Epigenetics reveals how environment and behavior shape gene expression without altering DNA. In this episode, Dr. Robert Philibert explores how these changes drive disease and how we can measure and modify them for better health outcomes.
Dr. Robert Philibert joins the show to unpack the fascinating world of epigenetics, where environmental factors like smoking, alcohol, and lifestyle reshape how genes are expressed. He explains how methylation, histone modifications, and chromatin structure act as regulatory layers on top of DNA, influencing disease risk far more than previously thought. The conversation dives into how technologies like bisulfite conversion and digital PCR enable precise measurement of these changes, transforming epigenetic signals into actionable data. Dr. Philibert also highlights real-world applications, from detecting behavioral risk factors to enabling early disease biomarkers, emphasizing how epigenetics can’t be “gamed” like traditional reporting methods, making it a powerful tool for precision health interventions.
From spilled drink mishaps to science fiction inspiration, the career corner brings humor and humanity. Dr. Philibert reflects on mentorship, passion, and the joy of seeing students turn ideas into impactful innovations, proving that science is as much about people as it is about discovery.
Jordan Ruggieri 00:12
Welcome to Gene-ius, a podcast series from Thermo Fisher Scientific. I'm Jordan Ruggeri.
Lisa Crawford 00:17
And I'm Lisa Crawford. Today, we welcome Dr. Robert Philibert for a dive into the world of epigenetics. Robert is a professor at the University of Iowa and the Chief Medical Officer of Cardio Diagnostics. He's also the founder and CEO of Behavioral Diagnostics, which uses epigenetic technologies to assess and manage substance use and substance use related disorders.
Jordan Ruggieri 00:38
We cover everything from PCR applications and epigenetics to the amazing complexity of the natural world. There's even some corn, yes, corn thrown in here and there for good measure. So thanks for lending us your ears, and we hope you enjoy our conversation.
Jordan Ruggieri 00:56
Rob, thank you so much for joining us on today's episode of Absolute Gene-ius. We are thrilled to have you. Can you give just a brief background on who you are and what your research is?
Robert Philibert, MD PhD 01:08
Oh, yeah, well, so I'm actually a genuine Iowa farm kid. I was born in Illinois, raised on a farm in Iowa. After graduating from high school, I went to St. Ambrose College, which is in Davenport, Iowa. And then after graduating from college, I was really caught between going to Johns Hopkins or to go to the University of Iowa. And it turned out there was a very pivotal trip to Baltimore, which I had never been to before, in which I was nearly mugged, that made me a Hawkeye for life. And since then, I went through the MD PhD program there, and then went through a psychiatry residency, then went off to the National Institutes of Health, where I was in the human genome headquarters building for six years, and then I returned to Iowa to pursue integrated clinical basic science research.
Jordan Ruggieri 02:07
That's awesome. And what are you looking at in your labs today?
Robert Philibert, MD PhD 02:12
So we're really looking at the role between modifiable behavioral traits and critical health outcomes. When I was at the National Institutes of Health, one of the things that was drilled into me that everything was genetic, genetic, genetic. But there was another revolution that was going on. Prior to really 2000, our understanding is that the vulnerability to most illnesses was genetic, and by sequencing the human genome, we would uncover a block, a medicine cabinet full of cures. That turns out not to be the case. And in fact, the vast majority of vulnerability to common diseases such as cardiovascular disease, cancer, diabetes, is actually acquired from the environment. That led me into looking for methods to better quantify that environment, which naturally led me to epigenetics.
Jordan Ruggieri 03:14
Can you describe a little bit for our listeners what is epigenetics, and how is it different than genetics?
