Methinks it is sort-of like two weasels

[Dan_Eastwood]

@lee_merrill

@Dan_Eastwood

ID methods are unique in that the probability of an event-type is considered to be smaller the more often it is observed. Normally we think that events which occur more often are more likely, not less.

The probability of evolution as a cause gets smaller the more we see convergent structures. Let’s say the probability of an eye evolving is .1. Then the probability of it evolving twice is .1^2, and so on. It gets smaller, exponentially smaller.

If the events were independent, and there were a multitude of ways to accomplish the same function, that might be so, but those are not reasonable assumptions. Various forms of eyes are thought to have evolved independently at least 40 times. Even algae can detect light and move towards it. Vision is clearly (heh) offers a big fitness advantage, or it would not have evolved so many times.

[RonSewell (RonS)]

@lee_merrill

The improbability of the eye evolving in the first place.

Response to light is ubiquitous in biomolecules. Even flowers face the sun; they do not have eyes because where are they going to run? For mobile surface and aquatic animals awash in light, any variation yielding competitive advantage in utilizing that environmental awareness would be subject to positive selection - in the land of the blind, the one-eyed man will be king. Populations which inhabit blackened situations such as caves often lose their sight, but to my knowledge this never happens in lit environments, demonstrating that vision is highly selective. The eye evolving in the first place is probably inevitable, and as the Nilsson Pelger study indicates, is likely rapid.

@lee_merrill

At step 6 a lens appears! By magic?

There is a selection of optically transparent crystallin proteins to choose from. Crystallin biomolecules serve other biological purposes as well. A refractive index is an inherent property of transparent materials, so a lens is entirely plausible by evolutionary mechanisms.

[Dan_Eastwood]

Do we have a citation for this “1 in 10^20” claim. I know it’s Behe, but not the rational.

[Art (Arthur Hunt)]

@Dan_Eastwood

Do we have a citation for this “1 in 10^20” claim. I know it’s Behe, but not the rational

Here is the complete passage from the review (White, N. J. 2004. Antimalarial drug resistance. J. Clin. Invest. 113:1084-92) Behe pulled the number from:

“Chloroquine resistance in P. falciparum may be multigenic and is initially conferred by mutations in a gene encoding a transporter (PfCRT) (13). In the presence of PfCRT mutations, mutations in a second transporter (PfMDR1) modulate the level of resistance in vitro, but the role of PfMDR1 mutations in determining the therapeutic response following chloroquine treatment remains unclear (13). At least one other as-yet unidentified gene is thought to be involved. Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 10^20 parasite multiplications.“

[Paul_King]

@lee_merrill

Let’s pick 500 heads in a row before the fact.

I’m glad that you agree with me that specifications should be chosen without reference to the data,

@lee_merrill

The probability of a sequence meeting a specification is what is relevant.

If the sequence has a valid specification of sufficiently low probability, the probability that it will meet that specification is 1.

@lee_merrill

But who talks about the probability of having a specification? Probability is about events.

That is an event, just as the sequence meeting a particular specification is.

[John_Harshman]

@lee_merrill

Several comments: if the steps are independent, it is indeed remotely unlikely to develop just once! 99%^2000 is 1.86 x 10^-9.

Where did this calculation come from?

@lee_merrill

At step 6 a lens appears! By magic?

I have to conclude that you didn’t actually read the paper. Is that correct?

@lee_merrill

But isn’t this assuming that the selectable variation per generation becomes fixed in each generation?

No, it doesn’t. It assumes that selection is acting on multiple loci in parallel to produce a net small change in various allele frequencies with a net small effect on the population each generation.

@lee_merrill

Finally, as they admit, the neural processing required for the more complex eyes was completely left out! This is a crucial factor, and would substantially reduce the probability.

Only if you assume that neural evolution happens in a way quite unlike the incremental steps of the eye evolution itself. And your probability calculations doesn’t seem based on anything.

@lee_merrill

Which makes it more surprising if evolution did it…

So in effect you’re saying that unique events can only be explained by design, whereas repeated events can only be explained by design. Is there anything that can’t only be explained by design?

