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Biotic Message by Walter Remine

Parsimony

Well-Known Member
Science for Creation, if I understand your argument correctly, you are saying that Haldane's Dilemma refutes the evolutionary idea that humans and chimpanzees descended from a common ancestor that existed 4-6 million years ago because the genomic differences between the two species is too large to be accounted for over such a short time period? Is that right?
 
Science for Creation, if I understand your argument correctly, you are saying that Haldane's Dilemma refutes the evolutionary idea that humans and chimpanzees descended from a common ancestor that existed 4-6 million years ago because the genomic differences between the two species is too large to be accounted for over such a short time period? Is that right?

No, that is not what I am saying. I am saying Haldane's Dilemma was never solved. Evolutionists commonly claim it was solved, but it was never solved.

Here is the problem, stated straightforwardly:

  1. Given, say, ten million years (which is two to three times the age of the said split between chimps and humans),
  2. Given a twenty-year generation-time on average, (that figure also comes from evolutionary geneticists for that lineage),
  3. Given the Haldane limit of 300 generations per beneficial substitution.
Given those three fundamentals (which all come from evolutionists), there could be merely 1,667 beneficial substitutions (=10,000,000/(20*300))since that split (plus some number of neutral substitutions, which do nothing for adaptation). (According to evolutionary geneticists, each substitution is typically one nucleotide.) All the uniquely human adaptations would have to be explained within a limit of 1,667 beneficial substitutions.
 
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ImmortalFlame

Woke gremlin
No, that is not what I am saying. I am saying Haldane's Dilemma was never solved. Evolutionists commonly claim it was solved, but it was never solved.

Here is the problem, stated straightforwardly:

  1. Given, say, ten million years (which is two to three times the age of the said split between chimps and humans),
  2. Given a twenty-year generation-time on average, (that figure also comes from evolutionary geneticists for that lineage),
  3. Given the Haldane limit of 300 generations per beneficial substitution.
Given those three fundamentals (which all come from evolutionists), there could be merely 1,667 beneficial substitutions (=10,000,000/(20*300))since that split (plus some number of neutral substitutions, which do nothing for adaptation). (According to evolutionary geneticists, each substitution is typically one nucleotide.) All the uniquely human adaptations would have to be explained within a limit of 1,667 beneficial substitutions.

Here's a brief article detailing a couple of refutations from talkorigins.org:

CB121: Haldane's Dilemma
 

Parsimony

Well-Known Member
No, that is not what I am saying. I am saying Haldane's Dilemma was never solved. Evolutionists commonly claim it was solved, but it was never solved.

Here is the problem, stated straightforwardly:

  1. Given, say, ten million years (which is two to three times the age of the said split between chimps and humans),
  2. Given a twenty-year generation-time on average, (that figure also comes from evolutionary geneticists for that lineage),
  3. Given the Haldane limit of 300 generations per beneficial substitution.
Given those three fundamentals (which all come from evolutionists), there could be merely 1,667 beneficial substitutions (=10,000,000/(20*300))since that split (plus some number of neutral substitutions, which do nothing for adaptation). (According to evolutionary geneticists, each substitution is typically one nucleotide.) All the uniquely human adaptations would have to be explained within a limit of 1,667 beneficial substitutions.
If that's only about beneficial substitution mutations, then what about beneficial deletion, insertion and frame-shift mutations? Did Haldane's calculations not cover those? If not, then that seems one way to solve the problem (if there is one). Let's also not forget that if each of the 1,667 mutations occured in different genes, then you could potentially generate 1,667 new genes (with humans having ~20,000 genes). That's an 8.3% change in total genes from the ancestral species, which is pretty significant. If chimps changed by the same amount from the common ancestor, then you can have a 16.6% beneficial gene difference between humans and chimps. That's not even counting neutral mutation differences in genes.
 
