Exploring weaknesses in evolution?

Oh, by all means.

David Shormann, Ph.D. takes on the notion of molecular clocks.

An example of real 21st Century science is the mounting evidence against the idea of molecular clocks. Scientists look at differences in genes along with fossil evidence to determine when two species diverged from a common ancestor. For the human species, scientists use molecular clocks to predict the date of "Mitochondrial Eve", our Most Recent Common Ancestor (MRCA) that supposedly originated in Africa.

Molecular clocks came into use in the 1960s. In the 1990 edition of Biology by Neil Campbell, an age between 200,000 and 400,000 years is given for "Eve" (p. 669). Moving ahead to 2004, we find in the 10th edition of Biology by Starr and Taggart that Eve is now only 100,000 to 200,000 years old (p. 471). The fact that the estimates were cut in half, on top of the huge error involved (50%), would make any reasonable scientist question molecular clocks.

That sounds rather telling on first glance. However, I have a couple of thoughts.

Firstly, molecular techniques were not terribly advanced in the 1960s, to say the least. It would be very interesting to compare the techniques used three decades apart.

A quick Google search shows that different molecular analyses will yield different ages for a last common ancestor. It turns out, for example, that:

A similar exercise has also been performed on the Xq13.3 region of the X-chromosome of the same individuals used in this study by Kaessmann et al.

The X-chromosome is the female sex chromosome in the nucleus, but because it is 'paired' with the tiny male Y-chromosome, it mostly doesn't recombine and is similar to mitochondrial DNA in that respect; but it is passed on by both fathers and mothers to offspring and so is different from mitochondrial DNA in that respect. Because the effective population size of the X-chromosome is three times that of mitochondrial DNA, the X-chromosome MRCA is predicted to be three times older than the matrilineal or mitochondrial MRCA. The age of the MRCA of Xq13.3 is found to be in agreement with the mtDNA data (mtDNA MRCA age: 171,500 years BP; Xq13.3 MRCA age: 479,000 years BP)

That's not very different from the 200,000 – 400,000 year range given in the 1960s-era textbook.

More searching: According to Wikipedia:

The notion of the existence of a so-called "molecular clock" was first attributed to Emile Zuckerkandl and Linus Pauling who, in 1962, noticed that the number of amino acid differences in hemoglobin between different lineages roughly changes with time, as estimated also from fossil evidence.[1] They generalized this observation to assert that the rate of evolutionary change of any specified protein was approximately constant over time and over different lineages.

It turns out the initial hypothesis of a fixed rate clock wasn't accurate. The clock can be speeded up or slowed down by a number of factors, including population size. If a species' population rises or falls significantly over time, this can affect the reading on the clock.

Molecular clocks are far from useless, despite this. We can tell a lot even if all we know is that event B happened between events A and C. Shorman misses this point where he writes:

The truth is, there will ALWAYS be confusion about what happened in the past because we cannot go back and verify it. Not only that, scientists believe up to 99.9% of the species that ever existed may be missing from the fossil record. .... finally, as Professor Jerry Coyne said on page 17 of Why Evolution is True, "By predictions, I don't mean that Darwinism can predict how things will evolve in the future."

Evolution is weak when it comes to explaining the past, present and future.

Many sciences make predictions about the past. For example, given evolution and continental drift, we predicted that fossils of ancestral marsupials – intermediate between Australian and South American marsupials – would be found in Antarctica. No marsupials live in Antarctica today, but their ancestors would have had to get to South America somehow, and Antarctica was the bridge between the two, before continental drift pulled them apart.

Guess what kind of fossils have turned up in Antarctica?

In fact, science can make predictions about things we already know. If we have a theory and exclude prior information, we can see if this information drops out of the theory. If it does, this is a valid test.

On top of that, genetic mutations are almost always neutral (see "neutral theory") or harmful, rarely beneficial, and never has a gene been observed to mutate and create a new and beneficial function.

This is just plain false. Antibiotic resistance is a new function, it's beneficial (for the bacteria), and it's the result of mutations. Bacteria have also picked up, through mutation, the ability to break down nylon and other completely novel molecules. And bacteria don't have recessive genes – if a function appears, it had to develop somehow, not appear from hiding somehow.

The blood clotting cascade is a complex and intricate molecular system. It was one of the poster children in Michael Behe's book, Darwin's Black Box. Behe's thesis was that systems like the blood clotting cascade were irreducibly complex, and therefore could not have arisen by Darwinian step-by-step modification of precursors. If any piece of the system is missing, or not yet ready, the whole system won't work.

Dr. Kenneth Miller has researched the development of the blood clotting cascade.

Using homology, he traces the molecules in the cascade back to a digestive enzyme in an ancestral form some 600 million years ago. Gene duplication would create a copy of this enzyme, which becomes the first step in the clotting cascade. It's pitifully inadequate for you or me, but it's perfectly adequate for a critter like a lobster.

Further gene duplication and differentiation gives us additional elements, which can then mutate to address different functions. An enzyme that does two functions well enough can be duplicated, and each copy can mutate to handle one function, even at the cost of losing the ability to handle the other.

Now, it would not be fair, just because we have presented a realistic evolutionary scheme, supported by gene sequences from modern organisms, to suggest that we now know exactly how the clotting system has evolved. That would be making far too much of our limited ability to reconstruct the details of the past. But nonetheless, there is little doubt that we do know enough to develop a plausible and scientifically valid scenario for how it might have evolved. And that scenario makes specific predictions that can be tested and verified against the evidence.

Now, what alternative theory does Dr. Shormann propose, and what (if any) are its strengths?