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.

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“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.

ResearchBlogging.org
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

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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.”

ResearchBlogging.org
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

#SfN13 Your coffee habit? Don’t fight it, embrace it.

Poster 236.10 The daily fix: habitual caffeine doses improve performance in attention and executive functions irrespective of food intake. JL Mariano, JCF Galduroz, S Pompeia. Univ. Federal De Sao Paulo, Brazil

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Coffee and I: 14+ years of history and counting.  Source: http://caravancoffee.com/

Here’s another reason to love coffee. Researchers from Brazil found that morning coffee consumption not only keeps you awake and alert, but also improves performance on cognitively demanding tasks. That is, if you’re already a habitual drinker.

People often start their day with a cuppa and breakfast. Carbohydrates in food gives the brains a shot of glucose, which is shown to positively affect cognition. Since caffeine also stimulates the brain, researchers wondered if stacking the two may lead to even better performance.

They recruited 58 young healthy coffee drinkers. After an overnight fast, half of the volunteers drank their usual cup (or two) of coffee, intaking 25-300mg of caffeine. The other half drank a placebo decaf. Some ate a cereal bar to chase the coffee, others didn’t. 30min later, researchers bombarded the volunteers with a series of mentally challenging tasks.

In one, volunteers tried to continuously call out numbers between 1 and 9 in a random fashion for 2 minutes straight – randomness and low repetition is the key. Here, volunteers had to actively inhibit our natural preference for number patterns (try it, it’s hard). In another test for  long term memory and recall, they named as many types of musical instruments or animals as possible in one minute. A whack-a-mole like game (hitting a button when a light comes on) tested their reaction speed while a zoo-navigating task tested for efficient goal-directed planning.

Surprisingly, food did not affect the performance on any of these tasks; but coffee certainly did. Coffee drinkers generated random numbers faster and repeated themselves less than controls. Their performance was also more stable within the task, consistent with less feelings of mental fatigue or weakness after the tests. However, these subjects were consistent coffee consumers, so it’s hard to say whether caffeine upped their smarts in a true nootropic-like manner, or if the placebo drinking group simply did worse due to caffeine withdrawal.

But for the average cup-a-day coffee consumer, if you’re in need of a quick boost in mental power (or avoid that nasty brain fog), it might help to go drink a cup. Scientists and lab techs, I’m looking at you.

 

PS Steve Miller, aka neuroscienceDC and fellow official #SfN13 blogger has a great post on the best time of day to drink coffee, check it out!

#SfN13 Stressed out mice turn to carbs for comfort food

Poster ZZ3 Ghrelin protects against stress by promoting the consumption of carbohydrates.T. Rodrigues. Z. Patterson. A. Abizaid. Carleton University, Ottawa, ON, Canada

In this world nothing can be said to be certain, except death and taxes.– Benjamin Franklin

Personally, I’d add stress to that.

There’s no question that chronic stress is a killer. Handled badly, stress can lead to anxiety, memory impairments, cardiovascular disease and sleep disorders. We all have our own strategies for coping with stress, some healthier than others. Me? I turn to food.

candy

Cavities galore or stress relief? Source: http://atomic-candy.com/ 

Apparently, so do bullied mice. Mice are social creatures; when housed together, larger and meaner ones will quickly assert dominance. The little guys have it rough, usually showing signs of anxiety, depression and increased body weight within weeks.

The reason for their weight gain can be traced back to an increase in ghrelin, a hunger-causing (orexigenic) hormone produced in the stomach. Once released, ghrelin travels to the brain and binds to its receptors to increase calorie consumption. But not all foods are equal; new research from Carleton University suggests that ghrelin promotes the intake of comfort foods – specifically, carbohydrates- because they decrease the level of circulating stress hormones such as corticosterone.

In the study, researchers first measured the amount of chow that mice ate per day for 21 days. They then chronically stressed out one group of mice by putting a dominant bully into every cage; the two mice were separated by a see-through glass wall to reduce violence. Every day, the mice had 24hr access to a standard, high-carb chow and a 4hr-window to a fattier alternative. Compared to non-stressed controls, the bullied mice drastically increased their total calorie intake, paralleled by an increase in ghrelin levels but surprisingly normal corticosterone levels.

