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Podcast: The sticky science of why we eat so much sugar

Stereo Chemistry shares a story from Tiny Matters

by Kerri Jansen
May 31, 2022

Graphic showing the Tiny Matters podcast logo.
Credit: Courtesy of Tiny Matters/C&EN
Credit: Tiny Matters/C&EN

Our bodies need sugar to survive. But most of us consume way more than we actually need, and many foods and beverages pack a dose of added sweeteners. So why are we eating all of this extra sugar? This month, Stereo Chemistry is sharing an episode of the podcast Tiny Matters that examines that question. In the episode, hosts Sam Jones and Deboki Chakravarti explore sugar’s impact on our bodies and trace how a genetic mutation that helped our distant ancestors survive is influencing our health today. And they dig into the debate around whether sugar can fairly be called addictive.

Note: This episode contains discussion of addiction and eating disorders.

Listen to Tiny Matters on the American Chemical Society’s website or on your favorite podcast platform. ACS also publishes Chemical & Engineering News, which is the independent news outlet that powers Stereo Chemistry.

Subscribe to Stereo Chemistry now on Apple Podcasts, Spotify, or wherever you listen to podcasts.

The following transcript was provided in part by Tiny Matters.

Kerri Jansen: You’re listening to Stereo Chemistry. I’m Kerri Jansen. We’re taking a short break on Stereo Chemistry to work on our upcoming season, which is all about the future of water. We’ll be back with new episodes later this summer. So this month, we’re sharing an episode from our friends at Tiny Matters. Tiny Matters is a new science podcast from the American Chemical Society, and it’s all about things that are small in size but big in impact. In the episode we’re about to hear, hosts Sam Jones and Deboki Chakravarti look at sugar, the family of molecules that sweeten our foods and beverages and can wreak havoc on our health when we consume too much of them. Sam and Deboki explore sugar’s impact on our bodies and trace how a genetic mutation that helped our distant ancestors survive is influencing our health today. And they dig into the debate around whether sugar can fairly be called addictive. Please note that this episode does contain some discussion of addiction and eating disorders beginning at about the 18-minute mark.

You can find more stories from Tiny Matters on the American Chemical Society’s website—we’ll put a link in the show notes. ACS also publishes Chemical & Engineering News, which is the independent news outlet that powers Stereo Chemistry.

And now, without further ado, Tiny Matters.

Sam Jones: The American Heart Association says people shouldn’t eat more than 100 to 150 calories of added sugar per day—that’s 6 to 9 teaspoons of sugar. But can you guess what the average American eats?

Deboki Chakravarti: I mean, just going off of my own habits and the amount of sugar I put in my coffee this morning, I’m going to guess a lot more than the recommendation.

Sam: Deboki, you would be right. Twenty-two teaspoons of added sugar a day—an extra 350-ish calories. That’s over 4 snickers bars worth of sugar. Every day.

Deboki: That’s a lot of sugar!

Sam: Yeah, and there’s zero nutritional need for this. People generally get plenty of sugar in their diets from fruits, veggies, dairy and different grains. We do not need all of that extra sugar. So, why are we eating it? Because it tastes good? Because we’re evolutionarily wired to like it? Or. . . because we’re addicted to it?

[intro music]

Deboki: Welcome to Tiny Matters, a science podcast about things small in size but big in impact. I’m Deboki Chakravarti and I’m joined by my co-host Sam Jones.

Today on the show we’re going to talk about sugar. How our bodies process sugar, why we need it, and, conversely, why a lot of extra sugar can be so bad. We’re also going to tackle the “is sugar addictive?” debate and talk about how an evolutionary adaptation that helped our ancestors survive millions of years ago is making life in today’s sugar-saturated world all the more dangerous.

And before we begin, we want to say that nutrition can be a really fraught topic because our diets and health are shaped by so many economic, social, and cultural factors that go beyond simplistic judgements of foods that are “bad” or “good” for you. Sugar gets talked about a lot in the context of our food choices, so our goal today is not to judge anyone’s diets, but to explore the science underlying those conversations.

Sam: Alright, Deboki, let’s kick things off with a quick sugar 101.

“Sugar” is kind of a catch-all term for a bunch of different molecules. But the ones that seem to come up the most, and that we’ll focus on today, are glucose, fructose and sucrose.

