In his book Genetic Entropy and the Mystery of the Genome, award-wining geneticist and young-earth creationist Dr. John C. Sanford argues that most mutations simply don’t produce a strong enough effect to influence natural selection. As a result, organisms continue to build up deleterious mutations as time goes on. This leads to an erosion of the genome. As he puts it:1
While selection is essential for slowing down degeneration, no form of selection can actually halt it. I do not relish the thought, any more than I relish the thought that all people must die. The extinction of the human genome appears to be just as certain and deterministic as the extinction of stars, the death of organisms, and the heat death of the universe. (emphasis his)
While he quotes a lot of experimental research to support his findings, he has never been able to demonstrate this effect directly…until now. He obviously hasn’t shown that the human genome is deteriorating, but last year he and young-earth creationist Dr. Robert W. Carter published (in a standard, peer-reviewed journal) the results of some of their research, which directly demonstrate that even when natural selection is working hard, it doesn’t seem to do a good job of getting rid of harmful mutations.
Carter and Sanford looked at how the genome of the H1N1 influenza virus has changed over time. The virus genome is fairly simple – it is made up of eight RNA segments that contain a total of 13,100 nucleotide bases. These eight segments code for up to eleven distinct proteins, since there are ways (like alternative splicing) that a single segment can code for more than one protein.
Believe it or not, there are published genomes of the influenza virus dating back to 1918! Obviously, people didn’t sequence the virus genome back then. However, samples of lung were taken from the frozen remains of someone who died of influenza at Brevig Mission, Alaska, in November of 1918. This sample and other preserved samples allowed scientists to sequence the genome of the virus from that time period. As the link discusses, when the 1918 virus was reconstructed based on this sequence, it was found to be much more virulent than current flu viruses. For example, mice who were exposed to the 1918 virus died, even though modern influenza viruses are not lethal to the same breed of mouse.
Why is the 1918 strain significantly more lethal? According to Carter and Sanford, it is because the virus has been accumulating mutations steadily since that time. Indeed, they show that the mutation rate of the influenza virus over time is remarkably constant. Most of those mutations are deleterious, but not so much that they can be weeded out by natural selection. As a result, the genome of the influenza virus is deteriorating, despite the natural selection that is clearly going on in the constant battle between the virus and the human immune system. They interpret their results as follows:2
We suggest that, while specific adaptive mutations commonly occur within the H1N1 virus, many more deleterious mutations are accumulating than beneficial mutations, even when there is strong selection. Consequently, H1N1 appears to have been in very gradual error catastrophe throughout its history.
In other words, even though natural selection was hard at work since 1918, it has not been strong enough to get rid of the deleterious mutations that have occurred throughout the virus’s 90+ year history. Because of this, the virus is becoming weaker.
If this idea is correct, it solves a puzzle that has plagued influenza research for more than 50 years: Why hasn’t any influenza outbreak in modern times matched the virulence of the 1918 pandemic? Researches have suggested that a combination of factors like herd immunity, advances in medicine, and advances in hygiene might explain this fact. In their paper, however, Carter and Sanford address each of these issues, suggesting that they have clearly played a role in the reduction of influenza virulence, but they cannot be completely responsible. Specifically, they argue that the steady decrease in virulence does not match the pattern one would expect from such factors. However, it does match the pattern expected from the accumulated mutation rate that their analysis shows.
Are Sanford and Carter correct in their contention that the influenza virus has actually gotten weaker over time? I have no idea. However, their data do seem to make a strong case for the fact that natural selection just wasn’t very good at getting rid of the deleterious mutations that happened over and over again throughout the known history of the virus. I hope this kind of study can be done for other cases to see whether or not it is a general trend.
For right now, however, I will have to say that Sanford’s contention that genomes deteriorate over time, despite the work of natural selection, now has even more evidence in its favor.
REFERENCES
1. John C. Sanford, Genetic Entropy and the Mystery of the Genome, Elim Publishing 2005, p. 83
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2. Robert W Carter and John C Sanford, “A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918”, Theoretical Biology and Medical Modelling, 9:42, 2012 (Available online)
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Fascinating. It does make sense that all genomes will eventually “wear out” due to mutations, since even beneficial mutations typically involve the loss of information. I have a question though. I’m under the impression that since viruses are not alive, the only way they can change is if the cell they have infected makes an error while producing new viruses. So when we say that a virus “mutates”, is that just short for “the virus is mutated by the cell”, or is there actually some sort of action performed by the virus itself in this process?
