Yet more in defense of Adam and Eve.

Adam and the Genome and “Predetermined Conclusions”
Evolution News | @DiscoveryCSC

In two previous posts (here and here), we saw that evolutionary genomicist Richard Buggs and biologist Dennis Venema have been debating online about Venema’s argument in Adam and the Genome that human genetic diversity refutes a traditional view of Adam and Eve. (Find the rest of our series of posts on the book here.)  Buggs explained that Venema’s allusion to human leukocyte antigen (HLA) genes (also called major histocompatibility complex, or MHC, genes) do not refute an original human couple. In his  Nature Ecology & Evolution blog post, Buggs writes, “Hyper-variable loci like MHC genes or microsatellites have so many alleles that they seem to defy the idea of a single couple bottleneck until we consider that they have very rapid rates of evolution, and could have evolved very many alleles since a bottleneck.” Buggs also explained in a  comment at The Skeptical Zone  that the ability of MHC genes to evolve rapidly isn’t a good argument for a large ancestral population size:

MHC loci are pretty exotic. Several studies show that they evolve fast and may be under sexual selection, pathogen-mediated selection, and frequency-dependent selection; they may also have heterozygote advantage (see e.g. [link]). The maintenance of MHC polymorphism is still “an evolutionary puzzle” ([link]). There is some evidence for convergent evolution of HLA genes ([link, link, link, link]). If the whole case for large human ancestral population sizes rests on MHC loci, I think this is inadequate to prove the point, given our current state of knowledge on MHC evolution.

Buggs isn’t the only qualified biologist who has looked at arguments from MHC genes against Adam and Eve and found them lacking. In the book Science and Human Origins, Ann Gauger considered the evidence, and found it compatible with an initial couple. She recounts her investigation of this topic:

When I began this study, I was prepared to accept that there was too much genetic diversity among these genes to have passed through just two first parents. To my surprise, I found that even this most polymorphic (most varied) region of our genome does not rule out the possibility of a first couple.

(Science and Human Origins, p. 106)

As Gauger points out, the evolutionary biologist Francisco Ayala had calculated that there were 32 different HLA alleles in existence when the human lineage diverged from chimps, requiring “that the minimum size of the ancestral population was no fewer than 4,000, with a long-term average effective population size of 100,000.” She explains why this supposedly refuted Adam and Eve:

Because of this minimal estimate of 4,000, Ayala claimed that at no time was it possible for the human population to have passed through a bottleneck of two. In his view, there is just too much ancestral diversity in HLA-DRB1.

(Science and Human Origins, p. 111)

After reviewing Ayala’s arguments, however, she found that his model had both explicit and implicit assumptions that were dubious:

These explicit assumptions include a constant background mutation rate over time, lack of selection for genetic change on the DNA sequences being studied, random breeding among individuals, no migrations in or out of the breeding population, and a constant population size. If any of these assumptions turn out to be unrealistic, the results of a model may be seriously flawed.

There are also hidden assumptions buried in population genetics models, assumptions that rely upon the very thing they are meant to demonstrate. For example, tree-drawing algorithms assume that a tree of common descent exists. The population genetics equations also assume that random processes are the only causes of genetic change over time, an assumption drawn from naturalism. What if non-natural causes, or even unknown natural causes that do not act randomly, have intervened to produce genetic change?

(Science and Human Origins, p. 112)

Gauger realized that in this case, Ayala had wrongly assumed a lack of selection on these genes, and wrongly assumed a constant background mutation rate. Another study that corrected for these problems found that only seven copies of HLA need have existed, which Gauger calls a “dramatically lower estimate for the number of HLA-DRB1 alleles in the ancestral population than the number Ayala found in his study (i.e. seven alleles versus thirty-two).” (p. 113) A later paper reported that HLA-DRB1 alleles numbered only four or five at the time of our supposed split from chimps. This number is low enough to have passed through a single couple.

Now of course Venema cites papers that looked at many other genes and their various alleles in the human genome. So there’s a lot more data that remains to be evaluated. But note why Gauger chose to study HLA genes:

I chose to look at the HLA-DRB1 story because it seemed to provide the strongest case from population genetics against two first parents. If it were true that we share thirty-two separate lineages of HLA-DRB1 with chimps, it would indeed cause difficulties for an original couple. But as we have seen, the data indicate that it is possible for us to have come from just two first parents.

(Science and Human Origins, p. 120)

For a short online summary of Gauger’s argument, see here.

A Prescient Warning

If perhaps the strongest argument against Adam and Eve — from population genetics — has fallen apart, what will happen when other genes are similarly scrutinized? Of course we should wait and see what the evidence says, but Gauger’s warning is prescient:

[O]ne thing is clear right now: Adam and Eve have not been disproven by science, and those who claim otherwise are misrepresenting the scientific evidence.

(Science and Human Origins, p. 121)

Indeed, much data remains to be examined. And Gauger and some of her colleagues, such as Ola Hössjer, have been addressing that data. They have published two peer-reviewed papers that present models for potentially testing population genetics arguments against a first couple at our origin: 

• Ola Hössjer, Ann Gauger, and Colin Reeves, “Genetic Modeling of Human History Part 1: Comparison of Common Descent and Unique Origin Approaches,” BIO-Complexity, Vol. 2016 (3).
• Ola Hössjer, Ann Gauger, and Colin Reeves, “Genetic Modeling of Human History Part 2: A Unique Origin Algorithm,” BIO-Complexity, Vol. 2016 (4).

Their papers evaluate the assumptions underlying the standard evolutionary model of human origins and find “it is full of gaps and weaknesses.” The authors maintain that “a unique origin model where humanity arose from one single couple with created diversity seems to explain data at least as well, if not better.”

