Award-winning journalist Maryn McKenna talks about her latest book, Big Chicken: The Incredible Story of How Antibiotics Created Modern Agriculture and Changed the Way the World Eats, and how the drugs helped increase the problem of antibiotic resistance. (Part 1 of 2)
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Mirsky: Welcome to Scientific American’s Science Talk, posted on October 17th, 2017. I’m Steve Mirsky. On this episode…
Maryn McKenna: I think most people think of antibiotics as only a thing that goes into humans in a medical context. But around the world, at least twice as many antibiotics go into livestock.
Mirsky: That’s Maryn McKenna. She’s a journalist and author specializing in public health, global health, and food policy. She’s the author of the award-winning Superbug: The Fatal Menace of MRSA, concerning antibiotic-resistant bacteria, which we talked about on the podcast back in 2012. Her new book is Big Chicken: The Incredible Story of How Antibiotics Created Modern Agriculture and Changed the Way the World Eats. She was in New York recently and we met at the Scientific American offices. Here’s part one.
The chicken that we take for granted, like so many other foods – I was thinking about tomatoes while I read Big Chicken. The chicken that we take for granted is nothing like the chicken that, for example, our grandparents grew up with, probably.
McKenna: Absolutely correct. Our chicken that we eat today that is so common to us, that we barely notice it, that is the meat that Americans eat more than any other, is the product, positively and negatively, of a whole bunch of technological innovation that takes place in sort of rolling waves across the 20th century. So, our chickens are bigger when they’re killed. They’re younger. They taste different. They behave differently. A chicken that our grandparents or great grandparents would have had out in their backyard does not look like the chickens that are coming out of industrial poultry production today.
Mirsky: It doesn’t look like it, it doesn’t behave like it, it doesn’t taste like it. We’ve basically modified chickens to be tofu. They’re not particularly flavorful. They’re soft. And you talk about eating chickens that you get in France that are completely different.
McKenna: That’s right. So chicken – our modern chicken – is, as you say, it’s sort of like a block of tofu with legs. It is big, it’s pale, it’s soft, it’s docile, because the type of production that we have built around it requires an animal to be docile. If they were not docile, they wouldn’t survive in those very large, very crowded sheds. Chicken elsewhere is different, because chicken elsewhere, among other things, has retained both different forms of production, but also different genetics that were sort of put on the shelf when the modern American chicken was developed, as not important or as not desirable.
Mirsky: Everything was sacrificed, like in the tomato, for quick marketability. Flavor was not really a factor in the choices that big agriculture made to make so many chickens. I mean, you have a figure in the book, 9 billion chickens in the US.
McKenna: Just 9 billion broilers.
Mirsky: Broilers.
McKenna: The United States produces almost 9 billion meat chickens every year. And that’s setting aside, you know, the birds that are hatched in order to be laying hens and produce eggs. So, yeah, so I think that tomatoes, actually, are a good analogy for what happened to the chicken, because our modern chickens have been bred and fed and dosed with antibiotics to produce certain effects. And the primary effect is that they can be produced very rapidly, very consistently, and very affordably.
Depending on your point of view, those are good things. You know, those are things that allow us to have the most consistent, most available, least expensive protein that has existed in American life, and increasingly in the life of the rest of the world, for a very long time. But in the journey toward the very available, very inexpensive, very reliable chicken, we sacrificed a bunch of things.
And among the things we sacrificed are what chickens taste like, because that fell way down the list of priorities for the people developing the modern chicken. We sacrificed their ability to express chickens’ natural behavior. So, if you think of those grandparents’ or great-grandparents’ chickens that we mentioned, the thing that you think of is that they’re kind of scratching around the barnyard and flapping up onto things.
Most modern broilers don’t do that. To some degree, most modern broilers are actually hurt by their inability to do that. They have leg problems because their bodies are so heavy. They have muscular problems because they develop so much muscle tissue that their circulatory systems can’t profuse the muscle. And so, after they’re slaughtered, it’s not uncommon to find necrotic areas of muscle, or what’s increasingly being called woody breast disease, which is hardened, whitened areas of muscle where the muscle couldn’t fully expand as it was growing.
So, while there are positives in terms of feeding the world with what we did to the world, there are a lot of negatives as well for biodiversity, for our experience of that protein, and for the chicken itself.
