Gambler’s ruin is Darwin’s ruin

Thanks, Sal. Very interesting and well laid-out post. There is, of course, an ongoing effort to deny that these principles apply to Darwinian theory, or if they apply, then evolutionary theory can overcome them. Nevertheless, the mathematical problems of the Darwinian paradigm bear repeating, and the more pressure that can be brought to bear the better. After all, if Darwinism is sound, it should be able to withstand, nay, it should even be supported by mathematical scrutiny; if not, it deserves to fall.

The contrast between a skilled gambler and natural selection is that a skilled player can wager small fractions of the money he sets aside for his trade. If a skilled gambler has $50,000, he might wager $100 at a time until the law of large numbers causes his statistical advantage to be asserted. He can attempt many many trials until his advantage eventually prevails. In this manner a skilled gambler can protect himself against the mathematics of gamblers ruin.
But natural selection is a blind watchmaker. It does not know how to perform risk management like a skilled player or the great math wizard, Edward Thorp.

Was surprised given the subject of the article that the “house advantage” was not mentioned once. How much skill does it take to put a 0 and 00 on a roulette wheel.

In natural selection would it not be the case that in the long run, mutations that confer any sort of advantage at all will predominate over mutations that confer no advantage. Certainly it is understandable how even mutations conferring a 1% advantage will be wiped out in huge numbers. But if you look at the mutations that have been preserved, the “house advantage” would seem to dictate that those conferring any sort of advantage should predominate drastically.

Truly novel and beneficial mutations are rare. They don’t repeat themselves very often, and when they arise, they will likely be wiped out unless there is fairly intense selection pressure
It seems that arguments against evolution often come down to the observed rate of mutation. So, does this mean there is some mutation rate that would have made the whole process viable? Is it possible that a huge amount of random genetic variation (a good bit of it pure garbage) was generated at the very start of the biological process on this planet, and it is that random genetic information that has been in the process of being sorted out ever since.

A further constraint on selective advantage of a given trait is the problem of selection interference and dilution of selective advantage if numerous traits are involved. If one has a population of 1000 individuals and each has a unique, novel, selectively-advantaged trait that emerged via mutation, one can see this leads to an impasse –selection can’t possibly work in such a situation since all the individuals effectively cancel out each other’s selective advantage.

So would this mean that if in a population of 1000 individuals each had a harmful dibilitating selectively-disadvantaged mutation, the disdavantages would be cancelled out and these mutations would be rendered neutral. If so, these traits would maintain the same ratio in relation to each other in the population, but the species would dwindle to extinction.

As far as beneficial mutations rendered “neutral”, if the entire population experiences a sharp peak, (IOW all traits are resulting in an increase in reproduction) then there are more chances for even “neutral” mutations to be preserved (right?)

Scordova, great article.

Great article indeed. I thumbed it up on stumbleupon.

I’m glad someone has done the research on the odds of a beneficial mutation taking over the population. But these statistics start out assuming a beneficial mutation has taken place.

Is there any research you could point me to to show the statistics of a mutation being beneficial? Or is that too broad of a term?

Thermodynamics and heat flow are two different areas of physics and mechanical engineering, with separately derived sets of equations for problem solution. Heat flow problems were classically defined for solids early on, but are also defined for other states of matter. The Black-Scholes-Merton equation is derived from the laws of heat flow. Thermodynamics is concerned with change of state, kinetic energy, potential energy, and energy conversion.

I’m glad someone has done the research on the odds of a beneficial mutation taking over the population.

This was done in the 1960s - N.T.J. Bailey gives the results in one of his books.

Is there any research you could point me to to show the statistics of a mutation being beneficial?

Yes - there was a review last year. It’s of the order of 1% or so, but the estimates vary, and it’s difficult to get really good estimates, because mutations are rare in themselves.

JH:

In natural selection would it not be the case that in the long run, mutations that confer any sort of advantage at all will predominate over mutations that confer no advantage. Certainly it is understandable how even mutations conferring a 1% advantage will be wiped out in huge numbers. But if you look at the mutations that have been preserved, the “house advantage” would seem to dictate that those conferring any sort of advantage should predominate drastically.

