Valerie and Michael on Todd Wood and Evolution

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Has Todd Wood ever said this? I’d like to see the quote.

Since you’re sharing dreams, my dream would be for evolutionists to see that evolution is not the strongest explanation for the diversity of life. :smiling_face:

That being said, my experience here was to be absolutely overwhelmed. I’m still amazed I stayed. :thinking: I’m just weird I guess. If you’re YEC, it’s going to be that way, based on the make-up off the regulars - maybe after these conversations it will change ever so slightly. If you affirm all of current, mainstream theories of evolution, you get to join the good’ol-boys club, which you did @Michael_Okoko. Either way I appreciate this thread. It’s tough for me wanting to be respectful of people who took the time to respond by responding back when you’re getting hit up with 5-6 responses based on one post.

Also, honestly what I’ve learned is that the mainstream responses to what y’all consider PRATTs only take a few months to cover. They’re now starting to look fairly similar to me. And I’ve also decided I’d rather stay to discuss new developments in science or discuss philosophy rather than origins as it’s annoying to cover the same stuff over and over and I’m not sure anyone will budge.

Any YEC lurkers, if there are such, aren’t going to learn anything new. They’re not going to think - shoot, I thought I had a good argument and such and such a person refuted that one. They’ve already heard it or seen it if they’ve lurked, I’m sure. So there’s really no point to considering such a person IMO. There may be a person who is new who hasn’t considered the arguments - but again they’re likely to log in, pose a question and be immediately overwhelmed. I’ve noticed a few posed ID questions and they didn’t even bother to engage very far into the thread after so many responses.

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Thanks I had read this before, but I find the blog to very different than saying he understands it’s the strongest explanation for the diversity of life. Perhaps he still does say that elsewhere.

Very much agree with him here:

Please don’t idolize your own ability to reason. Faith is enough. If God said it, that should settle it.

I have been watching his videos on evidence against evolution and it is a little odd that he seems to spend more time in each video giving evidence for evolution than against. :thinking::joy: But it’s in keeping with the spirit of the blog I suppose; he doesn’t fear evolution.

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Hahahaha, just keep on learning Valerie. Despite your refusal to let go of some misconceptions (like thinking evolution is solely based on random chance), you have certainly learned some things and have a somewhat better understanding of evolutionary theory than the average YEC.

Your dream is also extremely unlikely to come true. Evolutionary theories are pretty powerful and have been tested for decades.

My affirmation of evolutionary theory is irrelevant. What matters is why I do. I also affirm a globe earth, germ theory of disease and cell theory. Why? They are supported by mountains (if not galaxies) of evidence.

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I didn’t quote Todd in that comment I first mentioned him. Those were my words not his. By strongest, I meant best and by best, I mean most supported and Todd agrees with me:

“Evolution is not a theory in crisis. It is not teetering on the verge of collapse. It has not failed as a scientific explanation. There is evidence for evolution, gobs and gobs of it. It is not just speculation or a faith choice or an assumption or a religion. It is a productive framework for lots of biological research, and it has amazing explanatory power. There is no conspiracy to hide the truth about the failure of evolution. There has really been no failure of evolution as a scientific theory. It works, and it works well.”

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Btw, I don’t think this.

As far as I can tell, natural selection has barely been studied. As much as everyone bickers about DFE for various organisms and never references anything, it’s obviously not grounded in any “testing” yet.

Still not the same thing. Words mean something. “Works well” and “productive” do not mean “strongest” and “best”

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I don’t think you do, but you described evolution as purely random quite recently in another thread, to which I responded and said I was “irritated” (could someone help me search for it, because I tried but couldn’t locate that comment). You certainly know a bit better than the average YEC, but you sometimes repeat YEC canards which have been thoroughly debunked here.

Don’t let me change my mind about you knowing better than the average YEC.

Have you tried searching for these studies yourself? Or have you asked the experts here for those papers? The DFE for mutations in coding regions are a lot easier to measure, not so for non-coding regions, but there are studies that have looked at the DFE of new mutation for both parts of the genome. Seek for these papers and you shall find.

You ignored “most supported”.

