This continues our coverage on the 2020 annual National Conference on Christian Apologetics (NCCA), hosted by Southern Evangelical Seminary (SES) in Charlotte, NC. We focus mainly on faith-and-science and other natural theology issues. Previous posts in this series are:
Here we discuss a talk presented by John Sanford, titled Genetic Entropy – We are Going Down, Not Up! In this presentation it is claimed that deleterious mutations accumulate in populations faster than they can be removed by natural selection, and so all populations are degenerating at some significant rate. Not only is “upward” evolution impossible, but the implication is that life cannot possibly have existed on earth for millions of years. (This supports a young earth creationist perspective).
Dr. Sanford put forth a variety of scientific evidence to support this claim. We examine this evidence and find that none of it actually supports the claim of universal “genetic entropy”. Real world data for typical plants, animals, and microorganisms show that they do not demonstrate universal genetic degradation.
First, it is helpful to clarify the fundamental contention of this talk. All living things go through a life cycle of production (“birth”), growth, reproduction, and death. As long as individuals can keep surviving long enough to produce another generation of viable offspring, the population can continue. The production phases (e.g., making egg and sperm, in mammals) involve cell division, where one cell turns into two cells. Part of cell division is for the DNA-based genome of the original cell to get copied to become part of the new cell. There are error-correcting mechanisms in cells to ensure this DNA copying is done with great accuracy, but there can still be some differences between the new and original cell genomes. These changes are known as mutations, which can be passed down to the next generation.
A given mutation may have a positive or negative effect on the fitness of the next generation organism, or practically no effect at all (neutral). If a mutation is greatly detrimental, the child organism does not survive and reproduce, so that mutation is not passed on to the gene pool. That is natural selection in action. Deleterious mutations with lesser effects may or may not be eliminated.
The key claim in this talk is that harmful, heritable mutations accumulate from generation to generation AND that these deleterious mutations cannot be removed by natural selection and cannot be compensated for by beneficial mutations. Therefore, the genomes of all species everywhere are inevitably declining. For the human genome, a loss of fitness of around 1% per generation was claimed.
Most biologists, on the other hand, hold that in typical large populations there are enough beneficial mutations to compensate for whatever deleterious mutations are retained in the gene pool. Some of these beneficial mutations might be simply reversals of a previous deleterious mutation. This can explain why in real world observations, populations survive for many thousands of generations with no apparent decline in fitness. Small animals like rabbits have been around for thousands of years of human history encompassing thousands of generations, with no remarkable change in fitness. Fossil alligators of eight million years ago looked almost exactly like today’s gators, and were not much different even thirty million years ago. This contradicts Dr. Sanford’s claim that, due to relentless genetic decay, “no species can endure through millions of years”. (Most individual species actually only endure a couple of million years in the fossil record, but there is no evidence that they go extinct because of universal genetic deterioration; rather, they evolve into other, similar species or are eliminated by changes in environment or by competing species. But this is too large a topic to fully pursue here). Fish similar to today’s fish (not the exact same species) have been around for some 400 million years. (Yes, the earth really has been around that long).
These observations demonstrate that Dr. Sanford’s claim of universal genetic entropy is simply wrong. He claims it is universal, but there is typically no evidence for it. Mutational meltdowns only occur in unusual situations. But let us examine the scientific evidence he offers in support of his contention.
Five types of scientific evidence were presented in this talk, as listed on the following slide:
From the discussion above it is immediately obvious that the first four scientific evidences presented above are irrelevant rhetorical devices:
( 1 ) Yes, “energy dissipates” (i.e., heat flows from hot regions to cold regions) – – But how does that show that deleterious mutations will overwhelm beneficial mutations?
( 2 ) Yes,” matter tends towards disorder” (increase in entropy), in general and on average – – But how does that show that deleterious mutations will overwhelm beneficial mutations?
Dr. Sanford invoked examples of human-built devices like automobiles, which eventually rust and fall apart. But populations of living cells are not human-built devices. More importantly, Dr. Sanford did not tell his hearers is that this thermodynamic increase in disorder and entropy only holds for closed systems, and even there it only holds on average. Order can increase in some parts of a closed system, though it will always be offset by an increase in entropy in some other part of the system.