Created Founder Diversity

After reviewing five main mechanisms invoked by standard evolutionary models of population genetics to explain human genetic diversity (mutation, genetic drift, natural selection, recombination, and colonization and migration), the first paper observes:

Neo-Darwinism accounts for the above-mentioned mechanisms I-V, and among them germline mutations are essentially the only way by which novel DNA can arise. The theory does not allow for large amounts of new and suddenly appearing diversity. The reason is that neo-Darwinism is framed within methodological naturalism. This prevailing approach to science only allows for natural hypotheses. But if an intelligent designer is invoked as a possible explanation, and if humanity originates from one single couple, it is possible that their chromosomes were created with considerable diversity from the beginning.

Thus, the authors propose a sixth mechanism of genetic change, called created founder diversity. Created founder diversity is biologically plausible for DNA of non-sex chromosomes, and would allow for initial genetic diversity among all four sets of autosomes in the first couple.

The authors note that the “main argument against a unique origin is that the nucleotide diversity of human DNA data seems too high in order make a single founding couple possible.” But they argue it is possible that humans are descended from an initial couple if “they were created with genetic diversity in their autosomal and X-chromosome DNA.” They conclude: “Any common descent model faces a challenge to explain the genetic differences rather than the similarities with other species, the consequences of inbreeding depression and increased genetic entropy, human DNA mixture with archaic populations, and that our DNA resembles a mosaic of about four founder genomes.” Thus, they find, “The provisional conclusion is that a unique origin model seems more plausible.”

 Their second paper presents mathematical algorithms “for testing different historical scenarios of the human population,” including common ancestry models, and models where humans “all descend from one single couple.” Their mathematical approach can simulate human history by varying different parameters, including population expansion, bottlenecks, colonization and migration patterns, mating and reproduction schemes, and various types of mutations in autosomal chromosomes, sex chromosomes, and mitochondrial DNA. Additionally, “An important parameter of the model is the created diversity of the founder generation, since it facilitates a higher degree of genetic diversity for a relatively young population within autosomal and X chromosomal regions, and possibly also for mitochondrial DNA.”

Their algorithms incorporate what they identify as the six major mechanisms of genetic change: (i) genetic drift, (ii) genetic recombination, (iii) colonization and migration, (iv) mutations, (v) natural selection, and (vi) initial created founder diversity. They note that “common descent models only include the first five mechanisms, but (vi) is important in order to generate enough diversity for a population with only one founding couple.” Indeed, they observe that a “particularly important parameter is the created diversity, which makes it possible to obtain a substantial amount of genetic diversity for nuclear autosomal and X-chromosome DNA, during a relatively short period of time.”

After going through a detailed mathematical analysis of the model, they conclude, “In subsequent papers, we plan to simulate human DNA data from our proposed model in order to assess how well it fits real data,” with the ultimate goal of finding “the best fitting population history within a unique origin framework, and then to compare it with a best fitting common ancestry model.”

The Best Treatment of This Issue

Probably the best treatment of this issue found anywhere is the chapter “An Alternative Population Genetics Model,” by Ann Gauger, Ola Hössjer, and Colin Reeves in the book  Theistic Evolution: A Scientific, Philosophical, and Theological Critique. There, they find key human genomic diversity evidence is highly compatible with Adam and Eve:

Block Structure of DNA. A large part of our autosomal and X-chromosomes have apparently been recombined into blocks of varying length. Many of them are of the order 10,000 nucleotides long, but the variation in length is large. But even though the blocks are long, there is still very little variation within them. Each block comes in just a few variants, four for many parts of the genome. Our chromosomes are different mosaics of these block variants.

This DNA block structure is remarkably consistent with a unique origin hypothesis. If Adam and Eve were created with DNA diversity, there would have been four different copies of each autosomal chromosome — two in Adam and two in Eve. Their four chromosomes have since been scrambled by ancestral recombinations, and today each of us has one mosaic of the four founder chromosomes inherited from our father, and another one from our mother.

After reviewing various aspects of the genetic evidence, they conclude:

We have argued that a unique origin model (with a young or old age of humanity) with created diversity should have at least the same explanatory power for human genetic data as the most popular common descent scenario of today. Any model must be able to explain the big genetic differences between humans and other species, solve the problem of inbreeding depression, support the viability of human and archaic population admixtures, and give reasons why our DNA resembles a mosaic of about four founder genomes. The conclusion is that the unique origin model seems more plausible.

They end their chapter by discussing the models they are currently in the process of testing (the aforementioned technical papers).

We are currently working on implementing a model based on backward simulation. The intent is to validate it with real data. This is a long-term project, whose outcome we hope to publish elsewhere. Using this approach, it may be possible to demonstrate that a unique origin model is able to replicate current human diversity as well or better than the common descent model. That is the purpose of the model—to test this possibility. Therefore, if more than one plausible account of human origins can explain the data, the common descent model of our origin from ape-like ancestors can no longer be claimed as conclusive proof that there could not have been a single first pair. Thus, it would be premature to discard traditional interpretations of the reality and historicity of Adam and Eve.

Obviously  more work remains to be done. But if Venema wants to maintain that Adam and Eve are truly refuted, he’s going to have to contend with this modelling research, which isn’t complete, but already points in a promising direction.

In fact, Venema did respond — though only very briefly, and very dismissively — to this work.  As we explained here,  on the BioLogos website Venema called the papers “a (poor) attempt to argue for a predetermined conclusion that humans were specially created as a pair in the Middle East. It does not offer a mechanism to deal with the obvious problems of such an approach other than an appeal to ‘created diversity.’” University of Stockholm mathematician Ola Hössjer, who co-authored the papers, responded:

Venema basically criticizes the Middle East version of the unique origin model, saying the African DNA looks older than non-European DNA, both from single locus allele frequency statistics and from two locus linkage disequilibrium patterns. But we also point out that this is a drawback of the Middle East unique origin model (on the other hand we argue that a ME origin has other advantages, for instance less inbreeding depression). We offer some tentative explanations (reference 50, for instance) of why African DNA could look older even if humanity originated in the Middle East. Venema rules out these explanations as inadequate. This may very well be true, but it remains to be seen when the model is implemented.

