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But what about the evidence, and more importantly, what about the quest for what the real truth may be? If we already "know", then you aren't going to learn much else. Sort of like the folks who go to church. They aren't "seeking" anything, they already have their answer.
I find it interesting as well that you'd use a religious source in a discussion regarding the validity of mystical mumbo-jumbo vs. hard science.
Absence of evidence is not evidence of absence in this case - just because we have not found the 'missing link' does not indicate taht there never was one.
In fact, rapid evolution is sometimes theorized to have occured many times in the past, which would account for lack of a 'smoking gun' in the example of monotremes.
Every creature was created according to its kind. Each kind was made such that its genetic code carried all that was needed for the startling variety seen in subsequent generations.
I wasn't using the terminology in a mocking fashion, for the record... I apologize if you saw it as such.
I also note that you have not responded to the use of a biased source for your information.
Regarding the 'lack of evidence' train of thought, there is considerably more evidence for evolutionary science as opposed to a 'creator'.
What amazes me is that no matter how much fossil evidence is uncovered, it's always disregarded because we cannot recover evidence for every single species. Fossilization doesn't occur frequently, the conditions required aren't exactly common. It simply makes no sense to believe that every living thing that ever existed can have recoverable fossils.
I'd be interested to see what evidence you've gathered in support of some intelligent creator who had the foresight to allow minor changes for adaptability, but wouldn't allow for maximum felxibility in mutation.
...Believe it or not, orthodox evolutionists have tried to explain all the staggering variation both within and among species on the basis of these random changes in heredity called "mutations." What we know about mutations, however, makes them entirely unsuitable as any "raw materials for evolutionary progress."
As Ayala says, mutations in fruit flies have produced "extremely short wings, deformed bristles, blindness and other serious defects." Such mutations impose an increasingly heavy genetic burden or genetic load on a species. In her genetics textbook, Anna Pai makes it clear that "the word load is used intentionally to imply some sort of burden" that drags down the genetic quality of a species.3 The list of human mutational disorders, or genetic diseases, for example, has already passed 1500, and it is continuing to grow.
By elimination of the unfit, natural selection reduces the harmful effects of mutations on a population, but it cannot solve the evolutionists genetic burden problem entirely. Most mutations are recessive. That is, like the hemophilia ("bleeder's disease") gene in England's Queen Victoria, the mutant can be carried, undetected by selection, in a person (or plant or animal) with a dominant gene that masks the mutant's effect.
Time, the usual "hero of the plot" for evolutionists, only makes genetic burden worse. As time goes on, existing mutants build up to a complex equilibrium point, and new mutations are continually occurring. That is why marriage among close relatives (e.g. Cain and his sister) posed no problem early in human history, even though now, thanks to the increase in mutational load with time, such marriages are considered most unwise. Already, 1% of all children born will require some professional help with genetic problems, and that percentage doubles in first-cousin marriages.
Genetic burden, then, becomes a staggering problem for evolutionists trying to explain the enormous adaptive variation within species on the basis of mutations. For any conceivable favorable mutation, a species must pay the price or bear the burden of more than 1000 harmful mutations of that gene. Against such a background of "genetic decay," any hypothetical favorable mutant in one gene would invariably be coupled to harmful changes in other genes. As mutational load increases with time, the survival of the species will be threatened as matings produce a greater percentage of offspring carrying serious genetic defects.1,3
As the source of adaptive variability, then, mutations (and orthodox evolution theories) fail completely. As a source of "negative variability," however, mutations serve only too well. Basing their thinking on what we observe of mutations and their net effect (genetic burden), creationists use mutations to help explain the existence of disease, genetic defects, and other examples of "negative variation" within species.
Mutations are "pathologic" (disease-causing) and only "modify what pre-exists," as French zoologist Pierre-Paul Grassé says, so mutations have "no final evolutionary effect."4 Instead, mutations point back to creation and to a corruption of the created order.
There are 40-plus variants of hemoglobin, for example. All are variants of hemoglobin; that points back to creation. All are less effective oxygen carriers than normal hemoglobin; that points back to a corruption of the created order by time and chance...
How do you explain that we share the majority of our genetics with any other creature on Earth ?
...According to some reports, we share half our genes with a banana (New Scientist, 1 July 2000, pp4-5)! ! Is this evidence for a common origin?
Since 1859 the phenomena of homology has been cited by evolutionary biologists as providing one of the most powerful lines of evidence for the concept of organic evolution and to this day, the phenomena of homology has remained a mainstay argument for evolution (Denton, 1986).
In biology, two or more structures are said to be homologous if they are alike. In traditional biological thinking homology of say bone structure in the limbs of different mammals is associated with assumed shared ancestry - see quote from Darwin below.
In genetics, homology is used in reference to similar (or otherwise, e.g. non-homologous) DNA sequences, and again the assumption tends to be that sequences that are homologous share ancestry. Homology can also be used to describe similar protein sequences.
A common example of genetic homology is that we share about 98% of our genes with apes or chimpanzees. This is discussed later and also on the video clip DNA: Human and chimpanzee DNA (1:23 mins)...
...Similarity (‘homology’) is not evidence for common ancestry (evolution) as against a common designer (creation). Think about a Porsche and Volkswagen ‘Beetle’ car. They both have air–cooled, flat, horizontally–opposed, 4–cylinder engines in the rear, independent suspension, two doors, boot (trunk) in the front, and many other similarities (‘homologies’). Why do these two very different cars have so many similarities? Because they had the same designer"! Taken from "Human/chimp DNA similarity".
Anatomical homology. A well know example of anatomical homology linked to macroevolution is that given by Darwin above, e.g. "What can be more curious than that the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise, and the wing of the bat, should all be constructed on the same pattern, and should include the same bones, in the same relative positions"? What Darwin is basically saying is Why do virtually all vertebrate forelimbs have the same basic "pentadactyl" (five fingered) design, if not due to evolution?
In his book Evolution, A Theory In Crisis, the author Dr Michael Denton devotes a complete chapter to homology and discussed this issue in depth. His arguments against anatomical homology being related to shared evolutionary ancestry are in part summarised as below, and also later, when considering the homology of Cytochrome C protein sequences between different species.
"One of the most commonly argued proofs of evolution is the pentadactyl limb pattern, i.e. the five-digit limbs found in amphibians, reptiles, birds and mammals. However, they develop in a completely different manner in amphibians and the other groups. To illustrate, the human embryo develops a thickening on the limb tip called the AER (apical ectodermal ridge), then programmed cell death (apoptosis) divides the AER into five regions that then develop into digits (fingers and toes). By contrast, in frogs, the digits grow outwards from buds as cells divide". From "Ostrich eggs break dino-to-bird theory".
Sir Gavin De Beer in his book Homology: An Unsolved Problem says "Homologous structures need not be controlled by identical genes and homology of phenotypes does not imply similarity of genotypes".
Darwin did not know about gene or protein sequences in his day, so he could not see further than the visible anatomical features. If the pentadactyl limb did have a common origin though amphibians to reptiles, birds and mammals, then one would expect that the same genes would code for this structure in all these different animal groups.
To investigate this subject in more depth, please follow some of the links at the bottom of this page such as The Invalidity of Morphological Homology, or read Michael Denton's book Evolution, A Theory In Crisis...