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Ouroboros

Coincidentia oppositorum
If that's only about beneficial substitution mutations, then what about beneficial deletion, insertion and frame-shift mutations? Did Haldane's calculations not cover those? If not, then that seems one way to solve the problem (if there is one). Let's also not forget that if each of the 1,667 mutations occured in different genes, then you could potentially generate 1,667 new genes (with humans having ~20,000 genes).
And also, I think the possibility of beneficial retroviral infections also can play into this. And genetic add-mixture between different sub-species. Haldane was very fixed on a linear or sequential mutation rate. Today, we know there can be simultaneous chains of mutations and then crossing in between. And on top of that, there's the chance of our ancestral "ape" having dormant genes that were turned on again, and other genes turned off. It doesn't take much.

This whole "dilemma" argument sounds like someone would say that algebra should be questioned unless we can solve Fermat's last theorem. It was solved 15 years ago, but was the quadratic formula then invalid for 2,500 years since Pythagoras? Of course not. It was a problem in math that wasn't solved, but it didn't suggest that any other proof in algebra would also have to be wrong.

In this case, we know we are related to apes because of overwhelming evidence. The "dilemma" was questioned even by its author originally, and the responses over the years have been where and what Haldane was wrong, so there isn't really a dilemma.

It all also makes me think of moonlander conspiracy theorist who have all these tiny "dilemmas" they argue that have to be "solved" before they can believe we landed on the moon. Well, recently LRO took pictures (2013), remotely from space, of the landing site. Perhaps the whole world (all non-conspiracists) are all in it together to trick the true believers still... People just love a good conspiracy theory.


That's an 8.3% change in total genes from the ancestral species, which is pretty significant. If chimps changed by the same amount from the common ancestor, then you can have a 16.6% beneficial gene difference between humans and chimps. That's not even counting neutral mutation differences in genes.
If was thinking about that too.

The difference only have to be half of the 1667 since we're comparing to modern chimps that have evolved as well since the split. Haldane assumed chimps didn't evolve the past 10 million years, only humans. Also, he assumed chimps and humans aren't fertile until 20 yo, which is wrong. 15 or younger, especially in the past. The whole 20 year old is some puritan influence or whatever. You aren't old enough to have kids until 20 in our modern age, therefore the common ancestor must've also have had kids at 20. :areyoucra
 

Parsimony

Well-Known Member
I haven't read Haldane's paper, but what was the rationale behind the idea that it must take twice as long for two beneficial mutations to reach fixation than one? It's not like a second mutation has to "wait" until the first one reaches fixation before it pops up. If a second beneficial mutation comes into existence in a population while the first has already spread to 50% of the population, should that not allow both to reach fixation in less than double the time that the first one did?
 

Ouroboros

Coincidentia oppositorum
I haven't read Haldane's paper, but what was the rationale behind the idea that it must take twice as long for two beneficial mutations to reach fixation than one? It's not like a second mutation has to "wait" until the first one reaches fixation before it pops up. If a second beneficial mutation comes into existence in a population while the first has already spread to 50% of the population, should that not allow both to reach fixation in less than double the time that the first one did?
My understanding is that this is one of the major critiques of Haldane's paper.

Another point to make here is that a gene or mutation aren't exactly 1-to-1 relationship with a "beneficial" trait. There are many mutations happening not only in each generation, but also within ourselves while we live, and each mutation most of the time have no or little effect at all. Over time, there's a huge diversity of genetic code. The pool of variations in a population is what really is selected for or against, and also, all the "junk" DNA that is dormant, can go "live" by few mutations, so they can be there, for millions of years with variations, and suddenly come about in some offspring. Meaning, the "beneficial" mutations can already be there, but not in use. Haldane's model was based on a very limited view on how the changes really occurs. Point mutations are only one of them.

I was thinking. If we had a perfect situation where every mutation and permutation (recombination) were perfect, then wouldn't we have something like this:

3200 parents, giving birth to 4 kids each, each one with a perfect recombination of the parents genes.
Let's say one out of each 4 kids have one of the wanted, beneficial mutations we need for the end "product."
That means 1600 kids, each one carrying the mutation we want.
Now those 1600 live for 20 years, become fertile (very late) and have offspring, with perfect recombination, and no new mutations at all.
That means that one of every four kids will have two beneficial mutations. We have then 800 kids, each carrier of two end game genes.
Those 800, live 20 years, have kids, perfect recombination, no new mutations, four kids, one of each family have now four (4) of the end product genes we want.
I estimated something like 200-300 years to produce one offspring with the whole set of all 1600 mutations.
This, I think, would be the lowest of the low limits for a perfect sequence of mutations. It's of course based on a perfect scenario that doesn't happen in nature because of many other parameters, but it shows that it hypothetically could go much faster than 10 million years.
 
