The Fossil Record Proves Speciation, Not Evolution of Lifeforms Observed

[stevevw]

5 different nucleotides doesn't mean 5 different mutations. A single mutation can be as few as a single nucleotide or as large as an entire chromosome. Furthermore, you are focusing on unnamed specific functions again. Which doesn't even make sense, considering the fact that mutations are not truly random because certain mutations are far more likely to occur than others. Hence why a child being born with hemophilia without inheriting it from either parent is far more common than a child being born with an eye color they couldn't have gotten from either parent.

That’s true but is only highlighting the harmful effects. Common mutational changes are usually deleterious or neutral. The paper as with most papers on this topic do not state exactly what function needs to be changed. They are talking about any functional change that will be functional that requires more than one mutation.

-_- not sure why you are acting as if the only way to get a string of 5 nucleotides in a location they weren't before is if all 5 nucleotides are inserted.

Original sequence: ATGAATTAG
Insertion of 1 base: ATGAAATTAG- frameshift, entire protein product will change, earliest stop codon no longer applies. Sequence is entirely different, not just 5 nucleotides in practice.
Substitution of 1 base: ATGTATTAG - substitution, amino acid at this location in the protein liable to change, length of protein product unchanged, the codon is different, making all 3 nucleotides in the codon count differently. May influence the function of the protein product/s.

But, at a minimum, it would take only 2 substitution mutations to result in a sequence of 6 nucleotides that have a different effect. And considering that it is fairly common for entire genes to be duplicated and then subsequently get mutated (the most common mechanism by which new genes develop), it seems kinda manipulative to base the emergence of a "functional" sequence of 5 nucleotides as if it can only come about via 5 separate insertions.


-_- every human on this planet is born with 40-60 mutations unique unto themselves, so how do you figure? Do you seriously think they are all single base pair substitutions in irrelevant sequences all the time?

Their research is talking about the need for replacing two or more specific nucleotides changes for a new specific function that will require two or more linked mutations. It is also not just about the right mutations in the right place but about their amplification and fixation which can also take a long time.

Frameshift mutations result in abnormal protein products with an incorrect amino acid sequence that can be either longer or shorter than the normal protein. They are not talking about any single or double mutation substitution but a new functional change that requires multiple dependent mutational change. This does not have to be in one generation.

If a single substitution happens to have little effect, then it is of no benefit for a specific function change. Therefore, additional linked mutations need to happen and not another unrelated single mutation. Most single unrelated frameshift and substitution mutations are harmful, effect function of proteins or have no or little effect.

The authors gave a 10% reproductive fitness benefit to amplify the selective benefit when single substitution was added to the target string. So, in reality their results are underestimated. The tests also disregarded other factors that could interfere with the success of establishing these mutational changes such as selection interference from other mutational changes in other parts of the genome which would add more time.

Each value is the mean of 25 replicates. The population (10,000) and beneficial fitness effect (10 %) were held constant. The mutation rate was adjusted based on number of nucleotides in the string. For single point mutations (string length of one), numerous instances accumulated simultaneously in the population – such that many were superfluous to waiting time, resulting in extra instances arising prior to fixation.

Table 2 also shows the waiting times for creating and fixing genuine strings of 2–8 nucleotides. This data is also plotted in Fig. 2. Each additional nucleotide that was added to the target string substantially increased waiting time. Figure 2 shows that as string length increased linearly, the increase in waiting time was of an exponential nature. When there were as many as six nucleotides in the string, the average waiting time (4.24 billion years) approached the estimated age of the earth. When there were eight nucleotides in the string, the average waiting time (18.5 billion years), exceeded the estimated age of the universe.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/#CR15

Last I checked, humans are still apes. Time isn't an issue because your claim that it takes so long for a sequence to come into existence is immensely flawed. It doesn't take into account how common gene duplications are or how most genes in our genome are derived from such duplications accumulating mutations until their function is entirely different. Which can be as few as 1 single base pair substitution mutation, fyi.

It is not my claim but the scientific results of the work of scientists. I am not saying that specific functional gene change cannot happen. I am just saying that this may not happen by a Neo-Darwinian process of random mutations and natural selection, but rather other processes mentioned in the EES which seem to make more sense.

 

[stevevw]

Lol, genetic drift is just a matter of trends in how genes pass on to future generations in a population. Sure, by pure chance, a beneficial mutation can end up dying off without ever being passed down, but since over 1% of mutations are measurably beneficial, it is easy to see that eventually, some will persist.

Those rare beneficial mutations have to be the right ones in the right place that will be related to the specific change needed. So, it’s not just any beneficial mutation anywhere in the genome. That also reduces the chances.

