Early Complexity: A Case Study of Evolutionary Theory

6 Replies to “Early Complexity: A Case Study of Evolutionary Theory”

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   Dionisio says:

   January 28, 2018 at 2:05 am

   Very interesting. Thanks.
2. 2
   Dionisio says:

   January 28, 2018 at 2:07 am

   explaining important this doctrine was to Darwin

   explaining [how] important this doctrine was to Darwin

   ?
3. 3
   Truth Will Set You Free says:

   January 28, 2018 at 5:50 am

   I think some of the new Darwinian theories depart from Darwin on this point by allowing for jumps (genetic drift, emergence, etc.). Anything to keep the theory relevant.
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   bornagain77 says:

   January 28, 2018 at 7:21 am

   Although Darwinists refuse to accept falsification from mathematics and/or empirical evidence for their theory, their theory has, none-the-less, been falsified by mathematics and empirical evidence:

   The falsification from mathematics is particularly interesting. Besides the fact that probability calculations show Darwinian evolution to be beyond impossible,,, For example:

   HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION
   Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that the genes of E. coli contain over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance.
   http://www.pathlights.com/ce_e.....hist12.htm

   “In light of Doug Axe’s number, and other similar results,, (1 in 10^77), it is overwhelmingly more likely than not that the mutation, random selection, mechanism will fail to produce even one gene or protein given the whole multi-billion year history of life on earth. There is not enough opportunities in the whole history of life on earth to search but a tiny fraction of the space of 10^77 possible combinations that correspond to every functional combination. Why? Well just one little number will help you put this in perspective. There have been only 10^40 organisms living in the entire history of life on earth. So if every organism, when it replicated, produced a new sequence of DNA to search that (1 in 10^77) space of possibilities, you would have only searched 10^40th of them. 10^40 over 10^77 is 1 in 10^37. Which is 10 trillion, trillion, trillion. In other words, If every organism in the history of life would have been searching for one those (functional) gene sequences we need, you would have searched 1 in 10 trillion, trillion, trillionth of the haystack. Which makes it overwhelmingly more likely than not that the (Darwinian) mechanism will fail. And if it is overwhelmingly more likely than not that the (Darwinian) mechanism will fail should we believe that is the way that life arose?”
   Stephen Meyer – 46:19 minute mark – Darwin’s Doubt – video
   https://www.youtube.com/watch?v=Vg8bqXGrRa0&feature=player_detailpage#t=2778

   Bernard d’Abrera on Butterfly Mimicry and the Faith of the Evolutionist – October 5, 2011
   Excerpt:  renowned butterfly scholar and photographer Bernard d’Abrera considers the mystery of mimicry.,,,
   For it to happen in a single species once through chance, is mathematically highly improbable. But when it occurs so often, in so many species, and we are expected to apply mathematical probability yet again, then either mathematics is a useless tool, or we are being criminally blind.,,, Evolutionism (with its two eldest daughters, phylogenetics and cladistics) is the only systematic synthesis in the history of the universe that proposes an Effect without a Final Cause. It is a great fraud, and cannot be taken seriously because it outrageously attempts to defend the philosophically indefensible.
   http://www.evolutionnews.org/2.....51571.html

   The waiting time problem in a model hominin population – 2015 Sep 17
   John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
   Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
   Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
   While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
   It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.
   http://www.ncbi.nlm.nih.gov/pm.....MC4573302/

   Besides the fact that probability calculations show Darwinian evolution to be beyond impossible, Darwinian evolution is based on a materialistic view of reality which denies that anything beyond material reality exists. Yet, on the other hand, Mathematics, which provides the backbone for all of science, engineering and technology,,, Mathematics itself, exists in a transcendent, beyond space and time, realm which is not reducible any possible material explanation. This transcendent mathematical realm has been referred to as a Platonic mathematical world.

   Simply put, Mathematics itself, contrary to the reductive materialistic presuppositions of Darwinists, does not need the material world in order to exist. And yet Darwinists, although they deny that anything beyond the material realm exists, need this transcendent world of mathematics in order for their theory to be considered scientific in the first place. The predicament that Darwinists find themselves in regards to denying the reality of this transcendent world of mathematics, and yet needing validation from this transcendent world of mathematics in order to be considered scientific in the first place, should be the very definition of self-refuting.