Excellent question, Keith! You are correct that viruses are not alive, since they cannot reproduce on their own. Instead, they must use a cell’s chemical machinery in order to reproduce. Thus, it is the cell’s machinery that makes the errors that end up mutating a virus. So you are correct – when we say that a virus “mutates,” it is short for “the virus is mutated by the cell.”
A virus built on DNA is less likely to be mutated by its host cell, because the DNA-based virus can use most of the cell’s error-checking processes to make sure the DNA is copied correctly. As a result, DNA-based viruses don’t mutate very often. A virus built on RNA often has to bypass many of those same error-checking processes. As a result, the cell copies the genome in a sloppy way, producing lots of mutations. The influenza virus is an RNA virus, which is why it mutates so quickly.
Thanks for that clarification, Dr. Wile. I thought it was strange that people seemed to use active verbs with viruses so often. I guess it’s just easier to describe them that way.
I would also assert that even in the greatest of cases for natural selection (namely, macroevolution), the new specimen is going to be facing new mutations thanks to the fact that macroevolution is based on mutating organisms. So not only could natural selection be poor at rooting out mutations we currently have, but it is supposed to be creating new ones all the time.
I am not sure I understand, Jacob. Natural selection doesn’t create mutations. It acts on mutations. The serious question is how efficiently does it weed out the bad ones and keep the beneficial ones? Based on this study, the answer is “Not efficiently at all.”
I guess, now that I reread my statement, I am slightly confusing. Allow me to restate my intention. When I mean the “greatest of cases,” I mean the addition of information due to a mutation. Because new information is added, therefore that information is bound to have mutations of its own that will result in a loss of information. The new specimen, the one created from that information, therefore experiences exotic forms of mutation. I hope that makes more sense. :/
Ah…Now I understand what you mean. An evolutionist would say that those mutations are weeded out by natural selection, even though this particular study says that doesn’t work very well.
If the H1N1 virus has been degrading and becoming less virulent since 1918, shouldn’t there have been even more virulent strains before 1918? If there were any, I am not aware of them. The 1918 H1N1 strain seemingly came out of nowhere. The explanation must be more complex than a simple progression from more virulent to less virulent strains.
Greg, the paper gives background on the H1N1 virus and what the current thinking is on how new virus strains arise. It says that aquatic waterfowl are a natural influenza reservoir. They are not strongly affected by the virus, but they carry it. They say that all 14 influenza subtypes are maintained in this reservoir. According to them, the data demonstrate that most of the major innovations within the flu genome are the result of one flu strain recombining with another strain and getting RNA from the second strain. Thus, the idea is that those 14 subtypes are all hanging out in the waterfowl population. When the right situation occurs, this “reassortment” happens, producing a new strain. Once that new strain emerges and starts infecting different populations, it deteriorates due to mutation, losing virulence with time.
There’s a good reason why Dr. Sanford’s claims in his popular press book Genetic Entropy have been virtually universally rejected by the scientific community.
That some pathogens tend to reduce their virulence over time has been known to science for decades. There are several hypotheses for why this occurs, the best supported being the Trade-Off hypothesis. A pathogen that is 100% lethal will soon have no hosts and will die out itself. One that is too weak stands the chance of the host developing effective immunity. The evolution of virulence in the pathogens is thus a balance between the costs and benefits of virulence to the pathogen. It has nothing to do with the genome of the pathogen “degrading” (whatever that means) from some mysterious “perfect” original.
The trade-off hypothesis was tested and demonstrated with malaria by Mackinnon and Read(2004) and Paul et al(2004)
Mackinnon, M; A Read (2004). “Virulence in malaria: an evolutionary viewpoint”. Philosophical Transactions of the Royal Society of London Series B-Biological Sciences 359 (1446).
Paul, R; T Lafond, CDM Muller-Graf, S Nithiuthai, PT Brey, JC Koella (2004). “Experimental evaluation of the relationship between lethal or non-lethal virulence and transmission success in malaria parasite infections.”. BMC Evolutionary Biology 4.
