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Thanks Larry! If a species can lose its stomach, it must mean the mutation was neutral

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Larry actually had some rare kind words for me. He said here

Cordova is correct.

Thanks for the kind words, Larry!

Larry goes on to argue that organisms can tolerate lots of mutations and still reproduce.

Yes, I agree, but reproduction is not the real thing in question, it is the existence of designs. I’ve argued even with creationists the issue isn’t whether mutations are “beneficial” or “deleterious” in the sense of differential reproductive success, the question is whether neutral evolution and real selection in the wild will tend to destroy design rather than build it.

What’s the simplest fix to the problem of irreversibly accumulating bad mutations (as I illustrated here)? Simple, renormalize the selection coefficients and declare being sick as the new normal. Problem solved!

To solve the problem of deleterious mutations, evolutionists will argue loss of function is reproductively “beneficial” or neutral. Think I’m kidding? If you were a shark, you’d lose your stomach over the idea:

How the ghost shark lost its stomach

Animals from lungfish and ghost sharks to platypuses have lost their acid-making stomachs over evolutionary time, and researchers have now traced the genetic changes behind these stomach upsets.

True stomachs with digestive glands that concentrate acid and release protein-cutting enzymes called pepsins evolved with vertebrates. The gastric glands arose some 450 million years ago but have dwindled away at least 15 separate times across the animal tree of life, explains Filipe Castro of the University of Porto in Portugal.

More than a quarter of known bony fish species digest food without a true acid stomach. Picking out what drove the evolutionary change is tricky, says Jonathan Wilson, also at Porto. For instance, pufferfishes now repurpose their organ to store food and bloat with water for menacing spines-out displays.

After scrutinizing genes of 14 vertebrates with and without stomachs, Castro and his colleagues determined that none of the stomach losers has high-functioning genes for maintaining a highly acidic zone in their digestive tracts.

The animals also lack or have low-functioning genes for secreting the peptic enzymes that slice and dice proteins under acidic conditions, the researchers report December 4 in the Proceedings of the Royal Society B.

Losing one’s stomach is neutral at best and “beneficial” at worst, thus no need to worry that mutations are deleterious — solution via redefinition of good and bad. Some have called this genius insight Survival of the Sickest, Why We Need Disease.

So was the DNA that coded for the now missing stomach junk DNA? Since nature has shown we can knock the stomach out and the organism still reproduces for millions of years, does this mean their stomachs are junk and so was the DNA that coded them? This obviously has relevance to the junk DNA discussion today where sometimes the benchmark for determining if something is junk is whether we can sacrifice it and the organism still reproduces.

Larry argues elsewhere:

Because a large percentage of gene mutations are neutral, and because most of our genome is junk, we can easily tolerate 130 mutations per individual per generation without going extinct.

Genetic Load Neutral Theory and Junk

But tolerating the mutation isn’t the real question, it’s how such a scrambling process can be compatible with development of novel complexity. Larry answers a question that is not being asked. The problem is about irreversible loss of function, it’s not about the ability to keep making babies.

In light of these considerations, the problem of deteriorating design remains as I pointed out in my claim that high mutation rates create high breakage rates.

Evolutionists think of “beneficial” in terms of reproductive success whereas IDists and creationists think of beneficial in terms of function. Unfortunately, as happens in some creationists papers and books like Genetic Entropy, the creationists sometimes fall into the trap of using the Darwinists notions of “beneficial.”

Behe’s rule of adaptive evolution illustrates the problem — most of the radical sorts of adaptive evolution observed in real time are examples of functional loss, not gain. Behe’s rule is experimentally confirmed, and this casts doubts that this mode of adaptation can be an explanation for evolution of function in the first place.

The problem is, when we can freely say losing one’s stomach is a neutral mutation, then we are free then to insist neutral theory is correct because it is fundamentally unfalsifiable on such terms.

I’ve proposed the proper way to falsify neutral theory is if we can show mutations are increasing unabated in deeply “conserved” regions. If we show this, then both selectionist and neutralist theories are falsified properly, and design is vindicated. Right now, it’s still a tad too expensive to carry such research out, but because the question of genetic deterioration has medical significance, I expect the ID proponents will have their answers in due time and John Sanford’s genetic entropy thesis will be vindicated.