When researchers broke down in the increase in calories by the type of food, they uncovered an unexpected result: stressed-out mice did not eat more fat, but instead opted for more high-carb chow. In fact, this high-carb binge almost entirely accounted for the increase in total calorie consumption.

However, mice chow does contain ~50% of protein and fat. To rule out a preference towards these two macronutrients in combination, researchers repeated the experiment, but with sucrose solution as the alternative to high-carb chow. As before, stressed-out mice increased their intake of chow, but this time, they also doubled their intake of sugar water compared to their unstressed peers. At the same time, their corticosterone levels were normal, suggesting that they were coping fairly well in the face of daily terror.

Why is ghrelin triggering a preference for carbs? The answer might be internal stress management. When researchers feed both bullied and control groups the same standard chow (~50% carbs), effectively restricting access to stress eating, the bullied mice suffered numerous negative health effects. Their ghrelin and corticosterone levels shot through the roof. They had abnormally low blood sugar levels, signalling the onset of metabolic problems. They even showed signs of depression, refusing to swim when dropped into a deep container filled with water.

These data suggest that under stress, ghrelin levels rise and tip food preference towards high-carb rather than high-fat foods. To see if this is indeed the case, researchers turned to a strain of mice genetically engineered to lack ghrelin receptors. Normally, compared to wild-types, these mutants show similar patterns of eating and hormone regulation, although they tend to be slightly smaller. Once stressed, however, they didn’t respond by switching to the high-carb comfort chow, instead increasing their nibbling of fatty foods. Behaviourally, these mice could not cope – in the swimming task, they spent most of their time immobile, succumbing to their fates.

Researchers aren’t yet sure why ghrelin-induced carb – but not fat – intake helps to manage stress. One reason could be bioenergetics: stress alerts the brain that more energy is needed (and soon!) through ghrelin, which in turn increases the preference for glucose – a fast and efficient energy source. Or it could just be a matter of comfort. These mice grew up on standard mice chow, which just happens to be high in carbs. Perhaps, just like you and me, mice simply prefer familiar and comforting foods after a long, stressful day.

Feline Fever, Forever

Does Reddit have a case of the T. Gondii?

Does Reddit have a case of the T. Gondii?

Toxoplasma gondii is arguably one of the most interesting parasites known to nature. Packed in the single cell of this unassuming protozoan is the power to manipulate the most complex organ in the body – the brain- and remarkably, change the thoughts and behaviours of its unsuspecting host…

…by bringing on a case of the “cat crazy”, in mice and men.

While T. Gondii can infect almost all warm-blooded animals, they are only able to sexually reproduce in the gut of our favourite feline – the cat. Once orally consumed, T. Gondii produces egg-like “off springs” in the gut of cats, which gets released into the wild with poop. There they sit until another potential host comes along – say, mice sniffling for crumbs or human changing the litter box – and once in, disseminates widely in the body and the brain, eventually forming cysts that are observable under the microscope.

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T. Gondii cyst chilling in the brain. Can it really be harmless? Source: http://wiki.ggc.edu/

But now T. Gondii has a dilemma: to have a satisfying sexually active adult life (and continue the survival of the species), it HAS to get back into a cat. The best way to achieve this to get eaten. Astonishingly, T. Gondii evolved the ability to tweak its hosts’ brains and turn them into easily attainable catnip. Rodents, for example, loose their innate fear of cat urine, and may even become sexually aroused by cats.

While intriguing, previous behavioural studies mostly use the high-inflammatory Type II T. Gondii, which often leads to more infection-related complications and “sickness”-type behaviours in its host. This begs the question: is the parasite directly responsible for cat-love, or is the host’s inflammatory response that’s changing behaviour?

W.M. Ingram et al. (2013) Mice infected with low-virulence strains of Toxoplasma gondii lose their innate aversion to cat urine, even after extensive parasite clearance. PLOS ONE, doi:10.1371/journal.pone.0075246

The authors infected male mice with two low virulence strains (a genetically-altered Type I and a wild-type Type III) and waited between 3 weeks to 4 months for the parasite to “work its magic”. They then placed the mice into a box with cat urine on one end. The box was covered by a grid of infra-red beams; by tracking beam-breaks as the mice explored the box, researchers were able to closely track their position and movement.