It’s worth stating that these papers offer a model that can be used to test many scenarios, not just that of a single couple at our origin. The model will allow the examination of the effects of mutation rate, selection, recombination, population structure, and population history on patterns of genetic variability, in order to determine which scenarios best reproduce modern genetic diversity. As for the hypothesis of a single pair with created diversity, which Venema labels a “predetermined conclusion,” it is simply one hypothesis to be tested among many.

Moreover, initial “created diversity” is a legitimate, testable mechanism. We know how genetics works and we can decide whether (within the bounds of genetics) initial high diversity could account for present-day observations.

Unfortunately, critics of this work seem to want to reject the proposed model before it’s even been fully implemented. Dr. Venema complains of “predetermined conclusions.” But the criticism could be turned right around and applied to him, instead.

Trying to school God.

1)Wolf-Ekkehard Lönnig: Under Neo-Darwinism, the Recurrent Laryngeal Nerve Must Have a Rational Design

Casey Luskin 

In his book Why Evolution is True, evolutionary biologist Jerry Coyne claims that "Imperfectdesign is the mark of evolution; in fact it's precisely what we expect from evolution." (p. 81) He makes this prediction because "[n]ew parts don't evolve from old ones, and we have to work well with the parts that have already evolved. Because of this, we should expect compromises: some features that work pretty well, but some not as well as they might, or some features--like the kiwi wing--that don't work at all, but are evolutionary leftovers." (p. 81)

Thus according to Coyne, evolution predicts that some features will work well, some will work not-so-well, and some will work not at all. This is not exactly a useful set of predictions, but when he couples the argument with the dubious assertion that intelligent design (ID) requires "perfect design," then Coyne places evolution in a unique position to explain such examples of allegedly "imperfect design."

Coyne is by no means the first person to make this argument. In the largely anti-ID volumeIntelligent Design Creationism and its Critics, Kelly C. Smith states that "if a design in nature is clearly inferior to what a human engineer could produce, then we are entitled to [reject ID]." (p. 724) (Smith also purposefully mislabels ID as a form of creationism, but we'll ignore that for the moment.)

What both Coyne and Smith share in common is their granting of favored-argument-status to the recurrent laryngeal nerve (RLN) as an alleged example of this "imperfect" or "inferior" design. As the argument goes, the RLN innervates the larynx. However, instead of running directly from the brain to the voice box, as one might expect, the nerve path travels down past the larynx, with the RLN branching off the vagus nerve down near the heart, then looping around the aorta and traveling back up the neck to innervate the larynx from below.

Coyne calls this extra distance the RLN takes to get to the larynx "[o]ne of nature's worst designs," (p. 82) and Smith calls it "a very poor design for its intended purpose." (p. 725) Likewise, Richard Dawkins says in a National Geographic video, "Obviously a ridiculous detour! No engineer would ever make a mistake like that." They all go further and argue that the seemingly circuitous route of the nerve is easily explained if one understands that our body evolved from a fish body and must operate under those constraints.

But a new article by pro-ID biologist, recently retired from the Planck Institute for Plant Breeding Research in Germany,Wolf-Ekkehard Lönnig, titled "The Laryngeal Nerve of the Giraffe: Does it Prove Evolution?," explains that observed variation within humans implies that such so-called evolutionary constraints do not exist:

The fact is that even in humans in 0.3 to 1% of the population the right recurrent laryngeal nerve is indeed shortened and the route abbreviated in connection with a retromorphosis of the forth aortic arch. ("An unusual anomaly ... is the so-called 'non-recurrent' laryngeal nerve. In this condition, which has a frequency of between 0.3 - 1%, only the right side is affected and it is always associated with an abnormal growth of the right subclavian artery from the aortic arch on the left side" - Gray's Anatomy 2005, p. 644.; see also Uludag et al. 2009; the extremely rare cases (0.004% to 0.04%) on the left side appear to be always associated with situs inversus, thus still "the right side"). Nevertheless, even in this condition its branches still innervate the upper esophagus and trachea (but to a limited extent?). Although this variation generally seems to be without severe health problems, it canhave catastrophic consequences for the persons so affected: problems in deglutition (difficulties in swallowing) and respiratory difficulties (troubles in breathing) (see Rammerstorfer 2004; moreover "dysphagia (if the pharyngeal and oesophageal branches of nonrecurrent or recurrent inferior laryngeal nerve are injured)" - Yang et al, 2009)

Lönnig thus makes the following observations:

If mutations for such a short cut are possible and regularly appearing even in humans (not to mention some other non-shorter-route variations), - according to the law of recurrent variation (see Lönnig 2005, 2006), they must have occurred already millions of times in all mammal species and other vertebrates taken together from the Silurian (or Jurassic respectively) onwards. And this must also be true for any other (at least residually) functionally possible shorter variations of the right as well as of the left recurrent laryngeal nerve. Inference: All these 'short-cut mutations' were regularly counter-selected due to at least some disadvantageous and unfavourable effects on the phenotype of the so affected individuals (including any such mutants in the giraffes). Hence, they never had a chance to permeate and dominate a population except for the above mentioned very small minority of the (right) 'non-recurrent' laryngeal nerve, which is perhaps already accounted for by the genetic load ("The embryological nature of such a nervous anatomical variation results originally from a vascular disorder, named arteria lusoria in which the fourth right aortic arch is abnormally absorbed, being therefore unable to drag the right recurrent laryngeal nerve down when the heart descends and the neck elongates during embryonic development." Defechereux et al. 2000). Thus, even from a neo-Darwinian point of view, important additional functions of theNervus laryngeus recurrens should be postulated and looked for, not to mention the topic of embryological functions and constraints.

