State of the Debate

ID proponents say that Darwinian processes DO function BUT are only capable of making minor changes. The latest research by ID proponents is attempting to ascertain the exact limits of unguided Darwinian processes. This brings us to the State of the Debate, where I'll attempt to show you where events currently have taken us.

Now Darwinists will often cite medical advances as support for Darwinism. One common example, antibiotic resistance, falls well within the boundaries of ID (besides, Blythian evolution readily explains antibiotic resistance, not Darwinism). This is an attempt at conflating multiple issues. Because medical science has made many advances does not equate to Darwinism being valid.

….if truth be told, evolution hasn’t yielded many practical or commercial benefits. Yes, bacteria evolve drug resistance, and yes, we must take countermeasures, but beyond that there is not much to say. Evolution cannot help us predict what new vaccines to manufacture because microbes evolve unpredictably. But hasn’t evolution helped guide animal and plant breeding? Not very much. Most improvement in crop plants and animals occurred long before we knew anything about evolution, and came about by people following the genetic principle of ‘like begets like’. Even now, as its practitioners admit, the field of quantitative genetics has been of little value in helping improve varieties. Future advances will almost certainly come from transgenics, which is not based on evolution at all.

In science’s pecking order, evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics.

Jerry Coyne

Charles Darwin, perhaps medicine’s most famous dropout, provided the impetus for a subject that figures so rarely in medical education. Indeed, even the iconic textbook example of evolution—antibiotic resistance—is rarely described as “evolution” in relevant papers published in medical journals.
Catriona J. MacCallum

Doctors don’t study evolution. Doctors never study it in medical school, and they never use evolutionary biology in their practice. There are no courses in medical school on evolution. There are no ‘professors of evolution’ in medical schools. There are no departments of evolutionary biology in medical schools.

If you needed treatment for a brain tumor, your medical team would include a physicist (who designed the MRI that diagnosed your tumor), a chemist and a pharmacologist (who made the medicine to treat you), an engineer and an anesthesiologist (who designed and used the machine that give you anesthesia), a neurosurgeon (who did the surgery to remove your tumor), a pathologist (who studied the tumor under a microscope and determined what type of tumor it was), and nurses and oncologists (who help you recover and help make sure the tumor doesn’t come back). There would be no evolutionary biologists on your team.

I am a professor of neurosurgery, I work and teach at a medical school, I do brain research, and in 20 years I’ve performed over 4000 brain operations. I never use evolutionary biology in my work. Would I be a better surgeon if I assumed that the brain arose by random events? Of course not. Doctors are detectives. We look for patterns, and in the human body, patterns look very much like they were designed. Doctors know that, from the intricate structure of the human brain to the genetic code, our bodies show astonishing evidence of design. That’s why most doctors—nearly two-thirds according to national polls—don’t believe that human beings arose merely by chance and natural selection. Most doctors don’t accept evolutionary biology as an adequate explanation for life. Doctors see, first-hand, the design of life.

I do use many kinds of science related to changes in organisms over time. Genetics is very important, as are population biology and microbiology. But evolutionary biology itself, as distinct from these scientific fields, contributes nothing to modern medicine.

Without using evolutionary theory, doctors and scientists have discovered vaccines (Jenner, in the 18th century, before Darwin was born), discovered that germs cause infectious diseases (Pasteur, in the 19th century, who ignored Darwin), discovered genes (Mendel, in the 19th century, who was a priest and not a supporter of Darwin’s theory), discovered antibiotics, and unraveled the secrets of the genetic code (the key to these discoveries was the discovery of the apparent design in the DNA double helix). Heart, liver, and kidney transplants, new treatments for cancer and heart disease, and a host of life-saving advances in medicine have been developed without input from evolutionary biologists. No Nobel prize in medicine has ever been awarded for work in evolutionary biology. In fact, I think it’s safe to say that the only contribution evolution has made to modern medicine is to take it down the horrific road of eugenics, which brought forced sterilization and bodily harm to many thousands of Americans in the early 1900s. That’s a contribution which has brought shame—not advance—to the medical field.

