Did I miss the part where you presented any mathematical …

Comment on The Adventist Accrediting Association to Approve LSU’s Accreditation by Sean Pitman.

Did I miss the part where you presented any mathematical analysis or evidence of any kind for your evolutionary mechanism actually working at various levels of functional complexity? – as in systems that require a minimum of more than 1000 specifically arranged amino acid residues? vs. those that require, say, less than 200?

You continually present low-level examples of evolution like that somehow means something when it comes to explaining evolution beyond these low-level examples. It’s like arguing that since evolution between 3-letter words is easy it should be just easy to evolve between Shakespearean sonnets via function-based selection mechanisms.

cat-hat-bat-bid-did-dig-dog

This is easy because the ratio between meaningful vs. meaningless 3-letter sequences in the English language is about 1:18

However, when you’re talking about evolving something on the level of Dawkins’ “Methinks it is like a weasel” phrase, that’s not nearly as easy to do via any function-based algorithm because the ratio between meaningful vs. meaningless sequences at this length is truly miniscule. Do you not see this as a problem for the evolutionary algorithm?

You don’t seem to understand the exponential nature of the problem involved with your assertions for the creative potential of this mechanism of RM/NS. Each step up the ladder of functional complexity is exponentially more difficult to realize than the step that came before…

But, perhaps you’re too blinded by your confirmation bias and your chosen Darwinian fundamentalist heritage to consider such things in any real detail. Specifically, regarding your most current argument:

If after conceding that you believe that the evolution of all species from 2 of a kind occurred in a period 4000 years by a process of natural selection and random mutation,

What I said is that low-level allelic changes can be realized within a gene pool in very short order. The number of allelic options in the modern dog gene pool, for example, could easily be realized in just a few thousand years starting with just 2 individuals. The vast majority of these allelic changes only deal with quantitative functional differences, not qualitatively new traits. And, those traits that are qualitatively new are only based on novel systems that require no more than a few hundred specifically arranged amino acid residues. There simply are no examples of evolution in action that produce any qualitatively novel system that requires more than 1000 specifically arranged amino acids to function.

Consider something like the multi-protein rotary bacterial flagellar system. This system requires a minimum of over 5000 specifically coded residue positions, all working in a specific 3D arrangement relative to each other, to function. No such system has ever been shown to evolve. There’s not a single example in all of literature of such a thing. Not one. why not? Because of the odds, that’s why. The odds of the evolution of any system at this level of functional complexity, from any other pre-existing subsystems of any size or complexity, is extremely unlikely this side of trillions upon trillions of years of time.

that deleterious mutations in simpler species are removed by a process of natural selection,

This is most certainly true because the “simpler species” you reference have a very high reproductive/death rate… much much higher than can be tolerated by humans or any other mammalian species for instance. You still don’t grasp the concept that natural selection works through a mechanism of death before reproduction. Without death before reproduction natural selection cannot work at all. The greater this death rate, the more effective natural selection can be at removing deleterious mutations from the gene pool. Of course, this means that as the detrimental mutation rate increases in a linear manner, the required death rate needed to keep up increases exponentially (by 1 – e^-U where U is the detrimental mutation rate).

that our immune system is completely dependent on a process of natural selection from randomly produced diversity

Do you not understand how the immune system works? Let me present a few key facts for you just in case:

Each educated T-cell (that has already been taught not to attack “self” antigens) has only one type of receptor so only one specific non-self antigen can be recognized. But, how many possible antigens are there? “The total number of possible epitopes is, therefore, 20^B since there are 20 different amino acids.” Well, the typical length of an antigen epitope (“B” in the preceding formula) is about 20 amino acid residues. So, the total number of possible antigen epitopes is about 20^20 or 104,857,600,000,000,000,000,000,000 or ~100 trillion trillion.

Since there are so many trillions of different possible antigen epitopes, how does one’s immune system cope with such a variety of potential enemies? Well, there are many immune cells produced by the body. In humans, in particular, about 10^12 lymphocytes are present at any given time.

Not all the T-cells have different Y-shaped receptors, but many of them do. They have been pre-programmed to recognize a relatively large section of antigen “sequence space”. Therefore, the odds are very good that if enough non-self enemies get into the body that at least one of the immune cells will recognize the non-self marker sequences or “antigens” located on this invader as “foreign” to at least some useful degree. The odds that a single T-cell will recognize a random epitope to at least some useful degree is about 1 in 10^12. So, does this mean it would take a trillion different T-cells to cover all possible invaders? Well, no. The reason is because an average cell or foreign invader “bug” has about 10^12 different antigen epitopes. So, on average, a single T-cell will recognize at least one of the potential antigen epitopes of a foreign invader.