Mirsky: But the real key thing in terms of human health that we want to talk about and that your book goes into extensively is the antibiotic resistance that accompanied the growth of the Big Chicken agriculture industry, because they go hand-in-hand.
McKenna: So, chicken plays a fascinating role in the development of what we can call the sort of modern protein industrial complex, because that protein industrial complex has been built, since the late 1940s, on the routine use of antibiotics in meat animals. I think most people think of antibiotics as only a thing that goes into humans in a medical context. But around the world, at least twice as many antibiotics go into livestock as go into humans.
And unlike in the human context, most of those livestock are not sick. They’re getting the antibiotics either because they cause the animals to put on weight faster, or because they protect the animals from developing diseases in the confined, concentrated conditions that came about once it became clear that you could produce animals rapidly. The temptation to expand was almost, apparently, irresistible.
So, it’s my thought, now, looking at this history, that all of the things that we’ve come to critique about industrial-scale livestock production, that it treats animals like widgets, that it disrespects animal welfare, that it makes protein almost too cheap, that it exposes animals and therefore humans to a variety of diseases, to me all of that traces back to and is founded on the routine use of antibiotics. And all of those other things kind of flow from this.
And chicken really sort of brackets this entire story, because chickens were the first animals to experimentally get what came to be called growth-promoter antibiotics. And at least in the United States, it looks like chicken will be the first sector of what I guess we can call the protein economy that’s going to exit routine antibiotic use.
Mirsky: And that’s a really interesting story that’s a very recent development. But let’s talk about Jukes a little bit, and his influence, and then we’ll get into Congressman Whitten, who I had never even heard of, served in Congress for, like, 53 years, and, really, single-handedly kept a lot of the things that are now happening from happening sooner in terms of keeping our antibiotics a little bit safer by making sure we don’t overuse them with livestock. So, there’s Jukes the scientist and Whitten the congressman.
McKenna: Our two evil-doers. You know, that’s probably too strong, because for a variety of reasons, I think they thought they were doing good things. And, really, this whole story of how we came to give antibiotics to most of the meat animals on the planet is a story of unintended consequences, and of discovering down the road that there were negative effects that no one had really thought to look toward.
So, Thomas Jukes. All of the story starts with Thomas Jukes. He’s a Brit who leaves in the early part of the 20th century, he leaves England. He migrates across Canada. He ends up at the University of California. He’s working on – he’s a biologist and he’s working on the nutrition needs of chickens. So, back in that time that we talked about, back when our grandparents or great-grandparents had chickens, most places that grew chickens were fairly small, and they didn’t have all that many chickens.
And the primary point of chicken was to produce eggs. Meat chickens were really just kind of a side benefit, because a meat chicken would be either a hen that was sacrificed after its laying years, usually about two years, were done. Or, a rooster, that was hatched out and was not very useful to a farm that was going to be producing eggs. So, hens were old and chewy and not very tasty, and roosters were young and delicious.
In the mid-20th century, you see things called “spring chickens” on menus, and those are baby roosters that were fed for a few months and then killed because they weren’t useful to egg-laying farms. But one of the things that “spring chicken” sort of expresses is that chickens, as a meat crop, were not a year-round thing. And the reason is because farmers found it very difficult to keep chickens through the winter.
That when chickens were no longer able to go outside and get sunlight and scratch and peck and eat insects and plants and so forth, they had terrible difficulty keeping up the birds’ nutrition. So, the nascent industry of developing vitamins at the beginning of the 20th century turns out to be incredibly important, not just to the health of human beings, but to the health of livestock as well. And Jukes is one of those people.
And from his expertise in developing diets for livestock, he gets invited to work for a company that turns out to be one of the foundational companies of the beginning of the antibiotic era. So, the antibiotic era starts – I think people remember from high school that the history of Penicillin is that Alexander Fleming, Scottish bacteriologist working in London, recognizes the effect of the drug that they’re later going to call Penicillin in 1928.
But that compound doesn’t actually get developed into a drug until the 1940s. So, Penicillin comes out, it’s rolled out on the battlefields of World War II in 1943. It is released to the public in 1944. Almost immediately, the other drugs that start the antibiotic era are all released – streptomycin, chloramphenicol, and the tetracycline drugs. So, Jukes, our expert in the needs of chickens, happens to work for the company that is making Aureomycin, or chlortetracycline, the first of the tetracycline class.
