# Darwin’s Delusion vs. Death of the Fittest

Superficially, the phrase “survival of the fittest” seems undeniably true, but in the proximal and ultimate sense it is false. If this claim is false then Darwinism is also false. The notion of “survival of the fittest” is an illusion in the general sense though seemingly true in the Darwinian sense. Critical oversights in Darwin’s Origin of Species by Means of Natural Selection and in Dennett’s algorithm can be demonstrated. Finally, population genetics can be used to critique Dawkins Weasel, Avida and various other fallacious computer simulations that are used in promoting the falsehoods of Darwinism and Neo-Darwinism.

To demonstrate that “survival of the fittest is false” it is sufficient but not necessary to demonstrate “death of the fittest is true”. Is “death of the fittest” true? Yes, in the ultimate sense. There is the rather trivial argument from physics: the stars will burn out one day, the 2nd law will prevail, and all life will cease. The fittest along with the weakest will meet their end. QED.

But what about the history of life on Earth? Wasn’t “survival of the fittest” always true for the history of life on Earth? No. Dave Raup’s book Bad Genes or Bad Luck reveals that most extinction in the past happened through natural disasters and bad luck, not bad genes, not Darwinian selection.

The notion of “survival of the fittest” of a species presumes there are living members of the species to carry on, but if an entire species, genus, or orders are wiped out, the fittest don’t survive, but rather we have “death of the fittest” along with weakest. Hence, extinction by natural or other disasters is a counter example to the claim of “survival of the fittest”.

In what sense is “survival of the fittest” true? If we look at one generation of individuals and see that they had more offspring than their peers, it suggests that these individuals were more reproductively fit. For example, with anti-biotic resistance, certain “traits” over many trials in petri dishes suggests that individual bacteria with these traits are favored for reproduction. So “the fit” in that sense survive and it appears that “survival of the fittest” is unassailable, but this unassailabilty is a product of cherry picking, invalid sampling, equivocation and confirmation bias. More later on antibiotic resistance…

Using reproductive fitness as a metric for fitness can frequently run counter to intuitive notions of what it means to be functionally fit. And as much as I loathe to bring this up, consider the case of one of the most despised women in America Octomom, Nadya Suleman who has 14 kids.

Octomom is mentally unstable, lives on public assistance, bankrupted her parents who obviously sacrificed much for her, and then jeopardized 8 kids by having them all in one pregnancy. By most common sense metrics, Octomom is dysfunctional and parasitic.

Compare her to Oxford professor and millionaire Richard Dawkins who has 1 kid.

In one sense Dawkins is more functional than Octomom, but in the Darwinian view (which Dawkins subscribes to), Octomom outshines Dawkins in Darwinian virtuosity by a factor of 14. Poetic justice I suppose.

Doesn’t “survival of the fittest” imply continued improvement? No. Neither in the functional nor reproductive sense. Some examples would help illustrate.

Consider the scenario of Mutational Meltdown

From Wiki:

Mutational meltdown refers to the process by which a small population accumulates harmful mutations, which leads to loss of fitness and decline of the population size, which may lead to further accumulation of deleterious mutations due to inbreeding depression. A population experiencing mutational meltdown is trapped in a downward spiral and will go extinct

Here we have the situation where the ancestors are reproductively and functionally more fit than their descendants during their respective lifetimes. The “fittest within each generation” survive, but in the larger sense, the “fittest of all generations”, namely the ancestors, died long ago. Hence in the Darwinian sense, “the fittest survived” but in the functional sense across all generation, “the fittest died”.

How about humans? Were our ancestors more fit than we? Even though we are more technologically advanced than our ancestors were, we are more sickly. Consider this post from DLH at UD: Is human intellect degenerating

It is very likely that within 3000 years (~120 generations) we have all sustained two or more mutations harmful to our intellectual or emotional stability. Recent human genome studies revealed that there are, per generation, about 60 new mutations per genome and about 100 hetrozygous mutations per genome that are predicted to produce a loss of function [7], some of which are likely to affect genes involved in human intellect. . . .
we, as a species, are surprisingly intellectually fragile and perhaps reached a peak 2000-6000 years ago. . . .

This may seem shocking given that we are more technologically advanced than our ancestors, but it has been provident that even as our brains have declined, the collective knowledge and technology handed down from each generation has simultaneously improved.

But what about anti-biotic resistance and sickle cell anemia and blindness in cave fish? Don’t these show generational improvement? In the Darwinian sense of reproductive fitness yes, in the functional sense of being healthy complex creatures, absolutely not. Let’s start with blind cave fish. Blind cave fish presumably evolved to be blind. Living in totally dark environments, functioning eyes became a metabolic liability. Hence, fish that lost their eyesight became more reproductively successful, even though they are functionally disabled. This case highlights the contingent nature of “selective advantage” leading to such absurdities listed in the book Survival of the Sickest: Why W.e Need Disease. I gave a more formal treatment in Dennett’s Strange Idea.

Another example of “survival of the sickest” is sickle cell anemia where a defect in the blood enables African populations to better cope with malaria. Individuals suffering from sickle cell anemia would hardly view the condition as evidence of being “fit”. The most logical way to view sickle cell anemia is to view it as an example of how natural selection makes a disease persist. Instead of this logical view, Darwinists have spun this as some sort of vindication of their theory, when in fact it casts serious doubt on the potential of Darwinian evolution to create functionality since natural selection can also perpetuate dysfunctionality.

