Genome Lacks Compliance With Evolutionary Theory

Normally evolution does well with certain models along with assumptions (without observational data).  But according to a new research paper in nature not even models which hold to certain assumptions confirm evolution!

Four  universities conducted research on contemporary human populations in order to discover advantageous mutations, along with the rate of degradation by mutations. Trying to understand diseases from the present is one thing, it’s quite another trying to obtain knowledge of historical evolution which goes by the assumption of many millions of years.

In nature

“Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants…We estimate that approximately 73% of all protein-coding SNVs [single-nucleotide variants] and approximately 86% of SNVs predicted to be deleterious arose in the past 5,000–10,000 years. The average age of deleterious SNVs varied significantly across molecular pathways, and disease genes contained a significantly higher proportion of recently arisen deleterious SNVs than other genes.”    

 The researchers used the term “explosive population growth” because of its long age assumption whereby,  “selection has not had sufficient time to purge them from the population.” Researchers then claim that Europeans had stronger genetic drift, than Africans which is strange because genetic drift doesn’t know the difference. Obviously, they are fudging their assumptions in more ways than one!

They give an assessment of their findings…

“More generally, the recent dramatic increase in human population size, resulting in a deluge of rare functionally important variation, has important implications for understanding and predicting current and future patterns of human disease and evolution.”

“For example, the increased mutational capacity of recent human populations has led to a larger burden of Mendelian disorders, increased the allelic and genetic heterogeneity of traits, and may have created a new repository of recently arisen advantageous alleles that adaptive evolution will act upon in subsequent generations.

Advantageous mutations? Where are they? The researchers provide no examples in which they observed! They merely assumed it, because it’s part of evolution! This is what you call, “circular reasoning!” If the supposed evolutionary past doesn’t add up with the present data, how is this shed light on future patterns for evolution? When a theory displays a considerable pattern that shows increasing complexity in its explanation, the theory is not valid!

Rather than observing advantageous mutations, they observed a “larger burden of Mendelian disorders” afflicting mankind which is vital for understanding diseases not evolution. The research does however confirm a creation scientist’s (John Sanford) proposal which is known as genetic entropy where the genetic load increases dramatically. That would be a problem for evolution, because that observation makes it impossible for mankind to survive tens of thousands of years!

Here is more on the genome in this interview with John Sanford…

And here is part two of the interview with John Sanford…

The researchers are baffled by their finding as one can read by what they expected in the evolutionary framework verses what they observed!

“The site frequency spectrum (SFS) of protein-coding SNVs revealed an enormous excess of rare variants (Fig. 1a). Indeed, we observed an SNV approximately once every 52 base pairs (bp) and 57 bp in European Americans and African Americans, respectively, whereas in a population without recent explosive growth we would expect the SNVs to occur once every 257 bp and 152 bp in European Americans and African Americans, respectively (Supplementary Information).”

Thus, the European American and African American samples contain approximately fivefold and threefold increases in SNVs, respectively, attributable to explosive population growth, resulting in a large burden of rare SNVs predicted to have arisen very recently (Fig. 1b).”

“For example, the expected age of derived singletons, which comprise 55.1% of all SNVs, is 1,244 and 2,107 years for the European American and African American samples, respectively. Overall, 73.2% of SNVs (81.4% and 58.7% in European Americans and African Americans, respectively) are predicted to have arisen in the past 5,000 years. SNVs that arose more than 50,000 years ago were observed more frequently in the African American samples (Fig. 1b), which probably reflects stronger genetic drift in European Americans associated with the Out-of-Africa dispersal.”

 Their findings conflict with the whole long ages notion which comes from the ‘theory’ of evolution but does shed light on understanding diseases better while containing evidence for a population that has been around for 5,000 to 10,000 years! Which confirms what? Yes! It confirms creationism!

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17 thoughts on “Genome Lacks Compliance With Evolutionary Theory

  1. Michael: “Normally evolution does well with certain models along with assumptions (without observational data).”

    After such a completely untrue statement there is no point in reading any further.

