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Wednesday, July 06, 2011

Mutations are negative. Like energy turning to entropy, the genome runs downhill.

This is great news!  Creation-Evolution Headlines has redesigned their site (they are associated with Creation Safaris) and it is now up and running strong.  Let's highlight a recent post:

Genetic Entropy Confirmed

Posted on June 05, 2011 in Microbiology, Cell Biology, Genetics, Origins, Darwin and Evolution

In Darwinian evolution, variations must add new information to produce innovations.  Neo-Darwinism ascribes those variations to genetic mutations.  In 2005, geneticist John Sanford (Cornell) argued that the accumulation of mutations always decreases fitness in a process he called “genetic entropy.”1 The downhill trend is amplified by a number of factors, including selection interference and epistasis (interactions between mutations).2  Now, genetic entropy from epistasis has received support by two new papers in Science.

For mutations under epistasis to produce innovation, there must be a way for them to work together (synergistic epistasis).  This is often assumed but has not been observed.  Most experiments have shown beneficial mutations working against each other (antagonistic epistasis; see 12/14/2006), or causing even less fitness than if they acted alone (decompensatory epistasis; see 10/19/2004).  In a new paper in Science,3 Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.  The abstract said:

Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time. 

Within the paper, they said, “We observed an overall negative relation, indicating that epistatic effects became more negative as the expected fitness rose....”  Near the conclusion, they confirmed witnessing a type of genetic entropy: “A conspicuous feature of the mean-fitness trajectory for this population—and indeed for most experimental populations evolving in a constant environment—is that the rate of adaptation declined over time.”  The reason they gave was that “epistatic interactions contribute greatly to this deceleration by reducing the effect-size of the remaining beneficial mutations as a population approaches a fitness peak. In other words, epistasis acts as a drag that reduces the contribution of later beneficial mutations.”  No increases in adaptation or fitness were observed, and no explanation was offered for how neo-Darwinism could overcome the downward trend in fitness.

Another paper in the same issue of Science found similar bad news.  A group of researchers in Massachusetts put “diminishing returns” in the title of their paper.4  They introduced beneficial mutations into bacteria, but found them decelerating adaptation.  Their abstract said, “These results provide the first evidence that patterns of epistasis may differ for within- and between-gene interactions during adaptation and that diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation.”  Aware of the study by Khan et al,  they claimed that “across these two distinct model systems 7 of 10 alleles consistently showed antagonism, whereas only 2 exhibited synergy.”

A look in both papers, however, showed no clear examples of evolutionary progress in the experiments, and certainly no new species arising.  In fact, the experiments were more a test of artificial selection—studying which mutants adapted to contrived laboratory conditions.  In addition, fitness gains were measured by reproduction rates which, in some cases of adaptation, might have deleterious trade-offs, such as metabolic cost.

Commenting on these papers in Science,5 three authors from University of Pennsylvania noted that, “In Evolution, the Sum Is Less than Its Parts.”  The figure caption explained, “The mutations conferred smaller marginal benefits in combination than they did individually. This antagonistic epistasis causes progressively slower rates of adaptation over time.” Khryazhrimsky, Draghi and Plotkin referred to some microbe experiments that showed initial gains due to beneficial mutations (in isolated lab populations) that slowed to a crawl due to epistasis, or then “discover rare phenotypic innovations,” then diverge into populations that either coexist or compete.  More work will be needed, they said, to quantify these effects in the wild with different organisms, population sizes and natural ecologies.

Though hopeful that evolution can march onward in spite of these genetic brakes, they admitted that “the prevalence of antagonistic epistasis measured by the two groups ensures a predictable tempo of adaptation characterized by diminishing marginal returns.”  They pulled victory from the jaws of defeat, claiming that these experiments “represent resounding achievement for the reductionist approach to studying biology.

A pro-evolution article in Science Daily summarized the work of the first paper thorough the eyes of Tim Cooper [U of Houston], one of the participants.  “The more mutations the researchers added, the more they interfered with each other,” was one of the “surprising” results.  “It was as if the mutations got in each other's way as they all tried to accomplish the same thing.”  Hopefully readers will pardon Cooper for the anthropomorphism.  “The effect of their interactions depended on the presence of other mutations, which turned out to be overwhelmingly negative.”  What does this mean for evolutionary progress?  “These results point us toward expecting to see the rate of a population’s fitness declining over time even with the continual addition of new beneficial mutations,” Cooper said.

