Dr. Swamidass, who apparently calls himself “a new voice in the origins of life”, was a part a webinar with Jonathan McLatchie, a well known apologetic among the supporters of ID.
I think that the 2 hour discussion was actually very interesting, despite my earlier scepticism about it…I was wrong about Swamidass in some ways (I was wrong about his beliefs mainly), so it turned out to be interesting… Initially, I wasn’t going to join the webinar, as I usually take time off from any activities on Saturday, but my kids challenged me… So, I did, but I did miss the great majority of Swamidass’ intro…
Please note that no matter what question asked, Swamidass, if possible, refers it back to Behe… I’m sure it is obvious why… “
My questions are at 1:24.00 aa
It looks like my last update to the OP didn’t work. My questions to Swamidass are at 1:23.00 and 1:44.00
I don’t think it can be clearly heard the first part of my question at 1:44 though…
I’ve asked for the transcript that webinar…
Maybe someone can find a better link to the interview.
Maybe this No good for me. I’ve been boycotting Facebook since the Shenanigans with Brexit, Cambridge Analytica and Putin’s puppets.
I have an id without my name, with all privacy settings maximized, with no friends, and to which I never post. But it is useful for seeing some FB only posts.
I’ve configured my email to route “please post” stuff from FB to my junk mail.
I personally have no interest in spending 2 hours watching a video on this topic. It was interesting to put a voice with Joshua’s face. He’d be a good podcaster, IMHO, should he ever want to give up the forum-running biz.
J-Mac’s questions were inaudible for me. Which is an interesting meta on them at least.
.
LOL
My first question at about 1:22.45 was:
“Dr. Swamidass,
You have agreed that the polar bears’ “white” fur coats are due to the damaging mutations in the 2 genes responsible for the production of pigment in hair follicle cells, right? Therefore, Behe in fact was right in this case beyond any doubt, right?”
The provided link worked for me — in a private browsing window (in “opera” browser). And I’m not signed up for facebook anyway.
Ah, okay, when I try a private browsing window with “firefox”, it tells me that I must login first. But a private browsing window in “opera” still works.
Try the Brave browser. I believe it was produced by disgruntled FireFox people.
Didn’t watch the video. I was told there would be cats.
My second question at 1:44.00
Part A:
“Dr. Swamidass,
As a medical doctor, if 89 of your patients were on high fat diet and had extremely high cholesterol levels and no signs of heart disease, would you conclude that the lack of atherosclerosis in your patients was due to the beneficial mutations in ApoB protein?”
Is it me or was Swamidass stunned by the question? 😉
There’s nothing merely ‘apparent’ about it; he does call himself that. He’s a non-mainstream evangelical activist now ‘confessing’ himself as a self-proclaimed ’empty chair’ speaker on the topic of origins. He’s pushing both scientism & fideism at the same time & opening a new audience at PS in doing it. And he really doesn’t like me social psychologising about that, though it’s simply true.
My second question at 1:44.00
Part B:
“The researchers of the official paper published in Cell regarding polar bears concluded that the mutations in ApoB protein are linked to the LDL cholesterol transportation system prevent heart disease in polar bears and yet according to the same article in Cell the polar bears’ cholesterol levels are extreme. As a medical doctor, do you agree with the paper’s conclusion?
How could the conclusion be that mutations improve the LDL transportation clearance, if the same paper indicated that the polar bears’ cholesterol levels are extreme? Isn’t that a contradiction?
I have a feeling that someone here disagrees witn Dr. Swamidass’ answer to this question of mine. Rumraket??? 😉
Not necessarily.
If ApoB mutations increase it’s function by increasing fat transport and clearance from the bloodstream, but you eat extremely high amounts of fat, you might still have higher than usual blood cholesterol. As I wrote in the other thread, a hypothetical example could be that the function of the ApoB gene is increased 15%, but you eat 300% more fat than normal, you still end up with high blood cholesterol because cholesterol is involved in fat transport. So you still need all that cholesterol to transport the fat through the bloodstream. And now the ApoB gene is clearing it 15% faster than normal, but still not enough to reduce blood cholesterol levels below normal, because you eat 300% more fat.
You need to understand that there are relative magnitudes of effect at work here, and a better ApoB gene does not automatically translate into the nonexistence of LDL cholesterol in the blood stream.
Being 15% more efficient doesn’t fully compensate for a 300% increase in workload.
J-Mac,
I would like to hear more about how your kids “challenge” you, when it comes to acceptance of evolution.
Behe is essentially arguing that mountains shouldn’t exist because there is erosion. All he does is cite examples of erosion and ignores all of the examples of uplift. For evolution, Behe focuses on all of the mutations that damage genes while ignoring all of the mutations that improve or change function.
T_aquaticus,
I may be mistaken but both improve function and neutral mutations are mentioned in the book. Did you read the book? His point is that damaging mutations are more frequent and Art Hunt agrees with this.
Where did Behe do any calculations to show that the rate of gain of function mutations is not enough to make up for the rate of damaging mutations?
In brewers yeast, we can see that the rate of gene loss and gene gain is about the same, resulting in those yeast species keeping around 6,000 genes with a large flux of loss and gain.
https://onlinelibrary.wiley.com/doi/full/10.1111/evo.13710
T_aquaticus,
Where does it talk about gain of function variants?
