Editor’s note: Eric Anderson is an attorney, software company executive, and co-author of the recently released book, Evolution and Intelligent Design in a Nutshell.
This past week, science readers woke up to breathless headlines about our own continuing evolution. The evidence? An extra artery in the forearm of some adults. This time it wasn’t about some obscure bird on a remote island. This was us — hard evidence that humans are still evolving! Given this personal interest factor, the story quickly spread. “Evolution arms us with an extra artery,” as Cosmos quipped. A Science Alert headline was more direct, both about the observation and the implications: “More Humans Are Growing an Extra Artery in Our Arms, Showing We’re Still Evolving.”
Reporting in the Journal of Anatomy, scientists in Australia had uncovered that more adults now possess a “median artery of the forearm,” contrasted with studies over the past two centuries. Specifically, based on a sample of “78 upper limbs dissected at two different Australian Universities,” the researchers analyzed whether a median artery in the forearm was present. They then compared this number to those of prior studies and concluded that “the prevalence of median arteries of forearms” since 1846 had increased from approximately 10 percent to over 30 percent. The authors calculate that if the trend continues, nearly every person born after 2100 will have a median artery.
A Legitimate Cause for Concern
Prevalence of this additional artery may be of significance to modern medicine, because sometimes the “the median artery, when present, passes through the carpal tunnel, thus it can compress the median nerve, causing carpal tunnel syndrome.” Given that millions of us struggle with carpal tunnel syndrome in our device-infested world, this is potentially a legitimate cause for concern.
Setting aside for a moment the small sample size (as the authors acknowledge), let’s assume that the numbers reported in this study and in prior studies back to the mid 1800s are reflective of a genuine trend in the prevalence of the forearm median artery. Let’s further assume that the researchers’ projections for the future increase of this prevalence are spot on and that everyone born after 2100 will carry a median artery. What does this demonstrate about evolution? After all, it isn’t sufficient to simply observe a biological change and then declare that, therefore, humans are “evolving.” We must look at the underlying cause to understand what is really happening.
Regulating Embryonic Development
The authors of the study acknowledge that the cause of this change is unknown, but suggest it is likely the result of a mutation in a regulatory structure. Specifically, the median artery is “an embryonic structure, which normally regresses around the 8th week of gestation.” The median artery is therefore a perfectly normal aspect of human anatomy, present during early embryonic development and then typically fading or disappearing altogether as the radial and ulnar arteries on either side of the forearm develop and take over the job.
If we pause here and consider the facts, we can already see the clear outlines of a rational fact-based answer to the question at hand. The median artery is a normal (presumably essential) part of early embryonic development. After the artery has done its job, the developing embryo shuts down the median artery as it develops the radial and ulnar arteries. This speaks clearly to regulation and control. The kinds of things that are consistent with a planned and purposeful process. Indeed, the authors recognize that a regulated system is at work: “The mechanism for the regression of the median artery is initiated and regulated by specific genes. Persistence of the median artery into adulthood indicates the failure of the expression of these genes” (emphasis added). The researchers go on to suggest that this failure of the regression process “could have resulted from alteration of or damage to genes by mutations,” or perhaps an environmental factor, such as an infection of the mother, could have disrupted the regression process.
In either case, what we have is a carefully controlled process toward a particular outcome that has been disrupted. Unfortunately, the authors do not pursue this clear line of thinking, but instead immediately revert to the evolutionary paradigm within which they think the evidence needs to fit, arguing that the increased prevalence of the median artery “over the last 125 years means a true evolutionary process of the change in gene pools” and “the prevalence of persistent median arteries in adult forearms of people in many countries may be a trend associated with the evolutionary process.”
References to evolution are sprinkled throughout the paper. Yet despite the clear implication that the failure of median artery regression is due to a hitch in a sophisticated control process, little additional attention is paid to this fact. The authors do not mention “regulation” again, and there is no discussion of controls or outlines of additional research that could be pursued along these lines. Instead, the observations are shoehorned into a mental box of Darwinian thinking, with vague appeals to “selection pressure” as the cause of the observed change. There seems to be a collective blindness to the evidence right under our noses.
