The DNA Files:
Unraveling the Mysteries of Genetics

As heard on National Public Radio

Designing The Garden:
Food in The Age of Biotechnology

Hosted by John Hockenberry

Transcript

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JOHN HOCKENBERRY: It can be tough to decide what to buy at the supermarket these days. We hear a lot about genetically modified foods, but do you know which foods are modified or not? And what does genetically modified mean, anyway? This is The DNA Files. I'm John Hockenberry. Today's program is called, "Designing the Garden: Food in the Age of Biotechnology." Over the next hour, we'll visit coffee connoisseurs in California, soybean farmers in Ohio, and nutritionists in Southern India.

LAKSHMAN: So we are looking at the ultimate objective of "Are we able to reduce child mortality down to numbers, which are far lower than the kind of unimaginable numbers that we have today?"

JOHN HOCKENBERRY: We'll hear about scientists putting genes from daffodils into rice, DNA from mice into pigs, and a gene from bacteria into corn, all to better understand food created for the dinner table, coming up after the news.
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JOHN HOCKENBERRY: Welcome to The DNA Files. I'm John Hockenberry. And if there was like a theme park to food, it would be right here at the Fairway Market in Brooklyn, New York. I'm surrounded by produce--plums like an ocean of--oh, man, those are--yeah, I need this--and everybody's summer favorite, corn. Look at that. Look at that. Oh, man. Dinner.
JOHN HOCKENBERRY: Is this real yellow?

WOMAN 1: Is that real yellow?

JOHN HOCKENBERRY: Do they grow like this?

WOMAN 1: Yeah. Are you worried that it's like been genetically altered or something?

JOHN HOCKENBERRY: No. Do you worry about that?

WOMAN 1: I don't know. I don't really think about it so much, but that's--that's good.

JOHN HOCKENBERRY: That’s the real deal.

WOMAN 1: That's the real deal. [laughs]

JOHN HOCKENBERRY: Yeah, all right, thank you.

WOMAN 1: You're welcome.

JOHN HOCKENBERRY: Genetically modified foods, also called GM foods. That's when scientists modify a plant or an animal's genes in the lab. Sometimes they'll add new genes. Sometimes they'll turn off a gene so it stops working. Hardly any genetically altered plants wind up here in the produce aisle, maybe some yellow crookneck squash, an occasional papaya, but more than 70% of the corn grown in the U.S., and 90% of soybeans are genetically modified. And a lot of corn and soy shows up in processed foods.

Come with me. I'm going to head over to the cereal aisle here. We got Special K Protein Plus here, wheat bran soy grits, rice, wheat gluten, soybean oil, whole grain wheat, soy protein isolate, sugar, salt, high fructose corn syrup, malt flavor, natural ...

A lot of GM corn and soy is processed into these kinds of things--soy protein isolate, high fructose corn syrup, and it ends up in cereals, juice drinks, frozen pizzas, you name it.

LEE SILVER: So what? [laughs] I guess is the question.

JOHN HOCKENBERRY: Lee Silver is a professor of molecular biology and public policy at Princeton University. He's on one side of the GM food debate. He says pretty much everything we eat, processed or not, has been manipulated by humans. For example, he says corn as we know it today is essentially a human invention.

LEE SILVER: If you go out into the Midwest and you go outside of a farm, corn doesn't grow in the woods. It didn't exist before people in Central America took a weed, and began to select characteristics, which are actually bad for the corn, but good for people.

JOHN HOCKENBERRY: Ten thousand years ago, an ear of corn had no more than 12 little kernels. This ear of Silver Queen at the market today--umm, it's got to be 500 kernels. In Lee Silver's view, genetic engineering is just an extension of the plant breeding that's been going on for thousands of years. But another scientist says, "Unh unh, no. Selective breeding and genetic modification are very different. Mardi Mellon is with the Union of Concerned Scientists.

MARDI MELLON: I would argue that that's a radical departure from the technology of traditional or conventional breeding that's based on the selection of organisms and the controlled mating between organisms.

JOHN HOCKENBERRY: Mellon says traditional breeders work with plants that are closely related to those they're manipulating.

MARDI MELLON: Over time, we have accumulated an immense amount of experience with selective breeding, and one of the things we've learned is that if you stick with the set of genes that can be accessed through traditional breeding, i.e., the wheat that you want to modify can only be done by breeding the wheat plant with wheat or a near relative, that we have an idea of what kind of outcomes those limited genetic combinations produce.

JOHN HOCKENBERRY: Genetic engineers put daffodil genes into rice and bacteria genes into corn. Mellon says adding genes from unrelated species could create new risks to the environment and perhaps to people.

LEE SILVER: I think that's misleading.

JOHN HOCKENBERRY: Here's Lee Silver again.

LEE SILVER: The culture is such that people think GM food is dangerous. Now, the products that are on the market right now in the United States, there's no evidence that they've caused any detectable harm.

JOHN HOCKENBERRY: It's been more than a decade since GM products began making their way on to our dinner tables. In 1994, the Food and Drug Administration approved the “Flavor Saver” tomato. Consumers didn't like it. So you won't find it at the supermarket any more. But in 1996, the Monsanto Corporation came out with something that started a revolution in American farming. Today, more than 100 million acres of American farmland are planted with GM soy, corn, cotton, and a few other crops.

MAN 1: Today, agriculture is going far beyond Nature to produce new miracles for an even better, more abundant life.

JOHN HOCKENBERRY: Monsanto's innovation was the Roundup Ready soybean seed. Roundup is a well-known weed killer for homeowners and farmers alike. Monsanto came out with it more than 30 years ago, but now the company is selling is with a biotech seed that works together with the weed killer. Eric Sachs is chief of Monsanto's global scientific affairs group. He says that when someone sprays the Roundup weed killer, it binds with an essential enzyme in plants.

ERIC SACHS: That enzyme is critical for the production of certain amino acids.

JOHN HOCKENBERRY: And Roundup makes the enzyme inactive.

ERIC SACHS: So when it's inactivated in the weed, the weed eventually dies, because it's starved for those critical amino acids.

JOHN HOCKENBERRY: To create Roundup Ready seeds, scientists took a gene from a bacteria and added it to a plant's DNA. The new gene alters the shape of that critical enzyme.

ERIC SACHS: Think of something like a little kidney bean, where it has a small, little space in it where the Roundup molecule might fit. In the Roundup Ready gene, that space is altered slightly so that the molecule doesn't fit any more.

JOHN HOCKENBERRY: So in Roundup Ready plants, the weed killer can't bind, and it can't kill the plant. Farmers can spray all over a field of Roundup Ready corn or soy, and kill the weeds, not the crops. This Roundup Ready technology has been a huge boon for Monsanto. Sales of GM corn and soybean seeds totaled more than two billion dollars in the first half of 2007. That's in addition to almost 1.2 billion dollars in sales for the weed killer alone. But some U.S. farmers want to keep genetically modified plants out of their fields. These farmers worry that GM plants growing nearby could contaminate their fields and ruin their markets, and they think it's the government's responsibility to protect them. One of the biggest victories for anti-GM forces came in May, 2007. For the first time, farmers were forced to stop planting a biotech crop, because of a federal court ruling. DNA File's producer, Julie Grant, brings us the story of Roundup Ready alfalfa.

JULIE GRANT: Except for a few sprouts, most of us don't eat alfalfa, but cows do, and we drink milk and eat meat from those cows. If you want your milk and meat to be organic, your cows can't be eating genetically modified plants. The national organic rules are strict about that. In 2005, Monsanto put Roundup Ready alfalfa seeds on the market, and in just two years, nearly half of all alfalfa farmers switched to it.

A river flows around this farm in Northern California. Glenn Nakagawa has the trim build of a man who's worked a lifetime in these fields, but now Nakagawa's getting older. He wants a crop that won't take a lot of tending. He decided to plant Monsanto's new genetically modified alfalfa, because the Roundup Ready seeds are supposed to make it easier to keep weeds, such as lamb's quarters or wild mustard at bay.

GLENN NAKAGAWA: What's left is nice, green, thick stand of alfalfa.

JULIE GRANT: He's glad he chose Roundup Ready alfalfa.

GLENN NAKAGAWA: The nice thing is, you're paid on cleanliness of your hay. The more alfalfa you have in the bale, the more money you're going to get paid for that hay. If you have a lot of weeds [laughs], you're going to get paid for the weeds, and it won't be as much money.

JULIE GRANT: Nakagawa paid two to three times more for the biotech seeds, but he expects to use less herbicide. That will save him 30 to 50 dollars per acre. It also means less chemical run-off into the river. But ever since Roundup Ready alfalfa went on the market, it's pitted farmer against farmer. Glenn Nakagawa got his Roundup Ready alfalfa planted before the ban. Farmer Albert Straus wishes sales had been halted sooner. Nearly 15 years ago, Straus decided to have his family's farm certified organic.

ALBERT STRAUS: We do glass bottle organic milk, organic butter, yogurt. We make ice cream as well.

JULIE GRANT: In order to get the little round seal--the organic certification on his milk bottles and other products, everything he feeds his 270 cows also needs to be certified organic.

ALBERT STRAUS: We buy about 50% of our feeds every year. We probably buy about 3,500 tons of alfalfa a year, and that comes from either Northern California or Nevada.

JULIE GRANT: But when Straus tested the so-called organic corn in the feed he bought, more than a quarter of it was genetically modified.

ALBERT STRAUS: I was shocked. We verified with this higher standard test. I sent the sample to the lab, and they found that it was contaminated with three traits of genetically modified organisms.

JULIE GRANT: Straus was worried when he heard more farmers were starting to plant Roundup Ready alfalfa.

ALBERT STRAUS: They're not able to control the GM corn. They're not going to be able to control the GM alfalfa.

JULIE GRANT: But corn and alfalfa don't carry the same risk of cross-pollination. Each corn plant can produce millions of pollen. On a breezy day, corn can cross-pollinate plants hundreds of feet away. Alfalfa often pollinates itself, and when it does cross-pollinate, it's by bees. Honeybees don't spread pollen as far as the wind.

Dan Putnam is an alfalfa expert at the University of California at Davis. He wrote a brief to the court that was used by the U.S. Department of Agriculture and Monsanto to argue that alfalfa has low risk of gene flow. He and his colleagues tested non-genetically modified alfalfa growing 165 feet from GM alfalfa. The contamination levels were one-quarter of 1%. Putnam said bees just aren't very interested in alfalfa.

DAN PUTNAM: They do not like alfalfa, because it trips and hits them in the head.

JULIE GRANT: Putnam explains that when a bee lands on the flower, one of the petals tenses, jerks forward, and strikes the bees. He says there's another reason that cross-pollination or gene flow is unlikely from a field of alfalfa grown for hay.

DAN PUTNAM: Most growers manage gene flow just because of what they do with hay fields. They cut them frequently, and they don't allow them to flower very much, and they certainly don't allow them to set seed.

JULIE GRANT: Hay farmers want the plants' energy to go into making thick, green leaves, not into flowers. Putnam says that, coupled with the bees' dislike of alfalfa, make the potential for contamination in hay fields close to nil. But even the tiniest amount is too much for many organic farmers. The federal court that banned the GM alfalfa wanted more evidence. The judge instructed the USDA to prepare an environmental impact statement, something it hadn't done on any Roundup Ready crops. The study is expected to take up to two years. In the meantime, Monsanto has had to recall all the seeds from its distribution chain. For The DNA Files, I'm Julie Grant.

JOHN HOCKENBERRY: Coming up, how to reduce pollution with a genetically altered pig and how one scientist stops the coffee plant from making caffeine when we continue with "Designing the Garden: Food in the Age of Biotechnology" on The DNA Files.

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JOHN HOCKENBERRY: Welcome back to The DNA Files. I'm John Hockenberry. We just heard how the courts are forcing government agencies to do better research on the environmental effects of one GM crop. There's a lot at stake for biotech companies, for farmers, and consumers. So now, let's go back to the studio with Mardi Mellon and Lee Silver, our two experts who in some ways are acres apart on the subject of GM foods. All right, Mardi Mellon, who regulates genetically modified foods and crops?

MARDI MELLON: Three agencies do--the Food and Drug Administration, the United States Department of Agriculture, and the Environmental Protection Agency all have some piece of the biotech regulatory pie.

JOHN HOCKENBERRY: And they're all in total agreement about everything, Lee?

