Can the standard "Young Earth Creationist" model be falsified by genetics alone?

I said the following:
{I feel that so far, you misunderstand the extent to which their use of the chimp to represent the ancestral allele has affected your conclusions. And so far there are just far to many assumptions (one example - how to distribute the variations between A and DR) and too many variables (mutation rates, generations, % chimp that matches humans, division of mutations between DR and A, division of mutations between the 36 and the 1) and too many overestimations (mutation rate, no of mutation being 6271, no. of mutations in "A")}You replied that I make mistakes, without actually dealing with the many problems that I pointed out with your conclusions. Your 600 SNP's argument is affected by many factors, and to brush off those factors with sweeping statements leaves this discussion at a stalemate. You have to deal with EACH objection in a mature manner to back up your conclusions. Including lifestyle factors, and uncertainties regarding mutation rates, bit arguments which on their own destroy your point. Haha, they reduced the number from 6662 to 6271 due to the chimp comparison. They did cut down the number of variations, now are you saying they didn't? Ummm well. Are you saying that the chimp matched the reference sequence in 6271 positions. The study does not say if the chimp matched the reference sequence, but rather seems to indicate that the chimp's alleles matched the variants (the 36 individuals). Please back up your view from your link, because this needs clarification and without it your evidence is meaningless. You are focussing on the chimp, a point which you still have to show evidence for. But in addition to the chimp point, there are multiple other problems with your conclusions that you are just not dealing with.Edited by mindspawn, : fixing quote

sweeping statement when I asked you to be precise. Another sweeping statement, my concerns are legitimate and listed. That's with your interpretation of the study. Just because there are variants between two genomes, does not require that the variants are actual SNPs. No-one knows which genome has the ancestral allele, and which genome has the mutated allele. This principle applies when comparing "A" to the rest, and also when comparing the 36 to the reference sequence. My point is obvious, its accurate, and yet its ignored.Every time I mention this, you revert back to your "600 variants" argument in individual "A", should I then forget about your original argument, and we base your entire argument on individual "A"? Because you seem to be ignoring that the other 35 individuals have variants, and NOT all those variants are mutations, some of them are original alleles. This is obvious. Oh really. And how many of those 600 differences are mutations, and how many are original alleles? What if they used multiple individuals in the reference sequence, surely that would emphasize the number of differences? Or are we just to assume all parts of the reference sequence have exactly the same perfect proportion of mutations? Surely that's a huge assumption. Kindly focus on this point please. Admit it, Face it. Something. Explain why they dropped the number of variants from 6662 to 6271 using the chimp's loci? If you can explain this clearly, you will then succeed in explaining why the chimp is irrelevant.Please understand I am just taking the wording at its face value, the wording does not say they "extracted the ancestral loci" , the wording is saying they "extracted the ancestral allele" for the 6271 positions. Doesnt this mean they found the ancestral allele in all these positions, where though? In the reference sequence?Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.

Faith I feel that the link in the opening post does have legitimate claims to mutations, and therefore the mutation rate can have some significance. Each human on earth has DNA that is divided into 23 chromosomes. 22 chromosomes are in males and females, only males have the Y-chromosome.The reason we can be sure of mutations even under flood assumptions, is because there was only one Y-chromosome on the ark, Noah's. All his son's would have inherited the same Y-chromosome, as does science confirm that all men today derive from one single male ancestor. And so any variation now found in genes in the Y-chromosome are caused by subsequent changes to genes since Noah.(mutations in genes)My problems with Bluegenes assertions are numerous, because its now obvious even to you that if they find 6271 variations when comparing the DNA of 36 people with someone else, not all the variants will be mutations in the 36 individuals, some differences will be mutations in the reference DNA.
This basic and obvious point has not yet been acknowledged by Bluegenes.Another problem with his analysis is that mutation rates are not yet fully established.Another problem is that lifestyle factors affect mutations, and it is common knowledge that large portions of early society were hunter-gatherers. ie a more difficult lifestyle.Another problem, that I am still investigating, is that mutations are caused by radiation, during periods of high radiation mutation rates will be higher.And so I feel there are far too many uncertainties for definite conclusions at this point in time about the number of generations since the already acknowledged common male ancestor of all humans.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.

