The case of the poison potato

Maggie Koerth

8:15 am Mon, Mar 25, 2013

Frying a potato is a tricky proposition. Doing it right isn’t just about your skill as a cook, but also your partner, the potato itself. Waxy potatoes — high in sugar, low in starch — brown a little too easily as the sugar in them is altered by heat. By the time the interior is cooked through, the exterior is burnt to a crisp.

Good potato chips come from starchy potatoes. But to get just the right chip color — that perfect, buttery golden brown — you have to pay attention to a lot of different factors, from the types of sugar found in the potato, to the internal chemistry that happens as the potato sits in a sack post-harvest.

In the late 1960s, researchers from the US Department of Agriculture, Penn State University, and the Wise Potato Chip Company teamed up breed a very special potato, which they named the Lenape. More than 30 years later, one of their colleagues still thought fondly of that spud. “Lenape was [wonderful],” Penn State scientist Herb Cole told journalist Nancy Marie Brown in 2003. “It chipped golden.”

Yes, the Lenape made a damn fine potato chip.

Unfortunately, it was also kind of toxic.

Despite an almost boring reputation as the squishy white bread of the plant kingdom, potatoes actually come from somewhat nasty roots. Their closest relatives are innocuous enough. Potatoes have strong genetic ties to tomatoes and eggplants. But their more distant cousins include tobacco, chili peppers, deadly nightshade, and the hallucinatory drug-producing flower, datura.

This is a phylogenetic family that is ready to throw down, chemically speaking. Called Solanaceae, its members are known for producing a wide variety of nitrogen-rich chemical compounds, called alkaloids. Nicotine is an alkaloid. So are caffeine, cocaine, and a host of other plant-derived chemicals that humans have taken a liking to over the millennia. Depending on the dose, and on the specific compound, alkaloids can have effects ranging from medicinal, to far-out crazy hallucinatory, to deadly.

Potatoes produce an alkaloid called solanine. All potatoes have it, and it’s a feature, not a bug — at least as far as the potato is concerned. Like a lot of other plant-produced alkaloids, solanine is a natural defense mechanism. It protects the potato from pests. Think of potato blight, the fungus-like disease partly responsible for the Irish Famine of the 19^th century. The more solanine a potato contains, the less susceptible it is to blight. When a potato is put into a compromising situation — when it’s young and vulnerable, for instance, or when tubers get uncovered and, thus, more exposed to things that might eat it — solanine production can rev up.

Those triggers aren’t always the most convenient for the potato’s human predators. A sudden frost, for instance, can stunt the growth of tubers and promote the growth of vines and leaves, which mimics a younger stage of development and is accompanied by higher solanine concentrations. And if you leave potatoes exposed to the sun for too long after harvest, they start reacting as though they just got accidentally uncovered. They turn green and they produce more solanine. This is actually why you’re not supposed to eat green potatoes. Those spuds, and especially their skins, are rich in solanine. How much solanine varies; it might just be enough to make your stomach a little upset. Or, it could lead to serious illness accompanied by vomiting, diarrhea, loss of consciousness, and convulsive twitching. In very rare cases, people who ate green potatoes have even died.

Poor post-harvest handling was not the problem with the Lenape, however. In 1974, after Lenape potatoes had been recalled from agricultural production and relegated to the status of “breeding material”, the USDA published results of an experiment where they grew Lenape, and five other potato varieties, at 39 locations around the country. They carefully monitored growing and harvesting conditions and then compared the solanine content of all the potatoes.

The conclusion: Lenape was genetically predisposed towards producing an extraordinarily high amount of solanine, no matter what happened to it during growth and harvest. The average Russet potato, for instance, contained about 8 mg of solanine for every 100 g of potato. Lenape, on the other hand, was closer to 30 mg of toxin for every 100 g of food. That made it nicely resistant to a lot of agricultural pests. But it also explained why some of the people who were the first to eat Lenapes — most of them breeders and other professionals in the agriculture industry — ended up with severe nausea, like a fast-acting stomach bug.

What makes the Lenape really interesting, though, is its legacy as a cautionary tale. I first learned about it from Fred Gould, an entomologist at North Carolina State University, whom I met while I was working on a New York Times Magazine story about genetically modified mosquitoes.

He used Lenapes as an example of risk and uncertainty. Often, people frame genetically modified plants as this huge open question — a giant uncertainty, of the sort we’ve never dealt with before. There’s this idea that GM plants are uniquely at risk of producing unexpected side effects, and that we have no way of knowing what those effects would be until average consumers start getting sick, Gould told me. But neither of those things is really true. Conventional breeding, the simple act of crossing one existing plant with another, can produce all sorts of unexpected and dangerous results. One of the reasons Lenape potatoes are so infamous, I later found out, is that they played a big role in shaping how the USDA treats and tests new varieties of conventionally bred food plants today.

In fact, from Gould’s perspective, there’s actually a lot more risk and uncertainty with conventional breeding, than there is with genetic modification. That’s because, with GM, you’re mucking about with a single gene. There are a lot more genes in play with conventional breeding, and a lot more ways that surprising genetic interactions could come back to haunt you. “You try breeding potatoes for pest resistance, but you’re bringing in a whole chromosome from a wild potato,” he said. “We’ve found interactions between the wild genomes and the cultivated genomes that actually led to potentially poisonous chemicals in the potato.”

In 2004, a National Academies panel on the unintended health effects of genetic engineering reported that conventional potato breeders continue to try to increase the amount of solanine produced by the leaves and vines of their potato plants in hopes of making those plants more naturally pest-resistant. Because of that, the USDA actually has a recommended limit for solanine content of new potato varieties — but that limit isn’t strictly enforced.

Gould’s point isn’t that genetic modification is always better than conventional breeding. It’s not. Instead, they’re both tools — imperfect technologies that could produce unintended side effects. Which one you choose to use depends on what you’re trying to do. But, either way, you can’t say that one is scary and one is safe.