Science Friday - Contraceptive Failures, Future Of Combating Covid, Rapid Evolution In The Anthropocene. Nov 4, 2022, Part 1

Episode Date: November 4, 2022

Why Contraceptive Failure Rates Matter In A Post-Roe America Birth control options have improved over the decades. Oral contraceptives are now safer, with fewer side effects. Intrauterine devices can prevent pregnancy 99.6% of the time. But no prescription drug or medical device works flawlessly, and people’s use of contraception is inexact. “No one walks into my office and says, ‘I plan on missing a pill,’” said obstetrician-gynecologist Dr. Mitchell Creinin. “There is no such thing as perfect use, we are all real-life users,” said Creinin, a professor at the University of California-Davis who wrote a widely used textbook that details contraceptive failure rates. Even when the odds of contraception failure are small, the number of incidents can add up quickly. More than 47 million women of reproductive age in the United States use contraception and, depending on the birth control method, hundreds of thousands of unplanned pregnancies can occur each year. With most abortions outlawed in at least 13 states and legal battles underway in others, contraceptive failures now carry bigger stakes for tens of millions of Americans. Read the rest at sciencefriday.com. The Quest For New COVID-19 Solutions As we head towards our third pandemic winter, the nation still is facing about 2,500 weekly deaths from COVID, and over 3,000 people a day entering the hospital due to the virus. Dr. William Haseltine is chair and president of ACCESS Health International, a former professor at Harvard Medical School and Harvard School of Public Health, and the founder of several biotechnology companies, including Human Genome Sciences. “This thing knows everything about our immune systems,” Haseltine says. “We have to find new drugs that it has never seen before, and new combinations of those. That’s what’s worked for HIV. That’s what we have to do now—and we’re doing a very poor job of that.” Haseltine joins Ira to help explore the viral landscape, and where he sees viral research headed—from new vaccines to antiviral drugs and antibody cocktails.   Can Animals Evolve To Survive The Anthropocene? When you think of evolution, you might imagine a slow process that takes millions of years. Take Tiktaalik, for example: The ancient fish, an important human ancestor, took 375 million years from climbing out of water to get to the humans you see now.Now that we’re here, we’re changing the world at an unprecedented rate. Threats like climate change, deforestation, and pollution are wiping out entire animal species in just one generation. Can evolution punch back? Or are some species fighting a losing battle? Dr. Shane Campbell-Staton joins Ira to discuss rapid evolution in the anthropocene, and whether that’s enough to keep these species afloat.   Transcripts for each segment will be available the week after the show airs on sciencefriday.com.   Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

This is Science Friday. I'm Ira Flato. Since the Supreme Court decision overturning Roe v. Wade, we've been following the science behind reproductive health. Sci-fi producer Shoshana Bucksbaum, who's been focusing on reproductive health, joins me now to talk about a key option for healthy reproduction, contraception. Hi, Shoshana. Hi, Ira. I've been thinking a lot about how often contraception fails, how difficult it can be to access, and what this all means.

now that tens of millions of women live in states where abortion is a crime. And in order to help piece this together, I've enlisted the reporting expertise of Sarah Varney, senior correspondent with Kaiser Health News. She's a longtime health reporter who focuses on reproductive health. Welcome, Sarah. Thanks. Good to be here. So since the Supreme Court's overturning of Roe v. Wade,

some medical clinics have seen a spike in demand for more effective birth control. But you've been reporting on a very important fact. No contraceptive is 100% effective. That's exactly right. And I wanted to gauge just how many unplanned pregnancies can occur because contraception doesn't work flawlessly. So my first call was to a physician and researcher who wrote the textbook on contraceptive failure rates.

Mitchell Crennan, I am a professor and director of the Complex Family Planning Fellowship at the University of California, Davis. I put to Dr. Crennan an argument I've heard during my reporting on a board. And we had this idea, I think, that contraception should never fail, that there shouldn't be a need for abortion, perhaps, because people can always prevent pregnancy. When someone gets into their car, they don't go out and say, I think I'm going to get in a car accident today. The reason cars have seatbelts and airbags is because stuff happens even when we try our best not to have it happen. Same thing with using contraception. I asked Dr. Crennan to do some math with the failure rates of some of the most commonly used contraceptives.