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If that's only about beneficial substitution mutations, then what about beneficial deletion, insertion and frame-shift mutations?

Various types of beneficial mutations are already allowed into the analysis (for example, deletions, insertions, frame-shift mutations, unequal crossing-over, relocation of a gene, etc.) They are all allowed, each one counting as one substitution. Mix them however you like. Nonetheless, the total number of beneficial substitutions is still limited to less than 1,667. Evolutionists have not solved the problem.

Evolutionists have scarcely begun to deal with the new genetic data, which makes Haldane's Dilemma much more problematic. The ENCODE Project, for example, shows that a typical gene codes for seven different traits, and some of them up to 35 different traits. This phenomenon is known as pleiotropy. It is now known to be super abundant in genetics, and much more common than previously suspected. It makes the problem worse for evolutionists. It is vastly more difficult to "evolve a gene" when it simultaneously codes for many different traits, as in pleiotropy. (That is why evolutionary genetics textbooks ignore it when arguing for a greater speed (or greater plausibility) to evolution.)

Haldane favored evolution by completely ignoring pleiotropy. All Haldane's assumptions favored evolution, and modern data has made the problem worse for evolutionists, not better.

Evolutionists have scarcely begun to account for the organization of genes within the chromosomes. They completely ignore this when giving their repeated claim that chimps and humans are 98.5% genetically identical. From the beginning, that claim was highly misleading, but it is now known to be grossly false. It did not account for the reorganization of the genome, the organization of genes within chromosomes. It completely ignored that. Yet the organization of genes within the genome has long been known to be highly significant to the fitness and form of the organism. To this day, evolutionists ignore this in their discussions of Haldane's Dilemma.

Haldane's Dilemma was never solved.
 
And also, I think the possibility of beneficial retroviral infections also can play into this.

You are still trying to invent a solution on the fly. You ought to be able to find a solution -- a solution that evolutionary geneticists publically embrace and agree upon -- a solution they publically defend as realistic -- a solution that evolutionists consistently incorporate into their theory, explanations, and storytelling. No such solution exists. I challenge you to identify one.

(Note: If a retrovirus inserted something beneficial into the genome, and that 'beneficial something' goes to fixation (it substitutes into the population), then it would still incur a cost of substitution, and fall under the Haldane limit.)

Haldane was very fixed on a linear or sequential mutation rate. Today, we know there can be simultaneous chains of mutations and then crossing in between.

You are mistaken. Haldane allowed for mutations arriving at random, with their substitutions overlapping in time in any arbitrary fashion, with sexual reproduction, crossing-over, and recombination of chromosomes. It was all already taken into account.

And on top of that, there's the chance of our ancestral "ape" having dormant genes that were turned on again, and other genes turned off. It doesn't take much.

You are again trying to invent a solution on the fly. It doesn't work. The beneficial 'thing' that "turns on (or off) a dormant gene" must nonetheless incur a cost of substitution, and falls under the Haldane limit. You solved nothing.

This whole "dilemma" argument sounds like someone would say that algebra should be questioned unless we can solve Fermat's last theorem. It was solved 15 years ago, but was the quadratic formula then invalid for 2,500 years since Pythagoras? Of course not. It was a problem in math that wasn't solved, but it didn't suggest that any other proof in algebra would also have to be wrong.

You argued by false analogy. Fermat's Last Theorem wasn't solved, and then it was solved. Haldane's Dilemma was never solved. Evolutionists should own up to that. Mathematicians did!