Don’t forget about genetic drift. Genetic drift is the tendency of populations to become more homogenous over time — minority variations are wiped out by stochiastic processes. In order for a new mutation to take over a whole population, it has to be so advantageous that it overcomes the general tendency of populations to weed out such mutations.

Bottom line: genetic drift is another way the deck is stacked in favor of the original design, not the mutant.

Don’t forget about genetic drift. Genetic drift is the tendency of populations to become more homogenous over time

No, genetic drift is the tendency for allele frequencies to change randomly, because of finite sampling. The effect is for populations to become less homogeneous over time. Different “minority variants” become fixed in different populations.

Is there any research you could point me to to show the statistics of a mutation being beneficial?

“I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998). Therefore, I cannot …accurately represent how rare such beneficial mutations really are.” (Sanford; Genetic Entropy page 24)

The fate of competing beneficial mutations in an asexual population (Philip J. Gerrish & Richard E. Lenski)

“Clonal interference is not the only dynamic that inhibits the progression of beneficialmutations to fixation in an asexual population.Asimilar inhibition may be caused by Muller’s ratchet (Muller, 1964; Haigh, 1978), in which deleterious mutations will tend to accumulate in small asexual populations. As shown by Manning and Thompson (1984) and by Peck (1994), the fate of a beneficial mutation is determined as much by the selective disadvantage of any deleterious mutations with which it is linked as by its own selective advantage.”

http://myxo.css.msu.edu/lenski.....Lenski.pdf

Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon)

Abstract

……It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate.

http://www.nature.com/hdy/jour.....7270a.html

High Frequency of Cryptic Deleterious Mutations in Caenorhabditis elegans ( Esther K. Davies, Andrew D. Peters, Peter D. Keightley)

“In fitness assays, only about 4 percent of the deleterious mutations fixed in each line were detectable. The remaining 96 percent, though cryptic, are significant for mutation load…the presence of a large class of mildly deleterious mutations can never be ruled out. ”

http://www.sciencemag.org/cgi/...../5434/1748

” Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.”

Trying to find an actual “hard” number for the “truly” beneficial mutation rate is, in fact, what Dr. Behe tried to do in his book “The Edge of Evolution”.

Dr. Behe states in Edge of Evolution on page 135.

Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would explain the generation of the complexity we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite.

That order of difficulty is put at 10^20 replications (births) of the malarial parasite, by Dr. Behe.

Thus, the actual rate for “truly” beneficial mutations, that would account for the complexity we see in life, is far in excess of one-hundred-billion-billion mutational events.

Thus, this one in a million number, that is often bantered about for “truly” beneficial mutations, is actually far, far too generous for the evolutionists to be using for their hypothetical calculations.

In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biology, with no exceptions at all, and that the belief in “truly” beneficial mutations is nothing more than wishful speculation on the naturalists part that has no foundation in empirical science whatsoever:

The foundational rule of Genetic Entropy for biology can be stated something like this:

All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of the original integrated complex information in the parent species genome.

Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is clearly overwhelming, for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker).

“Mutations” by Dr. Gary Parker

http://www.answersingenesis.or.....ations.asp

Mutations: The Raw Material for Evolution?

http://www.icr.org/articles/print/3466/

“It is entirely in line with the al nature of naturally occurring mutations that extensive tests have agreed in showing the vast majority of them to be detrimental to the organisms in its job of surviving and reproducing, just as changes ally introduced into any artificial mechanism are predominantly harmful to its useful operation” H.J. Muller (Received a Nobel Prize for his work on mutations to DNA)

“But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution… There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution.” Jonathan Wells (PhD. Molecular Biology)

“The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume.” Dr. Lee Spetner (Ph.D. Physics - MIT)

cont..