   Darwinian Evolution vs Mathematics – video
   https://www.youtube.com/watch?v=q3gyx70BHvA

   And although Darwinian evolution has been refuted by many lines of empirical evidence,, for example,,

   What’s the matter with evolution? By Casey Luskin – April 25, 2015
   Science | A ranking of the top five scientific problems found in evolutionary theory
   Problem 1: No Viable Mechanism to Generate a Primordial Soup
   Problem 2: Unguided Chemical Processes Cannot Explain the Origin of the Genetic Code
   Problem 3: Random Mutations Cannot Generate the Genetic Information Required for Irreducibly Complex Structures
   Problem 4: Natural Selection Struggles to Fix Advantageous Traits into Populations
   Problem 5: Abrupt Appearance of Species in the Fossil Record Does Not Support Darwinian Evolution
   http://www.worldmag.com/2015/0....._evolution

   Part 2: What’s the matter with evolution? By Casey Luskin – May 2, 2015
   Excerpt: Five more scientific problems found in evolutionary theory
   Problem 6: Molecular Biology has Failed to Yield a Grand “Tree of Life”
   Problem 7: Convergent Evolution Challenges Darwinism and Destroys the Logic Behind Common Ancestry
   Problem 8: Differences Between Vertebrate Embryos Contradict the Predictions of Common Ancestry
   Problem 9: Neo-Darwinism Struggles to Explain the Biogeographical Distribution of Many Species
   Problem 10: Neo-Darwinism Has a Long History of Inaccurate Darwinian Predictions about Vestigial Organs and “Junk DNA”
   http://www.worldmag.com/2015/0....._evolution

   Although Darwinian evolution has been refuted by many lines of empirical evidence, two particularly devastating falsifications of Darwinian evolution from empirical evidence are, number one, Biological form is not even reducible to mutations in DNA in the first place:

   Darwinism vs Biological Form – video
   https://www.youtube.com/watch?v=JyNzNPgjM4w

   Simply put, since Darwinian explanations, i.e. reductive materialistic explanations, are grossly inadequate for explaining how any particular organism might achieve its basic form, then Darwinian speculations for how one type of organism might have transformed into another type of organism are based on pure fantasy and have no discernable experimental basis in reality.
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   bornagain77 says:

   January 28, 2018 at 7:22 am

   The second devastating empirical falsification for Darwinism comes from falsification of its randomness postulate. Firstly mutations are now shown not to be random as Darwinists had presupposed,,,

   How life changes itself: the Read-Write (RW) genome. – 2013
   Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences.
   http://www.ncbi.nlm.nih.gov/pubmed/23876611

   WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Fully Random Mutations – Kevin Kelly – 2014
   Excerpt: What is commonly called “random mutation” does not in fact occur in a mathematically random pattern. The process of genetic mutation is extremely complex, with multiple pathways, involving more than one system. Current research suggests most spontaneous mutations occur as errors in the repair process for damaged DNA. Neither the damage nor the errors in repair have been shown to be random in where they occur, how they occur, or when they occur. Rather, the idea that mutations are random is simply a widely held assumption by non-specialists and even many teachers of biology. There is no direct evidence for it.
   On the contrary, there’s much evidence that genetic mutation vary in patterns. For instance it is pretty much accepted that mutation rates increase or decrease as stress on the cells increases or decreases. These variable rates of mutation include mutations induced by stress from an organism’s predators and competition, and as well as increased mutations brought on by environmental and epigenetic factors. Mutations have also been shown to have a higher chance of occurring near a place in DNA where mutations have already occurred, creating mutation hotspot clusters—a non-random pattern.
   http://edge.org/response-detail/25264

   Secondly, although Darwinists presupposed that biological molecules would be based on ‘random’ Brownian motion and to therefore be “randomly colliding with each other”’.