As you can see in the graph below, uninfected mice avoided bobcat urine like the plague (solid red dots) while ignoring non-predatorial rabbit pee (empty red dots). The infected mice, on the other hand, didn’t think twice about approaching “dangerous” areas (solid triangle and solid square). This happened in an “all-or-non” manner regardless of how long they were infected, and didn’t disappear with time. A hidden cookie test revealed that their sense of smell was working fine.

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When researchers looked for the presence of the parasite in the mice’s brain after the behavioral tests, they detected Type III T. Gondii DNA (left below), but couldn’t find any signs of Type I (right below).

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Similarly, although Type III-infected mice had elevated white blood cells, suggesting an ongoing infection, Type I-infected had levels similar to those uninfected. Further probing confirmed that Type I did manage to established infection: parasite load was transiently detected between 5-20 days post-infection, along with molecular markers of a brain inflammatory response.

These results together suggest that (at least for Type I) T. Gondii can manipulate rodent behaviour even AFTER it’s gone and the brain no longer inflamed. Can the parasite still pull the cat-love strings 6 months after infection? What about a year? A lifetime?

T. Gondii thrives in 1/3 (!!!) of the human population, and once they settle, they stay for life. Once thought to be innocuous (other than the occasional  “crazy cat lady” joke), troubling evidence is emerging that links T. Gondii infection to higher suicide risk, schizophrenia, depression and even Alzheimer’s disease in humans – without apparent signs of brain inflammation. Types I, II and III are the most prevalent types in North America, though I’d love to know how often humans get a low-virulent Type I infection as used here. Nevertheless, this study suggests that the “latent” or non-inflamed stage of T. Gondii may not be as asymptomatic as previously thought.

HOW is T. Gondii playing master puppeteer? Previously people have pointed the finger at inflammation and disruptive cysts. Increased levels of immunomodulatory molecules called cytokines is linked to depression and suicidal thoughts and hypothesized to mediate T. Gondii’s behavioural effects in humans. Cysts may directly increase dopamine production or disrupt neuronal activity in brain regions associated with mood and innate fear.

The finding that a transient infection can cause persistent changes suggest some other factors, such as synaptic plasticity, T. Gondii-inserted parasitic proteins, or even parasite-induced epigenetic changes may be involved.

So next time you change the litter box, remember to wear a pair of gloves and wash your hands after. Or risk succumbing to a prolonged –if not forever – case of the feline fever.

PS. T. Gondii infection is on the rise world wide – so’s internet’s love for all things cat-related. Correlation or causation? #catconspiracytheory

ResearchBlogging.org
Wendy Marie Ingram, Leeanne M. Goodrich, Ellen A. Robey, & Michael B. Eisen (2013). Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance PLOS ONE DOI: 10.1371/journal.pone.0075246

The brain’s swan song: hyperactivity near death

TL;DR: Near-death experiences are ‘electrical surge in the dying brain? …But dude, what does it all mean?

Swan-Song-detail-2 copy

A last hurray before death? A biological basis for near-death experiences?
An experimental artifact? Or a simple observation blown WAY out of proportion?

We often think of death as flipping a switch: one minute you’re there, next all lights go out. But this is a simple caricature of the dying process: sparks of activity still linger in the brains of those undergoing cardiac arrest, in whom both breath and heartbeat flutter and abruptly halt. Researchers have long thought that these sad, sparse bouts of activity characterize the brain’s descent into permanent unconsciousness. However, a new study suggests that the complete opposite – a surge of heightened connectivity – paradoxically marks the final step towards death. Although a long (and I mean LOOOONG!) stretch, the authors propose that the observation may partially underlie the enigmatic near-death experience (NDE).

Reports of NDE are nothing new. The luckily revived few often re-emerge from “the other side” with realer-than-real stories of long tunnels, intensely vivid visions and meetings with those bygone. NDEs are treated by some as proof of an afterlife, or by others, the existence of a “mind” beyond the brain and body. Spiritual connotations aside, the biological underpinnings remain mysterious, although abnormal dopamine and glutamate transmission may be involved (and probably everything else – the brain IS dying!). Here, the authors turned the focus away from individual neurotransmitters, and instead asked: after the heart stops, what happens to the oscillating waves of neural activity in the brain?