    Michael, have you been living under a stone for the last 200 years ? There is something called a ‘library’, a place where you can borrow books, in which you will find a *lot* of observational evidence for evolution. More than you can possibly read in one lifetime …

  2. Fu et al. 2013. Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants. Nature 493(7431): 216-220.

  3. There is something called a ‘library’, a place where you can borrow books, in which you will find a *lot* of observational evidence for evolution. – Dear Eelco, what FIVE books would YOU recommend and could YOU give ONE practical example of lab tested NEW information increasing evolution?

  4. “We estimate that approximately 73% of all protein-coding SNVs [single-nucleotide variants] and approximately 86% of SNVs predicted to be deleterious arose in the past 5,000–10,000 years.”

    Creationists seem to be beyond their depth in basic arithmetic. If 73% and 86% of these SNVs arose in the past 10,000 years, then 27% of coding SNVs and 14% of potentially deleterious SNVs occurred longer ago than 10,000 years. Thus negating this argument that the Earth is only 10,000 years old.

    Stupid, Michael. Stupid. You knew there was a reason I suggested this topic, didn’t you?

  5. The researchers used the term “explosive population growth” because of its long age assumption[0] whereby, ”selection has not had sufficient time to purge them from the population.” Researchers then claim that Europeans had stronger genetic drift, than Africans which is strange because genetic drift doesn’t know the difference. Obviously, they are fudging their assumptions in more ways than one!

    Assume a large, static (Fischer-Wright) population Ne of a species. In this case, any mildly deleterious variants would occur at a constant rate by mutation, and disappear at a constant rate by purifying selection[1] in hundreds or thousands of generations down the line. Most variants will be “common” in the population, because they have been around for a long time.

    This scenario changes drastically for small populations that grow explosively. Although the old variants hang around for the same number of generations as selection eliminates them, their number does not increase, while the population size Ne does increase rapidly. At the same time, the frequency of new variants remains the same—say 100 variants/individual/generation. Thus, the total number of new variants will overwhelm the number of old ones.[2] Moreover, the new variants will be rare ones. For example, suppose Ne=5 million to begin, To simplify the math, consider a single old variant, in 1 individual. At the end of the explosion, about 1,000 people will carry that one old variant. But, for a young variant occurring at the end of the explosion, that variant will be present in only 1 individual, because it has not had time to spread. Thus, the older variants are fewer and “common” and the newer ones greater in number and “rare.” It’s a matter of simple math.[3] [4]

    .

    Michael also displays his profound ignorance of evolutionary theory. His statement that “genetic drift doesn’t know the difference” is not only false, it’s ludicrous.[5] Geneticists have known for many decades that drift, and its relative prevalence versus natural selection, depends highly upon population size. 10,000 years ago, the population of Africa was high, but the human population in Europe was very low. Thus drift played a much larger role in ancient Europeans than in Africans, where purifying selection dominated.[6] .

    ===================

    [0] Hunh???? Creationists are the ones who assume a huge population explosion: from 2 individuals to 7 billion in 6,000 years. Kind of knocks the wind out of that argument, doesn’t it?

    [1] Since Ne is assumed large, drift will not appreciably modify the selection rate.

    [2] Because purifying selection has not yet had time to dispose of them.

    [3] Think of an expanding balloon being spattered with paint droplets of different colors at a constant rate. Droplets landing when the balloon is small will be few, but will expand in size as the balloon inflates. Droplets landing when the balloon is large will be more numerous, because the area is much larger—but they will have more different colors. (That is, each color will be rarer.)

    [4] If this is so simple, why check it out and write a paper on it? Because, unlike creationists, scientists TEST THEIR HYPOTHESES. (Actually, a number of different interacting rates can influence this result, so it was not a foregone conclusion. In fact, the rate of rare variants was not expected to be as high as found. Another point: others have questioned the age of the rare variants, based upon different evidence of population growth.)

    [5] David Coppedge is also ignorant of this effect in the post that Michael cribbed his post from. In his comments, he says: “But how can they claim Europeans “probably” had stronger genetic drift at the same time Africans did not?

