Quirks and Quarks - Polar bears are thriving in Svalbard, and more...

Episode Date: January 30, 2026

Scientists spent nearly 25 years studying close to 800 polar bears in the Barents Sea region and discovered that those polar bears seem to be doing just fine, even though melting sea ice is also a major issue.PLUS:Sargassum seaweed is becoming such a problem, you can see it from spaceWhy some people only get mild sniffles with a cold and others get sickA woolly rhino's DNA found in an ancient wolf’s stomach reveals their quick demiseHow to change a memory — one scientist's quest to understand memory permanence

I am an actor, fresh out of theater school with big dreams and an even bigger drug habit. But things are pretty good. That is until my best friend is set up on a date with David Lee Roth. Yeah, from Van Halen. If you know, you know. From CBC's personally, this is Discount Dave and the Fix. The true-ish story about how a fake rock star led me to a real trial that held up a mirror to me. And okay, let's just say that not everyone in this story is who you think they are.

Personally, discount Dave and the Fix. Available now on CBC Listen or wherever you get your podcasts. This is a CBC podcast. Hi, I'm Bob McDonald. Welcome to Quarks and Quarks. On this week's show, why the common cold gives some the sniffles and others sickness. We were able to show that that was due to a warning signal put out by the infected cells called interferon. And the secrets of one animal's extinction discovered in the stomach of another animal.

Whatever happened to make them go extinct happened in a very short period of time. Plus, ocean algae you can see from space, polar bears that are actually thriving, and how to change a memory. All this today on Quartz and Quarks. If ever there was a poster animal for the species that best symbolizes the perils of climate, change, it'd be the polar bear. Long regarded as an icon of the north, polar bears now face ever bigger challenges from declining sea ice in a rapidly changing climate. What was driving it was that the date of sea ice breakup had impacts on the survival of bears of all age and sex classes. There's not much jiggle to this bear. On the fat scale, he's a two out of five.

It would have been rare to find bears in this condition back in the 80s. Canadian polar bears aren't doing that well because of melting Arctic sea ice, especially in western Hudson Bay, where populations are rapidly declining. Well, according to a new study, the dire situation we're seeing in parts of the Canadian Arctic is a stark contrast to polar bears north of Scandinavia and Russia in the Barents Sea. Scientists studied close to 800 bears in the region over nearly 25 years. They found that the population of polar bears is not only surviving, the rapidly melting sea ice, they're thriving.

So why are those polar bears doing so well when so many of ours are struggling? CBC science reporter Anan Ram has been looking into this and is with us in Toronto to tell us about it. Hello Anand, welcome to Quarks and Quarks. Thanks for having me, Bob. Tell me about this population of polar bears in the Barents Sea. What kind of shape are they in compared to the polar bears here in Canada? Well, I mean, some things are quite similar. These bears have been protected from hunting since 1973, but like polar bears everywhere,

nothing has protected them from the loss of sea ice brought on by a warming world. The bears in Svalbard, the archipelago, that's halfway between Norway and the North Pole. That's kind of the focus of this research. Well, they've depended on that ice, like all bears, to eat their preferred prey of ringed seals and bearded seals. And like bears everywhere, they really need to pack on the pounds in the warmer months to survive winter. Well, we're hearing a lot about the loss of sea ice in the Canadian Arctic. What's going on in the Barents Sea? Well, I mean, in the Barents Sea, it seems that compared to the global average,

we know that the Arctic is warming about five times faster. In the Barents Sea, the research estimates that it's a really different environment that these bears have experienced over the last quarter century or so. After about 2005, the ice is breaking up after winter at least a month earlier. And it's starting to freeze later, adding as much. much as a hundred more days on average for these bears of ice-free conditions. So are they losing as much ice as we are? Yeah, I would say so. And it's warming at the pace where they're having their frozen days,

of course, and there are bears that are very what they call pelagic in the sense that they traverse between the Barents Sea, the areas between the Norwegian and the Russian archipelagos. But they are losing, I would say, more in some sense for these local bear, these pelagic bears. versus the bears that sort of stay in Svalbard. Well, how did scientists go about investigating how well the bears are doing over there? I mean, to put it bluntly, they spent decades shooting these bears out of helicopters.

Shooting them? Yeah, they were tranquilizing them from the air. And of course, that's because, you know, you got to take their measurements. A researcher I spoke to Marie Oje Mette at the University of British Columbia says it's not a perfect way to understand populations, but it's the next best thing to sort of sedate them

and then take their measurements. So I think it's a great indicator. I mean, there are issues with body condition with polar bears because waiting a bear is difficult. So they have to like take the length and the girth and then estimate how big they are. It would be better to weight them. But I can tell you that that's not easy. And so they've been taking these measurements through these capture mark and recapture expeditions for 25 years. So what kind of differences have they seen?

