Has E. coli evolved in 31,500 generations?
BQ: In "The Greatest Show on Earth: The Evidence for Evolution," Richard Dawkins claims evidence for totally new, useful genetic information within DNA of an organism based on a study of 31,500 generations of E. coli bacteria. What is significant about this?
A: In the experiment, E. coli incurred a mutation which allowed them to process citrate ("Historical Contingency and the Evolution of a Key Innovation in an Experimental Population of Escherichia coli," Z. Blount, C. Borland, R. Lenski, Proceedings of the National Academy of Science), something that the original generation did not do.
In order for evolution to be true, it must overcome genetic entropy through the addition of novel genetic information, which Dawkins claimed happened in the experiment. However, the above mentioned scientists concluded that there were two possible explanations for what happened: a once-functional transporter gene already silenced by previous mutations was activated due to the selective, intelligent pressure (sans the gene, survival and reproduction were impossible) by the researchers, or, more likely, "an existing transporter was co-opted for citrate transport."
Both of these mechanisms use EXISTING genetic information. That is, they do not create new information at all within a genome. There is no evidence for evolution creating new information, and, even ignoring deleterious mutations, mutation/selection cannot even a single gene "within the evolutionary time scale." When deleterious mutations are factored in, we can see that a new gene cannot ever be created.
Dawkins tries to convince people that evolution creates new information, but his one, lone example, as it turns out, is nothing more than him trying to pull the wool over people's eyes.
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"For the entire Law is fulfilled in in this one word: "You shall love your neighbor as yourself."—Gal 5:14
Filtering by Tag: natural selection
Evolutionary cognitive dissonance.
Evolutionary admissions.
BQ: Today marks our last look at genetics for some time. I'd like to look at a few quotes from atheistic scientists and let them stand as they are.
F. Hoyle, a noted atheist, theoretical mathematician, and physicist, said, "...statements one frequently hears, to the effect that the Darwinian theory is as obvious as the Earth going round the Sun, are either expressions of almost incredible naivete or they are deceptions...with such widespread evidence of senescence [aging, destructively of the genome in this case—Lucas] in the world around us, it still seems amazing that so many people thing it is "obvious" that the biological system as a whole should be headed in the opposite direction."
Howell, a noted geneticist, used a mitochodrial mutational rate of .1-1.0, while our overall mutation rate is in the 100.00s to 1000.00s. He said, "We should increase our attention to the broader questions of how (or whether) organisms can tolerate, in the sense of evolution, a genetic system with such a high mutational burden."
Loewe, looking at mutations in only 1/200,000th of the genome, wrote, "A surprisingly large range of biologically realistic parameter combinations should have led to extinction of the evolutionary line leading to humans within 20 million years..."
Evolution is taught primarily from a philosophical, pseudo-scientific perspective. Why? Because the empirical evidence isn't the sort of thing you'd want in a textbook where evolution is being declared a "fact." The science is strictly against it.
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Possible objections to genetic entropy. (1-2)
Possible Objection I: Mega-beneficial mutations.
BQ: We are going to look at some "solutions" to the evolutionary paradox of genetic entropy. It is also correct to refer to these as "objections" to the entropy of our genome. The first objection is, "what about mega-beneficial mutations? What is one mutation was so strongly positive that it counteracted the harmful mutations?"
There are a variety of reasons why this objection fails to hold water, but I'll just provide two very short answers. First, it is true that one mutation can absolutely kill an individual. However, that's not the way beneficial mutations work, as we've seen before. It's like walking up a mountainside. You can trip and fall forward a couple of steps, but you won't fall all the way to the top. However, one slip can surely send you tumbling down a ways, if not to your death.
Second, that's not the way math or the genome works. If, say, the 100 good mutation can allegedly overcome 30,000,000 bad ones in, say, 3 billion nucleotides, we get a mathematical error. It's not possible to substitute a few mega-beneficial mutations for millions of others. Otherwise, we could have a genome as good as the human's 6 billion nucleotides but less than 1% of the length. This is not the way data/information works. It's like trying to improve a book by deleting 1000 words for every "super-awesome" word you write.
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Possible Objection 2: The failure of the primary axiom is no biggie.
BQ: Genetic entropy really wraps up almost all arguments. Since it is so fundamental to evolution, it MUST be overcome in order for a question to be valid. While I considered doing multiple questions from sites like atheistresources, ultimately they would be refuted by everything we covered so far. In order to avoid rehashing old proofs, we're going to look at what amounts to a "brush-off." It is stated as:
"The failure of the primary axiom (mutations+natural selection=progressive evolution) is not a serious challenge to evolutionary thought. Does it REALLY matter if this axiom is flawed? It's just one of numerous proposals and mechanisms for what we KNOW is true. We just need some time and we'll work out these kinks and evolution will be as factual as it has always been."