When this happens this particular T-cell sounds the alarm that the body has been invaded. Other immune cells, called B-cells, are also activated, but only those that specifically produce antibodies that have a pretty good match to the foreign antigen epitope expressed by the invading organism. The invader, with its non-self antigens, is attacked. However, if only a few immune cells recognize the invader upon initial exposure, the initial attack might be rather weak. The resulting sickness may linger on for some time before the body can kill off the offending invader. The good thing is that the immune system remembers this particular invader for the future so it can kill the invader more quickly if it ever sees its particular antigen marker again. But how does this memory work?

The B-cell that recognized the foreign antigen clones itself to make many nearly identical copies of itself – with slight variations. Now, there are many B-cells that will recognize this particular foreign antigen. If infected again by an invader with this particular antigen, the immune system is ready and produces many more specific antibodies than before. This kills the invader much more quickly – making the body “immune” to this particular bug.

So, you see, this is not an example of high-level evolution. It is only evolution within a sequence space size of 20aa or so… a sequence space that is easily covered by the immune system because of its relatively small size.

http://www.detectingdesign.com/immunesystem.html

its seems inconceivable that you would not understand why natural selection as a process has potency as a underlying premise of modern biology.

Natural selection does indeed have very strong potency when it comes to producing low-level functional changes. However, as already explained many times, this mechanism loses its potency, in an exponential manner, with each step up the ladder of functional complexity. You simply refuse to grasp this concept because of your preferred evolutionary bias. Otherwise, this concept is very simple and downright obvious.

You are simply inescapably captured by confirmation bias contingent on your fundamentalist heritage.

You’re the one with confirmation bias that prevents you from even trying to consider evolution beyond the lowest levels of functional complexity. You have no examples. You have no statistical argument. You have no science here.

Sean Pitman
www.DetectingDesign.com

Sean Pitman Also Commented

The Adventist Accrediting Association to Approve LSU’s Accreditation
This is the same language used by the Bible. Whatever “wiggle room” the Bible leaves open is still open when one uses this language. The Bible is not clear that the “creation of the heavens and the earth” means that the material of the Earth itself was created during creation week. Quite the opposite is true. The Bible seems to suggest that something was here prior to creation week. Or, at the very least, leaves this question open.


The Adventist Accrediting Association to Approve LSU’s Accreditation
Oh please. You do realize that there are difference kinds of “heavens” in Hebrew understanding? This is not a statement arguing that God made the entire universe…


The Adventist Accrediting Association to Approve LSU’s Accreditation
The question is if you or anyone else has even tried to explain how the evolutionary mechanism (RM/NS) can tenably work beyond very very low levels of functional complexity. The answer to that question is no. This means that this mechanism is not backed up by what anyone would call real science. It’s just-so story telling. That’s it. There is nothing in scientific literature detailing the statistical odds of RM/NS working at various levels of functional complexity. And, there is no demonstration beyond systems that require a few hundred averagely specified residues.

What is interesting is that no one who controls the mainstream journals will publish any observations as to why a real scientific basis for the Darwinian mechanism is lacking. The basic information is there. Contrary to Pauluc’s claims, a precise definition of “levels of functional complexity” has been published, along with what happens to the ratios of potential beneficial vs. non-benficial sequences. What no one is allowing to be published is the implications of this information.

Regardless, the implications should be clear to you. The math is overwhelmingly clear. If the ratio of beneficial vs. non-beneficial goes from 1 in 100 to 1 in 1,000,000,000,000 the fact that the average time to success will decrease quite dramatically doesn’t take a rocket scientist to figure out. Evolutionists, who have actually seriously considered this problem must recognize the implications here, but seem to be trying to brush it all under the rug because no one knows of any other viable mechanism (again, despite Pauluc’s unsupported claims to the contrary – to include his “life enzymes”).

In any case, it is possible for you to move beyond blind faith in the unsupported claims of your “experts” and consider the information that is available to all for yourself. Start at least trying to do a little math on your own and you will no doubt recognize the problem for yourself regardless of what your experts continue to claim – without any basis in empirical evidence or science.

Sean Pitman
www.DetectingDesign.com


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