They measured this body condition, this sort of proxy for how. how much fat the bear has. And they measured that as not really being affected. It declined a little bit initially, but then sort of bounced back and is doing fairly well. And this, they speculate, is because of a potential shift in their diet. Andrew DeRoshe at the University of Alberta is a veteran polar bear researcher, and he's a co-author on this study. As that ecosystem has warmed, the bears are spending more time on land. That's very clear. But they have exploited food resources that they've always used, but it seems like they're just using more often now. And so they're going after prey that they normally do go after, but in more greater ways.

So what kind of prey are they going after on the land? We're talking walruses, and walruses have a lot of blubber, very useful. They don't normally go after adult walruses because who wants a tusk in the face, but that population of walruses has been booming in the Swalbard area. and coming across a dead adult walrus and one that naturally dies can get you hundreds of kilos of fat, which is super useful. They also eat bird eggs, whale carcasses, and from observation, one of the authors, Yon Orr, who I spoke to in Swalbard,

says something else is showing up on the menu, and that's reindeer. And we look into what alternative food they eat, and then we do see that they take a lot of reindeer. And this has also been a big surprise. Twice I actually have been flying at the moment very, where you see a polar bear kill a reindeer. So we know that there have been a few bears that have taken a lot of reindeer

that have specialized and we see they do it in different ways. Wow. Okay, so that's over there in Spalbard. Why aren't we seeing similar strategies and weight gain in polar bears in Canada, especially around Hudson Bay? I mean, it's a very good question because we have walvers in our Arctic, we have seabirds, we have these sort of terrestrial resources

that our bears could access. When I spoke with John Whiteman, chief research scientist at Polar Bears International, he says the issue seems to be around energy expenditure. For example, in Western Hudson Bay, really neat series of studies in the last couple of years have shown us that, yes, polar bears there definitely eat terrestrial prey, terrestrial food items, but they spend almost exactly as many calories to get that food as they get back from the food. So it ends up being a net zero. It doesn't really matter if you terrestrial forage or not.

So it's the idea that if they go and hunt this food, they will probably use as much energy as they get out of it. And so for the small bard bears, these unusually rich alternatives, plus less energy spent hunting in a smaller landmass, that perhaps explains why those bears are doing okay and why our bears we're seeing here do have declines in body condition and subsequently their population and survival. Well, why are the bears over there spending less energy to get their food? is the geography? A little bit. And so I mentioned the difference between local and pelagic bears

in the sense that the ones that travel. Most of the 800 or close to 800 bears studied here are of the local variety. It's definitely the geography of normally they'd be out hunting these ringed seals out on the ice. If they don't have that, they're just going to be going up and down the coasts

in various places looking for food. They're very resourceful in the sense. So they find a richer source of food and they use less energy to traverse and find that food seemingly in Svalbard. So is this a good news story then? Could we see a similar situation eventually arising with Canadian polar bears where they will

adapt and get more food from the land? I mean, so far as we know, it's a good news story for the Svalbard bears. But everyone I spoke to reminded me that, listen, if bears could survive without sea ice, we'd see them everywhere. The last ice age, for example, they were in mainland Europe and as the ice retreated, so went the bears. But the thing we can trust to hope is that hungry polar bears are, as I said, remarkably resourceful. They're good at doing what's necessary to eat. And DeRoshe says, in his 40 years of

studying bears, he's been surprised more than once. So we could see these adaptation strategies, but it's very unique to the archipelago at the moment. Arnaan, thank you so much for your time. Thanks, Bob. That was CBC science reporter Anan Ram. There's an enormous algae mystery blooming in the ocean. Out in the Atlantic, there's a huge expanse a floating sargassum seaweed that stretches from the Gulf of Mexico all the way to the mouth of the Congo River in Western Africa. And there's so much of it, you can see it from space. It's called the Great Atlantic Sargassum Belt, and in satellite images it looks like a golden brown smear across the ocean. We don't hear about it often, unless it becomes a problem and washes up on

popular tourist beaches. Here's CBC's Susan Ormiston reporting on the extent of the problem, around Florida back in 2023. Last year, Sargasum exploded to a record-breaking 24 million tons, and this year it was tracking the same, leaving ugly, smelly and potentially harmful algae dumps from the Caribbean and Mexico right up to Florida. But Sargasum isn't the only type of seaweed algae floating on the ocean, or making its way onto land, and over the last couple of decades, this has become a global problem. Now, in the first major study of ocean algae, scientists found that the floating macroalgae is growing by 13.4% per year.

Dr. Chuan Min Hu is a professor of oceanography at the University of South Florida, who coined the term the Great Atlantic Sargassum Belt. He's the senior author in this study. Hello and welcome to Quarks and Quarks. Thank you for the opportunity to speak. First of all, how is this macroalamic? different from other algae that we hear about in the ocean, the microscopic stuff? This is a big algae that is visible to a human eye. Most of the ocean algae are invisible to human eye.

