Lawrence Krauss, Stephen Meyer, Denis Lamoureux: What's Behind it All? Problems with Intelligent Design not discussed by the debaters. Including “The Junk DNA Question,” “If I.D. were true,” “The Enzyme Fold Fallacy of Douglas Axe,” and, “Why I am not an I.D.ist”

The debate can be viewed here.

There were stronger responses to I.D. that were not mentioned. I am including them below along with highlighted links to their sources.

The Junk DNA Question

There is a considerable percentage of DNA that still appears to be junk, while other evolutionists views the glass as half full and view such DNA as raw material available for future use but of little to no functionality at present. Nor does the word “junk” need to be equated with garbage useful only for tossing in the bin, but instead one may view junk DNA like excess stuff for which on has no current use, like what one keeps accumulating in oneʼs garage or attic. Also, even if the majority of DNA were discovered to have some functionality the question remains to what degree or how essential its function is.

There are regions of DNA that are heavily methylated and hence inactivate, many of those are retro-viral DNA segments (inserted into the human genome by viruses long ago) which if unmethylated and activated have been shown to lead to cancers in rats or other disabilities. Also, consider the random means by which cells come into contact with viruses that insert such DNA into them. Viruses are blown about by the wind, or found on surfaces that organisms randomly cross, or viruses are carried by insects or other parasites that fly willy-nilly through the air. Yet our cells are filled with as many retroviral genes as the genes that we use to produce all the proteins that make up our bodies. Thatʼs a lot of randomly accumulated viral DNA! Doesnʼt sound like a particularly impressive argument for “design.” For more information on ERVs (endogenous retroviruses) found inside the human genome and how they demonstrate the truth of common ancestry and create headaches for I.Dists visit the science blog ERV, and the facebook group ERV that features an excellent FAQ with links to creationist and I.Dist attempts to deny the evidence (but which are shown time and again to ignore the most pertinent data).

Further facts pointed out by a professor biochemistry are these…

—Today, the majority of experts believe that most of our genome is junk in spite of the ENCODE publicity campaign from 2012.
-The ENCODE Consortium has backed off itʼs original claim and now agrees that they misused the word "function." Some of them blame the media for distorting their position.

If I.D. Were True

1. If I.D. were true then why did Lenskiʼs Long Term Evolution Experiment (LTEE) in which he bred generations of bacteria (in line after line and in bottle after bottle, keeping track of them all) to see whether a species of bacteria that does not digest citrate might evolve the necessary mutations to do so when fed citrate as their main diet—why did such an experiment take such a long time in “bacterial years” until apparently only a single bacterium in one bottle eventually developed the ability to digest citrate and soon filled the bottle with its descendants making the bottle cloudy, and even then it was discovered that the necessary mutations did not occur at once but in stages. If I.D. were true, then did the Designer reach down into a single bacterium in the midst of this experiment and nudge the one bacterium just enough to produce a first stage mutation and then nudge one of its descendants in some other bottle a second time until it could ingest citrate to some degree? (I did not say it ingested citrate as efficiently as known citrate-eating species of bacteria do, for there are different degrees of efficiency). Or, if the “direct nudge by the Designer” interpretation of I.D. is unappealing, then letʼs consider an alternative I.D. idea, namely that the Designer gave all bacteria the innate ability to “self-direct” their own mutations so that when citrate was the main food source present they could “self-direct” their own mutations that would allow them digest it. BUT THEN, why did only one bacterium in one line out of many lines and over a lot of time develop this ability? If they were all blessed with the same ability to self-direct their own mutations as needed, why did only one of them develop this ability?

   Such an experiment has shown that beneficial mutations are not evenly distributed but only arise in a few organisms at some times and then such a mutation spreads to the rest due to the advantages of such mutations, which is exactly what evolution predicts. Same with insect resistance to DDT. DDT was found to kill the vast majority of insects, and it still does kill the vast majority of insects, but some FEW insects survived exposure to DDT long enough to breed and produce new strains that were DDT resistant. Same with resistance to the many non-DDT pesticides that farmers use today on their crops and to which a FEW SURVIVING insects eventually bore plenty of offspring such that pesticides of increasing toxicity have had to be developed. These are examples of “evolutionary arms races.”