Likewise, in an open system, where there can be exchange of energy from outside that system, order can spontaneously increase (entropy can decrease). A simple example of this is a puddle of water outside when a mass of very cold air sweeps in. Because heat from the puddle is transferred to the air, you may come out in the morning to find some or all of the puddle frozen. Going from liquid water to crystalline ice is a definite increase in order (decrease in entropy) for the puddle; this is balanced by an increase in entropy of the air. We were likewise not told by Dr. Sanford that the earth is an open system, receiving light energy from the sun which drives photosynthesis, and we were not told that each cell is an open system, exchanging chemicals and heat with its environment. Cells routinely import nutrients to drive their metabolisms, and export waste products. This demolishes the whole entropy argument against evolution.
( 3 ) Yes, in humanly devised systems, information tends to get corrupted upon transmission and copying. And yes, there are mutations that accumulate in living things. We knew that already. But this observation does not address the key issue of the long-term net effect of these mutations (balance of beneficial and detrimental) on the fitness of the species.
( 4 ) Yes, humans and other long-lived animals accumulate thousands and thousands of mutations in the various cells in our bodies (especially skin cells), which are implicated in our aging and eventual death. This of course is quite dire and poignant for us as individuals, but this is just an emotional distractor by Dr. Sanford. He did not clarify that nearly all these thousands of mutations that occur in our bodies after birth have nothing to do with the evolution or degradation of the species.
With animals, mutations can occur in the genome of any cell in the body. The vast majority of these mutations cannot have any effect on the viability of the population as a whole. For instance, if at age 50 I suffer some skin cell mutation that leads to fatal cancer, that mutation is not something that would be passed down to my children. Only mutations in the genome of a “germ line” cell (e.g., egg or sperm) get passed to the next generation, and again the key issue is the net effect of beneficial and deleterious mutations.
The first four of the scientific evidences presented by Dr. Sanford are irrelevant distractors, which are easily disposed of. The fifth area, population studies, is more relevant and more complex, and requires more technical explanations for proper assessment.
The omission of key facts by Dr. Sanford becomes notable here. As we know from political ads and other examples, if you selectively present some facts and suppress others, you can “prove” practically anything you want.
Mutation Accumulation in Fruit Flies and Yeast
Under normal circumstances (large population, multiple offspring to allow for the unfit to be weeded out, no unusual environmental stress, etc.), species do not demonstrate genetic degradation. We mentioned above the examples of rabbits and alligators. The same holds true nearly anywhere we look. The effectiveness of natural selection depends in part on each generation producing a large number of offspring, such that less-fit individuals carrying deleterious genes get eliminated, and more-fit individuals can access a larger share of environmental resources.
In order to assess Dr. Sanford’s claims about the genetic degeneration of the human race, we must first establish the impact of doing things that reduce the normal operation of natural selection. Let’s start with the common fruit fly, genus Drosophila. The particular species often studied is Drosophila melanogaster. Fruit flies breed on life cycles as short as ten days from egg fertilization to adult, but let’s use 20 days as an average generation time. This gives about 18 generations per year.
There is no reason to believe fruit flies have not been around for at least the past 4000 years or so of recent human recorded history. In that timespan, there have been about 72,000 generations of fruit fly. Now let’s do a little math. Suppose the fitness of fruit flies were long-term declining by some tiny amount like 0.05% per generation. How would the fitness of today’s fruit fly compare to those in 2000 B.C., approximately the time of Pharoah Mentuhotep II in Egypt’s Middle Kingdom? If we raise 0.9995 (i.e., 1- 0.0005) to the 72000 power we find that the fitness of today’s fruit flies should be 0.000000000000000023 that of Mentuhotep’s flies. That is indistinguishable from zero fitness. In other words, if there were any meaningful consistent “genetic entropy” occurring with fruit flies, they would all be dead by now. Yet, they are still here.
