[00:00:00] “Decompose” Theme Music

[00:00:05] Anne Chappelle: We’ve been doing Adverse Reactions, and this is what our 

[00:00:08] David Faulkner: Fourth

[00:00:09] Anne Chappelle: Fourth

[00:00:09] David Faulkner: Season

[00:00:10] Anne Chappelle: Season

[00:00:11] David Faulkner: Amazing. 

[00:00:11] Anne Chappelle: So, David, do we have a theme? 

[00:00:13] David Faulkner: Everything is so much more complicated and interesting and more interconnected than we ever think it’s going to be. 

[00:00:22] Anne Chappelle: We’ve really kind of strayed from traditional toxicology in this season.

[00:00:28] David Faulkner: It’s true. We have been expanding the reach of what most people think of as toxicology because one of the things I love about this discipline is that it is a necessarily applied science and that means it touches basically everything—all the other sciences.

[00:00:44] Anne Chappelle: Have a listen.

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[00:00:52] David Faulkner: On this episode of Adverse Reactions, “Cardiovascular Risks from Low-Level Metal Mixtures” with Nivetha Subramaniam, a student at McGill University.

[00:01:02] Nivetha Subramaniam: So, it adds information, and now, we know where to go with it. Initially, when we were doing the study, we were expecting, “Okay, we’re going to see some stuff.” And as we were getting through it and we’re like, “No.” But then, everything is telling us the same thing. Whether we do in vitro or in vivo work, everything is telling us that at these doses, “No, we don’t actually see anything.” It sucks, but at least the science is making sense. 

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[00:01:26] David Faulkner: We are joined today by Nivetha Subramaniam, who is a PhD candidate in Koren Mann’s lab at the Lady Davis Institute for Medical Research School of Biomedical Sciences, McGill University in Montréal, Canada, on Earth, in the Sagittarius arm of the Milky Way galaxy. Thank you so much for joining us today.

[00:01:43] Nivetha Subramaniam: Thank you.

[00:01:44] Anne Chappelle: So, we don’t usually have graduate students on our podcast. Tell me a little bit about your research because we found it really to be interesting—and if you could explain it in the way that if you were talking to my mom at the grocery store.

[00:01:57] Nivetha Subramaniam: Sure. Thank you for inviting me. So, like you guys said, I’m a PhD student at McGill University. We’re basically a toxicology lab, and we primarily work with arsenic exposure. And my project really looks at low-dose metal mixtures and the risk of cardiometabolic diseases. As humans, we’re not exposed to just one agent in the environment, so really, it’s a combination of stuff. So, the idea behind my project is no longer to look at arsenic alone, but we’re also looking at arsenic as well as cadmium, which are basically two metals, and the risk of these metals when you’re exposed through drinking water to cardiometabolic diseases. And the two main diseases that I look at is atherosclerosis and as well as fatty liver disease. So, atherosclerosis is really when you have build up of fat in your artery that causes the blockage of your artery and at that point you end up with a heart attack. And with fatty liver disease is where you have at least five percent of your total liver which is accumulated with fat, and that could end up being where you have more and more damage and inflammation and you can eventually end up with fibrosis or liver cirrhosis. So, those are the two main diseases that I’m looking at.

[00:02:58] Anne Chappelle: So, why those two metals?

[00:03:00] Nivetha Subramaniam: Essentially, my project goes back to a human cohort data. There is a Danish diet cohort that we work with, and from there, we looked at the different metals that human population were exposed to. And because our lab primarily works with arsenic, and historically, we’ve already worked with a lot of projects on arsenic, where you’re like, “Okay, for sure, we’re going to do arsenic.” And that cohort specifically had so much data on cadmium, and cadmium is primarily found in cigarette smoke, but that population study was taken out of people that were not exposed to cigarette smoke. So, it was one of the largest studies that had that data. So hence, why we decided to do arsenic and cadmium and look at those two. And of course, the more and more you add variables, the more complicated it gets. So, we had to do first arsenic alone, and then cadmium alone, and then the combination of both.

