Intelligent Design

Back to School Part VIII

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We continue to examine the work of authors George Johnson and Jonathan Losos in their biology textbook, The Living World ((Fifth Edition, McGraw Hill, 2008). In their chapter on evolution and natural selection, these accomplished evolutionists begin by (1) misrepresenting the relationship between microevolution and macroevolution and biological variation here, (2) making a non scientific, metaphysical, truth claim that just happens to mandate the truth of evolution here, (3) making the grossly false statement that the fossils themselves are a factual observation that macroevolution has occurred here and here, (4) making a series of misrepresentations by carefully selecting the evidence to provide to the student and protecting it with circular reasoning here, (5) misrepresenting the molecular evidence here, (6) presenting the student with a blatantly false history of evolutionary theory here, (7) introducing the usual if-and-only-if evolutionary reasoning here, and (8) repeating the centuries old religious argument that bad design proves evolution hereRead more

19 Replies to “Back to School Part VIII

  1. 1
    bornagain77 says:

    Dr. Hunter, this quote of yours nails the situation!

    ‘Amazingly evolutionists think hemoglobin’s special amino acid sequence encoding for this machine is no different than any random list, such a list of birthdays. To be sensible Johnson’s and Losos’ analogy would need the list of birthdays to provide something fantastic, such as the answers to the biology class final exam.’

  2. 2
    kylefoley76 says:

    I’m trying to read this article but it requires a membership. Is there any someone can get this and post it on the web. This is one of the key articles for the ID movement.

  3. 3
    bornagain77 says:

    kylefoley76 I don’t have that paper but this full access one by Doug Axe may help:

    The Case Against a Darwinian Origin of Protein Folds – Douglas Axe – 2010
    Excerpt Pg. 11: “Based on analysis of the genomes of 447 bacterial species, the projected number of different domain structures per species averages 991. Comparing this to the number of pathways by which metabolic processes are carried out, which is around 263 for E. coli, provides a rough figure of three or four new domain folds being needed, on average, for every new metabolic pathway. In order to accomplish this successfully, an evolutionary search would need to be capable of locating sequences that amount to anything from one in 10^159 to one in 10^308 possibilities, something the neo-Darwinian model falls short of by a very wide margin.”

  4. 4
  5. 5
    bornagain77 says:

    kyle, this audio podcast may interest you as well:

    The Case Against a Darwinian Origin of Protein Folds – Douglas Axe, Jay Richards – audio

  6. 6
    kylefoley76 says:

    Born again, thank you for helping me out. By the way, does anyone know where the majority of the ID community stand on common descent?

  7. 7
    Joseph says:


    By the way, does anyone know where the majority of the ID community stand on common descent?

    I would say the majority of IDists would say the only way universal common descent is feasible is by design.

    But right now the major problem with UCD is no one knows where the information for determining form is nor how/ if it can be altered.

  8. 8
    bornagain77 says:

    kylefoley76, I don’t know where the majority stand right now, but I do know that the genetic evidence itself is turning against that position besides the lack of transitional fossils in the fossil record:

    First there is found to be a significant percentage of completely unique ‘ORFan’ genes in each new genome of each distinct species sequenced:

    ORFan Genes Challenge Common Descent – Paul Nelson – video – short version

    Microbial genomes multiply – Russell F. Doolittle – 2002
    Excerpt: It is precisely this point — the large numbers of putative genes with no known function — that has been the biggest surprise in genome sequencing.

    Analysis of Singleton ORFans in Fully Sequenced Microbial Genomes – Naomi Siew and Daniel Fischer – 2003
    Excerpt: Because there is no obvious evolutionary mechanism to account for the origin of single-member families, one might accept the explanation of their origin as extreme divergence. However, even if all ORFans correspond to highly divergent members of known families, a number of puzzling questions arise. For example, how have their sequences diverged to such an extent that no similar sequences are detected today? If evolution works through descent with modification, then why is it that no similar sequences are found in other organisms? Why is it that wedo not find today any of the necessary “intermediate sequences” that must have given rise to these ORFans?

    Estimating the size of the bacterial pan-genome – Pascal Lapierre and J. Peter Gogarten – 2008
    Excerpt: We have found >139 000 rare (ORFan) gene families scattered throughout the bacterial genomes included in this study. The finding that the fitted exponential function approaches a plateau indicates an open pan-genome (i.e. the bacterial protein universe is of infinite size); a finding supported through extrapolation using a Kezdy-Swinbourne plot (Figure S3). This does not exclude the possibility that, with many more sampled genomes, the number of novel genes per additional genome might ultimately decline; however, our analyses and those presented in Ref. [11] do not provide any indication for such a decline and confirm earlier observations that many new protein families with few members remain to be discovered.

    I like this following paper for though it is materialistic in its outlook at least Dr. Eugene Koonin, unlike many materialists, is brutally honest with the genetic evidence we now have.