In order to see them, you have to put a sample on a microscope. There's a tiny, but this macroalgae is really big, and a clump of this macroelgae is like a size of your hand. But many of these clums get together, you can see large mats, like a table or even bigger. Wow. Well, we're talking about the oceans here, which is a big place. How did you go about quantifying all that seaweed floating on the ocean? Well, this is not easy by any means.

If you have a boat, you can quantify in a small region, but you can never quantify in the entire tropical Atlantic. That's huge. That's 5,000 miles. or six, eight thousand kilometers long. So the only way to quantify is from space. But the problem is, although they appear large to human eye, they're really tiny to satellites. So we have to apply special technique to pick up this tiny signal from every image pixel and aggregate them together and paint a picture.

So how did you do that? It's a trick. So this macroalgae has a different way to reflect sunlight than background ocean water. So most background ocean water reflect very little sunlight, but this macroalgae reflects a lot of sunlight. So even if there's a tiny little bit in a certain area, we can detect an anomaly from space or from satellites. And then we have our technique to decipher this anomaly to say, okay, there is sargazen or seaweed in that place. Now, why is it important to get a global picture of this macroalgae? Why is that important? Because macroalgae serves two roles, good and bad.

In the open waters, more macroalgae would provide more habitat for better fisheries, for better survival of marine. animals. These animals use macroelage as a shelter, as a shade for sunlight, as a playground. So the more, the better for them. But if you have too much of good stuff at a wrong time and a wrong location, it can become very bad. That's what happened in the past decade in the Caribbean Sea. A lot of floating Sargassan seaweed has been inundated on beaches to cause many, many problems. So how much of this stuff is actually floating around in the oceans? All together, in its peak season, typically in summer, in June or July, it's huge. It's about 20 million metric tons if you can put everything together.

But these 20 million metric towns are spread over the entire ocean. If I was to look at a world map, where would I see it? Around the Caribbean, in the Gulf of Mexico, or now some people call Gulf of America, east coast of Florida, east China Sea, and the Yellow Sea of China and Korea. So you see a lot of macroalgae of different types. So what did you find when you looked at how quickly macroalgae is expanding in the oceans? That's quite a surprise, because if we look at the ocean, to look at anything in the ocean, there's a change.

Nothing stays static, but the change is pretty slow. That's what happened to the microalgae, the tiny little organisms. Slow change. But this macroalgae has changed very fast in the past 20 years. How quickly is it growing? On average, every year it has gone up by 13% for the past 20 years. And as a comparison, for those specific, types of microalgae, the tiny thing. When they aggregate on the surface, the change is only

1% a year. Wow. So what's making this macroalgae grow so quickly? There are different factors. For example, climate variability, including ocean warming, is a big factor. Other factors include nutrient sources, like human activities. We have more nutrients in coastal oceans. Plus, you know, people may ask, why do those two factors not impact the microalgae so fast? Well, they do, but many other things eat microalgae. So like a food chain, so it's recycled. But very few things eat macroalgae. So once they grow, unless they naturally die, they stay there.

Oh, I see. And when you say extra nutrients, are you talking about things like agricultural runoff from the land into the oceans? That's one contributor. And there are other nutrient sources. Like, well, many people don't know this, we have a nutrient from the air, the dust particles or smoke particles. They carry nutrients. And also, the water in the deep ocean carries a lot of nutrients. So once the conditions are okay, they can fuel the macroalgae and the microalgae at the same time. Well, what could be done then to try to manage this macroalgae? I'm just wondering if there would be a way to, to pull the macroalgae down to sequester the carbon that it does store into the deep sea?

Oh, that's a good point. Some people did think about this, and I think there are proposals to do this. So if you have a mechanical way to sink microalgae, then it will bring carbon down to the deep floor, to bury in the deep sediment. but the scale, no matter how much you can sink, compared to the vast ocean, the planting, this is a small amount. Right. But that doesn't mean it's not useful. Dr. Hu, thank you so much for your time.

Thank you for having me. Dr. Chuan Min Hu is a professor of oceanography at the University of South Florida. Well, it's cold season, and I'm not just talking about the weather. If you've ever had a common cold, through your household or workplace, you've likely noticed that the same virus can cause mild sniffles in some and severe illness in others. Recently, a team of researchers from the Yale School of Medicine wanted to get a detailed picture of what goes on during common cold infections

and how that may factor into how our bodies react to the virus. And it turns out, the secret is all in your nose. Dr. Ellen Foxman, is an associate professor of laboratory medicine and immunobiology at the Yale School of Medicine in New Haven, Connecticut. Hello, and welcome to our program. Hello, thank you for having me. First of all, give me the basics on the common cold. What virus actually causes it? Well, actually, a lot of different viruses can cause colds, but the main one is a group of viruses called rhinoviruses. And these are tiny little viruses that cause the vast majority of upper respiratory infections in people. Well, what makes the common cold so common? So what makes them so common,

we're not exactly sure, but a fascinating thing about rhinoviruses is that often when we get them in our nose, we don't actually get sick. So when modern techniques like PCR came about for virus testing, all of a sudden it became clear that, sure, a lot of people who have colds have rhinoviruses, but not everybody who has rhinovirus has a cold. In fact, about half the people who have rhinovirus don't have any symptoms. Well, why did you want to understand what happens when the rhinovirus infects us? The main reason is because it's a hugely impactful virus. So in addition to causing hundreds of millions of illnesses every year, this virus is also the number one cause. of asthma attacks and a worsening of disease and people with chronic lung diseases.

