Boom! When Evolutionary Biology and Toxicology Collide

[00:00:00] “Decompose” Theme Music
[00:00:05] Anne Chappelle: We’ve been doing Adverse Reactions, and this is what our 
[00:00:08] David Faulkner: Fourth
[00:00:09] Anne Chappelle: Fourth
[00:00:09] David Faulkner: Season
[00:00:10] Anne Chappelle: Season
[00:00:11] David Faulkner: Amazing. 
[00:00:11] Anne Chappelle: So, David, do we have a theme? 
[00:00:13] David Faulkner: Everything is so much more complicated and interesting and more interconnected than we ever think it’s going to be. 
[00:00:22] Anne Chappelle: We’ve really kind of strayed from traditional toxicology in this season.
[00:00:28] David Faulkner: It’s true. We have been expanding the reach of what most people think of as toxicology because one of the things I love about this discipline is that it is a necessarily applied science and that means it touches basically everything—all the other sciences.
[00:00:44] Anne Chappelle: Have a listen.
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[00:00:52] David Faulkner: On this episode of Adverse Reactions, 
[00:00:55] Anne Chappelle: “Boom! When Evolutionary Biology and Toxicology Collide,” with Noah Whiteman.
[00:01:02] Noah Whiteman: So, there’s an example of this intersection, like the eucalyptus are just doing this, making this eucalyptol. Pretty easy to make because lots of plants make eucalyptol actually. But they make a lot of it. And Aboriginal Australians were the first to turn to it and used it in many of the same ways that it’s used now. And so that’s another element. It’s like humans are tapping into these chemicals, these toxins that didn’t evolve with us in mind, but then we can use them as medicines. We can use them as weapons. We can misuse them and become addicted to some of them. 
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[00:01:39] David Faulkner: Welcome to Adverse Reactions. Today, we are joined by Noah Whiteman, PhD, Professor of Genetics, Genomics, Evolution, and Development, Director of the Essig Museum of Entomology at UC Berkeley, affiliations with The Helen Willis Neuroscience Institute, the Center for Computational Biology, the Museum for Zoology, the University in Jepson Herbaria, and many other things as well. Welcome to the show, Noah.
[00:02:03] Noah Whiteman: Thank you, David. It’s great to be here.
[00:02:05] David Faulkner: As an evolutionary biologist, how do you think about toxins—or poisons to use the vernacular—and how is that different from how most people think about them?
[00:02:16] Noah Whiteman: So, I came to the field of toxicology from a very different perspective, I think, than probably most people. And that’s because I was originally trained as an entomologist.
You mentioned the Essig Museum of Entomology. And, I was very early training as an undergraduate and then a master’s student in insect evolution, systematics—very kind of basic stuff. And then, for my PhD, I worked in the Galápagos Islands on birds because my PhD advisor, Patty Parker, is a behavioral ecologist and evolutionary biologist who studies bird behavior and mating systems of birds.
She had been working on the apex predator in the terrestrial part of the Galápagos ecosystem on most islands, and that is the Galápagos hawk. It’s an endemic bird, and it’s in the genus Buteo, which is in the same genus as the red-tailed hawk, the red-shouldered hawk, and the Swainson’s hawk.
What I was studying was coevolution between the parasites that lived on the hawk and that its ancestors brought with it to the islands when they colonized the islands hundreds of thousands of years ago. And I was studying how the hawk and its parasites were co-diverging across island populations. As the hawks themselves moved from island to island, they brought with them, of course, their parasites.
So, I was looking at the genetics of those two interacting things in a coevolutionary context. So, it’s like a trait in one species is influencing the evolution of a trait in another and vice versa. I became fascinated by that.
I switched to studying plants as hosts because they’re so much easier to work with than endangered birds. And so, we started working with the lab rat of the plant world, a little mustard called thale cress. So, the connection between these things is there’s like a parasite community attacking birds, there’s a parasite community attacking plants, and some of those parasites are insects, and we call them herbivorous insects.
And that is what I started really studying. And I would say the main challenge for an herbivorous insect that is colonizing or eating a plant are the specialized metabolites and other defenses—not just chemical. So, they could include physical defenses like hairs, trichomes, thorns, thick bark, wood, tannins that are part of the chemical milieu. But yeah, chemical defenses, and that is how I got into it. Because most of the—roughly half of the drugs in the modern pharmacopoeia are from nature, and most of those are from plants.
