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.

---

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

[ahayes]

Whee! Quickly, move that goal post! Faster, faster!

You are taking the exception that there are some overlapping open reading frames on the anti-sense DNA strand in a number of genes

What is really amusing here is that you granted the existence of something way more unusual than the garden variety situation and you don't even know it.

This is what we usually see:

5'-->-a-b->--->--3'
3'-->----->2-1>--5'

You say that this is impossible, yet you're granting that this happens:

5'-->-a-b->--3'
3'-->2----1>-5'

Overlapping orfs take place pretty frequently on the same strand, less commonly on the complementary strand because if you've got to make the sequence on one strand make a decent product, it's harder to make the complement make a decent product too because there's not a lot of flexibility in the possible sequence. These complementary overlapping orfs are seen most commonly in viruses since they need to cram so much information into such a short sequence. However, lucky you, I found an example in humans that you might find interesting.

So now we see that genes do occur on both strands by your own forced admission. I see that Ichneumon posted and find myself going OUCH! because of the fact that you got owned by Wikipedia. That's got to smart.

Given your disgruntled acceptance that both strands have genes and both are thus coding, given the fact that chemically there is nothing to distinguish one strand from the other, and given the fact that DNA can squiggle about from being linear to be supercoiled (an apparent earlier objection of your seems to be that DNA isn't flexible enough to be twisted around and joined up as it is), you have no rational reason to say that such rearrangments are impossible.

But you are still trying to say that although genes are on both strands, still (for some reason you are incapable of explaining) we can't flip a sequence and paste it back in. Unfortunately for you reality stands to testify against you. Inversions are quite common in our genomes. For instance, in just a single woman all of these variants were found:

We graphically mapped all sites with two or more discordant fosmids in the context of repeat, gap and duplication properties of each human chromosome (Fig. 1b and Supplementary Figs. 2,3, 4,5,6, 7,8,9, 10,11,12, 13,14,15, 16,17,18, 19,20, 21, 22,23,24, 25 and Supplementary Table 1 online). After elimination of clonal propagation and other assembly artifacts (Supplementary Note online), we identified 297 sites of putative structural variation, corresponding to 139 insertions, 102 deletions and 56 inversion breakpoints (Fig. 2 and Table 1 and Supplementary Table 1 online). Seventy-five percent (228 of 297) of these sites of putative structural variation also showed spanning fosmids consistent with the human genome reference sequence, in addition to two or more discordant fosmid pairs. This indicates that the diploid individual from whom the fosmid library was constructed is probably heterozygous with respect to these structural variants, and they probably do not represent genome assembly errors. We estimate that most of these putative structural rearrangements ranged in size from 8 to 40 kb. Deletions and inversions as large as 329 kb and 1.9 Mb, respectively, were also predicted (Supplementary Note online).

("Fine-scale structural variation of the human genome." Tuzun, E., et. al. Nature Genetics. 2005, 37, 727-732.)

This healthy woman has considerable segments of her genome reversed, yet she has no ill effects and all of her genes continue working correctly. The only case in which an inversion causes problems is when the inversion breakpoint hits the middle of an orf. If it is between genes, the ribosomes are perfectly happy to continue transcribing. After all, they can't tell one DNA strand from another anyway, so why would they care?

In one case a very long inversion is spreading through the population in northern Europe. Women with this inversion statistically have more children than the general population, indicating some reproductive benefit to the inversion. The human genome project has discovered multiple variants in our genomes in healthy individuals, with inversions, deletions, and multiple copies of genes being common.

Even worse, chromosomal rearrangements of this type and others commonly occur in mice. There are mice of the same species running around with as few as 22 chromosomes or as many as 40. Heck, I also ran across this page that lists a number of observed chromosomal remodelling events, including inversions.

It really would have been so easy for you if you had just checked on this when wyattearp called you on it initially instead of insulting him. Even if you had backed down when I posted explaining it wouldn't have been so bad. But you continued digging yourself in deeper and deeper. I'm pretty darn sure you haven't got a degree in biology, so why did you think you know better than those who do have such degrees? I would think that would give you pause. I also noticed that I've never seen this particular argument used before, which makes me think that either you probably made it up yourself or you stumbled across it in some source that even other YEC groups think is suspect. Did you think that you were the sole person in the world to realize this dilemma? If you find something to be a monstrous huge deal and obviously completely wrong yet nobody else agrees, odds are you're mistaken!

[PatrickHenry]

We await your retractions.

[Thunderous applause!]

[js1138]

Did you think that you were the sole person in the world to realize this dilemma? If you find something to be a monstrous huge deal and obviously completely wrong yet nobody else agrees, odds are you're mistaken!

For a small fee I will share with you the secret of squaring the circle.

[ahayes]

It doesn't. Bacteria do not live as single animals, but in huge colonies called a biofilm. Even if you tried to isolate one, you would not be sucessful, since they are constantly in the process of replication.

It's not that hard, I did it a couple weeks ago.

1. Get an agar plate.
2. Get a bacteria culture.
3. Pipet a few microliters of culture onto the plate.
4. Spread around thoroughly with a sterile inoculation loop.
5. Incubate overnight.

Voila! If you did it correctly, you have individual bacterial colonies spotted around. Each colony is clonal, the offspring of one initial bacterium. That's the entire point of doing this, for many bacterial culture applications you need to start with bacteria that are genetically homogenous. While it takes a bit of practice to streak a plate with elegance and finesse, your average high school kid can obtain clonal colonies in bio lab.

[RobbyS]

Well, if one starts with the premise that all reality is quantififiable, one comes up with many useful models which can at least be app;lied to reality. It is only when one claims that all these models are identitical to reality that one finds one self in a cul-de-sac.
.

[DannyTN]

"Response: Micropaleontology...

Associating fossils with certain strata and with oil formations is not the use of micro evolution. That's simply association and would work fine without theories of macro-evolution. Neither is using the condition of the fossils to determine exposure to heat and pressure. Although I am surprised it took 1000 posts for someone to bring up oil exploration.

I find your explanation of using certain micro-fossils as index fossils to time date ocean floor sediment interesting. It's my understanding that the ocean floor has more burrowing creatures per square foot than does land. Therefore, I question whether ocean sediment really lies there like dust undisturbed, at least until it's more than a few feet deep. I don't doubt that micro fossils can tell us things. But I do question the interpretations because the evolutionary bias is so strong.

[DannyTN]

Undeniable proof that wizard hats evolved into apples! But I see a lot of red x's. Those must be the transitionals that are assumed to exist but are yet to be found.

[b_sharp]

"No, I'm saying that Haldane's dilemma is a concern however genes move to fixation in a population. "

I understand that. What I am trying to get you to understand is that there are also many situations where the selection cost is not high enough to be a problem. I am also trying to get yo to understand that there are situations where there is no selection costs because the allele can fix without selection as is the case with drift.

"LOL! I warn you about dealing with things that aren't observable by definition and you give me an imaginary example.

I gave you an imaginary example to help clarify the definition not to prove that ERVs have been observed. That the example is imaginary does not change the definition.

Please take the time to try to understand my posts.

[b_sharp]

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

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

Yes I know, that is why, in the post you responded to, I said the following:

However, an immediately deleterious mutation quickly removes itself from the population.

"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.

Yes, and those alleles were not immediately deleterious.

Reread my post. You will see that I differentiated between recessive and dominant genes.

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

Again from my previous post:

Deleterious mutations don't accumulate unless the mutation is only deleterious when homozygous. Or if the mutation does not become deleterious until a change of environment.

You will note the qualification that the mutation does not accumulate unless it is deleterious only when homozygous. This is a reference to a recessive allele. There is no need for an allele to be homozygous if it is dominant.

This says that a dominant allele, which is subject to selection will not fix but that recessive alleles which are not deleterious until homozygous (both 'strands' have the same allele) can and do accumulate.

So you agree then that alleles can fix without selection so that selection costs are unimportant in those cases?

[Virginia-American]

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

The simplest explanation is common insertion points.

How would that explain the tree-like pattern? Are you claiming that these "insertion points" already mimic the phylogeny of the primates?

