It isn't rejected a priori. It just so happens that you have no evidence. There is nothing for science to investigate.
That is not assumed.
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There is no dichotomy, the problem is that the only alternative to naturalistic evolution is God, as cause of anything, is rejected a priori (without prior).
Obviously, an a priori assumption of universal common descent going all the way back to, and including, the Big Bang.
Why is it the only alternative? Saying it's either A or B when you have no idea if there could be a C is a blatant false dichotomy. I admit that I haven't followed all your arguments but it seems that they are about specific mechanisms of evolution. Is it not possible that even if you managed to show that these mechanisms didn't work as we understand them to that there could be other naturalistic mechanisms that we haven't yet discovered or understood?
Why do you call common descent an assumption? It's a conclusion drawn from observations, your bias is showing.
Oh but you don't do null hypothesis or we would be talking about the human brain.
Taxonomy is organized based on semantics and for the convenience of retrieving information. That is not an argument.
Scientific method relies on directly observed or demonstrated facts, not a priori assumptions.
Deleterious effects.
Again with the 'we', there is no one left LM. I'm going to tell you like I have Papias, they are all gone because the culture wars are over.
Now as far as the lab work I'm aware of the Phoenix virus and it can't even be reconstructed. The ERVs are a dead issue and chasing it in circles is a waste of time.
Nope, just bored to death with the circular fallacious logic.
Again with the we, you are performing in an empty theater.
You are rummaging a junk yard pretending to pass it off as a viable cause. Unless you are oblivious we are talking about adaptive evolution and I'm really tired of you trying to get me to chase a red herring.
They are a lame homology argument, nothing more.
I showed you what the null hypothesis is.
Unless you are oblivious, I have already addressed that. I pointed to the 40 million mutations that separate chimps and humans. Those mutations include those that are responsible for the differences in brain size and intelligence.
Please stop lying about my argument.
I have said over and over and over . . . IT IS A PHYLOGENETIC ARGUMENT.
It isn't rejected a priori. It just so happens that you have no evidence. There is nothing for science to investigate....
That is not assumed.
so, how is the scientific method going to explore something that isn't naturalistic? Is there a testable, falsifiable hypothesis for the supernatural?Nonsense, the a priori assumption of universal common descent by exclusively naturalistic means is the very epicenter of Darwinian logic:
so, how is the scientific method going to explore something that isn't naturalistic? Is there a testable, falsifiable hypothesis for the supernatural?
...I've obviously missed something. Could you give an example of the evidence please? and it is scientific evidence, right?The same way it explores anything, is deals with the actual evidence. Impossible is still impossible and the origin of life is still impossible by naturalistic mens.
The wrath of God is being revealed from heaven against all the godlessness and wickedness of people, who suppress the truth by their wickedness, since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse. (Rom. 1:18-20)That's kind of the point, the evidence follows.
Grace and peace,
Mark
The same way it explores anything, is deals with the actual evidence. Impossible is still impossible and the origin of life is still impossible by naturalistic mens.
The wrath of God is being revealed from heaven against all the godlessness and wickedness of people, who suppress the truth by their wickedness, since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse. (Rom. 1:18-20)That's kind of the point, the evidence follows.
Grace and peace,
Mark
...I've obviously missed something. Could you give an example of the evidence please? and it is scientific evidence, right?
Firstly, if you could prove that origin of life is impossibel by natural means then you would surely win the Nobel prize, as you cant, its just an empty assertion.
Secondly, biblical verses are not scientific evidence, its just preaching and should not be used in a scientific debate. But it do show that the only reason you argue the science is because of your religios belief.
Mark, I both know and understand the science perfectly fine, thats why I disniss your posts out of hand. You do neither.
Try to write a peer reviewed science article on the subject and see how that goes.
You get various mutation rates depending on ancestral population sizes and time. The thing is this is based on 1.33% divergence and because of the deleterious effects on fitness it's hard to reconcile such a high mutation rate.
Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common...Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33% (Table 1). (Estimate of the Mutation Rate per Nucleotide in Humans)
With the inclusion of the indels the divergence jumps from 1.23% to almost 5%.
human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial sequence of the chimpanzee genome and comparison with the human genome Nature 437, 69-87 1 September 2005)
That means that about 5mya the common ancestors would have had a wave of mutations that would have simply been too deleterious to be sustainable.
That's why evolutionists will never openly discuss the indels, the divergence is simply too great.
Mainly because of what would have to change in order to get a brain three times bigger then apes:
The 118-bp HAR1 region showed the most dramatically accelerated change, with an estimated 18 substitutions in the human lineage since the human;chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400 Myr ago
See FIGURE 2 from An RNA gene expressed during cortical development evolved rapidly in humans. (Nature 443, 167-172 14 September 2006)
Now if you really want to get into this I strongly suggest you learn something about fossils, that's when it get real interesting.
Have a nice day
Mark
Your all over the road and it's been a while since I took any of the convoluted mess seriously. Let's start with the fact that the OP and the proposal of the thread has been left unaddressed.
