Exploring breast cancer research

More episodes in the Science Sound Off Podcast

For breast cancer awareness month this October, listen to a breast cancer researcher explain her work on why some women get breast cancer, while others don't, and why they can have very different outcomes.

Episode Transcript

Christina Sumners: Welcome to Science Sound Off. I’m Christina Sumners.

Tim Schnettler: And I’m her co-host, Tim Schnettler.

Christina Sumners: And it is October, which of course means it is breast cancer awareness month. So we are here today with Dr. Robin Fuchs-Young, a professor in the Texas A&M College of Medicine who studies breast cancer. Welcome to the show.

Robin Fuchs-Young: Thank you so much for inviting me.

Christina Sumners: We’re thrilled to talk to you today about your research on breast cancer and everything that that entails. So I guess just to start, how did you first get into breast cancer research?

Robin Fuchs-Young: That’s a great question. I kind of was always interested in it. From when I first started graduate school and was trying to decide what kind of research I was going to do as part of my degree, I gravitated to breast cancer and stayed interested in it. It’s a little bit unusual, or at least it was back in those days, for someone to follow through on the same field or the same line of research all the way through. But I did, for good or ill, and it just … it really interests me. It interests me because it is a disease mostly, but not exclusively, that women get. There is male breast cancer, it’s an important problem for those folks who get it, but it is a very different disease.

Christina Sumners: Really?

Robin Fuchs-Young: And it represents a unique sort of breast cancer problem or set of problems. I’m very interested in why some women get breast cancer, some women don’t. Some women do very, very well and survive well. Other people unfortunately don’t. I’m very interested in that sort of very basic kind of discovery, so I’m interested mostly in risk and susceptibility. What are the determinants of risk and susceptibility? And I’m also interested in how those vary by race and ethnicity.

Christina Sumners: So some people of different races are more likely to get breast cancer than others?

Robin Fuchs-Young: Kind of, but not quite.

Christina Sumners: Okay.

Robin Fuchs-Young: It turns out that white women, women of European descent, are more likely to get breast cancer.

Christina Sumners: Okay.

Robin Fuchs-Young: But women of African descent are more likely to die.

Christina Sumners: Oh, interesting. Okay.

Robin Fuchs-Young: And that interests me.

Christina Sumners: Yeah.

Robin Fuchs-Young: So some of it is the whole psychosocial, SES, access to care.

Christina Sumners: Sure.

Robin Fuchs-Young: That’s an important part of that. But I don’t research that part. I research the biological underpinnings of that. If you dig into it carefully, you see that part of it is due to … part of this health disparity or what we call an outcome disparity is because women of African descent are more likely to get the kinds of breast cancer that are more aggressive, are earlier onset, and are more treatment refractory, or for which we have fewer good tools to treat or fewer good therapeutic regiments. So then it becomes a question of why.

Christina Sumners: Right.

Robin Fuchs-Young: Right? What is it that causes that kind of differential subtype development? So we’ve been looking at that fairly closely over the past few years, and our most recent work, which I think is pretty exciting, is based on diet.

Christina Sumners: Oh, okay.

Robin Fuchs-Young: We recently published a study, an animal model study, where we looked at the effects of diet during gestation, lactation, and post weaning, and this was the diet provided to the pup, right? We found that the diet to which the pup was exposed during gestation, and the diet to which the pup was exposed, the offspring was exposed, during post weaning or during the post weaning period, which is the rest of life, the two of those were the strongest impactors of the risk of cancer, of mammary cancer, in later life. In fact, we were able to change the incidence about fivefold.

Christina Sumners: Wow. Just by changing their diet?

Robin Fuchs-Young: Just by changing the diet. What we found was sort of surprising, and that is that if the mother was given free access, ad libitum, to a high fat, high sugar diet, and then the pup was mildly restricted on a healthy low fat, low sugar diet post weaning, that combination was very protective.

Christina Sumners: Protective?

Robin Fuchs-Young: Very protective.

Christina Sumners: Huh.