    The Biological Big Bang model for the major transitions in evolution – Eugene V Koonin – Background:
    “Major transitions in biological evolution show the same pattern of sudden emergence of diverse forms at a new level of complexity. The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin’s original proposal, remains the dominant description of biological evolution. The cases in point include the origin of complex RNA molecules and protein folds; major groups of viruses; archaea and bacteria, and the principal lineages within each of these prokaryotic domains; eukaryotic supergroups; and animal phyla. In each of these pivotal nexuses in life’s history, the principal “types” seem to appear rapidly and fully equipped with the signature features of the respective new level of biological organization. No intermediate “grades” or intermediate forms between different types are detectable;

    Biological Big Bangs – Origin Of Life and Cambrian – Dr. Fazale Rana – video

    This ORFan ‘surprise’ extends to the human genome:

    Human Gene Count Tumbles Again – 2008
    Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes.,,, Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate
    genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes. (The 1,177 ORFan genes in humans are completly unique to our lineage)

    In fact it turns out that the authors of the preceding ‘kick the ORFans out in the street’ paper actually did know that there was clear and unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore that strong evidence in favor of their preconceived evolutionary bias of forcing the genetic sequences of chimps and humans to be as similar as possible. That is EXACTLY how you ARE NOT suppose to practice science!!!:

    I would like to reiterate that evolutionists cannot even account for the origination of even one unique gene or protein, much less over one thousand completely unique ORFan genes:

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”

    “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” 2004: – Doug Axe ,,,this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.”

  9. 9
    bornagain77 says:

    Kyle as well,

    ,,,The significant percentage of completely novel ORFan genes plus the SEVERE polyconstraint of the polyfuntionality of each genome makes ‘top down’ design per each parent species far more reasonable than the ‘bottom up’ scenario of Darwinism, and this is true whether one currently considers theistic-Darwinism of any flavor, or neo-Darwinism proper, to be reasonable:

    Simplest Microbes More Complex than Thought – Dec. 2009
    Excerpt: PhysOrg reported that a species of Mycoplasma,, “The bacteria appeared to be assembled in a far more complex way than had been thought.” Many molecules were found to have multiple functions: for instance, some enzymes could catalyze unrelated reactions, and some proteins were involved in multiple protein complexes.”

    First-Ever Blueprint of ‘Minimal Cell’ Is More Complex Than Expected – Nov. 2009
    Excerpt: A network of research groups,, approached the bacterium at three different levels. One team of scientists described M. pneumoniae’s transcriptome, identifying all the RNA molecules, or transcripts, produced from its DNA, under various environmental conditions. Another defined all the metabolic reactions that occurred in it, collectively known as its metabolome, under the same conditions. A third team identified every multi-protein complex the bacterium produced, thus characterising its proteome organisation.
    “At all three levels, we found M. pneumoniae was more complex than we expected,”

    Scientists Map All Mammalian Gene Interactions – August 2010
    Excerpt: Mammals, including humans, have roughly 20,000 different genes.,,, They found a network of more than 7 million interactions encompassing essentially every one of the genes in the mammalian genome.

    Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information – David L. Abel and Jack T. Trevors – Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8
    “No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms’ genomes programmed?”

    Mammalian overlapping genes: the comparative perspective. – 2004
    Excerpt: it is rather surprising that a large number of genes overlap in the mammalian genomes. Thousands of overlapping genes were recently identified in the human and mouse genomes. However,the origin and evolution of overlapping genes are still unknown. We identified 1316 pairs of overlapping genes in humans and mice and studied their evolutionary patterns. It appears that these genes do not demonstrate greater than usual conservation. Studies of the gene structure and overlap pattern showed that only a small fraction of analyzed genes preserved exactly the same pattern in both organisms.

    Poly-Functional Complexity equals Poly-Constrained Complexity

    The primary problem that poly-functional complexity presents for neo-Darwinism, or even Theistic Evolutionists is this:

    To put it plainly, the finding of a severely poly-functional/polyconstrained genome by the ENCODE study has put the odds, of what was already astronomically impossible, to what can only be termed fantastically astronomically impossible. To illustrate the monumental brick wall any evolutionary scenario (no matter what “fitness landscape”) must face when I say genomes are poly-constrained to random mutations by poly-functionality, I will use a puzzle:

    If we were to actually get a proper “beneficial mutation’ in a polyfunctional genome of say 500 interdependent genes, then instead of the infamous “Methinks it is like a weasel” single element of functional information that Darwinists pretend they are facing in any evolutionary search, with their falsified genetic reductionism scenario I might add, we would actually be encountering something more akin to this illustration found on page 141 of Genetic Entropy by Dr. Sanford.

    S A T O R
    A R E P O
    T E N E T
    O P E R A
    R O T A S

    Which is translated ;

    This ancient puzzle, which dates back to 79 AD, reads the same four different ways, Thus, If we change (mutate) any letter we may get a new meaning for a single reading read any one way, as in Dawkins weasel program, but we will consistently destroy the other 3 readings of the message with the new mutation.

    This is what is meant when it is said a poly-functional genome is poly-constrained to any random mutations.