Drosophila populations have been studied intensively in laboratory for over a hundred years. In that timespan there have been something like 1800 generations. Fitness is measured in various ways. If there were a general trend of large control populations or of wild populations declining in fitness, surely it would be well-known by now. I was unable to find mention of this in the literature.
Everything changes, though, if the flies are not allowed to breed together in large numbers and purge the population of bad mutations naturally. Researchers have run various “mutation accumulation” experiments, where for each generation, a single brother-sister pair is randomly selected and mated. Every new mutation from each mating is added to all the previous mutations. There is no chance for letting less-fit individuals be out-competed by more-fit individuals, and thus there is no chance of weeding out bad mutations or favoring good mutations.
In these mutation accumulation experiments or small population studies, researchers typically find that the fitness of the flies declines significantly, sometimes to the point of a line of flies dying out altogether. For instance, in 2002 Avila and Garcia-Dorado found that out of an initial 200 separate lines of Drosophila maintained in mutation accumulation mode, 107 lines (more than half) had died out by generation 255. This dramatically illustrates the impact of not allowing normal natural selection to operate.
(Side comment on fruit fly mutations – – attempts to accelerate their evolution by inducing mutations by means of radiation and chemicals have been a failure. These massive, alien assaults on the genome can overwhelm the normal mechanisms of selection. Also, a successful organism like the fruit fly which has been around for a long time has likely evolved by now to a local optimum. Thus, in the timespan of human observation (hundreds or thousands of years) we would not expect to see much in the way of further large improvements in their genomes due to random mutations.)
One more mutation accumulation example: Common yeast, Saccharomyces cerevisiae, has been in play since ancient times for making wine. Yeast is a eukaryote, with the complex genome and internal cell structures (nuclear membrane) and organelles such as Golgi bodies, mitochondria, and lysosomal vesicles which are also possessed by plant and animal cells. It can double its count in as little as two hours, but let’s use 4 hours. Starting again from 2000 B.C, we find there have been nearly 9 million generations of yeast. As with the fruit fly, if there were any trace of the type of systematic genetic deterioration per generation as claimed by Dr. Sanford, we would have no yeast today. Thus, whatever the normal mechanisms are for weeding out deleterious mutations and promoting beneficial mutations, they seem to work just fine in normal populations of yeast.
As with fruit flies, however, if normal natural selection is curtailed, the fitness of a yeast population can decline fairly rapidly. A partial mutation accumulation experiment on yeast was run by Dickinson in 2008. In his experiment 48 separate lines of yeast were maintained for 4800 generations. Every 3-4 days, or approximately every 24 generations, the population in each line was reduced to a single individual, and asexual reproduction for that line was resumed from that individual. There were a total of 200 such population bottleneck cycles. The effect was about the same as if a constant population size of ten individual yeasts were maintained in each of the 48 lines. Fitness was assayed at the start and at three more points in the experiment.
Fitness Trajectories for 48 lines (populations) of yeast, from Dickinson (2008) mutation accumulation experiment. Copyright Genetics Society of America.
Though there was a clear trend on average towards reduced fitness, there was a wide variety in the responses of the 48 individual yeast lines, as shown in the figure above. The heavy line shows the average (mean) fitness of all 48 lines at each evaluation point. For any experiment that tries to quantitate fitness, some measurable quantity must be chosen as an estimator of fitness. Here, growth rates of samples from the experimental lines, compared to the parent, were used to estimate fitness. Most individual lines showed little change in fitness, some showed dramatic decline, and a few actually showed slight fitness improvement. Dickinson estimated that about 25% of the mutations occurring in this experiment were beneficial (which incidentally contradicts Dr. Sanford’s claim that beneficial mutations are very rare and ineffective). The average fitness declined significantly (by about 5%) over the course of this experiment which lasted about two years. As with fruit flies and many other species, when normal natural selection in yeast is curtailed, harmful mutations do accumulate and population fitness does decline. But if I told you that this shows that populations in general are inevitably declining, you would (or should) tell me that I was grossly misrepresenting matters.
