Two cups of coffee after learning may cure your forgetful streak

Like most junkies, I struggle to come up with excuses to justify my addiction. Lucky for me, increasing evidence is supporting my semi-hourly coffee habit: caffeine, the world’s favourite drug, not only keeps you awake and alert, but may also boost your memory.

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Here, have a memory-jolting Latte. Source:

Perhaps in an effort to excuse their own coffee addiction, many research groups have studied whether caffeine enhances memory. The results, unfortunately, are highly mixed. One study, for example, found that 200mg of caffeine – roughly the amount in two cups of drip coffee – consumed before a memory-taxing game enhanced working memory, the ability to flexibly maintain and manipulate information in your head to solve a problem. The catch? Only if you’re an extrovert. In a separate cohort of volunteers, 75mg of caffeine (roughly that in a cup of espresso) taken together with glucose on an empty stomach helped stabilize a new verbal memory. This is called “memory consolidation”, whereby new and unstable memories are moved into semi-permanent storage. However, in that study caffeine by itself had little effect on memory.

One problem with these previous studies is that caffeine was always given prior to learning or testing. This makes interpreting any improvements in performance difficult: is caffeine directly boosting memory or is it enhancing performance indirectly through increasing attention, vigilance and/or processing speed, thus giving the appearance of memory gain?

D Borota et al. Post-study caffeine administration enhances memory consolidation in humans. Nature Neuroscience, published online Jan 12, 2014. doi:10.1038/nn.3623 

To get to the bottom of this, researchers from University of California, Irvine* decided to see how caffeine consumed after learning affects memory consolidation. They recruited 160 uncaffeinated adults, a rare breed that drank less than 5 cups of coffee per week and showed no traces of caffeine or its metabolites in their saliva prior to the experiment. In fact, average caffeine intake of most of these “caffeine naïve” people lingered around 70mg a week, coming mostly from chocolate and soda rather than coffee per se. (*The research described in this post was done at Johns Hopkins before the lead author moved to UC Irvine)

The volunteers first looked at a series of images of various objects, such as a saxophone, a sea horse or a basket, and categorized them as either an indoor or outdoor object. Upon completing the task, they immediately popped a pill containing either 200mg of caffeine or a placebo and left the lab.

A day later, the volunteers returned. By now all traces of caffeine and its metabolites had washed out of their system; they were stone-cold sober. The researchers then showed them a new series of pictures, instructing them to identify whether they had previously seen the picture (“old”) or if it was new. To make things harder, researchers sneaked in several pictures extremely similar those shown before. For example, instead of the old picture of a svelte sea horse arching its back, they now presented a “lure” picture of the animal hunched over. This type of “pattern separation” task is considered to reflect memory consolidation to a deeper degree than simple recognition.

Regardless of caffeine intake, both groups had no trouble identifying the old and new pictures. However, as shown below, the caffeinated group outperformed their peers in picking out the lure, with a higher propensity of calling them out as “similar” rather than “old” (though the effect was small and barely reached significance, more on that later). In other words, caffeine seemed to help them retain minute details present in the original pictures. A similar boost in performance was seen when researchers repeated the experiment with 300mg of caffeine (~1 cup more than before), but the advantage disappeared when they dropped the dose down to 100mg. Remember that caffeine was administered after viewing the photos, hence the drug was not increasing attention to detail during the learning process.

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White bar is caffeine and grey bar is placebo. Notice the shorter white bar in the “Old” group (fewer lure images identified as old) and taller white bar in the “Similar” group (more images correctly identified as lure).

However, not everyone metabolizes the same 200mg caffeine pill to the same degree. When researchers accounted for individual differences in caffeine absorption and metabolism, they found that participants who broke down the largest amount of caffeine performed worse than those who metabolized slightly less. In other words, there is a sweet spot for caffeine’s memory enhancing powers – go either under or over and you loose that edge.

Finally, what if you waited too long after learning, only to remember to chug that Starbucks mocha the day after? In a separate study, researchers allowed 24hrs for volunteers to consolidate the memory of the initial picture stack before giving them the same caffeine pill, just one hour before the test. This time it didn’t work – these volunteers mixed up similar and old pictures just like the placebo control group. Whatever caffeine is doing, it has to be done during consolidation.

Researchers aren’t quite sure how caffeine induces memory gain, but they have a few ideas. The image discrimination task used here engages the hippocampus, a key brain area involved in learning and memory. It expresses high amounts of the caffeine receptor (adenosine A1 receptor) in its CA2 subregion, thus allowing caffeine to tweak (strengthen?) its function in memory consolidation. Caffeine can also indirectly boost the level of norepinephrine, a neurotransmitter that helps you lay down a memory for good.

