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The strange case of John Sanford, creationist

sayak83

Veteran Member
Staff member
Premium Member
An old discussion between @leroy and myself lead me to search the forum for older discussions on the number of mutations between humans and chimps and the like, and in a couple year old post Leroy referred to John Sanford.
Sanford is a former legitimate scientist, who had worked as a research horticulturist at Cornell and had a couple of patents. Then he became a creationist. And man, creationists love patents for some reason.
Anyway, he eventually wrote a book (as all such folk usually do) that made a splash a few years ago (I will not name it for I do not want to generate any publicity for it), and someone on a forum I was on at the time quoted from it. I couldn't believe the quote was real, so I Googled it and found a web site had hosted a couple of chapters for an advertisement, I guess, available to read for free on it for a while when it came out. I read those, found the quote, and chuckled (on p. 128-9):

"Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion years."​

Think about that for a moment. Really think about it -

"...1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise..."


Surely I am not the only one who, upon reading that, immediately thought "STRAWMAN!!!"?

I mean, does he REALLY think that Haldane (or anyone else, ever) actually posited that new genes are needed in evolution, and that new genes are made 1 beneficial mutation at a time, right next to each other???


Now, some may think that I am taking him out of context to make another creationist look like an incompetent fool (which, it turns out, is actually pretty easy). I thought about this, and so searched for the quote again, and was able to find the entire book online (a plain text version, to be sure) for free under a different name. So, with context:


Waiting on “Haldane’s dilemma”.
Once that first mutation destined to become fixed within the population has finally occurred, it needs time to undergo selective amplification. A brand new mutation within a population of 10,000 people exists as only one nucleotide out of 20,000 alternatives (there are 20,000 nucleotides at that site, within the whole population). The mutant nucleotide must “grow” gradually within the population, either due to drift or due to natural selection. Soon there might be two copies of the mutant, then four, then 100, and eventually 20,000. How long does this process take? For dominant mutations, assuming very strong unidirectional selection, the mutant might conceivably grow within the population at a rate of 10% per generation. At this very high rate, it would still take roughly 105 generations (2,100 years) to increase from 1 to 20,000 copies (1.1 105 = 20,000).
However, mutation fixation takes much longer than this because selection is generally very weak, and most mutations are recessive and very subtle. When the mutation is recessive, or when selection is not consistently unidirectional or strong, this calculation is much more complex, but it is obvious that the fixation process would be dramatically slower. For example, an entirely recessive beneficial mutation, even if it could increase fitness by as much as 1%, would require at least 100,000 generations to fix (Patterson, 1999).

Haldane (1957), calculated that it would take (on average) 300 generations (>6,000 years) to select a single new mutation to fixation, given what he considered a “reasonable” mixture of recessive and dominant mutations. Selection at this rate is so slow that it is essentially the same as no selection at all. This problem
has classically been called “Haldane’s dilemma”. At this rate of selection, one could only fix 1,000 beneficial nucleotide mutations within the whole genome in the time since we supposedly evolved from chimps (6 million years). This simple fact has been confirmed independently by Crow and Kimura (1970), and ReMine (1993,2005). The nature of selection is such that selecting for one nucleotide reduces our ability to select for other nucleotides (selection interference). Simultaneous selection does not help.

NOTE - Interesting that he provided citations for the rate of fixation according to Haldane, even though this is not controversial, but for his mere assertion re: simultaneous selection, he offers...... Nothing....ReMine did the same thing thoughout his book - all sorts of citations for trivial issues, not a one for his zany creationist claims.


Can Natural Selection Create?

At first glance, the above calculation seems to suggest that one might at least be able to select for the creation of one small gene (of up to 1,000 nucleotides) in the time since we reputedly diverged
from chimpanzee. There are two reasons why this is not true. First, Haldane’s calculations were only for independent, unlinked mutations. Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion
years.
One cannot select mutations that have not happened. Second, the vast bulk of a gene’s nucleotides are near-neutral and cannot be selected at all—not in any length of time. The bottom line of Haldane’s dilemma is selection to fix new beneficial mutations occurs at glacial speeds, and the more nucleotides under selection, the slower the progress. This severely limits progressive selection. Within reasonable evolutionary timeframes, we can only select for an extremely limited number of unlinked nucleotides. In the last 6 million years, selection could maximally fix 1,000 unlinked beneficial mutations, creating less new information than is on this page of text.* There is no way that such a small amount of information could transform an ape into a human....​


As the kids say, WHOOMP there it is! Context seals the deal (see the text in red).