This statement amounts to damage control and is false.
1.) Mutation/selection is the ONLY evolutionary mechanism. Period. Random drift is chaos. Since genetic entropy refutes it, all of progressive evolution must fall with it.
2.) Darwin did not have knowledge of molecular biology. He had no idea what was actually being "selected." He stridently advanced what was in therefore in effect a philosophical position.
3.) Degeneration is the antithesis of evolutionary theory, and it is demonstrably what defines our DNA and our destiny. It is 100% fatal for Darwinism. The null hypothesis of intelligent design is evolution. To disprove progressive evolution is to strongly support intelligent design.
This objection is like trying to fix a severed femoral artery with a Band-Aid.
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Genetic entropy's impact on evolution. (1-6)
Admissions of secular scientists 1: Millions of kids.
BQ: Stephen Gould quoted Thayer who said that natural selection was "pure, simple, and omnipotent." It is not necessary to believe in God to have a god to whom one submits. Richard Dawkins once said, "“The majority of children born into the world tend to inherit the beliefs of their parents, and that to me is one of the most regrettable facts of them all.” I absolutely agree with Dawkins in that regard. Atheists mostly remain atheists, Mormons mostly remain Mormons (I think!), etc. It is also true that evolutionists mostly remain evolutionists, even if they go to strange lengths to fabricate workable scenarios to get life to exist. (See F. Hoyle and R. Dawkins for further...)
We've been looking at what has become a god to many people, but we're going to look at statements from people who are researching their god, all of whom are leading geneticists, and all of whom are finding problems with it, yet ignoring the evidence of the man behind the curtain because, "it must be true." It is the same problem that Dawkins mentions, and it is valid.
Today, we look at M. Kimura who wrote about the number of offspring that would be needed for a population to maintain genetic stability. Kimura, an atheist, said, "under the assumption that the majority of mutation substitutions at the molecular level are carried out by positive selection...to maintain the same population number and still carry out mutant substitutions...each parent must leave...3.27 million offspring to survive and reproduce." (Evolutionary rate at the molecular level.)
Kimura realized that selection must occur slowly, unlike the way evolution is still taught today, and that it was very limited in how much it could affect at one time. He was able to calculate the absurdity of what we'd need to survive—over 3 million kids per parent! Yet instead of re-evaluating whether or not evolution was true, he decided to believe that most genetic information must be irrelevant. Read the quote by Dawkins again, because Dawkins got it right.
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Admissions of secular scientists 2: Muller's fear.
BQ: Today we look at "Muller's fear," which later led to "Muller's ratchet," a massive problem for evolutionary theory. In, "Our load of mutations," Muller writes about the evolution of man. Pay careful attention. Muller didn't know it, but his calculation of mutation rates were only 1/1000th of the actual value. Look at he describes us and our evolution.
"It would mean an ever heaping up of mutant genes...degradation into utterly unrecognizable forms, differing chaotically [from person to person]...it would in the end be far easier and more sensible to manufacture a complete man de novo, out of appropriately chosen raw materials, than to try to fashion into human form those pitiful relics which remained. For all of them would differ inordinately from one another, and each would present a whole series of most intricate research problems...if then the eliminated 10% failed involuntarily....the remaining 80%, although they contrived to reproduce would on the whole differ from the doomed filth but slightly....practically all of them would have been sure failures under primitive conditions."
Muller went on to point out that, were the mutation rate any higher than his calculation (which it is, because he was off by a thousand-fold), primitive man would never have evolved, but instead died off completely. So, dear reader, know that you are nothing but doomed filth, as admitted by Muller, and you allegedly came from a being that had only one scientific option: dying off. Muller later went on to discover "Muller's ratchet," which discerned that mutation-load was going in only one direction: vastly up. He was careful not to make any statement that would impact the "certainty of evolution," yet his counter-evolutionary discoveries disturbed him greatly.
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Admissions of secular scientists 3: Kondrashov's question.
BQ: In one paper, geneticist A. Kondrashov wrote, "Why have we not died 100 times over?" In fact, Kondrashov's question was an after-the-colon section of his research's title. He said, "I interpret the results in terms of the whole genome and show, in agreement with Tachida (1990), that VSDMs (very slight deleterious/harmful mutations)can cause too high a mutation load....conditions under which the load may be paradoxically high are quite realistic."
He went on to mention the paradox mentioned by others, such as Chetverikov, that indicates our genetic destiny is...death of the species (a paradox for an evolutionist). He also says, "accumulation of VSDMs in a lineage...acts like a time bomb...the existence of vertebrate lineages...should be limited to 10^6-10^7 generations.
Kondrashov came up for a theoretical answer, which he called "synergistic epistasis." We'll discuss that tomorrow.
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Admissions of secular scientists 4: Synergistic epistasis to the rescue.