The "dilemma" was questioned even by its author originally

The name, Haldane's Dilemma, wasn't coined until after his death. So he did not question the "dilemma" (your quotes there). On the contrary, Haldane saw a serious problem here. Haldane 1957 concluded, "I am convinced that quantitative arguments of the kind here put forward should play a part in all future discussions of evolution." (Underline added)

and the responses over the years have been where and what Haldane was wrong, so there isn't really a dilemma.

You are mistaken. Evolutionary geneticists, Crow, Ewens, Kimura, and Maynard-Smith, all took Haldane's concept seriously. They took it so seriously that they proposed radical new selection models (such as truncation selection) in an effort to solve the problem. Kimura wrote that "Haldane's Dilemma" (yes, he used that term) was the "main reason" why he proposed the theory of neutral evolution.

Also, he assumed chimps and humans aren't fertile until 20 yo, which is wrong. 15 or younger, especially in the past.

You're still trying to solve the problem yourself, on the fly. You're wasting your time. The key figure here is not the "age of fertility". Rather, it is the average-generation-time, which is a technical term in the practice of evolutionary genetics. Walter ReMine cited three different evolutionary geneticists for a figure of 20 years, for the lineage in question, over the said era of time.

It all also makes me think of moonlander conspiracy theorist who have all these tiny "dilemmas" they argue that have to be "solved" before they can believe we landed on the moon.

You're arguing by false analogy again. You're increasingly using personal attacks, and desperate tactics that do not serve you.

You're working too hard. For sixty years, evolutionists (falsely) claimed Haldane's Dilemma was "solved". All you have to do is identify a solution. It ought be easy.
 
I haven't read Haldane's paper, but what was the rationale behind the idea that it must take twice as long for two beneficial mutations to reach fixation than one? It's not like a second mutation has to "wait" until the first one reaches fixation before it pops up. If a second beneficial mutation comes into existence in a population while the first has already spread to 50% of the population, should that not allow both to reach fixation in less than double the time that the first one did?

Your question has been asked and answered many times, in various places.

Haldane allowed for mutations arriving at random times, with their substitutions overlapping-in-time in any arbitrary fashion. Haldane also allowed for sexual reproduction.

Haldane further assumed a selection model unrealistically favorable to evolution -- far more favorable to evolution than what nature provides. (But not as favorable, or as unrealistic as truncation selection.)

His result -- and it is a correct result -- shows that when multiple substitutions occur concurrently, the combined cost of substitution equals the sum of the their cost of substitution taken individually (or sequentially).

Therefore, no matter how the substitutions overlap (or don't overlap), the total cost of substitution (summed from the beginning of the first, to the end of the last), is the same, regardless of how they overlap. In short, there is no cost reduction for concurrent substitutions. So the Haldane limit applies, no matter how the substitutions overlap.

This technical result is well-agreed-to by leading evolutionary geneticists. I am aware of no evolutionary geneticist who disputes Haldane's Dilemma based upon this specific result. They attempt other disputes, but not this one.
 

Riverwolf

Amateur Rambler / Proud Ergi
Premium Member
No, that is not what I am saying. I am saying Haldane's Dilemma was never solved. Evolutionists commonly claim it was solved, but it was never solved.

Here is the problem, stated straightforwardly:

  1. Given, say, ten million years (which is two to three times the age of the said split between chimps and humans),
  2. Given a twenty-year generation-time on average, (that figure also comes from evolutionary geneticists for that lineage),
  3. Given the Haldane limit of 300 generations per beneficial substitution.
Given those three fundamentals (which all come from evolutionists), there could be merely 1,667 beneficial substitutions (=10,000,000/(20*300))since that split (plus some number of neutral substitutions, which do nothing for adaptation). (According to evolutionary geneticists, each substitution is typically one nucleotide.) All the uniquely human adaptations would have to be explained within a limit of 1,667 beneficial substitutions.

I ask again: define "beneficial".
 