So ‘Why would I want my doctor to have studied evolution?’ I wouldn’t. Evolutionary biology isn’t important to modern medicine. That answer won’t win the ‘Alliance for Science’ prize. It’s just the truth.

Michael Egnor, M.D.

Behe’s recent book “Edge of Evolution” is very important as it describes an observation (p. falciparum replicating trillions of times) where the ID hypothesis could have been falsified but instead was a confirmed prediction of ID (no complex (7) specified machines without intelligent agency). It’s hard to imagine a better test of Darwinian processes real-world ability than analyzing genetic change in a eukaryote at the nucleotide level over orders of magnitude more replications than all mammals that ever lived. The point is, if nothing of major interest is observed under these circumstances then how can Darwinists be so certain about their inference that these unguided processes are capable of producing, say, the changes between the chimp and man. (Note that this is not a slam against the potential of guided intelligent evolution!)

Now Behe made an estimate for an "edge" to unguided evolution of 2 CCC events. So if in the future someone "refutes" Behe's observation of a 2 CCC event "edge" then we should not be surprised. Obviously I’m doubtful observation will expand this “edge” enough to save Darwinism but if there is a minor expansion everyone (especially Darwinists) needs to keep in mind that potentiality won’t hurt ID. So the current estimate need not be defended overly much by ID proponents. Personally I think a generalized "edge" that applies in all situations will be either be 3 or 4 CCCs.

The "best" response to Behe's data I've seen so far consists of looking at various tyeps of HIV and cherry picking a speculative--not observed--evolutionary scenario out of several less favorable scenarios by comparing two viruses--NOT eukaryotic cells which have a mutation rate about 10,000 less!--then assuming that the mechanism for change in this case of evolution, assuming it did occur as speculated, was unguided Darwinian processes(4). The worst part is that this "refutation", even if accepted as valid, would not go far beyond Behe's "edge" and on top of that there isn't enough information content to be considered CSI!

A bundle of assumptions seems to be substituted for hard data. Reconstructing a speculative Darwinian pathway is not hard data. It would be best to stick to observed evolution known to have been caused by unguided Darwinian processes rather than perceived/inferred evolution (often referred to as "storytelling"). The worst assumption is the presumption that the only possible mechanism for this evolution scenario is unguided Darwinian processes. If they really want to challenge Behe they need to find observable evidence where the mechanism is KNOWN to be unguided Darwinian processes.

This is NOT impressive! Nor are other examples such nylonase (single frame shift)(3), the tuning of color vision in animals, cefotaxime antibiotic resistance in bacteria (1), pyrimethamine resistance in malarial parasites (2), mosquito resistance to pesticides (single nucleotide mutation) (3), anti-freeze protein in code (10), and computer simulations such as Avida(6). But at least in these cases we have observable evidence to work with.

http://www.biology-direct.com/content/2/1/15

Short version is that this Darwinist, Koonin, considers the unguided Origin Of Life (OOL) scenarios and as a conservative estimate he calculates one in 10e-1018 for the possibility that such a system could have arisen. He then appeals to the Multiple Worlds Interpretation (MWI) for curing these limited probabilistic resources. Read it through including the discussion and the appendices. In the discussion Koonin said there is a world in which Elvis is alive in 2007!

Funny thing is, an infinite multiverse (contrasted with a finite multiverse, but that isn't what is being proposed by Koonin) guarantees that there will be one in which all life is designed since every logically possible universe is actual. A Designer is logically possible; therefore in a multiverse the Designer is actual. So a question to pose to the materialist: if the infinite multiverse idea is true, why couldn't we be living in the one where the Designer is actual?

Essentially at this point Darwinists are attempting to counter observable evidence with trivial examples and massive amounts of storytelling. They are even trying to cloud the issues by appealing to the public with examples that "sound" scientific but are not (8). In short, the State of the Debate is that ID proponents, despite being persecuted (9) and having their research projects stymied or shut down, are winning the debate. Now the State of the Debate may change in the future...it IS possible that Darwinists or ID proponents may observe in nature Darwinian processes producing a 5 to 10 CCC event. But consider this...the age old example of the flagellum is comprised of 42 components!(5) Given this data I do not hold out much hope for our Darwinist friends.

