Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design

by Stephen C. Meyer

Scientists attempting to explain the origin of life must explain how both information-rich molecules and the cell’s information-processing system arose. The type of information present in living cells—that is, “specified” information in which the sequence of characters matters to the function of the sequence as a whole—has generated an acute mystery. No undirected physical or chemical process has demonstrated the capacity to produce specified information starting “from purely physical or chemical” precursors. For this reason, chemical evolutionary theories have failed to solve the mystery of the origin of first life—a claim that few mainstream evolutionary theorists now dispute.

and books have cast new doubt on the creative power of the mutation and selection mechanism.8 So well established are these doubts that prominent evolutionary theorists must now periodically assure the public, as biologist Douglas Futuyma has done, that “just because we don’t know how evolution occurred, does not justify doubt about whether it occurred.”

As science advanced in the late nineteenth century, it increasingly excluded appeals to divine action or divine ideas as a way of explaining phenomena in the natural world. This practice came to be codified in a principle known as methodological naturalism. According to this principle, scientists should accept as a working assumption that all features of the natural world can be explained by material causes without recourse to purposive intelligence, mind, or conscious agency.

Key

The term “phyla” (singular: “phylum”) refers to divisions in the biological classification system.

This pattern turns on its head the Darwinian expectation of small incremental change only gradually resulting in larger and larger differences in form.

Thus, unless Darwin’s evolutionary mechanism worked gradually by preserving the tiniest of random changes over many millions of years, it didn’t work at all.

Key point

First, the great profusion of completely novel forms of life in the Burgess assemblage (feature 3) demanded even more transitional forms than had previously been thought missing. Each new and exotic Cambrian creature—the anomalocarids (see Fig. 2.10), Marrella, Opabinia, and the bizarre and appropriately named Hallucigenia—for which there were again no obvious ancestral forms in the lower strata, required its own series of transitional ancestors. But where were they?

Nevertheless, the analogy holds at least insofar as the differences in form between any member of one phylum and any member of another phylum are vast, and paleontologists have utterly failed to find forms that would fill these yawning chasms in what biologists call “morphological space.”

In other words, the missing link is stil a key issue

He means, rather, that we have good reason to conclude that such discoveries will not alter the largely discontinuous pattern that has emerged.

Proponents of deep divergence don’t deny that the fossil evidence has come up short. Instead, they adopt one of the versions of the artifact hypothesis to account for that missing evidence. They then argue that there was no “explosion” of animal forms in the Cambrian, but rather a “long fuse” of animal evolution and diversification lasting many millions of years leading up to what only looks like an “explosion” of animal life in the Cambrian,

😂

Sometimes even different studies of the same or similar groups of molecules have generated dramatically different divergence times.

Key. But he doesnt extrapolate enough

Or as Valentine, Jablonski, and Erwin conclude, “The accuracy of the molecular clock is still problematical, at least for phylum divergences, for the estimates vary by some 800 million years depending upon the techniques or molecules used.”31

!!!

Evolutionary biologists typically exclude histones from consideration, because those times do not confirm preconceived ideas about what the Precambrian tree of life ought to look like. But that raises obvious questions. If we don’t have fossils documenting a common animal ancestor, and if genetic studies produce such different and contradictory divergence times, how do we know what the tree of life should look like and when the first animals began to diverge from a common ancestor?

Good questio

“The key assumption made when constructing a phylogenetic tree from a set of sequences is that they are all derived from a single ancestral sequence,

Good

They proposed, first, a mechanism called “allopatric speciation” to explain the rapid generation of new species.

In a television broadcast leading up to the Centennial celebration, Huxley captured the optimistic mood more succinctly: “Darwinism has come of age, so to speak. We are no longer having to bother about establishing the fact of evolution.”

What separates such organisms from a trilobite or a mollusk or even a lowly sponge? Clearly, all three of these higher forms of life are more complex than any one-celled organism. But exactly how much more complex?