And as they are trying to figure out what are all the possible markets for this new drug, something else is happening in the world, which is that World War II, which was so beneficial to making a market for antibiotics by demonstrating their incredible usefulness, World War II has changed food production, because there were millions of soldiers and sailors deployed all over the world, and they all need to be fed. That’s a guaranteed market for protein production that goes away as soon as the war is over.
So, suddenly there’s vast overcapacity in livestock production. Livestock producers have to cut their costs, or completely crash. They start feeding their animals much cheaper feed, and suddenly they need inexpensive supplements in order to keep the livestock market from completely bottoming out, or to keep their livestock from dying on the cheaper feed they’re feeding them.
So, Jukes gets the idea, based on some things that have been sort of percolating around through science that he should try a set of supplements, which are his special animal. And so, he takes – at the end of 1948, the takes a set of newborn chicks and he conducts an experiment, and he divides them up. He keeps a control group, and then he divides up the rest of the chicks, and he gives all those little smaller groups different supplements.
So, like brewers’ yeast and distillers’ grains and cod liver oil. And he gives one group of chicks the leftovers from making the drug chlortetracycline, or Aureomycin. Now, back then and even today, making an antibiotic is a lot like making beer. You take a carbohydrate, you inoculate it with the organism that makes to compound that you want, and then you let it cook.
And at a certain point, you drain off what you’re looking for. And if you were aiming for alcohol, for beer, you get alcohol and water. If you were aiming for an antibiotic, what you get is the compound expressed by a soil organism. And in either case, you’re left with a kind of sticky mass of leftover carbohydrate and exhausted bacteria, and some kind of brewing fluid.
So, Jukes takes that sticky mash and dries it, and gives it to the last group of chicks in his experiment. And when he goes to weigh the chicks on Christmas Day, 1948, he does it himself because since it’s the holiday, he’s given his lab assistant the day off. He discovers that the chicks that got the Aureomycin leftovers weigh three times what his control chicks did, and twice as much as any of the chicks getting any of the other supplements.
And there are several papers from 1949 and 1950 that all have almost have exactly the same title, and they’re all written by Jukes and his collaborators. And it’s because they kept doing the experiment over again to see if it kept working. And after they did it in chickens a few times, then they did it in pigs and so forth. And they kept getting this what they called a growth promotion effect.
And from that initial discovery, an entire industry is born. They don’t really know at first what’s going on. They have an idea, and they probably had more of an idea than they really admitted, too, because the patent paperwork that they file makes clear that they know that they are giving a tiny dose of antibiotic present in these manufacturing leftovers to these animals.
But at first, there’s this kind of hand waving about. “Well, it’s just our manufacturing waste, and maybe it’s just more nutritious. We’re not sure.” And they actually start selling the manufacturing waste before they’ve really figured out what’s going on. But within five years of Jukes’s experiment, livestock just in the United States are getting 500,000 pounds of antibiotics per year. And that’s just the beginning of a curve that has been endlessly rising.
The last federal data, which is out of date by about two years, was 34 million pounds of antibiotics going to livestock just in the United States.
Mirsky: [music] We’ll be right back after this.
Brian: Hey! Brian and Andrea, again, co-hosts of the Base Pairs podcast from Cold Spring Harbor Laboratory. We call it the podcast about the power of genetic information.
Andrea: That’s why we’re thrilled to share out latest episode, where we talk about how American science once took a wrong turn toward eugenics. Come find us on Apple podcasts, Stitcher, Sound Cloud, Google Play, or wherever else you get your podcasts.
Mirsky: Now back to Maryn McKenna, author of Big Chicken.
McKenna: When I look back, it’s very clear that there’s this, like, rapid step. Why is evolution? First, they think, “Oh, we can grow meat more rapidly.” First chickens, then it’s tried in pigs, and then they move on to cattle. Once you do that, I think, it’s almost irresistible to want to grow more in addition to growing them faster. And so we start to get the very large confinement farms that still are the mark of industrial scale animal production today.
