Does all of evolutionary theory rest on Fisher’s Fundamental Theorem?

The blogs of creationists and ID advocates have been buzzing with the news that a new paper by William Basener and John Sanford, in Journal of Mathematical Biology, shows that natural selection will not lead to the increase of fitness. Some of the blog reports will be found here, here, here, here, here, and here. Sal Cordova has been quoting the paper at length in a comment here.

Basener and Sanford argue that the Fundamental Theorem of Natural Selection, put forward by R.A. Fisher in his book The Genetical Theory of Natural Selection in 1930, was the main foundation of the Modern Evolutionary Synthesis of the 1930s and 1940s. And that when mutation is added to the evolutionary forces modeled by that theorem, it can be shown that fitnesses typically decline rather than increase. They argue that Fisher expected increase of fitness to be typical (they call this Fisher’s Theorem”).

I’m going to argue here that this is a wrong reading of the history of theoretical population genetics and of the history of the Modern Synthesis. In a separate post, in a few days at Panda’s Thumb, I will argue that Basener and Sanford’s computer simulation has a fatal flaw that makes its behavior quite atypical of evolutionary processes.

Was the mathematics of natural selection, and the mathematics of mutation, ignored in theoretical population genetics until Fisher’s 1930 book? Well, actually, no. Here is the major work on this before 1930:

1. In 1903, three years after the rediscovery of Mendel’s work, the mammalian geneticist William Ernest Castle showed in Proceedings of the American Academy of Arts and Sciences a numerical calculation of the elimination of a lethal recessive allele from population.

2. In 1915, in an Appendix to a book Mimicry in Butterflies by the well-known geneticist R. C. Punnett, H. T. J. Norton showed numerical calculations for a case of natural selection, showing that selection was effective in favoring an advantageous allele. Norton’s mathematical equations were not given until later, in 1928. Jennings (1916) and Wentworth and Remick (1917), in papers in Genetics, did further work on the elimination of recessive lethal alleles.

3. In 1922, R. A. Fisher published a major paper in the Proceedings of the Royal Society of Edinburgh, showing the algebra of natural selection for dominant alleles and for alleles of intermediate dominance, as well as the effects of mutation and of genetic drift (which he called the “Hagedoorn effect”). His treatment of genetic drift was pioneering, but made a technical mistake later corrected by Sewall Wright in 1929.

4. J. B. S. Haldane, starting in 1924, published a numbered series of papers under the general title “A mathematical theory of natural and artificial selection”, the first in Transactions of the Cambridge Philosophical Society and all the rest except the 10th in Proceedings of the Cambridge Philosophical Society. These treated many cases of natural selection and different mating systems.

5. In his 1927 paper in that series, whose subtitle is “Selection and mutation”, Haldane gives the probability of fixation of a new favored mutant when it is present in just a single copy in the presence of genetic drift. For infinite populations where genetic drift is absent, he derived the equilibrium frequency of a mutant allele when its increase is countered by natural selection.

6. In a paper in 1928 in American Naturalist, R. A. Fisher put forth an argument that natural selection would alter the degree of dominance of a deleterious allele that was recurring by mutation. Sewall Wright and he then debated this back and forth in that journal in 1929, with Wright arguing that the strength of selection on modifiers of dominance would be too weak to be effective, and that the recessiveness of many mutants was inherent in the biochemical kinetics of the genes. (Wright was backed up in this later by Haldane and by H. J. Muller).

7. Wright was already at work on the distributions of gene frequencies under natural selection, mutation, migration, and genetic drift. This work, which was the foundation of modern work using diffusion equations, was not published in full until 1931. An abstract Wright published in 1929 shows that Wright had many of the results by then.

Conclusion: the mathematics of mutation and natural selection had been well worked-out before R. A. Fisher published his 1930 book. That book puts forward many important and original arguments in addition to summarizing in verbal form the mathematics of natural selection and mutation. The Fundamental Theorem of Natural Selection is one of the least consequential things in the book — Fisher did not give a precise derivation, and what the terms mean has been the subject of a recent literature, with papers by the late George Price, by Anthony Edwards, and by Warren Ewens. The conclusions leave considerable doubt as to the fundamentalness of the theorem.

Thus the literature on the theory of natural selection, of mutation, and of their joint action, did not wait until 1930, and in its 1920s development did not rely at all on the Fundamental Theorem of Natural Selection. In addition, “Fisher’s Theorem”, so-called by Basener and Sanford, will not be found in Fisher’s work — he was in fact quite critical of Sewall Wright’s 1932 arguments that highlighted maximization of mean fitness as a major principle in evolutionary genetics.

I hope to follow this post up with one at Panda’s Thumb in the next few days, showing that the ineffectiveness of natural selection in Basener and Sanford’s simulations comes from an unfortunate choice of the parameters in their simulation.

126 thoughts on “Does all of evolutionary theory rest on Fisher’s Fundamental Theorem?

  1. So can we credit the Hagedoorns as being the first to document the concept of drift? I Googled quickly but I was unable fathom the paper I found. It was all Dutch to me!

    PDF

  2. Joe Felsenstein:

    natural selection will not lead to the increase of fitness

    I think it is more fair to say if a sufficient number of deleterious mutations are added in each generation, then natural selection will not be sufficient to increase fitness over time.

    My understanding is that Basener and Sanford’s conclusion actually agrees with your mutational load arguments in your book Theoretical Evolutionary Genetics pages 156-158 where you discuss the question : “Why we aren’t all dead“.

    http://evolution.gs.washington.edu/pgbook/pgbook.pdf

    From the standpoint of population genetics, the mutational load calculation is relevant. If there were 20 million genes, each subject to mutation at a rate 10−7 to deleterious alleles, the fitness of the population would be reduced to e−2 ≃ 0.15 of its potential value. If we assign an absolute meaning to the mutational load, this would mean either a 15% probability that a newborn would survive

    to adulthood (all risk coming from genetic disorders, with any death from environmental accident being on top of this) or else that fertility would be reduced by 85% by sterile or partially-sterile mutants, or an intermediate combination of these two. Clearly an organism with as much DNA as we have would be in severe trouble. Yet in humans well over 98% of all newborns survive to adulthood in most industrial countries


    The mutational load calculation continues to be relevant to understanding whether most eukaryotic DNA has any function that is visible to natural selection. Recent announcements
    (Encode Project Consortium, 2012) that 80% of human DNA is “functional”, based on finding some transcription or binding of transcription factors in it, are very misleading. Junk DNA is still junk DNA, however often its demise has been
    announced.

