[00:00:04] Speaker A: ID the Future, a podcast about evolution and intelligent design.
Are there prestigious ID friendly scientists out there who you've never heard of? I'm Casey Luskin with ID the Future, and the answer to that question is yes. In fact, a lot more than you might think. However, in the vast majority of cases, the identities of these scientists cannot be made public because. Because they fear for their careers. But every once in a while, one of these pro ID scientists finds themselves retiring or maybe no longer at risk for some other reason, and they decide to come out of the closet. Today you're gonna meet one of those ID friendly scientists. And so I'd like to introduce you to Carl Krueger. Hi, Carl, and welcome to ID the Future.
[00:00:46] Speaker B: Hi, Casey, how you doing?
[00:00:48] Speaker A: Great to have you on. Really great. Yeah. So I'll introduce you, Carl, and we'll get into some questions here.
Carl Kruger is a retired program director in the Division of Cancer Prevention at the National Cancer Institute of the NIH. He received a Ph.D. in biochemistry from Vanderbilt University and then continued doing research at the NIH as a postdoctoral fellow before he joined the faculty of Georgetown University School of Medicine. He then went to the National Cancer cancer institute in 2004 and retired at the end of 2022. He's also a supremely nice guy.
I want to start by just telling a little story here.
One day in the mid 2000, Carl and I think it was probably around the year 2013, Ann Gager and I were here at the downtown Seattle office of Discovery Institute, and we received a message that an ID friendly scientist was in town and wanted to meet us. That scientist turned out to be Carl Kruger, who at the time was still working at the National Cancer Institute. And. And we had a lovely time meeting Carl, and he then went back to the east coast and we loosely kept in touch over the years.
Well, a number of Years back, around 2020, after I got back from my PhD in South Africa, I reconnected with Carl and he mentioned that he was gonna retire fairly soon. And after retirement, he said that he wanted to do more work in the ID evolution domain. And so after Carl retired at the end of 2022, he began working on a couple of papers within his field of expertise, namely cancer.
Now, Carl had read Michael Behe's 2019 book, Darwin Evolves, which argued that when Darwinian evolution operates at the molecular level, it tends to break features at a much faster rate than it builds them. And this thesis from Michael Behe resonated with Carl's experience with the mechanisms that cause cancer and so he has now published in the last couple years two ID inspired papers in the journals Molecular Cancer Research and the Journal of Molecular Evolution about the molecular causes of cancer and how they generally breaking features at the molecular level. We're going to talk more about that today, but for now, let's get to know Carl. So, Carl, could you tell us a little about your own scientific background and your own kind of scientific journey?
[00:03:02] Speaker B: Okay. Well, you kind of summarized it already as, you know, I got my PhD in biochemistry from Vanderbilt University. That was 1981, so I'm probably dating myself. But since, you know, I'm retired, you know, that was a long time ago.
And then after leaving Vanderbilt, I went up to NIH and I've basically lived here in Maryland ever since.
I worked in the lab of Marshall Nirenberg. Many of you might know that name as the, you know, one of the pioneers who deciphered the genetic code. So I, I was with him for five years and then was able to land a faculty position at Georgetown University.
And it was actually in a pharmaceutical, a neuroscience institute that was funded by a pharmaceutical company.
So, you know, I kind of like had the best of both worlds because we had hard support from, from our company that was supporting us, plus, you know, we could still apply for NIH grants. And I stayed there for quite a while.
But eventually all good things must come to an end. And things, you know, slowly started to break down between the institute and Georgetown.
And you know, when I saw that this wasn't going to last forever, I realized, well, you know, I'm kind of getting tired of academia anyway. Research is great, but I feel like I'm so focused in one area of science, science. It'd be nice to kind of branch out and get a more global view.
And since I was still in the area, I said, well, you know, a lot of people actually leave, you know, local universities here and end up getting program director positions within the nih.
And I was able to find one such position within the National Cancer Institute. So that was 2004 when I moved there.
And so ever since then, that was really like a new field of science for me because while I was at Georgetown, I was specifically doing neuroscience. And in fact, I had to learn neuroanatomy myself. Being a biochemist, I knew nothing about anatomy. So to teach neuroanatomy to the medical students, I had to learn it myself. And that was quite an experience.