Surmises of Human Genome Deterioration in the Industrialized World
Armed with these insights on mutation accumulation when natural selection is artificially curtailed, let’s turn to Dr. Sanford’s claims about the human race. Here is how he presents the matter:
He presents quotes from leading geneticists such as James Crow and Michael Lynch and others who opine that the global human gene pool is rapidly declining in quality, and he claims that this supports his claim of universal “genetic entropy”. This seems impressive at first. But to claim that these conjectures support general genetic deterioration is misleading to the point of deception.
These researchers do not cite any hard evidence that the human race is actually deteriorating, and do not tie their assertions to any general failing of evolutionary processes. What they base their opinions on is this: in modern industrial society families are having fewer children, and improved nutrition and medical technologies are keeping less-healthy people alive. In the past, a female might have had four or five children, of whom several would die before reaching reproductive age or have difficulty in competing for mates. Now we have few children per family, and we keep nearly everyone alive (including those with obvious genetic vulnerabilities and disease conditions) such that their genes are passed along without much in the way of natural selection. In effect, we are now running a global mutation accumulation experiment. This is a very abnormal situation, and this abnormal condition is why geneticists are deeply concerned. Dr. Sanford withheld from his audience this crucial fact that the present human situation is not at all typical of natural populations or even of human experience before 1800 or so.
In his talk Dr. Sanford displayed a dire quote by Lynch (PNAS 107:961-968) saying that in the next few centuries there may be “…significant incapacitation at morphological, physiological and neurobiological levels.” But in that paper Lynch makes it clear that the only reason he raises his concerns is the recent low-selection regime we are in:
The motivation for this concern is the enormous change in the selective environment that human behavior has induced during approximately the past century. Innovations spawned by agriculture, architecture, industrialization, and most notably a sophisticated health care industry have led to a dramatic relaxation in selection against mildly deleterious mutations, and modern medical intervention is increasingly successful in ensuring a productive lifespan even in individuals carrying mutations with major morphological, metabolic, and behavioral defects…The fundamental requirement for the maintenance of a species’ genetic integrity and long-term viability is that the loss of mean fitness by the recurrent input of deleterious mutations each generation must be balanced by the removal of such mutations by natural selection.
Lynch holds that natural selection was operating adequately in pre-industrial human society. Indeed, the gene pools of the remaining “primitive” people groups may be valuable resources to help the rest of us cope:
The mean phenotypes of the residents of industrialized nations are likely to be rather different in just two or three centuries, with significant incapacitation at the morphological, physiological, and neurobiological levels. Ironically, the genetic future of mankind may reside predominantly in the gene pools of the least industrialized segments of society.
The full text in this paragraph above shows that Lynch’s statement regarding “significant incapacitation at the morphological, physiological, and neurobiological level” was wrenched out of its context (i.e., only industrialized, low-selection societies) by Dr. Sanford in his presentation and thus misused.
The same holds true for similar quotes that Dr. Sanford cites from James Crow, and for all the other geneticists who share Lynch’s fears for modern society. When Crow was made aware that young earth creationists like Dr. Sanford were using his conjecture (i.e. that agrarian and industrial lifestyles lead to mutation accumulation) to support their claims of rapid general genetic deterioration, Crow responded to clarify that his concern was only that “in recent years, as a result of environmental improvement, the effect of natural selection was diminished”:
Harmful mutations occur every generation, but are eliminated by natural selection. Although most mutations are harmful, some are favorable and these are retained and increased by natural selection. This has been going on for billions of years.
I suggested in the article that in recent years, as a result of environmental improvement, the effect of natural selection was diminished. If this is correct, there are probably more harmful mutations in the population than there were a thousand or so years ago…My comments had to do with only the recent past (a few thousand years). In the long run, harmful mutations are eliminated by natural selection. Both mutations and natural selection have been going on since life began, billions of years ago.
