Evolution Is Practically Useless, Admits Darwinist

Creation Evolution Headlines ^ | 08/30/06 | Creation Evolution Headlines

[DannyTN]

Evolution Is Practically Useless, Admits Darwinist    08/30/2006  
Supporters of evolution often tout its many benefits.  They claim it helps research in agriculture, conservation and medicine (e.g., 01/13/2003, 06/25/2003).  A new book by David Mindell, The Evolving World: Evolution in Everyday Life (Harvard, 2006) emphasizes these practical benefits in hopes of making evolution more palatable to a skeptical society.  Jerry Coyne, a staunch evolutionist and anti-creationist, enjoyed the book in his review in Nature,¹ but thought that Mindell went overboard on “Selling Darwin” with appeals to pragmatics:

To some extent these excesses are not Mindell’s fault, for, if truth be told, evolution hasn’t yielded many practical or commercial benefits.  Yes, bacteria evolve drug resistance, and yes, we must take countermeasures, but beyond that there is not much to say.  Evolution cannot help us predict what new vaccines to manufacture because microbes evolve unpredictably.  But hasn’t evolution helped guide animal and plant breeding?  Not very much.  Most improvement in crop plants and animals occurred long before we knew anything about evolution, and came about by people following the genetic principle of ‘like begets like’.  Even now, as its practitioners admit, the field of quantitative genetics has been of little value in helping improve varieties.  Future advances will almost certainly come from transgenics, which is not based on evolution at all.

Coyne further describes how the goods and services advertised by Mindell are irrelevant for potential customers, anyway:

One reason why Mindell might fail to sell Darwin to the critics is that his examples all involve microevolution, which most modern creationists (including advocates of intelligent design) accept.  It is macroevolution – the evolutionary transitions between very different kinds of organism – that creationists claim does not occur.  But in any case, few people actually oppose evolution because of its lack of practical use.... they oppose it because they see it as undercutting moral values.

Coyne fails to offer a salve for that wound.  Instead, to explain why macroevolution has not been observed, he presents an analogy .  For critics out to debunk macroevolution because no one has seen a new species appear, he compares the origin of species with the origin of language: “We haven’t seen one language change into another either, but any reasonable creationist (an oxymoron?) must accept the clear historical evidence for linguistic evolution,” he says, adding a jab for effect. “And we have far more fossil species than we have fossil languages” (but see 04/23/2006).  It seems to escape his notice that language is a tool manipulated by intelligent agents, not random mutations.  In any case, his main point is that evolution shines not because of any hyped commercial value, but because of its explanatory power:

In the end, the true value of evolutionary biology is not practical but explanatory.  It answers, in the most exquisitely simple and parsimonious way, the age-old question: “How did we get here?”  It gives us our family history writ large, connecting us with every other species, living or extinct, on Earth.  It shows how everything from frogs to fleas got here via a few easily grasped biological processes.  And that, after all, is quite an accomplishment.

See also Evolution News analysis of this book review, focusing on Coyne’s stereotyping of creationists.  Compare also our 02/10/2006 and 12/21/2005 stories on marketing Darwinism to the masses.

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¹Jerry Coyne, “Selling Darwin,” Nature 442, 983-984(31 August 2006) | doi:10.1038/442983a; Published online 30 August 2006.

You heard it right here.  We didn’t have to say it.  One of Darwin’s own bulldogs said it for us: evolutionary theory is useless.  Oh, this is rich.  Don’t let anyone tell you that evolution is the key to biology, and without it we would fall behind in science and technology and lose our lead in the world.  He just said that most real progress in biology was done before evolutionary theory arrived, and that modern-day advances owe little or nothing to the Grand Materialist Myth.  Darwin is dead, and except for providing plot lines for storytellers, the theory that took root out of Charlie’s grave bears no fruit (but a lot of poisonous thorns: see 08/27/2006).
    To be sure, many things in science do not have practical value.  Black holes are useless, too, and so is the cosmic microwave background.  It is the Darwin Party itself, however, that has hyped evolution for its value to society.  With this selling point gone, what’s left?  The only thing Coyne believes evolution can advertise now is a substitute theology to answer the big questions.  Instead of an omniscient, omnipotent God, he offers the cult of Tinker Bell and her mutation wand as an explanation for endless forms most beautiful.  Evolution allows us to play connect-the-dot games between frogs and fleas.  It allows us to water down a complex world into simplistic, “easily grasped” generalities.  Such things are priceless, he thinks.  He’s right.  It costs nothing to produce speculation about things that cannot be observed, and nobody should consider such products worth a dime.
    We can get along just fine in life without the Darwin Party catalog.  Thanks to Jerry Coyne for providing inside information on the negative earnings in the Darwin & Co. financial report.  Sell your evolution stock now before the bottom falls out.
Next headline on:  Evolutionary Theory