I wish I knew those secrets back when I was going through graduate school because you can't fool medical students. So you have to know your stuff. Cold leaving neuroscience, then I was able to basically enter the field of cancer, which really is a very broad field. Basically, we were being in the division of cancer prevention. Our group was primarily responsible for funding research that was trying to identify early detection biomarkers for cancer. I mean, it's a very difficult feat to accomplish now that I've seen what it takes.
I really was there up until 2022 when I finally retired.
[00:06:10] Speaker A: So, Carl, when you were at the National Cancer Institute, basically, and I just want to make sure I'm understanding this right, people would come to the NIH and the National Cancer Institute looking for grants to study cancer, the causes of cancer, these biomarkers and so forth. And you were basically, as a program director, part of your job was to evaluate those grant proposals and decide, you know, which were worthy of getting funding and sort of managing a major research budget to decide who would get funding to study cancer. Is that essentially right or sort of.
[00:06:45] Speaker B: In a sense, you're not exactly right. We weren't involved in the peer review process.
That, of course, is done by other faculty that are called into different study sections to review all the grants. But based on the scores that were received at those study sections, then, you know, we make the decisions from there. You know, we basically, you know, as most of the institutes, they basically take a certain percentage of the top scoring grants and say those are going to get funded. And then, you know, they're also given some liberty to kind of pick some more beyond that, so beyond the scoring threshold, so that, you know, they allow us to pick other grants that we think would be of value.
More than that, we were also able to kind of initiate our own programs.
You know, that is to, you know, when I got to the nci, I realized that really this area is very weak in carbohydrate chemistry. And I knew carbohydrates really play a very important role and in the biomarkers that we should be looking for. In fact, one of the best known cancer biomarkers, like for pancreatic cancer, is called CA99. It's actually a carbohydrate structure.
So, you know, I knew that there's going to be many more of those that should be available, but yet I knew the research wasn't being done. So I was able to get a program started to specifically look at cancer biomarkers that are based on carbohydrate structures. And, you know, we had that program running for over 15 years, you know, and, you know, they all went in five Year slots. And with each rendition of that program, it kept getting better and better because we started learning, okay, what are the. What are the types of projects that are really have the most success? So by our last round of it, you know, I was pretty pleased with the progress that had been made.
So that led us to the point where, you know, it was time for me to retire, and so I had to say goodbye to nci. And that's where I came to you guys and said, hey, I'm available now. What do you want me to do?
[00:09:05] Speaker A: Well, we said you should do whatever you want to do. But, yeah, I mean, it sounds like your experience there at the National Cancer Institute gave you a lot of just insights and understanding to cancer. So, Carl, maybe could you tell us a little bit about some of the insights you learned about cancer while working at the National Cancer Institute and how this led to your views about sort of this Darwin devolves take on cancer?
[00:09:32] Speaker B: Okay, yeah.
Just looking back and kind of, you know, pondering the two papers that I've written, I realized I really had a front row seat to what was happening in cancer research, because I got there in 2004. It wasn't long after that that the technology of next generation sequencing really started coming to the forefront.
And in fact, it was only. I was only there for two years when NCI started saying.
They started this program that they called tcga, the Cancer Genome Atlas. If you understand what the acronyms tcga, the four nucleotides that you see in DNA. The goal of TCGA was to pick a number of different tumors, actually excise the tumors from cancer patients, and then sequence the entire genomes of these cancer specimens.
So they started off with, I remember it was with glioblastoma, and I believe breast cancer was another one of the very early cancers they were looking at. But as time went on, they kept expanding to more and more tumors.
By the time TCGA had finished, they had sequenced over 16,000 tumors. And keep in mind, this is whole genome sequencing where they've sequenced tumor, the tumors as well as normal tissues from each patient. So you knew what the normal patient was essentially born with versus what the tumor was presenting with. And from that, we learned what's going on in cancer, that what has changed in the genome to produce this what I call a monstrosity of a beast that has arisen.