    [6] Genetic drift is not racist. It appears they are fudging assumptions. Has nothing to do with race, but everything to do with population size. When something runs counter to their beliefs, creationists not only reject it, they refuse to understand it

  6. The research does however confirm a creation scientist’s (John Sanford) proposal which is known as genetic entropy where the genetic load increases dramatically. That would be a problem for evolution, because that observation makes it impossible for mankind to survive tens of thousands of years!

    Here we go with “genetic entropy” again. First, no one, not even Sanford, has ever defined this quantity sufficiently to measure it, test it, or compare genomes for it. Sanford is an agricultural botanist with no background in the physical concept of entropy whatever. The concept genome entropy has been refuted many times[1] Based upon biblical accounts, Sanford claims that human lifespans have been decreasing since the age of the patriarchs. Of course, this will be major news to demographers, who have observed steady increases in human lifespans over at least the past thousand years.

    But why should we trust demographers? Do they have the faith? Are they biblical scholars? No.

    ===================

    [1] See my comment as recently as Oct. 26, 2012.

  7. Advantageous mutations? Where are they? The researchers provide no examples in which they observed! They merely assumed it, because it’s part of evolution!

    Creationists can’t seem to see past their paranoid delusion that every carpetbagger scientist, every flatlander biologist, writes papers only for the purpose of “proving” evolution.

    Michael himself quoted the purpose of this study just two paragraphs above:

    “More generally, the recent dramatic increase in human population size, resulting in a deluge of rare functionally important variation, has important implications for understanding and predicting current and future patterns of human disease and evolution.”

    Guess what, Michael. You find out about diseases by studying the bad genes, not the good ones. The “advantageous” genes are irrelevant to the purpose of the paper. [1] So the good ones were not discussed in detail.

    .

    BTW, although the age of many genes was less than 10,000 years, the authors do note that the SNVs shared between Europeans and Africans were more than 100,000 years old. That’s the average age.

    ================

    [1] Then, too, we could notice that the authors did not name any specific deleterious genes, either.

  8. Creationists can’t seem to see past their paranoid delusion that every carpetbagger scientist, every flatlander biologist, writes papers only for the purpose of “proving” evolution. Non-sequitur

  9. Olorin,

    You say, “First, no one, not even Sanford, has ever defined this quantity sufficiently to measure it, test it, or compare genomes for it.”

    Your either lying or you made an enormous error. I suspect you are lying given the fact how you look up information. Evolutionary biologist Kondrashov who wrote, “why aren’t we dead 100 times over” certainly could measure it. After the fall of Adam, the Bible says that nature is going towards deterioration, but in evolution nature is supposed to be going in the other direction! You can measure and test what direction nature is going in!

    Here is how one measures it and this work was done by mostly population geneticists who believe in evolution…

    Scientists have observed 10,000 to 1,000,000 harmful mutations for every one beneficial. That in itself tells you a downward trend (genetic entropy) By the way, this experiment wasn’t part of the genome research that I recently posted! Anyway, Sanford chooses to be conservative with the estimate. He uses population geneticist, Kimura’s data (he is also an evolutionist) for evidence for “zone of near-neutrality” on both the beneficial and harmful sides where natural selection doesn’t select for or against because mutations are point-nucleotide. Natural selection is unable to see those 99 percent of the time! Would you notice any difference if one prixel went out on your computer?

    The number of beneficiary mutations is so small that natural selection only selects one percent of them. This ensures that natural selection will never see 99% of the good mutations while allowing the bad which are vastly greater in number to accumulate. Thus, the genome will suffer from “genetic entropy”

    Genetic entropy is a fact, observable, testable, and one can make predictions with it! Errors in information causes chaos, not highly advanced engineered genes! The genome research hasn’t confirmed evolution (which surprised researchers with their modeling of the genome) nor made it clearer for your understanding…lol Evolution makes a prediction that information is increasing rather than increased complexity (information breaking down) where assumptions are being made to fill in the falsifications.

  10. Olorin,

    You say, “Guess what, Michael. You find out about diseases by studying the bad genes, not the good ones. The “advantageous” genes are irrelevant to the purpose of the paper. [1] So the good ones were not discussed in detail.”

