Vizion28 said:
In my years of study I have specifically focused on Evolutionists' claim that random mutations (coupled with natural selection) can turn a primordial cell to an ape in a few billion years. This is not scientifically supported, in fact science contradicts such a claim. For the sake of brevity I will just focus on this aspect of Evolutionary theory.
I will try to address most of your points. After reading several of them, I want to emphasize two points:
1) individuals do not evolve, populations do, and 2) evolutionary fitness is described by reproductive success, and not structural complexity.
Please keep these in mind as your read on. If you feel that I have missed anything, feel free to point it out. I implore, however, that you give my response the time I had given yours.
Most mutations are almost always deleterious or neutral to the organisms. That is why it is unbelievably silly to think mutations can be one of the mechanisms to get a primordial cell to an ape. Literally thousands of human diseases associated with genetic mutations have been catalogued in recent years, with more being described continually. A recent reference book of medical genetics listed some 4,500 different genetic diseases.
Yes, most mutations are deleterious (missense, nonsense) or neutral (silent). Severely deleterious mutations are either lethal, or render offspring infertile.
It is important to note, however, that neutral mutations can accumulate, and these form a basis of the available genetic material. Additionally, though beneficial mutations are rare, they exist. It would be just as silly, I would think, to dismiss the idea merely because it sounds foreign to you, and even more so if you are not completely familiar with it.
Let us go back to the idea of genetic diseases: of those how many categorized are both haploinsufficient and lethal before reproductive age? 4,500 plus observable genetic diseases is a surprising few given the tens of thousands genes we have.
Yes, there are some genetic mutations that may be beneficial for survival but still deleterious to the organism. For instance, the mutation responsible for sickle cell anemia has been put forward as an example of Evolution. The problems with this are obvious, as the sickle cell mutation, like the many other described hemoglobin mutations, clearly impairs the function of the otherwise marvelously well-designed hemoglobin molecule. It can in no way be regarded as an improvement in our species, even though its preservation is enhanced in malaria-endemic parts of central Africa by natural selection. But the mutation is nonetheless a loss of information. The hemoglobin's normal function is impaired, not improved, and the protection from malaria is simply an incidental side benefit the pathogen happens to be destroyed along with the person's own defective cells. This mutation does not introduce a new level of complexity; there is no new functional information or novel structural feature for evolution to build on. Considered in itself, this mutation is destructive and harmful, as are so many others. It is difficult to see how any genetic change of this sort could lead to a true evolutionary advance.
Evolution does not care about "improvement", and fitness is found not in structural complexity or wholeness, but
reproductive success. There was an incredible selective advantage for heterozygous carriers of sickle cell anemia. Compared to wild-type humans, they are able to reproduce, and more of their offspring can survive to reproduce in their given environment. That is all that matters.
As in the famous case of Theodosius Dobzhansky where he was bombarding fruit flies and moths with radiation in hope of mutating their DNA and producing improved creatures. These experiments were a total failure there were no observed improvements only weak, sickly, deformed fruit flies.
I admit that I am unfamiliar with the case, but there are some problems with using that as a case example: DNA is the mechanism through which evolution occurs, and placing it under such stress is like beating your mechanic and tearing up spare parts while he is fixing your car.
What can you expect? Well, generations of fruit flies, if exposed to moderate (nonlethal and nonsterilizing) amounts of radiation, may be adapted to reproduce in such an environment. They would look sickly, you say? Well, they're not dead; throw some wild-type flies in there after some generations and see how they fare in comparison.
If they die or cannot reproduce, then you have thrown them outside their possible range of tolerance. Sometimes populations of animals do not have the capability to sufficiently adapt to changing environments. which leads to extinction.
Random mutations are equivalent to noise, and noise only destroys information and degrades functionality. Ask any communications engineer - in the world of digital communication there is no example anywhere of adding noise to a signal and getting a better signal that contains more information and more functionality.
In Claude Shannon's information theory, noise is mathematically identical to entropy. Its damage to a signal is irreversible.
In other words mutations are a cause of degeneration not "upward evolution". In fact, we are "devolving". Genetic fitness is being reduced (entropy) every generation as mutations accumulate in the genome.