BQ: Kondrashov realized that, if we have existed for millions of years, we'd all be extinct due to an accumulation of harmful mutations. Harmful mutations, as it turned out, couldn't be selected away, and also outnumbered good mutations by an unthinkable amount. Kondrashov set out to "make evolution work" again. His "solution" was primarily synergistic epistasis. Synergistic epistasis (SE) is a phenomenon where the combined effect of mutations is greater than the sum of the individual mutations. Basically, he wanted the math for the good mutations to be 1+1=28, which could theoretically propel evolution forward.
This is obviously a good situation for beneficial mutations, but very bad for harmful ones. In harmful mutations, it can result in "synthetic lethality," a state where the combined effects of several deleterious mutations are potentiated by each other, resulting in such a bad effect that it kills the organism. Evolution needs SE to happen ONLY in beneficial mutations (keep the ratio of good-to-bad in mind), because if it happens in bad mutations, evolution is kaput.
Two recent studies have investigated the effects that beneficial mutations have on each other and both came to the same conclusion. The studies used E. coli and M. extorquens and were independent. Both studies proved the exact opposite of what Kondrashov said. That is, instead of SE occurring, a state called "antagonistic epistasis" (AE) happens. Under AE, beneficial mutations have math like this: 1+1=1/16th. That is, they have a negative impact on each other when found together. Furthermore, the only synergistic epistasis that has been shown to occur...happens in harmful mutations! Ouch!
Unfortunately, there is no way to overcome the slow but sure corruption of our DNA. Tomorrow we will look at "improvements" found in the studies mentioned above.
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Admissions of secular scientists 5: Impacts of Kondrashov’s false assumption.
BQ: Dr. J. Sanford, a geneticist, questioned Kondashov about "synergistic epistasis," but Kondrashov was willing to believe that something MUST be mysteriously overriding all the evidence that even he had discovered. As S. Doyle said, "Evolution thus has three strikes against it: most mutations are not beneficial, practically all mutations destroy specified complexity, and, now, even ‘beneficial’ mutations work against each other," and, "Mutations not only have to be beneficial, but they have to add biological information, i.e. specified complexity. However, practically all beneficial mutations observed have been losses of specified complexity , with only a few disputable examples of mutations increasing information ever found (e.g. bacteria that digest nylon, citrate or xylitol)."
The bacteria he mentioned were noted as "evolving" and being able to process another chemical in response to an artificially-controlled, hostile environment. These mutations were listed as being beneficial. However, they were not "novel." That is, they did not make new genes, but rather switched "on" part of an existing gene that was previously "off." No new information was ever added.
But in what setting were these mutations "beneficial?" In every environment, or just the hostile, controlled lab environment? As it turned out, in the "wild," the "evolved" bacteria was out-competed by it's "unevolved" relatives. That would be, to an evolutionist, the same as chimps being evolutionarily superior to humans!
In another experiment, the bacteria were already engineered by humans with splices from another species, so the difference wasn't analogous in the first place. Furthermore, specified complexity was lost, and the new bacteria grew far slower and was not competitive outside of their artificial environment. The studies reflected the consistent finding that lab-"evolved" populations experience a rapid deceleration of the rate of fitness increase.
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Admissions of secular scientists 6: Truncation selection.
BQ: In order to counter the evidence (which he had himself confirmed to be true), Kondrashov appealed to synergistic epistasis as a potential cure-all. We have seen that research now shows that what Kondrashov hoped would "fix" evolution not only doesn't exist, but in fact, the exact opposite is true! However, Kondrashov also hoped that "truncation selection" might be a fix for evolution.
In truncation selection, breeders use artificial selection methods. They select only the best organisms for breeding and remove the undesirables from breeding. This is done with certainty. However, and Kondrashov must know this, this does not exist in nature outside of a few very rare circumstances. (Bacteria in the presence of antibiotics.)
Furthermore, truncation selection causes long-term negative health impacts. This is the reason that purebred dogs usually have shorter lifespans than ones that are not purebred, and why mating a purebred with a non-purebred produces a state in the offspring called "hybrid vigor." Truncation selection improves certain traits immediately, but reduces long-term viability.
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Implications of genetic entropy. (1-3)
Implications 1: Genesis and decay. (See Figure 8)
BQ: Using everything we've learned about genetics, we're going ask, "What are some important implications of genetic entropy?" Well, we have seen that molecular evidence is 180 degrees off from evolutionary theory. Instead, as we go backward in time, useful information increases, and harmful mutations decrease.
Remember how we see improvements as we go back in time instead of forward? In the Bible, people in old testament times were recorded as having longer life spans the further back in history one looked. Holladay and Watt ran numerical simulations on the listed ages of these people vs. the dates the timelines compute to, and found that there was an exponential decay curve in lifespans. The correlation coefficient with Biblical data was shockingly close (.94), and the formula of best fit was y=386.6835(e^-0.00462214x)+70.065.
