Just had to say that this is excellent, David. I’m gonna steal this entire post & hang onto it. 
Cheers.
I’m not sure what you are calculating here. Just some back of the envelope calculations . . .
Using @glipsnort’s estimate of 150,000 recombination hotspots and 50 crossovers per meiosis, that’s a 1 in 30,000 chance of a recombination occurring at any given hotspot per meiosis. With a few million births in one generation you should get recombination at almost all hotspots in just one generation. Of course, some hotspots are hotter than others, but still, with a rather small population it should be quite easy to get all recombination events at hotspots in each generation.
That’s a bit of a loaded question since there are many claims attached to that term. Are there features where the removal of one part destroys the function of the whole? Yes, absolutely. Those are found throughout biology. However, I have yet to see anyone demonstrate that such systems can not evolve.
On top of that, science isn’t based on opinions. You subjectively believe that things in biology look designed, but subjective beliefs are not something science can gain traction with. What makes you believe in intelligent design is a question of psychology, ultimately. I don’t doubt that you believe this, but stating a belief is not very compelling evidence for those who don’t share your belief.
I will also echo what others have said. Truth doesn’t have to be scientific. Even as an atheist I don’t require Truth (with a capital T) to be scientific, empirical, or even materialistic in a narrow sense. However, when we have mountains of evidence for natural mechanisms playing out in biology it isn’t compelling when someone says we should just ignore them because of a belief they hold. Nor is it compelling when they claim those natural mechanisms can’t produce what we are looking at just because they say so. We need more than that. We need some data. We don’t need more rhetoric, semantics, and word definitions.
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As our informal intelligent design club insisted firmly, the moment you start arguing from a Designer you’ve stopped doing science.
I’m not sure why that is such a hard concept to grasp.
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According to YEC it does. They unknowingly measure truth according to scientific materialism.
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Plantinga’s essay on methodological naturalism might have something to do with it
I wouldn’t go that far. Hypothetically, there could be strong scientific evidence for a designer, even a natural designer like an alien species. It just so happens that the arguments we do get for design aren’t scientific. The reliance on rhetoric over data is one aspect of this. The constant Designer of the Gaps and burden shifting are other examples.
The real science stopper is ignoring the basic law of parsimony. This is best seen in the claim that it is somehow unfair that supernatural explanations are excluded from science. There’s a reason for that. We wouldn’t be able to explain anything if we threw out natural explanations (backed by mountains of evidence) just because we could imagine a supernatural being creating the same evidence. Since a supernatural being could do anything, then any evidence could be created. This is the type of argument ID proponents use to exclude evidence like the nested hierarchy or shared endogenous retroviruses. These types of ID arguments are meant to stop science.
It is an odd thing, isn’t it? They spend so much time calling science secular and atheistic, but they want nothing more than ID/YEC/OEC to be called scientific.
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I heard Richard Feynman make a startling admission about how an unending scheme of natural laws would be, I think he said, boring.
Something from nothing would also be an end to science, that is, it would be impossible to explain why it happened.
But the moment you bring in a Designer then aren’t you bringing in the supernatural?
Or at least to inoculate their audience against it.
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A dead end, rather, or a hole in the fabric; the rest of science would go on.
Here’s some complexity: I just finished watching Whiplash, which focuses on a hot drum student, and I just noticed that I’ve been typing out the rhythm of one of the numbers on the keyboard. I’m not sure I could have done it intentionally but that rhythm got into my head (and apparently my fingers) and out it came.
The reasoning here is that you always get what you need for the future.
It doesn’t seem that there is a tendency that you look into the specific features of the proteins (crystallins) that are needed to create a lens.
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How is that different from God causing an event?
I meant the argument we’re having about how rare protein function is. You didn’t introduce Axe’s paper yourself, but you did introduce a paper that relies on Axe’s work as a key step in its argument. You called the deeply impressive and wrote
Are you maintaining that claim – that a few undirected mutations can create entirely new functions – or not? Axe’s work doesn’t support that claim and your argument for it based on the rarity of catalytic function hasn’t stood up well.
