Another poor response to ERV evidence for common ancestry by a creationist.

[Zaius137]

Put Up or Shut Up…

“PS. Evolution has nothing to do with the origins of life.”

“In a letter to Joseph Dalton Hooker on February 1, 1871, Charles Darwin addressed the question, suggesting that the original spark of life may have begun in a "warm little pond, with all sorts of ammonia and phosphoric salts, lights, heat, electricity, etc. present, so that a protein compound was chemically formed ready to undergo still more complex changes". He went on to explain that "at the present day such matter would be instantly devoured or absorbed, which would not have been the case before living creatures were formed." In other words, the presence of life itself makes the search for the origin of life dependent on the sterile conditions of the laboratory.”

http://en.wikipedia.org/wiki/Abiogenesis#Pasteur_and_Darwin

And I believe Behe did an outstanding job in his argument.

 

[Zaius137]

(sfs)

“And my point is that insertions are marks of phylogeny regardless of their selective value.”

“I do remember that, and I also remember that you have been unable to offer any coherent reason for your rejection, nor for thinking that these are un-parsimonious explanations.”

Your hypothesis Is Only as Good as Your Null Hypothesis.

“Sequence similarity is an empirical observation, whereas the conclusion of homology is a hypothesis proposed to explain the similarity. Statistically significant sequence similarity can arise from factors other than common ancestry, such as convergent evolution due to selection, structural constraints on sequence identity, mutation bias, chance, or artifact manufacture. For these reasons, a skeptic who rejects the common ancestry of all life might nevertheless accept that universally conserved proteins have similar sequences and are "homologous" in the original pre-Darwinian sense of the term (homology here being similarity of structure due to ''fidelity to archetype''). Consequently, it would be advantageous to have a method that is able to objectively quantify the support from sequence data for common-ancestry versus competing multiple-ancestry hypotheses.”


http://www.evolutionnews.org/2010/11/douglas_theobald_tests_univers041021.html


"Hence the paleovirology nonsense" is not a place where evolutionary biologists have expressed an expectation that transposition rates have been constant over hundreds of millions of years. Now, could you answer the question?”

My observation said nothing about retrotransposition rates. I only made an observation that ERV insertion rates should be at least within an order of 10 in extrapolated time spans. It is up to you to show me why they shouldn’t be.

 

[Naraoia]

No actually the supervillain is the evolution lie but its new magic proof is the focus of our discussion.

"Lie" implies intent to deceive. Who is trying to deceive you with this "lie"?

Common ancestry, time of divergence and paleovirology is complete nonsense to me...

"To you" being the key words. The fact that you don't understand something doesn't make it "contrived", much less a "lie".

 

[Loudmouth]

Your hypothesis Is Only as Good as Your Null Hypothesis.

The null hypothesis would be a lack of orthology for the vast majority of ERV's. Instead, we observe what the hypothesis predicts, the vast majority of ERV's are orthologous, and orthology produces the nested hierarchy that the hypothesis predicts.

“Sequence similarity is an empirical observation, whereas the conclusion of homology is a hypothesis proposed to explain the similarity. Statistically significant sequence similarity can arise from factors other than common ancestry, such as convergent evolution due to selection, structural constraints on sequence identity, mutation bias, chance, or artifact manufacture. For these reasons, a skeptic who rejects the common ancestry of all life might nevertheless accept that universally conserved proteins have similar sequences and are "homologous" in the original pre-Darwinian sense of the term (homology here being similarity of structure due to ''fidelity to archetype''). Consequently, it would be advantageous to have a method that is able to objectively quantify the support from sequence data for common-ancestry versus competing multiple-ancestry hypotheses.”

So now you are claiming that ERV's are not from retroviral insertion? Really? What selective pressures are driving primate genomes to produce thousands of copies of reverse polymerases, repetitive LTR's, and viral proteins? Are you aware that retroviruses insert themselves into the host genome? Can you tell us why this is not a valid mechanism for putting these sequences into a genome? Do you really think that the homology between ERV's and real retroviruses is just a coincidence?

I only made an observation that ERV insertion rates should be at least within an order of 10 in extrapolated time spans.

You didn't observe that. You CLAIMED that. You need to support your claims with evidence.

 

[Loudmouth]

Put Up or Shut Up…

“PS. Evolution has nothing to do with the origins of life.”