[00:03:42] David Faulkner: Yeah, that’s what I was wondering about as I was looking through some of the research here, and obviously, this is the big problem in toxicology, right? It’s we tend to study things one at a time because that’s generally how you solve math problems, and how you do the scientific method, right? Are there other things you have to think about when you’re studying mixtures?

[00:04:00] Nivetha Subramaniam: Yeah. Really our exposures are through drinking water. So for in vivo, for animal work, I work with mice. We expose these mice to arsenic and cadmium via drinking water, but it’s not as simple because sometimes we control for it as much as we can, but again, there’s already basal levels of metals that you can find in tap water. So, we have to account for that as well by having controls while we do our exposures. But it’s not really 100 percent like true, right? Because of that basal contamination, we have to take that into consideration. And also, another thing in my project is that we’re working with really low doses. So, because it’s low dose, then even that basal contamination oftentimes becomes a question that everyone asks, whether it be in committee meetings or whether it be when I present my data, because if you’re working with a higher dose, then, having basal contamination, you can say you can neglect it, right? But when you’re working with really low doses, then, that basal contamination has an effect. But because we’re controlling for it at the same time, then, we can say that the effect is everywhere, but that is a caveat.

[00:04:57] Anne Chappelle: So, is this a low dose to a mouse, or is this low dose to humans?

[00:05:03] Nivetha Subramaniam: It’s low dose to humans, actually. So, basically, the maximum containment level for arsenic, for instance, in drinking water for humans is 10 parts of a billion arsenic, and I worked with five parts of a billion arsenic as one of my lower doses, so the half of that. We also included 50, which is higher, but that’s just because historically we’ve had data that we did 50, and we know that there’s a dose-dependent increase in the effects like the cardiovascular effects that we studied, so that was for arsenic.

For cadmium, the maximum containment level is three, and we did 1.5 and 5, and the lower limit and the upper limit that we chose are actually the 25th and 95th percentile that we got from the human cohort data. So, people are actually exposed to these doses.

And so, that’s how we set our lower and upper limit, so I had those four doses and then the combinations of those four. So, in total, I had nine different treatments, four singles and four combinations and then tap water. So, it was nine in total. 

To go back to your comment about it being low dose in mice versus humans. So, actually, a fun fact, mice actually metabolize arsenic much more faster than humans. They actually metabolize it a lot faster than the humans. And hence why now we’re extending our findings to a humanized mouse model for the gene that actually metabolizes arsenic. So, that’s a project that I’m currently working on right now.

[00:06:16] Anne Chappelle: So, I didn’t really think we metabolized metals. Is it really just making them more water soluble to get out of your body?

[00:06:24] Nivetha Subramaniam: So, arsenic gets metabolized. So, inorganic arsenic gets metabolized where it gets changed into like different metabolites and it gets excreted. You’re right about the excretion part but not all metals. Like, for instance, arsenic gets metabolized, but cadmium is a body burden. Like, you accumulate it.

[00:06:38] Anne Chappelle: Okay.

[00:06:39] Nivetha Subramaniam: And the half life of cadmium is like 15 to 30 years. So, as soon as it’s in you, it starts accumulating versus arsenic gets metabolized.

[00:06:47] Anne Chappelle: Now, tell me about the form of cadmium or the form of arsenic because that could also have a big effect on how it’s absorbed. Is there good arsenic versus bad arsenic or good cadmium versus bad cadmium? 

[00:07:01] Nivetha Subramaniam: Yeah. For arsenic, for example, there’s the inorganic and the organic form. So, the inorganic one is the soluble one and the one that were found in water, but there’s also organic arsenic that’s found in fish food, for example. You can accumulate arsenic that way as well. For instance, arsenobetaine, I believe it is, but arsenobetaine has we’ve seen where we didn’t see any effects with cardiovascular outcomes with cadmium, it does not get metabolized, and if you just accumulate it—and both in mice and humans you accumulate—and the amount that you absorb is actually less. So, you absorb about on average five percent, but it’s there in your body. So, it is a body burden, but the amount that you end up absorbing is a lot less than how much you would in terms of arsenic. So, for low doses, I do think there’s an effect, but I just think studies should be done at a chronic exposure really to understand what’s going on with cadmium effect versus arsenic. You can even study at lower exposure times.

