Episode Transcript
[00:00:04] Speaker A: ID the Future, a podcast about evolution and intelligent design.
Hello and welcome to ID the Future. I'm Casey Luskin and today we have on the show a very special guest, Dr. Udita Jayatanga, who is a medical doctor in the UK and a senior consultant in rehabilitation medicine with with expertise specializing in helping people to do rehabilitation after brain injuries. He was the Associate Clinical Director in Rehabilitation Medicine Department and previously been named a member of the NHS England Rehabilitation Medicine Clinical Reference Group. He's originally from Sri Lanka with a very strong Anglican background. He has had a long term interest in the subject of Intelligent Design and has spoken in Sri Lanka and the UK on this subject. Using his medical and bioscience background, he's done a comprehensive scientific analysis from the universe to cells and DNA to support intelligent design, especially looking at mathematical probabilities. And he's written a book titled Intelligent Design as Proof of Creation of scientific analysis. So, Dr. Jad Tunga, thank you so much for coming on the show with us today.
[00:01:16] Speaker B: Thank you very much for inviting me. It's a great pleasure to contribute to this exciting subject which I have been involved in over the last 10 to 15 years. So thank you very much for giving me that opportunity.
[00:01:29] Speaker A: Yeah, I know that you've been following this issue and doing your own research and investigations for many years, Dr. Jayatanga. And we just had the occasion to meet a few months ago in the UK when I was visiting there. We had a very lovely visit. We were introduced by a fellow friend and colleague, Dr. Richard Ganesakara at Biola University, who's a friend of yours and also a very close colleague and a fellow here at Discovery Institute and a wonderful guy. So it's really enjoyed meeting you and getting to hear about your story.
[00:02:00] Speaker B: Yes, I was pleased to have contact with Richard and through Richard to have contact with the Discovery Institute and you. It was a wonderful meeting.
[00:02:12] Speaker A: I want our listeners to get a little appreciation of how much our ID scientific community is growing. Meeting Dr. Jayatunga in the UK, who's a very prestigious and well respected medical doctor there with the NHS in the UK is a regular occurrence. We meet new scientists all the time and we have scientists in our network who are constantly introducing us to new scientists. Right after this podcast is over, I'm doing a zoom with a young electrical engineer who just got his PhD. This is somebody else who's introduced to us by a scientist in our network. This kind of thing happens all the time. It's very exciting time to be a part of Intelligent Design because our movement is growing. So fast keeps us very busy. And anyway, Dr. Jayatunga, we want to get into some of your arguments and some of your ideas that you put together in your book. So one of the things you start out talking about in your book is the complexity of the cell and some of the basic factors that are needed for life and why some of these pose an obstacle to a natural chemical origin of life. So can you tell us a little about from your own studies? Why does the complexity of the cell and these basic factors of life pose a challenge to a chemical origin of life?
[00:03:24] Speaker B: Yeah, so throughout the talk I want to make certain challenges to the evolution community on various aspects, starting with a cell. And all revolve around the complexity and the inability for the evolution of process to explain things.
So all of us have heard about ureth's experiment in 1950s and many don't know that. Even NASA has got a branch which is called center for Emergence of Life called Cell. And they have been trying to make a cell, self replicating cell, just like many other scientists across the world. And so during over the last 60 or 70 years, what has NASA done? They have sent people to the moon, they have sent people to the International Space Station, they have sent, they have explored distal planets millions of miles away.
But when it comes to a cell, they are still millions of miles away, a cell. So what, what it says is that a cell is much more complex than what all the things they have done, at least superficially, because they have not even come close to making a cell. Across the world, scientists also have been trying to make a cell. And if I take the current research on cell on, on creating a self replicating cell, if I say that a cell will be like an ocean, I think the scientists in my opinion may have progressed to a bucket full of water.
So there's much more to do. And it is unlikely in the near future that they will make a self replacement replicating cell. We have been told that a cell arose in a prior either primordial soup or deep thermal vents. But looking at what the scientists have tried with all their knowledge, all their expertise, all their analysis, all the pristine chemicals they have got, and all the analysis and research studies, they have not been able to make a cell even in a test tube. But we are asked to believe that in the vastness of the ocean a cell has come in the vastness of the ocean. That is, in my opinion, it is not logical because when we do experiments we can, we can change the parameters, we can go back and we can change their chemicals. To get it right. But in the vastness of the ocean, nothing such can happen.