In his talk, Dr. Sanford did mention in passing that these geneticists think that this degeneration only applies to recent times, but he did so in a very dismissive way, “They need to believe that sometime in the past we weren’t degenerating.” This would lead his hearers to think that that geneticists are being somehow arbitrary and unreasonable in holding that we weren’t degenerating in the past. That is gross misrepresentation. The reason geneticists believe that “sometime in the past we weren’t degenerating” is that trends in birthrates and mortality have hugely affected the operation of natural selection, so the human situation is far different now than it was hundreds of years ago. Also, we find that with normal, typical populations (e.g., with rabbits, alligators, fruit flies, yeast, etc., etc., etc.) natural selection is perfectly adequate to maintain population fitness. Furthermore, people looking like us have been around for over 100,000 years, and behaving like us for at least 50,000 years. Thus, it cannot be the case that human genomes in general have been rapidly deteriorating all that time, although naturally it is possible that small, inbred populations have suffered deterioration here and there. With nearly eight billion different versions of the human genome walking around the planet, it is clear that our genome can handle a wide variety of different mutations.
Dr. Sanford has been previously publicly corrected for misrepresenting geneticists’ concerns for human deterioration (e.g. here and here), so it is troubling that he continues to mislead his audiences in this regard.
The Lenski Long Term E. Coli Experiment
It is helpful to review the meaning of “beneficial” and “deleterious” mutations. These are mutations which make an organism either less fit or more fit, in some particular environment. There is no such thing as “fitness” in general, it can only be defined and measured in some defined environment. If a climate turned gradually colder and some sub-species developed white fur to blend in with all the snow, those mutations would be considered beneficial in that setting. But if the climate then suddenly warmed back to where it was, such that snow became rare, that white fur would be a liability, and all those lightening mutations would be now considered detrimental. But the mere possibility of future climate warming would not make the initial white-fur mutations “deleterious”.
Richard Lenski’s group has run a simple experiment for many years to monitor the spontaneous evolution of the common bacterium E. coli. They started with a certain strain of E. coli which was dispersed into twelve flasks contained liquid growing medium. Since then, every day a small sample is taken out of each flask and then placed in a new flask with fresh medium, allowing the culture of bacteria to keep growing. The main food for the E. coli is glucose, but not a lot of glucose is provided. The bacteria have therefore evolved to become highly efficient at digesting the limited glucose; laggards get out-competed and don’t survive. For simplicity, the flasks are kept at constant temperature and other conditions. Let’s see how the fitness of these populations have progressed under these conditions. Here are the fitness curves (as estimated by growth in cell volume) for all twelve populations for the first 12,000 generations:
Do we see “genetic entropy” here? No, not at all. We see the accumulation of beneficial mutations, making each of these twelve populations more fit for this environment. If we stretch the evaluation out to 50,000 generations, do we see evidence of universal genetic deterioration? No, the fitness of these populations just keeps rising, though at a slower rate:
Averaged fitness of evolved populations (compared to starting population) for first 50,000 generations of Lenski long-term E. coli experiment. Source: 13 December 2013 Vol 342 Science 1364-1367 M. J. Wiser, N. Ribeck, and R. E. Lenski. Black dots are experimental data, red and blue curves are fitted mathematical models.
This is typical behavior for populations which are put in a new environment. Their fitness may initially be low, but it moves up as beneficial (adaptive) mutations accumulate. Eventually they approach a fitness plateau or mutational equilibrium, when new beneficials are balanced by new deleterious mutations (and most mutations are effectively neutral). Dr. Sanford did not show his audience these plots of increasing fitness.
There is another interesting development in one of the Lenski experiment populations. Here is a blow-up of part of one of Dr. Sanford’s slides:
Notice that the liquid in all the flasks is fairly clear, except for A-3. That liquid is cloudy, indicating a large population (concentration) of bacteria in that flask. It turns out the growing medium contains a lot of a citrate chemical. Normally, under aerobic conditions like those used in this experiment, the E. coli are unable to metabolize citrate, though they can utilize it under anaerobic conditions. However, the bacteria in flask A-3 experienced a mutation involving making a duplicate copy of a gene with an altered regulatory region, plus other mutations elsewhere in the genome, all of which allowed this strain to feast on the large excess of citrate present in the growing medium.
