[0:00] Many bacteria, many viruses have evolved ways by which they infect a cell, they get to the center of the cell, they pull the substrates out of our own mitochondria and they use them for their own energy or for their own replication, which alters our energy metabolism, usually never in a good way.
[0:30] Thank you for coming on my podcast. I'd love to know all about you. I already know several things about you, but for everyone who's just perhaps meeting you for the first time, what's the elevator pitch on all things Dr. Amy for a while? Okay, so I'm a microbiologist, but I'm also the president of a nonprofit research organization that I founded with my partner, Mike Van Elziger, who's a neuroscientist at Harvard. And we run this nonprofit to study what we call either infection-associated chronic disease or post-acute infection syndromes. It depends what you want to call them, but basically we're studying the chronic consequences of infection. And what we're looking at is with every pathogen, with anything you could get, bacterial infections, viral infections, a subset of people who get the infection don't recover. Like they get sick and they get continual symptoms. And this can even last for a lifetime. With long COVID, that many people have probably heard of being a prime
[1:39] example of that. Like you get COVID and then for some reason, some people can't recover and they get really sick. So we're trying to study why that happens, right? And to do that, what we figured out early on, and this was even before COVID where we were already just studying these, you know, chronic consequences of infection, is we had to pull people into this field from related fields. Because in cancer, in HIV, there are teams using actually some pretty advanced technologies to be able to understand what viruses or organisms are doing. And they just weren't in this sort of post-acute infection space. So that's a lot of what we do is we network, we find teams who are doing a really good job in related spaces. And we pull them into this one to try to build collaborative projects. So that's what I spend a lot of my time on. And then as you know, I also am the scientific director for
[2:30] CORE, which is a clinic in Mount Sinai. And it is a clinic treating or working to treat patients with post-acute infection syndromes. And I really like my role there because what I want to do is make sure that I don't just sit with PolyBio with just all this academic knowledge falling on me, you know, that I know in my head. I want to make sure that we can apply it to the actual care of patients. So I actually want to know what's happening in that setting all the time so that we can figure out how to innovate it because it does need a lot of innovating, right? So those are the main things that I'm up to. Yes. I love it. The podcast is for general audiences. And I have a few questions I want to ask you, but I first want to establish a foundation of knowledge for them so that they can have some context for the questions I have to ask you. Can you tell me if we imagine our bodies as a
[3:23] community? People cells versus microbial cells. What is the balance numerically between them? Is it one to one? Is it one to 10? I've read things that said one to 10 and the more recent literature said one to one, but it's pretty substantial, right? Yeah. So this is what got me interested in studying organisms in the human body in the first place is that when I was first coming into the field of microbiology, this is over a decade ago, we didn't know, and we still don't know how many organisms inhabit the human body, but what we are learning and which really matters, like, of course, in any human chronic disease or in just how humans function is that humans are actually super organisms. We are actually a mix of our human genes and then millions of genes of our microbial inhabitants and those microbial inhabitants that form microbiome communities in our bodies include bacteria, fungi, archaea, and then there's even a viral component to these ecosystems, the human virome, because all
[4:38] bacteria in the human body are actually themselves infected by viruses called bacteriophage that infect and modulate their activity. And the scope of this is somewhat insane. There are millions of bacteria in the body. The estimate is about one to one. So for every human cell that you have, you have a bacterial cell, at least. For the viruses, the bacteriophage that infect the bacteria, bacteria, the estimate is there are about 10 times more phage than bacteria. So that's an incredible number of phage. In fact, phage, these bacteriophage are sometimes referred to by people as dark matter because we've characterized so few phage and it's similar to outer space where we've named and found a couple of planets, but really we know there's this vast solar system. It's similar to phage in the human body. We've named some, but we have these trillions of phage that are trafficking along with bacteria through our tissue, our blood all the time. And so really it does shift an understanding
[5:48] of what it means to be human, right? And then, so I recently posted something on Twitter and it was like this skit that this TikTok comedian put up and he was acting as a tapeworm. It was hilarious because it was a dialogue between the tapeworm and the human that it was inside. And the human took a probiotic gummy and the tapeworm was like, what was the intention behind that? Like basically like, dude, totally gaslighting gaslighting him. In fact, in the skit, he said, you're gastric lighting me, but we have parasites living inside of us too, that also influence our bodies too. And like, I want to talk about the relationship because they brought it up in that skit. He was like, you're thinking up here, but not, you're not thinking down here. So can we talk about that? Is it called the gut brain axis?