In order to keep the above article from being cluttered I've included some side discussions of various topics at the bottom:

(1)Point mutations confer cefotaxime resistance, but they compromise ampicillin resistance. Thus, selection for both drug resistances in a bacterium with two copies of beta-lactamase should favor the divergence of one copy to improve cefotaxime resistance while maintaining the other copy to preserve ampicillin resistance. This selection was performed on a bacterium with identical sequences of beta-lactamase on two separate, compatible plasmids. As expected, one plasmid evolved increased cefotaxime resistance when appropriately strong cefotaxime selection was applied. However, the cefotaxime-resistant plasmid maintained sufficient ampicillin resistance to tolerate the concentration of ampicillin used, and the other plasmid was lost. Hosts carrying both the cefotaxime-resistant and wild-type plasmids were then subjected to various higher concentrations of both drugs to find conditions that would ensure the maintenance of both plasmids. In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence.

(2) Pyrimethamine resistance is discussed on page 75 and 76 of Behe’s Edge of Evolution. But I'll provide a discussion of this point.

Pyrimethamine is a drug which works by binding to a very important enzyme of the parasite, DHFR. As it happens in bacterial antibiotic resistance, a single mutation which changes the structure of the enzyme can confer some resistance to the drug. Obviously, if we use the drug, mutants will be selected. Nothing new here. But listen to the fundamental novelty: the selected, mutant enzyme, can undergo other single mutations, usually just another one in different sites, which can further reduce the affinity to the drug and therefore confer more resistance. Obviously, if we continue to use the drug, the more resistant strain will be selected.

Well, is that unlikely? No. Is that an example of a CCC event as specified by Behe? No. Why? Because, again, like in bacterial resistance to antibiotics, here there is no new function created, no new functional information. There is only a modified structure of an enzyme, which in some way retains its original function, but loses the affinity of structure which was the target of the “weapon” against the parasite, that is the drug. In other words, in the beginning the drug “fitted” the enzyme, after one or more mutations, neutral enough not to affect seriously the enzyme function, it doesn’t fit anymore. A new function? No. Just a lucky loss of a recognizable structure. It’s exactly the same thing which happens when cancer cells, through accumulating mutations, become resistant to anti-cancer drugs which have been used in the patient, when the disease progresses. Resistance through random change of the target of an administered drug is certainly not an instance of information creation.

(3) Previously discussed here:

http://www.overwhelmingevidence.com/oe/blog/patrick/egnor_and_the_information_challenge

(4) http://www.uncommondescent.com/darwinism/ervs-challenge-to-michael-behe/

(5) http://www.nature.com/nrmicro/journal/v4/n10/fig_tab/nrmicro1493_T1.html

The flagellum consists of 42 proteins. 23 proteins are “thought to be” indispensable in modern flagella. Out of those 23, 2 are unique. Otherwise 15 other proteins are unique. So that’s 17 unique proteins with no known homologs. Years ago there were thought to be 30 unique proteins, which is what you'll see in a lot of old quotes from ID proponents. So in the last couple years 13 additional homologs have been found.

But before accepting those numbers note the sequence similarities. 14 of these homologs were found by BLASTing on non-default settings. Whether that should be considered acceptable I can’t say. So perhaps it’s debatable exactly how homologous/unique some of these proteins truly are (never mind Behe’s work on protein binding sites). But despite any bias in determining homology citing “30 unique proteins” is likely no longer correct.

(6) ”…our experiments showed that the complex feature never evolved when simpler functions were not rewarded.”
Lenski, Ofria, Pennock & Adami, “The evolutionary origin of complex features.” Nature vol 423, 139-144 (8 May 2003)

Essentially, they were awarding any type of complex code--even non-functioning code!--for the sake of complexity itself. This is the opposite of that found in nature.