    The puzzle I listed is only poly-functional to 4 elements/25 letters of interdependent complexity, the minimum genome is poly-constrained to approximately 500 elements (genes) at minimum approximation of polyfunctionality. For Darwinist to continue to believe in random mutations to generate the staggering level of complexity we find in life is absurd in the highest order!

    As to Theistic Evolutionists, who believe God guides evolution incrementally, all I ask of you is do you think that it would be easier for God to incrementally change the genome of a organism, maintaining functionality all the time, in a bottom up manner or do you think it would be easier for Him to design each kind of organism in a top down manner?

    further note:

    No Examples Of Gradualism In Molecular Biology – Doug Axe PhD.

  10. 10
    kylefoley76 says:

    I’m reading this paper which is a critique of Meyer over at Panda’s Thumb. It’s a very bad paper but I was astonished by this bold claim:

    The origin of new genes and proteins is actually a common, fairly trivial event, well-known to anyone who spends a modicum of effort investigating the scientific literature. The evolution of new genes has been observed in the lab, in the wild, inferred in great detail between closely-related modern species, and reconstructed in hundreds of cases by comparing the genomes from organisms sequenced in genome projects over the last decade.

    The author then cites this article

    I was wondering if any IDers have refuted this paper?

  11. 11
    bornagain77 says:

    Kyle, though I don’t know if he cites that particular paper, Casey Luskin deals with the substance of the ‘2003’ paper here:

    How to Play the Gene Evolution Game:

    you may find the paper in this article:

    Assessing the NCSE’s Citation Bluffs on the Evolution of New Genetic Information – Feb. 2010

    or this one:

    The NCSE, Judge Jones, and Bluffs About the Origin of New Functional Genetic Information – Casey Luskin – March 2010

  12. 12
    bornagain77 says:

    further notes:

    Asking the Right Questions about the Evolutionary Origin of New Biological Information – Feb. 2010
    As we’ve seen, it’s easy to duplicate a gene, but the key missing ingredient in many neo-Darwinian explanations of the origin of new genetic information is how a gene duplicate then acquires some new optimized function. Evolutionists have not demonstrated, except in rare specialized cases, that step-wise paths to new function for duplicate genes exist.

    Sanford Genetic Entropy Polyploidy – (Gene/Chromosome Duplication Fallacies)

    This following paper clearly reveals that there is a ‘cost’ to duplicate genes that further precludes the scenario from being plausible:

    Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model
    Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence.

    This recent paper also found the gene duplication scenario to be highly implausible:

    The Extinction Dynamics of Bacterial Pseudogenes – Kuo and Ochman – August 2010
    Excerpt: “Because all bacterial groups, as well as those Archaea examined, display a mutational pattern that is biased towards deletions and their haploid genomes would be more susceptible to dominant-negative effects that pseudogenes might impart, it is likely that the process of adaptive removal of pseudogenes is pervasive among prokaryotes.”

    and of course these tests:

    Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video

    Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness – May 2010
    Excerpt: Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken.

    Testing Evolution in the Lab With Biologic Institute’s Ann Gauger – audio

  13. 13
    kylefoley76 says:

    Bornagain, thanks again for all this great information. I really appreciate it. You sure know how to work.

  14. 14
    john_a_designer says:


    “By the way, does anyone know where the majority of the ID community stand on common descent?”

    Michael Behe does believe in UCD but he is clearly in the minority.

  15. 15
    Fross says:

    wow, what will they put in biology books next?

  16. 16
    Neil Rickert says:

    kylefoley76 (#2)
    I seem to have access to that paper from my office (on a university campus). Presumably the library has a subscription for the campus. If you have access to a computer on a university campus somewhere, you might try from there.

    From my home computer, I only see the abstract. From campus, I see the whole paper.

  17. 17
    bornagain77 says:

    kylefoley76, Casey Luskin has just ‘coincidentally’ wrote a article addressing every point of the supposed ‘overwhelming’ evidence for Common Descent:

    But Isn’t There a Consilience of Data That Corroborates Common Descent?

  18. 18
    Ilion says:

    KyleFoley:I’m reading this paper which is a critique of Meyer over at Panda’s Thumb. It’s a very bad paper but I was astonished by this bold claim: [excerpted quote] I was wondering if any IDers have refuted this paper?

    If you think carefully about it, you can see that the Darwinists themselves refute it. Or, at least, they deny its truth. Consider the ‘Science Daily’ article BA had referenced concerning ORFan genes – consider, specifically, the methodology of rejecting ORFan genes as not being “real genes,” seeing that they are unique to a lineage. Now, consider that methodology in light of the amusing Darwinistic assertion you quoted:

    The origin of new genes and proteins is actually a common, fairly trivial event, well-known to anyone who spends a modicum of effort investigating the scientific literature. The evolution of new genes has been observed in the lab, in the wild, inferred in great detail between closely-related modern species, and reconstructed in hundreds of cases by comparing the genomes from organisms sequenced in genome projects over the last decade.

    Can you not see the humor?

  19. 19
    jstanley01 says:

    Hey, if you’ve got the political muscle to teach whatever you want, why not flex it? I mean from a Darwinian perspective. After all, that’s what “survival of the fittest” is all about, right?

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