Also, it's not the simplest explanation. It is simpler to have one insertion event rather than half a dozen.

The phenomenon under discussion is the fact that, say, people, chimps, gorillas, and orangutans all have ERVs, some of which are unique to each species. However, if one is found in two species, then it will be found in others according to the tree-like pattern: if in gorilla and orangutan, then also in people and chimpanzee. If in gorilla and chimp, but not orangutan, then also in people, and not in gibbons. Etc Etc.

[b_sharp]

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

So you are saying that the 'dsigner' went to the trouble of inserting each of those 'thousands' ERVs rather than just placing it in a common ancestor? And that is the simplest explanation?

Placing the sequence in thousands of different organisms is easier than placing it one organism and using natural speciation. Hmmm. Interesting.

[csense]

LOL

It's also proof that my two year old nephew was bouncing off the walls while I was on the computer...

[b_sharp]

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

If we model weather on a computer does that mean weather is ID?

That humans can and do model phenomena, on computer and off, does not mean those phenomena are natural, neither does it mean those phenomena are artifacts. It says exactly nothing about their ultimate origin.

For someone so interested in pointing out other's errors of logic you should realize this.

[GourmetDan]

The goalpost is back at human chromosome 2, where it's always been.

The people moving the goalposts are the ones looking for 'flipped' chromosomes or evidence of coding structures on the anti-sense strand everywhere but at human chromosome 2 where it should be.

A key prediction of evolution has failed.

[GourmetDan]

No, imaginary examples are quite the problem, not the explanation.

Were real examples available, imaginary ones would not be necessary.

Please try to understand that reality is not defined by imaginary scenarios.

The selection costs of moving that many ERVs to fixation is huge. Neutral mutation is an entirely different thing altogether. ERVs are not always neutral and the study of their function is just beginning.

You're on the wrong side of this one.

The 'best' evidence for evolution always resides in the least understood areas of biology (like Haeckel's embyos). Once the attention focuses and the truth gets out, the support for evolution disappears like the proverbial pot of gold at the end of the rainbow. It never was there in the first place.

[GourmetDan]

You are merely defining the problem so narrowly that it becomes inapplicable to the issue at hand.

Even deleterious recessives don't move to fixation in anywhere near the numbers proposed for ERVs and your effort to try to use them to justify ERV fixation is inappropriate.

You need to wake up and see that the commonly-held scenario of single-infections moving to fixation is unrealistic.

[GourmetDan]

The 'tree-like' pattern has no organisms at the branches.

Can't you see that? It's a mental construct.

Just because there may be more than one insertion event in a preferred site doesn't make it simpler to have a single event followed by an impossible string of future events.

That's foolishness.

[GourmetDan]

No, the designer originally designed viruses as DNA-sharing mechanisms. They do that quite well.

It was the fall into sin that resulted in some of them becoming malevolent.

We have already seen that ERVs help moderate insulin activity in reproduction. More discoveries are sure to come as understanding grows in this area.

That's a design feature, not a 'lucky' accident of evolution.

[GourmetDan]

No, it means that you can make a computer program do whatever you want it to.

It means nothing except what the programmer designed it to do.

[Virginia-American]

The 'tree-like' pattern has no organisms at the branches.

OK, so what?

Can't you see that? It's a mental construct.

You find the homologous ERVs and the data organizes itself as a tree. Do you have a problem with this?

So either the ERVs are inheritance from common ancestors, or they were inserted independently. In the latter case, the insertion points exhibit the tree pattern.

Just because there may be more than one insertion event in a preferred site doesn't make it simpler to have a single event followed by an impossible string of future events.

You need to show that your scenario is more likely. That would involve lab tests of how much freedom there is in retroviral insertion into germ cells, and calculations showing that every one of these ERVs fixing in all the species involved (remember that's the phenomenon that need explaining - a tree-like structure doesn't have gaps in it - if the ERV is in both orangutan and gorilla genomes, it will also be in both people and chimps) is more likely than one fixation event followed by speciation.

That's foolishness.

Needs to be demonstrated. Perhaps DI or AiG or one of the other anti-evolution advocacy groups could sponsor some research for a change.