This sort of rare but highly beneficial set of mutations is the type of mutation which can move a population forward from its previous fitness plateau. In this flask A-3, for several thousand generations some of the earlier E. coli persisted alongside the new, citrate-eating strain. Eventually the old non-citrate strain died out, but it was not because of generic mutational meltdown; rather, it was simply out-competed by the newly evolved strain. This episode did not result in a whole new species, but it illustrates some of the general principles of speciation and extinction.
This is just the sort of hugely beneficial, complex mutation, giving new functionality, which opponents of evolution say cannot possibly occur. (It is entertaining to read their attempts to downplay this citrate mutation). Dr. Sanford failed to discuss this mutation.
In the face of all this data showing accumulation of beneficial mutations large and small, Dr. Sanford claimed instead that the whole Lenski experiment was “Clearly an example of genetic degradation”. How could he possibly say such a thing? His claim is based on two rhetorical moves. First, he notes that the mutations which are beneficial in the Lenski experiment mainly involve genomic simplifications, which deactivate metabolic functions that are useless drains in the simple Lenski experimental environment. But here Dr. Sanford has subtly switched criteria, by conflating fitness (which can only be defined relative to the current environment) with genetic complexity. These are two very different issues. Genetic complexity may be beneficial or it may be deleterious, depending on the environment. Evolution is driven by actual fitness effects for actual organisms in actual environments, not by some abstract scorecard of genetic complexity.
The other rhetorical move is to note that if the Lenski bacteria were placed back into its original “wild” environment (with a wider variety of conditions and predators), the evolved bacteria would fare poorly. Well, of course they would fare poorly compared to bacteria that were still adapted to that wild condition, but it is unreasonable to demand that a population that becomes adapted to some new condition must also retain its full adaptation to old condition. That like expecting a bear species which had evolved a white fur coat for an arctic environment to remain competitive (with brown bears) in some non-arctic environment. It makes no sense. That just isn’t the way the world generally works.
Influenzas That Come and Go
Most forms of life have DNA-based genomes. In DNA replication (e.g., for cell division) there is a proofreading mechanism involving an enzyme called exonuclease which recognizes and corrects most copying mistakes. This keeps the mutation rate low for typical lifeforms. RNA viruses, however, lack this proofreading mechanism, and hence their mutation rates are extremely high. In the short term, this high mutation rate can be advantageous; it can help a new, virulent strain of say human influenza virus quickly evolve to become highly infectious and it certainly makes vaccine development more challenging to keep up with all the changes in the virus. But this mutation rate can be so fast and drastic that it overwhelms natural selection and contributes to the disappearance of that particular strain.
This unusual nature of RNA viruses makes them a potential candidate for observing the type of genetic deterioration that Dr. Sanford proposes. He and Robert Carter compiled and analyzed data on the infamous “Spanish flu” that killed tens of millions in the 1918-1920 timeframe. This was a particular strain of the H1N1 sub-type of the influenza type A virus.
Preserved samples of that influenza strain were preserved and are available for most years from 1918 onward. Carter and Sanford found a linear increase in the mutations with time, and a steady decrease in virulence, as estimated by excess deaths in the population due to the flu. (Effectiveness at killing the host is not the greatest estimate of viral “fitness”, but we will let that pass). The data do seem to indicate that this particular strain mutated itself out of general circulation.
Is this evidence for general “genetic entropy”, as Dr. Sanford implied in his talk? Not at all. The mutation accumulation regime with RNA viruses is much different than normal (DNA-based) organisms. In his talk Dr. Sanford did not emphasize how unusual RNA viruses are, although in their paper Carter and Sanford themselves acknowledge that special aspect of RNA viruses:
The literature suggests RNA viruses should be inherently subject to mutational degeneration…It is well known that numerous factors can cause a breakdown in the selective removal of deleterious mutations. These factors include a high mutation rate, a high rate of random loss, limited sexual recombination, genetic bottlenecking, and mutations with very small fitness effects. All of these factors should be especially pronounced in an RNA virus such as influenza and all of these are either previously known or documented here.
