On I.D and the limits of science

Undesirable Intelligent Design is Still Intelligent Design
Casey Luskin February 29, 2012 6:01 AM

I thought I would add a few thoughts to David Klinghoffer's insightful comments on the "Centre for Unintelligent Design." Its proprietor, Keith Gilmour, offers a list of features from life and nature that he says show "unintelligent design" but in fact are best classified as illustrating "undesirable design." Looking at the website, I also noticed that Gilmour misunderstood and/or misrepresented an email exchange with University of Warwick sociologist Steve Fuller. Because this is a challenge that comes up often, it's worth clarifying.

Fuller wrote, apparently in response to Gilmour's sending him a link to the website:

Dear Keith,
Thanks for this. You might perhaps make more headway with ID people if you understood the position better. The problem of apparent "unintelligent design" in nature is one that people with ID sympathies have long tackled. Simply look up the literature on "theodicy."

Steve Fuller

To which Gilmour replies:
Dear Prof Fuller,
I am immensely grateful to you for your "stunning" reply to my recent email. In just one line, you inadvertently "destroy" the notion that ID is science:

"The problem of apparent 'unintelligent design' in nature is one that people with ID sympathies have long tackled. Simply look up the literature on 'theodicy.'"

By admitting that "unintelligent design" is a branch of theology, you necessarily admit that "Intelligent" Design is also a branch of theology.

Not quite what I was expecting, but absolutely priceless!

Many thanks again,

Keith Gilmour

The response from the "ID people" that Fuller mentioned is as follows: Those who cite alleged examples of undesirable design are making a theological argument, and since ID is a scientific argument, those theological arguments don't refute ID. Contrary to Gilmour's claims, "By admitting that '[undesirable] design' is a branch of theology," Fuller did NOT "admit that 'Intelligent' Design is also a branch of theology." That's because, if you take the time to read ID responses on this topic, they point out that "undesirable design" arguments do not refute ID arguments precisely because "undesirable design" arguments are theologically based, whereas ID is NOT!
As a science, ID doesn't address theological questions about whether the design is "desirable," "undesirable," "perfect," or "imperfect." Undesirable design is still design. Gilmour just doesn't like it because (in his own subjective view) it's undesirable. Here's a quick illustration of what I mean:

I'm writing this on a PC using Windows; this PC has crashed probably a dozen times in the past two weeks. Right now, I hate my PC. I consider it poorly designed, full of imperfections, and very undesirable. Does that mean it wasn't designed by intelligent agents? No. "Undesirable design" and "intelligent design" are two different things. "Undesirable," "poor," or "imperfect" design do not refute intelligent design.

In speaking of "unintelligent design," Gilmour misuses the term "intelligent," ignoring how ID proponents use it. By the word "intelligent," ID proponents simply mean to indicate that a structure has features requiring a mind capable of forethought to design the blueprint. Thus, ID proponents test ID by looking for complex and specified information, which is an indicator that some goal-directed process, capable of acting with will, forethought, and intentionality, was involved in designing an object.

We do not test ID by looking for "perfect design" or "undesirable design," because minds don't always make things that are "perfect," and sometimes they make things that are "undesirable" (to other minds, at least). Holding biological systems to some vague standard of "perfect design" where they are refuted by "undesirable design" is the wrong way to test ID. Examples like broken machinery, computer failures, and decaying buildings all show that a structure might be designed by an intelligent agent even if it subsequently breaks or shows flaws. Intelligent design does not necessarily mean "perfect design." It doesn't even require optimal design. Rather, "intelligent design" means exactly what it sounds like: design by an intelligent agent.

"Undesirable design" arguments share three general problems, some or all of which can be found in each of Gilmour's 130 examples. Here are the three main problems:
(1) An object can have imperfections and be undesirable, but still be designed.
(2) Critics' standards of perfection are often arbitrary. 
(3) "Bad design" arguments don't hold up under their own terms, as the objects often turn out to be well designed when we inspect them more closely.
Problem (1) applies to every single example Gilmour gives. Problems (2) and (3) apply to many, though not all, of his examples. In fact, some of them are legitimate examples of undesirable design. I mean, who likes "easily worn out knees" or hernias -- both examples of how our bodies break down? Objectively speaking, those are flaws or imperfections. But as much as you might not like "undesirable design," they don't refute ID because ID is a scientific argument that isn't concerned with the moral value, perfection, or desirable/undesirable quality of a structure. Computers break down but were still intelligently designed. In the same way, the fact that our bodies break down doesn't mean they weren't intelligently designed.

Gilmour's website implies designers must always design things so they NEVER break down. But I'm not aware of a single example of human-designed technology that never breaks down. Undesirable qualities, breakdowns, and imperfections are a normal part of intelligently designed objects; they don't refute intelligent design.

I would say to Keith Gilmour and the many others who adopt his approach: Stop playing games and just lay your cards on the table. You are arguing against the idea that an all-perfect, all-knowing, all-powerful God created everything, because you claim that if such a God existed then there would be no flaws in nature. In essence, you are raising the "problem of evil." So you're arguing against a different, much broader thesis than intelligent design. You are making a theological argument, not a scientific one.

For millennia, the Judeo-Christian theistic tradition has offered theological explanations for how a perfect God can exist, even as we observe undesirable and evil things in nature. But these issues are separate from ID. Oxford philosopher Richard Swinburne wrote, "It seems to be generally agreed by atheists as well as theists that what is called 'the logical problem of evil' has been eliminated, and all that remains is 'the evidential problem.'" Obviously, I don't deny that evil can be hard to cope with, which is why I like C.S. Lewis's words when he wrote in The Problem of Pain:

[T]he only purpose of the book is to solve the intellectual problem raised by suffering; for the far higher task of teaching forgiveness and patience I was never fool enough to suppose myself qualified, nor have I anything to offer my readers except my conviction that when pain is to be borne, a little courage helps more than knowledge, a little human sympathy more than much courage, and the least tincture of the love of God more than all.

So I think one can be a traditional theist and a scientific proponent of ID -- I personally fit into this category. But again, these questions are separate questions from the science of ID, as ID doesn't specify the "desirability" or "perfection" of the design. Familiarizing himself with ID arguments would help Keith Gilmour to better understand why Dr. Fuller was right to note that "You might perhaps make more headway with ID people if you understood the position better." I hope Gilmour and other likeminded folks take that piece of good advice and come to understood the ID position a bit better.

Another failed Darwinian prediction XII

Genomic features are not sporadically distributed:

A fundamental concept in evolutionary theory is the inheritance of genetic variations via blood lines. (Forbes) This so-called vertical transmission of heritable material means that genes, and genomes in general, should fall into a common descent pattern, consistent with the evolutionary tree. Indeed, such genes are often cited as a confirmation of evolution. But as more genomic data have become available, an ever increasing number of genes have been discovered that do not fit the common descent pattern because they are missing from so many intermediate species. (Andersson and Roger 2002; Andersson and Roger 2003; Andersson 2005; Andersson, Sarchfield and Roger 2005; Andersson 2006; Andersson et. al. 2006; Andersson 2009; Andersson 2011; Haegeman, Jones and Danchin; Katz; Keeling and Palmer; Richards et. al 2006a; Richards et. al 2006b; Takishita et. al.; Wolf et. al.)