If you look at my background, it seems strange that I went from, like, wasps and beetles and then feather lice to things like caterpillars and leaf miners. What’s the thread? And the thread is coevolution between species.
[00:04:59] Anne Chappelle: How big is your field in terms of people looking at stuff like you’re looking at it? 
[00:05:05] Noah Whiteman: I would say that in the people who study plant-herbivore interactions, it’s a pretty small community. We have a Gordon Research Conference that runs every two years, and I’m chair this year. It’s 200 people will show up from around the world. A lot of them are from the agricultural or ecological side. And then some of us are from the evolutionary side. I would say it’s not a huge field, but people who do study natural products that arise because of these interactions, that’s a much bigger field.
And if you think about why is the plant making this chemical, we never know why it evolved to do that. We can dissect maybe what it’s doing now to some extent for the plant from the plant perspective or the fungus’s perspective of that. From an evolutionary perspective, it’s hard to reconstruct what happened in the past, but we try to do that in a variety of different ways.
And now, it’s a golden era for doing this, for using DNA sequence information to trace the origin of a genetic change to a particular point in time. We can do that to some extent. We can guess-timate when a pathway evolved the ability to say, make caffeine—that happened at least six times independently in plants. And did they all do it the same way? No, but some of them pretty much did. Very similar genes got duplicated in this particular transferase pathway that allows them to create these methylxanthines that include caffeine. Now, we have the ability to sequence genomes, figure out the metabolic capacity of these plants. And then, at the same time, from the insect’s point of view, we can try to understand why. 
[00:06:27] David Faulkner: There’s so many interesting questions that come out of that. First of all, the idea that caffeine independently evolved six times is really fascinating. 
[00:06:35] Anne Chappelle: It shows you how important it is if it evolved six times. Things that only evolve once, you know, you can kind of write that off. But six?
[00:06:43] Noah Whiteman: That’s right. It tells you that is targeting something important, maybe in the animal nervous system, like an adenosine receptor, or dopamine in the case of insects. So yes, I think you’re right that when lightning strikes more than once in nature, in organisms, we think that is suggestive that the trait has a lot of adaptive value, enhancing the fitness of its bearers. And so, this is true for things that re-evolve over and over. But the other side of it is interesting, too. Just as the six plant lineages independently evolved caffeine, many insects independently colonize those plants and have evolved the ability to resist the caffeine in different ways.
And that’s true for the things that eat the milkweeds, too. It’s not just monarchs. All of these different insects, from different insect orders—which just means anciently diverged from each other, like aphids, beetles, leaf-mining flies, monarchs, tussock moths—they all attack milkweed. They all evolve the ability to resist it. Sometimes in the same way, sometimes in different ways.
But sometimes, and this is what we learned from studying the genetic basis of resistance in these insects to the cardiac glycosides—which target the sodium pump, the sodium-potassium ATPase that is maybe consuming half of our ATP right now, resetting the resting membrane potential of cells, pumping sodium out and potassium in—the toxin targets that pump.
And it turns out, that’s a big constraint. So many of these insects have evolved not only mutations in the same gene but have fixed—in other words, everyone has them in that species, and it becomes a trait of the species because it’s adaptive. But the same mutations in the same place have evolved to block the cardiac glycoside from binding to the cardiac glycoside binding pocket in the sodium pump.
So, we found that the black-headed grosbeak—which actually was at my bird feeder two days ago; my husband noticed it and it was eating suet—birds are resistant to the monarchs, and they eat them there. They eat millions of them potentially there. And how do they do this? They have evolved the same resistance mutations in their sodium pump that some of these milkweed-village insects have. Yes, lightning keeps striking when the constraint is high or the advantage is high enough.
Unfortunately, people are born with new mutations in the sodium pump gene that change the amino acid that’s encoded by a codon. Every coding mutation in the sodium pump gene will result in some kind of neurological trait or disease in humans, including seizures.
And sure enough, in these little fruit flies where we engineered them to carry the monarch mutation in their sodium pump using CRISPR gene editing—we did this in my lab—yes, these three mutations can make a fruit fly basically totally resistant to levels of the toxin that would kill a room full of elephants. Not that I would ever want to do that, but it caused them to have seizures when you shake them up. They basically can’t recover easily from being shaken, and that’s called a bang-sensitivity phenotype. And again, it’s nice to work on fruit flies because, like plants, no one really cares what you do to a fruit fly.