    It seems to me Basener and Sanford are recasting your mutational load arguments into Fisher’s equation.

    Your solution to the dilemma is to say ENCODE is wrong. It echoes Graur’s comment, “If ENCODE is right, evolution is wrong.” Basener and Sanford’s re-framing of Fisher’s Theorem arrives at a conclusion everyone seems to agree on: “If ENCODE is right, evolution is wrong.”

    Thank you any way for discussing Bill and John’s paper and taking time to read it. All of us have the highest respect for you even when we sharply disagree.

  3. I look forward to your Panda’s Thumb post.

    I had a look at the Basener and Sanford paper. To my mind, the problem is their choice of distribution for s’, the selection coefficient of a new mutation. In the region near zero, where drift dominates, alleles will have been fixed more or less at random, and hence the probability of a new mutation being deleterious should be about 1/2, not 999/1000. Near zero, the distribution should be very nearly symmetrical. It will become increasingly asymmetric in favour of deleterious mutations as you go away from zero.

    I wouldn’t describe this as ‘an unfortunate choice of the parameters in their simulation’ though, so I guess you’re thinking of something else?

  4. Graham853:
    I look forward to your Panda’s Thumb post.

    I had a look at the Basener and Sanford paper. To my mind, the problem is their choice of distribution for s’, the selection coefficient of a new mutation. In the region near zero, where drift dominates, alleles will have been fixed more or less at random, and hence the probability of a new mutation being deleterious should be about 1/2, not 999/1000. Near zero, the distribution should be very nearly symmetrical. It will become increasingly asymmetric in favour of deleterious mutations as you go away from zero.

    I wouldn’t describe this as ‘an unfortunate choice of the parameters in their simulation’ though, so I guess you’re thinking of something else?

    When you look at the references on which they based the 1000:1 ratio, they are all to chapters that Sanford wrote in the creationist book “Biological Information: New Perspectives”. I have my doubts regarding the neutrality of those citations. 🙂

  5. Graham583:

    the probability of a new mutation being deleterious should be about 1/2

    Isn’t anyone going to challenge this? This is the Skeptical Zone after all. John Harshman, are you going to let that claim slide?

  6. stcordova: Isn’t anyone going to challenge this? This is the Skeptical Zone after all. John Harshman, are you going to let that claim slide?

    If you actually read what he’s saying instead of cherry-picking two or three words, it’s perfectly reasonable. He’s assuming a continuous distribution of fitnesses, very locally symmetrical about 0, which seems entirely reasonable to me. If few mutations are absolutely neutral, it seems reasonable that very slightly deleterious mutations ought to be about as common as very slightly advantageous ones. In any large population, of course, they’re all effectively neutral. So, to sum up: try reading and trying to understand what is actually said rather than collapsing onto your fainting couch.

  7. stcordova: Isn’t anyone going to challenge this? This is the Skeptical Zone after all. John Harshman, are you going to let that claim slide?

    He’s saying that the ratio depends on the magnitude of the selection coefficient. That very close to neutral the ratio is 1 beneficial for every 1 deleterious, but as the magnitude of the fitness effect moves further away from neutral, the proponderance of deleterious mutations will rise.

    I simply don’t know whether such a view is correct. I’d like to see reference from anyone who makes claims about the ratios. Including from Sanford’s claims about the 1:1000 ratio.

  8. stcordova: Isn’t anyone going to challenge this? This is the Skeptical Zone after all. John Harshman, are you going to let that claim slide?

    Shouldn’t you also be skeptical about Basener and Sanford’s numbers? Have you asked them where they got them from?

  9. Rumraket:

    Shouldn’t you also be skeptical about Basener and Sanford’s numbers? Have you asked them where they got them from?

    You mean like the figures from evolutionists they cited in their paper:

    The predominance of deleterious mutations over beneficial ones is well established. James Crow in (1997) stated, “Since most mutations, if they have any effect at all, are harmful, the overall impact of the mutation process must be deleterious”. Keightley and Lynch (2003) given an excellent overview of mutation accumulation experiments and conclude that “…the vast majority of mutations are deleterious. This is one of the most well-established principles of evolutionary genetics, supported by both molecular and quantitative-genetic data. This provides an explanation for many key genetic properties of natural and laboratory populations”. In (1995), Lande concluded that 90% 90% of new mutations are deleterious and, the rest are “quasineutral” (Also see Franklin and Frankham (1998)). Gerrish and Lenski estimate the ratio of deleterious to beneficial mutations at a million to one (Gerrish and Lenski 1998b), while other estimates indicate that the number of beneficial mutations is too low to be measured statistically (Ohta 1977; Kimura 1979; Elena et al. 1998; Gerrish and Lenski 1998a). Studies across different species estimate that apart from selection, the decrease in fitness from mutations is 0.2–2% % per generation, with human fitness decline estimated at 1% 1% (See Lynch 2016; Lynch et al. 1999). Estimates suggest that the average human newborn has approximately 100 de novo mutations (Lynch 2016). Research using finite population models has been driven by the need to understand the impact of the buildup of deleterious mutations (called mutational load) in small populations of endangered species (See Lande 1995; Franklin and Frankham 1998). Of special interest is the mutational load in the human species given the relaxed selection due to social and medical advances (Kondrashov 1995; Crow 1997; Lynch 2016).

    Ok, how many beneficial mutations do you think are happening per human per generation? Give your best number. Then give an estimate of how many deleterious are happening per human.

    If you don’t know, or if no one knows, well, I think that’s a problem for evolutionary theory which claims to know, but which doesn’t really know. In that sense, evolutionists walk by faith, not sight, just like creationists.

  10. Alan Fox: It was all Dutch to me!

    It is about inbreeding depression (degeneration), correctly explained as an increase in the expression of recessive deleterious variants. Genetic drift is not explicitely mentioned, but perhaps Fisher saw a connection with loss of genetic variation in small inbreeding populations?

  11. Joe,

    I think you’re going to get a response along the lines of “Well, yeah, sure, that’s true, but the usual interpretation of FTNS by biologists, including teachers addressing students, was [something stupid, which we have corrected].”

    Have biologists been saying stupid stuff about FTNS? Has FTNS been played to rhetorical effect by people intent on “proving” that “Darwinian evolution works”?