The human genome, according to Bill Gates the founder of Microsoft, far, far surpasses in complexity any computer program ever written by man. The data compression (multiple meanings) of some stretches of human DNA is estimated to be up to 12 codes thick (Trifonov, 1989)! No line of computer code ever written by man approaches that level of data compression (poly-functional complexity). Further evidence for the inherent complexity of the DNA is found in a another study. In June 2007, a international team of scientists, named ENCODE, published a study that indicates the genome contains very little unused sequences and, in fact, is a complex, interwoven network. This “complex interwoven network” throughout the entire DNA code makes the human genome severely poly-constrained to random mutations (Sanford; Genetic Entropy, 2005; page 141). This means the DNA code is now much more severely limited in its chance of ever having a hypothetical beneficial mutation since almost the entire DNA code is now proven to be intimately connected to many other parts of the DNA code. Thus even though a random mutation to DNA may be able to change one part of an organism for the better, it is now proven much more likely to harm many other parts of the organism that depend on that one particular part being as it originally was. Since evolution was forced, by the established proof of Mendelian genetics, to no longer view the whole organism as to what natural selection works upon, but to view the whole organism as a multiple independent collection of genes that can be selected or discarded as natural selection sees fit, this “complex interwoven network” finding is extremely bad news, if not absolutely crushing, for the population genetics scenario of evolution (modern neo-Darwinian synthesis) developed by Haldane, Fisher and Wright (page 52 and 53: Genetic Entropy: Sanford 2005)!

http://www.genome.gov/25521554

BETHESDA, Md., Wed., June 13, 2007 -” An international research consortium today published a set of papers that promise to reshape our understanding of how the human genome functions. The findings challenge the traditional view of our genetic blueprint as a tidy collection of independent genes, pointing instead to a complex network in which genes, along with regulatory elements and other types of DNA sequences that do not code for proteins, interact in overlapping ways not yet fully understood.”

http://www.boston.com/news/glo.....ed/?page=1

“The science of life is undergoing changes so jolting that even its top researchers are feeling something akin to shell-shock. Just four years after scientists finished mapping the human genome - the full sequence of 3 billion DNA “letters” folded within every cell - they find themselves confronted by a biological jungle deeper, denser, and more difficult to penetrate than anyone imagined.”

Your spreadsheet doesn’t reflect the Gambler’s ruin problem exactly: a path which reaches zero should stay at zero.

As well, what is crushing to the “beneficial mutation scenario” is “slightly deleterious mutations” are far below the power of natural selection to remove from the genome. Thus if a hypothetical “truly” beneficial mutation, it would be of no benefit from a progressive Darwinian scenario since this multitude of slightly deleterious mutations will be far below the power of natural selection to remove from the Genome (Sanford 2005)

Bob O’H,

“No, genetic drift is the tendency for allele frequencies to change randomly, because of finite sampling. The effect is for populations to become less homogeneous over time. Different “minority variants” become fixed in different populations.”

I just want to clarify something. When you use the word ‘populations’ it is in the plural. Are you referring to separate populations of the same species that may be separated from each other as opposed to using it in a general way to refer to populations of several species.

Within a population of a species, genetic drift will cause the population to become more homogeneous as certain variants of an allele are eliminated but it will be non homogeneous with other sister populations that faced different situations.

And as a population breaks off from a mother population wouldn’t the sub population become more homogeneous a large percentage of the time. It may not have some of the variants of the mother population and being smaller would be more likely to succumb to genetic drift and natural selection might eliminate certain alleles faster if it is in a new environment.

Bob Oh:

No, genetic drift is the tendency for allele frequencies to change randomly, because of finite sampling. The effect is for populations to become less homogeneous over time. Different “minority variants” become fixed in different populations.

You’re adding a second variable — multiple isolated populations — that confuses the issue.

Individual populations become more homogenous over time due to genetic drift, because minority variants are weeded out.

If you have multiple isolated populations, each of the isolated populations will become more homogenous over time — although they will likely become homogenous with respect to different sets of traits from other, isolated populations.