In his textbook, Crennan distinguishes between typical use and perfect use. That's when contraception is used without any error. There is no such thing as perfect use. We are all real-life users. And for real-life users in real-life circumstances, the failure rate for oral contraceptives is 7%. Here's the simple math. There was 1 million women in the United States using a birth control pill, for example.

At the end of one year, 70,000 unplanned pregnancies would occur. in people saying I'm using a birth control pill to prevent pregnancy. More than 6.5 million women of childbearing age use oral contraceptive pills. That means the potential of about 460,000 unplanned pregnancies each year. And if that seems like a high number, wait until you hear about condoms. The typical failure rate is double that of oral contraceptives, 13%. Right. And that's still better than not using anything. but that would mean for a million couples using condoms, there would be 130,000 unplanned pregnancies within one year.

And even the most effective forms of birth control are no guarantee. The IUD, or hormonal intrauterine device, releases a hormone that thickens the mucus on the cervix, creating a barrier for sperm. There are electron microscope studies that show the sperm just kind of hit this brick wall of mucus and can't get past it. Copper IUDs work a bit differently. The high concentration of copper kills the sperm. Another highly effective method is an implant placed under the skin of the upper arm that slowly releases a hormone that prevents the ovaries from releasing an egg. Hormonal IUDs have that typical use failure rate of about 0.1 to 0.4, and copper IUDs have a typical use failure rate at about 0.8.

Nearly 5 million women in the U.S. rely on IUDs and implants, which means that even for those using top-notch birth control, up to 19,000 will become pregnant within a year. At the Planned Parenthood in Little Rock, Arkansas, nurse practitioner Gordon Lowe has treated these shocked patients. We have had women come through here for abortions who had an RUD in, and they were the one in a thousand. Abortion has been completely outlawed in Arkansas

since the Supreme Court's ruling in late June. The only exception is when the death of a pregnant woman is imminent. There is nothing that is a 100% effect short of never having sex. That is it. All right, Sarah, you just walked us through some really sobering stats. But why can't scientists develop a contraceptive that works all the time every time? That was my question exactly. I called up one of the world's leading researchers on contraception and asked her that question.

Well, first I would say that in medicine, there is never any 100%. This is Regine Citric Ware. I'm a reproductive endocrinologist, and I work at the Population Council in New York. Dr. Citric Ware says an IUD might fail because the health care provider didn't place the device properly. Or, in other situations, you can have people who take specific drugs for other disease that would interfere with, the molecule, the hormones that is in the system, and therefore this contraceptive is less active, and so there is a failure. For example, some HIV and tuberculosis medications, and even the herbal supplement St. John's Ward

can intervene in the processing of certain birth control pills. And then there's just daily life, which is hectic. The perfect use is always very difficult. You may have delay in taking your next pill or delay in inserting the next pill. month of the vaginal ring. And then there are factors like weight. Certain emergency contraception, including Plan B, may not work in people who weigh more than 165 pounds because the single dose of hormone is weight dependent.

Even vasectomies have a failure rate. Here's Dr. Crennan again. A vasectomy is removing a small part of the tube that takes the sperm from the storage facility that's right above the testicle where all the sperm that is. made is stored. And the body naturally wants to heal. That's right. If you get a cut on your finger and you just put a band-aid over it, the skin seals back up. So if you have a gap in a tube, the body naturally wants it to grow back together. And that's one of the ways in which it fails. For now, vasectomies and condoms are the only birth control options for men. But Dr. Citric Ware is

developing a new method, a gel that a man applies to his shoulders, where the skin is thinner and generally less hairy, that can temporarily block sperm production. At this stage, we saw really good acceptability by the couple and no pregnancy so far. About 350 couples are in the transdermal gel study so far, and Dr. Citric Ware is on track to begin a large-scale trial next year. You've come much further in the development of a new male contraceptive than people have in decades. There's always been this promise of a male contraceptive. Is the difficulty in developing male contraception more of a scientific problem, or is it more of a social or a cultural one? I think we can say all of it.

Scientifically, it takes more time to suppress the sperm production 90 days than suppressing ovulation in women, which is every month. Also, it's a social situation where the male contraception is taken by the men, but if there is a failure, His female partner is at risk of pregnancy. But this type of male contraception is still a long way away from hitting pharmacy shelves. And there have been so many fits and starts in this area of research. But there are other dynamics at play here, too. And Sarah, you looked into something that many straight women may be familiar with, but don't talk about publicly.