LEE SILVER: No. They're supposed to regulate different aspects of the process. Obviously the Environmental Protection Agency is looking at impact of growing crops on the environment, and you have the USDA, which is looking at agricultural levels. The Food and Drug Administration is looking at the outcome, the product.

JOHN HOCKENBERRY: Do you think genetically modified foods and crops are well regulated in the United States?

LEE SILVER: In the United States, I think they're well regulated, meaning the unlikelihood that something will reach the commercial market that is harmful to people, I think yes, in that sense, they're well regulated.

JOHN HOCKENBERRY: Mardi? Are you satisfied with the regulatory process as it exists now?

MARDI MELLON: I'm not satisfied with the regulatory process as it now exists. I think it is fundamentally ill conceived. It's far too voluntary. The FDA regulations really require nothing of any company in terms of providing evidence to the government before a product goes on the market to establish whether it is one of the safe products of biotechnology or perhaps one of the few--and I agree that they're not likely to be many--that's not safe.

LEE SILVER: The regulations are based on agency mandates that existed before biotechnology matured into what it is today, and I think that they can all be brought together in a way that's much, much less cumbersome.

JOHN HOCKENBERRY: So far, we've been talking about food from genetically modified plants, but what about animals? The U.S. doesn't have specific regulations for GM animals. You won't find any GM salmon at the fish counter yet or hamburger at the meat case or bacon either. Canadian scientist Cecil Forsberg has been working for years to market his ““Enviropig”s.” They would have a tough time getting to market in the U.S., because they've been engineered using e-coli. In Canada, GM animals are called "novel foods," and even there, the ““Enviropig” have been stuck in the pen. The DNA Files producer Brian Mann has the story.

BRIAN MANN: A mile outside of Guelph, Ontario, the tree lined streets give way to fields and stretches of wood. Microbiologist Cecil Forsberg points me down a gravel drive towards what looks like a modern industrial farm.

CECIL FORSBERG: You make a left turn. I'd stay away from the front door where your vehicle can pick up the smell.

BRIAN MANN: It's a rental. So I don't mind the smell. [Cecil laughs.]

BRIAN MANN: We park a safe distance away. Despite the wind, there is an odor--cows and mowed grass, but overwhelming it all, the sickly sweet stench of pig manure. Forsberg opens the door to a sprawling barn operated by the University of Guelph. The building is part pigsty, part high tech laboratory. Massive fans churn constantly, maintaining the temperature and easing the odor. Pigs are famous for eating a lot, and it turns out they're not very efficient at digesting the kind of corn and soybeans that make the cheapest livestock feed. As a consequence, their poop is thick with undigested waste products, including phosphorous. For 11 years, this has been Cecil Forsberg's obsession.

CECIL FORSBERG: We thought this would be an ideal project to undertake, because of the extensive phosphorous pollution one finds within areas where there's very intensive livestock production.

BRIAN MANN: The phosphorous problem is a conundrum of modern agriculture. As the human population grows, we require more and more food. That means more cows and pigs, which industrial farmers have supplied pretty handily. But the side effects of those huge factory farms can be devastating.

MARY WATZIN: Oh, we have a creme de la creme spot. We're right on the waterfront in Burlington.

BRIAN MANN: Mary Watzin is director of the Rubinstein Ecosystems Science Laboratory on Lake Champlain. The lake is beautiful, a huge craggy waterway that cuts between Vermont, New York State, and Canada. But phosphorous run-off from large pig and dairy farms has triggered disgusting algae blooms.

MARY WATZIN: You wouldn't miss it, if you saw it. The water looks like there's green stuff in scums on the surface.

BRIAN MANN: Algae can create conditions that gobble up a lake's oxygen, Watzin says, suffocating fish, and throwing the natural ecology into a tailspin. In recent years, toxic concentrations have risen, and several animals exposed to the algae have died.

MARY WATZIN: There are two toxins, actually, produced in Lake Champlain. One is the neurotoxin or brain toxin, and that's been responsible for most of the dog deaths.

BRIAN MANN: Half a dozen dogs have died, Watzin says. The other toxin found during autopsies destroys liver tissue. No humans have been affected so far, because the algae looks so gross that people won't go near it. But a lot of towns along the shore still draw their drinking water from the lake, and as industrial agriculture spreads around the world, producing more and more phosphorous, Watzin says precious water sources are gumming up with this algae soup, which brings us back to Cecil Forsberg's “Enviropig”.

Forsberg wades into a pigpen, waist deep in what looked like everyday Yorkshires, pale skinned, rubbery nosed pigs. The unique thing about these animals isn't their voracious appetites, but a genetic modification with their salivary glands. Remember how pigs aren't very good at digesting the phosphorous in corn and soybeans? Well, it happens that some bacteria are great at it. They naturally produce an enzyme that dissolves the phosphorous.

Forsberg's team managed to introduce this clever enzyme from the bacterium into these animals. They even managed to arrange the DNA so that the gene is expressed in the pig's salivary glands. So when an “Enviropig” munches corn, the enzyme in its saliva digests the phosphorous. As a result, Forsberg says, the “Enviropig” produces 60% less phosphorous than a normal pig. That's twice the reduction that farmers achieve even when they use better and more expensive grains, and when they feed their pigs costly dietary supplements. Even better, Forsberg says, these pigs seem normal in every other way.

CECIL FORSBERG: Although we haven't eaten any of the pork--in fact, it's illegal until there's regulatory approval--I am 99.9% confident that the flavor of the pork from these pigs will be equivalent to that from conventional pigs.

BRIAN MANN: But there's a wrinkle. Pig farmers in Ontario helped to fund the first round of “Enviropig” research, but the project still faces years of testing and regulatory hurdles, and the big grants from an industry group called Ontario Pork have dried up.

CECIL FORSBERG: I'm embarrassed to admit it, but we have no genuine commercial interest in these pigs.

BRIAN MANN: Could I have a ham and swiss? Actually I'd rather have a BLT, please.

BRIAN MANN: After touring the farm, he takes me to a Tim Horton's restaurant. The fast food chain is everywhere in Canada, one more link in our industrial food economy. Forsberg looks around at the crowd grabbing a quick lunch. As the world's population grows, so will our hunger for those BLT and ham sandwiches, which means more pigs, more polluted waterways, and more toxic algae blooms.

CECIL FORSBERG: I don't view this scientific advancement as being one to increase the quantity of food. I view it as a trait within an animal that reduces its environmental impact. Sustainability, I think, is the key issue, which I would raise.

BRIAN MANN: For The DNA Files, I'm Brian Mann.

JOHN HOCKENBERRY: “Enviropig”. This gives new meaning to the term "green eggs and ham." I mean, you've got a pig that helps the environment. You can have your bacon. Come on, this sounds like a great idea. Lee?
LEE SILVER: I think it is a great idea.

JOHN HOCKENBERRY: Mardi? Come on, you've got to be pro “Enviropig”, right?

MARDI MELLON: I'm underwhelmed by the pig. I'm definitely pro environment, but before I signed on to this one, I wanted to know what impact it might have on the pig, and then I'd want to see what the alternatives are. Is it possible to just adjust the feeding ratio of how much corn to other components of the food, and reduce phosphate that way? The other thing I'd want to look at is the system. Concentrating so many pigs in such small spaces and ask if we couldn't think about environmental benefits that we might achieve by changing the system.

JOHN HOCKENBERRY: So the “Enviropig” might help reduce pollution, and genetically modified crops are supposed to ease the farmer's work load. But what's in this genetic engineering for us, consumers? Scientists are trying to create cows that will have more marbling in their beef. That's for us. They're developing soybean oil that's lower in trans fats, allergy-free peanuts, and gluten-free wheat, and for people who just want a good cup of--get this--decaffeinated coffee, DNA Files producer Julie Grant tells us about scientists who are genetically modifying coffee plants to grow without caffeine.

JULIE GRANT: If you want to know the best ways to grow, roast, and serve coffee, or if you just want a really good cup, this is the place. It's the Specialty Coffee Association of America's annual conference. This year, it's at the Long Beach Convention Center in California. The center floor is lined with row after row of more than 500 vendors, looking to buy and sell their gourmet coffee goods. Some are showing off different beans they grow--a rainbow of pale greens, caramel colors, and deep browns. Some vendors are displaying huge stainless steel roasting machines, and others are serving up coffee--drink after drink after drink. It's enough stimulation to make you reach for a decaf--that's unless you're wary of the chemicals used to decaffeinate coffee beans.

JOSEPH RIVERA: We're going to talk about what goes on with roasting --

JULIE GRANT: Joseph Rivera is director of science and technology for the Coffee Association. He's teaching a class in decaffeination. Here's how it works. The green beans are steamed to soften and swell them. Then they're mixed in big stainless steel chambers with solvents.

JOSEPH RIVERA: It's just kind of a big laundry mat, if you will. Things are being mixed up and swirled around.

JULIE GRANT: During all of that swirling, the caffeine molecules separate from the beans and attach to the solvents. They're siphoned out of the chamber, and what's left inside are the decaffeinated beans.

JOSEPH RIVERA: You have to realize that these beans have gone through a lot. They've been stressed out. They've been steamed. They've been beat up in these containers. They've been subjected to chemicals.

JULIE GRANT: Rivera says the chemical used in 60% of coffee decaffeinated in the U.S. is methylene chloride, the same stuff used in paint strippers and degreasers.

JOSEPH RIVERA: People don't like to hear that. [laughs] They don't like to hear that it's in paint remover. It's used in a number of different things.

JULIE GRANT: And Rivera says there's no denying that once you change the chemical make-up of the beans like this, you change the flavor of the coffee. That's where one scientist walking around the coffee conference sees his opening.

JOHN STILES: I'm John Stiles. I'm chief scientific officer for Integrated Coffee Technologies.

JULIE GRANT: What is Integrated Coffee Technologies?

JOHN STILES: We're a small--I guess you'd say a boutique biotechnology company that focuses on coffee and a few other tropical crops.

JULIE GRANT: Stiles says he prefers regular coffee to the decaf on the market today, including the decaf that's processed with water.

JOHN STILES: There's some really good methods for decaffeinating coffee now, but all of them change the flavor. There's no method that can take out just caffeine. You're never going to have the full flavor we all really love about really good coffee using a chemical process to take out the caffeine. Our approach--well, let's just not make caffeine, have everything else the same.

JULIE GRANT: Apparently, it's not as easy as it sounds. So far, it's taken more than 15 years of development in the lab. Stiles grinds up the leaves of the coffee plants and extracts strands of a plant's DNA. From that, he says they've been able to locate the one gene that begins the plant's process of making caffeine.

JOHN STILES: We take the gene, and sort of turn it around backwards, and make it work in reverse.

JULIE GRANT: Normally, that caffeine-making gene sends out what's called messenger RNA, which goes from the nucleus into the body of the cell. There it's translated into the key enzyme that starts the caffeine making process. Flipping the gene around stops the process.

JOHN STILES: And so the enzyme doesn't get made. No enzyme, it can't do that first step, so no caffeine can be made.

JULIE GRANT: Stiles hopes to plant his decaf coffee trees in the field next year, and that's the next step in getting them approved for market. For The DNA Files, I'm Julie Grant.

JOHN HOCKENBERRY: No one knows yet whether coffee connoisseurs will go for the GM decaf. If it gets to market, it may go the way of the “Flavor Save” tomato, which only lasted about three years. But as long as GM crops like corn and soybeans make life easier for farmers, they'll keep turning up in the form of high fructose corn syrup and other additives on the supermarket shelves. It's the cost benefit analysis for farmers though that may be in for a change, as evidence emerges that GM groups may be creating a problem. If you use a chemical weed killer on your lawn, you may have noticed the ingredient, glyphosate.

MARK LOUX: Glyphosate may be the best herbicide we've ever had to work with.

JEFF STACHLER: Glyphosate is the best herbicide ever discovered.

JOHN HOCKENBERRY: Jeff Stachler and Mark Loux are specialists in weed science at the Ohio State University. They love glyphosate, because it kills nearly everything green. Even Charles Benbrook, chief scientist for an organization called The Organic Center in Oregon thinks it's not a bad weedkiller.

CHARLES BENBROOK: It's not acutely toxic. It has not been shown to cause cancer or birth defects. It breaks down fairly quickly in the environment to benign chemicals.

JOHN HOCKENBERRY: Lots of companies sell products with glyphosate. Monsanto's brand is called Roundup. The company also created genetically altered seeds. The seeds grow into plants that can survive Roundup. This is called the Roundup Ready system. Ohio State's Jeff Stachler says the Roundup Ready package is supposed to make work easier for farmers. They can spray glyphosate all over a field. The weeds die; the crops live.