Robin Fuchs-Young: On the other hand, if the gestating mother was mildly restricted, very mildly, but had a very low fat, low sugar diet, and then the pup was provided with as much really high fat, high sugar food as it wanted, that those animals were very susceptible. They had much higher levels of mammary cancer.

Christina Sumners: Much later in their life … obvious, or-

Robin Fuchs-Young: Right.

Christina Sumners: Okay.

Robin Fuchs-Young: Not right at that time, but as adults.

Christina Sumners: Sure. Okay. So that persists. What happened when they were young-

Robin Fuchs-Young: What happens during that time persists.

Christina Sumners: Interesting.

Robin Fuchs-Young: So we’ve been studying the mechanisms of that and we have found, as we expected, that there’s two things going on. One is that it changes the number and proportion of early developmental cells called mammary stem cells and other early developmental cells called progenitor cells, luminal progenitor cells. It increases the proportion of those two types of cells, and those cells are carcinogen targets and are also what we call … they can be cancer initiating cells. So basically, the diet increases the proportion of cancer initiating carcinogen targets, and so then the question is, how is that happening? It turns out that the diet is also changing the epigenetic markings or the epigenetics of certain genes that are protumorigenic, and one of the genes that it’s changing the epigenetics of is IGF-1

Christina Sumners: And what is IGF-1?

Robin Fuchs-Young: IGF-1 is insulin-like growth factor 1.

Christina Sumners: Okay.

Robin Fuchs-Young: It’s a very important peptide in the body that regulates growth. It’s the effector of growth hormone, so it’s important for the development of many organs and tissues. It’s highly impactful on overall body stature, height, for example. But it also has some very interesting and unique effects in the breast or mammary tissue, and it turns out that we were able to demonstrate that it also has an impact on the number and activity, activation, if you will, of mammary stem and luminal progenitor cells. Now, it’s not the only thing-

Christina Sumners: Sure.

Tim Schnettler: Right.

Robin Fuchs-Young: … that affects those, certainly. So this is not the only thing that is at work, but it is one of the things that is apparently at work.

Christina Sumners: So the difference in epigenetics, we’re not actually changing the genome of any organism, we’re actually just changing how it’s expressed? Is that …

Robin Fuchs-Young: Well, it affects … It’s not a mutation.

Christina Sumners: Okay.

Robin Fuchs-Young: Right? So I think what you’re referring to, the fact is that epigenetic modifications are not, quote, “mutations”, end quote. They’re modifications of the genome that do end up resulting in differential expression of particular genes, and they’re very … turned out to be incredibly important and have changed, at least for me, the paradigm of cancer, because cancer no longer really requires a mutation. Now, you can certainly change susceptibility quite a lot by altering the epigenetic modifications of particular important genes. You can either reduce or increase susceptibility. That doesn’t mean that at a later incident oncogenic insult has to occur, but changing susceptibility is kind of important because we all get exposed to oncogenic insults throughout our lifespan.

Christina Sumners: Sure.

Robin Fuchs-Young: Right? Every time we walk into a smoky room, or breathe the air in a somewhat polluted environment, or get exposed to chemicals, all of us are being exposed to various potential carcinogens, and all the time. Sometimes they’re very weak carcinogens and our body deals with them extremely well, but those insults are still there. I mean, anybody who’s ever roasted marshmallows over the campfire, eaten a good char broiled steak, every time we grill out, that’s what’s happening. But most of us would rather have some grilled meat than not, and so … or some of us, anyway, and so this is just the way that the world is. We don’t live in a completely pristine environment.

Christina Sumners: Sure.

Robin Fuchs-Young: So those changes in susceptibility are important.

Christina Sumners: Yeah. You look like you had a question.

Tim Schnettler: Well, I was going to … You mentioned early on about male breast cancer and how it’s a little bit different.

Robin Fuchs-Young: It is different.

Tim Schnettler: I mean, I think that all of us in this room probably know a female who’s been affected by breast cancer-

Robin Fuchs-Young: Sure. It’s very common.

Tim Schnettler: … and a lot of people still don’t know that there is male breast cancer. Talk a little bit about the differences between the two that you mentioned earlier.