[00:07:51] David Faulkner: Okay. So, this raises the question of how do you get from metal exposure to heart disease? Because you hear about like, Arsenic and Old Lace. We know that arsenic is bad for you. We know that cadmium is bad for you. But the specifics of how does a metal cause heart disease?

[00:08:06] Nivetha Subramaniam: Yeah, of course, because before you get to atherosclerosis, there are also the proatherogenic mechanisms. So, those include ROS generation, endothelial cell activation, lipid accumulation. So, arsenic on its own can generate ROS. So, we studied that in a dish where we have the cells of interest, we add arsenic, and we look at their effects. Do they increase ROS? Do they increase lipid uptake? So, all these, yes, same thing with cadmium. It has been done. Really, it’s the early on proatherogenic mechanisms where they can have an effect and that could eventually lead to your atherosclerosis. And we’ve actually characterized the plaque size and the plaque phenotype in these mice. So, we’ve done the early proatherogenic mechanisms in a dish. And then, the mouse models, what we do is actually we expose them at the end point. We sack these mice and look at the plaques in the aorta and as well as in the heart. So, that’s how we look at the cardiovascular outcomes.

[00:08:56] David Faulkner: So, is it that the heart tissue is just more metabolically active and that’s why you see more damage and more reactive oxygen species being generated there? What is the targeting there? Or is there targeting because why wouldn’t you see necessarily plaques and other blood vessels like the brain?

[00:09:12] Nivetha Subramaniam: In humans, it’s actually coronary artery that you see more. In mice, it’s a little less feasible to look at other arteries. So, we look at the aorta, which is the largest artery, and as well as the sinus, which is inside the heart. So again, there’s a little bit of a differences, but the end outcome is same. You still see increased athero and increased atherogenic properties.

[00:09:31] David Faulkner: Incredible. So, how did you get into researching metals? 

[00:09:34] Nivetha Subramaniam: I never thought I would end up in toxicology, actually. That was never where I was headed. I was born and raised here in Canada, and I did my undergrad at Concordia University. And initially, I always thought about med school. So, I always wanted to go for pediatrics. That was really my initial thought. So, I went into biochem at Concordia University. When I started, I really thought, “Okay, at the end of my undergrad, I’m going to apply for med school and go to med school.” So, that was the game plan. And I wanted to co-op because I needed a backup plan. I’m like, “What if I don’t get into med school? What am I going to do then?” And I also wanted to know what else can I do if I ever end up changing my mind? So, I worked at Agilent for almost a year, almost a year-and-a-half, actually. So, I did all three work terms at Agilent Technologies. I started off as an scientific inside sales associate, and I realized that I can’t do that. I was like, “Nope.” It paid me great. I made quite some money being a student, but I did not like that. I did not like making the calls even though it was about instrumentations and all that stuff. It wasn’t enticing. 

But one thing I am grateful for is that, so the way the Concordia program is that if you’re at the same place for all three work terms, your third work term, you have to do a different position. So, I had to change position, and so then, I was actually working in a lab. So, I was working with a application scientist at that time, and we were working on some pesticide samples related to some government work. And so, I worked with some LCGC instruments. I did a lot of sample prep. Then, I realized, “Okay, I actually enjoy working in the lab.” And then, after that internship, I went back and did an honors project because I was only a specialization student, so I didn’t have to do a one-year honors project. But then, I decided maybe I should try it out before I consider grad school. So, I did that for a year in the labs. I did it in the Chair of the chem and biochem at Concordia, and it was a biophysical chemistry lab. So, I worked with Langmuir troughs and looked at air-water interface. Please do not ask me any follow-up questions on that; I don’t remember. 

But anyway, so I did that, and then, it was the lockdown; it was COVID, and I still applied to med because that was still the goal, but I did not get in. So, then, I was like, “Okay, so what should I do?” And I started applying for labs. And because it was COVID, it was a lot more difficult. I reached out and everyone was like sure come, but they were like we don’t have really funding So, I did not hear back from a lot of professors. The only person that I really did—I had two or three offers, I think—but the one person I got to actually talk to in person was Koren. 