It seems quite likely that there are mutational pathways to a more efficient route for the RLN. Under neo-Darwinian thinking, this implies this pathway should have evolved. At the very least, it shows that there are no in-principle constraints based upon our alleged fish-ancestry which prevent this route from evolving. The fact that the pathway remains--under evolutionary logic--that there's some benefit to the current design, which implies that the current design isn't so imperfect after all.

In the next post and subsequent posts, we'll explore some potential benefits to the current design of the innervations of the larynx.

2)The Recurrent Laryngeal Nerve Does Not Refute Intelligent Design

Casey Luskin October 14, 2010 1:10 PM

In the prior post, I discussed challenges to the claim that our supposed fish-ancestry dictates that the recurrent laryngeal nerve (RLN) must take a circuitous route from the brain to the larynx. Let's assume, for the sake of argument, that common ancestry between mammals and fish is the best explanation for the nerve's path. Would that refute intelligent design? Evolutionary biologist Jerry Coyne assumes that ID is incompatible with common ancestry, which it isn't. As one pro-ID biologist wrote me on this topic, "this is only a problem for design if one assumes design means designed from scratch for each taxon, and if one believes that the designer would necessarily use the shortest distance between two points (in other words, that the designer thinks like we do), and that there are not other design considerations at play."

But if we set aside the question of whether evolutionary history explains the RLN's path, it's also never been clear to me why "imperfect design" should refute design. I've complained before about the breakdowns and flaws I've had with computers, but obviously computers are designed. In fact, every piece of technology that has ever had a flaw shows that imperfect designs are was still designed! "Imperfect design"--a term used by Coyne--is still design.

Regardless of whether evidence for common ancestry or evidence of imperfect design actually do refute design, both Jerry Coyne and Kelly C. Smith admit that if we find some rational function or a reasonable purpose for a design, then the "imperfect" or "inferior" design objection falls apart. Coyne tells us that imperfect design doesn't refute evolution because evolution predicts that both highly functional or poorly-functional parts may exist. Therefore it seems to actually really predict nothing whatsoever on this matter.

While Coyne's argument may not be coherent, one way to refute it is to to find rational function for the RLN's pathway in normal humans.

Indeed, hints of important functions for the RLN nerve can be seen in the old authority, Gray's Anatomy, which states regarding the normal human design:

As the recurrent nerve hooks around the subclavian artery or aorta, it gives off several cardiac filaments to the deep part of the cardiac plexus. As it ascends in the neck it gives off branches, more numerous on the left than on the right side, to the mucous membrane and muscular coat of the esophagus; branches to the mucous membrane and muscular fibers of the trachea; and some pharyngeal filaments to the Constrictor pharyngis inferior.

So it seems that the RLN is innervating a lot more than just the larynx. Pro-ID biologist Wolf-Ekkehard Lönnig, in his article "The Laryngeal Nerve of the Giraffe: Does it Prove Evolution?," quotes a passage from a much more recent 1980 edition of Gray's Anatomy stating much the same thing:

As the recurrent laryngeal nerve curves around the subclavian artery or the arch of aorta, it gives several cardiac filaments to the deep part of the cardiac plexus. As it ascends in the neck it gives off branches, more numerous on the left than on the right side, to the mucous membrane and muscular coat of the oesophagus; branches to the mucous membrane and muscular fibers of the trachea and some filaments to the inferior constrictor [Constrictor pharyngis inferior].

(Gray's Anatomy, 1980, p. 1081, similarly also in the 40th edition of 2008, pp. 459, 588/589)

Lönnig further states: "I have also checked several other detailed textbooks on human anatomy like Sobotta - Atlas der Anatomie des Menschen: they are all in agreement. Some also show clear figures on the topic. Pschyrembel - Germany's most widely circulated and consulted medical dictionary (262 editions) - additionally mentions 'Rr. ... bronchiales'."

So the RLN's sole purpose, or as ID-critic Kelly Smith put it, its "intended function," is not simply to innervate the larynx, as it provides innervations for the heart and even for the esophagus. And for those organs it takes a direct, or as Coyne might put it, "rational" route from the brain.

All of this this would seem to satisfy what Kelly Smith called evidence of a "global" function, which Smith admits makes "an instance of local imperfection" (i.e. the circuitous route of the RLN) more acceptable in an argument for design (See Smith's article in the volume "Intelligent Design Creationism and Its Critcis," p. 725). So what is Smith complaining about?

Embryological Considerations for the RLN's Design

Lönnig also hints that there may be embryological reasons for the design of the RLN:

However, just to refer to one possible substantial function of the Nervus laryngeus recurrens sinister during embryogenesis: "The vagus nerve in the stage 16 embryo is very large in relation to the aortic arch system. The recurrent laryngeal nerve has a greater proportion of connective tissue than other nerves, making it more resistant to stretch. It has been suggested that tension applied by the left recurrent laryngeal nerve as it wraps around the ductus arteriosus could provide a means of support that would permit the ductus to develop as a muscular artery, rather than an elastic artery" - Gray's Anatomy, 39th edition 2005, p. 1053.

Another pro-ID thinker commented to me privately about this matter as follows:

So according to this description, nerve filaments emanate along its length from the cardiac plexus to the esophagus, which if accurate might well dictate its positioning. Whether due to a requisite embryogenic sequence, for optimal nerve routing, or even an evolutionary carryover, it is a workable routing in all mammals, and therefore lacks substance as an argument against design based upon "poor design."