Key info follows

Imagine someone producing a series of zeros and ones by reaching into the bag and placing them one by one on a game board. The probability of choosing a zero on the first pick is just 1 in 2. But the probability of choosing two consecutive zeros after placing the first back in the grab bag (and shaking the tiles) is 1 chance in 2 × 2, or 1 chance in 4. This is because there are four possible combinations of digits that could have been chosen—00, 01, 10, or 11. Similarly, the probability of producing any three-letter sequence as a result of choosing consecutively in this manner is 1 in 2 × 2 × 2, or 1 in 23 (or 1 in 8). The improbability of any specific sequence

Although Shannon’s theory measures the amount of information in a sequence of symbols or characters (or chemicals functioning as such), it doesn’t distinguish a meaningful or functional sequence from useless gibberish. For example: “we hold these truths to be self-evident” “ntnyhiznslhtgeqkahgdsjnfplknejmsed” These two sequences are equally long and equally improbable if we imagine them being drawn at random. Thus, they contain the same amount of Shannon information. Yet clearly there is an important qualitative distinction between them that the Shannon measurement does not capture. The first meaningful sequence performs a communication function, while the second does not.

Cool

Eden argued that much the same problem applied to DNA—that insofar as specific arrangements of bases in DNA function like digital code, random changes to these arrangements would likely efface their function, while attempts to generate completely new sections of genetic text by random means were likely doomed to failure.5 The explanation for this inevitable diminution in function is found in a branch of mathematics called combinatorics. Combinatorics studies the number of ways a group of things can be combined or arranged. At one level, the subject is fairly intuitive. If a thief slips round the corner of a dormitory after hours looking for a bike to steal, he will scan the bike rack for an easy target. If he spots a basic bicycle-style lock with only three dials of ten numbers each, and on the rack beside it one with five dials of ten numbers each, the thief wouldn’t need a degree in mathematics to realize which one he should attempt to open. He knows that he would need to search fewer total possibilities with the three-dial lock.

Consequently, there are four possible bases that could occur at each site along the DNA backbone and 4 × 4, or 42, or 16 possible two-base sequences (AA AT AG AC TA TG TC TT CG CT CC CA GA GG GC GT). Similarly, there are 4 × 4 × 4, or 43, or 64 possible three-base sequences. (I’ll refrain from listing them all.) That is, increasing the number of bases in a sequence from 1 to 2 to 3 increases the number of possibilities from 4 to 16 to 64. As the sequence length continues to grow, the number of combinatorial possibilities corresponding to sequences of increasing length inflates exponentially. For example, there are 4100, or 1060, possible ways of arranging one hundred bases in a row.

The amino-acid chains are also subject to such inflation. A chain of two amino acids could display 202, or 20 × 20, or 400 possible combinations, since each of the twenty protein-forming amino acids could combine with any one of that same group of twenty in the second position of a short peptide chain. With a three-amino-acid sequence, we’re looking at 203, or 8,000, possible sequences. With four amino acids, the number of combinations rises exponentially to 204, or 160,000, total combinations, and so on.

This is embarrassing imho for evolutionusts

In his presentation at the conference, Eden himself acknowledged a possible way of resolving this dilemma. He suggested that it was at least possible that “functionally useful proteins are very common in this [combinatorial] space so that almost any polypeptide one is likely to find [as the result of mutation and selection] has a useful function.”

During the late 1970s and early 1980s, however, molecular biologists developed technologies for making customized synthetic DNA molecules. Robert Sauer used these techniques to make site-directed changes to DNA sequences of specific genes of known function and then to insert those variants into bacterial cells. He could then evaluate the effect of various targeted alterations to a DNA sequence on the function of their protein products within a bacterial cell culture.

Thwy need a architect to creaye the controls to "test"

though many different combinations of amino acids will produce roughly the same protein structure and function, the sequences capable of producing these functional outcomes are still extremely rare. He showed that for every functional 92-amino-acid sequence there are roughly another 1063 nonfunctional sequences of the same length. To put that ratio in perspective, the probability of attaining a correct sequence by random search would roughly equal the probability of a blind spaceman finding a single marked atom by chance among all the atoms in the Milky Way galaxy—on its face clearly not a likely outcome.

!!!

Yet Axe’s calculations only hint at the full problem for neo-Darwinian theory. By bending over backwards not to overstate the improbability of generating a new protein fold and by focusing narrowly on that one aspect of the challenge confronting evolutionary theory, his figures vastly understate the improbability of building a Cambrian animal. There are several reasons for this.