So, when Koren told me about her project, I was actually really hesitant at first because I do not like animals. I’m very scared because of what happened when I was young. I got chased by a dog and, then, it jumped on me, and I have a phobia. But it’s funny because it’s been four years that I’m handling mice, but that’s going fine. 

So, at first, I was very not too sure, but I started as a master’s and then, I really liked my project. So, my project was going to extend into three years at that point. I decided, “Okay, I like the project I’m doing, and I would like to see where it’s headed. So, then, I decided to fast track into PhD and here I am.

[00:12:21] Anne Chappelle: Well, you’re not just fast tracking. You’ve got a lot of publications; it’s great to see you as a first author on your work versus some other labs where you might be, “I’m sorry, no, you can’t be first author.” And that’s got to be really empowering. It’s one thing to do it, but it’s another thing to speak in front of the Society of Toxicology or my mom or whatever it happens to be.

[00:12:44] Nivetha Subramaniam: Yeah, it’s really on Koren. Koren’s very encouraging. She is very pushing for like, “Oh, it’s your work. You should present it.” Like when I got the offer to present, I did ask Corin. I was like, “Do you want to present it? I don’t mind.” And she was like, “No, it’s your work. You’re presenting it.” And I’m like, “Sure.” So, that’s where that is.

[00:12:59] David Faulkner: Wow. 

[00:12:59] Anne Chappelle: How do you change the message of your research when you are presenting it in a public forum? How do you have to think about your research differently when you’re trying to present it?

[00:13:10] Nivetha Subramaniam: It is really about the audience, who we’re presenting to. For general public, the one thing we always—and I think with my project, it gets a little bit easier just because of the doses that we work with—one thing I always like to highlight is how even sometimes the first part of my project, a lot of it was negative. It wasn’t really like we were seeing, “Oh, at these doses, it’s really bad,” but it was good to know. Like, it’s information that should be out there, and it helps with policies as well because the doses that we’re working with is actually what doses people are exposed to. So, that makes it a lot easier for me to connect what I’m doing and to rationalize why it’s important to do what we’re doing right now.

[00:13:42] David Faulkner: Yeah. I think that touches on something that I think is really important is the importance of negative data. More specifically, the importance of publishing negative data, which is usually a thing that doesn’t happen. And then that’s, I think, it’s a big problem, right? Because then, people are like, “Yeah, but there’s no evidence that at this level it, it’s fine.” And it’s like, “Well, maybe there is.” 

[00:14:00] Anne Chappelle: I’m not going to shout from the rooftops, “I didn’t see anything!” I mean, unless you’ve got a really good positive control, but I agree: Finding opportunities to present data that’s well conducted, but it does not show a particular effect that you’re looking for is really important.

[00:14:17] Nivetha Subramaniam: Yeah, it adds to the story, especially when we have data for the upper limit or for the higher doses. Like no one has looked at this, so now, it’s done. It’s there so we know. So, it adds information, and now, we know where to go with it. Initially, when we were doing the study, we were expecting, “Okay, we’re going to see some stuff.” And as we were getting through it and we’re like, “No.” But then, everything is telling us the same thing. Whether we do in vitro or in vivo work, everything is telling us that at these doses, “No, we don’t actually see anything.” It sucks, but at least the science is making sense. But then, there are other limitations to our exposures and everything. So, hopefully, with the humanized mice, we’ll see what happens.

[00:14:53] Anne Chappelle: What do you think you want to do now with the rest of your life?

[00:14:55] Nivetha Subramaniam: That’s a great question.

Honestly, so, right now I think in a year or so, I should be done with my PhD. So, that’s one thing. I don’t really think I will be in academia for long. I don’t think academia is what I’m thinking—becoming a supervisor and having my own lab. I don’t think I’m really interested in that. I love my project, but I don’t think I have the drive to ask a new question and to keep digging for the answer. It’s not for me, but I would like to do a postdoc just to learn a new technique, a short postdoc to learn something outside of what I’ve done for the past five years during my PhD. I think it will be a good learning experience as an independent researcher just to get hands on onto something else, but then, I would like to, in the long run, work either for the government in policy or regulations or something like that or even benching, if possible. I’m not sure how it works in terms of what labs in the government, but I’m also open to industry. So, I don’t know. I feel like I can’t sit at a desk all day long, so I need something that’s a little bit hybrid that would allow me to do some experiments and then maybe come back and work on my computer or look at data or something. So, yeah, but I think what I ruled out is really academia at the moment.