“In a letter to Joseph Dalton Hooker on February 1, 1871, Charles Darwin addressed the question, suggesting that the original spark of life may have begun in a "warm little pond, with all sorts of ammonia and phosphoric salts, lights, heat, electricity, etc. present, so that a protein compound was chemically formed ready to undergo still more complex changes". He went on to explain that "at the present day such matter would be instantly devoured or absorbed, which would not have been the case before living creatures were formed." In other words, the presence of life itself makes the search for the origin of life dependent on the sterile conditions of the laboratory.”

http://en.wikipedia.org/wiki/Abiogenesis#Pasteur_and_Darwin

And I believe Behe did an outstanding job in his argument.

I still don't see anything in there showing how evolution is dependent on abiogenesis. Care to explain? Are you saying that a supernatural deity could not have formed very simple replicators that evolved over time into the biodiversity we see today?

Can you name a single scientific theory you do accept? I am willing to bet that theories you do accept suffer the same "problem" (as in lack of a problem) that evolution does.

 

[Zaius137]

Reply to Loudmouth…Yes I have problems with this speculation.


“So now you are claiming that ERV's are not from retroviral insertion? Really? What selective pressures are driving primate genomes to produce thousands of copies of reverse polymerases, repetitive LTR's, and viral proteins? Are you aware that retroviruses insert themselves into the host genome? Can you tell us why this is not a valid mechanism for putting these sequences into a genome? Do you really think that the homology between ERV's and real retroviruses is just a coincidence?”

I would like to examine a particular case that bothers me…

There is always a substitution cost. Not only does the new insertion need to be incorporated into a population but also the removal of the previous allele must be accomplished from that population (substitution cost is incurred). By the way this may take longer than predicted by Haldane’s dilemma (that deals with incorporation limit of beneficial mutations). “ReMine’s suggestion”

“Using the neutralist approach, ReMine shows that, in 10 million years, a human-like species could substitute no more than 25,000 expressed neutral mutations and this is merely 0.0007 per cent of the genome — nowhere near enough to account for human evolution. This, ReMine says, is the trade secret of evolutionary geneticists. Evolutionary genetics textbooks avoid mentioning the problem”.

http://creation.com/images/pdfs/tj/j11_3/j11_3_292-298.pdf

But Alu’s are determined to constitute about 10% of the current human Genome.

‘‘’Previous estimates for the retrotransposition rate (RR) of Alu elements in humans of one new insertion every [FONT=AdvTT6120e2aa+22]∼100–125births were developed prior to the sequencing of the human and chimpanzee genomes.’’[/FONT]

“Both methods consistently yielded RR on the order of one new Alu insertion every [FONT=AdvTT6120e2aa+22]∼20births, despite the fact that the evolutionary-based method represents an average RR over the past [FONT=AdvTT6120e2aa+22]∼[/FONT]6million years while the mutation-based method better reflects the current-day RR. These results suggest that Alu elements retrotranspose at a faster rate in humans than previously thought, and support the potential of Alu elements as mutagenic factors in the human genome.”[/FONT]

“Population genetics theory predicts that the probability of fixation of any element under neutral evolution is 1/2Ne, where Ne is the human effective population size (Graur and Li, 2000). Thus, the expected total number of Alu insertions (i.e. encompassing insertions that ultimately became fixed or lost, as
well as currently polymorphic elements) that must have occurred in humans to produce n fixed human-specific elements at the time of observation (present-day) is n2Ne.”

http://batzerlab.lsu.edu/publications/Cordaux_2006_Gene_retrotransposition%20rate.pdf

Look at the last paragraph of my citation. The examination uses the “neutral” formula for fixation and yet another inconsistency by this mutation being deleterious. This case for HERV is typical and typically flawed.


http://www.geneticorigins.org/pv92/aluframeset.htm

http://www.somosbacteriasyvirus.com/ERV9.pdf

http://www.evolutionnews.org/2011/05/do_shared_ervs_support_common_046751.html

 

[Loudmouth]

I would like to examine a particular case that bothers me…

There is always a substitution cost. Not only does the new insertion need to be incorporated into a population but also the removal of the previous allele must be removed from the population (substitution cost is incurred). By the way this may take longer than predicted by Haldane’s dilemma (that deals with incorporation limit of beneficial mutations). “ReMine’s suggestion”

Where did you show that it takes too long? Why can't genetic drift produce ubiquitous ERV's? There are other neutral mutations in the human genome that have moved to fixation, so I really don't see why you have a problem with it.