Glucose is the type of sugar our bodies use for fuel and it’s found in tons of different foods. Fructose is naturally found in fruits, honey and a few other foods, but also in a lot of processed foods—think “high fructose corn syrup.” Sucrose is one glucose molecule and one fructose molecule joined together. Sucrose is what’s used as table sugar and it usually comes from sugarcane or sugar beets.

Deboki: And we absolutely need sugar to survive, but in the form of glucose. We’re not going to die without sucrose or fructose, but they both get added to a ton of things. There’s the obvious foods like soda, juice, yogurt and candy, but they’re even in things you might not necessarily consider sugary—like bread, soup, ketchup, and even cold cuts!

When you eat sugar it is processed by your digestive system, which is made up of your gastrointestinal tract, pancreas, liver and gallbladder. We’re going to focus on the liver and pancreas.

Your pancreas is right below your stomach and makes a liquid called “pancreatic juice” that’s secreted into your small intestine to help digest a bunch of things including proteins, fats and carbohydrates like starches. Many different types of cells all throughout our bodies can metabolize glucose, but your pancreas plays a really important role in regulating glucose in your blood by producing insulin.

Sam: Your liver can store glucose and release it when your blood glucose levels get low. Think of it as insurance, so that you don’t starve to death. It also creates a fluid called bile which breaks down fats.

And your liver is the only place in your body where fructose is metabolized. Bombarding your liver with a bunch of extra fructose is bad because it will stimulate fat production and lead to something called nonalcoholic fatty liver disease where fat accumulates in your liver cells. It can usually be reversed if a person changes their behavior early enough, but it can destroy your liver and be deadly if it’s not treated.

Laura Schmidt: One of the biggest concerns in the world of sugar and metabolic health is fatty liver and a pretty substantial proportion of the American population has some degree of fatty liver, children are getting fatty liver. And once the fat gets clogged up in your liver, it causes all manner of mayhem when it comes to your metabolic regulation.

Sam: That’s Laura Schmidt, a professor of health policy at the University of California at San Francisco.

What’s wild is that fatty liver caused by excess fructose is the same disease as fatty liver caused by alcohol. Fructose and alcohol—specifically ethanol—are processed by the liver in the same way.

Laura Schmidt: The problem is that we regulate alcohol. We don’t give alcohol to children. We don’t sell it to people under 21. We tax it, we put warning labels on alcohol, and we do none of that for sugar, even though they have this common pathway through the liver.

Deboki: Laura is part of the team of scientists who developed, a totally free resource for people to access the latest information on sugar and its impacts on health. Laura told us that SugarScience is all about creating transparency when it comes to sugar research.

Laura Schmidt: It was motivated by this unfortunate reality in nutrition science that a lot of what we know about sugar is based on industry-funded research. So scientists that are paid by the sugar association or whomever to essentially conduct research on sugar that may or may not be biased on the basis of who funds the work. And we know that this is a massive problem in the nutrition science space because we have an archive of internal industry documents at UCSF and we know from studying internal industry documents—most are obtained either through litigation against these companies or through scientists within them who pass on and leave their archives to universities—we know that scientists have been for many, many decades paid off by sugar interests to downplay concerns about the health impacts of sugar.

Deboki: One of the early studies that Laura and her fellow researchers conducted was on a bunch of documents from nutrition scientists in the 1960s who were paid by the sugar industry to downplay the role of sugar in cardiovascular disease, and instead focus on saturated fats. Those nutrition scientists published a bunch of studies that seemed to make a big public impact, based on the shift away from eating fats to eating foods that were fat-free but loaded with sugar.

Laura Schmidt: And so we know that this whole downplaying of sugar had roots in the scientific community in very influential scientists. And that’s a huge problem. So from that we started to think, okay, what if we got a bunch of scientists together—a panel of a dozen people who do everything from bench science to clinical science to population science—and we got them to look at what we know about sugar only based on studies that are not industry-funded, studies that are neutral from a funding standpoint and have no scientific conflicts of interest associated with them. And from that, we generated a set of conclusions and materials that are available at

Deboki: Laura told Sam and I that studying and drawing conclusions about sugar can be difficult, because there’s a lot going on beyond just digestion.

Laura Schmidt: The other thing that’s a little tricky about something like sugar is that there are also hormones that are designed to regulate our appetite. Excess sugar affects them.

Sam: An example of one of those hormones is leptin, which acts as an appetite suppressant, telling our brains, “Hey, you’re full! Stop eating!” And when a person has a lot of extra sugar in their diet, particularly fructose, leptin levels can decrease to the point where your brain’s not getting that “you’re full!” signal, so you’ll continue eating when you don’t actually need to.