[GourmetDan]

Sorry, only dominant deleterious alleles impact the phenotype and expose themselves to selection.

http://www.scientia.org/cadonline/Biology/genetics/mutation.ASP

Doesn't look like it 'takes care of itself' to me. That's why each person has a load of deleterious mutations in their genome.

As for 'loss of function' being considered evolution, that's merely a case of 'evolution' being defined in a manner consistent with a created biology that is in decline because that's what scientists are really looking at. Not good for evo. And read the link. Deleterious mutations do not 'quickly remove themselves' from the population. That would be a lethal mutation. Mildly deleterious recessive mutations are nearly impossible to get rid of. That's why they persist as genetic load.

Recessive mildly deleterious mutations are everywhere. You really are uninformed if you think they are rare. They are more common than lethal mutations.

You know, you just really don't understand what I'm talking about. I'm not saying that 'large portions of the population are so poorly fit that they die off'. I'm saying that they must die off regardless of how fit they are for the ERV to move to fixation. And recessive deleterious mutations do accumulate. That's why populations have genetic loads.

And the numbers you use for 'beneficial' mutation fitness increase are simply laughable. Doesn't happen like that. Fitness increases are on the order of 1% for a significant one.

You do know that a 'beneficial' mutation with a 1% fitness increase has a 98% chance of being lost through drift, don't you? I think it was Haldanes calculation.

[GourmetDan]

Here you go dear.

http://www.genome.gov/glossary.cfm?key=non-coding%20DNA

You just can't 'flip it'.

The second strand doesn't code. It is known as anit-sense. It won't work. That's the problem.

[ahayes]

Goodness! Please immediately email the people who did the human genome project and tell them they have it all wrong!!

You have no explanation for the things I pointed out showing you are exactly wrong?

[ahayes]

You're operating from a junior high understanding of genetics. As I pointed out earlier, coding/noncoding and sense/antisense only have meaning if applied to a particular gene. Both strands are coding for some genes and noncoding for others.

[GourmetDan]

Well, now you are merely assuming that because the fault-tolerant, error-correcting design of the genetic code exists, it therefore must have 'evolved'.

That would be a logical error.

[GourmetDan]

Nope.

Your 'pattern' is imposed through a belief in common descent. Common insertion points in a common-design immune system does the same thing.

We have been discussing the problems of single-infection moving to fixation. There are *thousands* of these things in humans alone requiring *thousands* of 'single-infection moving to fixation' scenarios. The cost of substitution for such scenarios is tremendous and you haven't even begun to add any 'beneficial' mutations yet.

It is simply ludicrous to believe such scenarios.

[js1138]

Well, now you are merely assuming that because the fault-tolerant, error-correcting design of the genetic code exists, it therefore must have 'evolved'.
That would be a logical error.

I'm not sure what you are responding to, but it isn't anything I said.

[GourmetDan]

No, you are merely overstating your case by orders of magnitude.

You are taking the exception that there are some overlapping open reading frames on the anti-sense DNA strand in a number of genes and misapplying it to the problem at hand.

The fact that these O-ORF's exist does not mean that flipping the 5' to 3' orientation to allow head-to-head joining of 2 chromosomes wouldn't destroy the information on the coding strand.

The human chromosome 2 does not have the coding and anti-sense strands flipped as would be required if it were the result of 2 primate chromosomes joining head-to-head.

The problem still exists.

To say that 'both strands are coding for some genes and non-coding for others' may be 'correct' in a technical sense, but it is extremely disingenious and completely inappropriate for solving the problem at hand.

Nice try though.