  12. Nothwithstanding Joe Felsenstein’s comments on Basener and Sanford’s paper, I think, as far as I know, for a given reproduction rate and a given deleterious mutation rate, fitness will decline. This is known as mutational meltdown. It’s not like Basener and Sanford are the first to hypothesize this:

    https://en.wikipedia.org/wiki/Mutational_meltdown

    Mutational meltdown (not to be confused with the concept of an error catastrophe[1]) is the accumulation of harmful mutations in a small population, which leads to loss of fitness and decline of the population size, which may lead to further accumulation of deleterious mutations due to fixation by genetic drift.

    A population experiencing mutational meltdown is trapped in a downward spiral and will go extinct if the phenomenon lasts for some time. Usually, the deleterious mutations would simply be selected away, but during mutational meltdown, the number of individuals thus suffering an early death is too large relative to overall population size so that mortality exceeds the birth rate.

    So to repeat Joe Felsenstein’s question, “why aren’t we all dead? ” Actually it’s also Kondrashov’s question too.

    I have my fix to the problem: auto renormalization of the S-coefficients. Ok, so lets say a deleterious mutation gets fixed into the population by drift. The S-coefficient only measures the trait’s relative performance to other traits in a competitive environment with other traits. It says little of whether the species will become less prolific on the whole if the competition is removed for that trait by that trait becoming fixed.

    So that’s my answer to why we aren’t all dead. The S-coefficients of the traits changed so as not to cause mutational meltdown.

    Modelling populations with immutable S-coefficients seems kind of silly any way, and is mostly done for the sake of mathematical tractability. Just because it is easier to model stable S coefficients doesn’t make stable S coefficients true. Elegance and simplicity like that only seems to work in physics, not in evolutionary questions.

  13. Alan Fox:
    So can we credit the Hagedoorns as being the first to document the concept of drift? I Googled quickly butI was unable fathom the paper I found. It was all Dutch to me!

    I cannot read Dutch myself. Hagedoorn and Hagedoorn are credited with being the first to mention the existence of genetic drift. They did not do any theory on it.

  14. Corneel: It is about inbreeding depression (degeneration), correctly explained as an increase in the expression of recessive deleterious variants. Genetic drift is not explicitely mentioned, but perhaps Fisher saw a connection with loss of genetic variation in small inbreeding populations?

    Interesting. Were they talking about inbreeding owing to the finiteness of the population? That would be connected.

  15. Maybe it’s just me, but if Sanford’s hypothesis predicts that all life should go extinct, but all life has NOT gone extinct, doesn’t that mean his numbers are wrong?

  16. Faizal Ali:
    Maybe it’s just me, but if Sanford’s hypothesis predicts that all life should go extinct, but all life has NOT gone extinct, doesn’t that mean his numbers are wrong?

    You’re assuming that there have been millions or billions of years for this to happen. If you’re Sanford, you only admit maybe 6022 years available for this to happen. And you’re pretty sure that The End Is Nigh.

  17. I should add that genetic drift is also credited to the snail evolutionist Thomas Gulick in 1873. Of course, without any understanding of genetics on his part.

  18. Faizal Ali: Maybe it’s just me, but if Sanford’s hypothesis predicts that all life should go extinct, but all life has NOT gone extinct, doesn’t that mean his numbers are wrong?

    stcordova has an answer to that. Not a very good answer, but an answer nonetheless.

  19. Faizal Ali: Maybe it’s just me, but if Sanford’s hypothesis predicts that all life should go extinct, but all life has NOT gone extinct, doesn’t that mean his numbers are wrong?

    He’s a young-Earth creationist, and the author of Genetic Entropy. Part of what he’s doing is to provide evidence that the End Time is nigh. That is, the human species cannot survive much longer.

    John Sanford is not, as best I can tell, one of God’s Own Prevaricators. He seems to believe his own claims, which is to say that he’s not to be lumped with most of the leading advocates of intelligent design. He has put a lot of time and energy into what is essentially the elaboration of a delusional system. I do not know whether he suffers from psychosis at times. And I do not mean to denigrate people suffering from extreme psychiatric illness (as is someone dear to me). But when someone fits an exponential curve to the ages at death of various figures in the Bible, including Jesus, something bizarre is going on.

    There are a couple of other religious takes allowed by Basener and Sanford. One is that the conditions for life on Earth are fine tuned. The other is that life requires constant sustenance by God. That is, if life has existed for billions of years, then it is only because God has intervened all along.

    ETA: Joe posted while I was composing. He’s generally a helluva lot quicker than I am.

  20. Tom English:

    There are a couple of other religious takes allowed by Basener and Sanford. One is that the conditions for life on Earth are fine tuned. The other is that life requires constant sustenance by God. That is, if life has existed for billions of years, then it is only because God has intervened all along.

    That wouldn’t work, however, with his claim that deleterious mutations far outnumber beneficial ones. Or is he saying that this is just what we’re seeing now, because God has withdrawn his protective hand?

    BTW, has anyone heard of this Basener guy before? His name is new to me.

  21. Even aside from Basener and Sanford, others including Nobel Prize winner Hermann Muller pointed out the human race cannot tolerate very many mutations per individual per generation. The number Muller arrived at was about 1 bad mutation per generation per individual as the limit the human genome can tolerate.

    Additionally, so what if an individual has a good mutation if he has 10 bad to go with it. This is like have a slight increase in intelligence while having 10 heritable diseases to go with it. You go one step forward and ten steps back.

    Can natural selection arrest the problem? Only if there are enough reproductive resources relative to the number of offspring per couple.

    For human populations there was something published by Nachman and Crowell and Eyre-Walker and Keightley using a Poisson distribution as reasonable model for the probability of a eugenically clean individual appearing in the face of various mutation rates.

    If it is improbable that an eugenically clean kid can be reproduced by a couple, this makes it hard to weed out the bad. So this is an alternative way to arrive at Muller’s conclusions, which are also Sanford and Basener’s conclusions, and really everyone else’s conclusions as summarized by Dan Gruar: “If ENCODE is right, evolution is wrong.”

    This is a simpler argument than the one Basener and Sanford put forward, but to Sanford’s credit, he’s also put the simpler version in his book Genetic Entropy, although the following derivation isn’t in his book, it’s something I ginned up myself. 🙂

    So how can we estimate the probability a kid can be born with no defective mutations?

    The following derivation was confirmed in Kimrua’s paper (see eqn. 1.4)

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1211299/pdf/1337.pdf

    which Nachman and Crowell, and Eyre-Walker and Keightley reference as well.