Ouroboros

Coincidentia oppositorum
Multiple Simultaneous Substitutions Lower the Cost Even Further
It is easy to see that the substitution cost is lowered when multiple substitutions are occurring in a population. The reason for this is very simple. If two beneficial mutations are moving towards fixation in a population, whenever an organism that carries neither of those mutations dies, the cost of substitution is exactly half what it would have been had the two substitutions occurred at different times from one another. One organism has died to "pay the cost" for two substitutions. If you prefer to look at the cost from the perspective of the number of individuals that must be born to carry the mutation to fixation, then one individual which is born with two beneficial genes (and survives to reproduce) pays the cost that would have been required of two organisms if the substitutions had occurred separately. As more substitutions are going on at the same time, the more the cost will be lowered (compared to what the cost would have been had the substitutions occurred separately. Evidence that this actually occurs in nature has recently been discovered. Scientists have recently determined that the genes driving the speciation of a particular group of aphids lie very close to one another on the same chromosome. When genes are closer together on a chromosome (tightly linked), they are more likely to move together as a single unit because they are not broken up by recombination. This will lower the substitution cost even more than the simultaneous substitution of unlinked genes.

Haldane did address the issue of multiple simultaneous substitutions in "The Cost of Natural Selection" (see the fifth paragraph of page 511). However, because he considered only substitutions occurring in the deteriorating environment scenario, he did not think that very many substitutions could occur simultaneously. He gave the example of a change in the environment that suddenly favored 10 rare alleles, leaving the fitness of any individual carrying all 10 of those alleles unchanged and reducing the fitness of all individuals not carrying all 10. If each of the 10 alleles is rare, the vast majority of the population would carry none of the 10. If the fitness of an organism is reduced by 1/2 for each of the 10 beneficial alleles it does not have, then the fitness of the vast majority of the population would be reduced by a factor of 1024. Haldane pointed out that such a fitness reduction could not be tolerated by the vast majority of species in the world. However, when substitutions occur that are truly beneficial (when the environment is not deteriorating), then the fact that the vast majority of the population does not possess any of the beneficial mutations does not lead to any reduction in fitness. Individuals without the beneficial mutations have the same fitness that they did before. Individuals that do not have the beneficial mutations will only see a decrease in fitness when the individuals carrying the beneficial mutations become more common in the population and begin to out compete those without the beneficial mutations for resources.
Robert Williams. From here: Haldane's Dilemma

Or Wiki:
Haldane stated at the time of publication "I am quite aware that my conclusions will probably need drastic revision", and subsequent corrected calculations found that the cost disappears. He had made an invalid simplifying assumption which negated his assumption of constant population size, and had also incorrectly assumed that two mutations would take twice as long to reach fixation as one, while sexual recombination means that two can be selected simultaneously so that both reach fixation more quickly.[2][3][4]

Oh. I'm just inventing stuff "on the fly." *rolleyes*

(Clicked on "ignore" for good now.)

Grant, Verne & Flake, Robert, "Solutions to the Cost-of-Selection Dilemma", Proc Natl Acad Sci U S A. 71(10): 3863–3865, Oct. 1974.

Nunney, Leonard, "The cost of natural selection revisited", Ann. Zool. Fennici. 40:185–194, 2003. (This paper describes computer simulations of small populations with variations in mutation rate and other factors, and produces results that are dramatically different from Haldane's low substitution limit except in certain limited situations).

(Also from Wiki. It's easy to find these refutations.)
 
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My understanding is that this is one of the major critiques of Haldane's paper.

That particular critique is made frequently by amateurs, and internet posters. Leading evolutionary geneticists, especially Crow, Kimura, Ewens, and Maynard-Smith, all accepted the point -- that under the selection model used by Haldane, the costs during concurrent substitutions sum together.

and also, all the "junk" DNA that is dormant, can go "live" by few mutations, so they can be there, for millions of years with variations, and suddenly come about in some offspring. Meaning, the "beneficial" mutations can already be there, but not in use. Haldane's model was based on a very limited view on how the changes really occurs. Point mutations are only one of them.

Can you cite even one evolutionary geneticist who embraces your fantasy solution to Haldane's Dilemma?

