Big Lie Number 2 - Evolution is accepted fact - continued
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Another problem for macroevolution involves the nature and structure of life. In fact, the entire Darwinist narrative is missing a great deal of information:
1) Where did the Universe come from?
It just happened? There was nothing and then there was something
2) How did life begin?
It just happened? There wasn't life and then, voila, there was!
3) Where did the information come from?
It simply appeared out of nowhere.
Truly, the idea that the Universe just kind of happened by chance and that life just kind of happened by chance and that information just kind of happened by chance...does that sound like science?
INFORMATION
I've blogged a great deal about the lack of a logical explanation from a naturalistic point of view about the beginning of the Universe and the beginning of life itself. Sometimes Darwinists will complain that those are questions that predate the concept of evolution. Well, if you are a atheistic naturalistic materialist you will have to address those concepts at some point, but, okay, lets let those go for now. But then you come upon the problem of information.
All life has a great deal of information contained within. Rather than the generic "stuff" that scientists thought might comprise a typical cell, it is actually a wondrous array of micro-machines carrying out all sorts of processes, all run by coding in the DNA of the cell itself. It isn't just a matter of a blop of goo forming into the right shape and being zapped by a bolt of lightning, within that first supposed organism that began life has to be INFORMATION. Information is organized and precise and, in the case of a cell, if it is not correct the cell will not carry out functions properly and will likely die.
We've considered how unlikely it would be for a tornado to blow through a junkyard and assemble a 747. Yet, that scenario is more likely than the structure of a living cell simply happening out there in some puddle on a rock. But even if such a thing happened, it wouldn't be life. You see, a 747 needs fuel and electricity and crew members. It needs specific switches to be flipped and levers to be adjusted, pedals to be pushed, all sorts of operations in order for it to start up and taxi out to the runway and fly and then land. Not only would a tornado need to assemble a 747, it would have to assemble a crew and a school to send them to in order to learn to fly it and a staff of teachers to teach them and a source of power for the batteries to be charged and an entire oil company to pump up the crude oil and refine it into airplane fuel and transport it to the plane and of course it would have to have assembled a working fuel truck and a crew to design the airport and a work crew to lay out and pour the concrete for the airfield and...well, it just goes on and on.
Evolutionists have no explanation for where information, which is quite organized, may have come from. Without information, a cell is just a blop. Before we can even be awed by the incredibly intricate designs involved in a Paramecium or the remarkable series of systems involved in the process of Photosynthesis, we have to ask where the original information came from to run such things. Every living being, every process of that being, the very blueprint of every being that is DNA - all bear the hallmarks of being designed and all depend on very specific information.
MUTATION?
Could information have evolved? Did chaos mutate into information? Frankly, the idea is absurd on the face of it, is it not? We know that the Universe is running down, changing from order into disorder according to the Laws of Thermodynamics. For information to have taken the opposite path makes no sense, especially since Darwinists can show no means by which it may have occurred.
Incidently, you won't find any transitional forms in the fossil records, either. No race of animals with two-thirds of a working eye have been found in the fossils. No woodpeckers with half-formed tongues. No, when animals are found in the fossil record they appear to have fully-formed systems.
You will also not find macroevolution occurring in today's living creatures. All instances of change in the gene pool are either zero sum or losses of information. In order to have macroevolution you need gains in information, new information being added to the gene pool to form a new creature.
Neo-Darwinists will make claims that they have found something that supports their ideas in living organisms from time to time and then you never hear of it again because those claims always prove to be false. Let me give an example:
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"Gene duplications followed by subsequent mutation of the duplicated genes are often cited by evolutionists as a mechanism for adding new information to the genome and providing new functions to the organism. Over millions of years this is thought to lead from molecules to man. Sean Carroll, author of a recent article in Nature on gene duplication in yeast,1 states, “This is how new capabilities arise and new functions evolve. This is what goes on in butterflies and elephants and humans. It is evolution in action.”2 However, to my “surprise,” Carroll’s research showed exactly the opposite—the complete impotence of gene duplication and mutations as a force driving molecules-to-man evolution.
Investigating 100-million-year-old Events
Carroll and others studied the galactose use pathway in Saccharomyces cerevisiae, commonly known as baker’s yeast. This pathway enables yeast to metabolize the sugar galactose. S. cerevisiae is thought to have evolved from the yeast Kluyveromyces lactis 100 million years ago.1 Supposedly, the whole genome of K. lactis was duplicated—some of the duplicated genes were lost, and some were kept. This resulted in the formation of S. cerevisiae.
The focus of the research was two specific genes found in S. cerevisiae, GAL1 and GAL3, which code for proteins that function in the galactose use pathway. In the “ancestral” K. lactis one gene (called GAL1) serves the function of both GAL1 and GAL3. Carroll’s team believes that this is evidence of the past duplication event which led to S. cerevisiae.1
It is important to note that the two genes in S. cerevisiae do not perform any new or different function than the one gene in K. lactis. This has been observed in other studies of supposed gene duplications—rather than resulting in “neofunctionalization” (new functions) the result is “subfunctionalization” (dividing of the functions among two or more genes).1 A model that has been developed to account for this is called duplication-degeneration-complementation (DDC) and “. . . explains the preservation of duplicate genes by a neutral mechanism in which each paralogue [duplicated gene] accumulates loss-of-function mutations (degeneration) that are complemented by the other copy.”1
Let us look at an analogy to better understand this. Suppose I have a TV, and one day it loses the ability to produce sound, although it still has the ability to produce pictures. I go to a used TV shop and find the exact same make and model of TV as the one I have at home, though this one produces sound but not pictures. I purchase the broken TV, take it home, and put it beside my broken TV. The two broken TVs complement each other (they have different defects), and together make it possible for me to see the picture and hear the sound for any given TV program. However, my broken TVs are not doing anything new. So, obviously the DDC model is not sufficient alone for evolution to occur, since no new functions are being gained and this is a requirement for molecules-to-man evolution. Rather, DDC is seen as a first step to preserve the duplicated genes, as non-functional genes would not be selected for and are lost via genetic drift (just as most people would probably throw away the broken TVs).