    So now the details:

    let U = mutation rate (per individual per generation)
    P(0,U) = probability of individual having no mutation under a mutation rate U (eugenically the best)
    P(1,U) = probability of individual having 1 mutation under a mutation rate U
    P(2,U) = probability of individual having 2 mutations under a mutation rate U
    etc.

    The wiki definition of Poisson distribution is:

    $latex=\large f(k,\lambda ) = \frac{\lambda^k e^{-\lambda } {}}{k!}$

    to conform the wiki formula with evolutionary literature let

    $latex \lambda = U$

    and

    $latex f = P$

    Because P(0,U) = probability of individual having no mutation under a mutation rate U (eugenically the best), we can find the probability the eugenically best individual emerges by letting:

    $latex k = 0$

    which yields

    $latex \large \large P(k,U) = P(0,U) = \frac{U^0 e^{-U }}{0!} = e^{-U}$

    Given the Poisson distribution is a discrete probability distribution, the following idealization must hold:

    $latex \large \sum_{n}P_n =\sum_{i=0}^{\infty}P(i,U) = 1$

    thus

    $latex=\large \large P(0,U) + \sum_{i=1}^{\infty}P(i,U) = 1$

    thus subtracting P(0,U) from both sides

    $latex=\large \large P(0,U) + \sum_{i=1}^{\infty}P(i,U) -P(0,U) = 1 – P(0,U)$

    thus simplifying

    $latex=\large \sum_{i=1}^{\infty}P(i,U) = 1 – P(0,U)$

    On inspection, the left hand side of the above equation must be the percent of offspring that have at least 1 new mutation. Noting gain that $latex=P(0,U) = e^{-U}$, the above equation reduces to the following:

    $latex \sum_{n}P(i,U) = \sum_{i=1}^{\infty}P(i,U) = 1 – P(0,U) = 1- e^{-U}$

    which is in full agreement with Nachman and Crowell’s equation in the very last paragraph and in full agreement with an article in Nature: High genomic deleterious mutation rates in homonids by Eyre-Walker and Keightley, paragraph 2.

    http://www.lifesci.sussex.ac.uk/CSE/members/aeyrewalker/pdfs/EWNature99.pdf

    The simplicity and elegance of the final result is astonishing, and simplicity and elegance lend force to arguments.

    So what does this mean? If the bad mutation rate is 6 per individual per generation (more conservative than Gruar’s estimate if ENCODE is right), using that formula, the chances that a eugenically “ideal” offspring will emerge is:

    $latex=\large \large P(0,6) = e^{-6} = 0.25\%$

    This would imply each parent needs to procreate the following number of kids on average just to get 1 eugenically fit kid:

    $latex= \frac{1}{e^{-U}} = \frac{1}{e^{-6}} = 403.42$

    Or equivalently each couple needs to procreate the following number of kids on average just to get 1 eugenically fit kid:

    $latex=\large \large 2 * \frac{1}{e^{-U}} = 2 * \frac{1}{e^{-6}} \approx 807$

    For humanity to survive, even after each couple has 807 kids on average, we still have to make the further utterly unrealistic assumption that the eugenically “ideal” offspring are the only survivors of a selective process.

    Hence, it is absurd to think humanity can purge the bad out of its populations — the bad just keeps getting worse.

    In truth, since most mutations are of nearly neutral effect, most of the damaged offspring will reproduce, and the probability of a eugenically ideal line of offspring approaches zero over time.

    Muller’s number of only 1 new bad mutations per generation per individual. So if anything I understated my case.

    There are some “fixes” to the problem suggested by Crow and Kondrashov. I suggested my fix. But the bottom line is to look at what is actually happening to the human genome over time. Are we getting dumber and sicker? I think so. It’s sad.

    We can test Basener and Sanford’s prediction by observing whether human heritable diseases continue to increase with each generation. Whether their derivation is right or not, the conclusion is testable.

    On some level, I suppose even Basener and Sanford wished it were not so because it is a tragic conclusion.

  22. Faizal Ali,

    I meant to distinguish interpretations of the particular paper by Basener and Sanford from the personal beliefs of Sanford.

    Basener has long been an affiliate of the Evolutionary Informatics Lab. Marks, Dembski, and Ewert included a long quote of a publication of his in Introduction to Evolutionary Informatics (without giving any indication that they understood what he was saying). I don’t know whether he’s a YEC, but he certainly quacks like one in comments at UD. Judging by his prose (which is a good way to judge), he’s very bright.

    In my mind, the clearest indication that intelligent design is a religio-political movement, and not science, is the accommodation of YECs. No one is going to take ID as a genuine attempt at science, let alone as science, when many ID “scientists” are bent on supporting their Biblical view that the Earth has been around for less than ten thousand years.

    I find myself wondering how many models Basener and Sanford have investigated, and whether they would report on models that do not lend support to their Biblical views. Perhaps the ultimate reason they ended up with a crummy simulation model was that it “said” what they wanted to “hear.” (But I won’t be getting into discussion of this matter until I see what Joe has to say in his next post.)

    Basener has emphasized the worldviews of scientists in a comment at UD (emphasis added):

    There are good lessons in that, and I don’t mean only for those with a Darwinist view of the world. Scientists are people trying to form a big picture out of a collection of observations/measurements/facts. I think it was Henri Poincare who said that a collection of facts are not more a theory than a pile of rocks is a house. We are trying to assemble the rocks into a form that makes sense to us on a larger scale. It is human insight and some level of belief in something beyond the rocks themselves that makes us believe they form a house. All scientists have a faith that there is *some* overall house, some order to the universe.

    The greater house is constructed as scientists argue of how the rocks go together – hypothesis are posed and refuted – but it is critical to distinguish between the hard observations of rocks and our view of how they should go together. Everybody has a philosophy or worldview that informs the lines of investigations and hypothesis they pose, but we have to check that view when it comes to validating experimental results, otherwise we are just validating preconceptions instead of doing science. Properly done science works.

    There is a long discussion that can take place about what the best worldview for building hypothesis is, but for the interested reader I’ll defer to Pearcey and Thaxton’s book “The Soul of Science.”

    He follows that up immediately with:

    Adding to the above conversation – I believe there is no better view of the universe from which to make hypothesis and assemble rocks than that of a universe designed by an biblical Creator.

    His “Properly done science works” reminds me of a remark by Richard Feynman:

    We’ve learned from experience that the truth will come out.