[GourmetDan]

Yes, it was.

You just didn't understand that saying, "The point is that evolution included both beneficial and neutral changes. There are lots of mutations and chromosome changes that are synonyms or which have no immediate noticable effect.

Brings the whole reason as to *why* there are so many 'neutral' changes. That is a function of the fault-tolerant *design* of the triplet-codon, diploid, information-coding system.

[Virginia-American]

Your 'pattern' is imposed through a belief in common descent.

No, the pattern exists. The hypothesis of common descent is the simplest explanation for it.

[DaGman]

" How many generations before the deleterious mutation is removed from the population?

How many generations before the beneficial mutation fixes in the population?

What is the least number of members experienced by the population?"

You're asking way too much from a creationist, but let's see what happens.

[Ichneumon]

f you think only one strand contains genes, please go here and examine the sequence of the human chromosome. You can see that some genes are oriented in one way and some in the other. Examination of the tooltip there says, "Orientation--Down arrow: Positive strand, Up arrow: Negative strand." You might also examine this viral DNA. You can see one open reading frame runs the opposite direction from the other two. That's because it's on the other strand. Some viruses have to pack the information in so tightly that they've managed to overlap open reading frames, so one segment of DNA will produce one product and its complement on the other strand will produce a different product. The presence of genes on both strands is easily demonstrated by examining a variety of different plasmids. Now we can also go back and zoom in on a gene in the Y chromosome. You can see here that the selected gene, SRY (the sex-determining master switch, errors in this gene can result in a female with and XY genotype), runs in the opposite direction from the surrounding genes (SRY is on the minus strand, the others on the plus strand). Of course you know that this means they can't be on the same strand, since strands are transcribed 5'->3'.

Game, set, and match. GourmetDan's assertion that all transcription is done from one DNA strand and not from the complementary strand is, of course, completely bogus.

He has made the mistake of thinking that the terms "sense" and "antisense" strands are global, when in fact they are merely local -- i.e., for any one transcription coding (typically, one gene) one strand has the encoding for that gene and is considered the "sense" strand FOR THAT GENE and the complementary strand is the "antisense" strand (again, FOR THAT GENE). The next gene down the pike, however, may be coded on the *other* strand, at which point the "sense" and "antisense" strands for that region will be vice versa.

It's fascinating that GourmetDan thinks that the ape -> human chromosome fusion was done "head to head" and that other chromosome fusions (in other animals) is done "head to tail". The reason his claim is fascinating is because I don't know where in the heck he could have gotten such an impression, because it's not true and doesn't even make any freaking sense. Chromosomes don't have "heads" and "tails". There's nothing, biologically or chemically speaking, to distinguish one end from the other. BOTH ends terminate in a matched pair of DNA strands which are 5' on one strand and 3' on the other strand.

And you can end-to-end fuse a pair of chromosomes in any of four configurations (p-p, p-q, q-p, q-q) and all of them will remain functional. Nature doesn't "care" about the orientation of the strands. And even a moment's thought should have revealed this -- think about it: when transcribing some gene in the middle of a megabase DNA helix, the ribosomes haven't a clue what strand is which or what "direction" either one is oriented relative to the ends or any other sequences (or entire chromosome) might be pasted onto it twenty million bases away. For an analogy, think of pulling a loop of string out of the middle of a gigantic ball of string -- there's no way to know which "direction" your loop of string is oriented (i.e. no way to know which direction you'd have to follow the string in the loop to get to the "north" or "south" end of the huge length of string making up the big ball of string. Nor, if the string consisted of two thinner fibers twisted together, would you have any way of knowing which fiber in the loop was which, even if you had them labeled as "A" and "B" at one of the ends.

The cellular "machinery" which transcribes, copies, repairs, and pefforms other functions on DNA strands has no way of telling these things either. There is no "preferred" strand, because there's no way to distinguish one from the other.

Another way of looking at it is that if one chromosome works properly by itself, i.e. if ribosomes can jump into the middle of it and transcribe genes from it, it'll *still* work fine when another chromosome is "pasted" onto it end-to-end, because transcription is done locally and doesn't "know" or "care" (because it can't "see") what might or might not be attached to the former "end" of the DNA helix it's transcribing. Of course, the same argument applies to the *other* chromosome in the fusion as well. So no matter *what* order or direction they're fused into, mid-chromosome transcription (and all other local processes) will continue to work as well after the fusion as before, because the mid-chromosome regions are unchanged and untouched.