See (ERVs put chimp/human common ancestry beyond any reasonable doubt.) The ERVs are a dead issue, I have not the slightest intention of chasing this around the mulberry bush with you.
If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. (On the Origin of Species, Chapter 6 - Difficulties on Theory)
The Phylogentic Argument is a waste of time it's already been dealt with at length. Taxonomy is a highly subjective means of organizing details, nothing more.
The inverse logic is intuitively obvious, if the homology argument for things in common can prove common ancestry then . . .
What makes this such a lackluster argument is that the Darwinian will just keep repeating that ERVs are the result of germline invasions, something that has simply been assumed as far as I can tell.
. The researchers got the 'Phoenix Virus' to work, it had 20 amino acids and just one frameshift. In order to understand why this is important you would need to know how protein coding works on a molecular level.
The HERV-K (HML2) is less then 1% of the human genome and yet it is the most studied. When they revive this sequence they actually manage to reconstruct it but with one frameshift. What is interesting about the results is that only two are within genes. The explanation being that they are probably deleterious so their are defenses that prevent this.
Doesn't it make sense that the germline cells would be protected as well?
The amino acids need an open reading frame. When they got it working they they wanted to see how it would interact with living cells and it was introduced to live T cells. Guess what, it really can get into the DNA but I'm still waiting for the part where it's demonstrated that massive germline invasions are possible.
Let's take a look at a little Darwinian mythology and try to picture what they believe happened here. Our supposed ancestors from about 25 million years ago would have been inundated with a massive dose of these pathological ERV viruses.
As a result the ERVs would replicate at random in the genomes until random mutations disrupted the reading frame, leaving fragments like the HERV K. Getting this far into the ancestry of apes in Darwinian evolution leaves you following a lot of long 'ghost lineages' but geographically always go back to the East African Rift valley. (Nature, 30 May 2013)
This is an area that has made a number of paleontologists famous, especially the Leaky family who found so many of the Homo habilis and Homo erectus fossils in and around this area. So in case you were wondering when this supposed ERV onslaught of germline invasions would have happened it would have been right around there. What the Darwinian desperately wants to prove is a correlation between the molecular evidence and the fossil record. What they are doing is taking this highly technical ERV research, molecular clock age estimates and reconcile it with the fossil record. My positive argument here will simply be this, no matter how many ways it's reconstructed ERVs are just another homology argument.
That's about it, Talk Origins wants you to accept the assumption that ERVs are the result of germline invasions then drop a probability argument in your lap. The essence of the argument is the strongest argument against germline invasions in the first place. They are rare and they are pretty much random. Once they hook you with the assumption that they must be the result of a germline invasion they use the probability argument for common ancestry.
It's just another homology argument buried in highly technical viral research but it really comes down to a false assumption and some anecdotal comparisons.
You can't look at the actual fossils and comparative genomics in adaptive evolution so you pick the most convoluted argument available.
Nonsense, the a priori assumption of universal common descent
When you get done with your peer reviewed article let me know. What I never quite understand is how a person can think themselves the voice of science without even so much as reading the literature, let alone thinking about the details. If you know and understand so much about science then why have you managed to say nothing substantive, let alone scientific. The approach you are using is about all evolutionists have, it's called an ad hominem fallacy, it's an argument that never happened.
You understand science perfectly? I don't think you know what the word means
Have a nice day
Mark
/
They seemed to have reconciled it just fine: "suggests that synergistic epistasis among harmful mutations may be common". What they are saying is that individuals with two or more mutations are strongly selected against which increases the rate at which deleterious mutations are removed from the population.
Why is that a problem?
Why is that a problem?
Sometimes it is rather sad that you lack a sense of irony.
Heh, no that is not how this works. You make the claim that the science is wrong, you back it up. As you obviously cant its just empty preaching.
I already addressed it. The differences between the human and chimp brain is due to the mutations that separate the two species.
Will you address my response or not?
Then don't question common ancestry between humans and chimps unless you are willing to address the evidence that supports it. Also, if you have to deny the direct observation of retroviruses producing ERVs, what does that say about your argument?
So where have you been shown that the human brain could not have been produced by numerous, successive, and slight modifications?
That is simply untrue. Phylogenies are objective.
You can't simply ignore the evidence.
We are using a phylogenetic argument. Please stop misrepresenting our argument.
How many times do we need to go over this?
Do you have to assume a suspect is guilty in order to get a DNA match from a blood sample at a crime scene? Do we have to witness a suspect leaving his DNA at a crime scene in order to use it in court?
The evidence that germline invasions occurred are heritable ERVs. ERVs are the evidence that germline invasions leave, just as the DNA at a crime scene is what a criminal leaves.