Two final points of particular note.
Darwin Devolves — Again
First, no new biological structures were observed and there is no evidence that evolution produced any new biological feature. Quite the contrary. A functional structure, necessary for early embryonic development, failed to be removed when it would normally be eliminated in the developmental process. If this counts as “evolution,” as the authors say and the eager headlines proclaim, then it certainly is not evolution as Darwin envisioned it. Evolution needs to explain (and Darwin thought he was explaining) the origin of new biological features, and eventually completely new biological forms. Observing that a pre-existing structure remains on the scene after it was supposed to depart stage left tells us nothing about the structure’s origin.
Instead, what we seem to be observing in the case of the human median artery is a breakdown of a pre-existing system and a failure of a regulatory process to proceed along its pre-programmed lines. In spite of the evolutionary narrative, breakdown of existing systems and disruption of genetic programming is precisely what we can expect from mutations. If it turns out that the persistence of the median artery into adulthood is indeed the result of mutations, then what we will have is yet another example of broken genes and a broken process — another example of loss-of-function mutations, just as Michael Behe argued in Darwin Devolves. Such de-evolutionary changes may be interesting, but they are of no comfort to the evolutionary story. Indeed, they are precisely the opposite of what evolutionary theory has to explain.
Natural Selection to the Rescue?
Second, despite suggestions in the researchers’ paper to the contrary, the persistence of the median artery can hardly be viewed as an example of natural selection acting on variations. If it is, then it seems to be exactly backwards from what the theory states. As already mentioned, potential negative implications for carpal tunnel syndrome are at hand. Additionally, the authors note the disadvantages of the persistent artery in terms of potential “thrombosis, aneurysm, calcification or traumatic rupture,” and acknowledge that “a median artery is usually considered a disadvantage when complications arise due to its presence.” Why then would natural selection aggressively select for the median artery in the course of just a few generations? The best the authors can offer for a selection advantage is that “in rare instances,” the median artery could act as a backup “emergency vessel” if damage to the radial or ulnar arteries occurs.
On balance, the authors’ own cited evidence points to an overarching disadvantage in the persistence of the median artery, suggesting (one might reasonably conclude) that there was a purpose in the first place for the regression of the artery after it had done its job in early embryonic development. In order to shoehorn the persistence of the median artery into the evolutionary narrative, the authors can come up with little more than a possible contingent advantage that might occur in “rare instances” as an emergency backup (precisely the kind of thing, by the way, that natural selection would be blind to in all but the most unusual circumstances).
Succumbing to evolution’s siren song and ignoring the weight of the own evidence they have presented, the authors’ evolutionary explanation consists of little more than a vague reference to “selection pressure,” coupled with a curious blindness to the fact-based observation they previously made about the disruption of a pre-existing regulatory structure. This simplistic shout-out to Darwin is not anything that can be taken seriously as a scientific explanation. Rather, it hampers our understanding.
A Better Understanding
By all accounts, the researchers have done excellent work and have presented good information. I do not in any way denigrate their research efforts. Indeed, there are a number of valuable design-related questions that naturally flow from this research. What is the initial biological purpose of the median artery? Why is the embryo pre-programmed to eliminate the median artery, and what design and engineering constraints necessitate this regression? How is the regression controlled and initiated? If persistence of the median artery is due to a breakdown in a regulatory switch, are there ways to re-activate the switch?
Yet with evolution as a guide, there is little of significance. This is plainly not an example of evolution producing a new biological structure or a novel anatomical feature — precisely the kinds of things that evolution must be able to explain. If anything, this is an example of devolution. Nor is it at all clear, despite the authors’ appeals to a “selection pressure,” that this change in the human population has anything to do with natural selection — the regular go-to explanation for these kinds of observations. This appears to be a non-beneficial change, with natural selection failing to prevent the negative persistence of the artery, and certainly not responsible for producing the artery in the first place.
So much for natural selection “daily and hourly scrutinizing, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good,” as Darwin wrote in the Origin of Species. From an evolutionary perspective, natural selection seems to have been caught napping on the job.