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In science it kind of does. Scientific theories have descriptive, predictive and explanatory power. If something explains a lot of our observations, it ‘works well’ because it has descriptive power. If it makes testable predictions that have not been falisifed with evidence (I know, others, Popper is not everything…), it is ‘productive’ in terms of generating new scientific inquiries. And if it offers explanations for the phenomena it describes and predicts, it works well and is productive.

I’m not sure how ‘strongest’ and ‘best’ could be defined differently for scientific theories. Do you have an approach to suggest?

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The deleterious DFE in coding regions for multiple organisms has been studied quite extensively. We don’t know exactly what the distribution is because it’s difficult to measure and is transient. However, we do know the DFE used by GE is not supported by the best available data. We also know the beneficial DFE used by GE is not supported by the best available data. We additionally know the DFE for coding regions is different from the DFE for non-coding regions and therefore the DFE is multimodal.

The deleterious DFE in humans looks closer to this:

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The SNVs were derived from whole-genome sequencing of 9 YRI individuals (Yoruba in Ibadan, Nigeria).

Racimo F, Schraiber JG (2014) Approximation to the Distribution of Fitness Effects across Functional Categories in Human Segregating Polymorphisms. PLoS Genet 10(11): e1004697. Approximation to the Distribution of Fitness Effects across Functional Categories in Human Segregating Polymorphisms

You might notice there appears to be at least two groups of distributions. Each group [edit] may correspond to the coding versus non-coding. You should also notice the mean deleterious DFE used by GE (from Kimura) is 0.001. You would need to extend the x-axis on this figure over 3 times to find that value.

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This statement suggests a lack of curiosity and desire to learn on your part.

Natural selection has been the subject of intense study in a wide variety of contexts using different tools and types of data for many decades now.

Does that mean that we know everything–or even most things–about how it operates in all situations? Not at all. There is a lot left to learn. That’s why we do science, and science is hard.

But to suggest that it has “barely been studied” is absurd and false. Frankly, it is an insult to the thousands of researchers who have spent literally millions of hours studying how selection works.

If you want to gain a small inkling regarding what is known about natural selection (among other things), might I suggest that you read Graham Coop’s free electronic textbook, Population and Quantitative Genetics. It is a well written and relatively accessible, if brief, introduction to the topic.

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Well, I qualified the statement - it was based on what I read in a paper that was linked here in the forum that mentioned not much observational study had been done, as well as general observation based in what people have shared in the forum on posts. I’m happy to be wrong if that’s not the case.

But let me be defensive for a minute so you can get to know me better: I have a part-time job, I have two little kids who seem to want to trash my house so I feel like I live in chaos. In the middle of that I have about two months in of studying biology after my kids go to bed, but I’m trying out of curiosity and a new interest in science. For almost the last two weeks and probably for the next two+ months I get to feel like I have the flu every day because I’m silly enough to want to increase my fitness (I tried before but no one got/acknowledged the joke). I’m feeling almost normal right now, so I’m in a really good mood. But yeah, with all that, I feel like I’m allowed to be a little defensive and say that I think “lack of curiosity” doesn’t describe my personality. :smiling_face: But you did say “suggests” so you qualified your statement as well. :slightly_smiling_face:

Thank you for the link! So much to read already… Merry Christmas! :christmas_tree:

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Please keep in mind that understanding the distribution of fitness effects of new mutations is one very small part of studying how natural selection works. Moreover, it’s become much easier to examine the DFE in recent decades because mutations are much easier to measure and track. Fitness effects of individual mutations are still challenging to examine, but there are plenty of systems where they can be assessed directly (bacteria, yeast, etc.), and lots of useful methods for indirectly measuring fitness effects in in less cooperative organisms. There are now lots of empirical data on the DFE (for example, check out some of the roughly 1,000 papers that have cited the Eyre-Walker and Keightley 2007 review paper that gets mentioned a lot).