Robert Philibert, MD PhD 03:22
Conceptually, epigenetics is very easy, and I just tell people to raise their right hand. And I say, my right hand is just like your right hand. It has four fingers and an opposable thumb. Now, at the same time, if I would scrape the DNA from my finger, and scrape the DNA from their finger, I would find out that at the genetic variation level, we differ at millions and millions of positions. But the DNA in my hand is identical in sequence to the DNA in my brain, and yet my brain I have, well, some sclerosing neurons and glia. And in my hand, I have bone muscle and squamous. All epigenetics is, is a modifiable program that goes on top of the DNA architecture to make sure that no matter what genetic variation we have, we get the right cells, at the right place, at the right time. Now, the fundamental breakthrough really was, is understanding that we all start as single cells with really a limited epigenetic signature. But as we mature from that single cell into complex organisms, these cells acquire epigenetic signatures, which dictate their fate. Moreover is, as we develop disease, except for cancers, it is not the genetic variation that changes, it's the epigenetic regulation that changes. And starting at about 2008, 2009, we started to use epigenetics to search for and eventually harvest that signature so we can identify modifiable traits that can, if changed, can prevent disease. But finally, in 2016 we developed a technology that could use the epigenetics to actually diagnose the presence of disease.
Jordan Ruggieri 05:28
Interesting, what is that exact, like, more, more on the technical side, right? You know, we have our four bases. We have the deoxyribo backbone, right? We have all these things, what, what is that exact kind of modification that tells a gene, “Hey, turn on or turn off?” Right. Is that the right, is kind of the right way of thinking about it?
Robert Philibert, MD PhD 05:50
You know, at the base level, that is absolutely it. But conceptually, when we think about epigenetics, we really can think about three distinct layers. The easiest one to conceptualize is what we refer to as the methylome. And the methylome generally refers to the presence or absence of methyl groups. You know, carbon and three, three hydrogens that can be placed or not placed on cytosine residues that are part of cytosine phospho guanine residues. In the human genome, there are about 27, 28 million of these sites. And you're quite right, you know the they serve as more as on off switches for local transcriptional regulation. But they also, this methylation signature, also occurs in harmony with other types of epistemic signatures, particularly the histone code. And the histone code is a set of modifications that is put on the proteins that directly bind to DNA and nucleosomes, referred to as histones, that control how tightly or loosely DNA is contained within nucleosomes. And then finally, and really, we've only begun to really appreciate this in the past decade or so. There is the tertiary space coat, or where a gene is in the nucleus. Prior to 30 years ago, we thought just the DNA is shoved in there, wound up into nucleosomes. It turns out that that's just our foolishness. Actually, nature partitions each of the chromosomes into chromosomal domains and the amount of water or amount of hydration in that area of the nucleus and its relative location with respect to the nuclear pores, which are sort of the in-out gates of the nucleus, dictate how much transcription goes on. So it's actually a very complexly regulated, and we're only really scratching the surface of understanding the role of epigenetic modifications in the cell cycle and viability.
Jordan Ruggieri 08:22
How do these actually impact let’s say, different disease states? Does it actually come in and say, you know, you have an environmental factor, let's say you're a smoker, right. Does that go in and change how the DNA is wound around histones or the different methylation groups that are on the DNA to then change the cellular, let's say, output and structure that ends up coming from protein translation? Is that that correct, an accurate way of, kind of describing how this might change or interact with your environment?