For example, let's say 100,000 people have been born thus far today, and assume that each of them were only born with 10 mutations (despite the human average being much higher than that). That makes for a million new mutations introduced into the human population today, and even if only 1% of them were beneficial, that would mean the human population has gained 10,000 benign mutations TODAY. Not only that, but by definition, these mutations make individuals that have them more likely to survive and reproduce than those who don't, so to behave as if genetic drift is just going to eliminate all of them is ridiculous.

I never said that. I said it can be a contributing to some loss of beneficial mutations. But also, drift can encourage the fixation of dexterous mutations as well.

-_- what the heck? No, 100% no, just looking at the methodology of Behe's "experiment", he should have concluded, just as everyone else has, that within a few hundred years, starting off with a population of 10,000 humans, all decedents down the line would share many of those original 10,000 ancestors if not all of them. Think about it, you have 2 parents, 4 grandparents, 8 great grandparents, and so on. It takes about 14 generations for that number to so solidly exceed 10,000 that it would be strange for a person not to have all the lineages that survived in their family tree somewhere. If we consider a human generation to be 25 years, it would only take 350 years for the population to reach that point if it started with 10,000 individuals, assuming that all of those individuals reproduced and had lineages that persisted all 14 generations. It'd take 30 generations if you started with 1 billion people, or 750 years. Thus why even large populations can have beneficial genes become fixed in the population in a relatively short period of time. And this is counting how long it takes for a modern human generation, can you even imagine how short that time frame is for organisms that have a new generation every year?


This statement in his paper is factually incorrect: "single DNA sub-string of minimal length (2–8 nucleotides). This sort of minimal genomic modification would alter only one (or a few) specific amino acids, or might conceivably result in one new specific protein fold."

Any insertion/deletion that isn't a number divisible by 3 has the inevitable effect of changing the reading frame of a gene, making it produce entirely different proteins despite the change to the genome being minimal.

They are not talking about any single mutation being fixed anywhere in the genome but a specific connected mutation being fixed in the same short DNA section. This means that further mutations not only have to be rare benefits but adds to the existing one and fits specifically for the future establishment of that specific function that requires several mutational and string changes. It would be like a jig saw puzzle where the entire genome may have thousands of different puzzles with a number of different pieces for each. The right piece and not just any piece (mutation) has to occur in the right place (right puzzle) within the right time frame. Then increase the odds/time with each extra piece (interconnected mutation).

Furthermore, Behe is very obviously doing his calculation based on the probability of a specific spot in the DNA receiving a mutation, and he is doing it poorly. He acts as if the population he has set up is some sort of evolutionary ideal, but it is not. Fluctuating between large population sizes and small population sizes is far better for improving the probability of both a given mutation occurring and becoming fixed within a population within a relatively short amount of time, not a population staying small.

The paper I was quoting from is talking about a hominin population which will not fluctuate between large and small population because it is relatively small especially when considering the time from apes to humans when it would have started out very small and still be small when humans were established. The paper showing that mutations need to be in a specific spot for a new function that requires a string of 5 nucleotides is not Behe’s work but Behe’s has similar findings and do several non-religious papers.

Lol, the Lynch paper Behe quotes directly contests his own conclusions. That is, Lynch even calls the dude out by name, hahahahahahahahahaha.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253472/

That is not Behe quoting the paper but the one from here.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/#CR15

As mentioned in previous post they state that even Behe’s critics that disagreed with some aspects of his work also agreed with the findings for when two or more linked mutations are needed to produce a specific functional change it will take too long a time for evolution. In fact, Lynch’s findings are even longer that the paper I linked which you want to discredit.

These authors then suggest they have largely resolved that problem. However, that paper again suggests that for a hominin-type population, waiting times are much longer than we report in this paper. Figure 1 in that paper suggests that to establish two specific co-dependent mutations in a population of 10,000 (given that the first mutation to arise is neutral) requires roughly 10–100 million generations. In a hominin population this would be roughly 0.2 to 2 billion years – just to fix two specific mutations. Figure 1 in that paper also suggests that for the same population of 10,000, when the intermediate mutation has a deleterious effect of 1 %, the waiting time is nearly 100 billion generations (2 trillion years).