Robin Fuchs-Young: Well, let me start by saying that I’m not an expert in male breast cancer.

Tim Schnettler: Right.

Robin Fuchs-Young: It’s rare, thankfully, and it is … in some cases, it looks a lot like certain types of female breast cancer and is treated, in some cases, similarly, with anti-estrogens for example, or SERMs. But I think what’s really not well understood is the etiology of it, is why that happens.

Tim Schnettler: Right.

Robin Fuchs-Young: I think that that’s an area of very active and important research, trying to understand that, but I think all of us, as basic scientists, we’re really interested in understanding why cancer happens, and understanding also that it’s incredibly complex. So understanding male breast cancer is … even though the number of people who get it is small, understanding the basic mechanisms is very, very important. I will say that the survival in male breast cancer is not as high as in female, at least in females of European origin, ethnicity. That’s a lot because we really don’t understand.

Tim Schnettler: That’s what I was going to ask. Is it because there hasn’t been as much research into male breast cancer?

Robin Fuchs-Young: I think that’s true, and there’s not as much known about it.

Tim Schnettler: Right.

Robin Fuchs-Young: Or at least I’m not as knowledgeable about those things. Men actually have breast tissue, but it’s just not developed the same way that it is in females, so their risk is going to be a lot lower just because they have fewer cells to transform. So what’s going on there is an important problem.

Christina Sumners: So you mentioned different types of female breast cancer. Could you just explain a little bit more about what that means?

Robin Fuchs-Young: Sure. So that turns out to be … I guess it was discovered maybe 12, 10-12 years ago. Very, very important group of scientists in a couple of different places, one of them in North Carolina, did massive analyses of different breast cancers from a large group of women in various places, and were able to determine that there were certain specific signatures, molecular signatures, and subtype phenotypes that grouped together and had defined characteristics.

Those characteristics were really important because they determined the characteristics of the disease, how quickly it progressed, or how aggressive it was, how well-differentiated it tended to be. So that goes to grading how and what cells were probably involved, and so they’re … The basics …

I mean, I’m going to give you the overview here. There’s been a lot of work done since then, but the basic subtypes are called luminal A, luminal B, HER2 negative, basal and normal type. So what it turns out, in terms of health disparities this is an important component, that women of European descent are more likely to get the so-called luminal A type of breast cancer. Luminal A type of breast cancer, again, this is all tends to be, these are not absolutes.

Christina Sumners: Sure.

Tim Schnettler: Right.

Robin Fuchs-Young: It’s not zero and a hundred, right, percent. So women of European descent tend to get post-menopausal luminal A breast cancer, for which the five year survival, if it’s stage one, is 100%, essentially.

Christina Sumners: Okay.

Robin Fuchs-Young: These are ER-PR positive, HER2 negative. They do not have an appreciable level of basal phenotype. They respond well to standards of care for those types of tumors, which involve anti-estrogen therapy or hormonal ablation, and the survival is very good. They tend to be the least aggressive. On the other side of the scale, or close to the other side of the scale, is so-called basal, which is almost the same as triple-negative, but not exactly.

Christina Sumners: Okay.

Robin Fuchs-Young: Triple-negative is a molecular signature, basal is a phenotypic description. The Venn diagram is pretty close to being overlapping, but there are variances at the side, and women of African descent have a greater likelihood to get premenopausal basal type triple-negative tumors. Okay, so what are the characteristics of those kinds of tumors? The characteristic is that they are aggressive. Highly aggressive. They are treatment refractory.

Christina Sumners: So we don’t have any good way to … okay.

Robin Fuchs-Young: Fall back on the old bad cytotoxics.

Christina Sumners: Sure.

Robin Fuchs-Young: In between are the luminal Bs and the HER2 negatives. Both ethnicities, multiple ethnicities and races get those. They do have a larger choice of therapeutic approaches, which are sometimes extremely effective. So those are sort of the gross … the biggest differences. I’ve laid it out. There’s a lot of blurring of the lines.