   As for the bacterium species mentioned in the debate that was found in the bin of a nylon factory that had partially digested nylon turning it into slippery goo, please note that if all bacteria had some specially designed ability to direct their own mutations, this would be happening a whole lot more often because thereʼs a lot of plastic on the earth that could provide food for the worldʼs bacteria. Just that little strain of bacteria in that one factory apparently developed such an ability. Even then, itʼs digestion process was not very efficient.

2. If I.D. were true then how efficiently did the Designer design things? Did the Designer conclude, “Oh, thatʼs good enough, why go to any more trouble?” Meyerʼs migraine headache during the debate is a case in point. What a marvelous organ is the brain, until you suffer a migraine headache that affects oneʼs vision and memory. Or maybe, just maybe, evolution can explain matters better? The evolution of big heavy brains sitting atop thin cervical vertebrae got to be a bit too much for some of us who spend a lot of time sitting, traveling, and/or bent over reading and engaging in tense debates with one another.

   Humans are two-legged upright creatures whose anatomy is based on the same skeletal plan of four-legged creatures. Evolution elucidates some of the obvious drawbacks to the evolution of upright posture, i.e., lower back pain, foot, ankle, and knee problems. Not to mention…

   “To effect upright posture based on the skeletal system of four-legged animals the human femaleʼs sacrum had to be pushed down somewhat, so that its lower end is now below both the hip socket and the upper level of the pelvic articulation… This has resulted in an encroachment on the female pelvic cavity, thereby narrowing the birth canal and rendering it too small for comfortable birthing. The result is that human childbirth is generally painful and often dangerous. The process of giving birth exposes both the mother and her infant to sizable risks of accidents and infections. For a woman with a small pelvis the rigors of childbirth can be excruciating, even fatal. No other animal has this problem.” [Wilton Krogman, “The Scars of Human Evolution,” Scientific American, 1951 - as cited in Timothy Andersʼ “The Evolution of Evil”]

   Only in recent times has the mortality of women and children during childbirth been greatly reduced due to advances in obstetrical medicine. Even today, however, a womanʼs chances of dying from complications during childbirth remain greater than dying from complications due to having an abortion during her first trimester of pregnancy. If only the Designer had employed a uniquely improved design instead of just jury-rigging the old four-legged skeletal system to make us walk erect.

   Another flaw (albeit one not involving risk of death or infection as mentioned the above), designed into the upright skeletal system of human beings are “two major blood vessels, going to the legs, that must cross a sharp promontory bone at the junction of two lower vertebrae in the spine. The organs in the pelvis exert great pressure on those two blood vessels. During pregnancy, this pressure may build up to such an extent that the vein is nearly pressed shut, making for very poor blood drainage of the left leg. This is the so-called ‘milk leg’ of pregnancy. Four-legged animals experience no such problem.” [Wilton Krogman, “The Scars of Human Evolution,” Scientific American, 1951 - as cited in Timothy Andersʼ “The Evolution of Evil”]

The Enzyme Fold Fallacy of Douglas Axe

Meyer brought up the work of fellow I.Dist Douglas Axe. Axe claims that new genes and/or protein folds are too improbable to evolve by random mutations and hence inaccessible to evolution:

Basically every gene, every new protein fold… there is nothing of significance that we can show [that] can be had in that gradualistic way. Itʼs all a mirage. None of it happens that way.

However, the evidence from Lenskiʼs ongoing experiment demonstrates that new genes can indeed arise as FCTs recombine, and the genomics evidence that suggests that this mechanism is widespread. If indeed new genes can be produced by recombining FCTs to create new proteins with new properties, it now falls to Axe to explain why this is not a threat to his claim that new genes/protein folds cannot be produced through evolution.