This type of pattern is also found for genome architecture features which are sporadically distributed and then strikingly similar in distant species. In fact these similarities do not merely occur twice, in two distant species. They often occur repeatedly in a variety of otherwise distant species. This is so widespread that evolutionists have named the phenomenon “recurrent evolution.” As one paper explains, the recent explosion of genome data reveals “strikingly similar genomic features in different lineages.” Furthermore, there are “traits whose distribution is ‘scattered’ across the evolutionary tree, indicating repeated independent evolution of similar genomic features in different lineages.” (Maeso, Roy and Irimia)

One example is the uncanny similarity between the kangaroo and human genomes. As one evolutionist explained: “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order. We thought they’d be completely scrambled, but they’re not.” (Taylor)

It is now well recognized that this prediction has failed: “Vertical transmission of heritable material, a cornerstone of the Darwinian theory of evolution, is inadequate to describe the evolution of eukaryotes, particularly microbial eukaryotes.” (Katz) And these sporadic, patchy patterns require complicated and ad hoc scenarios to explain their origin. As one paper explained, the evolution of a particular set of genes “reveals a complex history of horizontal gene transfer events.” (Wolf et. al.) The result is that any pattern can be explained by arranging the right mechanisms. Features that are shared between similar species can be interpreted as “the result of a common evolutionary history,” and features that are not can be interpreted as “the result of common evolutionary forces.” (Maeso, Roy and Irimia)

These common evolutionary forces are complex and must have been created by evolution. They can include horizontal (or lateral) gene transfer, gene loss, gene fusion, and even unknown forces. For instance, one study concluded that the best explanation for the pattern of a particular gene was that it “has been laterally transferred among phylogenetically diverged eukaryotes through an unknown mechanism.” (Takishita et. al.) Even with the great variety of mechanisms available, there still remains the unknown mechanism.

References

Andersson, J., A. Roger. 2002. “Evolutionary analyses of the small subunit of glutamate synthase: gene order conservation, gene fusions, and prokaryote-to-eukaryote lateral gene transfers.” Eukaryotic Cell 1:304-310.

Andersson, J., A. Roger. 2003. “Evolution of glutamate dehydrogenase genes: evidence for lateral gene transfer within and between prokaryotes and eukaryotes.” BMC Evolutionary Biology 3:14.

Andersson, J. 2005. “Lateral gene transfer in eukaryotes.” Cellular and Molecular Life Sciences 62:1182-97.

Andersson, J., S. Sarchfield, A Roger. 2005. “Gene transfers from nanoarchaeota to an ancestor of diplomonads and parabasalids.” Molecular Biology and Evolution 22:85-90.

Andersson, J. 2006. “Convergent evolution: gene sharing by eukaryotic plant pathogens.” Current Biology 16:R804-R806.

Andersson, J., R. Hirt, P. Foster, A. Roger. 2006. “Evolution of four gene families with patchy phylogenetic distributions: influx of genes into protist genomes.” BMC Evolutionary Biology 6:27.

Andersson, J. 2009. “Horizontal gene transfer between microbial eukaryotes.” Methods in Molecular Biology 532:473-487.

Andersson, J. 2011. “Evolution of patchily distributed proteins shared between eukaryotes and prokaryotes: Dictyostelium as a case study.” J Molecular Microbiology and Biotechnology 20:83-95.

Haegeman, A., J. Jones, E. Danchin. 2011. “Horizontal gene transfer in nematodes: a catalyst for plant parasitism?.” Molecular Plant-Microbe Interactions 24:879-87.

Katz, L. 2002. “Lateral gene transfers and the evolution of eukaryotes: theories and data.” International J. Systematic and Evolutionary Microbiology 52:1893-1900.

Keeling, P., J. Palmer. 2008. “Horizontal gene transfer in eukaryotic evolution,” Nature Reviews Genetics 9:605-18.

Maeso, I, S. Roy, M. Irimia. 2012. “Widespread Recurrent Evolution of Genomic Features.” Genome Biology and Evolution 4:486-500.

Richards, T., J. Dacks, J. Jenkinson, C. Thornton, N. Talbot. 2006. “Evolution of filamentous plant pathogens: gene exchange across eukaryotic kingdoms.” Current Biology 16:1857-1864.

Richards, T., J. Dacks, S. Campbell, J. Blanchard, P. Foster, R. McLeod, C. Roberts. 2006. “Evolutionary origins of the eukaryotic shikimate pathway: gene fusions, horizontal gene transfer, and endosymbiotic replacements.” Eukaryotic Cell 5:1517-31.

Takishita, K., Y. Chikaraishi, M. Leger, E. Kim, A. Yabuki, N. Ohkouchi, A. Roger. 2012. “Lateral transfer of tetrahymanol-synthesizing genes has allowed multiple diverse eukaryote lineages to independently adapt to environments without oxygen.” Biology Direct 7:5.

Taylor, R. 2008. “Kangaroo genes close to humans,” Reuters, Canberra, Nov 18.

Wolf, Y., L. Aravind, N. Grishin, E. Koonin. 1999. “Evolution of aminoacyl-tRNA synthetases--analysis of unique domain architectures and phylogenetic trees reveals a complex history of horizontal gene transfer events.” Genome Research 9:689-710.

Another failed Darwinian prediction XI

             MicroRNA:


Genes hold information that is used to construct protein and RNA molecules which do various tasks in the cell. A gene is copied in a process known as transcription. In the case of a protein-coding gene the transcript is edited and converted into a protein in a process known as translation. All of this is guided by elaborate regulatory processes that occur before, during and after this sequence of transcription, editing and translation.

For instance, some of our DNA which was thought to be of little use actually has a key regulatory role. This DNA is transcribed into strands of about 20 nucleotides, known as microRNA. These short snippets bind and interfere with RNA transcripts—copies of DNA genes—when the production of the gene needs to be slowed.

MicroRNAs can also help to modify the translation process by stimulating programmed ribosomal frameshifting. Two microRNAs attach to the RNA transcript resulting in a pseudoknot, or triplex, RNA structure form which causes the reading frameshift to occur. (Belew)

MicroRNAs do not only come from a cell’s DNA. MicroRNAs can also be imported from nearby cells, thus allowing cells to communicate and influence each other. This helps to explain how cells can differentiate in a growing embryo according to their position within the embryo. (Carlsbecker)

MicroRNAs can also come from the food we eat. In other words, food not only contains carbohydrates, proteins, fat, minerals, vitamins and so forth, it also contains information—in the form of these regulatory snippets of microRNA—which regulate our gene production. (Zhang)

While microRNAs regulate the production of proteins, the microRNAs themselves also need to be regulated. So there is a network of proteins that tightly control microRNA production as well as their removal. “Just the sheer existence of these exotic regulators,” explained one scientist, “suggests that our understanding about the most basic things—such as how a cell turns on and off—is incredibly naïve.” (Hayden)

Two basic predictions that evolutionary theory makes regarding microRNAs are that (i) like all of biology, they arose gradually via randomly occurring biological variation (such as mutations) and (ii) as a consequence of this evolutionary origin, microRNAs should approximately form evolution’s common descent pattern. Today’s science has falsified both of these predictions.

MicroRNAs are unlikely to have gradually evolved via random mutations, for too many mutations are required. Without the prior existence of genes and the protein synthesis process microRNAs would be useless. And without the prior existence of their regulatory processes, microRNAs would wreak havoc.

Given the failure of the first prediction, it is not surprising that the second prediction has also failed. The microRNA genetic sequences do not fall into the expected common descent pattern. That is, when compared across different species, microRNAs do not align with the evolutionary tree. As one scientist explained, “I've looked at thousands of microRNA genes and I can't find a single example that would support the traditional [evolutionary] tree.” (Dolgin)

While there remain questions about these new phylogenetic data, “What we know at this stage,” explained another evolutionist, “is that we do have a very serious incongruence.” In other words, different types of data report very different evolutionary trees. The conflict is much greater than normal statistical variations.