And those attacks are what put people in the hospital and really put them in a life-threatening situation. Well, how did you go about studying why some people are affected more than others? Well, it's been a challenge in the field of rhinovirus because there is no animal that gets infected and gets sick from rhinovirus the way the people do. So we had to come up with a different way to recreate the infectious. in the lab so that we could then study it and understand what makes people sick on a molecular level. So you basically get normal nasal cells from healthy people and you can grow them in a lab

with the top of them exposed to air. And then over the course of the next month, they will turn into a complicated tissue that looks just like the lining of our noses and the lining of our airways. And how it changes is it turns into this complicated community of cells that are all interacting and they get infected with viruses just like our regular noses. And they can also fight viral infections like our noses. So we could really study in detail what was happening. That's amazing. Yeah. You have noses in a petri dish.

Sort of. Yeah, exactly. So people have figured out that technique a while ago, actually. but there's another new technique we were able to apply called single cell sequencing. And this fancy technique allows you to basically take a group of thousands of cells and look inside each one of them and ask what's happening in every cell at the same time as they're responding to an infection. So you can see in a really detailed fashion what's going on during the infection. Okay, so you have these culture no cells in your patriot dish. You infected them with a cold, with a rhinovirus? What happened?

Well, different things happen depending on the conditions. So if we just infected them with a small amount of rhinovirus like you would normally get, and as I said, these cells were all from healthy people. By your eye, you hardly see a difference. These cultures have beating cilia, which we have in our nose and all these special features, and none of it seemed to change. All the cells seemed healthy. But if we looked with this detailed method I described, we could tell that about 1% of the cells were. infected with the virus, and all the cells around them were responding by having their antiviral defenses up. And we were able to show that that was due to a warning signal put out by the infected cells called interferon. Oh, so the infected cells are calling for help, in other words. Exactly. So that's how everything happens when things go perfectly during a viral infection is that the first few cells that get infected put out these interferons, put up a warning flag to the other cells and they all turn on their defenses. So then the virus is just can't spread anymore and it can't cause illness. Okay. But the really interesting thing was when we

blocked that interferon from being produced, that was when it got really interesting because then what we saw was a lot more cells getting infected. And we also saw specialized cells from the inside of the nose, start producing a bunch of mucus and a bunch of molecules associated with inflammation, which really looks so much like what happens in the body when you get one of these bad infections that cause a lot of symptoms. So you're saying that the interferon is a key here. If it's blocked or if it slows down, you get a worse cold? Yes, that's true. But I would say the most novel thing about this study was not finding out that. interferons are important in defending against viruses. That's been known for a long time. The most novel thing

about this study was figuring out when things go wrong because the interferons fail and you're on to the next, you know, then the virus gets through the first gate. Then what happens? And then we could identify molecules involved in the mucus production and inflammation. And those represent potential drug targets. So it was sort of figuring out, well, when things go awry, and you can now recreate this bad viral infection in a dish, how would you stop those symptoms? So that was the real novelty of the study. But what does this tell you about why some people get sicker than others? It tells us that that's something very important to look into is what are the factors that make someone more likely to have a really rapid, successful interferon response versus the factors that make it delayed or diminished?

For example, certain bacteria, if they're present in your nose or your lung might push you towards having the bad response rather than the good response. And actually, there is scientific evidence that a slightly cooler air when you're inhaling that, that does lower the speed and the strength of the interferon response, it might predispose you to getting a worse cold. And another thing that we found out some years ago is recent exposure to a virus might actually pump up the interferon response so that you have a good, fast response when you get a second infection. So that's been known, but what isn't known is what are the molecules you could actually target with drugs to flip a bad response back to a good response. So that's what we're able to go after with this new experimental method. Dr. Foxman, thank you. much for your time. Yeah, thank you so much. It was nice to talk to you.

Dr. Ellen Foxman is an associate professor of laboratory medicine and immunobiology at the Yale School of Medicine. I'm Bob McDonald, and you're listening to Quarks and Quarks on CBC Radio One and streaming live on the CBC News app. Just go to the local tab and press play wherever you are. Coming up later in the program, How to Change a Memory. The big success story here is being able to artificially turn those brain cells on and off to thereby turn that corresponding memory on and off as well. If you sold somebody a loaded gun who you knew was in a vulnerable state and they shot themselves, I think it is murder. Just because you're using the internet doesn't mean you get away with murder.