Robert Philibert, MD PhD 09:02
Well, absolutely, absolutely. You're right on the mark about tobacco smoke. Tobacco smoke contains polyaromatic hydrocarbons which, if you didn't have the enzymatic capability of detoxifying these enzymes, you would die after smoking a pack of cigarettes. Now, however, to accomplish that task, the human body, cells in the white blood cells and the cells in the liver, have to change their transcriptional repertoire in the cells. They have to change what proteins are being expressed, and as part of that change, the epigenetic signature changes. And it turns out one of the most critical changes is at a pathway called the aryl hydrocarbon receptor repressor. And the best way to understand this particular locus is that it acts like an old-fashioned governor in a 1970s car to keep it to going too fast. The system it regulates is called the aryl hydrocarbon receptor, or the xenobiotic pathway. And the xenobiotic pathway is essential to the survival of humans and our primate species. As our ancestors evolved in the forests, they would pick up strange foods, they would and they ingest them. And many of the foods have toxins in them that are specifically produced by the plants in order to defend the plants from other, from foraging. Well, fortunately, humans and our primary forebears developed enzymes that could break down those toxins. And those toxins are part, are toxic, detoxification enzymes are part of the xenobiotic pathway. But nature never gives anything without a catch. The catch is that many of the toxins that we find in the environment that we're trying to break down look very much like the nutrients in our cell. So there has to be a way to make sure that we don't turn on a system irrevocably and accidentally metabolize ourselves, and that's where the aryl hydrocarbon receptor repressor comes in. In response to smoking, it slowly demethylates at that locus, allowing transcription of the AHRR protein. This protein goes out and serves as a decoy receptor blocking activation. So at a certain point there more and more and more activation doesn't get you, of that pathway, doesn't get you more and more detoxification. There is a limit. And then as the toxin goes away, it combats activity at that pathway to make sure we don't digest ourselves accidentally. And it turns out that this critical nature of this pathway is recognized by, actually defects in the real hydrocarbon receptor itself are associated with some forms of cancer. Nature is doing a balancing act with epigenetics, and it that is particularly evident at the aryl hydrocarbon receptor pathway. Now, however, it's not the only environmental toxin that changes our epigenetic programming. Everything we eat and drink does, and it turns out, one of the most potent toxins in our environment is carried at our local liquor store. The sad aspect is, is that using actually machinery produced by Thermo Fisher, what we're doing is we're demonstrating that it is not smoking, it is alcohol, which is far and away the leading preventable cause of death in the United States. Now, why is that important? Both smoking and excessive consumption of alcohol are treatable. They're easily treatable through psychotherapeutic or medical interventions. I think we all recognize nobody is born and grows up wanting to be an alcoholic. But I believe through developing diagnostic tools to recognize individuals early in the pathway, having difficulties with smoking or having difficulties with drinking, that we can use precision epigenetic tools to change their behavior, benefiting them, but benefiting everyone.
Lisa Crawford 13:48
That leads to a question that I had, which was, you know, you're talking about these modifiable behavioral traits or environmental influences like smoking or living somewhere that's polluted, or, you know, drinking. These have, you know, fundamental cellular changes. And, you know, I've heard a lot about that being an inheritable thing. Is that, like, are these things inheritable? Or is that still something that you guys are looking into? Because, for example, you know, we talk about generational trauma, even affecting epigenetics. And like everyone on a cellular level, and then their children have those changes and reflect those changes further down the line. Is that something that you guys feel confident in, or is that something that's still being looked into?
Robert Philibert, MD PhD 14:30
Well, in a strict sense, most epigenetic signatures are not intergenerationally transferable in the classical sense. Now I see in the classical sense, because when a, you know, when the sperm and the sperm cell enters into the female cell, it actually the first thing that the female cell, the female gamete does, is actually demethylate, erase the male signature, and that's to protect the future pregnant woman from having selfish genes inside the male damage the female. Now, having said that, so really, do epigenetic signatures, are they transferred to the germline? No. Okay, but the largest factor that predicts whether a child will smoke is whether the mother or father smokes. Okay. The truth of the matter, it has to be a very strong emphasis on promoting health throughout the life cycle, and understand that probably, perhaps, the most critical portion in all of our lives is our in utero phase.
Jordan Ruggieri 15:48
My next question is, maybe, how can we then use some of these findings and information for the betterment of life, right? Is there ways to maybe detect early if somebody might have an epigenetic marker that predisposes them for certain behaviors or conditions? Or are there ways to take a look at that for treatment and research into different treatments for disease states? Is that?