Edge of Evolution pg. 276

In Avida, acquiring new abilities is only one way for an organism to get computer food. Another way is by simply acquiring surplus instructions, whether or not they do anything. In fact, instructions that aren’t ever executed - making them utterly useless for performing tasks - are beneficial in Avida because they provide additional food without requiring any additional consumption. It’s survival of the fattest!

It’s also very unrealistic. Biological organisms show the opposite behavior - genes that are useless in the real world are not rewarded; the genes are rapidly lost or degraded by mutation. Why, then, was Avida programmed to do the opposite? As explained on the Avida website, the counterbiological feature was needed, “Otherwise there is a strong selective pressure for shorter genomes.” In other words, otherwise the program wouldn’t give the desired results.

I should note that there apparently is a mechanism for conserving large chunks of information that apparently does not have an immediate use.

http://www.uncommondescent.com/intelligent-design/ultra-conserved-dna-with-no-evident-immediate-purpose/

Dr. Marks, in an interview:

“Teleological” means that there is a goal in mind for the evolution process. Any time we go to the computer and actually simulate the evolution we have some sort of goal in mind, yet if you go over into the biology area, they say Darwinian evolution is not teleological — it has no goal. It’s just a process of meaningless, random events and, boom!, all of a sudden you have something which appears designed. Yet, intererestingly, in my limited exposure to some if the literature in biology, everything they do in computer modeling of evolution is teleological. And so, one of the things that I would like to see, and I have [as] a[n open] challenge, is to actually show me an emulation of a computer model that is nonteleological. And I don’t believe that there is one. We have looked at some different programs in the area of biology, and one of the things that is often claimed is that there is a magical design which occurs with the computer doing the evolution — again, not paying attention to all of this information that is snuck into the side. And what we have done, [is] we’ve been able to look at, for example, a paper from Tom Schneider at NIH, which actually proposed a[n] evolutionary program, ev, and we’re actually able to show that the amount of added information that he was using was incredible! There were two stages to it. One where he actually put together the program, and then he used an evolutionary program to do a search of this model, and it turns out his model was so information-rich that he didn’t even require an evolutionary program. He could have done it just by blind queries and it works better, and we actually were able to show this, and have it on one of our papers at evolutionaryinformatics.org — and we actually showed that the amount of added information that he placed into his algorithm was such that there only was required 8 bits of information that he needed to search for.
…
The other one we’ve looked at, which we haven’t published as of yet, is the Avida program. Now the Avida program has been written by some very top people in the area of computational intelligence and biology. They purported to show through this process that, gosh, evolution can, indeed, happen on the computer. And it was [Avida researcher, philosopher Robert] Pennock who was one of the witnesses that testified at the Dover trial. There was reference made [at Dover] to this program called Avida. And Avida, like many of these other programs that we see in the evolutionary literature, said “Wow! Look at the magic of evolution. Look at all this information that we gained without having information.” I am actually starting to believe that there’s a law — a type of law of conservation of information. That is, you can’t get much more information out of an evolutionary program than you put in. Well, we have also done an analysis of Avida and will very soon be publishing a paper showing that the amount of information that was snuck in from the side was such that the program would not have a snowball’s chance if it didn’t have this extra information placed into the side. They also talk about it being “non-targeted.” It does have a target. And they even say, “It looks like it has a target, but it doesn’t have a target.” Well, it does have a target, and we’ll be showing that and actually giving measures of the amount of information — in bits — that was added to the Avida program.

(7) In reference to an increase in complexity, a Darwinist challenged me thus: How about an actual example where a more complex organism is less fit than its simpler counterpart?

Depends on the complexity being looked at it, does it not? Let’s take a look at Talk Origins’s example of people with “monkey tails”. I have no problem calling that “complexity” in a generalized sense (as in, not CSI). I’m not sure what positive effects they do have. They’re not articulated and cannot serve as an additional limb. But I’m pretty sure they’d act as the opposite of a peacock’s feathers, dramatically reducing those individual’s chances of reproducing. Ditto goes for additional/non-functioning mammary nipples and other examples that turn off the opposite sex.