So we know that a cell, life on Earth needs so many parameters, about 200 parameters for life to start on Earth. But if you take the complexity of the cell now, last common ancestor, Luca, they have said that it has got 2,600 proteins. The smallest bacteria is Mycobacterium genitalium, which has got about 482 genes and 600 proteins. Proteins. Now, there are lots of discussions, debates going on whether it was a DNA or the RNA which was the first, but I'll keep away from that discussion. But it is important to ask, how did Luca get 2,600 proteins? I mean, these are not isolated proteins. They are interactive proteins. So they had to come together.
And how can a random selection, random mutations, or natural selection can select these proteins?
So this becomes an impossibility. And Professor Vikramasinghe has looked at this problem and said some bacteria have got about 2,000 proteins. And he has said that the chances, the random chances of this coming together is 10 into the minus 40,000. This is amazing, amazing numbers. Can't even think of how minute those numbers are.
[00:08:40] Speaker A: Dr. Jaytanka, you have a great quote in your book where you describe the complexity of the cell. And I think it really gives an appreciation of how difficult it would be for this kind of a complex feature to arise naturally. You say beyond DNA and rna, a cell has many other complexities. Every cell in the body is a chemical factory making hundreds of proteins, enzymes, hormones, energy substances, and have absorption and excretion, excretory pathways. It also has got its own protective mechanisms to make sure it does not get destroyed easily. In other words, the mechanisms in a cell could be described as having complex circuits, sliding clamps, transport channels, storage compartments, turbines for energy generations, and an actual multitude of miniature machines. These are nanotechnologies within cells. And I just thought that was such a wonderful picture of the complexity of the cell and what the evolutionary scientist is up against. You know, you said NASA trying to explain how does this come about by blind and unguided mechanisms. They're trying to explain technology that is far more complex than the technology that they use to go to the moon. You know, so it just. There's a problem there. Yeah, go ahead.
[00:09:53] Speaker B: Yeah, yeah. So even, even if you, if you take the cell wall, it has got about a thousand types of lipids.
So all those need to be explained on a random basis. And I cannot see any way a random process or natural selection selecting those proteins. There's no Mechanism. And also you describe some of those. If you take the most complex electrical circuit you can think of, the cellular biochemistry is much more complex than some of the most complex electrical circuits you get. So do such electrical circuits come on a random basis? And can you make any changes on a random basis? You can't, because if you change one, you had to change another ten or fifty or hundred of things to, to, to accommodate that change. So one of the things I want to stress is that there, there has to be, there has to be. Life is not add on process. And many things have to arise simultaneously because they are interlinked, interlinked processes. And it is starting from a, from, from a cell. And it cannot be accidental process or cannot have a blind beginning. Even with all the technologies we have, if we can't get even close to making a cell, including NASA, it is not right for us to say that it arose in the vastness of sea or primordial soup or things like that.
[00:11:38] Speaker A: And when you look at sort of what progress they have made, you talk in your book about the insignificance of the Miller Urey experiment. Okay, yes, they made a couple amino acids, but they're not getting the right chirality. They're not able to link them up to form proteins in an aqueous environment. As you say, you know, trying to form life in an undersea hydrothermal vent would be a terrible place to try to form longer peptides because that reaction isn't favored in water. And then of course, even if you could form all these proteins, getting all the amino acids in the right order in order to create functional proteins, to create these molecular machines is just, it's just beyond belief that this could happen by unguided natural mechanisms. I actually took a, A class from Stanley Miller when I was an undergraduate at UC San Diego, Udita. And it was very interesting. I should call you Dr. Jay Tonga. So. But it was very interesting as an undergraduate student to take this course. And I remember Stanley Miller telling our class that making amino acids or making proteins is not the same as making life. Even he recognized that his experiments were a far cry from making life. And so I think that you have really hit on something very fundamental here in, in your book. I, I'd like to move also to, you know, once, let's say, you know, for the sake of the argument, we could say that, okay, somehow life arose. Well, then the next part of the evolutionary story is that Darwinian evolution, natural selection and random mutation takes over and that is supposed to then build all the Complex features that we see in living organisms. After you get that first self replicating life form, one of the things that you talk about is the likelihood of getting a positive mutation and how difficult it is. So based upon your studies, why is it so difficult to get what you call a positive mutation or a beneficial mutation? From what we know of biology, yes.
[00:13:38] Speaker B: So many times when evolutionists discuss things, they say that mutations happen and they will bring changes, but no one discusses the chances of having a positive mutation.
Now bacterial studies have shown that the chances of getting a positive mutation is about 1 in 10 million. So that's just for one mutation. Now when, if you want to think of a complex structure or even complex biochemical pathway, you have to think of at least hundreds of mutations or some genes. But even so, at that rate, 1 in 10 million for one mutation, the organism to have two simultaneous mutations will be 1 in 10, 1 in 100 trillion. So these, these, these factors are not being discussed when, when evolution is. Evolution seem to imply that if you get a mutation you can have a change. It is not like that. They never take the rate of positive mutations into account. And in fact, many are neutral and some are negative. I mean, some give rise to diseases. So the chances of the species dying of a disease due to negative mutations are much higher than progressing to a new change.