    And in the context of that remark, Feynman said:

    The first principle is that you must not fool yourself — and you are the easiest person to fool.

    People who believe that scientific investigation is necessarily guided by a worldview, and who furthermore believe with all conviction that their worldview is True, cannot possibly abide by Feynman’s first principle. We’ve learned from experience that creationists do not take no for an answer from nature. They are not open to learning that they’ve fooled themselves on matters of fundamental importance.

  23. stcordova: You mean like the figures from evolutionists they cited in their paper:

    They only mention a single number (a million to one), and it doesn’t take much to see that number was picked because of how skewed a ratio it suggests. That’s a red flag in my opinion.

    They quote Keighley & Lynch 2003 for a statement that isn’t in dispute. The vast majority of mutations (in functional DNA) are quite certainly deleterious. But it is the specific ratio (along with the magnitude of the effects) that is in question. The “vast majority” can just as well be 19/20, 49/50 or 99/100 that are deleterious. Those could just as well qualify for the statement Keighley and Lynch are cited for.

    Regardless, the particular paper that number comes from (Garrish and Lenski 1998) doesn’t actually say what Basener and Sanford claims it says. Their claim is:
    “Gerrish and Lenski estimate the ratio of deleterious to beneficial mutations at a million to one (Gerrish and Lenski 1998b)”.

    They say it is the ratio of deleterious to beneficial. As in for every one beneficial mutations, there is a million deleterious ones.

    Yet this is not actually what Gerrish and Lenski 1998b says. Here’s a direct quote: “We have estimated parameters α and µ from these data by finding the point of intersection between the solution curves of equations (8). The solution for this system of equations is α = 35 and µ = 2.0×10^-9 beneficial mutations per replication. Given that the genomic mutation rate of E. coli is approximately 3×10^-3 mutations per replication (Drake, 1991), one can infer that the proportion of mutations that are beneficial is roughly one in a million. We emphasize that these estimates depend on (i)the assumption of an exponential distribution of beneficial mutational effects, and (ii) the assumption that α and µ remain constant even as mean fitness increases. The empirical fitness trajectories referred to in this section show a decreasing rate of increase, suggesting that assumption (ii) is false if the environment is constant. (See Assumptions of the models.)”

    That statement could be interpreted as saying that a large fraction of mutations could be neutral. In other words, while there would still be many more deleterious to beneficial, it could be 100.000 to 1, or 10.000 to 1, with the rest being neutral. Besides, what a rather obscure reference to pick just to hunt down such a quote. I suspect cherrypicking.

    That same paper also says the averate fitness increase resulting from a beneficial substitution is 0.1. A ten percent (10%) increase. But the paper isn’t cited for that number. I wonder why?

    Yet they don’t actually use the million-to-one number in their simulations, electing instead to go by a 1 in 1000 ratio. With that switch they can pretend to have gone for an extremely forgiving ratio. First try to present an extremely conservative estimate as if it is a normal one, then switch to a much more forgiving one in comparison so it looks like you have gone out of your way to be lenient to the opposition. That’s really clever of course.

    The whole thing smells like an exercise in rhetoric and deception. Almost all of their citations that directly address the proportion of deleterious to beneficial mutations, and the magnitudes of their selection effects, are to studies in the late 1990’s, where sequencing technologies were a far cry from what they are today. Again, I smell cherrypicking.

    The paper looks to me like Basener and Sanford’s designed it to mislead laymen who don’t check the references. A culture-war publication. The papers cited are cited only because the parts that are cited sound so damning when not put into context and the papers referenced aren’t actually read(and understood). A nice little thing that your average creationist know-nothing can read and find extremely impressive-sounding. The whole thing is designed to be quotable by people who lack the qualifications to assess the work, and lack the skepticism and therefore motivation (or the means) to dig into the references. A piece of carefully crafted creationist propaganda.

    A minor point, and I’m sure just a small mistake, but the reference to Garrish & Lenski 1998a is wrong. The title is from a different paper (Thomas Bataillon, 2000): Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations?. But this paper is mistakenly attributed to Lenski & Garrish 1998.

  24. stcordova: Are we getting dumber and sicker? I think so.

    Actually mean IQ’s are rising, curiously enough.

    Though yes we are accumulating genetic diseases because modern medicine, technology, agriculture and industrialization has made life expectancy and survival rates go totally off the “normal” curve for animal species.

    We can test Basener and Sanford’s prediction by observing whether human heritable diseases continue to increase with each generation. Whether their derivation is right or not, the conclusion is testable.

    No, you can’t test their prediction about general evolutionary phenomena by observing what is happening to the human population. We are in a very atypical situation with the inventions of civilization, modern medicine, agriculture and industrialization. The kinds of phenomena that would provide the selective “purging” of deleterious traits we see in wild populations of animals is not really in effect on Homo sapiens. Luckily, the solution is the very same phenomenon that has created this unusual situation in the first place: Medicine, industrialization, and biotechnology. We will have to edit our genomes in the coming generations with new upcoming biotechnologies (like CRISPR) to correct many of these accumulated genetic diseases.

  25. Rumaket,

    Fair enough, and thanks for the response.

    But going back to the paper, given there are disagreements of the Deleterious to Beneficial ratio, would it be correct to say if the ratio were 1000 deleterious to 1 beneficial, would the results of the derivation be accurate?

    I’ve posed the question before to evolutionists, “can you cite some mutations which are unequivocally benefical that have arisen in recorded history?” Eh, sickle cell anemia? Ok, name some others. Eh, Tay Sachs. Hey, how about the ability to digest milk as an adult? How about a beneficial which you expect to get fixed into the human population that isn’t the majority allele already?

    Well maybe no one really knows the number, that’s why I pointed out the simpler argument which many agree with and which I just provided some derivation for and which is essentially Gruar’s argument: “If ENCODE is right, evolution is wrong.”

    So I feel all this theory stuff is like beating a dead horse. Many have already agreed to the terms of the experiment: “If ENCODE is right, evolution is wrong.”

    Sanford agrees with that, Graur agrees with that, Larry Moran agrees with that, and as far as I know, Joe Felsenstein agrees with that.

    So rather than rehash theory, we can just proceed from what is agreed upon regarding ENCODE and then find out if ENCODE is right. We may know in due time which side is closer to the truth.

  26. Rumraket:

    The kinds of phenomena that would provide the selective “purging” of deleterious traits we see in wild populations of animals is not really in effect on Homo sapiens.