Also, not all human ERV's are ubiquitous:

However, some members of the human endogenous retrovirus (HERV)-K family are remarkably intact and display high genetic homology to mouse mammary tumor virus (MMTV), a retrovirus causing breast cancer in mice. Two full-length HERVs (K113 and K115) have been reported to show insertional polymorphism. We used PCR to investigate the presence of these two HERVs in 102 female breast cancer patients and an equal number of age-matched controls with no history of malignancy (age range: 25-92 years). The two groups showed no significant difference in frequency (HERV-K113, 16.7% vs. 12.7%; HERV-K115, 4.9% vs. 9.8%) and no apparent association with histology, age at diagnosis, receptor status, HER-2/neu status, or TNM stage at diagnosis.
Insertional polymorphisms of endog... [AIDS Res Hum Retroviruses. 2004] - PubMed - NCBI
​

The authors were looking for a potential link between these HERV's and breast cancer. However, they found that only a minority of people carry these HERV's.

Also, you have done nothing to cast doubt on the viral source of ERV's. Do you really think that ERV's are a case of convergent evolution as you proposed in an earlier post.

“Using the neutralist approach, ReMine shows that, in 10 million years, a human-like species could substitute no more than 25,000 expressed neutral mutations and this is merely 0.0007 per cent of the genome — nowhere near enough to account for human evolution. This, ReMine says, is the trade secret of evolutionary geneticists. Evolutionary genetics textbooks avoid mentioning the problem”.

http://creation.com/images/pdfs/tj/j11_3/j11_3_292-298.pdf

Remine ignores the effects of neutral substitutions that are linked to beneficial mutations. The closer a neutral substitution is to a beneficial mutation the higher the chance that the neutral mutation will hitchhike along with the beneficial mutation.

Real peer reviewed research demonstrates just the opposite:

The results are in good agreement with indirect estimates, obtained by comparison of orthologous human and chimpanzee pseudogenes. The average direct estimate of the combined rate of all mutations is 1.8x10(-8) per nucleotide per generation, and the coefficient of variation of this rate across the 20 loci is 0.53.
Direct estimates of human per nucleotide mutation ... [Hum Mutat. 2003] - PubMed - NCBI

​

These authors found that the observed human mutation rate in their study matches very well with the estimation of the mutation rate derived from a comparison of neutral mutations in the human and chimp genomes.

But Alu’s are determined to constitute about 10% of the current human Genome.

Retrotransposons are not endogenous retroviruses. Please stay focused.

This case for HERV is typical and typically flawed.

Again, where have you cast any doubt on the viral origin of ERV's? Where have you presented anything that casts doubt on this hypothesis:

Given the size of vertebrate genomes (>1 × 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14).
Inaugural Article: Constructing primate phylogenies from ancient retrovirus sequences

​

 

[Zaius137]

“Where did you show that it takes too long? Why can't genetic drift produce ubiquitous ERV's? There are other neutral mutations in the human genome that have moved to fixation, so I really don't see why you have a problem with it.”

I did not show it takes too long, others did. Did you read ReMine’s argument? If not in his chapter devoted to neutral selection at least read summations on the web…

“The authors were looking for a potential link between these HERV's and breast cancer. However, they found that only a minority of people carry these HERV's.”

If they don’t exist in all human’s I need your citation. Alu’s are among the most studied. And no Alu’s are a major part of the human genome from what I read (the sequenced genome) some 10% of it.

“Also, you have done nothing to cast doubt on the viral source of ERV's. Do you really think that ERV's are a case of convergent evolution as you proposed in an earlier post.”

I did not propose anything, others did.

“Retrotransposons are not endogenous retroviruses. Please stay focused.”

The Alu was considered from an ERV… Please read my citations…

“Given the size of vertebrate genomes (>1 × 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14).
Inaugural Article: Constructing primate phylogenies from ancient retrovirus sequences”

A speculation lacking a null hypothesis as I posted before.