The most likely result of an indel in an open reading frame would be a frameshift, the likely hood of a triplet codon replacement would be astronomical. I refuse your assumption as mythical, not methodological.I have forgotten more about protein translation than you have ever known. I am not the one who incorrectly thinks that an indel outside of an open reading frame will result in a frame shift mutation. That would be you. I am not the one who incorrectly thinks that a 3 base indel occuring in an open reading frame will result in a frame shift mutation. That would be you. I am not the one who incorrectly thinks that frame shift mutations can occur in an RNA gene that is never translated into protein. That would be you. I am not the one who incorrectly thinks that a 10 base indel indicates 10 separate insertion or deletion events. That would be you.
96% at best and you have seen the actual research enough times to know that. Now if you just mean the actual protein coding genes it's, on average, on substitution per genome per gene on average. Given the deleterious effects of mutations it's a statistical impossibility by even the most conservative estimations. It's only believed because it's assumed.You are the LAST person who should be pointing any fingers when it comes to knowledge of protein translation, RNA transcription, or even DNA replication. You can't even figure out that finding a 2% difference between genes does not refute the argument that there is 98% similarity.
Which assumes they are the result of germline invasions rather then actual reading frames simply broken by mutations. The odds of mutations breaking the reading frames fall into expected averages, the odds of them happening as the result of viral infections are laughable.No. The explanation is that insertions which occur within genes are almost always deleterious, SO THEY ARE SELECTED AGAINST THROUGH NATURAL SELECTION. ERV insertions that happen outside of the 2-3% of the genome made up of coding regions can be completely neutral, so they are not selected against or for. There are also indications that some ERVs are actually beneficial, and they are selected for.
You are imagining things that don't exist.
Why aren't they possible?
Reference?
Or do you not realize that they are spread out through time and did not occur all at once?
It seems that you are making a lot of stuff up.
Its rather sad to see that deleterious effects are inevitable is absent from the language.
Two reasons, selective constraints and deleterious effects.
Because for obvious reasons mutations, especially on this scale, always result in devastating disease and disorder.
What is truly sad is the lack of scientific acumen on the part of those who pretend to be it's defenders.
You categorically assumed they were the result of mutations, you demonstrated nothing.
The direct observation of an ERV producing a germline mutation in the human genome when?
Bear in mind I mean modern times not some assumed germline invasion from a mythical natural history.
The effects of mutations on human brain relate genes, they are always deleterious.
They are semantics.
I am the only one in this thread actually appealing to actual evidence, something you manage to ignore. Every single time.
No you are using semantics to avoid actual evidence.
Till you get dizzy enough from arguing in circles that you argument finally collapses which is usually not that long.
You need two good samples and a direct comparison.
Unless the invasion is simply impossible due to deleterious effects. Which is the case.
The most likely result of an indel in an open reading frame would be a frameshift, the likely hood of a triplet codon replacement would be astronomical.
96% at best and you have seen the actual research enough times to know that.
Now if you just mean the actual protein coding genes it's, on average, on substitution per genome per gene on average. Given the deleterious effects of mutations it's a statistical impossibility by even the most conservative estimations. It's only believed because it's assumed.
Which assumes they are the result of germline invasions rather then actual reading frames simply broken by mutations.
The odds of mutations breaking the reading frames fall into expected averages, the odds of them happening as the result of viral infections are laughable.
The stone age ape man myth is laughable.
More circular questions, points refuted a thousand times.
I at least have source material, something you cannot be bothered with.
I made no such assumption. The evidence is conserved sequence within functional parts of the genome, and a phylogeny of DNA differences and similarities. That is the evidence which allows us to CONCLUDE that those differences are due to mutations. Again, we have the evidence. We aren't assuming.
The direct observation of a retrovirus producing an ERV in a human cell. We have directly observed it. Why do you have to run away from this observation?
Then why ask for any modern observations if you are just going to ignore them?
Still waiting for evidence to back this up.
No, they aren't. We are using a phylogenetic argument, not a homology argument. Please stop lying about the argument we are using.
Where is the evidence that every single mutation is deleterious?
Why are you ignoring the direct observation of retroviruses creating ERVs as shown in this scientific paper?
http://www.ncbi.nlm.nih.gov/pubmed/15314653
Why are you ignoring the PHYLOGENETIC ERV evidence supplied in this paper?
http://www.pnas.org/content/96/18/10254.full
My other irony meter just exploded.
You are ignoring the phylogenetic argument by calling it semantics.
Then lets see your probability calculations and the science that backs it. Why is a 3 base indel nearly impossible while a 1, 2, 4, or 5 base indel completely possible?
And yet you would point to a 4% difference as a refutation of the 96% similarity. Do you see the problem with your argument or not?
We only assume that human and chimp genes are 98% identical? We haven't held them up side by side and compared them?
We assume no such thing. We have the evidence of germline invasions. We have the ERVs. It is no different than finding a criminal's DNA at a crime scene.
And yet you haven't shown us those odds, or that they even need to be broken in order to insert into a germline cell and become heritable.
And you avoid the evidence once again.
You haven't produced a single source demonstrating that every single mutation is deleterious.
Just produce a single peer reviewed paper which states that every single mutation is deleterious. Just one.
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