In contrast to the depressing news in Science, three authors in Nature claimed hopeful news with mutations under epistasis.6  “Cryptic genetic variation promotes rapid evolutionary adaptation in an RNA enzyme” was the optimistic title of their paper, but a close look at their experiment shows it was a case of artificial selection on RNA ribozymes only.  It did not involve a real cell culture, and the gains from “cryptic variation” only showed adaptations to contrived conditions in the lab.  They explained the adaptation as a case of “pre-adaptation” or “exaptation” with mutations hiding out till an opportunity arrived for them to show some adaptation in the scientists’ contrived environments.  Their simplified model substituted for real evidence, because “this facilitating role for cryptic variation has not been proven, partly because most pertinent work focuses on complex phenotypes of whole organisms whose genetic basis is incompletely understood.”  Nevertheless, they claimed by extrapolation that “Our results highlight the positive role that robustness and epistasis can have in adaptive evolution.”  This paper came out in print a day before the pessimistic papers in Science.

Speaking of mutations, researchers at USC discovered “a chromosomal mutation responsible for a very rare condition in which people grow excess hair all over their bodies” (see Medical Xpress). While the benefit of such a condition might only count in the arctic, it shows that some mutations can have drastic effects.  Even if a hairy female could survive the cold, though, what male would want to marry her?   Such mutations would probably not become fixed in a population or else Eskimos would all have it.  Most mutations are nearly neutral and invisible to natural selection, as Sanford explained in detail in his book.  Because they are not eliminated by purifying selection, they therefore accumulate in the genome, dragging it into genetic entropy.  Mutations are not good material for natural selection.
1.  John Sanford, Genetic Entropy and the Mystery of the Genome (Ivan Press, 2005).
2. Ibid., pp. 109-111.
3. Khan et al., Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population, Science, 3 June 2011: Vol. 332 no. 6034 pp. 1193-1196. DOI: 10.1126/science.1203801.
4. Chou et al., Diminishing Returns Epistasis Among Beneficial Mutations Decelerates Adaptation, Science, 3 June 2011: Vol. 332 no. 6034 pp. 1190-1192, DOI: 10.1126/science.1203799.
5. Khryazhrimsky, Draghi and Plotkin, In Evolution, the Sum Is Less than Its Parts, Science, 3 June 2011: Vol. 332 no. 6034 pp. 1160-1161, DOI: 10.1126/science.1208072.
6. Hayden, Ferrada and Wagner, Cryptic genetic variation promotes rapid evolutionary adaptation in an RNA enzyme, Nature, 474  (02 June 2011), pages 92–95, doi:10.1038/nature10083.
Only an evolutionist can find hope in this bad news. Re-read the 12/14/2006 and 10/19/2004 entries to see evolutionary hopes get further dashed.  And even if an evolutionist can claim a real fitness innovation arose spontaneously, the organism will face newer and bigger hurdles (see 04/09/2007).

Mutations are like weights on a swimmer, loading him down.  Beneficial mutations are so small, they are mere bubbles providing a tiny bit of buoyancy.  Now get other swimmers with weights clinging to him to illustrate epistasis; do you think he will evolve wings and fly?  Get real.  Even if one of them has lifeguard training, it will only delay the inevitable.  Remember, evolution has no direction and cannot see the shoreline.

Get John Sanford’s book; it will scare some genetic sense into any Darwinist.  Sanford was asked what has been the reaction to his book by Darwinists.  His answer was, “complete silence.”


Can anybody say,  "Haldane's Dilemma?"

The slow, painful death of junk DNA

Published: 9 June 2009(GMT+10)
Image stock.xchng

So-called “junk DNA” has fallen on hard times. Once the poster child of evolutionary theory, its status has been increasingly challenged over the past several years. Functions for junk DNA have been cited at other places on this website1 and in the Journal of Creation2. In The Great Dothan Creation Evolution Debate,3 my opponent’s main argument, to which he returned again and again, rested on junk DNA. I warned that this was an argument from silence, that ‘form follows function’, and that this was akin to the old vestigial organ argument (and thus is easily falsifiable once functions are found). We did not have to wait long, however, because a new study has brought the notion of junk DNA closer to the dustbin of discarded evolutionary speculations. Faulkner et al. (2009)4 have put junk DNA on the run by claiming that retrotransposons (supposedly the remains of ancient viruses that inserted themselves into the genomes of humans and other species) are highly functional after all.