And there are other things going on at the same time that make this easier. Nutrition continues to improve. Genetics start to improve. There start to be breeds of chickens specifically developed for these conditions. But it’s really antibiotics that starts it rolling, and also protects animal agriculture from the effects of what it’s doing.
Because if you are producing animals rapidly and you are effectively distorting them so that they are growing mostly the tasty muscle that you most want, and then you are jamming them into barns that are larger and larger and larger year by year so that now we’re, you know, in the modern era, we’re looking at chicken sheds that are as long as a football field that will have 20, 25, 30,000 birds in them at a time.
It is natural that diseases would spread. And them, just slightly larger doses of antibiotics protect the animals from those effects of all that expansion. And it’s important to say that at no point here are we talking about a dose that’s big enough to actually cure an infection.
And that’s one of the things that’s so interesting to me, and so bizarre about this story is that if you talk to medicine about antibiotics, you will hear, “We should never take antibiotics if we are not sick. We should always take the right antibiotic for an organism. We should never take doses that are too small or too short.” But that’s almost all of what agriculture does.
There certainly is in agriculture use of antibiotics therapeutically to make animals well. But the vast expansion of antibiotic use in agriculture is going into animals that are not sick, for purposes that are not treatment.
Mirsky: Jukes, to the end of his life, argues that there’s no detrimental aspects of this at all. But even when this was first getting stared in the ‘40s, there were some people who were saying, “You’ve got to be careful with this, because there’s an evolutionary process that will occur, and you are going to drive the advent of antibiotic resistant microorganisms.”
McKenna: That’s right. In fact, Alexander Fleming himself warned against this. You know, one year after Penicillin was released to the open market, he and his collaborators were awarded the Nobel Prize in medicine. And he stood up in Oslo in December 1945, and while they were celebrating his drug, he said, “The time may come when Penicillin is sold in the shops, and there is the danger that the ignorant man may underdose himself, and by doing that, make his organisms resistant.”
So, that was a warning that medicine heard. But it’s striking to me to look bad and realize that what Fleming was describing is exactly what agriculture was going to do – open over the counter access – up until very recently, animal antibiotics were not sold by prescription – and vast under-dosing.
And Jukes himself admits in a sort of memoir that he writes in 1985 that the veterinarians within his own company in 1948 and ’49 told Jukes and his – the head of the company that they shouldn’t do this, that is was a mistake, that they were circulating antibiotics too freely. And Jukes is very candid about saying we needed to do this for the profit. He says, “Competition was right on our heels.”
Mirsky: And what people didn’t know was that bacteria can exchange genes. They can just trade things with each other, and if one type of bacteria developed resistance, it could just give that resistance to another type that had not even had to go through the evolutionary trials to develop it on its own. And you start to see human beings who are exposed to these antibiotic resistant bacteria, who never went near a farm. You see them at the farm, but never went near a farm, because it’s in the food now.
McKenna: Right.
Mirsky: And over – this takes a couple decades now to really rev up, but by the ‘70s, we’re seeing it.
McKenna: I don’t want to make it sound like people at the start of this process did this irresponsibly. I think it’s more correct to say they just did it very confidently. They didn’t really think there were any downsides to their science. And if you look back at their scientific publications from the ‘40s and the ‘50s, they are trying to interrogate. Is resistance going to arise in animals?
And what they conclude is if the gut bacteria that everybody knows are present in the guts of animals and every living thing – we’re not at this point talking about the concept that we’ve now come to call the microbiome, but they know that there are bacteria resident in the gut – they assume that if those bacteria become resistant because of this persistent dosing, the growth promoter effect is just going to stop working.
And so, it has a built-in failsafe, and they don’t have to worry about it. What they never seemed to have considered is that the resistant bacteria wouldn’t stay with the animals, that it would leave the animals, either by the meat that those animals become, or in the manure, while the animals are still living, and that those resistant bacteria could move freely through the environment in ground water and surface water, dust on the wind, on the clothes and bodies of farm workers, and move out into the wider world.