I'm Damon Fairless, host of Hunting Warhead. This season, I take you inside the business of suicide and the places desperate people go when they can't find what they need in the real world. Hunting the Suicide Salesman. Available now wherever you get your podcasts. In 2011, hunters near the village of Toomat in Siberia discovered an exceptionally well-preserved 14,400-year-old mummified wolf puppy that had been trapped in permafrost.

And a few years later, they found her sister just a few meters away. These Toomat wolfpups have been an absolute treasure trove for scientists looking to understand what life was like before the end of the last ice age, and not just for wolves either, because inside their stomachs, researchers discovered their last meal, including a hunk of meat covered in golden fur. Recently, biologists extracted DNA from this meat, and for the first time they reconstructed the entire genome

of an extinct woolly rhinoceros, from undigested remains in another animal. Dr. Camilo Chakhan Duque is a bioinformatician at Opsala University in Sweden. He was part of the team behind the work. Hello and welcome to our program. Hello, Welp, and thank you very much for inviting me. First of all, tell me about these wolves. How are they so well preserved?

They were trapped in permafrost, basically. So the theory that some researchers have, including some of our collaborators, is that they're then collapsed. They were litter mates, probably sisters, and apparently they then collapsed and they got trapped in there. And since they lived in such northern latitudes, they got pretty much immediately frozen. So what exactly did you find in their stomachs? Our colleagues did an autopsy, a biopsy of the animal, hoping to analyze the stomach contents. And to their surprise, they found a very intact piece of meat, a piece of tissue that looked like muscle tissue.

and it even had some fur attached to it, so it really looked like it wasn't digested at all. So then you do the DNA work and you find out it's a woolly rhino. What would that animal have looked like? It basically looked like very similar to rhinoceros nowadays, especially to Sumatran rhinoceros, which is the closest living species. But they had very big horns. They had a bit of a hump, and they were covered in a thick forest. like Willie mammoths.

Yeah. Okay, so how is a wolf puppy able to swallow a rhinoceros? Based on the investigations that the other colleagues have done on these puppies, they have been hypothesizing that this was probably a young, a wilded dinosaur, probably a cow that was preyed upon by the adults on this den, so probably the parents of these wolves. and that food was probably given to them via their parents or some adults from the pack.

Oh, I see. Okay, so the parent comes in and hands them a piece of meat or regurgitates a piece of meat for the pup. Yeah, exactly. Okay. How were you able to map the full genome of the woolly rhino just from that piece of mead? Okay, so basically, when we work in this field of ancient DNA,

samples can be contaminated with many things, with the humans that manipulate them, with soil, bacteria, they've been underground. In this case, with DNA from the wolf or some other stomach contents, so we needed to make sure that we got some reliable and high-quality information out of it. Well, that's quite remarkable because we often hear that DNA does not preserve well over time, usually it breaks apart. Yes, precisely. And one of the interesting things about permafrost is that it obviously

allows for a longer preservation, but since these animals are so old, it will still be very degraded. So it was very fragmented and degraded, and we also needed to account for that. So once you got the genome

of the woolly rhinoceros, what were you hoping to learn from it? We were just hoping to have like a sort of a window to that time in the history of the species. This woolly rhinoceros happened to be 14,400 years old. So we are talking here that this individual existed somewhere around 400 years before the species disappeared. So we wanted to see if this individual already showed us some signs of genetic impact on, like an impact on their genetic. because of that population declined. We had some previous evidence from previous studies

that at least up until 18,000, 19,000 years ago, they were doing okay, they were stable for several thousand years and everything. So we were maybe expecting that this individual will start showing us some signs of decline, but we didn't find that. The only thing this genome tells us with a lot of confidence is that whatever happened to make them go extinct happened in a very short period of time,

let's say 400 years. Boy, so you say they were stable for many thousands of years and then all of a sudden they go extinct. So what does that say to you about sort of the possible causes of their extinction to happen in such a short time? Yeah, that basically tells us that first that something very big,

should have happened, something that really changed their environments or their health or the way they used to live. Since this coincides very well, like this sort of window of 400 years, matches kind of well with the beginning of climate warming that happened at the end of that last ice age. We sort of hypothesized that climate change probably was the biggest or the most important aspect that should have caused this final extinction. Well, tell me more than about that climate change that happened at that time. Basically, there was warming in general. The temperatures raised considerably, and the habitats that the wilder rhinoceros inhabited

were transformed from like tundra-step kind of environment to more shrubs and small trees and eventually taller trees and snow melted, and they were probably just very confined to small areas where they could still find their preferred habitat. So the first step was probably that they were confined to specific places. That could have been also associated with humans dispersing around and everything, but definitely the climate should have played a big role here. Well, why is it important to have the woolly rhino genome from this time mapped out like this?