“There have to be,” added another evolutionist, “other explanations.” One explanation is that microRNAs evolve in some unexpected way. Another is that the traditional evolutionary tree is all wrong. Or evolutionists may consider other explanations. But in any case, microRNAs are yet another example of evidence that does not fit evolutionary expectations. Once again, the theory will need to be modified in complex ways to fit the new findings.

In the meantime, scientists are finding that imposing the common descent pattern, where microRNAs must be conserved across species, is hampering scientific research:

These results highlight the limitations that can result from imposing the requirement that miRNAs be conserved across organisms. Such requirements will in turn result in our missing bona fide organism-specific miRNAs and could perhaps explain why many of these novel miRNAs have not been previously identified. (Londin)

Evolutionary theory has been limiting the science. While the common descent pattern has been the guide since the initial microRNA studies, these researchers “liberated” themselves from that constraint, and this is leading to good scientific progress:

In the early days of the miRNA field, there was an emphasis on identifying miRNAs that are conserved across organisms … Nonetheless, species-specific miRNAs have also been described and characterized as have been miRNAs that are present only in one or a few species of the same genus. Therefore, enforcing an organism-conservation requirement during miRNA searches is bound to limit the number of potential miRNAs that can be discovered, leaving organism- and lineage-specific miRNAs undiscovered. In our effort to further characterize the human miRNA repertoire, we liberated ourselves from the conservation requirement … These findings strongly suggest the possibility of a wide-ranging species-specific miRNA-ome that has yet to be characterized. (Londin)

The two microRNA predictions have been falsified and, not surprisingly, the evolutionary assumption has hampered the scientific research of how microRNAs work.

References

Belew, Ashton T., et. al. 2014. “Ribosomal frameshifting in the CCR5 mRNA is regulated by miRNAs and the NMD pathway.” Nature 512:265-9.

Carlsbecker, Annelie, et. al. 2010. “Cell signalling by microRNA165/6 directs gene dose-dependent root cell fate.” Nature 465:316-21.

Dolgin, Elie. 2012. “Phylogeny: Rewriting evolution.” Nature 486:460-2.

Hayden, Erika Check. 2010. “Human genome at ten: Life is complicated.” Nature 464:664-7.

Londin, Eric, et. al. 2015. “Analysis of 13 cell types reveals evidence for the expression of numerous novel primate- and tissue-specific microRNAs.” Proc Natl Acad Sci USA 112:E1106-15.

Zhang, L., et. al. 2012. “Exogenous plant MIR168a specifically targets mammalian LDLRAP1: evidence of cross-kingdom regulation by microRNA.” Cell Research 22:107-26.

The brand of the beast.

If Patients Were Pets
Wesley J. Smith February 29, 2016 2:44 PM

A Canadian government panel -- charged with recommending terms for the Supreme Court-imposed right to euthanasia -- wants MDs (and nurses) to have lower conscience rights than veterinarians. What do I mean? If someone presents a pet to be euthanized, the veterinarian can say no if she thinks the condition of the animal does not warrant that extreme action.

But if the panel gets its way, not so with doctors. It wants all MDs required by law to either kill the legally qualified patient or -- if they have a religious or other predicated conscience objection to committing homicide -- to provide an "effective referral" to a colleague to perform the lethal injection.

"Effective referral" will likely mean procuring a death doctor they know will be willing to do the deed, which is the law in Victoria, Australia, around abortion. From the report:

RECOMMENDATION 10 That the Government of Canada work with the provinces and territories and their medical regulatory bodies to establish a process that respects a health care practitioner's freedom of conscience while at the same time respecting the needs of a patient who seeks medical assistance in dying. At a minimum, the objecting practitioner must provide an effective referral for the patient.

Some objecting doctors might try to get around the effective referral requirement by claiming they didn't find the patient legally qualified medically. But conscientiously, religiously, or morally objecting nurses would have no such wiggle room.

The panel wants nurses to be allowed to kill. But since they wouldn't be the ones determining whether a patient was qualified legally for euthanasia, nurses would face the stark choice of administering the lethal injection when directed by a doctor, or being insubordinate and losing their livelihood. The same would no doubt apply to pharmacists who would concoct the death brew.

Not only that, but religious medical institutions will be required to permit euthanasia in their facilities if the panel has its way. This includes Catholic nursing homes if they receive government funding, which, I am told, is how Canada's system works. Again, from the report:

RECOMMENDATION 11 That the Government of Canada work with the provinces and territories to ensure that all publicly funded health care institutions provide medical assistance in dying.

Here's the bottom line: If the panel's recommendations are enacted, to practice medicine, nursing, pharmacy, or run a nursing home or hospice in Canada will require participation or complicity in the killing of sick, disabled, and mentally ill patients.


There's a word for that. Hint: It is the antithesis of liberty.

The case for design is as plain as nose on your face.

The Physics and Biology of Olfaction
Evolution News & Views March 1, 2016 3:26 AM 

If you've seen Living Waters, you were undoubtedly amazed at the complexity of operations going on inside a salmon's nose. Yet that animation vastly oversimplifies the olfactory sense. New findings continue to bring scientists closer to understanding how it works, adding to what we previously reported in September.

Last time we focused on the olfactory epithelium, the tissue that receives the odor molecules. We saw how it is organized into a hierarchical pattern that provides the best possible reception for different kinds of odorants. Each nostril's epithelium contains half a million olfactory sensory neurons (OSNs), long cells with cilia at one end and an axon at the other end. The cilia are where the odor molecules make contact with olfactory receptors (ORs). When a molecule "fits" just right, the receptor responds, triggering a cascade of activity. But what makes a good fit?

Vibrating Locks and Keys

There's been a lively debate about that. The leading view was that the molecule's shape fits the shape of the receptor like a "lock and key." In the 1990s, however, Luca Turin and others proposed a "vibrational" theory to account for shortcomings in the shape model. Why, for instance, do different shapes produce similar smell sensations in some cases, and similar shapes produce different sensations in others? Because the debate between the "shapists" and "vibrationists" has remained unsettled, the animators at Illustra alluded to both possibilities, showing the molecule fitting like a glove but also vibrating. (It's possible, too, that both theories are partly right.)

The vibration theory was thought to be down for the count last year when a team failed to find evidence for it in an experiment with mouse olfactory receptors in a petri dish. The receptors didn't react differently to two molecules with the same shape but different vibration frequencies. Now, though, the vibration theorists are back with a vengeance. John Hewitt tells about this at PhysOrg. A team from Italy, publishing in Scientific Reports, found evidence for discrimination between molecules with identical shapes but different vibrations. Four pairs of odorant molecules were carefully designed to be identical except that some hydrogen atoms were replaced with deuterium (heavy hydrogen, containing an extra neutron). The slight mass difference in these "isotopomers" ("same topology") alters the vibration frequency of the molecule. These same-shaped odorants were wafted into the noses of honeybees while the scientists monitored their brains in real time.

Sure enough, the bees appeared able to discriminate them, showing very different responses to the same-shaped pairs. "Considering the close structural correspondence between isotopomers," Hewitt writes, "the experimental truths observed here would be difficult for even the most ardent adherent to the shapist receptor philosophy to sweep under the rug." The implications are interesting for design theorists. Hewitt continues:

The authors observe that the shape-independent discrimination capabilities they found can not be dismissed as idiosyncratic to a few peculiar olfactory receptors, rather, they are a more general feature of ligand-receptor interaction. Much of the palpable in-house derision that members of the larger olfactory and neuroscience communities routine reserve for the vibrational theory might be traced to a deeper, more insidious fear: despite exhaustively focused efforts, they have no idea how receptors actually work. [Emphasis added.]