Moreover, for RNA viruses in general, if rapid genomic deterioration were really such a universal problem, all RNA viruses such as Type A influenza should have disappeared long ago. But they are still here. Although the particular Spanish flu strain has disappeared, related viruses (including other H1N1 variants) keep circulating and evolving and appearing in birds, pigs, and humans. “Horizontal” transfer of DNA/RNA between microorganisms is a common and important component of how they evolve. Here is a mapping of the relationships of some of these strains:
Source: Wikipedia (Click to enlarge image)
We noted earlier that with plants and animals, a particular species may go extinct, but often some offshoot of that species has evolved into a different species, so there is some ongoing continuity of genes. As it turns out, that is the case with the 1918 Spanish flu genome. As illustrated in the figure above, although the full embodiment of the original Spanish flu is not longer apparent, some of its genome is still present in the current seasonal flu:
You can still find the genetic traces of the 1918 virus in the seasonal flus that circulate today…Every single human infection with influenza A in the past 102 years is derived from that one introduction of the 1918 flu.
This lack of “genetic entropy” in global RNA viruses is something to ponder as you roll up your sleeve for your new flu shot next fall.
Dr. Sanford and his colleagues have devised a program which performs genetics calculations. The user can input various parameters and starting conditions, including levels of beneficial and deleterious mutations, and the program can calculate trajectories of population growth and decay. Dr. Sanford displayed calculation results that showed genetic decay for a given set of assumptions. There is no reason to doubt that it carries out its designated calculations with mathematical exactitude. But a model is only as good as the assumptions that go into it. If this model does not match all the real world displays of genetic robustness in decent sized populations of normal DNA-based organisms, the proper response is the correct the model, not to deny the real-world data.
Summary and Conclusions
Judging from the chat comments on this talk, Dr. Sanford’s presentation seemed to his lay audience to present a compelling cumulative case for rapid general genetic deterioration. All points of this the case fall apart, however, upon closer examination. The first four scientific evidences (energy dissipation, general tendency towards disorder, corruption of information in human-produced systems, and deleterious mutations in our body cells) have appeal to the imagination, but they are irrelevant distractors. They do nothing to address the key issue of whether natural selection plus the injection of new beneficial mutations is able to compensate for new deleterious mutations in a population.
The only empirical evidence for actual catastrophic accumulation of deleterious mutations presented by Dr. Sanford was for an RNA virus which is known to mutate wildly. He did not clarify to his audience that this virus is quite unrepresentative of normal living things. (In fact, biologists debate whether viruses should even be considered to be “alive”). The other example he offered was the speculation of geneticists that the human race is declining; he did not clarify to his audience that this is merely a speculation which is not based on actual data, and that this speculation is based on the very abnormal birth/death situation of modern industrial society. One can probably find evidence of harmful inbreeding in various small, isolated populations, but no evidence was offered that populations in general are suffering inexorable genetic decline.
In his treatment of the Lenski long term E. coli experiment, he did not show key results from that experiment which include a steady increase in fitness at the experimental conditions, and which show that some bacteria evolved a complex novel beneficial mutation which gave a significant new functionality. Instead, he downplayed the Lenski results by illogically conflating fitness with genomic complexity, and illogically complaining that a bacterial population that has adapted to a new environment will now be more poorly adapted to its old environment.
Dr. Sanford’s claim of universal genetic entropy is disproven by practically all known information on plants, animals, and microbes, as we have discussed above. His claim that beneficial mutations are “vanishingly rare” is likewise refuted by real world studies. A more extended critique of Dr. Sanford’s position is here.
In contrast, there is lots of hard data supporting evolution and the long-term history of life. For instance, the signature of viruses inserted into our genomes shows beyond reasonable doubt that humans and chimpanzees evolved from a common ancestor. The topic of fossils did not come up in the talk, but it is worth noting that, despite the attempts of opponents to deny it, the fossil record we have thoroughly supports evolution. See here for a discussion of how recent whale genetic and fossil results confirm specific predictions from evolutionary theory.