We want to understand more about what are the genetic consequences of population decline and of extinction. So we want to understand these natural evolutionary processes from the data itself. because so far we've been relying mostly on proxies, on simulated studies on mathematical modeling. But nowadays, there's a lot of studies on modern-day species that are in danger of extinction or that are going extinct. We can actually try and draw some parallels with that information from the information we get from species that are still around. Dr. Chacon Duque, thank you so much for your time. Thank you for having me, Bob. It was a great conversation.

Have a nice day. Dr. Camillo Chacon Duque is a bioinformatician at Uppsala University in Sweden. The ability to change our memories might sound like something out of a science fiction movie, like the 2004 film Eternal Sunshine of the Spotless Mind. Here at Lacuna, we have perfected a safe, effective technique for the focused erasure of troubling memories. In a matter of ours, our patented non-surgical procedure, will rid you of painful memories and allow you a new and lasting peace of mind you'd never imagined possible.

And as fictional as that sounds, altering our memories is an active area of scientific research because our memories may not be as infallible as we think. In fact, there could be a lot of ways to manipulate memories to erase them or activate long-dormant ones. Dr. Steve Ramirez is the author of How to Change a Memory. one neuroscientist's quest to alter the past. It's partly a deep dive into his scientific research on the matter and part memoir about dealing with difficult memories of his own.

Dr. Ramirez is an associate professor in the Department of Psychological and Brain Sciences at Boston University. Hello and welcome to Quarks and Quarks. Hi, thank you so much for having me. First of all, how realistic are movies like Eternal Sunshine of the Spotless Mind in terms of permanently changing or removing memories? So it's realistic in the sense of being able to identify memories in the brain and being able to change the contents of memories in the brain.

It's unrealistic in the sense of going into the brain and finding the exact brain cells that hold on to one memory in the human brain and killing those brain cells to thereby kill that corresponding memory. We think this is partly because memories are not located in one single point in the brain, but the sights and sounds and smells and emotions associated with the memory recruit all parts of the brain. So it's a distributed phenomenon that exists throughout the brain in three dimensions, which is something that the movie gets a little bit wrong. So in that sense is a bit unrealistic.

Oh, I see. So our memories aren't in some hard drive somewhere that we can just dip into and pull out the file. Right. Unfortunately, biology is a little bit messier. Well, before we get to your work, how do we even form memories? So it's funny you ask because we have a pretty good idea of many of the processes that happen when you form a memory, but we don't yet quite know all of the rules of the game here. So, for example, whenever you experience something, let's say you had a particularly good dinner last night,

there's corresponding bits of sensory information, like what did the dinner taste like, who were you with, what was the conversation like? And all of those parts of the experience leave some kind of enduring change in the brain. And that's important because that enduring change can happen at the level of DNA, at the level of individual brain cells, at the level of thousands of brain cells, orchestrating activity with each other to fire in particular patterns to make that memory possible. So no matter where you look, you're going to see echoes of the past in the brain. And we know that experience changes the brain from DNA all the way up to our cognition and behavior.

But the rules that it follows, we're filling in that rule book, I think, with extraordinary detail, but we certainly don't have a complete picture yet. Well, what parts of the brain actually store memories? I like to think of it as it's not that memories are stored in one brain area and are then shuffled off to another brain area. but memory is what the brain does. So all aspects of that memory are going to recruit all types of cells in brain areas and systems in the brain to make that particular memory possible. So in that sense, you're going to find traces of that memory no matter where you look,

but what aspects of that memory you're looking for, that may give us hints as to where to look, such as the smell of the dinner that you had last night or the people that you were interacting with. then we, I think, can begin to narrow that search down within the brain a bit more. Now, we experience a lot of things in a day, but we don't remember all of them, or some are more important than others. So what's the difference between where and how the memories are stored in terms of short-term versus long-term memories? Yeah, I mean, all we have to do is think about the last time we met someone and tried to remember their name. And five seconds later, that information was lost, right? So what our brain chooses to encode or to store so that we can later remember it is an entire line of research in neuroscience.

We know that it's important to attend to the thing that you're trying to remember. So if someone tells you their name, for example, you try to rehearse their name in your head. And we also know that emotionally significant events, my wedding day, for example, are particularly memorable. but there's always bits and pieces of seemingly irrelevant information that piggyback on top of memories. I remember my wedding day, but I also remember more or less what I was doing the day before, maybe even the outfit that I was wearing, and why that information has piggybacked onto my wedding day is something that we're now making headway in with research that the brain

tends to link these kinds of memories over time. But how and why it does that is where we hit the forefront of where we are. are in the neuroscience. So you're still trying to figure out why I can remember all of the words to a song out of the 70s, but I can't remember what I had for lunch yesterday? Yeah, right. There's a lot of competing theories that it could be because you've rehearsed the song endless times since the 70s, or it could be that for some reason the first time you heard that song, you thought, man, like this song, it just, I'm tapping my feet to it. The rhythm of it is amazing. The lyrics particularly stick. There's something that emotionally drew you to the magic of music that made that information

