Making the Most of Your Midnight Toast

Image Credit: Alex Brown.

It’s been a slow news week for science. The days between Christmas and New Year’s Eve can be a wasteland of year-in-review lists and other fluff concocted to facilitate holiday vacations. But all it took was an animated short on the science of sparkling wine from the American Chemical Society to stop my grumbling and get me on board with the lightness of the season. Forget real discoveries and real news and real whatever else. Let’s talk champagne.

What makes Champagne and other sparkling wines special is, of course, their bubbles. These are not only fun to observe, they also release aromas as they reach the liquid’s surface and burst, increasing the whole sensory experience thing. Dissolved carbon dioxide (CO₂) gives champagne its sparkle. Higher pressures and lower temperatures allow more CO₂ to be dissolved into wine than the liquid could hold in standard conditions. Your chilled bottle of champagne is under a good deal of pressure (thus the signature pop made when the cork is removed). Once uncorked, this pressure drops, and the amount of CO₂ that can be crammed into the liquid drops with it. CO₂ gas makes a break for it through the surface of the beverage and voila – festive bubbles. The trick to enjoying a glass of sparkling wine is too maximize the spectacle of bubbles without losing the molecule that makes them too quickly. Nobody likes flat Champagne.

Putting the Bubbles in the Bottle

The simplest way to get bubbles into liquid is just to inject CO₂ gas, which is how soda is made. But sparkling wines can take advantage of fermentation to form their fizz. Officially, Champagne is only Champagne if it comes from the Champagne region of France. But the “méthode traditionnelle” (aka méthode champenoise, when in France) by which it is made isn’t proprietary information. Spanish Cava for instance (my preferred bubble water) is also made using the Champagne method.

Here’s how it works. All wines are made through fermentation, that process where yeast metabolizes sugar and turns it into ethanol (drinkin’ alcohol) and CO₂.* This “primary fermentation” occurs in tanks and CO₂ generated is allowed to dissipate into the atmosphere. Champagne and its ilk, however, undergo a second fermentation once already tucked into their bottles.† Some other gunk also accumulates in the process (dead yeast cells and such) and must be ousted before the final corking. To collect and remove the “lees”, the bottles are stored at an angle, cork-side facing downward, and periodically prodded so that the stuff pools near the mouth of the bottle and can be removed with minimal wine loss. These are some of the bells and whistles that can make Champagne pricier than more crudely made sparkling beverages, even before the retail mark-up.

Ideal Glass Law

In late November I served my father, a wine enthusiast/wine snob, sparkling wine in a juice glass. For this transgression I was rewarded with an early Christmas gift – a set of champagne flutes. The most obvious reason why stemware is the best choice for sparkling wine is that the stem helps keep your sweaty hands off the bowl of the glass. Holding a glass from its stem prevents heat transfer to the liquid (recall that increasing heat speeds up CO₂ escape).

But the shape of the glass matters too. The two dominant vessels for sparkling wine serving are the flute (the tall one) and the coupe (think Champagne fountain). Scientists have done a lot of gas measuring to help you choose your glass, and mostly the flute wins. Being taller and narrower, flutes not only keep beverages cooler, they also offer less surface area for CO₂ gas to launch. Coupes basically hemorrhage CO₂ for the first few minutes after being poured and then calm down, by which time the wine has lost a lot of its fizz. Flutes maintain a steadier movement of bubbles. Flutes are also better designed to showcase the bubbles. The entire vertical column is filled with bubbly movement, whereas coupes have a less effervescent “dead zone” at the portion of the bowl furthest from the center.

Less than half of the CO₂ exiting the liquid departs in the form of aesthetically pleasing bubble. Much of it disappears through unceremonious “invisible diffusion” into the air. This too is higher in the coupe, though less so than expected, given that glass’s abundant surface area. This finding can be attributed to the greater bubbling going on in the flute. The bubbles travel further and mix more vigorously, and thus more gas is lost per unit of surface area. But overall, unless you have your heart set on that champagne fountain, you’re better off with the flute.

Right Angles

Now that you have the perfect glass, don’t ruin everything by pouring the wrong way. It turns out that the angle at which the glass is held during the pour also impacts how much CO₂ escapes before you even get the flute to your mouth. While champagne is normally poured like any other wine – into a glass standing straight up on a table – painstaking experimentation has demonstrated that you’re better off holding the glass at an angle – as if you were pouring a beer. The pour is a turbulent time for newly uncorked Champagne, and an angled glass minimizes the CO₂ loss during this vulnerable stage, leaving more bubbles to bounce around once you’re finally drinking your drink.

Well cheers then. And don’t forget to hold the glass from the stem. In addition to the temperature issues we discussed, you’ll also get a better clink that way. Clink!

* There are more steps, but just face it, if I started telling you about glycolysis, you would stop reading.

† Another method, used for sparkling wines like Prosecco, does a second fermentation in tanks and then bottles the wine under pressure before it loses its pop.

Terror from the Tap: How a deadly amoeba can sneak into your neti pot

Image Credit: Antonio Foncubierta.

Last summer, when a friend told me about a brain-eating parasite that lurks in warm freshwater swimming areas and can kill you in just one week, I thought, “Hmm, interesting, but a bit obscure even by my standards.” A quick check with the CDC website confirmed that such infections were absurdly rare – only 32 were reported in the United States in the entire decade from 2001 to 2010 – and so the topic was shelved in favor of more newsworthy science. But now, with two people in Louisiana dead at the (figurative) hands of the grisly microbe, and the state issuing a warning about the perils of improper neti pot usage, Naegleria fowleri is suddenly looking more relevant. 

The Louisiana cases are peculiar in that their victims didn’t have to dive into a warm lake or pond to encounter the parasite. Rather, it came to them, straight from the tap they used to fill a neti pot – a popular device for irrigating the sinuses.

How does this happen?

The microorganism responsible for all this trouble, Naegleria fowleri, is an amoeba that inhabits warm fresh water (a sustained 80˚F or above is its preferred aquatic climate). While content to live in water, it can also make its way into the human body via the mucosa in the nasal cavity, i.e., if you happen to get water up your nose. After gaining entry, it crawls along the olfactory nerves into the brain, where it chows down on vital central nervous system tissue. The ensuing illness is dubbed Primary amoebic meningoencephalitis (PAM).

The standard way to contract PAM is swimming in warm, amoeba-friendly waters (the microbe is found through the world, though is most common in warmer areas). Activities that increase the chance of water getting into your nose – such as diving or jumping – also up the risk of being infected by Naegleria fowleri.

Genie? No. Brain-eating amoebas? Maybe. Image: Kurt Yoder.

The amoeba can live in lakes, rivers, ponds and hot springs. It occasionally even crops up in poorly maintained swimming pools. It isn’t considered common in tap water, which undergoes a purification process to render it potable. Yet apparently, Naegleria fowleri has turned up in Louisiana’s tap water at least twice this year* And the neti pot, which is used to pour water through the nostrils (with the head tilted sideways, not directly up the nose) provides an interaction with the tainted water similar to that experienced splashing around in lakes during the summer months.

Could it happen to me?