While exciting, this study cannot end the debate on whether caffeine improves memory. The effect sizes were small, with some only scraping significance – that is, researchers were only barely able to say with some confidence that the effect is real. This doesn’t reflect the quality of the research, but most likely represents individual variance among the volunteers: different gene variants for faster caffeine metabolism, BMI, basal metabolic rate, oral contraceptives and so on. It would also be interesting to see if caffeine boosts memory reconsolidation: when you retrieve a memory, it temporarily becomes labile. Can coffee help the memory restablize?

Unfortunately, we don’t known if caffeine-induced memory gain applies to caffeine junkies like me. But to quote the lead author: one needs to do the experiment with habitual drinkers to find out, but my guess is that it’s why we’re so awesome!

Many thanks to the principal investigator @mike_yassa for patiently answering my questions over Twitter. You can check out our full conversation in my timeline.
Borota D, Murray E, Keceli G, Chang A, Watabe JM, Ly M, Toscano JP, & Yassa MA (2014). Post-study caffeine administration enhances memory consolidation in humans. Nature neuroscience PMID: 24413697

Top 10 science stories I wish I’d blogged about in 2013

As 2013 grinds to an end, the internet fills with reminiscence of the year’s top stories and moments. I, for one, especially can’t resist ruminating about the past, especially when packaged in a brain-tickling, “top n”  list form. Without further ado, here is my Top 10 list of the year: Science Stories I Wish I’d Blogged About.

Bonus. A List of Reasons Why Our Brains Love Lists. By Maria Konnikova.

To start off, why are we drawn to lists anyway? Is it due to the clean, structured organization that helps us navigate the material efficiently? Or is it more a product of our current “bite-sized” information culture? Maria has the answers.

10. Can we lessen the effects of fearful memories while we sleep?

Sleep therapy can change bad memories. By Helen Shen (original paper here)

Spontaneous activation of memories during sleep is generally thought to strengthen them. However, when researchers in Northwestern University repeatedly brought up a recently learned fear memory in their sleeping participants by presenting a fear-associated odour, the participants showed a smaller fear reaction to the odour after they awoke. According to the researchers, this is the first time emotional memories have been successfully manipulated in humans.

Similar: A gene for forgetting. MIT researchers identified a gene Tet1 that is critical for memory extinction in mice. Original paper in Neuron.

9. Men and women’s brains are wired differently. Is THAT why men can read maps better (or so the cliché goes)?

Here‘s one cover of the study that would let you believe that (gasp) it is indeed so!

Here are a few level-headed analyses that tackle the nitty-gritty of the study and how its conclusions got blown out of proportion. The bottom line? Brain scans don’t tell us anything about behaviour. Here’s the original paper for reference.

Are men better wired to read maps or is it a tired cliché? By Tom Strafford.

Men, Women and Big PNAS Papers. By Neuroskeptic.

Getting in a Tangle Over Men’s and Women’s Brain Wiring. By Christian Jarrett.

8. Mice inherent fears of their fathers. (And update) By Virginia Hughes.

You know how you are what your grandpa ate? Epigenetics offers an answer to how our interactions with the environment can influence the expression of our and our offspring’s DNA. However there is little evidence that stress and fear can directly change the germline, so that offsprings inherit the fear memory (or something akin to it) of their parents. (There was this interesting report earlier in the year on how cocaine-addicted sires lead to cocaine-resistant male pups through a purely epigentic means, though I remain skeptical.)

Virginia Hughes broke this story at the 2013 Society for Neuroscience conference. Since then, it has garnered plenty of attention from media and neuroscientists alike, with opinions from “deep scepticism” to “awe-inspiring”. Here’s the original paper if you’d like all the juicy details.

7. From Club to Clinic: Physicians Push Off-Label Ketamine as Rapid Depression Treatment. By Gary Stix

Ketamine, the clubbing sweatheart and horse tranquillizer, is now being repurposed as a fast-acting antidepressant; this is perhaps THE most breakthrough new treatment for depression in the last 50 years. In this 3-part series, Gary Stix explains the uprising of grassroots ketamine prescriptions, big pharma interest in the drug and how ketamine is directly the development of next-generation antidepressants.

6. Computer Game-Playing Shown to Improve Multitasking Skills. By Allison Abbott.

Rejoice, gamers of 2013! Not only has the year given us PS4 and Xbox One, this study from Nature has also given us an excuse to game (uh, or not): in subjects aged 60-85, playing a 3-D race car-driving video game reduced cognitive decline compared to those who didn’t.