They aren’t pseudogenes. They are functioning genes.
Are you asking that because you think that in order to show that Behe is wrong, we need to show that the number of gain of function mutations must quantitatively equal or outnumber the loss of function mutations?
To answer your question, it doesn’t speak of gain of function variants because the analysis they did wasn’t capable of finding them. They only looked for premature stop codons and frameshift mutations, and reasoned that these were more likely to be loss of function mutations.
No conclusion about relative rates of all adaptive losses versus adaptive gains can be derived from it.
T_aquaticus,
Your claim is that they were originated from random mutation?
I didn’t know that J-Mac was Jonathan McLatchie. McLatchie comes across as a stupid but decent human being, whereas the J-Mac persona shows astounding stupidity mixed up with a level of self-unaware arrogance that makes him come across as an authentic ass-hole. Self-ridiculing ass-hole, but ass-hole nonetheless. Far away from something I’d call a human being.
Wait, what? That can’t be true. I’m pretty sure J-mac isn’t Jonathan McLatchie. I think McLatchie was reading from a set of written questions, of which J-mac had submitted some.
Rumraket,
That makes better sense.
Why would you imagine that? Beneficial mutations prevail beyond random expectations because of natural selection.
Speaking of someone making an ass of himself… Congratulations ! 🤣 Happy Ass-Entropy Day!!!
I asked Swamidass this question:
““Dr. Swamidass,
As a medical doctor, if 89 of your patients were on high fat diet and had extremely high cholesterol levels and no signs of heart disease, would you conclude that the lack of atherosclerosis in your patients was due to the beneficial mutations in ApoB protein?”
Swamidass seemed stunned by the question and said that medical doctors don’t test for ApoB protein mutations…
Why not test for ApoB in humans if polar bears apparently benefit from them? Maybe Dr. Swamidass wouldn’t have to prescribe statins to many of his patients if he knew they had the ApoB protein mutations…😉
Rumraket,
I agree. Thanks.
Or that’s what Darwinists must blindly believe…otherwise…what else is left of evolution? Fairy tales? 😉
I have a distinct feeling that that Jonathan McLatchie would like to be me now…😉
Are you really that stupid J-Mac? It’s an obvious inference. So fucking obvious that some creationists complain that it’s a tautology, which then they’re stupid enough to mistake for a tautological fallacy.
Do you really think that organisms with beneficial mutations would not have a better chance to survive that organisms with harmful ones? Really? Really, really?
It’s amusing that, despite I keep telling you that you’re shooting yourself in the foot with these kinds of comments, you insist on shooting yourself in the foot. You fight evolution because you want to be left with nothing but your fairy tales!
Not that I expect you to notice the irony any time soon.
Stop your unfounded speculations and read the original paper in Cell! ” Polar bears’ cholesterol levels are extreme” ! Get it?!
Do you know another way of conveying the message or by another adjective?!
I don’t.
Stop wasting my time with your blind self-deceptions… I don’t care what you wish the reality were like.. You can’t change it no matter how much you pray to Darwin…Get a life!
As I said, J-Mac will forever insist on shooting (him/her)self in the foot.
I believe the main reason why Behe has ignored Swamidass and Lents is not because they are less known in comparison to Lenski… They have embarrassed themselves to the point that if Behe responded to them, it would be like you responding to Byers…
Lents with Human Erros, polar bears being white and 17 mutations being not damaging…
Swamidass has no clue about the difference between dermis and epidermis pigmentation vs hair follicle pigmentation…
Same applies to the cholesterol “paradox”… Why would Swamidass support the conclusion of the authors of the original Cell paper that the ApoB mutations improved the clearance of LDL cholesterol, if the same paper clearly says that polar bears cholesterol levels are extreme?
Someone is not being truthful… If cholesterol levels in polar bears are extremely high, how could the clearance of cholesterol be improved by the beneficial mutations?
Thus starts the rapid moving of the goal posts.
As of now, a doctor can’t change a person’s genome, so they can’t fix a broken ApoB gene. What they can do is use medications to lower blood cholesterol. If drug companies discover a medication that specifically treats ApoB mutants then they may start sequencing ApoB genes. However, there is no reason to do so right now.
T_aquaticus,
In order to have goal posts you need a claim first. Just asking what it is.
When you attack the person instead of their arguments you demonstrate that you can’t address their arguments.
It’s a purposeful red herring meant to distract attention away from the argument.
I thought you agreed with Swamidass that the ApoB gene mutation was a beneficial one? Or are you confused, again? 😉
All I do is expose nonsense, just like I did now with your confusing about ApoB protein mutations…
I can’t fix optimism bias and certainly not evolutionary blindness… 😉
Isn’t that the pot calling the kettle black…? 😉
Atlantic summary of recent stuff on fish and anti-freeze, which is possibly an example of “irreducibly complex”. Convergent for sure.
https://www.theatlantic.com/science/archive/2019/03/how-fish-evolved-antifreeze-junk/585226/
BruceS,
What luck!
You whacky skeptics. Nothing is too serendipitous for you.
Imagine all the frozen cod before they got their last lucky accident.
More or less lucky than how the designer did it?
Oh yes!
I don’t know how the NASA people designed the spaces shuttles…
According to the ingenious analogy NASA designers must not exist… 😉
It’s beyond stupidity…