I see. You mean in the small font text directly beneath the figure? It seems your expert usage of the Socratic Method had me utterly confused as to what you had a problem with there.
I agree that ‘accumulation’ is talking about fixation and not about individual occurrences of mutations. I’ll correct that ASAP.
Thanks.
Wouldn’t correcting that and making it abundantly clear demolish the very point of the article?
No, I don’t think it would. Why do you say so?
Because you are posting the results of both massive natural (in people) and artificial (preparation for sequencing) selection of the mutant viruses, nothing about mutation itself.
My point is that while “accumulated” is more accurate than your legend, it’s still very inaccurate given the conclusions you are claiming it supports.
There’s also the irony of your citing the results of many observational studies of real-time evolution at the same time you are denying that such studies exist–in this very thread.
Where did the sequences come from?
I appreciate your desire to be brief, but could you explain a bit more what you mean by this? What Carter and Sanford did was to plot the accumulation of fixed mutations over time based upon the available data for the H1N1 (Spanish Flu) genome. They showed this increase of mutational load correlated with the drop in virulence and eventual extinction of the strain.
There’s also the irony of your citing the results of many observational studies of real-time evolution at the same time you are denying that such studies exist–in this very thread.
This is indeed an equivocation on the meaning of ‘evolution’. Creationists don’t deny that ‘allele frequencies change’ and other such overly broad definitions of the term. What I mean by evolution is universal common descent.
Where did the sequences come from?
The answer is found in Carter & Sanford’s paper in the Methods section. I did not participate in that paper so I don’t have firsthand info beyond what is reported there.
It does not suit the YEC narrative that scientists can be just fair minded folk who simply understand the evidence in favor of an ancient earth and mainstream knowledge of biology as a context for their research. In the lab, out in the field, it is their working reality. In conferences, when submitting papers, it is their job to defend the findings and their place in the body of scientific knowledge. Their PhD’s were obtained with the criteria of extending human knowledge.
YEC do not just misunderstand science, but also scientists. To correct this, one, no there is not some groundswell among scientists broadly questioning Darwin or the established scientific model of the universe or any such thing. This is settled science for the vast majority, including practicing Christians in research or resource geology. Further, the adoption of mainstream science is freely embraced, it is the weight of evidence, not coercion, which is at the base of consensus.
Two, while some scientists do seem to have an anti-christian axe to grind, the common motivator of almost all scientists is curiosity. Most have little interest in theology and are just trying to get an answer as to the why’s and how’s in the focus of their specialty. There is no big humanist agenda for most.
Lastly, scientists are not drooling village idiots in lab coats who are too thick to evaluate what they are told and are too smart for their own britches. When YEC adherents say, “Hey, I’ve never studied this but I know these guys are all wrong”, that is pretty much the implication. Not all YEC has this attitude but many do.
“Accumulation of fixed mutations” is not accurate. They plotted the number of newly fixed (by neutral evolution and selection) mutations over time.
They only did the former.
First, mutations that have been fixed are not in any way a load.
More importantly, the virus never became extinct. If you disagree, please explain how you think they measured extinction. If the virus became extinct, how did it come back multiple times? How did empirically eliminate the possibility that the virus was just attenuated to a state of nonpathogenicity?
Extinction is permanent. Using that term is incredibly misleading.
That’s not what biologists mean by it. So are you saying that when influenza returns from these alleged extinctions, is it not descended from earlier influenza strains?
And I would suggest that you read up on defective interfering particles before you scoff. You don’t have the slightest clue that most of the virus particles produced by any cell infected by an RNA virus are defective; it’s literally how the virus attenuates its pathogenicity to allow greater transmission and reproduction.
This is especially amazing in the case of rabies, as rabies also modifies the behavior of its host to increase transmission. This is all about real-time evolution.
And precisely how is the phage paper I cited above not an observational, experimental study of evolution?
I already know, Paul; my graduate training was in virology, so it’s likely that I know more about it than Carter and Sanford combined. Viral isolates are plaque-purified before sequencing. Plaque purification is extreme artificial selection to get rid of DI particles.
It was a question for you to answer, so that you can comprehend how much selection was involved in obtaining the data that you are misrepresenting as “mutational load”! If you looked into it, you’d see my point.
Amen. And most importantly, contrary to YEC rhetoric, it is not believed.
Amen again. What YECs demonstrate in spades is a severe lack of curiosity. To a scientist, their lack of curiosity comes off as pathological.
Sanford’s “genetic entropy” story is directly and empirically refuted in this study:
https://royalsocietypublishing.org/doi/full/10.1098/rspb.2015.2292
I would refer you to this article addressing that argument:
https://creation.com/genetic-entropy-and-simple-organisms
I don’t see how it does so. Shouldn’t bacteria be suffering fitness decline, rather than increase?
