Behe has posted the third and final installment in his series of posts about recent research results supporting his Edge of Evolution position.

Undirected evolution may not be able to easily to move from one structure even to a related structures.

First, thanks for jumping in with some clarification. I hope you continue to participate at UD.

That said, I would like to comment on your statement:

“If expression levels increase to the point that they’re harmful (as can apparently happen in Pif), fitness goes back down and there are fewer or no descendents. If the ones with a moderate level of this new gene reproduce a lot and the ones with too much or too little reproduce less- voila! The appearance of tuning and design, all from natural selection.”

It is clear enough that natural selection can weed out cases where excessive expression has become harmful to reproduction. But the natural selection itself never, ever produces anything at all. It merely filters, weeding out the relative losers. It explains survival, not arrival of new beneficial features.

To explain the design of any regulatory mechanism within a realistic time and number of generations, it is necessary to account for its appearance. Before it can be preferred by natural selection, it must first appear.

The question begging assumption is that undirected variations are able to produce any mechanism (regulatory or otherwise) that might be needed or helpful. If this can be done in sufficiently small, incremental and preservable beneficial steps, this is feasible and realistic.

However to approach it scientifically, it is not enough to merely assume that this small, stepwise, unbroken staircase always exists.

Have you read Michael Behe’s The Edge of Evolution?

It turns out that even Richard Dawkins has now (indirectly) acknowledged Behe’s point about how certain kinds of changes can be very difficult to come by.

Other research has supported Behe’s observations that this process can be actually quite limited, e.g. see the first and second posts in a series.

The Darwinist’s very accusation of “bad design” implies a recognition that “design” exists – for which the Darwinist has no explanation.

As an engineer, I usually find the argument of “bad design” comes from a woeful misunderstanding of the design process and a very limited understanding of the science or evidence involved.

I know of features like the eye that Darwinist’s claim are “bad design” when more detailed understanding of the design requirements, like response speed, provide the design parameters that result in the feature actually being an excellent design.

“When an IDist looks at something and considers it as “good design”, that is now a nice little pro-ID argument?”

See “Blink” by Malcolm Gladwell

Those skilled in design can often quickly recognize a good design but it would take a while to explain.

The reasons for it being a “good design” would need to be explored in depth to provide the quantitative objective basis for that argument.

Sanford spends most of the book systematically going through the consequences of known genetic processes and the major population models.
1) The genome is the book of life. Where did it come from?
2) Are mutations good?
3) How much mutation is too much?
4) All-powerful Selection to the rescue?
5) Can Genomic Selection problems be solved?
6) A closer look at noise.
7) Crow to the rescue?
Man to the rescue?
9) Can natural selection create?
10) Is the downward curve real?
Personal Postlude What Hope?
Appendix 1 What other scientists say
Appendix 2 How many mutations can be selected against simultaneously?
Appendix 3 The phenomenon of Unity, and the concept of Integrated Complexity.
Appendix 4 Three Possible Objections
References

In Appendix 1 Sanford reviews the major population models and their consequences.

Sanford has one figure “Declining Lifespan – Noah’s descendants” with a paragraph including:
“we see a dramatic decline in life expectancy, which has the strong appearance of a biological decay curve. Fitting the data to the “line of best fit” reveals an exponential curve following the formula: y=5029.2*x^-1.43. The curve fits the data very well – having a correlation coefficient of 0.90.”
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See Scordova’s review on endorsements:
On the Snaford’s back cover:

In the Mystery of the Genome Cornell University researcher John Sanford lifts the rug to see what evolutionary theory has swept under it. He shows that, not only does Darwinism not have answers for how information got into the genome, it doesn’t even have answers for how it could remain there.

Michael Behe

Other back cover endorsements are from John Baumgardner, Henry Morris, and Phillip Johnson.
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You can download Mendel’s Accountant for free along with the associated articles.

Previous UD posts indicate that Behe, Dembski and Johnson have all endorsed this book. Is this true?

One of the glowing Amazon reviews states:

Sanford concludes that the degeneration of the genome is unstoppable and Darwinism could never have gotten off the ground. Contrary to one reviewer’s beliefs about this book, Sanford only spends a few paragraphs on the declining life-spans of the generations of men after Noah. He shows that the life-spans of post-flood man, as recorded in the Bible, follow a curve that is eerily similar to a declining fitness curve found in earlier chapters of this book.

Is this statement accurate?

Thanks

When an IDist looks at something and considers it as “good design”, that is now a nice little pro-ID argument? Consider me confused.

ID is left with the difficult question of why the designer did so much more to prevent early in life cancer than late in life cancer.

Would it not make sense that design provides greater effort to preserve the design on to the next generation?
There are also extensive systems to repair DNA damage that fit in with the ID perspective. NeoDarwinism has the severe challenge of explaining how any of those complex systems came into being with random mutations and “selection”, on top of its huge presupposition of the incredible complexity of self reproducing cells. It has

Distinguish between the problem of suffering versus that of preserving the species.

On further reading, Cheng stated: “. . moderate over expression of PIF1, which is only mildly toxic on its own, causes growth defects in strains with mutations in genes involved in DNA replication and the DNA damage response.”

i.e., Overexpression of PIF1 compounds other mutations.

Further Cheng et al.

“DNA damage caused by high levels of Pif2 induce the accumulation of ssDNA. . . the damage is not specifically localized to telomeres. . .

. . .Pif1 removes telomerase from telomeres and DNA DSBs . . . overexpression of PIF1 inhibits cell growth in a dose dependent manner. . . .
Elevated levels of Pif2 interfere with DNA replication: . . . overexpression of PIF1 is toxic to . . . mutants with defects in lagging strand synthesis. . .
. . .our studies strongly suggest that elevated levels of Pif1 disrupt lagging strand DNA synthesis . . .
. . .deletion of several kinetochore genes renders cells sensitive to PIF1 overexpression (Table 2). . .”

“…our work shows the importance of carefully regulating the protein levels of Pif1 in the cell. We propose that overexpression of PIF1 impairs lagging strand synthesis resulting in DNA damage. At telomeres, telomerase activity is needed to repair this damage.”

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You claimed: “If a protein picks up a new function, it may help its descendants and they grow faster/reproduce more.”
That is an astronomically big “IF”.

Neo-Darwinian evolution has to demonstrate how complex systems come to be formed by random mutations when there are such harmful effects until the those complex systems are in place.

Degradations by mutations from normal base operation would be expected from ID.

Please review the population models reviewed in Genetic Entropy and the Mystery of the Universe.
Please try your hand at Mendel’s Accountant.
See if you can find any way under realistic parameters how the numerous mutations needed to create PIF1 and telomerase, compared to dominance of accumulated “neutral” and harmful mutations.

PS My misunderstanding that all mutations were not viable does not constitute “lying”. Please refrain from accusations of moral perversity when you have no clear evidence.

DLH at 21
“All the greater reason to see this as ID as Darwinism has no explanation for systems with such obvious lack of “evolutionary selection”.

Huh? Late in life cancer is pretty common (much more so than in child bearing years and earlier) and not something that we can expect evolution to solve since it happens after a person has offspring. ID is left with the difficult question of why the designer did so much more to prevent early in life cancer than late in life cancer.