Counterintuitive though it may sound, tap water teeming with Naegleria fowleri is still safe to drink. That’s because the microbe needs to enter your nose rather than your mouth to cause PAM. And neti pots are okay too, just not for use with tap water. Additionally, the illness is not communicable from person to person and the amoeba doesn’t live in saltwater. Although pouring ocean water through your nose doesn’t sound like a great idea either.

With so many other pathogens out there, how seriously should you take this one? Well, as with many splashy media maladies – such as mad cow disease – PAM is scary not for its prevalence (extremely low) but rather for its prognosis (extremely grim). The disease is usually fatal, and rapidly so at that. Initially symptoms are similar to those of bacterial meningitis – headache, fever, nausea, stiff neck – but these will soon progress to confusion, loss of balance, hallucinations, seizures and the like. By the time these second wave symptoms set in, there has already been significant destruction to brain tissue. So, yeah, you want to avoid getting this infection in the first place.

Its rareness means that the odds are already on your side. You can improve your chances even more by using a nose plug when swimming underwater, and by sticking to distilled (or thoroughly boiled) water when loading up your neti pot.

* The first case occurred in June of 2011, the second in October. Caveat alert: the cases are still under investigation.

It came from outer space

Image Credit: Ed Sweeney.

Guess who’s coming home for the holidays? Russia’s broken 15-ton Mars probe. Well, probably. You know how unreliable malfunctioning probes can be. Early reports claimed the unmanned spacecraft would reenter the Earth’s atmosphere around November 26, just in time for Thanksgiving leftovers, but now it’s looking more like late December or early January (which could still qualify for Christmas if you go by the Russian Orthodox calendar).* All this, of course, is assuming that the prodigal probe doesn’t change its mind again and decide to complete its originally scheduled mission to Mars.

You might be interested to know that Russia has been aiming various contraptions at the Red Planet for about half a century without much luck (I know, kind of ironic during the Soviet years). Following a 1996 mission failure, the past 15 years have been silent of Mars attempts, but on November 8^th, Russia got back on the horse and launched Phobos-Grunt into space. The space-bot’s goal was a lofty one: land on the surface of Phobos – Mars’s largest moon – collect soil samples, and then bring them back to Earth.† To achieve this, the probe needed to fire a second set of engines after its initial launch, which would direct it toward Mars. Everything went swimmingly for the launch, but the probe failed to activate those second phase engines. Now it’s stalled in Earth orbit, circling the planet as though it can’t find the on-ramp to the freeway.

Russian scientists are frantically working to reestablish communication with the probe. It’s seemingly intact and its fuel tanks are full and ready to complete the journey. Russia would like nothing more than to reboot the probe and send it on it way, but Phobos-Grunt is not taking their calls.

With the window to set the wayward spacecraft back on track narrowing, what you should really be asking yourself is how and where Phobos-Grunt will land, should it fall back to Earth. Because it was suited up to go all the way to Mars and back, most of the probe’s 15-ton mass is composed of fuel, which would allegedly burn up upon reentry (probably generating an impressive fireball for anyone watching). But if any of the rocket fuel does reach the ground it’s not very reassuring to know that it’s composed of toxic hydrazine. Plus there’s still the possibility of probe shards to contend with. Early projections of likely landing sights included “most of the U.S., part of Europe, all of Africa and Australia and virtually all of South America and Asia”, which pretty much translates into “somewhere on Earth”.

Before you start accusing Russia of imperiling us all, I should mention that Phobos-Grunt is poised to be the third uncontrolled spacecraft reentry this season. NASA’s UARS satellite crashed into (probably) the Pacific Ocean on September 24, and just a month later, Germany’s ROSAT came down somewhere in Southeast Asia on October 23. ‡

Coincidentally, Phobus-Grunt was launched on the same day our planet had its much-publicized near miss with the asteroid 2005 YU55. The 400-meter (1,300-foot) diameter asteroid got within about 200,000 miles of Earth (which is closer than our moon, FYI). § The last time a huge asteroid got uncomfortably close to us was in 1976, so this isn’t exactly a once-in-a-lifetime occurrence. According to the Washington Post, NASA spends 5 million dollars annually keeping an eye out for asteroids capable of, you know, killing everything on the planet. (None scheduled for the near future, in case you’re wondering.)

So are you more likely to get hit by a satellite or an asteroid? Ugh, that question has far too many variables. Any satellite or asteroid? A specific one? Any person on earth or just you? I can tell you this much, apparently your odds of being killed by an asteroid are greater than the odds of being struck by one. And, if it’s any consolation, in all the years our species has been lobbing metal into outer space, only one person has ever been hit by the stuff on its return. That person was Lottie Williams of Tusla, Oklahoma, who in 1997 was clocked on the shoulder by a chunk of the Delta II rocket. She was fine.

* Russia being my place of birth, I use this excuse annually when presenting cards and gifts well after the western version of “the holiday season” is over.

† Hence the probe’s name. “Grunt” translates into soil. (It’s pronounced groont by the way.)

‡ ROSAT’s plunge was particularly threatening because it had primarily functioned as a telescope and, as such, was equipped with massive (over 1.5 tons total), and very heat-resistant mirrors – exactly the kind of thing you don’t want falling on your house… or your head.

§ If 400 meters sounds like an abstract and unimpressive figure to you, then you might prefer Purdue University professor Jay Melosh’s description of its potential impact, “If a space rock the size of 2005 YU55 ever hit Earth, it would explode like 500 nuclear bombs, trigger a 7.0 magnitude earthquake and, if it splashed down in the ocean, generate a 70-foot tsunami.”

Got a fever? Best to cool it on the pills.

Thermometer by Andres Rueda, pills by Tyler Sparks, collaging by yours truly.

It’s time to wake up and smell the cough syrup, people; cold and flu season is here.* Soon everyone you know will be hacking and sneezing and generally assaulting you with their horrible germs. Illness is inevitable. You will get sick. And what to do then? If you’re like me, you probably gave up on store bought cold remedies ages ago. What’s the point? They merely suppress symptoms in exchange for other side effects. All you need to battle a run-of-the-mill virus is rest, fluids and maybe some over-the-counter pain reliever (Advil or Tylenol or the like) to reduce the fever, which is really the bulk of what’s making you feel so crappy. Right? After all, blowing your nose is just inconvenient, while a fever is incapacitating.

Well, you may want to reconsider even such modest medicating, because fever does more than just make you miserable, it also restores your health. This isn’t exactly news. It’s well known that an increase in body temperature can slow down bacteria and other microscopic invaders while the immune system mobilizes against them. Fever can even help accelerate the clearing of the parasite that causes malaria. In addition to thwarting cooties, fever can also improve the body’s pathogen fighting mechanisms. A recent study in the Journal of Leukocyte Biology found that a 2 degree centigrade increase in body temperature in mice resulted in improved differentiation of the lymphocyte CD8+ T – one of the cells involved in the immune response to viruses. While it may be detrimental to your performance of normal daily tasks (like staying awake and sitting upright), a fever actually makes your immune system more efficient.

