And Ebola becomes less fit when funeral practices change in the face of an outbreak, changing the virus’s environment.
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I agree of course. Sanford actually does equate virulence with viral fitness in his paper. It is like saying that the steroid addled bodybuilder who has sterilized himself is fitter because he is muscular.
Sanford (bold is mine):
We suggest H1N1 has been undergoing natural genetic attenuation, and that significant attenuation may even occur during a single pandemic. This process may play a role in natural pandemic cessation and has apparently contributed to the exponential decline in mortality rates over time, as seen in all major human influenza strains.
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This is understandable as it falsifies evolutionary theory. The quick dismissal of contridictory evidence is troubling to me. @Joe_Felsenstein disagreed but did not dismiss. He wrote a thoughtful counter hypothesis.
Sanford is not the only biologist interested in this theory. The question is why they disagree and I don’t see a compelling counter argument. I think 1000 deleterious mutations to every beneficial one that the model is based on is conservative. I think what slows this down is aggressive purifying selection. We see this with comparing sequences of critical proteins such as alpha actin. As such, I do not think it supports 6000 years of animal life.
he newest edition of Genetic Entropy (2014), has shown that genetic degeneration is not just a theoretical concern, but is observed in numerous real-life situations. Genetic Entropy has reviewed research that shows: a) the ubiquitous genetic degeneration of the somatic cells of all human beings; and b) the genetic germline degeneration of the whole human population. Likewise Genetic Entropy has reviewed research that shows rapid genetic degeneration in the H1N1 influenza virus. Genetic Entropy also documents “evolution in reverse” in the famous LLEE bacterial experiment (article available here).
A new paper (Lynch, 2016) written by a leading population geneticist, shows that human genetic degeneration is a very serious problem. He affirms that the human germline mutation rate is roughly 100 new mutations per person per generation, while the somatic mutation rate is roughly 3 new mutations per cell division. Lynch estimates human fitness is declining 1-5% per generation, and he adds; “most mutations have minor effects, very few have lethal consequences, and even fewer are beneficial.”
Our new book “Contested Bones” (available at ContestedBones.org) cites evidence showing that the early human population referred to as Neanderthal (Homo neanderthalensis) was highly inbred, and had a very high genetic load (40% less fit than modern humans) (Harris and Nielsen, 2016; Roebroeks and Soressi, 2016). See pages pages 315-316. This severe genetic degeneration probably contributed to the disappearance of that population (PrÜfer et al., 2014; Sankararaman et al., 2014).
Similarly, the new book Contested Bones (pages 86-89), cites evidence that the early human population referred to as “Hobbit” (Homo floresiensis), was also inbred and apparently suffered from a special type of genetic degeneration called “reductive evolution” (insular dwarfing) (Berger et al., 2008; Morwood et al., 2004). This results in reduced body size, reduced brain volume, and various pathologies (Henneberg et al., 2014).
Contested Bones (pages 179-210) also cites evidence that the early human population referred to as Naledi (Homo naledi), was likewise inbred and suffered from “reductive evolution”, again resulting in reduced body size, reduced brain volume, and various pathologies.
Contested Bones (pages 53-75) also cites evidence that many other early human populations, broadly referred to as Erectus (Homo erectus), were inbred and suffered from “reductive evolution” (Anton, 2003). However, it seems the genetic degeneration of Erectus was less advanced—generally resulting in more moderate reductions in body size, brain size, and pathologies. Indeed, many paleoanthropologists would fold both Hobbit and Naledi into the more diverse Erectus category.
An important but overlooked paper, written by leading population geneticists (Keightley et al., 2005), reported that the two hypothetical populations that gave rise to modern man and modern chimpanzee both must have experienced continuous genetic degeneration during the last 6 million years. The problems associated with this claim should be obvious. Their title is: Evidence for Widespread Degradation of Gene Control Regions in Hominid Genomes, and they state that there has been the “accumulation of a large number of deleterious mutations in sequences containing gene control elements and hence a widespread degradation of the genome during the evolution of humans and chimpanzees.” (emphasis added).