How do we classify that - sleight of hand? Bait and switch? Strawman? Lie? Confusion factor?

To sum up - Haldane's model was about the time needed to fix beneficial mutations (i.e., mutant alleles, or genes that had acquired novel function via mutation) given the understanding at the time (1957). IF all of Haldane's parameters were 100% applicable to all large, slowly reproducing populations, he calculated that it would take 300 generations for that mutant allele to reach fixation (be present in all members) of a population. That is all. It was not REMOTELY about making a brand new gene one mutation at a time, so why did Sanford take the time to set up a scenario indicating how impossible it would be?
This was considered a 'dilemma' at the time due to the current beliefs/understandings - that humans had more than 100,000 genes, that evolution occurred only or primarily via selection, etc.

And a mere 1000 or so such mutations since we split from chimps? PREPOSTEROUS! Humans are so special and so different from the apes that there HAD to have been much much larger changes to explain it all! Or so Sanford's hero ReMine claimed (without evidence), and so Sanford perpetuates.

Couple of problems....

1. Not all population geneticists accepted Haldane's model as accurate or universally applicable. Warren Ewens, for example, said in an interview (italics mine):

"...There was an interest in two load concepts. The first was the mutational load, and interest in that concept came from the concern about genetic damage caused by atomic bombs. This was discussed in detail by the great geneticist Muller in 1950. Jim Neal and Jack Schull had gone to Japan shortly after the 1939-45 war to conduct an examination of the mutational effects of the atomic bomb. Their work on this matter was very well known, and so the question of how much genetic damage had been produced by the bomb was uppermost in many people’s minds. That damage became analyzed mathematically as a mutational load.

A second form of the load concept was introduced by the British biologist-mathematician Haldane who claimed, in 1957, that substitutions in a Darwinian evolutionary process could not proceed at more than a certain comparatively slow rate, because if they were to proceed at a faster rate, there would be an excessive “substitutional load.” Since Haldane was so famous, that concept attracted a lot of attention. In particular, Crow and Kimura made various substitutional load calculations around 1960, that is at about that time that I was becoming interested in genetics.
Perhaps the only disagreement I ever had with Crow concerned the substitutional load, because I never thought that the calculations concerning this load, which he and others carried out, were appropriate. From the very start, my own calculations suggested to me that Haldane’s arguments were misguided and indeed erroneous, and that there is no practical upper limit to the rate at which substitutions can occur under Darwinian natural selection."​

Interestingly, ReMine had interviewed Ewens for his 1993 book, but did not seem to care much about his disagreement with Haldane and Crow, for what are obvious reasons.

2. Experiments demonstrated that Haldane's model had flaws, 1 example:

Proc. Nat. Acad. Sci. USA Vol. 71, No. 10, pp. 3863-3865, October 1974
Solutions to the Cost-of-Selection Dilemma
(substitutional load/gene substitution/evolutionary rate)​

3. The notion that some large number of genetic changes is required to produced notable phenotypic change is false:

Am J Hum Genet. 1998 Sep;63(3):711-6.
Mutations in Fibroblast Growth-Factor Receptor 3 in Sporadic Cases of Achondroplasia Occur Exclusively on the Paternally Derived Chromosome

Abstract
More than 97% of achondroplasia cases are caused by one of two mutations (G1138A and G1138C) in the fibroblast growth factor receptor 3 (FGFR3) gene, which results in a specific amino acid substitution, G380R. ..​

I present that only to show that a single mutation can affect all limbs as well as the skull and other structures. No huge suite of mutations required.

I am shocked that Sanford would not have had the sense to do a lit review prior to writing his creationist pap.
What is so strange about the fact that a creationist is being intellectually dishonest?
 

tas8831

Well-Known Member
Well, ah . . . they know how to calculate probabilities very well. The problem is the assumptions that they based calculations on their desire to justify their religious creationist beliefs, and not science..
I've seen creationist employ numbers they pulled out of thin air in 'probability calculations', and when challenged on the numbers they used, they dismissed the criticisms, claiming that we were so desperate that we were attacking "established mathematics"...
 

tas8831

Well-Known Member
What is so strange about the fact that a creationist is being intellectually dishonest?
Good question - I'm sure most of us that have been involved in this 'debate' for more than a few months will have discovered a very obvious and far-too-common tendency for professional creationists to act this way. In this case, it is primarily due to the fact that this guy was used as a resource by a certain creationist....
 

tas8831

Well-Known Member
Really? More excuses to avoid an answer?
Found this from the old thread, dated Jan.29, 2019:

Why " evolution vs creationism"

You ran off and never answered. When I mentioned it in another thread, you just engaged in burden shifting like are doing in this thread. Was that an admission? I'd say yes. Here it is again, your words in red:



You don’t seem to understand the point made by the article that I quoted, the point was that even in a far too convenient and unrealistic scenario, you can add a maximum of 500,000 beneficial mutations.