Tim Schnettler: Right.

Christina Sumners: Sure.

Robin Fuchs-Young: So it’s a tad of an oversimplification, but for most part it’s reasonable to think about it in that way. So our work is really about, why? Why do these different subtypes … What are the mechanisms by which these different subtypes occur? And the reason that that’s valuable is because that gives us insight into prevention and treatment strategies. Because if you don’t know how something’s happening, it’s really hard to prevent it.

Tim Schnettler: Right.

Christina Sumners: Right, or to treat it, really. Yeah.

Robin Fuchs-Young: Well, you can treat it based on what you see at the time.

Christina Sumners: I see. Okay.

Robin Fuchs-Young: But I think in terms of prevention, we really need to understand mechanism, and no one is naive enough to think that we’re going to prevent 100% of breast cancer, but if we understand why it happens and how it happens, we might be able to do a good job in terms of reducing risk.

Christina Sumners: Other than the diet-based risks, what other risks have you been studying?

Robin Fuchs-Young: Well, we’ve looked at IGF-1 by itself, without having a diet …

Christina Sumners: Okay.

Robin Fuchs-Young: Okay, so this would be a genetic risk. We have a model, an animal model, that allows us to look at just IGF-1 that doesn’t actually end up resulting from dietary changes. So we’ve found that but, but IGF-1 is … Women can have different amounts of IGF-1, just based on the regulation, the endogenous regulation, of their IGF-1 gene and growth hormone.

So we’ve been looking at that, and what we think is that it links into some risks that we know about. So for example, large babies, babies that are born, that are just big babies when they’re born, females, have an increased lifetime risk of breast cancer.

Christina Sumners: Huh.

Robin Fuchs-Young: Huh, right? Women who have large stature, who are very tall, also have increased risk of breast cancer on the lifetime. So this starts you thinking about IGF-1, right?

Tim Schnettler: Right. Yes.

Christina Sumners: Sure.

Robin Fuchs-Young: So we have a model that allows us to very closely investigate the effects of IGF-1. We’ve also looked at, over time we’ve looked at the role of p53. We’ve looked at the interaction of p53 and estrogen receptor. We did some work on that a few years ago. So we look at whatever we can think of to try to see if there is a contribution to susceptibility that we can do something about, or an association that wasn’t recognized previously.

Christina Sumners: And then figuring out the … You see in the population that tall women are more likely to get breast cancer, then you investigate some of the reasons behind that. That’s fascinating.

Robin Fuchs-Young: Correct.

Christina Sumners: Okay.

Robin Fuchs-Young: And also, we’ve known for some … So it’s a little bit more complicated than what I’ve tried to … than what I’ve explained to you, so-

Christina Sumners: It always is, yeah.

Robin Fuchs-Young: It always is. So I don’t want to leave you without letting you know, so the complication is that not only is there increased risk for large female babies, there’s also increased risk for small.

Christina Sumners: Wow, okay.

Robin Fuchs-Young: Okay. So it seems like the two, the extremes, carry with them an increased risk. Now, what that tells me is that those are going to be very different mechanisms. So therein lie some of the complications.

Tim Schnettler: We talked about ethnicity playing a role in this. How much does family history play into a disease like this-

Robin Fuchs-Young: A lot.

Tim Schnettler: … as far as maybe great-grandmother had it or someone?

Robin Fuchs-Young: Yes.

Tim Schnettler: How far down the line and how much is that a factor?

Robin Fuchs-Young: That’s a really good question. So what they call first-order relatives are incredibly important if you want to determine risk. Some of that is due to known mutations in the BRCA1 and two genes, for example.

Christina Sumners: Right. You hear a lot about those, yeah.

Robin Fuchs-Young: So those are detectable, are passed in families. Those risks are passed genetically and they can … But even they do not have what’s called a 100% penetrance.

Tim Schnettler: Right.

Robin Fuchs-Young: So even they do not … Not every woman gets breast cancer, even if they have various types of mutations in one of those genes. Now, part of that could be because the gene … the mutations have more or less effect on gene function, but it also suggests that, as with most diseases, you have a genes times environment situation, where it’s not all one thing, it’s a combination of effects.