This is unexpected and amazing because it is a biological decay curve. Either the data was recorded faithfully by the writer of Genesis, or he fabricated the info using advanced mathematics and a desire to show exponential decay. But why would someone want to show such a decay curve, especially without knowledge of genetics and mutations, and with no understanding of such advanced math? Is this an elaborate, stone-age fraud? Given that no reason is given for listing the numbers in the Bible, and the impossibility of someone at time having that sort of foreknowledge, it can't be be a fraud. Empirical evidence supports genetic entropy, while philosophical hand-waving about natural selection presents nothing. I'll leave the conclusion up to you—why does the Bible model genetic entropy in the same way that our molecular makeup does?
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Figure 8
Implications 2: Size of the genome.
BQ: In our look at the implications of genetic entropy, we can see that we have a problem: mutations accumulate at a rate of 600-6000 per generation. But wait, we have 6 billion nucleotides, so losing one ten-millionth of our information per generation isn't that bad, is it?
Well, as it turns out, out genome is much like a computer program. Computer programs can be millions and billions of bytes in size, yet can fail because of a single error. Much like like us, most sturdy programs can continue to function even with multiple errors. Luckily for us, our genome is incredibly robust and able to withstand many, many errors. However, in the evolutionary timespan since we allegedly evolved from chimps, we would have accumulated a minimum of 90,000,000 errors. It is inconceivable that we would still be functional with a 3% data loss in the genome.
Like any information, there must be an engineer/designer for it, and also like any information, it WILL decay. Consider the Chinese telephone game you played when you were a child: as the whisper was passed down the line, it was changed, and the net information was lost and distorted.
The very existence of the genome is a mystery in evolutionary terms. Information and polyfunctional complexity which far surpass our ability to understand are programmed into space impossible to see with the naked eye. It should be obvious that our genome did not arise spontaneously, which leads to only one conclusion: it is an engineered masterpiece. The engineer has been known since ancient times. He has written the book using genetic language of who we are. It is perfect in every sense to see Acts 3:15 describe Him as "the Author of life," as that is exactly what He is.
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Implications 3: The Titanic is doomed.
BQ: The messages on genetics so far have been two-fold, but a major portion of them focus on the fact that we are on board a sinking ship. It is horrific to think that every species is eroding away, like a sand castle on a beach, a beautiful creation that is slowly losing its form. Yet it is necessary to KNOW the bad news in order to know how to respond.
So how does someone respond? If the evidence is ignored, there is only one response: death and decay. Morality becomes meaningless other than to live physically a little bit longer, to avoid an early death. If your hope is in a sinking ship, your best response is merely to be on the last part that sinks.
But if the logical evidence is followed, and if you recognize that there is an "Author of life," as Acts 3:15 states, suddenly there is a lifeboat! There is no need to go down with the sinking ship. You see, apart from Jesus, there is no hope. There is only the inevitability of death. Science and physics cannot conquer it, but rather ensure it. Yet God made you alive. He made the heavens and the earth in the first place, so He can make you alive again, and when He promises a new heaven and new earth, He is able to meet that promise. Because He rose from the dead, we can also have that hope. And apart from that, there is no hope.
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Can natural selection create novel genetic info? (Pt 8-11)
Can natural selection create: Part 8: Irreducibly complex. (See Figure 6)
BQ: We recall from our recent line of questioning that being irreducibly complex means that a particular item needs all of its parts to function, like a mousetrap that, missing any single part, simply does not function at all.
There is a counter-proposition that each part functions quite well as something else if we take the mousetrap apart. One scientist explained that all the parts of the mousetrap could be used as various things—a hook, a paperweight, etc.—and then happen to come together at the same time in a synergistic evolutionary co-opting. For some, this seems like the needed answer! Tthese parts can do other things! But looking at the idea holistically, it quickly becomes apparent that it's an appeal to, well, making an infinite number of fairy tales. "Perhaps this did this, this thing did this, and this did...and then BAM, they all became one." From our previous look at poly-functional DNA and other concerns, we can now soundly refute this sort of idea. It doesn't work that way in genetics, and it doesn't even work that way with a mousetrap! Furthermore, that proposition still requires simultaneous synthesis, which is the problem in the first place.
So let's think about an old example we used of a red wagon, which has a limited number of parts. We were hand-copying instruction manuals (DNA), and seeing if the wagon would ever become a space shuttle over billions of years of hand-copying and keeping only the best instruction manuals to copy from each time. It didn't of course, even with intelligence thrown in. But what if we delete a wheel on accident and make a tricycle? Well a 3-wheeled wagon is not a tricycle, it's simply a broken wagon! This is the problem of irreducible complexity: as complexity increases, the need for intermediary forms would require massive reworking of the instruction manual (GENEtic code) and component parts.