[6:42] Well, yeah. So first, I mean, I think the important thing first is that we, we all have, let's call it the human microbiome, these ecosystems of bacteria and viruses. And under conditions of health balance, they, you know, we live with them in a state of homeostasis. And so they, in fact, they metabolize a lot of our foods, their activity contributes to a lot of our signaling. Obviously people who are healthy climbing mountains, whatever have these organisms, but this is a thing under conditions of inflammation or imbalance. Some of these same organisms can shift their gene expression. They can shift what proteins they turn on off to start to act in their own interest instead of ours. And so a lot of chronic diseases are actually tied to what's called microbiome dysbiosis or imbalance, where a lot of the organisms in the human bodies start to change their gene expression.
[7:39] And the proteins they're making in a way that's not so great anymore, it can drive inflammation or problems. And now you have issues. So the main thing there is that microbiome can actually start to cause problems for us and can be really important thing that's understudy as a driver of a lot of human chronic disease processes. But within that, you also get your sort of single pathogens that themselves are, you know, definitely like a tapeworm. If they infect the human body, they are just purely acting in their own interest. They're hijacking us. I mean, literally pathogens will feel substrates from our mitochondria. In fact, I wrote a paper on this with my colleague, Mike Van Aelziker, a few years ago.
[8:24] Our mitochondria that make energy in every cell, many bacteria, many viruses have evolved ways by which they infect a cell. They get to the center of the cell. They pull the substrates out of our own mitochondria and they use them for their own energy or for their own replication, which alters our energy metabolism, usually never in a good way and keeps them going. Right. So in other words, they hijack us. Right. So that's what we study is we study not just how collective organisms are impacting humans, but also how select pathogens, which include everything from tapeworm type organisms to bacteria, like the Lyme disease organism that people get from tick bites to the SARS-CoV-2 virus, can really start causing problems as single infectious agents. And the thing is so many forms of chronic disease are becoming tied to the activity of these pathogens, including even Alzheimer's disease, including neurodegenerative disease. And part of that gets into what you mentioned before with like a gut
[9:31] brain access. The thing is that organisms in our bodies, for one thing, some of them can get into the brain directly. And from there they can modulate even human cognition or neuroinflammatory or neurosignaling processes, or they can, for example, change the way important nerves in our body signal. For example, the vagus nerve is this really important nerve. It innervates every trunk organ of the body. So it connects to the gut and the heart and the lungs. And then it also connects to the brain and it's conveying all these signals between the brain and the body all the time to regulate functions like even autonomic function, which is basically the ability to move from sitting to standing. You get, you're laying down, you get up, you, everything adjusts. But if you have, so vagus nerve is part of like the signaling that allows that to happen. But if you have problems and the organisms in your body
[10:26] are problematic or you get a pathogen, for example, into your gut that persists and, and, and causes problems, it can throw off the signaling of that vagus nerve. And now you have that access between the gut and the brain is dysregulated. So that is under study in the range of conditions, even can have a role in long COVID where we think, you know, we see the SARS-CoV-2 virus potentially having detrimental effects on signaling of vagus nerve and other things like that. You mentioned Alzheimer's disease. Can you expand on that a little more? Definitely. So infection as a driver of Alzheimer's disease is just one of the most important and fascinating topics out there. If you think about it, but rates of Alzheimer's disease are skyrocketing. They have been skyrocketing for a while now. It's really crazy. I think someone develops a new case of Alzheimer's every 30 seconds, something like that. So as we're talking,
[11:21] maybe during this podcast, people are being diagnosed with new cases of Alzheimer's. It's just, the rates are out of control. So the current thinking on Alzheimer's, there's probably something wrong. Like we're, let's just say maybe then we need to think through what's causing Alzheimer's disease to best understand, are we doing something wrong? Right. And the current thinking on like the mainstream sort of textbook still thinking on Alzheimer's disease is that there's this plaque in the brain, this amyloid plaque. I mean, we know it's there that this amyloid plaque forms in Alzheimer's brain. The current textbook thinking is that plaque is the driver of the disease.
[11:58] So many drugs have been created in the last years to remove that plaque from the Alzheimer's brain with the hope that that would get people better. And none of these drugs have worked just in a series. They just failed. They failed. They failed. Is it around the cells or is it aggregation inside of the cells? It is sometimes between and sometimes even in the cells, but it's more like between aggregates in the brain tissue. This is the thing though. There's a researcher who was actually a mentor of mine. His name is Rob Moyer. And he started to realize that this amyloid plaque, it's really conserved, like evolutionary. It's been found in zebrafish. It's been found in animals really early on in the human evolutionary scale, right? So if it's so damaging, like if it's so bad, why isn't it being weeded out? Like why is amyloid being conserved as animals continue to develop?