JEFF STACHLER: It's a very good system.

JOHN HOCKENBERRY: Which brings us to where we are today. Stachler and Loux are walking through a field of yellow flowers as high as their shins, weeds. The yellow flowers are Cressleaf Groundsel. They're mixed in with Giant Ragweed. The owner of this Ohio soybean farm contacted Stachler and Loux in 2004, because his weedkiller didn't seem to be working any more.

JEFF STACHLER: One of the things we want to determine is whether these plants are truly surviving from the glyphosate.

JOHN HOCKENBERRY: The scientists sectioned off part of the field and planted 1,400 pink flags, each marking a Giant Ragweed plant. They sprayed the area with glyphosate. Stachler says it killed all the Cressleaf Groundsel, but what about the Giant Ragweed?

JEFF STACHLER: You can see that this plant here that was flagged is dead. There's some others around it that are dead, but if we take a look at some of these others, and some that were flagged, you can see that they are still alive.

JOHN HOCKENBERRY: Stachler says that this was the only farm in Ohio reporting glyphosate resistance in Giant Ragweed in 2004. By the end of the 2006 growing season, they'd confirmed sites in ten Ohio counties. That doesn't surprise Charles Benbrook. Before he came to The Organic Center, he headed up the National Academy of Sciences board on agriculture.

CHARLES BENBROOK: Farmers typically rotate soybeans, cotton, and often corn, but in recent years, it's been Roundup Ready soybeans followed by Roundup Ready cotton followed by Roundup Ready corn, back to Roundup Ready soybeans. Well, obviously those weed populations were getting hammered year in and year out with a single herbicide active ingredient.

JOHN HOCKENBERRY: But all that glyphosate favors the growth of those few weeds that aren't susceptible to the chemical. The next year, those weeds have more seedlings. When the farmer applies more Roundup, those weeds do well again. And so they have even more seedlings and so on and so on until we're looking at a field full of weeds.

JEFF STACHLER: It's the same way with antibiotics or anything. When you do the same thing over and over again and take the easy way out, Mother Nature's going to find a way to combat that, and that's really what we're dealing with here. It's no different from any other type of resistance. We've just done the wrong thing too long, and we need to do more things.

JOHN HOCKENBERRY: There are now seven weeds in the U.S. that have become glyphosate resistant, and according to USDA data, in the last ten years farmers are reacting by spraying the chemical more often, almost doubling the amount they spray on each acre. But Monsanto's Eric Sachs says weeds become resistant to any herbicide that works well and becomes popular.

ERIC SACHS: It still controls more than 100 weeds, and that's why farmers continue to use the Roundup Ready system even though they do face some resistant weed problems in some areas in the United States or other parts of the world.

JOHN HOCKENBERRY: Sachs and other GM proponents argue that these technologies will become more and more important. We'll tell you why in a moment, when we return with The DNA Files.

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JOHN HOCKENBERRY: Welcome back. You're listening to The DNA Files. I'm John Hockenberry. Our show today is called, "Designing the Garden: Food in the Age of Biotechnology." One of the biggest claims made in favor of genetically modified foods is that they can offer better diets to people in the developing world. Eric Sachs is chief of the global scientific affairs group at Monsanto.

ERIC SACHS: We will be able to make crops more nutritious. We'll also be able to increase the productivity of those crops by helping to resist not only diseases, pests, and weeds, but also to help them resist drought and temperature stress, and salt stress, and other conditions that limit the development of crops in different areas around the world. So I think in 10, 20, 30 years, we'll see agriculture much more productive. We'll see the food crops being developed more nutritious and healthier for us, and in the end, hopefully we'll be seeing a reduction in people around the world that are hungry, because there's more healthy and prevalent food available to feed the world.

JOHN HOCKENBERRY: Sachs is talking about the future, but genetically engineered crops have been around for more than a decade. Have any of them begun to live up to this potential? And if the answer is no, why not?

Let's take one example, rice, the staple crop of hundreds of millions of people around the world. Plant geneticist Ingo Potrykus grew up struggling in postwar Germany, and had to steal food to survive. That's one reason why he set out more than 15 years ago to create a rice plant, which would help nourish people in poor countries. He wanted it to be fortified with beta-carotene, an essential nutrient that our bodies convert to Vitamin A. Without it, people can go blind, and even die. This isn't a big problem in the U.S. We've got lots of nice orange vegetables--carrots, sweet potatoes, along with leafy greens that provide beta-carotene. But around the world, 250 million preschool children don't get enough Vitamin A. Potrykus began to look at rice plants, which already make beta-carotene, but only in the outer green stems, and leaves. He says the grain, the part we eat, also has genes for beta-carotene, but they're turned off. Funded by the Rockefeller Foundation, he spent most of the 1990s figuring out how to turn them on.

INGO POTRYKUS: And you can imagine a staircase of, say, ten steps, and four of these steps were not there. So we had to rebuild these four steps. For this purpose, you need four enzymes, and for these enzymes, you need four genes.

JOHN HOCKENBERRY: Potrykus and his team took the genes from a daffodil and from a soil bacterium. After more than seven years of work, they were making rice that was slightly orange in color, an outward sign that the grain was now producing beta-carotene. They called it "Golden Rice."

INGO POTRYKUS: Golden Rice, when it could be used, could save millions of lives, and prevent blindness in hundreds of thousands of cases.

JOHN HOCKENBERRY: Potrykus and his colleagues were hailed for their breakthrough, but it's been another seven years since then, and Golden Rice still isn't available in developing nations. DNA Files producer Julie Grant traveled to India to find out why.

JULIE GRANT: Just a few minutes drive outside the southern Indian city of Madurai, the crowded streets of food vendors, auto rickshaws, and cars give way to small villages and green countryside. It's a patchwork of farm after farm. There are no barns or outbuildings. There's hardly any tractors. People here do most of their farm work by hand. 77-year-old Dr. Lakshmi Rahmathullah has been working with people in these villages for most of her career. Today, she's gathered some of the children in Arasakulam village. Six-year-old Karthik Kumar bravely walks to the front of the group as an adult holds his head steady for Dr. Lakshmi.

DR. LAKSHMI RAHMATHULLAH: If you look at his eyes, you will see brownish folds on the white part of the eye, which shows that is an indication of Vitamin A deficiency.

JULIE GRANT: Another child here, a 10-year-old girl said she couldn't see at night. She said it was scary. Everyone looked like ghosts. These symptoms, if left untreated, can lead to much worse problems. Her cornea could have literally shriveled away, leaving her totally blind. But the kids here were lucky. They got high dose Vitamin A supplements. This 10-year-old girl got her eyesight back within four months.

International aid organizations estimate that fully a third of children under age 5 in India and Southeast Asia have some level of Vitamin A deficiency. Anand Lakshman is manager of Child Survival Interventions for an aid agency called The Micronutrient Initiative with an office in New Delhi. He says Vitamin A deficiency can lead to diarrhea and make otherwise minor illnesses into life threatening problems.

ANAND LAKSHMAN: So we are looking at the ultimate objective of are we able to impact on child mortality? Are we able to reduce child mortality down to numbers which are far lower than the kind of absolutely unimaginable numbers that we have today.

JULIE GRANT: About two-thirds of Indian children under age five get Vitamin A supplements. They line up twice each year at health clinics to receive a spoonful of the serum. A mega dose of Vitamin A is stored in the child's liver, and is slowly released through the months. Lakshman says it's reduced the child mortality rate 23%. But there's debate in India over the need to continue the supplementation program. Dr. HPS Sachdev is former president of the Indian Academy of Pediatrics. He's a small man in a dark blue turban. Sitting in his medical office, he says most children these days don't need the mega doses

DR. HPS SACHDEV: I view it as a medicine. God did not intend us to take a pill off and on.

JULIE GRANT: Sachdev says many Indian families have gained the education and financial means to meet their Vitamin A needs the way people in richer countries do--through those orange vegetables and leafy greens. So children should only get the mega doses if there's an obvious lack of Vitamin A in their diet. Sachdev says there's another way to meet low level needs - golden rice. That's the rice genetically engineered to express beta-carotene. Sachdev says children could just eat a little rice regularly.

DR. HPS SACHDEV: A small lower dose mimics the daily requirements or is much closer to the daily requirements and its chances of toxicity are much lower as compared to a huge pill based on the mega dose approach.

JULIE GRANT: Ten years ago, Dr. S.R. Rao, director of India's department of biotechnology, was touring laboratories in Switzerland, and met geneticist Ingo Potrykus. Potrykus was still experimenting then, trying to make rice express beta-carotene. Rao says he wanted that rice for India, because he thought it could go a long way to reduce Vitamin A deficiency in regions where rice is a staple in the diet.

DR. S.R. RAO: So I'm from the southern part of India, and we only eat rice and rice and rice.

JULIE GRANT: Rao says they often eat rice for breakfast, lunch, and dinner. But why would farmers in India want to plant Golden Rice? Dr. Rao is a leader in efforts to transfer the genes for Golden Rice into varieties Indians already eat. Dr. Rao takes us to what's called a phytotron. It's a building used to grow plants, but it doesn't receive natural light like a greenhouse. That sound is a sterilizer. Before you enter the phytotron, you've got to spend a couple of minutes in this chamber. It blows super high air pressure to clean off contaminants that could ruin the experiments.

DR. S.R. RAO: To really get clear of your dust and all the organisms and you just come to this side. Now they're coming out. Okay? So Julie's smiling, that you are sterile, Julie.

JULIE GRANT: Sterilized. He means sterilized. It's just air.

DR. S.R. RAO: Sterilized. Yeah, that's the correct thing. [laughs] I am sorry. You are sterilized.

JULIE GRANT: The phytotron's main room has row after row of huge aqua colored refrigerators that keep the young plants at a constant temperature. Inside are Indian hybrids of Golden Rice. The genetic modification, the beta-carotene, was originally bred into a Japanese rice variety. Rao says in his phytotron they bred the Golden trait into some popular Indian varieties.

DR. S.R. RAO: That is in terms of their yield, in terms of resistance to diseases and pests. Such varieties have been taken, and where we put this traditional trait of Golden Rice.

JULIE GRANT: So traits that farmers like?

DR. S.R. RAO: Traits farmers like.

JULIE GRANT: Because they're going to grow better. They're not going to have as many pests.

DR. S.R. RAO: Yes, exactly.

JULIE GRANT: What he expects farmers to like even more is that the government plans to give Golden Rice seeds free to those making under $10,000 a year. This is possible, because of a deal struck between Ingo Potrykus, the scientist who created Golden Rice, and the seed company, Zeneca. There are some 70 patents on the various technologies involved in making Golden Rice. Zeneca, which is now part of Syngenta, owns many of those patents. The company was interested in selling Golden Rice to the U.S. and European health food markets. So in exchange for the right to do that, the company agreed to give the seeds away free to developing nations. But those free seeds are making some people angry. Vandana Shiva is famous worldwide for her opposition to genetically modified foods and the companies that pervade GM seeds. She calls Golden Rice a hoax, and says there are more natural ways for Indians to get Vitamin A.

VANDANA SHIVA: You can add a few micrograms of Vitamin A to a white, polished rice, and be thrilled that you have added nutrition. But again, food is not just rice, and definitely for anyone who has even a kindergarten knowledge of nutrition, polished rice is not where you turn to for meeting your Vitamin A needs. You turn to your greens. You turn to your coriander, your curry leaves, something very, very central to our eating.

JULIE GRANT: 60% of Indians are farmers, but many don't grow food for themselves any more. Ever since the Green Revolution brought pesticides and fertilizers to India in the 1960's, Shiva says farmers have been growing cotton and rice for the commodities market instead of food for their families. She says they need to be reeducated to grow and eat those leafy greens and other vegetables rich in Vitamin A.

But farmers aren't unified in what will be the best future for Indian agriculture. Some are clamoring for the latest technologies. There's a black market for genetically modified cotton seeds. But other farmers and activists agree with Shiva. Last year, GM opponents convinced the Indian Supreme Court to temporarily ban any new genetically modified crops from being planted, saying the crops were bad for human health and the environment. The ban has since been lifted. Some farmers worry GM crops could destroy their export market.