Robert Philibert, MD PhD 16:18
Well, I'm a firm believer in precision epigenetic approaches for addressing behavioral changes. And the wonderful, you know, there was a very nice paper by a University of Pennsylvania group in the 2016 New England Journal of Medicine that used financial incentives to get people to quit smoking. What the authors in that paper recognized is the symbolism of an external reward to them was important. And what they found is that financial incentives, or contingency management, worked well in inducing smoking cessation. The challenge was that when the when Halpern and Associates analyzed their data, they noticed, “Hmm, it looks like maybe up to about 20% of the people that enrolled the study really weren't smokers,” but had faked smoking by smoking immediately beforehand or using co- and, you know, nicotine gum, or things like that, to appear to be smokers, thus qualifying for the rewards. I mean, it's easy to be rewarded for quitting smoking if you never start it. The second thing that they also notice is, is that when they stopped reward is that people relapsed. Now, the wonderful thing about epigenetics is you can't fool it. We can tell exactly how much you're smoking and how much you're drinking. And so it takes the ability to game the system out. And more importantly, is if people have, if employers or insurers have a financial stake in this, they're going to want to make sure that their money is well spent. And at the same time, is there is a psychological principle that shows that is, is if a person knows that they're going to be tested and that they can't fool the test, that they actually will comply with the measure, they'll, they'll, they will follow it. Epigenetics, because we can precisely tell that the change in behavioral intensity allows us to gamify changes in behavior and to both reward the subject or the client being treated and ensuring the investment of the insurer or the government underwriting the behavioral program.
Jordan Ruggieri 18:59
Are there particular drugs or treatments that can actually go in and change a certain epigenetic target? Can you actually get that specific, you know, in this particular pathway, or this particular gene has an epigenetic marker we want to change? Is that, is that doable?
Robert Philibert, MD PhD 19:16
Well, you know, the truth is for me, yes. However, I know that many scientific groups, particularly in cancer, are interested in using epigenetic modifiers to change gene transcription to affect outcomes. You know, epigenetics is always they talk about readers, writers, and erasers, okay. And, you know, using techniques that are analogous and, and both analogous to and inspired by CRISPR, we can target specific areas of the genome with epigenetic modifiers which turn on or turn off that gene locus, changing a cell behavior and sometimes creating a cure.
Jordan Ruggieri 20:03
Moving into maybe some of the technology used to study epigenetics. I mean, initially my question is around looking at things like qPCR and dPCR. I mean, if it's not a change in the in the base of, or even sequencing, right, if it's not a change in the base of DNA that you're using to study, how do you actually know that there's an epigenetic marker that that might be at play?
Robert Philibert, MD PhD 20:31
Well, you know, the most common technique is, uses a, uses a process called bisulfite conversion. And it's conceptually very easy to, to visualize. As we talked about previously, in the in the human, in each of us have about 3 billion base pairs. And if you look linearly along this this genome, you'd find out at about 28 million places there are cytosines followed by guanine residues. Now those cytosines can be, have a methyl group stuck on, stuck on them or not. But if we think back to our college and we think about methyl groups, well, we always know methyl groups stabilize. They're, they withdraw electrons actually. And what the bisulfite modifications do is they use, I believe, a nuclea-, to selectively modify those cytosines which don't have the stabilizing influence of cytosines and those which are modified by sodium bisulfite are interpreted by DNA polymerases as T's. Whereas the, the methylated groups stay as C's. So what we've taken is an epigenetic difference, and we've made it into a genetic difference. And if there's one thing we're good at in science is measuring genetic differences. And using this process, we now take tens of thousands of strands of DNA and measure at each one of those strands, “Did sodium bisulfite modify that strand or not modify that strand?” And so by this process, we can tell give very precise estimates of the methylation ratio at any of these 28 million CpG sites.
Jordan Ruggieri 22:31
Okay, is there any way to, I mean, that sounds like the sequencing is, is heavily involved in a lot of study here, if you're, if you're, you know, converting a base and you're comparing right where, where the changes were, you need to look at the sequence level. Is there a way to easily look at this, using PCR or qPCR, digital PCR as well? Are there methods around for things like that?