You are specifically referring to the distribution between "A" and the 35, which is your fixation.
How do you distribute the 6271 mutations between the 36 and the reference individual? You keep ducking this question. Aah you are reverting back to the 615 again because you cannot explain how to distribute the mutations in the 6271 variant loci between the reference individual and the 36. This point would only stand if they really did compare two individuals. Unfortunately your reference sequence contains bits and pieces of DNA from more than one individual which throws out your logic. It could be 150 and 450, we just don't know. Haha, you are missing the point. Do you even understand the study? Haha all your calculations are irrelevant because they were left with 6271 variable loci when comparing with the reference sequence. Just because the loci VARY WITH THE REFERENCE SEQUENCE does not mean the variants are mutations.In addition if there was exposure to radiation, or lifestyle factors , this could greatly affect mutation rates, and my compressed timeframes view REQUIRES exposure to radiation due to my claim that radioactive isotopes actually decayed far faster than is currently measured.In addition the Y chromosome mutation rate is approximately 4.8 times higher than elsewhere, however this figure "4.8" I found in Wikipedia, and cannot verify it elsewhere. The mutation rate in the Y-chromosome is an unknown, and until you give more precise figures on specifically the Y-chromosome mutation rate this whole thread is irrelevant to actual reality.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.

I need links, I need calculations. I don't care about the source of information, if the information makes sense then I respect it.Could you kindly give me your sources.

You are in fact incorrect.Not only are you incorrect, I already pointed this out in my post 76:"Thus, despite the small number of individuals, there was good geographical representation of global populations and of the haplogroup tree. After QC and validation, we extracted 6662 high-confidence variants (i.e., sites that differ from the Y chromosome reference sequence)"SITES THAT DIFFER FROM THE Y-CHROMOSOME REFERENCE SEQUENCE. Not differences from each other, but differences from the reference sequence. These comments are based on your misunderstanding of the study. As pointed out above, they did not compare with eachother , they compared the 36 with the reference sequence. Now its up to you to explain where the mutations are in 6662 variant loci. The reference sequence , or the 36 individuals? How do we divide the mutations between them? Your conclusion of 5:3 is way too simplistic and does not acknowledge the full range of factors that increase mutations in the y-chromosome:
"The Y chromosome is passed exclusively through sperm, which undergo multiple cell divisions during gametogenesis. Each cellular division provides further opportunity to accumulate base pair mutations. Additionally, sperm are stored in the highly oxidative environment of the testis, which encourages further mutation. These two conditions combined put the Y chromosome at a greater risk of mutation than the rest of the genome"
Also a lack of recombination in the Y-chromosome.The following study seems to indicate a much higher Y-chromosome mutation rate than either of us has quoted so far, but does not focus on SNP's. This study claims the field needs further study to establish y-chromosome mutation rates:
http://www.ncbi.nlm.nih.gov/...s/PMC1378017/pdf/10762544.pdfI don't find your simplistic ratio of 5:3 very convincing, seems like a thumbsuck to me. Wishful thinking on your part 1) Scientists themselves still claim Y-chromosome mutation rates are uncertain
2) You are still showing a misunderstanding of where those 6662 variants come from, this along with other factors directly affects your mutation count on which your argument is based.
3) You are ignoring the possibility of lifestyle factors , which have been proven to affect rates
4) My compressed timeframes view requires more radiation, which has a direct effect on mutations. Could you post a link. This is very interesting for me.Edited by mindspawn, : No reason given.