A new paper (Gaur, 2017), shows that if a substantial fraction of the human genome is functional (is not junk DNA), then the evolution of man would not be possible (due to genetic degeneration). Gaur states that human evolution would be very problematic even if the genome was 10% functional, but would be completely impossible if 25% or more was functional. Yet the ENCODE project shows that at least 60% of the genome is functional.
A new paper (Rogers and Slatkin, 2017), shows that mammoth populations were highly inbred and carried an elevated genetic load (likely contributing to their extinction due to “mutational meltdown”).
A paper (Kumar and Subramanian, 2002) shows that mutation rates are similar for all mammals, when based on mutation rate per year (not per generation). This means that mammals (both mice and men) should degenerate similarly in the same amount of time. This suggests that the major mutation mechanisms are not tightly correlated to cell divisions.
A new paper (Ramu et al., 2017), shows that the tropical crop, cassava, has been accumulating many deleterious mutations, resulting a seriously increasing genetic load, and a distinct decline in fitness.
Another paper (Mattila et al. 2012), shows high genetic load in an old isolated butterfly population. “This population exemplifies the increasingly common situation in fragmented landscapes, in which small and completely isolated populations are vulnerable to extinction due to high genetic load.”
Another paper (Holmes, E. C. 2003), shows that all RNA viruses must be young—less than 50,000 years. This is consistent with our H1N1 influenza study that show that RNA virus strains degenerate very rapidly.
True. When Europeans came to the new world, the viral smallpox they transmitted to Native Americans wiped out large proportions of the population. The virus was the exact same pathogen, the obvious difference is that one population has a history of exposure and built up resistance, and the other population had no such defence. So two points; one, fitness has nothing to do with virulence; two, fitness has everything to do with the relationship of the organism to its specific environment. In view of smallpox, what was Sanford thinking when he came up with genetic entropy in the context of epidemiology?
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If you’re going to quote something, either give a complete citation or a link or both.
And you still aren’t confronting the paradox in your thinking. If genetic degradation is real, lineages can’t be millions of years old. Strong purifying selection is irrelevant, as the degradation supposedly results from the accumulation of many weakly deleterious mutations, each individually invisible to selection. Nothing you’re saying on this subject makes sense.
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Pretty difficult to assess the several points following from the book when we do not have access to the book or the referenced papers.
If this is going to be your excuse every time your new pet favorite idea is rejected(they reject it because it disagrees with them) then there’s no reason to even have this discussion with you. We can just say the same about you, you think GE is right because you already believe evolution is false.
The quick dismissal of contridictory evidence is troubling to me. @Joe_Felsenstein disagreed but did not dismiss. He wrote a thoughtful counter hypothesis.
There have been numerous lengthy rebuttals to people advancing Sanford’s claims here.
Okay, but then you flat out disagree with Sanford, because Sanford thinks purifying selection is incapable of removing weakly deleterious mutations. So if some proteins have been conserved unchanged for hundreds of millions of years, that implies they’ve either never suffered a weakly deleterious mutation in any individual(what are the odds of that?), or that selection IS strong enough to remove them. Either of which should be close to impossible according to Sanford.
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He was walking in the footsteps of Arch-charlatan Henry Morris, who wrote that when reality and doctrine differ, reality is wrong and doctrine is right.
“…the main reason for insisting on the universal Flood as a fact of history and as the primary vehicle for geological interpretation is that God’s Word plainly teaches it! No geologic difficulties, real or imagined, can be allowed to take precedence over the clear statements and necessary inferences of Scripture.”
– Henry Morris, Biblical Cosmology & Modern Science, pp 32-33 (1970)
Real or imagined. Real, even if real. He really wrote that. They still write some similarly subnormally encephalitic poppycock on AIG’s website.