Thanks for your comment, Thorton. I suspect there is a reason why Dr. Sanford’s claims have been rejected. However, that reason isn’t based on evidence, as the evidence supports his claims.
I think you need to read those studies you cite more carefully, as they don’t talk about pathogens reducing their virulence. They discuss how pathogens increase their virulence up to a point, and then it levels out. As the first reference you give says:
The second reference tests the idea. It finds some inconsistencies, but in the end, it concludes:
This is quite different from what Sanford and Carter demonstrate in their paper. The claim in the references you cite is that virulence increases to an upper limit. However, Sanford and Carter show a constant rate of mutation, and many of those mutations are deleterious, but only slightly. However, as predicted in Sanford’s book, as those slightly deleterious mutations build up (because natural selection cannot weed them out), the fitness of the virus decreases. As a result, it constantly becomes less virulent.
jlwile
I suspect there is a reason why Dr. Sanford’s claims have been rejected. However, that reason isn’t based on evidence, as the evidence supports his claims.
Sanford opined that the human genome is somehow “degrading” and claimed that as a result human life spans are decreasing. However, for his primary “scientific” evidence of this he offered the supposed ages of Noah and his descendants as recorded in the Bible.
Like I said, there’s a good reason why Dr. Sanford’s claims have been virtually universally rejected by the scientific community.
However, as predicted in Sanford’s book, as those slightly deleterious mutations build up (because natural selection cannot weed them out), the fitness of the virus decreases.
You seem to be just as confused as Sanford. The virulence of the virus does equate to its evolutionary fitness. Indeed, if a less virulent strain allows the host to live longer and gives the pathogen more time to reproduce in greater numbers and infect others the pathogen’s evolutionary fitness would be increased, not decreased.
Like many well meaning YECs, Sanford is so desperate to prop up his literal Biblical beliefs he makes a total shambles out of the science. Not the first time it’s happened by far, and sadly it probably won’t be the last.
Thanks for your reply, Thorton, but I do think you need to read Sanford’s book. He does not use the ages of Noah and his descendents as evidence for his views. The book is 202 pages long, and the discussion of Noah and his descendents takes up less than 2 pages of content. Thus, he is not building his case with those data. He doesn’t even take up the discussion of Noah and his descendents until page 148, by which time he has already built his case for genomic decay.
What is the purpose of showing the data relate to Noah and his descendents? Sanford tells you himself:
Of course, that is a false dichotomy. There are other possibilities, such as the author was just really lucky. However, the most reasonable conclusion is that the ages are real. Rather than using the ages as evidence of his views, then, he shows that the ages are consistent with the other data that indicate genomic decay, which adds evidence to their veracity.
I do think you are rather confused about viruses and their virulence. As the papers you cited in your first comment state, natural selection is supposed to increase virulence of a virus to a specific value, and then it is supposed to maintain that value. That way, the fitness of the virus is maximized. That’s clearly not what happened in the case of H1N1. As Sanford and Carter show, the deleterious mutations increased, and with them, the fitness of the virus decreased. That’s why no H1N1 outbreak has ever come close to the scale of the 1918 outbreak. This fact, of course, confirms Dr. Sanford’s view, which the data presented in his book also confirm.
Like many well-meaning evolutionists, many have rejected Sanford’s views not because of the evidence, but because they are devastating to the evolutionary worldview. Indeed, Sanford himself says that when he followed the evidence, he was forced to give up the evolutionary worldview. Unfortunately, this isn’t the first time evolutionists have ignored the data, and sadly it probably won’t be the last.
As Sanford and Carter show, the deleterious mutations increased, and with them, the fitness of the virus decreased.
Of course Sanford showed no such thing. He had no way to measure the evolutionary fitness of either the original strain of the more recent ones. If makes a great hand-waving story to gull untrained laymen, but that’s about all it does.
Sanford’s use the Bible for his “scientific” data is one of the reasons (and not the only one) he and other YECS aren’t taken seriously by the scientific community. It’s great for selling popular press books to the true believers but only elicits chuckles from professional researchers.
Why is the DNA of Otzi the Ice Man who lived some 5300 years ago virtually identical to the DNA of extant humans and shows no sign of being closer to some “perfect” ideal? Why were the fragments of DNA recently recovered from two 7000 year old human remains in Spain also identical to extant humans?