   No, Scientists in Darwin’s Day Did Not Grasp the Complexity of the Cell; Not Even Close – Casey Luskin – June 6, 2013
   Excerpt: We have always underestimated cells. Undoubtedly we still do today. But at least we are no longer as naïve as we were when I was a graduate student in the 1960s. Then, most of us viewed cells as containing a giant set of second-order reactions: molecules A and B were thought to diffuse freely, randomly colliding with each other to produce molecule AB — and likewise for the many other molecules that interact with each other inside a cell. This seemed reasonable because, as we had learned from studying physical chemistry, motions at the scale of molecules are incredibly rapid. Consider an enzyme, for example. If its substrate molecule is present at a concentration of 0.5mM,which is only one substrate molecule for every 105 water molecules, the enzyme’s active site will randomly collide with about 500,000 molecules of substrate per second. And a typical globular protein will be spinning to and fro, turning about various axes at rates corresponding to a million rotations per second.
   But, as it turns out, we can walk and we can talk because the chemistry that makes life possible is much more elaborate and sophisticated than anything we students had ever considered. Proteins make up most of the dry mass of a cell. But instead of a cell dominated by randomly colliding individual protein molecules, we now know that nearly every major process in a cell is carried out by assemblies of 10 or more protein molecules. And, as it carries out its biological functions, each of these protein assemblies interacts with several other large complexes of proteins. Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines.”
   – Bruce Alberts, “The Cell as a Collection of Protein Machines: Preparing the Next Generation of Molecular Biologists,” Cell, 92 (February 6, 1998): 291-294)  Editor-in-Chief of Science (2009-2013). Dr Alberts served two six-year terms as the president of the National Academy of Sciences
   http://www.evolutionnews.org/2.....72871.html     

   Flailing Blindly: The Pseudoscience of Josh Rosenau and Carl Zimmer – Jonathan Wells – April 17, 2014
   Excerpt: The new animation (like the old) also includes a kinesin molecule hauling a vesicle, but this time the kinesin’s movements are characterized (in Zimmer’s words) by

   “barely constrained randomness. Every now and then, a tiny molecule loaded with fuel binds to one of the kinesin “feet.” It delivers a jolt of energy, causing that foot to leap off the molecular cable and flail wildly, pulling hard on the foot that’s still anchored. Eventually, the gyrating foot stumbles into contact again with the cable, locking on once more — and advancing the vesicle a tiny step forward. This updated movie offers a better way to picture our most intricate inner workings…. In the 2006 version, we can’t help seeing intention in the smooth movements of the molecules; it’s as if they’re trying to get from one place to another. In reality, however, the parts of our cells don’t operate with the precise movements of the springs and gears of a clock. They flail blindly in the crowd.”

   But that’s not what the biological evidence shows. In fact, kinesin moves quickly, with precise movements, to get from one place to another. A kinesin molecule takes one 8-nanometer “step” along a microtubule for every high-energy ATP molecule it uses, and it uses about 80 ATPs per second. On the scale of a living cell, this movement is very fast. To visualize it on a macroscopic scale, imagine a microtubule as a one-lane road and the kinesin molecule as an automobile. The kinesin would be traveling over 200 miles per hour!
   https://iconsofevolution.com/flailing-blindly/

   Although Darwinists presupposed that biological molecules would be based on ‘random’ Brownian motion and to therefore be “randomly colliding with each other”, the fact of the matter is that Brownian motion in biology is, for all practical purposes, not to be found in biological life. In fact, it is now found that “living organisms have a certain order. A structure to them that’s very different from the random thermodynamic jostling of atoms and molecules in inanimate matter of the same complexity. In fact, living matter seems to behave in its order and its structure just like inanimate cooled down to near absolute zero.”

   Jim Al-Khalili, at the 2:30 minute mark of the following video states,
   “,,and Physicists and Chemists have had a long time to try and get use to it (Quantum Mechanics). Biologists, on the other hand have got off lightly in my view. They are very happy with their balls and sticks models of molecules. The balls are the atoms. The sticks are the bonds between the atoms. And when they can’t build them physically in the lab nowadays they have very powerful computers that will simulate a huge molecule.,, It doesn’t really require much in the way of quantum mechanics in the way to explain it.”
   At the 6:52 minute mark of the video, Jim Al-Khalili goes on to state:
   “To paraphrase, (Erwin Schrödinger in his book “What Is Life”), he says at the molecular level living organisms have a certain order. A structure to them that’s very different from the random thermodynamic jostling of atoms and molecules in inanimate matter of the same complexity. In fact, living matter seems to behave in its order and its structure just like inanimate cooled down to near absolute zero. Where quantum effects play a very important role. There is something special about the structure, about the order, inside a living cell. So Schrodinger speculated that maybe quantum mechanics plays a role in life”.
   Jim Al-Khalili – Quantum biology – video
   https://www.youtube.com/watch?v=zOzCkeTPR3Q