GourmetDan should have been able to figure this out for himself, if he had any clue about biology in the first place. Funny that even though he doesn't have such a clue, he still frequently feels qualified to lecture *us* on it...

You know GourmetDan's error is an elementary one (and inexcusable) when even a quick check on something as elementary as the Wikipedia entry for DNA has the information necessary to learn the error of his ways:

This merely confirms that there is no biological distinction between the two strands of the double helix. Typically each strand of a DNA double helix will act as sense and antisense in different regions.

I wonder how you got the idea that only one strand has information on it, and why you think this is required.

Yeah, I'd like an answer to that one too... Did he get it from some clueless (or dishonest) anti-evolution source, or did he just make it up?

If we mentally examine the two DNA strands of a duplex, both strands are pretty much the same so far as a ribosome is concerned--they both have the four bases and they both run 5'->3'. An open reading frame on either strand will be transcribed.

Bingo.

So, GourmetDan, would you care to retract the following bogus claim you made in post #676?

Take the gorilla-chimp/human 'chromosome fusion' argument as an example. One problem that I've never seen answered is how scientists explain away the 5' to 3' problem of joining 2 chromosomes head-to-head? It would seem to be critical to the claim, yet I have never seen that addressed.

How about this bogus claim in post #709?

The observed type of chromosome fusion is not the *assumed* head-to-head fusion of the evos. That has never been observed. The head-to-head issue presents a unique problem because of the 5' to 3' structure. You don't seem to adequately understand the problem and merely propose generic 'chromosome fusions' as solving your inadequate understanding of the 5' to 3' problem. They do not solve it because they are a different type of chromosome fusion that avoids the 5' to 3' problem. It is the proposed head-to-head joining that is the issue.

Ready to retract this bogus claim from post #870?

The hypothesis is that human chromosome 2 is a fusion of 2 primate chromosomes joined head-to-head. The 5' to 3' structure makes this impossible, yet the problem is glossed over in favor of 'banding pattern' similarities (which mean nothing). http://www.evolutionpages.com/chromosome_2.htm If you twist the chromosome, you join the anti-sense strand to the sense strand and the anti-sense strand does not code.

How about this bogus claim from post #993?

Nope, strand 2 is non-coding.

Or this bogus claim from post #995:

Good grief dude. You know absolutely nothing about this subject. One strand does code and the other does not. Do some research.

We await your retractions.

[Ichneumon]

There are *thousands* of these things in humans alone requiring *thousands* of 'single-infection moving to fixation' scenarios.

Yes indeed. So?

The cost of substitution for such scenarios is tremendous and you haven't even begun to add any 'beneficial' mutations yet.

Son, once again, there is no "cost of substitution" for neutral fixation. Period. Deal with it, and stop repeating falsehoods that don't get any more true the louder and more often you repeat them.

You haven't a clue what you're talking about, you're just flinging buzzphrases around with no understanding of when they do and do not apply, but that doesn't stop you from blathering on about them endlessly. Why do you behave this way?

It is simply ludicrous to believe such scenarios.

I'm sure it looks that way to someone who doesn't understand them in the least. But they make fine sense to those of us who do.

[GourmetDan]

No, the hypothesis of common descent is not the simplest explanation.

The simplest explanation is common insertion points.

Common descent requires too many individual infections in single organisms moving to fixation to be plausible.

There are thousands of these things in the human genome alone.

[Ichneumon]

Brings the whole reason as to *why* there are so many 'neutral' changes. That is a function of the fault-tolerant *design* of the triplet-codon, diploid, information-coding system.

You mean the *evolution* of fault-tolerance...