[00:09:43] Anne Chappelle: I remember doing a gene-tox lab back in college a gajillion years ago, and it is hard to get them to sit still enough to look at their phenotypes. How do you do it when they’re having little seizures? That would make me seasick when I’m trying to look at them, and they’re, like, vibrating across.
[00:09:58] Noah Whiteman: I know. We, yeah, they’re in vials, and you vortex them in a vortexer. And then you start a stopwatch, and then, you just count the number of seconds until they’re upright and walking. You can see them seizing, just looking at them with the naked eye. It’s quite remarkable. And when they have these one to three mutations, it can take them over two minutes to recover. 
[00:10:17] Anne Chappelle: It makes my brain kind of boil over a little because you start your conversation. Then, you start saying, “what could this happen on another planet or place? And how does all that fit together?” And my little brain can’t handle it. 
[00:10:29] Noah Whiteman: What’s amazing to me is when I look out at that eucalyptus grove behind me, and I think of the species interactions that are happening, both between the eucalyptus and the plants that aren’t able to grow under it that well, probably because of specialized metabolites that are in the soil. There’s allelopathy; there’s evidence of that. And also, the insects that attack it—or don’t—or go to Australia, where they’re native, and there’s a koala that’s specialized in eating them. And that’s a hard life. And then I think of the mistletoes in the sandalwood family that attack the eucalyptus there, that look like the eucalyptus because they evolved crypsis to match the leaves so that you could not tell them apart.
I think about chemicals driving all of this, especially specialized metabolites that end up being toxic to varying degrees, like eucalyptol. I think poison control centers in Australia—by far one of the biggest for children—deal with eucalyptol. And that’s used as a home remedy for respiratory infections and things like that. But to a small person? It’s the dose that makes the poison, and they’re often more sensitive, these developing people.
So there’s an example of this intersection. The eucalyptus are just doing this, making this eucalyptol—pretty easy to make because lots of plants make eucalyptol, actually—but they make a lot of it. And Aboriginal Australians were the first to turn to it and used it in many of the same ways that it’s used now. 
And so that’s another element. It’s like humans are tapping into these chemicals, these toxins that didn’t evolve with us in mind, but then we can use them as medicines. We can use them as weapons. We can misuse them and become addicted to some of them. Not most of them, but some of them. And so this co-evolutionary dynamic between organisms that are mediated by toxins are probably the most diverse type that is out there of these interactions mediated by these chemicals, and that’s why I study them.
And so if we have knowledge about that co-evolution mediated by toxins, we have, then, general knowledge about why there are so many species of life on Earth. Most of the, I would say, traits that interest me—things like toxins and resistance mechanisms—those themselves can lead to the origin of new species, we think, through this process of co-evolution. And so maybe by understanding something about how organisms make and use toxins in defense and offense and co-opt them, we can understand something about how life evolves. Why there are so many species. Why are there so many species maintained in the tropics, for example? And this crucible of evolution is mediated often by toxins as weapons.
[00:12:59] Anne Chappelle: The words that you’re using to describe, these different scenarios, they bring forth a very good visual picture of, “Ah, yeah, that makes sense.” I can see what you bring to the table can really flip someone’s perspective on poisons and just even the other stimuli that we’re going through right now like global warming and how is that affecting genes and diversity—and unfortunately, or fortunately, we may not be able to be around long enough to really see how that really plays out. 
[00:13:31] Noah Whiteman: Going back to your first point, I do think part of it is that I don’t come from this field of toxicology. So, I come at it from this really different angle, and I feel like I’m a visitor, a guest, like it’s not my field. 
When we think about the evolution of these specialized metabolites, they’re almost always building off of preexisting pathways, and this constantly happening in every generation and every set of seeds, right? There’s some mutation that is causing either say a duplicated version of that gene. So, there’s twice as much enzyme now, or there’s a mutation in one of them that changes the substrate binding affinity for something or creates a new substrate. This is just happening. And most of the time it’s bad because they’re already on a fitness peak, the population, and it’s selected against that’s the most common kind of natural selection—keeps the ancestral character state, keeps the sequence the way it was. This is why our sodium pump gene is so similar to the fruit fly’s. 
[00:14:21] Anne Chappelle: Well, it’s perfection. Why mess with perfection? 