Now let's consider a gene. A single gene has about 50,000 component parts! That's more than a car, and yet we can't create a linear path to make a car piece-by-piece, with each stage doing something USEFUL. For example, a pitman arm and drag link do nothing by themselves other than flop around. Yet this gene needs to have 50,000 parts, and is itself a minute portion of irreducible complexity within a galaxy of irreducibly complex parts, all of which must be working in an orchestrated way. Combine that with what we know about natural selection's ability to create a gene, and it's clearly impossible.
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Figure 6
Can natural selection create: Part 9: Nearly neutral positively kills. (See figure 7.)
BQ: In our ongoing look at what we have demonstrated as natural selection’s inability to create even a single useful new gene, we need consider something that is often not discussed.
In earlier writings, we saw that most harmful mutations are nearly neutral. That is, they are relatively insignificant in terms of the health of a being. If the mutation is not massively harmful (such as a genetic disease that kills a child within 8 months), other selection factors make it hard to remove from the genome, and it is passed on. Think of it like this: if you make a copy on the copier, the copy isn't as good as the original. It has slightly negative qualities. These "harmful" mutations, however, are not enough to make the copy non-viable. The copy will still be used, and itt would take a very bad copy to be rejected.
However, a minuscule proportion of the time (note: this tiny proportion is a mutation within an already-existing gene; to create a new, useful mutation is infinitely rarer to the point of impossibility), there is a chance for a positive mutation occurring. We need these beneficial mutations during the construction of our new gene. The problem we encounter is that they, like the harmful near-neutrals, are almost certainly going to have little impact. Let's do some analogous math using brain-friendly numbers.* For every 10,000 harmful mutations, 9,900 of them are nearly neutral—not good, but not too harmful. 100 of them are fatal. As a ratio, we'll say that for every 100,000,000 harmful mutations, we have 10,000 helpful mutations. Unfortunately, of those 10,000 helpful mutations, 9,900 of them are also nearly neutral—slightly helpful, but nothing entirely useful.
Now step back and look at this in light of our new gene: the vast majority of our new gene is going to be defined by these nearly-neutral mutations! The nature of these nearly-neutral beneficial mutations presents compelling evidence for genetic design, as there is simply no way to build a gene one nucleotide at a time through natural selection.
*For the hard numbers, see our previous looks at this topic.
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Figure 7
Can natural selection create: Part 10: Bad mutations are real and other considerations.
BQ: In our look at creating a new gene, we've excluded deleterious (harmful) mutations so that we'd have a leg up. However, in the real world, deleterious mutations outweigh beneficial mutations by perhaps a million to one. Ouch! Now let's look at other considerations.
Muller's ratchet: We've mentioned this before, so I won't define it here. In a strand if DNA, recombination of material happens mostly between entire genes, and not between nucleotides. Mutations happen as individual nucleotides. This means that good mutations and bad ones can't be separated. Bad mutations, as above, outnumber good ones by an unconquerable amount. If we DID manage to get 100 good mutations, time would actually be our ENEMY in evolution, as good mutations would start to back-mutate into harmful ones while we tried to get enough good mutations to make a good new gene. Thus term, "Muller's ratchet." (See Muller, Loewe, Gabriel et al., Tishkoff, and Verrelli.)
Too much cost: If we could identify half of the population with the worst problems and kill them off, we could calculate the "selective cost" and remove bad mutants. We have seen before that this cost would actually destroy the species in the long run, as reproduction wouldn't keep up. If the selection cost to remove harmful mutants is too much, we certainly can't "pay" for the removal of them and ALSO have genetic "funding" to pay for progressive/beneficial selection.
Non-random mutations: Mutations actually aren't entirely random. In fact, some genomic areas are far more likely to mutate than others. This is actually a problem. While we can get a good mutation in a "hot spot," we have to wait for the cold spot to also produce a good mutation. Again, time is our enemy. The hot spot will back-mutate and, ironically, this non-randomness slows down progressive selection and is antithetical to novel genetic architecture.
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Can natural selection create: Part 11: Wrapping it up.
BQ: Research, reason, and applied genetics show that natural selection cannot innovate new genes within the evolutionary timespan, even when harmful mutations aren't present. When harmful mutations are present, backward-mutations outnumber forward mutations by such an amount that eventual termination awaits every species. Information decay exists all around us, and no amount of counter-intuitive, hand-waving theory can change that fact.
Information theory (Gitt) and numerical simulation (Sanford et al) show that information within our own genome is eroding. We can witness the future of these mutations in inbreeding: recessive mutations that have built up in the genome are expressed. The inbred individuals have worse health problems, die sooner, and function less well. . Much like with cloning, this is a glimpse into the future of information decay and the future of our species.