[00:15:58] David Faulkner: Do you think you want to continue to work on metals mixtures? Do you have sense of that?

[00:16:02] Nivetha Subramaniam: Yeah, I think I’m open to working in metals mixtures. It’s not something I thought I would be, but it’s rather interesting. And I think mixtures research is pretty important, and I think it’s a growing field right now. We have so much information about single agents, but as mixtures, it’s pretty limited. I would be happy to continue.

[00:16:19] David Faulkner: So, as far as mixtures go, this is, I guess, the trillion-dollar question, honestly, is just how do we account for so much environmental exposure? So, then outside of humanized mouse models. What do you think about other technologies or strategies for studying mixtures?

[00:16:34] Nivetha Subramaniam: So, basically, in the cohort that my project is part of the human data, I don’t know how they do it, these biostatisticians and epidemiologists, but I know they try to run these cool analyses that takes into account the different components and how they can have a weighted effect across multiple components. I do not know, honestly. I’ve only done one and two agents right now, so I have no idea, but I think it will be difficult even as soon as you add a third component. Things will get difficult in wet lab, per se. So, I’m not sure if I’m answering your questions, but I really, I don’t know. 

[00:17:05] David Faulkner: So, you mentioned that there’s a really long latency time with cadmium in the body. Where does it store? Where does it hang out?

[00:17:13] Nivetha Subramaniam: Cadmium is primarily kidney and liver. So, more kidney than liver, but those two are the top. 

[00:17:18] Anne Chappelle: With the whole push towards reducing animal usage, how do you take your research and translate it to a nonanimal model? Is it a computational model, potentially? Or I’m of the vein that there’s some things you just have to test in vivo, but there is a big push for that.

[00:17:37] Nivetha Subramaniam: Yeah, like I mentioned in my work, yes, we have the mouse studies, and we do want to do as much as possible to reduce the amount of animal use. But for instance, the early proatherogenic mechanisms, there was all done in dish, right? So, those were all with cell lines, and they were done in a dish where we looked at this and characterized it and realized, “Okay, no, there isn’t an effect.” Versus with the in vivo exposures, we had no choice. But then when we did, that’s also the reason why we collected all the organs. So, I have the bone marrow, I have the spleen so that we limit if ever we have to go back and ask, “Okay, what happened to the kidneys?” Then, I have them, so we don’t have to redo the exposures. So, that’s the idea behind collecting everything and storing them appropriately, so that when we have another question or someone else would like to explore, then, we have these resources. 

[00:18:19] David Faulkner: On the topic of things that are contingent on animal models, did you see sex differences in the ways that the exposures affected the mice?

[00:18:26] Nivetha Subramaniam: That’s a great question. So again, because it was my stuff it turned out largely negative right now. At least for the cardiovascular outcomes. We did not see any effects, but it is known actually that in mice, female mice have larger plaques than male mice despite the dosing. And it’s the opposite in humans. So, men are more prone to the risk of cardiovascular diseases than women. So, there is that caveat once again, differences between mouse model versus humans. Right now, I’m working on the liver stuff. The fatty liver disease outcomes, and I actually see more of an inflammatory phenotype in the liver in the male mice than the females. So, it’s a little bit of a differences.

[00:19:03] Anne Chappelle: Do you think it has anything to do with estrogen and testosterone and cycling mice?

[00:19:08] Nivetha Subramaniam: Honestly, for the cardiovascular outcomes, yes, there’s a lot of studies that have supported that, maybe it is related to sex hormones, but it hasn’t been established. There’s a lot of controversy in the literature as well, so I’m not sure. Some say it is related to sex hormones, others say not really, so I don’t know if I can really answer that for sure, but there is controversy in the literature.

[00:19:28] Anne Chappelle: See and that was a really good response because you didn’t dig yourself into a hole, claiming something that you didn’t know about. And that was a really good way to address that question. Well done.