And then getting into the ‘60s and ‘70s, we discover that the problem is not just the movement of the organisms themselves, but that the resistance DNA present in these organisms that’s been forced into existence by the constant exposure to low levels of antibiotics can break free of those organisms, so that it’s not only a question of resistance passing down mother cell to daughter cell vertically, but also that that DNA resident on what comes to be called a plasmid – though at first they’re called R-factors and R stands for resistance – but a free loop of DNA that can be exchanged among bacteria or released freely into the environment, and so can move what you can say is horizontally through the same generation.
And that accounts both for the very rapid expansion of resistance once a resistance factor comes into being, and also that people who have no contact with the farm, who have never eaten meat from that farm, who could be on the other side of a country or across a national border from a farm, nevertheless are subject to infection with resistant bacteria that can be traced back to an antibiotic-using farm.
Mirsky: And the agricultural practices whereby multiple animals can wind up, you know, if you eat hamburger, it might be beef from 20 different cows in that hamburger that just get mashed together, and to try to trace where the outbreak began, and then go back and bring all that – recall all that meat, that can be a huge detective story, and a huge problem.
McKenna: Right, exactly. So, the first outbreaks that are really kind of traced back to his agricultural use of antibiotics expose that just as antibiotics have entered into livestock production post-World War II, the entire food production system has been changing, so that livestock are raised in much larger amounts than ever before, but also the products that those livestock become travel much greater distances than ever before.
You know, in our grandparents’ time, back when they had the chickens in the backyard, if someone got sick as a result of a food-borne illness, somebody would probably notice and know what caused it, because it might be, you know, a dozen people in a family, 50 people at a church supper, 17 people who went to the same butcher in their small town. Now, you know, once we get to the ‘70s, food is traveling hundreds and thousands of miles from its origin.
And in the case that you were describing, this is one of the first really big outbreaks that explains how complicated this has gotten, you could have a cow that, along with a bunch of other cows, travels to a slaughterhouse and then is broken down. And then part of that cow or part of that herd is sold to another middle man that makes some products out of parts of that cow.
And then they might sell the scraps, say, to yet another middle man that makes hamburger out of the parts of that cow, and all the other lots of cows that have come in. So, if you have one herd, or even just a few members of a herd that are carrying antibiotic-resistant bacteria because of the way they were raised, they could be combined with lots and lots of other meat from many other herds into giant batches of thousands of pounds of ground meat, say, that then are subdivided and sold to various stores or various chains that might subdivide them further.
So, finding the origin of an outbreak and also understanding how far the outbreak has spread becomes incredibly challenging. And it also becomes a means by which the parts of the industry that doesn’t want to think there’s anything wrong with antibiotic use is given plausible deniability for the any of the negative effects of routine antibiotic use.
Because how could those people, thousands of miles away from this farm, have any – how could their illness have any connection to this farm that, as far as we know, is raising its animals up to proper scientific standards. And the answer is there is a connection. But it takes a lot of hard detective work to elucidate it.
Mirsky: And we’ve had a few of these really well-known outbreaks – the Jack in the Box hamburgers….
McKenna: So, the Jack in the Box hamburger outbreak, 1993, that bacteria was not actually antibiotic resistant, but it was really lethal. What it was was the first perception in the United States of the problem of e-coli 0157H7, which is an e-coli that expresses a particular toxin that is really destructive to red blood cells and to the kidneys.
And that outbreak, which occurred mostly on the West Coast, but did move east into the center of the country, made more than 100 people sick, and killed four children. That really was the one that helped the United States to understand how diverse and how geographically stretched food-borne outbreaks could be.
After that come outbreaks that are also antibiotic resistant, and have these same characteristics of tracing back to one farm or one production company, but having their meat distributed over, you know, in some cases literally from coast to coast, and posting a really significant challenge of putting all of those pieces back together again and finding what the source is.[music starts]
Mirsky: I’ll be back in a moment.
Andrea: Hi. Brian and Andrea one last time. Before you go, we want to tell you why we’re so excited about the power of genetic information. It helps us put food on our tables. It tells us about out ancient ancestors. And it can even help us map the brain with DNA barcodes.
Brian: We cover a whole swath of subjects, anywhere the power of genetic information plays a role. So, check out Base Pairs, the official podcast of Cold Spring Harbor Laboratory. Search for Base Pairs wherever you get your podcasts to learn more.
Mirsky: That’s it for part one with Maryn McKenna about her book, Big Chicken. We’ll be back in no time with part two.