But what about anti-biotic resistance and superbug bacteria? Superbugs are more reproductively successful, but in the overwhelming majority of cases, reproductive success was the result of dysfunction, not increase in integrated complexity. In his article, Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?, Kevin Anderson lists 40 of the major cases of anti-biotic resistance, and almost all were the result of broken pumps, bad expression of proteins, etc. More recently we have Michael Behe’s peer reviewed paper: The First Rule of Adaptive Evolution where Behe documents that most observed instances of adaptive evolution in the lab are through loss of function, and that as general rule, the first line of adaptation is loss of function, not gain of function. Thus, “death of the fittest” better characterizes evolution than “survival of the fittest”.

There are two notions of survival of the fittest, the formal definition, and the implicit one in Darwinian literature. One notion is true and the other is false.

notion #1. “survival of the fittest” means certain individuals relative to their peers in the same generation have a better chance of reproductive success (true statement)

notion #2. “survival of the fittest” means each generation is functionally fitter than the previous one (false statement as shown by counter examples above)

Darwinists equivocate these notions. A true statement (#1) is often equivocated with a false statement (#2), giving the false impression that notion #2 has been proven because notion #1 has been proven. This equivocation is Darwin’s delusion, a delusion of inevitable progress toward biological complexity and diversity. Philosopher Daniel Dennett’s ideas suffer from the same failures. Darwinism is not a universal acid. It’s not even a coherent theory.

Though Herbert Spencer coined the term, “survival of the fittest”, it summarizes Darwin’s delusion. Darwin articulated his delusion in Origin of Species:

Natural Selection is daily and hourly scrutinising, throughout the world, the slightest variations; rejecting those that are bad, preserving and adding up all that are good.

C.DARWIN sixth edition Origin of Species — Ch#4 Natural Selection

As hinted above, there is plenty of empirical evidence to the contrary. Nature has rejected the bad as well as the good (in mass extinction events) and there are documented cases where selection preserved the bad rather than the good. There are cases where selection is precluded from preserving and adding up the functionally fit if the most functionally fit were the long dead ancestors during their lifetime. And last but not least, selection is frequently outdone by random luck as I showed in Gambler’s Ruin is Darwin’s Ruin. Thus, “survival of the fittest” is universally true except when it’s false.

It is almost understandable that Darwin thought the next generation had to be better. When we see kids, they look so healthy relative to their grandparents. But now that we understand the mechanisms of inheritance better than Darwin in his day, we now realize that even though a grand kid’s youthful looks demonstrate that he is healthier in his youth than his grand parents in their elderliness, that does not imply the grand kid’s inherited genes are better than his grand parents’ genes. Yet, such failures of insight permeate Darwin’s ideas. Darwin didn’t seriously account for the possibility that ancestors on average are more functionally fit than their kids.

To further demonstrate that “death of the fittest” (fittest as in the more functionally fit ancestor) is a more accurate characterization of evolution than “survival of the fittest” I appeal to population genetics.

I will first illustrate “death of the fittest” with a simple model and then later augment it with more sophisticated considerations based on the Poisson distribution and papers by Kimura, Nachman and Crowell, Eyre-Walker and Keightley.

The following video is a crude 1-minute silent animation that I and others put together. God willing, there will be major improvements to the animation (including audio), but this is a start. Be sure to watch it in full screen mode to see the details.

The animation asserts that if harmful mutation rates are high enough, then there exists no form or mechanism of selection which can arrest genetic deterioration. Even if the harmful mutations do not reach population fixation, they can still damage the collective genome.

The animation starts off with healthy gingerbread parents. Each parent spawns 2 gingerbread kids, and the red dots on the kids represent them having a mutation. To simplify the animation, the reproduction was depicted as asexual, but the concept can easily be extended to sexually reproducing species.

The missing gingerbread limbs are suggestive of severe mutations, the more mild mutations are represented by gingerbread kids merely having a red dot and not having severe phenotypic effects of their mutation. The exploding gingerbread kids represent natural selection removing the less functionally fit from the population. 4 generations are represented, and the fourth generation has three mutations per individual.

Note the persistence of bad mutations despite any conceivable mechanism of selection.

When I posted this video earlier at UD, I got complaints about the simplicity of the model. I will suggest two refinements which will show that even with moderate rates of mutation per individual per generation, genetic deterioration will happen. Further, this claim is reinforced by the work of Nobel Prize winner Hermann Muller who said a deleterious mutation rate of even 0.5 per individual per generation would be sufficient to eventually terminate humanity. So the simple model I present is actually more generous than Muller’s. Current estimates of the number of bad mutations are well over 1.0 per human per individual. There could be hundreds, perhaps thousands of bad mutations per individual per generation according to John Sanford. Larry Moran estimates 56-160 mutations per individual per generation. Using Larry’s low figure of 56 and generously granting that only about 11% of those are bad, we end up with 6 bad mutation per individual per generation, 6 times more than the cartoon model presented, and 12 times more than Muller’s figure that ensures the eventual end of the human race.

The first refinement of the cartoon model comes from Nachman and Crowell’s paper Esitmate of the Mutation Rate per Nucleotide in Humans and The Mutational Load by Kimura. Nachman provides a way to relate mutation rates with the probability of having a eugenically “ideal” child.

I hypothesized Nachman and Crowell were using a Poisson distribution as reasonable model for the probability of a eugenically clean individual appearing in the face of various mutation rates. And sure enough, with a little sleuthing help from my UD colleague “JoeCoder”, it was confirmed in Kimrua’s paper (see eqn. 1.4) which Nachman and Crowell, and Eyre-Walker and Keightley referenced.