    You didn’t read the paper did you? Much like you didn’t read Stanford’s research and how he came up with his conclusion! You just ranted some abstract of your own that was irrelevant to the conclusion! In other words, a straw man’s argument! Here is the abstract of that paper published in nature…

    “Establishing the age of each mutation segregating in contemporary human populations is important to fully understand our evolutionary history…” The abstract of the paper continues…“and will help to facilitate the development of new approaches for disease-gene discovery.”

    So the purpose was two-fold, fully understanding evolution’s story (not just one side of the curb) AND coming up with new approaches for diseases! What they discovered was, the human genome could not have lasted tens of thousands of years as told in the story of evolution so they had to invoke something to explain why the evidence wasn’t matching up with the story.

    How could researchers then claim that Europeans had stronger genetic drift if they were just studying bad genes? Here again is a quote from the paper…

    “More generally, the recent dramatic increase in human population size, resulting in a deluge of rare functionally important variation, has important implications for understanding and predicting current and future patterns of human disease and evolution.”

    Not relevant according to you because they didn’t go into detail about functionally important variation which are good genes by the way, they are supposed to be focused on the bad genes for diseases only according to you. Since they didn’t go into detail about functionally important variation, do you think they were still scientists? lol What nonsense you come up with!

    But what is quite remarkable is when they think “genetic entropy” happened. They could have said 15,000 years ago, 20,000 years ago…But remarkably 6,000 to 10,000 years which is what? The age range of creationism!

  11. Entropy, in the context of information theory (Shannon entropy) quantifies the expected value of the information contained in a message. Thus, in a message that is 10 times longer than a previous message in the same symbol ensemble has 10 times as much information as the first message. It doesn’t matter whether the message is good or bad or indifferent—or, as applied to genomes, advantageous, deleterious, or neutral. So Michael’s statement—

    Evolutionary biologist Kondrashev who wrote, “why aren’t we dead 100 times over” certainly could measure it.

    —is irrelevant to a “measure” of any recognized kind of genetic entropy. Kondrashev did not measure it—he spoke only of “mutational load”; not the same concept at all. I have not read the book, but none of the reviewers seem to have any idea how to measure genetic entropy in the way that Sanford bandies that term about. Perhaps Michael can enlighten us: What genetic events affect entropy? How do you calculate the amount of entropy produced or subtracted by such an event? What relation does genetic entropy have to Shannon entropy?

    The major failing of Sanford’s book seems to be that it is contradicted by the evidence. If the entropy of humans reduces us to a genetic slag heap in 10,000 years—about 300 generations—then entropy of mosquitoes, with a generation time of about 20 days, will have more than 150,000 generations in the same time—enough tp make them extinct many times over. But, so far ….

    Sanford laughably relies upon the biblical age of the patriarchs as showing modern declines. But other species should be affected as well. If the genomes of rats were declining at a very small rate (say, 0.1%/year) then they should be down to only 5% of their fitness since 1,000BCE. Yet we do not read of any super-rats in the age of the patriarchs. Nor about any other species having exponentially longer lives during that period.

    Sanford’s model of selection presents another glaring error. He selects only the most fit breeding pair from a generation, then allows the population to build. Then he selects a single pair from that population, and so forth. This is a patently ridiculous model of natural selection. Garbage in, garbage out.

    You can measure and test what direction nature is going in!

    Yes we can. And it does not go in the direction Sanford predicts. In humans, for example, the average lifespan has been increasing for the past 1,000 years, and the world population has risen from 400 million to more than 6,000 million during that time. Besides, a steady stream of papers demonstrates positive selection in humans[1] In Lenski’s E. coli experiment, each of the 12 starting populations increased in fitness over the first 10,000 generations; this, of course, is very well documented.[2]

    Almost every number that Sanford presents has been refuted. His citations omit and distort an amazing breadth of genetics.[3] Population genetics is a difficult area; opportunities for errors abound. With Michael’s ignorance of basic biology, he really does not want to play in that sandbox.

    ========================

    [1] Michael filters comments with a plethora of links See “Detecting Natural Selection” for a description of how this is done.

    [2] Sanford had to be aware of this result, but withheld it from his readers. The fitness increase slowed down thereafter, because the bugs were already near 100% by that time- their fitness certainly dii not ever decrease at all.