NOTES

1. Larry, couldn’t you have picked April 2 instead of April 1 to say something nice about what I said? 🙂

2. Thanks any way, Larry.

3. Here I suggested in 2007, there will be almost unabated growth of mild, almost undetectable defects accumulating in the genome.

JoeCoder, to my surprise, informed me that just last year:
Past 5000 years prolific for changes to human genome

Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. On average, 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. ‘There’s so many of [variants] that exist that some of them have to contribute to disease,’ says Akey

As I predicted, the deep sequencing made possible by Solexa technology is paving the way to vindicate ID claims over the competing theories of selection and neutral evolution in the past.

Thanks JoeCoder. You made my day, even if it means the human race is dying, at least I got something right.

4. I accept neutralism as a better description of evolution in the present day, but I reject it as an explanation of design and the fundamental structures of biology. Neutral evolution is real, it wins out over Darwinian selection, but it’s not the mechanism of design. Neutral evolution destroys design, it much less does it explain it.

5. Here is an excerpt form the paper in question. Note how the problem of harmful mutations is nicely renormalized away. Just redefine the loss of an organ as a good thing or neutral thing, and problem solved!

We propose that relaxation of purifying selection in pepsinogen genes and possibly proton pump genes in response to dietary changes led to the numerous independent events of stomach loss in gnathostome history. Significantly, the absence of the gastric genes predicts that reinvention of the stomach in agastric lineages would be highly improbable, in line with Dollo’s principle.

Recurrent gene loss

Translation, “we propose neutral evolution”. And lo and behold, on top of that we have fixation of this neutral trait in all those species who’ve lost their lunch.

6. The fundamental problem with evolutionary theory as compared to theories of physics is that the most fundamental concept “selective advantage” is not well-defined compared to physical notions like mass, charge, length, and time. The ambiguity, imho, is fatal to evolutionary theory. I tried to demonstrate the problem in this essay: Dennet’s Strange Idea is a bad idea for recognizing design. The article about sharks losing their stomachs serves to highlight this problem.

7. HT JoeCoder x10

25 Replies to “Thanks Larry! If a species can lose its stomach, it must mean the mutation was neutral

  1. 1
    scordova says:

    The reason I suggest tests of sequence divergence in the present day is that the numbers are unambiguous when we make a measurements. Selection coefficients even in the present day, when dealing with weakly detectable traits, are pretty much hard to define much less measure as Lewontin and Andreas Wagner rightly point out. How much less can we say what the selection coefficients were in the past!

    These questions can be settle by science, by observation. So far so good for John Sanford.

  2. 2
    wd400 says:

    This is so… all over the place that it’s very hard to see exactly what you are trying to say.

    What does this mean?

    I’ve proposed the proper way to falsify neutral theory is if we can show mutations are increasing unabated in deeply “conserved” regions

  3. 3
    scordova says:

    I’ve proposed the proper way to falsify neutral theory is if we can show mutations are increasing unabated in deeply “conserved” regions

    Take the regions that both mice and men or men and men have conserved. Sequence the mice and men over a generation or more (father, son, grand son, great grand son), see if they start to have more SNP’s in the conserved regions over that short span. To detect the grown, one need large samples of humans since novel SNPs (or whatever) are rare.

    If the SNPs grow and grow, it means they aren’t subject to selection, which then is a problem for arguing the regions are somehow conserved by selection.

    I’m sure someone as smart as you could figure out the proper observational parameters to make a valid measurement. The question obviously has medical significance.

    If the conserved regions are grown in mutations, it then raises the question, “why are they conserved to begin with?”

  4. 4
    CentralScrutinizer says:

    Here’s the deal. Can we have a thread where the neo-darwinists can post their bests arguments and/or evidence that small mutations can be selected to emerge novel cell types, tissue types, organs or body plans. (Examples of deleterious mutations excepted, like cancer cells.)

    Isn’t that the bottom line here?

    If they can’t, what’s all the debate about?

    Forget ID. Stop trying to argue ID. The “modern synthesis” is bankrupt. All reasonable people should be forced to acknowledge this first.

  5. 5
    wd400 says:

    You don’t need to sequence thousands of people mice – selection changes allele frequency distirbutions so you can sample populations instead. There are quite a few papers on this sort of thing – generally showing that (a) selection is still acting on conserved regoins (b) selection is somewhat repaxed in apes relative to rodents (presumble due to the smaller effective population sizes near our branch of the tree)

    Here’s one such, which will probaly lead you to more: http://www.nature.com/ng/journ.....g1710.html

  6. 6
    scordova says:

    Great comment WD400, thanks for the info.

  7. 7
    JoeCoder says:

    Sal, if you really wanted to drive home the point I would’ve focused on this part from Dr. Moran:

    It’s probably less than two (2). It’s probably not as low as 0.5. It should be no more than 1 or 2 deleterious mutations per generation.

    And compared it with various studies that estimate the number of conserved sequences or strict function from other means. I cited a couple in the other thread but I don’t know of any that are low enough to get it at or below two deleterious mutations per generation.

    I’m not sure if I agree with Dr. Moran that 1-2 is the limit–the math I described in the first comment of the other thread would allow it to be much higher than that, and I’m not sure if it’s possible to even get accurate results with formulas instead of simulations. For the record I do think genetic entropy is real in higher organisms but establishing that is much more complicated than any of us are doing here.

  8. 8
    JacobyShaddix says:

    Sal,

    I’m struggling to find your point in this rant or are you just gloating about the fact that you and a Professor of Biochemistry agree on something?

    Yes, I agree, but reproduction is not the real thing in question, it is the existence of designs.

    Perhaps you could start by telling us what a design is because I have never encountered this term in the scientific literature?

    in the sense of differential reproductive success

    Reproductive success is all that matters. The question of whether a lungfish has a stomach or not is completely irrelevant. The matter of function is completely irrelevant if that function is no longer required.

    Simple, renormalize the selection coefficients and declare being sick as the new normal.

    So lungfish are sick now? Have you ever asked a lungfish how it felt? I get the impression that they’re quite quite content and that they have everything they need for reproductive success.

    More than a quarter of known bony fish species digest food without a true acid stomach. Picking out what drove the evolutionary change is tricky, says Jonathan Wilson, also at Porto. For instance, pufferfishes now repurpose their organ to store food and bloat with water for menacing spines-out displays.

    After scrutinizing genes of 14 vertebrates with and without stomachs, Castro and his colleagues determined that none of the stomach losers has high-functioning genes for maintaining a highly acidic zone in their digestive tracts.

    The animals also lack or have low-functioning genes for secreting the peptic enzymes that slice and dice proteins under acidic conditions, the researchers report December 4 in the Proceedings of the Royal Society B.

    They probably lost that function due to their feeding habits and environment. They weren’t using it and so didn’t need it. This meant that there was no selective pressure to maintain those genes and so they freely started accumulating mutations. What is the issue here? I fail to see your point.

    Here is another example you can add to your menagerie: The Mexican Tetra. It is a fish with no eyes and no pigmentation. This is because it lives in the dark and both of these features would be useless to it. At one point it had an ancestor with eyes and pigmentation, but these were eventually lost due to random mutations due to the fact that there was no selective pressure to maintain these features.

    The Mexican Tetra is not sick. It is perfectly suited to its environment. If you were to change its environment, it wouldn’t compete very well with other fish, but why should unguided natural selection care about that?

    So was the DNA that coded for the now missing stomach junk DNA?

    In all likelihood, yes. They could be pseudogenes in the lungfish or they might be missing altogether due to deletions. We have pseudogenes too for functions that no longer contribute to our genetic fitness. They are junk DNA – you should look into that.

    Since nature has shown we can knock the stomach out and the organism still reproduces for millions of years, does this mean their stomachs are junk and so was the DNA that coded them?

    Like I said Sal. IT DEPENDS ON THE ENVIRONMENT. I doubt an ape would survive long without stomach acid, but clearly a lungfish can. If the selective pressure exists to maintain a function, it will be maintained.

    it’s how such a scrambling process can be compatible with development of novel complexity

    This is something else you need to read up on. Here is a good place to start. A major contributor of novel complexity is gene duplication, followed by point mutations. There are plenty of examples of where this has likely occurred in the scientific literature.

    This has also been observed in simulations.

    Evolutionists think of “beneficial” in terms of reproductive success whereas IDists and creationists think of beneficial in terms of function

    Which is daft because “functional” is a relative term. Function is relative to the environment. An F1 racing car floating in orbit is non-functional because it needs pressure on its wheels in order to be able to function.

    The problem is, when we can freely say losing one’s stomach is a neutral mutation, then we are free then to insist neutral theory is correct because it is fundamentally unfalsifiable on such terms.

    What would falsify neutral theory would be if creatures kept the organs they no longer needed and if pseudogenes were non-existent. If the Mexican Tetra kept their eyes even when they no longer needed them, that would falsify neutral theory.

  9. 9
    JacobyShaddix says:

    Sal said:

    If the SNPs grow and grow, it means they aren’t subject to selection, which then is a problem for arguing the regions are somehow conserved by selection.

    And what if these SNPs simply produced functional alleles?

  10. 10
    Joe says:

    Jacoby:

    A major contributor of novel complexity is gene duplication, followed by point mutations.

    Not enough time for unguided evolution to pull that off:

    Waiting for TWO Mutations

  11. 11
    JacobyShaddix says:

    Joe:

    The link I gave lists three papers which discuss instances where we see evidence for this occurring:

    > Two enzymes in the histidine biosynthesis pathway that are barrel-shaped, structural and sequence evidence suggests, were formed via gene duplication and fusion of two half-barrel ancestors (Lang et al. 2000).

    > RNASE1, a gene for a pancreatic enzyme, was duplicated, and in langur monkeys one of the copies mutated into RNASE1B, which works better in the more acidic small intestine of the langur. (Zhang et al. 2002)

    > Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further. (Brown et al. 1998)

    There are many others

  12. 12
    bornagain77 says:

    JacobyShaddix, since the histidine example is pretty much pure speculation, I’ll skip it, but as to your other two examples:

    Hopeless Matzke -David Berlinski & Tyler Hampton August 18, 2013
    Excerpt: RNASE1

    A gene destined for the short-term glory peculiar to genetic publicity campaigns. “The origination of new genes,” Zheng et al write, “was previously thought to be a rare event at the level of the genome … However, it does not take many sequence changes to evolve a new function (emphasis added). [W]ith only 3% sequence changes from its paralogues, RNASE1B has developed a new optimal pH that is essential for the newly evolved digestive function in the leaf-eating monkey” (emphasis added).

    This is interesting, exciting and false.

    a) The new and improved optimal pH promoted by RNASE1B does not involve a new function, let alone a new protein fold. The fold remains the Ribonuclease fold. Colobines are old world monkeys that that eat leaves and employ symbiotic bacteria in their foregut to digest cellulose. The bacteria are themselves digested in the small intestine. To efficiently recycle nitrogen from RNA in quickly growing intestinal bacteria, it is better that the expression levels of RNASE1B be higher in the small intestine than in the foregut. And better that the optimal pH for its enzyme be lower, since the intestinal environment itself has a pH of between 6 and 7. The adaptation involved in lowering the optimal pH from 7.4 to 6.7 is accomplished principally by three forward mutations, something Zheng et al demonstrated by reconstructing and then expressing the ancestral sequence in bacteria. Do the mutations altering RNASE confer a tangible benefit? They do not. There is no increased catalytic activity for the enzymes operating at the lowered optimal pH as opposed to the raised optimal pH. The mutations that lowered the optimal pH caused the enzyme to lose other features. Nothing in Zheng et al. account suggests that the mutations represented a complex adaptation.

    b) Long’s assertion that lowered optimal pH was essential for digestive function is a more urgent claim. It suggests the existence of tight functional constraints on changes leading to a complex adaptation. But whatever Long may suggest, the facts are otherwise. They so often are. “Although unproven,” Zheng et al. write, “it is generally believed that foregut fermentation and leaf-eating emerged in the common ancestor of all colobines. Fossil evidence suggests that these changes occurred at least 10 Myr ago predating the duplications of RNASE1.”

    What follows is emphatic: “The shift in optimal pH of the pancreatic RNases was not necessary for the changes in diet and digestive physiology of colobines.”

    Not necessary, meaning not essential. “Rather, the latter changes provided a selective pressure for more efficient digestive RNases in acidi?ed environments, while gene duplication offered raw genetic materials that enabled this functional improvement.”

    Only the monkeys are apt to remain impressed.
    http://www.evolutionnews.org/2.....75631.html

    Can Random Mutations Create New Complex Features? A Response to TalkOrigins – Casey Luskin June 22, 2012
    Excerpt: In another study, the TalkOrigins Page states, “Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further.” Assuming the description is correct, we see more of the same — nothing “new” is evolving. The key to gene duplication isn’t explaining how you can get more of the same, but rather how you can get something that wasn’t there before.
    http://www.evolutionnews.org/2.....61221.html

    Related notes:

    Evolution by Gene Duplication Falsified – December 2010
    Excerpt: The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality. Contrary to Darwin’s view of the plasticity of biological features, successive modification and selection in genes does indeed appear to have real and inherent limits: it can serve to alter the sequence, size, and function of a gene to an extent, but this almost always amounts to a variation on the same theme—as with RNASE1B in colobine monkeys. The conservation of all-important motifs within gene families, such as the homeobox or the MADS-box motif, attests to the fact that gene duplication results in the copying and preservation of biological information, and not its transformation as something original.
    http://www.creationsafaris.com.....#20110103a

    The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway – Ann K. Gauger and Douglas D. Axe – April 2011
    Excerpt: We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions. But evolutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth.
    http://bio-complexity.org/ojs/.....O-C.2011.1

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://biologicinstitute.org/2.....t-collide/

  13. 13
    Joe says:

    Jacoby- Perhaps that is because A) gene duplication is assumed in all those cases or B) gene duplication is a design mechanism- see “Not By Chance” Spetner 1997

  14. 14
    JacobyShaddix says:

    Joe:

    If two genes have a remarkably similar structure but there are differences leading them to produce different proteins, then gene duplication is the most rational explanation.

  15. 15
    Joe says:

    Jacoby:

    If two genes have a remarkably similar structure but there are differences leading them to produce different proteins, then gene duplication is the most rational explanation.

    Is it? In a common design that is what happens anyway. Functioning genes are duplicated and modified for another organism or for a slightly different function in the same organism.

    However in the context of blind processes gene duplication followed by function altering mutations is a pipe dream tnat requires too many coincidences. Along with the gene you need to have a binding site and promoter. And in the beginning you will just be pumping out a copy of an existing protein which could get in the way of normal activity.

  16. 16
    scordova says:

    Perhaps you could start by telling us what a design is because I have never encountered this term in the scientific literature?

    Perhaps then you should advise a Nobel Prize winner in science not to use the word “design” to describe biology because she used the term in her 2009 Nobel lecture. She used the phrase “ingenious design” to describe the ribosome. 🙂

    http://www.nobelprize.org/nobe.....ecture.pdf

    There is a graduate student program at Arizona State:

    http://www.biologicaldesign.asu.edu/

    Biological Design attempts to mimic or harness natural processes by understanding the rules by which nature designs highly adaptable and efficient systems.

    And last but not least, anti-IDist Ken Miller:

    A Brown University biologist says the best way to communicate evolution in a religious America is to acknowledge that there is indeed a “design” in living things. He says scientists should embrace the concept of “design” in a way that supports evolutionary theory. He argues that science itself, including evolutionary biology, is predicated on the idea of “design” — the correlation of structure with function that lies at the heart of the molecular nature of life.

    http://www.sciencedaily.com/re.....143838.htm

    And Kenny Miller is a biology textbook author for high school students:

    Miller will argue that science itself, including evolutionary biology, is predicated on the idea of “design” — the correlation of structure with function that lies at the heart of the molecular nature of life.

    Miller defines it as the correlation of structure with function.

    This is a nice paper by the way it says DNA has 10 of 13 counterparts to design features of human language.

    [update, here is the link]
    http://www.conformon.net/wp-co.....of-DNA.pdf

  17. 17
    scordova says:

    I fail to see your point.

    Because you define biological function in terms of immediate reproductive success. Function transcends reproductive success. That’s why sickle cell anemia is viewed as a sickness by the medical profession but Darwinists view it as a beneficial mutation. That’s why you look at losing a stomach as either neutral or beneficial, but anyone else losing their stomach would view it as a tragedy.

  18. 18
    Upright BiPed says:

    Sal, what “nice paper” were you referring to?

  19. 19
    scordova says:

    Cross posted from VJTorley’s thread on neutral theory and human evolution:

    RodW
    1. Are there good reasons to think that there have been muutations/genes that have been positively selected in the human lineage or is this just evolutionists making stuff up?