The situation is complicated enough that there can’t be blanket statements. There can be increments in complexity where the tradeoff is more positive than negative. But that’s why ID doesn’t have blanket statement…there is a complexity threshold. And that’s why Behe is trying to find an “edge of evolution”. While an estimate has been arrived at I don’t think that “true final edge” has been found yet. Personally I think it “might” be greater than where some ID proponents envision it to be. But I could be wrong.

As an aside, the problem with these loose definitions comes about when any type of complexity itself is rewarded for the sake of complexity…then you get things like AVIDA. We're also looking for a combined increase of complexity and specification, which is the mark of an intelligent agent. To refer to only "increases in complexity" is not an argument against ID. Producing more Shannon information can easily be "white noise", which is not CSI.

(8) Exhuming the Peppered Moth Story

http://www.discovery.org/a/4198

Dawkins refers to the dog breeding as an example of the "power of Darwinian processes":

http://www.uncommondescent.com/intelligent-design/dog-breeding-proof-that-darwin-was-right-hardly-says-prof/

(9) The latest evidence of persecution of ID proponents:

http://www.uncommondescent.com/intelligent-design/media-coverage-baylor-robert-marks-and-the-evolutionary-informatics-lab/

If the case for Darwinism is so strong why not allow ID proponents to do their research? In fact, some Darwinists claim that the Darwinian mechanisms RM+NS are not enough. That being the case, shouldn't Darwinists themselves desire to see this research continued? In fact, why couldn't they offer to help the research of Dr. Marks and ensure their is not any bias in the results?

(10) hen L, DeVries AL, Cheng CH. 1997. Evolution of antifreeze
glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish. Proc Natl
Acad Sci U S A 94:3811-3816.
Cheng CH, Chen L. 1999. Evolution of an antifreeze glycoprotein. Nature

Behe discusses this in Edge of Evolution. In short, he says that it looks reasonably convincing, but that it's a relatively minor development, and probably marks the limit of what Darwinian processes can reasonably be expected to do in vertebrate populations.

At length, if you read the literature, the antifreeze protein is not a normal protein, but is made up of a simple repeating 9-nucleotides coding for Thr-Ala-Ala. The gene has a "simple structure" because it is "made up of 4 to 55 repeats of just three amino acids." Most genes don't consist solely of repeats of amino acids, and have a much more complicated sequence structure. (It seems that a 9 nucleotide region upstream from the trypsinogen gene, when in the right reading frame, can code for this simple sequence.)

One can envision the original trypsinogen gene duplicating, experiencing a reading frame shift, and the 9-nt segment duplicating multiple times. None of those are huge steps, and each of them could conceivably confer a benefit of lowering the freezing point of the fish's fluids (first in the digestive track, then in blood). The resulting protein, however, is not globular -- not a "folded" protein as most normal proteins are. Furthermore, there are several such genes for the protein, of varying lengths (not discrete), and the polypeptide product gets chopped into fragments of varying length. Thus it is much less like a molecular machine, as other proteins are, and much more like a blood additive, like the glycerol and other small molecules that also are added to fish blood to lower its freezing point.

It's also useful to consider the enormous evolutionary resources that would have gone into it. Antarctica started freezing about 10 million years ago. Since that time there have been perhaps 10^15 fish. Yet with all that time and all those organisms and with relentless selective pressure, the evolutionary result is arguably very modest. Although, evolving a functional antifreeze gene would still require the simultaneous duplication of the 9-letter stretch plus the evolution of a start sequence, a stop sequence, and any introns and regulatory domains associated with the gene. To evolve a unique and functional polyprotein would require the simultaneous evolution of both the polyprotein and its associated cleaver protease enzyme. Behe has discussed the irreducibly complex nature of protease - substrate interactions and the difficulties involved in their evolution elsewhere:

http://www.discovery.org/scripts/viewDB/index.php?command=view&id=442

But, again, this scenario presumes--does not observe--the mechanism for evolution as being unguided Darwinian processes.

Thanks to everyone on UD, evolution news, discovery institute, and other sources I used in the writing of this article.