[13:00] And so he started to question why amyloids there. And what he thought is, wait, maybe it's forming for a reason. In other words, maybe the plaque is forming in response to something. And so he started to look and see if he could find viruses in the brain. And indeed, what he started to realize in a really incredible series of experiments at Harvard Medical School is that if they took viruses, like a herpes virus, and put them in a neuron in a dish model, the amyloid plaque forms in response to the herpes virus. In other words, the plaque has a function, which is that when viruses or bacteria get into the brain, it forms as an antimicrobial peptide in order to capture them. And that's why the plaque is there, right? So we've been removing this plaque, but it's actually supposed to be trapping these organisms, right? And the root cause driver is infection, right? So the thing is, we now need
[13:56] to switch in Alzheimer's to a new paradigm where we are trying to do research and treatment to look at the viruses that can be drivers of Alzheimer's. So for example, as part of our nonprofit right now, we have a team who studied the impact of the SARS-CoV-2 virus on Alzheimer's disease. You know, just showing that if SARS-CoV-2 gets into the brain, it can again seed the formation of these amyloid or tingles that are part of the Alzheimer's. So really, it's a paradigm shift in which, you know, and that gets down to it. Like we've thought too long that humans are sterile. And we keep blaming things like the plaque itself or the immune system alone for human chronic disease without considering that these organisms or pathogens that we're infected with can themselves be the drivers. And what that opens up to us now is a new world in which if we're able to really document the activity of pathogens in
[14:59] these diseases, we can switch a lot of medicine to a more root cause type treatment where instead of just using palliative drugs that a lot of people get on, like immunosuppressive drugs like Humira or something that shut down the immune system, but don't really cure you when people are on them for life, we can maybe get at the root causes of these diseases and actually treat them with antivirals or antibiotics. And that's again, part of what I work on. That is incredibly fascinating. And I know that this is going to really shift a lot of people's perceptions of infection. I want to talk about this notion that scientists should have already known this because I feel like when people learn this information for the first time on this podcast, they're going to say, well, why haven't, like, why don't we have these answers if they're so, if these organisms are so prevalent in our bodies,
[15:58] like, why is our knowledge further along? And of course, people are going to try to fill in the gaps with their own thoughts and feelings. And that kind of leads people down to this path of conspiracy theory of like, well, then something's being hidden from us. What do you have to say to those people just really moved by the idea that we don't know so much about the body? So this is the thing. It's not conspiracy theory that we don't know that the thing is that science takes a lot of time to change. So I'll be honest, I forget who said it. But there's a saying, you know, science sometimes even advances one funeral all the time. I know that's a brutal way to say it.
[16:40] But the truth is that you have these old ideas. And sometimes those ideas get into the textbooks, right? And there are years of fresh studies, and it just takes time for them to be replaced. The thing is, a lot of the work that's tied infection to these chronic diseases like Alzheimer's, it's been done in recent years before some of our main textbooks were written. So people were trained in medical school 10 years ago, like, it's just not in their book. So we're in this period first where it's changing, and it is. But second, the reason that there's a lot of, it's challenging to study infection and chronic disease, because it, this is the key thing. Like, when we're studying persistent pathogens, and a lot of these diseases, they're not found easily in your blood. So let's say, for example, that we are trying to study the impact of viruses on Alzheimer's disease, we have to get people's brain tissue. And we have to do that in a very specific kind of study. And we
[17:43] have to set up the ways to get the tissue, and the tissue has to be well preserved. And then we have to use specific technologies to find the genetic materials. So you have to set up these actually big research projects to be able to find it. And someone, meanwhile, with Alzheimer's can come in, and you have no idea that there's a virus in their brain if you're just running standard tests. We've had to collect a lot more types of samples from people with chronic disease. So that's a lot of what PolyBiomine Nonprofit does, is in patients with chronic symptoms after infection, we've set up and helped teams set up infrastructures where they can collect gut tissue, say via endoscopy, or lung tissue via bronchoscopy procedure, or even lymph node tissue, because those are the parts of the body where pathogens tend to hide out. They tend to get into our tissue or our nerves. And they're not in our
[18:30] blood, like the blood, the immune system is the most robust, you're most likely to get targeted there. So if the pathogens there, it's not usually there. So this is the thing, there's not a simple blood test for these pathogens. And I think that's one of the main reasons that that's also sort of harder to prove is we have to find them in tissue samples. And sometimes we have to use really advanced tools to be able to find small amounts of their genetic material or little amounts of their proteins. And those tools are still in development. So the thing is, what we kind of know in science by doing these studies has yet to trickle into the clinic, where doctors are just running the same panels on people and none of those panels yet contain any of this kind of testing or anything like that.