    What do you mean positively selected, selected before they were functional or after they were functional. A heart is “positively” selected for after it exists otherwise you die, but it says zero about it being positively selected for before you have it. A Stanley Salthe observed, if you ask a biologists what traits are most likely to evolve, they’ll say the ones under least selection. 😯

    Are they just making it up? It looks that way. Example:

    Did the shark stomach that is now missing in sharks evolve via selection or neutral evolution?

    Here is the problem of logic.

    If an organ (like a stomach) is vital, then how can it evolve since the organism would be dead! The alternative then is to assume the organ is not vital so that it can evolve. But to the extent it is not vital, it then casts doubts that it was under any sort of selective pressure except via pure assumption (making it up as you say). You just have to assume it is not vital but just advantageous enough that it evolves. But then, why did it lose the stomach? It casts doubt that it was selectively favored in the first place!

    So yes, it sure looks like the narratives are just made up with no justification aside from maintaining the narrative.

  20. 20
    scordova says:

    Upright BiPed,

    Sorry, I forgot to add the link. You’ll love it. Right up your alley of semiotics!

    [update, here is the link]
    http://www.conformon.net/wp-co.....of-DNA.pdf

  21. 21
    Upright BiPed says:

    gracias

  22. 22
    Evolve says:

    scordova,

    ////Losing one’s stomach is neutral at best and “beneficial” at worst///

    You entire argument breaks down with this poor statement. Losing the stomach can be beneficial at best if the organism takes to a new diet that doesn’t require enzymes working under acidic conditions. The very paper in the article you cited mentions this:

    “We propose that relaxation of purifying selection in pepsinogen genes and possibly proton pump genes in response to dietary changes led to the numerous independent events of stomach loss in gnathostome history.”

    “Presumably, there is a high cost in maintaining a complex organ like the stomach; however, estimates of these costs from specific dynamic action measurements remain ambiguous. Nevertheless, acid pumping by the H+/K+-ATPase, protection of the stomach lining from the acid and neutralization of the acid in the intestine will all contribute.”

    “We consistently found numerous cases of ongoing pseudogenization in gastric species. For example, CYM is inactive in humans as a possible consequence of the lower level of proteins in human milk, although it is suggested to be essential for neonatal milk digestion in mammals.”

    The same is true for blind cave fish who have lost their eyes. As they adapted to a new environment where eyes are useless and has a high cost of maintenance, they lost it.

    It’s such a shame these are the best arguments ID creationists can come up with. No wonder ID failed so miserably.

  23. 23
    scordova says:

    Evolve,

    there is a high cost in maintaining a complex organ like the stomach

    Which argues selection doesn’t like complexity, the very thing Darwin and Dawkins say Natural Selection is supposed to make. You’re so focused on reproduction you don’t even realize you’re helping argue for selection’s failure to maintain design, much less make it in the first place.

    Just as I said, you think survival of the sickest is some genius insight. You revel in the loss of eyes (cave fish), the loss of stomachs (sharks), the loss of wings (beetles), the loss of legs (snakes), the loss of functioning blood (sickle cell anemia), etc. and think “Wow, Natural Selection is such a great theory to explain the evolution of complexity because we have so many examples of how selection destroys things for the sake of reproductive success.”

    Walter Remine told me of a parasite that essentially lost all of its functions and all that was left was essentially an anus. If someone knows what creature that was that suffered such a fate of reductive evolution, please post, that should be the poster child of Darwinian evolution.

  24. 24
  25. 25
    Evolve says:

    scordova,

    ///Which argues selection doesn’t like complexity///

    You’re under the wrong impression that selection should always build complexity. Selection is not trying to build anything, it’s only trying to ensure reproductive success. In some cases that means new organs, in other cases that means loss of existing organs.

    ///you think survival of the sickest is some genius insight///

    “Sick” here is a relative term. An animal without a stomach would be sick if the stomach is required for its survival. On the other hand, an animal without a stomach would be more fit and efficient if the stomach is not required for its survival.
    Why do you think the human appendix shrunk in size? Because a change in diet made carrying around that organ a waste of energy. Losing the structure only made humans more efficient in their new environment. It didn’t make them sick.

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