Northern India in the shadow of the Himalayas is the main world region for growing basmati rice. Basmati is a huge export crop for Indian farmers. Gurnam Singh is leader of the BKU Farm Union in this state, Haryana. Last year, he got wind that one of the multinational biotech companies had planted an experimental plot of genetically modified rice in the midst of the basmati region. Today, he rides up to that plot on his motorcycle, but there's no genetically modified rice here any more. Singh rallied a group of farmers, at least 100 by some counts. They piled straw over the small test site, poured some kerosene, and basked in the heat of the message they were sending to Monsanto.

GURNAM SINGH: (In Punjab)

TRANSLATOR: He's saying they met here basically as a sign of protest towards the company, because they were doing something--something which would harm the farmers, and so basically this was supposed to be a sign of protest for them by burning.

JULIE GRANT: That same day, Monsanto telephoned Dr. MS Swaminathan to tell him what had happened. Swaminathan is largely credited for bringing modern farming to India in the 1960s, and for leading efforts to bringing genetically modified crops here today. But when he heard farmers had burned the GM rice plot --

DR. MS SWAMINATHAN: I was happy, because I thought it was wrong.

JULIE GRANT: He says the company shouldn't have planted genetically modified rice in India's basmati rice region, because of the possibility of cross-pollination.

DR. MS SWAMINATHAN: It was foolish to have gone there, in the heartland of the rice exporting region, basmati rice, because we all know genetic pollution, gene flow, genetic contamination.

JULIE GRANT: Swaminathan says contamination could ruin India's rice trade with Europe, Japan, and other countries that don't accept genetically modified imports. But he says there are many places in India where genetically modified crops do make sense, and will be necessary to grow enough food for India's growing population.

DR. MS SWAMINATHAN: Genetic modification is one more tool, which can help you to overcome certain problems.

JULIE GRANT: He remembers when his family couldn't get rice. It was rationed by the government. People were asked to fast one day a week, because there wasn't enough food in India. He says it's time for the government to make policies that will provide enough food.

DR. MS SWAMINATHAN: Why, because we've got 1.1 billion people today--it will be 1.5 billion--the largest population in the world. Who is going to feed us? A country like India cannot depend on others to feed this population. And I think it's the fundamental duty of a government to ensure the daily bread to everybody.

JULIE GRANT: If Syngenta is serious about giving away Golden Rice for free, Swaminathan says it should drop its patents. Syngenta says poor farmers in India will never have to pay for Golden Rice, but the company may want to use the technology elsewhere. So it's holding on to its patents.

There are also questions about how much it will cost to complete development, to distribute seeds, to ensure children actually eat it, and that it provides enough Vitamin A. Back in Araskulam Village in southern India, Dr. Lakshmi Rahmathullah wouldn't mind seeing Golden Rice on these small farms, but she says for the sake of its children, it's too soon for the Indian government to stop offering Vitamin A supplements.

DR. LAKSHMI RAHMATHULLAH: There is no best solution. Offer families fortified rice, offer families fortified salt, offer families Vitamin A solution. Multiple solutions are the best answer.

JULIE GRANT: Dr. Lakshmi says the most important thing to offer malnourished families is food they can afford. For The DNA Files, I'm Julie Grant.

JOHN HOCKENBERRY: You know, in India, some people greet visitors to their home by placing a smear of rice mixed with turmeric on their forehead. It's a sign of respect and welcome. In all cultures, there are different ideas about what is sacred, about the meaning of food, and what it symbolizes. So the debate over genetically modified food is informed by culture, our values and beliefs as well as by science. That's true for all of us, including our scientists, Mardi Mellon and Lee Silver, who with their very different viewpoints helped us navigate the debate over GM foods. Hey, what kind of foods do you guys eat, by the way? Lee?

LEE SILVER: I could answer it very quickly. I only eat inorganic food.

MARDI MELLON: And I am a strong supporter of organic agriculture as a scientifically advanced vanguard of the kind of agriculture I think we're going to need if we're going to deal with global warming in the future.

JOHN HOCKENBERRY: I'm not hearing hot dogs and Twinkies on your table. Am I right about that? Mardi?

MARDI MELLON: You're right, but someday, I hope Lee and I can sit down and have ourselves a nice cup of strongly caffeinated coffee.

LEE SILVER: Fair trade.

MARDI MELLON: I'll buy.

LEE SILVER: That's right.

JOHN HOCKENBERRY: We'll hold you to that. I'm John Hockenberry. Thanks for listening to The DNA Files.

To find out more about genetically altered food, visit our website at dnafiles.org where you can download a podcast of this program. This series, The DNA Files, was produced by SoundVision Productions with funding by the National Science Foundation, U.S. Department of Energy, National Institutes of Health, and the Alfred P. Sloan Foundation. This program, "Designing the Garden: Food in the Age of Biotechnology" was produced by Julie Giant and Elizabeth Kulata. The field producer in India was Adam Burke. The DNA Files is managing editor, Loretta Williams, editor, Deborah George, science content editor, Sally Lehrman. Research director is Adi Gevins. Production support by Noah Miller, Julie Caine, and Jenn Jongsma. Office support provided by Steve Nuñez and Beverly Fitzgerald. Our web director is Ginna Allison. Technical engineer and music director is Robin Wise. Our host is John Hockenberry. Our theme music was composed and performed by Steve White. Additional music by Conrad Praetzel and Robert Powell. Marketing of The DNA Files is by Schardt Media. Legal services by Cooper, White and Cooper, and Spencer Weisbroth. Special thanks to Murray Street Productions. Send your responses and letters to feedback@dnafiles.org. For CDs and transcripts, call 888-303-0022. That's 888-303-0022. The executive producer is Bari Scott. This has been a SoundVision production.

The DNA Files:
Unraveling the Mysteries of Genetics

As heard on National Public Radio

Beyond Human

Hosted by John Hockenberry

Transcript

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and the Alfred P. Sloan Foundation.
JOHN HOCKENBERRY: This is The DNA Files. I'm John Hockenberry. What does it mean to be human? Philosophers have asked that question for hundreds of years. Now scientists consider the question by comparing the DNA of humans to other species.

SEAN CARROLL: The more you look at the genetics, the less unique we are. You know, we don't even have more genes than a puffer fish. So you know, you're just going to have to get over that.

JOHN HOCKENBERRY: We share most of our DNA with chimps, a lot with mice, and even a good bit with animals that seem quite remote like sea urchins and sea slugs.

ROSS HARDISON: There's no reason to think that every nucleotide or every base pair in the human genome is important in making you human. It is possible, maybe way more than half of the DNA in our genomes is doing nothing.

JOHN HOCKENBERRY: Coming up in this hour of The DNA Files, "Beyond Human." We'll be right back after the news.
...
JOHN HOCKENBERRY: All right. Let's talk for a minute about gorillas and chimpanzees. How different do you think they are from us? How different do they seem?

GIRL 1: This sounds kind of cheesy, but when we were at the gorilla exhibit, and the little baby gorilla looked you right in the eye, you could just tell that they were making connections with you, and that you were similar to them, really like making judgments about you.

JOHN HOCKENBERRY: This is The DNA Files. I'm John Hockenberry, and this program is "Beyond Human."

GIRL 2: I guess we're more advanced, like our world, but I doubt a lot of us would be able to survive in the wild, how they do.

JOHN HOCKENBERRY: About 10 feet away, there's a family of Western Lowland gorillas walking through the woods. Well, 10 feet plus some pretty thick glass that we're looking through. Welcome to the world famous Bronx Zoo in New York. I'm here with some 8th graders from Owego, New York in the Congo Gorilla Forest.

GIRL 3: There's a lot of similarities that you can see, but there's also a lot of differences, just structural, like their brain case is smaller.

JOHN HOCKENBERRY: Half a century ago, biologists compared species by looking at body parts and brain size, behavior. Now we have something else to look at, the entire DNA sequence inside our cells, our genomes that help make us us and chimps chimps, aardvarks aardvarks, and algae algae.

JOHN HOCKENBERRY: What percentage of similarity do you think, just guessing between chimps and humans, if you're looking at DNA?

GIRL 4: Probably like 80 or 90?

JOHN HOCKENBERRY: 80 or 90? So that would be like a 10% difference?

GIRL 4: Yeah.

JOHN HOCKENBERRY: What do you think?

GIRL 5: 75, 80%.

JOHN HOCKENBERRY: 75, 80%? Do you know what it really is? Are you ready? Are you sitting down? [laughter]

GIRL 6: Yes, we are sitting down.

JOHN HOCKENBERRY: 99%.

GIRLS: Oh, my gosh. I would have never guessed.

JOHN HOCKENBERRY: I mean, probably there are people in your class that you don't even think are 99% similar to you, right? [laughter] Ooh, touched a nerve.

GIRL 8: Ouch.

JOHN HOCKENBERRY: Okay. Thanks. We'll go down to this end of the table now.

ROSS HARDISON: We have a wonderful resource of many, many new genome sequences that are being determined. Of course, the sequence of the human genome was a revolutionary event for our field.

JOHN HOCKENBERRY: Comparative genomics is a relatively new science. Researchers line up and compare the genetic sequences of different species.

ROSS HARDISON: For comparisons, you need at least two, but we are putting together with our collaborators our alignments among 28 different vertebrate species -- that'd be human and mouse, chimpanzee and macaque and other monkeys --

JOHN HOCKENBERRY: Ross Hardison is director of the Center for Comparative Genomics at Penn State University. The Center analyzes patterns in genomes that contain millions, sometimes billions of bits of information.

ROSS HARDISON: The dog genome is in very good shape, and has been a spectacular resource for study. The cat genome is catching up, and the horse is quite similar to the human genome. We can move over to another continent, Africa, the elephant sequence --

JOHN HOCKENBERRY: As they compare these genomes, scientists are finding subtle differences and surprising similarities in everything from birds to baboons to bacteria.

ROSS HARDISON: And then happily, we're getting several other vertebrate species that are great for certain types of comparisons. Chicken has been published for about two years now. I see a lizard that's coming along that's going to be very useful, and frog -- the frog genome sequence is available, and I think five different fish.

SEAN CARROLL: So we can decode a bacterium. We can decode a virus. We can decode a -- a redwood. We can decode a human using all the same genetic code, and that's just terrific.

JOHN HOCKENBERRY: In the next hour, we'll cross the country visiting the labs and people who are pioneering this new way to look at ancient patterns in DNA. Sean Carroll is a molecular biologist at the University of Wisconsin in Madison.

SEAN CARROLL: So comparative genomics. What do we see when we gaze into genomes, and especially about evolution?

JOHN HOCKENBERRY: Carroll studies how various species evolved to have particular shapes, and what DNA can tell us about how that happened. He's the author of popular books, Endless Forms, Most Beautiful and the Making of the Fittest.

SEAN CARROLL: So the genome is the complete DNA information of an individual, and in us, it contains about three billion bits of individual pieces of information. And what scientists are able to do now is inventory all that information for an individual species. Now this DNA record can tell us about species relationships. It can tell us about how species are different from their ancestors, and of course, it also tells us about the operating instructions for making new individuals. So the DNA record is written in a very simple alphabet, that of just four letters, A, C, G, and T, but it's almost the infinite permutations of those four letters that gives us all the complexity of the living world.

ROSS HARDISON: If you can imagine three billion characters -- and there are only four types of characters -- A, G, C, and T -- and it's the order that they are along these three billion positions that's important.

JOHN HOCKENBERRY: Again, Ross Hardison of Penn State's Center for Comparative Genomics.

ROSS HARDISON: If you line up the genomes of two species, and you find segments that are still quite similar, we say they are conserved. It's an inference that we're drawing.

JOHN HOCKENBERRY: These conserved DNA segments give us a glimpse into the past we share with other species. Researchers are finding similar DNA sequences doing similar tasks in very dissimilar animals.

ROSS HARDISON: That means that they were the same sequence and the last common ancestor, and they're still similar enough for us to line them up. Almost the entire genome has that property between humans and chimp. You go out to mouse and it's a lot less. So we can line up of the order of -- depending on how you do it, maybe 40%. So you can say that 40% of human is conserved with mouse. Then if you line up human with chicken, it's a very small percent of human that lines up with chicken.

So the fact that something is conserved in human and chimps doesn't mean much. It sure means a lot if you can find it conserved between humans and fish or humans and chickens. And in fact what we see, if we look at thousands of regulatory regions, you see that a small fraction of them, about 2% align all the way from humans out to chickens, and they have some very interesting properties. I mean, not only has selection been working on them really hard, so they don't change much, they regulate a certain category of genes. They are the genes that encode proteins that control the fundamental early stages of development.

SEAN CARROLL: How is it that the head is put at the right end of the animal, and you get the right number of digits, and you get this beautiful bilateral symmetry that exists in a lot of animals?