[19:15] What a lot of scientists know and are working on, and this is one of the things we try to break down these barriers, there's this knowledge, but a couple people have it in these institutions and everything like that. And it hasn't trickled down yet for people to get. And it hasn't permeated medical school or the system yet where it's going to be actually taught to the doctors that are out there. Without that happening quite yet, people just don't know. And I also, like when you mentioned that, I think about clinical trials and I think about the kinds of people that tend to participate in them. It feels like it's kind of rare to see a clinical trial that has a really diverse representation of humanity. And I think what you just said really just lends itself to the importance of people participating because we need to learn these things. I don't know, it just, we, we've talked about so many things on this podcast, including like, I talked to a dolphin
[20:11] expert and I asked them about dolphin menstrual cycles and like, do dolphins have menstrual cycles? And they said, well, we actually don't do a lot of research on female dolphins. And I was like, you don't do a lot of research on female people. That's what I was told. And like, she even told me that most of the lab rats that people use are male lab rats. I know. I know. No. I mean, that's in, in humans as well. Diseases, women's conditions that affect women are way more underfunded, you know, just understood like, like endometriosis or interstitial cystitis. So these diseases that are just so painful, like there's so few teams working on those conditions compared to what there could be. I mean, and also just teams that are not in a lot of cases doing logical work. So one of the studies we're doing is where, when people are undergoing surgery for endometriosis, when women are, we're getting their tissue. We're saying like,
[21:11] don't throw it out. Like this is one of the things of like a lot of our studies. We find surgeons who are working on a people with a certain condition. And we literally like, like they would take this tissue, otherwise maybe preserve it or send some of it, you know, to be analyzed quickly and then get rid of it. We just say, no, like stabilize it and send it to our research teams. Now we can use all kinds of these extra tools to profile the whole immune genetic and infectious landscape of this tissue. Maybe like the third group in the world to just do this with endometriosis tissue. It's insane, right? So that does come from this history, you know, of, of chronic disease with women where, you know, women have totally been considered hypo, you know what I'm saying? Like where MS, not that long ago, I mean, was attributed to hysteria, right? Like, in other words,
[22:06] no way for doc, this is the problem. Like there's a lot of conditions that includes even long COVID now or ME-CFS, which is a condition related to long COVID where people become really sick after viral or bacterial infections often. They look fine. So they go to the doctor and the doctor runs, I don't know, like four blood tests that are pick up on like 0.1% of things that could be wrong in the human body. And when those don't come back with some signal, they just start, they're like, oh, you know, this must be in your head or something like that. And that, that is, that's still an attitude in medicine that, you know, it's getting better, but it's, it's there. There's this too much implanted idea that, oh, with women, like, well, I mean, it could be some physical problem, like a virus in your brain or something, or it could just be, I don't know.
[22:58] Like it's literally in your head. Yeah. No, that's the thing. That's, you're exactly right. Robin, like, I mean, Raven, like you're, you're, you are right. But like, people will tell women, you know, it's all in your head. And the truth is like, yeah, you're right. The infection is probably all in their head or, you know what I'm saying? Like, like there's something in their head, but it's just not, it's an actual driver, physical driver of disease, like a, like a virus, not some kind of, you know, thoughts, right. Or like inability to cope. Like, so psychiatry, in other words, has kind of overtaken, like it's overstepped its bounds. Psychiatry needs to just chill out.