"To support their contention of the implausibility of adaptive protein evolution by Darwinian processes, Behe and Snoke started with an ad hoc non-Darwinian model with a highly restrictive and biologically unrealistic set of assumptions. Such extreme starting conditions guaranteed that the probability of neofunctionalization would be reduced to a minimal level. An alternative approach, adopted here, is to rely on a set of biologically justified premises and an explicit population-genetic framework. When this is done, contrary to the assertions of Behe and Snoke that neofunctionalization events involving multiple amino acid residues require 10^8 or more generations and population sizes in excess of 10^9 individuals, it is readily demonstrated that this process can go to completion with high probability on time scales of 10^6 yr or less in populations >10^6 in size. As is discussed below, this is a highly conservative conclusion with respect to both the time and population-size requirements. To put this into perspective, a span of 10^6 yr is small on the total evolutionary time scale (in years) of ~3.8 × 10^9 for all of life, ~2 × 10^9 for eukaryotes, ~7 × 10^8 for metazoans, ~4 × 10^8 for tetrapods and land plants, and ~2 × 10^8 for mammals (e.g., Knoll 2003). In addition, a population size of 10^6 is minuscule for most microbes (the species whose genome structure is most compatible with the Behe-Snoke model) (Finlay 2002)"

In turn Lynch’s paper has been shown to miscalculate things as well. The claim that Lynch’s has resolved the waiting time problem has been challenged.

The most recent attempt to resolve the waiting time problem is the paper by Lynch and Abegg [25]. The findings of that paper have been challenged by Axe [21].

Lynch and Abegg [25] also analyzed the waiting time required for strings longer than 2 nucleotides. They argue that beyond two mutations, longer string length has only a marginal effect on waiting time, especially in small populations. This conclusion is very counterintuitive and is strongly contradicted by our own findings (see our Fig. 2). Similarly, the findings of Durrett and Schmidt [16], and Axe [21], seem to directly contradict that claim. Even if the claim by Lynch and Abegg regarding string length were valid, all of their waiting times for strings longer than two were extremely prohibitive for a population of 10,000 (see Fig. 4 of that paper – also note, that plot employed a heightened fitness benefit of 2 %).

In light of all this, it is clear that there are multiple lines of evidence that support our findings.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/#CR15

By the way, none of the figures in the Lynch paper referenced in Behe's paper are actually in Behe's paper. Behe has some giant testicles for quoting Lynch's paper as if the math in it is anything like his own.

I never said they were and have been quoting another paper that refers to Behe and states that his critics including Lynch and the others I linked agree with the waiting time problem despite criticizing Behe’s methods.

 

[stevevw]

-_- John Sanford, the "big name" in that article (also from Theoretical Biology and Medical Modelling journal) is also a YEC. Wesley Brewer seems to be a physicist at best, but "Fluid Physics International" seems to purely exist on Linked In or something, I can't find info on it.
Franzine Smith is a member of the FMS Foundation, which stands for "false memory syndrome", so she's in psychology. John Baumgardner is a geophysicist and YEC. So what we got here is a group of creationists essentially doing the exact same math as Behe without any adjustments or criticism, and 3/4 of them don't even have careers relevant to genetics, and the one who does, John Sanford, specializes in plant genetics.

You aren't impressing me in the slightest.

This is still a logical fallacy that all scientists associated with religious connections work are automatically wrong. It is also a logical fallacy to say that the journal and any work it produces and the scientists who perform the peer review process which follows the valid processes for peer review to validate the work published is all wrong. That would mean every scientist associated with the journal, all the work produced by the journal and all the scientists who check the work are all wrong. That is a massive fallacy.

What you failed to mention perhaps because your aim is to discredit everyone associated with these results is that John Sanford is a geneticist and also famous for inventing the Gene Gun so he should know what he is talking about as the paper is directly associated with genetics. What you also failed to do was continue to check out the other papers that supported the results that I mentioned that come from non-religious mainstream scientists and journals such as GENETICS, Protein Science and Molecular Biology and Evolution Journals. ie just hit the links it references.[15–17, 25]

Virtually all of the papers subsequent to the work of Behe and Snoke have confirmed that waiting times can be prohibitive – depending upon the exact circumstances. Some of the subsequent papers have been critical [15–17, 25]. Yet even those papers show that establishing just two specific co-dependent mutations within a hominin population of 10,000 can require waiting times that exceed 100 million years (see discussion). So there is little debate that waiting time can be a serious problem, and can be a limiting factor in macroevolution.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/#CR15

AS stated they may criticize the methods of Behe but they agree with his and Sanfords findings. In fact, Sanford allows a 10% fitness advantage which underestimates the time factor and Lynch, Abegg, Durrett and Schmidt's findings have even longer times.

The waiting time problem in a model hominin population

The most recent attempt to resolve the waiting time problem is the paper by Lynch and Abegg [25]. These authors then suggest they have largely resolved that problem. However, that paper again suggests that for a hominin-type population, waiting times are much longer than we report in this paper. Figure 1 in that paper suggests that to establish two specific co-dependent mutations in a population of 10,000 (given that the first mutation to arise is neutral) requires roughly 10–100 million generations. In a hominin population this would be roughly 0.2 to 2 billion years – just to fix two specific mutations. Figure 1 in that paper also suggests that for the same population of 10,000, when the intermediate mutation has a deleterious effect of 1 %, the waiting time is nearly 100 billion generations (2 trillion years).