If genetic entropy is the claim that natural selection cannot maintain fitness because weakly deleterious mutations accumulate, shouldn’t fitness be going down? Then why is it going up?
You seem to be saying, effectively, that bacteria don’t suffer genetic entropy. Their fitness is increasing, the opposite of genetic entropy.
You write:
When living things reproduce, they make a copy of their DNA and pass this to their progeny. From time to time, mistakes occur, and the next generation does not have a perfect copy of the original DNA. These copying errors are known as mutations. Most people think that ‘natural selection’ can dispose of harmful mutations by eliminating individuals that carry them. But ‘natural selection’ properly defined simply means ‘differential reproduction’, meaning some organisms leave more progeny than others based on the mutations they carry and the environment in which they live. Moreover, reproductive success is only affected by mutations that have a significant effect. Unless mutations cause a noticeable reduction in reproductive rates, the organisms that carry them will be just as successful in leaving offspring as all the others. In other words, if the mutations aren’t ‘bad’ enough, selection can’t ‘see’ them, cannot eliminate them, and the mutations will accumulate. The result is ‘genetic entropy’. Each new generation carries all the mutations of previous generations plus their own. Over time, all these very slightly harmful mutations build up to a point that, in combination, they start to have serious effects on reproductive fitness. The downward spiral becomes unstoppable, because every member of the population has the same problem: natural selection can’t choose between ‘fit’ and ‘less fit’ individuals if every member of the population is, more or less, equally mutated. The population descends into sickness and finally becomes extinct. There’s simply no way to stop it.
All that text to describe the phenomenon of accumulating fitness decline. While any one single mutation will have an almost imperceptible fitness loss associated with it, in conjunction the fitness losses build up, and the implication is straightforward and obvious. Fitness should be declining.
If one mutation has a small fitness loss, two mutations should have a greater fitness loss still, four mtuations even greater, etc. etc.
So why is fitness increasing in bacteria?
I am gathering you’re saying there was a fundamental problem with the data that Carter and Sanford used in their study. If this is the case, I think the appropriate thing for you to do would be to have a Comment to that effect published in Theoretical Biology and Medical Modelling . This way Carter and Sanford will have the opportunity to publicly address that concern.
To my knowledge nobody in the peer-reviewed literature has ventured to criticize this paper, and it has been cited in other works.
Thanks for sharing this. I’ll look into it.
First, mutations that have been fixed are not in any way a load.
I’m curious why you would say this. For example, in this phage study we see that language being employed (even in the title):
“The main result is clearly the decline in average burst size, supporting a conclusion of a high load of deleterious mutations.”
According to the CDC, you’re wrong. The image below comes from them, and the strain marked red is the one that Carter and Sanford say went extinct in 2009.
It is considered extinct because it has stopped appearing in the databases. Of course that’s not proof positive of extinction (can’t prove a universal negative), but to the best of our knowledge it is extinct.
I’m only aware of it ‘coming back’ one time in 1977. The answer to your question would be impossible to know outside of speculation, but I’m quite sure you could come up with some potential theories to explain what happened there.
How did empirically eliminate the possibility that the virus was just attenuated to a state of nonpathogenicity?
Read the paper for yourself; the study was based upon database information, not on direct experiments (the strain is extinct anyway meaning it’s not available for direct study).
Why is it not going down in these bacteria? That question is addressed in the article I linked to. Why is it “going up”-- probably due to factors we mentioned at creation.com/fitness as it regards the misleading nature of the word ‘fitness’ as it’s used in these cases.
No, it’s not addressed. At all.
You don’t explain why fitness is increasing in bacteria. You spent a lot of words trying to explain why it should be going down SLOWER in bacteria, compared to humans. You never explain why we are seeing an INCREASE in bacterial fitness.
So since genetic intropy is the idea that most mutations are weakly deleterious, and natural selection can’t remove them because such single mutations are almost invisible to selection. Why is fitness then increasing instead of going down?
Why is it “going up”-- probably due to factors we mentioned at creation.com/fitness as it regards the misleading nature of the word ‘fitness’ as it’s used in these cases.
It’s not misleading at all. It is entirely sensible to speak of relative fitness in the context of a particular environment, in terms of the reproductive success of mutant descendants compared to non-mutant ancestors. That’s a simple and straightforward way to understand the concept.
If the mutants have higher relative fitness in the same environment, compared to their ancestors without those mutations, then fitness has increased. The opposite of genetic entropy.
You’ll have to read the article at creation.com/fitness because what is counted as an “increase of fitness” is not really what genetic entropy is all about. I think if you read that article in its entirety you’ll come out of it understanding the answer to this question you’re asking, and how it does not refute genetic entropy.
So now you’re saying you’re employing a sort of bait-and-switch to understand what constitutes “deleterious” mutations under genetic entropy?
You’re now suddenly NOT talking about the accumulation of weakly deleterious fitness effects of mutations on reproductive success of carriers, even though you claimed you were in that wall of text I quoted earlier? Can you get your story straight?