[Mercer (John Mercer)]

[quote=“lee_merrill, post:142, topic:15043”]

@lee_merrill

@Mercer

How much money would you bet that there is single mutation documented in the primary literature that increases resistance and is therefore selectable?

[/quote]

I agree with this,
[/quote]

Then we agree that Behe is wrong.

No, this only shows that there are subsequent mutations that improve resistance, once resistance is in place.

If Behe is correct, no single mutation can possibly increase resistance over that of wild-type by itself.

How much money are you willing to bet?

[quote=“lee_merrill, post:142, topic:15043”]

@Mercer

@lee_merrill

“But these could be separated into two main lineages” is indeed two pathways.
[/quote]

Not ONLY two pathways, as you claim.

Only two that seem to be probable enough to occur.

The paper did not address probability. Have you noticed that Behe’s citations often fail to support his claims?

@lee_merrill

@Mercer

Show me how Behe accounted for existing variation MATHEMATICALLY.

Again, he observed what evolution actually did, starting with existing variation. Thus all that is needed is to observe the rate at which resistance evolves.

No, Behe both ignores existing variation and the vast majority of the primary literature on chloroquine resistance (that’s why he quote-mined a review). You have tacitly acknowledged this by responding to my request for math with words.

[Roy (34-year veteran)]

@lee_merrill

@Paul_King

It is not billed as or intended to be a simulation of biological evolution and Dawkins says that it is not accurate as such.

But I was responding to people here defending it.

This isn’t true.

But that’s a minor sideshow in anticipation of the main event:

@lee_merrill

@Paul_King

@lee_merrill

“An irreducibly complex evolutionary pathway is one that contains one or more unselected steps (that is, one or more necessary-but-unselected mutations). The degree of irreducible complexity is the number of unselected steps in the pathway.” (Behe here)

That is certainly not a definition of design. Nor can it be considered evidence of design. After all, unselected steps will occur (quite frequently) and evolution is hardly going to care about whether it is including unselected steps or not.

This is definitely a definition for design, you may say it doesn’t work, but it’s still a definition.

It is not a definition of design, because it does not contain the word “design”, or anything similar to the word “design”.

It is a definition of the term “irreducibly complex evolutionary pathway”.

[Roy (34-year veteran)]

@lee_merrill

@Roy

Neither Behe nor you has any idea what alternative paths to chloroquine resistance there might be, that are not included in his or your calculations.

Again, Behe is observing what evolution actually did, where all paths were open to evolution.

Exactly. Neither Behe nor you has any idea what alternative paths to chloroquine resistance there might be, that are not included in his or your calculations.

You don’t understand the problem, do you?

[Rumraket (Mikkel R.)]

Regardless, chloroquine resistance evolved, and you can’t generalize from how chloroquine resistance evolved to say that other adaptations would have to evolve in a similar way or be equally restricted.
There are other adaptations known to have many hundreds to thousands, or even millions of pathways by which they could evolve.

Alternate evolutionary histories in the sequence space of an ancient protein

Contingency and chance erase necessity in the experimental evolution of...

[T_aquaticus]

@lee_merrill

That’s one probability. Another would be the probability of evolution generating a given structure.

That’s the Sharpshooter fallacy.

@lee_merrill

Are you saying we can’t observe what evolution does, and compute a rate from that?

Using your same logic, we can observe what lotteries do.

Let’s say the chances of winning the lottery are 1 in 100 million. For 10 straight lotteries we have 10 winners. The chances for each of those people winning is 1 in 100 million. The chances of those specific 10 people winning is 1 in 100 million to the 10th power, or 1 in 1x10^80. For each lottery there were 300 million tickets sold, so it isn’t surprising that people won in 10 straight lotteries, yet the probability of those specific people winning is nearly impossible.

This is the type of faulty logic you are using. What did happen was nearly impossible.

@lee_merrill

But Behe looks at what evolution did, including neutral mutations and existing variation.

That’s the Sharpshooter fallacy.

[T_aquaticus]

@lee_merrill

But Behe is interested in the limits of what evolution can do,

That’s laughable.

Why doesn’t he compare the human and chimp genome and tell us which differences evolution could not produce?