The Cambrian animals exhibit structures that would have required many new types of cells, each requiring many novel proteins to perform their specialized functions. But new cell types require not just one or two new proteins, but coordinated systems of proteins to perform their distinctive cellular functions. The unit of selection in such cases ascends to the system as a whole. Natural selection selects for functional advantage, but no advantage accrues from a new cell type until a system of servicing proteins is in place. But that means random mutations must, again, do the work of information generation without the help of natural selection—and, now, not simply for one protein, but for many proteins arising together.

The sensitivity of proteins to functional loss, the rarity of proteins within combinatorial sequence space, the need for long proteins to build new cell types and animals, the need for whole new systems of proteins to service new cell types, and the brevity of the Cambrian explosion relative to rates of mutation—all conspire to underscore the immense implausibility of any scenario for the origin of Cambrian genetic information that relies upon random variation alone, unassisted by natural selection.

If only one out of every 1077 of the alternate sequences are functional, an evolving gene will inevitably wander down an evolutionary dead-end long before it can ever become a gene capable of producing a new protein fold. The extreme rarity of protein folds also entails their isolation from each other in sequence space.

Huge point

Let’s take a closer look at the article that allegedly shows “how new genetic information arises.”

Key material follows

These papers assume the existence of significant amounts of preexisting genetic information (indeed, many whole and unique genes) and then suggest various mechanisms that might have slightly altered or fused these genes together into larger composites.

!

Remember: ORFans, by definition, have no homologs. These genes are unique—one of a kind—a fact tacitly acknowledged by the increasing number of evolutionary biologists who attempt to “explain” the origin of such genes through de novo (“out of nowhere”) origination.

Long does cite at least one type of mutation that does not presuppose existing genetic information, the de novo origination of new genes. For example, one paper he discusses sought to explain the origin of a promoter region for a gene (the part of the gene that helps initiate the transcription of the gene’s instructions) and found that “this unusual regulatory region did not really ‘evolve.’ ” Instead, it somehow snapped into being: “It was aboriginal, created de novo by the fortuitous juxtaposition of suitable sequences.”

The only thing missing is God. Can’t do that.

extreme specificity

extreme rarity

As molecular biologist Ann Gauger explains, “Thus, [alpha] helices and [beta] sheets are sequence-dependent structural elements within protein folds. You can’t swap them around like Lego bricks.”44

In the absence of such demonstrations, evolutionary biologists have taken to offering what one biologist I know calls “word salad”—jargon-laced descriptions of unobserved past events—some possible, perhaps, but none with the demonstrated capacity to generate the information necessary to produce novel forms of life.

“recruited”

“unknown source”

“extensive refashioning”

“fortuitous juxtaposition

“fortuitous acquisition”

“rapid, adaptive evolution”;

“cobbled together

How does convergent evolution occur, given the improbability of finding even one functional gene in sequence space, let alone the same gene arising twice independently? No one knows exactly, but perhaps it was a “fortuitous juxtaposition of suitable sequences,” or “positive selection,” or “de novo origination.” Need to explain two similar genes in more closely related lineages? Try “gene duplication,” or “chimerical gene fusion,” or “retropositioning,” or “extensive refashioning of the genome,” or some other scientific-sounding combination of words.

In fairness, neo-Darwinian biologists have mathematical models of their own—models indicating to them that nearly unlimited evolutionary change can occur under the right conditions. The assumption that these models, which are based on the equations of population genetics, accurately represent how much evolution can occur has left many evolutionary biologists confident in the creative power of various mutational mechanisms. But should they

He knew that almost any biological structure of interest—the inner ear, the amniotic egg, eyes, olfactory organs, gills, lungs, feathers, the reproductive, circulatory, and respiratory systems—possesses multiple necessary components.

As the number of necessary components increases, the requisite number of coordinated changes increases too, rapidly driving up the difficulty of maintaining the functional integrity of the system while modifying any of its parts.

And that was the problem, as Frazzetta understood it. Any system that depends for its function on the coordinated action of many parts could not be changed gradually without losing function.

Yet this is always downplayed in discussions

Not only must the end product—the final machine—be feasible, but so must be all the intermediates.