Again, the mutations that sufficiently 1) destroy information and 2) degrade functionality sufficiently tend to lead to nonviable offspring. List any functional organ in the human body, and we likely know of a more primitive, yet functional precursor. Do not expect evolution to do otherwise.
A signal is incorrect comparison because there is no ideal form, no specific image as to what an organism should be.
Scientists say it themselves:
<A lot of quotes.>
Forgive me if I do not address all the quotes individually. Please, select three at a time and I will discuss them at your leisure.
Michigan State University evolutionary biologists Richard Lenski and his colleagues searched for signs of evolution in bacteria for 20 years, tracking 40,000 generations. In the end, the species that they started with was hobbled by accumulated mutations, and the only changes that had occurred were degenerative. University of Bristol emeritus professor of bacteriology Alan Linton summarized the situation:
Is it the same Lenski, who, upon introducing groups of bacteria to a citrate solution, eventually yielded a population that could metabolize it? I see you address this later, but apparently the mutations were not all degenerative, were they?
But where is the experimental evidence? None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of 20 to 30 minutes, and populations achieved after 18 hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another, in spite of the fact that populations have been exposed to potent chemical and physical mutagens and that, uniquely, bacteria possess extrachromosomal, transmissible plasmids. Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic to eukaryotic cells, let alone throughout the whole array of higher multicellular organisms.
The definition of "species" is fairly eukaryote-biased, and the author fails to be cognizant of the idea that categorizations are a human tool to organize data. How many, and what type of changes would you like to see in a strain of bacteria before you call it a different species?
In a recent study, also published in Nature, University of California Irvine researcher Molly Burke led research into the genetic changes that occurred over the course of 600 fruit fly generations. The UCI lab had been breeding fruit flies since 1991, separating fast growers with short life spans from slow growers with longer life spans.
The UCI scientists compared the DNA sequences affecting fruit fly growth and longevity between the two groups. After the equivalent of 12,000 years of human evolution, the fruit flies showed surprisingly few differences.
I am not familiar with the paper in question, but longevity is likely a multifactorial trait. And of course, "few" does not mean "none."
One requirement for Darwin's theory is that the mutational changes that supposedly fuel evolution somehow have to be "fixed" into the population. Otherwise, the DNA changes quickly drift right back out of the population. The researchers found no evidence that mutational changes relevant to longevity had been fixed into the fruit fly populations.
The study's authors wrote, "In our sexual populations, adaptation is not associated with 'classic' sweeps whereby newly arising, unconditionally advantageous mutations become fixed."
They suggested that perhaps there has not been enough time for the relevant mutations to have become fixed. They also suggested an alternativethat natural selection could be acting on already existing variations. But this is not evolution, and it is actually what creation studies have been demonstrating for many years.
You are looking for an instance of a fixed gene in a multifactorial trait. Glossing over UCI's article, it appears they did find some 500 genes associated with the trait for rapid development, but not all 500 are required. Given the genetic complexity of this vague trait, how can you expect any given one to be completely fixed?
Evolution was not observed in fruit fly genetic manipulations in 1980, nor has it been observed in decades-long multigenerational studies of bacteria and fruit flies. The experiments only showed that these creatures have practical limits to the amount of genetic change they can tolerate. When those limits are breached, the creatures don't evolvethey just die.
Evolution: the change in allele frequencies over time. Have allele frequencies changed?
Although the experimental results from these studies were given titles with an evolutionary "spin," the actual experiments demonstrate undoubtedly that bacteria and fruit flies were created, not evolved.
http://www.icr.org/article/5779/
One example I come across on the internet of random mutations adding a new function of an organism is Lenskis supposed evolution of the citrate ability for the E-Coli bacteria after 20,000 generations of the E-Coli:
Multiple Mutations Needed for E. Coli Michael Behe
Excerpt: As Lenski put it, The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions. (1) Other workers (cited by Lenski) in the past several decades have also identified mutant E. coli that could use citrate as a food source. In one instance the mutation wasnt tracked down. (2) In another instance a protein coded by a gene called citT, which normally transports citrate in the absence of oxygen, was overexpressed. (3) The overexpressed protein allowed E. coli to grow on citrate in the presence of oxygen. It seems likely that Lenskis mutant will turn out to be either this gene or another of the bacteriums citrate-using genes, tweaked a bit to allow it to transport citrate in the presence of oxygen. (He hasnt yet tracked down the mutation.),,, If Lenskis results are about the best weve seen evolution do, then theres no reason to believe evolution could produce many of the complex biological features we see in the cell.