Sanford is well meaning but severely self-deluded by his religious views. He sees only what he wants to see, as do most YECs. Fortunately real science doesn’t work from those narrow ideological restrictions.
Thorton, you must not have read the paper that this OP describes, as Sanford and Carter make a very strong case that the fitness of the virus decreased with time, in perfect harmony with Sanford’s genomic decay model. Since this paper was peer-reviewed, it obviously convinced more than “untrained laymen.”
You obviously haven’t read Sanford’s book, either, because he doesn’t use the Bible for scientific data. Instead, he uses the data to show that the Bible’s reporting of patriarchal ages is reasonable.
I think you need to read a bit more about Otzi the Ice Man, because his DNA is quite different from modern humans. For example, his mitochondrial DNA is so different from modern humans that one of the scientists who published the sequenced mitochondrial DNA says:
In addition, the Spanish DNA you mention is also completely consistent with Dr. Sanford’s views. As the article that reports on the DNA says:
So the mitochondrial DNA indicates not nearly as much variety as we see today, because there hadn’t been a lot of decay. In addition, the nuclear DNA is so different that its owners cannot be related to the current populations in that area.
Most evolutionists are well meaning but severely self-deluded by their commitment to the evolutionary worldview. They see only what they want to see. Fortunately, real science follows the data, so in time, this narrow viewpoint will be corrected.
Very cool. The first thing I thought of was how gonorrhea was so deadly at first and then slowed down to annoying. It’s a good thing everything is decaying together or we’d be really sunk!
Excellent point, Cheri!
Thorton, you must not have read the paper that this OP describes, as Sanford and Carter make a very strong case that the fitness of the virus decreased with time, in perfect harmony with Sanford’s genomic decay model.
LOL! They didn’t do any testing of the evolutionary fitness at all. The term is only mentioned twice in the whole paper, where they claim with zero evidence the genetic changes are “tightly correlated with rapid fitness decline”.
You obviously haven’t read Sanford’s book, either, because he doesn’t use the Bible for scientific data.
LOL again! Of course he and Carter did. From the book
Sanford: “A recent paper by a mathematician and a theologian presents some fascinating data (Holladay and Watt, 2001 [Evangelical Theological Society Papers; 52nd Natl. Conf., Nashville TN]). Their paper compares the lifespan of early Biblical characters to how many years they were born after the patriarch Noah. This Biblical data (recorded thousands of years ago) clearly reveals an exponential decay curve).”
Carter even has an article on CMI defending his use of the Bible data and referencing Carl Wieland’s equally scientifically vacuous claims.
I think you need to read a bit more about Otzi the Ice Man, because his DNA is quite different from modern humans.
Here is the whole article you quote-mined.
Complete mitochondrial genome of 5,000-year-old mummy yields surprise
Including “The surprise came when we found that the lineage of the Iceman did not fit any of the three known K1 clusters,” Rollo said. His team has informally named the newly discovered branch on the human family tree “Ötzi’s branch.”
“This doesn’t simply mean that Ötzi had some ‘personal’ mutations making him different from the others but that, in the past, there was a group—a branch of the phylogenetic tree—of men and women sharing the same mitochondrial DNA,” Rollo said. “Apparently, this genetic group is no longer present. We don’t know whether it is extinct or it has become extremely rare.”
Nothing in there at all about Otzi having a “non-degraded” human genome. Looks like you imagined that part.
So the mitochondrial DNA indicates not nearly as much variety as we see today, because there hadn’t been a lot of decay.
LOL yet again! We didn’t see as much variation then as today because the human population was 1400X smaller than today (5 million v. 7 billion). It has nothing to do with any imagined “decay”.
The way you can twist and cherry-pick evidence to fit your narrow pre-conceived religious notions is quite remarkable.
BTW, how do these discoveries fit in with the YEC supposed Noah’s Ark timeline? Why don’t we see evidence of a severe genetic bottleneck in all animal species if they all came from the lucky few who survived the Flood?
