I definitely feel your pain on the too many books on the reading list side of life. A benefit of being single is the ability to spend more time reading, but even then there just isn’t enough time. Just figured that it would be good to not just rely on a rebuttal paper without reading the book itself to see if the criticisms are fair.
Not always doable with limited time, though
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No, it still doesn’t. You’ve had this explained to you multiple times. You can’t generalize one part of the mitochondrial genome to the entire mitochondrial genome, just like you can’t generalize the y-chromosome to all other chromosomes.
And then you have to factor-in the long-term effects of natural selection. Deleterious mutations will be weeded out by natural selection. Hence the long-term mutation rate must be lower. This result is so basic and unassailable only an insane person would seek to oppose it.
If a mutation lowers your reproductive rate compared to others(and some mutations do), then that mutation will eventually be outcompeted and go extinct.
There are no ifs or buts here. If you deny it, you have left the arena of rational discourse.
I don’t know which or to what extend ignorance or something else explains your apparent inability to put two and two together here, I’ll leave that to your own devices to figure out. Suffice it to say you’re not impressing anyone by making the same easily debunked, vacuous assertions every time.
No, still no. You can’t generalize the D-loop of the mitochondrial genome to the rest of the mitochondrial genome. No, you can’t just ignore the effects of natural selection. No, natural selection isn’t an assumption, it’s a demonstrable reality. It is so basic one can know it from reason alone.
The attributes of organisms are encoded in their DNA.
Changing that DNA changes their attributes(such as survival and reproductive success).
Those attributes can get worse.
Hence some mutations unavoidably, logically necessarily must have deleterious fitness effects. You can’t get around it. It won’t go away just because you don’t want to think about it.
You can ignore it, which you seem to be doing. But that only reflects badly on you.
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Have you read Genetic Entropy? In chapter 4, Sanford explains scientists have been taught evolutionary theory this way, but he says this is absolutely wrong and not how it works. But I need to read the whole book and some others before I want to argue this. Just wondering if you have read the whole book.
Sanford does not argue that deleterious mutations are not weeded out by selection over time. He argues that not all deleterious mutations are weeded out, which is an argument that is irrelevant to @Rumraket’s point.
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He says that, it’s nuts to say that. Sanford can’t argue reality away. Use your own brain, think.
Is it possible to get a mutation that affects your survival and reproductive success? Just to pick one of the most obvious examples, imagine you get a mutation that makes you sterile. Will you be passing that mutation on?
Think ! Use your brain and think.
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Have you read the book?
And @evograd is right, there’s clearly a conflict even between Sanford’s understanding of population genetics, and Jeanson’s vacuous dismissal of the time-dependent mutation rate.
Sanford’s thesis is that among deleterious mutations there is a large fraction that are so weakly deleterious they can accumulate to large numbers before they start showing their effect in bulk. But he doesn’t argue anywhere that deleterious mutations of more strong effects don’t exist. At all.
It is logically unavoidable that deleterious mutations of more significant effects will get removed more quickly by natural selection.
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Can you use your own brain or have you dug it out and installed Sanford’s book in it’s place? Are you afraid of allowing yourself some thought? Do you need to be coached into what to say, or can you try reasoning for yourself just for a moment?
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Here’s a section from the book:
Natural selection has a fundamental problem. This problem involves the enormous chasm that exists between genotypic change (a molecular mutation) and phenotypic selection (selection on the level of the whole organism). There needs to be selection for billions of almost infinitely subtle and complex genetic difference on the molecular level of the whole organism. When “Mother Nature” selects for or against an individual within a population, she was to accept or reject a complete set of 6 billion nucleotides - all at once! It is either take all the letters in the whole book or none.
Then he goes on to talk about homeostasis and how that makes mutations invisible to selection, so that deleterious mutations won’t be selected away.
That’s how far I’ve read, so I can’t argue beyond that. 
I don’t understand what you’re distinguishing between here.
You should answer the question. Have you read the book? Yes or no?
Yes, this is where he is describing this assumption he has that most mutations have very tiny deleterious effects.
That doesn’t change anything about what I have been saying.
The magnitude of the deleterious effect. The degree to which a mutation is bad. Some are worse than others.
Sanford is imagining that most mutations(but not all) are deleterious (bad), and that the majority(but not all) deleterious mutations have effects so small that they’re basically invisible to natural selection on their own, and so their “badness” only starts to take effect when they have accumulated in large numbers (because many small bad effects add up into a large bad effect).
But he doesn’t say there are no large-effect bad mutations. They’re still part of his model. Even in his model, they get removed by natural selection because of their large effect.
Now clearly we don’t even have to consult his model to know and understand that there are organisms born with very bad mutations. Stillbirths, Siamese twins, and many other things like that. For all organisms including humans. These unlucky individuals don’t get to pass on their genes. Some individuals with bad mutations don’t die at birth, they survive to adulthood, but they’re still strongly affected by their bad mutations. For organisms “In the wild” they don’t survive or reproduce as well. These individuals are extremely unlikely to pass their mutations on for many generations.
Among such mutations are those that cause sterility, or very low fertility. Some men produce very few (or no) viable sperm for example. Some women have similar problems with their eggs. Clearly such people are very unlikely to successfully reproduce. Their mutation is therefore very likely not passed on to coming generations, it is thus effectively removed by natural selection because of the effect the mutation had. So even though we would be able to measure their mutations as having occurred, they need to be subtracted from the long-term rate of mutation. And we can add many others to the list. Mutations that affect survival and reproduction in many other ways than a direct effect on fertility.