Based on the work of J.B.S. Haldane (Haldane 1957)5 and others, who showed that natural selection cannot possibly select for millions of new mutations over the course of human evolution, Kimura (1968)6 developed the idea of “Neutral Evolution”. If “Haldane’s Dilemma”7 was correct, the majority of DNA must be non-functional. It should be free to mutate over time without needing to be shaped by natural selection. In this way, natural selection could act on the important bits and neutral evolution could act randomly on the rest. Since natural selection will not act on neutral traits, which do not affect survival or reproduction, neutral evolution can proceed through random drift without any inherent ‘cost of selection’.8 The term “junk DNA” originated with Ohno (1972),9 who based his idea squarely on the idea of Neutral Evolution. To Ohno and other scientists of his time, the vast spaces between protein-coding genes were just useless DNA whose only function was to separate genes along a chromosome. Can you see how the idea of junk DNA came about? It is a necessary mathematical extrapolation. It was invented to solve a theoretical evolutionary dilemma. Without it, evolution runs into insurmountable mathematical difficulties.

Junk DNA is a necessary mathematical extrapolation. It was invented to solve a theoretical evolutionary dilemma. 

To recap for emphasis: Junk DNA is not just a label that was tacked on to some DNA that seemed to have no function; it is something that is required by evolution. Mathematically, there is too much variation, too much DNA to mutate, and too few generations in which to get it all done. This was the essence of Haldane’s work. Without junk DNA, evolutionary theory cannot currently explain how everything works mathematically. Think about it; in the evolutionary model there have only been 3–6 million years since humans and chimps diverged. With average human generation times of 20–30 years, this gives them only 100,000 to 300,000 generations to fix the millions of mutations that separate humans and chimps. This includes at least 35 million single letter differences,10 over 90 million base pairs of non-shared DNA,10 nearly 700 extra genes in humans (about 6% not shared with chimpanzees),11 and tens of thousands of chromosomal rearrangements. Also, the chimp genome is about 13% larger12 than that of humans, but mostly due to the heterochromatin that caps the chromosome telomeres. All this has to happen in a very short amount of evolutionary time. They don’t have enough time, even after discounting the functionality of over 95% of the genome—but their position becomes grave if junk DNA turns out to be functional. Every new function found for Junk DNA makes the evolutionists’ case that much more difficult.

Without Junk DNA, evolution runs into insurmountable mathematical difficulties.

One of the important classes of “junk DNA” is retrotransposons, which were thought to be leftovers from ancient virus infections where bits of DNA from the viruses had been randomly inserted into the DNA of humans (for example).
The idea that huge stretches of human DNA are useless junk left over from evolution is itself having to be progressively junked.
The idea that huge stretches of human DNA are useless junk left over from evolution is itself having to be progressively junked.

Enter Faulkner et al. (2009). Working in human and mouse, they discovered that between 6 and 30% of RNAs13 start within retrotransposons. Their distribution is clearly not random. This was a shock in itself, but they added that these RNAs are generally tissue-specific, as if there were different classes of retrotransposons involved in regulating gene expression in different tissues. From the start, their conclusions do not seem to support the idea that retrotransposons are evolutionary junk, but it gets better from there. It turns out that retrotransposons coincide with gene-dense regions and occur in pronounced clusters within the genome, emphasizing the non-random distribution pattern. When they occur upstream of protein coding genes, they provide an abundance of alternative start sites for transcription, producing abundant alternative mRNAs and non-coding RNAs. On the downstream end, over one quarter of RefSeq (protein-coding) genes14 have a retrotransposon in their 3’ UTRs,15 and these reduce the amount of protein synthesized. They concluded that these 3’ UTRs are the site of intense transcriptional regulation. This is hardly something one would expect from junk DNA! Based on the distribution of retrotransposons, they identified a whopping 23,000 candidate regulatory regions within the genome. In addition, they found 2,000 examples of bidirectional transcription caused by the presence of retrotransposons (where the DNA is “read” in both directions, not just one direction, which is thought to be the norm).