So, you know, at one point we had Bert Vogelstein come down from Johns Hopkins University. He was one of the leaders in this field. And it was just amazing to see him you know, kind of talk about some of his earlier studies where he shows, you know, the mutational profiles of different tumors. He was working primarily on colon cancer at the start because that's what his lab was specializing in. You know, and he was showing things where, you know, he'd show certain mutations that just show up repeatedly in cancer. He would call those mountains, and then he'd show a lot of other mutations that occur, and he would call those hills. So these. This was the terminology he started off with, you know, the mountains and the hills. Well, obviously, the mountains were very important mutations, because you see them repeatedly in cancer.
So that's saying that there's something important about that particular mutation that cancer likes. But you couldn't throw away all the hills either. Most of the hills are what are called passenger mutations. I mean, most tumors really have thousands of mutations within them, but most of them really play no role. But yet there are still a few of them that do play roles.
As time went on, what they found out is a lot of these hills, a lot of these mutations that are kind of in low abundance, what they're actually doing is they're actually knocking out what are called tumor suppressor genes. So it's very easy to do that. You know, just put in a termination codon early in the coding sequence, and you've knocked out that gene.
Another way is to just put any. In any kind of mutation that alters or, you know, disables the function of that protein.
So basically, things have broken down to you've got tumor promoter genes and tumor suppressor genes in tumor promoters. What you find is that the mutations basically hyperactivate those proteins, but then the tumor suppressors, which far outnumber the tumor promoters, all you gotta do is knock it out any way you can.
And so things were kind of broken down in that kind of a way. And here I was getting a front row seat, you know, watching this develop, and then actually seeing some of our own researchers as well, getting into their own aspects, trying to go a step further. Because TCGA was based on tumors that had already metastasized. You know, the patients were already presenting with symptoms. In our division, we wanted to catch cancer before it got to that stage. You know, you want to get it before it metastasizes. So we had a lot of our investigators actually actually looking at what are called precancerous lesions. They're a lesion that could develop into a tumor, but ultimately you don't know if it will develop into a tumor or not.
So, you know, we started Looking at, you know, that our investigators started looking at a lot of these pre cancer lesions. And in fact, that.
That meeting when I met you in Seattle, that was the same meeting where our investigators were starting to show the first data they were getting off of sequencing these precancerous lesions.
And I think I emailed you the day after that when I said, you should see what our investigators are finding. This is amazing.
And that's really what kind of got me started thinking this way. Because it's like, now I could see, while I never believed in Darwinian evolution, I could see, wait a minute, there's a way right here that this looks like Darwinian evolution to me.
So, you know, that's kind of the direction I had taken since then. And of course, you know, where that led.
[00:15:13] Speaker A: Yeah. So let's maybe help our listeners and our viewers understand kind of the context here and how this applies to Darwinian evolution, because.
Okay, so Carl, we've often heard people say that cancer shows how evolution works. Okay. And you would actually agree that cancer is Darwinian evolution in action. You've got sort of all these cells in an organism, and they're competing for resources, they're competing to survive. However, under. And I want to make sure if I'm getting anything wrong here, please correct me or feel free to, you know, restate everything in your own terms, of course. But you know, you've got all these cells in a multicellular organism, like a human being, okay. Now, under normal circumstances, these cells have various genetic checkpoints and inhibitory mechanisms and barriers that prevent those cells from replicating out of control. Okay? So these are like stop points or checkpoints that prevent cells from just starting to multiply. But if you start to break those inhibitory mechanisms, then you can progressively get closer and closer to. To sort of this out of control growth stage. And when that does happen, if you break enough of those mechanisms, you will get out of control growth and you'll start to grow tumors or other things, and you will get cancer. And so in that sense, the cell that wins the genetic lottery by getting these right mutations to break all these inhibitory mechanisms, that is sort of like winning the contest to survive and reproduce in the context of the host organism. And that is sort of a Darwinian process. However, in this case, to survive and reproduce, you've got to break these normal mechanisms that prevent out of control growth, that inhibit growth.
And only when you do that do you actually get cancer. And so over the years, we've had other folks who have made this comparison between Darwinian Evolution and cancer. You know, when you, when you brought this argument to our attention, Carl, this was not the first time we'd heard it. I could think of some folks at biological.