In very simple terms, we are biologic machines. We have incredible processes to fix and repair damage, and to reproduce. But like every machine, we operate at less than 100% efficiency. This inefficiency is a measure of entropy, or the universal tendency of things to run down or degrade apart from intelligent intervention. While biologists have philosophically argued for decades that special qualities of natural
selection can reverse the biological effects of the second law of thermodynamics, making life effectively immortal, we have shown that this is not true.
If the genome must degenerate, and it must, then the assertion that natural selection + mutation=improvement must be wrong. Why is this? Because mutation/selection cannot prevent the loss of genetic information. Selection occurs on the level of the organism, not the molecular level. It's like trying to fix a computer with a hammer: the microscopic complexity of the computer makes the hammer mostly irrelevant. In the same way, the microscopic complexity of the genome makes selection on the level of the whole individual largely irrelevant. (Sanford)
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Can natural selection create novel genetic info? (Pt 4-7)
Can natural selection create: Part 4: Waiting for other mutations: Lots of colons!
BQ: We are considering the question, "Can natural selection CREATE even a single useful gene?" Remember, it's quite easy to modify existing genetic code, and your body does all the time. That's why we get cancer. It's why we are all, in fact, unique mutants. But can natural selection CREATE novel information?
It took us 12,000,000 years to stabilize our first desired mutation, and we saw that such presented a large problem with the evolutionary timeline. But keep in mind, it took us that long to encode a SINGLE useful nucleotide. Genes are at a minimum 1000 nucleotides in length, and that's about 50 times too generous, as we're ignoring regulating elements and introns.
However, to give ourselves the best chance of creating new, useful information, we're setting up this advantage. We'll call it a nice, linear, piece-by-piece process. Our first change took 12,000,000 years, and now we need to do it at least 1,000 more times, and it has to be useful. How long will that take? Well, multiply 12,000,000 times 1000 more times and you get, 12,000,000,000 years. That's a little bit under the time that the Big Bang took place, and we just made one single, useful gene, in a world with no harmful mutations and perfect selection.
Tomorrow, we need to look at even MORE factors that we're leaving out. Also, remember, this is making a new, useful gene only 1000 nucleotides long. Our genome is composed of 6,000,000,000. How long would it take to make such a genome if it takes so long just to create one new gene? And, from a while ago, we found out that creating the first "life" exceeds the probabilistic resources of the entire universe for its stated "life"span. From that we saw that M-theory was a fallback, because if we have multiple (in this case, infinite) universes, then such an infinitely small (by definition, impossible) chance of it happening would have to take place. Oh, and in one universe you, dear reader, are the Pope, and have a miniature llama as a pet.
(F. Hoyle, Mathematics of Evolution. M. Lynch, J. Conery, R. Burger, Mutation accumulation and the extinction of small populations. J. Neel, The rate with which spontaneous mutation alters the electrophoretic mobility of polypeptides. J. Adell, J. Dopazo, Monte Carlo simulation in phylogenies: An application to test the constancy of evolutionary rates.)
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Can natural selection create: Part 5: Surprisingly slow.
BQ: We are continuing to answer the question, "Can natural selection create even a single useful gene?" Yesterday we "made" our first cool, new nucleotide. It took us just this side of forever to do so. What we didn't mention is that the human genome occurs in large "chunks" of between 20K-40K nucleotides within which we have no recombination. This means that the nucleotides are not moving around. Essentially, this reduces the probability that we can easily create the gene, and adds even more billions of years into the calculation. (The nucleotide mutations have to occur in such a way that they adjoin each other.)
But now we have our mutant nucleotide and are trying to get it to "survive" reproduction and to be passed on; since we have 20K possible nucleotide alternatives within our population of 10K, we have a tough goal. We want to go from two copies of the mutation in the population to four, and then more from there. If the mutation managed to be reproduced at 10% per generation (this is an awesome mutation that turns you into a supermodel and gives you just the best qualities ever), it would take us ~105 generations (2100 years) to increase from 1 to 20K copies. (1.1^105=20K).
The problem is these advantages are unrealistic. According to Patterson in "Evolution," a recessive beneficial mutation that would increase fitness by 1% would take 100,000 generations to fix. Haldane in, "The cost of natural selection," estimated that the most nominal time for fixation of a beneficial new mutation to take place is at least 300 generations, or >6000 years. This is called, "Haldane's dilemma," as it is so slow that it means there is effectively no selection taking place.
But if we can create one new nucleotide in 6000 years, can't we create a new gene in 6 million, the time since we supposedly evolved from apes? No. Haldane's dilemma concerns unlinked, non-adjacent mutations. For 1000 specific, adjacent mutations, it would take well over 6 billion years; furthermore, selecting for one nucleotide reduces our ability to select for others, which is called "selection interference."
We can conclude from all this that we cannot create even one new gene within our evolutionary timeframe, even without harmful mutations to boot.
