Why are We Disagreeing with ID?

But you do know that cars are produced in factories, and do not come about thru unguided natural processes the way that rivers or mountains or trees or birds or bacteria come into existence. Correct? The distinction between the two is not based on “irreducible complexity” “specified complex information” or any other such vacuous ID buzz words.

And the way they do this is by comparing to things that they know are naturally produced.

You might find the article below illuminating. It describes how, when radio telescopes were first developed and the first pulsar detected, it was at first thought that this was a message from an extraterrestrial intelligence, because there was no natural object that was known to produce such a regular signal. However, when other such signals were detected, it was decided that this was much more likely coming from a previously unknown natural sources, rather than that intelligent beings far distant from each other in the universe were by coincidence sending the same sort of signal.

So even though ID’ers often talk about SETI, it is actually a very good example of how ID does not describe the process by which design is detected.

if you still disagree, please explain how the concept of “irreducible complexity” would be used to determine that a radio signal was sent by intelligent beings.

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why not? after all, we see many people around us and we never seen someone who start to evolve a new organ. so i think that one in 1000 births to get a new anatomical trait is very generous.

For the first, that would depend on the fossil. Modern placental mammals or birds in the Permian or earlier would be extremely problematic.

For the second, it depends entirely what you mean by a “reproducing watch”, and what evidence is available.

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100%, because it happened.

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The receptor is not unique to humans. Binding is trivially easy to alter and evolve.

Genes aren’t fixed; alleles are. If you don’t know the difference between them by now, it’s hopeless.

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That doesn’t really help Behe’s argument,

You specified 2 mutations, so there’s no need to worry about cases where more are required. Lynch’s point here is also relevant - it’s entirely possible that the first steps of some 2-step mutations are already in the population. So the time needed in that case would be the time for one of those to acquire a second mutation that produces a new function.

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there is no problem to push back birds origin by 100 my. we already seen that with flowering plants. so why not with birds?

a watch that is made of organic components and can reproduce like a living thing.

The same way as any zoonotic spillover. The same way as coronavirus diseases SARS and MERS made the jump. Does this really have to be spelled out?

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Agreed. Are you arguing for acceptance of evolution? -because this is exactly as would be expected by biologists.

Given that birds are derived theropod dinosaurs it would be an extreme problem to push them back to before the earliest dinosaurs.

That pushes it towards the natural side - a little. But far more would be needed. Is the “watch” functionality beneficial to the organism? A side effect of some beneficial functionality? Is the “watch” capable of surviving and reproducing without human aid? Do we have evidence of plausible ancestors of the “watch” species? And I’m sure that there are many more factors to be considered.

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How do you know? What does it look like for someone to “start to evolve a new organ”? Please be as specific as you can.

I think there is a more subtle problem with your argument: How can a fossil be said to be “out of place” to begin with, unless there is an overall pattern that shows evolution to have occurred?

I ask you the same question I asked @scd. How do you know that there are not millions of people walking around right now with mutations that could potentially lead to new organs at some point in the distant future, (even if only a very few of then actually do)?

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Making the “jump” is not the same as how they made the “jump”.

It hurts Lynch’s argument because many proteins are not mutating neutrally.

Behe’s argument included adaptions of 2 or more changes. Existing in the population and becoming fixed in the population are very different.

Polydactyly?

That is obtuse. How do you think spillover happens?

Sure. My comment was directed at someone who evidently does not understand the distinctions between cell expression, tissue, and organ, and seems to think that evolution posits that complete organs just pop up whole.

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They only need to exist.

Also, fixed neutral mutations dating back 10’s of millions of years already exist in the human genome.

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I’ll assume that you meant genes, since genes mutate and proteins don’t. Yet what proportion of genes don’t mutate neutrally?

But your comment specifically talked of a 2 mutation adaption. So that’s what we are discussing.

Indeed, but the time taken for an adaption to become fixed once it occurs can be less than millions - or even thousands - of years. And the existence of potential first mutations in the population will substantially reduce the time it takes for an adaption to occur.

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That probably shouldn’t be considered a new organ. Just an additional copy of a structure that already existed. “New organs” most likely start with mutations that have very little, if any, noticeable functional or phenotypic effect. That’s what I would expect, anyway.

I guess he should clarify for himself. I thought he was referring to some initial stub or simple structure that is not yet a lung or heart or liver or whatever, but which can be identified as the first step towards this. Not identified in retrospect, mind you, but whose eventual function we would be able foresee tens of thousands of years, if not more, into the future. If so, I’d be very interested to hear the method @scd would use to identify such things.

Maybe this is a better way to approach this question: @scd, can you tell us exactly when the wing of a bird could be said to “begin to exist” in the fossil record?

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Hi Ron
Sorry for the curt response. You seemed to be asserting “split over as the cause”. It may be possible but seems unlikely.

Infectious diseases are emerging at an alarmingly rapid pace, faster than any other time in human history. Virus Spillover and Emerging Pathogens Pick Up Speed

With so many variables, such as complex pathogen life cycles, modes of transmission, and random susceptible hosts’ interaction, an initial spillover event resulting in ongoing transmission into a new host is relatively rare and usually an imperfect process. Most mammalian viruses lack the ability to infect humans .

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