Tim Schnettler: Right.

Robin Fuchs-Young: The environmental piece, it plays an important … These both play an important role in determining susceptibility. So we’re always working with whatever the environment is that we live in, we’re always working with genetic susceptibility. But keep in mind that genetic susceptibility is not necessarily based on mutation. It can be based on polymorphic variants, which are perfectly normal, but do not … but code for variances in the way that certain genes are expressed.

So you can have an important difference in susceptibility because a gene that detoxifies something is expressed at a somewhat lower level than in another person who’s more resistant because their detoxifying genes actually are expressed at a higher level. That’s a simple explanation or a simple example, but it … I think it’s illustrative.

So there’s a whole lot of interaction, and now that we know that epigenetics can play an important role, so this is one of the mechanisms whereby diet and other environmental factors play a role in susceptibility to not only cancer, but other diseases as well.

Tim Schnettler: Right.

Christina Sumners: So you mentioned these treatments, these drugs that can block estrogen.

Robin Fuchs-Young: Yeah.

Christina Sumners: I know you worked on developing one of those.

Robin Fuchs-Young: I did.

Christina Sumners: Could you tell us a little bit about that experience?

Robin Fuchs-Young: Sure. So that was … I spent several years at a big pharma drug company and we were working on what’s called a SERM, a selective estrogen receptor modulator. The beauty of those drugs, or those compounds, is that they have different effects in different tissues. So in some tissues they’re estrogenic, and in other tissues they’re actually anti-estrogenic. So that’s quite valuable if you can find just the right profile, right, where it’s anti-estrogenic in some tissues and estrogenic in the tissues that you want it to be.

So for example, tamoxifen, which was not the drug I worked on, is sort of the archetypal SERM. It’s been used for many years, still the most widely used breast cancer drug in the world, and because it is anti-estrogenic in the breast. The good news is that it doesn’t have … it actually is bone sparing. So it’s partially estrogenic in the bone. The downside to tamoxifen is that it’s also estrogenic in the endometrium. The drug that we worked on, which is raloxifene, is not as estrogenic in the endometrium, so it has a slightly improved profile from that point of view.

So it was really an interesting experience being part of a development team. I learned a lot about how that works and how that goes, and working … I had the great pleasure of working very closely with some of our chemists who were really knowledgeable, much more knowledgeable than I, in chemistry. I learned a lot about chemistry, which I never knew, and just how things get moved along, and what are the kind of discussions that are had, and what are the regulatory components you learn about those. I really enjoyed it, and we were successful, which is a somewhat unique experience because a lot of drugs don’t make it through.

Tim Schnettler: Right.

Christina Sumners: Right.

Robin Fuchs-Young: So I felt very privileged to have the opportunity to work on something that actually was successful and made it to market. So that was sort of a unique experience.

Christina Sumners: Yeah.

Tim Schnettler: How long did that process take? Because we hear all the time about drugs in development and it takes a while to get from step to step. So from the start to when it finally was made available to the public, about how long was that?

Robin Fuchs-Young: Well, raloxifene was a somewhat unique thing, okay. It had actually been synthesized many years previous and didn’t really excite people enough to bring it forward, so it sort of sat around. In the chemistry labs, there are these massive shelving units with all these little boxes, and there’s just drugs, there are these compounds in all of these boxes, right?

So what’s really fun is you can say, “I wonder what this would do,” and you can go in and you can ask the chemist for a little bit of this or a little bit of that, and they’ll give it to you, and you can do experiments with it. It’s sort of really … that part is incredibly cool. This is a long time ago. Now, of course, there are much more sophisticated screens that are ongoing all the time. But that was a little bit before that, so the screening was what we sort of did in the laboratory. But now it’s done in a completely different way, so it’s much more sophisticated and much more productive.

So the story of raloxifene is a little bit different than the story of a drug that is made and tested for a particular application within a relatively short time. So we were able to take this drug that had already been safety tested and all that sort of stuff, and we knew something already about the kinetics, the biokinetics of it, and slot it into a particular application. So it was much more quick.