I totally understand it. It is just that tossing out big numbers like that, and extrapolating specific conclusions, is unwarranted.
The claim is that 500,000 mutations are not even near the amount of mutations required to produce a modern human and a modern chimp from a common ancestor who lived 10M years ago.

Yes, an unsubstantiated, ignorance-based claim.

You can falsify the argument by:

Showing that 500,000 mutations are enough to explain the differences between chimps and humans


OK - humans and chimps exist. Evidence indicates we shared a common ancestry. Proved.
You and your sources appear to put mathematical models above actual evidence when it suits them (funny how the same folks are typically dismissive of climate change mathematical models).
What I NEVER see in such essays are an accounting of WHY they claim x-number of mutations is too few - i.e., I NEVER see any explanation as to how they know it is too few. I NEVER see an accounting of how many mutations they know it would take to get B-trait from A-trait in an ancestor.
This is the fail of ALL of these proclamations, from ReMine to Sanford to creation dot com. They merely seek to argue via big numbers with no actual rationale.
Showing that there is a realistic scenario that would produce much more beneficial mutations.
You need to explain how you determined that 500,000 mutations IS too few. All I see are assertions.
And even more important, rather than cherry picking minor details in the analysis, can you make a positive case explaining how chimps and humans evolved from a common ancestor by a process of random mutations + NS? (consider the low rate of beneficial mutations, and the low rate of reproduction in primates)
The case has already been made.
If creationists want to counter it using models and assertions, they will only impress and convince those that do not understand the biology.
Here is why I am very confident that such a large number of beneficial mutations is NOT needed to produce the relatively minor phenotypic changes we see between extant chimps and humans as derived from a common ancestor:
1. These arguments seem to imply that any particular trait is brand new and thus must be accounted for by some large number of mutations. This exposes the multi-level ignorance of those making them.
Look at the generic mammal body type - what specific trait does a human have that, say, a lemur or a dog does not? All human traits are essentially variations on a theme, not brand new. Developmental tweaks are all that is actually needed, not some suite of new beneficial mutations to get, say, the human shoulder joint from an ancestral primate shoulder joint.
There is the case of familial achondroplasia (dwarfism) - a single point mutation causes alterations in limb proportion (to include all muscle/nerve/soft tissue/etc. changes), joints, facial features, etc. All from a single point mutation. I am not saying that this is beneficial or adaptive, I am merely explaining that some huge number of mutations is NOT needed to produce relatively large-scale phenotypic changes. THIS is what your Haldane's dilemma-spewing creationist sources can't or won't understand or mention - usually because THEY don't know this, or because they don't want their target audience to know about it.
2. These arguments imply that some huge number of beneficial mutations MUST HAVE BEEN required for this transition to take place. Given that we know that single point mutations can affect multiple body systems and overall morphology, other than a desire for it to be so, what do these Haldane's dilemma types present that actually supports their position?
I've read ReMine's book - he offers nothing in that regard. I've read more recent treatments of it - more of the same.
I mentioned that a creationist once claimed that just to get the changes in the pelvis for bipedal locomotion a million mutations would have been required. Do you think he provided a million 'changes' that had to have been made? Nope. He could not provide A SINGLE example, but as is is the way of the creationist, he merely insisted that he was correct.

My argument against such claims are 1. that there is no argument (see the Ewen's quote); 2. that the arguments are based on ignorance of developmental biology; 3. that they are premised on the argument from awe (big numbers).​


It was nice that back then you were directly paraphrasing ReMine with his bogus, totally made up 500,000 thing - you've now moved to 30 million using grade school maths, but hey, you go with what you know, I guess.
 

shunyadragon

shunyadragon
Premium Member
Well then show that random mutations (rather than othe rmechanisms) where mainly responsible for larger brains, upright posture, cooperative behavior etc.