[23:37] Yeah. Remove itself from, like, we're at a point now where psychiatry got involved in a lot of conditions because we didn't have data. You know, we didn't have imaging yet to get at the brain or we could show actual inflammation. And so psychiatry would come in and say, oh, maybe now for most conditions, we can show actual signs of dysfunction. And now we need them to pull back and not be as quick to jump to these, you know, honestly, kind of ridiculous psychosomatic explanations for the disease. I talked to Dr. Shannon Delaney on a different podcast and she enlightened me to the facts around Lyme disease and specifically how it can manifest mood changes in young children. And then I was taught about how prevalent ticks are, especially in the Northeast. And ticks are transmitters of the bacteria that causes Lyme disease. So we talked about what are the chances that one of us has been bitten by a tick in
[24:46] our life. And she was like, well, it's actually quite high, especially if you've been frolicking in grass or in nature. It doesn't take much. And she told me a story of one of her patients. It was literally her first time ever, like being out in nature. And she went and had a picnic and got bit by a tick and then experienced long-term effects of Lyme disease. I think about children who are, I ran barefoot in the grass. I was like outside girly, loved playing in the dirt. I wonder how many kids are experiencing chronic diseases, but maybe don't find out until they're adults. And we haven't been taught to be tested for that. If you don't have a tick attached to you, or if you don't have that hallmark bullseye rash, we wouldn't know. And that doesn't always happen. And if you have darker skin, you might not even see it. So what are your thoughts on this? No, it's a huge problem. And here's the thing is we have to
[25:53] take all pathogens way more seriously. Like this is the truth that whenever we get infected with things, and this even comes to the viruses that infect, you know, children now in schools like RSV or hand, foot and mouth disease or strep, you know, it actually, all those pathogens can cause serious problems and sometimes really bad long-term consequences. So it's not, I think we need a cultural change where, first of all, where just getting an infection is like, ah, you know, oh, I just got strep. It's like, no, I got strep and it matters. And I'm not saying that like all of us have to be paranoid, but I think that there's a lot of chronic diseases and a lot of people who feel sick out there and don't know what's wrong with them. And there's a lot of pathogens. And I think we need to merge that understanding a little bit closer that for people who have symptoms and they're not
[26:49] sure what's going on, especially children where you see changes in behavioral issues, that we have to consider that infections may play a role in their case because strep is one pathogen that sometimes acts along with the Lyme pathogens that you mentioned to cause this syndrome called PANS-PANDAS, where kids develop really bad OCD. So we have, we know that in other words, pathogens, these viruses and bacteria can sometimes be drivers of not just physical symptoms like flu-like symptoms, but actually neurological changes in thinking, anxiety, you know, depression, OCD, right? And that's not even really understood either. So like, first of all, so first we just need general respect for, for infection more. This is something I truly think to be true. But when it comes to the, the tick-borne, vector-borne pathogen, it's like where we're doing the worst job. Like if you want to go to just the place where we are most ignoring infections that could matter, that's where it is. Like the ticks
[27:51] do carry the Lyme pathogen, but here's the, the interest. And sometimes this is the important part. They also even carry other bacteria that can cause a lot of chronic symptoms and problems. For example, Babesia is a parasite of Bartonella, an intracellular pathogen that can cause neuropathy, anxiety, a lot of, of serious problems. So if you get by, by a tick, it's not even just Lyme. You can get like multiple problems that happen from this tick, right? So I know that people are going to, as soon as they hear this be like, okay, well, what can I do? Is Babesia on the Lyme test or is that a separate, can you get tested for that? And is it separate?
[28:33] It's separate. So you'd have to ask your doctor to test you for Babesia. And this is the part that gets hard that our current testing for these pathogens is not great. First of all, I just want to make the point that the Babesia and the Bartonella, you don't even have to get a tick bite to get infected. They're actually vector-borne pathogens, which means that they can be carried by fleas, by spiders, by just other organisms too. So for example, you can get a spider bite or you could interact with a cat that had, it's for Bartonella. One of the types of Bartonella, one of the strains of it is the driver of an illness called cat scratch fever, where you just get it from, unfortunately, interacting with a cat that has fleas. So you think about how many kids or people sometimes have interactions where you don't even need a tick bite. You just need interactions with,
[29:23] so that's, it's just, there's no understanding of that out there at all. Like not even for the stereotype is like, oh, you have to have gone camping. You can get bit, first of all, with a tick in a urban area playground. There's been studies that have found ticks in LA playgrounds. Like you don't even have to go deep into the woods. And second, you don't even need to get a tick bite to get some, you can just, you know, have a spider issue or bite or something. So there's definitely way more ways to get them. But this is, that is the crux of the problem is that the testing for them is not great because especially for Lyme, because Lyme, it's like a little bit like SARS-CoV-2 that we study in long COVID now. It's a really tissue-based pathogens. What Lyme loves to do is infect connective tissue.