So why are we still so quick to swallow fever-reducing pills? Certainly part of it is comfort (nobody likes feeling awful), but another problem is the perception the fevers are dangerous. While fever can be a part of serious illness, many high fevers result from minor ailments (and conversely, serious illness may present with only a mild fever). 103°F is a figure frequently given as an appropriate panic point (i.e., when call a doctor). But haven’t you had a 104° fever at some point in your life and not sought medical attention? And you were fine, right? The fever didn’t keep rising exponentially until it broke the thermometer and literally cooked your brain? Same here. The reason for concern over high fevers has more to do with possible complications of elevated body temperature than the fever itself. Dehydration, seizures – these are issues that might benefit from the presence of health care professionals.

“But can’t a fever be life-threatening?” you ask, “I’m sure I saw it on television once.” You are perhaps confusing cold/flu-induced fevers with something like heatstroke. Heatstroke occurs when the body has been pushed by strenuous exercise and ridiculously hot weather (think football practice in August) to the point where standard mechanisms for thermoregulation (sweating, dilating blood vessels, etc.) aren’t doing the trick anymore. The individual’s temperature rises not as defensive response to pathogens, but because the body has lost control of its internal environment. It’s potentially fatal, and gives one a sense of what reptiles have to worry about daily.

And while we’re empathizing with snakes and lizards, it’s worth noting that ectothermic animals (often described as “cold-blooded”†) also respond to infection with fever. How? While they can’t regulate their body temperatures internally like we do, reptiles can raise or lower their temperature behaviorally – for instance, by choosing a sunnier or shadier rock to lounge on. Research has shown that reptiles injected with bacteria will aim for a slightly higher temperature than non-infected control animals. Basically, when lizards get the sniffles, they cope with a behaviorally-induced fever rather than a bottle of ibuprofen.

The fact that even reptiles exhibit a fever response tells us that it’s a pretty old strategy for fighting infection. It’s certainly been around longer than NyQuil, echinacea, and chicken soup. While nothing cures the common cold, toughing out one its more uncomfortable symptoms is more likely to speed the healing process than your favorite home remedy.

Does this mean you have to forgo the pills entirely? Hey, I’m not your mom. Do whatever you like. There are plenty of good reasons for attempting to pull yourself together for a few hours despite being sick (birthdays, rock concerts, possibly even jobs). You just need to accept that you’re in for a certain volume of misery regardless. The only real decision is whether to spread the suffering out over more days, or just get it over with already.

* Well, at least here on the northern side of the Equator. I’m guessing that might not be the case elsewhere. Feel free to tune this one out for now, Southern Hemisphere.

† Their blood isn’t actually cold, they just have to stay warm behaviorally (by basking in the sun and that sort of thing) rather than with the fancy metabolic tricks of endotherms like ourselves.

Get Your Fats Straight

Image Credit: Dawn Huczek

Last week, in an attempt to curb obesity rates and their related health complications, Denmark rolled out what quickly became dubbed the “fat tax” – a price hike targeting foods specifically by saturated fat content. Critics of the tax – and there are many – are taking aim from several directions, including social inequity, the uncertain efficacy of sin taxes in general, and the singling out of saturated fats over other dietary dangers (processed foods, refined sugars etc.). But throughout the reports and editorials, terms like “saturated fats” and “fatty foods” have been used almost interchangeably, as though there were no other fats in existence besides saturated ones. Denmark’s new food rules aren’t the only sign of triglyceride confusion. In my workplace on the other side of the Atlantic, a jar of reduced fat peanut butter has been loitering in the break room for months. Part of a coworker’s good intentioned but misguided attempt to eat healthier, the odious product is another reminder that we could all use a refresher course on our metabolic macromolecules.

Some fats are better than others

Let’s travel back in time (figuratively at least) to high school biology, where we learned that the structure of fats involves fatty acid chains, each composed of a long carbon skeleton decorated by a bunch of hydrogen atoms. The hydrogen to carbon ratio is what makes fats different both in physical form and nutritional function. If the carbons on the skeleton are all single-bonded to one another, this allows for the maximum number of hydrogens to be attached to the chain. The resulting fats are called saturated because the carbon chain is holding as much hydrogen as it can fit. Saturated fats (found mostly in foods from animal sources, such as butter) are solid at room temperature, which makes them desirable ingredient for sandwiches, baked goods, etc. Unfortunately, they have also been widely linked to cardiovascular problems like atherosclerosis. Unsaturated fats, on the other hand, are one or more hydrogens short of a full set. This occurs because at least one pair of carbons in the skeleton is double-bonded. These double bonds create fatty acid chains that have kinks in them. They can’t pack together as tightly as the straight chains of saturated fats and are thus usually liquid at room temperature. Rounding out the list of contrasts, unsaturated fats (found in foods like vegetable oils, nuts and fish) are linked to health benefits, such the lowering of bad (LDL) cholesterol.

This would be easy enough to keep straight if the food industry hadn’t come up with the idea of turning liquid vegetable oils into solid fats by “hydrogenation”, a process that breaks those carbon double bonds and sticks more hydrogens on there. In the best-case scenario, the fatty acid is fully hydrogenated and the consumer is rewarded with a product whose higher saturated fat content renders it solid enough to be applied to toast. But if unsaturated fats are only partially hydrogenated, the process can warp the stereochemistry on any remaining carbon double bonds and the dreaded trans fat is born.* In short, “unsaturated” means safe, whereas “saturated”, “hydrogenated” and “partially hydrogenated” means varying degrees of scary.

Reduced fat peanut butter: the devil’s lunch spread

So what’s so bad about reduced fat peanut butter? Given all the other unhealthy atrocities lurking in your local supermarket – chocolate-covered Oreos, frozen chicken pot pies, 2-liter jugs of soda the color of antifreeze – it may seem odd to single out reduced fat peanut butter for nutritional derision. But what is especially evil about this product is that it takes something that is initially healthy (peanuts are naturally low in saturated fat and high in unsaturated fat) and defiles it with a host of questionable ingredients that render it less so, which is then advertised as an improvement.

And then there's portion size...  Image Credit: Dan McKay

Ideally everyone would wise up and purchase plain, unadulterated peanut butter such as the reasonably affordable Central Market store brand I’m using as a reference point. It contains a single ingredient: peanuts. Pulverized peanuts serve up 190 calories, and 16 grams of fat per 2 tablespoon serving (which is more than enough to make a sandwich).

Because the oil in pure peanut butter tends to separate out after it’s packaged and apparently some people find stirring to be a task too daunting to undertake, many national brands add a dash of hydrogenated vegetable oil to keep things all homogenized. They also add sugar. Go figure.

Sugared and hydrogenated peanut butter is already not great, but let’s have a look at the ingredients of reduced fat Skippy (they own the domain name “peanutbutter.com”, so it seems only fair to pick on their brand): roasted peanuts, corn syrup solids, sugar, soy protein, salt, hydrogenated vegetable oils (cottonseed, soybean and rapeseed), mono and diglycerides, minerals (magnesium oxide, zinc oxide, ferric orthophosphate, copper sulfate) vitamins (Niacinamide, pyridoxine hydrochloride, folic acid).

Oh, peanut butter, what have they done to you? To break things down a bit, many of the additional names are vitamins and minerals (strangely absent from the original Skippy product and not touted on the reduced fat version label). The remainder are additional texturizers and emulsifiers (if you’re going to take out peanuts, you’ve got to fill out the space with something) and even more sweetener, this time in the form of corn syrup solids, the second ingredient, sandwiched between peanuts and sugar. The resulting mess weighs in at 180 calories and 12 grams of fat per serving.