[00:14:24] Noah Whiteman: And I would say that perfect is local because there are other probably faster, better ways of moving sodium and potassium across the cell membrane, Evolution hasn’t found it yet, that pathway. Or this is good enough, so you gotta think about these fitness peaks also as relative and local is what I would say.
[00:14:42] David Faulkner: Perfection is local is just such powerful and succinct phrase. An immediate thought that I had was sickle cell disease and resistance to malaria, where in the right dosing of those gene mutations, that’s highly adaptive, but in any other circumstance, actually not great. 
[00:14:59] Noah Whiteman: Exactly. And it’s adaptive against malaria because it makes it very hard for the malarial parasites to reproduce in the red blood cell, to live in the red blood cell when it’s sickle-shaped. And there are ideas now about why that is. They may not have access to the actin that’s in there because this hemoglobin mutation causes changes to the structure of the cytoskeletal structure of the cell, and that has this trade-off.
It causes debilitating illness for people who have two copies, but people who have one copy—and one copy that isn’t sickle trait—they have resistance against malaria, and they have enough hemoglobin that doesn’t have that resistance mutation to avoid the symptoms of sickle cell trait that are debilitating.
That heterozygote advantage, as it’s called—where either homozygote is selected against because you die of malaria as a baby, or you have sickle cell trait so badly that you have a shorter life—how could evolution maintain this? And it’s because the heterozygote has higher fitness. And in Sub-Saharan Africa, in Saudi Arabia, in Southern Asia, where malaria is endemic, all of those populations not only have evolved things like sickle cell trait but many other traits in the blood that allow resistance against malaria.
Things like favaism, which is a mutation—it’s the most common enzyme deficiency in humans, the G6PD deficiency. And it can cause mortality in babies that have an adverse reaction to something like vicine alkaloids that are in fava beans that, to most people, are easily processed. But people who have a certain set of mutations in the G6PD gene that results in an enzyme that has some different amino acid changes, that causes the red blood cells to basically not have enough NADPH, and they can’t process or deal with the cytotoxic properties of the vicine alkaloids very well. So they end up lysing, or they get removed by the spleen. And so these babies have these severe anemias, and they can die from this. Guess what? They’re also resistant to malaria. And so, the favaism is a problem in the presence of fava beans and on its own in some ways, but then, it allows for resistance against malaria. And if malaria exacts a higher cost than just having this trait, that’s going to evolve. The resistance trait is going to be favored, and that’s exactly what happened.
But there are all kinds of other mutations that have also risen in frequency. Those alleles—just the genetic variants—that are ultimately caused by mutation, that natural selection increases in frequency in the presence of these malarial parasites. And it usually has negative consequences for some other function of that protein.
[00:17:33] David Faulkner: What I really appreciate about the research you do the book that you wrote, and the way that it talks about the idea of toxins is that it’s not just this moralized, “This substance is bad.” Because we talk about like, “Ah, it’s poison. It’s evil.” But that’s a moral judgment. And what you present, and I think as a really interesting and valuable perspective, is this idea that when it comes to the field of evolutions and natural products and things like that, it’s actually a lot more complicated than that because the toxins-as-tools concept has existed in molecular biology for the last few decades, but evolution has been doing that for millennia. This idea of, “Oh, this is really poisonous to insects, but we do consume caffeine on a daily basis.” In certain circumstances for certain organisms, these are poisons, but there’s just so many of them that are useful to us.
[00:18:23] Noah Whiteman: Exactly. And then if you think of it this way, David, it also allows us to see humans as two sides of the same coin. On the one hand, we have these big brains, and we make choices. On the other hand, we’re also animals still, and we’re susceptible to many of the same sensitivities that these insects are. And we have to remember that, right? We are part of the web of life. We are not apart from it. We’re part of it; it’s us. 
[00:18:49] Anne Chappelle: We are not in control.
[00:18:51] Noah Whiteman: We are not in control, Anne. At the same time, we do have the capacity to change and to make decisions and to get help and things like that. So, it’s not like we’re automatons. It’s not like we’re just on this path. So, that’s the other thing—we make choices even in the midst of this very strong biological imperative, this gravity, this chemical gravity. But, at the same time, it’s also hard for some people, and some people die because they fail at this, fighting that gravity. They fall. And so, it’s like both things are true at the same time.