Hewitt sees a possible overarching principle at work in biological sensing. How did living things apply themselves to the task of "quickly (in evolutionary time) coming up with and artfully deploying 'universal detectors'" that are applied for diverse inputs, in everything from olfaction to vision to touch? Even the suntan response to UV light deploys this strategy. "Nature has unleashed her unbridled imagination," he quips -- and artfully so.

Score one for the vibrationists. The debate will continue, undoubtedly, but more to our interest, it illustrates the complexity of the olfactory sense and its extreme precision that has baffled scientists for decades. Imagine a honeybee, fruit fly, or salmon being able to discriminate twin molecules that differ only by one or two atomic mass units. Design doesn't get better than that.

Dynamic Switchboard

Meanwhile, a recent paper in Nature Communications takes us down the other end of the olfactory neuron to the tip of the axon. As shown in the Illustra animation, the nerve endings of a million OSNs converge on a remarkable organ, the olfactory bulb (OB), which is studded with connection points called glomeruli. In an amazing example of preprogrammed networking, these axons "know" during development somehow which glomerulus to attach to, depending on the type of odorant receptor they express (and there are hundreds of those). Axons for one receptor might grow toward a glomerulus on top of the bulb; axons for another to the backside. Between top-bottom, front-back, and left-right, the OB has three axes by which to discriminate connections coming from different classes of receptors. This is the first stage of sorting and classifying odorant types. (Note: it gets even more complicated from there.)

These scientists from the NIH and Carnegie Mellon University wanted to find out how malleable the olfactory inputs are. Once set up, is the olfactory tissue set for life? Can the olfactory bulb be rewired as conditions change or the fish grows older? When a new neuron replaces an old one, does it wire up the same way? The short answer is that rewiring is not only possible, but it occurs throughout adult life. Why might that be?

Incorporation of new neurons enables plasticity and repair of circuits in the adult brain. Adult neurogenesis is a key feature of the mammalian olfactory system, with new olfactory sensory neurons (OSNs) wiring into highly organized olfactory bulb (OB) circuits throughout life. However, neither when new postnatally generated OSNs first form synapses nor whether OSNs retain the capacity for synaptogenesis once mature, is known. Therefore, how integration of adult-born OSNs may contribute to lifelong OB plasticity is unclear. Here, we use a combination of electron microscopy, optogenetic activation and in vivo time-lapse imaging to show that newly generated OSNs form highly dynamic synapses and are capable of eliciting robust stimulus-locked firing of neurons in the mouse OB. Furthermore, we demonstrate that mature OSN axons undergo continuous activity-dependent synaptic remodelling that persists into adulthood. OSN synaptogenesis, therefore, provides a sustained potential for OB plasticity and repair that is much faster than OSN replacement alone.

Notice that reference to the "highly organized olfactory bulb circuits." Unlike Hewitt, who verged off into evolutionary speculations in his article after describing those "artfully deployed" sensors, these scientists didn't go the storytelling route. Their approach was to observe a phenomenon and find a purpose for it.

So what is the purpose of rapid structural remodelling of OSN synapses? Synapse turnover clearly plays an essential role during circuit formation (and in the case of the OB, incorporation of newborn neurons into existing circuits) by enabling selection, refinement and error correction. Hence, transient pre- or post-synaptic structures may represent those that fail to locate a synaptic partner, or form inappropriate connections that are rapidly eliminated. This may explain why immature OSN presynaptic terminals are formed and eliminated more rapidly than their mature counterparts (Figs 4, 5). Alternatively, these transient synaptic structures may represent short-lived synaptic contacts that temporarily contribute to network function, or play other roles such as promoting axon branch stabilization. Whatever the role of transient synaptic structures, ongoing synapse formation and elimination endows OB circuits with a plasticity potential that can be harnessed when needed, such as during learning or in response to altered experience.

That's the spirit. There must be a role, a purpose, a potential. At first, it would appear startling that so much rewiring takes place. What chip manufacturer would alter integrated circuits while they are in use? Maybe manufacturers could learn something from the way life does things.

Clearly a salmon is undergoing a lot of "learning" and "altered experience" as it grows from fingerling to adult, swimming downstream through a welter of new sensory experiences, memorizing hundreds of new odors and mapping them into its memory. It's possible that the brain and the olfactory bulb are triggering some of that rewiring in elaborate feedback loops, strengthening the connections to weak signals or reducing the connections to overpowering signals. It brings to mind a skilled technician on a sound board turning knobs and moving sliders to get the ideal overall experience in auditory space. In olfactory space, though, the salmon's sliders are automated. "Whatever the role" of these transient connections, we can infer from the results -- such as that a salmon can detect odorants at parts per trillion -- that they contribute to the spectacular performance of the olfactory system.

We've discussed "plasticity" before as a challenge to Darwinism. Why would a blind evolutionary process create "plasticity potential" that can be "harnessed when needed" in case of an altered experience? Darwinian evolution has no foresight. Plasticity makes perfect sense, though, from a design-based perspective on biology. There's no better example than right there in a salmon's nose, where the olfactory system will be encountering numerous new environments over a period of years. The scientists' expectations of roles for synaptic plasticity were confirmed in their conclusions (readers can find the details in the open-access paper).

One more thing. The scientists found that rewiring is "much faster" than replacement. While OSNs are replaced throughout life, the rewiring "plasticity potential" provides a more rapid response, giving the animal both high-speed (transient) and low-speed (permanent) fine tuning of its olfactory system. Since this is true of mice, it's undoubtedly true for us as well.


Now go out and smell the roses.

Homology vs. Darwin

The Types: Why Shared Characteristics Are Bad News for Darwinism
Michael Denton February 29, 2016 3:28 AM 

Editor's note: In his new book Evolution: Still a Theory in Crisis, Michael Denton not only updates the argument from his groundbreaking Evolution: A Theory in Crisis (1985) but also presents a powerful new critique of Darwinian evolution. This article is one in a series in which Dr. Denton summarizes some of the most important points of the new book. For the full story, get your copy of Evolution: Still a Theory in Crisis. For a limited time, you'll enjoy a 30 percent discount at  CreateSpace by using the discount code QBDHMYJH.

One of the major achievements of pre-Darwinian biology was the discovery that the living world is organized into a hierarchy of ever more inclusive classes or Types, each clearly defined by a unique homolog or suite of homologs possessed by all the members of the Type and which in many cases have remained invariant in divergent phylogenetic lines for tens or hundreds of millions of years.

Seeking an explanation for the distinctness of the Types and determining their ontological status was seen to be one of the major tasks of 19th-century biology. Virtually all pre-Darwinian biologists, and many after Darwin, saw the Types as immanent and invariant parts of the world-order, no less than crystals or atoms.

There is currently a widespread impression that pre-Darwinian biologists derived their discontinuous-typological conception of nature from all sorts of discredited metaphysical beliefs. This view has been severely criticized by recent researchers and shown to be largely a myth created by twentieth-century advocates of the neo-Darwinian evolutionary synthesis1 -- what Ron Amundson calls "Synthesis Historiography."2 As Amundson shows, whatever their metaphysical leaning, pre-Darwinian biologists did not derive their view of the Types as changeless components of the world order from any a priori metaphysics but from solid empirical observations.

The 19th-century structuralist conception of the Type, and of an ascending hierarchy of taxa or Types of ever-widening comprehensiveness as immanent features of nature, was close to the classic Aristotelian worldview. But it was based on the facts of biology, not on a philosophical a priori assumption -- Aristotelian, Platonic, or otherwise.

Today, 150 years after Darwin, Owen's "biological atoms" are as distinct as ever. The vast majority of all organisms can be assigned to unique classes based on their possession of particular defining homologs or novelties that are not led up to via Darwin's "innumerable transitional forms."