I don't think any biologist is sort of immune to that wonder at how a single fertilized egg becomes a complete complex individual with all of its body parts. And this process we refer to as development or embryonic development.

So only a small fraction of all the genes in our genome are devoted to body building and organ building and sort of the patterning of the way we look. You can sort of think of them, if you want, metaphorically speaking, as the sculptors and painters in our genome. And over the course of a couple of decades, developmental biologists have defined what we call a genetic tool kit for development. It's changes in this tool kit that underlie the diversity of everything we see. A lot of what's going on in evolution is we're just changing the number and identity of particular body parts.

So once sort of making vertebrae was figured out, it's just tinkering with the number of vertebrae or the identity of vertebrae or what's sort of erected on that sort of chassis, and that would be true, whether we're talking about snakes versus humans or even humans versus chimpanzees. You know, the anatomical resemblance between ourselves and the chimps is pretty obvious, but you know, we've got bigger brains, different facial shape, different arm length, and these are really perceived as minor tweaks of anatomy. We're just a remodeled ape, I think. That's what I boil it down to. And this process of remodeling involves using these genes in either slightly to dramatically different ways in the course of evolution.

So it's demystifying a lot of what we found mysterious about biology and about evolution by making lots more connections between the simple and the complex, and this is what we can do through genomes, and this what we can do through developmental biology. We can trace the origins of structures. We can trace the relationships among structures, and we can see all sorts of gradations from really very, very, very simple versions of some structures to what we think is, you know, the more complex grand versions that we carry. So we're finding much more in common with the whole animal kingdom than we ever thought before. And you know, humans wanted to hold themselves out as something unique. Well, the more you look at the genetics, the less unique we are. You know, we don't even have more genes than a puffer fish. So you know, you're just going to have to get over that.

JOHN HOCKENBERRY: So 99% similarity. What does that say to you?

BOY 1: Well, for how much we have, 1% is still a lot.

JOHN HOCKENBERRY: What do you think?

BOY 2: Chimps and their DNA, all of it, all of their chromosomes, it's 1% different. But you have to realize that not all of the DNA actually controls something. A lot of it's just left over from whatever. So in that 1% that's different could be a lot of stuff that controls traits and the brain size and the body hair and the body structure and --

ROSS HARDISON: [laughs] If you try to talk about a percentage human or a percentage chimpanzee, that's a hard thing to define. There's no reason to think that every nucleotide or every base pair in the human genome is important in making you human. It is possible, maybe way more than half of the DNA in our genomes is doing nothing. So what does it mean, if 98% of something that doesn't do anything [laughs] lines up? Right? That's not such an interesting question. The interesting question is: What's different?

JOHN HOCKENBERRY: One clue can be found in our genes. Researchers have found that chimps do share almost all their genes with humans, but they work differently.

ROSS HARDISON: When they see genes whose coding sequences are substantially more different than you would expect, we say, "Well, wow, maybe this has something to do with making humans uniquely human or making chimps uniquely chimp."

GIRL 1: Their eyes are like exactly the same as ours -- the same shape and the same flat face, and 10% of like communication is only words, like only 10%. So it's all about body language and how you act.

JOHN HOCKENBERRY: What do you think the chimps are thinking? Do you think if they knew that you'd actually pay money to watch them stand around? [laughter]

GIRL 2: They probably think we're weird. [laughter]

GIRL 3: And they're kind of like -- they're probably wondering, just like we are, like, "What are they doing?" and like "How do they live?" and stuff.

BOY 2: We're just a little bit more advanced with the speaking, but they can do sign language, which a lot of people can't do.

WILLIAM FIELDS: Here comes Liz. Come up here and talk on this keyboard, okay? Come tell the visitor what you said. So is there anything you would like after the Wasserman test, Panbanisha?

COMPUTER: Coffee.

WILLIAM FIELDS: You'd like some coffee? You would?

JOHN HOCKENBERRY: Coming up, we talk to the animals, and evolve an eye. You're listening to The DNA Files. We'll be back in a minute.

FIELDS: All right. So -- all right.

...
JOHN HOCKENBERRY: This is The DNA Files. I'm John Hockenberry. That's a bonobo, one of the chimpanzees genetically most similar to humans. As our bright young students mentioned, there are some pretty big differences between chimps and us. For example, my human DNA has given me the ability to talk, which is why I can host this program. [laughs] Digging around in genomes may one day help us explain how language works, but to get a better picture now, we first need to widen our view.

WILLIAM FIELDS: Come up here and talk on this keyboard, okay? Come tell the visitor what you said.

JOHN HOCKENBERRY: At the Great Ape Trust, just outside Des Moines, Iowa, researchers communicate with bonobos using symbols or lexigrams. The bonobo sits at a large touchscreen. When she presses a lexigram on the screen, the computer speaks its name.

COMPUTER: Coffee.

JOHN HOCKENBERRY: William Fields is director of research and co-author of the book, Kanzi's Primal Language. No one trained Kanzi and his sister, Panbanisha to use the keyboard. They just watched the older bonobos listen to the humans and learned on their own.

WILLIAM FIELDS: This is Panbanisha. She's the real life of genius.

LIZ: Here you go, Panbanisha.

WILLIAM FIELDS: Okay, it's ready. Come do it. Come do it. She's going to match to sample.

COMPUTER: Brush.

LIZ: Good. Do 15 of them.

COMPUITER: Sue, Sue.

WILLIAM FIELDS: The lexigram comes up, and there's spoken English, and then Panbanisha matches the lexigram and the spoken English to the photograph. She gets several selections of photographs there, and she's really good. The only time she's wrong is when she wants to make a point, and she'll just hit one to be wrong. She's never wrong without intention.

COMPUTER: Popsicle, Popsicle.

WILLIAM FIELDS: She learned just the way children learned language. She acquired it just by being exposed to it, and humans using the lexigrams around her.

COMPUTER: Marshmallow, marshmallow.

WILLIAM FIELDS: We're getting ready to test her receptive vocabulary for English. We know it has to be in the thousands of words, and we'll never really know. We'll just have an idea of the dimension, because it's unlimited. I mean, I know that she knows "microphone," because I've asked her to hand me the microphone before, and she's handed it to me. We don't have a lexigram for microphone. Or I can ask her to go over and see the visitor with blond hair. She knows blond hair. We don't have "blond" on the keyboard. She has all kinds of competencies that we're unable to measure at the moment, because of limitations of the keyboard.

LIZ: I know you're upset, but we're not going to do that.

WILLIAM FIELDS: There you go.

LIZ: This is "clippers."

COMPUTER: Clippers, clippers.

LIZ: Do you want me to come in?

WILLIAM FIELDS: Yeah, Panbanisha got mad at us. We got a little too involved in the whole human conversation thing, and like I told you earlier, they enforce the social rules. The best way she could express her frustration with us was to hit the wrong key for "clipper." I mean, we all know she knows "clipper," just like she knows her name. And she hit it twice for us, just so it would make that noise. [laughs]

COMPUTER: Coffee.

WILLIAM FIELDS: Okay, well, I'm going to get the coffee when you're through.

AL: The order's been placed. [laughs]

WILLIAM FIELDS: What are you hanging around for, Coffee Boy? [laughter] A decaf caramel macchiato is a favorite. Panbanisha and I have spent a lot of time in the forest together. We've made stone tools together. We've camped out. We've made fires, drank a lot of coffee together. She's a really good friend. You're doing good. But they're not human. They are persons, but they're not human. They're bonobos. They have identity. They have autobiographical memory. They have episodic memory. They can identify themselves in photographs. They identify themselves in the mirrors. It's not just that they identify themselves. If you have two of them in the mirror, they can point to themselves, and they can point to the other one in the mirror. They know who they are. They have a history, and they can tell you about it.

Humans are wonderful and special, but they're not any more wonderful and special than any of the other Great Apes or the biodiversity on this planet. Even though we have wonderful talents -- or I think that they're wonderful -- that may just be -- that's just a bias. I mean, I happen to like mathematics, but the bonobos don't seem to do mathematics, even though they can do quantity judgments, and they can do numerosity and ordinality. They're not interested in differential equations, but now that I think about it, neither is my mother.

All right. After you do your Wasserman test, we'll have some coffee, okay?

COMPUTER: Coffee.

JOHN HOCKENBERRY: How would you prove to a chimp that you're more advanced or do you maybe think that you're not?

BOY 1: I think it's -- a lot of it that the main argument is language.

JOHN HOCKENBERRY: Language?

BOY 1: They probably do have vocal chords, but just like not --

BOY 2: They don't know how to use them yet.

BOY 1: Not -- it's being developed.

BOY 2: They're probably just not as developed yet.

JOHN HOCKENBERRY: For years, we've assumed that humans have language, because we've mastered abstract concepts like grammar, symbols, and syntax. But we also know that the human voice box, and brain, are built differently than in most other species. So how do we sort out what's happening in our heads and bodies that's different from other animals?

ERICH JARVIS: To actually answer that question, we have to take a comparative genomic approach.

JOHN HOCKENBERRY: Erich Jarvis studies that genes and brains of vocal learners at Duke University in North Carolina. These aren't animals that can talk, but they are animals that learn to make more than the growls and whistles they're born with, animals that communicate by complex vocalizations. You know some of these animals.

ERICH JARVIS: There are three vocal learning groups of mammals at least and three vocal learning groups of birds. Amongst the birds, these are parrots, hummingbirds, and songbirds, and what we discovered is that these vocal learning birds have very similar brain pathways to control their learned sounds. We argue that the bird brain pathways are similar to humans. The mammalian part of the story is similar. In humans, bats, and dolphins, these are all vocal learners, and yet they are separated by vast genetic differences, but yet you have a chimpanzee, a very close relative to the human, 98% identical in its sequence, is not a vocal learner. So we're also doing genomic comparisons on chicken and chimpanzee and bat to ask the question, "Will bats and humans have a similar type of mutation as you find in songbirds, parrots, and hummingbirds?"

DONALD KROODSMA: We're listening now to a song sparrow singing here, and there's a close relative, a swamp sparrow, both in the same genus.

JOHN HOCKENBERRY: Donald Kroodsma has been studying vocal communication in birds for over 30 years. He's one of the best guys on the planet to take us for a stroll in the woods. He likes to be there before sunrise, of course. That's when the birds sing the best, apparently. So imagine it's 5 AM. You're in the Quabbin Reservoir, a wilderness area in central Massachusetts, shh. Here we go.

DONALD KROODSMA: And what's so intriguing about these two -- they're members of a group called songbirds. And songbirds learn to sing like we learn to speak. And I can say that a thousand times, but wow, then I can show you a sequence of my daughter's babbling and how she babbled at a year and a half to two, and that's something that we've all done to get to where we are so we could speak. Then you compare that babbling of that child to the babbling of a baby bird, and it's exactly the same process, because these songbirds have to hear other adults in order to develop normal songs. If they didn't, they'd just sing absolute nonsense. It's like taking a human child and not ever letting it hear language -- why, it would not speak a language [laughs], recognizable a language either.

And then there's -- there's this bird over here. It's an oven bird, singing on the forest floor. And the mnemonic that we read in the field guides is, "Teacher, teacher, teacher, teacher." It's a crescendo. It's just shattering, and our ears just can't capture what these birds are doing. And these songbirds have ears that are a lot better than ours. They can resolve sounds in time far better than we can.

Any small songbird like the winter wren, once you start to slow it down, it develops this richness, because now we're starting to hear the individual elements, and we're lowering it to a frequency where our ears can pick it up. And you take a tiny little 10-gram wren, and slow it down far enough, it starts to sound like a humpback whale.

ERICH JARVIS: All the research that I've been doing in the past 10 years has been leading up to one conclusion for me, that language or vocal learning in general, what's unique about it in those species that have it -- humans, songbirds, parrots -- is the motor skill part of it.

JOHN HOCKENBERRY: Again, Erich Jarvis.

ERICH JARVIS: And the neurobiology of our results are suggesting that the vocal learning pathways, what's unique about them is they're coming out of a pre-existing motor pathway, not in a perceptual one, or one might call a conscious one or something else.

DONALD KROODSMA: Oh, getting these songs right is an extraordinary athletic endeavor. And a friend of mine published a paper many years ago entitled, "Vocal Gymnastics in Wood Thrush Songs," and that really captures it. If you watch a gymnast flipping and turning in the air, and you think, "What did it take to get her there?" Why, she had to practice and practice and practice, and drive that routine into the neurons and into the brains so that she could do it without thinking. That's what these songbirds do, too.

