Bill Cole points out a good test for the "FI" hypothesis

It only “came in” that way because you ignored its polymorphism, Bill.

You even made the prediction that there were only “a few” alleles, which falsifies both your and @gpuccio’s hypotheses.

You’re not testing the correlation between conservation and functional information if you’re not bothering to calculate the degree of conservation.

“The past was alterable. The past never had been altered. Oceania was at war with Eastasia. Oceania had always been at war with Eastasia.”


I disagree. Your assertion is duly noted.

The polymorphisms being very different in a single animal but very similar across animals is very strong evidence the polymorphisms were designed. There is no good evolutionary explanation for this result.

Oh you disagree, then where is the hypothesis that predicts the observed result?

So where is the design hypothesis that predicts this?

Data cannot be evidence for a hypothesis if the hypothesis does not actually predict the data. And you do not have an ID hypothesis that has predicted this result, hence it’s not evidence for ID.

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What you really mean is things Bill doesn’t understand are evidence of design to Bill. To the rest of us it’s just chuckle-bait.


The hypothesis is the data will supports design (mind) as a mechanism. It does that exactly. Just as starlight curving around the sun supported mass(energy) as a mechanism. How many times do I have to repeat this :slight_smile:

But the data can only “support design (mind) as a mechanism” if you have a hypothesis that predicts the data. And you don’t.

Where? Where is the prediction of the data Bill?

Even if you repeated it an infinite amount of times, that wouldn’t make it true. Where is the predict of the data Bill? Where is the design model that says “due to a mechanism that qualitatively and quantitatively functions in the following way X, we should expect there to be data patterns like this Y” ?

Nowhere, it is nowhere. Such a model does not exist. You do not have a predictive theory of ID, hence the patterns in the data (such as some particular degree of conservation of some gene between different species, or distributions of types of DNA mutations) isn’t evidence for it.

Why don’t you just accept this, what you must at some level know is true, and move on with your life? Do something else with your life, find some other basis for your beliefs.

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As was your false assertion that there were only “a few” MYH7 variants.

How many do you think there are, btw? Feel free to limit yourself to different protein sequences.

That’s not a hypothesis. Science is about preventing yourself from engaging in wishful thinking.

Your ID hypothesis predicted only a few MYH7 variants. That’s not true, so your hypothesis has been disproven.

Always back to the disembodied mind used magic to POOF life into existence. You need a new writer Bill, that joke has gone stale.

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But they aren’t for MYH7. Yet another of your hypothesis’s predictions falsely presented as a fact, and yet another disproof of your ID hypothesis.

Keep those false predictions comin’, Bill!

Bill’s “poof” hypothesis has made three very strong predictions:

  1. Different tissues will have different myosin heavy chains.

  2. There will be only “a few” MYH7 variants.

  3. The polymorphisms being very different in a single animal but very similar across animals.

All three are false. That’s a perfect record, Bill.


Nevertheless, it is still as good or better than any other ID supporting evidence - which makes it (equal) best.


Wrong analogy. The correct one would be “The hypothesis is that the data will confirm general relativity.” Think anyone would have taken Einstein seriously if that was all he had?

Also, if we had no observation of mass causing curvature in space, how would that have confirmed a hypothesis that mass causes curvature of space?

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As others have noted, that’s not a hypothesis. A hypothesis predicts what observations we should see AND what observations we should NOT see. You don’t have that. You simultaneously claim that design will result in many polymorphisms and conservation of sequence which only begs the question of what design won’t produce. Until you have a null hypothesis you don’t have a hypothesis.


The prediction is that the evidence will show ultimately what we are observing is the direct product of a mind. If you found a mechanism in the prokaryotic cell that could generate complex functional information de novo then you would strongly challenge the hypothesis.

I have been discussing this for 4 years and in the beginning I was merely an evolutionary skeptic. I now believe science is getting to the point it needs to re engage the old design argument given what we are observing in biology.

You can make nit picky arguments as no analogy is perfect but that’s all you guys have at this point. Design is a much better explanation for the origin and evolution of life then any evolutionary theory be it Darwinian, neutral theory or the Shapiro group…

I do believe that common descent explains some of the data but it is only a partial explanation. It certainly does not explain the origin of the mechanism that it is touting that explains the data: sexual and a sexual reproduction.

No, that’s the HOPE, not a prediction of a hypothesis. It’s something you hope will one day happen.

You don’t have an actual hypothesis that predicts “the direct product of a mind”. Because you genuinely have no idea what that would be.

Sure the design argument does. You should understand that by now.

No, it does not. There is no “design argument” that predicts that “there should be some entity with X properties because that’s what some mind would want to make”.

A mind is able to put together a long string of meaningful symbolic sequences. I have seen evolutionists try to explain how the cell can do this for 4 years. We can test a minds ability to do this with human minds.