    [3] I won’t even mention the travesties he commits on Notoo Kimura’s papers.

  12. Olorin,

    What are you talking about? Are trying to impress me with you jargon which is not relevant? You didn’t address a very fundamental question, if the human genome is degrading (genetic entropy) shouldn’t lifespans get shorter? Modern technology has enabled people to live longer, more so than they would have lived before the technology was invented, but that isn’t measuring the maximum lifespan!

    One-celled organisms are almost ‘immortal’ because a bacterial cell is able to reproduced by dividing into two where there was one, those two then become four, those four become eight and so on…On the other hand, human cells tend to divide some 50 times before they stop. Reaching their genetic limit. However, human tumour cells can divide themselves for any length of time without stopping. There is an upper limit on age (maximum lifespan) which has not been increased. Around 120 years!

    Lenski’s E. coli experiment did nothing of the sort in providing evidence for increase maximum lifespan! In fact, the comparison is fatal to your argument. In 2010, researchers published in nature, their work on artificial selection much like the E. coli experiment. Researchers were hoping to observe and then document beneficial mutations becoming fixed in the fruit fly population. So they produced 600 generations under ideal conditions without any harsh environmental pressures which would favor upward, and onward supposed evolution. But what did they discover? Any beneficial mutations? No! In fact, the paper said,“selection did not lead to the fixation of newly arising unconditionally advantageous alleles.”What they did find was the fruit flies became more resistant to change and not only that, but started going in “reverse” or what is known as “reverse evolution.”

    Science Daily on October 12, 2012, published this…

    “The last common ancestor of man and fruit flies lived about 600 million years ago,” says Werner. “All the genes needed to build a body were already present in that ancestor, and today we still share virtually all of our body-building genes with fruit flies. This is why we are able to study human diseases like cancer in fruit flies.”

    Since fruit flies are that similar with human genes and yet fruit flies resist change after 600 generations before going backwards, it disqualifies your whole argument for evolution and your position against genetic entropy!

  13. What are you talking about? Are trying to impress me with you jargon which is not relevant? You didn’t address a very fundamental question, if the human genome is degrading (genetic entropy) shouldn’t lifespans get shorter?

    I’m trying to get it through your head that what you are talking about is not “entropy.”[1] It might be “mutational load,” which is not the same thing at all. If it is something else, then you need to define it—and state how to quantify it.

    Why should “entropy” of any kind shorten lifespans? As I said, Shannon entropy represents the amount of information in a message. Is it your position that more information in a genome—i.e. bigger genomes—shortens lifespan?

    .

    Lenski’s E. coli experiment did nothing of the sort in providing evidence for increase [sic] maximum lifespan!

    So what? Sanford’s claim is that lifespans will *decrease*—in fact that, they will decrease to the point of extinction. Hasn’t happened.

    On the other hand, human cells tend to divide some 50 times before they stop. Reaching their genetic limit. However, human tumour cells can [sic; “cannot”??] divide themselves for any length of time without stopping. There is an upper limit on age (maximum lifespan) which has not been increased. Around 120 years!

    And again, so what? The claim is that lifespans are decreasing, not that they are not increasing.[1] However, over evolutionary periods, lifetimes of proto-humans has increased quite a bit.[2]

    .

    The rest of your comment has no relevance whatever to any of Sanford’s claims.[3]
    ================

    [1] The cell-division limit is an unproven hypothesis. Many biologists hold that no such limit exists.

    [2] One of the proposed drivers of increased human culture was the invention of grandparents a hundred thousand years ago, because humans began to live long enough to aid parents in raising children.

    [3] For example, why would “reverse evolution” shorten lifespans? Why would chickens with alligator-like snouts shorten their lifespan?

  14. Michael’s logic in his comment follows this paradigm:
    *** God is love. Love is blind. Stevie Wonder is blind. THEREFORE, Stevie Wonder is God.

    Here is the paradigm as it applies to Michael’s comment:
    *** Entropy is disorder. Disorder is bad. Shortened life spans are bad. THEREFORE, entropy shortens lifespans.

    Can you say “non sequitur, non sequitur, non sequitur, THEREFORE non sequitur”?

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