Random mutations are not responsible for anything except the diversity of the genes in a population. There are many long science threads citing scientific research that address the details backing up evolution as a process if you wish to read them. At present you have not grasped the basics.
 
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tas8831

Well-Known Member
Your math seems wrong (or perhaps I am the one who cant understand what you are trying to represent)
Yes, pretty sure it is you, unless I plugged in the wrong number..
upload_2020-5-27_11-48-33.png

The mutation rate is in mutations per site per year. Multiply the rate times the number of sites times the years. The number of sites and the number of years came from YOU, so if the numbers are out of whack (as I already indicated they could well be), it is likely due to my use of YOUR numbers.

But assuming a mutation rate of 2.2x10^-9/site/year you need 23M years to accumulate 30,000,000 mutations (or 1% of the human/ape genome)
Please show your work as I did. Because that seems utterly nonsensical.
but irrelevant lets simply agree on that the "human line" evolved faster that average ¿ok? (answer yes or no)
Not a yes or no question - what do you mean "evolved" - what is your measure?
The relevant point is that you don’t seem to understand my point,
Entirely possible, as you never really seem to make one.
The point is that you have to show that the mechanism of random mutation natural selection and genetic drift (Darwinism)
Darwinism contained drift? huh...

Wow, OK...

The mechanism of random mutation is primarily replication error during DNA replication/synthesis:

Mutations arise spontaneously at low frequency owing to the chemical instability of purine and pyrimidine bases and to errors during DNA replication. Natural exposure of an organism to certain environmental factors, such as ultraviolet light and chemical carcinogens (e.g., aflatoxin B1), also can cause mutations.

A common cause of spontaneous point mutations is the deamination of cytosine to uracil in the DNA double helix. Subsequent replication leads to a mutant daughter cell in which a T·A base pair replaces the wild-type C·G base pair. Another cause of spontaneous mutations is copying errors during DNA replication. Although replication generally is carried out with high fidelity, errors occasionally occur. Figure 8-5 illustrates how one type of copying error can produce a mutation. In the example shown, the mutant DNA contains nine additional base pairs.​


There are other factors as well, but the bulk of mutations are produced by errors. They are random with respect to fitness. That is, any given mutation can be neutral, beneficial, or deleterious. Most mutations are neutral. Of the rest, most are bad. But more are beneficial than previously believed.


The statement that mutations are random is both profoundly true and profoundly untrue at the same time. The true aspect of this statement stems from the fact that, to the best of our knowledge, the consequences of a mutation have no influence whatsoever on the probability that this mutation will or will not occur. In other words, mutations occur randomly with respect to whether their effects are useful. Thus, beneficial DNA changes do not happen more often simply because an organism could benefit from them. Moreover, even if an organism has acquired a beneficial mutation during its lifetime, the corresponding information will not flow back into the DNA in the organism's germline. This is a fundamental insight that Jean-Baptiste Lamarck got wrong and Charles Darwin got right.

However, the idea that mutations are random can be regarded as untrue if one considers the fact that not all types of mutations occur with equal probability. Rather, some occur more frequently than others because they are favored by low-level biochemical reactions. These reactions are also the main reason why mutations are an inescapable property of any system that is capable of reproduction in the real world. Mutation rates are usually very low, and biological systems go to extraordinary lengths to keep them as low as possible, mostly because many mutational effects are harmful. Nonetheless, mutation rates never reach zero, even despite both low-level protective mechanisms, like DNA repair or proofreading during DNA replication, and high-level mechanisms, like melanin deposition in skin cells to reduce radiation damage. Beyond a certain point, avoiding mutation simply becomes too costly to cells. Thus, mutation will always be present as a powerful force in evolution.​

I should have thought that someone so well-versed in evolution and genetics - such as yourself - might have taken the time to learn some of this stuff. Regarding selection and drift:

Genetic drift

Natural Selection


So yet again I address your demands, you still run off when challenged.
are mainly responsible for this “evolution” my point is and has always been that given that the speed of evolution is much faster than the speed that would be possible by the mechanism of random mutation natural selection and genetic drift, there must be other nonrandom mechanisms that made mayor contributions to the process of evolution (being Darwinism just a minor contributor)
Is that your point? Odd then that you seem incapable of presenting any actual rationale, much less supporting evidence, for your "point." That is standard - Sanford and ReMine didn't either. They think assertions and made-up stories work. They don't.