The results of other researchers [20–24] are generally consistent with our own results. Interestingly, even the previous studies that have strongly argued against the waiting time problem [15–17] still indicate that for a hominin population, the fixation of two co-dependent mutations is extremely problematic. For example, in the analysis of Durrett and Schmidt [16], they studied the waiting time to first appearance (first instance) of various string types within a hominin-type population (a population essentially identical to our own simulated population and with exactly the same mutation rate). Yet for a string of 8, when a perfect match was required, they still calculated a waiting time to first instance of 650 million years. For a beneficial effect of 1 % they estimate that the time to the effective instance (followed by final fixation), would be about 100-fold higher (this would be about 65 billion years). Their results, when adjusted as they prescribe, make our own findings for a string of 8 seem quite modest (just 18.5 billion years). The primary reason our waiting time was less than their corrected waiting time was apparently because we used an over-generous fitness benefit 10 times stronger than what they were assuming.

In a second paper by Durrett and Schmidt [17], they examined a more limited problem – how long does it take to create two co-dependent mutations within a hominin population. Yet their calculations indicated the average waiting time for establishment of these two mutations was still 216 million years (their simulations suggested a somewhat shorter time – 162 million years). Their waiting times again appear to be substantially longer than our own average waiting time for two co-dependent mutations (84 million years – Table 2). This again appears to be primarily because we used a ten-fold stronger fitness benefit. Their data is in good agreement with our own waiting time for two co-dependent mutations when we reduced our fitness benefit to a more reasonable 1 %. We then observed a waiting time of 270 million years (Table 3), which is in the same ballpark as their findings.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/#CR15

I have noticed you have gone a long way to try and discredit the findings by trying to undermine the scientists and journals involved rather than deal with the content that produces the findings. So because these non-religious scientists from non-religious mainstream journals directly associated with evolution agree with the long waiting times that Sanford and Behe have stated I think this supports their findings even though I should not have to go to these lengths to support my case.

 

[Speedwell]

That’s true but is only highlighting the harmful effects. Common mutational changes are usually deleterious or neutral. The paper as with most papers on this topic do not state exactly what function needs to be changed. They are talking about any functional change that will be functional that requires more than one mutation.

That's not how evolution works. It's just a creationist straw man. If a variation is selected it is because it produces increased fitness, period. That's all there is to evolution. There is no requirement that the next variation add to fitness in any particular way. There is no requirement that if the first variation increases fitness in a particular way that a second variation increases fitness in that same direction. Some other direction will do just as well, as long as the variation increases fitness in some way with each step. Evolution has no long-term targets which require a particular series of variations. If functional structures emerge which are built of a particular series of variations, that is purely contingent and if you let the creature evolve again under the same conditions you would most likely get something entirely different. All that can be predicted is increased fitness, not how that fitness is increased.

 

[stevevw]

That's not how evolution works. It's just a creationist straw man. If a variation is selected it is because it produces increased fitness, period. That's all there is to evolution. There is no requirement that the next variation add to fitness in any particular way. There is no requirement that if the first variation increases fitness in a particular way that a second variation increases fitness in that same direction. Some other direction will do just as well, as long as the variation increases fitness in some way with each step. Evolution has no long-term targets which require a particular series of variations. If functional structures emerge which are built of a particular series of variations, that is purely contingent and if you let the creature evolve again under the same conditions you would most likely get something entirely different. All that can be predicted is increased fitness, not how that fitness is increased.

They are talking about a specific functional change that may require linked multiple mutations on the same short DNA over several generations. Therefore the mutations will not be any mutational change on any place in the genome but a specific mutational change that needs to be made that is needed to produce a change where more than one mutation is needed. If this is not a part of evolution then why are there so many papers talking about this as mentioned in my previous posts ie

Lynch and Abegg suggests that to establish two specific co-dependent mutations in a population of 10,000 (given that the first mutation to arise is neutral) requires roughly 10–100 million generations.

This is summed up in the paper from Sanford.

In the biological realm, much information is transmitted within the cell based upon long strings of either nucleotides or amino acids. The information within an RNA or protein string almost always traces back to DNA strings. Within DNA, a primary unit of functional information is the gene, which is a very long text string that can range in size from about 1000 to more than one million nucleotides long. No geneticist believes that these very long nucleotide strings could ever arise directly, from scratch, via the mutation/selection process. Rather, a new gene is thought to arise from a previously existing gene, with the mutation/selection process establishing mutations within the long text string that is already established and functional. If sets of mutations (or short sub-strings) can be established within the preexisting longer string, then a new gene might arise, having a new biological function. Since a typical human gene is roughly 50,000 nucleotides long, to form a new gene with a new function should typically require the establishment of multiple mutations (or multiple sub-strings) within a pre-existent gene.