Robert Philibert, MD PhD 22:58
Absolutely, absolutely. And it really that before you engage in a technique, you just simply have to ask yourself, “Do you need breadth, or do you need depth?” Now, if you need breadth, companies such as GRAIL use sequencing, okay, because they're interested at hundreds and hundreds of sites. But for companies such as companies that are interested in a few sites, such as Cardio Diagnostics, Behavioral Diagnostics, any of a number of, Cologuard, which is only interested in a couple sites. There's a number of Chinese firms that are actually starting to use digital PCR to measure methylation. And the wonderful thing about digital PCR is how it makes previously developed PCR techniques more precise and quantitative. Prior to really about 2015 to 2016, the only option for scientists that they really wanted to use PCR to quantify things was to use quantitative PCR. And we do quantitative PCR, there's two problems. First of all is that we always have to have an external reference. In other words, a solution that has the molecule we're trying to measure at a known concentration. Well, that's hard to do to start with. And the second thing is, is that, shockingly, we can't pipette as accurate as we like. So if we're really dealing with 10 microliter volumes in some of these wells, which you have to keep things affordable, “Did you really get 10 microliters? Or was it eight? Or was it 12?” This introduces a huge amount of error. Now, the beautiful about digital PCR approaches are, is that they are reference free. In other words, we're not looking at other wells to see, understand what the level of signal was in them and comparing. The only thing we care about is what's in our tube. So like sequencing, it is a reference free method. It is something we actually can use to calibrate other systems, such as qPCR. And it's, it is truly a transformative technique. And as you well know, over the past five to years, there has been a, you know, a great acceleration in these digital PCR technologies. We've moved from droplet technologies to chip technologies. Now, why are chip technologies superior? Is, first of all, is because all the wells are the same size. Okay, you don't have the variation of droplet size. Number two is, it's easy. It's just the chip tray. You're done. And what it really does is, if you, particularly, if you compare it to the prior qPCR methods for quantifying methylation, it's quicker, it's faster. And in the end, if it gets you the data you want, it's cheaper.
Jordan Ruggieri 26:19
Yeah, how does that work on the PCR, for a PCR level epigenetic quantification experiment? Is it. is it mostly still in that primer design that's designed around epigenetics? Or is there still some sort of conversion that maybe changes how the primer and probe bind so you get, not detected, detected, and can compare?
Robert Philibert, MD PhD 26:41
So the first step, once again, though, is the bisulfite conversion. In other words, you keep your methylated C's, C's, the other ones are interpreted T's. Now the strategy really then goes to is, “Can you do a PCR amplification directly? Number one.” And number two is how, “What is the type of signal that you're going to use to quantify the ratio of C's and Ts?” Well, there was some love in many, many decades ago for techniques such as differences in melt temperature. But they turned out this turned out to be too friable. Almost everyone in the world uses fluorescent technologies, hydrolysable fluorescent probes to quantify the amount of C's or T's. And you know, quite honestly, it works very well. Typically, you have a reference dye in the tube that tells you if you have PCR reagents in the tube, and then you have one fluor that is specific for the C allele, one fluor that is a specific the T allele. And then, you know, the beauty about digital technology is, conceptually, all you're looking is for a zero or a one. Okay, so if you have signal which means you either have one or more copies of your target in the, in the well, or you see no signal which means zero. And because digital technologies such as that allow us to use techniques such as Poisson distributions. By measuring enough wells, we can very precisely estimate the methylation of any locus that we can target with PCR in the human methyl quickly, and I might put affordably.
Lisa Crawford 28:41
So Jordan, when people think about qPCR, they usually think about just the instrument, but it's really an entire ecosystem, right?
Jordan Ruggieri 28:50
Exactly Lisa. A great qPCR experiment starts long before the run. Thermo Fisher Scientific offers a complete qPCR ecosystem, from sample prep and reverse transcription kits to the Applied Biosystems TaqMan™ assays, master mixes, software and the QuantStudio™ instruments, all designed to work together.
Lisa Crawford 29:08
That integration helps simplify assay design, improve reproducibility and support applications from gene expression analysis to genotyping and pathogen detection.
Jordan Ruggieri 29:18
So whether you're scaling up, standardizing across labs, or optimizing a new assay, the Applied Biosystems qPCR ecosystem is built to support you and your research.
Lisa Crawford 29:27
You can explore the full qPCR ecosystem at thermofisher.com/qpcr. And be sure to check out our latest promotions at thermofisher.com/promotions. Products are for researchers only, not for use in diagnostic procedures.
Jordan Ruggieri 29:42
All right, let's jump back into the conversation.
Jordan Ruggieri 29:49
Well, I'll pass it over to Lisa for our Career Corner.