So now it s your turn - present your model that accounts for this mysterious, unnamed, 'additional factor', supported by evidence, of course.
But feel free to prove me wrong, my statement is testable, all you have to do is show that “Darwinism” can account for such a fast speed of evolution in mammals.
I just did - using YOUR numbers.

But please do explain what is so 'fast' - what is the evidence, other than your zany heroes pulling numbers out of thin air and arguing via personal disbelief.

You say it is 'too fast', but you can never explain why that is (eagerly awaiting some inaccurate paraphrasing or creationist/fringe sources). The ONLY way it seems "too fast" is if you are still clinging to the mere assertion-based claim that 500,000 or now 30 million 'beneficial mutations' are too few, which not even the professional creationists can seem to explain or support. It is mere assertion.

Yes, that is part of my point “transposons” while the can contribute to the diversity of the genome and can create very fast changes in the phenotype in a very small little amount of time, this mechanism is not random

Your point? You've never mentioned transposons to me before. But I did find this from you from November:

Non random mechanisms like NGE, epigenetics, transposons etc. can create brand new functional and selectively positive proteins in 1 generation, this makes some scientists wonder that perhaps some of these non-random mechanism play a more important role than the process of random mutations and natural selection. Other scientists would argue that random mutations and natural selection play the most important role and that these other mechanisms provide a minor contribution.​

Isn't it precious that you have glommed onto "non-random". Yes, this causes some fringey-types that are out for name recognition to make all kinds of wild extrapolations.
But do tell me about how this "non-randomness" works in this context - tell us all how transposons are non-random, for example.

My point is and has always been that organism changing and adapt mainly by nonrandom mechanism (being random mutations just a minor contributor)

Really? Odd - all I can ever remember from you are paraphrasings of creationists like ReMine. That is where your earlier 500,000 mutation nonsense came from. And if that was really your point all along, one has to wonder why you expended so much energy NOT clearly indicating this, and instead spent most of your time demanding we address ReMine/Sanford's fantasies and disinformation.
Trasposons is just 1 of many other non random mechanism that could have played a mayor role.
Major role, according to you.

Interesting thing - part of my graduate research was on the evolution of a gene family in mammals. There are multiple genes in the family, all mutated copies of each other. One of the major duplication events was facilitated by the insertion of a LINE between 2 of the genes.
The most common LINE in mammals is L1, and it is able to recognize the hexanucleotide "TTAAAA"
and use that to insert itself into a genome. In that sense, it is non-random, since it uses a specific DNA sequence.

Would you like to guess how frequently that sequence shows up in genomes? Just for kicks, I searched GENBANK for the sequence for human chromosome 3. It is about 200 million BP, and my browser kept crashing, so I only downloaded 20 MB of it ( quick back of the envelope calculation indicates that 20 MB = only about 10 million 'letters' representing nucleotides, or about 1/20 of the chromosome in question). Once it loaded, I did a simple search for TTAAAA...........................
How many times do you think TTAAAA showed up?

22,679 times.

That is, there are potentially 22,679 insertion sites for the L1 LINE in about 1/20 of just 1 chromosome.
But sure, transposon insertion is totally 'non-random'....wrt fitness....

It is not that I do not think they play a role in evolution or fitness or selection - they clearly do (I have referred to one such insertion that conferred DDT resistance to fruit flies), but this genotype STILL has to spread throughout a population for it to become fixed, just like plain old SNPs. So your "speed" issue... isn't.

Given that you seem to believe that organisms evolve mainly by random mutations and natural selection (Darwinism) you have to show that this mechanism is enough to account for the speed of evolution in mammals describe in your paper. (or correct me if I am misrepresenting your view)
I have done this repeatedly, even using YOUR numbers.

That you keep re-asking me to do this for you - even as you seem 100% incapable of providing your rationale for asking over and over, and seem 100% incapable of providing any kind of counter model or rationale for whatever it is your actually think about it - and that tells everyone that you are amazingly disingenuous/dishonest about this whole subject. You seem unable or unwilling to explain or answer simple questions related to your anti-'Darwinism' claims, such as how many mutations would have been required if evolution were true according to your claims - again, dishonest.
 
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tas8831

Well-Known Member
No, I cant,
And yet you demand that I do ... Huh...
But the evidence seems to be consistent with the idea that evolution was caused mainly by non random variation, if you would affirm the opposite (random mutations are the mayor contributor) we can have a discussion where you present your arguments and I present mine.