[00:15:19] Speaker A: I want our listeners to really appreciate what you have just said, Dr. Jayatanga. It's unlikely to get even one mutation that can give you a benefit to survive and reproduce under domino elution. But maybe sometimes one mutation can help you. But, but what you're talking about is there are many of these complex features that will require more than one mutation before you get some kind of an advantage to survive and reproduce. And in fact, some of those intermediate mutations, so to speak, they, they may not give you any advantage. They may be neutral or they may even be deleterious. They may cause some deficiency or make it harder to survive and reproduce. So when you have to get multiple mutations before you get some kind of an advantage, I think you talk about this in terms of coordinated mutations or these complex mutational features. That is really where Darwinian evolution gets stuck. Because as you said correctly, the odds begin to multiply, right? If it's, say we could come up with some number one in a trillion to get one single beneficial mutation, okay, maybe that can happen every once in a while. There's a big population, there's a lot of mutations going on. But when you need multiple mutations, then to get, you know, and that's multiple Mutations to get any advantage, then you've got to multiply one in a trillion times one in a trillion and you very quickly start to run out of probabilistic resources to get those kinds of complex traits. Your, your, your comments on that?
[00:16:44] Speaker B: Yeah, absolutely right. So they have done the Drosophila fly study and they have estimated to get two positive mutations to change one enzyme to a better enzyme based on that study. If you extrapolate those data to humans, they say it will take hundred million years in humans to get two to have those enzyme changes of two mutations.
So these things are extremely rare and almost impossible.
[00:17:24] Speaker A: So Dr. Jayatanka, another topic that you cover in your book a little bit is junk DNA. How does junk DNA play into this debate? And what, what role does it play in terms of the, the whole question of intelligent design versus evolution.
[00:17:40] Speaker B: So that is another important aspect which I have thought about and I simply can't get the evolutionary evolution explanation on that. So coding is done only by about 2% of DNA and the rest is previously called junk. But all about 80% of that has been found to have some function like repair regulation, aiding in folding maintenance, epigenetics.
So my next issue is if you get a, we'll say you get a positive mutation.
That positive mutation cannot act on its own. It needs all the supporting mechanisms for it to be effective in the next generation. It is like if you have a good tennis player, right, you give him a new racket, right? So that's, we say that's a new mutation. Just by giving him a racket, you can't get him to be an international tennis player. You need all the supporting mechanism, the trainer, the diet, the physiotherapist, the backup systems, finances, all the kids, other kids. So when you, so even if you have a new positive mutation, it needs to be followed up with many supportive DNA mechanisms for it to act in the next generation. So again, that sort of thing has not been explained as far as I know.
[00:19:24] Speaker A: Yeah, you're exactly right. I've often heard these arguments of what they call de novo gene origination, where supposedly a stretch of junk DNA will spontaneously, you might say, magically transform into a functional gene. And my response is always, okay, well, maybe, but let's do some calculations. What is the likelihood that you could transform basically a junk sequence, a sequence that's not, apparently according to you, doing anything that is supposed to just basically, according to you, be a randomized sequence of nucleotides? What is the likelihood that you could spontaneously transform that into a functional sequence or a functional gene. It was what they'll even say, functional protein coding gene. So I find these kinds of explanations to be very unlikely, but especially more importantly lacking in detail. They never explain, you know, what is the likelihood of this happening and, and how does this happen. So let's talk about what you call some amazing or I think you say magical animal complexities and I think you're using that, that phrase kind of tongue in cheek. But you, you go over in your book many, many incredible examples of complex biological features that we find in animal species. And I'm not, we don't have time to go through all the examples of your book. A very fun read. But one of the examples that intrigued me because I'd actually never heard about this before is special features that allow for the freezing of the Alaskan wood frog. And you talk about the fact that there would be many simultaneous mutations that would be needed for this to function. It kind of reminded me a little bit of metamorphosis where you know, sort of an organism goes through all these complex changes and if it's not, if the whole process is not pre programmed then you're going to end up with a dead organism at the end of this. So can you tell us a little bit about this Alaskan wood frog, how it actually freezes to survive and what would be necessary for an ability like that to evolve to random mutation.
[00:21:20] Speaker B: So I want to stress on the need for simultaneous changes. Life is not an add on system. You need many simultaneous changes. So I have given some, some examples now as you say Alaskan wood frog, even if they have to survive one season, that the freezing of the Alaskan wood frog, all the systems have to be there even for them to survive to the next generation.