Joshua Swamidass, who is a computational biologist at Washington University of St. Louis, he has compared Darwinian evolution to cancer. Perry Marshall, very nice guy, kind of from an ID 3.0 perspective, who I know pretty well. Joshua Swamidas, also a very smart biologist. These are very good biologists. And they have said, look, cancer shows the sort of creative power of Darwinian evolution. And our response is, yeah, you're right, it actually does. However, when you understand what cancer is doing and what the Darwinian quote unquote, you know, process is doing at the molecular level, it's not creating new features at the molecular level. It's breaking inhibitory mechanisms that are normally there.
So eventually you get out of control growth. So again, this is where the Michael Behe's Darwin evolves thesis comes in. Because you get, you know, Michael Behe proposed that when Darwinian evolution does act, it tends to break things much more easily and much more rapidly than it's going to build new molecular mechanisms. That seems to be exactly what we see going on with cancer. So did I get that kind of right, Carl? Is that going to the right direction?
[00:18:41] Speaker B: Right. You were majoring on the tumor suppressors. Don't forget we also have tumor promoters.
[00:18:47] Speaker A: Okay.
[00:18:47] Speaker B: There it's a different story. Because what we find happening is that with tumor promoters, quite often you see the same mutations or very small set of mutations that repeatedly show up in different patients. Even the example of, I think you saw one of my papers where I had the braf, where there's basically one mutation that shows up in tumors that's more than 20 fold higher than any other mutation that is found in the tumor promoter. Braf. Well, that one mutation, what you're doing is substituting a Valine for a glutamic acid. You're converting a neutral amino acid to, to a negatively charged amino acid that constitutively activates that protein. So now it's always act, you know, it's always working. It's always phosphorylating other signaling proteins. Basically, you're turning on growth by doing that. It's sort of like, you know, another analogy that they use for cancer progression is it's kind of like driving a car. You can either step on the gas pedal or you can step on the brake.
Tumor suppressors are basically applying the brake. And that's very important because there's many ways that you need to suppress cell growth.
There's generally less ways that you need to increase growth. And that's what happens when you activate a tumor promoter by that one mutation in braf. Yeah, you convert that one amino acid to a glutamic acid. Now it's constitutively activated and before you know it, tumor growth or the cell growth has increased. And it's not just one mutation that does it. Cancer requires multiple mutations.
So you've actually got several chances to get by before you actually get a full fledged tumor. What you hope for is that you don't keep losing the lottery in this case.
I mean, cancer season, as it wins the lottery, you know, you're hoping that you don't get those mutations that just add onto the growth processes of the cell.
[00:21:08] Speaker A: So you've got a lot of expertise in cancer and the mechanisms behind cancer. And I would like to maybe rewind a little bit. We actually jumped ahead in the script here a little bit. You mentioned that you have been a skeptic of Darwinian evolution for a long time. So maybe I could ask you originally in your career and your studies were what made you become a skeptic of Darwinian evolution?
[00:21:30] Speaker B: Okay, well, I guess to start off with, I should say that, you know, even though I was brought up in the Lutheran church, I really didn't become a Christian until I was 16 years old.
So that kind of like sets the stage for my state before I actually got into college.
But, you know, going into college, you know, undergraduate school, I was kind of waffling between majoring in biology and chemistry. So I really kind of heavily intensified in both of those subject areas.
Ultimately I got my bachelor's in biology, but of course, you know, I went into biochemistry when I went to graduate school.
But before going into undergraduate school, I decided, well, you know, about this evolution debate, you know, which really wasn't such a high profile thing back then. I just said, I'm just going to let learn about science and let, you know, let me make my own decisions about which way I'm going to go on this.
[00:22:30] Speaker A: Well.
[00:22:33] Speaker B: As my sophomore year of high school, I had to take organic chemistry. So that's a very important background to have. And then finally in my junior sophomore years, I had various different courses. Basically that's where I learned things related to biochemistry and what would become molecular biology. Know, by the time I had that background knowledge, I said, okay, it's very clear to me, Darwinian evolution is really not possible. You can't create such magnificent structures by just random chance. You know, and this holds for origin of life. You can't create life just by mixing chemicals together and expect to, you know, pop out a living cell. That's not going to happen.