 

[Speedwell]

They are talking about a specific functional change that may require linked multiple mutations on the same short DNA over several generations. Therefore the mutations will not be any mutational change on any place in the genome but a specific mutational change that needs to be made that is needed to produce a change where more than one mutation is needed.

That is the straw man I'm talking about. There is no such "need."

If this is not a part of evolution then why are there so many papers talking about this as mentioned in my previous posts ie

All I've seen from you are hack creationist papers promoting the straw man.

 

[stevevw]

That is the straw man I'm talking about. There is no such "need."All I've seen from you are hack creationist papers promoting the straw man.

So you didn't even bother to check out the non-religious mainstream scientists and journals that agree with the findings that were linked. This shows you had already made your mind up and immediately dismissed things without any checking. This is an example of the bias against good scientists and their work all because of their associations which is unfair and biased.

 

[Speedwell]

So you didn't even bother to check out the non-religious mainstream scientists and journals that agree with the findings that were linked.

They don't. That is your misapprehension because you were deceived by the straw man.

 

[Speedwell]

They are talking about a specific functional change that may require linked multiple mutations on the same short DNA over several generations. Therefore the mutations will not be any mutational change on any place in the genome but a specific mutational change that needs to be made that is needed to produce a change where more than one mutation is needed. If this is not a part of evolution then why are there so many papers talking about this as mentioned in my previous posts ie

What you are doing is analogous to looking at scientists calculating the odds of a particular individual winning the lottery and concluding that because they are so small it is impossible for anyone to win it. Yes, the odds of a particular series of mutations leading to a particular functional outcome are very small. Everybody agrees to that. But the odds of a series of mutations leading to some functional outcome are actually quite favorable.

 

[tas8831]

How is it a strawman.

Because they are indicating that 1. evolution had a goal and that goal was 2. a specific set of mutations.

They are, in effect, taking a current state, and back-calculating the probability of that state arising after the fact.

As I have written on here, I once saw a fellow, to show how silly such calculations are, calculate the probability of his own existence premised on several improbably events (such that one sperm out of hundreds of billions produced by his father, who was one of 5.5 billion, etc.) and numerically showed that he did not exist.


Have you ever wondered why creationists NEVER actually do research on creation?

 

[tas8831]

This is still a logical fallacy that all scientists associated with religious connections work are automatically wrong.

Yes it is. It becomes less fallacious when the religious connection is fundamentalist Protestantism and young earth creationism (since such folk are, in effect, 'duty bound' to reject anything that does not conform to their views) , and even less so when the scientists in question have track records of dishonesty or incompetence in the area that they are writing about.
At what point is is not fallacious to dismiss the latest work of a crank? It is sort of like a reverse little boy cried wolf - the crank might be right 1 in 100 times, but by then it is too late, their credibility is gone.

What you failed to mention perhaps because your aim is to discredit everyone associated with these results is that John Sanford is a geneticist and also famous for inventing the Gene Gun so he should know what he is talking about as the paper is directly associated with genetics.

Are you familiar with the fallacy of argumentum ad verecundiam? Because you just made it. The Gene Gun is cool, but is 100% irrelevant to, say, population genetics, or evolutionary biology. And given that Sanford - whom, according to you, "should know what he is talking about as the paper is directly associated with genetics" - wrote, in his book, regarding mutations and genes:

"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."

That was regarding Haldane's dilemma, for which Sanford had cited electrical engineer YEC Walter ReMine, who had in turn played the 'I won't quote the guy that I put forth as the ultimate expert when he says Haldane;s dilemma was never a dilemma because it was wrong' in his book.

If you don't see the problem in that quote, then I suspect that may explain why you find his work so convincing.

What you also failed to do was continue to check out the other papers that supported the results that I mentioned that come from non-religious mainstream scientists and journals such as GENETICS, Protein Science and Molecular Biology and Evolution Journals. ie just hit the links it references.[15–17, 25]

Virtually all of the papers subsequent to the work of Behe and Snoke have confirmed that waiting times can be prohibitive – depending upon the exact circumstances. Some of the subsequent papers have been critical [15–17, 25]. Yet even those papers show that establishing just two specific co-dependent mutations within a hominin population of 10,000 can require waiting times that exceed 100 million years (see discussion).