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No, but I am familiar with what it says. I don’t need to read his book. I have argued extensively with apologists who come here to talk about it. I have read both his papers in the peer reviewed literature, and his non-peer reviewed papers published in various creationist venues. I’ve read pretty much all the articles dealing with the subject of GE on AIG and CMI’s websites.
Now, I also happen to be able to just think. Nothing that it says in any book is going to affect how the real world works. Deleterious mutations of strong effect clearly exist, and they logically necessarily will be very unlikely to proliferate in any population.
Why subtract them?
He says,
A few rare mutations have profound biological effects…Natural selection against these types of major mutations is an obvious “no-brainer.” But the bowling ball (semi-lethal) mutations are very rare, and such nucleotide sites carry only a miniscule amount of the total information in the genome. Most of the information in the genome is carried by nucleotides whose effects are much more subtle…It is the origin and maintenance of all those nucleotides that we are trying to understand.
Have you read the book?
Please just think. If we are trying to count the long-term rate of mutation, then mutations that get removed in the short term will not be there to be counted in the long-term, will they?
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The whole point is that they are accumulating. They are not removed.
Can sterility mutations accumulate? Infertility?
Edit: I apologize for my tone. It’s uncalled for.
Obviously not.
I have many friends who’ve had trouble conceiving. After beginning to read this book, I wonder if this will be accumulating. Societal implications like autism ( a big implication in my life)…endometriosis for many of these female friends…The book’s implications are huge. This matters obviously.
Definitely selectable.
In nature, these would be.
No. Given the quality of Sanford’s paper on H1N1 and his articles on lifespan decay, I have no intention of reading his book, now or ever.
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Okay good. We can agree on this at least. So these would be deleterious mutations of very strong effect, and they will not be able to accumulate. When they occur, they won’t be passed on by their very nature.
We can see that there are infertility/sterility-type mutations. These will be lost again quickly when they occur. So if we count the rate of mutations that accumulate over the long-term, these won’t be among them. Already now we can see that there is a time-dependency to mutation rates. Some mutations with extremely strong deleterious effects are lost immediately.
So now we can go a step further. There are lethal mutations too. Mutations that are lethal to the organism before they get to reproduce. They may be lethal already at the single-cell stage. A cell divides into two, the daughter cell suffers one or more mutations, the mutation completely inactivates one or more genes absolutely critical for the life of that cell. That mutation occurred, but does not get passed on to any further cells.
Or there are lethal mutations that take effect during embryonic development. Or after birth, some time during childhood. Such as a brain-cancer causing mutation that a young child is born with. This mutation also won’t accumulate in the population, because the child will die before being able to pass it on. It’s a tragedy, but sadly a reality. They happen. So this type of mutation also does not contribute to the long-term rate of mutation. We will not be able to count that mutation among those having been passed on many generations down the line.
And we can go on and on. Mutations that take effect later in life, that aren’t immediately lethal, but also affect the survival and reproductive rates. Mutations that cause individual organisms to have fewer offspring than “normal”. Mutations that make organisms have a hard time surviving in the wild.
Over the long term, such mutations are unlikely to accumulate because their negative effects are too strong.
It follows logically that there really is and must be a time-dependent mutation rate. Over longer and longer periods of time, more and more mutations will be lost to natural selection.
So observing a pedigree rate of mutation measured over single or double generations can’t be the actual long-term rate of mutation. It logically must be lower. How much lower depends (among numerous things) partly on how long term we look(centuries? millennia? eons?), and partly on the distribution of fitness effects of mutations (how many of them have strong deleterious effect, and how strong are those effects?).
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I want to emphasize this. @evograd in part 6 of his review documents several predictions of time dependent slowdown, all of which have been verified:
As I said, this model can continue to be tested, for example with studies estimating mutation rates by calibrating with medium-term events known from archaeology. If estimated mutation rates keep falling on that curved line (Figures 5 and 6), this is further support for the time-dependent rate slowdown hypothesis. For example, consider the results of Rieux et al . (2014). They estimated mutation rates using calibration points of ancient DNA sequences that were independently dated to between 2,500 and 64,500 years old. Not only did their overall estimated mtDNA mutation rate come out to a value intermediate between the fast rate from pedigree studies and the slow rate based on more ancient divergences, but they also observed a time-dependent trend within their own dataset.
Another prediction this hypothesis can make is that synonymous sites should display far less signature of time-dependence than non-synonymous sites, as mutations in these sites would be less likely to cause any fitness effect that could be acted upon by natural selection. For example, mutation rates estimated from 3rd codon positions should be fairly similar regardless of timescale, while the estimates from 1st and 2nd codon positions should differ, following the trend in Figure 5. This is a prediction that has been fulfilled ([Endicott and Ho, 2008); (Subramanian et al ., 2009). Put more simply, deeper (older) branches in the phylogeny should display a lower ratio of non-synonymous to synonymous mutations than more recent branches, which is what we find (Kivisild et al . 2006.)
If Jeanson genuinely believes testable predictions are the bread and butter of real science, he needs to deal with these confirmed predictions of time-dependency. Im sorry, but Jeanson does not get to decide these fulfilled predictions don’t count simply because he came up with his model after the fact. He needs to explain why these predictions are not validations of the model and how they fit his own. We know he lurks here, so I’d frankly like to see an explanation.
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