Replies

As you probably know, anthropoid primates all have the same genetic defect that causes a lack of the L-GLO enzyme, preventing them from synthesizing ascorbic acid. In this case, the hypothesis that the common defect is a result of common descent - inheritance from a common ancestor -

The conclusion of common descent is built into the bare assumption that the lack of the L-gulano-g-lactone oxidase gene is a "defect", or "nonfunctional" version of a gene that was purportedly functional at some point in human history. But even if that could be proven to be the case, it says nothing about nothing about whether it descended from a universal common ancestor or was a descendant of many independently created organisms or was itself created independently. In fact, the very (claimed) persistence and identifiability of these supposed pseudogenes millions of years after they supposedly ceased functioning could indicate that they have some as yet undiscovered function; (why else would they persist for so long?) It simply cannot be said definitively at this point that these types of genes have no function. In short, NDT can accommodate this evidence but it can also accommodate it's absence, which doesn't say very much for the utility of this alleged prediction of common descent.

Cordially,

"The conclusion of common descent is built into the bare assumption that the lack of the L-gulano-g-lactone oxidase gene is a "defect", or "nonfunctional" version of a gene that was purportedly functional at some point in human history."

Because the rest of the gene is still there. The defect is in the same spot on the gene cross species. Other than common descent there is no other plausible explanation.

That's not an assumption. The purpose of the gene is well established.

It simply cannot be said definitively at this point that these types of genes have no function.

That is true. It can however be said definitively that they have lost the function they previously had, and as a result that humans and the great apes lack the ability to make vitamin C, but still carry the relic gene. It is not inconceivable that the pseudogene was coopted for some function yet to be discovered, and it's unlikely we'll be doing knockout experiments on humans or great apes to rule out that contingency, not because we can't, but because there are ethical issues.

However, the ID explanation is unfalsifiable; an inscrutable deity could have done whatever he wanted for whatever ineffable reason he liked.

"(why else would they persist for so long?)"

Once turned off the retention of the inactive gene had no reproductive cost.

Ascorbic acid can be acquired through food. An inactive gene is not recognized by selection.

Why assume the more untenable stance, that it will mean something in the future?

Is it not more reasonable to conclude that its function matches that in other organisms where it is turned on?