Laura Schmidt: And so there’s a lot of tricky harmonies between these different chemicals that regulate our appetite and regulate our sense of satiety and regulate our sense of pleasure. And they’re all designed, unfortunately, for a species that is living in a sugar-scarce environment. But in today’s environment, we’re just not rigged for this kind of sugar saturation in our food supply.

Deboki: So let’s dive into that idea—that we humans are, evolutionarily-speaking, not meant to be eating this much sugar.

We’re going to talk about one example in particular and it starts with uric acid—a compound found in your blood.

A high amount of uric acid is commonly associated with a painful arthritis known as gout as well as obesity and diabetes. For many years, physicians thought that elevated uric acid levels and diseases like gout were the consequence of being obese or diabetic.

But based on some initial experiments done in rats, a group of researchers found evidence that the reverse was true—that uric acid could actually play a role in causing obesity and diabetes.

Humans have higher uric acid levels than most mammals because of a genetic mutation millions of years ago. That mutation meant we no longer were able to produce an enzyme called uricase, that breaks down uric acid, which means that we’re more at risk for uric acid piling up in our bloodstream.


Sam: And scientists already had an inkling that fructose could lead to higher uric acid levels.

To test if fructose alone could lead to higher uric acid levels and their negative consequences like obesity and diabetes, the research team, led by Rick Johnson, a physician and professor of nephrology at the University of Colorado, blocked uricase production in rats—to mimic what’s happening in humans—and then they fed those rats fructose.

I like to think of this as the rat equivalent to drinking tons of soda.

Richard Johnson: And they became obese and they became diabetic and developed kidney disease and they developed all the features of metabolic syndrome. And it was clear that fructose was doing it. If I fed them other foods so that they were getting the exact same number of calories, only the fructose-fed animals would develop diabetes, only they would get fatty liver, only they would get hypertension. It was apparent that fructose was the culprit.

Sam: That was Rick you just heard, who actually just published a book that includes this story that we’re telling. It’s called “Nature Wants Us to Be Fat.”

Ok, so back to it—Rick and his colleagues found those results really interesting, but they were also left wondering: why don’t we produce uricase? I mean, if we did, we could break down a lot of the uric acid that’s caused by the extra fructose in our diets and we wouldn’t struggle as much with obesity and other health conditions. In other words, why have our genetics essentially set us up to suffer?

So first Rick wanted to know, when during evolution we lost the ability to make uricase. When did that genetic mutation occur?

Those questions led him to the Miocene—the period of time 5 to 23 million years ago.

Deboki: It was a time when our ancestors—early primates—were living in Africa, eating fruit, which—remember—is rich in fructose. And then the climate started to change. It got a lot cooler, things started freezing, and sea levels fell, opening up areas that these ancient primates wouldn’t have been able to explore in the past. But as they headed north towards what is now Europe, they found a lot less food.

Richard Johnson: Especially during the cooler months, there wasn’t any fruit available. And what happened was the apes started showing seasonal starvation, meaning that for those cooler months they ran out of food and you could show that by these rings on their teeth of enamel hypoplasia of, you know, poor enamel—basically the teeth can’t grow very well during the time when there’s no food. And so these animals develop these like tree rings on their teeth and each tree ring represents a seasonal starvation.

Sam: Many of these ancient primates died, but some of them survived and made it back to Africa. Many researchers believe that these primates were the ones who gave rise to more modern primates, including humans. How they survived might have been because they no longer produced uricase. A new genetic mutation meant that, instead of breaking down uric acid, it stuck around, and allowed these ancient primates to store more fat that could be used as a kind of reservoir to live off of during times of starvation.

Deboki: So Rick and his colleagues were able to actually recreate that original gene and put it in liver cells in a dish. And they found that those cells would produce some fat when you gave them fructose, but if you mutated that gene to the human version and then gave the liver cells fructose they would produce a lot more fat.

Richard Johnson: We are all susceptible to sugar, but those who eat a lot of sugar are the ones who raise their uric acid the highest. And they’re the ones that are most likely to develop obesity and diabetes. Now this of course does not mean that there aren’t many other factors like genetics, other genes and so forth. So this is just one major factor.

Deboki: Like Rick said, we humans are all susceptible to sugar. But, on top of that, we are eating an unbelievable amount of sugar.