So reduced fat peanut butter shaves of 4 grams of fat (an underwhelming 25%) and 10 calories (pfff) and replaces it with increased sweeteners and fillers. Oh, and they throw in a secret multivitamin pill for your trouble.

What brings this to the level of absurdity is that reduced fat peanut butter is marketed toward those trying to control their weight. However nuts, though high in fat, have been linked to weight loss rather than gain as well as an array of other health benefits.

Something rotten in the state of Denmark

Image Credit: Bryan Ochalla.

Now while replacing unsaturated fats with processed sweeteners is a terrible idea, lowering saturated fat consumption is, in theory, a good one. That’s why, when I first heard about Denmark’s tax on saturated fats, I was totally ready to be on board. Sure, I said, make such foods more expensive and they will be used only as luxury items. Daily staples like butter and cheese will be saved for special occasions and replaced with foods high in healthy fats like olive oil and nuts. But it turns out to be a bit more complicated. The specific form of the Danish tax, as reported in the press, is a price increase equivalent to just under $3 (16 Kroner to be exact) per kg of saturated fat, and affects those foods whose saturated fat content exceeds 2.3%.

That 2.3% struck me as a bit low. While vegetable source fats are generally much lower in saturated fats than their animal derived counterparts, they are not completely absent of such fats. And with something like cooking oil, the calorie content comes exclusively from fat (as opposed to proteins or carbohydrates). A trip to the kitchen and some basic math revealed that both my preferred oils – olive and sesame – were comprised of 15% saturated fat.† But these are not unhealthy foods. The remaining 85 percent of their caloric make-up comes from a mixture of mono and poly-unsaturated fats (remember, unsaturated fats are linked to health benefits).

Where did this 2.3% cut-off come from? It seems so precise and yet so arbitrary. I seriously considered that it might be a typo, the intended figure being 23%. But no, every article thorough enough to report a percentage stated it as 2.3%. If Denmark’s tax is rigidly enforced, many foods considered to be healthful would also be subject to the price increase. Nutritious foods like walnuts and avocados would be too high in saturated fat to make the cut. Yet the okay list would include Cracker Jacks (too few peanuts to tip the scales) pretzels, and gummy bears (as well as every other fat-free candy out there). Considering that a healthy diet should contain some fat (20-35 percent of total daily caloric intake is the usual recommendation) that 2.3% limit seems illogically restrictive – an attempt to cut out not just saturated fat, but all fat.

While obesity is, in part, a problem of too much energy in and not enough out (i.e. lots of calories and little exercise), diseases associated with it are also influenced by the kind of calories input. One would think that the idea behind a tax aimed at saturated fat would be to encourage replacing foods high in saturated fats with those containing mostly unsaturated fats. But if even “good fats” are included in the tax, people might reach for other options. Some may reach for fruits and vegetables (though not avocados, it seems) but others may just follow the example of Skippy’s reduced fat products and replace fat with sugar. Perhaps I’m missing something. Denmark is welcome to check my math ^‡ but for now I’m just going to go ahead and declare this tax almost as stupid as reduced fat peanut butter, which, by the way, is still too high in saturated fat to escape Danish taxation.

* You probably recall cis/trans isomers more from Chemistry class. It’s about the carbon-to-carbon double bond again and how atoms and molecules can end up on the same or opposite sides of that bond. In this example, both hydrogens on the same side yields a cis fatty acid, whereas hydrogens on opposite sides yields a trans fatty acid. The two isomers have different properties. Long story short, trans fat are bad for you. Very, very bad.

† As butter contains over 60% saturate fat, 15% is relatively low.

‡ Formula: (Grams of fat per serving)(9 [the calorie content of 1 gram of fat])/total calories per serving = percent fat, expressed as a decimal.

For instance olive oil: (2 grams saturated fat)(9 calories/gram)/120 calories = 0.15 = 15%

What’s Listeria?

Image Credit: Clay Irving.

By now you’ve surely heard about the latest food-borne illness freak-out: cantaloupes contaminated by Listeria monocytogenes. Originating in Colorado’s Jensen Farms, the fruits have already caused 72 illnesses and 13 deaths in a total of 18 U.S. states. And those are just the numbers as of this writing, they’ll probably be higher by the time you read this. For reasons that I’ll explain momentarily, cases are expected to keep rising for some time.

Listeria doesn’t make headlines very often. Usually it’s the more familiar pathogens E. Coli and Salmonella that are responsible for outbreaks of food poisoning. As with these more famous cooties, Listeria is a bacterium with a propensity for turning up in animal feces (though it can also be found in soil), which then comes in contact with our food. But it has a few additional qualities that distinguish it from our friends E. Coli and Salmonella. For one thing, Listeria can reproduce in colder conditions, rendering it unfazed by all our fancy refrigeration technology. A dash of Listeria on a cantaloupe (or on the cheese or cold cuts that more typically serve as its intermediate home*) will gleefully multiply into a teeming hoard of bacteria without ever being improperly stored.

Another important difference is the Listeria bacterium’s lengthy incubation period in the gut of its human host. It can take several weeks for someone who ingested the microorganisms to manifest symptoms of Listeriosis – the actual illness caused by Listeria. The good news is that most people who eat Listeria-tainted food won’t get this malady; a healthy immune system generally destroys these pathogens before they have a chance to do any real damage. But in those with weaker internal defenses – older adults, pregnant women (and their newborn babies) and anyone with a compromised immune system – Listeria can escape the intestinal tract and cause serious illness. Symptoms include fever, muscle aches and diarrhea, but life-threatening complications like meningitis can also occur.

Given that the initial symptoms of Listeriosis are best described as “flu like”, we’re ensured an extra special flu season this year, as every under-the-weather individual with recollections of cantaloupe consumption rushes to the ER. Not that they shouldn’t. Listeria may not account for many food-borne disease outbreaks, but when it does cause illness, the fatalities are high, even when treated with antibiotics. When dealing with E. Coli and Salmonella, we’re accustomed to hearing figures in which hundreds or thousands of people are sickened but only a handful die. Listeriosis, on the other hand, can be fatal in as many as 25% of cases. If I’m doing my math correctly, this current outbreak is at about 18%. Pretty scary.

The textured rind of a cantaloupe. Image Credit: Bruno Girin.

And what can you do to protect yourself from killer cantaloupe? Clearly peeling it doesn’t do the trick. The trouble with produce of this sort is specifically that it does have a thick rind. People tend to view it as safe and forgo the more thorough washing they would give to something like lettuce. I’ve been scrubbing fruits with peels for ages (except bananas, one has to draw the line somewhere) and others in the kitchen act like I’m insane. But as I’ve explained again and again, the peel touches things that touch other things that end up in your mouth. It touches the knife that slices through the rind and right into the fruity center, it touches the plate onto which you place the sliced fruit, it touches your hands. Ugh, cooties everywhere! Just wash your fruit, okay. And if you fall into any of the high risk groups mentioned above, I’d recommend also having a look at the CDC’s prevention page for Listeria for a complete list of foodstuffs to avoid. It’s a pathogenic world out there.