There is nothing wrong, in principle, with attempting to calculate the proportion of sequence space that will yield functional proteins/protein folds. It is just very difficult to do (e.g. How do you determine a priori whether a given protein is “functional?” And to what degrees of functionality?) and so itʼs quite easy to generate numbers that are meaningless. The bottom line is that such a calculation is very difficult to make with any high degree of accuracy. Also, Axeʼs calculation was based on erroneous assumptions that cause it to be off by several orders of magnitude. See Arthur Huntʼs evaluation of Axeʼs paper that Meyer cited, and that shows where Axe went wrong.

Axe claims that the research he cites, “The Evolutionary Accessibility of New Enzymes Functions: A Case Study from the Biotin Pathway,” tests an evolutionary hypothesis, i.e., by studying whether one extant enzyme in a family of enzymes could have evolved from another extant enzyme in the same family. But that is not what evolutionists propose, they propose that both evolved from a common ancestor enzyme, not from another enzyme in the same extant family. Axe and Gauger are making precisely the same error that creationists Comfort and Cameron made when they came up with their Croco-Duck argument against evolution, namely that they think “common descent” means that related modern day species evolved from each other rather than from a common ancestor. Thatʼs like claiming “common descent” means that I am descended from my living cousin Keith.

Even young-earth creationist biochemist Todd Wood rebutted that particular claim more than a year ago. Wood wrote:

“Instead of ancestral reconstruction, Gauger and Axe focused directly on converting an existing enzyme into another existing enzyme. That left me scratching my head, since no evolutionary biologist would propose that an extant enzyme evolved directly into another extant enzyme. So theyʼre testing a model that no one would take seriously? Hmmm.”

Axe and Gauger quite simply didnʼt test an evolutionary hypothesis in the paper Axe cited, but Axe continues to claim that it says something about the limits of evolution. But when even an honest young-earth creationist sees the error, persisting in it is no more than perverse. For further comments click here.

Douglas Axe also wrote Chapter 2 of Science and Human Origins by the Discovery Institute house press, in which Axe claims that unless we can identify each and every mutation between humans and our common ancestor with chimps and exactly how each arose and why they were favored, thereʼs room for a Designer. That argument is addressed here, and here.

Those like Douglas Axe who claim itʼs impossible to turn a chimpanzee into Homo Sapiens via random mutations and natural selection donʼt seem to be aware that the common ancestorʼs DNA would most probably be nearer to both chimp and human DNA than either are presently to each other, because when thereʼs a fork in the road that leads to two different destinations you have to go back to the fork in the road to study where things began to change. In fact the distance from the fork to each rival destination (chimp or human) is half as far as the distance back down one line to the fork and up the other line to the rival destination.

Does Axe consider in his calculations that there may be natural restraints concerning how things naturally interact within the cell, with some mutations being more common than others? Such natural restraints need not be due to “intelligent design,” but to ways molecules and entire molecular processes interact. (Speaking of which see the book Lifeʼs Ratchet.)

Does Axe consider that the vast majority of mutations are neither deleterious nor beneficial but neutral, so we cannot predict all the possible ways neutral mutations may accumulate until something new and at least semi-functional develops?

Does Axe consider that enzymes are arranged into groups that are similar to one another, which suggests a common ancestor enzyme that underwent duplication and further minor mutations, allowing it to fit into an already ongoing process?

Can Axe predict how many or few mutations, or what types of mutations, may lead to a similar benefit Thereʼs a wide variety of possible mutations that a single bacterium can undergo that increase its resistance to antibiotics, same with insect resistance to pesticides. Sometimes a gene is omitted, and that helps protects them, sometimes a gene is duplicated, and that helps protect them. Some mosquitoes resistant to DDT were found to have multiple copies of the esterase genes that help them detoxify it; some cotton budworms were found to no longer possess the same biochemical target that the DDT poison aims at inside the insect; and some houseflies were found to have proteins that no longer transport the poison to its target inside the insect. So there are a variety of possible mutations that can reduce the killing effects of a pesticide on an organism, and only one of those different types of mutations has to occur in order for the organism to develop some form of DDT resistance. This increases the odds that such resistance could occur via random mutations. The study of insect resistance to insecticides as well as bacterial resistance to antibiotics, as well as the human immune systemʼs ability to produce random keys till one fits the lock of an invading microorganism (like an internal version of mutation and natural selection in action), are fascinating.