Fault tolerance naturally arises through selection in evolutionary processes. See for example:

Evolution of mutational robustness

Abstract: We review recent advances in the understanding of the mutation-selection balance of asexual replicators. For over 30 years, population geneticists thought that an expression derived by Kimura and Maruyama in 1966 fully solved this problem.However, Kimura and Maruyama’s result is only correct in the absence of neutral mutations. The inclusion of neutral mutations leads to a wealth of interesting new effects, and, in particular, to a selective pressure to evolve robustness against mutations.We cover recent literature on the population dynamics of asexual replicators on networks of neutral genotypes, on the outcompetition of fast replicators by slower ones with better mutational support, and on the probability of fixation at high mutation rates.We discuss empirical evidence for the evolution of mutational robustness, and speculate on its relevance for higher organisms.

Evolution of Robustness in Digital Organisms

Abstract: We study the evolution of robustness in digital organisms adapting to a high mutation rate. As genomes adjust to the harsh mutational environment, the mean effect of single mutations decreases, up until the point where a sizable fraction (up to 30% in many cases) of the mutations are neutral. We correlate the changes in robustness along the line of descent to changes in directional epistasis, and find that increased robustness is achieved by moving from antagonistic epistasis between mutations towards codes where mutations are, on average, independent. We interpret this recoding as a breakup of linkage between vital sections of the genome, up to the point where instructions are maximally independent of each other. While such a recoding often requires sacrificing some replication speed, it is the best strategy for withstanding high rates of mutation.

[Ichneumon]

No, the hypothesis of common descent is not the simplest explanation.

Sure it is.

The simplest explanation is common insertion points.

Uh huh. Sure. You betcha. Except that there is absolutely no plausible mechanism for "common insertion points", and absolutely no evidence (in the field, or in experiments) for retroviral insertions ever having any method for, or any history of, ever performing a "common insertion" (i.e. ending up in identical locii in independent insertion events).

Nice try.

Look, admit it -- you just won't accept the overwhelming evidence of the origin of matching ERVs because you refuse to admit the possibility of common descent. You're rejecting the data because of your dogmatic bias.

Common descent requires too many individual infections in single organisms moving to fixation to be plausible.

No it doesn't. Feel free to try to produce calculations supporting your wild-assed guess, though. This should be highly amusing.

There are thousands of these things in the human genome alone.

Yeah, so? Feel free to show us your math indicating why this is somehow incompatible with their having gotten there in ancestral infections.

By the way, son, if they're *not* there by way of common descent, you've just made your "implausibly many" claim even WORSE, not BETTER, because you've *reduced* the time and population in which these ERVs could have been acquired. If there's any kind of "wow there's too many ERVs in the human genome" problem as you assert (but have provided no argument for), the common descent scenario REDUCES the problem, not makes it worse.

OOPS!

Now, show us your math. I could use a laugh.

[GourmetDan]

Let's see. You neglected to include this part of the Wiki article. It was just before the part you snipped and posted so disingenuously.

"A small proportion of genes in prokaryotes, and more in plasmids and viruses, blur the distinction made above between sense and antisense strands. Certain sequences of their genomes do double duty, encoding one protein when read 5' to 3' along one strand, and a second protein when read in the opposite direction (still 5' to 3') along the other strand."

Hmmm, 'a small proportion'. Simple oversight, I'm sure.

The fact is, there are sense and antisense strands on the DNA and flipping the chromosome to fuse it head-to-head simply won't work.

And the fusion of the primate chromosome was head-to-head. The long arm points down and the chromosome that is supposed to have fused has been flipped in orientation so that the long arm is up.

[GourmetDan]

Now neutral fixation is a different thing that a single-infection moving to fixation.

Single-infections moving to fixation follow the same path as beneficial mutations (according to the claim) even though they are not. This makes their fixation even more problematic, not less.

[GourmetDan]

No, the presence of fault-tolerance does not mean that it 'evolved'.

One of your links is an ID computer program. Are you saying that life is ID?

The other link says that organisms that are fault-tolerant do better than those that are not. No big whoop there, but that doesn't explain how fault-tolerance 'evolved'.

Most evos can't get past the idea that, because something is beneficial, it must have evolved.

That doesn't logically follow.

[GourmetDan]

Here's an example of an HERV that is involved in insulin regulation during human reproduction.

How convenient that this 'random' infection just 'happened' to help regulate this insulin gene and the reproductive process.

http://www.biolreprod.org/cgi/content/full/68/4/1422

No evidence, yeah right.