Allow me to change focus for a second:

"Virtually all of the papers subsequent to the work of Behe and Snoke have confirmed that waiting times can be prohibitive – depending upon the exact circumstances. "

Durrett in particular pointed out the silly circumstances employed by the 'too much time' crowd (weird, isn't it, that genetics expert Sanford has not yet written a book providing the evidence and mechanism for God making DNA sequences...) in his amazingly cited papers:

"To be precise, the last argument shows that it takes a long time to wait for two prespecified mutations with the indicated probabilities. The probability of a seven of eight match to a specified eight-letter word is 8(3/4)(1/4)7 ≈ 3.7 × 10−4, so in a 1-kb stretch of DNA there is likely to be only one such match. However, Lynch (2007, see p. 805) notes that transcription factor binding sites can be found within a larger regulatory region (104 – 106 bp) in humans. If one can search for the new target sequence in 104 – 106 bp, then there are many more chances. Indeed since (1/4)8 ≈ 1.6 × 10−5, then in 106 bp we expect to find 16 copies of the eight-letter word."

"One obvious problem with their [Behe and Snoke] analysis is that they do their calculations for N = 1 individual, ignoring the population genetic effects that produce the factor of

."

There is much more. And later in his response to Behe's whining:

"
This conclusion is simply wrong since it assumes that there is only one individual in the population with the first mutation. There are on the order of

individuals with the first mutation before the second one occurs, and since this event removes only one individual from the group with the first mutation, it has no effect on the waiting time.

Behe is not alone in making this type of mistake. When Evelyn Adams won the New Jersey lottery on October 23, 1985, and again on February 13, 1986, newspapers quoted odds of 17.1 trillion to 1. That assumes that the winning person and the two lottery dates are specified in advance, but at any point in time there is a population of individuals who have won the lottery and have a chance to win again, and there are many possible pairs of dates on which this event can happen. The probability that it happens in one lottery 1 year is ∼1 in 200 (Durrett 2009)."

And so on...

But no - you keep hawking probability calculations premised on strawman as your go-to anti-evolution knockout.

 

[Heissonear]

They are talking about a specific functional change that may require linked multiple mutations on the same short DNA over several generations. Therefore the mutations will not be any mutational change on any place in the genome but a specific mutational change that needs to be made that is needed to produce a change where more than one mutation is needed. If this is not a part of evolution then why are there so many papers talking about this as mentioned in my previous posts ie

Lynch and Abegg suggests that to establish two specific co-dependent mutations in a population of 10,000 (given that the first mutation to arise is neutral) requires roughly 10–100 million generations.

This is summed up in the paper from Sanford.

In the biological realm, much information is transmitted within the cell based upon long strings of either nucleotides or amino acids. The information within an RNA or protein string almost always traces back to DNA strings. Within DNA, a primary unit of functional information is the gene, which is a very long text string that can range in size from about 1000 to more than one million nucleotides long. No geneticist believes that these very long nucleotide strings could ever arise directly, from scratch, via the mutation/selection process. Rather, a new gene is thought to arise from a previously existing gene, with the mutation/selection process establishing mutations within the long text string that is already established and functional. If sets of mutations (or short sub-strings) can be established within the preexisting longer string, then a new gene might arise, having a new biological function. Since a typical human gene is roughly 50,000 nucleotides long, to form a new gene with a new function should typically require the establishment of multiple mutations (or multiple sub-strings) within a pre-existent gene.

The more molecular biology we learn the more we see such new information does not support the foundation that living things have evolved.

All of the biochemistry about even physiological diseases (particularly neuropathic of spine and brain) the complexity displays multiple mutations in sequence and time in order for the known physiological cause to exist. No one single mutation can account nor continue without the string of other mutations for such said complex physiological "systems" of biochemical interactions and intergrations to exist.

 

[Heissonear]

Some have displayed what they think are transition fossils showing morphological changes. The did not truely present a succession of morphological changes in the fossil record over time. Only macro-assemblages that weere force fit to align into a scheme of "features evolved".

Once drunk on koolaid many find macro assemblages sufficient. Hard evidence void of conjecture is not what they walk by, nor post.

 

[Heissonear]

Some posters who like Googlism info need to first look in paleontology texts printed prior to 1970 to see how macro-assemblages were already presented as the existing evidence that the fossil record shows evolution occurred.

They knew of the massive gaps of morphological changes that had to occur between the presented macro-assemblages. But they did not have any better fossil record evidence to present.

Such as a fish fin turning into an arm-like assemblage. And eventually with a primative forked hoof or hand.

A lot of conjecture (missing evidence- and assumed reality) that such mix and match fossil features really did occur and is evidence of evolution.