* This is the first case of Listeria being found on cantaloupe.

Why Florida should stick to cats and dogs

As someone who spends a lot of time researching animals, I’ve read my share of articles on invasive species and I’ve noticed a certain pattern. In peer-reviewed journals and Cracked top-10 lists alike one word comes up again and again: Florida. I’ve been speculating as much for ages and now scientific research has confirmed that Florida does, in fact, have the worst invasive reptile and amphibian problem on the entire planet.

A recent study published in the journal Zootaxa after almost two decades of critter cataloging came up with a startling total of 137 introduced herpetofauna (a fancy, though also easier to type, word for retiles and amphibians) lurking in Florida’s great outdoors. An additional 3 species were intercepted before they could get too comfortable. Of the 137 outdoor dwelling herpetofauna, 56 are “established”, meaning they’re reproducing and, in many cases, pretty much taking over the place.

How did all these non-native beasties end up in the wild? The study examined animal introduction incidents in the Sunshine State from 1863 through 2010 and found that for the first half of the timeline, invasive species mostly trickled in as accidental stowaways on cargo ships, much like Guam’s infamous brown tree snake. But once the exotic pet trade took off in the latter 20^th century, things got a lot messier. Whether the animals got outside through stealth or by owner abandonment – some of these animals prove to be far higher maintenance than their owners anticipated – the pet trade ultimately accounted for 125 (about 84%) of the 137 species described in the study.

Part of the problem is Florida’s laws regarding such pets. While it is illegal in the state to release non-native animals into the wild without a permit, this is obviously not the easiest law to enforce. The authors of the study stress the importance of creating better legislation to prevent further species introduction. Personally, if I were running the show in Florida, I would just go ahead and immediately ban the acquisition of any new exotic pets. It’s just too accommodating of a climate for fugitive herpetofauna. The warm, humid weather, the luxurious tree coverage, the abundant insects… it’s ectotherm paradise. Ironically, some colder states like New York, where delicate exotic pets would freeze to death or get run over by a taxi within an hour of their escape into the world, have stricter laws about animal ownership.

Some of Florida’s more well-publicized invasive herpetofauna include the Burmese python, which grows to an average of 12 feet in length and can strangle prey as large as an alligator, and the Nile monitor – a muscular 6-foot long lizard with alarming sharp teeth and claws, not to mention its formidable swimming, climbing and running abilities. It is lizards that comprise most of the troublesome species plaguing Florida – 43 of 56 established invaders (and the state only has 16 native lizard species). While viewed by many people with less dread than snakes, lizards can be the more destructive of the two reptiles, devouring both plants and animals and compromising manmade structures with their incessant burrowing.

The charming Nile monitor. Image Credit: Chris Eason

The study’s authors begin by noting that, “Introduced species are second in negative effects only to human-mediated effects on native species, habitats, and whole ecosystems.” It’s a reminder that for all the accidental monsters visited upon the native flora and fauna of Florida, the biggest problems are ultimately created by the same invasive species that has caused widespread damage to so many other parts of the world – Homo sapiens.

Advice from mice, trade in your weekend benders for moderate daily tippling

Image Credit: Daniel Farrell.

Is consuming alcohol good for you or bad for you? The research often seems contradictory. Drinking is linked to health benefits one day and ghastly diseases the next. Amount of alcohol consumed seems to be one predictor of relative help or harm, but how much is too much? For example, is 14 drinks per week a lot or a little? Before you answer that question, you may want to ask about when (and how often) those drinks are being drunk, as patterns of drinking may play as large a role in determining how alcohol affects health as the actual amount consumed. To better understand the relationship between drinking and cardiovascular disease, University of Rochester scientists recently spent a month sousing up mice and found that different drinking schedules yielded very different health impacts.*

The advantage of working with mice is that, unlike human subjects who tend to choose when and how much to drink, alcohol consumption of experimental rodents is determined solely by their lab-coated bartenders. The mice were thus divided into three groups. A “daily-moderate” group received the mousey equivalent of two drinks per day seven days a week, while a “weekend-binge” group were instead assigned seven rodent-sized cocktails in a sitting, but on only two days each week.† A control group of teetotalling mice received a non-alcoholic cornstarch mixture (in order to match the caloric intake of the boozers). Additionally, all three groups were subjected to an “atherogenic diet” a high calorie, high fat menu designed to induce atherosclerosis – a thickening or “hardening” of the walls of the arteries caused by fatty deposits, which impedes blood flow and potentially leads to heart attacks and strokes. Essentially, they ate like average Americans.

While the daily-moderate mice consumed the same total amount of alcohol per week as the weekend-binge group (and ate the same unhealthy meals), their bodies fared considerably better. Mice in the moderate group actually emerged with healthier blood vessels than those in the non-drinking control group on the same diet, with 40% less build-up of plaque on their arteries. Meanwhile, the binge group had pretty dismal numbers with a 60% increase in arterial plaque build-up compared to the control mice.

The binge-drinking mice not only sustained more damage to their arteries, they also got the fattest. While all three groups were fed the same junk food diets, changes in body weight varied with different alcohol intake schedules. Over the course of 4 weeks, non-alcoholic control mice increased in mass by about 8.5%, while the moderate-daily-drinking mice only increased by about 5%, a modest improvement. The binge drinkers, however, gained double the weight of the control group and more than triple that of the moderate drinking mice, adding a mighty 17.5% to their initial body weight.

How can the same amount of alcohol protect the cardiovascular health (and figures) of the daily drinkers while doing so much damage to the bingers? While exact mechanisms of action are yet undetermined, part of the difference lies in how the two patterns affect cholesterol in the blood. While both groups of boozing mice experienced an increase in HDL (the “good cholesterol” associated with removing build-up from arterial walls) their drinking regimens produced opposite effects in LDL levels (“bad cholesterol” that can cause build-up). Relative to the control group, the daily-moderate group showed a 40% decrease in LDL while the unfortunate binge group experienced a 20% increase in LDL.

Alcohol metabolism itself differs in moderate versus binge drinking episodes. While much to-do has been made over demon alcohol, its metabolite acetaldehyde is the more damaging molecule. When alcohol is consumed, the body breaks it down so that it can be removed. It’s a two-step process, first to acetaldehyde and then to acetate (a nontoxic chemical similar to vinegar). This is all fine and well except that the supplies needed to do the second step (breaking down nasty acetaldehyde into benign acetate) run out after a few drinks worth of metabolizing. So with binge drinking, acetaldehyde hangs around causing problems until the materials required to deal with it can be replenished.‡

Of course cardiovascular disease isn’t the only health concern out there. This study does not aim to address the overall effect of drinking patterns on all systems in the body. But it’s information worth noting for those who believe that abstaining from alcohol during the week is sufficient to balance out weekend bacchanalian excesses. That and it might be a good idea to lay off the cheese fries.

* The study will be published in a forthcoming issue of the journal Atherosclerosis. If you’re too impatient to wait for it, you can download the accepted manuscript in all its unformatted, un-copyedited majesty.

