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.