In fact, I would say origin of life really defies organic chemistry. And, you know, organic chemistry really hasn't changed since the day when I took it.
And I would hope that anybody who has gone through that level of chemistry should understand by now that, yeah, you're not going to get life just by mixing, you know, organic chemicals that you might find on a prebiotic Earth. That's not going to happen.
And then, you know, I also learned through biochemistry that proteins have very specific sequences, just like our language. You know, any. Anything you want to communicate has a very specific sequence of letters. It's the same way with proteins. If you modify, if you change those sequences, you've basically wiped out the function of that protein.
And I realized, well, to get it that exact, that also requires some sort of. I didn't think of it in that time, but nowadays that's. I use the term, yeah, that would take a designer, some intelligence that would actually have to put that protein together, that would have to engineer it to actually carry out this particular function.
So I saw it back then in undergraduate school, and my mind hasn't changed since then. Okay. Nobody has convinced me yet, and I'm talking about even going through graduate school, you know, being a faculty at the university. Nobody has convinced me that Darwinian evolution is even possible because you're really breaking the laws of thermodynamics. You're going from something very simple to something very highly complex.
Well, you're, you're basically decreasing your entropy. But also, that takes a lot of energy to actually put things in that state of order.
That's not going to happen through random chance.
And it wasn't until, you know, I saw what was happening with cancer that I realized, well, wait a minute, here's a system where it does seem like Darwinian evolution is happening, but it's going in the opposite direction. It's going downhill. It's not going uphill.
[00:25:27] Speaker A: That's great. So, Carl, when you and I have spoken, we've talked a lot about your interest in Michael Behe's book, Darwin of all.
Maybe could you share about when you read that book, how did that resonate with your thinking and how did that impact you?
[00:25:41] Speaker B: Okay, well, just to clarify it, you know, as I was telling you back in those days, what I was seeing with what was happening in cancer, it was you who suggested to me, Carl you need to read the book Darwin devolves, which I did right away. I bought it from Amazon and started reading it.
[00:26:00] Speaker A: I forgot about that. But I probably did say that to you, that that sounds quite reasonable.
[00:26:05] Speaker B: No, that is.
And I mean, I absolutely agreed with everything that Michael Behe said. I said, yeah, this, this is exactly what's happening in cancer, because when you think of it, it's very hard to improve upon a protein.
Now, when you look at the tumor promoters that I was talking about, and yet cancer is specifically selecting just certain mutations that show up repeatedly in different patients.
The evolutionists like to call that a gain of function mutation, because now you've basically increased the activity of the enzyme.
What's actually happening is, no, it's still a loss of function mutation. They only call it gain of function because the activity is increased. What is broken is you've broken the break for that enzyme. It seems like all these enzymes have their own inhibitory mechanism. In some cases, the confirmation of the protein, the shape of it, keeps it in a closed state, or certain enzymes require to be dimerized in order to be activated. One way or another, the enzyme is in an inactive form.
And these cancer mutations, the driver mutations that we find in the tumor promoters, they all find ways to basically break that inhibitory mechanism so that now the. The enzyme is constitutively activated.
[00:27:34] Speaker A: Interesting. So.
[00:27:35] Speaker B: So both evolutionists like to call it a gain of function. I say, sorry, guys, no, this is a still a loss of function. You call it what you want, but you've broken something. And, you know, that's what my second paper looks at, the one that I published in the journal Molecular Evolution, where I looked, well, can you find any of these hyperactivating mutations anywhere in any species? You know, can you find those mutations in the germline of any species anywhere? So I looked through everything that was available, you know, within the, you know, the databases at the National Cancer of Bioinformatics Institute. And no, you don't find them at all. And it made perfect sense to me because if you did find that mutation, that organism probably would not survive because you would have rogue cells going that would not contribute to the survival of the organism as a whole.
[00:28:33] Speaker A: So you would argue that both the mutations that break the tumor inhibition mechanisms and the mutations that essentially are tumor promoter mechanisms, that they both ultimately are breaking things, and they both represent Darwin devolves kind of in action.
Let's talk real quick about the two papers that you published, Carl. The first one was in the journal Molecular Cancer Research. Maybe we can show this up on the screen here. The title is Neo Darwinian principles exemplified in cancer genomics. And you talk about the fact that yes, neo Darwinian mechanisms are at work in cancer, but you go on to talk about how essentially your braking features. The second paper is in the journal of molecular Evolution and it's titled Survey for activating oncogenic mutation and metazone Germline genes. And so we'll probably write about these two articles on evolution news. But Carl, maybe could you very briefly just take us through some of the highlights of these two papers?
[00:29:40] Speaker B: Okay, so the one that was in molecular cancer research, it's interesting because I didn't know, but one of the groups that we were funding at Johns Hopkins, you know, we were funding this group in another one of the programs that I wasn't directly involved with, but our group was funding them in another program, had just published a paper that showed up in the journal, the same journal in the issue before my paper came out. And they were proposing a better definition for cancer, basically defining cancer as a disease that is evolving.
They're basically saying the same thing that I'm saying, and yet the two of us didn't know that we were writing our own papers. And here they are showing up in the same journal, one issue right after the other, really back to back issues.
They're giving more of a clinical perspective as to what tumors are doing. And I was giving more of a molecular biological aspect. And you know, and my title says it all, the neo Darwinian principles that are exemplified in cancer genomics.
So, you know, so basically, you know, we did the cancer genome just says it all. I mean, you can basically predict how that cancer has evolved over its time by looking at the mutations and the older other kinds of alterations that occurred in its genome.
And it's not just mutations. Cancer quite often shows a lot of rearrangements of chromosomes, a lot of chromosomal abnormalities to the point where you get significant deletions, where parts of chromosomes are deleted.
In that case, quite often what you're deleting are tumor suppressor genes.
You might have one tumor suppressor gene deleted from one chromosome, but you've still got another tumor suppressor gene on another chromosome that may have been inactivated by a mutation.
You've also got areas where you might have chromosomal amplifications.
The segments that get amplified tend to have tumor promoter genes on them. There again, there you have the principle. Well, you're stepping on the gas even harder by putting more tumor promoter genes in the genome.
So it can actually get going faster than it is even humanly possible.
So, you know, so these are the principles that cancer relies on and it selects them specifically.
But, you know, it selects events that are all detrimental in nature.
Okay. It's, it's great for the cancer cell if the cancer cell wants to grow, but it's harmful for the individual.
[00:32:29] Speaker A: Well, I have to say that, you know, reading your papers, I learned a lot about the mechanisms and the mutations that potentiate cancer. It's really, really fascinating. And I highly recommend your papers and we'll try to summarize them on evolution news. But I highly recommend them to anybody who just wants to sort of get a nice review of some of the molecular mechanisms that can cause cancer. And one of the things that really struck me as I was reading your paper, your papers, Carl, is that there has been so much research done on cancer. I mean, thankfully, there's a lot of very good biologists out there trying to understand this horrific disease and how we, how it, why it happens and how we can stop it. So we've got a lot of data on cancer, which, this is one of those areas where, you know, when you have a very data rich field, you can really drill down into the molecular details and understand what's really going on. Whereas in a lot of other, you know, even evolutionary articles, when I read about, oh, this protein evolved to do this, we don't have this much data. A lot of it is just, you know, frankly, it's data poor. Whereas this field is so data rich that you were able to drill down into the mechanisms or talk about, you know, this particular mutation shows up in this type of cancer x percent of the time, 40, 80%, whatever it might be. There's just so much that we know. And so this actually allows us, I think, to use this as a nice case study of, of what mutations and Darwinian evolution really is doing and can do and does do at the molecular level because we have so much research that's been done. And so, I mean, kudos to you, Carl, for being so fluent in the literature. I mean, I was just amazed at how many papers you would cite. It's like you knew exactly where to go to figure out, you know, what's going on at the molecular level with this, you know, this or that mutation. And it was just really, really an incredible review that you wrote digging into these details. So. So, I don't know, I just want to recommend your, your papers to anybody who wants to learn about cancer, you know, much less understand, you know, there are winning Implications. But so. So thank you for the great work that you've done here.
[00:34:34] Speaker B: Okay, well, it's been a pleasure. You know, like I said, I had a front row seat being in the nci and it was just amazing to see this all happen right in front of my eyes.
[00:34:44] Speaker A: Well, you're. Yeah, you were definitely the right person to write about this and talk about it.
So tell us. You know, there's some other lines of evidence. You talked a little about the complexity of life and you know, how you, even before you got involved with cancer research, thought that many of these complex features, they couldn't evolve by blind mutation and random mutation, natural selection, etc. Etc. But what are some. There's some other lines of evidence that you think challenge the Darwinian evolution model and support intelligent design that come to your mind.
[00:35:17] Speaker B: Okay. Yeah. One thing that I've been thinking about lately is, you know, I've become keenly aware of what are called the cancer risk genes. Cancer risk mutations. That is, people are often born with, you know, one mark against them. They might have a mutation most often, and this will be in a tumor suppressor gene. You know, BRCA1, BRCA2 are the most famous right now, but there's many, many more.
And you know, they're born with this mutation. They have no idea that they have it. They grow into adulthood, they have children. By the time they're in their 40s, 50s, 60s, they might develop a cancer. You know, if you're talking BRCA1, BRCA2, it could be breast cancer or ovarian cancer. You know, then now, because of, you know, the, you know, robust sequencing technologies that we have now, they just go ahead and sequence your genome. You know, you can get it done for 250, $300 right now, of course, for a patient, you know, they'll go do it because they're going to find out exactly what needs to be, you know, how they can maybe try to attack the tumor. And you know, and, and that is where they find that quite often a lot of these cancer patients were actually born with a mutation to, to start with, you know, if you take BRCA1 as a, as an example, you know, a person finds out they have a BRCA1 mutation, they realize, Geez, I already have four kids. Did I pass this gene on to them? Well, you can check and see whether you have. It has been passed on to them. You know, now we have that capability. But it's like the best you can do is try to, you know, undertake any preventive measures.
So.
But you know, that that's an aspect where Darwinian never saw. Darwin never saw this coming.
You know, he had some great ideas for how natural selection can, you know, can basically promote certain features.
Yeah, but he didn't. He had no concept that, no, there's other things that are still happening that you don't even see that the organism can still live fine into adulthood, they can still reproduce, but yet still transmit some detrimental mutations to your progeny.
And, you know, since every generation accumulates another hundred mutations that the parents did not have, these kinds of mutations are just mounting up, you know, every generation. You know, it's not. Things are not getting better, they're getting worse. You know, we're just. The number of dysgenic mutations in any species just keeps growing.
So I, you know, I see it as, you know, basically, you know, falling in line with the term of genome genetic entropy, where, no, even our genomes are really tending towards, you know, a decrease in complexity. You know, we're actually losing that information that's critical.
[00:38:21] Speaker A: And this again gets to the idea that Darwinian mechanisms, you know, blind mutations, they don't tend to improve things, they tend to degrade things.
And, you know, getting back to cancer, we all know people who have just been had their lives ended or, you know, harmed terribly by this terrible disease of cancer. And I think that your insights, Carl, I hope that they will lead us to a better understanding of this disease and maybe lead us closer to being able to push back on it and combat it.
Carl, we're going a little bit long on time here, so I want to just close this up by asking you a question because you. You spent a lot of years in the mainstream scientific community as a scientist who was skeptical of the standard evolutionary model and was sympathetic towards intelligent design, but you were not able to say anything publicly due to your career concerns. You were friends behind the scenes. And we've, like I said at the very beginning of this podcast, we. We know a lot of folks who are in a position like yours where they are ID friendly, they're at some mainstream institution, and they just cannot be public about their views. I mean, the number of people we know is sadly very, very high.
But so. So there's a lot of folks out there who I think can resonate with you and your position and what you're going through, what you've been through. What would you say to a scientist in this position who is, you know, struggling with, you know, seeing a long career ahead of them where they. They know that they're ID friendly or they're questioning the Darwinian view, but they. They don't feel that freedom to speak out. How would you advise a person in that position?
[00:39:58] Speaker B: Yeah, I mean, you know, when I was in that position, I didn't try to make a big thing of it. You know, I would.
I wouldn't try to bring up evolution and try to bang it, you know, bash it in front of my colleagues.
Occasionally I might kind of dispute some things, but I wouldn't take a strong stand. But, you know, I would be. I would basically be low key and don't really try to draw a lot of attention to yourself. Just leave it at that. I mean, by and large, most of them are just scientists and they really want to, you know, delve into science deeper that doesn't involve evolution. You know, it's important that we increase our knowledge in science. And, you know, that is the general push that most scientists are going towards.
You know, it's. It's just only now that, you know, since I'm basically free, it's like, okay, now I'll. I'll say what I. What I want to say. The way I really feel, the way I see reality. And, you know, that's why I'm. I'm taking the stance now, you know, using you guys as my springboard to do that. But, yeah, I would say just hang low and enjoy the science. Keep pushing forward and work together with your colleagues, because you're all working for the same goal. Just like all those cancer researchers out there.
It's amazing what they have been able to find.
I didn't even touch even what I thought were some of the best studies as to what has been accomplished in, you know, cancer research. But, you know, it's. It's just amazing that how much we know about cancer right now, and it fits beautifully with the model of Darwinian evolution. But, you know, like I have to say to Darwin, hey, everything's been going in the opposite direction that you said, you know, and in his book, he talked about monstrosities as, you know, like domesticated species that look so different from the. Their species in the wild. He would call those monstrosities. I feel like saying to him, you don't know what a monstrosity is like. Look at cancer. There's a monstrosity that evolution created for you. So that's what you should be considering, you know, not these domesticated species where, you know, it's just minor adaptations.
[00:42:22] Speaker A: Yeah, Carl, I think that you just gave great advice. The vast majority of scientists out there, even, you know, scientists who don't support intelligent design and accept the standard evolutionary model. They're not ideologues, you know, they're not looking to whatever promote an agenda. They're just trying to do their research, do good science, do good research, help benefit humanity. You know, the folks that you worked with were trying to help cure cancer. What a noble goal. This is like science at its best, right? It's not political, it's not ideological, it's just trying to help humanity. And we know so many people in those positions and many of us have done science research in those contexts. So just trying to help us better understand the world that we live in and make a positive contribution to the world. That's great.
And the difference though is that even in those very positive, good scientific contexts, you have some folks who are free to speak their views when it comes to questions about origins and other folks who are not view, sorry, who are not free.
And if they were to speak their views, they could be ousted or their careers could be at risk. And so we're speaking right now to those folks who are coming from that ID friendly view who, you know, don't have that freedom. And your advice, Carl, is very good. You know, basically do good research, work hard, don't rock the boat.
And, and you know, maybe someday, hopefully they will reach a point in their career where like you, they can speak publicly. And we want folks to know that we're here for you. At Discovery Institute we have a very large network of ID friendly scientists and Darwin Dowding scientists and we'd love to have you come join that network and maybe not feel so quite alone so that you can, you know, you can talk amongst friends behind the scenes and be able to express your views. That's, that helps a lot as well I think to make friends with folks who are like minded and sort of feel that camaraderie in that community and that you don't feel quite so isolated and know unable to speak your views when you can say them privately to friends in a safe environment, in a safe space. So we would love to help connect you with that community if that's you.
Carl, we're really glad that you made it to the point in your career where you're now able to freely speak your views. And we wish you only the best whatever the future holds. We appreciate the work you've done and just, and just how you've modeled what it looks like to be a good scientists coming from the pro ID perspective in the scientific community. So thank you for your work. And, and we look forward to, you know, working with you in the future as well.
[00:44:55] Speaker B: Okay. Well, thank you very much, Casey. It's been a great pleasure working with you and getting to know you.
[00:45:00] Speaker A: The feeling is very mutual, Carl. Okay. Well, I'm Casey Leskin with ID the Future. Thanks for listening. And if you are an ID friendly scientist who doesn't feel free to speak, your views reach out to us. We'd love to hear from you. We, we're not going to put you on ID the Future unless it's something that you really want to do. And in Carl's case, he was 100% sure this is what he wanted to do. But we would love to connect with you behind the scenes, help you to find resources where you can not feel so isolated and alone and connect you to a larger community where you can be private and confidential, but also, you know, be your real you. So anyway, thanks for watching. I'm Casey Gluskin and thanks again.
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