For readers subjected to popular and pervasive claims by evolutionary biologists that there are innumerable transitional forms of organisms, it might come as something of a surprise that there are unique taxon-defining novelties not led up to gradually from some antecedent form, and that remain invariant after their actualization for vast periods of time.

There is indeed something incongruous about the very notion of distinct taxa and genuine immutable "taxon-defining novelties" in the context of the functionalist Darwinian framework, which implies that all taxa-defining traits should be led up to via long series of adaptive transitional forms! On such a Darwinian model, taxa-defining novelties should not exist; neither should distinct Types in which all members possess unique defining novelties not shared by the members of any other taxa.

Let me reiterate: If evolution has occurred as conceived of by Darwin, invariant taxa-defining novelties, not led up to via long sequences of transitional forms from some antecedent structure, should not exist.

Ironically, it is only because organisms can be classified into distinct groups on the basis of their possession of invariant unique homologs that descent with modification can be inferred in the first place. If it was not for the invariance of the homologs and the Types they define, the common descent of all the members of a particular clade from a common ancestor would be in serious doubt. The living realm would conform to a chaotic network rather than an orderly branching tree.

Types are still as distinct today as they were for Richard Owen, Agassiz, and the other typologists and structuralists in the pre-Darwinian era and even for Darwin himself.3 They are still clearly defined by homologs or synapomorphies that are true evolutionary novelties without antecedent in earlier putative ancestral forms.

References:

(1) Mary Winsor, "The Creation of the Essentialism Story: An Exercise in Metahistory," History and Philosophy of the Life Sciences 28 (2006): 149-174.

(2) Amundson, The Changing Role of the Embryo in Evolutionary Thought, 11.


(3) Charles Darwin, Origin of Species, 6th ed. (London: John Murray 1872), 264 (Chapter 10): "The distinctness of specific forms, and their not being blended together by innumerable transitional links, is a very obvious difficulty."

Another failed Darwinian prediction X

Similar species share similar genes:

The only figure in Darwin’s book, The Origin of Species, showed how he envisioned species branching off of one another. Similar species have a relatively recent common ancestor and have had limited time to diverge from each other. This means that their genes should be similar. Entirely new genes, for instance, would not have enough time to evolve. As François Jacob explained in an influential paper from 1977, “The probability that a functional protein would appear de novo by random association of amino acids is practically zero.” (Jacob) Any newly created gene would have to arise from a duplication and modification of a pre-existing gene. (Zhou et. al.; Ohno) But such a new gene would retain significant similarity to its progenitor gene. Indeed, for decades evolutionists have cited minor genetic differences between similar species as a confirmation of this important prediction. (Berra, 20; Futuyma, 50; Johnson and Raven, 287; Jukes, 120; Mayr, 35)

But this prediction has been falsified as many unexpected genetic differences have been discovered amongst a wide range of allied species. (Pilcher) As much as a third of the genes in a given species may be unique, and even different variants within the same species have large numbers of genes unique to each variant. Different variants of the Escherichia coli bacteria, for instance, each have hundreds of unique genes. (Daubin and Ochman)

Significant genetic differences were also found between different fruit fly species. Thousands of genes showed up missing in many of the species, and some genes showed up in only a single species. (Levine et. al.) As one science writer put it, “an astonishing 12 per cent of recently evolved genes in fruit flies appear to have evolved from scratch.” (Le Page) These novel genes must have evolved over a few million years, a time period previously considered to allow only for minor genetic changes. (Begun et. al.; Chen et. al., 2007)

Initially some evolutionists thought these surprising results would be resolved when more genomes were analyzed. They predicted that similar copies of these genes would be found in other species. But instead each new genome has revealed yet more novel genes. (Curtis et. al.; Marsden et. al.; Pilcher)

Next evolutionists thought that these rapidly-evolving unique genes must not code for functional or important proteins. But again, many of the unique proteins were in fact found to play essential roles. (Chen, Zhang and Long 1010; Daubin and Ochman; Pilcher) As one researcher explained, “This goes against the textbooks, which say the genes encoding essential functions were created in ancient times.” (Pilcher)

References

Begun, D., H. Lindfors, A. Kern, C. Jones. 2007. “Evidence for de novo evolution of testis-expressed genes in the Drosophila yakuba/Drosophila erecta clade.” Genetics 176:1131-1137.

Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.

Chen, S., H. Cheng, D. Barbash, H. Yang. 2007. “Evolution of hydra, a recently evolved testis-expressed gene with nine alternative first exons in Drosophila melanogaster.” PLoS Genetics 3.

Chen, S., Y. Zhang, M. Long. 2010. “New Genes in Drosophila Quickly Become Essential.” Science 330:1682-1685.

Curtis, B., et. al. 2012. “Algal genomes reveal evolutionary mosaicism and the fate of nucleomorphs.” Nature 492:59-65.

Daubin, V., H. Ochman. 2004. “Bacterial genomes as new gene homes: The genealogy of ORFans in E. coli.” Genome Research 14:1036-1042.

Futuyma, Douglas. 1982. Science on Trial: The Case for Evolution. New York: Pantheon Books.

Jacob, François. 1977. “Evolution and tinkering.” Science 196:1161-1166.

Johnson, G., P. Raven. 2004. Biology. New York: Holt, Rinehart and Winston.

Jukes, Thomas. 1983. “Molecular evidence for evolution” in: Scientists Confront Creationism, ed. Laurie Godfrey. New York: W. W. Norton.

Le Page, M. 2008. “Recipes for life: How genes evolve.” New Scientist, November 24.

Levine, M., C. Jones, A. Kern, H. Lindfors, D. Begun. 2006. “Novel genes derived from noncoding DNA in Drosophila melanogaster are frequently X-linked and exhibit testis-biased expression.” Proceedings of the National Academy of Sciences 103: 9935-9939.

Marsden, R. et. al. 2006. “Comprehensive genome analysis of 203 genomes provides structural genomics with new insights into protein family space.” Nucleic Acids Research 34:1066-1080.

Mayr, Ernst. 2001. What Evolution Is. New York: Basic Books.

Ohno, Susumu. 1970. Evolution by Gene Duplication. Heidelberg: Springer.

Pilcher, Helen. 2013. “All Alone.” NewScientist January 19.

Zhou, Q., G. Zhang, Y. Zhang, et. al. 2008. “On the origin of new genes in Drosophila.” Genome Research 18:1446-1455.

The first protein vs. Darwin

Yockey and a Calculator Versus Evolutionists

Zero Probability is Not a Problem

In a 1977 paper published in the Journal of Theoretical Biology, Hubert Yockey used information theory to evaluate the likelihood of the evolution of a relatively simple protein. Yockey’s model system was cytochrome c, a protein consisting of about one hundred amino acids. Cytochrome c plays an important role in the mitochondria’s electron transport chain (ETC) which helps to convert the chemical energy in carbon-carbon and carbon-hydrogen bonds, in the food we eat, to an electrochemical potential energy in the form of hydrogen ions (or protons) stored within the mitochondria’s inner membrane. Like water pressing against a dam and turning its turbines to generate electricity, the high-concentration hydrogen ions drive the ATP synthase “turbine” to create the high-energy ATP molecule. Like the electrical outlets in your house, the ATP molecule provides a standardized form of energy that is used for a wide range of applications in your body, such as muscle contraction and nerve signals. There is no scientific explanation for how the ETC evolved. There also is no scientific explanation for how a single protein, such as cytochrome c, evolved. Yockey explained this in 1977, and since then the problem has only gotten worse.

Given 20 different amino acids to choose from, then for a protein with a sequence of 101 amino acids, such as cytochrome c, there are 20 raised to the power of 101, or 20^101, different possible amino acid sequences. That represents an astronomically (and impossible) number of sequences for evolution to search through to find a functional cytochrome c protein.