You claim a lengthy stretch of DNA lays within organisms, "dormant for millions of years" -- getting plugged repeatedly with random mutations for "millions of years", and because it is "dormant" there is no purifying selection to prevent this scrambling of the DNA -- and eventually this lengthy stretch of DNA can "go live" (by a few more mutations...). This random lengthy stretch of DNA goes "live"! It will kill the organism, and make the problem worse. You suggest that by some phantasm miracle that it doesn't kill the organism, but is actually "beneficial"! ??? Is that your claim? Well, it still has to substitute into the population, and incur a full cost of substitution -- and falls under the Haldane limit. You didn't reduce the problem one iota. You made it worse.

You are struggling too hard. If trained evolutionary geneticists haven't solved the problem after sixty years, then it's unlikely you can either. On the other hand, if they solved it, then you should easily find a solution! They've surely done the work for you.
 

Ouroboros

Coincidentia oppositorum
Recommended read, wikipedia's discussion behind the wiki-page: Talk:Haldane's dilemma - Wikipedia, the free encyclopedia

(ReMine is also in it, but I'm not sure under what screen name. I think his name is XXXXXXed out.)

This quote was especially interesting:
While Haldane(1957) apparently did pose a "dilemma" in the past, it is (a) different from what ReMine claims and (b) largely solved. The real impact of Haldane's cost model was that adaptations could not explain the whole of molecular evolution. But genetics discovered that most of the DNA in our genes is not under constraint, i.e. only a small part of our genome codes for proteins (and even those parts experience many silent mutations). In other words, adaptations do not need to explain all of evolution because the actual genetic information forms only a fraction of the DNA in most species. Most of our DNA can change freely with little or no effect on phenotype.
and
Besides, it seems that molecular evolution is largely caused by gene duplications. ReMine insists that we should concentrate on point mutations, because they are the most common type of mutation. But ReMine ignores the fact that a gene duplication can involve tens of thousands of nucleotides (counting introns and exons). So duplications don't need to be common at all, and they still may well beat point mutations in importance in molecular evolution. For example, I believe that the better part of molecular differences between humans and chimps are attributed to the about 1,500 fixed duplications that these species have experienced since their divergence. So far as ReMine's argument is about molecular evolution, then gene duplications and neutral evolution can easily explain the quick molecular changes, and Haldane's cost model has little to say about it. Presumably this debate is about morphologic adaptations, however, because otherwise Haldane's paper would likely not be under focus. (Of course, gene duplications likely play a relevant role in morphological adaptations as well, because they are a source of new genes. But ReMine's argument deals with the quantity of adaptations rather than the quality. Admittedly, protein dosages seem to be selected, in which case some gene duplications could fit under Haldane's cost scenario.)

Also
Average mutation rate per nucleotide site: Mutation rates estimated for a range of divergence times and ancestral population sizes fall between 1.3 × 10−8 and 2.7 × 10−8 assuming a generation time of 20 years (Table 3) or between 1.6 × 10−8 and 3.4 × 10−8 assuming a generation time of 25 years. We suggest that 2.5 × 10−8 is a reasonable estimate of the average mutation rate per nucleotide site (but caution that the actual rate may be between 1.3 × 10−8 and 3.4 × 10−8). The human diploid genome contains 7 × 109 bp (MARSHALL 1999) and thus ~175 new mutations per generation (range 91–238)
From here: http://www.genetics.org/content/156/1/297.full

So 10 my, 25 y between generations, 175 new mutations per, is 70,000,000 mutations to pick from. If 3 of 4 of those are detrimental and immediate death (if I understand some other numbers in that paper), that still leaves 17,500,000 neutral or beneficial mutations. So we could have had 1667 beneficial mutations up to 10,500 times... ???
 
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Let it go on record that evolutionists here routinely cite (and post links to) material that is not peer-reviewed (and which is actually internet web pages, where the sources are anonymous).

******

Also, the following highly relevant paper was cited here by evolutionists. Yes, highly relevant!!!

From here: Estimate of the Mutation Rate per Nucleotide in Humans

That abstract says, "The average mutation rate was estimated to be ... 175 mutations per diploid genome per generation."

But what does that mean? A helpful evolutionist here tells us!