This was important because up until that realization, I felt uncomfortable not knowing how those probabilities were derived. But now that it is clear that professional population geneticists are using the Poisson distribution to estimate probabilities, there is transparency in their model, and that makes the cartoon model defensible. The Appendix Notes in the comment section will provide a justification for the Poisson distribution.

So now the details:

let U = mutation rate (per individual per generation)
P(0,U) = probability of individual having no mutation under a mutation rate U (eugenically the best)
P(1,U) = probability of individual having 1 mutation under a mutation rate U
P(2,U) = probability of individual having 2 mutations under a mutation rate U
etc.

The wiki definition of Poisson distribution is:

$\large \large f(k,\lambda ) = \frac{\lambda^k e^{-\lambda } {}}{k!}$

to conform the wiki formula with evolutionary literature let

$\large \large \lambda = U$

thus

$\large \large f(k,\lambda) = P(k,U) =\frac{U^k e^{-U }}{k!}$

Because P(0,U) = probability of individual having no mutation under a mutation rate U (eugenically the best), we can find the probability the eugenically best individual emerges by letting:

$\large \large k = 0$

which yields

$\large \large P(k,U) = P(0,U) = \frac{U^0 e^{-U }}{0!} = e^{-U}$

Given the Poisson distribution is a discrete probability distribution, the following idealization must hold:

$\large \large \sum_{n}P_n =\sum_{i=0}^{\infty}P(i,U) = 1$

On inspection, the left hand side of the above equation must be the percent of offspring that have at least 1 new mutation, and this reduces to the following:

$\large \large \sum_{i=1}^{\infty}P(i,U) = 1 - P(0,U) = 1- e^{-U}$

which is in full agreement with Nachman and Crowell’s equation in the very last paragraph and in full agreement with an article in Nature: High genomic deleterious mutation rates in homonids by Eyre-Walker and Keightley, paragraph 2. The simplicity and elegance of the final result is astonishing, and simplicity and elegance lend force to arguments.

So what does this mean? If the mutation rate is 6 per individual per generation, using that formula, the chances that a eugenically “ideal” offspring will emerge is:

$\large \large P(0,6) = e^{-6} = 0.25\%$

This would imply each parent needs to procreate the following number of kids on average just to get 1 eugenically fit kid:

$\large \large \frac{1}{e^{-U}} = \frac{1}{e^{-6}} = 403.42}$

Or equivalently each couple needs to procreate the following number of kids on average just to get 1 eugenically fit kid:

$\large \large 2 * \frac{1}{e^{-U}} = 2 * \frac{1}{e^{-6}} \approx 807}$

In other words parents would have to be acting roughly like 100 Octomoms or 800 Richard Dawkins just to make one eugenically “ideal” baby that doesn’t have any new mutation (but still has all the bad mutations inherited from mom and dad). These calculations suggest, if Darwinism is true, the world needs far more women with the virtues of Octomom.

For humanity to survive, even after each couple has 807 kids on average, we still have to make the further utterly unrealistic assumption that the eugenically “ideal” offspring are the only survivors of a selective process. Hence, it is absurd to think humanity can purge the bad out of its populations — the bad just keeps getting worse.

In truth, since most mutations are of nearly neutral effect, most of the damaged offspring will reproduce, and the probability of a eugenically ideal line of offspring approaches zero over time. Therefore the cartoon model which assumes at least 1 new mutation per individual per generation is reasonable, and as I pointed out, the cartoon model is actually generous given Muller’s number of only 0.5 new mutations per generation per individual. The cartoon however graphically conveys the gravity of the problem.

Finally, how does this relate to the flaws in Dawkins weasel, Avida or any other conceivable genetic algorithm falsely used to defend Darwinism? These models notoriously don’t allow the offspring to move progressively farther from a desirable ideal with each generation (as illustrated in the cartoon model). Dawkins assumes cumulative selection, but this suffers from the flaw of assuming the all descendants are at least as good as the ancestor (the implementation of Dawkins Weasel disguises this fact). Computer simulations that assume offspring are at least as good as parents are obviously flawed, and more subtly, simulations that allow offspring to be on average better than their parents are also flawed. I leave it to the developers of these simulations to fix their bugs and conceptions. This is the 2nd refinement to the cartoon model. Let developers of evolutionary simulation incorporate the above considerations into their programs.

We have models from nature that show “death of the fittest” better describes what’s going on in nature, and the notion of “survival of the fittest implies inevitable improvement with each generation” is Darwin’s, Dennett’s, and Dawkins’ delusion (DDDD).

ACKNOWLEDGEMENTS:

Walter ReMine, JoeCoder, JGuy, DLH as well as my friends, colleagues, critics and detractors at UD, PandasThumb, ARN, TheSkepticalZone, NCSE and the Discovery Institute.

## 43 Replies to “Darwin’s Delusion vs. Death of the Fittest”

1. 1
scordova says:

[APPENDIX NOTES]

1. The concept of Natural Selection was actually pioneered by the creationist Blyth, and Darwin plagiarized much of Blyth’s work.

2. There is a beautiful illustration of the Poisson distribution, it discusses the probability P(k,r) of getting k deaths in a given year by horse kicks if the rate of death is r. That example can easily be ported, using different math symbols to the probability P(k,U) of getting k number of mutations with a mutation rate U.