That wood thrush, when they sing, they actually have two voice boxes, and it really is precision breathing, because they open and close those voice boxes, change the tension, puff the air through one voice box or the other to create this beautiful harmony. And if you're out with them at the right time in August and September, you hear them practicing. You can hear the wavering quality to their songs as they're bringing their whole body back up into singing condition. Everything has to peak for the spring and summer season to create these -- these masterpieces that we're hearing now. So I like to look at each one of these animals out here -- each one of these birds and say to myself, "Each one of those birds has an equal claim to success as I do." This oven bird, he is every bit as much a success as we are, an extraordinary success in the world that he lives in.

JOHN HOCKENBERRY: It's nice to think we might share something as complicated as language with songbirds, and that chimps like Panbanisha try to communicate with us. It makes me feel one with the universe and all. But let's face it. Our tax dollars aren't being spent on science research to make us feel warm and fuzzy. No, all this sequencing and lining up is really big.

FRANCIS COLLINS: This is a landmark occasion. Here in the very month of the 50th anniversary of the discovery of DNA's double helix, I am pleased and honored -- perhaps I should say "exhilarated" to declare the goals of the Human Genome Project to be completed. [applause]

JOHN HOCKENBERRY: That's Francis Collins who helped lead the Human Genome Project, announcing the completed sequence in 2003.

FRANCIS COLLINS: But then the Chinese proverb comes to mind, "Behind one high mountain lies yet a higher one," and so tomorrow, we will be looking beyond the mountain called the Human Genome Project to the next phase of how it is that we can apply this to the betterment of humankind for advances in medicine, which were after all, always the point.

ANTON NEKRUTENKO: When the human genome was sequenced, I think CNN had these headlines that now we're going to solve all the problems. All the diseases will be cured and everything. But in fact, it's very difficult to decode this information. So the only way you can effectively do that is by comparison with something else. Only by comparison you can actually make sense of genomic sequences, and so I'm doing a lot of analysis related to mammals, and Steve is doing a lot of analysis related to flies.

JOHN HOCKENBERRY: Anton Nekrutenko and Steve Schaeffer are colleagues at Penn State's Center for Comparative Genomics. Even before the human genome sequence was finished, scientists started lining up what pieces they could get their hands on with other animals and insects. We've gotten hints about our immune system from the primate genome. From dogs, we're learning about the roots of cancer, diabetes, and epilepsy. Oh, and about Steve Schaeffer's flies.

STEVE SCHAEFFER: It turns out that a lot of the genes that you find in humans, albeit they're distantly related, are found in flies, things that are important for segmentation and the formation of our nervous system and the vertebral column are basically similar between flies and humans. And the beauty of a fly is its generation time is only about two weeks in length, and it turns out that many of the genes that actually are involved with cancer can be manipulated and studied in a fly and nobody really has – you know you don't see PETA coming in and releasing the fruit fly. So the Human Genome Project wasn't just about humans. It was about looking at diverse organisms, developing genomes for model systems that can be experimentally manipulated so that if there are human counterparts in those organisms that we can study them in a laboratory.

***

JOHN HOCKENBERRY: When you look into the eyes of a chimp, do you see anything even remotely human?

GIRL 1: Well, I think we have a lot of similarities, physical and emotional.

JOHN HOCKENBERRY: Emotional?

GIRL 1: Well, just in their eyes. You can just tell how they're feeling some of the time.

GIRL 2: It's more than that, though. Like if you look at their faces, even they have expressions like in the lines of their faces, too, like one of the gorillas we saw out there, he almost looked like he was sitting there thinking about all of us out looking at him, like it was in his eyes, too, but you could kind of see it in the contours of his face.

JOHN HOCKENBERRY: How about -- what do you think?

GIRL 3: I think that chimps like humans have different like intelligence levels. So some might look more intelligent through their eyes than others do.

SEAN CARROLL: For many, many decades, in fact, leading all the way back to Darwin, biologists have been contemplating the origin of eyes.

JOHN HOCKENBERRY: Remember Sean Carroll? He says it wasn't easy to see how evolution came up with something as sophisticated as the eye. That is, until comparative genomics came along with a whole new way to look at the question.

SEAN CARROLL: So one of the most spectacular discoveries I think that's emerged from comparative genomics and developmental biology is that body parts that initially seem so different can have a very similar genetic recipe. And let's take, for example, the eye. One of the most spectacular discoveries made a little over 10 years ago in a very unexpected way is that some medical scientists have been studying mutations that affected the development of the normal human eye, and the counterpart of that gene was known in the mouse. Well, biologists in Switzerland came upon a gene necessary for making the fly eye, and when they scrutinized its sequence, lo and behold, it's the same gene involved in making the human and the mouse eye.

So the fruit fly eye -- the compound eye that's sort of 800 little individual light sensing units and very different from our beautiful, you know, human eye, these are to anatomists entirely different types of eyes, and it's hard to see any connection between them. But yet their formation requires the same gene, and subsequently, several more genes were found that are common ingredients to all eyes. Well, what it's telling us is that a long time ago, when eyes first evolved, they had these genetic ingredients, and that has told us a lot about how evolution works with available materials. It rarely invents from scratch. It starts from something that works, and elaborates upon it. It works from a simple pair of cells, these light sensitive cells, and just makes a lot more of those cells, and arranges them in some pattern on the surface of the animal, and now you've got what looks like a more full-fledged eye.

JOHN HOCKENBERRY: So again the recipe for the eye, if you will, take some light sensitive cells, sort of mush them all together, and pour in lots and lots of time.

SEAN CARROLL: It does stretch the human mind's capacity to think about 1,000 years, 10,000 years. That's a whole history of civilization. A million years. I think that's actually -- humans can throw that number around, but it's inconceivable in human experience what a million years represents. But when I'm talking about the origin of eyes, I'm talking about something that probably got rolling about 600 million years ago. It's had a long time to wind up with compound eyes of flies and camera eyes of other animals, etcetera, and we can trace this by finding sort of the roots of the process in very simple organisms and in very simple organs, and what we're having to do is sort of take away so much bias that's been around in humans for centuries about we being more complex and about we requiring more special explanations, and understanding that our organs and our bodies are just an elaboration of a game that's been going on at least in the animal kingdom for 600 million years.

JOHN HOCKENBERRY: Coming up, my brother, the bacterium. That's in a minute on The DNA Files. I'm John Hockenberry, and this is "Beyond Human."
...
JOHN HOCKENBERRY: Welcome back to The DNA Files. I'm John Hockenberry. We're exploring comparative genomics. We line up our human DNA with the fruit flies, with the chimpanzees. Some stuff lines up. Some stuff doesn't. It's not like looking eye to eye.

They're so much the same and lots different. Let's go back to Erich Jarvis, the neurobiologist from Duke University. He compares genes to the brain pathways of vocal learners like parrots, songbirds, and bats, and me. I'm a vocal learner, but am I closer to a parrot or closer to my dog?

ERICH JARVIS: When you take this comparative approach, you start to realize, "Okay, what's really unique about language?" Spoken language is the ability to produce sequences of non-innate sounds, and yes, and have meaning to them. Well, there's something called auditory learning, the ability to make sound associations, and your dogs have it, your cats have it. So say, "Come here, boy" or "Fetch the newspaper" or "Sit" in English. "Osuwari" in Japanese also means "sit." These are not part of a dog's innate repertoire. Yet it has the ability to understand these human speech sounds and even some syntax, but those dogs cannot say it. But a parrot can and a human can, and the difference between a parrot and a human -- they're vast, but the difference between a parrot and a songbird is equally, if not more vast.

So to think that, okay, mammals are more advanced. So their brains are going to be more advanced. Well, whoever said mammals were more advanced? That kind of thinking led people to come up with these terminologies that had those definitions in it of lower to higher order and behavior complexity and intelligence. Pervasive throughout the field of science, even today, is the terms like lower vertebrates, higher vertebrates or lower primates, higher primates, and they look for brain structures or brain pathways that fit that kind of view. But when you really look, you can't find them.

JOHN HOCKENBERRY: When scientists start tearing down their assumptions, setting aside things they think they know and start asking questions in a new way like Jarvis is doing up there, well, [laughs] prepare to be surprised.

ERICH JARVIS: When we found that these brain pathways for vocal learning were so similar, more than we would have had expected, in these various different animals, we thought that it seems to be something simple that should drive this evolution of this brain pathway, but the answers that we're coming up with, it seems to maybe involve more than just the genetic change, but how an animal interacts with its environment. So we think that females of certain species or even the males like a male who produces a variable song with variable syntax, and the more variability you have, the more likely she's going to mate with you, like a jazz singer. Think about it in that way. And so that female selecting for that behavior then influences which genes get selected for in the next generation.

So with vocal learning behavior, these songs as our language is passed on culturally from one generation to the next. So here you have a non-genetic inheritance of a behavior. Well, how is that behavior actually then selecting upon the genes? And so I argue that there's a positive feedback loop. The behavior gets passed on in a learned way from one generation to the next without the direct influence of genes except the control of the behavior itself, but then that behavior then gets selected upon to become more and more variable through this cultural transition from one generation to the next.

JOHN HOCKENBERRY: Surprise. Maybe you thought only humans had culture, like table manners, poetry, symphonies. Jarvis says birds can pass songs down the generations. That's culture. Culture affects the way songbirds choose mates and evolve just like us. I wonder. Is lining up genomes really the best tool for identifying our similarities and our differences? I mean, where's the romance? Boy meets birds, bird meets song, chimp meets whatever.

BOY 1: No other animal really looks like -- at all like us, and chimps sort of do.

GIRL 2: Like we're their bald ancestor or something. [laughter] When you think about us, our only advantage is the fact that we're smart. I mean, you look at humans, we're like this scrawny, hairless, little thing, and almost any animal could overpower us physically. Our only advantage is intelligence. That's the main thing that sets us apart.

GIRL 3: But we're not sure of that.
DANIEL POVINELLI: Hey, how are you doing, huh? Huh? How's it going? How's it going?

JOHN HOCKENBERRY: Even without peering into anyone's DNA, it's pretty obvious that humans are not the same as chimps. I mean maybe as babies, we look an awful lot alike -- round head, flat foreheads, small jaw, but as we grow up, the paths diverge. We start thinking differently. At the University of Louisiana, cognitive researchers are trying to find out when that happens. They compare how children learn with how chimps learn. They asked, "When did children start to develop the kind of abstract concepts that chimps can't grasp?"

DANIEL POVINELLI: My name is Daniel Povinelli. I'm a professor at the University of Louisiana, and we're here at the Cognitive Evolution Group's chimp testing facilities n New Iberia, Louisiana.

JOHN HOCKENBERRY: Povinelli has been testing a group of chimpanzees since 1991. Many of these chimps were born and raised right here in this indoor/outdoor facility. Outside, they're free to swing and spit and be their chimp selves. Inside, researchers test the chimps' cognitive skills. Can they put round objects in round holes? Can they separate heavy objects from light ones? Young human children at the nearby Center for Child Studies take the same tests. The kids quickly master general concepts like shape or weight. Yes. The chimps can, too, but might have to learn them all over again the next day. [laughs] Povinelli wrote a book about his work called Folk Physics for Apes: The Chimpanzee's Theory of How The World Works.

DANIEL POVINELLI: I think the problem we have as human beings in getting our mind around, "Well, how can we be so similar to apes in our DNA profile, in our bodies, in the way we move through space and our gestures, etcetera -- how can we be so similar to them and at the same time apparently so radically different?" And so it tempts us into this zone of saying, "Well, maybe we've just sort of souped up the basic ape mind, and we're just quantitatively, massively better than chimps at all of these areas." But you know, when you really look hard at the experimental data that scientists have been struggling to accumulate about the similarities and the differences between humans and chimps, it really looks as if there's a qualitative, fundamental difference in this abstract, symbolic level of thought.

JOHN HOCKENBERRY: But what causes that fundamental difference? All our human bravado about being more intelligent, knowing mathematics, knowing architecture are just symptoms of something deeper. Is it even possible to find the source of this difference between humans and chimps?

DANIEL POVINELLI: So a lot of people want to know, "Well, if there is this qualitative difference, where is it encoded? Is it in the genes? Can we identify a particular segment of the genome or regions of the genome? Can we identify the brain areas that are different that support this level of abstract thinking?" And they really want something that concrete. But of course, biologists know better, that these are complex developmental systems that don't necessarily code one for one in a simple fashion, but rather set up a brain system, a mind system that can, depending on the environment it's raised in, can form different kinds of abstract thoughts. But it's all nested within this potential, this developmental potential to become a part of the human species.

