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And so then how do you detect the wolves in sheeps clothing? Because the wolves also lay claim to the title.
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And so then how do you detect the wolves in sheeps clothing? Because the wolves also lay claim to the title.Why not settle, arguendo, for the definition provided by Christian Forums?
A person who insists on laying claim to the title probably doesn't deserve it.And so then how do you detect the wolves in sheeps clothing? Because the wolves also lay claim to the title.
But if two mutations need linked over time to produce a beneficial result, then why would the body continue to preserve and waste energy on an appendage that is non functional?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.
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.
View attachment 235472
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
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.
Yes, that is exactly the "straw man" we're talking about. Thank you for giving us such an easily understandable example of creationist perfidy so we can better explain the idea to Steve.But if two mutations need linked over time to produce a beneficial result, then why would the body continue to preserve and waste energy on an appendage that is non functional?
From some point from development from flippers to legs, it neither grants advantage to water travel or land travel, but is in fact a hinderance to both. It is working against survival. This is the problem that must be overcome not once, but billions of time in the mutational view. At every stage there is a point lasting unknown eras where the mid-development is working against survival, not for it.
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.
But if two mutations need linked over time to produce a beneficial result, then why would the body continue to preserve and waste energy on an appendage that is non functional?
From some point from development from flippers to legs, it neither grants advantage to water travel or land travel, but is in fact a hinderance to both. It is working against survival. This is the problem that must be overcome not once, but billions of time in the mutational view. At every stage there is a point lasting unknown eras where the mid-development is working against survival, not for it.
Indeed.Because from any given starting point there are so many possible functional outcomes, not just the one which happened to develop.
Those rare beneficial mutations have to be the right ones in the right place that will be related to the specific change needed.
This does not make sense. In your previous reply you sayBecause from any given starting point there are so many possible functional outcomes, not just the one which happened to develop.
Not for the same thing to happen. Not for a particular functional outcome, but for any one of the many other possible functional outcomes which may be reached from that same first "mutation."This does not make sense. In your previous reply you say
Speedwell says
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.
On the one hand you say the odds of a particular series of mutations leading to a particular functional outcome are very small. Then you contradict this by saying the odds are very favourable for the same thing to happen.
That's a hard question, because most of us don't divide evolution into "Darwinian" and "EES" processes like you do. Let's just say that random variation is mostly random or it wouldn't plot to a bell curve like it is most often observed to do.How do we know that these functional outcomes are the result of Darwinian evolution and or from other processes such as with the EES and the like.
Biological information is completely different to Shannon info. Comparing this to there being several paths down a hill is too simplistic and perhaps shows how some try to simplify things so that they can account for what we see which has proven very hard to explain by this logic. AS I said if mainstream biologists use the same hindsight logic to calculate the chances then they are also perpetrating the wrong idea about evaluating evolutionary processes.Indeed.
It is like rolling a pebble down a hill - it may or may not reach the bottom. If it does, there are any number of paths it could have taken. The arguments Behe and Snoke and steve and Sanford are making is that because the pebble reached the bottom, it is impossible to have done so by chance because it needed to take the path it did.
Why?Biological information is completely different to Shannon info.
Not if they make the distinction between the odds of a particular favorable outcome and the odds of any one of all possible favorable outcomes.Comparing this to there being several paths down a hill is too simplistic and perhaps shows how some try to simplify things so that they can account for what we see which has proven very hard to explain by this logic. AS I said if mainstream biologists use the same hindsight logic to calculate the chances then they are also perpetrating the wrong idea about evaluating evolutionary processes.
But they don't assume--as you appear to do-- that it was the only thing which could have happened.As far as I can see this method of looking back and trying to evaluate what processes and how it happened occurs in just about every field of science from archeology to astrophysics. They do exactly the same thing in beginning with assumptions about how things happened and then mapping out how it actaully happened according to those assumptions.
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.
If only the transition from ape-ancesor to human 100% relied on 2 pre-specified mutations in regulatory sequence occurring one after the other...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. ... 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.
Biological information is completely different to Shannon info.
Isn't it odd - I use a simple analogy to make a point, and the creationist, excuse me, not a creationist has a fit.Comparing this to there being several paths down a hill is too simplistic and perhaps shows how some try to simplify things so that they can account for what we see which has proven very hard to explain by this logic.
Yes, YOU said that. But you failed to see why these 'mainstream biologists' are discussing it. I sincerely doubt that any mainstream biologists think that evolution proceeds solely via a series of 2 pre-specified mutations occurring in regulatory sequence. Unless you have examples?AS I said if mainstream biologists use the same hindsight logic to calculate the chances then they are also perpetrating the wrong idea about evaluating evolutionary processes.
And when their assessments demonstrate that their models do not comport with reality, then only creationists cling doggedly to them at all costs. D&S took the assumptions of others and applied them to the Behe assertions and showed how silly they were.As far as I can see this method of looking back and trying to evaluate what processes and how it happened occurs in just about every field of science from archeology to astrophysics. They do exactly the same thing in beginning with assumptions about how things happened and then mapping out how it actaully happened according to those assumptions.
This does not make sense. In your previous reply you say
Speedwell says
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.
On the one hand you say the odds of a particular series of mutations leading to a particular functional outcome are very small. Then you contradict this by saying the odds are very favourable for the same thing to happen.
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.
That is putting a different context on things and widening the scope of what is being analysed. They are talking about these specific changes requiring specific mutations in a small section of DNA and not the entire genome.Not for the same thing to happen. Not for a particular functional outcome, but for any one of the many other possible functional outcomes which may be reached from that same first "mutation."
I am not the only one who supports the EES processes and there is a growing number of scientists who do. This is part of the problem. By not determining how variation is produced you would not know and therefore because people assume that it is derived from Neo-Darwinism (random mutation) their results will also be based on assumptions. This will taint the way they see things and influence the outcomes. IE if variation or a particular change in function is caused by a development process (development bias or plasticity) that is directed will be seen as random and the result of Darwinian processes.That's a hard question, because most of us don't divide evolution into "Darwinian" and "EES" processes like you do. Let's just say that random variation is mostly random or it wouldn't plot to a bell curve like it is most often observed to do.
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".
You like to yammer about these issues as if you are an expert of some kind.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.
LOL! Evidently you didn't read that paper clear though, or didn't understand it--all standard undergraduate inferential statistics.The bell curve is not well suited to biological info and cannot determine random and non-random processes. Many results of non-random variations can appear random because each individual creature is subject to different conditions. Plasticity can produce varying phenotypes that are no based on gene change and therefore have no effect on survivability. Other factors associated with extra genetic inheritance and niche construction can appear random because individual living things are subject to different environmental conditions and may also respond differently in how they change but still achieve the same end result.
In reality, most biological data do not conform to a perfect bell-shaped curve, and, in some cases, they may profoundly deviate from this ideal.
http://www.wormbook.org/chapters/www_statisticalanalysis/statisticalanalysis.html
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