Lisa Crawford 29:52
So we'd like to talk a little bit more about you specifically, after getting insight into your research and your work. Um. You gave us a little bit of an introduction at the beginning, but I kind of want to go into more depth about your career path and your journey and just kind of how you ended up where you are. So I guess a question I would have is, you know, what age do you remember being interested in science? And what was it that kind of guided you in that direction to begin with?
Robert Philibert, MD PhD 30:21
Oh, you know the and this is, I grew up in the age of Star Trek, so to see the potential for technology and science to change our future. I mean, I cannot tell you, I mean, I almost, I tried, You know, when I got my PhD, I wanted to see if Leonard Nimoy would sign it. But the inspiration of Star Trek and science fiction were transformative. At the same time as my parents were both very well educated. My father eventually ended up with a master's. My mother actually got a PhD. But you know, one of the things they bought me was, I don't know if you remember a company called Skil-Craft in the basement of our farmhouse, which occasionally had snakes. I had a Skil-Craft chemistry set. And I still remember the little blue tube with sodium bisulfite. And the rest was the powerful influences of tremendous mentors that actually, you know, quite honestly, shape my scientific but my personal viewpoint towards education. And you know, one of the things I'm always grateful for is to Professor Arthur Serianz, formerly of St. Ambrose College, because, you know, there's, there's always those kids in your class which are annoyingly bright, and I was at least half that, I was annoying. So when I got to St. Ambrose, I really never had to study. And unfortunately, the being a very political type, I was in student government, out partying every night, and just one day in class after I got, got my first D, ever, ever, I had never got anything but A's on tests. He just, he just said, “You know, Mr. Philibert, you drink too much. You know.” And but it was said in a loving way, in a very embracing way. And, you know what? I turned from a biology major to essentially measure, essentially major in chemistry there. And I took every one of those instructor’s courses and that is what powers my scientific career today. The analytical and organic chemistry and instrumental analysis that I learned at St. Ambrose powers my understanding of how to develop, to design primer probes, and also the understanding of how the technology it works. And then, when I got into my MD PhD, I had the most wonderful, wonderful mentor named Gary Dutton. You know, Gary was kind of an odd bird in American academia. Actually, he was an American, but he's British trained, and he took me into his lab. I was the first neuroscience PhD to graduate from the University of Iowa. And more importantly is he worked with me to teach me how to write. And now, what do I do as a professor? Very often, a lot, all I do is fly a keyboard. I was exposed to some of the greatest scientific minds on the planet. They were inspirational. They were extremely, extremely supportive. And you know what? They were really nice individuals.
Lisa Crawford 33:34
That's such an interesting thing about science. As a non-scientist, that I've learned getting into this world is a lot about it can be isolating in ways. You know, especially if you're a research scientist, you're kind of in your lane and you're focused, but it's such a community at the same time. And then the more that you reach out and interact with that community and, you know, exchange ideas, that's really where I guess the magic happens, you could say.
Robert Philibert, MD PhD 33:57
It is the community that is magic. We progress as a community. Yeah, I got a few more papers than most and things like that. But you know, you know, I didn't discover the English language, I didn't discover digital PCR, and I didn't discover DNA methylation. All I did was put a couple hopefully useful bricks in the wall. And you know, there's some people that are, but there's other people that made the mortar to put those bricks together, and other people sitting telling me where I should put those bricks.
Lisa Crawford 34:30
Do you have words of advice for scientists who are maybe just starting out today? I know the world isn't the kindest place to science at the moment. But you know, something that you learned that you wish you had known, or something you would just want to say to someone who may be interested, especially in getting into epigenetics?
Robert Philibert, MD PhD 34:48
Well, you know, I would just tell people to find out what you're passionate about and get somebody else to pay you to do it. The funny thing is, I'm here almost every day of the week in my academic office or, you know working in some aspect. Why? I absolutely enjoy it. It's a privilege to do what I do. You have a chance to change the world.
Jordan Ruggieri 35:09
I have one question that I always like to ask, just because I feel like it gives a great, great insight into you and your career as well. It's a two parter, what was the most embarrassing thing that stands out to you? Maybe it's in the lab or, you know, something embarrassing that happened to you, well, you know, in your career? And then the second side is, what's your proudest moment?