[00:21:48] Speaker A: Dr. Jaitanka, explain to us how does it work? So this frog actually freezes at certain seasons of the year. Can you tell us a little bit about what do they do? Because our listeners may not be familiar with it.
[00:21:58] Speaker B: So they stop breathing, heart and blood circulation stops completely.
You get antifreeze substance in each cell. And 60% of the water is drawn out of the cell. The cells, because the water is drawn out, the tissues solidify, liver produces lot of glycogen and urea which is sort of cryoprotective. And all the, every body system is protected. You know you can think of something like the cornea of the eye. They're so vulnerable, they're so frail. But and the brain tissue, the lung, gut, kidneys are all are protected by this mechanism. And then when the weather improves, it reverses within two hours. So that whole whole process needs not one or two mutations, I'm sure hundreds of genes for it to act that way. Because you can't have one of these features coming one at a time over a long period of time, ten or hundred or thousand years, it cannot come in a stepwise manner. All the systems have to come together for it to work. So these huge metabolic changes, physiological changes, biochemical changes, muscle function, heart function, they all cease. And it can be reversed within a few hours for when the weather improves. So this sort of thing cannot come one at a time. It's not an add on thing. All the systems have to come at the same time or within a very, very short time, even if they have to survive one season.
[00:23:58] Speaker A: Yeah, I mean, normally organisms don't want to freeze. When you freeze, that usually means you die, especially in something as complex as a frog. I mean, maybe a bacterium or a single celled organism, but I mean, a complex animal like a frog is not going to be able to survive that unless many, many traits are there to enable this. Sorry, go ahead.
[00:24:20] Speaker B: So this is a unique feature. I think that's why it needs to be explained. It's a unique feature and as you say, most of the animals and the tissues die in this sort of environment because they can't migrate. This is what they have got and it works out perfectly well for them. And so it hasn't got an evolutionary tree to support it. And there are similar other things. Like pregnancy of seahorses.
[00:24:50] Speaker A: Yeah, let's talk about that one. Dr. Jaytonka, I know that we're probably gonna have to do a second podcast here with you, which is great because you've got so many fascinating examples of animal complexity. But let me just give an intro on this and then I want to hear your explanation of male seahorse pregnancy. In seahorses, it's the male that gives birth to young. And I was doing some research on this for this podcast and I came across this, this Reddit thread that asked a very reasonable question. It said, if the male seahorse is the one who has the babies, why isn't that just called the female seahorse? And of course it's because the male seahorse is still the one providing the sperm, not the egg. And so these male seahorses, they have sort of this very special incubator pouch and the, and the females will actually lay their eggs in the male's incubator. Incubator pouch. And the male then gives sort of gestates the young and gives birth to them. But tell us, Dr. Jaytonga, and this will be our last one for this podcast and we'll do a second one. Why is this so complex and what are some of the, you know, the changes that would need to happen, simultaneous changes, as you say, in order to convert pregnancy to go to the male and the seahorses?
[00:25:56] Speaker B: Yeah, so. So this is, again, a very unique situation, unique change. There is no evolutionary tree to back it up. So it's for pregnancy and procreation. All the systems have to be there perfectly. If you don't have any of the systems, it may not work. So for the male seahorse pregnancy, what are the changes? It needs? It needs a brood pouch, it needs muscles, it needs elongated body, it needs new hormones, it needs different immune response, it needs different behavior called courtship dance. Now, all they cannot come one at a time. That whole system change has to happen en bloc because halfway stages will not work if they want to reproduce even one generation. So studies have shown that this process needs 3,000 extra genes. 3,000 extra genes. So it's not extra mutations, but 3,000 extra genes. So this is the enormity of such changes. And these things cannot come one by one over thousands of years. They had to arise simultaneously within a short time for it to work.
[00:27:24] Speaker A: Okay, well, Dr. Jaytonga, this has been a fun conversation. You have many more examples of amazing animal complexities. So let's stay tuned for a second podcast if you can stay with us and we will talk Additional examples of Dr. Udita Jayatunga's explanations of how animal complexity challenges evolution. So will you stay with us, Dr. Jayatanga?
[00:27:45] Speaker B: Yeah, sure, sure.
[00:27:47] Speaker A: Okay, great. So stay tuned for more with Dr. Ujita Daytonga on animal complexity and why it challenges evolution. I'm Casey Laskin with ID the Future. Thanks for listening.
Visit us at idthefuture.com and intelligentdesign.org this program is copyright Discovery Institute and recorded by its center for Science and Culture.