Yeah. You know, we talked about condom use earlier. And getting a partner to use a condom can require negotiation or persuasion. Those are skills that Jennifer Evans, an assistant teaching professor at Northeastern University, studies closely. So, SELFING or Non-Consual Condom Removal is where one partner puts on a condom, but then removes the condom either before or during sexual intercourse without the other partner's knowledge or consent. When I spoke to Evans, I had just been interviewing girls about teen pregnancy for another story. One of the teens described how a guy pretended to rip the condom wrapper open, but then apparently never used it. She became pregnant and now has a four-month-old baby.

A lot of these stealthing cases, women don't necessarily know that the condom has been used improperly. It means that they can't engage in any kind of preventative behaviors like taking a plan B or even going and getting an abortion in a timely manner. In any of your research, have you asked men what their motivation would be to even do this? Generally, what we find in the research and the literature says that, you know, men, usually engage in this behavior whenever they have a more severe history of sexual aggression towards women or that men are doing it for the thrill of engaging in a behavior

that they know is not okay. And a lot of them also report that they do it from a physical pleasure standpoint. The consequences were already severe before, but now that Roe v. Wade has been overturned, I would argue that they're even more worse right now. I mean, that's just sort of heartbreaking in a lot of ways. Controception is really more complicated than I'd previously thought. And of course, unfortunately, no conversation about American health care would be complete without some nod to how many people struggle to get even the basic care that they need. So how does that whole dynamic affect access to birth control?

There are 7.9 million women of reproductive age in the U.S. who are uninsured. So they have no coverage for birth control. The states that have banned or severely restricted abortion in general have far higher rates of people without health insurance. That includes Texas, where one in five people have no health coverage. Alina Salganikoff is the director of women's health policy at the Kaiser Family Foundation. She has spent decades studying this issue. We have a patchwork of programs and services that provide contraceptive care in the United States. We have private insurance, we have Medicaid.

We also have the federal Title X family planning program. But Sliganikov says this patchwork has gaps. Not everyone has private insurance or Medicaid or lives near one of these federally funded clinics that provide free or low-cost birth control. So there is definitely cases where these women fall through the gaps and lose coverage and have problems accessing and affording birth control. So, Sarah, we've covered a lot of ground here, how the numbers of unintended. attended pregnancy, adds up when birth control fails, a possible male contraceptive, and the difficulties of navigating sexual relationships. So has the overturn of Roevi-Waid affected access to birth control? We're starting to get some hints from around the country of how the court's

ruling might affect birth control. I spoke to several clinic directors in Arkansas, for example, who are no longer prescribing emergency contraception because they're not sure how the state's abortion ban will be enforced. And recently, the University of Idaho issued legal guidance to faculty and staff that they can no longer offer any birth control to students. Condoms can only be provided, quote, for the purposes of helping prevent the spread of STDs, but not for birth control. This is something we'll be following closely. Thanks so much, Sarah. Oh, thank you, Shoshana. Sarah Varney is a senior correspondent with Kaiser Health News, and I'm Shoshana Bucksbaum. If you want to dig deeper into the data on contraceptive failure rates and read more of Sarah's reporting, go to sciencefriday.com slash contraception.

We have to take a break. And when we come back by a medical pioneer, William Hazeltine, on our COVID past and future. Stay with us. This is Science Friday. I'm Ira Flato. As we head towards our third winter with COVID, this may be a good time to reflect on the paths taken to deal with the pandemic, the development of the vaccines, the distribution, and what may lie ahead. Case in point, Pfizer announced last week that your vaccines may no longer be free next year. Retail price, about 130 bucks per shot. So what does this all mean? Here to help explore the viral landscape is a scientist who has spent a lifetime researching and battling viruses and who frequently writes about where he sees viral research headed. Dr. William Hazeltine,

chair and president of Access Health International, former professor of Harvard Mid-School and Harvard School of Public Health, founder of several biotechnology companies, including human genome sciences. Dr. Hazeltine's writings appear regularly on Forbes Online. Welcome back to Science Friday. Well, thank you, as you said. It's been 20 years, so I'm happy to be back. It certainly has. Lots have happened. Let's talk about some of this stuff. What is there about this disease that the public needs to know that you spend so much of your time writing about? I think the first thing to know about what it is. And I think most people don't really have a good grasp of that.

It's a virus, like the flu virus, is very well adapted to infecting an adult, healthy animal, and then reinfecting them shortly thereafter. And we know that because its natural habitat are bats. Now, something most people don't know about bats, they live a long time. but they're about the size of a mouse or a rat, but they can live 20 to 30 years. And these viruses infect them every year, year in and year out, kind of like our colds. But what does that mean? It means the ecological niche for this virus is an adult healthy person that infects

again and again and again, even if it infected them before. And that means it's got lots of tools to do that. It's niche. We happen to be the new target, the new ecosystem. So we shouldn't be surprised then about how many times we can get infected. No, just like the flu. It comes back and it changes. This is even more subtle than the flu. It's bigger. And Science Magazine had it right on the front of its cover, a beautiful issue a couple of weeks ago, calling it an immune saboteur. Not only does it change its coat, but it's got, we're still counting, and I'm counting up to 35 to 40 different ways, it can jimmy our immune system.

So once it gets in, it shuts down your ability to see it until it gets out. And then it doesn't care what happens to you. Some of us doesn't kill 10% of us. Some of its cousins kill 30% of us. We're very lucky. This one only kills about 1% of us. Earlier in the pandemic, there was an idea circulating that as the virus, It tends to get less severe. Has that been the case here?

You know, there's arguments about that. But let me just put it into that myth. Think about tuberculosis. Think about malaria. Think about what smallpox did what it was rolling on. Did it get, after thousands of years, any less horrible? No. That is not the way pathogens go. They don't generally get weaker. So that's a myth, and it's, I think, a dangerous myth. What's the case for this? It's very hard to tell because a population has changed. There's tremendous experience of the population now with this,

and there is some partial protection. There's one other thing I think people should know. Right now, we're in an era of complacency. I live amongst other places in New York City, and the city is as there's no virus around. There is virus around. But the important thing to know is the vaccine will protect you for about two to three months from infection.

It will protect you pretty well for five to seven or eight months from ending up in the hospital or dead, but then all bets are off. The idea that there's perpetual protection from the worst thing this virus can do to you is not right. The latest data that's coming out says, that protection from hospitalization and even worse ends or actually wanes, it just wanes more slowly. And that's what you would expect for a virus like this.

It's a lot of all these tricks to come back and get you again and again. So the last thing I'd like to say that people should know is this things around to stay. Unless we learn how to put it to bed like we're learning for HIV to use drugs. as well as our immune system to fight it. This thing knows everything about our immune systems. It knows how to fight it. We've got to find new drugs that it's never seen before, and combinations of those.

That's what's worked for HIV. That's what we have to do now, and we're doing a very poor job of that. What do you mean we're doing a very poor job of that? Please tell us what you're talking about. Well, you can count on your one hand, the number of drugs we have, and those aren't really great to.

Those aren't really great drugs. As somebody who's worked on developing HIV drugs, both the theory and the practice, we now have super drugs. We now have a drug that you can get injected once every two months and you won't get infected and you got the virus, HIV. It won't make you sick. We're on the brink of having a shot that'll do that every six months. We are so far away from that for this disease. For example, Paxilvid, Paxliv. Paxlivet doesn't stop you from getting infected. Paxlovit does have an impact on keeping you out of the hospital, but only about 50%.

We'd like you to wipe out the virus completely. You know, I had COVID last May, and I talked Paxilvid for, and I mentioned Paxilvind because it's our best part. I took Paxilvid for 10 days, and it was a virus positive for 15. So is that a good viral drug that's wiping out? No. Yes, it's an important drug to have, and I urge everybody who gets infected to take it, because it does reduce your chance of ending up in the hospital. But it's not the powerful drug that we want. Why don't we have that powerful drug like we have with HIV?

Well, it's taken us 40 years to get where we are. I think we can do it in five or six years if we really put our mind to it. But, you know, developing drugs is a complicated business. I've been at it for a long time. And the way I like it to is like, say, we've got to fix my Ferrari by throwing a wrench into the engine. Okay, it's a complicated machine. There is a small chance that will get better.

There's a lot bigger chance of messing up that I don't know about yet. So drug development is tough, and you've really got to have a lot of knowledge. Now, there's one or two little pieces of the SARS-CoV-2 virus that we know well enough to begin to do really rational, of design. One of us how it puts a cap on, because it's completely differently from most other viruses and cells, but it gives us a great juicy target. We know every atom involved in that process, and so we can start to make drugs. But we know very little. This thing has a giant replication machine. It's got many moving parts. You can probably mess it up every single, a lot of different ways.

We only have one way to mess it up, which is scurrying up, which is polymerase a little bit, not working as well as we'd like. And so we just need a lot more research on this. We have the tools now, thank goodness. We have so much better tools that we had at the outside of HIV that it's just incomparable, a bunch more we could do in the time we can do it. But we've got to do it now. Who's the we we we're talking about here?

Is it drug companies, the NIH? I mean, is there money? It's really not the drug companies yet. No. Drug companies are able to take something. that academics have shown will work and then turn it into a drug. We need the companies. And actually, we need the companies to work closely together. You know what really worked for HIV? First of all, money. The United States was willing to spend two to three billion

dollars a year on HIV research. Second, a collaboration, a very tight collaboration between academia and business. In fact, I remember working with Dr. Fauci to create a special series of grants in which the federal government would give an academic laboratory money, provided they have an industrial partner, which would develop their drug. That's the kind of programs that really work. We have a couple of those, but we need to expand them. We don't even give money now for preparing our society for the next attack of a virus, right? We're going to get into a series of politics and other questions, but it is the case. And I've been working on health policy for a long time now, too. That they're great, report.

It's a Commonwealth Fund just did a really important report on the need for a powerful national public health service. We don't have it. It's all balkanized. And that is a Commonwealth Fund report. My friend Peggy Hamburg shared it. She was former head of the FDA. It's a great report. It tells you what we should do.

Will we do it? Same thing, the National Academy at Medicine did a wonderful report on how we have to integrate our health care services. care services across the nation to help people who are underserved and talk about the way we deliver health care now. Beautiful report tells us a clear idea of where to go. It's now up to us as American citizens to make sure that our politicians do follow the directions. We need them to follow. But you know as well as I do that this country's in a difficult spot right now.

Yeah. You've written, just moving on a bit, that new research published in science translational medicine suggests an MRI vaccine that targets both the SARS-CoV-2 spike protein as well as something called the nucleocapsid protein may offer stronger and broader protection than current spike-only vaccines. This research opens the possibility that one vaccine may protect against current and future variants. I'm asking, is it possible to create? a universal COVID vaccine? Well, you know, thank you for asking, I write.

That's a topic I'm really very close to my heart. And I do think it's possible. Let me just tell you what I was working on just before we started talking. It's a great paper, a wonderful group, Dr. Sapphire in La Jolla, has done some very beautiful work on developing antibodies, cocktails of antibodies, that neutralize two really important viruses. When everybody knows about Ebola, and she's developed drugs that will probably work against this new Sudan strain. Very exciting.

She just recently published one on another nasty critter out there called Lhasa. And she's got a cocktail of three antibodies that, you know exactly atom to atom, which ones it touches, and can lock the thing up and probably stop that, too. So I think we can do this. There are cocktails now of molecule antibodies that are very broadly neutralizing. They neutralize not only SARS-CoV-2, but SARS-1 and MERS and some of these crazy bat viruses. You can do this. Now, they're also beginning to use that knowledge to design vaccines. Is it possible to design vaccines?

But let me talk a little bit about some of the mRNA vaccines. We're really excited that RNA can now be used directly as a vaccine. vaccine because it's really simple to make, totally chemical process, and it's really fast and flexible. But the way it's currently being used with these modified nucleotides, you stick it in, the RNA lasts a couple of days, the proteins there for no more than two, three days, and then your immune system can't see it anymore. There's now something called self-amplifying messenger RNA. Really exciting. You put a little bit of the RNA, and it makes a lot of the RNA. You don't put it in the muscle, you put it in the layer of the skin where most of your immune systems can see it.

And that is giving very, very good results. The antibodies last for up to a month. Your body gets to see it, and you can add lots of different proteins, very, very easily, including what you mentioned, the nucleocapsi. And when you do that, you get some broad reactions that could react all the way across most of the SARS variants, in fact, all of them that I know about, the MERS, as well as SARS-1. So I think there's some good things coming, both with the vaccines and with monoclon antibody cocktails, and hopefully, eventually, with small molecule drugs. It's not impossible to put

this thing behind us. It's just hard. This is Science Friday from WNYC Studios. In case you just joined us, we're talking with Dr. William Hazeltine about the future of the COVID pandemic and lessons learned. You've worked with many different viruses. as we're talking about, and many people, as you say, know of your work with HIV. And I'm wondering what you can tell us, what we can learn from those other viruses about living with COVID. Well, we live with flu, and we've lived with flu all our lives. I've been in bed for five, 10 days, five times from the flu. I've lived with flu. I haven't liked it, but I've lived with it. I get my flu shots, and most years they work, and some years they don't.

But the difference between this and flu is this is a worst virus. It's much more lethal. It's already killing, on average, every year a lot more people than the flu does. It's not seasonal. It doesn't come along only in the winter. It comes along fall, spring, summer, and winter. So it's not seasonal life, though, which makes it nasty. And it affects many more organs.

So, yeah, we can live with it. But right now, we're living. sort of a low, and the average is about five, six hundred people a day are dying. What would we do if an airplane fell out of the sky and killed five, six hundred people every day? We wouldn't like it, right? But that's what's actually happening right now. And it's not seasonal. It's been pretty constant from me.

And so, yeah, we can live with it. Hopefully it won't get worse. You know, the real nightmare for somebody like me who thinks about what these viruses can do is I know. that with some very subtle change, this could move from killing 1% of us to 20% to 30% or more. We don't know that's not going to happen. So the reason you hear people like me say, we've really got to control this as much as possible, is to reduce that possibility. The more viruses that are out there in humans, the more they get into our animal environment,

the more likely it is that something worse will happen, not better, worse. And I can give you enough examples to curl your hair about how viruses get worse. One of the questions you asked me in the very beginning. We know how it happens. We know it can happen. And we're just praying it won't happen now. I would say something else to think about and why we really have to pay attention to this. This is happening to us, not because we're moving into new ecosystems, but because we are a new ecosystem.

When I was born, there might have been two billion people in the world. They're eight billion today. That's a lot more people. There are five billion single airplane flights, people taking flights, a year. We move around a lot. Think of us as bats congregated together in a cave when you're on one of those cramped airplanes. That's like being in a bat cave. And these viruses are taking advantage of a brand new.

ecosystem. We're great food for viruses, and we've got to be able to protect ourselves. Dr. Hazeltine, you've given us a lot to think about, both scary and hopeful. You know, in the end, I have more hope. And the reason I do what I do is I think that there's a lot of hope that are a lot of great people out there that I work with. And we have really great scientists and great people working on this. So would it be fair to say you're more hopeful than fearful? Yes, cautiously optimistic that we can do better. Thank you very much for taking to have to be with us today. You're welcome, thank you.

Dr. William Hazeltine, chair and president of Access Health International. We're going to take a break when we come back, how animals evolve in the age of human change. Stay with us. This is Science Friday. I'm Ira Flato. When you think of evolution, you might imagine a slow process that takes millions of years, right? I mean, it took 375 million years from the first fish climbing out of the water to get to the humans you see now. And now that we're around, we're changing the world at an unprecedented rate.

Threats like climate change, deforestation and pollution are wiping out entire animal species in just one generation. So scientists are wondering, can evolution act fast enough to keep up, or are some species just doomed for extinction? Here to discuss is Dr. Shane Campbell-Staten, assistant professor of ecology and evolutionary biology at Princeton University in Princeton, New Jersey. Dr. Campbell-Staten wants to figure out how humans drive evolutionary change. He studied all sorts of critters, from lizards to elephants.

Welcome back to Science Friday. Thank you so much for having me. I appreciate being back. Nice to have you. Let's start with the basics. shall we? What are some of the big questions you are trying to answer? So the major questions that my group is trying to answer have to do with how humans act as engines for evolutionary change in other species across the tree of life. So we are changing the planet in a lot of different ways, everything from pollution to hunting and fishing

to climate change, global warming, all these different ways that are both intentional and unintentional. And in doing so, we are putting all of these pressures on the other organisms that share space and time with us. And we want to know not just how they're being affected now in terms of population declines, but how they will continue to be affected through the process of evolutionary response

to all these different things that we're doing into the future. I note that to get at these questions, you've looked at a type of lizard. Is that right? What did the lizard tell you about evolution? Yes, so we've been studying a small lizard called the Crestodinole, which occurs across the island of Puerto Rico. And we've been studying how these lizards have adapted to cities across the island. So it's a very abundant lizard that occurs in multiple cities across the island. island where it's colonized from the surrounding forests. So myself and my collaborator, Kristen Wintzel, have been really interested in how these urban environments are acting as selection pressures for these very small, thermally sensitive animals. So one of the things

about cities is that they are very hot, you know, because of all the concrete and metal, a lot of reflective surfaces. Yeah, they call them heat islands, right? Exactly, right? This is what we call the urban heat island effect. And we've been studying how thermal tolerance, how heat tolerance in the noles that occur in cities has changed from their forest counterparts. And we've shown that again and again, every time these lizards colonize cities, that they become more heat tolerant. And this effect seems to have a very significant genetic component, suggesting that it is evolution by natural selection that's driving this change. So the lizards have evolved over generations you're saying to better tolerate the heat? Exactly. Huh. And so what about when it gets cold? Do they

die out quicker? So there doesn't seem to be a trade-off in terms of cold tolerance. So urban anoles and forester noles are just as cold-tolerant. So they've been able to increase their heat tolerance without sort of sacrificing their ability to perform at the other end of the temperature spectrum. So are these lizards then an example of rapid evolution? Yes, absolutely. So we're talking about the oldest cities in Puerto Rico, so like Old San Juan, maybe a couple, 100 years old. But a lot of these cities are even younger. So, you know, we're talking about a hundred or less generations.

you know, this urban heat island effect is a much more recent urban effect, which means that they've had to evolve even more rapidly. You know, I find this is amazing because when I learned about evolution as a student, I remember the teacher drilling into our heads that evolution takes place over many, many, many generations, but you're saying it can happen fast. Yes. How do you know that it's evolution that's happening? So we know that it's evolution because we can actually look at the signatures

of selection at the genetic level. We can actually read the story of a population in its DNA. And over and over again, we see that that story is a story of evolutionary response by way of natural selection. So it leads distinctive footprints at the genomic level that we can identify and pick up on. So they pass these traits down. Exactly. Yeah.

I understand that you're also showing how elephants are evolved. evolving in response to poaching, sort of the same thing. Can you tell us more about that? Yes. So when we're talking about rapid response, things like lizards are better equipped to deal with those sorts of pressures, right? Because they have short generation times, they have really large population sizes, they're able to respond to selection pressures more quickly than larger, more long-lived organisms just because it takes them longer to reproduce. They have smaller population sizes. All of that is working against them. But we see that even in species like elephants, we can look at the effects of human-mediated selection and evolution. So in this case, with

African elephants, almost all African elephants have tusks. So all males have tusks. The vast majority of females also have tusks, but there's a small proportion of females that are naturally born without their tusks and they never grow them. But in regions where there has been intense hunting for ivory, we've seen an increase in the frequency of tuskless females in those populations. So in Gorongosa National Park, during the Mozambican Civil War, which happened between the late 70s and early 90s, there was large-scale hunting of all of the large mammals and the elephants specifically were being hunted for their ivory. Before the Mozambican Civil War, about 18% of the females in the park were tuskless, which is already a pretty high number versus what we see in other parts of

the range. Then after the war, half of the surviving females were tuskless. This seems to be, again, due to a selection response. If you're living in an environment where individuals are being disproportionately killed because they have tusks, not having those tusks gives you a selective advantage. You're more likely to survive, reproduce, and then pass on those genes for tuscllessness to the next generation. The oldest elephants in the park, those are the elephants that actually live through the Civil War. Like, they're still around. And then amongst their offspring, we still see an increase in the frequency of tusklessness amongst their daughters. About 33% of their daughters are still tuskless, which is still

significantly higher than what we saw before the war. Even though those offspring themselves, they never experienced the war at all. And that didn't take very long. You're talking about a 15-year Mozambique Civil War? Did it happen in one generation? Yes. Exactly. It happened in a single generation. So, you know, when we talk about evolution, most people know evolution by natural selection, right? But natural selection plays out within a generation, right? It can happen almost instantaneously. As long as there's some event that disproportionately favors some individuals over others, then that selection can play out in the course of days. or months, in extreme cases, maybe even hours. But it's not until those survivors have offspring, until they pass those genes on to the next generation, that you actually get evolutionary response to selection, right?

And that is evolution by way of natural selection. Would that mean that for you to see this change or for the elephants to really exhibit this tuscllessness, that there would have to be many, many elephants killed who had the tusks for the other ones to survive? Yes. So in a lot of these stories, I think we have a tendency to see them as success stories,

and they are in a way in terms of like the resilience of life, but selection always comes at a cost, and that cost is death. So the stronger selection pressure is, the more individuals have to die in order to get a response to that selection pressure. Yeah, I get it. And just to be clear, these species aren't evolving because they're developing new adaptations like Lamarck would say, right?