Richard Johnson: Way back in 1700, the average intake of sugar was four pounds a year per person. And it got up to 150 pounds a year in 1990 or so. So that’s a huge difference. You take that sugar and you add it with that mutation and now you’ve got this epidemic that’s affecting people.

Sam: So that’s a good lead into the last thing we want to talk about—why we humans eat so much sugar and if we are actually “addicted” to it.

Maggie Westwater: Even just a quick Google search will lead to thousands of hits showing, you know, articles or blogs or even scientific literature suggesting that there are addictive properties to sugar. And I think it’s a very compelling narrative. It’s something that a lot of folks say kind of feels like it has to be right. And I think this does tie back a little bit to what you were saying about how we use the term addiction. And I think we have to draw a distinction between how, you know, the general population might use the term to describe something that’s distressing or kind of feels hard to control versus how we as scientists use the term. We need to be careful about how we use it.

Sam: That’s Maggie Westwater, a cognitive neuroscientist at Yale University. Maggie told us that “addiction” to a substance means seeking it out and taking it, even if there are negative consequences for doing so, all while the person feels a loss of control and a negative emotional and physical state when they can’t get their hands on whatever they’re addicted to.

Maggie Westwater: So to go back to the history of sugar addiction, it really kind of piggybacked on this emergence of the notion of food addiction, which you’ve also probably heard of. And food addiction really has been with us for quite some time, at least over 60 years. And it really gained prominence towards the end of the 20th century when the rates of overweight and obesity started to rise in the United States and other Western countries. And a lot of scientists really wanted to look for an explanation, you know, why is this happening? And of course there’s so many different factors—there’s genetic factors, there’s environmental factors, all sorts of factors that go into someone’s body mass. But the idea that perhaps there’s something in the foods that have become more and more commonly consumed is actually driving overeating, which is leading to weight gain.

This put these researchers in a bit of a tricky position because they had to identify something in these foods that could trigger overeating. So the idea that, well, maybe, you know, a lot of foods that are highly palatable and that we might find ourselves eating more than we would like tend to be quite high in carbohydrate, they’re high in fat. But the idea that, “oh, well, sugar might be the mechanism in these foods is actually leading to weight gain” started to gain a lot of prominence. And this also coincided with some studies in mice and rats which showed that under very specific experimental conditions rodents would develop addictive-like consumption of sugar.

Deboki: Ok, Sam let’s talk about these studies. In some of these studies, rodents were fasted for 12 to 16 hours and then given access to food or a sugar solution and they would totally binge on the sugar. There were also studies showing that if you give rats a choice between sugar and cocaine, they choose sugar.

Maggie Westwater: So you can only imagine the headlines that came from these studies, you know, “oh my gosh, we’re giving our kids sugar, it’s more addictive than cocaine,” which of course we recognize as a highly addictive substance. So those were kind of two types of studies that came out in animal models that really led to the conclusion that sugar could be considered addictive like certain drugs of abuse.

Sam: And Deboki, I’m sure you’ll agree that that looks bad—mice choosing sugar over a highly addictive substance like cocaine. But, as it turned out, there were more variables in there that made things a lot less straightforward than they appeared.

Maggie Westwater: So a few years ago, my colleagues at the University of Cambridge where I did my graduate training and I reviewed the literature on models of drug addiction in rodents—comparing findings from rodents who are given access to sugar and rodents who are given access to cocaine or heroin.

And we did compare the evidence across those three phases—the binging phase, the increased motivation to seek the drug, and then the compulsive drug seeking. And what we found in that literature was that, first of all, there was very little evidence beyond drug binging that sugar had similar properties to cocaine and heroin at a behavioral level. But the other more important point: in order for sugar to be considered an addictive agent that’s akin to something like cocaine or heroin, we have to consider, why is it rewarding? What part of consuming sugar is rewarding to us?


Sam: In other words, is sugar rewarding because of a neurological change that happens as our bodies process the sugar? Like is the case with cocaine or heroin? Are mice choosing to eat tons of sugar because their bodies are saying “These calories are good! We need these calories!” Or is there something else going on?

Maggie Westwater: Actually what these models show is that when you give a rodent access to a calorie free sweetener, it will also develop binge-like consumption of a calorie free sweetener.

Deboki: So mice want something that tastes like sugar even though it doesn’t have calories.

Maggie Westwater: Another line of research shows that if you give the rodent access to a sugar solution but it’s immediately drained from the stomach that it will still develop a binge-like consumption of sugar. So what these data suggests is that it’s actually sweet taste alone that is sufficient to lead to the emergence of these addictive-like behaviors in rats. And that’s a really important distinction. It’s so critical that the effects of sugar have to be post-ingestive if we’re going to use this model of addiction.