[00:19:41] Nivetha Subramaniam: Thank you.

[00:19:42] David Faulkner: Yeah. It is refreshing the amount of “Actually, I’m not sure. The research isn’t clear on that” because it’s very easy, especially in today’s media environment for people, such as myself even, to speak with great authority on things. It’s actually, we don’t really know

[00:19:57] Anne Chappelle: Was going to say, overall, do the baseline levels of arsenic and cadmium in water, is it lower in Canada versus the US? Should I move to Canada to protect my heart?

[00:20:09] Nivetha Subramaniam: No, I, honestly, no, I think you’re fine. Don’t worry. Actually, there are some regions in both Canada and US where there are higher metal exposure than others. So, in Canada, there was a recent report in one of our territories—so I think it was Northwest Territory or Yukon, I’m not sure which one of them. I can’t remember off the top of my head—where there was actually arsenic exposure, like contamination, over the last few years because of a mine that was there. So, there’s that in U S in North Carolina, there has been studies that have shown that there is a little bit more arsenic exposure than the maximum containment level. Same for cadmium. And honestly, there’s a lot more exposure in like India, Thailand, Bangladesh, like in higher PPP, PPM ranges even. So, like Canada and US, Some regions are better than the others. 

[00:20:57] Anne Chappelle: When you’re thinking about some of these in vivo models, I would think that the actual formation of a plaque might take a while. Are there other markers that you’re considering that are earlier to evaluate plaque development? I mean, you mentioned looking at inflammation. Is that a good marker?

[00:21:14] Nivetha Subramaniam: Yes, for sure. For atherosclerosis, inflammation, it is known as an inflammation-prone disease as well, but what I was talking about earlier for inflammation was liver. But you’re right. We did a 13-week exposure where we see pretty much a fully grown plaque, but we’ve also looked at earlier time points, for instance, at eight-week exposure. So that was one thing that we’ve done to look at it earlier on. We usually look at the circulating lipid levels as well when we sack to see if those have increased over time or not. But really, earlier on , we haven’t really done anything more than just looking at the plaque and looking at serum levels and, yeah, really at end point. 

[00:21:50] David Faulkner: Well, it’s interesting that it’s inflammation that’s the boogeyman here. It makes me wonder is there a third metal that maybe you have your eye on?

[00:21:58] Nivetha Subramaniam: That’s, honestly, that’s a great question. Do I have a third metal I have my eye on. Really, no. Especially not in terms of toxic metal. Like, one thing I was curious to see is because there’s been more recent studies on zinc and cadmium because zinc being more essential and how zinc and Cadmium tends to mimic zinc also. So, that was one thing that I did think about adding in. So, initially, we did think about adding essential nutrients and looking at the effects of essential nutrients and as well as metals, toxic metals at the same time. So, that kind of went down, like we decided not to really go more just because the first part of the project was already largely negative. So, we decided we will change gears a bit and look at something else.

[00:22:35] Anne Chappelle: It sounds like you’ve had a really positive experience leading you into this laboratory and a research career. Do you think your experience was a lot different because you started within COVID that you maybe couldn’t take classes the same way or be in the lab the same way?

[00:22:53] Nivetha Subramaniam: Yeah. In undergrad, when they get the chance to do like a thesis project or something and they get to go into labs for the year or a course even, I think that’s a great opportunity for them to learn as well. I would suggest students that are thinking about grad school to see if they can do those courses even because that gives them an idea. I’ve had through my year so far, a few students that came in—at least I think about four now—and I’ve had some that were really great and awesome. But then at the end of it, they’re like, “Oh, maybe I don’t want to do this kind of work.” And I have others that weren’t so great, but they were still very motivated to give it another shot. So really, I think that helps as well, doing the experience because I think the idea that you have from learning from textbooks is quite different than what it is like when you’re actually doing the work. So, I think that’s really important, especially for students that are maybe, I don’t know if it works in the US, but here you can actually go from undergrad to PhD even. But I would really suggest give it a shot before, try to get a short-term commitment, see if you like it, and then try to aim for something that’s more long term. 