All this is beside the point, however. The point is that new mutations tend to be weeded out by genetic drift, and in order to survive, a mutation would need to be sufficiently advantageous to overcome this “stacking of the deck” by genetic drift.

bornagain77,

“As well, what is crushing to the “beneficial mutation scenario” is “slightly deleterious mutations” are far below the power of natural selection to remove from the genome. Thus if a hypothetical “truly” beneficial mutation, it would be of no benefit from a progressive Darwinian scenario since this multitude of slightly deleterious mutations will be far below the power of natural selection to remove from the Genome (Sanford 2005)”

If this is true, then these deleterious mutations should show up in the genomes of various related species. For example, there are speculations that there are as many as 300,000 species of beetles. All these deleterious mutations should be in evidence in their genomes.

If they are not found in these genomes or genomes of other related species or only represent a small insignificant part of the genomes then Dr. Sanford’s ideas may be suspect. Also by studying the genomes of various related species one will eventually be able to determine just what makes each different since the vast majority of the genomes will probably be very similar.

This research is getting to be within the reach of modern biology as over 4500 genomes have been mapped and more are coming on line each day. There is speculation that the cost to map a genome may get as low as a thousand dollars in the near future and the computer programs to easily analyze them may be forthcoming too. So the proof will be in the pudding. Meanwhile the beetles seem to be doing just fine.

Jerry:

Within a population of a species, genetic drift will cause the population to become more homogeneous as certain variants of an allele are eliminated but it will be non homogeneous with other sister populations that faced different situations.

Bingo.

You’re adding a second variable — multiple isolated populations — that confuses the issue.

In your original post you referred to populations in the plural, which I interpreted, incorrectly, as meaning several populations.

All this is beside the point, however. The point is that new mutations tend to be weeded out by genetic drift, and in order to survive, a mutation would need to be sufficiently advantageous to overcome this “stacking of the deck” by genetic drift.

Unless the relative fitness is large, this is the wrong way round. A new mutation is always going to suffer from drift, regardless of the population size. In a small population, however, it does not have to drift as far to get to fixation. So, the probability of fixing a new mutant increases as population size decreases. The smaller the population size, the larger the effect of drift, so the higher the probability that a new mutant becomes fixed.

For a neutral mutation the probability of fixation in a diploid population is 1/2Ne, where Ne is the effective population size. For an advantageous mutation, the probability increases, but not significantly unless the relative fitness is quite large.

The full analysis will depend on Ne and s, and I’m not going to check it right now!

Jerry you stated:

If this is true, then these deleterious mutations should show up in the genomes of various related species. For example, there are speculations that there are as many as 300,000 species of beetles. All these deleterious mutations should be in evidence in their genomes.

If they are not found in these genomes or genomes of other related species or only represent a small insignificant part of the genomes then Dr. Sanford’s ideas may be suspect.

In the few studies I have been able to look at this “Genetic Entropy” principle holds up, i.e. loss of information (genetic diversity) is always found for younger “species”.
In fact, the differences of human races we find that the younger races (Chinese, Europeans, American Indians, etc.. etc..) are losing genetic information for skin color when compared to the original race of humans that is thought to have migrated out of east Africa some 50,000 years ago.

“We found an enormous amount of diversity within and between the African populations, and we found much less diversity in non-African populations,” Tishkoff told attendees today (Jan. 22) at the annual meeting of the American Association for the Advancement of Science in Anaheim. “Only a small subset of the diversity in Africa is found in Europe and the Middle East, and an even narrower set is found in American Indians.” Tishkoff; Andrew Clark, Penn State; Kenneth Kidd, Yale University; Giovanni Destro-Bisol, University “La Sapienza,” Rome, and Himla Soodyall and Trefor Jenkins, WITS University, South Africa, looked at three locations on DNA samples from 13 to 18 populations in Africa and 30 to 45 populations in the remainder of the world.