The problem is more complicated than this, however, since the different amino acids are not equally likely and there are many different sequences that will form a functional cytochrome c protein.

Yockey accounts for these factors to determine the effective number of sequences evolution would have to search through to find cytochrome c. For instance, Yockey uses the known cytochrome c proteins at the time, from many different species, to get an idea of the different amino acids that are possible at each position, within the sequence of 101 residues. Some residues allow for quite a few different amino acids while others seem to be more stringent.

This approach is reasonable, but by no means the only way of estimating the number of different amino acid sequences that could work. One way or another, the bottom line is this: while the number of different sequences that could form a successful type of protein, such as cytochrome c, is a pretty big number, it doesn’t solve the problem.

Yockey found that the probability of evolution finding the cytochrome c protein sequence is about one in 10^64. That is a one followed by 64 zeros—an astronomically large number. He concluded in the peer-reviewed paper that the belief that proteins appeared spontaneously “is based on faith.”

Indeed, Yockey’s early findings are in line with, though a bit more conservative than, later findings. A 1990 study of a small, simple protein found that 10^63 attempts would be required for evolution to find the protein.

A 2004 study found that 10^64 to 10^77 attempts are required, and a 2006 study concluded that 10^70 attempts would be required.

These requirements dwarf the resources evolution has at its disposal. Even evolutionists have had to admit that evolution could only have a maximum of 10^43 such experiments. It is important to understand how tiny this number is compared to 10^70. 10^43 is not more than half of 10^70. It is not even close to half. 10^43 is an astronomically tiny sliver of 10^70.

Furthermore, the estimate of 10^43 is, itself, entirely unrealistic. For instance, it assumes the entire history of the Earth is available, rather than the limited time window that evolution actually would have had. And it assumes the pre existence of bacteria and, yes, proteins. In fact, the evolutionists assumed the earth was covered with bacteria, and each bacteria was full of proteins. That of course is not an appropriate assumption for the question of how proteins could have evolved in the first place. In fact, it is circular.

Of course the evolution of a single protein is only one of many problems for evolution. Consider, for example, the cellular apparatus that constructs proteins—the protein synthesis machinery. One paper used a back-of-the-envelope, simple and conservative calculation to show that the probability of such an apparatus evolving by chance is one in 10^1018. That’s a one followed by 1,018 zeros. Normally in science this would be considered far beyond impossible, so therefore evolutionists are considering an infinite universe, or multiverse, to solve the problem. In such a universe, it does not matter how improbable any event is, it will eventually occur:

Origin of life is a chicken and egg problem: for biological evolution that is governed, primarily, by natural selection, to take off, efficient systems for replication and translation are required, but even barebones cores of these systems appear to be products of extensive selection. The currently favored (partial) solution is an RNA world without proteins in which replication is catalyzed by ribozymes and which serves as the cradle for the translation system. However, the RNA world faces its own hard problems as ribozyme-catalyzed RNA replication remains a hypothesis and the selective pressures behind the origin of translation remain mysterious. Eternal inflation offers a viable alternative that is untenable in a finite universe … In an infinite universe (multiverse), emergence of highly complex systems by chance is inevitable. Therefore, under this cosmology, an entity as complex as a coupled translation-replication system should be considered a viable breakthrough stage for the onset of biological evolution.

There you have it. Probabilities don’t matter. You can point out how unlikely evolution is, and evolution remains a fact. Science is done by people, and people seek certain answers, regardless of the data.

Religion drives science, and it matters.

Posted by Cornelius Hunter 

Gilded smoke

Recession proof.

The invincible enemy?:A prequel

Extreme poverty the invincible enemy?

A clash of Titans X

Another failed Darwinian prediction IX

Biology is not lineage specific:

Evolution expects the species to fall into a common descent pattern. Therefore a particular lineage should not have highly differentiated, unique and complex designs, when compared to neighboring species. But this has been increasingly found to be the case, so much so that this pattern now has its own name—lineage-specific biology.

For example, transcription factors are proteins that bind to DNA and regulate which genes are expressed. Yet despite the importance of these proteins, their DNA binding sites vary dramatically across different species. As one report explained, “It was widely assumed that, like the sequences of the genes themselves, these transcription factor binding sites would be highly conserved throughout evolution. However, this turns out not to be the case in mammals.” (Rewiring of gene regulation across 300 million years of evolution) Evolutionists were surprised when transcription factor binding sites were found to be not conserved between mice and men, (Kunarso et. al.) between various other vertebrates, and even between different species of yeast. So now evolution is believed to have performed a massive, lineage-specific “rewiring” of cellular regulatory networks. (Pennacchio and Visel)

There are many more such examples of lineage-specific biology. Although flowers have four basic parts: sepals, petals, stamens and carpels, the daffodil’s trumpet is fundamentally different and must be an evolutionary “novelty.” (Oxford scientists say trumpets in daffodils are ‘new organ’) Out of the thousands of cockroach species, Saltoblattella montistabularis from South Africa is the only one that leaps. With its spring-loaded hind legs it accelerates at 23 g’s and out jumps even grass hoppers. (Picker, Colville and Burrows) An important immune system component, which is highly conserved across the vertebrates, is mysteriously absent in the Atlantic cod, Gadus morhua. (Star, et. al.) The brown algae, Ectocarpus siliculosus, has unique enzymes for biosynthesis and other tasks. (Cock) And the algae Bigelowiella natans has ten thousand unique genes and highly complex gene splicing machinery never before seen in a unicellular organism. It is, as one evolutionist explained, “unprecedented and truly remarkable for a unicellular organism.” (Tiny algae shed light on photosynthesis as a dynamic property)

Another fascinating example of lineage-specific biology are the many peculiar morphological and molecular novelties found in disparate, unrelated unicellular protists. As one study concluded, “Both euglenozoans and alveolates have a reputation for ‘doing things their own way,’ which is to say that they have developed seemingly unique ways to build important cellular structures or carry out molecular tasks critical for their survival. Why such hotspots for the evolution of novel solutions to problems should exist in the tree of life is not entirely clear.” (Lukes, Leander and Keeling, 2009a) Or as one evolutionist exclaimed, “this is totally crazy.” (Lukes, Leander and Keeling, 2009b)

References

Cock, J., et al. 2010. “The Ectocarpus genome and the independent evolution of multicellularity in brown algae.” Nature 465:617-621.

Kunarso G., et. al. 2010. “Transposable elements have rewired the core regulatory network of human embryonic stem cells.” Nature Genetics 42:631-634.

Lukes, J., B. Leander, P. Keeling. 2009. “Cascades of convergent evolution: the corresponding evolutionary histories of euglenozoans and dinoflagellates.” Proceedings of the National Academy of Sciences 106 Suppl 1:9963-9970.

Lukes, J., B. Leander, P. Keeling. 2009. “The corresponding evolutionary histories of euglenozoans and dinoflagellates: cascades of convergent evolution or accumulation of oddities?.” The National Academies. http://sackler.nasmediaonline.org/2009/darwin/julius_lukes/julius_lukes.html

“Oxford scientists say trumpets in daffodils are ‘new organ’.” 2011. BBC News February 28. http://www.bbc.co.uk/news/uk-england-oxfordshire-12598054

Pennacchio, L., A. Visel. 2010. “Limits of sequence and functional conservation.” Nature Genetics 42:557-558.

Picker, M., J. Colville, M. Burrows. 2012. “A cockroach that jumps.” Biology Letters 8:390-392.