† The blood alcohol levels attained by moderate vs. binge drinking mice were roughly 0.07% and 0.23% respectively. This placed the moderate daily drinkers at a level where they could still legally drive in most U.S. states….if they weren’t mice, that is.

‡  Lingering acetaldehyde is also a major contributor to hangovers.

The Evil Genuis of Toxoplasma

Image Credit: Rosa Pomar.

Just when you thought it was safe to clean the cat box, Toxoplasma gondii is back in the news. In the August 17^th issue of the journal PLoS One, scientists reported the latest creepy details about how the Machiavellian parasite tricks host organisms into doing its bidding.

For those unfamiliar with the brilliant and disgusting life cycle of Toxoplasma gondii – the microorganism that causes the disease toxoplasmosis – a brief review (feel free to skip to the next paragraph if you already know this)….

Toxoplasma is a single-celled protozoan with both sexual and asexual phases of reproduction. The sexual phase occurs in one place only – the small intestine of a cat. Here’s how it works: after the micro-sex act, the resulting oocysts make their way into the world in the form of cat feces. There they sporulate for a few days until they’re ready to infect the intermediate host (such as a rat). The rat eats the cat feces, which allows the parasite to complete its last phase of asexual development before lodging itself into the host’s brain or muscle tissue. Then it just hangs out there as a cyst until the host is eaten by a cat and ferried to the feline digestive tract, where a circle of life begins anew.

Getting rats to eat cat shit is no problem; they’ll eat anything. But convincing them to offer themselves up at cat treats is a bit more challenging. Healthy rats have an innate fear of cats, and typically run in the opposite direction the moment they detect catty smells. This is evolutionarily advantageous for rats since cats tend to view them as food. But rats infected with Toxoplasma lose their cat-avoidance instincts. Past experiments exposing normal and Toxoplasma -infected rats to cat urine found that the parasite-carrying rodents not only didn’t show a fear response, they actually seemed somewhat intrigued by the odor of cat pee. Somehow the parasite had tampered with these rats’ brains and was causing them to recklessly place themselves in harm's way, thus ensuring that the parasite-harboring rodents would find their way into a cat’s belly. Curiosity kills the rat.

Image Credit: Luke Hayfield.

In the latest study, researchers showed that infected rats had abnormal responses not just in their behavior, but in subregions of the amygdala – a part of the brain associated with emotions, including both fear and attraction. While healthy rats encountering the smell of cat urine showed more activity in the fear pathway of the amygdala, the Toxoplasma-infected rats also had responses in the attraction pathway. Their brains lit up in pattern more like that of a rat confronted with a potential mate than a potential predator.

While Toxoplasma that make their way into neural tissue do often land in the amygdala, the method by which they confuse its emotional pathways is still unknown. But the behavioral results suggest that the seemingly dormant cysts are turning prudent fear into foolhardy interest. Also rather telling is the observation that infected rats display normal behavior in other situations, even those involving non-feline predators. It would seem that Toxoplasma has no interest in finding its way to the intestine of an eagle or a snake. Just cats please.

So what? Too bad for the rats, you may say, but humans too can harbor Toxoplasma. While most of us don’t go out of our way to eat cat crap, our species can become infected with the parasite through ingesting undercooked meat (remember, the cysts can also end up in muscle tissue) or by just not washing our hands well enough after cleaning the cat box. Once the parasites enter our bodies, they linger just like they do in rodents. Infection rates vary considerably by region, but up to a third of the human population carries the parasite.* Toxoplasmosis is generally mild in otherwise healthy humans, causing little or no symptoms; you might get some flu-ish aches and pains, but that’s about it. However in it can be life-threatening for anyone with a weakened immune system.

But for the healthy, asymptomatic hosts of the parasite, is there anything to be concerned about? Humans have amygdalas too, which can house parasitic cysts just like those of rats. What might Toxoplasma be up to in our brains? Researchers have been increasingly drawn to this question. Studies have linked Toxoplasma in humans to a variety of behavioral changes, cultural differences (since infection rates vary from one country to the next) and even schizophrenia. Such research is hardly at the point of being universally accepted, but it is suggestive of the possibility that toxoplasmosis may not be as asymptomatic as we’ve been led to believe. Perhaps the symptoms are just more psychological than physical. Perhaps Toxoplasma is subtly affecting our behavior in ways that haven’t even occurred to science. I’m not saying that the parasite is causing people to live alone with upwards of ten cats so that it might one day be able to reproduce if, say, the cat owner dies and the pets start eating the body before anyone discovers it.† But we can’t rule it out.

* Before you lock yourself in the house with a box of sani-wipes, please recall that the parasite only reproduces in cats, so you can’t get it from ordinary human contact. However, the disease can be passed from a pregnant mother to her child, or (though this is quite rare) via organ transplants or blood transfusions.

† For a more thorough exploration of “postmortem predation”, have a look at The Straight Dope, where no question is too obscure or too gross to be answered.

Crazy From The Heat: The Crime-Temperature Connection

Image Credit: Julius Schorzman

 

In just a few days I’ll be vacating my overpriced studio apartment in Austin’s tree-lined Hyde Park area and moving to the ‘hood (aka, the east, east side). 

 

In the typical hailstorm of calamity that precedes a move, the house in which I’ll soon be hanging my hat was broken into a week ago and we’re currently in the process of, uh, upgrading security a bit.

And then there’s the weather. The temperatures in Austin have been hitting record highs all summer and are intensifying this week in apparent anticipation of my impending move. We’ve opted to do most of the heavy lifting Saturday evening when the sun should be slightly less blazing. Still, it is guaranteed to suck.

This means two things for you the reader, 1) I don’t have time to write one of my longer, more researched pieces right now and 2) I’m currently obsessed with a the dual waves of heat and crime. So naturally this article in Wired about the possible link between hot weather and violent crime caught my eye.

Anecdotal evidence and much of Spike Lee’s oeuvre seems to bear out a connection between hot days and aggression. I mean, who among us hasn’t thrown a malfunctioning electric fan across the room at some point in their lives? But is there any data supporting such a correlation, or any reason to believe that thing one causes the other?

The Wired article discusses a study conducted by Ellen Cohn and James Rotton, psychologists at Florida State University, examining assault rates over a two-year period in Minneapolis, Minnesota. I’m guessing they were referring to this study, yet for some reason they linked to this other study by the same authors, which deals with property crime during the same period in the same city (also interesting, given my recent break-in issues, but let’s stick with assault for the moment).

Cohn and Rotton reported several noteworthy observations.

1) Assault rates were higher in summer than in winter.

2) Assault rates were higher at night than during the day. (Remember this detail, as it will become important in a minute.)

3) Overall assault rates initially rose with temperature, but as the mercury neared 80F, such crimes leveled off and even decreased.

This last point runs contrary to our expectations that things continue to get worse as heat and heat-related frustrations rise. Perhaps people were just too exhausted from the heat to pick a fight?

But you don’t have accept Cohn and Rotton’s interpretation of their own data, because another group of psychologists – Brad Bushman, Morgan Wang, and Craig Anderson – also had a go at it. They concluded that the original study failed to properly consider time of day. The major issue is that both crime rate and temperature vary with time of day, but in opposite directions. Crime is higher at night, while temperature is higher during the day. So things seem to level off after 80F because it’s usually not that hot in Minneapolis by midnight (excluding July 2011, of course). When focusing on the data specifically between the angry hours of 9pm and 3am, there is no fall off and assault rates continue to rise as the nights get hotter.