So 10 my, 25 y between generations, 175 new mutations per, is 70,000,000 mutations to pick from. If 3 of 4 of those are detrimental and immediate death (if I understand some other numbers in that paper), that still leaves 17,500,000 neutral or beneficial mutations. So we could have had 1667 beneficial mutations up to 10,500 times... ??? (emphasis added)

The data says, on average, every progeny receives 175 new mutations (plus the mutations it inherits from its parents). Of these, the evolutionist tells us "3 of 4 of those are detrimental and immediate death." 175 x 3/4 = 131.25 mutations per progeny that are "detrimental and immediate death"! In other words, Each progeny receives enough harm to cause immediate death over 131 times! And he claims it's a solution to Haldane's Dilemma! What a hoot!!!

This evolutionist has (quite by accident) bumped into another central unsolved problem in evolutionary genetics. The problem is known as "error catastrophe" or "mutational meltdown" -- where harmful mutations accumulate faster than the population can be rid of them. (ReMine's book was the first to bring this issue into the origins debate in a form that pedestrian audiences could understand.)

The problem is now acute. Depending on which evolutionist you care to cite, they are now measuring a mutation rate in humans of between 100 and 300 new mutations per progeny. Not only have evolutionists not solved Haldane's Dilemma, they have not solved the problem of error catastrophe, where populations would undergo genetic deterioration, generation after generation. Evolutionists now have a morass of central problems they are hiding from the public, and falsely claiming are "solved".
 

Riverwolf

Amateur Rambler / Proud Ergi
Premium Member
I'm going to assume that beneficial has not yet been defined because it's not understood.

Well, here's the solution: the number of "beneficial" mutations is wholly dependent on the immediately previous, current, and near-future states environment of the organism. It's beneficial if it allows better reproductive opportunities than the previous state of the organism in the new environment, and will continue to be better long enough for the older state to be selected out.

As a result, the number is not going to be static, since environments are always changing, sometimes at slow paces, sometimes at fast ones. Only 10,000 years ago, the Sahara was wetland and Britain was a peninsula connected to Europe via Doggerland (which is now submerged).

Evolution is reactive, not static.
 

Simurgh

Atheist Triple Goddess
Let it go on record that evolutionists here routinely cite (and post links to) material that is not peer-reviewed (and which is actually internet web pages, where the sources are anonymous).

You use that to assert your right to quote what exactly? Religious drivel? Or creationist scientific confusion? OK, they’re the same.

Also, the following highly relevant paper was cited here by evolutionists. Yes, highly relevant!!!

From here: Estimate of the Mutation Rate per Nucleotide in Humans

That abstract says, "The average mutation rate was estimated to be ... 175 mutations per diploid genome per generation."

But what does that mean? A helpful evolutionist here tells us!.......................Evolutionists now have a morass of central problems they are hiding from the public, and falsely claiming are "solved".
Well, you first problem is that you act as if Haldane’s paper, which was published in 1935, is the end-all of genetics.

We all know that the field of genetics has progressed greatly since then. Also, Haldane studied hemophilia, and while his results are –to this day—found fairly accurate, it is also true that not all genes mutate at the same rate. Research further shows that not all mutation is necessarily harmful and is considered neutral. Blue eyes are a mutation that happened about 6 to 10,000 years ago and I venture to assert that they hurt no-one.

And if you want to actually understand what you are debating ever so cleverly with all those red herrings and pseudo-truths, then read Nachman’s article that deals with Haldane’s findings regarding hemophilia. Then you might have a better understanding of what goes on in regard to mutations, good, bad, and neutral. http://www.ias.ac.in/jgenet/Vol83No3/231.pdf . (Nachman is the author of the 2000 article)


Then there are the gene switches that determine if any gene is actually expressed or not; and then there are some noncoding DNA sequences that determine the expression levels of various genes; and transcription factor sites operators, enhancers, promoters, and insulators too that play roles in how genes are expressed.
So getting all bent out of shape over hemophilia research that happened roughly 100 years ago and applying it across the board to prove that evolution cannot be right is a touch presumptuous…but totally within the purview of creationist ideology.