Robert Philibert, MD PhD 35:35
Well, the one most embarrassing was when I was a graduate student. And like said, as I, you know, studying was, you know, not a big thing for me. Never was, you know. And I had to give my second graduate seminar, a book Journal Club seminar. Now, why second? Because the first one did not go so well, and my professor said, “You need to do better on this one.” So now the tradition of the Journal Club is the person that was hosting the Journal Club, the graduate students hosting it had to bring in treats. It just so turned out that a cola called Jolt Cola, which was really, really, really high caffeinated, just came out in the market. And so I went out and got a, you know, a 12-pack of that. And, of course, the usual donuts for morning Journal Club. So Saturday morning comes, and I have stayed up most of the night. I had gone through every reference in that scientific paper to make sure I've done it. And then at about three o'clock in the morning, went out to get treats and everything else. So I'm sleep deprived and but I, you know, I give a wonderful seminar, as one of the professors noted, “Yeah, you gave a full seminar in 22 minutes.” So I was speeding along. But you know, the good news, it went through without problem. And I was cleaning up in the area and left in the room was our, the chairman of our department, who was known for being extraordinarily strict and occasionally very harsh, talking to his favorite grad student. And he was bent over a chair talking to the student, just gesturing, you know, wildly. They talked about their work and endocrinology, and I was picking up all the journal, the heavy books, and I had an open can of Jolt Cola, and I'm going like, “I'm a poor graduate student. I'm not going to waste this.” So I put it in my teeth and started to head out the door. When I turned, it fell off my teeth hit the chair and sprayed my chairman all across the butt, and he turned around, and he looked like the I was dead. I just went. And he saw that I was so frightened I could not have intended to do it, and he just looked at me, said, "Just go clean it up." And so I got the nickname as a graduate student, “The spiller.” So that's probably my most embarrassing thing. You know, quite honestly, there's been so many gratifying parts of my career. But you know, as much as I'm ratified by publications, patents, forming companies, I think probably one of the most things that I'm, that brings me to heart is to watch someone take an idea and run with it. And that, you know, this probably brings me to Meesha Dogan. Meesha Dogan was, came to the United States from Malaysia as a high school student, came into my lab, went through undergrad in biomedical engineering, and then did her, decided to stay in my lab to do her thesis. Now together, we made the discoveries that formed Cardio Diagnostics, and that was basically that we could use genetically contextual methylation signals to assess and diagnose heart disease. And actually it works better than any known technology. Just using the DNA from half a mL of blood. Now to see her go from coming to the United States to making these fundamental discoveries, taking them out of the lab, and transforming them into a publicly traded company that's like a farmer that was looking at his is at his crop, and he's got corn that's giving you a 400 bushel an acre. It just doesn't get any better. And it probably tells me, “I, you know, I may not be the world's best mentor. But I'm not the world's worst either.” So it is actually very gratifying to know that, you know, the you know, this technology isn't staid. I'm not going to be remembered just because I had my citation in, just where I published these papers, but actually, that what I did helped contribute to making people better.
Jordan Ruggieri 40:24
I think that is the perfect ending to this conversation. Rob, thank you so much for joining us on our episode today. Absolutely fascinating conversation. I learned a ton. I hope our listeners did as well, and we really appreciate your time.
Robert Philibert, MD PhD 40:39
Well, thank you. I very much enjoyed being here.
Jordan Ruggieri 40:43
That was Dr Robert Philibert, Professor of Psychiatry at the University of Iowa in Iowa City. We've got more great conversations and corny jokes around the corner in upcoming episodes. So, stay curious and we'll see you next time. This episode of Absolute Gene-ius was produced by Sarah Briganti, Matt Ferris and Matthew Stock. Products mentioned in this episode are for Research Use Only, not for use in diagnostic procedures.
Lisa Crawford 41:08
That was really corny, Jordan.
Jordan Ruggieri 41:11
Oh the puns.
Lisa Crawford 41:11
Low hanging fruit, low hanging vegetables.
Jordan Ruggieri 41:14
Low hanging ears.