This fact is totally contrary to what we would expect to find if the variation found in the sub-species were truly wrought by random mutations in the DNA generating novel information for variability! And this result is to be totally expected if the parent species were indeed created with a certain amount of flexibility for adaptation to differing environments already programmed in its genetic code! Yet, naturalists conveniently ignore the hard conclusive fact that the variation in the sub-species or pure breed is severely limited when it is compared to the much larger variability that is found in the parent species.

as well as this:

African cichlid fish: a model system in adaptive radiation research

http://www.pubmedcentral.nih.g.....id=1635482

of special note:

Interestingly, ecological opportunity (the availability of an unoccupied adaptive zone), though explaining rates of diversification in radiating lineages, is alone not sufficient to predict whether a radiation occurs. The available data suggest that the propensity to undergo adaptive radiation in lakes evolved sequentially along one branch in the phylogenetic tree of African cichlids, but is completely absent in other lineages. Instead of attributing the propensity for intralacustrine speciation to morphological or behavioural innovations, it is tempting to speculate that the propensity is explained by genomic properties that reflect a history of repeated episodes of lacustrine radiation: the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages.

Thus as you can see, the evolutionists are mystified that the radiations are not happening for “sub-species” of cichlids but are always radiating from the “more ancient” lineage. This fits in perfectly with Genetic Entropy.

This principle also holds for the genetic studies of wolfs/dogs and sheep I have looked at i.e. sub-speciation always comes at a loss of genetic diversity from the more ancient lineage. (loss of genetic information)

As well this following study is very interesting in that it shows genetic entropy being obeyed in trilobites over their 270 million run in the fossil rcord:

In fact, i think The principle of Genetic Entropy allows us to trace the CSI to point of implementation with a large amount of confidence.

A Cambrian Peak in Morphological Variation Within Trilobite Species
Mark Webster

http://www.sciencemag.org/cgi/.....7/5837/499

This following study is excellent for Genetic Entropy proof! It is a study of trilobites over their 270 million year history in the fossil record since their “abrupt” appearance at the beginning on the Cambrian explosion. Of special note: It studies within species variation instead of just among species variation. Within species morphological variation, over deep time, for the entire spectrum of trilobites, gives us a peak at CSI “degeneration” within trilobites over their 270 million year history.

It follows Genetic Entropy to a “T”!

“Early and Middle Cambrian trilobite species, especially, exhibited greater morphological variations than their descendants. This high within-species variation provided more raw material upon which natural selection could operate, Webster says, potentially accounting for the high rates of evolution in Cambrian trilobites. Such findings may have implications for our understanding of the nature of evolutionary processes, he says.

Why the early trilobites were so morphologically diverse is a whole different mystery.”

Guess what we know the answer to the mystery! CSI degeneration aka Genetic Entropy! (Sanford 2005)

And it gets even better if you go into the actual studies themselves you find all trilobites that branch off the “parent” trilobites species quickly lose variability that is found in the parent stock of trilobites.

I am extremely confident that this study, when it is fully fleshed out in all its detail, will fit the ID/Genetic Entropy model perfectly (as well as supporting environmentally driven adaptations).

http://www.geotimes.org/july07.....72707.html

Unless the relative fitness is large, this is the wrong way round. A new mutation is always going to suffer from drift, regardless of the population size. In a small population, however, it does not have to drift as far to get to fixation. So, the probability of fixing a new mutant increases as population size decreases. The smaller the population size, the larger the effect of drift, so the higher the probability that a new mutant becomes fixed.

True. On the other hand, the smaller the population, the less individuals are available to “host” the new mutation. That is to say, if you’ve got a population of 10,000,000, you’ve got a much better chance of getting some lucky mutations than if you’ve got a population of 10.

Seems like something of a catch 22. To get the mutations you have to have a large population, but having a large population prevents the new mutation from setting, and ultimately wipes it out unless there’s a substantial selection advantage.

The diluvial model, of course, accounts rather admirably for the population bottleneck necessary to set characteristics in isolated population. If 7 pairs of primal “cats” of substantial heterozygosity stepped off the boat, genetic drift would “set” them into a numnber of distinct species within a matter of a few generations.

Scordova:

Thank you for the very interesting article, which adds more fuel to the arguments against darwinian evolution, and clarifies many important aspects.