The evangelical opposition to evolution derives not from genuine science or even from the Bible, but from a particular (human) interpretation of the Bible. This creation/evolution controversy is reminiscent of the Galilean controversy of four hundred years ago. Although there were other political and philosophical issues involved, the core driver there was taking a literal interpretation of the many passages which describe the sun moving and the earth standing fixed on its foundation. The Roman Catholic Cardinal Roberto Bellarmine, a prosecutor of Galileo, stated in 1615: “…to affirm that the sun is really fixed in the center of the heavens and the earth revolves swiftly around the sun is a dangerous thing, not only irritating the theologians and philosophers, but injuring our holy faith and making the sacred scripture false.” Note well: “…injuring our holy faith and making the sacred scripture false.” That is exactly what today’s creationists say about an old earth and evolution, i.e., that these concepts injure our faith and make the sacred scripture false.
If we don’t get this right, we risk losing even more of our youth. If they are told in home and church that the Bible and evolution are incompatible, they will be pushed away from their faith once they get exposed to actual science and discover in high school or college that evolution is true. Also, the larger culture has turned against biblical Christianity with surprising rapidity. There are many key cultural and theological disputes that command careful attention. Maintaining an obviously ridiculous stance on a verifiable issue like evolution gives legitimate grounds for outsiders to distrust our treatment of other factual issues such as the evidence for the resurrection. Thus, evangelical Christians who desire to handle accurately God’s revelation in his works would do well to rethink their opposition to evolution.
The counsel of Saint Augustine in this regard is worth heeding:
Usually, even a non-Christian knows something about the Earth, the Heavens, and the other elements of this world, about the motion and orbit of the stars and even their size and relative positions, about the predictable eclipses of the sun and moon, the cycles of the years and the seasons, about the kinds of animals, shrubs, stones, and so forth, and this knowledge he holds to as being certain from reason and experience. Now, it is a disgraceful and dangerous thing for an infidel to hear a Christian, presumably giving the meaning of Holy Scripture, talking nonsense on these topics; and we should take all means to prevent such an embarrassing situation, in which people show up vast ignorance in a Christian and laugh it to scorn.
The shame is not so much that an ignorant individual is derided, but that people outside the household of the faith think our sacred writers held such opinions, and, to the great loss of those for whose salvation we toil, the writers of our Scripture are criticized and rejected as unlearned men. If they find a Christian mistaken in a field which they themselves know well and hear him maintaining his foolish opinions about our books, how are they going to believe those books in matters concerning the resurrection of the dead, the hope of eternal life, and the kingdom of heaven, when they think their pages are full of falsehoods on facts which they themselves have learnt from experience and the light of reason?” – St. Augustine, The Literal Meaning of Genesis (408 A.D) Book 1, ch.19. Bolded emphases added.
Appendix. More on Sanford’s H1N1 publication:
I later found this evaluation of the paper discussed above:
“…they manage to get everything wrong. Here’s a short list of the errors the authors commit:
They ignored neutral mutations.
They claimed H1N1 went extinct. It didn’t. Strains cycle in frequency. It’s called strain replacement.
They conflated intra- and inter-host selection, and in doing so categorize a bunch of mutations as harmful when they were probably adaptive.
They treated codon bias as a strong indicator of fitness. It isn’t. Translational selection (i.e. selection to match host codon preferences) doesn’t seem to do much in RNA viruses.
They ignored host-specific constraints based on immune response, specifically how mammals use CpG dinucleotides to recognize foreign DNA/RNA and trigger an immune response. In doing so, they categorized changes in codon bias as deleterious when they were almost certainly adaptive.
They conflated virulence (how sick a virus makes you) with fitness (viral reproductive success). Not the same thing. And sometimes inversely correlated.
Related, in using virulence as a proxy for fitness, they ignored the major advances in medicine from 1918 to the 2000s, including the introduction of antibiotics, which is kind of a big deal, since back then and still today, most serious influenza cases and deaths are due to secondary pneumonia infections. “