for 5 minutes before chewing and spitting each bite into a napkin. Blood samples were taken before and after feeding (or chew and spit) for analysis, and the subjects were asked to fill out the Three Factor Eating Questionnare (TFEQ) to assess their eating behavior.

Here’s what they found:

1)   Patients with AN had higher levels of ghrelin before and after chew and spit compared to controls. Both groups showed a spike in ghrelin secretion within 30 minutes of chew and spit, but AN women showed a much higher peak than controls.

2)   AN women had higher obestatin levels compared to control women, and showed a much sharper DECREASE in blood obestatin levels 30 minutes after chew and spit.

3)   Blood sugar levels didn’t significantly change after chew and spit – there was also no difference in blood sugar levels between AN and control women both before and after chew and spit.

4)   Ghrelin levels after chew and spit correlated with TFEQ factor 2 in all women, and TFEQ factor 3 in women with AN.

So what does this mean?

In healthy women, chew and spit can cause an increase in ghrelin and a simultaneous decrease in obestatin. As mentioned above, ghrelin promotes hunger and food seeking, while obestatin may counteract its effect. Together, these hormonal changes may represent the body’s normal response to the presence of palatable food, promoting the initiation of food intake. To support this idea, increased ghrelin levels correlated with TFEQ factor 2, which measures the tendency to lose control over eating.

In AN patients, base levels of both ghrelin and obestatin were increased, and the hormonal responses to chew and spit were significantly enhanced. This amplification of ghrelin increase and obestatin drop might result in an amplified signal of hunger for at least 30 minutes after chew and spit. This is supported by the eating behavior data in AN patients that shows a correlation between enhanced ghrelin levels with TFERQ factor 3, which measures hunger. Hence, it is conceivable that chew and spit may increase hunger levels in AN patients, leading to feelings of a lack of control over eating. This may counteract the patients’ rigid control over food intake and promote more chewing and spitting (or binge eating), resulting in a downward spiral.

While this is an interesting study, there are some problems with it. First, subjects may have swallowed food unconsciously  – a nurse monitored their chew and spit session, but a more subjective measure would be to look at cholecystokinin levels (released by the small intestine), which increases during feeding but stays stable during chew and spit. Second, the number of subjects is quite small, hence I’m not sure how generalizable it is to a greater population. And finally, note that this study looks at AN patients undergoing chew and spit in a controlled setting – they did not ask whether these patients engaged in chew and spit outside the experiment. It is conceivable that chronic chew and spit may alter the body’s response somewhat.

Nevertheless, this study shows that AN patients have enhanced ghrelin and obestatin responses after chew and spit, and this may be a strong factor in promoting hunger and loss of control over eating, ultimately leading to more chew and spit sessions and/or binging behavior.
Monteleone P, Serritella C, Martiadis V, & Maj M (2008). Deranged secretion of ghrelin and obestatin in the cephalic phase of vagal stimulation in women with anorexia nervosa. Biological psychiatry, 64 (11), 1005-8 PMID: 18474361

Méquinion, M., Langlet, F., Zgheib, S., Dickson, S., Dehouck, B., Chauveau, C., & Viltart, O. (2013). Ghrelin: Central and Peripheral Implications in Anorexia Nervosa Frontiers in Endocrinology, 4 DOI: 10.3389/fendo.2013.00015
This is a recent review on ghrelin in AN in general, and a good read for those interested in exploring the subject further. Note the authors argue that AN can be viewed as an addictive disorder – I’m not fully on board.

Chewing and spitting – a neglected symptom?

This is a cross-post from the wonderfully informative Science of Eating Disorders blog. ScienceofED covers a broad range of peer-reviewed research articles related to all aspects of eating disorders. Head over and check it out!

Eating disorders come in all shapes and sizes, but all of them are characterized by the same goal: to avoid weight gain or induce weight loss. While behaviors such as food restriction, purging and laxative abuse are relatively well studied, chewing and spitting (CHSP) is a  less studied symptom. A simple Google search, however, reveals over 1.5 million results for the term “chewing and spitting..  Results often links to blog posts or Tumblr pages where CHSP sufferers confess their guilt, disgust and obsession with the behavior.

What is chewing and spitting? How does it relate to other disordered eating behaviors, such as restrictive eating or binge eating?