Since my position is the standard one, how about your provide your evidence that most change occurs via "non random" mutations.

But first., define what you mean by "nonrandom"mutations, and specifically how these can somehow spread faster that random ones, as you have implied.

By this is what I mean by random (just anticipating possible semantic games from your part)
"whether a particular mutation happens or not is generally unrelated to how useful that mutation would be."

When have I ever indicated differently?
I sense a strawman in the making....
 

tas8831

Well-Known Member
Well then show that random mutations (rather than othe rmechanisms) where mainly responsible for larger brains, upright posture, cooperative behavior etc.
It is really something to watch you alter your supposed arguments within single threads even as you pretend your new twists were your original claims.

So why not show us all up, and provide your evidence that transposons allowed for obligate bipedalism, etc.? Wouldn't that be more effective than playing games?
 

tas8831

Well-Known Member
By old discussion, it appears you mean where @leroy claims science is wrong and ID is right, but refuses to support that while doing everything to shift the burden of proof. That is what I see growing here.
Indeed. I also like how he moves his goal posts/alters his 'argument' all sneaky-like, hoping nobody will notice. This all started out with his claim about 500,000 'beneficial mutations' not being enough, then it became 30 million, then it became 30 million is too many... Now it is nonrandom mutations are what he was referring to all along...
And they wonder why people think of them the way we do...
 

leroy

Well-Known Member
So now it s your turn - present your model that accounts for this mysterious, unnamed, 'additional factor', supported by evidence, of course

t.
No is my turn? You haven provided your proof nor your evidence yet.

Prove that the mechanism of random mutations and natural selection (and perhaps genetic drift) can account for the genetic differences between chimps and humans, or more specifically between humans and the common ancestor. (given you only have 5M years)

You are just making random and unrelated question, and dancing around irrelevant stuff which seems to be your tactic, your strategy seems to be “hey I will make this discussion long, tired and boring so that my opponent get tired, abandons the discussion and claim victory.
 

shunyadragon

shunyadragon
Premium Member
No is my turn? You haven provided your proof nor your evidence yet.

First, you nave not understood nothing is proven in science.

Your not even qualified to understand the evidence presented, nor have you explained how you concluded concerning that the evidence is not demonstrated.

Prove that the mechanism of random mutations and natural selection (and perhaps genetic drift) can account for the genetic differences between chimps and humans, or more specifically between humans and the common ancestor. (given you only have 5M years)

You are just making random and unrelated question, and dancing around irrelevant stuff which seems to be your tactic, your strategy seems to be “hey I will make this discussion long, tired and boring so that my opponent get tired, abandons the discussion and claim victory.

This has been done in terms of the falsification of the hypothesis of evolution by the evidence, and you have failed to demonstrate why it is not.falsified. There have been many research articles cited concerning human evolution and you have not responded to the evidence.

Since you lack a knowledge of genetics, paleontology, and the biology evolution and your ENRON bookkeeping probability is as phony as a three dollar bill. What are you basing you estimate of insufficient time for the evolution of primates that evolved to chimpanzees and humans?

Still waiting . . .
 
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Bear Wild

Well-Known Member
Random mutations are not responsible for anything except the diversity of the genes in a population. There are many long science threads citing scientific research that address the details backing up evolution as a process if you wish to read them. At present you have not grasped the basics.
Thank you. It is finally time to realize that random mutations play one of many roles in evolution. There are many aspects of genetics that are not just random and even epigenetics that can pass on traits without changes in the DNA. This old tiring argument of just random mutation should be put in its place as only one of the amazing ways that diversity occurs and allows evolutionary changes to continue.
 

Bear Wild

Well-Known Member
No is my turn? You haven provided your proof nor your evidence yet.

Prove that the mechanism of random mutations and natural selection (and perhaps genetic drift) can account for the genetic differences between chimps and humans, or more specifically between humans and the common ancestor. (given you only have 5M years)

You are just making random and unrelated question, and dancing around irrelevant stuff which seems to be your tactic, your strategy seems to be “hey I will make this discussion long, tired and boring so that my opponent get tired, abandons the discussion and claim victory.