No, not at all. But I’m saying that an attenuated strain can have higher ‘fitness’ despite the fact that it is actually harboring a high load of deleterious mutations and may well be near mutational meltdown. In fact that’s what we see here:
The authors claim that fitness increased despite also saying this:
“The main result is clearly the decline in average burst size, supporting a conclusion of a high load of deleterious mutations.”
Mind blown? 
It doesn’t.
How was fitness measured in the article I cited? In which is it misleading?
Yes you are. You deliberately change the argument away from fitness, to speaking in some vague sense about deterioration, while deceptively retaining the vocabulary of “beneficial” and “deleterious” when speaking about the effects of mutations.
The deception is yours. You write an article on genetic entropy, with this nice fat paragraph about what you mean:
When living things reproduce, they make a copy of their DNA and pass this to their progeny. From time to time, mistakes occur, and the next generation does not have a perfect copy of the original DNA. These copying errors are known as mutations. Most people think that ‘natural selection’ can dispose of harmful mutations by eliminating individuals that carry them. But ‘natural selection’ properly defined simply means ‘differential reproduction’, meaning some organisms leave more progeny than others based on the mutations they carry and the environment in which they live. Moreover, reproductive success is only affected by mutations that have a significant effect. Unless mutations cause a noticeable reduction in reproductive rates, the organisms that carry them will be just as successful in leaving offspring as all the others. In other words, if the mutations aren’t ‘bad’ enough, selection can’t ‘see’ them, cannot eliminate them, and the mutations will accumulate. The result is ‘genetic entropy’. Each new generation carries all the mutations of previous generations plus their own. Over time, all these very slightly harmful mutations build up to a point that, in combination, they start to have serious effects on reproductive fitness. The downward spiral becomes unstoppable, because every member of the population has the same problem: natural selection can’t choose between ‘fit’ and ‘less fit’ individuals if every member of the population is, more or less, equally mutated. The population descends into sickness and finally becomes extinct. There’s simply no way to stop it.
So genetic entropy is the inescapable accumulation of mutations with weakly deleterious fitness effects.
But then in your “fitness” article, you write this:
We know that mutations happen, and we understand that most mutations are bad. So how does evolution work? One way evolutionists get around the problem is to ignore the discussion of mutations. They appeal to an increase in ‘fitness’ as a counter to any claim of genetic deterioration. If fitness has increased, they argue, then deterioration has not occurred. But in cases like sickle cell anemia, where the corruption of an important gene just happens to allow people to better survive malaria, children who carry the disease are more likely to live to adulthood. This is a bad change. The sickle cell trait is deleterious . It hurts people. But it helps them to survive. What do we do with this? Is it an example of natural selection? Yes. Is it good for the individual? Yes, but only if you live in places where malaria is present. Is it good for humanity? Not in the long run. “Fitness” in this case is subjective.
There are other cases where entire sets of genes have been lost in some species. They are able to survive because they have become fine-tuned to a specific environment. They have ‘adapted’ by becoming more specialized, but the original species could live in more diverse environments. Sometimes this is oxymoronically called ‘reductive evolution’. In this way, evolutionists never have to admit that genetic entropy is actually happening. But this is what natural selection does. It fine tunes a species to better exploit its environment. Since natural processes cannot ‘think’ ahead, the result is short-sighted. If the loss or corruption of a gene helps the species to survive better, it should be no surprise that this happens regularly. Species end up getting pigeonholed into finer and finer niches while at the same time losing the ability to survive well in the original environment. Natural selection goes the wrong way !
So here we see the bait-and-switch right before our very eyes. The change from speaking about the fitness effects of mutations, their effect on reproductive success, to some nebulous idea about how the mutation works at the biochemical or cellular level.
So in order to maintain Sanford’s claim that all populations are suffering “genetic entropy”, which you spent lots of words defining as fitness decline, you are forced to change the subject to include the maintenance of the molecular and cellular phenotypic functions of the systems the genes encode. The shapes of cells, the structural integrity of certain molecular complexes, and so on.
Sanford levies the prestige and opaqueness of a mathematically heavy field like population genetics to prove that the accumulation of reproductively deleterious mutations should cause inescapable fitness decline, but then when the real world contradicts this deceptive use of population genetics and the correct usage of the terms fitness (when in the real world fitness goes up), he (and you) turn around and start weakly waving your hands in the direction of broken genes and “bad” sickle-cells, and you have the temerity to accuse evolutionary biologists of being the deceptive ones.
You’re confused. Nobody is disputing that genetic load is, or can be, a real thing that happens.
What they are disputing is the claim that “genetic entropy”(inescapable and persistent fitness decline) is always happening, that life could not have existed on Earth for billions of years because of it, and that all populations are suffering constant and unavoidable fitness decline because of the accumulation of weakly deleterious mutations.