Guarda AS et al. Chewing and spitting in eating disorders and its relationship to binge eating. Eating Behaviours 5 (2004) 231-239

What is CHSP?

Chewing and spitting describes the pathological eating behavior where the individual chews a variety of enjoyable foods, and spits it out to avoid undesirable consequences of weight gain (Mitchell et al, 1988). This seemingly “smart” workaround allows them to enjoy the taste of foods they usually deny themselves. However, CHSP is described as “driven and compelling,” often leading to uncontrollable episodes in which the individual chews and spits out large quantities of food. This type of behavior often results in social isolation, severe food obsession and financial difficulties.

Given the phenomenological similarities between CHSP and binge eating, CHSP was previously mostly examined in the context of bulimia nervosa (BN). While chew and spit is fairly common in patients with BN (64.5% of 275 patients with BN over the course of their lifetime), few patients engaged in the behavior continuously (Mitchell, 1985). In fact, chew and spit was considered an intermittent purging behavior used in place of self-induced vomiting or laxative abuse. A more recent survey  of individual with anorexia nervosa (AN), BN and eating disorder not otherwise specified (EDNOS) revealed that chew and spit was not limited to patients with BN (Kovacs, 2002). Patients who reported engaging in this type of behavior in the AN and EDNOS group demonstrated more disturbed eating behavior than their non-chewing and spitting counterparts.

In a study by Guarda and colleagues, , the authors set out to evaluate the prevalence and frequency of chew and spit in patients with AN, BN and EDNOS, and compare psychometrics between individuals who have this behavior compared to those who do not. Self-report questionnaires included the Beck Depression Inventory (BDI), which measures depressive symptomatology, and the Eating Disorder Inventory-2 (EDI-2) questionnaire, which measures eating disorder symptomatology. Overall, 301 patients were surveyed.

So what did they find?


1)   Overall prevalence: 34% admitted to one episode of CHSP in the month prior to admission, with 19% engaging in the behaviour several times a week (CHSP+).

2)   Overall, compared to patients who did not CHSP or did so once a week or less (CHSP-) CHSP+ patients were younger, significantly more likely to abuse diet pills, engage in excessive exercise, skipping meals and restrict fat and calories. The authors further examined if this difference in disordered eating occurred in all groups (AN, BN and EDNOS), and found that it was seen only in the AN group,. In other words, AN patients who engaged in CHSP reported more of the above behaviors than AN patients who did not. On the other hand, CHSP did not significantly alter eating behaviors in BN and EDNOS groups.

3)   Overall BDI scores were not different between CHSP- and CHSP+ patients, although CHSP+ patients were more likely to have considered suicide.

4)   There were no significant differences in mean length of stay as an inpatient, race or current employment between CHSP groups.

5)   There were no significant differences in BDI or EDI-2 in CHSP+/- patients who also engaged in binge eating.

Making sense of these results:

Contrary to previous belief, chewing and spiting is not limited to BN patients, but appears in similar frequency in patients with eating disorders in general. AN patients who engaged in CHSP tend to be more pathological in their disorder than AN patients who did not. CHSP did not influence eating behaviors of patients with BN or EDNOS. Surprisingly, CHSP is more commonly associated with other restricting eating behaviors than binging and purging.

However, as the authors noted, a limitation of this study is that they did not assess the amount of food consumed during each chew/spit episode or associated loss of control. Patients generally choose sugary or high fat food to chew and spit, hinting at a reward system deregulation that is also found in patients with binge eating disorder.  Future studies should address the macronutrient composition and amount of food consumed in a sitting as well as the individual’s state of mind to characterize this frequent eating disordered behavior and its reinforces.


Mitchell J et al. 1985. Characteristics of 275 patients with bulimia. American Journal of Psychiatry, 142, 482-485.

Mitchell J et al. 1988. Chewing and spitting out food as a clinical feature of bulimia. Psychosomatics, 29(1), 81-84.

Kovacs D 2002. Chewing and spitting out food among eating-disordered patients. International Journal of Eating Disorders, 32, 112-115.
Guarda AS, Coughlin JW, Cummings M, Marinilli A, Haug N, Boucher M, & Heinberg LJ (2004). Chewing and spitting in eating disorders and its relationship to binge eating. Eating behaviors, 5 (3), 231-9 PMID: 15135335