And what about that study on property crime, (a reasonable concern for those of us about to relocated our earthly belongings to a part of town where folks kick in doors with some regularity)? Once again weather is a factor (more break-ins in summer, with rates rising according to temperature), but so is time of day (more break-ins at night).

It’s a lot of information to process with July temperatures melting one’s fragile brain. It has also been suggested that weather affects crime rates not as much by pissing people off, but by driving them outdoors in the first place, where they are more likely to encounter each other and the poorly lit back door of your house. It’s too cold for crime in January. Property crimes in particular are often opportunistic, which requires that the individuals committing them venture outside to find said opportunities.

As is often the case, more research on the subject would be needed to understand any psychological causes behind the correlations. For now, a freshly installed metal door will be welcoming me to the neighborhood.

The Trouble With Sprouts

Image Credit: Jessica Reeder

Remember the carefree days when you thought you only had to worry about E. coli if you were eating hamburgers? Good times those were. The salad days. Well, after weeks of media speculation around the possible involvement of sprouts in Europe’s E. coli outbreak,* I’ve finally accepted what health officials have been saying for some time; sprouts – like raw fish and un-pasteurized milk – are a high-risk food. It’s been an unhappy realization. I love sprouts. They are awesome on everything; salads, sandwiches, breakfast tacos. But they are dangerous, more dangerous it turns out than other raw vegetables, such as the cucumbers that were originally blamed (but later exonerated) for this recent spell of food-borne illness.

Some Numbers For You:

According to the FDA, at least 30 outbreaks of food poisoning in the U.S. since 1996 have been linked to sprouts.† And those are just outbreaks – large scale incidents in which enough people get sick from the same foodstuffs to have any chance of tracing the illness to its source. But only 5% of food poisoning cases are associated with outbreaks, while the remaining 95% fall under the heading of “sporadic” cases in which only one or two people develop symptoms severe enough to report and the cause is never isolated as anything more specific than “something I ate…”

One of the worst E. coli outbreaks in recent history occurred in Japan in 1996. At least 10,000 people fell ill. The culprit? Tainted radish sprouts.

How Good Food Goes Bad

We’re all familiar enough with stories in which raw meat, which usually gets the cooties cooked out of it, contaminates raw vegetables that don’t receive the same protective heat sterilization. It’s why we keep raw chicken far from the salad bowl and thoroughly wash any cutlery than comes into contact with it. Contamination, of course, isn’t isolated to kitchens; it can also occur during various stages of agricultural production. But why should sprouts be any different from the other components of a salad? 

Image Credit: Little Blue Hen

Part of the problem is in how they are grown. Sprouts start as seeds, like other vegetables. However, instead of being planted in the ground, these seed are soaked in water and grown indoors in a warm, humid space. These are coincidentally the same conditions that favor bacterial growth. Under such optimal circumstances, even a single E. coli bacterium on a single seed can multiply into millions of disease-causing microorganisms, infecting an entire batch of delicious sprouts.

But how do the seeds get contaminated in the first place? Here we return to the same problem that causes the more familiar undercooked-hamburger-induced food poisoning – animals, namely cows. E. coli bacteria live in the intestinal tracts of these mammals and often find their way into food through the ubiquitous medium of cow crap. Cows are everywhere. Try as you might to keep the animals on one side of the farm and the plants on the other, run off from cattle is a constant threat to vegetable hygiene.

Making matters worse, cow manure is sometimes used as fertilizer. Call me an ignorant city person (you’d be right), but this does not sound like a good idea for growing any produce that might be consumed raw. Sprout seeds can also be contaminated by the water used to irrigate them (again, cow crap runoff). And, further down the line, they can pick up bacteria in the harvesting and shipping process. Remember, it only takes a teensy bit of bacteria tracked in areas containing meat or manure to multiply into an enormous problem once the sprouting commences.

Can Anything Be Done?

There’s a lot working against the production of pathogen-free sprouts. Even if they are grown on a farm that houses no livestock and uses no animal-derived fertilizer, sprout seeds may already have picked up enough harmful microorganisms to doom a truckload of produce. Seeds can be treated with a germ-killing chlorine solution before sprouting, but this is a recommendation rather than a requirement. Additionally, not everyone wants their produce soaked in nasty chemicals. Spouts and other vegetables are also tested for pathogens (as is meat), but clearly this process doesn’t catch every instance of bacterial contamination.

Further adding to the “you’re screwed” factor is the knowledge that the FDA currently only considers one strain of E. coli to be worthy of a recall – O157:H7, the bug responsible for the notorious 1993 Jack in the Box food poisoning fiasco.‡ This is not the same contaminant implicated in the current European outbreak. That honor goes to E. coli O104:H4, which is similarly deadly but rarer and hasn’t yet caused a high-profile poisoning in the U.S. Therefore the FDA does not mandate recalls if it should be found in U.S. food. No flaws in that perfect logic, right?

Editorial Tangent

So basically, sprouts are a scary biohazard but they’ve come to be this way largely as a result of our planet’s insistence on consuming enormous quantities of animal products. In my utopian society, in which livestock farming would account for a fraction of the food supply and be kept a good distance from plant-based agriculture, sprouts would be mostly safe (nothing in life is 100% safe, so you’ll have to live with some level of uncertainty).

I was aiming to avoid a lot of editorializing here about the issue of meat consumption, but while doing my research I ran into a Huffington Post piece ostensibly discussing the risks of eating sprouts and what might be done about them. The author writes,

Many people who love sprouts seem to be in denial, touting their taste and health benefits, and as I have learned in writing about the subject, they are having difficulty understanding the real risk.

Fine, but then he goes on to say,

But attacking the meat industry is not likely to solve the problem. We are not going to be able to ban meat or significantly reduce consumption. People love to eat meat and will not likely give it up in significant numbers. In fact, the trend is going the other way as meat consumption is rising around the world.

Really? So consumers of vegetables should take a good, hard look at their eating habits and wake up to reality, but meat eaters should continue full steam ahead in denial of the negative impact over-consumption of animal products can have on their bodies and, more importantly, the planet? Because people like meat?

I’m unmoved by this lazy, pessimistic reasoning. People have been fond of a lot of stupid and dangerous things over the years and we still try to dissuade them rather than throwing our hands up and saying, “What can we do? People like ______ (fill in the unhealthy habit of your choice).” And, yes, completely eliminating meat is unlikely and probably even unnecessarily rigid. But reducing consumption should be a priority.§

This summer’s headline-grabbing story of high fatality food poisoning seems to be subsiding, but the threat of a replay lingers. If the cause of the illness was sprouts and if these sprouts were contaminated with E. coli as seeds (the prime suspect is currently fenugreek seeds grown in Egypt) then those seeds are still out there, waiting to be sprouted. And our modern system of agriculture is convoluted enough (additional rant about factory farming averted) to make tracking them down pretty impossible. The best guess as to when Europe will be safe from this particular batch of tainted seeds is around their expiration date – about three years from now. 