[00:19:23] Anne Chappelle: The title of your book is pretty interesting, and I’m always interested in why did you write the book? You don’t sound like you have a lot of extra time on your hands. What was it like to write a book? What was the desire, the drive? Tell me about the book.
[00:19:37] Noah Whiteman: Well, we can start with the title, Most Delicious Poison, which is from Shakespeare, from a play, Anthony and Cleopatra, and there’s a scene where Cleopatra’s really lovesick for Anthony the whole time in the play. And he’s away at war, and she instructs her handmaiden, Charmian, to bring her the mandragora tonic, which is mandrake, which is in the Solanaceae in the tomato family, and produces things like hyscocine, scopolamine, these anticholinergic alkaloids, and soporific, which means you lose track of what’s happening. You have this kind of amnesia. So, Shakespeare knew that about the mandrake. And she said, “Bring me the mandragora so that I can sleep away Anthony’s absence.” And she said, “Bring me my most delicious poison.” To me, it illuminates this two sidedness that these chemicals have for us: that one hand, we want to drink that beer; on the other hand, we now all know that actually doing that increases our risk of cancer. There’s no safe amount of alcohol that you can drink. I do it anyway.
[00:20:36] Anne Chappelle: Way to end it on a bummer. Thanks for that, Noah. Boom! It’s all gonna kill you.
[00:20:43] Noah Whiteman: So, as I was drinking my Kölsch last night—I promise this intersects with the topic—I locked myself out of my house. And my husband was teaching a night class, and I was like, what am I going to do? So, I went to this pub, I ate dinner by myself, and I bellied up to the bar.
Of course, as I ordered the beer, I’m like, I picked the low ABV one. That’s one way of dealing with this—the lowest alcohol by volume. And so, okay, I’m making a healthier choice than it would have been if it was an IPA. I only had one. I’m trying to moderate it a little bit. Yet, I still did it. I still did it, even though it killed my dad.
He died of alcohol use disorder, which is the clinical term for alcoholism now. That term, I think, was invented to take away the stigma. It’s like he wanted to stop. He couldn’t. So, it killed him. Complications of it did.
I think about this every time I drink. I’m like, should I just abstain because I have this family history? I don’t. I usually have one drink if I’m going to drink, but it’s not that often. But I’m so lucky that I didn’t fall into the same spiral that he did because, by the time he was my age, he was well on his way. He was drinking 12 beers a night just to feel normal.
This is why I wrote the book. I started thinking about those yeasts that make that ethanol, this amazing toxin that is also an energy source for them—also a way to outcompete others that can’t handle the toxicity, like this toxic larder, I call it. And I started thinking about that.
And then the monarchs we were studying, that are also tapping into a toxin made by, in this case, a plant and using it against their enemies, the birds. And then I thought about my research on that intersecting with my dad’s death. When he died in 2017, I was set on this course I didn’t choose, and then, it eventually ended with the book being written.
So, what I would say is, it’s this thing that I felt compelled to do, and I’ve never felt compelled to write a book before. And it was this thing that got me moving. And then, without talking to anyone, I wrote a Guggenheim fellowship application. I sent it in, and they chose it. 
[00:22:42] David Faulkner: Wow.
[00:22:43] Noah Whiteman: And then, I was like, “Wow, so I guess I have to do this now.”
[00:22:46] David Faulkner: Yeah. Yeah.
[00:22:47] Noah Whiteman: I do feel like incentives and that kind of good pressure helped—it encouraged me because that meant that people I didn’t know thought it was a good idea and that it needed to be written. And it wasn’t just the story of nature’s toxins, which is an amazing story on its own. One of the threads that’s woven through the book is my own experience being the child, not just of my dad being an alcoholic, but of my maternal aunt, my maternal grandmother, and some other relatives. It’s throughout my family tree. And then I studied these things. I never thought that there was even a reason, a connection. I didn’t ever see it until this book, right? And so, the ability to write the book and weave these threads together was the most rewarding thing I’ve ever done.
And I’ve had some amazing experiences. I’ve been to the Galápagos four times, caught 200 Galápagos hawks, banded them, live-captured them, caught Darwin’s finches. Our lab was the first lab to engineer these kinds of coding mutations using CRISPR to trace an adaptation in an animal. I’ve done all these things that I’m so lucky to have done, usually working for or with people who actually did it with me—always collaborative. This was different because it was just me. It was just me writing the book.
