How do you call the acquisition of genes that actively pump out drugs that kill them devolution? How do you call the development of systems that routinely change their antigens so that they escape the host immune system devolution?
I work in a lab that studies E. coli and these bugs will be put in the same test tube for months and still survive. All of the nutrients deplete, yet they evolve in order to survive the nasty environment. And when you plate them after a long incubation, they look completely different than E. coli. That’s not “devolution”, that’s speciation at the bacterial level.
(cont.)
Also, You should ask yourself, How is it that malaria so easily gained a resistance to chloroquine but is unable to defeat the sickle mutation? Are there problems that are even harder for evolution than dealing with sickle hemoglobin? Problems that are for all intents and purposes beyond the reach of RANDOM mutation? The answer is that Darwinian (random) mutation can deal quickly and easily with some problems, but slowly if at all with others. There is a mathematical limit to what random mutation is able to achieve in nature.
In the
Edge of Evolution, Michael Behe helps clarify this point:
Let’s compare the two numbers for the odds of achieving resistance to atovaquone, where just one mutation is needed, versus chloroquine, where (presumably – since if a single mutation could help, chloroquine resistance would originate much more frequently) two are needed. The odds are, respectively, one in a trillion (10^12) and one in a hundred billion billion (10^20). The ratio of the two numbers shows that the malarial parasite is a hundred million times (10^8) less likely to develop resistance to chloroquine than to atovaquone. This is reasonable since the genome size of the malarial parasite is in the neighborhood of a hundred million nucleotides. The implication is that if two amino acids in a protein have to be changed instead of just one, that decreases the likelihood of resistance by a factor of about a hundred million.
Even though the odds are tremendously stacked against it, P. falciparum (malaria) was able to develop chloroquine resistance because there are an enormous number of parasitic cells (about a trillion) in an infected patient’s body, and about a billion infected people in the world in a year. So the parasite has the population numbers to get around the terrible odds. Spontaneous resistance to atovaquone can be found in roughly every third sick person. Spontaneous resistance to chloroquine can be found perhaps in every billionth sick person, and since there are usually close to a billion sick people on the planet every year or so, that means chloroquine resistance is usually waiting to be found in at least one person, somewhere in the world, at any given time.
Suppose that P. falciparum were not quite as prodigious as it actually is. What if, instead of a trillion malarial cells in the typical sick person, there were only a million? How long would it then take for chloroquine resistance to pop up? If all other things were equal, it would take about a million years. The reason is that if there were fewer parasites per person, and therefore fewer in the world’s population, then the parasite would have to wait a proportionately longer amount of time for the right combination of mutations to come along. The number of players in the lottery would be decreased a millionfold, so the length of time needed to get a winner would be increased a millionfold.
This straightforward example carries an obvious implication. Species in which there are fewer living organisms than malaria (again, other things being equal) will take proportionately longer to develop a cluster of mutations of the complexity of malaria’s resistance to chloroquine. Let’s dub mutation clusters of that complexity – 1 in 10^20 – “chloroquine-complexity clusters,” or CCCs. Obviously, since malaria is a microbe, its population is far more vast than any species of animal or plant we can see with the unaided eye. Virtually any nonmicroscopic species would take longer – perhaps much, much longer – to develop a CCC than the few years in which malaria managed it
Behe goes on to conclude that:
No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian (random) evolution in the line leading to humans in the past ten million years. Instead of concentrating on us humans, we can look at the odds another way. There are about five thousand species of modern mammals. If each species had an average of a million members, and if a new generation appeared each year, and if this went on for two hundred million years, the likelihood of a single CCC appearing in the whole bunch over that entire time would be only about one in a hundred. Let that sink in for a minute. Mammals are thought to have arisen from reptiles and then diversified into a spectacular array of creatures, including bats, whales, kangaroos, and elephants. Yet that entire process would – if it occurred through Darwinian mechanisms – be expected to occur without the benefit of a single mutation of the complexity of a CCC. Strict Darwinism requires a person to believe that mammalian evolution could occur without any mutation of the complexity of this one.