Natural selection is happening. Yes, this is natural selection. So it's selection on standing genetic variation. When most people think about evolution, you think about like a novel mutation popping up in a single individual and then sort of being slowly spread, which does happen, but it takes a very long time. The examples that we're talking about, you already have variation that exists in populations or in species that then become adaptive under specific circumstances and then drive those traits and their genetic underpinnings to higher frequencies in a population. And that occurs much faster. So evolution is like having a toolkit. Exactly.

And if you have a full toolkit, you get better results. Yeah, so genetic diversity is essentially the toolkit that any species has to respond to any type of pressure that it would possibly encounter. So the more genetically diverse you are, the more potential tools you have to respond to any given challenge. The thing about natural selection and evolution is it's not a forward-looking process. It's not trying to predict anything. it's not planning on anything. It's a responsive process. So something happens and then you get an evolutionary response.

So the more tools you have in your toolkit to deal with whatever may come, the more adaptable a species or a population is. But again, once you go through a large selection event, because that selection requires death, it also requires a lot. of genetic diversity. So in the case of the lizards in Puerto Rico, like they may be very heat tolerant, the survivors in cities, but what happens if an extreme cold snap comes through? Well, the genetic diversity that may be needed for the physiological traits that would be able to survive that type of event may be very different than the traits that have been selected for in the past, but you've also lost a lot of the population, and a lot of that genetic diversity may then be gone. So selection always comes at a cost. This is Science Friday from WNYC Studios.

In case you're just joining us, we're talking to Dr. Shane Campbell-Staten about how climate change is driving animal evolution. I guess you were talking about some of these elephants being really, really old, and I'm thinking, you know, if I'm one of these older elephants, I must have been around to watch this massive die-off of the other elephants who couldn't survive. Yes. Yes. So it's one of the things that I learned very quickly when I undertook this project. So when I started the elephant project, I'd never worked on elephants before.

I'd never been to continental Africa before, you know, which is a big deal for me as, you know, as an African-American. So everything was brand new. And seeing an elephant up close and personal, a sedated elephant right in front of me, it was a completely different experience than anything I'd ever experienced before because I'm looking at this adult female who's, you know, she's in her 40s or 50s. She actually lived through the Mozambique and civil war and survived while literally 9 out of 10 of the individuals and her species died during this 15-year period, and she survived,

and then went on to have children and grandchildren became the matriarch of a herd, and now she's still living her life. That sort of an individualistic story, right? I mean, that is, it's such an intense, it's such an intense point of connection that I think we can have when it comes to the organisms that are responding to the different things that were that we're doing. But those individual success stories, they're always marred in some sort of a tragedy. And ultimately, we happen to be the cause of a lot of those tragedies in the Anthropocene in the age of humans. I imagine, and from talking with you, I can see that you have been through and watched a lot

that has been going on in the Anthropocene. Has your research changed your perspective on what biodiversity might look like in the world we leave behind? It has. I think it's really driven for me the idea, this sort of conundrum that is life, right? So life is both incredibly resilient and incredibly fragile at the same time and simultaneously. You know, I spend my life studying all these examples of the strange,

incredible, amazing, weird ways that organisms have figured out how to respond to all of the things that we're doing. And it makes me hopeful and it makes me proud to some extent to be a part of this story that is life. But ultimately, I feel like a lot of these organisms, if things don't change, as much as they're doing, they may be fighting a losing battle because we're just, changing the planet so quickly in so many different ways simultaneously that even the most diverse toolkit, I have no idea how a species would be able to survive all of the different things that were throwing at the planet all at once. So will life survive the Anthropocene? Absolutely. I have almost no doubt in that. I mean, it survived five major extinction events in the

past and I think it will survive us. But what that biodiversity looks like that comes out on the other side, it may be very different than the diversity that we know now. Yeah, yeah. Well, that is the state of affairs, isn't it, Dr. Campbell-Staten? Exactly. Thank you very much for joining us today. Thank you so much for having me. It's been a pleasure. Dr. Shane Campbell-Staten is an assistant Professor of Ecology and Evolutionary Biology at Princeton University. One last thing. Did you know that SciFri hosts events both in person and online? If you want to pop open a cold one made with science or go stargazing or hear about tech that could help us better understand animals, we have an event for you. Here's how to find out.

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