* The going explanation for the outbreak is contaminated sprout seeds, but we may never know for sure. Evidence disappears quickly in cases against food-borne disease.

† This isn’t just E. coli. Salmonella and another animal-carried cooties account for a good chunk of food poisoning cases. But, for the sake of brevity, I’m focusing on E. coli here.

‡ And apparently even getting that strain listed as an “adulterant” was a major chore. The whole sordid story was recently chronicled in the book Poisoned, by Jeff Benedict. I’m itching to read this thing, if anyone has a copy they’d like to lend me.

§ Sorry, meat enthusiasts, I do try to be tolerant of your choices and, like I said, I would never ask you to give up meat altogether. I just want to keep cow feces off of my vegetables.

Shakes on a Plane: Can Turbulence Kill You?

Image Credit: Jason Pratt

See that plane on the upper left?

Airplanes are scary. This indisputable fact originally came to my attention somewhere during college, when my relationship with flying matured from irritated ambivalence to full-blown phobic terror. There is something profoundly disturbing about being suspended thousands of feet in the air in a metal tube piloted by someone you’ve never even met. When I explain this to people who aren’t bothered by air travel, they foolishly try to persuade me with statistics about how flying is safer than driving blah, blah, blah…as though irrational fears could be soothed by something as banal as data.* Really, the only way to take my mind off my impending death is to pretend I’m not in an airplane at all. Distractions like food and music and in-flight magazine crossword puzzles go a long way toward accomplishing this, but all their hard work is undone the instant the plane encounters even a little turbulence. Turbulence has a way of snapping you back into the present moment, its every lurch and bump an unwelcome reminder that you’re hurtling through the stratosphere at over 500 miles per hour.

...this is what I think of every time I look at it.

My spring vacation† involved a total of 7 flights and amounted to something like 25 hours of time in the scary skies. Mercifully, every flight was smooth and trouble free, except for the very last one – a short jaunt from Dallas to Austin. I could tell the final phase of the trip was going to be less compliant than the previous portions. Thick clouds hung over the airport while we waited to board the plane. As soon as we were in the air, the pilots announced that there would be no beverage service due to some rough weather ahead. Throughout the next terrifying 40 minutes or so, we received various ominous announcements from the cockpit as the plane shuddered in increasingly malevolent winds, “We’re going to fly low today and try to stay below this storm,” and “Okay, so still pretty bumpy even at this altitude, but we should hopefully be there soon” etc. After we were safely back on the ground, I apologized to my boyfriend for all my in-flight whimpering, calling upon the mantra I’d heard dozens of times, “I know it’s just turbulence and it can’t hurt the plane, but it really feels like you’re about to crash.” But instead of laughing at me for being such a sissy, he launched into a lengthy discussion of how severe turbulence can cause plane crashes, and how the turbulence we’d just experienced had been pretty rough, and something about “wind shear” being capable of tearing planes in half.‡ I was really glad he didn’t share any of this with me during the flight.

Say It Isn’t So

Since anecdotal boyfriend babble is not always accepted as a reliable source, I’ve done some research on the question of whether turbulence can cause aviation disasters. The answer turns out to be a heavily-caveated yes. Turbulence can lead to plane crashes, but it is exceedingly rare. By some estimates, turbulence takes down about one plane per decade.§ This chaotic air movement - and its effects on the movement of the aircraft - is classified in degrees of light, moderate, severe and EXTREME (emphasis added by author). There’s also something called “chop” which is a more rhythmic bumpity-bumpity effect that comes in light and moderate flavors. Passenger perception of turbulence tends to be direr than that of experienced crew, so if you think you’ve been on the worst flight of your life, it’s likely you only witnessed moderate turbulence.

The good news is that airplanes are designed to withstand extreme turbulence (as well as lightning). The bad news is that, like all machines, airplanes age. Wear and tear that is no problem under normal circumstances can make aircraft less resilient to ridiculous levels of turbulence. Additionally, flying a plane that is being pummeled by rogue air masses isn’t the easiest thing in the world. Planes can be pretty much out of control during these episodes and, while temporary, the pressure is really on the pilot to react (but not overreact) in a way that keeps the aircraft from flying into the side of a mountain. If you think this all sounds melodramatic, consider a 1966 incident in which a BOAC (now British Airways) Boeing 707, flying near Mt Fuji, broke up in midair and crashed amidst harsh winds.

Your Wake, My Funeral

As frightening as that is, you should probably be more concerned about something called “wake turbulence”. Unlike turbulence created by naturally occurring differences in air flow (bad weather, pressure variations near mountains, jet streams, etc.), wake turbulence is caused by other airplanes, sort of like the wake created by a boat, except with air and much scarier. The worst part of wake turbulence is the creation of “wingtip vortices”, tornadoes of bumpy air generated by a plane’s wings that can take several minutes to dissipate.

Image Credit: NASA Langley Research Center

As with boat wake, this form of turbulence is not a problem for the planes creating it, but rather for the planes near it. Airports enforce strict limits regarding how much time must pass in between take-offs and landings to prevent one plane from getting caught in another’s wake. However, airports are increasingly crowded places with limited runway resources. Since they are travelling at slower speeds and pitched at awkward angles, planes that are taking off or landing are more vulnerable to turbulence. And, unfortunately, take off and landing are exactly the times when planes fly closest to one another.

As with other forms of turbulence, wake turbulence is more of a threat to small planes (especially when caused by the significant wakes of large commercial jets). Probably the largest aircraft to crash as a result of the phenomenon was a McDonnell Douglas DC-9 that got caught in the wake of a Lockheed L-1011 in 1972, prior to the implementation of the above-mentioned spacing regulations.** Wake turbulence allegedly also contributed to the 2001 demise of American Airlines Flight 587, though this crash is officially attributed to pilot error in response to the wake.

Reality Check

And now let me stress how very, very rare these occurrences are. Finding examples with which to freak you out was no easy task. Really, the biggest of your worries in the realm of bumpy air is encountering clear air turbulence (CAT) when you don’t have your seatbelt fastened. This is the surprise turbulence that occurs on a sunny day in seemingly smooth skies. The major impact of turbulence is not the causing of plane crashes, but rather bodily injury from all that jerking around. Every year, dozens of un-seatbelted passengers are seriously injured (and occasionally even killed) from being thrown around the cabins of twitchy planes. Your pilot isn’t just being an overbearing nag when he (or she) asks you to keep your seatbelt fastened when you aren’t walking around the cabin. CAT can come out of nowhere and knock the #%$ out of a plane. So buckle up, people.

* By the way, I’m afraid of cars too, making such logic even more useless to me.

† I went to Spain. It was lovely, thanks for asking.

‡ Wind shear turns out to be variations in speed and direction of air movement, which often leads to turbulence. Possibly he was talking about wake turbulence rather than wind shear. Maybe he even said wake turbulence. I don’t know, I was still a bit rattled (pun not intended, but permitted) at the time.

§ This was reported in the Guardian (via the aviation consultant Ascend) and they didn’t elaborate on what types of planes – or types of turbulence for that matter –were involved in these disasters.

** The DC-9 is still relatively small compared to a wide-body behemoth like the Lockheed L-1011.