You know, a lot of people engage in debates back and forth about, "Well, should we start with the supposition that they're similar, or should we start with the supposition that they're different?"Well, I just think that that's fundamentally the wrong way of looking at it. Let's just start with the supposition that we don't know, and let's develop the best possible tests -- and admittedly, they're crude at this point in our understanding of the mind -- but the best possible tests for elucidating what the similarities are and what the differences are. Because let's face it, the human mind is incredibly powerful. It wants to go out and reshape the world in its own image. But is that really what we want to hinge our understanding of chimps on, is the way in which our minds work? I don't think so.

I think we want to create a space, an intellectual space, which gives them the opportunity to say, "Yeah, we're very much like you here. No, we have no idea how you think here." And it's that intellectual space in science that's ultimately going to allow us to understand our place on this planet -- what makes us similar and grounded to the other species on this planet, and also the obvious radical ways in which we've departed from the natural world.

JOHN HOCKENBERRY: Maybe we're asking the wrong questions of our DNA, or maybe our DNA doesn't have all the answers. What are we really trying to find out anyway? We want to understand evolution. We want to know why we're here, why birds sing, how chimps think. We know we're all related, descended from one ancient ancestor, and that random genetic differences are handed down through generations -- that is, if they turn out to be useful for that population. So why are we the ones that survived? Why us? Evolution, a struggle to survive, a competition to adapt. Is that really what's written in our genes? Maybe we should be thinking of evolution in a different way. I kind of like the idea that I'm cousin to a chimpanzee, choir mate to a chickadee, yeah. That's nice. But nephew to a mold? Have you ever thought about all the species that live in our guts and on our skin and alongside our eyeballs? Yeast and E. Coli were some of the first species to be sequenced. Am I a bacterium's brother?

MARK MCMENAMIN: We represent a bacterial community on foot, [laughs] so to speak, all bacteria.

LYNN MARGULIS: The fundamental unit of life is bacteria, absolutely. The bacteria got together into communities, and made all kinds of things, but one of them is the ancestor to all the nucleated organisms.

MARK MCMENAMIN: Yes.

JOHN HOCKENBERRY: Lynn Margulis and Mark McMenamin see the world in terms of relationships, of cooperation, a web, not an ancestral tree. These two worry that scientists will get stuck looking at genomes, comparing one to another like life is lined up on a ladder, and then they might miss what's right in front of their faces, like moss on trees, bacteria in our guts.

LYNN MARGULIS: So the basic idea is that what we think is an individual is in fact a community of many individuals in a coordinated way. It's an evolution.

MARK MCMENAMIN: Yeah, it's an evolution. So what we're walking around now is our corporeal bodies, which are microbial communities that are inside of us. They represent an ancient ecology that has become fixed in place, so to speak.

JOHN HOCKENBERRY: Lynn Margulis is an important contributor to what's called "GaiaTheory." The concept that sediment, air, water, and living beings form one vast interdependent system. She says life is one big bundle of symbiosis -- organisms working together. Paleobiologist Mark McMenamin looks at life that way, too. What's more, according to these two scientists, we don't just live together, we move in together. We cohabitate, and we become something altogether new. Together. That's what they call “symbiogenesis.”

MARK MCMENAMIN: Symbiogenesis is when a sea anemone picks up some kind of photosynthetic microbe, and the photosynthetic microbe lives inside of its tissues and starts creating sugar. Suddenly the sea anemone has so much energy, it doesn't know what to do with it all, and it forms a coral reef.

LYNN MARGULIS: Exactly, but what he didn't tell you is sea anemone is not an anemone like a flower. It's an animal. So what he's talking about is the evolution of a green animal. An animal can be photosynthesized. It's as if we shaved your head, and we took little algae, little plant things or plants, and put them under your scalp, and you sat in the lights, and you didn't have to go running around, looking for food.

JOHN HOCKENBERRY: You might call that brain salad surgery. You know, I think I have that album somewhere in my basement still. I'm not sure I'd like that, but it could be handy. Evolution is all about adapting like this to an environment, and cooperation can be as important as competition. While walking through Harvard Forest in western Massachusetts, Mark McMenamin with his daughter, Jenny, and Lynn Margulis talked about the evolutionary effects of cooperation. Species don't just help each other; they share their operating systems, their genomes.

MARK MCMENAMIN: Instead of evolution being a process of one organism saying to another, "You're in my space. I'm going to kill you," it's about a group of organisms wanting to perpetuate an ecology.

LYNN MARGULIS: Look at this tree.

MARK MCMENAMIN: You see how this dead tree is just --

JENNY MCMENAMIN: Ew, it feels weird.

MARK MCMENAMIN: Covered with shelf fungi.

JENNY MCMENAMIN: Oh, it feels really weird.

MARK MCMENAMIN: We're looking at a dead tree that has white shelf fungus all over it, coming out of the bark, and this is not a situation in which a spore of the fungus has floated through the air and landed on the tree and started growing, but rather this is fungus that was inside of the tree that is now coming out, because a tree cannot live on land without its fungi. It is creating an environment for the fungus, but the fungus is sustaining the tree as well. The connection here is totally symbiotic. You can't have life on land without it.

JENNY MCMENAMIN: It needs the fungus to live?

MARK MCMENAMIN: It needs the fungus to live, yes. 90% of all trees --

JENNY MCMENAMIN: That's weird. I thought it just needed like sunlight and water.

MARK MCMENAMIN: No, it needs more. It needs the mineral nutrients. Once it gets them, it can produce so much sugar that it passes this down to the fungus, and so sugars are being pumped into this fungal ,bodies in the soil, and in exchange, the fungus is pumping mineral nutrients into the trees, and so there's a two-way flow. Minerals going up, sugars going down.

JENNY MCMENAMIN: Daddy, look at the inside.

MARK MCMENAMIN: Yeah, there's the inside of the shelf fungus.

JENNY MCMENAMIN: What's that called?

MARK MCMENAMIN: Those are the spores, yeah.

JENNY MCMENAMIN: Weird.

MARK MCMENAMIN: Yeah.

JENNY MCMENAMIN: It feels weird. It feels like a bone.

MARK MCMENAMIN: You -- you can't really distinguish the individual in the plant fungus situation. It's the -- the extension of the marine bio to coming on to deadly, dry land habitat and terraforming it, transforming it, and it can only happen with the symbiosis.

JOHN HOCKENBERRY: If Lynn Margulis and Mark McMenamin are right, comparative genomics might only be a starting point here. Stay with me now. Lining up genomes and checking for mutations, sorting out what's been added and what's been lost over the millennia, that can tell us a lot. I mean, we can see ancient similarities in our operating machinery, how an amazing structure like the eye developed, how the life forms we see today took shape, but to really understand evolution, we might need to throw out some old ideas, old ideas about the meaning of our differences, about competition. Maybe we're not just in this for ourselves. The story of life is written in our genes, but not just in our genes. DNA is only part of the story. Evolution and the way we think about it continues to evolve.

Thanks to Houghton Mifflin for allowing us to use the birdsong CD from Donald Kroodsma's book, The Singing Life of Birds. Thanks also to our students from Owego, New York, and thanks for listening to The DNA Files. I'm John Hockenberry.

To find out more about comparative genomics, visit our website at dnafiles.org where you can download a podcast of this program. This series, The DNA Files, was produced by SoundVision Productions with funding by the National Science Foundation, U.S. Department of Energy, National Institutes of Health, and the Alfred P. Sloan Foundation. This program, "Beyond Human" was produced by Barrett Golding. The DNA Files is managing editor, Loretta Williams, editor, Deborah George, science content editor, Sally Lehrman. Research director is Adi Gevins. Production support by Noah Miller, Julie Caine, and Jenn Jongsma. Office support provided by Steve Nuñez and Beverly Fitzgerald. Our web director is Ginna Allison. Technical engineer and music director is Robin Wise. Our host is John Hockenberry. Our theme music was composed and performed by Steve White. Additional music by Jeff Arntsen, Conrad Praetzel, and Robert Powell. Marketing of The DNA Files is by Schardt Media. Legal services by Cooper, White and Cooper and Spencer Weisbroth. Special thanks to Murray Street Productions. Send your responses and letters to feedback@dnafiles.org. For CDs and transcripts, call 888-303-0022. That's 888-303-0022. The executive producer is Bari Scott. This has been a SoundVision production, distributed by NPR, National Public Radio.

The DNA Files:
Unraveling the Mysteries of Genetics

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Rewriting Heredity: Environment and the Genome

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JOHN HOCKENBERRY: This is The DNA Files. I'm John Hockenberry. In the next hour, a collision with the American diet leaves an indigenous people reeling from runaway obesity.

PETER BENNETT: They had an extremely high prevalence of diabetes that was estimated to be eight to ten times higher than in any other population in that particular time. In truth, we had really no idea what the underlying causes were.

JOHN HOCKENBERRY: Meanwhile, in the Court of Long Beach, an asthma epidemic, but the sufferers tend to be related.

KARENA HAMILTON: My mom takes daily medicine for it, an inhaler, and my sister does as well and her daughter.

JOHN HOCKENBERRY: And scientists are learning that our genes and the environment are entangled in an embrace that may alter our legacy to our children and our children's children. Join us for "Rewriting Heredity: Environment and the Genome" after the news.
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JOHN HOCKENBERRY: This is The DNA Files. I'm John Hockenberry.

Welcome to New York City, eight million sharp elbowed homo sapiens, crowded together, breathing, eating, jostling.

JOHN HOCKENBERRY: Hi, how are you doing?

JOHN HOCKENBERRY: Each one a little different, but all immersed in the same complex environment. Truck exhaust. [laughs] There's somebody smoking over there. That means I'm smoking.

JOHN HOCKENBERRY: Sorry. It's okay. It's fine. I don't want to cause a fight.

JOHN HOCKENBERRY: Like pedestrians in a crowded city, the chemistry of the human body is constantly being bumped and elbowed by the environment -- pollution, pathogens, stress --

JOHN HOCKENBERRY: Whoa. Hey. What are you trying to do, kill me? Hey, you almost ran over me, what's going on?

JOHN HOCKENBERRY: Even what you eat and drink affects the chemistry inside your body where the crucial genetic machinery does its work. From the gene's point of view, your diet is part of the environment, but each one of us responds to this environment a little differently. Hang on a second.

JOHN HOCKENBERRY: Hot dog? Hot dog?

VENDOR: Hot dog? How many?

JOHN HOCKENBERRY: Yeah, with everything. One.

VENDOR: Okay.

JOHN HOCKENBERRY: With everything.

VENDOR: Okay.

JOHN HOCKENBERRY: I mean, everything.

VENDOR: Okay.

JOHN HOCKENBERRY: Take this New York delicacy, for example.

JOHN HOCKENBERRY: Oh, yeah.

VENDOR: 2, 3, 4, 5. Thank you very much.

JOHN HOCKENBERRY: Change.

VENDOR: Have a nice day.

JOHN HOCKENBERRY: All right. Thanks so much

JOHN HOCKENBERRY: A hot dog wolfed down on the street isn't on anybody's celebrity diet plan, but some people can eat anything, and never gain a pound, while others diet constantly, and just can't seem to lose weight. Well, no mystery there. It's genetic, right? Some people are just naturally slim. So, then why is America suddenly in the midst of an obesity epidemic? Are we all changing genetically?

For nearly a century, geneticists have searched for the code that makes one person fat, another thin, one sickly, the other robust. The quest has drawn them into a labyrinth of genetic pathways and environmental turning points, the plan of which is still unknown. In the American Southwest, one historically isolated population has been devastated by unprecedented rates of obesity and diabetes. For more than 40 years, scientists have been asking why. Producer Vicki Monks reports from Arizona.

VICKI MONKS: An hour before sunrise, 15 Tohono O'odham runners leave their encampment on the sacred mountain southwest of Tucson, Arizona, descending the mountain, moving across the desert floor. The runners are lean, athletic, conditioned to the Sonoran desert heat that's pushing over 100 degrees before 10 AM.

Runs similar to this one have been part of sacred ceremonies going back longer than memory. Not so many years ago, nearly all the Tohono were as fit and healthy as these runners, but now, too many people are overweight, in wheelchairs. Some have amputated feet or legs from diabetes. Tohono are Pima Indians who have inhabited what is now the American Southwest for millennia. Their cousins, a bit to the north, occupy reservations on the Salt and Gila Rivers bordering the Phoenix metropolis.