Coming up, we'll look at the implications of endless fitness valleys, deleterious mutations, and poly-constrained mutations, all in our attempt to make evolution act the way "it's supposed to." We have about two or three questions left on this, and they should be easier to understand.
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Can natural selection create: Part 6: Inferiority and fitness.
BQ: Continuing to see if natural selection can create a single useful gene, we now need to look at the conclusion of some known facts that we've left out. We know that man and ape differ by approximately 150,000,000 nucleotides. As we've seen, as a percentage, that's not too much, but as a genetic change in raw nucleotide numbers, that's massive. These changes account for at least 40,000,000 mutations.
If we assume that man came from chimp-like creatures, there must have been 20,000,000 nucleotide fixations within the human lineage (40,000,000/2), but we found out yesterday that natural selection could maximally have accounted for ~1000 of these in 6 million years, and they would have been non-sequential. What does this mean? It means that the rest would have been fixed by random drift, not a natural "enhancement" by selection, which would make them...you guessed it, nearly-neutral but HARMFUL mutations. We'd have on the best of days 1000 "good" mutations and millions of harmful ones, which would mean that man DEVOLVED from chimps! In fact, we'd be statistically dead!
Before we move on to poly-constrained DNA tomorrow, we need to briefly consider fitness valleys. Evolutionists can show that the creation of a new gene takes a great deal of experimentation. When the gene is being developed, there is a period of time when the species' fitness declines. This is called a "fitness valley." A partially-completed gene is not neutral, and it's not helpful...it's harmful. The species, then, must be harmed in order to be enhanced. We can imagine a situation where a species could survive fitness valleys if they were rare and short-lived, but continuous evolutionarily-positive innovation of novel genes would mean continuous, harmful fitness valleys, or one longer valley with a negative trajectory. Indefinitely number, indefinitely long fitness valleys ultimately would destroy all species.
(PN242)
Can natural selection create: Part 7: Polyfunctional DNA (See Figure 5—Polyfunctional Complexity)
Continuing to see if natural selection can create a single useful gene, we now need to look at the conclusion of some known facts that we've left out. We know that man and ape differ by approximately 150,000,000 nucleotides. As we've seen, as a percentage, that's not too much, but as a genetic change in raw nucleotide numbers, that's massive. These changes account for at least 40,000,000 mutations.
If we assume that man came from chimp-like creatures, there must have been 20,000,000 nucleotide fixations within the human lineage (40,000,000/2), but we found out yesterday that natural selection could maximally have accounted for ~1000 of these in 6 million years, and they would have been non-sequential. What does this mean? It means that the rest would have been fixed by random drift, not a natural "enhancement" by selection, which would make them...you guessed it, nearly-neutral but HARMFUL mutations. We'd have on the best of days 1000 "good" mutations and millions of harmful ones, which would mean that man DEVOLVED from chimps! In fact, we'd be statistically dead!
Before we move on to poly-constrained DNA tomorrow, we need to briefly consider fitness valleys. Evolutionists can show that the creation of a new gene takes a great deal of experimentation. When the gene is being developed, there is a period of time when the species' fitness declines. This is called a "fitness valley." A partially-completed gene is not neutral, and it's not helpful...it's harmful. The species, then, must be harmed in order to be enhanced. We can imagine a situation where a species could survive fitness valleys if they were rare and short-lived, but continuous evolutionarily-positive innovation of novel genes would mean continuous, harmful fitness valleys, or one longer valley with a negative trajectory. Indefinitely number, indefinitely long fitness valleys ultimately would destroy all species.
(PN243)
Figure 5—Polyfunctional Complexity
Can natural selection create novel genetic info? (Pt 1-3)
Can natural selection create: Part 1? (See Figure 1—Genes; Figure 2—Irreducibly complex)
BQ: Based on the independent research of Haldane, Gabriel, Tishkoff, Verrelli, Crow, Kimura, ReMine, and other scientists, I'd like to start a deeper look at natural selection’s ability to create useful information. We'll start off with the question, "can natural selection create even a single useful gene?" Furthermore, we'll work our way slowly, recalling past research and questions, and give ourselves a favorable scenario to create an "origin of species."
Let's take a look at defining our first desirable mutation by asking, "is any particular nucleotide more valuable than any other?"
A: By itself, no nucleotide (A, T, C, G) has any more value than any other, in the same way that no letter in the English alphabet has any particular value outside of the letters around it. That is, a letter's value is defined by the context we find it in, and so are nucleotides. A change to a single letter in this sentence can only be evaluated by the surrounding letters.