“Rewiring of gene regulation across 300 million years of evolution.” 2010. ScienceDaily April 12. http://www.sciencedaily.com/releases/2010/04/100409093211.htm

Star, B., et. al. 2011. “The genome sequence of Atlantic cod reveals a unique immune system.” Nature 477:207–210.

“Tiny algae shed light on photosynthesis as a dynamic property.” 2012. ScienceDaily November 28. http://www.sciencedaily.com­ /releases/2012/11/121128132253.htm

Another failed Darwinian prediction VIII

Serological tests reveal evolutionary relationships:

Early in the twentieth century scientists studied blood immunity and how immune reaction could be used to compare species. The blood studies tended to produce results that parallel the more obvious indicators such as body plan. For example, humans were found to be more closely related to apes than to fish or rabbits. These findings were said to be strong confirmations of evolution. In 1923 H. H. Lane cited this evidence as supporting “the fact of evolution.” (Lane, 47) Later in the century these findings continued to be cited in support of evolution. (Berra, 19; Dodson and Dodson, 65)

But even by mid century contradictions to evolutionary expectations were becoming obvious in serological tests. As J.B.S.Haldane explained in 1949, “Now every species of mammal and bird so far investigated has shown quite a surprising biochemical diversity by serological tests. The antigens concerned seem to be proteins to which polysaccharides are attached.” (quoted in Gagneux and Varki)

Indeed these polysaccharides, or glycans, did not fulfill evolutionary expectations. As one paper explained, glycans show “remarkably discontinuous distribution across evolutionary lineages,” for they “occur in a discontinuous and puzzling distribution across evolutionary lineages.” (Bishop and Gagneux) These glycans can be (i) specific to a particular lineage, (i) similar in very distant lineages, (iii) and conspicuously absent from very restricted taxa only.

Here is how another paper described glycan findings: “There is also no clear explanation for the extreme complexity and diversity of glycans that can be found on a given glycoconjugate or cell type. Based on the limited information available about the scope and distribution of this diversity among taxonomic groups, it is difficult to see clear trends or patterns consistent with different evolutionary lineages.” (Gagneux and Varki)

References

Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.

Bishop J., P. Gagneux. 2007. “Evolution of carbohydrate antigens--microbial forces shaping host glycomes?.” Glycobiology 17:23R-34R.

Dodson, Edward, Peter Dodson. 1976. Evolution: Process and Product. New York: D. Van Nostrand Company.

Gagneux, P., A. Varki. 1999. “Evolutionary considerations in relating oligosaccharide diversity to biological function.” Glycobiology 9:747-755.

Lane, H. 1923. Evolution and Christian Faith. Princeton: Princeton University Press.

On the limits of intelligent design theory

Good Questions on the Nature of Intelligent Design
Ann Gauger February 25, 2016 6:01 AM

Earlier, Evolution News responded helpfully to a question from an email correspondent. Here are more questions and answers. A reader writes with a few good queries on the nature of ID theory.

Question:

On the complexity and specificity arguments, I've read that there are two arguments used as evidence for a designer's existence. However, do such arguments entail that the designer is still intervening in the ongoing development of the universe and of life within it? Or does ID only state that there was a designer at least at the very beginning, and ID as a theory does not categorically state (or necessarily entail) that this designer is still interested in making changes? Thus, are the complexity and specificity arguments examples rather than actual requirements?

Answer: ID is about design detection, and makes no statements about ongoing design or a design mechanism. We simply say that there are elements in the universe that give evidence of being designed. Anything further goes beyond what we can say. For example, we can say nothing about how (by what mechanism) design is instantiated. As for specified complexity and irreducible complexity, they are methods of design detection. I see irreducible complexity as a special case of specified complexity. There are probably other valid arguments for design, such as the fact that the universe is intelligible to us when there is no logical requirement that it be so.

Question:

Does ID associate any particular attributes with this "designer"? I am aware that various prominent ID proponents have said, on different occasions, yes and no -- and I do see a difference between a) ID theory itself, and b) personal opinion on aspects of the theory. The first is a necessary contingent on the theory itself. The second is not. My analogy for this is -- Christians believe certain things. Catholics accept the main Christian belief, plus a few other things.

Answer: ID posits nothing about the attributes of this designer, other than the fact that the designer must be capable of carrying out design at the appropriate scale. Anything more is personal opinion. As one leading ID scientist has written:

I myself do believe in a benevolent God, and I recognize that philosophy and theology may be able to extend the argument. But a scientific argument for design in biology does not reach that far. Thus while I argue for design, the question of the identity of the designer is left open. Possible candidates for the role of designer include: the God of Christianity; an angel -- fallen or not; Plato's demiurge; some mystical New Age force; space aliens from Alpha Centauri; time travelers; or some utterly unknown intelligent being. Of course, some of these possibilities may seem more plausible than others based on information from fields other than science. Nonetheless, as regards the identity of the designer, modern ID theory happily echoes Isaac Newton's phrase "Hypothesis non fingo"(I make no hypothesis).

(Michael Behe, "The Modern Intelligent Design Hypothesis," Philosophia Christi, Series 2, Vol. 3, No. 1 (2001), pg. 165)

Question:

Inherent in ID theory, is there the idea that there was purpose in the design? And, if so, what specific purposes?

Answer: ID also does not say anything about purpose, aside from the fact that things, especially biological things, look like they were made to carry out some particular function. They work together as a whole to make a functional organism. That functional organism is part of an ecosystem, and contributes to the functioning of that system. But is there an overall purpose to that system? To make a biosphere? This can be pushed out only so far; as to the reason for the existence of all of this -- why there should be such a planet, or the reason for our existence on the planet -- that goes beyond what ID can say. Final ends belong in the realms of philosophy and theology.

Question:

A personal question regarding how the ID debate has been fought. Why oh why was it based on biology??? IMHO, that was a terrible starting point! I would suggest later iterations and discussions focus on even more fundamental aspects of the universe. Time (apparently) is constant and measurable (not random and chaotic); the universal constant is just that -- a constant -- and without such a very, very limited range of variation, we could not exist (at least, not as we do now). Mathematics works -- again, in my thinking, a sign that this universe is rational; and if rational, designed (rationality and order from chaos...???). I know Plato et al. discussed this, but it seems to have been ignored in the ID debate. As I hope I have clearly indicated, I'm after answers that clearly differentiate ID as a theory in general from any personal takes on it (e.g., characteristics of the designer).

Answer: ID is not based purely on biology, though it may appear to be sometimes. The extreme fine-tuning of the universe for life; the fact that mathematics is rational and elegant, and fits the needs of science; the fact that chemistry is ordered so as to make its discovery possible, and that the planet is ordered so as to permit intelligent life to discover science at all (see The Privileged Planet) -- all these are arguments for design, design that is detectable by minds such as ours. I suggest reading A Meaningful World, by Benjamin Wiker and Jonathan Witt.

The reason it often appears that the argument is all about biology is because it is from there that the majority of pushback comes.


Thanks for your questions, and I hope my response helps.

Darwinism vs, the real world XXXI

The Digestive System: The Stomach and Beyond
Howard Glicksman February 26, 2016 11:24 AM

Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." For the complete series,  see here. Dr. Glicksman practices palliative medicine for a hospice organization.


Except for molecular oxygen (O2), which comes in through the lungs, everything else the body needs to survive enters through the gastrointestinal system. This includes things like water, sugars, amino and fatty acids, cholesterol, electrolytes, minerals, and vitamins. But most of the nutrients the body needs are trapped inside more complex molecules, like carbohydrates, proteins, and fats, and are too large to enter the body. The gastrointestinal system must first break down these large molecules into much smaller ones, in a process called digestion, so it can then absorb the nutrients the body needs into the blood. In my last article I showed that digestion is similar to how a pulp and paper mill works. They both use mechanical and chemical means to break down large things into smaller ones and only use their equipment and chemicals when needed.