The other thing that’s important to remember about the model we discussed with drug addiction is that the effect of drugs on the brain is very, very different from an animal or an organism’s normal physiological state. And when we talk about drugs “hijacking the dopamine system,” this really does mean that they lead to a huge release in dopamine.

Deboki: Dopamine is a molecule that sends messages between our neurons. It plays a big role in us feeling pleasure and happiness and—like Maggie said—dopamine is totally hijacked by amphetamines like meth and opiates like heroin and oxy.

Maggie Westwater: So there were some studies in the eighties that actually showed that when you gave different rats all these different classes of drugs, giving them amphetamine would lead to an increase of dopamine that was nine times greater than baseline dopamine levels. And for something like cocaine, which has more nonspecific effects in the brain, it was about three times greater. But when you look at sugar and not so many of these studies have actually focused on this aspect of what is the magnitude of change in dopamine, it’s much less pronounced. It is leading to an increase in dopamine, which I, as it should, right? When we’re consuming food, it should be reinforced. It should be a positive experience so our species doesn’t die out. But the magnitude of this change is simply not equivalent to what we see with drugs of abuse.

Deboki: Although Maggie’s not convinced that people are addicted to sugar in the traditional sense of what “addiction” is, she says that absolutely does not mean people don’t struggle with regulating how much they eat.

Maggie Westwater: This isn’t to say that folks don’t experience distress and dysfunction related to their eating. So I think that’s important to keep in mind—that just because we see something doesn’t seem to map onto addiction, it doesn’t mean that it’s not a real experience that someone’s feeling, and there are other possible explanations. This is not the only explanation. We really just need to keep moving forward with our research to try and find, you know, appropriate interventions for folks.

Sam: Maggie’s interest in understanding and evaluating the “is sugar addictive” debate comes, in part, from the work she does on objective binge eating episodes—when someone eats a very large amount of food in a short amount of time and feels completely out of control and unable to stop what they’re doing.

Maggie Westwater: There are a lot of arbitrary examples, but it could be, you know, someone has a bag of carrots, um, like several bowls of cereals, several bagels, um, you know, several, maybe ice cream cones, there’s a variety of foods. Some folks do tend to consume more of these energy dense, highly processed foods, but not everybody. And, you know, the experience of binge eating is extremely distressing because in many cases the person wants to stop eating. Um, and sometimes it’s described as kind of this feeling like a snowball rolling down a hill and gaining mass, gaining momentum, and it just feels impossible to stop what you’re doing.

My research is primarily studying binge eating in the context of bulimia nervosa, which is the mental health condition that’s characterized by binge eating as well as compensatory behaviors, which could be fasting or excessive exercise, or self-induced vomiting as well as preoccupation with one’s body shape and weight. And I’ve also examined this in patients with anorexia nervosa who suffer with binge eating, which is a very understudied disorder. And we often associate binge eating with health-harming weight gain, which in many cases can be true, but we actually do see this behavior across the full weight spectrum. So I’ve been very interested in why that happens and what might be underlying these very distressing experiences for patients that really significantly reduces their quality of life.

Food is such a central part of our existence. You know, so many of our relationships revolve around food. You know, we go out to eat with friends, we go on first dates to restaurants. And it’s important that we try to get people to the best treatment as soon as possible. And one thing that I have seen is unfortunately, I think some folks latch onto the idea of I have a food addiction, I have sugar addiction, but we have no treatment for that. So if you kinda believe that this is what you have, and maybe it’s actually keeping you from seeking help that is supported by data, empirically-based care, that really bothers me. And I think that, you know, we all have to do our best to try and help folks live the lives that they want to lead.

Sam: Alright. Deboki, we went through a whole lot in this episode, so let’s briefly recap: not all sugars are the same and not all sugars are processed the same way. One of those sugars—fructose—can lead to fatty liver disease and also a buildup of uric acid which leads to things like obesity and diabetes. Unfortunately, we humans have trouble breaking down uric acid because of a mutation many millions of years ago that allowed our ancient primate ancestors to store more fat and survive starvation. Today it’s making life more dangerous in a world filled with super sweet, super processed foods.