From this, we see an example of irreducible complexity. Irreducible complexity presents a problem for evolutionary thought, though circularly many try to arm-wave it away with the all-powerful, "natural selection." By irreducible complexity, we mean, "a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition non-functional.’ (Behe)
If we look at the problem with creating these sentences (the DNA of this BQ), we'll see we have a very basic bit of irreducible complexity. To create new information, we need to select for our first beneficial mutation, but...we can only define the value of the nucleotide/mutation as compared to its nucleotide neighbors. By changing the nucleotide, we inherently also change the overall meaning of the neighbors; we have therefore created a circular paradox as we keep destroying the context on which we are trying to build.
Tomorrow, we'll start off from here and look at the problem of fundamental inter-relationships of nucleotides, known as "epistasis." If you have any questions at this point, shoot me a message and I'll be glad to explain it better. :)
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Figure 1—Genes
Figure 2—Irreducibly complex
Can natural selection create: Part 2. (See Figure 3—Epistasis)
BQ: We are considering the question, "Can natural selection create even a single useful gene?" We are giving ourselves a massive advantage by assuming that we have no negative mutations ever (IRL, the neg/pos ratio of mutations is pretty much "vast-to-none"). Yesterday we learned that no nucleotide (DNA building block) is more useful than another by itself. We also learned that they are only useful in the context of the other "building blocks" around them, and that any mutation inherently affects context. Therefore, we inherently have irreducibly complex DNA.
Today we need some background information clarified, so we're going to look at epistasis. Epistasis is a problem with the fundamental inter-relationship between nucleotides. Essentially, this inter-relationship between nucleotides is infinitely complex. When we define epistasis, we say that, "Different mutations that affect the same trait often interact, so a harmful mutation may be much more or less harmful depending on the absence or presence of other mutations." This "noise" in the DNA makes natural selection of genetic benefits almost impossible, like trying to get only internet with Comcast, yet having to buy a bundle with overpriced phone and TV. Genomes are a package deal; we can't just take that nice internet deal for super cheap.
Genetic language, like any language, is not a product of chance. Having letters randomly fall into meaningful places is not statistically feasible (in fact, as we saw before, it exceeds the probabilistic resources of the entire universe), and the same can be said for our genetic language. We know from computational models than strings of nucleotides (and just dozens of them, not billions as found in our DNA) cannot randomly fall into place, but we're going to look and see if we could accomplish this one nucleotide at a time, giving ourselves another advantage.
With this background information out of the way, tomorrow we'll examine the timespan we'd have to have for our first mutation within human evolution to become "fixed," and we're going to give ourselves the benefit of having no "package" deal with mutations, though epistatically we know that we would HAVE to have many bad mutations attached to any "improvement mutation." We'll use the assumed population model proposed by evolutionary theory and see how long it'd take us if everything was perfectly in our favor.
Attached is a picture I made to help you visualize what we're talking about when we say "epistasis."
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Figure 3 —Epistasis
Can natural selection create: Part 3, The waiting game. (See Figure 4—Extrinsic Factors.)
BQ: We now know what the concept of irreducible complexity is as well as the tough problem of epistasis. We continue to move forward with our question, "can natural selection create even a single useful gene?" Today, we're assuming no harmful mutations exist or would exist, and that we have a pristine human population to pull from, using the evolutionarily accepted figure of about 10,000 individuals.
The mutation rate for any given nucleotide is about 1 chance in 30,000,000. So if we assume 100 mutations per person per generation, we need about 3000 generations, or 60,000 years, to expect a specific nucleotide within our population of 10,000 to mutate. About 66% of the time, it will mutate into the "wrong" building block. So for a specific site to get a beneficial mutation, it'll take about 3x as long, or 120,000 years. Once we do get it, we need to "fix" it—that is, make sure that all individuals will have two copies.
Our challenge is then genetic drift. That is, a mutation needs to be exceedingly noticeable and beneficial to counteract the extrinsic factors and genetic noise. In other words, it's hard to "keep the mutation ball rolling," because most reproduction will not be based upon this one beneficial mutation, but rather other aspects. So perhaps the mutation gives our individual nice abs, but because of the way he was "raised," he is obnoxious and no other individual mates with him to produce offspring which might pass the mutation on. According to population geneticists, the new mutation has 1 chance in 20,000 (total number of non-mutant, location-specific nucleotides present in the population) of not being lost via this genetic drift.
At least 99% of the time, even a good beneficial mutation will be lost via drift. So even a BENEFICIAL mutation needs to happen about 100 times before it "sticks around." On average, then, we would need 120,000 years times 100, or 12,000,000 years to stabilize a first desired genetic mutation. But remember, this is ONE nucleotide segment, and we need MANY of these to build just one desired mutational gene. It supposedly took us 6,000,000 years to evolve from ape-like creatures, but we can see that we can only realistically expect to fix one good mutation in twice that long, and that's without harmful mutations thrown in.
Next, we'll look at the wait for other mutations in building our gene, because one nucleotide base pair does not a gene make.
(PN239)
Figure 4—Extrinsic Factors