The classic Poisson example is the data set of von Bortkiewicz (1898), for the chance of a Prussian cavalryman being killed by the kick of a horse. Ten army corps were observed over 20 years, giving a total of 200 observations of one corps for a one year period. The period or module of observation is thus one year. The total deaths from horse kicks were 122, and the average number of deaths per year per corps was thus 122/200 = 0.61. This is a rate of less than 1. It is also obvious that it is meaningless to ask how many times per year a cavalryman was not killed by the kick of a horse. In any given year, we expect to observe, well, not exactly 0.61 deaths in one corps (that is not possible; deaths occur in modules of 1), but sometimes none, sometimes one, occasionally two, perhaps once in a while three, and (we might intuitively expect) very rarely any more. Here, then, is the classic Poisson situation: a rare event, whose average rate is small, with observations made over many small intervals of time.

Let us see if our formula gives a close fit for the actual Prussian data, where r = 0.61 is the average number expected per year for the whole sample, and the successive terms of the Poisson formula are the successive probabilities. Remember that our formula for each term in the distribution is:

p(k) = r*k / (k!)(e*r)(5)

We may start by asking, given r = 0.61, what is the probability of no deaths by horse kick in a given year (module of observation)? For k = 0, we get by substitution

p(0) = (0.61)*0 / (0!)(e*0.61) = 1 / (1)(1.8404) = 0.5434

Given that probability, then over the 200 years observed we should expect to find a total of 108.68 = 109 years with zero deaths. It turns out that 109 is exactly the number of years in which the Prussian data recorded no deaths from horse kicks. The match between expected and actual values is not merely good, it is perfect.

3. The human immune system B-Cell Maturation has been used to prove Darwinism. Their conclusions that somatic cells like B-cell somehow prove Darwinism are based on cherry picking, and if they carried out their ideas to all somatic cells, they ought to logically conclude somatic cell development and death actually refutes Darwinism and affirms death of the fittest, not survival of the fittest.

4. Bertrand Russell beautifully articulated the death of the fittest

Such, in outline, but even more purposeless, more void of meaning, is the world which Science presents for our belief. Amid such a world, if anywhere, our ideals henceforward must find a home. That man is the product of causes which had no prevision of the end they were achieving; that his origin, his growth, his hopes and fears, his loves and his beliefs, are but the outcome of accidental collocations of atoms; that no fire, no heroism, no intensity of thought and feeling, can preserve an individual life beyond the grave; that all the labours of the ages, all the devotion, all the inspiration, all the noonday brightness of human genius, are destined to extinction in the vast death of the solar system, and that the whole temple of Man’s achievement must inevitably be buried beneath the debris of a universe in ruins — all these things, if not quite beyond dispute, are yet so nearly certain, that no philosophy which rejects them can hope to stand. Only within the scaffolding of these truths, only on the firm foundation of unyielding despair, can the soul’s habitation henceforth be safely built.
Bertrand Russell
http://www3.nd.edu/~afreddos/courses/264/fmw.htm

5. Dennett was wrong about Darwinism being a universal acid, his philosophical pH estimates were way off. He should stick to philosophy instead of philosophical chemistry.

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JGuy says:

This reminded me of the of the movie Idiocracy. … Where unintelligent people (first depicted as the likes of a promiscuous uneducated jock having babies with all the women he slept with) were out reproducing smarter people (depicted as a fully educated couple obsessed with planning how many children to have & when). And hence the future is fully over-run by only stupid people.

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JGuy says:

Sal,
This looks somewhat relevant enough that it may add to any discussion & be on topic. From the ICC link you recently linked to:

Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle – “Haldane’s Ratchet”
– Christopher L. Rupe and John C. Sanford.

In 1957, Haldane first described a fundamental problem with evolutionary theory. This problem eventually became widely known as “Haldane’s Dilemma”. The essence of this problem is that even given a steady supply of beneficial mutations plus deep time, the rate that such mutations reach fixation is too slow to achieve meaningful evolution. After more than 50 years, this fundamental problem remains unresolved. ReMine has gone far beyond Haldane’s original mathematical analysis, and has developed “cost theory analysis” which strongly supports Haldane’s thesis. Here we examine this long-standing problem using an entirely different approach. We employ advanced numerical simulation of the mutation/selection process to empirically measure the fixation rates of beneficial, neutral, and deleterious mutations. We do this employing both realistic and optimized population parameters. In our numerical simulations, each new mutation is tracked through time until it is either lost due to drift or becomes fixed in the population.

We first confirm that our numerical simulations correctly tallying the fixation of neutral mutations. We show that neutral mutations go to fixation just as predicted by conventional theory (i.e., over deep time the fixation rate approached the gametic mutation rate). We also show that the reason the vast majority of neutral mutant alleles fail to go to fixation, is because they lost due to drift, and this rate of loss rapidly approached 100% as population size is increased.
We then show that given realistic distributions of mutation fitness affects, the vast majority of all mutations (including deleterious and beneficial mutations), are similarly lost due to random drift. In terms of fixations, deleterious mutations went to fixation only slightly slower, while beneficial mutations went to fixation only slightly faster, than neutral mutations.

We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage.
Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as “Haldane’s Dilemma” is very real.
Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon “Haldane’s Ratchet”.

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Sal:

Good thoughts and plenty to chew on. I’ve already exhausted my energy in the past addressing the nonsense (or is that non-sense?) that is natural selection. The exceptions to the supposed progression of natural selection are so frequent and significant that in any particular case it becomes difficult to say whether natural selection had anything to do with it. Unless, of course, we define natural selection so broadly as to encompass everything that happens to a species, including mass extinction events. My sense is that the modern tendency is to do just that: everything is natural selection.

More problematic are the frequent claims that natural selection actually does something, as though it were some kind of natural force or natural law. It isn’t. It isn’t a force. It isn’t a law. It doesn’t do anything.

It is just a convenience label assigned to the results of processes that are seldom identified and rarely understood.

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scordova says:

JGuy regarding Haldane’s ratchet,

There are several separate problems with Darwinian theory, some are harder to conceive of.

1. The U-paradox problem (subject of the cartoon), Darwin’s Delusion vs. Death of the Fittest

2. Haldane’s dilemma (the speed limit of natural selection in the wild)

3. Muller/Haldane’s ratchet (the problem of irreversible, bad traits in a population)

4. Lewontin’s challenge, Survival of the Sickest and Dennett’s strange idea (the unstable, unusable, absurd notions of what it means to be “fit”)

5. No Free Lunch theorems. Ha! And some many Darwinists thought if they defeated this one, their problems were solved.

6. Irreducible Complexity

7. Origin of Life (Darwinism fails without the assumption of life first), but this is debatable if should be used as a critique of Darwinism, so you can strike it if you don’t like it

Any of the above are in-and-of themselves fatal to the claim of mindless evolution.

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scordova says:

Sal:

Good thoughts and plenty to chew on. I’ve already exhausted my energy in the past addressing the nonsense (or is that non-sense?) that is natural selection.

Thanks for the kind words, especially since you’re worn out seeing a dead horse beaten. But I’ve tried to figure out more creative ways to do beat that dead horse, and the Darwinists keep figuring out ways to protect that dead horse.

Finding that Poisson distribution clarified so much for me. The paradox of inevitable decline really is as simple as I had conceived even without the math. But seeing the math gave me the confidence to state things more forcefully.

FWIW, even though I intuitively knew of the problems with Natural Selection, it’s another thing to be able to articulate it in a way I feel makes sense to me. It’s only after a few years of thinking about it that things have become clearer.

Often I knew something was unwholesome in evolutionary theory, but I couldn’t quite put my finger on it.

Sal

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bornagain77 says:

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bornagain77 says:

Walter ReMine on Haldane’s Dilemma – interview
http://kgov.com/Walter-ReMine-on-Haldanes-Dilemma

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scordova says:

Unless, of course, we define natural selection so broadly as to encompass everything that happens to a species, including mass extinction events. My sense is that the modern tendency is to do just that: everything is natural selection.

I have an unpublished draft post somewhat along those lines. If we assume that we can describe natural selection purely in terms of physics and chemistry, we can make certain statements about what nature will really “select” versus what Darwinists want it to select.

Say we have a pool of lifeless chemicals on a lifeless primordial Earth, will nature “select” for the formation of the first life or not. 🙂

If we look to the end of the universe, the universe “selects” for the end of all species, the fit and unfit.

But Darwinists have then equivocated “nature selects for yet-to-be realized complexity” with “natural selection”.

They’ve equivocated

1. “nature selects for existing complexity like the human heart”

with

2. “nature selects of yet-to-be-existent complexity like the human heart from the reptilian heart”

One statement is true, the other unproven and likely false. But through equivocation, Darwinists make it appear #2 is proven since #1 is true. Not so. Such are “proofs” of Darwinism.

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Sal wrote:

If we assume that we can describe natural selection purely in terms of physics and chemistry, we can make certain statements about what nature will really “select” versus what Darwinists want it to select.

Exactly. And in that case we can describe and explain the whole process of what happened in the population without ever even invoking the words “natural selection.”

If we know what is going on, we don’t need to invoke natural selection — we can refer to the real physical processes. We only need to invoke natural selection if we don’t really know what is going on. The invocation of “natural selection” serves as a surrogate for an explanation.

Worse, it gives the intoxicating impression that some explanation has actually been provided and some valuable insight set forth, when in fact it has just obscured. As a result, in so many instances the concept of natural selection is not just incomplete information or even wrong information; rather, it ends up being what we might call anti-information: a non-explanation wrapping itself in the garb of verbiage and seducing the listener into thinking that it is a real explanation.

This anti-information has a telling result, namely that the person sincerely seeking to understand what really happened in a given instance is generally worse off for having entertained the idea of natural selection.

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Andre says:

Great article

I’ve always wondered how deleterious and bad mutation which is almost all of them have somehow conspired to build complexity. This idea is not only illogical its just plain stupid.

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scordova says:

Thanks for the kind words Andre.

For the reader’s benefit, Elizabeth Liddle graciously offered me the opportunity to post at TheSkepticalZone.

At Mark Frank’s request for authors to be more concise, I posted a much shortened version there:

“Darwin’s Deluision” Consice Version

which gives a different perspective than the long version.

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[…] LONG WINDED VERSION AT UD: Darwin’s Delusion vs. Death of the Fittest […]

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scordova says:

I’m reposting a comment I made at TSZ because it justifies the 11% number JoeCoder suggested for the percent of bad mutations relative to all mutations:

” you acknowledge deleterious mutations, but ignore beneficial mutations.”

Thanks for raising the objection.

For proteins, only a very small fraction (less than 0.1%) of mutations are conceivably beneficial because of the scarcity of functional proteins in the space of all possible amino acid polymers. The rest of the mutations are neutral to deleterious. The ratio of beneficial to non-beneficial is negligibly small. So as you can see, there is justification for not weighing in beneficial mutations.

Codon Bias suggests every nucleotide that codes for a protein has importance, and even supposing it doesn’t have importance, it then raises the equally difficult question of why it is there in the first place. Either interpretation of its existence (functional or non-functional) is equally difficult in terms of random mutation and natural selection.

Even though a silent mutation and sometimes a missense mutation might not immediately affect reproductive fitness, many such mutations that go unchecked, will compromise the organism like a slow oil leak eventually compromising an airplane.

To illustrate, losing a spare tire in a car or spare navigation device in an airplane may not be noticeable in terms of immediate performance, but the system is functionally compromised nonetheless. Similar analogies apply to functional systems in biology with respect to slightly deleterious mutations.

Notes:
Consider E. Coli Frail Hypothesis in Evolution

the deleterious/beneficial mutation ratio is assumed to be as high as four to five orders of magnitude, implying that E. coli’s genome is fully optimized with respect to single nucleotide substitutions. The deleterious mutation rate would be higher than 2×10?4 per genome replication, or about one tenth the mutation rate. On the other hand, “the proportion of mutations that are beneficial is roughly one in a million”

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Objector via Sal @15:

you acknowledge deleterious mutations, but ignore beneficial mutations

Well, in the genetics class I took we did calculations on mutation rates generally (deleterious/neutral), but when it came to beneficial mutations the professor said, in effect, “These are so rare that we aren’t even going to bother trying to calculate anything here,” and we just moved on.

Perhaps some knowledgeable evolutionist can come along and give us the answer. Pray tell, what is the rate of beneficial mutations? Go ahead, pick an organism, any organism . . .

Saying “you acknowledge deleterious mutations, but ignore beneficial mutations” is tantamount to saying: “You acknowledge that normal natural processes can’t produce these biological systems, but you ignore miracles.”

17. 17
scordova says:

Here are the opinions of the TSZ scientists and my response:

RBH:

That’s a point I’ve made in Sal’s presence more times than I care to remember, going way back to ARN days. The random search metaphor for evolution by natural selection is a snare and a deception. It snares the unwary, and is used deceptively by Dembski & Marks and their acolytes, Sal among them.

hotshoe:

“That is not a correct statement. Mutations in existing life are NOT exploring the space of all possible amino acid polymers. They are exploring the immediate next-door neighbors of already-existing functional proteins.”

Lizzie:

This is circular Sal: you only know if a protein is “functional” if you know whether it can be “beneficial”. So your ratio doesn’t mean anything.

I responded in general:

didn’t say it explores all possible amino acid polymers, I said the space of functional proteins occupies only a small space of amino acid polymers. But I wasn’t being clear and I failed to actually engage your first objection. So I will try again.

Let me take you up on your suggestion. How about exploring the immediate neighbor? Say the neighbor only involves changing simultaneously a measly 3 amino-acids, That specificity will require 1 out of 20^3 amino acid combinations to hit the target, or 1 out of 8000 (it’s a bit more complicated than that because of codon degeneracy, but that’s a rough estimate). So, that’s a 0.01% chance which is less than 0.1% that I suggested. That’ also renders RBH objection moot as well since this is only a small step to the neighbor. 0.01% is pretty generous given the E. coli study gave a probability that is 0.0001% (1 in a million).

As far as ARN days, I was posting on origin-of-life. So it’s rather inappropriate to invoke evolution from a pre-exiting protein that doesn’t pre-exist.

A protein isn’t functional without being a part of larger system, like a key without a lock or password without a system to incorporate it. So even supposing you can make a key an infinite number of ways, there is still the probability associated with making a corresponding lock.

You can look at it like the probability of building a key and a corresponding lock via random matching. There might be an infinite space of possible lock and key combinations, but for a specific key you need specific lock. That corresponds to proper binding. So when one says functional protein, it really implies a functional protein system.

A given lock that enables a key to be functional with a specificity with a mere 3-amino acids will yield probabilities of the order suggested above.

The improbability of biology isn’t solved by saying we can build a lock-and-key system an infinite number of ways, it is the improbability of building lock-and-key systems with various levels of specificity for each other that we see in living organisms.

But perhaps to settle the argument, everyone is invited to provide their estimate of beneficial, neutral, and deleterious mutations.

Is the ratio of beneficials relative to all mutations:
0.01%
0.1%
1.0%
10%

But even granting we have new innovations, that doesn’t solve the problem of fixing broken parts. This is like getting a new fancy set of wipers but the battery starts to degrade. The addition of good doesn’t heal the broken parts.

Anyway, I appreciate everyone’s criticism of what I asserted. Thank you for taking the time to read and respond to what I said.

I apologize for being verbose, but I was trying to respond to multiple criticisms at once, and I think they are good criticisms. Thank you.

I think my original thesis is holding up well.

I’m not going to go after every objection they offer. I think those can be dealt with.

But I leave it to UD readers to decide for themselves if the U-paradox as depicted in the cartoon is correct.

18. 18
scordova says:

BTW,

I don’t think it’s quite dawned on RBH, I’m not making the No Free Lunch arguments of Dembski and Marks, this is the U-paradox argument of ReMine and Sanford.

Dembski and Marks address the problem of creating new function, ReMine and Sanford address the problem of retaining existing function.

Here is the list of objections to Darwinian evolution, any of which could be sufficiently fatal:

1. The U-paradox problem (subject of the cartoon), Darwin’s Delusion vs. Death of the Fittest

2. Haldane’s dilemma (the speed limit of natural selection in the wild)

3. Muller/Haldane’s ratchet (the problem of irreversible, bad traits in a population)

4. Lewontin’s challenge, Survival of the Sickest and Dennett’s strange idea (the unstable, unusable, absurd notions of what it means to be “fit”)

5. No Free Lunch theorems. Ha! And some many Darwinists thought if they defeated this one, their problems were solved.

6. Irreducible Complexity

7. Origin of Life * (depends on who you ask if this is relavant)

I don’t think RBH has figured out that this is a different criticism than the No Free Lunch criticisms of Dembski and Marks.

19. 19
JGuy says:

Sal @ 17

Is the ratio of beneficials relative to all mutations:
0.01%
0.1%
1.0%
10%

&lt .00000001% where beneficial is an actually selectable non-destructive benefit.

20. 20
Joe says:

Sal,

The TSZ denizens don’t have any evidence to support the claims of their position- they cannot demonstrate that natural selection can produce multi-protein configurations and living organisms contain many of those.

As for Lizzie- we know a protein is functional because we observe it doing some function.

21. 21
Joe says:

Lizzie sez:

The cartoon does not apply to sexually reproducing organisms, in which genes can propagate independently from each other.

Your position cannot account for sexual reproduction, Lizzie. It can’t account for meiosis.

Biological fitness is a perfectly well defined concept and can be measured and used.

Biological fitness refers to reproductive success. And in order to figure out anything from that you would have to follow the offspring and see how they reproduced, and then their offspring and their offspring etc.

And outreproducing others in your population still doesn’t produce new multi-protein configurations.

Lizzie on IC:

Not a theoretical problem (see Lenski and Avida), and not easy to demonstrate that it is a practical problem (how do you prove a negative?)

Neither Lenski nor AVIDA demonstrate that blind and undirected process can produce IC. Lizzie is still sadly mistaken.

22. 22
scordova says:

I responded to Liz’s criticism of sexual reproduction.

The cartoon can be extended to sexually reproducing species because it deals with NUMBER of mutations, not specific mutations that can drift out because of sexual recombination. If Mom has 10,000 bad nucleotides and Dad has 10,000 bad nucleotides, when they have junior, junior on average will get 5,000 from Mom, 5,000. Then junior will get 6 brand new ones (if U=6).

Even if mom and dad have the same mutation in the same loci on the same chromosome, that means junior will become homozygous in that defect. The defect doesn’t go away just because of recombination, in the case of homozygosity, junior now has a double dose of the defect, and the U-paradox still holds.

Mutation ACCUMULATION is a separate problem form Muller’s ratchet which is mutation FIXATION. Accumulation implies that even if most specific mutations are drifted out of the population, there are plenty of new bad mutations to take their place, so to speak.

The issue of fixation (as in Muller’s ratchet) is separate, we’re talking about the lack of purification for all bad mutations (fixed and non-fixed).

23. 23
scordova says:

By the way Muller himself gave U=0.5 for the termination of humanity, so Muller did have in mind sexually reproducing species!

The cartoon model was at U=1.0, so if Muller says meltdown happens at U=0.5, how much more then will it be for U=1.0, or U=6.0 or U = 100!

24. 24
25. 25
scordova says:

Joe,

Yes! And that’s what started all this, and this was 5 years before John Sanford entered the scene. At first I thought that was Walter’s Website until I realized it was Fred Williams (Scott Paige constant reference to ReMine and Williams website let me confuse the two).

Sanford used to be an evolutionist, and he was a recent convert to creation at the time. He didn’t accept ID until Behe’s Black Box came out, so maybe around 1998 was when Sanford began to join the ID ranks.

Because of Sanford’s reputation, the genetic deterioration argument got revived around 2005, and suddenly Walter ReMine’s credibility began to rise because a mainstream scientist of Sanford’s stature affirmed ReMine’s work.

Btw, do you sense the debates are getting easier these days. I remember when I used to debate RBH, it was difficult even though he usually lost. Nowadays, because of the defections out of Darwinism (like Sternberg, Shapiro, Sanford, Nei, etc.), it would be really easy to debate RBH because there is so much more data. Tons of it.

When I first debated RBH, the issue of DNA being mostly junk seemed settled, Neo-Darwinism seemed settled, and few would openly question OOL — all that has changed. A new day is dawning.

26. 26
Joealtle says:

Hey, which one of you guys is Ray “the banana man” Comfort?

27. 27
scordova says:

Say the neighbor only involves changing simultaneously a
measly 3 amino-acids, That specificity will require 1 out of 20^3 amino acid combinations to hit the target, or 1 out of 8000 (it’s a bit more complicated than that because of codon degeneracy, but that’s a rough estimate

There is a reason the 3 amino-acid assumption is generous.

When proteins act through binding (think lock-and-key methapor), if specificity were low (let a variety of keys open the same lock), then proteins would be interacting and binding with all sorts of things they shouldn’t and there results a conflict.

To conceptualize the problem, if the human has 30,000 proteins, the body needs to discriminate 1 from the other, hence the address space must be at least 30,000 large, and preferably just for safety. To discriminate between 30,000 proteins one needs more than 3 amino acids (20^3.44 = 30,000). It is reasonable to suppose more are needed to ensure sufficient discrimination between proteins.

By way of analogy, a 32-bit computer has more addressable space than a 16-bit computer. High specificity (high improbability) isn’t an option, it’s a requirement for a complex system. Hence, a smooth gradient for selection from one protein to the next isn’t reasonable even in principle when dealing with systems that require high specificity.

But, that’s not even the end of it. Locks are usually far more complicated than keys, and a single protein specificity is nowhere near the complexity of the structure that must integrate it. If proteins are the basic building blocks, then the infrastructure that integrates it is more complex just like buildings are more complex than the building blocks that integrate the building blocks. Changing 3-amino acids and finding a way to use it is like creating a new sized brick and trying to integrate it into an existing building…the few times we see this works out in organisms, where 3 amino acid changes are significant, is the rare exception, not the rule.

Though we might have an exception to this once in a while where change in 1 or 2 amino acids is significant, it is the exception rather than the rule. To extrapolate such isolated cases as some sort of general principle, is the fallacy of hasty generalization.

28. 28
scordova says:

I posted this at The Skeptical Zone:

Regarding Muller’s value of 0.5

see page 155 paragraph 3 of

“if Ut should rise above 0.5, the amount of selective elimination required for the maintenance of equilibrium, would as we have seen, be greater than the rate of effective reproduction…[for reprodcution of 2 per couple] the upper or critical mutation rate, that beyond which any equilibrium is impossible, must be much lower than 0.5 and, a we have seen, perhaps lower than 0.1”

This pertained to Muller’s research on the effects of radiation on the next generations. That was his immediate concern and for his related work in understanding x-ray mutagenesis, he won the Nobel prize. He unwittingly gave creationists a lot of ammunition.

and also see paragraph 2 of page 1344
Mutational Load by Kimura and Mayurama

If U=.5 then even for fruit flies, the load is too much as Kimura showed, if so, then for U=1 or greater this will be even more true.

The cartoon model attempted to show that for U=1 or higher, the derivations become simpler, and for U=6, selection becomes pretty much irrelevant because one would have to presume selection is 99.75% accurate in eliminating the new bad mutations for every generation, which is unreasonable as Sanford’s former Cornell colleague, Kondrashov, demonstrated.

29. 29
scordova says:

To be fair, Sal’s reference is 63 years old. That seems fairly typical of ID references.

To be fair, Nachman and Crowell’s paper cited Muller’s 1950 paper in 2000, and Michael Lynch referenced it in 2010 Proceedings of the National Academy. Rate Spectrum in a way favorable to Muller’s hypothesis of grave challenges for the human genome.

Lynch went to the trouble of defending Muller. Does that Lynch’s paper suggest humans are getting progressively healthier? No. It describes the failure of Natural Selection.

If you say, “NS no longer operates because of industrialization”, it only goes to prove the point Nature is under no obligation to make populations behave according to a Darwinian model, there are tons of counter examples starting with those identified by Raup to the present day. NS works, except when it doesn’t.

But as I said, we’ll all know the answer in far less than geological time if the human genome is indeed deteriorating….no need to settle the issue in this discussion, the facts could tell us in the next couple of decades (they already have, but some haven’t caught on).

Michael Lynch:

“it is difficult to escape the conclusion that the decline in fitness is at least %1 in humans and quite possibly as high as 5%”.

And this is telling:

“a full reassertion of the power of natural selection would be incapable of returning the population to a state better than that represented by the least loaded chromosomal segment”

Criticize what I’ve said, but the data will be the final judge. We’ll know the answer in due time. Blame the problem on industrialization, but it goes deeper than that. If U=6, even with 99.75% effective selection and each female giving birth to 807 kids, the genome won’t get better.

I’ve given what I think is true. No need to try to settle the issue by more debate, observation and testing will judge who is right.

30. 30

[…] demonstrated the fallacy of survival of the fittest in Death of the Fittest, and that real evolution is where function is lost over time, not gained. Fault tolerance is a […]

31. 31

[…] meltdown, genetic deterioration, blind cave fish, sickle cell anemia, wingless beetles. Reality is Death of the Fittest not survival of the […]

32. 32

[…] meltdown, genetic deterioration, blind cave fish, sickle cell anemia, wingless beetles. Reality is Death of the Fittest not survival of the […]

33. 33

[…] evidence says even if lunches were free, nature would eventually dispose of them anyway (see: Death of the Fittest), hence not only are Darwinists up against the ropes because of NFL theorems, even if Darwinists […]

34. 34

[…] evidence says even if lunches were free, nature would eventually dispose of them anyway (see: Death of the Fittest), hence not only are Darwinists up against the ropes because of NFL theorems, even if Darwinists […]

35. 35

[…] evidence says even if lunches were free, nature would eventually dispose of them anyway (see: Death of the Fittest), hence not only are Darwinists up against the ropes because of NFL theorems, even if Darwinists […]

36. 36

[…] NOTES: I pointed out other ridiculous equivocations and rhetorical ploys here: Death of the Fittest […]

37. 37

[…] are pointing out the “science” of Darwinism is based on rhetorical ploys (see: Death of the Fittest and Blind Watchbreaker and Selection falsely called a […]

38. 38

[…] See my derivation with the Poisson distribution in Death of the Fittest to see how the bad that is purged is replaced with more bad in addition to the ratcheted mutations […]

39. 39

[…] See my derivation with the Poisson distribution in Death of the Fittest to see how the bad that is purged is replaced with more bad in addition to the ratcheted mutations […]

40. 40

[…] the fittest relative to the healthier parents. (I delved into this less-than-honest equivocation in Death of the Fittest.) When ReMine set the default to non-renormalization, the populations went […]

41. 41

[…] Darwin’s delusion vs. Death of the Fittest […]

42. 42

[…] Death of the Fittest […]

43. 43

[…] NOTES Excerpt from Death of the Fittest […]