Let me repeat my quote from the actual study:
"Thus, despite the small number of individuals, there was good geographical representation of global populations and of the haplogroup tree. After QC and validation, we extracted 6662 high-confidence variants (i.e., sites that differ from the Y chromosome reference sequence)"Your response:
"the loci on which the reference differs from all 36 of the real people are its own mutations"You say that they "automatically exclude" the mutations in the reference sequence. Please quote from the study to prove your point, I have had the courtesy to back up my statements with actual quotes. You would be surprised how many time scientists miss some logic in making their conclusions and devising their studies. Applying what you think is logical to a document that explains things differently is just not good enough to make your point.And even if you were correct, your reference to another common ancestor further back in time ruins your mutation count, because its possible that all 36 individuals had the mutation, and the reference sequence has the original allele. The only method in which to tell the difference is to actually have the ancestral sequence, which they do not have, and they had to use the chimp to estimate the ancestral alleles.I believe the more unique variants found in small proportions of the population are more likely to be true mutations, and so referring to your graph, we can be pretty confident after the 52/41 , that these are all true mutations. But the 54, the 13 , the 41, the 185 and the 285 have a high chance of being ancestral alleles and not mutations which ruins your count. You are looking at one generation, however you need to factor in long term selection through variation via recombination. De-selection is limited regarding the Y-chromosome because it does not recombine.regarding my 4 points,
1) Ok the point is partially accepted, they are beginning to define an acceptable range that is currently applicable. This however does not reflect on past rates.
2) We are still in total disagreement.
3) You write: Not at all. I've pointed out the reality of variant rates along lineages, and that you can see by how much lineages can vary for a prolonged period of time on the chartsYou seem to miss my point here, its possible that ALL humans had a worse lifestyle during the first generations after the flood. They were also having children at older ages. The accumulation of mutations in the first few generations could have been dramatic compared to today, based on age and lifestyle factors.4) You say: And a direct effect on disease. Your model requires a very healthy population in order to spread rapidly around the world before the end of the stone age, whenever you think that was.This was a weak reply, we are looking at the number of germline mutations already existing in populations and how rapidly they were formed. Even now with these mutations, populations can grow rapidly, so your point that populations would not have been healthy with many germline mutations does not apply, because we are healthy enough to expand rapidly. Did mankind rapidly gain its germline mutations during a period of high radioactivity? I believe its possible.

Bluegenes, thanks for the civil discussion. I am not sure why it took you so long to point out the reference sequence, but other than that particular delay you have communicated well which is more than I can say for nearly everyone else in this forum.There are so many variables that do affect your stance, but I have probed and probed for weaknesses in your argument that would have a major effect and generally feel that you have answered well.The chimp does play a significant role in the study, but even so it has the role of reducing the mutations to a more reliable core and so even though there are some flaws in using the chimp I do see your 98.3 % point and your earlier point about the same logic being applicable under common design or common ancestry.So to conclude I generally agree with you on your points regarding my questions 1 and 2, despite the uncertainty regarding some variables. So your opening post makes sense regarding current rates, so we are now disputing the application of those rates to times past. I'm not getting you here, could you explain this again please. I don't see how we can work out mutation rates from that study itself, we need outside mutation rates to determine the timespans involved. I did post a link that showed that lifestyle effects mutation, and so my claim is not unsupported. I added an additional claim that age of parenthood affects mutations, which is widely known, here is a link to support that claim:Just a moment...
Abstract
"The number of de novo mutations in the germline can be expected to increase with age in males, therefore females might decrease mutation load in their progeny by avoiding mating with older males. Here, I propose that female polyandry can be more effective in decreasing the risk of genetic disorders in progeny than pre-copulatory mate choice, particularly if sperm competitiveness declines more steeply with age than other traits affecting chances of males to mate. If faster ageing of spermatogenic tissue causes older males to transfer inadequate numbers of functional sperm, polyandry would also benefit females directly."Now the bible claims that the males were vastly older than today when having their first offspring during the early post-flood years, so the accumulation of germline mutations during a difficult lifestyle and also from older males per generation would have been much higher during the first few generations. Shem was 100 years old, most others had their FIRST child in their thirties, later Terah had his children in his seventies, Abraham at a late age as well.Paternal age effect - Wikipedia
The population geneticist James F. Crow said that the fact that DNA in sperm degrades as men age and can then be passed along to children in permanently degraded and irreparable form, which they likely pass on as well, means that the "greatest mutational health hazard to the human genome is fertile older males"Eight times as many mutations in a 70 year old compared to a 20 year old, so there is some exponential effect occurring:
Fathers bequeath more mutations as they age | Nature
"A 36-year-old will pass on twice as many mutations to his child as a man of 20, and a 70-year-old eight times as many, Stefnsson’s team estimates." Bluegenes, we are looking at the existing germline mutations that exist in all of us. We still survive and breed even with these mutations, whether they came at the human population rapidly or slowly. The early population would have had less mutations than us, whether gained rapidly or slowly. We survive, of course they would have survived having even less than us. High radioactivity causes mutations. If rocks decayed faster in the past, the resulting radiation would have caused more mutations.I believe current rates of radioactivity are slowed down by the muon effect. Muons when colliding with earth generate many neutrons, which in turn prevent the decay of heavy elements. Under past conditions the magnetic field was stronger, preventing many muons from striking earth, the background neutrons were less and hence parent isotopes decayed at a faster rate, producing radiation that would have affected the mutation rate.Edited by mindspawn, : No reason given.