 

[Zaius137]

“Where did you show that it takes too long? Why can't genetic drift produce ubiquitous ERV's? There are other neutral mutations in the human genome that have moved to fixation, so I really don't see why you have a problem with it.”

I did not show it takes too long, others did. Did you read ReMine’s argument? If not in his chapter devoted to neutral selection at least read summations on the web…

“The authors were looking for a potential link between these HERV's and breast cancer. However, they found that only a minority of people carry these HERV's.”

If they don’t exist in all human’s I need your citation. Alu’s are among the most studied. And no Alu’s are a major part of the human genome from what I read (the sequenced genome) some 10% of it.

“Also, you have done nothing to cast doubt on the viral source of ERV's. Do you really think that ERV's are a case of convergent evolution as you proposed in an earlier post.”

I did not propose anything, others did.

“Retrotransposons are not endogenous retroviruses. Please stay focused.”

The Alu was considered from an ERV… Please read my citations…

“Given the size of vertebrate genomes (>1 × 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14).
Inaugural Article: Constructing primate phylogenies from ancient retrovirus sequences”

A speculation lacking a null hypothesis as I posted before.

 

[Zaius137]

“Remine ignores the effects of neutral substitutions that are linked to beneficial mutations. The closer a neutral substitution is to a beneficial mutation the higher the chance that the neutral mutation will hitchhike along with the beneficial mutation.”

That is patently wrong and a misrepresentation…

 

[Loudmouth]

I did not show it takes too long, others did. Did you read ReMine’s argument?

Is this a recommended reading forum? Present the info.

If they don’t exist in all human’s I need your citation.

I just supplied it. Here it is again:

Insertional polymorphisms of endog... [AIDS Res Hum Retroviruses. 2004] - PubMed - NCBI

Also notice that this is a peer reviewed paper, not a book.

In that study they found that 12-16% of humans carry HERV-K113 and 4-10% of humans carry HERV-K115.

Alu’s are among the most studied.

Most studied what? Alu's are not ERV's.

The Alu was considered from an ERV

Alu's move within the genome all on their own. ERV's are from exogenous sources which are retroviruses.

A speculation lacking a null hypothesis as I posted before.

Already answered that as well. The null hypothesis is that humans and chimps do not share a common ancestor if the vast majority of ERV's are not found at orthologous positions as would be expected from independent insertions.

 

[Loudmouth]

“Remine ignores the effects of neutral substitutions that are linked to beneficial mutations. The closer a neutral substitution is to a beneficial mutation the higher the chance that the neutral mutation will hitchhike along with the beneficial mutation.”

That is patently wrong and a misrepresentation…

Then show why it is wrong.

 

[Zaius137]

Sorry LoudMouth but we will not make any ground on this without you having the courtesy of reviewing my posts in a detailed manner (a few minutes don’t cut it). I spend a great deal of time reading and studying other person’s thoughtful posts. What you would reduce this forum to is simple “trolling”. I will not go there…

Please address my posting and we can reason further.

 

[Loudmouth]

Sorry LoudMouth but we will not make any ground on this without you having the courtesy of reviewing my posts in a detailed manner (a few minutes don’t cut it). I spend a great deal of time reading and studying other person’s thoughtful posts. What you would reduce this forum to is simple “trolling”. I will not go there…

Please address my posting and we can reason further.

Let's review, shall we? I wrote the following:

"The null hypothesis would be a lack of orthology for the vast majority of ERV's. Instead, we observe what the hypothesis predicts, the vast majority of ERV's are orthologous, and orthology produces the nested hierarchy that the hypothesis predicts."

Several posts later you wrote:

"A speculation lacking a null hypothesis as I posted before."

I have posted the null hypothesis twice now. Perhaps you can address it?