   Quantum coherent-like state observed in a biological protein for the first time – October 13, 2015
   Excerpt: If you take certain atoms and make them almost as cold as they possibly can be, the atoms will fuse into a collective low-energy quantum state called a Bose-Einstein condensate. In 1968 physicist Herbert Fröhlich predicted that a similar process at a much higher temperature could concentrate all of the vibrational energy in a biological protein into its lowest-frequency vibrational mode. Now scientists in Sweden and Germany have the first experimental evidence of such so-called Fröhlich condensation (in proteins).,,,
   For their protein, the researchers chose the enzyme lysozyme, .,,,
   The real-world support for Fröhlich’s theory took so long to obtain because of the technical challenges of the experiment, Katona said.
   https://phys.org/news/2015-10-quantum-coherent-like-state-biological-protein.html

   Darwinian Materialism vs Quantum Biology – video
   https://www.youtube.com/watch?v=LHdD2Am1g5Y

   Thus, although Darwinists have refused to accept falsification for their theory from mathematics and empirical evidence, Darwinian evolution has, none-the-less, been thoroughly falsified by both.

   2 Corinthians 10:5
   Casting down imaginations, and every high thing that exalteth itself against the knowledge of God, and bringing into captivity every thought to the obedience of Christ;

   Darwinian Evolution: A Pseudoscience based on Unrestrained Imagination and Bad Liberal Theology – video
   https://youtu.be/KeDi6gUMQJQ
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   bornagain77 says:

   March 28, 2018 at 11:45 pm

   and let’s not forget Dr. Michael Behe’s (via White) empirical falsification of Darwinian evolution:

   Michael Behe – Observed (1 in 10^20) Edge of Evolution – video – Lecture delivered in April 2015 at Colorado School of Mines
   25:56 minute quote – “This is not an argument anymore that Darwinism cannot make complex functional systems; it is an observation that it does not.”
   https://www.youtube.com/watch?v=9svV8wNUqvA

   “The number I cite, one parasite in every 10^20 for de novo chloroquine resistance, is not a probability calculation. Rather, it is a statistic, a result, a data point. (Furthermore, it is not my number, but that of the eminent malariologist Nicholas White.) I do not assume that “adaptation cannot occur one mutation at a time”; I assume nothing at all. I am simply looking at the results. The malaria parasite was free to do whatever it could in nature; to evolve resistance, or outcompete its fellow parasites, by whatever evolutionary pathway was available in the wild. Neither I nor anyone else were manipulating the results. What we see when we look at chloroquine-resistant malaria is pristine data — it is the best that random mutation plus selection was able to accomplish in the wild in 10^20 tries.”
   Michael Behe

   An Open Letter to Kenneth Miller and PZ Myers – Michael Behe July 21, 2014
   Dear Professors Miller and Myers,
   Talk is cheap. Let’s see your numbers.
   In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White’s straightforward estimate that — considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) — the development of chloroquine-resistance in malaria is an event of probability about 1 in 10^20 malaria-cell replications. Okay, if you don’t like that, what’s your estimate? Let’s see your numbers.,,,
   ,,, If you folks think that direct, parsimonious, rather obvious route to 1 in 10^20 isn’t reasonable, go ahead, calculate a different one, then tell us how much it matters, quantitatively. Posit whatever favorable or neutral mutations you want. Just make sure they’re consistent with the evidence in the literature (especially the rarity of resistance, the total number of cells available, and the demonstration by Summers et al. that a minimum of two specific mutations in PfCRT is needed for chloroquine transport). Tell us about the effects of other genes, or population structures, if you think they matter much, or let us know if you disagree for some reason with a reported literature result.
   Or, Ken, tell us how that ARMD phenotype you like to mention affects the math. Just make sure it all works out to around 1 in 10^20, or let us know why not.
   Everyone is looking forward to seeing your calculations. Please keep the rhetoric to a minimum.
   With all best wishes (especially to Professor Myers for a speedy recovery),
   Mike Behe
   http://www.evolutionnews.org/2.....88041.html