[30:11] It infects the tissue that infects the joints. It infects the nerves, right? When it gets into someone's body, they're causing like pain, connective tissue issues, joint problems. But again, it's not in your blood, this is the problem. You can, we don't have a test to find it. And then some doctors order antibody testing. So basically like seeing it, the immune system created a response to Lyme, but that doesn't tell you really if you had it or if you have it because antibodies, here's the worst part is Borrelia. The Lyme pathogen debilitates the immune response over time as it persists in you in a way that can actually make you make less antibodies. So the worst part is the sickest person who might have the, you know, deepest case of Lyme in their connected tissue and their nerve isn't even making the antibodies that are part of the test, right? So like one of the biggest things again, that our nonprofit works on is innovating the testing diagnostics for Lyme and
[31:13] tick-borne disease. It's just, it's like one more place where we need to build better tests. Those tests either need to be able to find smaller amounts of the pathogens, genetic material, or we have to even be able to potentially get a tissue sample from patients and just look like sometimes we can do a punch biopsy. We have a study where you can get a little piece of thigh punch biopsy that contains a little bit of tissue and peripheral nerves from a patient. And we're seeing if we can find Bartonella in those samples. And so, so for example, and, and people say like, okay, well then you'd have to do a tissue biopsy for diagnosis. Well, fine. I mean, whenever we think there's, you know, in cancer, we're more than happy to do a biopsy if we think there's an issue with a tumor. So we, we shouldn't, you know, in my opinion, we should be using that same paradigm on patients who could have
[32:01] these kinds of illnesses. If needed, we could do a biopsy or something like that. So that's part of what we're looking at. I think one of the things is you actually can go off symptoms sometimes to consider if you might have a Lyme or Babesia Bartonella infection. There's a questionnaire created by a Lyme doctor named Richard Horowitz. It's probably, I bet you can Google it and you can fill it out and it starts to just give you an idea, at least if your symptoms fall into the types of symptoms experienced by people with Lyme or Babesia Bartonella. And at least that gives you like a, all right, maybe I should head down this road, try to get some testing done. You know, there, there are some companies you have to pay out of pocket that have testing. The problem is they're not covered by insurance. And that's a whole other, you know, crazy issue is that that's one of the
[32:50] things at Sinai that we're trying to work on when we're creating a clinic for patients with issues after infection is we're doing clinical trials and a lot of research studies because that helps for the tools or the drugs that we're trialing to get covered by insurance because we can publish a paper that gets attention that shows signal in patients. Otherwise, a lot of what's being developed for things like Lyme or other conditions are by a biotech company that might come into the space and develop a test. It's a little bit better and it costs $3,000. And that's the problem is then it becomes only able to be accessed by a few. And that's good. At least the test exists. And yet I want to build a medical system that everyone can access. And so that's the challenge too, is developing diagnostics, but making sure that they don't end up in just the hands of companies that charge huge
[33:49] amounts that only a few people can get. Like we have to make diagnostics that are open source, that are affordable, that everyone can get. So that's part of the whole challenge in the space. This is really important. And it ties into what I was reading about the history of how we understand this field, because from what I learned, we've known that there has been some sort connection between our overall human health and pathogens or like organisms, infections. Once we figured out, hey, antibiotics can knock out certain pathogens, and that works, then the attention sort of went away from infectious diseases toward non-infectious diseases like cancer. And so then we've seen like, I mean, I guess it's kind of feels like that's how that's when the, the modern biotech industry was born.
[34:49] But you're drawing, you're kind of circling back and drawing this important funding and attention toward, hey, we're actually like, the story is not done. We need to continue furthering our knowledge here because it's, it's simply not done. How do you feel about the current climate and the contrast between what work gets funded and what work doesn't get funded in this space? Yeah, that's a big issue. You know, going back to the history of connecting infection to chronic disease, one of the hardest periods for that was when the theory of autoimmunity gained hold. I mean, it's easy to call something autoimmune, because you measure an immune response in people, people are inflamed, and you blame the immune system. And then that's sort of an easier paradigm for the pharmaceutical industry to come on. They can come make blockbuster drugs that knock down the immune response without asking why is the immune response dysregulated in the first place. So the problem is
[35:57] that infections connections to chronic disease got sort of pushed to the side while autoimmunity was, to be honestly, over assumed in a lot of conditions. And I think that now that's changing. In fact, when it comes to cancers, you know, a good number of cancers are driven by viruses. So I think at least 10% of cancers, like Epstein-Barr virus is a cancer oncogenic driving virus, they transform that the cancer itself. So this is the thing about viruses is they can pack the cells that they infect and transform their metabolism. There's got to be drivers of why things are happening. And viruses are beautiful drivers. Whenever you see things changing, transforming viruses, because they're able to push our own cells to be moving in this more detrimental direction. But I think that when it comes to grants and funding for this, it's been really difficult. I think that a famous story does come down to Alzheimer's disease and infection.