As to fixation rates, they fit just fine as show in this paper. The authors found that there are 113 human specific HERV-K insertions with 8 of them being polymorphic (i.e. not fixed). They plugged these values into their population models and these are the results:

HERV-K(HML2) copying events lead to novel elements that are present initially only in a single host individual. The frequency of these elements in the host population may then increase as a result of genetic drift (we exclude here cases of co-option, which we assume are rare). If the HERV-K(HML2) family is still active and producing new copies at present, we expect to find elements that have inserted recently and are present in only a proportion of the human population. The actual number of insertionally polymorphic elements that we would expect, assuming the scenario of present-day activity, can be determined by using standard population genetic models.
We therefore calculated a frequency distribution (see Materials and Methods) for the expected number of loci in the published human genome sequence that would be insertionally polymorphic when compared to our sample of 19 individuals, assuming activity of the HERV-K(HML2) family until the present. Parameters used were our estimated insertion rate since the divergence from chimpanzees (μ = 3.8 × 10−4) and the previous estimate of long-term effective population size (Ne) of 10,000 (17, 36). Given that a polymorphism has a probability of 0.72 (78/108) of being detected in our survey (i.e., is in a region of the genome that can be amplified by PCR), the model predicts a mean of 10.6 polymorphic insertions, with 95% bounds of 5 and 18.
Genomewide Screening Reveals High Levels of Insertional Polymorphism in the Human Endogenous Retrovirus Family HERV-K(HML2): Implications for Present-Day Activity
​

The number of predicted unfixed HERV-K insertions in their model was 5 to 18. The real value is 8. It fits just fine. If you want to discuss their methodology I would be happy to do so. I am sure that sfs would have some comments as well.

Also note that I am citing a peer reviewed paper. I would suggest that you do the same.

 

[Naraoia]

The Alu was considered from an ERV… Please read my citations…

As far as I can tell, Alu elements are copied pieces of host DNA that hijack other retrotransposons' machinery to jump. Nothing to do with viruses, endogenous or otherwise.

Good thing I went away and wised up a bit about human retrotransposons when the ERV subject came up!

“Given the size of vertebrate genomes (>1 × 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14).
Inaugural Article: Constructing primate phylogenies from ancient retrovirus sequences”

A speculation lacking a null hypothesis as I posted before.

The very first sentence of your quote gives you a brief rundown of a hypothesis test. The null hypothesis is that ERVs in different genomes inserted independently. Given what we know about retroviral insertions, we can assign a p-value on the order of 10[sup]-9[/sup] to two retroviruses independently inserting in the same place in two vertebrate-sized genomes*. Taking the low probability of fixation into account, the p-value is even smaller. A p-value of <10[sup]-9[/sup] is good reason to reject the null by anyone's standards, and that's just one pair of matching ERVs in orthologous locations.

Now, compare that to the alternative given by the above text: common ancestry. If the two ERVs were derived from a single insertion in a common ancestor, the probability of seeing them in orthologous locations is close to 1**.

*A p-value being the probability of observing a given set of data IF the null is correct.

**Not quite 1, because you could technically have one or more of the copies retro-jump somewhere else and be deleted from the original insertion site.

 

[Zaius137]

Loudmouth&#8230;


&#8220;As to fixation rates, they fit just fine as show in this paper. The authors found that there are 113 human specific HERV-K insertions with 8 of them being polymorphic (i.e. not fixed). They plugged these values into their population models and these are the results:&#8221;

&#8220;If the HERV-K(HML2) family is still active and producing new copies at present, we expect to find elements that have inserted recently and are present in only a proportion of the human population. The actual number of insertionally polymorphic elements that we would expect, assuming the scenario of present-day activity, can be determined by using standard population genetic models.&#8221;


I really need to point out how bad the assumptions are in this article. They use a constant population (Ne) of 10,000. That number is highly controversial number and its range varies in estimates of at least 20x by evolutionists. If this is current infection with a current infective agent then we can use current populations. You must use the real figures within 10,000 years and the stable population is 4 million. http://en.wikipedia.org/wiki/Population_growth#Human_population_growth_rate

Also to date there is no evidence of the HERV-K retro virus infecting humans. As all these models prove is that evolutionists can never fit the evidence without extraordinary exaggeration.

 

[Zaius137]

By the way thanks for the thoughtful consideration. I endeavor to be as considerate.

 

[Zaius137]

Reply to Naraoia..


&#8220;As far as I can tell, Alu elements are copied pieces of host DNA that hijack other retrotransposons' machinery to jump. Nothing to do with viruses, endogenous or otherwise.&#8221;

I think you win this point. I can&#8217;t locate where I dredged up this one.

