Common Descent (CD) has been offered as a scientific theory and must therefore be judged as such. Its status as a scientific theory, however, has never been properly established. Without a theory showing that speciation is reasonably probable in the available time, all the circumstantial evidence proffered for CD by its advocates is for naught, and the evidence of proteins such as vitellogenin (the subject of some discussion here lately) is no more than circumstantial evidence. Circumstantial evidence can support a conclusion only when there is a theory to connect the evidence with the conclusion.
By the beginning of the twentieth century, Charles Darwin’s suggestion for the variation on which he meant for natural selection to act was rejected because it turned out to be nonheritable. In the first third of the 20th century several replacement suggestions for the variation were offered only to be later rejected. In 1941 a project was launched to establish the theory of evolution on a sound basis by bringing together facts and methods from all branches of science, and a decade later was considered fully established. The modern synthesis (MS) embraced natural selection and took the variation to be mutations and recombinations in the chromosomes, although exactly what these were was not clearly understood at the time.
The discovery of the structure of the DNA in the mid 20th century was thought to solidify the MS. The random mutations were identified with random changes in the DNA sequence attributed to DNA-copying errors and genetic recombination. The variation was no longer a vague genetic effect that it had been: it was now an understood random process.
With a known random mechanism now available for the variation on which natural selection could operate, the randomness became subject to mathematical investigation. Mutation rates could be measured and in principle the probability of an evolutionary event could be calculated. For the first time it became possible to check if Darwin’s celebrated mechanism of random variation and natural selection could really account for CD. But the advocates of CD never picked up the challenge to publish any probability calculations. Some who questioned CD, however, did calculate and found the probabilities of speciation under random mutation and natural selection in the available time to be negligibly small and essentially zero. These results were never competently rebutted. The conclusion is inescapable that CD has no theoretical backing, has been refuted, and is not a valid scientific theory.
The discovery of the structure of DNA followed closely on Claude Shannon’s discovery that information was quantifiable. It was quickly grasped that the order of the nucleotides in the DNA molecule was the defining information of the organism. The DNA base pairs played the role of symbols carrying information and the base-pair sequence was immediately assumed to carry a program that controlled the development and functioning of the organism. Evolution was soon recognized as a process whose job it was to build this information.
Toward the end of the 20th century and in the beginning of the 21st, new phenomena of genetic change were discovered to have important implications for evolution. Epigenetic effects were found to produce phenotypic change, but without changing the base sequence of the DNA. Transposable elements (TE’s) were found to produce phenotypic change and did change the base sequence. A movement is currently underway among evolutionists to extend (or replace) the MS to include these effects but there is so far no consensus on just how to do it. TE activity in the genome is known to lead to microevolutionary phenotypic effects. But the activity is not random: it is under cellular control. This is nonrandom evolution driven by environmental change. In my book Not by Chance (1996), I suggested what I called the Nonrandom Evolutionary Hypothesis(NREH) and elaborated on it in a later book, The Evolution Revolution (2014). Environmental stress induces activation of TE’s, which in turn produce an adaptive phenotypic response in individuals. TE’s are activated both in somatic cells and in the germline and are therefore heritable.
TE activity can be the basis of a theory of evolution — but one that does not include CD. It cannot include CD because the mechanism for TE activation is endogenous in the organism. There is no way presently known to explain how that mechanism might have evolved. Its evolution could not be explained by random mutations for the reasons explained above.
CD must therefore be abandoned as a failed theory. All the evidence given for CD — fossils, molecular similarities, junk DNA, pseudogenes, vestigial organs, and vestigial molecules — is circumstantial, for which there may be explanations better than the invalid theory of CD. In many cases of vestigial organs, vestigial proteins, pseudogenes, and “junk” DNA, better explanations have been found. There is reason to suppose that better explanations for remaining “evidence” for CD will be forthcoming. In the meantime, bringing “evidence” for CD is a futile endeavor.