How much can evolution really accomplish?

How much can evolution really accomplish? Editor's Note: In 2020, Michael Behe published the book A Mousetrap for Darwin, in which he collected his articles and his responses to critics. Biochemist Lawrence Moran argued that Behe misinterpreted the evidence and misunderstood the importance of chloroquine resistance. Biochemist Michael Behe dared in 2007 to ask a question, which should have been asked with urgency and sincerity repeated by all biologists since the ink of what Darwin first wrote dried up on his manuscript: what can evolution really achieve? This question is very plausible and fundamental in the evolutionary story. But it has often been overlooked in the history of evolutionary thought. The firm assumption of almost all evolutionists is that evolution can do everything. Because ultimately we are here, right! So there is little point in asking the question. To be honest, such an inquiry has been carried out from time to time for decades, but these efforts have usually fallen into the practice of requisitioning, which simply presupposes that evolution must have this great creative power. We are here, and if we do not understand the exact mechanisms of evolution, if we are still trying to complete the details, if there is an evolutionary mechanism yet to be discovered, then evolution must simply possess this great creative power. The paleontologist Stephen Jay Gould famously used this tactic, arguing that if we don’t understand exactly how evolution works, we still have to consider evolution as a reality, because things have already evolved. Philip Johnson exposed Stephen Gould for using this circular self-serving attempt to support evolution. Johnson’s careful analysis of Gould’s “truth” of evolution turned out to mean nothing more than theory itself. Because Behe was not satisfied with the circular logic of evolution and lazy thinking, he decided to ask his question based on real-world data. What does the actual evidence show about what evolution can do? Behe approached the problem from several angles, most famously his analysis of the emergence of chloroquine resistance in the single-celled malaria parasite Plasmodium falciparum. Lots and lots of cells. In short, Behe noted that the antimalarial drug chloroquine was far more successful than other antiparasitic drugs, as resistance to chloroquine arose only in one cell out of roughly 10 x 20 parasitoid cells, as estimated by immunologist Nicholas White, a well-known expert on malaria research. This figure is difficult for us to absorb but by comparison astronomers estimate that there are only between 10 x 11 and 10 x 12 stars in our galaxy. Although molecular details of chloroquine resistance were still ambiguous at the time of the 2007 Behe book, Edge of Evolution, based on then available malaria data, Behe suggested that chloroquine resistance might require two mutations working together. A dot mutation (as we have seen with some other drugs) or a series of individual repeated beneficial mutations should have arisen much more closely than White's 10x20 estimate. The bottom line is that they argued that resistance to chloroquine could also be achieved through a series of useful step-by-step point mutations. We will not go into that claim as completely contradictory to the data because that is not our topic. It was not lost on careful observers that, paradoxically, Behe suggested that the perceived might actually gain two coordinated mutations along an evolutionary path. However, determined to maintain the tradition of "one small step at a time for evolution," Quinn and Carroll rejected Behe's suggestion of two coordinated mutations. Arguments over the next few years floundered back and forth, and more ink was wasted by the debaters than by a clumsy intern at the printing press. Yet, despite the selection of definitions, mathematical argumentation, and repeated accusations that Behe certainly does not understand how evolution really works, those who followed the battle of intelligence without taking part in it have noticed that Behe’s fundamental question has remained unanswered by his critics: how much evolution actually works? Moran Lottery One of the most reactive critics of Behe's argument was Dr. Larry Moran, a renowned biochemist at the University of Toronto. Moran seems to agree with the broader evolutionary narrative, but does not consider himself a Darwinian. Shortly before Behe published his book The Edge of Evolution, Moran published a detailed description of his views as well as his blog Sandwalk's "Evolution by Chance." By and large, I agree with Moran’s assessment of the randomness of evolution, and my basic argument is that Moran does not go far enough in recognizing the role of chance in the evolutionary narrative, particularly in the case of so-called selective events. After careful analysis, Darwin’s selection mechanism also ends up being something that is often based on chance, so the effort to distance itself from Darwin’s shadow by embracing random evolution is a real distinction. The main point he made to readers here was that Moran, armed with his coincidental view of evolution, had indulged in Behe’s debate about chloroquine resistance. During the summer of 2014, Moran and Behe (and their supporters and critics) took a broader approach than is detailed here. To silence the false accusation that he was not responding to his critics, in November 2020 Behe published his book The Mousetrap of Darwin, a collection of numerous refutations of the critics of his previous three books. In The Mousetrap he cited several responses to Moran. Moran quickly wrote a quick response to his Sandwalk blog arguing essentially that Behe was wrong about how chloroquin resistance occurred and misinterpreting the mechanisms of evolution. A misunderstanding by Behe or a misunderstanding of Behe's point of view? Notably, Moran acknowledges the main thrust of Behe's argument, noting that: Behe correctly identified [sic] an extremely unlikely evolutionary event. i.e. the development of chloroquine resistance in the malaria parasite. This is an event close to the edge of evolution, which means that more complex events of this kind are beyond the edge of evolution, and cannot occur naturally. [emphasis added.] That's a very important statement, and Moran's Edge of Evolution reader might say, "Welcome to our ship!" Instead, Moran's main objection (convinced at different times by BZ Myers, Kenneth Miller, and their companions) seems to be that Behe misunderstood how malaria resistance originated. Moran admits that "none of us object to guessing [one mutation 1 in 10 x 20 malaria cell division], but many of us object to how it is interpreted from Behe". Going back to 2007, we recall that Behe suggested that the simplest explanation for the extreme scarcity of chloroquine resistance is that at least two coordinated mutations are needed. This was in stark contrast to the drug atovaquone, for example, which requires only one point mutation, against which resistance arose faster than the time it takes for the average person to learn to pronounce "Plasmodium falciparum" (the Latin name for sicklephed conception). Casey notes to Skin that some critics of Behe have brought much disaffection to Behe's use of the word "simultaneous", but it was clear to any sane reader of The Edge of Evolution that Behe never claimed that the two mutations must originate at the same moment in a single stroke, i.e. occur in the exact same breeding cycle. His view was simply that the two mutations must ultimately be together at a particular point in time. What are reasonable guesses? It was not at all clear in 2007 - as far as I know it is still not entirely clear - exactly the generally available mutant methods of perception in humans, nor all the other factors or nuances that may affect the problem. Moran himself points out that "there are a lot of complexities and many unknown variables" and that we can "make estimates" but "we can't give exact calculations". The best thing to do while waiting for more specific research in 2007 was to make an educated guess as to the exact pathway(s) of chlorcocque resistance. The question is what are the plausible guesses in light of malaria data? An important paper by Summers and colleagues in 2014 showed new things in the evolution of chloroquine resistance. Although this research is limited to experiments involving frog eggs in the laboratory, it provided strong empirical evidence detailing the specific mutations involved. The researchers identified two primary pathways to chloroquine resistance, with additional mutations leading to "full transport activity". In fact, the most important key finding of Sommers’ and colleagues’ research is that chloroquine resistance is a multi-mutation event, requiring both specific methods of resistance “at least two mutations” to begin with. In the second part of this response, we will examine the data and implications of chloroquine resistance for the broader evolutionary story. Source: How Much Can Evolution Really Accomplish - Eric Anderson - Translated by Abdullah Dabgen — Source: Brahin Center website - Published 2022-06-03 (archived at the Internet Archive) https://braheen.com/articles/evolution-design/ما-القدر-الذي-يمكن-للتطور-أن-يحققه-فعلا