Clearly, you do not understand what Nachman actually said when he confirmed that Haldan’s hemophilia derived data is fairly accurate and holds up with some caveats. The point is he did not know anything about what we so eloquently refer to as “junk DNA” and its role in gene expression.
 

Parsimony

Well-Known Member
Your question has been asked and answered many times, in various places.

Haldane allowed for mutations arriving at random times, with their substitutions overlapping-in-time in any arbitrary fashion. Haldane also allowed for sexual reproduction.

Haldane further assumed a selection model unrealistically favorable to evolution -- far more favorable to evolution than what nature provides. (But not as favorable, or as unrealistic as truncation selection.)

His result -- and it is a correct result -- shows that when multiple substitutions occur concurrently, the combined cost of substitution equals the sum of the their cost of substitution taken individually (or sequentially).

Therefore, no matter how the substitutions overlap (or don't overlap), the total cost of substitution (summed from the beginning of the first, to the end of the last), is the same, regardless of how they overlap. In short, there is no cost reduction for concurrent substitutions. So the Haldane limit applies, no matter how the substitutions overlap.

This technical result is well-agreed-to by leading evolutionary geneticists. I am aware of no evolutionary geneticist who disputes Haldane's Dilemma based upon this specific result. They attempt other disputes, but not this one.
What does "cost" mean in this situation? Do neutral mutations have a cost as well? If not, why not? Also, why did you say in an earlier post that a neutral mutation can reach fixation faster than a beneficial one? A neutral mutation does not have selective pressures acting on it to increase its frequency in a population. If a neutral mutation becomes fixed, it's a chance event (genetic drift). A beneficial mutation, on the other hand, does have selective pressures which drive it towards fixation. If anything, any given neutral mutation should reach fixation much more slowly than any given beneficial one (unless the neutral mutation is closely linked to a beneficial one in the genome such that the two are likely to be inherited together).
 

Ouroboros

Coincidentia oppositorum
MUTATION is the ultimate source of genetic variation; it is both the substrate for evolution and the cause of genetic disease. Most previous estimates of the human mutation rate have utilized one of three approaches. Two of these approaches rely on phenotypic differences associated with diseases and the third approach relies on direct comparison of DNA sequences without function. These phenotypic and molecular methods are fundamentally different and rely on different assumptions. The first approach, pioneered by HALDANE (1932, 1935), assumes diseases are in mutation-selection balance. For recessive mutations, the equilibrium frequency of mutant alleles is Formula , where μ is the mutation rate and s is the selective effect of the deleterious mutation (HALDANE 1927). The mutation rate can be estimated if the frequency of mutant alleles and the strength of selection are known. Using this method, HALDANE (1932) calculated that the per locus rate of mutation for hemophilia in humans is ~10−5 per generation. The second approach involves counts of affected individuals born to unaffected parents for dominant disorders (COOPER and KRAWCZAK 1993). This method has been used for many dominant diseases in humans, and rates per locus vary from 10−6–10−4 per generation (summarized in VOGEL and MOTULSKY 1997). Methods that rely on screens of disease phenotypes may provide an underestimate of the actual mutation rate because not all nucleotide changes in a disease gene will result in disease. On the other hand, some disease genes are likely to have been identified and studied in part because they have high mutation rates. The third approach to measuring the human mutation rate takes advantage of the well-known result that for neutral mutations, the mutation rate is equal to the rate of evolution (KIMURA 1968). A direct comparison of stretches of DNA without function can provide an estimate of the mutation rate per generation between species whose divergence time and generation length are known. Comparisons of pseudogenes and of synonymous sites between humans and chimpanzees have suggested mutation rates on the order of 10−8 per site per generation (e.g., KONDRASHOV and CROW 1993; DRAKEet al. 1998). Since many genes may contain ~103 nonsynonymous sites, this estimate is in reasonable agreement with per locus rates of 10−5 (VOGEL and MOTULSKY 1997).
http://www.genetics.org/content/156/1/297.full

Not going to add any comment to is since it's just another "evolutionist's opinions" if I do, except that it concludes that the mutation rate is reasonable for the difference between chimps and humans (and that Haldane only used one approach).
 
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