I would try to make a brief summary of some important points, as we often discuss them separately, and can’t see them in their logical relations:

1) Random variation (RV) is the only available engine of variation in theories which exclude design. All the recognized causal mechanisms of variation (sinlge point mutations, deletions, inversions, duplications, genetic drift, and so on) are in essence random.

2) The power of RV to create new useful complex information (CSI) is strictly dependent on the ratio of functional results to the whole serach space. The transition from a preexisistng condition to a new condition which exhibits new CSI (and which, therefore, could be in theory selected) is, as far as we can judge, a completely negligible possibility, due to the huge search space of even the simplest proteins. The probabilities become even more prohibitive for any multiple level of information, involving for instance multiple proteins in specific relation.

3) If the new level of functionality is irreducibly complex (IC), then it cannot be deconstructed in simpler functional units (with the same function), and should be achieved in its entirety before being selected. The alternative of “cooption” poses even more formidable improbabilities, having to realize a critical concurrence of independent functions in the huge space of all the possibilities.

4) Anyway, most mutaions seem to be neutral, and therefore cannot be selected. Neutral mutations can be “fixed” only by genetic drift, which, being a totally random process, adds nothing to the considerations of point 1 and 2.

5) Even if, overcoming the impossibilities of the first 4 points, some beneficial muation can emerge in an individual, its probabilities of being selected are extremely small, as well shown in the above article. It could be useful to remember that, when we speak of a beneficial mutation giving a 1% advantage of reproduction, we are assuming a lot. Most single mutations, even if potentially beneficial, would not be able to generate really a 1% reproductive advantage. A reproductive advantage, even small, is really a big thing, and usually would require a lot of new, coordinated CSI. The only exception (and, indeed, the only examples really known of natural selection) are scenarios of extreme selective pressure (like antibiotics) combined with the possibility that simple, essentially destructive mutations can protect from the pressure. In that case, and only in that case, many of the difficulties described in the above points do not apply.

6) All those mechanisms however, even if improbable or quite impossible, require anyway lots of reproducing beings and short inter-reproductive time. To try to apply them to complex, and rare, and slow animals, like mammals, is not only a fairy tale, but a really bad one.

Regarding the frequently asked question of how Sanford’s genetic entropy concept may be compatible with the actual survival of biological beings, we could perhaps consider that intelligently designed mechanisms to preserve DNA information are universally active in the biological world. Those mechanisms are a fundamental part of the real scenario, because the real scenario is one of constant interaction (and fight) between design and purpose on one side, and chance and entropy and meaninglessness on the other.

Scordova:

Exactly!!!! Spetner was keen to realize this. His book highlights the catch-22.

Fun! I’ll have to read the book.

Scordova:

Exactly!!!! Spetner was keen to realize this. His book highlights the catch-22.

I was just thinking, and there’s a counterpoint to this catch 22 — the larger the population, the less intense the pressure from genetic drift. That might permit new mutations to survive long enough to get picked up by natural selection. Did Spetner address this in his book to your knowledge?

bornagain77:

In your last post, you stated: “The human genome, according to Bill Gates the founder of Microsoft, far, far surpasses in complexity any computer program ever written by man.”

I’ve seen this statement before in the literature. Do you, or does anyone else, know the source? I’m just curious.

Here’s the source:

The understanding of life is a great subject. Biological information is the most important information we can discover, because over the next several decades it will revolutionize medicine. Human DNA is like a computer program but far, far more advanced then any software ever created.

The Road Ahead; Bill Gates pg. 188

I believe Bill Gates wrote that in 1995, yet all comprehensive studies conducted by ENCODE have back his claim up immensly.