Conjecture cannot be avoided by those stating the fossil record proves evolution occurred.

There is zero fossil record evidence that show evolution happened. How one lifeform changed into another lifeform over time in the fossil record.

This thread has showed many do not want to face up to this reality.

 

[Kylie]

Some posters who like Googlism info need to first look in paleontology texts printed prior to 1970 to see how macro-assemblages were already presented as the existing evidence that the fossil record shows evolution occurred.

They knew of the massive gaps of morphological changes that had to occur between the presented macro-assemblages. But they did not have any better fossil record evidence to present.

Such as a fish fin turning into an arm-like assemblage. And eventually with a primative forked hoof or hand.

A lot of conjecture (missing evidence- and assumed reality) that such mix and match fossil features really did occur and is evidence of evolution.

Conjecture cannot be avoided by those stating the fossil record proves evolution occurred.

There is zero fossil record evidence that show evolution happened. How one lifeform changed into another lifeform over time in the fossil record.

This thread has showed many do not want to face up to this reality.

So you want to limit science to what was known prior to 50 years ago in order to show your position is true?

Funny, I thought that if evolution was wrong, it wouldn't matter what science we used, since it would have to be wrong no matter what if your argument is true. But you don't seem to want to do that...

 

[stevevw]

What you are doing is analogous to looking at scientists calculating the odds of a particular individual winning the lottery and concluding that because they are so small it is impossible for anyone to win it. Yes, the odds of a particular series of mutations leading to a particular functional outcome are very small. Everybody agrees to that. But the odds of a series of mutations leading to some functional outcome are actually quite favorable.

why is that

 

[stevevw]

Because they are indicating that 1. evolution had a goal and that goal was 2. a specific set of mutations.

They are, in effect, taking a current state, and back-calculating the probability of that state arising after the fact.

As I have written on here, I once saw a fellow, to show how silly such calculations are, calculate the probability of his own existence premised on several improbably events (such that one sperm out of hundreds of billions produced by his father, who was one of 5.5 billion, etc.) and numerically showed that he did not exist.


Have you ever wondered why creationists NEVER actually do research on creation?

Then why is it not only what you say are creationists doing the research and debating about the probabilities of evolution evolving specific mutations that are needed for a specific function but also mainstream scientists. They respond to what Behe says and say that his calculations are wrong and then go about setting him strait on the very same scenarios by looking back at the probability of this happening. Some end up coming to the same conclusions as what Behe and Sanford has shown. For example Durrett and Schmidt are mainstream scientists publishing in mainstream Journal GENETICS state

Results of Nowak and collaborators concerning the onset of cancer due to the inactivation of tumor suppressor genes give the distribution of the time until some individual in a population has experienced two prespecified mutations and the time until this mutant phenotype becomes fixed in the population. In this article we apply these results to obtain insights into regulatory sequence evolution in Drosophila and humans. In particular, we examine the waiting time for a pair of mutations, the first of which inactivates an existing transcription factor binding site and the second of which creates a new one. Consistent with recent experimental observations for Drosophila, we find that a few million years is sufficient, but for humans with a much smaller effective population size, this type of change would take >100 million years.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581952/

100 million years far exceeds the 6 million years it took for apes to become humans.

 

[Warden_of_the_Storm]

Some posters who like Googlism info need to first look in paleontology texts printed prior to 1970 to see how macro-assemblages were already presented as the existing evidence that the fossil record shows evolution occurred.

They knew of the massive gaps of morphological changes that had to occur between the presented macro-assemblages. But they did not have any better fossil record evidence to present.

Such as a fish fin turning into an arm-like assemblage. And eventually with a primative forked hoof or hand.

A lot of conjecture (missing evidence- and assumed reality) that such mix and match fossil features really did occur and is evidence of evolution.

Conjecture cannot be avoided by those stating the fossil record proves evolution occurred.

There is zero fossil record evidence that show evolution happened. How one lifeform changed into another lifeform over time in the fossil record.

This thread has showed many do not want to face up to this reality.

The fact you want science, and thus knowledge too, to go BACKWARDS, really says everything about you.

 

[stevevw]

Yes it is. It becomes less fallacious when the religious connection is fundamentalist Protestantism and young earth creationism (since such folk are, in effect, 'duty bound' to reject anything that does not conform to their views) , and even less so when the scientists in question have track records of dishonesty or incompetence in the area that they are writing about.
At what point is is not fallacious to dismiss the latest work of a crank? It is sort of like a reverse little boy cried wolf - the crank might be right 1 in 100 times, but by then it is too late, their credibility is gone.