Tim Schnettler: Okay.

Robin Fuchs-Young: So I’m recollecting that it was about five or six years from when we started to when it actually was made available.

Tim Schnettler: Wow. And that’s one of the shorter times?

Robin Fuchs-Young: That was … be very short.

Tim Schnettler: Wow.

Christina Sumners: That’s really quick, yeah.

Tim Schnettler: Yeah, that is … Right.

Robin Fuchs-Young: Yeah, that’s incredibly short. Six years, five or six years, I’m guessing, and because there was already so much known about it. But it was developed for actually not a breast cancer. It was marketed for an anti-osteoporotic because it was bone sparing.

Tim Schnettler: Right.

Robin Fuchs-Young: And that’s what it actually went to market for. Now, after it went to market, there was a lot of people who recognized its potential use as a breast cancer treatment, and that’s … I think it’s being used for that a lot. It has a somewhat better profile than tamoxifen in terms of uterine side effects, and it has the bone sparing effect, which is good, and it has the anti-estrogenic effect, which is what you’re looking for for breast cancer treatment, in the breast. So it has a good profile.

Christina Sumners: And so this is only for certain types of breast cancer, right?

Robin Fuchs-Young: Very good, yes, that’s exactly right. So the so-called luminal A type we talked about before, which is ER and PR positive.

Christina Sumners: Okay.

Robin Fuchs-Young: So it’s an anti-estrogen, so it’s going to be effective in those tumors that express the estrogen receptor, and for which … but quite frankly, the estrogen receptor is functional. Because you can have failures where the estrogen receptor is expressed, but in fact the signaling machinery is not functional for whatever reason, and then you’re going to have a less of a effect, less of a positive anti-tumor effect if that’s the case.

So to determine that, one way of thinking about that is to test whether something is PR-positive, because progesterone receptor is actually regulated by estrogen, so estrogen actually upregulates the PR. So if you have both estrogen receptor and progesterone receptor, not only do you have the estrogen receptor that’s there to interact with the drug, with the SERM, you also have evidence that that pathway, that regulatory machinery, is actually functional.

You can get fooled even under those conditions, okay, where you have dysregulation of the estrogen, your network, gene network, the expression system and the regulatory system that’s activated by estrogen. But usually, that’s been a pretty good guide.

Tim Schnettler: We all know the importance of breast cancer awareness, so talk a little bit about how you get this out to the community, and different ways you get the community involved in this.

Robin Fuchs-Young: One of the things that I’ve been so privileged to be able to do for about the past 20 years is work with medically underserved communities that … and it’s not just about breast cancer.

Tim Schnettler: Right.

Robin Fuchs-Young: Obviously, we do general health promotion, disease prevention, education, and we also work with the … we work through the schools, is how we do it. There’s lots of ways of accessing communities for engagement mechanisms, through which you can effectively engage communities. We use the schools because generally, if you provide opportunities for their kids, it’s a good way of breaking the ice.

Tim Schnettler: Right.

Robin Fuchs-Young: And of building trust, because that’s the most important component, is building trust and understanding where folks in the community are coming from and what their wants and needs are, and meshing them with what we can provide.

Over the years we’ve had various sources of support for this, NIH, Howard Hughes Medical Institute, DOD, a variety of different sources. What we do is we start with the students and teachers, and we talk about disease susceptibility and progression and healthy lifestyles, and we go into not only … It’s not only about, “Oh, you should do this and, oh, you should do that.”

It’s actually about working this kind of information into the science curriculum, and into the health curriculum, and into the activities that happen in the classroom every day, and also giving … trying to recruit some new young scientists and physicians-

Tim Schnettler: Right.

Christina Sumners: Yeah, future scientists. Yeah.

Robin Fuchs-Young: … future scientists and-

Tim Schnettler: Get them excited.

Robin Fuchs-Young: … and get them excited, and also demonstrate that these are not just careers for someone else. These are careers for you if this is what you … If you’re interested, if it turns you on, you can do this.

Tim Schnettler: Right.

Robin Fuchs-Young: Our predominant target audiences are down at the border, and we’ve been working down there for over 20 years, and have been able to establish some really good relationships with the schools in the area. We have a program right now called MENTORS, Model Education Networks to Optimize Rural Science, and that has been supported by the NIH. We also work with the PATHS-UP Engineering Research Center. They support this, the PI of that is Gerry Coté, and we also work with the new Texas A&M Center For Environmental Health Research. The PI of that is David Threadgill, and we do the community outreach, community engagement in K-12 education for those other big center type grants.

I’ll just tell you one, I think one of the coolest things that has come out of all of this. We thought a lot about how to get health information that’s usable and accessible and not off-putting to folks, and we came up, myself and my collaborator, co-PI, Carolyn Cannon, came up with this idea of training health ambassadors in the community. So we offer a competitive opportunity for the students, the high school students, in Mercedes, Texas, to apply to become health ambassadors.

They apply, we make a selection, and then for the entire school year, after the application year, we train them to be health ambassadors. So we train them about the pathophysiology of the most common diseases in that community, and those are … and all the students, by the way, know what they are. We didn’t have to tell them that.

Tim Schnettler: They knew.

Robin Fuchs-Young: They knew. So they are obesity, diabetes, cardiovascular disease, and asthma. So we talk to them for … we meet once a month, we have reading assignments, we have discussions about what … why these diseases are common in the area, and what are the reasonable preventive strategies that can be discussed. Evidence-based.

Tim Schnettler: Right.

Robin Fuchs-Young: The other thing we try to teach people is, or educate them about, is the fact that not every claim of miracle whatever is accurate. So we talk about evidence-based information, and we train these kids to do it, and they’re amazing. Then we have a big health expo that’s open, obviously, to the entire area. We’ve had two health expos so far. Somewhere around 400 people have come to participate in those, and the students do the noninvasive screenings.

So they do the screening for obesity, they do the screening for cardiovascular disease, they do the screening for asthma, and then they act as health educators and help the folks who have participated in those screenings to understand what the results mean. Also, too, they talk to them about some strategies that can be used to prevent or reduce the severity of …

Christina Sumners: Of the conditions.

Robin Fuchs-Young: … of the conditions.

Christina Sumners: Wow.

Robin Fuchs-Young: They can’t do the diabetes screen because it’s invasive.

Christina Sumners: Taking blood, right.

Robin Fuchs-Young: It’s a blood-take.

Tim Schnettler: Right.

Christina Sumners: Okay, yeah.

Robin Fuchs-Young: But they can certainly do the diabetes education and they become quite knowledgeable. So the reason that we think that that’s a good approach is, first of all, the students who participate learn a lot. They can decide whether maybe health care, health education, community engagement is maybe their thing.

Tim Schnettler: Right.

Robin Fuchs-Young: And it is sustained in that community, so it’s not over when we leave because the money’s gone, right. It’s a sustained situation, plus we work with the teachers and the schools to get this information incorporated into science, and physiology, and anatomy, and health, and other classes. Biology, certainly. Chemistry, certainly. So, that way, the goal here is for the effects to be as sustained as possible and not be limited by just the time that we have, the money.

Christina Sumners: That sounds incredible.

Robin Fuchs-Young: Pretty gratifying.

Christina Sumners: Yeah, I can imagine.

Robin Fuchs-Young: It’s a team effort, by the way. It’s not me. We have a wonderful team that includes, like I said, Carolyn Cannon, Tim Lightfoot. We have wonderful folks that come to us from … work with us from the School of Public Health, Natalie Johnson and folks like that. So it’s really a team effort, and the program coordinators, Alyssa Palacios and Simon Schmitz, are also important. Very important. Like, maybe the most important when it comes to that.

Christina Sumners: Well, thank you so much for taking the time to join us today.

Robin Fuchs-Young: It was a pleasure. Thank you for giving me the opportunity.

Christina Sumners: And thank you all so much for listening, and we’ll see you next time.