The process of digestion begins as soon as food enters the mouth. Its presence, along with its taste and smell, are detected by the nervous system, which stimulates the release of saliva from the glands in the mouth. Saliva contains the enzymes amylase and lipase, which begin the chemical breakdown of carbohydrates and fats respectively. As the food mixes with saliva, it is mashed by the teeth and the tongue, formed into a small mushy lump called a bolus, and moved back toward the pharynx.

Sensors in the pharynx detect the bolus and send information to the brain, initiating the swallow reflex. Swallowing involves the coordinated action of about twenty-five different pairs of muscles to protect the airway and propel the bolus into the esophagus, where it is moved by peristalsis down into the stomach. This article will show how the body follows the rules and takes control to continue digestion and absorption within the stomach and beyond.

Seeing, smelling, and tasting food causes the brain to send nerve messages to the stomach, which begins the first or cephalic phase of gastric secretion. This causes the release of mucous, hydrochloric acid, and pepsinogen. The mucous protects the cells that line the stomach from its own chemicals. The acid both kills microbes and converts pepsinogen into a powerful digestive enzyme called pepsin, a protease that begins to chemically breakdown protein. This phase also results in specialized cells in the stomach secreting a hormone called gastrin,which travels in the blood and tells the stomach cells to send out even more mucous, hydrochloric acid, and pepsinogen.

As the stomach fills up and distends with fluid, the stretch-sensitive mechanoreceptors in its walls send out more nerve messages. These stimulate the cells in the stomach to send out even more mucous, hydrochloric acid, and pepsinogen in what is called the second or gastric phase of gastric secretion. The contents of the stomach are then churned and mixed to further help in the digestive process, creating an acidic liquid called chyme.

It is important to note here that besides playing a major role in digestion, the stomach does two other important things: use its acid to help iron be absorbed later on and produce intrinsic factor to protect Vitamin B12 from being broken down by its acid. Both of these nutrients are needed for the production of hemoglobin.

The stomach absorbs very few nutrients (mainly water) and once it has done its part of digestion it passes the chyme into the first part of the intestine called the duodenum. To prevent damage to the duodenum and allow for more efficient digestion and absorption, it is important that the stomach control how fast it releases the chyme. This is accomplished by the pyloric sphincter, a ring-like band of muscle at the end of the stomach that is able to constrict and relax to send out the right amount of chyme for the right situation. Sensors in this region send messages to nerve cells, which help to control gastric emptying. In general, the more fat and protein is present and the more acidic the chyme, the slower the stomach empties its contents into the duodenum. This is why, when you have a heavier meal, your stomach feels full for a longer period of time.

As the stomach works on the acidic chyme and slowly sends it into the duodenum, the stretching of the intestinal walls signals it to start producing its own fluid. Intestinal juice mainly contains saline (NaCl), mucous, bicarbonate (HCO3-), and digestive enzymes. The alkaline bicarbonate begins to neutralize the acidic chyme that the intestine receives from the stomach. The enzymes produced in the lining of the intestine mainly help to break up the bonds between molecules that contain two sugars. Maltase breaks up the bonds between the two glucose molecules that make up maltose, lactase breaks up the bonds between glucose and galactose which make up lactose, and sucrase breaks up the bonds between glucose and fructose which make up sucrose. The intestine also produces enterokinase, a protease that is important for activating many of the enzymes that come from the pancreas.

As the chyme moves from the stomach into the duodenum, sensors on specialized gland cells detect simple molecules, like fatty and amino acids. The gland cells respond by sending out two hormones, secretin and cholecystokinin, to tell the pancreas to deposit its fluid into the digestive tract. Pancreatic juice contains high amounts of bicarbonate and is very alkaline. The addition of the alkaline pancreatic juice helps to further neutralize the acidic chyme that has entered the intestine from the stomach. The pancreatic juice also contains most of the enzymes needed to finish off the digestion of carbohydrates, fats, and proteins. In addition to amylases and various lipases, the pancreatic juice contains many different proteases that break down proteins. This includes trypsin, chymotrypsins, elastases, and carboxypeptidases. All of these proteases are produced inside the pancreatic cells in the inactive form so they won't digest the pancreas itself.

Trypsin enters the intestine as trypsinogen and becomes activated by its alkaline environment and enterokinase, which, by snipping a few atoms off, changes its shape so it is ready to go to work. Trypsin then activates the other enzymes and proteases, mentioned above. Finally, since lipids are not very soluble in water, they require the presence of bile from the liver and gall bladder to help in fat digestion. The presence of fatty acids in the duodenum contributes to the release of cholecystokinin, which tells the pancreas to release its juice and the gall bladder to contract and send its concentrated bile into the intestine to help in fat digestion.

The intestine, which consists of the duodenum, jejunum, and ileum, is where most of digestion and absorption take place. In addition to water, glucose, amino acids, cholesterol, and simple fats, the intestine also absorbs other vital chemicals, such as minerals, like calcium and iron, electrolytes, like sodium and potassium ions, and vitamins like A, C, D, E, K, and all of the B vitamins, including Vitamin B12. About 1.5 liters of fluid makes its way from the intestine into the colon daily, where mostly water, sodium, and chloride ions are reabsorbed. The remaining 100-150 gm of feces that daily exits the gastrointestinal tract through the rectum and anus usually consists of about 70 percent water and 30 percent solids from undigested plant fibers, like cellulose, cells shed from the lining of the gastrointestinal tract, and bacteria.

A quick review of gastrointestinal function shows that, to do its job properly, it needs separate control systems to turn on different organs, each using enough fluids and chemicals to adequately digest food and absorb enough nutrients. The cephalic and gastric phases of gastric secretion, along with gastrin, make sure the stomach sends out enough acid to activate pepsin for the digestion of proteins to begin. The amount of fatty and amino acids and the acidity of the chyme determine the rate of gastric emptying to help in proper digestion and absorption.

These chemicals also stimulate certain gland cells to release secretin and cholecystokinin, which together tell the pancreas to release its juices into the intestine and the gall bladder to release concentrated bile. Alkaline intestinal and pancreatic juices neutralize the acid coming from the stomach, which, with the help of enterokinase, activates trypsin. Trypsin then activates many other pancreatic enzymes that do most of the work of digestion. Bile from the liver and the gall bladder are needed to help fat digestion as well. Having completed digestion, the intestine then absorbs the nutrients that have been freed up. Finally, the intestine and colon reabsorb most of the water, sodium, and chloride ions that have been previously secreted so that very little is lost through the feces.

The total absence or significant deficiency of any one nutrient would have made it impossible for our earliest ancestors to survive long enough to reproduce. The gastrointestinal system demonstrates irreducible complexity because every component has to be present for it to be able to do its job. It also demonstrates natural survival capacity because each of its components has to provide enough of the right fluid and chemicals to cause adequate digestion and allow for the absorption of what the body needs for survival. Evolutionary biology usually points to similar systems within simpler organisms to explain how the gastrointestinal system may have come into being. Of course, this does not explain how the simpler systems developed in the first place or how it must work within the laws of nature to allow for survival.


The body must breathe in air every few seconds because its need for oxygen is so acute that without it, it dies in just a few minutes. When it comes to water, because the body is able to move some of it from its cells into the blood to compensate for its loss, it only has to drink fluids every few hours. What about glucose? After all, we know we don't have to take in glucose as often as oxygen or water to stay alive. So, how does the body go about making sure it has enough for its energy needs and how does evolutionary biology explain the development of the system it uses? That's what we'll start to look at next time.