[36:59] So the National Institute of Health or NIH funds most research on science. And they had a panel, you decide you come up with an idea for a study, what you want to do, you write it up and you submit it to the NIH to be reviewed for consideration for funding. And there's a panel of people there that review the grants and make the decisions on whether they get funded or not. It turns out that for years, for Alzheimer's, there was kind of this click and basically one journalist called it a cabal, honestly, of people who just were not into the idea of, I mean, infection and Alzheimer's.
[37:34] Partly because their own work didn't show it. This is the biggest problem. Like you have people often on these grant committees where their research is something new actually goes through and they're the experts, then their work could be less relevant. This is a big problem in science. So the people on the committees are often very unlikely to let the new ideas or the breakthroughs go through because they kind of want to keep that sort of old guard stuff part of it. Sometimes it's just human nature like that. The grant committees and Alzheimer's knocked down grants on infection for years. You just couldn't get one. This was just well known. And then finally, due to patient advocacy, due to all kinds of issues, they finally started to just change it recently, where they now let a few grants through on this topic that, quite frankly, is the most important topic. So that's the thing is government funding can be
[38:32] extremely conservative. And also, you know, it's difficult sometimes to break into sort of like the circles that you need to do to get government funding. We at PolyBio, we get funding from private donors because I realized when I started PolyBio that we were just not going to be able to move research on infection and these conditions forward fast enough with just government grants. And so what we do is we build projects, make slide decks showing like the team, the project, what we're going to do, the tools we're going to use. And we get it out there and we actually see if people who have private funding want to make it happen. And that's an okay model and it's been working for us, but we need more support from government. So what government needs to do then is, you know, create a better, more like sort of fast track grant mechanism because a current government grant can take over two years
[39:30] to get funded. This is what people don't realize either. Like you submit, it takes so long to get reviewed. Then it comes back with feedback. Then you have to answer. I mean, often this happens and you answer the feedback that takes another eight months. I mean, it really is, can be well over a year before a person gets a decision on a grant. I mean, that timeline is just not feasible. It's just not okay. I mean, especially for example, let's say with long COVID that we've been studying now, we have this pandemic and new novel virus just rips through the world and people start developing chronic symptoms and chronic symptoms. And we're supposed to put grants into a, you know, this slow stepwise mechanism. I mean, that's, that's madness. So they, they need to create a government system for that, that turns grants around more quickly and actually just favors new novel ideas.
[40:29] There's one government agency called ARPA-H that does that, but the level, we're not sure if they're accepting grants along the infection side. We just turned one in. We'll find out. We'll see. I know. I know. Yeah. So, but the ARPA-H model, this, this sort of like faster turnaround time, you know, we are actually looking for truly new things has to become like the whole government model. Like, like it really should be, it shouldn't be this one group that, that does that. It should be the whole NIH that does that. Is it weird for me to say that white supremacy is slowing down scientific research and just like the notion of elitism and ego, like egocentric, um, you know, our way or the highway, you know, we want to dominate the space type energy. I feel like if we were just, if the culture was more collaborative and accepting of diverse opinions, we wouldn't necessarily be here. Like exactly right. I mean, look, I just, uh, white supremacy,
[41:43] but like the, one of the things that, that we do at PolyBio that I've done is, is just network with people. Like, I do not care if someone has a fancy title. I don't care if they're like the head of seven departments. I don't care. I really actually only care if they have a good idea, if they are doing good work. Right. And I don't, this kind of just comes from my own life where, you know, I've read papers and I've kind of partially, even before I got a PhD, I taught myself a lot of the science by just reading in this. So I started to learn about what works in science based off the, just the ideas, not what other people were telling me was right. And so that's, so we do, we just, we, we, we have cool conversations with everyone out there and we figure out who's doing what, and then we get people
[42:37] together and we, we say like, look, like your lab is right next to this lab. You guys could share tools. You could share samples. And, and when people start engaging like that, it's, it's so much better. First of all, we, we, we are learning way more. We're, we're definitely like the new ideas are, are going more fast, more quickly. And, and yeah, when things don't work, it's kind of more acknowledged and we're able to adapt more quickly. And, and that kind of culture can absolutely move things forward. So, so what we, what we definitely need in science is just, is less of this, like, yeah, you can only succeed if top people and, you know, government accept your grant and it has to be that like this, we need like panels of, of diverse people exactly with different from the community, from different backgrounds, from different walks of life. They're in government looking over proposals that come in and, and, and, and ranking them off, off logic,