stick a bit more. And there's theories behind why that information sticks a bit more. But I think everyone is actually a bit different in what they encode and what they remember. And music is a great example of that since we all have our bits and pieces of musical flavors that we enjoy. Well, tell me about how you study manipulating memories in the laboratory. Yeah. So we work with mice to try to find individual memories in the mouse brain and to look at those brain cells under microscopes to see what are they doing? What are these brain cells doing when a memory is being formed? What are those brain cells doing when a memory is being recalled? So the first line of research that my lab embarks on is to try to visualize the cellular landscape of memories

in the brain. Just what does it look like? And then can we take a small enough ruler to start measuring bits and pieces of those memories to see what kind of information we can extract from it. The second part is given now that we can visualize memories at the level of individual brain cells, the next part is to trick those brain cells to become artificially activatable so that we can go on and test, does activating this set of brain cells activate the particular memory? does inactivating those particular sets of brain cells, inactivate or suppress that memory? And by and large, the answer is yes to all of the above,

that we can trick brain cells to become artificially modulatable. This can be through lasers and lights or drug-based approaches. And contemporary neuroscience has an amazing Swiss army knife of tools to turn brain cells on and off. But the big success story here is being able to artificially turn those brain cells on and off to thereby turn that corresponding memory on and off as well. Well, take me through your setup. How do you establish memories in mice and then how do you manipulate them? Yeah, so there's a handful of ways of doing it reliably. And one of the ways that

we started off with was by exposing our animals to a, what we call a context, which is essentially a box, the size of a shoe box that these animals go and explore. And we teach them something in that box. We can teach them, for example, that a particular part of that box is negative. So if the animals get some aversive stimuli that they temporarily won't like, then they'll learn to avoid that part of the box. It's kind of like going to a restaurant and getting food poisoning. You're very unlikely to go back there anytime soon. Alternatively, we can also go in and say, well, if the animal goes to this corner of the box, let's give them a bit of a food reward. Animals will work to get either more food, or sugar water or even condensed milk in Nutella, they tend to go wild over.

And they will learn that that corner of the box now has this rewarding stimulus there. So they will learn to go back there again and again. And they'll remember that this is where I've received the reward. So go back here repeatedly. Now, the beauty of that is that it gives us a very straightforward readout of whether the animal is recalling a memory or not. If it's a negative memory, we think that the animal should be freezing in place. so they remain immobile so as not to be detected by a potential threat.

And if it's a positive memory, they'll go towards the small opening in the side of the box that is where they will get a reward, for example. And we can find the brain cells that correspond to all of those. Then we use a handful of genetic tricks that installs a light-sensitive switch in just those cells that hold on to just that memory. That way, finally at the end, we can go in and deliver later, laser light into the brain to activate only those brain cells that hold on to only that positive or negative memory and thereby drive that memory to become reactivated and the animals will behave

accordingly. They'll go to the corner of the box with the hole to receive a reward, for example, when we reactivate the positive memory or they will freeze in place when we reactivate the negative memory. Wow, that's astounding. So you train these mice to learn one side of the box is good, the other side is bad. They remember that. You look into their brains. You find out what cells are activated during those memories. And then you use light to turn the memories on artificially.

You're actually able to turn them on or turn them off. Exactly. And the beauty of it is that we're able to turn them on or off and ask, how did the brain just do that? Like, we know that if we were to walk by a bakery, for example, and the slightest odor of a cupcake might transport us back to a time that we were involved in a brain. bake sale in high school, for example. And that was just because of one small odor. We're trying to do by analogy that within the brain, where rather than relying on the external stimulus of an odor, we're trying to access it internally by activating the brain cells directly to see if that's

enough to trigger the process of recollection. And that was profound to us because it let us know that these key brain cells were enough to trigger the recollection of a negative experience. So what can we learn from that from both a basic science perspective of how memory works? We learned that it takes a surprisingly little number of brain cells that need to be activated to drive a given memory. And we can also ask, well, what good is that basic knowledge for ourselves? And we know that negative memories and emotions are core components of PTSD, generalized anxiety, depression, and many related psychiatric disorders. And now that we have an understanding of what that cellular landscape that is enough to trigger those emotions and memories look like, we can go in and ask, of course, can we turn them off and try to get rid of the unwanted components of given memories and so on. Well, now that you've done this in mice, you've been able to manipulate their memories, how close are you to doing this in humans?

Maybe erasing traumatic memories like PTSD. PTSD is an interesting example in particular because it's that emotional oomph, that debilings, that debilings. Emolitating emotional impairments that come about as a result of PTSD, that's what we're trying to target and turn the volume down on those components of a memory, not necessarily getting rid of the entirety of the memory like in Eternal Sunshine, because most people, I think it's about 80% of people would not want their memories erased. They're the thing that threads and unifies our sense of being. They're inextricably intertwined with our sense of identity. And most people agree that those memories forged are strength and resilience of who we are today as well. Now, all that said,

there are still, of course, people who are dramatically impaired by the particularly debilitating components of any given disorder. And now that's where we want to ask, well, we don't necessarily have to get rid of the entirety of the memory. Can we go in and chisel out just the components that we think are doing the most damage internally, such as the traumatic emotional components of a given memory. In rodents, we can certainly do that, and we hope that that work now can inspire what those experiments may look like in humans by trying to do something similar as well, ideally just as non-invasively and ethically bound as possible. So in other words, you're saying you're not trying to get rid of the memory itself, but how that memory affects us.