http://behe.uncommondescent.com/page/3/
I am not sure what Behe expects: evolution builds on what exists, and doesn't bow to some irrational human demand for complete novelty.
Lenskis e-coli Analysis of Genetic Entropy
Excerpt: Mutants of E. coli obtained after 20,000 generations at 37°C were less fit than the wild-type strain when cultivated at either 20°C or 42°C. Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates. Such a reduction can be beneficially selected only as long as the organism remains in that constant environment. Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment.
http://www.answersingenesis.org/articles/aid/v4/n1/beneficial-mutation s-in-bacteria
Fitness is only relevant to reproduction, and reproduction was only relevant in that given environment. The fact that they were less fit at 20C or 40C is equivalent to saying dolphins are less fit than humans on land.
New Work by Richard Lenski:
Excerpt: Interestingly, in this paper they report that the E. coli strain became a mutator. That means it lost at least some of its ability to repair its DNA, so mutations are accumulating now at a rate about seventy times faster than normal.
http://www.evolutionnews.org/2009/10/new_work_by_richard_lenski027101. html
In reality there is no "evolution". The mutant E. coli had reduced fitness. How can a mutation which results in reduced fitness be held as an example of random mutations involved in "upward evolution"?
Fitness: an individual's ability to propagate its genes. Nothing else. See above.
Another example used by evolutionists as "evolution" caused by random mutations are microorganisms attaining resistance to antibioitics.
Dr. Lee Spetner, author of Not By Chance:
Some microorganisms are endowed with genes that grant resistance to these antibiotics. This resistance can take the form of degrading the antibiotic molecule or of ejecting it from the cell... [T]he organisms having these genes can transfer them to other bacteria making them resistant as well. Although the resistance mechanisms are specific to a particular antibiotic, most pathogenic bacteria have... succeeded in accumulating several sets of genes granting them resistance to a variety of antibiotics.
The acquisition of antibiotic resistance in this manner... is not the kind that can serve as a prototype for the mutations needed to account for Evolution
The genetic changes that could illustrate the theory must not only add information to the bacterium's genome, they must add new information to the biocosm. The horizontal transfer of genes only spreads around genes that are already in some species
... [A] microorganism can sometimes acquire resistance to an antibiotic through a random substitution of a single nucleotide... Streptomycin, which was discovered by Selman Waksman and Albert Schatz and first reported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. But although the mutation they undergo in the process is beneficial to the microorganism in the presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed by NDT [Neo-Darwinian Theory]. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and degrades its molecular match with the antibiotic molecule.
This change in the surface of the microorganism's ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution
cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.
"To sum up, a mutation impinging on a bacterium's ribosome makes that bacterium resistant to streptomycin. The reason for this is the "decomposition" of the ribosome by mutation. That is, no new genetic information is added to the bacterium. On the contrary, the structure of the ribosome is decomposed, that is to say, the bacterium becomes "disabled." (Also, it has been discovered that the ribosome of the mutated bacterium is less functional than that of a normal bacterium.) Since this "disability" prevents the antibiotic from attaching onto the ribosome, "antibiotic resistance" develops."
"...there is no example of mutation that "develops the genetic information." Evolutionists, who want to present antibiotic resistance as evidence for evolution, treat the issue in a very superficial way and are thus mistaken."
In adapting to sudden changes in environment, selection favors those that can survive and reproduce in the short term. In an analogy, if you needed to do long division in five minutes or die, would you build a calculator or grab a paper and pencil? Likewise, the genetic material of the bacteria has no cognition: a random deleterious mutation, which would have otherwise been disadvantageous in the natural environment, is suddenly the phenotype that is able to resist a sudden change in environment.