Some scientific papers brag that Darwin’s universal tree of life is coming into sharper focus, but as the data increase, so do the problems.
Case in point: Maximilan Telford in Science Magazine presumed to write about “The Animal Tree of Life” as if one such tree exists, but ended up showing that results of tree-building are highly dependent on the methods used. He spoke of a “strengthening consensus” emerging 150 years after Darwin moaned to Huxley that he would not live to see his tree of life established.
The earlier disagreements derived from varying interpretations of the morphological and embryological characteristics of animals. Many of these characters have evolved repeatedly in unrelated lineages as adaptations to similar selective pressures or have been lost from certain groups through disuse. Today’s strengthening consensus is almost entirely thanks to the use of molecular genetic data in reconstructing trees. Heritable changes in nucleotides and amino acids are abundant and generally much less prone to the problems of convergent evolution and loss than are morphological characters.
Some morphologists may disagree with that assessment, but Telford basically confessed long-standing disputes between the morphologists and the molecular evolutionists, despite his apparent favoritism for the latter. A distant view appears to show a tree, but the devil is in the details. He digressed into various “surprises” and taxonomic tricks to get the trees to match up:
If we consider a summary of the trees produced from these data…, we find some familiar groups (arthropods, chordates, and echinoderms), as well as some surprises. For example, almost all premolecular phylogenies supposed a close link between the brachiopods (lamp shells) and the deuterostomes (chordates and echinoderms). Yet in Field et al.‘s tree, the brachiopods are placed far from the deuterostomes in the Lophotrochozoa, which include annelids and mollusks. This major rearrangement suggests that certain “deuterostomian” characters of brachiopods may have evolved more than once….
Other surprises in the tree were less welcome. Probably the most striking result, and the one that provoked the strongest reaction at the time, was the conclusion that the multicellular animals evolved on two separate occasions from unicellular relatives…. It quickly became clear that this conclusion was incorrect and that it resulted from the cnidarians being misplaced in the tree. A second error—the placement of the flatworm Dugesia (Platyhelminthes) as a branch outside of the main groups of animals… took longer to resolve. We know now that its correct place is within the lophotrochozoans…. Both errors arose because the 18S rRNA genes of the misplaced groups evolve at an unusually high rate, resulting in “long branch attraction,” whereby rapidly evolving species are incorrectly placed close to the long branch leading to the species used to root the tree….
In other words, the resolution of the tree depended on human choices made in forcing the data to match expectations. It’s like the tree was in the mind, and the methods had to be adjusted to force “surprises” to cooperate. A gardener can trim a bush to look like a giraffe (an artform called topiary); that doesn’t mean the plant would grow that way naturally.
Telford went on to describe newer fit-forcing methods, such as “probabilistic methods that can accommodate the systematic biases present in real sequences, such as unequal rates of evolution.” Who could know, though, the rates of evolution without already having in mind a picture of how the evolutionary saga was supposed to unfold?
Skeptics might complain that tree-building exercises like this do not “carve nature at its joints” but rather confirm a preconceived bias. They might also point out that confirming that bias required radical reorganizations of earlier visions of the tree, casting doubt on the lasting credibility of version 2013 that relies more heavily on molecular data than how the animals actually look:
These studies have led to a widely accepted phylogeny of all animal phyla that has radically changed our views of animal evolution. Premolecular phylogenies generally envisaged a gradual increase in complexity from the earliest animals without a body cavity or coelom (acoelomate flatworms) via pseudocoelomate worms (such as nematodes and rotifers) to coelomate protostomes (annelids, arthropods, and mollusks) and deuterostomes (echinoderms and chordates) with a sophisticated mesoderm-lined coelomic body cavity.
In contrast, today’s tree divides bilaterally symmetrical animals into protostomes and deuterostomes…. Within the deuterostomes, the simple urochordates (sea squirts) are closer relatives of the vertebrates than the more fishlike cephalochordates (amphioxus); a third phylum of deuterostomes, the hemichordates (acorn worms), are the sister group of echinoderms and not of the chordates.
A view that “radically changed our views of animal evolution” does not indicate scientific progress. Just because something is “widely accepted” (by whom?) does not make it scientifically valid, either. Alchemy was widely accepted for centuries. An explanation that requires believing that features as important as the coelomic body cavity has been “gained and lost multiple times” should raise eyebrows.
In conclusion, Telford appealed to the “future research” escape clause to clean up today’s messes:
Although much of the animal tree is now resolved, a number of problems remain. These problems tend to involve relationships either of taxa with extreme systematic biases or among groups that seem to have originated in a rapid radiation, resulting in a lack of signal supporting individual nodes. Future progress will depend on increasing useful signal with larger “phylogenomic” data sets from the widest possible taxonomic sample and on continued improvement in the correspondence between real data and the models used when reconstructing trees.
Thus Telford confessed a lack of correspondence between models and the real data. Are the “extreme systematic biases” in the data or in the scientists’ world views?
In “Following the footprints of positive selection,” a press release from the Broad Institute of MIT promised to showcase examples of real evolutionary progress: “genetic changes [that] have conferred an evolutionary advantage” if such an oxymoronic phrase has any meaning (i.e., only a rational mind can determine what is advantageous).
Surprisingly, it took another radical rethinking to figure out how to find positive selection. The article calls it a “turning point” and a “shift” to try this new method: “the genome itself can be used as a starting point to guide scientists to important genetic locations, leading to hypotheses about human health and disease.”