Why I am Not An I.Dist

If science does anything well, it is the manner in which it has sought and later discovered connections throughout nature, not discontinuities. DNA mutates via known natural forces (such as cosmic rays that penetrate each cell, or natural mutagenic chemicals already within each cell, as well as mutations that occur during replication which is not a perfect process even with copy-reading enzymes on hand).

Moreover, organisms have to leap over a heap of natural hurdles before they can pass along their genes to the next generation, most organisms donʼt make it, or they reproduce to a far less robust extent compared with other members of their species. And all those natural hurdles are what alter or maintain what genes a species has after it has undergone mutations, i.e., population genetics.

Moreover, the tiniest organisms, microbes, reproduce at a far faster pace than multi-cellular organisms. A single bacterium that reproduces each minute, if none died and all ate well, could produce enough offspring to equal the mass of the entire planet in a matter of days. But bacteria die in massive amounts. And bacteria exchange DNA with each other freely, as well as absorb DNA passively when they run across it, so they thrive on exchanging DNA, which as I said, is subject to mutations from natural sources.

Furthermore, according to both the fossil record and morphological considerations, bacteria preceded the far larger and more complex types of cells that make up the worldʼs multi-cellular species. In fact bacteria were around for maybe two billion years before the first larger and more complex type of cell evolved, the eukaryotic cell with its organelles and well defined nucleus. That means a lot of DNA mutations (and DNA exchanges) went on for a long time before the evolution of larger more complex cells than bacteria took place.

In fact the world was filled with nothing but single-celled organisms for a far longer time than it has been filled with multi-cellular organisms. The time from the earliest replicators to the very first multi-cellular organisms was far longer than the time from the Cambrian explosion until humans.

Viruses, which are mere strings of RNA in a protein shell, have also been around a long time, and they donʼt have any copy-reading mechanisms when it comes to the replication of their DNA, so for viruses mutations occur more often, mutations are in fact their bread and butter, and look how successful viruses are! There are more viruses than any other type of DNA-based thing on earth (I wonʼt call them living things, but I will call them DNA-based things). Some viruses are mega-sized, even bigger than bacteria and they invade even some of the largest single-celled organisms like amoeba! And some of those mega-sized viruses have special mechanisms inside them to aid further in their reproduction. And some of those mega-sized viruses get invaded by smaller viruses! DNA always wants more of itself it seems. Naturally.

On the Complexity of Each Cellʼs Inner Architecture

The cost of discovering beneficial mutations is paid by very different reproductive ratios which include countless numbers of dead organisms that leave behind no offspring at all—that is the price paid in order to produce and sustain beneficial mutations via random mutations and natural selection generation after generation. And even then, with all that price paid, most species still go extinct over time. For every species that thrives, dozens of cousin species, close offshoots, go extinct, and not just in mass extinction events but in individual extinction events throughout time. The price for evolutionary change is death on a tremendous scale, countless dead ends for every success story. Thatʼs the price paid for the ratcheting of life.

Also, if the most amazing complexity is found inside the molecular architecture of single cells thatʼs not unexpected after you consider the way the world of nothing but single-celled organisms existed on earth for far longer than the time of multi-cellular organisms from the Cambrian to humans. Back then only single cells ruled the earth, bacteria and viruses were mutating, and bacteria were exchanging DNA and passively absorbing DNA when they ran across it for a couple billion years, and reproducing so fast and dying so fast as well, all quite expected if evolution via random mutation and natural selection is true.

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Also check the topic labels below to read additional pieces on the “fine-tuning” argument, the “Cambrian Explosion,” and “intelligent design.”