[00:23:51] Anne Chappelle: So, we like to ask our guests, we ask the same kind of question, which is, what is the greatest adverse reaction that you’ve ever had?

[00:24:00] Nivetha Subramaniam: Is it weird that I think this is the toughest question that you guys have asked so far?

[00:24:04] Anne Chappelle: No, I don’t think it is weird at all.

[00:24:06] David Faulkner: We go for it.

[00:24:07] Anne Chappelle: My biggest adverse reaction was getting a question about my biggest adverse reaction

[00:24:11] Nivetha Subramaniam: reaction.

[00:24:11] David Faulkner: This right here. 

[00:24:14] Nivetha Subramaniam: Uh, no, I actually don’t know. 

[00:24:17] David Faulkner: Yeah, the title of the show, we got to ask it. The other question that I’m always interested in is the alternate reality, timeline, divergence where you don’t end up becoming a toxicologist, where does your path lead? What would you be doing if you were not doing what you’re doing right now?

[00:24:31] Nivetha Subramaniam: I think I mentioned it earlier, but I think if I didn’t find the happiness or the satisfaction I get now doing research, I think I would be trying to get into med school. I think I would be probably trying other routes. I did think about it at one point before I started grad school about if I should do another undergrad maybe that would help me get in. ’Cause I don’t know if it’s the same thing in US, but here, it’s they do weigh your undergrad more than grad school. So, I think once you’re done grad school, if you decide to do med school, you get an added one point or two point, depending on whether you have master’s or PhD, but largely it’s your undergrad that they take into consideration. So, I was like, “Oh, maybe I should do another undergrad.” So, I think really if I didn’t find the satisfaction I have right now doing what I’m doing, I think I would be either maybe enrolled in another undergrad or like probably studying to do the MCAT so that I can go elsewhere to do med school. 

[00:25:17] David Faulkner: Interesting. Interesting. Pursuing medicine. Well, thank you so much.

[00:25:21] Nivetha Subramaniam: Thank you. Thank you for having me.

[00:25:23] “Decompose” Theme Music

[00:25:29] David Faulkner: On the next Adverse Reactions, 

[00:25:32] Anne Chappelle: “Boom! When Evolutionary Biology and Toxicology Collide,” with Noah Whiteman, a professor at the University of California Berkeley.

[00:25:41] Noah Whiteman: We can guesstimate when a pathway evolved the ability to say, make caffeine. That happened at least six times independently in plants. And did they all do it the same way? No, but some of them pretty much did. Very similar genes got duplicated in this particular transferase pathway that allows them to create these methylxanthines that include caffeine. Now, we have the ability to sequence genomes, figure out the metabolic capacity of these plants. 

[00:26:04] “Decompose” Theme Music

[00:26:09] Anne Chappelle: Thank you, all, for joining us for this episode of Adverse Reactions presented by the Society of Toxicology.

[00:26:15] David Faulkner: And thank you to Dave Leve at Ma3stro Studios,

[00:26:18] Anne Chappelle: that’s Ma3stro, with a three, not an E,

[00:26:21] David Faulkner: who created and produced all the music for Adverse Reactions, including the theme song, “Decompose.”

[00:26:27] Anne Chappelle: The viewpoints and information presented in Adverse Reactions represent those of the participating individuals. Although the Society of Toxicology holds the copyright to this production, it has,

[00:26:39] David Faulkner: definitely,

[00:26:40] Anne Chappelle: not vetted or reviewed the information presented herein,

[00:26:44] David Faulkner: nor does presenting and distributing this podcast represent any proposal or endorsement of any position by the Society.

[00:26:50] Anne Chappelle: You can find out more information about the show at adversereactionspodcast.com

[00:26:56] David Faulkner: and more information about the Society of Toxicology on Facebook, Instagram, LinkedIn, and Twitter.

[00:27:02] Anne Chappelle: I’m Anne Chappelle, 

[00:27:03] David Faulkner: and I’m David Faulkner. 

[00:27:05] Anne Chappelle: This podcast was approved by Anne’s mom. 

[00:27:08] “Decompose” Theme Music

[00:27:14] Episode Ends