Dr. Lönnig thus concludes:

To innervate the esophagus and trachea of the giraffe and also reach its heart, the recurrent laryngeal nerve needs to be, indeed, very long. So, today's evolutionary explanations (as is also true for many other so-called rudimentary routes and organs) are not only often in contradiction to their own premises but also tend to stop looking for (and thus hinder scientific research concerning) further important morphological and physiological functions yet to be discovered. In contrast, the theory of intelligent design regularly predicts further functions (also) in these cases and thus is scientifically much more fruitful and fertile than the neo-Darwinian exegesis (i.e. the interpretations by the synthetic theory).

To sum up: The Nervus laryngeus recurrens innervates not only the larynx, but also the esophagus and the trachea and moreover "gives several cardiac filaments to the deep part of the cardiac plexus" etc. (the latter not shown below, but see quotations above). It need not be stressed here that all mammals - in spite of substantial synorganized genera-specific differences - basically share the same Bauplan ("this infinite diversity in unity" - Agassiz) proving the same ingenious mind behind it all.

Lönnig goes on to make a devastating critique of Dawkins and others who use the alleged poor design of the laryngeal nerve to refute ID. See Lönnig's article, "The Laryngeal Nerve of the Giraffe: Does it Prove Evolution?," for details.

The next post in this series will show that the exact form of direct innervations of the larynx from the brain--demanded by ID-critics--in fact exists.

3)Direct Innervation of the Larynx Demanded by Intelligent Design Critics Does Exist

Casey Luskin October 15, 2010 1:33 PM

Intelligent design (ID) critics Jerry Coyne, Kelly Smith, and Richard Dawkins have all argued that the allegedly circuitous innervations of the larynx from the brain by the recurrent laryngeal nerve (RLN) is an "imperfect design" that refutes ID. What they rarely disclose, however, is that there are in fact nerves that innervate the larynx directly from the brain through the superior laryngeal nerve (SLN), without taking the longer path of the RLN--exactly as they demand.Thus, the larynx is in fact innervated from both above and below, by both the RLN and the SLN. This is clearly seen in the diagram below, from Elsevier's Atlas of Regional Anesthesia, 3rd ed., hotlinked from here:

As noted here, damage to the SLN can in fact affect the ability of people to swallow, yell, sing, or properly control voice pitch.

Thus, the preferred design of Coyne, Dawkins and Smith actually DOES exist in our bodies, as the larynx is innervated from above, directly from the brain.

Given the different medical conditions encountered when the laryngeal nerves (such as the SLN and RLN) are damaged, it seems that the two nerves are performing distinct functions. The SLN--which innervates from above--has something to do with producing higher-pitched sounds, and the RLN--which innervates from below--has something to do with producing lower-pitched sounds.

Rather than being an "imperfect design," perhaps the dual innervation of the larynx from both above and below is a good design principle -- a form of redundancy, or complementation to help minimize the impact upon function if one of these two nerves is damaged. Thus we see hints of function and design optimization in the innervation of the larynx. Again, this is evidence of optimization for a "global function," which ID-critic Kelley C. Smith admits is a good design principle.

In the final post we'll explore some medical considerations for the design of the RLN.

4)Medical Considerations for the Intelligent Design of the Recurrent Laryngeal Nerve

Casey Luskin October 16, 2010 8:31 AM

In the previous three posts (see part 1, part 2, and part 3), we've seen that the arguments of intelligent design (ID) critics based that the recurrent laryngeal nerve (RLN) is an "imperfect design" fail for a variety of reasons. These include:

(1) There is evidence that supposed fundamental evolutionary constraints which would prevent loss of the circuitous route of the RLN do not exist. This implies that there is some beneficial function for the circuitous route.

(2) The path of the RLN allows it to give off filaments to the heart, to the mucous membranes and to the muscles of the trachea along the way to the larynx.

(3) There is dual-innervation of the larynx from the SLN and RLN, and in fact the SLN innervates the larynx directly from the brain. The direct innervation of the larynx via the superior laryngeal SLN shows the laryngeal innervations in fact follows the very design demanded by ID critics like Jerry Coyne and Richard Dawkins. Various medical conditions encountered when either the SLN or RLN are damaged point to special functions for each nerve, indicating that the RLN has a specific laryngeal function when everything is functioning properly. This segregation may be necessary to achieve this function, and the redundancy seems to preserve some level of functionality if one nerve gets damaged. This dual-innervation seems like rational design principle.

To add another reason, pro-ID professor of neurosurgery Michael Egnor has suggested that the RLN may have a medical function which gives the organism a warning that it is sick, and needs to heal from an internal infection or disease originating in the chest area. Dr. Egnor offered me some insightful comments about function of the design of the RLN pathway from his vantage as a doctor and professor of medicine:

There is actually a design advantage to the course of the recurrent nerves, if one wishes to pursue this line of argumentation. The course of the nerves brings them through the mediastinum, where the heart and lungs meet. There are many lymph nodes there, and enlargement of these lymph nodes from processes such as cancer or infection (e.g. tuberculosis) often irritates these nerves and causes hoarseness or coughing. The course of the nerves reveals disease in an otherwise hidden part of the body (deep in the chest) by interfering with a process (speech) that is readily evident. It serves as an early warning to get medical care (or, with infectious diseases, as a warning to others that this person is ill), and this early warning has saved many more lives than the redundant course of the nerves has cost lives. The risk/benefit ratio needs to be examined comprehensively before one claims that the course of the nerves is biologically disadvantageous.