The above is an illogical considering that the work that some of these scientists present is in peer reviewed mainstream journals which is reviewed for its honesty and validity to published in the first place. Unless you want to say that the journals themselves are disonsts and then question their entire process. These papers are then open to critical analysis by other scientists.

I don't think it is a case of dishonesty but more about the assumptions one uses to base the results on. This is the difference in debate with one side taking more favourable assumptions and the other more unfavourable ones. The problem is it is hard to determine what really happens especially in more complex living things such as humans as the process cannot be observed.

Are you familiar with the fallacy of argumentum ad verecundiam? Because you just made it. The Gene Gun is cool, but is 100% irrelevant to, say, population genetics, or evolutionary biology. And given that Sanford - whom, according to you, "should know what he is talking about as the paper is directly associated with genetics" - wrote, in his book, regarding mutations and genes:

"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."

That was regarding Haldane's dilemma, for which Sanford had cited electrical engineer YEC Walter ReMine, who had in turn played the 'I won't quote the guy that I put forth as the ultimate expert when he says Haldane;s dilemma was never a dilemma because it was wrong' in his book.

If you don't see the problem in that quote, then I suspect that may explain why you find his work so convincing.

My point was that people wanted to take the position that Sanford was religious and therefore his science was wrong. I pointed out that he is also a genetic scientist and his paper is about genetics which makes him qualified to know what he is talking about. Some chose to focus on his religious connections rather than his scientific ones which is a fallacy when determining his ability to write on the topic he is trained in.

The problem with your reference that Sanford cites a YEC is also an unbalanced view of his work in that he also cites non religious main stream scientists from main stream journals that support his results which kind of negates what you are implying.

Allow me to change focus for a second:

"Virtually all of the papers subsequent to the work of Behe and Snoke have confirmed that waiting times can be prohibitive – depending upon the exact circumstances. "

Durrett in particular pointed out the silly circumstances employed by the 'too much time' crowd (weird, isn't it, that genetics expert Sanford has not yet written a book providing the evidence and mechanism for God making DNA sequences...) in his amazingly cited papers:

This is irrelevant to the time problem in his paper which is based on the biological and genetic processes.

"To be precise, the last argument shows that it takes a long time to wait for two prespecified mutations with the indicated probabilities. The probability of a seven of eight match to a specified eight-letter word is 8(3/4)(1/4)7 ≈ 3.7 × 10−4, so in a 1-kb stretch of DNA there is likely to be only one such match. However, Lynch (2007, see p. 805) notes that transcription factor binding sites can be found within a larger regulatory region (104 – 106 bp) in humans. If one can search for the new target sequence in 104 – 106 bp, then there are many more chances. Indeed since (1/4)8 ≈ 1.6 × 10−5, then in 106 bp we expect to find 16 copies of the eight-letter word."

Yet Lynch supports Sanfords findings that it would take a prohibitively long time for human evolution to do this. Lynch als takes a more favourable approach to the possibilities by assuming neutral and beneficial mutations for other results associated with larger populations in microbes. Like I have said this is a matter of assumption. Some may say that the evidence showns there is a high chance of some of those mutations and even one being deleterous which then compounds things and increases the time.

"One obvious problem with their [Behe and Snoke] analysis is that they do their calculations for N = 1 individual, ignoring the population genetic effects that produce the factor of

."

There is much more. And later in his response to Behe's whining:

"
This conclusion is simply wrong since it assumes that there is only one individual in the population with the first mutation. There are on the order of

individuals with the first mutation before the second one occurs, and since this event removes only one individual from the group with the first mutation, it has no effect on the waiting time.

Behe is not alone in making this type of mistake. When Evelyn Adams won the New Jersey lottery on October 23, 1985, and again on February 13, 1986, newspapers quoted odds of 17.1 trillion to 1. That assumes that the winning person and the two lottery dates are specified in advance, but at any point in time there is a population of individuals who have won the lottery and have a chance to win again, and there are many possible pairs of dates on which this event can happen. The probability that it happens in one lottery 1 year is ∼1 in 200 (Durrett 2009)."

And so on...

But no - you keep hawking probability calculations premised on strawman as your go-to anti-evolution knockout.

the above is an unreal comparison. The mutations for a specific function need to be specific and happen in a specific area of the DNA and not just anywhere and any time. Lottery winners are based on one number coming out. Lotto would be more of a suitable comparison where there are several numbers. But even this is not really a good comparison as each number is subject to other conditions that may work against it happening. But besides all that Durrett has supported the results of time being a prohibitive problem in human evolutin anyway as shown in my above post.

but for humans with a much smaller effective population size, this type of change would take >100 million years.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581952/

 

[Speedwell]

why is that

Because from any given starting point there are so many possible functional outcomes, not just the one which happened to develop.