    Given we’re in what appears to be a rapid rate of extinction, Sanford’s general thesis outside of his paper, namely Genetic Entropy, looks pretty accurate to me. If a species line is wiped off the face of the Earth, that is genetic deterioration in the ultimate sense. The net average direction of evolution in field and lab observations is destructive, not constructive.

    Do you have direct evidence in the lab and field that most evolution observed is constructive? Even Jerry Coyne had to concede, on average, lab observed evolution is loss of function — aka Behe’s first rule of adaptive evolution.

    https://whyevolutionistrue.wordpress.com/2010/12/12/behes-new-paper/

    I think that while Behe’s summary of the results of these short-term lab experiments is generally accurate,

    Coyne unfortunately adds:

    one would be completely off the mark to extend his conclusions to evolution in general—that is, evolution as it has occurred in [sic] nature, be it in microbes or eukaryotes.

    Coyne would have been more accurate to say:

    one would be completely off the mark to extend his conclusions to imagined evolution in general—that is, evolution as it has occurred in our imagination

    Coyne doesn’t actually have direct evidence supporting his claim, it’s all based on his inferences which are based on his premises, all of which can be wrong. He seems to have an unfortunate habit of equating unobserved ideas as if they were actually observed and measured data points.

  27. stcordova: “If ENCODE is right, evolution is wrong.”

    You realize that this statement actually means “if ENCODE is right, population genetic estimates of the ratio and magnitude of deleterous mutations, is wrong”. Right?

    You seem to think it means “if ENCODE is right, then the theory that all species on Earth evolved by a branching genealogical process of descent with modification while subject to natural selection over billions of years, is wrong”.

    No amount of ENCODE being right can make the consilience of independent phylogenies, or the fossil record, and countless other lines of evidence for macroevolution, magically not exist. ENCODE simply doesn’t have the power to overturn that evidence.

  28. stcordova: Rumraket:

    The kinds of phenomena that would provide the selective “purging” of deleterious traits we see in wild populations of animals is not really in effect on Homo sapiens.

    Given we’re in what appears to be a rapid rate of extinction

    Of what? There’s very significant climate change going on (caused by us) and we are massively disturbing Earth’s ecosystems, among other things by incurring very substantial habitat loss. Forests and grasslands are converted to farms and cities. Abyssal plains, coral reefs and significant portions of the water column are rendered barren deserts due to industrial overfishing with massive and deep-reaching trawler-nets, not to mention other forms of pollution. Those are the primary drivers of biodiversity extinction being witness in the present, not “genetic entropy”.

    Sanford’s general thesis outside of his paper, namely Genetic Entropy, looks pretty accurate to me.

    Not to me.

    If a species line is wiped off the face of the Earth, that is genetic deterioration in the ultimate sense.

    Not really. If you’re run over by a car, that isn’t genetic deterioration. Wiping out a forest to make room for a field of wheat and potatoes isn’t genetic deterioration.

    The net average direction of evolution in field and lab observations is destructive, not constructive.

    You’ve confused the average fitness of a population with the phenomenon of genomic and structural complexification. How very deceptive of you.

    A species can continously increase in fitness, while simultaneously losing genes and genetic material that is being shedded because it isn’t needed and therefore no longer maintained by purifying selection.

    Do you have direct evidence in the lab and field that most evolution observed is constructive?

    I don’t think it needs to be constructive, in the sense of causing increased complexity, in order for it to have the net effect of increased fitness, or for it to be able to maintain a population healthy and avoid extinction.

    Even Jerry Coyne had to concede, on average, lab observed evolution is loss of function — aka Behe’s first rule of adaptive evolution.

    Yes, but all lab-observed evolution is also in static lab-environments designed to minimize the number of factors that confound analysis of what factors contribute to evolutionary change.

    I think that while Behe’s summary of the results of these short-term lab experiments is generally accurate,

    So do I. That is what happened in those experiments. And we know why that is what happened in those experiments. In fact I would go so far as to say we would predict that to happen. If you remove the majority of the factors that persist in natural environments, to which organisms have adapted, then the population will in turn shed those adaptations, over subsequent generations, as they are no longer needed.

    Coyne unfortunately adds: one would be completely off the mark to extend his conclusions to evolution in general—that is, evolution as it has occurred in [sic] nature, be it in microbes or eukaryotes.

    Coyne would have been more accurate to say:

    one would be completely off the mark to extend his conclusions to imagined evolution in general—that is, evolution as it has occurred in our imagination

    Except it isn’t imagined of course, as all evidence ever collected demonstrates beyond rational doubt.

    Coyne doesn’t actually have direct evidence supporting his claim

    29+ Evidences for Macroevolution
    The Scientific Case for Common Descent.

    it’s all based on his inferences which are based on his premises, all of which can be wrong.

    All inferences can be wrong. How truly novel a philosophical statement.

    He seems to have an unfortunate habit of equating unobserved ideas as if they were actually observed and measured data points.

    This is funny reading, coming from a guy who thinks the entire planet’s geology and the light of all the stars in the entire cosmos is lying to him when it contradicts his favored literalist interpretation of a book containing a mish-mash of old and ancient religious myths and fables. I’ll have to go replace that irony meter again.

  29. stcordova: Do you have direct evidence in the lab and field that most evolution observed is constructive? Even Jerry Coyne had to concede, on average, lab observed evolution is loss of function — aka Behe’s first rule of adaptive evolution.

    I will repeat something I wrote here earlier today:

    This highlights something that creationists have a hard time appreciating about the Lenski experiment: It provides clear cut empirical refutation of many of the key claims of ID. The ID creationists can try all they want to play with their pocket calculators and come up with big numbers that supposedly show that evolution is impossible. However, Lenski has shown that all you need to do is put a bunch of bacteria in a bottle and watch them. Evolution will then happen right before your eyes.

    From one clonal population, 12 completely distinct populations have emerged. If speciation was impossible, we wouldn’t see that.

    And the fact that every single one of those populations is better adapted to their environment shows that evolution can produce beneficial new genetic information. There just is no other explanation.

    So when.e.g. Michael Behe decides to invent his own new category of “gain of function” mutations and argues that these did not occur in Lenski’s lab, it is irrelevant. All it shows, is that, even if Behe’s definition means anything, evolution does not require such “gain of function” mutations to proceed.

  30. Rumraket:

    Of what? There’s very significant climate change going on (caused by us) and we are massively disturbing Earth’s ecosystems, among other things by incurring very substantial habitat loss. Forests and grasslands are converted to farms and cities. Abyssal plains, coral reefs and significant portions of the water column are rendered barren deserts due to industrial overfishing with massive and deep-reaching trawler-nets, not to mention other forms of pollution.

    Sounds to me like an excellent test (from a scientifcal standpoint anyway) of what actually happens when selection pressures on organsims are substantially increased. That is, the struggle for existence and competition for resources has become very acute.

    So contrary to Darwin’s predictions, more selection results in less species, it doesn’t originate more of them! Observations disagree with Darwin’s theory, it confirms natural selection de-originates more species than it creates under increased selection pressure.

  31. To some creationists, when the legs of terrestrial mammals evolved into the flippers of whales, that would effectively qualify as a loss of function mutation. Because you see, maybe that change required some deletion mutations, or reduced activity of some regulatory element, and of course there’s the phenotypic effect of the loss of ability to run around on dry land. So, “loss of function”.

    By some creationist definitions of “loss of function”, the entire diversity of life could evolve from a self-replicating molecule of RNA by such “loss of function” mutations. 🙂

  32. stcordova: Sounds to me like an excellent test (from a scientifcal standpoint anyway) of what actually happens when selection pressures on organsims are substantially increased.That is the struggle for existence and competition for resources has become very acute.

    So contrary to Darwin’s predictions, more selection results in less species, it doesn’t originate more of them! Observations disagree with Darwin’s theory, it confirms natural selection de-originates more species than it creates under increased selection pressure.

    Oh, so when human beings remove 10 million square kilometers of natural habitat in a couple of decades, you expect that to drive up selection pressures to change the species so they can… wait, they don’t even have a place to even exist. C’mon, don’t be silly.

    A species that doesn’t have an area to exist in, can’t evolve. There’s a net loss of habitat, not merely a gradual change in the nature of that habitat.

  33. Graham853: I had a look at the Basener and Sanford paper. To my mind, the problem is their choice of distribution for s’, the selection coefficient of a new mutation. In the region near zero, where drift dominates, alleles will have been fixed more or less at random, and hence the probability of a new mutation being deleterious should be about 1/2, not 999/1000. Near zero, the distribution should be very nearly symmetrical.

    I haven’t read Basener and Sanford’s paper, but that sounds right. And it seems to me there’s a fairly clear example of this: synonymous substitutions. When a mutation changes a codon into another that codes for the same amino acid, it doesn’t change the resulting protein at all. But it can have a slight effect on fitness because different synonymous codons aren’t all translated at the same speed and accuracy. As a result, they’ll often have selection coefficients very close to — but not quite equal to — zero.

    As a result… well, here’s an excerpt from the wikipedia article on codon usage bias:

    It is generally acknowledged that codon biases reflect a balance between mutational biases and natural selection for translational optimization. Optimal codons in fast-growing microorganisms, like Escherichia coli or Saccharomyces cerevisiae (baker’s yeast), reflect the composition of their respective genomic tRNA pool. It is thought that optimal codons help to achieve faster translation rates and high accuracy. As a result of these factors, translational selection is expected to be stronger in highly expressed genes, as is indeed the case for the above-mentioned organisms. In other organisms that do not show high growing rates or that present small genomes, codon usage optimization is normally absent, and codon preferences are determined by the characteristic mutational biases seen in that particular genome.

    If a particular codon is optimal, a synonymous mutation to it will be deleterious; if it’s pessimal, synonymous mutation will be beneficial. In the absence of codon bias, both situations will occur at the same rate, so (as you said) the overall probability of one of these mutation being deleterious should be about 1/2.

    In terms of Sanford’s “genetic entropy”: where there’s no initial codon bias, the genetic entropy on these nearly-neutral degrees of freedom is already maximized, so further mutations cannot increase it. And clearly it’s not a big problem, because many species (including humans) get along fine in this maximum entropy state.

  34. Boiling down the questions at hand as best as I see.

    1. Independent of Fisher’s Theorem, is there a Deleterious to Beneficial ratio at which fitness is guaranteed to decline? What is that ratio?

    2. If yes, what are the theoretical ratios and how do real ratios compare with the theoretical ones. Are the real ratios ratios above the theoretical ratios, and thus decline is predicted?

    3. If yes to all the above, can Fisher’s theorem be recast to reflect the above insights.

    So those are questions to ask independent of Sanford’s paper. If yes to all three, then we can ask if Basener and Sanford’s paper carry the above out correctly.

    Intuitively, it would seem there is a ratio of deleterious to beneficial that cannot lead to improvement, but to inevitable decline. Experiments to that effect might be subjecting germline cells to mutation such as radiation or mutagenic chemicals. It think all evidence points to the fact such a ratio should exist at least in principle given certain other parameters.

  35. In support of the derivations I just carried out with the Poisson Distributions, consider if we have 45 bad mutations in the genome. Using the formula I derived, let the number of bad mutations per individual be U = 45. Then the number of kids each person must have in order to make one bad-mutation-free child on average is:

    1/ (e^-U) = 1 / exp(-45) = 3.4 x 10^19

    how about U = 82?

    1/ (e^-U) = 1 / exp(-82) = 4.1 x 10^35

    Well, these numbers were close enough to Gruar’s figures.

    https://arxiv.org/ftp/arxiv/papers/1601/1601.06047.pdf

    In his scientific paper, Gruar uses the word Bonkers! I love it. Bonkers Gruar:

    If 80% of the genome is
    functional, as trumpeted by ENCODE Project Consortium (2012), then 45-82 deleterious mutations arise per generation.

    For the human population to maintain its current population size under these conditions, each of us should have on average 3 × 10^19 to 5 ×
    10^35 (30,000,000,000,000,000,000 to
    500,000,000,000,000,000,000,000,000,000,000,000) children. This is clearly bonkers.

    Hence, Graur vigorously argues, “If ENCODE is right, evolution is wrong.” Ironically Sanford agrees. It’s a much more straightforward calculation than the one involving Fisher’s theorem.

    Perhaps because of the simpler derivation of a genetic entropy argument such as Graur’s, Sanford was emboldened to find alternative proofs of Genetic Entropy based on the ratio of deleterious to beneficial. The above simpler calculations I provided don’t consider those ratios at all, just the simple count of bad mutations…..

  36. Intuitively, it would seem there is a ratio of deleterious to beneficial that cannot lead to improvement, but to inevitable decline.

    Here’s how to look at it.