"Oh your god" Leroy! There has been so much evidence documented in this forum with no reliable evidence to contradict. The evidence is contained in more than enough journal to keep you reading for a life time. You just need open your mind. Despite ridiculous claims that are unsupported by ID and creationists, evolution theory just grows stronger. Time to get on board with the truth.
 

blü 2

Veteran Member
Premium Member
Ok if creationist can only do strawmans and false assumptions.... Why don you provide your own correct model with correct assumptions, and show that humans and chimps could have evolved from a common ancestor 5Mya through the mechanism of random mutations and natural selection.

Or you can simply admit that such model doesn't exist
What would be the point?

You appear to have no intention of being persuaded by any evidence at all that the theory of evolution is correct.

And it would follow that your approach to any answer would be to consider how best to attack it; and if nothing handy occurred to you, to remain silent.

Please correct me if that's wrong.
 

leroy

Well-Known Member
[
First, you nave not understood nothing is proven in science.

Your not even qualified to understand the evidence presented, nor have you explained how you concluded concerning that the evidence is not demonstrated.

More semantic games? Honestly aren’t you tired of repeating the same dishonest tactic?

Ok let me reformulate my question

Can you provide evidence that shows that the model that states that organisms evolve mainly by the mechanism of random mutation and natural selection is “almost certainly true”?


This has been done in terms of the falsification of the hypothesis of evolution by the evidence, and you have failed to demonstrate why it is not.falsified. There have been many research articles cited concerning human evolution and you have not responded to the evidence.

You are a liar such thing has never been done in this forum. Provide a single article that concludes beyond reasonable doubt, that organism evolve mainly by the mechanism of random mutations and natural selection .


l. What are you basing you estimate of insufficient time for the evolution of primates that evolved to chimpanzees and humans?

. .

We know roughly* the mutation rate in humans and primates

We know roughly* the ration of beneficial / selectable mutations vs non beneficial mutations

We know roughly* the probability of fixation of beneficial and neutral mutations

From this 3 numbers we get an approximation of how fast can primates evolve through the process of random mutations and natural selection

And we know roughly* how different are humans from chimps, and from that we can infer the differences between humans and the common ancestor.

From this values one can evaluate if 5M years is enough time

Given the values that I estimated the answer is “NO” 5M years is not enough time. (Feel free to correct me and make your own math with the correct values)

Given that the human line evolved much faster than the maximum speed allowed by random mutations and natural selection , it is fare to hypothesis that maybe* there was another main mechanism that caused this “super fast evolution” (being random mutatons and NS just a minor part of the process.
 

leroy

Well-Known Member
"Oh your god" Leroy! There has been so much evidence documented in this forum with no reliable evidence to contradict. The evidence is contained in more than enough journal to keep you reading for a life time. You just need open your mind. Despite ridiculous claims that are unsupported by ID and creationists, evolution theory just grows stronger. Time to get on board with the truth.
That simply is not true, while it is uncontrovertialy true that we evolved from other primates, scientists are still discussing on which mechanism (s) where responsible for such an event and they are still discussing on which mechanism played a minor role and which played a mayor roll.

Except from fanatic evolutions, nobody in the academia would claim that this issue has been solved; it is still an open question.
 

leroy

Well-Known Member
What would be the point?

You appear to have no intention of being persuaded by any evidence at all that the theory of evolution is correct.

And it would follow that your approach to any answer would be to consider how best to attack it; and if nothing handy occurred to you, to remain silent.

Please correct me if that's wrong.
In fact a single paper that concludes that evolutionary theory* is likely to be true would convince me. I would simply trust the scientists and the peer review process even if I myself can’t understand the math or the methodology of the paper.

· *With evolutionary theory it is meant that “organisms evolve mainly by a mechanism of random variation and NS.”
 

leroy

Well-Known Member
In fact a single paper that concludes that evolutionary theory* is likely to be true would convince me. I would simply trust the scientists and the peer review process even if I myself can’t understand the math or the methodology of the paper.

· *With evolutionary theory it is meant that “organisms evolve mainly by a mechanism of random variation and NS.”
The problem is that such a paper doesn’t seem to exists and the proof is that there are over 100 posts in this forum where I ask for such a paper, and evolutionist simply ignore my recuest or answer something to else
 

leroy

Well-Known Member
Thank you. It is finally time to realize that random mutations play one of many roles in evolution. There are many aspects of genetics that are not just random and even epigenetics that can pass on traits without changes in the DNA. This old tiring argument of just random mutation should be put in its place as only one of the amazing ways that diversity occurs and allows evolutionary changes to continue.
Agree, glad to see that you are un my site
 
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