As much as this might sound like following the evidence without bias, in fact, nothing has been accomplished yet. The press release merely states that researchers are “poised” to make great discoveries with their chosen tools and datasets. Some candidate high-level findings were put forth: “Several important categories of pathways emerged from the team’s analysis, including pathways tied to metabolism, skin pigmentation, and the immune system.” Only the last one got any elaboration. Alas, the elaboration only mentioned suggestions and possibilities for counter-intuitive observations, like the fact that “The particular variant that the researchers uncovered makes the immune system respond less dramatically to invaders, which, paradoxically, seems to help in the fight against them.” How is that evidence of positive selection? With imagination, the data can be made to fit the theory:
We were thinking, ‘Why would decreasing the signal be important?’” Grossman recalls. “One possibility involves the role of TLR5 in facilitating certain bacterial infections. It turns out that in order for these bacteria to enter the host organism, they have to invade activated immune cells and hitch a ride to the lymph nodes. If the receptors are never activated, the bacteria have much more difficulty infecting the host.”
It would be hard to defend a loss of function as evidence of positive selection. Even so, this represents only “one possibility” to explain a conundrum – not a signal of positive selection that jumps out of the data. The article concluded with more promissory notes. “With this new data, we – and others – can examine numerous mutations and search for biologically meaningful outcomes,” one researcher hoped. No clear-cut example came from this hunt intended on “Following the footprints of positive selection.”
Elizabeth Pennisi’s article in Science Magazine, “How Did Humans Evolve? Ask a Mouse” is another example of a headline that fails to deliver. She discussed a Harvard study celebrated by the previously-cited press release about positive selection: a mouse study at Harvard that focused on a gene for hair and sweat glands:
Mice carrying human disease genes have proved valuable for learning what goes awry in people. Now, researchers have tapped the rodents to understand human evolution. Mice with a human version of a gene called EDAR have more sweat glands than normal, providing clues to how East Asians adapted to a humid environment 30,000 years ago.
Certain people groups, such as Native Americans and East Asians, have thicker hair, Pennisi said, but it should be obvious that there’s a lot of difference between living members of ethnic groups that do not necessarily tell anything about “human evolution” from mice. Since mice and humans already have sweat glands and hair, what’s the point, Darwinly speaking?
Then we find that the Harvard team cheated: they used intelligent design to insert the human EDAR gene into mice. Then they bred the resulting mice for several generations:
The mice had thicker hairs in their fur, as expected. But they also had more sweat glands, denser mammary glands, and smaller fat pads around those mammary glands. “This study was able to show there are other, more subtle effects” beyond hair thickness, says Joshua Akey, an evolutionary biologist at the University of Washington, Seattle, who was not involved with the work.
But why would this be surprising? They were grown with a human variant of a gene. This only provides a mouse model of a possible evolutionary change that might have helped certain people in certain habitats. Pennisi boasted that the study “pushes the field in novel ways,” but no matter the wishful thinking among the evolutionary biologists, she confessed at the end that the implications of this study are not at all clear:
The group’s analyses and computer simulations looking at how 370A arose and spread indicate that the mutation creating the variant gene happened more than 30,000 years ago in central China. China had been relatively warm and humid between 40,000 and 32,000 years ago and then got cooler and drier. But Kamberov thinks that summer and winter monsoons still created high enough humidity that those people who were able to cool their bodies with extra sweat glands would have done better. Alternatively, or in addition, the increased branching in the mammary glands could have provided an advantage for raising infants. “It’s not clear which one of those [traits] resulted in differences” in survival and reproductive ability, Akey says.
Surely easterners know from experience that more sweat glands do not help in areas of high humidity; and if the rest of the year were drier and cooler, the people would have had other worries on their minds than sweating. If “increased branching in the mammary glands” could have provided an advantage, why do infants survive outside China? Why didn’t the genes revert after the climate change? At best, these “evolutionary advantages” are of a very meager sort, considering the major overhauls Darwinism requires to get from mouse to human.
The requirements of natural selection are very stringent. Only what promotes immediate survival counts. The advantage has to be so great that all the other members of the population must die so that the favored variant proliferates — this is called the “cost of selection.” This issue was not addressed in the article. Instead, Pennisi ended with a quote that says evolutionary theory can never solve it:
The work “pushes the field in novel ways, Akey adds, as very few studies have pinned down the functional consequences of genetic changes that have been selected for. Although “the mouse model brings you closer” to understanding how modern humans have changed through time, Enard says, “without a time machine we will never get all the relevant data.“
One might expect then, that to “ask a mouse” how humans evolved, the only answer would be, “Squeak, squeak.”
We can dub this last story (the tale of a tail) the “Mighty Mouse Theory of Evolution” – not because the mouse is mighty (it’s only hairy and sweaty) – but because it Might help bring evolutionists closer to their coveted “understanding” of how humans evolved. But even if evolutionists think with all their might about their mighty mice, they might, instead, never understand anything about evolution, because it’s not a mouse with a human gene injected into it they need, but a time machine.
The next best thing to a time machine is an Eyewitness who was there who can tell us how mice and humans “emerged” (and it wasn’t by a blind, unguided process of natural selection).
We hope these three articles expose to the world the shenanigans of the Darwin Party: imagination, suggestion, and empty promises. Find one clear evidence supporting molecules-to-man evolution (or even a clear-cut case of “positive selection”) in any of these studies or models, or any any of the hundreds of other examples we have reported since fall of 2000. Time’s up. If this is the best the Darwiniacs can put forward after over 150 years of hunting for a magic tree that emerges by chance, they lose. Let them get out of the way of the researchers who have the resources to understand the origin of “complex things that appear to have been designed for a purpose,” as Dawkins described life.