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Sure. And if God came down and gave us all mutations that allowed us to breathe underwater, that wouldn’t be a REAL beneficial because it wouldn’t help us survive on the surface of the sun.
Right?
The paper Bill referenced, by William F. Basener and John Sanford, is yet another peer reviewed publication where the phrase “genetic entropy” does not appear! It does not show in Sanford’s H1N1 paper either. Sanford’s brand is genetic entropy, yet his own publications in peer reviewed literature seem to take pains to avoid specifically referencing the very concept.
The fundamental theorem of natural selection with mutations
Please, search it yourselves. Not even among the footnotes.
So to answer the original post, not according to Sanford at any rate.
Isn’t “genetic entropy” just the old (but still valid) idea of mutational load, but done wrong?
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Absolutely, Sanford did not invent or materially contribute to the concept. For instance, it has been long known that the shared inability of anthropoid primates, including us, to synthesis vitamin C is a mutational load which was masked by the abundance of vitamin C in the available diet given the environment to which they were confined. The effect of this loss of genetic function became most manifest when the environment changed to ships at sea for months. Once the gene function was lost, selection pressure made no difference to further genetic mutational load, and the mutations piled up so that the gene function is probably irretrievable. Strangely, you do not hear Sanford appeal to this example.
The Genetics of Vitamin C Loss in Vertebrates
What genetic entropy means as Sanford promotes it in his popular writings, is that 6000 years ago all creation enjoyed pristine DNA like some platonic idealized creature carved in marble as a Greek statue, and by today we are a mess on the cusp of an eschatological genetic last gasp. That, of course, is a vision far removed from what is observed in biology.
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Naturalism?
That’s true; but these mutations which increased fitness are few compared to the much larger number of mutations that have been accumulating like rust in a car. As a result, the mutations we see in figure 4 correspond overwhelmingly to these rusting mutations that have nothing to do with fitness gain. So Sanford is right when he says that there is a perfect match between figures 4 and 5.
It happens that this vision of the human genome as a platonic ideal is much closer to the reality than you think. Here is a quote from Maynard Olson that illustrates this point
« A model for human genetic individuality is emerging in which there actually is a “wild-type” human genome—one in which most genes exist in an evolutionarily optimized form. There just are no “wild-type” humans: We each fall short of this Platonic ideal in our own distinctive ways »
https://science.sciencemag.org/content/331/6019/872.3.full
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What you are referring to here is nothing more than momentary adaptive blip probably caused by the fixation of a few impactful mutations. But that doesn’t change the fact that beneath this superficial phenomenon, a much deeper phenomenon is constantly at work that is irreparably eroding viral fitness, ie the linear and clock-like accumulation of slightly deleterious mutations.
What does that mean?
And if you knew anything about the study itself, as opposed to the lies being force fed to you by religious propagandists, you would know that is not true:
https://science.sciencemag.org/content/342/6164/1364
Experimental studies of evolution have increased greatly in number in recent years, stimulated by the growing power of genomic tools. However, organismal fitness remains the ultimate metric for interpreting these experiments, and the dynamics of fitness remain poorly understood over long time scales. Here, we examine fitness trajectories for 12 Escherichia coli populations during 50,000 generations. Mean fitness appears to increase without bound, consistent with a power law. We also derive this power-law relation theoretically by incorporating clonal interference and diminishing-returns epistasis into a dynamical model of changes in mean fitness over time.
(My bold.)
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Do you ever provide anything besides just rote repetition of Sanford’s own long demolished talking points? If the overall reproductive fitness of the organisms increased then their genomes are not “degrading” they are improving WRT to the local environment. That ridiculous comparison to two completely different graphs shows how Sanford will do anything to try and rationalize his delusions.
The bottom line is - since beneficial mutations providing fitness increase are empirically observed to occur then Sanford’s MA which produces zero beneficial mutations, only deleterious ones, does not accurately model actual biological processes.
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Basic question, @Giltil: How is fitness defined and measured in Lenski’s study?