    A long time ago — assuming common descent — our ancestors (bacteria) were 100% of the biosphere. Now we are only a tiny fraction of the biosphere.

    Obviously our fitness has declined. So there have been deleterious mutations. We are the result of deleterious mutations.

    Incidentally, this is why I am not a Darwinist. The notions of “fitness”, “beneficial” and “deleterious” are not well defined. The biosphere is too dynamic, and the usual definitions assume something nearer to being static.

  37. Faizal Ali: I will repeat something I wrote here earlier today:

    This highlights something that creationists have a hard time appreciating about the Lenski experiment: It provides clear cut empirical refutation of many of the key claims of ID. The ID creationists can try all they want to play with their pocket calculators and come up with big numbers that supposedly show that evolution is impossible. However, Lenski has shown that all you need to do is put a bunch of bacteria in a bottle and watch them. Evolution will then happen right before your eyes.

    From one clonal population, 12 completely distinct populations have emerged. If speciation was impossible, we wouldn’t see that.

    And the fact that every single one of those populations is better adapted to their environment shows that evolution can produce beneficial new genetic information. There just is no other explanation.

    Ali, you have not so skillfully completely avoided Sal’s question.

    Lenski’s experiments don’t show accumulation of new functions. That’s completely misleading. An artificial environment was created for the bacteria, an environment which was so lethal, that only bacteria which were only suited for one very specific environment could survive. Its the equivalent of saying that we are going to employ people to chop off the feet of everyone in some village of people, such that they would bleed to death. It would just so happen, that if you were born with no feet, you would be spared this death. This anyone with a mutation which deformed their feet have a new beneficial mutation. That’s not evidence of the power of natural selection that anyone finds useful.

    We could come up with literally millions of such scenarios. But they are not informative as to how NEW functions appear. If you have to destroy functions for everything to become useful, how could that have worked in the past? It couldn’t. You are not going to create any eye that way.

    I think you aren’t even close to understanding the evolution problem. Its sounds like all you have really done is read Pandas Thumb or Talk Origins. That’s like trying to learn inside a not so warm cocoon.

  38. Rumraket: A species that doesn’t have an area to exist in, can’t evolve. There’s a net loss of habitat, not merely a gradual change in the nature of that habitat.

    Yea, sort of like Lenski’s experiments.

  39. Using math, corect paremeters or not, is still just using math to make biological historical conclusions.
    its like when they USE MATH to settle there is other life in outer space and use math to settle there is not. i’ve seen both sides do it.
    It settles nothing but the presumptions behind it al. Since one is wrong then thats what must first be settled,. Before the math.
    Anyways.
    Does natural selection lead to increased fitness. ?
    Artificial selection does not!
    I don’t think NS has ever had any influence in biology even if possible on minor occassions.
    Yet if a selection did occur then it would maintain a fitness.
    Would it increase fitness?
    No! why would it do this? its just holding the fort.
    Anyways. A new year and another good famous creationist punch to the body of a unlikely hypothesis called EVOLUTIONISM.
    All the math just shows how little actual biology is behind evolutionism.
    it really is just a line of reasoning on very raw data.

  40. Joe Felsenstein: Interesting. Were they talking about inbreeding owing to the finiteness of the population? That would be connected.

    Not explicitely no. They recognise that inbreeding (close breeding of relatives) increases the homozygosity. I guess you could make a case that this concerns inbreeding by drift rather than assortative mating.

    But I note that the paper Alan linked to is from 1944, so I guess Fisher referred to a different older manuscript. That may be hard to come by 🙂

  41. stcordova: I’ve posed the question before to evolutionists, “can you cite some mutations which are unequivocally benefical that have arisen in recorded history?” Eh, sickle cell anemia? Ok, name some others. Eh, Tay Sachs. Hey, how about the ability to digest milk as an adult? How about a beneficial which you expect to get fixed into the human population that isn’t the majority allele already?

    Can you cite some mutations that are unequivocally deleterious that got fixed in the human population in recorded history?

    Any signs of mutational meltdown yet?

  42. Corneel: But I note that the paper Alan linked to is from 1944, so I guess Fisher referred to a different older manuscript.

    There we go. It is in “The Relative Value of the Processes causing Evolution” by Hagedoorn and Hagedoorn, published in 1921.

    Through Kimura:

    As early as 1921, Hagedoorn and Hagedoorn pointed out that the group of organisms destined to become the parents of the next generation is usually considerably smaller than the number of individuals of their species so that some genes will be lost by chance. According to their opinion, reduction of potential variability is automatic, being independent of any sort of selection. They considered that this is the most important gain in knowledge that we owe to Mendel’s work and to the biomechanical interpretation of it.

  43. stcordova: So contrary to Darwin’s predictions, more selection results in less species, it doesn’t originate more of them!

    Where did Darwin claim that selection increases the speciation rate?

  44. Neil Rickert: A long time ago — assuming common descent — our ancestors (bacteria) were 100% of the biosphere. Now we are only a tiny fraction of the biosphere.

    Obviously our fitness has declined. So there have been deleterious mutations. We are the result of deleterious mutations.

    Unless you want to claim all ancient bacterial lineages as our ancestors, it follows that our distant ancestors were a tiny fraction of the biosphere as well.
    Perhaps you were referring to the very beginning of cellular life, but then of course our “fitness” decline was an inevitable consequence of the expansion of this ancient lineage, and mutations had nothing to do with it.

    I submit that our definitions are fine, but that you need to adjust your view of them 😉

  45. phoodoo: Yea, sort of like Lenski’s experiments.

    There is not a net loss of habitat, nor a gradual change in habitat, in Lenski’s experiment. So it isn’t clear what you are trying to say.

  46. phoodoo: An artificial environment was created for the bacteria, an environment which was so lethal, that only bacteria which were only suited for one very specific environment could survive.

    And, yet, they somehow managed to survive for over 30,000 generations without the ability to metabolize citrate. Explain that.

    At the beginning ot the experiment, no bacteria had the ability to metabolize citrate aerobically. Now, two of the populations do. No matter what kind of creationist Humpty Dumpty reasoning you try to employ, that is a new function by any rational definition of the term.

    Also, there is a misconception that this is the only beneficial trait that arose during the study. There are literally hundreds of others, though none as spectacular as citrate metabolism. Every single one of the 12 lines is more fit than the ancestral population, even those without the ability to metabolize citrate.

    It seems the only way creationists can refute this experiment is to lie about it.

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