The next step in this model is additional mutations that modify the genes so that they perform their current function “optimally” and eventually perform completely new functions (although the latter was not observed in the yeast study). DDC is thought to relieve an “adaptive conflict”.1 Genes (and their proteins) typically perform multiple functions (i.e. they may serve in multiple metabolic pathways, etc.). Thus, many mutations that might optimize one function of the gene would harm another function of the gene (the adaptive conflict), and so, the majority of mutations would be detrimental and selected against.
The situation resembles a stalemate in which the genes essentially do not change. Duplication resolves this conflict by allowing each duplicated gene to perform a singular function. The overall function of the genes in a given pathway is preserved, and now mutations in the genes can be selected for that will optimize that specific function. This supposedly happened in S. cerevisiae with the GAL1 and GAL3 genes (duplicate of the GAL1 gene in K. lactis), and this led to “. . . more complex and, in some ways, [a] more optimal genetic pathway.”1
Were You There?
Once again we have a classic case of circular reasoning. The scientists must assume evolution is true to claim that duplication events 100 million years ago led to the species S. cerevisiae, but then claim that these duplication events are evidence of “evolution in action.” It cannot be evidence for something if you must assume that something is already true to interpret the evidence!
The DDC Model and Creation
The DDC model by itself may potentially fit within a creation framework. The model encompasses mutations in genes that lead to loss of information and/or function. These mutations could potentially compensate for each other if this were occurring in two copies of the same gene. This would resemble a case where individuals are carriers for certain recessive genetic disorders: they have two copies for every gene (one from mom and one from dad); one copy is defective (mutations), and one is normal (no mutations). The normal gene compensates for the defective gene, and thus, the individual does not have the disease. Duplication of genes followed by compensatory mutations may be a mechanism for survival of organisms in a post-Fall world.
The problem comes with the next step, which involves mutations that supposedly lead to “optimization” of the singular functions of the genes (and eventually to new functions of the genes). Natural selection does not occur at the DNA (genotypic) level—only at the whole organism (phenotypic) level.3 The mutations in the duplicated genes would need to lead to proteins that significantly alter the fitness or survival of the whole organism. The article indicated that the fitness differences in the yeast studied were very small, requiring an extremely sensitive assay.1 Thus, it is likely that these “optimization” mutations would not accumulate and be lost by genetic drift.
Not “Evolution in Action”
What is clearly not shown in the article is evidence for molecules-to-man evolution. Instead, we observe just how powerless duplication and mutation really are for adding new information that leads to the gain of new functions. However, the authors of the article seem to think otherwise. Carroll states, “They [GAL1 and GAL3 in S. cerevisiae] became optimally connected in that job [their role in the galactose use pathway]. They’re working in cahoots, but together they are better at the job the ancestral gene held. Natural selection has taken one gene with two functions and sculpted an assembly line with two specialized genes.”2 The Nature article also states, “After whole-genome duplication, S. cerevisiae GAL1 and GAL3 were integrated into a more complex and, in some ways, more optimal genetic pathway.”1
These statements are a clear example of prejudicial conjecture on the part of the scientists and not based on fact. The terms optimal, better, and more complex are based solely on their conjecture or assumption that the more “advanced” S. cerevisiae evolved from the more “primitive” yeast K. lactis 100 million years ago. The preferred evolutionary scenario would seem to be just the opposite: S. cerevisiae would be the ancestor, since it requires two genes for the same job that K. lactis manages to do with just one gene.
Carroll states, “We retraced the steps of evolution.”2 “Retraced”? What they did was concoct an evolutionary scenario with which to interpret the data in order to get an evolutionary conclusion! Evolution infers a gain of new information and new functions. All of the mutations they think have occurred in the GAL1 and GAL3 genes in S. cerevisiae are loss of information and/or function mutations when compared to the GAL1 gene in K. lactis. They involve the loss of binding sites for proteins, the loss of enzymatic activity, and the loss of orientation of the binding sites. So, no new information, no new functions, and yeast are still yeast!
Carroll also states, “When compounded over time, these very small changes [that have led to the formation of GAL1 and GAL3 in S. cerevisiae] make one group of organisms successful and they out-compete others.”2 Within a creationist framework it is possible that K. lactis and S. cerevisiae are members of the same kind of yeast and that alterations (including duplications and mutations) occurred in the past leading to the formation of S. cerevisiae from K. lactis or vice versa. Both K. lactis and S. cerevisiae exist today; so, it may be that certain environmental conditions have led to their formation from each other.
The evidence seems to fit the creationist orchard model of variation within a kind while not supporting the evolutionary tree of life model of evolution from one kind to another. It is also possible that S. cerevisiae and K. lactis are representatives of different created kinds of yeast and that the genetic differences in GAL1 and GAL3 are merely part of the original created genetic diversity. Once again we are presented with evidence of God’s amazing design and provision in a post-Fall world for even some of the smallest members of His creation."
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Footnotes
Chris Todd Hittinger and Sean B. Carroll, “Gene Duplication and the Adaptive Evolution of a Classic Genetic Switch,” Nature 449 (2007): 677–682.
John Sanford, Genetic Entropy and the Mystery of the Genome (Lima, New York: Elim Publishing, 2005).