And as a modern scientist, it’s never just you. And, of course, the experiences weren’t just me, but the writing process was. And yes, I had editors. Yes, all of that, who were amazing and really made it what it was. But the rewarding feeling I got was from the writing process, and it was like this thing that had to come out of me. And when I handed the manuscript in, I said to my husband that day—and I was not being facetious, I wasn’t joking—I said, “I feel like it would be okay if I died now.”
[00:24:30] David Faulkner: Wow. 
[00:24:31] Noah Whiteman: That was the feeling I had. And so I think it was this compelled thing that needed to emerge. And that was very strange because I don’t think I’d ever felt that way before about something that I had done. So, I was—I don’t want to use the word possessed—but something had to really compel me to do this because it took a lot of energy to do it while I’m running my lab. I’m on sabbatical, so I did have a break from teaching and service. But I treated it sort of like a job. I did it every day for a while, and I also had to run my lab. So, I was doing that, too, but it was like, I could do those two things, but I couldn’t do this on a regular basis without some protected time.
[00:25:08] David Faulkner: I like that. I think that’s a good way to wrap up. The one last thing that we like to do is we like to ask questions to everybody. One of the questions is what would you be doing in the alternate universe where you’re not doing what you’re doing right now? What is alternate-universe Noah Whiteman doing? 
[00:25:23] Noah Whiteman: I know what it would be.
[00:25:24] David Faulkner: Okay.
[00:25:25] Noah Whiteman: I would be an airline pilot.
[00:25:27] David Faulkner: That is a very different thing from what you do,
[00:25:30] Noah Whiteman: I know, I know. I almost went to commercial airline pilot school. The thing that tipped me away from it is that I’m red-green colorblind. Because of that, it’s more challenging to be a commercial airline pilot, depending on the severity of that colorblindness. So, that’s the answer to that. 
And it’s a pitch for my next book, which is about color vision and colorblindness. And we have a color vision research part of our lab, too, that I’m not going to talk about today, but that’s a teaser about what the next book is about. Coming out is colorblind. One out of 10 XY people are red-green colorblind.
[00:26:06] Anne Chappelle: So, thank you so much for your time today. I really appreciate this, and I’m going to go think about all of these things and try and process them—and I may have some follow up questions.
[00:26:17] David Faulkner: Oh, yeah.
[00:26:18] Noah Whiteman: It was my pleasure, Anne and David. Thank you for having me. And, I’m happy to follow up.
[00:26:23] “Decompose” Theme Music
[00:26:29] David Faulkner: On the next Adverse Reactions,
[00:26:31] Anne Chappelle: “Testing the Waters,” with Kari Sant, an Associate Professor at Michigan State University.
[00:26:37] Kari Sant: So, a lot of what we’ve been looking at is when these get into our waterways—because they undoubtedly do when it rains—is that going to lead to issues in the aquatic ecosystem? So, we’ve looked at basically a bunch of product types and compared them to conventional cigarettes, and I will say vaping products, there’s a lot of liquid left in those when they’re discarded typically, and they definitely dump a bunch of nicotine into the environment. So, yeah, we’re finding a lot of toxicity there.
[00:27:02] “Decompose” Theme Music
[00:27:07] Anne Chappelle: Thank you, all, for joining us for this episode of Adverse Reactions presented by the Society of Toxicology.
[00:27:13] David Faulkner: And thank you to Dave Leve at Ma3stro Studios,
[00:27:16] Anne Chappelle: that’s Ma3stro, with a three, not an E,
[00:27:19] David Faulkner: who created and produced all the music for Adverse Reactions, including the theme song, “Decompose.”
[00:27:26] Anne Chappelle: The viewpoints and information presented in Adverse Reactions represent those of the participating individuals. Although the Society of Toxicology holds the copyright to this production, it has,
[00:27:37] David Faulkner: definitely, 
[00:27:38] Anne Chappelle: not vetted or reviewed the information presented herein,
[00:27:42] David Faulkner: nor does presenting and distributing this podcast represent any proposal or endorsement of any position by the Society.
[00:27:48] Anne Chappelle: You can find out more information about the show at adversereactionspodcast.com
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[00:28:00] Anne Chappelle: I’m Anne Chappelle, 
[00:28:01] David Faulkner: and I’m David Faulkner. 
[00:28:03] Anne Chappelle: This podcast was approved by Anne’s mom. 
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[00:28:13] Episode Ends