[Mercer (John Mercer)]

@lee_merrill

Well, Behe also examines the HIV virus, where one new protein-protein binding site did evolve, as it turns out.

Yet he claimed in the book that no such sites had evolved, citing a paper that had nothing to do with his false claim.

Why would he do that?

Also, “HIV virus” is redundant. Do you not know what the “V” stands for?

@lee_merrill

If it’s all that easy to produce a new binding site, then HIV could be cranking them out right and left.

It is easy, but I don’t see why it would need to crank any out. It seems to be hanging around with no problem.

It seems that you have no understanding of mutation and selection at all.

@lee_merrill

But again, I’m sure if we saw a flagellum-in-process somewhere, we’d hear about it.

Why? And how many completely different flagella do we already know about?

[Mercer (John Mercer)]

@T_aquaticus

Just looking at life in general will tell you there are many, many potential pathways for evolution to take, not just 1 or 2.

Even looking at the primary literature on chloroquine resistance will tell you that there are not just two.

[colewd (Bill Cole)]

@T_aquaticus

This is the type of faulty logic you are using. What did happen was nearly impossible.

He is talking about probability before the event or looking at the pattern after the event and judging the cause. If you see a distribution of bullets that is highly unlikely to to be random then you can infer aiming. If you see a highly organized arrangement of parts you can infer design.

If you sat down at a poker table and 3 straight flushes were dealt could you infer the cause of this extraordinary event? What if it happened 3 times in a row? Would you infer a shuffled hand or a stacked deck?

@T_aquaticus

Why doesn’t he compare the human and chimp genome and tell us which differences evolution could not produce?

The splicing changes and gene expression differences are unlikely to be from reproduction and random variation.

[Rumraket (Mikkel R.)]

If it wasn’t already, this thread is now ruined and any further discussion is pointless.

[CrisprCAS9]

@colewd

The splicing changes and gene expression differences are unlikely to be from reproduction and random variation.

Show your work…

[Dan_Eastwood]

@colewd

He is talking about probability before the event or looking at the pattern after the event …

You came so close to describing Bayes’ Theorem …

… and judging the cause.

… yet managed to miss it. Still relevant to the discussion though, I’m surprised no one has mentioned it before this.

Affirming Design this way is Affirming the Consequent.

@colewd

If you sat down at a poker table and 3 straight flushes were dealt could you infer the cause of this extraordinary event? What if it happened 3 times in a row? Would you infer a shuffled hand or a stacked deck?

BEFORE the event and having observed the cards being dealt this is indeed unlikely. BUT if you come across a card table with 3 straight flushes laid out and no players about, that is not cause to infer a stacked deck.

Does this remind anyone else of Maverick, or is it just me?

[T_aquaticus]

@colewd

He is talking about probability before the event or looking at the pattern after the event and judging the cause.

But that isn’t the case. We are talking about the probability of specific functions evolving after they have already evolved, such as the bacterial flagellum.

@colewd

If you see a distribution of bullets that is highly unlikely to to be random then you can infer aiming.

Not if we use ID logic. Random processes would always produce unlikely results using ID methods because any outcome of a reasonably complex system will be unlikely. If I shuffle a deck of cards and deal them out 1 at a time the result will have a probability of 1 in 10^67. An ID proponent will tell us that the order of cards had to be designed because the chances of that occurring are so low.

@colewd

If you sat down at a poker table and 3 straight flushes were dealt could you infer the cause of this extraordinary event?

Any three hands of any 5 cards is equally unlikely.

@colewd

The splicing changes and gene expression differences are unlikely to be from reproduction and random variation.

Yet another bald assertion with zero evidence and zero science.

[lee_merrill]

@Dan_Eastwood

The sample mean is a Maximum Likelihood Estimator - it is not a likelihood.

Fine, I meant (and have said) that the likeliest estimate of the mean is the sample mean, for binomial / exponential / normal distributions in particular.

@Dan_Eastwood

My not sure what you are trying to do, but you probably want a proportion or a rate, not the mean.

Behe calculates a mean from the rate at which chloroquine resistance arises, a probability of such an event.