At one point Faulkner et al. try to downplay their results. They point out that only some retrotransposons contain active promoters and that only some of these are functional. They do not advocate a universal function for retrotransposons. However, as Faulkner et al. also point out, retrotransposons are highly abundant, with thousands of retrotransposon promoters immediately adjacent to protein coding genes, influencing their regulation and, they assume, their evolution. They concluded that retrotransposons have a key influence on transcription genome-wide, that they are “multifaceted regulators of the functional output of the mammalian transcriptome”, that they are “a pervasive source of transcription and transcriptional regulation”, and that they “must be considered in future studies of the genome as a ‘transcription machine’.”

Evolutionists just lost one of their favorite pieces of evidence: the ‘presence of ancient deactivated viruses in the genome’

These results are stunning. With genome regulation becoming more and more complicated, and with more and more of the genome being demonstrated to be functional, one wonders how long evolutionists can hold to the idea of junk DNA? However, hold on to it they must, for without it they lose one of their best arguments. But they just lost one of their favorite pieces of evidence: the presence of ancient deactivated viruses in the genome. Rather than being functionless vestigial remnants of our past, retrotransposons turn out to be functionally integrated into the amazingly complex regulatory apparatus of mammalian genomes!

I’d like to point out that young-earth creationists do not require the entire genome to be highly functional. While I suspect that direct and indirect controls of transcription will eventually be found for most of it, there may be very large stretches of the genome that just add temporal structure to the functional parts. Think of them as scaffolding in a three-dimensional genomic skyscraper. Even these portions will be functional (because of a need for structure), though they may not contribute directly to genome regulation, and their sequence specificity might be very weak. We’ll have to wait to see how it all works out in the end. For now, let us take heart that one more weak link in the evolutionary line of arguments has been exposed.

Related articles

Further reading


  1. ‘Vestigial’ Organs Questions and Answers; see especially No joy for junkies Return to text.
  2. e.g., Woodmorappe, J., Potentially decisive evidence against pseudogene ‘shared mistakes’. Journal of Creation 18(3):63–69, 2004. Return to text.
  3. The Great Dothan Creation/Evolution Debate; The Great Dothan Debate; Return to text.
  4. Faulkner G.J., et al., The regulated retrotransposon transcriptome of mammalian cells. Nature Genetics 41(5):563–571, 2009. Return to text.
  5. Haldane, J.B.S., The cost of natural selection, Journal of Genetics 55:511–524, 1957. Return to text.
  6. Kimura, M., Evolution rate at the molecular level, Nature 217:624–626, 1968. Return to text.
  7. Batten, D., Haldane’s Dilemma Has Not Been Solved. Journal of Creation 19(1):20–21, 2005. Return to text.
  8. Batten, D., The Biotic Message: Evolution versus Message Theory. Journal of Creation 11(3):292–298, 1997. Return to text.
  9. Ohno, S., So Much “Junk” DNA in our Genome. Evolution of genetic systems. Brookhaven Symposia In Biology, no. 23 (Smith, H.H., ed.) pp. 366–370, 1972. (available at Return to text.
  10. Varki A. and Altheide T.K., Comparing the human and chimpanzee genomes: searching for needles in a haystack. Genome Research 15:1746–1758, 2005. Return to text.
  11. Demuth J.P., et al., The evolution of mammalian gene families. PLoS One 1:e85, 2006. Return to text.
  12. According to the Genome Size Database (, the human genome size (reported as "C-value", a unit of weight that is [theoretically] directly proportional to genome size) is 3.2. Chimp C-values have been recorded as 3.46, 3.63, 3.76, and 3.85. They all indicate the human genome is smaller (8–17%). Return to text.
  13. RNAs are an intermediate step between DNA and protein. They are manufactured from DNA via the process of transcription. Not all RNAs are turned into protein, however, as they serve a myriad of other functions in the cell. Return to text.
  14. A standardized catalog of protein coding genes. Return to text.
  15. UTRs (“untranslated regions”) are portions of mRNA that are not translated into protein. There are generally two UTRs per mRNA transcript, one at each end. The 3’ UTR is on the downstream end, after the protein coding portion, and generally contains a termination signal, a polyadenalation signal, and other features. Return to text.


Really, the entire Darwinist myth is falling apart at the seams.   At the Macro level of the Universe, where Big Bang ideas are becoming a parody of themselves (gravity forced matter to appear?  What?!) or, when stated seriously they consist primarily of energy and mass that cannot be found.   At the Micro level, where we see that DNA and RNA become more obviously designed with every study done on them.  In every field of science the Creationists have the better explanation.