Deboki: We also talked about the sugar addiction debate and learned that, although people can display addiction-like behaviors when eating, sugar is not addictive in the same way well-known drugs of abuse like cocaine or heroin are addictive. I’m sure that conversation is far from over, but I definitely feel like we got a lot of clarity by talking with Maggie.

Sam: Whew. Lotta stuff there. So now, Deboki and I have a surprise—something we just want to try out—and if you, our listeners, love it, we’ll have it at the end of each episode.

Deboki: This is the 60-second science show and tell! That is not necessarily the official name, but that is just what we’re working with right now. So if you all have suggestions for names that you think would be better, they are very welcome. They probably are better. We welcome all of your suggestions.

We are each gonna get 60 seconds to share a science thing we learned about in the last few weeks. Maybe it’s a news story, maybe it’s just a weird fact. It’s a total free-for-all, it’s science anarchy, we’re gonna see what happens. And we’re gonna start with Sam because I’ve decided that that’s how we’re gonna start. So Sam, you wanna go first ‘cause I’m not giving you a choice?

Sam: Yeah, sure. Why not?

Deboki: Okay. You have 60 seconds on the clock. Ready? Go!

Sam: Okay. So I’m gonna talk about super ancient cannibals. To start off, scientists were pretty certain that there were cases of cannibalism hundreds of millions of years ago, but now they think that they’ve found the earliest case yet—514 million years ago. This cannibalism was in slash by creatures called trilobites. So I think of a trilobite as, you know, if you took like a pill bug or roly-poly and you combined it with a horseshoe crab, that’s what a trilobite looks like to me. And they went extinct like 250 million years ago. So anyways, what these scientists found is there were a couple of different species, some were larger, some were smaller when they saw in the larger ones is that they had scars all over them, like they had been fighting, but then in their poop—or what they think was their poop—there were the little trilobites meaning they were eating their trilobite brothers and sisters. And yeah, that’s my first 60 second show and tell!


Deboki: I love a thing found in trilobite poop.

Sam: Okay, Deboki, now it’s your turn. You got 60 seconds starting now.

Deboki: Okay. So today for my science show and tell, I am bringing to you all drama within the paleontology community specifically within the T-Rex community. It is maybe a little unfair to call this drama because what it actually is, is a scientific debate that has been going on in many different communities, many different biological communities about how we specify species, how we actually define them, how we differentiate between what different species are. In this case, there’s a study where researchers suggested that T-Rex—what we consider T-Rex—is actually three different species. T-Rex, T-Regina, and T-Imperator, which are all great names, but this is based on studying 37 specimens and their bones. However, there are a lot of T-Rex researchers who don’t necessarily accept this result. They say that actually the difference is that these researchers are identifying between the different species are just like individual variations within a species like, you know, those little minute differences that we all have between each other. And I love this because this is just like an ongoing thing that we just don’t know how to deal with when we’re coming up with species and how to differentiate them. If you say the last few words really, really fast, the time doesn’t mean anything.

Sam: Amazing. That’s really interesting. I didn’t not know about this, so thanks for sharing. I just learned something new.

Deboki: I’m catching my breath from speaking really fast, but that was exciting. That was a lot of fun. That was the end of our first 60-second science show and tell. So tell us what you think, tell us if you learned something new from it, and if you enjoyed it. And also, again, if you have a better name, otherwise we’re sticking with science show and tell for a while.

Sam: Thanks for tuning in to this week’s episode of Tiny Matters, a production of the American Chemical Society. I’m your exec producer and host, and I’m joined by my co-host Deboki Chakravarti.

Deboki: This week’s script was written by Sam, edited by me and by Rubén Rodríguez Pérez, and fact-checked by Michelle Boucher. The Tiny Matters theme and episode sound design are by Michael Simonelli and our artwork was created by Derek Bressler. Thanks to Rick Johnson, Laura Schmidt, and Maggie Westwater for chatting with us.

Sam: If you haven’t rated and reviewed us on Apple Podcasts, Spotify, Stitcher, Google Podcast, iHeartRadio, or wherever else you listen, please, please do! And if there are some tiny things that you think matter and that you’d love us to explore in an episode, or if you’d like to tell us you do or don’t like our new show and tell addition, please shoot us an email at Links to the show and tell stories are in the episode’s description.

Deboki: We’ll see you next time.

Kerri: You’ve been listening to an episode of Tiny Matters, presented by Stereo Chemistry. Stereo Chemistry is the official podcast of Chemical & Engineering News. C&EN is an independent news outlet published by the American Chemical Society. Thanks for listening.


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