You seem to have missed my point, so I will try to clarify it. Haplotype blocks are small compared to chromosomes and they are many compared to the rate of functional mutations. Say the rate of deleterious mutations per human birth is 4 (even though it’s probably lower than that). That’s two per genome copy. Those two will be more or less randomly distributed among the 150,000 blocks that occur between hotspots. Almost always they will occur in different blocks, which means that they are effectively unlinked, with free recombination between them. So the normal process of recombination + purifying selection will operate to remove them from the population. That takes some time, so we all are carrying some load of deleterious mutations, but the number of those is still much smaller than the number of blocks, meaning that new deleterious mutations are effectively unlinked from existing ones, as well.
Sure, occasionally a new deleterious mutation will occur within the same block as an existing one, but not often. This means that the ratcheting effect of hotspots is five or ten thousand times less than if entire chromosomes were non-recombining, meaning it’s negligible.
For the same reason, new beneficial mutations will also almost always be effectively unlinked from deleterious mutations.
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It wouldn’t be unreasonable to believe in a designer obviously, and I don’t think you are making that claim.
My basic understanding of ID arguments could be wrapped up in the view my professor in philosophy of religion, Paul Draper, had. That a designer is highly probable due to the apparent design in the world, but it’s also highly probable that a designer doesn’t exist in the God sense due to the apparently needless suffering that happens in the world. Now that I think about it, the apparently needless suffering could be tied in with evolution easily.
This double sided probability was the basis for his agnosticism. That was 20 years ago, and I think he has changed his view somewhat, but I haven’t kept up with him.
No, you don’t always get what you might possibly have use for in the future. But if you get something useful, you can often hang onto it because natural selection favors it. Then a variation of it might be better, and likely to be retained. In other words, complexity is reducible.
You don’t need crystallins to make a lens; glass and plastic and any other transparent material will do. The crystallins have other biochemical functions and so have been handy options for many organisms to use for lenses, from simple and blurry to more advanced. But other options exist as well. Trilobites used calcite for their lenses, for example.
Proving intervention-style ID has the difficult task of showing that a particular feature is not simply one of myriad possibilities. For example, given that there are 20 standard amino acids, the probability of a specific 8 amino acid sequence being generated randomly is 1/(20^8) , about 1 in 26 billion. Should I conclude that the sequence glycine-alanine-isoleucine-asparagine-phenylalanine-isoleucine-serine-threonine must have had an intelligent designer intervening to make it? Not only does it serve as part of an essential protein in many freshwater mussels, it also spells a message using the standard one-letter abbreviations: GAINFIST. But the same essential protein is found in practically all eukaryotes and some bacteria, with variations in the amino acid sequence; the mussels would survive with any number of different exact sequences, though not all spell a two-word phrase. And we have no idea how many alternative ways there might be to make multicellular living things that don’t depend on having functional mitochondria.
Again, disproving that some intervention-style design occurred is similarly difficult. But I have not seen any claims that biological features couldn’t be produced by evolution that struck me as good, given my background in paleontology and molecular systematics.
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I’m not. I’m questioning a specific claim about the rarity of functional proteins in protein space.
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I was sceptical about the claim that betalactamase activity raised from random peptides with a chance of 10^-9. And I think that this was right. Catalytic activity isn’t intitiated by random peptides but by coding part of the genome. However, while studying in the literature about abzymes, I realized that some functions can be performed by simple structures and that sometimes, hydrolysis is easily done. However, many functions require very complex structures or sequences of events, for which it’s for me not possible to imagine that this occurs by chance (and selection of course). Betalactamase activity seems to be a relative simple function.
Thank you for that. You are clear. Of course, I understand that with presence of many haplotype blocks, ratching is much lower, however, does this realy mean that it is negligible? The second point is that you compare actually mutations (4 may be) with all haplotype blocks present, however, only a very very small part of the recombination hotspots are used at the same time. Is this a correct comparison? The third point is, that it seems unlikely that nature is able to select against 4 mutations per individual per generation, which means that undesirable mutations accumulate.
Perhaps some you can elaborate on the opposite situation, where a mutation does something that might seem deleterious at first, but actually must be beneficial for the organism to not have to expend resources on it. Thinking of the broken vitamin C enzyme in humans and apes, and the blind eyes of cave dwelling organism.
Those would seem to be a hard sell for ID.
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I wrote:
And you said:
I don’t see the connection.
I’m envious.
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