&#8220;The very first sentence of your quote gives you a brief rundown of a hypothesis test. The null hypothesis is that ERVs in different genomes inserted independently. Given what we know about retroviral insertions, we can assign a p-value on the order of 10-9 to two retroviruses independently inserting in the same place in two vertebrate-sized genomes*. Taking the low probability of fixation into account, the p-value is even smaller. A p-value of <10-9 is good reason to reject the null by anyone's standards, and that's just one pair of matching ERVs in orthologous locations.&#8221;

Aside from what ReMine postulated:

&#8220;Using the neutralist approach, ReMine shows that, in 10 million years, a human-like species could substitute no more than 25,000 expressed neutral mutations and this is merely 0.0007 per cent of the genome &#8212; nowhere near enough to account for human evolution. This, ReMine says, is the trade secret of evolutionary geneticists. Evolutionary genetics textbooks avoid mentioning the problem&#8221;.

My Null hypothesis would not include common decent but creationism.


http://creation.com/images/pdfs/tj/j11_3/j11_3_292-298.pdf

 

[Loudmouth]

I really need to point out how bad the assumptions are in this article. They use a constant population (Ne) of 10,000.

No, they use an effective population size of 10,000. This does not mean that the actual population size is 10,000. Rather, this is the population size once inbreeding and temporal variation are considered. The effective population size will always be smaller than the actual population size for most models (if I understand it correctly, sfs can correct me if I am wrong).

You must use the real figures within 10,000 years and the stable population is 4 million.

Why? What is wrong with using the effective population size?

Also to date there is no evidence of the HERV-K retro virus infecting humans.

113 human specific HERV-K insertions are the evidence.

As all these models prove is that evolutionists can never fit the evidence without extraordinary exaggeration.

Why aren't you leveling the same criticisms at Remine? He also uses assumptions.

Added in edit: More information on human effective population sizes

This abstract states that the effective human population size was ~18,000 over the last 2 million years using Alu insertions:

There are estimated to be ~1000 members of the Ya5 Alu subfamily of retroposons in humans. This subfamily has a distribution restricted to humans, with a few copies in gorillas and chimpanzees. Fifty-seven Ya5 elements were previously cloned from a HeLa-derived randomly sheared total genomic library, sequenced, and screened for polymorphism in a panel of 120 unrelated humans. Forty-four of the 57 cloned Alu repeats were monomorphic in the sample and 13 Alu repeats were dimorphic for insertion presence/absence. The observed distribution of sample frequencies of the 13 dimorphic elements is consistent with the theoretical expectation for elements ascertained in a single diploid cell line. Coalescence theory is used to compute expected total pedigree branch lengths for monomorphic and dimorphic elements, leading to an estimate of human effective population size of ~18,000 during the last one to two million years
Alu Evolution in Human Populations: Using the Coalescent to Estimate Effective Population Size

​

This paper calculates ~3,000 to ~7,500 effective population size based on SNP's from the HapMap project (which comes from modern populations):

Phase I of the HapMap project produced between 18 and 22 million SNP pairs in samples from four populations: Yoruba from Ibadan (YRI), Nigeria; Japanese from Tokyo (JPT); Han Chinese from Beijing (HCB); and residents from Utah with ancestry from northern and western Europe (CEU). For CEU, JPT, and HCB, the estimate of effective population size, adjusted for SNP ascertainment bias, was &#8764;3100, whereas the estimate for the YRI was &#8764;7500, consistent with the out-of-Africa theory of ancestral human population expansion and concurrent bottlenecks.
Recent human effective population size estimated from linkage disequilibrium
​

Here is a good resource into what goes into calculating the Ne:
Lect. 7. Eff. pop. size, Ne

 

[Loudmouth]

Aside from what ReMine postulated:

“Using the neutralist approach, ReMine shows that, in 10 million years, a human-like species could substitute no more than 25,000 expressed neutral mutations and this is merely 0.0007 per cent of the genome — nowhere near enough to account for human evolution. This, ReMine says, is the trade secret of evolutionary geneticists. Evolutionary genetics textbooks avoid mentioning the problem”.

Can you please cite the peer reviewed paper that contains this information?

My Null hypothesis would not include common decent but creationism.

First, it is descent with an s, although our ancestor may have been decent fellows.

Secondly, can you please tell us why the proposed null hypothesis is not viable?

Thirdly, how do you include creationism in the hypothesis? What observations with regards to ERV's would falsify creationism? Please be specific and spell out the mechanisms that allow you to make these predictions.