[43:44] you know, off, just practical, like, just practical, like, like, no, I don't think you're asking for too much. Like, yeah, exactly. Like, yeah, you're exactly right to take all the snobbery out the whole thing. Like, just, just take it down and, and, and, and let everyone talk and, and make it and make it cool. I, I know that people are going to be so comforted knowing that someone like you, with these values and notions of how science should be done is behind such an important organization, the Polybio Research Foundation. Yes, okay. Yeah, that's us. The Polybio Research Foundation. I, I think it's just so important that you are leading this effort, because I know you're going to have the impact that you've already had the impact that you're looking to make, and it's going to be successful because you're doing exactly what needs to be done to move our knowledge of the roots of these diseases and then the treatments of these diseases
[44:45] forward. So I'm, I'm excited. I'm really happy to be, you know, tangentially even a part of what what you're doing. Um, and it's really cool to, to get more of your perspective on the bigger picture, because it is fascinating. And so how can people support you? I think like what, how can we support what you're doing? I mean, funding, you know, donations are helpful, but I think beyond that, the main thing is, is to share what we're doing and, and get out to the extent that's possible. Even this, just doing interviews, um, or sharing other interviews or other papers that we've written more widely is helpful because we want to, you know, like in, in terms of changing paradigms and getting people more accustomed to the, the, you know, ties to infection and the stuff that we're doing, the more that we can just get a word out, the more that that helps us, you know, get a seat at the table where we,
[45:51] where we want it and where we can be able to talk further. Right. So I think that, that, that at the very least, just like go to our website, read through our projects. There's interviews on there. There's, there's lots of stuff and just check out our materials and start to, start to learn. This was what I think is, is cool, especially for, for patients, you know, or for people who themselves might be affected by a condition tied to infection. It's just, just, it's empowering to learn about it. Right. Don't think that, you know, that you can't get it, that some expert has to get it. You know, there's, that's absolutely untrue. Like some of the most basic parts of, of what goes wrong when people, you know, get sick, like, like we studied, for example, a lot pathogen persistence, right?
[46:40] Like we study now in long COVID, how a lot of people who are infected with the SARS-CoV-2 virus might not even fully clear it. And that might be part of why some people develop symptoms after long COVID. That that's really straightforward, right? Like the idea that you get an infection, and then part of why you develop chronic symptoms is because you still have the, I mean, it like, it doesn't take a genius to get this right. It's their concepts are actually really straightforward. Right. And that's one of the things that I also dislike about academic medicine. It tries to make it seem like a, oh, it's so, no, it's not like the main trends.
[47:15] I really, you can get them, you can understand them. And if you start to read about it, and if you start to read, especially about infection in the microbiome, those ecosystems of the human body, it's totally fascinating. I mean, it just gives you a new, you know, understanding of so many, you know, as you're going through life, like, like, don't you want to know, you know, like, that all these organisms are in and on you? Like, don't you even want to be thinking? Yeah. So my, my thing to people is just start reading and listening and learning. And in that, you'll find so many clues already to be able to sort of better navigate through a lot of, you know, what's going on in this space and to be able then to be one of the voices that helps move it forward.
[48:07] Amy, this is so exciting. And your website is polybio.org. Can people follow you and polybio online if you are interested in catching up and keeping up with all that's going on? Yes. My Twitter is microbe-minded too, which I know is really cheesy, but it's true. I always have microbes on my, if you, if you know me, if you like my husband, I'm, I, I never to stop talking about infection. It's a, it's a joke, but it's true. Um, so microbe-minded too is my Twitter. And then polybio's Twitter is polybio rf. So yeah, follow me or us. Oh yeah. Oh, they're going to love all of them. Yes. Well, thank you, Amy. I learned so much and I'm, I've got a million more questions, of course, but that's exactly what science is. Like you, you get answers and then those answers don't solve everything. You just are left with 100 additional questions.
[49:05] Yep. But that's why we do what we do because it's just this never ending journey. And it's very rewarding when the questions that we answer help us answer also questions about life and help us to get solutions for other people that might be suffering. So thank you for the work that you do. Um, and thank you for your time. I know everyone's going to love this. So if you have any questions for Dr. Amy Proal, um, leave them, you can leave them to me and I'll give them some answers to her and maybe I can get you some answers. Um, yeah.