Epidemiologist Peter Bennett visited the Pimas at Gila River in the 1960s to study rheumatoid arthritis, hoping to find arthritis free populations in this hot, dry climate. The study was a disappointment. There was plenty of rheumatoid arthritis among the Pima, but he noticed something else.

PETER BENNETT: They had an extremely high prevalence of diabetes that was estimated to be eight to ten times higher than any other population in that particular time. Of course, we didn't know why it was so frequent. One hypothesis was simply that the Pimas might have been a genetic isolate, and for some unknown reason, those few people with diabetes genes had multiplied and formed the Pima tribe. That was one hypothesis.

VICKI MONKS: Another hypothesis was that some environmental agent was responsible.

PETER BENNETT: Another pretty wild idea, but nevertheless one that we examined at least to some extent was that perhaps the toxins provided by scorpion bites would precipitate diabetes, because there was some fractional evidence that the toxins in scorpion bites would actually cause hypoglycemia in I believe it was mice, if I recall correctly. So, that was one possibility, and of course, that fell flat on its face, too. We could find no evidence that there was an excess of scorpion bites among those who had diabetes as compared to those that did not. In truth, we had really no idea what the underlying causes were.

VICKI MONKS: Diabetes and obesity are closely linked. Obesity is the greatest risk factor for adult onset diabetes that usually develops after age 35. Bennett began to look for high rates of diabetes or obesity in other populations. By that time, he had been joined by other researchers with their work funded through the National Institutes of Health. The team discovered another desert tribe with extraordinarily high rates of both diseases -- the Tohono O'odham, closely related by language and culture, to the Pimas at Gila River. That discovery reinforced the plausibility of a genetic explanation, but what was it, and how might it work? Eric Ravussin, a young specialist in obesity joined the team in Phoenix to investigate how the Pima might be examples of the thrifty gene hypothesis, first postulated in 1962 by pioneering human geneticist, James Neel.

ERIC RAVUSSIN: And he postulated the hypothesis that diabetes has to be associated with a survival advantage. He didn't know what it was.

VICKI MONKS: According to Neel's scenario, the ability to store fat conveyed an evolutionary advantage.

ERIC RAVUSSIN: Larger weight was a good thing in the history of mankind. It's only over the past 70 years that it's becoming a bad thing. Our genome, which has been modified over thousands of years have been adapted to scarcity of food and not abundance.

VICKI MONKS: Eric Ravussin and other NIH researchers embarked on a more than 40 year quest to find evidence of a thrifty gene operating in the Pima Indians. Along the way though they discovered several things about how and why people gain weight, and why it's so difficult to lose it. But to understand, we need to back up and follow the path the Pimas took into the modern world.

WOMAN: Squash, cheese, uh shredded beef, green chile, corned beef, red chile burro, and bean and cheese, and soda.

VICKI MONKS: In Sells, Arizona, on the Tohono O'odham reservation, everyone drives cars these days. So, it's the parking lots where vendors do their best lunchtime business. You can buy pork tamales, pizzas, sodas -- high fat, high calorie quick food.

TERROL DEW JOHNSON: You know, I used to drink at least a 12-pack of soda a day. Two, three in the morning, two, three for lunch, two and three or four for dinner.

VICKI MONKS: At 6 feet tall and 300 pounds, Terroll Dew Johnson seems an unlikely figure to be the leading health advocate on the reservation, but over the past 12 years, his organization, Tohono O'oodham Community Action or TOCA has been fighting some of the more destructive effects of modern life by helping people reclaim traditional diets.

TERROL DEW JOHNSON: This is the food the Creator gave us. This is what kept the people in a desert, where there's hardly any rainfall, alive for thousands of years.

DANIEL LOPEZ: Sometimes we just walked out in the desert to look for mesquite bean when they were in season. That was our sweet. The mesquite sap called usabi

VICKI MONKS: Daniel Lopez was born in 1936 when most Pimas still held to traditional ways, relying on desert plants for food. Cholla buds, mesquite beans, wild spinach, the sweet red fruit of the saguaro cactus, and there was plenty of physical activity.

DANIEL LOPEZ: Well, we didn't have TV. We didn't have Game Boys, but our playground was the desert, and the girls were over there by this clearing near the ceremony house, and they're playing the woman's game called Toka. I mean, you're running back and forth -- that's a very active, strenuous game, the same thing with the kickball that the boys played. We ran all the way up there, barefooted, you know. But we did it back then.

VICKI MONKS: But changes were coming fast.

DANIEL LOPEZ: Maybe around the 1940s, the cotton field era came in, and the farmers would come out and recruit O'odham families to go and pick cotton. That's when I say the traditional farming began to decline, because so many people were gone, because to go to the cotton field, chop cotton, starting May, then pick cotton, starting about September, and yet you plant in the summer time. That's when you plant it traditionally with corn, beans, and squash, but now the farmer take it to the store, and you can purchase your canned goods, your bread, your soda, your candy, probably the things that we shouldn't have been eating, but this was things available, you know. We had no choice. That's the only thing we could eat, you know.

VICKI MONKS: Then came World War II.

TERROL DEW JOHNSON: My grandfather was in the Navy. He was taken from his farm and put on a boat where he learned how to cook doughnuts.

VICKI MONKS: When the war ended, Terrol Johnson's grandfather couldn't find a job on the reservation. So he improvised.

TERROL DEW JOHNSON: He made doughnuts in the village and would sell them to people to make maybe one cents or two cents. People loved it, because it was something different.

VICKI MONKS: By the 1950s, the pressures to abandon traditional lifestyles intensified and the disruptions that began with the cotton fields and the war accelerated. As Arizona cities grew, so did demands for water. So the federal government stepped in with money to dam the rivers. That brought traditional farming to an end, and pushed Pimas into the cash economy, earning the lowest wages. Healthy eating can be expensive, and there was the pressure to fit in.

DANIEL LOPEZ: We could eat like you guys, you know -- eggs and ham and all that. The thing is mindset, you know. But we wanted to be like the dominant culture -- dress like them and talk like them, eat like them.

VICKI MONKS: Of course, Pimas value modern innovations as much as anyone else. The Internet's an important tool on the reservation, and without cars to travel vast expanses of desert, it could be nearly impossible today for the Tohono O'odham to hold jobs or carry on business. But changes over the past 60 years have been disastrous for Pima health. College professor Tony Chana recalls his own diagnosis with diabetes in 2002, when he was 63 years old.

TONY CHANA: My blood sugar was over 500. They put me on IV and said that I was critical. And when I was lying there, taking the IV, I thought about all the kinds of things that people who have diabetes seem to go through -- many of my friends who have diabetes where they've lost their toes, some of them who eventually died from failure of heart or something like that -- diabetes related, I'm sure. Now I see it in people younger than myself, and it's tragic, even kids who have diabetes.

VICKI MONKS: More than three-quarters of older Pima adults have diabetes, and this adult onset disease is now showing up in Pima children as young as 7. Obesity among children is the culprit.

JOHN HOCKENBERRY: When The DNA Files returns, measuring a metabolism. This is "Rewriting Heredity: Environment and the Genome." I'm John Hockenberry. We'll be back in a minute.

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JOHN HOCKENBERRY: Welcome back. This is The DNA Files. I'm John Hockenberry. It was a promising hypothesis -- a tribe living where food was scarce might harbor a thrifty gene that promoted fat storage. One way such a gene might work is by lowering the rate of metabolism. Perhaps the Pima was fat, because they conserve more calories. Investigator Eric Ravussin's team began the painstaking work of measuring the metabolic rate of the Pimas, one individual at a time. And in Phoenix, they built a special sealed room called a metabolic chamber to do the measuring, a facility much like this one, back on the streets of Manhattan, at Columbia's New York Obesity Research Center.

DR. ALLAN GELIEBTER: A metabolic chamber is used to measure the amount of energy that an organism consumes by measuring the amount of oxygen consumed and carbon dioxide produced.

JOHN HOCKENBERRY: Dr. Allan Geliebter is a senior research scientist to Columbia University. In metabolism, you'll remember, the body consumes oxygen, and produces carbon dioxide. Got it? So a person in a sealed room gradually changes the composition of the air. You may have noticed this. The faster their metabolism, the faster the change. So as the air in the room is gradually refreshed, scientists can measure the gases in this outgoing air.

JOHN HOCKENBERRY: It looks like a regular hospital room, sort of, but uh we've got the vacuum door there.

JOHN HOCKENBERRY:There's a sink and other necessities for a 23 hour visit. Tasty meals arrive periodically through an airlock.

DR. ALLAN GELIEBTER: No, we'd rather people in here are not bored. We do have some nice videos.

JOHN HOCKENBERRY: The Abyss, Special Edition, Fargo.

DR. ALLAN GELIEBTER: It's one of my favorites, Fargo. There's a window they can look out.

JOHN HOCKENBERRY: And if you put up a little "Help Me" sign, you can just put it up to the window there.

JOHN HOCKENBERRY: In Phoenix, more than a thousand people spend up to a week in Eric Ravussin's metabolic chamber, but the researchers found no evidence that the Pima had a thrifty metabolism. Then the investigation took an unexpected turn with the discovery of another native population in a remote part of Mexico. They were also Pima, and they were thin. Vicki Monks picks up the tale.

VICKI MONKS: The village of Maycoba nestles beneath dramatic cliffs in Mexico's Sierra Madre Mountains. Traveling there can be risky. Livestock or fallen rocks often block the narrow highway. In the mid-90's, when scientists first came here, the road had just opened. Before that, if you wanted to get to Maycoba, you could drive down a steep gorge and through the river or take your chances on a rickety footbridge.

In a highland meadow near Maycoba, Pima elder Jose Angel Galaviz is constructing a wooden plow for planting corn. It's built on the same design used by his ancestors who inhabited this region for at least 500 years, when it's believed they drifted apart from their Pima cousins in Arizona. Wiry, thin, and muscular, like most of the Pimas here, Angel is fit by default. Survival for Maycoba Pimas depends upon constant work.

JOSE ANGEL GALAVIZ: (speaks Pima)

INTERPRETER: One person turns the ground with burros or with oxen, and the other goes to plant, and then the corn is born. When the cobs are there, then you start to pick -- to pick the corn. So from there, we can feed all of the indigenous companions for the whole rest of the year.

VICKI MONKS: Scientists working with the National Institutes of Health who had been studying the Arizona Pimas wondered if the Maycoba Pimas could help prove the thrifty gene theory. They reasoned that even though intense physical labor and a limited food supply kept the Maycoba group thin, the Pimas there might still be genetically susceptible to obesity. In 1995, the scientists hauled a trailer into the mountains to set up a makeshift research station. It's been shuttered now for several years, and locks were rusty when Julian Esparza and Leslie Schulz opened it again last spring, their first visit in more than a decade.

LESLIE SCHULZ: Yeah, it was pretty fancy at the time. [laughs] Now it doesn't look quite so fancy any more.

JULIAN ESPARZA: You see?

LESLIE SCHULZ: Yeah.

VICKI MONKS: Esparza and Schulz are both specialists in the nutritional aspects of diabetes and obesity. Collaborating with other scientists under a grant from NIH, the team ran the same battery of tests here in 1995 that they’d used earlier in Arizona. If the Maycoba Pimas had thrifty genes, the resting metabolic rate should be lower than that of non-Pimas. Eric Ravussin was part of the team.

ERIC RAVUSSIN: And in the same environment, there are people calling themselves "blancos" or "mestizos" who are not Pimas, and they are different genetically, but they live in the same environment. And we're hoping to find a difference between Pima in this environment versus non-Pimas.

VICKI MONKS: But as it turned out, there was no difference. The Maycoba Pimas didn't have thrifty metabolisms. The research team in Mexico now expanded the investigation to include environmental factor, such as diet and physical activity Leslie Schulz turned to doubly labeled water, a technique for measuring energy burned as people carry on their daily lives A research subject drinks a short glass of special water containing heavy isotopes of hydrogen and oxygen that can be tracked as they're gradually eliminated from the body.

LESLIE SCHULZ: It's perfectly safe. It sounds terrible when you say you're giving people this water that has isotopes in it, but they're both stable, and they're perfectly safe to consume.

VICKI MONKS: A few hours after someone drinks the water, researchers collect a urine sample, then wait one week, and collect another. By comparing the ratios of hydrogen to oxygen in