Commercial companies have claimed for years that brain-training games help improve cognition; yet whether their games actually work is hotly debated (I’m looking at you, Luminosity!). In this new study, researchers from UCSF show that a game carefully tailored to a specific cognitive deficit can be useful, even months later. Unfortunately this doesn’t mean any ole’ video game will do. Shame.

5. 23andme versus the FDA.

I’m sure by now you’ve heard about the fight of the year.

David Dobbs has a full page of links over the 23andme and FDA food fight. What’s the big deal? Why did the FDA issue a cease and desist order? Is it simply a clash of cultures between the company and government department? Or are we selling out our own genetic data to the next-generation Google, and should we fear the services the company offers?

4. Sleep: The Ultimate Brainwasher? By Emily Underwood (Here’s another cover by Ian Sample).

Why do we sleep? Reasons range from learning and memory, metabolism and body-weight regulation, physiology, digestion, everything. A study this year proposes that sleep has another function: nightly cleaning, in which the cerebral spinal fluid washes a day’s worth of brain waste down the sewers. That is, if you’re a rat.

3. Death by sugar? by Scicurious.

With fat making a come-back, sugar and/or carbs are the devil this year. This study in Nature Communications says yes: when mice consumed a diet that has an equivalent amount of sugar to that of many people in the US, the animals’ health and reproductive ability declines.

However, as Scicurious astutely asked, can we really directly translate conclusions derived from mice to humans? Is sugar really that evil?

Here is another article on the topic by Ferris Jabr that’s well worth a read.

2. False memories implanted in mouse’s brain by linking portions of two real memories together. Wow. Just, wow.

False memory planted in mouse’s brain. By Alok Jha

Scientists Plant False Memories in Mice–and Mice Buy It. By Joel N. Shurkin

This is one paper I REALLY wish I had the time to cover when it first came out. An MIT group artificially connected the memory of a safe box and the memory of a footshock in another box to generate a new hybrid memory. This is not “implanting” a de novo memory – that is, researchers didn’t use electrical stimulation (or something similar) to generate a memory from scratch. The study also can’t tell us how false memories are generated biologically in our brains (ie linking imagined material to actual memories), but the study is genuinely fascinating all the same.

Here is a link to the paper, and here is the lead author doing an “ask me anything” interview on Reddit.

1. Knockout blow for PKMzeta, the long-term memory molecule. 

Single protein can strengthen old faded memories, Exposing the memory engine: the story of PKMzeta, and Todd Sacktor talks about the memory engine by Ed Yong

In a nutshell, previous studies have identified a single protein called PKMzeta that helps maintain long-term memory. Unlike other kinases (a type of protein involved in many cellular processes, including memory) PKMzeta is always active, and seems to help sustain the strengthening of connections between neurons during memory formation. Inhibit PKMzeta, and the memory’s gone.

These results spurred HUGH interest in the “memory molecule”, often with references to Eternal Sunshine of the Spotless Mind. However, things went for a downward spiral at the 2012 Society for Neuroscience conference, when researchers presented the first evidence that mice without PKMzeta had no impairments in LTP (long-term potentiation, widely considered a cellular mechanism for learning and memory) could still form memories. The two groups published their findings in early January 2013 in Nature (here and here).

These observations don’t necessarily mean that PKMzeta is not a memory molecule – it very well could be one of the MANY memory-associated proteins. Given the redundancy that often comes with evolution, it’s hard to believe that one particular molecule would be the sole guardian of our memories. The question remains whether PKMzeta is a MAJOR player, but overall, the debate is a cautionary tale against putting one molecule on the pedestal. So if (or when) you see another article with the headline “erasing a bad memory”, remember there’re plenty of other players in memory that you haven’t been told about.

Christmas food for thought: Feed me, all 100 trillion of me

The morning before Christmas eve, I’m sitting here in the dining room munching happily on the bits and pieces of what’s left of our gingerbread house that was only erected to its full glory the night before. I have not consumed this amount of carbohydrates in over a year.

Inside, a few species of my extensive gut microbe community are screaming bloody murder.

E. coli bacteria

FEEEEED ME!!!! Source:

When you eat, you’re not only feeding your own fleshy vessel, but also the 100 trillion of microbugs that thrive in your intestines. Hardly “along for the ride”, these bugs not only help us digest foodstuff, ferment carbohydrates and proteins but also heavily impact our metabolism and general health. Depending on their composition, they tweak our risk of cardiovascular diseases, Type II diabetes and may even cause obesity in humans. There’s tantalizing evidence that their reach extends to the brain, influencing mood, anxiety and cognition in mice.