Jimo Borjigin et al. 2013. Surge of neurophysiological coherence and connectivity in the dying brain. PNAS. doi: 10.1073/pnas.1308285110 

Researchers fitted 9 rats with electrodes to measure their brain waves – rhythmic brain activity generated by feedback connections between large numbers of neurons that differ in frequency. Alpha activity, for example, is often detected during relaxed wakefulness, while the faster theta activity is linked to cognitive processing. Gamma waves – the most recently discovered component – are particularly interesting to cognitive neuroscientists (and pseudo-science marketers) studying consciousness.

Why? The low gamma band, oscillating at 25-55Hz, has long been linked to visual consciousness, or the perception and awareness of visual stimulation. It seems to promote associative learning, and is also present during REM sleep (and slow wave sleep/deep sleep as well), which involves dreaming and complex visuals. Gamma bands also appear during transcendental mental states, as measured in Tibetan monks told to generate feelings of compassion as they meditated. Some even propose that gamma bands are behind the heightened sense of consciousness and bliss following a meditative bout. Sounds pretty magical, eh? As things goes, it’s also a tough band to measure with EEG – in fact, there are even skeptics who doubt its existence.

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Back to the study. After fitting rats with electrodes, researchers monitored changes in each brain wave component as the rats passed through three states: awake, under ketamine-induced anesthesia and after cardiac arrest. Unsurprisingly, after the loss of heartbeat and oxygen flow, the strength (“power”) of all brain wave frequencies measured tanked – except for low gamma bands, which spiked in power and became the dominant frequency in the spectrum as you can see above.

After cardiac arrest, gamma waves also showed higher levels of synchrony – that is, the neural activity in various brain regions became more “in tune”, even compared to an awake state. This high level of coherence between different brain regions is often associated with a highly “aroused” brain – that is, a state in which high levels of information processing may occur. Thus the authors concluded that the brain might exist in a hyper-conscious state for tens of seconds after the heart stops.

Sounds a bit too philosophical? I feel you. Where to start? First, the data really doesn’t tell us much. We already know that for a brief time following clinical death (which will most likely be redefined in the future), the brain remains active – so that’s nothing new. The increase in gamma wave power and synchrony is intriguing, especially since it appeared in all 9 rats (but really, just 9?), and the magnitude of the changes were large. But to link those changes to hyper-consciousness (what does that even mean?) and near-death experiences (NDEs) is going a step too far.

For one, there is absolutely no direct proof that gamma waves reflect NDEs. It has never been recorded in people there-and-back-again. While it’s true that high power gamma activity is often measured during conscious brain activity (and dreaming), its presence does not “lead to” conscious perception. Hence we can’t conclude, for example, that the rats were experiencing heightened awareness like NDEs – if they even have the ability to – because they show increased gamma oscillation. Along the same lines, higher gamma activity in the visual cortex does not necessarily mean there is more visual awareness and sensation. It may let you watch your life flash before your eyes, or it might just be a random quirk in the brain before all lights go out.

I’m not bashing research on consciousness. I just dislike interpretations that take data completely out of the realm of scientific discussion. I’d perk up if the authors repeated this experiment on people who have undergone cardiac arrest and experienced NDEs, and found the same pattern of changes in gamma waves. But even then it wouldn’t really tell us much. Now if only we had the ability to experimentally manipulate gamma (or any other) bands and “implant” an NDE in those still alive…

Note: I’d love for the EEG experts out there pitch in. How hard is it to measure and isolate gamma band from noise? What conclusions (if any) would you make out of this study?

ResearchBlogging.org
Borjigin J, Lee U, Liu T, Pal D, Huff S, Klarr D, Sloboda J, Hernandez J, Wang MM, & Mashour GA (2013). Surge of neurophysiological coherence and connectivity in the dying brain. Proceedings of the National Academy of Sciences of the United States of America PMID: 23940340

Is the taste of beer dangerously intoxicating?

IMG_2211 (from Melville)

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.

ResearchBlogging.org
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