Exactly, exactly. Like we're trying to keep the what, when, and where of that memory intact, but while trying to dial down or dial up the volume on the components of the memory that we think are debilitating us in some capacity. You talk about how memories are actually formed in our brains in your book. Tell me about that. How do we recall? We don't think that you can actually recall the exact same memory twice, the same way that the old aphorism goes, that you can't step in the same river twice. That's true of memory, that every time you recall it, it's almost like a save.

VAS version of the previous memory. So the implication here is that every memory is only as real as the last time that you recalled it. And the last time that you recalled it, there's bits and pieces of that memory that transformed and changed to enable it to be processed and stored yet again and save as in the brain once more. Well, if we're changing the memories when we recall them, how much can we actually trust our memories? I think that it really depends on the context because our biology is imperfect.

Like we're built on unstable parts. Our skin sheds, our new cells are growing every single day. Our biology is constantly changing literally every single second that we're alive. And the brain is no different. So for memory, they're certainly flooded with imperfections, no matter, memory we're recalling, but oftentimes it doesn't really matter because we're just storytelling around the campfire at a friend's cabin during holiday break. And we might remember our past slightly differently, a particular event in high school, let's say, or in college. We all have our different version of that story. But it makes for good laughs and maybe some disagreements and it's reasonably inconsequential. Society still thrives despite having imperfect memories.

Now, when those imperfections, though, are the kind of evidence or testimonials, for example, that can be used in either the court of law or somewhere where we need objectivity, certainly, that's where it can be a little tricky because I think that one way of answering how to trust our memories is to say, well, let's lean into our biology be an imperfect. and we probably remember our memories and the gist of those memories with pretty extraordinary detail. But let's be safe. If there's something that we're recalling about, let's say to go back to our graduation in high school, for example, and if me and five other friends have slightly different versions of that story, then we got to go to the data. We have to go to the data that's independent of our biological imperfections. So we pull up the videos, we pull up the text messages,

We pull up the photos. We pull up all of the evidence that we can accumulate to triangulate what the actual truth is. And then we can see that the truth is probably an amalgam of all of our experiences here somewhat. So I think that's the best way or a way of relying on our memories is to triangulate them for the truth when necessary. If it's something rather inconsequential like a given story, then it might not matter as much. What about your own brain? Do you have a memory that you'd like to change or erase all together? There's nothing that I would want to erase entirely by any means.

I remember that some of the more difficult memories that I have or just some of the harder life experiences that I've gone through, even in the moment, like I certainly wish that I had the button that made it go all away. In retrospect, though, I really don't think I would have grown into the person that I am today had I not figured out how to confront that kind of adversity. For example, when either losing someone or when kind of stuck overusing a particular drug like alcohol, for example, certainly there are ways of trying to get out of that rut and try to resolve that kind of grief

or that kind of addiction. And what I learned was that one of the most powerful ways of addressing that was by connecting with other people and listening to their memories and listening to their lived experience, that connected me with so many other groups and people and communities that I'm so eternally thankful for. And I wouldn't want that to get thrown out the window if I could rewind time and say, well, I have a pill right now that will help me just erase this memory or erase this moment of my past that is currently causing me grief, for example. But I can certainly think of instances where when I was closer to the feelings of loss or grief or addiction, that I wish that I had something that could help me expedite that process a bit more.

And I think that that will never be a bad thing to lend a helping hand, but it might not be as magical as like a secret pill that we can take that gets rid of any aspect of our past. Well, Dr. Ramirez, I have to say this has been a memorable conversation. Thank you so much for the book. And thank you for your time. Thank you. This was such a pleasure. I really appreciate it.

Dr. Steve Ramirez is the author of How to Change a Memory, one neuroscientist quest to alter the past, and an associate professor in the Department of Psychological and Brain Sciences at Boston University. And that's it for Quirks and Quarks this week. If you'd like to get in touch with us, our email is Quirx at cbc.ca. You can find our web page at cbc.ca.ca.

Where you can read my latest blog or listen to our audio archives. You can also follow our podcast, get us on SiriusXM, or download the CBC Listen app. It's free from the App Store or Google Play. Quarks and Quarks is produced by Rosie Fernandez, Amanda Buchowitz, Livia Diring, and Dan Falk. Our intern is Dion Sudial. Our acting senior producer is Sonia Biting. I'm Bob McDonald. Thanks for listening. For more CBC podcasts, go to cbc.ca.ca slash podcasts.