While it's impossible to get into the mind of the designer and there's a lot we still don't understand about development, it's equally clear that the RLN's pathway allows it to serve a variety of functions. We do have solid positive evidence for multiple important functions of the RLN. Indeed, Michael Egnor wrote an elegant explanation of why it is the evolutionists who are basing their arguments upon our ignorance, not facts, of developmental biology:

Of course ID advocates have never claimed perfect design. But the argument that the anatomy of the recurrent laryngeal nerve is evidence for 'bad design' fails on many levels. The descent of the recurrent nerves below the aortic arch and subclavian artery is the result of patterns of coalescence and movements of components of the aortic arch during embryogenesis. It appears that proximity of various layers and structures in the embryo serve to guide embryogenesis (it's called induction). The details of this process are only beginning to be understood, and the Darwinist argument that the relationship between the recurrent nerves and the aortic arch is evidence of bad design fails to take into account the enormous complexities of embryonic development. It's analogous to a 3 year-old taking apart a computer and asserting that it was designed badly because some of the circuit board patterns were 'curvy' instead of straight. The design wisdom of the anatomy of the recurrent nerves can only be judged by someone who knows all of the design specifications necessary for that region of the human body. Even the best embryologists are pre-schoolers when it comes to that.

Conclusion
Clearly, the RLN is performing many jobs, not just one. Its "intended function" is much more than simply innervating the larynx; and the larynx is in fact innervated directly, exactly as ID-critics say it should be.

All of this this would seem to satisfy what Kelly Smith called evidence of a "global" function, which Smith admits makes "an instance of local imperfection" (i.e. the circuitous route of the RLN) more acceptable in an argument for design ("Intelligent Design Creationism and Its Critics," p. 725). The argument against intelligent design of the RLN has collapsed.

If anything is clear here, it's that we don't know enough to presume that the RLN is "[o]ne of nature's worst designs" (Coyne's words), but that we do know enough to see that it's definitely not "a very poor design for its intended purpose" (Smith's words).

Ancient whale may have eaten Darwin defenders home work.

A Whale of a Problem for Evolution: Ancient Whale Jawbone Found in Antartica
October 14, 2011 Posted by Jonathan M 

MSNBC.com is reporting on the discovery of a jawbone of an ancient whale in Antarctica: the oldest fully aquatic whale yet discovered. The news story reports,

The jawbone of an ancient whale found in Antarctica may be the oldest fully aquatic whale yet discovered, Argentine scientists said Tuesday.

A scientist not involved in the find said it could suggest that whales evolved much more quickly from their amphibian precursors than previously thought.

Argentine paleontologist Marcelo Reguero, who led a joint Argentine-Swedish team, said the fossilized archaeocete jawbone found in February dates back 49 million years. In evolutionary terms, that’s not far off from the fossils of even older proto-whales from 53 million years ago that have been found in South Asia and other warmer latitudes.

Those earlier proto-whales were amphibians, able to live on land as well as sea. This jawbone, in contrast, belongs to the Basilosauridae group of fully aquatic whales, said Reguero, who leads research for the Argentine Antarctic Institute.

“The relevance of this discovery is that it’s the oldest known completely aquatic whale found yet,” said Reguero, who shared the discovery with Argentine paleontologist Claudia Tambussi and Swedish paleontologists Thomas Mors and Jonas Hagstrom of the Natural History Museum in Stockholm.

Paul Sereno, a University of Chicago paleontologist who wasn’t involved in the research, said that if the new find withstands the scrutiny of other scientists, it will suggest that archaeocetes evolved much more quickly than previously thought from their semi-aquatic origin in present-day India and Pakistan.

“The important thing is the location,” Sereno said. “To find one in Antarctica is very interesting.”

As many readers will doubtless be aware, the evolution of the whale has previously raised substantial problems because of the extremely abrupt timescale over which it occurred. Evolutionary Biologist Richard von Sternberg has previously applied the population genetic equations employed in a 2008 paper by Durrett and Schmidt to argue against the plausibility of the transition happening in such a short period of time.  Indeed, the evolution of Dorudon and Basilosaurus (38 mya) from Pakicetus (53 mya) has been previously compressed into a period of less than 15 million years.

Such a transition is a feat of genetic rewiring and it is astonishing that it is presumed to have occurred by Darwinian processes in such a short span of time. This problem is accentuated when one considers that the majority of anatomical novelties unique to aquatic cetaceans (Pelagiceti) appeared during just a few million years – probably within 1-3 million years. The equations of population genetics predict that – assuming an effective population size of 100,000 individuals per generation, and a generation turnover time of 5 years (according to Richard Sternberg’s calculations and based on equations of population genetics applied in the Durrett and Schmidt paper), that one may reasonably expect two specific co-ordinated mutations to achieve fixation in the timeframe of around 43.3 million years. When one considers the magnitude of the engineering fete, such a scenario is found to be devoid of credibility. Whales require an intra-abdominal counter current heat exchange system (the testis are inside the body right next to the muscles that generate heat during swimming), they need to possess a ball vertebra because the tail has to move up and down instead of side-to-side, they require a re-organisation of kidney tissue to facilitate the intake of salt water, they require a re-orientation of the fetus for giving birth under water, they require a modification of the mammary glands for the nursing of young under water, the forelimbs have to be transformed into flippers, the hindlimbs need to be substantially reduced, they require a special lung surfactant (the lung has to re-expand very rapidly upon coming up to the surface), etc etc.

With this new fossil find, however, dating to 49 million years ago (bear in mind that Pakicetus lived around 53 million years ago), this means that the first fully aquatic whales now date to around the time when walking whales (Ambulocetus) first appear. This substantially reduces the window of time in which the Darwinian mechanism has to accomplish truly radical engineering innovations and genetic rewiring to perhaps just five million years — or perhaps even less. It also suggests that this fully aquatic whale existed before its previously-thought-to-be semi-aquatic archaeocetid ancestors.

Another day; another bad day for Darwinism.

No free will,no civil liberty?