But let me be defensive for a minute so you can get to know me better: I have a part-time job, I have two little kids who seem to want to trash my house so I feel like I live in chaos. In the middle of that I have about two months in of studying biology after my kids go to bed, but I’m trying out of curiosity and a new interest in science. For almost the last two weeks and probably for the next two+ months I get to feel like I have the flu every day because I’m silly enough to want to increase my fitness (I tried before but no one got/acknowledged the joke). I’m feeling almost normal right now, so I’m in a really good mood. But yeah, with all that, I feel like I’m allowed to be a little defensive and say that I think “lack of curiosity” doesn’t describe my personality. :relaxed: But you did say “suggests” so you qualified your statement as well.

I get that everything is chaotic (and congrats on the impending baby!). And I’m sorry if it seems like I’m jumping down your throat. I may be a bit grumpy about the fact that I’m not seeing any family in person this Christmas.

That said, you don’t actually have to express opinions on topics that you don’t understand. I try to avoid doing that most of the time, though I’m sure I don’t always succeed. We could probably all do a better job of exercising intellectual humility.

Thank you for the link! So much to read already… Merry Christmas!

Merry Christmas to you too!

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Sorry, I wasn’t clear - I wasn’t correlating the two even though they are related even and I mentioned them together. It was meant to be 1) natural selection 2) DFE

Thanks for getting my joke. I find it amusing to refer to it as fitness.

I’m really sorry you’re not getting to see family.

True. It’s a personality flaw. I’m trying to avoid it though.

Science would probably be the better for it. But we’re all human. It’s a good thing to remember at Christmas.

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Then why the hell is Sanford claiming he knows what the DFE of mutations is really like, and that it supports GE? You can’t have it both ways.

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Adam and Eve with perfect genomes. He doesn’t say it, but we know its most likely what he wants to.

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You haven’t bothered to look.

How is that obvious?

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By the way, here’s an article on the DFE for three different catalytic functions for a single enzyme.

Pay special attention to figure 4:

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( a ) The DFE of missense and nonsense mutations for ACT (cranberry), PR (orange) and IB (cyan) growth selections. The dashed vertical line demarcates the wild-type fitness metric ( ζ =0.0). ( b ) DFE for beneficial mutations identified in the ACT, PR and IB selections, respectively. Overlain curves are best-fit exponential distributions estimated from the data.

Somehow this massive number of mutations of invisibly small fitness effect are absent, most mutations have significant effects tunable by selection, and the proportion of mutations that are beneficial range from about 22% to 5%.

Missense mutations were on average deleterious for the ACT and PR selections, with 75.8% and 74.2% of variants yielding at least 20% reduction in growth rate relative to wild-type, respectively. By contrast, only 45.4% fell below this threshold for the IB selection. Remarkably, 21.5% ( n =1,394) of missense mutations had above wild-type fitness metrics for the IB selection, with 483 (7.5%) variants having at least 10% increased growth rate ( ζ >0.15). There were appreciably less enhanced variants found in the ACT and PR selections, with 4.7% and 5.1% ( n =306 and 328) having fitness metrics above wild-type, respectively.

Wrap your head around those numbers. While most mutations are deleterious, the proportions are enormously removed from those assumed in Sanford’s work on GE, who is usually operating on the assumption that one in one million mutations are beneficial, with the rest being deleterious. Sanford will some times relax that assumption down to a range where 1 in 1000 mutations are beneficial, but considers basically any higher proportion to be physically unrealistic.

Price stated that proportions such as those measured(not drawn from analogies or assumed, measured in experiments) above are “self evidently false”. Well, I guess creationist intuitions about how “computers” work are of no real value in understanding the phenomenon of life, or the relationship between genetic mutations and the fitness effects of genotypes.

Notice something else there. The proportion of beneficial mutations is much higher for a non-canonical enzyme substrate the enzyme has not normally been selected on (fig4 a, blue color distribution). Which again supports the concept I have brought up multiple times before in GE discussions, which is the concept of diminishing returns epistasis, whereby the distribution of fitness effects of mutations changes as a function of fitness and gradually shifts the distribution towards more deleterious at higher fitness levels because the magnitude of effect and the pool of fitness-improving mutations gets closer to becoming exhausted for individual fitness-contributing functions, such as those of enzymes.

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Also by the way, there’s a button linking to the free full-length paper:

It looks as though your claims have been thoroughly and objectively falsified.

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