Thorton, it’s unfortunate that you aren’t willing to read the paper to look at the evidence. Sanford and Carter bring up several lines of evidence to support their case, including rapid and monotonic accumulation of mutations during a single pandemic, continuous and rapid accumulation of mutations over the entire history of the virus, a steady increase in nonsynonymous amino acid substitutions, and a significant decline in codon bias. They then show that these characteristics are correlated with a decline in the survivability of the virus. Thus, they do show a lot of evidence to support that fitness decreases over time. This, of course, is why the peer-reviewers allowed them to write:
And once again, you clearly haven’t read Sanford’s book. The quote you give is followed by the quote I gave:
So Sanford is not using the Biblical data to support his claim. He is showing that the Biblical data fit the expected pattern, which adds weight to the Biblical data’s veracity. Also, the quote you cite makes it clear that the analysis was not even his. He is mentioning it as a sidelight – a way that his views intersect the work of other scholars. This, of course, is evident, because he spends less than two pages discussing it. You claimed it was his “primary” evidence. Obviously, that’s not true.
Thanks for linking the excellent article by Carter, but you really need to read the articles before you link them. Nowhere does Carter even mention the Biblical data. He is simply making the distinction between a person’s maximum lifespan and his actual lifespan to explain why human lifespans are currently increasing. It is an excellent response, of course, clearing up confusion that often exists in evolutionary circles. It does not even touch on the Biblical data, however. Also, you might want to note that Dr. Carter is not Dr. Sanford. Thus, if you are trying to make the case that Dr. Sanford uses Biblical data to support his claims, you should probably stick to the writings of Dr. Sanford!
Regarding Otzi the Ice Man, the article you link is not the article from which I quoted. I linked the article from which I quoted, and you didn’t seem to read it, just as you haven’t read the Sanford and Carter paper, Sanford’s book, or the excellent article by Dr. Carter that you linked. I think I am detecting a pattern….
However, the quotes you give accurately summarize the issue and demonstrate that you are wrong. Remember what you wrote regarding Otzi the Ice Man:
As the quotes you provide demonstrate, the DNA of Otzi the Ice Man isn’t anywhere close to “virtually identical” to the DNA of extant humans. Thanks for demonstrating yourself to be wrong. That makes my job much easier!
Indeed, Otzi the Ice Man’s DNA is so different that the authors have to imagine that everyone who shared his DNA went extinct! That’s the only way they can think to explain the significant difference that exists between Otzi the Ice Man and modern humans. However, that’s simply because they are constrained by their narrow view. Since they are forced to believe in evolution, they have to come up with some way to explain around the fact that Otzi the Ice Man’s DNA is so significantly different from modern humans. However, the difference is more easily explained by genetic entropy.
The main point, however, which your own quotes demonstrate, is that you were quite wrong in claiming that Otzi the Ice Man’s DNA is “virtually identical” to that of extant humans. It is significantly different, which is just one more piece of evidence on the large pile of evidence that supports Dr. Sanford’s view.
In terms of the Spanish DNA, you claim that the supposed small population of humans back then explains the uniformity. However, I suspect that the authors of the paper which presents the DNA results believed in a small population back then, and yet they say that their result “…suggests a remarkable genetic uniformity and little phylogeographic structure over a large geographic area of the pre-Neolithic populations” (emphasis mine). The word “remarkable” suggests that they didn’t expect such strong uniformity.
Nevertheless, even if you want to explain around the uniformity by positing a smaller population, the fact is that this result is exactly what one would expect using Sanford’s model, so once again, this is simply more evidence to support Dr. Sanford’s claim. Also, the data once again demonstrate that you were wrong in claiming that the Spanish DNA is “identical” to modern human DNA.
You ask about evidence of a genetic bottleneck caused by the Flood. Of course there is strong evidence for just such a genetic bottleneck. In the human population, where the DNA is studied extensively, we see exactly the genetic bottleneck you would expect from a Flood event. In addition, the fossil record provides strong evidence for a genetic bottleneck in animals. After all, in the YEC model, the majority of the fossil record comes from the Flood. Thus, it is a “sample” of the phenotypic diversity at the time of the Flood. We see an enormous amount of diversity among all phyla in the fossil record. We don’t see nearly that kind of diversity in the extant species. This is exactly what you would expect from a genetic bottleneck.
I admire your patience and civility, Dr. Wile.
Thank you Greg.