Free Will Denial and PreCrimes
Michael Egnor

Tamler Sommers, an associate professor of philosophy at the University of Houston who blogs at Naturalism.Org,  argues that we don’t really have free will, and that giving up the idea of moral responsibility would be beneficial to society:

[T]he idea that criminals do not morally deserve punishment is tough to accept… In fact, giving up on the idea of deep moral responsibility has no … anarchical or distressing consequences. Let’s suppose we did start viewing terrible crimes as we do natural disasters. Would this mean we would not try to prevent future crimes?  Of course not, no more than it would suggest that we not tape our windows or retrofit buildings to protect ourselves from hurricanes and earthquakes. It would mean only that we cease to relentlessly blame criminals (or political figures) for their behavior.

Sommers inadvertently points out the most dangerous consequence of the denial of free will. If we deny free will and treat criminals as we would treat natural disasters, then preemption of crime becomes the logical goal, just as preemption of damage from natural disasters is smart public policy. As Sommers candidly admits, we should “try to prevent future crimes.” We tape our windows before hurricanes, reinforce our buildings before earthquakes, and evacuate our trailer parks before tornadoes. We don’t blame hurricanes and earthquakes for the damage they cause, in any moral sense; natural disasters aren’t guilty of anything. They’re just physical events. A consequence of this pragmatic approach is that we preempt the damage caused by natural events. We act before the natural disaster has happened, to mitigate its effects.

If we treat criminals the way we treat natural disasters — as physical events without moral culpability — the pragmatic approach is preemption as well. Why wait for a murderer to commit murder? In order “to prevent future crimes,” by Sommers’s reasoning, we can identify people with a statistical propensity to commit murder (based on race, age, sex, prior behavior, etc.), and incarcerate them before their crime, and prevent the damage.

Of course, Sommers would argue: you should’t incarcerate innocent people for crimes they haven’t committed! But if Sommers is right, and free will is not real, then there are no innocent people, any more than there are guilty people. There is no innocence or guilt at all, because innocence and guilt only have moral meaning if we have free will. If there is no free will and no innocence and guilt, there are just natural systems (us) doing what natural systems do. And, as with natural disasters, it’s prudent to preempt.

The preemption of crime is the theme of the Tom Cruise film Minority Report, which describes an imaginary world several decades in the future in which people are arrested and incarcerated (in a virtual reality world) before they commit crimes, based on the skills of experts who can visualize the future. The “crimes” of which they are convicted are called PreCrimes.n Sommers’s society in which free will is denied and guilt and innocence are rendered meaningless, there is no moral reason not to incarcerate people for PreCrimes. Of course, they’re not guilty, but they aren’t guilty even after they commit a crime, and they are never innocent either. Why wait to incarcerate people predisposed to crime? Why wait to board up your windows and evacuate your home with the approach of a hurricane? Why wait until a man has committed a crime to incarcerate him?

Hannah Arendt  observed that a hallmark of totalitarian states is the eclipse of the concept of guilt and innocence. In a totalitarian state, masses of people are managed like livestock, irrespective of any imputation of personal guilt or innocence. Hitler didn’t kill Jewish children because they were guilty of crimes. He cared not whether they were guilty or innocent. Stalin didn’t starve millions of Ukrainians because they were individually guilty. He starved them as a matter of public policy, without regard for individual moral culpability.

The denial of free will, and the denial of moral culpability that follows on it, is the cornerstone of totalitarianism. The denial of free will does not, pace Dr. Sommers, herald an era of tolerance and understanding. It heralds an era of human livestock management, and the early experiments based on denial of free will and moral culpability — in Germany and the Soviet Union — have already been run.

Darwinists summon cancer to the ramparts.

Sick of the Oxygen Theory of the Cambrian Explosion? Here’s the Cancer Theory
Evolution News | @DiscoveryCSC

You thought you’d heard it all? All the desperate materialist theories seeking to explain the burst of biological novelty some 530 million years ago that Meyer writes about in Darwin’s Doubt? You were wrong. Along comes Lund University in Sweden with a “Novel hypothesis on why animals diversified on Earth.”  Get ready for the cancer theory of the Cambrian explosion.

Can tumors teach us about animal evolution on Earth? Researchers believe so and now present a novel hypothesis of why animal diversity increased dramatically on Earth about half a billion years ago. A biological innovation may have been key. 

Not many of us who have seen friends suffer or die from cancer would sanctify tumors as “biological innovations” leading to anything good.

The new hypothesis holds that the dramatic diversification of animals resulted from a revolution within the animals’ own biology, rather than in the surrounding chemistry on Earth’s surface.

This will be a hard sell, but charitably, let’s give them their slot on the Cambrian Gong Show and try to understand their act. It’s good to see they toss out the oxygen theory, the runner-up for worst explanation. Agreed, “a causal relationship between the Cambrian explosion and increasing atmospheric oxygen lacks convincing evidence.” With itching ears we await their convincing evidence for the new hypothesis.

The leader figure behind the cancer theory is geobiologist Emma Hammarlund. She got in touch with a tumor biologist, Sven Påhlman, to consider how cancer acts like a multicellular organism.

“I wanted to learn what tumor scientists observe on a daily basis, in terms of tissue growth and how it relates to oxygen. Tumours are after all, and unfortunately, successful versions of multicellularity”, explains Emma Hammarlund.

OK, so we have multicellularity. Tumors don’t seem to automatically grow eyes and articulated limbs, though. As far as we can tell, tumors only seem to be good at killing their hosts. What’s up with this new hypothesis?

The team, including also tumor biologist Dr. Kristoffer von Stedingk at Lund University’s Paediatrics division, tackled the historic question of why animals developed so late and dramatically with novel clues from the field of tumour biology.