However, the gut microbiota* is a fluid, ever-changing beast. In one previous study, researchers transplanted gut-free mice with fresh or frozen human poop to inoculate them with a microbiome of known composition. When researchers switched these mice’s plant-based diet to a high-fat, high-sugar one, the structure of the established microbiome changed within a single day: some species dwindled in number, while others exploded onto the intestinal stage, bringing with them their particular metabolic tricks. (*The word “microbiome” refers to the set of genes in the gut bugs).

Similar diet-induced changes have been found in humans. When babies are weaned from their mothers’ milk and switch to solid food, their gut bug community simultaneously go through tumultuous changes. The gut bugs of African hunter-gatherers vastly differ from those in people grown on a Western diet. But these changes take weeks, even lifetimes. Just how fast can the microbiome adapt and change to a new diet?

In a new study, researchers recruited ten volunteers and put them on two drastically different extreme diets for 5 days – as you can see below, the plant-based diet was rich in grains, fruits and vegetables (high-carb and high-fibre), while the animal-based diet consisted of meats, eggs and cheeses (high-fat, high-protein and low/no-fibre). Each day, the volunteers handed in a poop sample for the researchers to monitor.

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In general, the animal-based diet had a greater impact on gut flora than the plant-based one. It significantly increased the diversity of gut flora, enriching 22 species whilst decreasing the fibre-intake associated Prevotella in a life-long vegetarian on this meaty diet. The plant-based diet, on the other hand, only increased the abundance of 3 species, mostly those associated with carbohydrate fermentation.

Many of the changes made sense. An animal-based diet enriched putrefactive microbes, shifting carbohydrate fermentation into amino acid digestion, thus helping the body break down the onslaught of heaps animal protein. Several strains of immigrant bacteria – particularly those used for cheese- and sausage-making –settled down and made themselves comfortable in the native gut flora community. The meat-heavy diet also triggered microbes to activate pathways that degrade cancer-causing compounds found in charred meats, and enhanced the synthesis of vitamins.

On the other hand, several strains of potentially health-negative bacteria also multiplied in the meat-eaters. On a high-fat diet, we excrete more bile – a bitter fluid that may ruin a good fish dish – to deal with the digestion of fat. Bile is toxic to many gutbugs, but not to the mighty Bilophila (“bile-loving”) wadsworthia – a bile-resistant bacterium stimulated by saturated fats in milk that may cause intestinal inflammation, at least in mice. The high-fat content in the animal-based diet also triggered increased levels of microbe-produced DCA, which is previously linked to liver cancer in mice. However, as of now there’s no evidence that these risks also apply to people, and researchers caution against making health-related judgments (although some can’t resist the temptation).

On the whole, plant- and animal-based diets induced changes in host microbiome gene structure that resembled those of herbivorous and carnivorous mammals within a few days. Furthermore, the volunteer’s microbiome reversed back to their previous composition only 2 days after the end of the experiment. Researchers believe we might be looking at a fast-forwarded movie of millions of years of co-evolution between humans and their microbugs: when animal food sources fell scarce, our ancestors were forced to switch to a plant-heavy diet; a flexible gut-bug community could quickly and appropriately shift their repertoire and function to help digestion, thus increasing the flexibility of human diets and chances of survival.

Thus, when you gobble down the vast selection of Christmas dishes this year, remember to thank the flexibility of your gut flora for your diverse digestive powers. And remember that we can’t say one diet is better than the other for our microbiota; the take-home message is that they are incredible flexible, more so than we previously thought. In the end, it still comes down to the age-old wisdom: you are what you eat.
David LA, Maurice CF, Carmody RN, Gootenberg DB, Button JE, Wolfe BE, Ling AV, Devlin AS, Varma Y, Fischbach MA, Biddinger SB, Dutton RJ, & Turnbaugh PJ (2013). Diet rapidly and reproducibly alters the human gut microbiome. Nature PMID: 24336217

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?

photo (19)

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

Scientific American Best of the Blogs Video

I’m over at #SciAm videos, talking about the (potential) neuroprotective effects of a ketogenic diet. The short clip is based on a blog post The Fat-Fueled Brain I wrote a while back for their Guest Blogs (the article’s older sibling, Brain, living on Ketones can be found here).

The talented Dr. Carin Bondar, host of the series, suffered through the process of piecing my camera-dodging, hair-pulling, face-making video clips together (I’m EXTREMELY camera shy). She has my deepest respect.


SciAm also has a great video series called Instant Egghead that’s worth checking out. Fun – and super random- science info in ~2min clips with great graphics. Here’s an example: why toothpaste makes OJ taste bad.