As well;

There are about….
Three-billion letters of code on that six feet of DNA. The DNA contains the “complete parts list” of the trillions upon trillions of proteins that are in your body, plus, it contains the blueprint of how all these countless trillions of proteins go together, plus it contains the self-assembly instructions that somehow tells all these countless proteins how to put themselves together in the proper way.If you were to read the code aloud, at a rate of three letters per second for twenty-four hours per day (about one-hundred-million letters a year), it would take you over thirty years to read it. The capacity of a DNA molecule to store information is so efficient that all the information needed to specify an organism as complex as man weighs less than a few thousand-millionths of a gram. The information needed to specify the design of all species of organisms that have ever existed (a number estimated to be one billion) could easily fit into a teaspoon with plenty of room left over for every book ever written on the face of earth. For comparison sake, if mere man were to write out the proper locations of all those proteins in just one human body, in the limited mathematical language he now uses, it would take a bundle of CD-ROM disks greater than the size of the moon, or a billion-trillion computer hard drives, and that’s just the proper locations for the protein molecules in one human body, that billion-trillion computer hard-drives would not contain a single word of instruction telling those protein molecules how to self assemble themselves.

The coding system used for living beings is optimal from an engineering standpoint. Of all possible mathematical combinations, the ideal number for storage and transcription has been calculated to be four letters. This is exactly what has been found in the DNA of every living thing on earth—a four-letter digital code. As Werner Gitt states: “The coding system used for living beings is optimal from an engineering standpoint.”

The atoms in a human being are the equivalent to the information mass of about a thousand billion billion billion bits. Even with today’s top technology, this means it would take about 30 billion years to transfer this mass of data from one point to another. That’s twice the age of the universe.

There are about…..
One-hundred trillion cells in the average person.Every human spent about half an hour as a single cell Each cell has over a million unique structures and processes (a complexity comparable to a large city ). Each cell consists of artificial languages and their decoding systems, memory banks for information storage and retrieval, elegant control systems regulating the automated assembly of parts and components, error fail-safe and proof-reading devices utilized for quality control, assembly processes involving the principle of prefabrication and modular construction and a capacity not equalled in any of our most advanced machines, for one of our most advanced machines would have to be capable of self-replicating its entire structure within a matter of a few hours. Every one of those trillions of cells (except for the brain cells) is regenerated and replaced on average of every seven years! Each cell has about ten-thousand times as many molecules as our Milky Way galaxy has stars.

When considering this absolutely staggering level of complexity it is apparent that life “accidentally” evolving is absolutely impossible by unintelligent means.
Darwinian Evolution is sheer fantasy of the highest magnitude as far as hard science and evidence is concerned.

DLH wrote:
a designed system would be expected to exhibit some degree of optimization. (Apparent lack of full optimization would likely be caused by failure to recognize the full design and optimization involved.)

The challenge for evolution is how to “jump” from one configurational mountain to the next configurational mountain - when then the variation required to move away from the local mountain results in substantial variational regional of negative slope in function or a reduced fitness.

So, the premise of everything you wrote, if I understand correctly, is that species tend to be highly optimized for a specific niche, so any varation away from that will be detrimental in the short run, so how would this obstacle be surmounted.

But it seems there are multitudinous examples of species that are highly optimized in certain ways and yet regularly make forays into other environments where they are comically ill-equipped to do so. In such areas there could be change without at all effecting the areas where they were optimized already.

With marine mammals and birds this is very much in evidence. A walrus is highly optimized and graceful in the sea, but lumbers around like a big slug on the land where it spends most of its time. Would not marginal increase in land motility give male walrus’s competing with others males for breeding purposes a big advantage, without effecting at all their means for making a living in the sea. Same example with birds that dive beneath the surface of the water for fish. (not increase in land motility but possibility something that increases capability in the sea.) Then you have polar bears, with webbing between toes and other adaptions for swimming and yet capable of interbreeding with grizzlies. Also, occasionally you can see a roach fly, but they’re not all that good at it. The more I think about your idea the less sense it makes. Would an increase in lung capacity decrease the level of optimality of a dolphin? Apologies if I’ve missed your point.

Bob O’H:

(quoting Sal)

Is there any research you could point me to to show the statistics of a mutation being beneficial?

Yes - there was a review last year. It’s of the order of 1% or so, but the estimates vary, and it’s difficult to get really good estimates, because mutations are rare in themselves.

Bob, I can only get the abstract of the article you cite. But looking at a similar article from a year earlier, it appears that i