Basically, they looked at stem cells to see how they respond to oxygen. Generally, low oxygen (hypoxia) is a threat to a cell, and stem cells are particularly sensitive to hypoxia (are you still following?). Stem cells, therefore, have various mechanisms to deal with fluctuating oxygen levels. Well lo and behold, tumor cells do, too!

These systems involve a protein that can ‘fool’ cells [to] act as if the setting was hypoxic. This can also fool cells to get stem cell-like properties.

Tumor cells, they say, are able to maintain their stem-cell-like traits in spite of low oxygen. This gives them the freedom to evolve, just like microbes found a way to use sunlight. (What?) You may have to read this news several times to see how they get from point A, an uncontrolled tumor cell, to point B, a trilobite.

The new hypothesis that gives credit to a biological innovation to have triggered animal diversification is similar to how we think of biological innovations changing life in the past. Just the presence of free oxygen is the result of some microbes finding a way of using sunlight to get energy. This was also a biological event.

Dr. Hammarlund is a little clearer about what she means in her article at The Conversation, “Cancer tumours could help unravel the mystery of the Cambrian explosion.”

Could tumours help us explain the explosion of life of Earth? Scientists have typically explained the period of history when large animal species became much more diverse very quickly as the result of the planet’s rising oxygen levels. But my colleagues and I have developed a new idea that the change might have started within animals’ own biology, based on evidence from proteins found in tumours. It wasn’t until animals developed these proteins that they could take advantage of the oxygen and start diversifying.

This new hypothesis appears partly motivated by the failure of the oxygen theory to account for the Cambrian explosion. Here’s how it goes. In short, proteins “developed” out of nowhere. By chance, they gave cells the opportunity to “take advantage” of oxygen. This set them free to diversify. And there you go: trilobites.

Does she explain exactly how they diversified into animals with multi-system, hierarchical body plans with complex systems and behaviors? Not at all. Take a look at this newly discovered Cambrian bristle worm from Marble Canyon in Canada and see if it looks like the product of a tumor set free to diversify (Live Science).

Maybe the original paper in Nature Ecology & Evolution can clarify things. The title is, “Refined control of cell stemness allowed animal evolution in the oxic realm.” The peer-reviewed explanation follows:

Animal diversification on Earth has long been presumed to be associated with the increasing extent of oxic niches. Here, we challenge that view. We start with the fact that hypoxia (<1 a="" achieved="" action="" adult="" allowed="" and="" animal="" animals="" at="" be="" biology="" can="" cell="" cells="" cellular="" challenges="" concentrations.="" conditions="" consistent="" continuously="" control="" cope="" diversification="" enabled="" evidence="" evolution="" evolve="" factors="" fluctuating="" from="" geological="" how="" hypoxia-inducible="" hypoxia-response="" i="" illuminate="" immaturity="" in="" insights="" into="" is="" life.="" machinery="" maintains="" multicellular="" nevertheless="" new="" novel="" o2="" of="" on="" onset="" over="" oxic="" oxygen-sensing="" oxygen="" oxygenated="" paradoxically="" perspective="" provided="" provides="" realm.="" refinement="" regenerate="" regenerating="" settings.="" stem="" stemness="" suggest="" that="" the="" them="" then="" these="" this="" through="" thus="" tissue.="" tissue="" to="" transcription="" tumour="" unprecedented="" view="" we="" whereas="" with="">

From this, you see that all they are really doing is “enabling” microbes to evolve into animals, no matter how much oxygen is present. The authors endow microbes with new transcription factors that don’t restrict the action of their stem-cell properties as oxygen levels rise. Microbes can now become “successful versions of multicellularity” like cancerous tumors, and thus evolve into the Cambrian animals. Are we missing something? Do the judges want to gong this show yet?

In his recent book, Zombie Science, Jonathan Wells already gonged the cancer act when it played in a different venue. Evolutionists feel depressed at the lack of enthusiasm for Darwinism in medical science. A recent paper in PLOS ONE admits this:

Evolutionary biology currently has a marginal place within medicine. There is even a significant tendency to avoid the ‘e-word’ in the biomedical literature when referring to antimicrobial resistance.

In his chapter on antimicrobial existence as an icon of evolution (Chapter 8), Wells discusses the cancer hypothesis as another proposed example of “speciation” of sorts. This claim goes back to Julian Huxley in 1958, and continues today. Most recently, Joshua Swamidass used cancer not as an example of speciation, but of evolution by mutation and selection of the “fittest variants” (not fittest for the host, obviously). Swamidass and others try to view tumor cells as innovators. Wells looks into the examples provided by evolutionists and finds them lacking true novelty. They only rewire existing complex functions, but already have existing complex resources to draw on (p. 166). This is not innovation. It’s more like theft.

Evolutionary theory, furthermore, does little to guide medical science into new treatment options for cancer patients. Its value is “questionable, at best,” Wells concludes (p. 167). It certainly fails as evidence for evolution.

But some people argue that cancer is at least of value in providing evidence for evolutionary theory. Something doesn’t seem right here. According to evolutionary theory, the human body originated by mutation and selection, though the evidence shows that those processes cannot produce anything like a human body. Now we have evidence that mutation and selection can produce cancer, which destroys the human body. How does that support evolutionary theory? (pp. 167-168).

Applying this reasoning to Hammarlund’s cancer hypothesis for the Cambrian explosion, one finds no evidence that tumors can innovate the body plans of Cambrian animals. Jonathan Wells’s last paragraph applies here as well:

Darwinian evolution needs examples of biological processes that build new forms and functions. Cancer destroys these things. Saying cancer is evidence for biological evolution is like saying that I have a theory that explains the rise of modern civilization, and the evidence for my theory is the night of the living dead. (p. 168).

So to the cancer theory for the Cambrian explosion, the most desperate yet, we hit the gong and await the next act.