From now on I will restrict my replies to posts that contain no personal attacks, even if somewhere in the post there are some facts or good questions.

Nonukes, that's a 444 page document. Could you kindly quote the portion that you feel is relevant.
http://www.icr.org/i/pdf/research/rate-all.pdf None on those rebuttals deal with my muon hypothesis. Muons are currently slowing down decay by producing many neutrons on impact with the earth. (neutrons are known to slow down the decay of heavy isotopes). During past periods of strong magnetic fields, the muon effect would have been less, the decay more rapid.

That's a whole thread. Could you kindly summarise your point and refer me to a specific link. I haven't got the time to look through all those posts, and at this stage I'm not even sure what I would be looking for.

I suggest you think that through. Rates are slow now. This means that they overestimate time periods when comparing ratios of parent to daughter isotopes. Without the slowdown, rocks would rapidly decay into daughter isotopes which I believe is what happened from about 4400 years ago until about 1700 years ago. (approximately).

Please note there are so many variables, that I am agreeing only that current rates in that 3.2 mb section do not conform with a 4500 year time period. The extent is largely unknown.
The use of the genome of only one individual "A" to establish most of those variants has insufficient scope to be truly confident in the conclusions. If they had used 35 "A" individuals and 35 of the rest, we could be more confident that they matched the sections/sequences before comparing them. Remember 600 of the ~2000 variants were found in the "A" individual. Any error in matching sequences would have been exacerbated through the low numbers in the sample (one rare individual, 35 common ones). I know they are confident of their results, nevertheless there is a principle that the smaller the sample the less confidence we have in the results.In addition the exact rate of accumulation of germline mutations in the y-chromosome compared to the elimination through recombination in other areas of the genome is unknown, unless you can find a study to show the differences in germline accumulation over time. I cannot find clear figures anywhere on this effect of the lack of recombination over time. Ok but of course I'm disputing your 50% variance through 3 additional factors in the past:
A) Lifestyle
B) Paternal age
C) RadiationSo I feel your point above is irrelevant due to our ongoing discussions about factors that would increase the mutations rates above the modern observed range of mutation rates. Lol! I assume you promote promiscuity if its "nice to see".I understand your maths, however its not that simple if you take into account the exponential effect with age, ie the number of mutations approximately double up every 16 years:3 mutations at 20
6 mutations at 36
12 mutations at 52
24 mutations at 68 (8 times the mutations at age 70 )
48 mutations at 82
96 mutations at 98A couple of ancient fathers in each lineage would have a dramatic effect on the gaining of germline mutations, especially if there were exacerbating factors like excess radiation during their lifetimes. But I do admit that on its own, paternal age is not enough to explain the observed germline mutations.
. I understand this, but looking at my radiation argument, this relates specifically to the strength of the magnetic field which was stronger for quite a long period of time. (~2000 years). Its possible that higher birth rates and the length of time would have minimized the effect you are referring to, unless you have more exact figures that can strengthen your case. Cool, looking forward to your figures. I'm not sure of the proportion of the population that does have disabilities or reduced fitness levels, apparently about 2.5% are born with noticeable disabilities, but nearly everyone inherits some weakness that could result in slightly higher chances of death from a certain affliction. Even if early populations had a far higher proportion of disabilities, about 10%, I believe they would have coped. We can picture a scenario in which a farming family has about 10 offspring with 1 of those with a disability, there is no reason why that family would not survive, and the other 9 have offspring. And so 10% compared to 2.5 % would not wipe out the population.

Outward changes and the establishment of new race groups can occur without any significant genetic change whatsoever. Allele frequencies can determine many changes, and allele frequencies can occur over a few generations.Homo erectus, homo ergaster, and Neanderthals are merely extinct human race groups, nothing more. Its a big assumption to see an extinct race group and assume their bones are earlier then the early Sumerian civilization. We need very careful dating methodology to establish earlier dates, if you present your findings on the dating methods used for homo ergaster we can discuss this further but its probably more relevant to another thread.Homo australopithus is quite simply an extinct ape.

Bluegenes, due to admin's attitude to moderation I will no longer be participating in these forums. You are welcome to message me privately and we can continue this discussion, thank you for your civility during our discussion.This is a quote from admin, he is allowing both sides a "free for all" which obviously is to my disadvantage: