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New information, Genetic entropy and Junk DNA blablabla

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New information, Genetic entropy and Junk DNA blablabla
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Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post New information, Genetic entropy and Junk DNA blablabla

I have come in contact with a creationist youtuber Standing For Truth (SfT) and he wants to have a talk with me and others in the near future, although I have yet to get a response from him to know exactly when he wants to talk. I have listened to him multiple conversations with people like Jackson Wheat, Crispr and Scientist Sam and I can summarise his tactic of discourse as such:
JAQing off (short for "Just-asking-questions")
It’s a way to phrase claims as questions in such a way that completely disregards the answers that could be given and is only intended to influence the views of spectators. For example, if an 9/11 truther asks questions about how you can explain their perceived evidence of a controlled demolition, it implies that IF you or someone else is unable to answer the question on the spot then they are seemingly winning the point automatically, hence it WAS evidence of a controlled demolition. It’s a clever way to shift the burden of proof. So SfT often asks questions with claims and assertion hidden within them. That's one thing to watch out for. SfT also employs changing topic constantly by asking new questions immediately after previous one is answers and once he is pinned into a corner (the opponent won't let him change the subject), he apparently begins to freak out and starts spouting a string of nonsense all at once just to flabbergast the opponent and distract them with this steaming pile of BS. A discussion with him would be quite some experience. And I believe that his tactic would work more effectively with people who aren’t prepared to answer his loaded/leading questions, so here I have prepared some answers/rebuttals to his questions/assertions.

One of his main talking points is new genetic information, in which he seems to define as “new functional DNA popping out of nothing”. Note the “out of nothing” caveat. It doesn’t matter if you have a completely new gene forming from non-coding DNA which previously didn’t do anything, it doesn’t count as new information since the template was already there. Of course, Evolution doesn’t entail nor require that things pop out of thing air. Evolution is more like tinkering. Rather than inventing new things it uses old stuff and modifies it to make the new. A good example of this is the GPCR (G-coupled Protein receptors) superfamily. They bind to molecules outside the cell and when that happens they activate an internal signal transduction pathway. It is an extremely fast way for cells to respond to external stimuli. The first GPCR got duplicated, and the duplicated version got duplicated in turn, and so forth, creating this protein super family.
Image
Each duplicated version was slightly modified such that they would react to different molecules. This produced a wide variety of different GPCRs with completely different functions in many systems. There are those that bind to hormones, regulate the immune system and inflammation, some are involved in our sense of smell and taste because they bind to flavour and odour molecules. Some GPCRs even got modified such that they could react to light and are now the opsins in the rod cells of our eyes. It's rather odd that creationists are asking us to show new information, i.e. show how DNA can pop into existence from nothing.
That’s the creationists view, God making things from nothing. So they should be asking this question to themselves, not us.
It also shows that they have this conception that these biological systems just HAD to come from nothing. They couldn't have evolved gradually by slight modification of existing systems, but the example above is just one example that completely discredits this notion.

The second talking point of his is the idea of genetic entropy. SfT thinks that the genome is somehow under influence of the second law of thermodynamics so it should break down over time, even though the genome is part of an open system and it doesn’t have anything to do with the “order” of a system. Thermodynamic entropy has to do with the amount of energy that is able to do work. This doesn't apply to the "order" or "disorder" of DNA.

The man behind genetic entropy is John Sanford, who is the scientist that co-invented the gene gun, which makes him a respectable scientists in the field of plant genetics. Though, that doesn’t mean all of his ideas are respectable. There are many scientists with ground breaking ideas like Lynn Margulis (Carl Sagan’s first wive) who proposed endosymbiosis, but she was also an HIV denials and 9/11 truther. Likewise Sanford has also some wacky ideas that aren’t supported, like genetic entropy. Sanford claims that genomes are deteriorating over time. This is because in every individual of every generation, there are numerous small deleterious mutations, a good fraction of which have almost no influence on fitness such that selection is ineffective to weed them out. Thus these small harmful mutations will accumulate due to genetic drift, generation by generation. This would inevitably deteriorate the genome over time and populations could never increase in fitness. They will always decrease in fitness. You might think “what about beneficial mutations? Wouldn't they cause an increase in fitness and counter act this "genetic entropy"?” Well, John Sanford simply dismisses the influence of of beneficial mutations, because he thinks that they are too rare and practically all of them are also effectively invisible to selection. He also claims that because of this, beneficial mutations cannot play the role in evolution according to the scientific consensus. More on that later.

One of the things that discredits genetic entropy is by pointing out that most mutations are completely neutral since most stretches of the genome is non-functional. But then, of course, SfT brings up ENCODE to claim that 80% of the human is functional and not junk DNA. However, most of the human genome is actually not functional (don’t have any effect on phenotype or fitness). SciShow did a recent video on this:

ENCODE defined “functional” as any region of DNA that interacted with a binding protein of some sort. It doesn’t matter if anything else happened. If something sticked to the DNA, the DNA is functional according to that ENCODE paper. It’s like (as Jackson Wheat put it) saying that a piece of gum on the ground is functional to your shoe because it can stick to the bottom of your shoe. The genome is a large molecular chain(s) of four different monomers. Simply by change, there would be large sections of DNA that are very similar to protein binding sites. Not entirely identical but similar enough such that proteins will occasionally bind to them and nothing else happens. And when we actually define functional as “DNA that has an effect on fitness or at least the phenotype of the organism” which is more reasonable and useful, we see that the majority of our genome is not functional. But whenever someone explains this SfT he begins to assert that we just assume that the DNA doesn’t have any function simply because we don’t know what it does. That’s not true, we can look at the DNA tell what they do and determine whether they do anything, and we have for most of the genome.

In the functional category we have:
Functional parts of protein coding genes, non-coding RNAs, regulatory sequences, SARs, Origins of replication, centromeres, telomeres, and conserved sequences of unknown function is about 8.7% (essential/functional). Non-functional includes transposable elements, viral DNA, pseudogenes and introns is about 65% (non-functional Junk). The remaining 26.3% is non-conserved intergenic regions of unknown function (probably mostly junk too).

Note: There are very few exceptions such as co-opted viral or pseudo genes that have acquired a new function secondarily, but these are just a fraction of a percentage of all these categories. Creationists will often jump on these exceptions which only account for less than 0.0001% of the genome and use that to claim that the entire genome is functional, which is like cherry picking one cherry on a tree and then claiming that the entire tree is edible. And there are also fractions of a percentage on the functional categories that are actually non-functional, so these small differences won’t change these overall percentages.

So 65% is KNOWN to be non-functional, but we can actually determine how much is likely to be non-functional by other means. There is this thing called genetic load, which sounds similar to the idea of genetic entropy but it is different. It’s real for one thing. The principle behind this is the fact that a population can only tolerate a finite number of deleterious mutations. And it is not like if we went beyond this limit, we would slowly deteriorate (even while increasing our population size) like according to genetic entropy. No, the population couldn’t increase in or maintain its size. We would go into extinction much quicker if we only had four couples (each man related to the same father), like with Noah’s family, because there there is almost nothing that increases the genetic load MORE than incestious inbreeding. But somehow, genetic entropy doesn’t apply with Noah’s family allowing them to produce thousands of offspring in a few generations without deteriorating because….reasons. Anyway..... a paper by Dan Graur published in genome biology and evolution shows how he calculated that we can only have 25% of our genome to be functional at the upper limit. But even this is absurdly generous. A more reasonable value is 10-15%, which is roughly correspond to the previous figure of 8.7% that is known to be functional. Remember, if it was functional over this limit, we would’ve dwindled into extinction a long time ago. Simply of this reason, most of our mutations would be within non-functional regions of the genome and be entirely neutral.

So what more does John Sanford use to support genetic entropy. He often cites various scientists like Michael Lynch and James F. Crow who supposedly all agree that the human genome (or any genome in general) is deteriorating (just like Sanford does):
J. Sanford wrote:“Subsequently, they realise that genetic information is currently being lost, which must eventually result in reduced fitness of our species. This decline unfitness is believed to be occurring at 1-2% per generation (Crow 1997)”
“The most definitive findings were published in 2010 in the Proceedings of the National Academy of Science by Lynch. That paper indicates human fitness is declining at 3–5% per generation.”

However, Sanford is misrepresenting the views of these scientists. Crow, Lynch and other scientists who are similarly quoted by Sanford are concerned with what is called “Relaxed natural selection”. In order for natural selection to fully operate, populations must produce lots of offspring only some of which would survive and reproduce. But when there are only few offspring per individual and each offspring is kept alive through artificial means, there is little opportunity for deleterious mutations to be purged or beneficial mutation to be rewarded and the fitness of the population declines for this reason. When we observe populations with large individuals and differential reproduction, fitness holds up just fine due to selection having full effect. But when selection is shut down, fitness and genomes deteriorate. And this is what Lynch and Crow are publishing about regarding human populations in industrialised societies which have few offspring per family and each offspring largely being kept alive by medial intervention.
James F. Crow wrote:“However efficient natural selection was in eliminating harmful mutations in the past, it is no longer so in much of the world. In the wealthy nations, natural selection for differential mortality is greatly reduced. A newborn infant now has a large probability of surviving past the reproducing years. There are fertility differences, to be sure, but they are clearly not distributed in such a way as to eliminate mutations efficiently. Except for pre-natal mortality, natural selection for effective mutation removal has been greatly reduced.”

Michael Lynch wrote:“the mean phenotypes of the residents of industrialised nations are likely to be rather different in just two or three centuries, with significant incapacitation at the morphological, physiological, and neurobiological levels. Ironically, the genetic future of mankind may reside predominantly in the gene pools of the least industrialised segments of society.”

But this doesn’t support Sanford’s claims. Sanford is specifically claiming that even natural selection cannot prevent genetic entropy. Obviously, the work of Lynch and Crow specifically apply to situations without natural selection, but the way Sanford cites these scientists is grossly misleading, such that it sounds like they are saying that the human genome is deteriorating regardless of selection. And there are other researches that shows evidence against the notion that humans are deteriorating due to a lack of selection, which is obviously ignored by Sanford and his ilk.

Sanford also likes to cite his own adapted figure for the frequency distribution of mutations and their effect on fitness from the 1979 paper of Motoo Kimura, here below, to argue for why beneficial mutations are too rare and too low impact to be selected for and counter genetic entropy
Image
Here is the figure of the original article, figure 1.
Image
His “adapted” figure is fudged in a subtle way. The “no selection zone” is significantly enlarged in his graph, as sanford boundary is closer to the -0.001 mark while the original is closer to the 0.00 mark. There is also the fact that the original doesn’t show anything on the positive (beneficial mutation) side of the fitness scale, while Sanford has added a tiny curve on the right to represent the beneficial mutations, which are apparently infrequent and always inside the “no selection zone”, just as he claims. If John presented this figure as his own speculative hypothesis, to illustrate his ideas, it would be fine. But no, he claimed that this tiny curve also represent what Kimura would have put in for beneficial mutations:
Sanford wrote:“In Kimura’s figure, he does not show any mutations to the right of zero – i.e. there are zero beneficial mutations shown. He obviously considered beneficial mutations so rare as to be outside of consideration.”
“So selection could never favor any such beneficial mutations, and they would essentially all drift out of the population. No wonder that Kimura preferred not to represent the distribution of the favorable mutations!”
"Kimura does not show the beneficial distribution, which is essential to the question of net gain versus net loss! When I show the beneficial distribution (while Kimura did not do this, I suspect he would have drawn it much as I did), anyone can see the problem: the vast majority of beneficial mutations will be un-selectable"

But what does Kimura actually say in the article?
Well….
Motoo Kimura wrote:“Note that in this formulation, we disregard beneficial mutants, and restrict our consideration only to deleterious and neutral mutations. Admittedly, this is an oversimplification, but as I shal show later, a model assuming that beneficial mutations also arise at a constant rate independent of environmental changes leads to unrealistic results.”
“Under the present model, effectively neutral, but, in fact, very slightly deleterious mutants accumulate continuously in every species. The selective disadvantage of such mutant (in terms of an individual’s survival and reproduction - i.e., in Darwinian fitness) is likely to be of the order of 10^-5 or less, but with 10^4 loci per genome coding for various proteins and each accumulating the mutants at the rate of 10^-6 per generation, the rate of loss of fitness per generation may amount to 10^-7 per generation. Whether such a small rate of deterioration in fitness constitutes a threat to the survival and welfare of the species (not to the individual) is a moot point, but this can easily be taken care of by adaptive gene substitutions that must occur from time to time, say once every few hundred generations.”

Thus Kimura actually believed that there would be selectable beneficial mutations that compensate for the accumulation of deleterious mutations. So if he did draw a line for beneficial mutations, the curve would extend beyond the non selection zone. The reason why Kimura omitted beneficial mutations in his figure is that, in his primitive mathematical model, the presence of any beneficial mutation would make it blow up, i.e. he omitted them NOT because (as Sanford claims) Kimura believe they were negligible, but because their effect was too strong. (See citations: 11 and 12)
So what does Sanford have left to speak about? Are there laboratory experiments with populations that show clear genetic entropy (regardless of selection)?

John Sanford wrote:“It is true that most lab experiments do not show clear degeneration. But Scott should realize that anything alive today must have been degenerating slowly enough to still be here, even in a young earth scenario. All three of the downward decay curves I show in my book indicate that degeneration slows dramatically as it becomes more advanced. If a species is alive today and has been around for thousands of years, the rate of degeneration must be very slow (too subtle to measure in most cases). Obviously, genetic degeneration is not going to be clearly visible in most lab experiments.”

The answer seems to be “no” at least not most experiments. But we do have an interesting caveat here. Genomes are relentlessly deteriorating, yet at the same time it is happening so slowly that we cannot detect it? Notice that the “slowness” of entropy is added just to explain away how species could have survived thousands of years of genetic entropy (especially considering that they all started from just an incestious gene pool right after the flood 4000 years ago). Trying to have your cake and eat it too it seems. About the “downward decay curves” that he cites in his book, I have no better response to this than Dr. Scott Buchanan.
Scott Buchanan wrote:"The claim here is that genomes are relentlessly deteriorating, but we cannot detect it. I’m sure that genetics simulation programs can be adjusted to show that the fitness of all sorts of organisms, from bacteria to elephants, starting from some idealized mutation-free state, could fall dramatically from 4000 B.C to say around 500 B.C., then almost level out. I do not find that compelling support for genetic entropy."

In his book (fourth edition), Sanford makes an attempt to support his claims with actual data (emphasis on "attempt"). He compared his figure 14 (results of Sanford’s mendel’s accountant algorithm, that models his genetic entropy, showing a fitness decline over time) and compares it to figure 15, the data of is comes from influenza viruses from the paper by Simonsen et al a rare example of Sanford referencing to real world data. He presents that figure as - “Actual biological data, showing mutation accumulation and fitness decline in human influenza virus”.
John Sanford wrote:“This graph illustrates the pathogenicity (i.e., fitness) of the H1N1 strain, as well as the other two pandemic-causing strains during the last century.”

But this is, just like with the Kimura figure, completely misrepresenting the original figure 1 from Simonsen et al. That figure doesn’t quantify pathogenicity nor fitness like Sanford is claiming. As Gerard Jellison said in his review on Amazon:
Gerard Jellison wrote:“…the figure shows a ratio: the number of influenza-caused deaths of people under 65, divided by the total number of deaths. The point of the paper is that the flu epidemic of 1918-1919 was unusual in that it killed mostly young people. The authors studied how this ratio varied with time, and modeled the results in terms of different immunity in the two age cohorts. Thus, the curves in Sanford’s plot merely show that, as time goes on, flu strains kill a greater proportion of elderly people. This makes sense, since young people have more vigorous immune systems [….] Sanford’s Figure 15 is invalid, since it does not illustrate declining viral “fitness” at all. This blunder is an absurd misuse and/or misunderstanding of scientific data.”


To make matters even worse for Sanford, there are experimental data that actually disproves the idea of genetic entropy. The most famous one is the long Long Term Evolution Experiment by Lenski et al. wherein in one paper they show that even after 50.000 generations, all 12 separate populations still increased in fitness relative to their ancestors following a power law model. This shows that surprisingly fitness can increase indefinitely (or at least for a very long time) even in a constant environment. This flies completely in the face of genetic entropy which says that populations must always decline in fitness over time. In other studies, they also show that beneficial mutations with the same effect occur independently in different populations. (see citations 15 and 16) So these beneficial mutations aren’t too rare nor are they invisible to selection. And of course, the most famous beneficial mutation of the LTEE experiment led to a completely new phenotype in one of the 12 populations. The ability to utilise citrate when oxygen is present.

Now creationist like SfT like to downplay the significance behind this mutations by claiming that it already could digest citrate so it is not “new information” and sometimes go as far to claim that it is actually a decrease in information (SfT specifically said it is a loss of "control") since it now lost its specificity to express these genes only when no oxygen is present. Now it is "unspecific" or "uncontrolled" such that the genes are active all the time. But that is all wrong. The ability to digest citrate under aerobic conditions wasn’t present before, so the phenotype is NEW by any reasonable definition of what count as new. It is also not the case that genetic information was lost since the mutation that was responsible for this new phenotype was a duplication. Well, now you can already hear the creationists yelling “duplications aren’t new information!!!”, but this duplication DID create something new, see diagram here below
Image
Picture from this
The section that was duplicated included the CitT (the gene which produces a membrane transporter that allows citrate into the cell) at one end and the RNK promotor (which expresses the RNK gene when oxygen is present). The duplication was tandem, meaning the duplicated section was directly put next to the original section. This ended up with a duplicated CitT gene being controlled under a duplicated RNK promotor. Notice that the original genes are still there and still being controlled by the same promoters. There is still a CitT gene controlled by a promoter that is activated when no oxygen is present and there is still an RNK gene controlled by a promoter that activates when oxygen is present. Hence NOTHING WAS LOST. What was gained was a novel regulatory module.

First you had these regulatory modules:
1. Promotor (activate when no oxygen is present) —> CitT
2. Promotor (activate when oxygen is present) —> RNK

After the duplication, you have:
1. Promotor (activate when no oxygen is present) —> CitT
2. Promotor (activate when oxygen is present) —> RNK

3. promotor (activate when oxygen is present) —> CitT
It’s an novel (new) module. No specificity was lost, no loss of control. Control and specificity was gained at the molecular level and a novelty was gained at the phenotype level.

Now I am done. I think that this pretty much shows that Genetic Entropy is complete bollocks as well as other talking points of creationists like “there is no junk DNA” and “no new information”. The sum of the sources are here below.

SOURCES:
1. Stevens, Raymond C., et al. "The GPCR Network: a large-scale collaboration to determine human GPCR structure and function." Nature reviews Drug discovery 12.1 (2013): 25.
2. Sandwalk: What's In Your Genome? - The Pie Chart
3. Sandwalk: Theme: Genomes & Junk DNA
4. Graur, Dan. "An upper limit on the functional fraction of the human genome." Genome biology and evolution 9.7 (2017): 1880-1885.
5. http://sandwalk.blogspot.com/2017/07/revisiting-genetic-load-argument-with.html
6. http://sandwalk.blogspot.com/2009/11/genetic-load-neutral-theory-and-junk.html
7. Rands, Chris M., et al. "8.2% of the human genome is constrained: variation in rates of turnover across functional element classes in the human lineage." PLoS genetics 10.7 (2014): e1004525.
8. Dr. Scott Buchanan "Letters to creationists" Junk_DNA_Design
9. Crow, James F. "The high spontaneous mutation rate: is it a health risk?." Proceedings of the National Academy of Sciences 94.16 (1997): 8380-8386.
10. Lynch, Michael. "Rate, molecular spectrum, and consequences of human mutation." Proceedings of the National Academy of Sciences 107.3 (2010): 961-968.
11. Dr. Scott Buchanan "Letters to creationists" Gen_Entropy
12. Gerard Jellison - Amazon Customer Review for the book "Genetic Entropy" by J. Sanford
13. Simonsen, Lone, et al. "Pandemic versus epidemic influenza mortality: a pattern of changing age distribution." Journal of infectious diseases 178.1 (1998): 53-60.
14. Lenski, Richard E., et al. "Sustained fitness gains and variability in fitness trajectories in the long-term evolution experiment with Escherichia coli." Proc. R. Soc. B 282.1821 (2015): 20152292.
15. Cooper, Tim F., Daniel E. Rozen, and Richard E. Lenski. "Parallel changes in gene expression after 20,000 generations of evolution in Escherichia coli." Proceedings of the National Academy of Sciences 100.3 (2003): 1072-1077.
16. Cooper, Tim F., et al. "Expression profiles reveal parallel evolution of epistatic interactions involving the CRP regulon in Escherichia coli." PLoS Genetics 4.2 (2008): e35.
17. Blount, Zachary D., et al. "Genomic analysis of a key innovation in an experimental Escherichia coli population." Nature 489.7417 (2012): 513.
18. A Duplication Mutation and a New Arrangement: E.coli Cit+ phenotype
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Last edited by Nesslig20 on Mon Jan 07, 2019 12:32 pm, edited 11 times in total.
Sat Sep 29, 2018 11:05 pm
RumraketUser avatarPosts: 1263Joined: Fri Jun 25, 2010 7:49 am Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Outstanding post Nesslig.
"Nullius in verba" - Take nobody's word for it. https://en.wikipedia.org/wiki/Nullius_in_verba
Extraordinary claims require extraordinary evidence.
Sun Sep 30, 2018 12:27 am
RumraketUser avatarPosts: 1263Joined: Fri Jun 25, 2010 7:49 am Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Nesslig20 wrote:To make matters even worse for Sanford, there are experimental data that actually disproves the idea of genetic entropy. The most famous one is the long Long Term Evolution Experiment by Lenski et al. wherein in [url]one paper they show that even after 50.000 generations, all 12 separate populations still increased in fitness relative to their ancestors following a power law model.[/url] This shows that surprisingly fitness can increase indefinitely (or at least for a very long time) even in a constant environment. This flies completely in the face of genetic entropy which says that populations must always decline in fitness over time.

Heh, this is also a point I've raised before to Sanford and his fans. You will find his response hilarious, paraphrasing: The ratio of beneficial to deleterious mutations in the particular species of bacteria used in the experiment under the unique experimental conditions, is different from humans and lots of other organisms where genetic entropy must be the case in the wild.

That's it, that's essentially his response. So basically he will just respond to evidence that contradicts his claim with special pleading.

So if you show evidence of fitness increase in experiments, he will just say this is consistent with a model where fitness can increase in response to selection in the particular species used and with the particular experimental environment(and then he'll try to deflect by pointing out that many of the mutations are "loss of function" mutations)*, but that his genetic entropy claims are still true for everything else in the wild.

So we have to basically prove him wrong with experiments for all 10 million species on Earth in conditions that are pretty much exactly equal to whatever it is in the wild, or he's going to keep claiming genetic entropy must be the case for everything. Essentially he's saying "here's how everything is in my view, prove me wrong". Not understanding that it's HIS job to prove his claims right. :roll:

* This one is his get-out-of-jail-free card. He operates with two significantly different senses of genetic entropy in mind, and will casually switch back and forth between them as he sees fit. In the one sense he will argue that
1. Genetic entropy means there are too many deleterious mutations for selection to ever be capable of countering their cumulative effects, and
2. In the other sense he will say that loss of function mutations (or even just nucleotide deletions) are also examples of genetic entropy, even if they have positive fitness effects. That way he has basically defined his position in very specious fashion so he will always be able to argue that what we're seeing is "genetic entropy". That's what he does in response to the LTEE, because the majority of the beneficial mutations in the experiment were either loss of function mutations or deletions.

It is extremely dishonest.
"Nullius in verba" - Take nobody's word for it. https://en.wikipedia.org/wiki/Nullius_in_verba
Extraordinary claims require extraordinary evidence.
Sun Sep 30, 2018 12:45 am
Dragan GlasContributorUser avatarPosts: 3214Joined: Mon Dec 14, 2009 1:55 amLocation: Ireland Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Greetings,

I agree with Rumraket:, excellent post, Nesslig.

Given Sanford's claim regarding deleterious and beneficial mutations being "invisible" to evolution, this would place them in the "neutral' category. Of course, his claim that beneficial mutations are rare in comparison with deleterious ones, allows him to claim his idea is right. However, since he hasn't provided any positive evidence for this claim of genetic entropy, his claim can be held as unproven, if not dismissed outright as wrong.

Regarding Lynch's paper, and its misinterpretation/misrepresentation, this was used before in the Onceforgivennowfree thread.

Dandan had cited it - having first attempted to get me to agree that, if he could provide scientific evidence of his claim that deleterious mutations were more frequent than beneficial ones, would I admit I was wrong?

I initially dealt with it here - Inferno's two subsequent replies also dealt extensively with it. Aron and HWIN also addressed it - and DutchLiam pointed out that dandan's definition of "real science" was whatever he thought agreed with his own worldview, which may be what Sanford is doing!?

When it was pointed out by Inferno that dandan hadn't understood his own paper, and asked by myself if he'd read the three I cited in response, he admitted to not having read any of them.

I - along with others - attempted to point out that he'd failed to prove his claim here, and all he could do was complain that we weren't using his definition of "information" (Dembski's).

If you read that part of the discussion from the first post to which I linked, you'll get a good sense of what the problem is, along with some good information/answers from those taking part in the discussion.

Kindest regards,

James
Image
"The Word of God is the Creation we behold and it is in this Word, which no human invention can counterfeit or alter, that God speaketh universally to man."
The Age Of Reason
Sun Sep 30, 2018 1:28 pm
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

So, yesterday I had a conversation with Crispr Cas9 about what I wrote here to check my mistakes. A few hours later Standing for Truth had his conversation with Immutable Destiny.

The conversation starts at 26:16


Standing for Truth then left a commont on my hangout, so I will respond here.


Standing For Truth wrote:Here's what I stated in my discussion tonight with Immutable Destiny and Crispr, and I will say it again. We know AND agree that genomes of several organisms have been sequenced. We also know and hopefully agree that only a small portion of the human genome is used to code for proteins. And so here is the question: what does the remaining “non-coding” DNA do?
If you would read my previous comment, you'll see that I already answered this question.
I wrote:In the functional category we have: Functional parts of protein coding genes, non-coding RNAs, regulatory sequences, SARs, Origins of replication, centromeres, telomeres, and conserved sequences of unknown function is about 8.7% (essential/functional). Non-functional includes transposable elements, viral DNA, pseudogenes and introns is about 65% (non-functional Junk). The remaining 26.3% is non-conserved intergenic regions of unknown function (probably mostly junk too).
Note: There are very few exceptions such as co-opted viral or pseudo genes that have acquired a new function secondarily, but these are just a fraction of a percentage of all these categories. Creationists will often jump on these exceptions which only account for less than 0.0001% of the genome and use that to claim that the entire genome is functional, which is like cherry picking one cherry on a tree and then claiming that the entire tree is edible. And there are also fractions of a percentage on the functional categories that are actually non-functional, so these small differences won’t change these overall percentages.
So 65% is KNOWN to be non-functional...
About 1.0-1.8 % is protein coding DNA, which is part of the larger 8.7% portion that contains non-coding RNA's, regulatory sequences, etc. So we know that there are "non-coding" DNA that do have function (nobody is saying that all non-coding DNA is non functional), but these still amount to just 8.7%. 65% is KNOWN to be non-functional, and the remaining 26.3% is largely unknown. And as the paper by Dan Graur) shows, the genome can only be (at the upper limit) 25% functional, otherwise we would've gone extinct due to genetic load a long time ago. And that is still being very generous. It's most likely just 10-15% functional.


Standing For Truth wrote:I think it's quite evident that evolutionists have assumed and stated that it was inactive, redundant, or left over from the evolutionary process.
That's complete nonsense and a blatant straw man. No scientist has said that all non-coding DNA was non-functional. Junk DNA was never used as a synonym for non-coding DNA.


Standing For Truth wrote:I have also stated many times that based on pre-existing heterozygosity and built in designed variation or built in genetic algorithms, some genes are activated by environmental conditions and not typically expressed. This is evidence of the handiwork of our Creator.
First, you are starting with an assumed conclusion, i.e. there is "build in designed variation or built in genetic algorithms", and then you conclude with your assumed conclusion, i.e. "This is evidence of the handiwork of our creator".That's called Circular Reasoning. You are already beginning with the assumption that there is design to argue for design. That's not evidence at all, except for your poor reasoning skills. Also, how can anything be evidence of a magical man's handiwork? Think about it. God can do literally anything for any reason, meaning there is no possible scenario were we can say "Oh, this wasn't the handiwork of God". This means that God is an unfalsifiable hypothesis, and something that is unfalsifiable can't make specific prediction. Thus, saying that something is evidence for God is utterly meaningless since ANYTHING can be evidence for God by simply stating "That's just how god Didit". That doesn't mean you can't believe that there is a god or that there isn't a god or that god didn't do anything, it's just means that we cannot have evidence for it.


Standing For Truth wrote:I also ask how scientists perform experiments to conclude what functions some genes may have. The answer is that they do "knock-out" experiments. What does this mean? Well, simply put, it means that sections of DNA are removed from the genome of an organism to see what effect its removal will have. This will help us determine what sections of our DNA are doing, specifically in the non protein coding regions. Now here's what's MOST important: We know that extensive knock-out experiments for a mammal have yet to be performed, so it is premature and arrogant to make the claim that the majority of non-coding DNA is non-functional (“junk”).
Now your are doing in the same that John Sanford is doing as Rumraket was describing in a previous post:
Rumraket wrote:So if you show evidence of fitness increase in experiments, he will just say this is consistent with a model where fitness can increase in response to selection in the particular species used and with the particular experimental environment(and then he'll try to deflect by pointing out that many of the mutations are "loss of function" mutations)*, but that his genetic entropy claims are still true for everything else in the wild. So we have to basically prove him wrong with experiments for all 10 million species on Earth in conditions that are pretty much exactly equal to whatever it is in the wild, or he's going to keep claiming genetic entropy must be the case for everything. Essentially he's saying "here's how everything is in my view, prove me wrong". Not understanding that it's HIS job to prove his claims right. :roll:
In response to the overwhelming evidence for the majority (75% at the upper limit) of of the human genome to be non-functional, now you are saying that you wouldn't be convinced that this is the cause UNLESS we do knock out experiments that covers a significant portion of mammalian genomes, completely disregarding other experiments that would demonstrate the same thing. This is an absurd demand to falsify your claim, which was probably the point since you don't want to be proven wrong. There are other means to determine functionality/non-functionality than just knock out experiments. For example, the majority (44%) of our genome consists of transposable elements: transposons, retrotransposons (SINES and LINES). These are easily recognisable and we know what they do, they just jump around the genome or they make copies of themselves. That's it. Most of these are just broken fragments of complete (active) transposable elements. A fraction are active, but they simply jump around. Occasionally, like <0.01%, a (fraction of a) transposable element is evolutionarily co-opted for a new purpose, like in the evolution of adaptive immune systems.
Image
But this doesn't support your assertions, because (1) coopted TE's consists of just a fraction of a percentage of the transposable elements and (2) it supports the evolutionary origins of these complex biological systems.


Standing For Truth wrote:Now in regards to the ENCODE project that is being talked about in this hangout, the ENCODE project examined 1% of the non-coding DNA of the human genome for possible function. What did they find? They found that at least 80% of the noncoding DNA was transcribed into RNA, SUGGESTING function.
WRONG!! First, you are talking about the ENCODE pilot project that only examined 1% of the non-coding regions. The ENCODE project with that "80% functional" result examined essentially the entire genome. Second, even transcription doesn't suggest function. Random DNA sequences can easily become promotor like with a few mutations, which is a factor that causes spurious transcription. In fact, natural selection has to keep most of our DNA from being promotor like to avoid too much spurious transcription.
There are also many pseudogenes that are transcribed, like the human MYH16 gene, which is a broken primate gene that codes for jaw muscle proteins. It even makes a protein, but it's broken and it doesn't work (It's non functional), which is the reason why our jaw muscles are so pathetic compared to other primates (Rhetorical question: why would we have broken monkey genes?). So even though it is transcribed and even though it is translated, it is still non-functional. Secondly, Encode did not define functional as "anything that is transcribed into RNA". This was their definition of "biochemical function"
The ENCODE Project Consortium, 2012 wrote:Operationally, we define a functional element as a discrete genome segment that encodes a defined product (for example, protein or non-coding RNA) or displays a reproducible biochemical signature (for example, protein binding, or a specific chromatin structure).
Notice that in order to qualify as "functional" it doesn't necessarily have to be transcribed. As PZ Myers noted:
PZ Myers wrote:That isn’t function. That isn’t even close. And it’s a million light years away from “a critical role in controlling how our cells, tissue and organs behave”. All that says is that any one bit of DNA is going to have something bound to it at some point in some cell in the human body, or may even be transcribed. This isn’t just a loose and liberal definition of “function”, it’s an utterly useless one.
And as Jackson Wheat said to you. It's like saying that a piece of gum under your shoe is functional with respect to your shoe, because it sticks to it. And there is good reason to think that the leaders of the ENCODE project deliberately used their misleading usage of "biochemical functional" as a PR stunt to get the attention of the journalists. And unfortunately, they were successful in getting that attention.
Laurence A. Moran wrote:See What did the ENCODE Consortium say in 2012? for more details on what the ENCODE Consortium leaders said, and did, when their papers came out. The bottom line is that these leaders knew exactly what they were doing and why. By saying they have assigned biochemical functions for 80% of the genome they knew that this would be the headline. They knew that journalists and publicists would interpret this to mean the end of junk DNA. Most of ENCODE leaders actually believed it. That's exactly what happened...aided and abetted by the ENCODE Consortium, the journals Nature and Science, and gullible science journalists all over the world.
In other words, don't read too much into this 80% functionality of ENCODE nonsense.


Standing For Truth wrote:It has been found that the non-coding regions of genomes correlate with biological complexity better than the protein coding regions, suggesting that the non-coding regions do indeed carry significant information, probably for regulatory activity.
Eh? I going to need a citation for that one....
EDIT after posting:
Thanks to someone called "Ration alMind" I got the paper that StandingForTruth is referring to. This is what he told me about it.
Ration alMind wrote:he’s referring to the finding of papers like this one by John Mattick, who publishes tirelessly to insist that huge swathes of our genome is functional. While it’s true that this correlation exists, it’s premature to say that this means that most or all of the non-coding regions are functional. For example, it could be that 10% of non-coding DNA is consistently functional, so in order to get an extra 1% functional non-coding DNA you have to increase your non-coding genome size by 10%. This would produce the same correlation. Another glaring gap in this paper and others like it is the failure to consider population dynamics at all. It seems likely that the reason more complex organisms have more non-coding DNA is because more complex organisms (e.g. humans) tend to have smaller population sizes and longer generation times that less complex ones (e.g. bacteria) - this places different pressures on the genome. Bacteria are able to reduce their genome size to the bare minimum to increase efficiency, since their population sizes can handle it. Humans don’t have the same luxury - the selection coefficients to remove non-coding DNA are too low to efficiently remove extraneous sequences, and as you’ve pointed out with Graur’s 2017 paper, we can’t have anywhere close to a 100% functional genome, so a lot of non-coding DNA is needed as a “buffer”.
....and it better be a good one since there are numerous indications that this is completely wrong. For example, another reason for why most of our DNA is most likely non-functional ("junk") (a reason I didn't touch because I thought my post was already overkill) is the cleverly named "onion test". It is named after the observation that among the onion genus (Allium) there are species that have 2 times the amount of DNA that humans, another one has 5 times the amount of DNA and another one has 9 times of the amount.
T. Ryan Gregory wrote:Image
Left, A. altyncolicum (7 pg = 2 times human DNA); centre, A. cepa (17 pg = 5 times human DNA); right, A. ursinum (31.5 pg = 9 times human DNA).
So the question is, if you think that most of the genome is functional and the amount is correlated with biological complexity, then why do some onions have several times more DNA than us? And if you think that onions are actually special, they do require that amount, then what explains this range in genome sizes from 7 pg to 31.5 pg among the species of the onion genus? Especially considering that these species belong to the same genus and are thus very similar to each other. And this conundrum is made even worse when we consider other species. Lungfishes have 40 times more DNA than us. Salamander genomes fall between a range of 4 to 35 times more DNA and some single celled eukaryotes have over 200 times the human genome. One the other extreme end, the puffer fish has almost no "Junk" DNA (transposable elements are rare in Fugu). If "junk DNA" like transposable elements are so important, then how can they survive without it?
Genome Size and “The Onion Test" wrote:There are several key points to be understood regarding genome size diversity among eukaryotes and its relationship to the concept of junk DNA. First, genome size varies enormously among species [18], [19]: at least 7,000-fold among animals and 350-fold even within vertebrates. Second, genome size varies independently of intuitive notions of organism complexity or presumed number of protein-coding genes (Figure 1). For example, a human genome contains eight times more DNA than that of a pufferfish but is 40 times smaller than that of a lungfish. Third, organisms that have very large genomes are not few in number or outliers—for example, of the >200 salamander genomes analyzed thus far, all are between four and 35 times larger than the human genome [18]. Fourth, even closely related species with very similar biological properties and the same ploidy level can differ significantly in genome size.
Image
Figure 1. Summary of haploid nuclear DNA contents (“genome sizes”) for various groups of eukaryotes.
This graph is based on data for about 10,000 species [18], [19]. There is a wide range in genome sizes even among developmentally similar species, and there is no correspondence between genome size and general organism complexity. Humans, which have an average-sized genome for a mammal, are indicated by a star. Note the logarithmic scale.
These observations pose an important challenge to any claim that most eukaryotic DNA is functional at the organism level. This logic is perhaps best illustrated by invoking “the onion test” [20]. The domestic onion, Allium cepa, is a diploid plant (2n = 16) with a haploid genome size of roughly 16 billion base pairs (16 Gbp), or about five times larger than humans. Although any number of species with large genomes could be chosen for such a comparison, the onion test simply asks: if most eukaryotic DNA is functional at the organism level, be it for gene regulation, protection against mutations, maintenance of chromosome structure, or any other such role, then why does an onion require five times more of it than a human? Importantly, the comparison is not restricted to onions versus humans. It could as easily be between pufferfish and lungfish, which differ by ∼350-fold, or members of the genus Allium, which have more than a 4-fold range in genome size that is not the result of polyploidy [21]. In summary, the notion that the majority of eukaryotic noncoding DNA is functional is very difficult to reconcile with the massive diversity in genome size observed among species, including among some closely related taxa. The onion test is merely a restatement of this issue, which has been well known to genome biologists for many decades [18].
The simple answer to all of this is that most of the genome is non-functional.


Standing For Truth wrote:Now why do I say that these regions do play important roles in the placenta and embryo? I talked about this tonight with Immutable Destiny, and therefore, I highly recommend watching it.
I have watched some of it and I am not impressed. For one thing, you presented a quote from Michael Ruse wherein he supposedly said that evolution is a religion. Later at this time stamp 1:00:26 You finally presented your source for this quote...and this is what it says:
Michael Ruse wrote:
Evolution is promoted by its practitioners as more than mere science. Evolution is promulgated as an ideology, a secular religion — a full-fledged alternative to Christianity, with meaning and morality. I am an ardent evolutionist and an ex-Christian, but I must admit that in this one complaint — and Mr. Gish [Duane T. Gish the Creation Scientist] is but one of many to make it — the literalists are absolutely right. Evolution is a religion. This was true of evolution in the beginning, and it is true of evolution still today.
Well, what quote of yours do you want to have on your gravestone?!
I think this paragraph, the introduction to a book review (for which I was never paid) in a Canadian newspaper some 10 or so years ago, has received more attention and more repetition (especially on the Internet) than anything else I have ever written. More even than my claim that morality is an illusion put in place by the genes to make us social animals. No matter that I qualified it then and have qualified it before and ever since. “Ruse recants! Evolution is a religion! Read all about it!” Or more accurately, don’t read all about it, because then you might find that that is not quite all that I had to say.
How can you possibly quote mine someone, while that person is correcting the quote mine right in the next paragraph?. Remember what you said about creationists quote mining Darwin about the evolution of the eye and they ignored the piece he wrote right after? And remember when you were insisting that you aren't doing the same thing? Well, you did something that's even worse. What an embarrassment.


Standing For Truth wrote:But ENCODE did not look at the portions of the genome involved exclusively in development; such DNA would only have function then.The trajectory of discovery favors genome-wide functionality.
What trajectory of discovery? You don't cite any discovery. All you have done is parroting the nonsense of the ENCODE 80% functionality (point refuted a thousand times), and make numerous assertions that are not substantiated by anything and often easily proven to be erroneous.


Standing For Truth wrote:So what does all this mean? And why is this consistent with Biblical Creation and Common Design.
Once again, if you believe in a magical character that can literally do anything, then anything can be consistent with your pet beliefs. Whatever happens is just the way that God did it. This means that there is no meaning behind any of it.


Standing For Truth wrote:We can infer and conclude that non-coding DNA is probably involved in regulatory functions (when and how fast to make specific proteins), embryonic development, the timings of protein manufacture, stagings of proteins for construction of molecular machines, switches, etc. Some non-coding DNA is transcribed into short chain micro-RNA that binds to specific sites in DNA thereby regulating transcription of those sites. Some RNA is involved in the splicing of mRNA before it is translated in the ribosome.
An inference based on nothing is not worthy to be considered.


Standing For Truth wrote:We are just beginning to understand the development process, how coding and non-coding DNA coordinate when, where, and how structures are sequentially put in place to produce a fully functional organism. So all in all, this suggests that our genome is both Poly-functional AND Poly-Constrained. This means that any change no matter how small it is will ultimately be deleterious.
Considering fact that all the evidence that we have examined so far points towards the exact opposite conclusion that you are asserting here. And considering the fact that you are arguing in a circle, starting with an assumed conclusion. This means that all you have said so far is nothing but fallacious and unsupported nonsense or fallacious nonsense already disproved. For the most part, it is the latter.
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Last edited by Nesslig20 on Fri Jan 04, 2019 3:27 pm, edited 14 times in total.
Sun Sep 30, 2018 2:02 pm
SparhafocPosts: 2658Joined: Fri Jun 23, 2017 6:48 am

Post Re: New information, Genetic entropy and Junk DNA blablabla

Rumraket wrote:Outstanding post Nesslig.



High praise. Marking thread to read for when my head consists of more than 3 pounds of disparate mush.
"a reprehensible human being"
Beliefs are, by definition, things we don't know to be true.
Sun Sep 30, 2018 3:32 pm
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

UPDATE: A while back, Standing For Truth and I with a few other people previously named (Sam the scientist, Jackson Wheat, Crispr Cas9 and Ration alMind) were together in a google hangouts chat talking about some of the stuff that I addressed here......almost every single day. Usually it happens after I went to bed when Standing says something that is totally asinine and then gets fact checked by the other people and then after a few back and forts it dies down and I get to see in the morning that a few dozen more comments were made that I missed. .......Good times, good times.......
Sometimes I participated it live and almost everything I was like "I already addressed it here on the League of Reason, you should read what I wrote and if you want to respond you should do it here on the league of reason where we can discuss point by point". I have heard that he would join a few days ago, so I don't know when he will join. But in the mean time he did a solo hangout and made a few comments in the comment section (one directed at me) as a response to me and the others.

TL:DR His response in a nutshell: For the most part, it is the same stuff re-stated that has already been refuted by me in this thread or in the google hangouts chat. Repeating your claims without while omitting the the counter points doesn't count as a response. Regarding the parts that are new, he mentions some things that are also easily debunked and/or reveals the dishonesty in his position.

So first the comment directed at me:
StandingForTruth wrote:This one is for Nesslig: It is universally accepted that duplication, whether within a written text or within the living genome, destroys and degrades information. The effect of a gene often depends on gene copy number. If an organism appears with extra copies of a certain gene, it may not be able to control the expression of that gene and an imbalance will occur in its physiology, decreasing its fitness (e.g. trisomy causes abnormalities such as Down syndrome because of such gene dosage effects). Sure, rare EXCEPTIONS may be found where a duplication is beneficial in some minor way (possibly resulting in some "fine tuning"), but this in no way changes the fact that random and deleterious duplications overwhelmingly destroy information. Duplications are no different than other types of mutations. As I stated, mutations are destruction and NOT construction. After a given gene has been accumulating deleterious mutations for a long time, it is in a partially degenerated and deteriorated state. If that gene is then duplicated, the deleterious mutations are duplicated with it. Does such duplication in any way slow down the degeneration process? The answer is an obvious no! Remember, it is all about NET LOSS versus NET GAIN. I said this to Jackson Wheat, and I will say it to Nesslig, even if Nesslig presents us with 1000 examples of adaptation via beneficial point mutation, he has still failed to address the key issue, which as I just said, is net gain versus net loss.
StandingForTruth has asked numerous times (in various discussions) for examples of "new information" as mentioned in my opening post. He usually dismisses these by asserting that they don't count as "new information" simply because he hasn't defined what he means by "new genetic information" such that he can shift the goal post however he likes. But he has been given numerous examples of unambiguous genetic novelties that arise via gene duplication and other means, such that he has to make another excuse, which basically is stating that it doesn't matter how many examples I or anyone can provide. It simply doesn't solve the problem that isn't even demonstrated to be a problem, which I will go into later. However, if StandingForTruth thinks that new information doesn't solve his problem, then why was he asking for examples in the first place? This just shows that he is willing to shift the goal post (or in this case remove the goal post entirely) just to avoid making the admission that his question has been answered. One telling example of his blatant dishonesty. Secondly, he is making some strong assertions with no evidence to back it up. No, It's NOT universally accepted that duplication "degrades the information" in the genome just as does in written text. This is one of many conceptual problems that he has, probably due to a severe lack of eduction. He makes these analogies for genetics that simply aren't applicable. A genome is not at all like a written text. It doesn't contain semantical information in the same way a romantic novel does. Thus a duplicated section of a text doesn't have the same effect as a duplication in a genome. And here he conflates the semantical "information" of "meaning" within a text with the genetic information that codes for protein - as he also often asked for new "MEANINGFUL" information in the genome - which is also not remotely comparable. I don't mind analogies to elicit a point, but when you are constantly arguing from false analogy, it becomes a fallacy. It's true that most duplicated version of genes will become pseudogenes, which is why we have many pseudogenes in our genome. And we share many of these broken copies (which are broken in the same way) with chimpanzees and other species. One good example is the NANOG pseudogene family, explained in this video at 2:41.
Evolution of the NANOG pseudogene family in the human and chimpanzee genomes wrote:The NANOG gene is expressed in mammalian embryonic stem cells where it maintains cellular pluripotency. An unusually large family of pseudogenes arose from it with one unprocessed and ten processed pseudogenes in the human genome. This article compares the NANOG gene and its pseudogenes in the human and chimpanzee genomes and derives an evolutionary history of this pseudogene family. The NANOG gene and all pseudogenes except NANOGP8 are present at their expected orthologous chromosomal positions in the chimpanzee genome when compared to the human genome, indicating that their origins predate the human-chimpanzee divergence. Analysis of flanking DNA sequences demonstrates that NANOGP8 is absent from the chimpanzee genome. Based on the most parsimonious ordering of inferred source-gene mutations, the deduced evolutionary origins for the NANOG pseudogene family in the human and chimpanzee genomes, in order of most ancient to most recent, are NANOGP6, NANOGP5, NANOGP3, NANOGP10, NANOGP2, NANOGP9, NANOGP7, NANOGP1, and NANOGP4. All of these pseudogenes were fixed in the genome of the human-chimpanzee common ancestor. NANOGP8 is the most recent pseudogene and it originated exclusively in the human lineage after the human-chimpanzee divergence. NANOGP1 is apparently an unprocessed pseudogene. Comparison of its sequence to the functional NANOG gene's reading frame suggests that this apparent pseudogene remained functional after duplication and, therefore, was subject to selection-driven conservation of its reading frame, and that it may retain some functionality or that its loss of function may be evolutionarily recent.
Which fully supports common ancestry. But Standing wants to focus, for obvious reasons, on the duplications that result in abnormalities like trisomy or more subtle negative effects from gene dosage, which are rare compared to the majority of gene duplications, most of which don't do anything (at first). While he focuses on the negative effects even though they are rare, he wants to ignore the beneficial aspects of gene duplication, because they are rare. An obvious double standard. And his assertions about "degrading genomes" has been addressed here in my previous posts, which he hasn't even attempted to respond to. People have said this to him many times and I will repeat here again: No matter how many times you assert things like "duplication are mutations overwhelmingly destroy and degrades information" it doesn't become fact, no matter how many vague analogies you are making in the process. You have to provide supporting data. In the real world, scientists have provided a coherent definition of what counts as "biological information" in the genome, (unlike SFT, who can only understand genetics in weird analogies). The genes of an organism can tell you how an organism is adapted to its environment, what kind of food it can digest, how it will respond to changing temperatures, etc. Thus genes "carry" information about the environment to which the organism is adapted to live in. Natural selection is the mechanism that transfers information in the genome about the environment, specifically its niche. And according to computer models, information does increase when selection is involved. And gene duplication isn't like any other mutation (duplications are the opposite of deletions for instance) and it is a mechanism that has been demonstrated to provide an adaptive advantage. And there are specific examples of complex biological structures for which there is strong evidence that they came about mainly via gene duplication followed by mutations to produce new functions or sub-functions. My previous example in the first post was the GPCR superfamily. There are also the genes involved in metabolism, coagulation, haemoglobin and even the bacterial flagellum. So all of these examples shows that relatively rare events aren't rare over long periods of time when beneficial mutations persists and are inherited by a large group of organisms that are still around, thereby rendering SfT's points moot.

So, next up is the solo hangout itself.

Addressing every single sentence will be too tedious so I will address only the main points he made, which is still a lot so I will try to keep it short (no promises).

1. From beginning to about 4 minutes in the video. I previously stated that Standing for Truth thinks that the genome is somehow under influence of the second law of thermodynamics so it should break down over time. In response, he begins his video response by stating that this is a straw man. He stated that genetic entropy while not the same as the 2nd law of thermodynamics increase in entropy, it is consistent with it. But it is not. He still believes that entropy (of the 2nd law) is the same disorder and thus “consistent with” genetic entropy that the genome is increasing in disorder just like the 2nd law, which isn’t much really different from what I previously stated. He also said in reference to the second law that everything else will go towards disorder - apart from intelligent intervention. Which is stupid since engineers and physicists know that nobody can stop the 2nd law, otherwise we would be able to make 100% efficient motors or build perpetual motion machines. I have already said this before, but this correction has to be stated again apparently. While he is right that the term “entropy” can have different usages, under the 2nd law of thermodynamics it has one usage. It means the total amount of energy within a system that is unable to perform work. This has no relationship with the concept of “genetic entropy” in which case “entropy” means “disorder” even when it is taken at face value.

2. Between previous point to about 6:10 minutes in the video. He said the following:
Standing For Truth wrote:Nucleotide cannot be neutral. They take up space, they affect spacing between nucleotides sites. DNA folding, nucleosome building. Believe it or not, even if a nucleotide contains no information, it is still not neutral. It still slows down cell replication and wastes energy.
This point is completely rendered moot by the existence of point mutations, which doesn't affect spacing. But even so, a single nucleotide more/less in a 3 billion nucleotide genome size isn't (for all intent and purpose) a difference that affects the fitness of an organism whatsoever. Even larger deletions/duplications of completely neutral regions of the genome (no genes included) might not even take up more energy since cellular mechanisms are very robust. If something happens that takes a little bit more energy, cellular processes can change in such a way that compensates for it without any noticeable effect. The metabolic noise caused by spurious processes would have a greater difference in energy consumption compared to a neutral duplication. And how does this even relate to the genetic entropy argument? Would a genome deteriorate by continuously growing bigger with duplication and thus eventually consume too much energy? To me, Standing is now grasping at straw when he defines "neutral mutation" in such a way that no biologists would find it useful. Some papers on the effects of mutations (some of which are neutral and some are beneficial):
And apparently, these beneficial mutations (however rare they may be), with the help of selection, are sufficient to counter the negative effect of harmful mutations. Even in cases of asexual populations that are subject to muller's ratchet, as this paper shows:
Dynamic Mutation–Selection Balance as an Evolutionary Attractor wrote:The vast majority of mutations are deleterious and are eliminated by purifying selection. Yet in finite asexual populations, purifying selection cannot completely prevent the accumulation of deleterious mutations due to Muller’s ratchet: once lost by stochastic drift, the most-fit class of genotypes is lost forever. [so if there is any truth to the concept of "genetic entropy" it must apply here or it simply cannot apply to anything else] If deleterious mutations are weakly selected, Muller’s ratchet can lead to a rapid degradation of population fitness. Evidently, the long-term stability of an asexual population requires an influx of beneficial mutations that continuously compensate for the accumulation of the weakly deleterious ones. Hence any stable evolutionary state of a population in a static environment must involve a dynamic mutation–selection balance, where accumulation of deleterious mutations is on average offset by the influx of beneficial mutations. We argue that such a state can exist for any population size N and mutation rate U and calculate the fraction of beneficial mutations, ε, that maintains the balanced state. We find that a surprisingly low ε suffices to achieve stability, even in small populations in the face of high mutation rates and weak selection, maintaining a well-adapted population in spite of Muller’s ratchet. This may explain the maintenance of mitochondria and other asexual genomes. [much to the dismay of Sanford and Standing].

Provided that beneficial (back and compensatory) mutation rates do increase as fitness declines, Muller’s ratchet will eventually come to a halt. Once the fraction of beneficial mutations is high enough to counter the ratchet, the population will remain in a stable dynamic equilibrium state, as illustrated in Figure 1.

Figure 1
Image
The relationship between the fraction of mutations that are beneficial, ε, and the absolute fitness of the population, ω. A poorly adapted population (green) with Embedded Image and ε < εc will adapt toward the dynamic equilibrium “attractor” state (gray) with higher fitness and lower ε. Conversely, an “overadapted” population (red) with Embedded Image and ε < εc will decline in fitness toward the dynamic equilibrium state due to Muller’s ratchet.

We have shown that for any population size, mutation rate, and selection pressure, there exists a proportion of beneficial mutations, εc, which balances the accumulation of deleterious mutations. Because beneficial mutations are favored by natural selection, a small-fraction beneficial mutation can suffice to maintain stability, εc ≪ 1. We have demonstrated this by explicitly calculating εc as a function of population size, mutation rate, and the strength of selection. There are two qualitatively different regimes for εc, as shown in Figure 6. In the slow-ratchet regime, selection stabilizes the fittest subset of the population at the nose of the distribution, so εc is small and depends exponentially on the population parameters Ns and λ. On the other hand, in the fast-ratchet regime, εc must be larger to balance rapid accumulation of deleterious alleles, and it depends more weakly on the population parameters Ns and λ. The boundary of the two regimes is approximately given by Nse^−λ = 1.

Figure 6
Image
The fraction of beneficial mutations εc necessary to maintain the dynamic mutation–selection balance in a population with parameters Ns and λ = U/s. The dashed line separates the slow- and fast-ratchet regimes. Experiments with various model organisms with different population parameters are represented as points.

Examining the properties of the dynamic mutation–selection equilibrium over the full parameter range, shown in Figure 6, has revealed a strong asymmetry between beneficial and deleterious mutations. For example, for a small population Ns ∼ 103 with high mutation rate λ ∼ 8, just 2% beneficial mutations are enough to counteract the effect of deleterious mutations. This indicates that purifying selection is remarkably effective even for conditions where Muller’s ratchet would proceed extremely quickly in the absence of back and compensatory mutations. Populations with ε > εc should adapt, while populations with ε < εc should decline in fitness. Experimental evolution of model organisms in controlled laboratory environments appears to be consistent with this expectation. [Once again, much to the dismay of Sanford and Standing]


3. Between previous point to about 9 minutes. Standing is once again claiming that the accumulation of near neutral mutations is inevitable which means fitness will always increase. But as previously shown in my first post in the section on the Lenski experiment, we see that fitness not only doesn't decline but continues to rise in all 12 separate populations. In response to criticism, Standing for Truth has a tendency to repeat the same claim over and over again. Often paraphrased, but still not proving any supporting data and constantly dismissing data that contradicts his claim. Furthermore, StF also brought up non-coding DNA as if it was interchangeable with non-functional DNA. No standing. We don't think that all non-coding DNA is functional and scientists have been aware of functional non-coding DNA for a long time. This has been explained to you numerous times. The existence of some functional coding and non-coding DNA does not mean that all non-coding DNA is functional as well. (see my first and second post on this thread).

4. Between previous point about 10:30 minutes in the video. Standing for Truth is straw manning scientists. They don't say something is non-functional simply because they don't see a function. There are multiple reasons to why most experts think that most DNA cannot be functional (especially the onion test and genetic load, again explained in previous posts). But Standing simply ignores these as well and continues on with this straw man. And again, citing the encode project. Standing, we aren't straw manning you since you did state (at one time) that Encode found out that 80% of the genome was functional as "RNA or Protein". Encode found out that 80% of the genome was biochemically active in at least one cell type at one time. This doesn't equate with functionality whatsoever (also explained in previous posts). Nor does this equate with Standing's so-called "trajectory" (addressed in the following point).

5. Between previous point about 11:50 minutes. Standing says the following:
Standing For Truth wrote:We only understand less than 5% of the DNA “language” or 1% if we include the gold standard, gene knock out test. We still don’t know what most of the genome does and it would be arrogant to do so. Tiny clues from DNA functions, point strongly to the vast majority of DNA to be functional [which he likes to call a "trajectory"] It is likely that most of the non-coding genes are guiding embryonic development
But it is not arrogant to say that most of it is functional without any evidence whatsoever? Calling someone "arrogant" for making a claim isn't a counter argument. It's an emotionally charged fallacy. Standing thinks that gene knock out tests are the "golden standard" for determining whether it is functional. But it isn't. I have seen that gene knockout experiments are described as the golden standard for uncovering what function a particular gene has, not whether it is functional at all and certainly not whether large regions of the genome is functional since knockout experiments would be impractical on that scale. Which is of course the reason why Standing wants to bank on knockout experiments since nobody would bother doing this experiment that would disprove his position. A better method would be deletions of large sections of randomly chosen regions that aren't known to have any function, which has been done and doesn't really show the results Standing for Truth wants to hear.
Megabase deletions of gene deserts result in viable mice wrote:The functional importance of the roughly 98% of mammalian genomes not corresponding to protein coding sequences remains largely undetermined1. Here we show that some large-scale deletions of the non-coding DNA referred to as gene deserts2,3,4 can be well tolerated by an organism. We deleted two large non-coding intervals, 1,511 kilobases and 845 kilobases in length, from the mouse genome. Viable mice homozygous for the deletions were generated and were indistinguishable from wild-type littermates with regard to morphology, reproductive fitness, growth, longevity and a variety of parameters assaying general homeostasis. Further detailed analysis of the expression of multiple genes bracketing the deletions revealed only minor expression differences in homozygous deletion and wild-type mice. Together, the two deleted segments harbour 1,243 non-coding sequences conserved between humans and rodents (more than 100 base pairs, 70% identity). Some of the deleted sequences might encode for functions unidentified in our screen; nonetheless, these studies further support the existence of potentially ‘disposable DNA’ in the genomes of mammals.
There are also other means to finding these things out, and thus we actually do know a lot about what the functional and non-functional regions of the genome as I said in my first post.
Nesslig20 wrote:In the functional category we have: Functional parts of protein coding genes, non-coding RNAs, regulatory sequences, SARs, Origins of replication, centromeres, telomeres, and conserved sequences of unknown function is about 8.7% (essential/functional). Non-functional includes transposable elements, viral DNA, pseudogenes and introns is about 65% (non-functional). The remaining 26.3% is non-conserved intergenic regions of unknown function (probably mostly non-functional as well). Note: There are very few exceptions such as co-opted viral or pseudo genes that have acquired a new function secondarily, but these are just a fraction of a percentage of all these categories. Creationists will often jump on these exceptions which only account for less than 0.0001% of the genome and use that to claim that the entire genome is functional, which is like cherry picking one cherry on a tree and then claiming that the entire tree is edible. And there are also fractions of a percentage on the functional categories that are actually non-functional, so these small differences won’t change these overall percentages. So 65% is KNOWN to be non-functional, but we can actually determine how much is likely to be non-functional by other means.
Also, Standing is often claiming that since we keep discovering new regions of the genome that turn out to have some function, this "trajectory" points towards a reality that most of the genome is functional. However, such an argument is inherently flawed for several reasons. First, we already know that huge regions of the genome is entirely made of broken bits of transposable elements (TE's) (see previous posts). No matter how many new regions with functions we find in the genome, that won't suddenly change these broken TE's into something that is functional. It's like saying that most of the earth will eventually turn out to be mostly gold since gold miners keep finding more of it. Secondly, the new regions with functionality we do find are increasingly smaller. First we discover huge portions of the genome that is regulatory and coding for protein, then we found out about non-coding RNA genes. Nowadays, when we find new regions they are just tiny fractions of the genome. If we were to interpret a so-called trajectory with this, we should conclude that we are currently scrapping for more functional regions at the bottom of the genomic barrel. Exactly the opposite of what Standing wants to assert.

6. Between previous point to about 16 minutes Standing makes.....once again.....the mistake of saying that the 80% of the ENCODE project's "functionality" or better put biochemical activity is transcribed. That's not what the paper itself says:
The ENCODE Project Consortium, 2012 wrote:Operationally, we define a functional element as a discrete genome segment that encodes a defined product (for example, protein or non-coding RNA) or displays a reproducible biochemical signature (for example, protein binding, or a specific chromatin structure).
Meaning, in order for something to qualify as "functional" it doesn't even have to be transcribed. All it has to do is sometimes "stick" to some protein at some point. Whether that sticky action does anything useful is omitted. But even transcription doesn't necessarily mean functionality since spurious transcription is a thing. In fact, spurious transcription is likely a starting point of the evolution of new functional regions since even among random sequences, there is a high likely hood that there is at least one section that happens to function as a weak promotor. Ford Doolittle explains it best:
We simply cannot go on being so vague about ‘function’ wrote:A recent study in Genome Biology by the Salzberg laboratory reported on the assembly of a new human gene catalog, based on an exhaustive transcriptomic survey of 31 tissues from hundreds of human subjects. After the removal of transcripts that overlapped with those found in RefSeq or GENCODE databases and additional filtering, they found what appeared to be 224 new protein-coding genes and 116,156 new non-coding transcripts that they deemed to be functional. [oh boy, new function. Undoubtedly, that would be cherry picked by Standing or some other creationists, but there is more to this...] More surprising is their claim to have also detected over 30 million additional non-functional transcripts, revealing an overwhelming amount of “transcriptional noise” in human cells.

[...] most of many genomes is transcribed, albeit infrequently. It is about this process and its products that there is disagreement, and two schools of thought. [...] The first school, which may be called ‘functionalist’, imagines that these RNAs comprise a vast interconnected network of subtle regulatory and evolutionary capabilities (evolvability), realized and potential. [...] The second school, which could be called ‘skeptics’, regards ncRNAs (especially lncRNAs) as mostly transcriptional noise. [...]

The two schools came into conflict in 2012, after investigators associated with the ENCODE project claimed that 80.4% of our genome is functional, and thus we might at last “write the eulogy for junk DNA”. After all, that claim was largely based on evidence that most of our DNA is transcribed, in one tissue or another. Indeed, tissue-specific transcription is considered proof of function in many studies. However, there are several reasons why tissue-specific transcription could happen without providing evidence for tissue-specific ‘function’. Indeed, Graur et al. criticized the ENCODE consortium for often falling into the logical error of “affirming the consequent” (i.e., taking a true statement and invalidly concluding its converse), in particular assuming that because functional genes are transcribed, transcribed regions must be functional genes.

ENCODE investigators responded to critics by admitting that assessments of ‘function’ were not easy to make, and that in the case of low-abundance transcripts it was possible that simple presence is not enough for such ascription. They admitted the need to use multiple biochemical criteria in order to elucidate “genome function in human biology and disease”. Still, the functionalist viewpoint seems at odds with the conclusions of Pertea et al. which, compared to those of Lloyd et al. using machine learning models, are based on very straightforward methods. For instance, unlike Mattick, Salzberg and colleagues dismiss pseudogene transcripts by fiat and declare all protein-noncoding RNAs to be non-functional if they (1) were assembled in fewer than ten samples (of almost 10,000) unless at high levels in these, (2) contained only a single exon, or (3) overlapped known genes (on either strand). By these, and a few additional tests that functionalists might consider arbitrary and biased, they declared that over 30 million transcripts at over 650,000 genomic loci were likely nonfunctional—that is to say, transcriptional noise.

This last concept is of course well-grounded. Struhl calculated from first principles that more than 90% of the Pol II initiation events in yeast are noise in the sense of not having a ‘biological function’, by which he presumably meant not honed by natural selection in order to contribute to organismal fitness. Accuracy in any informational transfer process such as transcription comes at a cost and perfect accuracy is unattainable. In any case, the number of ‘mistakes’ surely increases with the number of opportunities to make them, particularly with genome size.
At another point in time, standing claims that
Standing for Truth wrote:much of the 80% was found to be controlling the expression levels of protein coding DNA
He also claimed in the previous section #4 that it is likely that most of the non-coding genes are guiding embryonic development. But he doesn't provide any citations for either of these claims. And then there is this:
Standing for Truth wrote:They regulate DNA replication and regulate transcription. They mark cites for program and rearrangement of genetic material. They influence the proper folding and maintenance of chromosomes.....blablabla
He is quoting directly from The Nature of Nature: Examining the Role of Naturalism in Science by Bruce Gordon, William Dembski. But again, no citations given. Just parroting. So what can be asserted without evidence can be dismissed without evidence.

7. Between previous point to about 17:30 minutes Standing is claiming that, unlike our books, DNA can be read forwards and backwards. Depending on what he means by that, he is either trivially correct or completely wrong. DNA cannot be read backwards. RNA polymerase can only transcribe DNA in the 3 to 5 direction (making mRNA in the 5 to 3 order). At the very best, one gene on one strand can overlap another gene on the opposing strand, which isn't exactly "read" in the opposite direction in the same way two pages of a book that are stacked (with the text side of both pages facing each other) aren't read in the opposite direction either. But oddly enough, there are books, one in particular called "Hopscotch" by Cortazar, the chapters of which can be read in many different orders, including in the opposite direction. There are also poems that can be read backwards (line by line) that says something different. So I don't know what Standing's point of this was, but I can make a good point of it. While writing the Hopscotch, Cortazar often used used the "cut-up technique" which is performed by taking a finished and fully linear text and cutting it in pieces with a few or single words on each piece. The resulting pieces are then rearranged into a new text. This is analogous to another evolutionary mechanism by which new genes are formed in the genome called Exon Shuffling Image
In this process, exons from different genes are co to form a new combination of exons within a gene or create a new gene altogether as with the TPA gene (see picture above). It's similar to gene duplication in that no "new information" is added in the sense that "it didn't came from nothing" which isn't a problem for evolution since it doesn't state that new genes pop out of nothing. But new information got added since it created a different gene with a completely different function that didn't exist before, such as the TPA gene.

8. (skipping some redundant parts) Between 28 to about 33 minutes. Standing's last commentary is about the Lenski experiment, most of which could be addressed by my very first post in this thread. Standing claims that the Lenski experiment actually DOES support genetic entropy.....despite the fact that it shows that the fitness increases in all 12 separate populations indefinitely (or at least for a very long time). This is how Standing squares that circle: Standing asserts that since the genome shrank in size, that's evidence for genetic entropy happening in these populations. He also says that most of the "so-called" adaptations of these bacteria were always by loss of function or loss of regulation. This is because these bacteria are living in an artificial environment that allows for this "adaptive degeneration" (his words, not mine). In other words, if these bacteria lived in the wild (not in the lab) they would be declining in fitness.
Standing for Truth wrote:...the silencing of these temporarily expendable genes and the elimination of all non-relevant functions will continue….indefinitely until the bacterial genome is stripped down to its minimal functionality in several centuries.
1) Genome size shrinking genome sizes is evidence of genetic entropy? I thought that genetic entropy means that fitness decreases despite selection, not that genomes shrink despite selection. Does smaller genome mean lower fitness and bigger genome mean higher fitness? eh, no. It doesn't. If it does, it would imply an increase in genome size by duplication would be an automatic increase in fitness.
2) Loss of function and regulation The assertion that all the adaptations of these bacteria were always by loss of function or loss of regulation is also wrong. The most famous adaptation that is seen in one population is the ability to utilise citrate under aerobic conditions. Standing thinks that this is a "loss of regulation" since the genes that make the bacteria import citrate from the environment are normally expressed only when oxygen is absent, but now the regulation is lost such that they are always expressed. As I showed previously, this is not the case. It was a duplication that created a novel regulatory module, in other words regulation wasn't lost, it was gained.
I wrote:First you had these regulatory modules:
1. Promotor (activate when no oxygen is present) —> CitT
2. Promotor (activate when oxygen is present) —> RNK
After the duplication, you have:
1. Promotor (activate when no oxygen is present) —> CitT
2. Promotor (activate when oxygen is present) —> RNK
3. promotor (activate when oxygen is present) —> CitT
It’s an novel (new) module. No specificity was lost, no loss of control. Control and specificity were gained at the molecular level and a novelty was gained at the phenotype level.
3) Artificial environment Why is it relevant to genetic entropy? The environmental conditions is what defines the selective pressure on organisms. It's likely that the bacteria wouldn't be as fit as the wild-type under the conditions that are found outside the laboratory, but this is completely expected from natural selection. Organisms are adapting to the environment they are found in at the time, which often comes at a cost for losing adaptations to other environments. When foxes loose most of their thick insulating fur in order to live in a desert environment, they increase their fitness to that environment, but they wouldn't be as fit if they are put in a cold climate. That is completely in agreement with natural selection since the environment determines the selective pressure, but genetic entropy completely omits selection, hence it omits the conditions of the environment. It's thus completely irrelevant to genetic entropy. Also, Rumraket preemptively responded to the same excuse Sanford pulled:
Rumraket wrote:So if you show evidence of fitness increase in experiments, he will just say this is consistent with a model where fitness can increase in response to selection in the particular species used and with the particular experimental environment(and then he'll try to deflect by pointing out that many of the mutations are "loss of function" mutations)*, but that his genetic entropy claims are still true for everything else in the wild. So we have to basically prove him wrong with experiments for all 10 million species on Earth in conditions that are pretty much exactly equal to whatever it is in the wild, or he's going to keep claiming genetic entropy must be the case for everything. Essentially he's saying "here's how everything is in my view, prove me wrong". Not understanding that it's HIS job to prove his claims right. :roll:
4) Extendible genes are eliminated until the genome is stripped down to it's minimal functionality after a few centuries The entire point of genetic entropy is that (no matter what) the accumulative harmful effects of nearly neutral mutations will inevitably make the individuals of a population less able to survive and reproduce, i.e. fitness will always decrease until the population dies out. And since fitness is not only NOT observed to decrease, it's observed to increase 12 independently. Standing has no other option but to completely ignore that and pulls up red herring after red herring to distract us from the fact that genetic entropy isn't supported at all. It's also very telling that Standing is now claiming that "minimal functionality" is maintained in a population for several centuries, despite E.coli's fast rate of reproduction. Does that mean that genetic entropy (at first) only effects the expendable parts of the genome......for some reason..... allowing the organisms to maintain fitness until AFTER SEVERAL CENTURIES there is no expendable part of the genome left and only then does fitness decline?? If that's true, the claim of genetic entropy becomes even more dubious. Believe me, it's true! Just watch them for several centuries and you will see!! I promise!!!
Image
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Last edited by Nesslig20 on Tue Jan 08, 2019 10:30 am, edited 8 times in total.
Thu Jan 03, 2019 7:00 pm
RumraketUser avatarPosts: 1263Joined: Fri Jun 25, 2010 7:49 am Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Anyone find it ironic that these creationists say that most mutations are destroying function and are deleterious, yet simultaneously claim that it just cant' be the case that most DNA is junk? Junk created by an accumulation of mutations resulting in dead retrotransposons, degrading retrovial elements, and pseudogenes?
"Nullius in verba" - Take nobody's word for it. https://en.wikipedia.org/wiki/Nullius_in_verba
Extraordinary claims require extraordinary evidence.
Fri Jan 04, 2019 7:38 am
RumraketUser avatarPosts: 1263Joined: Fri Jun 25, 2010 7:49 am Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

StandingForTruth wrote: It is universally accepted that duplication, whether within a written text or within the living genome, destroys and degrades information.
No, that isn't universally accepted. In fact that very point is directly contested by experts in information theory, such as Jeffrey Shallit:
http://recursed.blogspot.com/2009/01/test-your-knowledge-of-information.html

Creationists think information theory poses a serious challenge to modern evolutionary biology -- but that only goes to show that creationists are as ignorant of information theory as they are of biology.

Whenever a creationist brings up this argument, insist that they answer the following five questions. All five questions are based on the Kolmogorov interpretation of information theory. I like this version of information theory because (a) it does not depend on any hypothesized probability distribution (a frequent refuge of scoundrels) (b) the answers about how information can change when a string is changed are unambiguous and agreed upon by all mathematicians, allowing less wiggle room to weasel out of the inevitable conclusions, and (c) it applies to discrete strings of symbols and hence corresponds well with DNA.

All five questions are completely elementary, and I ask these questions in an introduction to the theory of Kolmogorov information for undergraduates at Waterloo. My undergraduates can nearly always answer these questions correctly, but creationists usually cannot.

Q1: Can information be created by gene duplication or polyploidy? More specifically, if x is a string of symbols, is it possible for xx to contain more information than x?

(...)

The answer to each question is "yes". In fact, for questions Q2-Q5, I can even prove that the given transformation can arbitrarily increase the amount of information in the string, in the sense that there exist strings for which the given transformation increases the complexity by an arbitrarily large multiplicative factor. I won't give the proofs here, because that's part of the challenge: ask your creationist to provide a proof for each of Q1-Q5.

Now I asserted that creationists usually cannot answer these questions correctly, and here is some proof.

Q1. In his book No Free Lunch, William Dembski claimed (p. 129) that "there is no more information in two copies of Shakespeare's Hamlet than in a single copy. This is of course patently obvious, and any formal account of information had better agree." Too bad for him that Kolmogorov complexity is a formal account of information theory, and it does not agree.
Case closed, game over.
"Nullius in verba" - Take nobody's word for it. https://en.wikipedia.org/wiki/Nullius_in_verba
Extraordinary claims require extraordinary evidence.
Fri Jan 04, 2019 7:50 am
RumraketUser avatarPosts: 1263Joined: Fri Jun 25, 2010 7:49 am Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

StandingForTruth has asked numerous times (in various discussions) for examples of "new information" as mentioned in my opening post. He usually dismisses these by asserting that they don't count as "new information" simply because he hasn't defined what he means by "new genetic information" such that he can shift the goal post however he likes.

When creationists refuse to define their terms, I have decided to do it for them. They always refuse to define new, so here I will do it for them: If it's different from what it was before, then it's new. If it's slightly bigger, slightly smaller, slightly darker, slightly longer, slightly thinner, slightly more curved, if it has changed in ANY measurable way, then I say it's new. That goes for physiological, mental, and molecular changes of any and all kinds. Changing a T nucleotide into a G nucleotide is change, and therefore new. An ever so slightly taller person is different, so also new.

There we go, "new" has now been defined and any measurable change qualifies as new.

With respect to new information: New information is any change in a sequence such as a polymer like DNA, or a string of abstract symbols used in writing (including it's length, or the order of arrangement of monomers or symbols within it) that wasn't there before. If it wasn't there before, it's new. So any mutation is new information. All duplications are new information. All substitutions are new information. All deletions are new information, because they all constitute change that wasn't there before.

Using this simple, intuitive definition of what would be "new", all mutations cause new information. If creationists don't like this definition, they're going to have to come up with one they think is better.
"Nullius in verba" - Take nobody's word for it. https://en.wikipedia.org/wiki/Nullius_in_verba
Extraordinary claims require extraordinary evidence.
Fri Jan 04, 2019 8:03 am
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Rumraket wrote:Anyone find it ironic that these creationists say that most mutations are destroying function and are deleterious, yet simultaneously claim that it just cant' be the case that most DNA is junk? Junk created by an accumulation of mutations resulting in dead retrotransposons, degrading retrovial elements, and pseudogenes?
A striking contradiction.
Rumraket wrote:
StandingForTruth has asked numerous times (in various discussions) for examples of "new information" as mentioned in my opening post. He usually dismisses these by asserting that they don't count as "new information" simply because he hasn't defined what he means by "new genetic information" such that he can shift the goal post however he likes.
When creationists refuse to define their terms, I have decided to do it for them. They always refuse to define new, so here I will do it for them: If it's different from what it was before, then it's new. If it's slightly bigger, slightly smaller, slightly darker, slightly longer, slightly thinner, slightly more curved, if it has changed in ANY measurable way, then I say it's new. That goes for physiological, mental, and molecular changes of any and all kinds. Changing a T nucleotide into a G nucleotide is change, and therefore new. An ever so slightly taller person is different, so also new.

There we go, "new" has now been defined and any measurable change qualifies as new.

With respect to new information: New information is any change in a sequence such as a polymer like DNA, or a string of abstract symbols used in writing (including it's length, or the order of arrangement of monomers or symbols within it) that wasn't there before. If it wasn't there before, it's new. So any mutation is new information. All duplications are new information. All substitutions are new information. All deletions are new information, because they all constitute change that wasn't there before.

Using this simple, intuitive definition of what would be "new", all mutations cause new information. If creationists don't like this definition, they're going to have to come up with one they think is better.
They all to often rely on an "intuitive" notion of "information" like how a textbook contains semantic Information about a subject of study, which is why Standing demands new information that is - quote - "meaningful". Information scientists are smart to avoid semantics, but creationists aren't. At some time, Standing implied that if a genetic sequence like a gene originated from something that already existed (even if it was non-coding), it still doesn't count as "new" since there was something already there. By inference, his definition of "new" means "creation ex nihilo" but that doesn't apply to evolution since it doesn't state that anything came from nothing. On the contrary, it's descend with modification. Creationists are the ones who believe this so they should be answering their own question.

We should also define how to measure the exact amount of genetic information and in what unit. Even if they would accept your definition of "new", they would state something like "well, even if it's new, it is now LESS information compared to the prior state". So now the questions now become: how do you measure the amount of information that was lost? How can you tell the difference between losing and gaining information? How do you measure the amount of information in the first place?

But they don't answer these types of questions either...
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Fri Jan 04, 2019 10:52 am
he_who_is_nobodyBloggerUser avatarPosts: 3508Joined: Tue Feb 24, 2009 1:36 amLocation: Albuquerque, New Mexico Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Rumraket wrote:Anyone find it ironic that these creationists say that most mutations are destroying function and are deleterious, yet simultaneously claim that it just cant' be the case that most DNA is junk? Junk created by an accumulation of mutations resulting in dead retrotransposons, degrading retrovial elements, and pseudogenes?


Just about everything intelligent design creationists do is ironic. That is what you get when one actively refuses to learn about a subject, yet still wants to speak on it as if they know the first thing about it.
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Fri Jan 04, 2019 5:08 pm
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SparhafocPosts: 2658Joined: Fri Jun 23, 2017 6:48 am

Post Re: New information, Genetic entropy and Junk DNA blablabla

It's par for the course.

Evolution works like Pokemon. You can't show evidence for Pokemon evolution, therefore it's false!
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Beliefs are, by definition, things we don't know to be true.
Fri Jan 04, 2019 5:19 pm
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

UPDATE Standing for truth had a live youtube debate with Jackson Wheat.

Unsurprisingly, Standing didn't really had any of substance to show. It wasn't original either as his arguments are directly parroted from creationists website like AiG, specifically the claims from John Sanford's "Genetic Entropy" and Nathaniel Jeanson's "Replacing Darwin", mixed with some stupidity of Kent Hovind's rhetoric. So a lot of his claims in that debate was already addressed here. Standing has said to me, and I quote:
Standing For Truth wrote:I made my opening to Jackson in response to some of what you said there so look out fr some debunking of it
Which is really weird considering that he is supposed to begin the debate by making arguments backed with evidence that support his claims, not begin by making a response to me. But his opening didn't debunk any of my rebuttals in this thread at all. It's just rehashing the same thing that was already debunked.

Furthermore, Standing for Truth having conniptions in the comment section is also pretty hilarious.

Standing For Truth wrote: Just to clarify, I'm not entirely sure why people are confused about the whale genetic marker. If common ancestry is true, then why do whales have a water echo-location system lacking in land mammals specific to the whale lineage? Junk echo location genetic markers in the whale lineage to be specific (maybe thats the confusion?). Because since most land animals don't need it, it should have been made junk by evolution. But instead we found those same exact genetic sequences on other animals so far away from the whale lineage? How can they evolve the exact same genetic sequences so far apart? Thanks.
brogner wrote:Why would a common ancestor of a whale need this water echolocation system if that ancestor was a land dwelling animal? BTW not all whale species has this ability. I believe only whales with teeth have this ability.

Standing For Truth: Okay listen, you atheists need to STOP pretending you don't know what I am talking about. Jackson either pretended or misunderstood what I said, which means he left my rebuttal open and therefore justified. Echolocation genetic marks on the WHALE (while evolving) don't show echolocation markers evolving, but instead a completely non evolving markers show up somewhere far beyond the whale lineage with PRECISE genetic sequences. How can evolution MAGICALLY create precise nucleotide level genetic markers of the exact same echolocation far apart in its tree? Unless ALIENS came down and did it, or God did it. So QUIT pretending. Jackson CHERRY PICKED his data, his genetic markers in his fancy charts DO NOT demonstrate common ancestry.

John Petersen: You don't understand the science well enough to realize that your question is nonsense.
James Downard wrote:Because it developed AFTER they were in the sea, SFT. If you'd paid more attention the fossil sequence (and had a working Map of Time in your head) you might have spotted this.

Standing For Truth: Send me a paper on that.

James Downard: Haven't you done any research on this previously? You mentioned "echolocation" markers. We'll have to fill you in some of the work your creationist secondary filters avoided for you. https://royalsocietypublishing.org/doi/ ... .2016.0060 Park's 2016 paper tracks the acquisition of echolocation aptitude. Of course since you SFT need to crunch everything into the YEC frame, the sequence of things wouldn't be so apparent to you.
I find it difficult to determine what the hell Standing is getting at. At first he seems to be asking why whales have echolocation genes specific to the whales that aren't present in any terrestrial mammal......as if it goes against common descent....which it doesn't. As Downard already explained, only one subset of whales have echolocation, the toothed whales (odontocetes). The baleen whales don't have it, and don't appear to ever had any ancestor with echolocation the way odontocetes have. So echolocation in whales evolved in odontocetes AFTER it split from baleen whales. And then Standing is asking why the exact same genetic sequences of echolocation are found in other animals far away from the whale lineage, but he doesn't specify what the "other animals" are. I guess he is talking about bats since this reminds me of an old argument that someone else used on the League of Reason, which I already debunked.

EDIT: Furthermore, this claim about echolocation of bats and whales is based on this particular paper but the results of that aper were apparently based on a flawed test as pointed out by this particular paper.


Standing For Truth wrote:Jackson is just plain wrong on the H1N1 virus as in the HUMAN version of the H1N1 virus. Yes, the swine flu version is currently circulating. In fact, H1N1-related human mortality has declined very dramatically and very systematically [2]. Apart from the 1917 pandemic, H1N1 has failed to cause any severe global pandemic, and human H1N1 essentially went extinct from 1957–1977.Oct 12, 2012 patterns of mutation accumulation in the human H1N1 ... - NCBI - NIH https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507676/ H1N1 went from a RED HOT pandemic to a WIMPER to an EXTINCTION event in 90 years....PLUS all the other forms of evidence I provided for genomic degeneration = CASE CLOSED. I'm sick of people ignoring the obvious. Mutation accumulation IS detrimental. Thanks again for having me on James! You were a great moderator as usual. Looking forward to another.
Crispr CAS9 wrote:H1N1 went from a RED HOT pandemic to a WIMPER to an EXTINCTION" The 2009 H1N1 resulted from a recombination between a swine-adapted avian virus and a direct descendant of the 1918 strain! In any event the idea that host mortality is synonymous with viral fitness is laughably idiotic.
More on that later...

And there were also some replies he made to the comments that I made (one admittedly just a snarky joke).
Nesslig20 wrote:12:00 even the internet couldn't process that much nonsense...
Standing For Truth wrote:All new innovations, structures, body plans, and novel information, cannot be the result of natural selection acting upon random variation and random mutations. But I firmly advocate for the rights to your religion! You have a very fancy science fiction religion complete with plenty of IMAGINATION (hence my Spongebob icon:)).
Nesslig20 wrote: 1:23:24 That reaction from Jackson is priceless, when Standing accused him of "Straw manning" him for pointing out that haplogroups M and N are SUBSETS of L which would mean that.....according to standing.....two of the three wives of Noah's sons would be the descendants of the third wive. A very awkward family.
Standing For Truth wrote:BRO C'MON! This is why the atheists were angry in the chat. The Biblical Model was not falsified. Any biblical creationist who understands the data has NO REASON to give up the biblical based model, and any theistic evolutionist has ZERO excuse for compromising God's Word for a dumb theory. The N and M didn't come from L BECAUSE the L M N are very close together compared to other haplogroups. HOW can three haplogroups L M N that are CLOSE together be descended from one another? If they are close together, that means everyone descended from them instead. PLUS, the L that is connecting M and N shows a much larger genetic differences from the rest of the L's like L1, L2, L0. SO how can the L come from the other L's if they are separated by so huge amount of genetic differences? PLEASE just study the haplogroups, and that way, when doing these debates, I can be given an appropriate rebuttal. The atheists deserve strong rebuttals to my points, or else...they may CONVERT to biblical creation, do you want that?

Crispr CAS9: I notice you didn't mention L4, because if you take L3'4, L3, and L4, you have 3 differences from L3'4 to L3 and 3 from L3'4 to L4, for a total of 6, compared to 4 differences from L3 to L3M and 5 from L3 to L3N for a total of 9. So by your own logic of "If they are close together, that means everyone descended from them instead." that would make the 'three groups' L3'4, L3, and L4, not L3, L3M, and L3N.

James Downard: SFT, its likely NOTHING could ever persuade you, especially when all you do is repeat the tropes you've copied from secondary sources you seem reluctant to fact check.


So Standing seems to be really upset about the responses he got for what he said on Mitochondrial DNA Haplogroups (watch the debate at 14:30 minutes in). Standing parroted these claims from Nathanial Jeanson. First some background. The Human matrilineal lineages (lines of descent that only involves women: your mother to her mother to her mother, etc) can be traced using inherited Mitochondrial DNA mutations that are unique to each lineage, which can be treated as genetic markers of shared matrilineal ancestry. The genetic markers that are shared by many individuals are dubbed "haplogroups", which is similar to the concept of clades as haplogroups are divided into subsets that are also haplogroups. How does all this relate to the claim? Well, Jeanson and hence Standing are claiming that the three major haplogroups - designated as L, M and N - are the result of the matrilineal lineages that started with the 3 wive's of Noah's sons after the flood. Basically, one wive was the post-flood matrilineal ancestor of everyone belonging to haplogroup N and another was the ancestor of M and the third one of L. As.....ehum...""evidence"" for this claim, they say that biblical creationism (specifically Noah's flood myth with 3 sole surviving females) predicts that all extant humans should be composed of three major haplogroups, hence L, M and N are evidence for creationism. They also say that the fact that these three ancestral nodes of L, M and N (see figure below pointed by three green arrows) are very close together on the phylogeny and at the same time are far apart from their modern descents, is also predicted by biblical creationism. The wives are closely related to each other since their pre-flood ancestors of these wives had very long generation times and the descendants became very distantly related as a result of a time period when evolution went into overdrive. Which is also their explanation for how a few thousand animals gave rise to millions of species within a few centuries. Furthermore, Jeanson also says that "Africans and Asians may have traced their ancestry back to different women". It's better if you don't think too much about that.
Answers in Genesis article by N. Jeansons wrote:The resultant tree (Fig. 1; see also Supplemental Fig. 1 to zoom in on individuals within the tree) depicted results consistent with previous studies—the longest branch lengths belonged to African individuals. However, the highest divergence (117 nucleotides) resulted from a comparison, not between two Africans, but between an African San individual and an Asian Taiwanese Aborigine (Table 3; see also Supplemental Table 3). From a biblical perspective, Africans and Asians probably split after the Flood, likely due to the events at the Tower of Babel. Going back to the time of the Flood, modern ethnic groups would have all traced their maternal ancestry back to the three wives of Noah’s sons (Jeanson 2015a). Consistent with this historical record, three major nodes were visible in human mtDNA trees (Fig. 1).4
Image
Fig. 1. Human mtDNA tree for 369 individuals of varying ethnicities. The 369 human mtDNA sequences clustered into three major nodes, which were indicated by green block arrows. One of the nodes spawned almost exclusively sub-Saharan African individuals, whereas the other two nodes gave rise predominantly to non-African and North African individuals (identities of individuals are more readily visible in Supplemental Fig. 1). The positions of the six South African individuals analyzed in Table 4 were indicated with blue block arrows and underlines. The positions of the individuals from the primarily African node with shorter branch lengths were indicated by gold arrows (two of the individuals were South African; hence the overlap). The most divergent pair of individuals was between the San and Taiwanese Aborigine individuals, denoted by the red block arrows and underlines.
In theory, among these three wives, Africans and Asians may have traced their ancestry back to different women. Consistent with this hypothesis, the highly divergent San and Taiwanese Aborigine individuals traced their ancestry back to different mtDNA nodes (Fig. 1). Thus, not only did the San and Taiwanese Aborigine not share a common ancestor after the Tower of Babel incident, they also appeared to have different maternal ancestors at the time of the Flood.

But there are some problems with this:
First problem: If you look at any phylogenetic tree (based on haplogroups or otherwise), there will always be "3 main lineages" that you can pick arbitrarily. You can arbitrarily pick 2 or 4 nodes on a tree and call those the main lineages. Jeanson doesn't give any reason for why there are specifically 3 main haplogroups. It just happened to be that Jeanson wants the number to be 3 since he believes there were just three surviving women after the flood, so he just arbitrarily picks 3 nodes on this unrooted tree and call those the main lineages. That's not prediction, that's postdiction.
Second problem: Jeanson is specifically using an UNROOTED radial tree. You cannot determine which node is ancestral to any other node from an unrooted tree. Unrooted trees don't infer the direction of ancestry between nodes. That's what it means to be an unrooted tree. So that tree doesn't show that Jeanson's tree handpicked nodes are in fact the ancestors of all humans. We actually need a ROOTED tree in order to infer the direction of the ancestor/descendant relationships. So when we do this with these mitochondrial haplogroups, this is what we get:
Courtesy of Ration alMind:
Image
Whoops...
Third problem:The specific nodes that Jeanson picked are not L, M and N. They are L3, M and N. The latter two actually descended from L3 which is one specific lineage of the larger L haplogroup.
Maternal ancestry and population history from whole mitochondrial genomes wrote:Image
Figure 2: mtDNA haplogroup tree and distribution map. Haplogroup labels are reported according to the http://www.phylotree.org/ nomenclature [14]. Only a single branch defining marker, preferably from the coding region, is shown. The main geographic features of haplogroup distribution are highlighted with colour.
As you can see in the diagram above, the root lies on the left. THAT is haplogroup L and it encompasses all human matrilineal lineages that are connected by the most recent matrilineal common ancestor (mt-MRCA) or often dubbed "mitochondrial Eve". So when we plot these matrilineal lineages on a world map, this is what we get.
Image
mmmhhhh......a pattern of human migration that began in Africa. Jee, I wonder.....what theory predicted that result? ;)

So the nodes that Jeanson picked don't even encompasses ALL of humanity, as there are lineages like L0, L1 and L6 that did not descent from any of them. And since one node is the ancestor of the other two, they couldn't' have been contemporary matrilineal ancestors like the three wives. This is the point that Standing got very upset about in the comments. Haplogroups M and N came from the larger L3, which in turn came from the total L haplogroup as you can see. His specific response:
Standing For Truth wrote:...HOW can three haplogroups L M N that are CLOSE together be descended from one another? If they are close together, that means everyone descended from them instead. PLUS, the L that is connecting M and N shows a much larger genetic differences from the rest of the L's like L1, L2, L0. SO how can the L come from the other L's if they are separated by so huge amount of genetic differences?...
Is really dumb. It just shows how poor his understanding of the subject really is. "HOW can three haplogroups L M N that are CLOSE together be descended from one another? If they are close together, that means everyone descended from them instead."? That makes no sense at all. As previously pointed out, unrooted trees don't show any direction of ancestry, which also means that the lengths of the branches don't tell you which nodes are ancestral. By his logic, if I take a look at my pedigree (projected as unrooted) and see that my great great great great grandpa is closer to his father than he is to me or any of his descendants alive today, I should think "how can my great great great great grandpa and his father that are close together be descended from one another? If they are close together, that means everyone descended from them instead."
Image
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Thu Jan 10, 2019 11:43 pm
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

FOLLOW UP In the previous post I addressed some of Standing's youtube comments, mainly the claims on the mitochondrial haplogroups. I also wanted to address the comments on the H1N1 virus, but I figured that the post was getting long enough so it would be better if I did this in a separate post.

Just to recap, this is the comment that Standing made under the debate about the virus.
Standing For Truth wrote:Jackson is just plain wrong on the H1N1 virus as in the HUMAN version of the H1N1 virus. Yes, the swine flu version is currently circulating. In fact, H1N1-related human mortality has declined very dramatically and very systematically [2]. Apart from the 1917 pandemic, H1N1 has failed to cause any severe global pandemic, and human H1N1 essentially went extinct from 1957–1977.Oct 12, 2012 patterns of mutation accumulation in the human H1N1 ... - NCBI - NIH https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507676/ H1N1 went from a RED HOT pandemic to a WIMPER to an EXTINCTION event in 90 years....PLUS all the other forms of evidence I provided for genomic degeneration = CASE CLOSED. I'm sick of people ignoring the obvious. Mutation accumulation IS detrimental. Thanks again for having me on James! You were a great moderator as usual. Looking forward to another.
And after that debate with him and Jackson, Standing said this in a chat on google hangouts.
Standing For Truth wrote:The virus started out more human in its codon usage, and ended up more randomized. Natural selection that is weaker is not the same thing as no selection at all and it got worse at interacting with human DNA over time. If it isusing the wrong codons, that means it will be less efficient at replicating in human hosts. That is a decline in functionality, and matches exactly with genetic degernation. It really helps explain why the mortality rates went down, and it also helps to explain why the strain went extinct. Its due to harmfel negative mutations. The viruses became less lethal because they got worse, not better, at doing their one and only job: replicating themselves.
And to summarise his response to me showing him what I wrote here about Sanford's claims on the H1N1 virus.
Standing For Truth wrote:You are grasping at STRAWS nesslig. All your arguments against GE are weak and sad. Tell Modern Day we will debate formally ONLY the topic of GE. We can talk Synergistic epistasis, MCM, H1N1, lenski, junk DNA, and so on...
You are a science denier. You cannot explain why H1N1 virus is extinct in huans. Adaptation evolution DOES NOT cause extinction events. Your semantic wordplay on fitness is just an attempt to move the goalpoasts Nesslig.
The viruses became less lethal because they got worse, NOT better, at doing their one and ONLY job, replicating themselves. GE in real time TONS of examples, just keep denying my friend. H1N1 the human version went from a RED HOT pandemic to a wimper to an EXTINCTION event in 90 years. Tell me, why is the H1N1 human version extinct right now?
I have noticed that creationists often feel the need to challenge me to a debate in response to a rebuttal. It's an obvious attempt to be intimidating. Aside from this petty posturing, I said to Standing that I will write a full explanation for this here, on the league of reason, so we can talk as much as we want about it on this forum. To which he agreed. So, after all this time, he may join, but don't hold your breath.

As I noted in my first post, Sanford's claim about the H1N1 virus in relation to his notion of genetic entropy is highly flawed. In his book, Sanford tries give evidence for his assertion that the H1N1 virus supports genetic entropy by contrasting figure 14, a Graph made by Sanford's Medel's Accountant algorithm showing theoretical fitness decline as a function of time, with figure 15 that is dubbed "Actual biological data, showing mutation accumulation and fitness decline in human influenza virus.".
Sanford wrote:“This graph illustrates the pathogenicity (i.e., fitness) of the H1N1 strain, as well as the other two pandemic-causing strains during the last century.”
However, the data Sanford's figure 15 comes from figure 1 from the paper by Simonsen et al, and that figure does NOT show either "mutation accumulation", "fitness decline" NOR "pathogenicity (i.e. fitness)" of these viruses over the last century. The data points are plotted on a graph as a ratio: the number of influenza-caused deaths of people under the age of 65, divided by the total number of deaths. The paper itself notes that the epidemic of 1918 was unusually deadly for young people, and in the following decades, the virus killed a greater proportion of elderly people. Thus, the figure isn't about the fitness of the virus at all, thereby invalidating Sanford's argument.

This was pointed out by Gerard Jellison in his review on Amazon. I have quoted him in my first post, but here below is the full segment on this specific issue. (click on "show more")
When Standing for Truth says that the decline of H1N1-related human mortality shows genetic entropy, he is making the same mistake that Sanford Carter made in their paper.
Sanford and Carter wrote: Despite this common perception, a more lethal version of H1N1 has not arisen via mutation within the human population during the last 90+ years. This is significant. The two major human influenza pandemics since 1918 [...] were also less lethal than the 1918 version. It is true that the population had a degree of residual immunity and was not as immunologically naïve as it was in 1917–18, but selection has still not been able to generate a devastating pandemic from the remnants of that which swept the world at the close of WWI.

They are erroneously equating the capability of the virus to harm or even kill its host (virulence) with the ability of the virus to replicate and spread to new hosts (fitness). Virulence is certainly a factor that relates to the fitness of the virus, but a decrease in virulence doesn't equate to a decrease in fitness. Sanford and Standing may believe that the purpose of viruses is to cause devastating pandemics, killing as many people as possible. (So God is a huge prick after all?) This misconception is almost exactly the opposite of the reality.

Viruses do need to cause some virulence. In order for them to reproduce, they have to hijack the genome of living cells, forcing them to make new copies of the virus, destroying them in the process. The destruction of cells is a necessary consequence of virus reproduction, which in turn would cause some harm to the host often in the form of uncomfortable symptoms. And when viruses hijack more cells of its host, it will produce more offspring. Many offspring is also necessary since it needs to increase its chance of transmission to other hosts since the host will eventually produce immune defences against the virus. So it seems that killing more cells would increase the fitness of the virus, HOWEVER...... if the virus reproduces too quickly, it will kill the host before it has the chance to spread to a new host. Even if it doesn't kill, the virus still reduces its chance to spread if it makes the host too sick such that he/she won't come in contact with many people.
Image
So a little virulence is necessary to reproduce enough offspring which are able jump to a new host, but being too virulent is not better. Natural selection favours a balance between the two, which would be the condition that provides the highest fitness. The balancing point depend on the properties of the virus as well as other conditions. If the virus cannot spread very easily, it needs to keep its host alive and active long enough in order to guarantee transmission. This is especially the case with pathogens that transmit via sexual activity between their hosts. They tend to not produce noticeable symptoms for a very long time, even if they end up being lethal to their hosts. However, if the virus can spread very easily, the virus is free to evolve a high level of virulence in order to produce more offspring.

However, if it's in the best interest for the virus to not be very virulent, then why do we have deadly outbreaks and pandemics? Well, there are several factors that can chance or disrupt the balance between virulence and transmission. One simple explanation is the simple fact that a balance has yet to be achieved. When a virus makes the first jump to a new population, one that hasn't experienced the particular pathogen, the virus can be quite deadly since the individuals of that population don't have any immune defences against it. This is what happened when smallpox devastated the natives of America during the Spanish conquest who brought the virus with them. It's also the reason why modern pandemics tend to be zoonotic, meaning they jumped from other animals to us. Another reason is the selective pressure changed due to the behaviour of the hosts. Normally, when someone gets infected with a highly virulent virus, the person is less active which makes transmission less likely to occur. However, during the 1918 H1N1 pandemic, there was a world war going on. When soldiers were infected with a mild virus, they stayed on the battle field. But if soldiers were infected with a highly virulent form of the same virus, they were send home giving the virus a higher chance to spread. In this case, selection favours high virulence. This is hypothesised to be one factor that explains the high virulent nature of the 1918 pandemic.
Why Was the 1918 Influenza So Deadly? wrote:In his book Evolution of Infectious Diseases (1996), Paul Ewald hypothesizes that through our actions we can favor the evolution of infectious agents that are either more or less pathogenic. According to this idea, in a given population of pathogens, there exists variability. Some organisms will cause severe symptoms in their hosts, while others will occasion only mild symptoms. If a pathogen needs its host to spread (i.e., it cannot be spread by vehicle or vector transmission such as by contaminated water), then the health status of the host will play a part in the spread. If a host is infected with a particularly virulent pathogen, then that host is incapacitated, and the spread is halted. If a host is infected with a mild form of the pathogen, then the host can continue functioning, is more likely to be in contact with other potential hosts, and the pathogen is more likely to spread and replicate. erefore, natural selection will favor strains that only mildly a ect the host. However, there was a potential reversal of conditions during World War I. If a soldier on the war front was infected with a mild form of influenza, he stayed on the war front, only contaminating others around him. However, soldiers who were infected with a particularly virulent form of influenza were removed from the trenches and transported in crowded troop trucks to crowded clinics or hospitals, giving the virus ample opportunities to infect many more hosts. us, the evolution of a virulent strain of influenza was favored, and this newly emerged pathogenic virus devastated the world (as reported in Gladwell, 1997).
Scientists also have identified a specific mutation that made the virus 1918 H1N1 so virulent. Viruses with this mutation induces elevated levels of cytokines in their hosts. Cytokines are involved the immune response, but over-secretion of cytokines can lead to a "cytokine storm" that makes the immune system go haywire. This is suspected to have been the main cause of mortality of the 1918 pandemic as it explains why deaths uncharacteristically occurred among healthy young people, since they have immune systems that is able to produce stronger reactions. So if Standing still wants to insist that the initial strain started with a high level of fitness, equating that with its high virulence, then this high "fitness" (emphasis on the quotes) was the result of this mutation and likely many others. Not something Standing would like to accept, but that's irrelevant to the truth of the matter.

We see that the balance between virulence and transmission is an important aspect of virus evolution. However, viruses also evolve in order to avoid the immune system of its host. After prolonged exposure, the immune system will develop receptors and antibodies that bind to specific antigens of a virus. So the virus needs to constantly produce new strains with different antigens, which aren't recognised by the immune system. This mainly happens via mutations that happens within the genes that code for these antigens, which is called antigenic drift. It's the reason why we have to constantly make new flu vaccines. Another more dramatic mechanism is Antigenic Shift caused by reassortment, which happens when two (or more) strain of the same virus OR strains from two (or more) different viruses combine their genomes to form a new virus with different antigens. So a decline in fitness of a particular virus strain doesn't mean that it's genome is deteriorating. The host population will eventually develop immunity to a particular strain, regardless wether its genome is deteriorating or not. So Standing's argument "the extinction of human H1N1 virus shows genetic entropy" is rendered moot. It's also committing the fallacy of affirming the consequence. But it gets worse for Standing.

The H1N1 is technically not extinct. While the original strain is gone, as expected from how viruses continuously evolve new strains after the population acquired immunity to the old strains, the human H1N1 virus that was present back then in 1918 gave rise to almost all of the later influenza A viruses. Including those that aren't called H1N1 (H and N refer to the glycoprotein antigens haemagglutinin and neuraminidase), because their antigens changed either by antigenic drift of shift. Some of these descendants caused all of the subsequent pandemics.
1918 Influenza: the Mother of All Pandemics wrote:All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics.
The Persistent Legacy of the 1918 Influenza Virus wrote: Image
Genetic Relationships among Human and Relevant Swine Influenza Viruses, 1918–2009.
Yellow arrows reflect exportation of one or more genes from the avian influenza A virus gene pool. The dashed red arrow indicates a period without circulation. Solid red arrows indicate the evolutionary paths of human influenza virus lineages; solid blue arrows, of swine influenza virus lineages; and the blue-to-red arrow, of a swine-origin human influenza virus. All influenza A viruses contain eight genes that encode the following proteins (shown from top to bottom within each virus): polymerase PB2, polymerase PB1, polymerase PA, hemagglutinin (HA), nuclear protein (NP), neuraminidase (NA), matrix proteins (M), and nonstructural proteins (NS). The genes of the 1918 human and swine H1N1 and the 1979 H1N1 influenza A viruses were all recently descended from avian influenza A genes, and some have been “donated” to the pandemic human H1N1 strain.
This includes the human H1N1 (swine-origin Influenza Virus) S-OIV, that caused the 2009 "swine flu" pandemic. It's a dramatic example of antigenic shift as it originated via a series of reassortment events, including one "triple reassortment", from 4 different viruses that circulated between humans, birds and pigs!
- 2 pig strains: Eurasian "Avian-like" Swine H1N1 and Classical Swine H1N1
- 1 bird strain: Avian H1N1
- 1 human strain: seasonal H3N2 virus
Image
Image source
Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic wrote:Image
Figure 1: Reconstruction of the sequence of reassortment events leading up to the emergence of S-OIV.
Shaded boxes represent host species; avian (green), swine (red) and human (grey). Coloured lines represent interspecies-transmission pathways of influenza genes. The eight genomic segments are represented as parallel lines in descending order of size. Dates marked with dashed vertical lines on ‘elbows’ indicate the mean time of divergence of the S-OIV genes from corresponding virus lineages. Reassortment events not involved with the emergence of human disease are omitted. Fort Dix refers to the last major outbreak of S-OIV in humans. The first triple-reassortant swine viruses were detected in 1998, but to improve clarity the origin of this lineage is placed earlier.


To summarise, all of this doesn't any give credence to genetic entropy whatsoever. Virulence doesn't correlate to the fitness nor genome functionality of viruses, since causing deadly pandemics is not their primary function. For this reason, saying that a decrease in mortality during a pandemic is evidence of genetic entropy is completely erroneous. Populations will eventually acquire sufficient immunity against the strain that caused the outbreak, which are replaced by newer strains. So strains don't go extinct by building up too many mutations, nor do they just go extinct. Viruses, including the 1918 H1N1, kept and keeps evolving into new strains with different antigens in order to avoid our immune system, which is why we have to keep making new vaccines.

In other words, Standing for truth...
Image
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Fri Jan 18, 2019 4:33 pm
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

So….ehum…..well. As I said previously, Standing agreed to join the forum once I made a post addressing his claims on the H1N1 virus. So I did, after which I notified him that I made that post and asked him to join. This was the following back&forth discussion with him.
Standing: I have a lot of debates and discussions planned in the future on Modern Day Debates channel (they have been a blast and i love presenting the strength of our model for everybody to see), and so I really don't have time for blogs, maybe one day brother, maybe one day. Well what I will do is continue reading your blog, writing responses, and present my responses in a video. Hows that sound? Or when I finish the response, I can post it in the League of reason.

Me: Do I really have to debunk every 40 minute solo hangout that you are making?

Standing: No. You wrote a lot in your blog.

Me: Okay then, wouldn't you agree that a back and forth discussion where we address each point one by one (without making videos as an intermediate medium) would be more effective and productive? If you would have joined from the start, then I wouldn't have to write such long posts.

Standing: I am working on it, plus working on stuff for future debates/discussions (one is with Stefan Frello), and when I am done, I will either make a video addressing your blog, or just join the blog, and post it directly to it for you to read. Or maybe both.

Me: sigh.....apparently, you don't want to do this the easy way. 

Standing: Whats the easy way? You don’t want me to address everything at once?

Me: NO, I specifically told you the very opposite. One by one. Come on the league of reason and we can discuss each point one at a time. First we (or you) pick one point. So that would be the easy way. Wouldn't you agree?

Standing: Yes I agree. Do people join this anonymously, or is real names and what not required?

Me: I am anonymous on that forum so yeah, you can be anonymous. Better using the same name that you are using now, so people can see that it is really "Standing for Truth".

Standing: Okay. Sounds good. Ill talk to you guys later though got Sunday chores to get done. Peace for now.
:o I thought…Yes, finally! He can be persuaded to have a productive conversation after all this time. Perhaps we will finally get somewhere…….there is some hope after all!?……sadly, no. A few hours after having this agreement, he went on having a 2 hour hangout with other people, attempting (but failing) to debunk some things I said here and also some things that was said by Ration alMind.

:facepalm: Why would he do this after we both agreed to do this discussion using a written format? Well, my guess would be that he got very upset after he read my posts. He probably got also upset about what Ration alMind said in a separate discussion. Here is what Ration alMind has to say about the hangout (click on “show more”)
So I asked him if he is now expecting me to respond to this 2 hour hangout. And does he still want to continue with the written discussion, which (remember) he agreed to have.

Well, his response…..in a nutshell:
Standing For Truth wrote:Would you like me to set up a debate between you, Jeremy and myself? You can bring Ration. If not then thats fine but Im not joining your blog Ive looked over it and the arguments are sad. I will continue making videos debunking anything you put in it. I don't do this for you and the other BIASED atheists. I've chosen to do this to show FELLOW brothers in Christ that you evolutionary heavyweights of YouTube are not as smart as you think. I am enjoying this too much. Joining a forum is not something I am interested in. Debates are quick and easy and people can see both sides and come to a valid conclusion on whose side is better in light of the evidence. You have all fallen one by one, Jackson, RJ & the rest of the crew. You guys should retire because theres a new sherrif in town. This is Standing For Truths territory now. And Jeremy wiped the floor with you guys. You vs Jeremy on Haplogroups. Bring it. Chicken.
Firstly, He is completely wrong about debates. They are easy for people who are good in arguments with appealing rhetoric, but wether they actually have evidence to back up those arguments is incidental. Debates aren’t easy for discussing the evidence. So, more often than not, people won’t be able to come to a valid conclusion on who side is better. This is why debates are a venue more for entertainment rather than a venue for the academics. For this reason, you don't see scientists discuss their findings by having live debates. They carefully discuss the data in the literature, i.e. in a written format NOT in live debates. This is also the reason why declining an offer to a debate does NOT mean that the person is a coward!

And it appears that Standing has suddenly decided to not do the written discussion, despite the mutual agreement. What gives?? Standing says that he doesn’t want to join the forum (not blog) because my arguments are, quote…..sad….(not wrong, just "sad"?)...but they aren’t sad enough to not have live debates? They aren’t sad enough to not make hours of response videos that he is going to make? This excuse simply doesn’t add up.

He is obviously doing the same thing that Hovind tried with Aron. He realised that he can’t succeed with a written discussion, because under that format his claims are easily proven false. But he also cannot just ignore my rebuttals, since people might get the idea that he is unable to address them. That’s why he engages with filibusters and desperate posturing towards me. He is going to make the conversation as inconvenient as possibly by making hours upon hours of response videos and challenge me to random debates, while hoping that I won’t bother with all of that since practically nobody would.

And if I refuse to address his long videos or accept his debate challenges, he seizes the opportunity to call me a coward….and that's what he already did, calling me a chicken at the end......Yeah, really…..he refuses my proposal for a written discussion, yet he calls me the chicken. Hypocrisy, has never been that stark.

He also suffers from psychological projection. On numerous occasions in response to valid criticism, Standing has accused me (and others) of being biased…as if merely asserting that would prove that we are biased. As if proven bias would invalidate the actual criticism. And yet, here he demonstrates that he is absurdly biased by admission. He admits that he doesn’t do what he does in order to engage his opponents with the intend to discuss the evidence in a productive conversation. He does all of this JUST to show-off in front of his fellow creationist sycophants in order to gratify his ego. The association between his claims and his name “Standing for Truth” always seemed to be a contradiction to me, but this just sealed it.

I am still going to make a post about the points he made in that hangout that are directed at me, but Standing’s intellectual honesty, or rather the lack thereof, was a bigger issue that needed to be addressed first. Standing isn’t just wrong about practically everything, he is absurdly biased, annoyingly dishonest and a massive hypocrite. He may publish countless response videos, constantly challenge me to debate him and calling me a chicken for refusing to debate him live on youtube, but all of that is just a very sad attempt to hide the fact that…in response to my invitation for a written discussion on the league of reason forum….he is basically doing this
Image
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Last edited by Nesslig20 on Fri Jan 25, 2019 2:35 pm, edited 2 times in total.
Tue Jan 22, 2019 12:07 am
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Follow up. So, here I am going to address some of the things that were said in the 2 hour hangout and also the subsequent hangout that Standing made. I won’t bother with all of it, just the points that are mostly directed to me.
Standing has no right to complain about me not willing to address all the points he made in the hangouts.

Most of his counter points are just the same tired claims restated that were already addressed somewhere in this thread. Of course, I don’t expect him to remember everything I wrote here, which is why it would be more efficient to do this via a written format. If he wants me to address a specific point he made that I haven’t addressed yet, he must join the forum to have a written conversation, just as we agreed to do in the first place.

Okay first hangout (2 hour one)


5:52 - 10:20
As the first issue, he shows the piece I wrote about how Sanford misrepresented Kimura’s paper. Standing is dishonestly avoiding this very issue by calling it a “rabbit trail” for obvious reasons. He cannot admit that his hero, Sanford, used misrepresentation to support his claims. As a response, he is simply reasserting the same claims that I already addressed here: Why beneficial mutations just too rare to outweigh harmful mutations, why selection isn’t sufficient, or that we aren’t given the numbers of beneficial mutations.

I already mentioned, in my THIRD post, papers that explains how beneficial mutations outweigh the harmful ones with the effect of selection (even with Muller’s ratchet) and I also cited several papers on the distribution of mutations and their effects, including the numbers of those that are beneficial. But all of this is irrelevant to whether or not Sanford misrepresented Kimura, which is the point of contention. Stay on topic Standing.

10:21 - 11:53
Standing is still avoiding the issue that I mentioned in that specific section he screen shared. Standing previously stated that Kimura was simply speculating without evidence when he said that beneficial mutations are enough to counter the harmful mutations. You don’t give any evidence for that assertion Standing, however even IF I granted this for the sake of the argument, Sanford still misrepresented Kimura.

As you said yourself, Kimura believed that beneficial mutations were enough to counter the harmful effects of the deleterious mutations. As shown in this quote from his paper:
Motoo Kimura wrote:“Note that in this formulation, we disregard beneficial mutants, and restrict our consideration only to deleterious and neutral mutations. Admittedly, this is an oversimplification, but as I shal show later, a model assuming that beneficial mutations also arise at a constant rate independent of environmental changes leads to unrealistic results.”
“Under the present model, effectively neutral, but, in fact, very slightly deleterious mutants accumulate continuously in every species. The selective disadvantage of such mutant (in terms of an individual’s survival and reproduction - i.e., in Darwinian fitness) is likely to be of the order of 10^-5 or less, but with 10^4 loci per genome coding for various proteins and each accumulating the mutants at the rate of 10^-6 per generation, the rate of loss of fitness per generation may amount to 10^-7 per generation. Whether such a small rate of deterioration in fitness constitutes a threat to the survival and welfare of the species (not to the individual) is a moot point, but this can easily be taken care of by adaptive gene substitutions that must occur from time to time, say once every few hundred generations.”
But Sanford stated this:
“In Kimura’s figure, he does not show any mutations to the right of zero – i.e. there are zero beneficial mutations shown. He obviously considered beneficial mutations so rare as to be outside of consideration.”
“So selection could never favor any such beneficial mutations, and they would essentially all drift out of the population. No wonder that Kimura preferred not to represent the distribution of the favorable mutations!
"Kimura does not show the beneficial distribution, which is essential to the question of net gain versus net loss! When I show the beneficial distribution (while Kimura did not do this, I suspect he would have drawn it much as I did), anyone can see the problem: the vast majority of beneficial mutations will be un-selectable"
Notice the difference between what you just stated about Kimura’s view on beneficial mutations and what Sanford says here. This is a clear misrepresentation of Kimura's actual views on this issue. Sanford said that Kimura would agree with him on these points, but it’s quite clear that he wouldn’t, even according to you Standing!

24:47 - 26:14
Practically every paper that discusses the rooting of the mitochondrial haplogroups identifies the L node as the last common ancestor of all matrilineal lineages.
The Dawn of Human Matrilineal Diversity wrote:Image
Figure 1. Simplified Human mtDNA Phylogeny
The L0 and L105 branches are highlighted in light green and tan, respectively. The branches are made up of haplogroups L0–L6 which, in their turn, are divided into clades. Khoisan and non-Khoisan clades are shown in blue and purple, respectively. Clades involved in the African exodus are shown in pink. A time scale is given on the left. Approximate time periods for the beginning of African LSA modern- ization, appearance of African LSA sites, and solidization of LSA throughout Africa are shown by increasing colors densities. For a more detailed phylogeny, see Figure S1.
Evaluation of Group Genetic Ancestry of Populations from Philadelphia and Dakar in the Context of Sex-Biased Admixture in the Americas wrote:Image
Mitochondrial DNA phylogenetic tree.
Tree of mtDNA haplotypes based on median joining network with African American cases (yellow), African American controls (orange), Senegalese (white), European American cases (light green), and European American controls (dark green). Node sizes are proportional to the sample sizes, indicated by numbers within the node, with the exception of haplogroups H and K labeled by numbers in red. Variable positions typed for these samples in coding, HVS I, and HVS II region are distinguished by red, black and grey font, respectively. The main continental location is indicated by the background color with ochre indicating predominantly African, green West Eurasian, grey Asian, and pink Amerindian haplogroups. The raw data can be found in File S1.
The root of a tree can also be found by other means. For example, the first rooted tree that I showed was made by Ration alMind, from his blog. He simply used the “midpoint” of the unrooted tree as the root. Basically, this tree is based on the rather reasonable assumption that all lineages are on average equally distant from the root in terms of genetic differences. Ration alMind points out that this is also the same method Jeanson used to root the mt-trees of other animals in chapter 10 of his book. But with humans, Jeanson doesn’t pick the midpoint....because that would give inconvenient results......Jeanson's root ends up making the lengths of the branches of the African haplogroups substantially longer than the non-africana ones, because most of the human diversity lies in Africa. Jeanson gives the ad hoc explanation that all Africans simply reproduced much faster than all non-Africans or that they simply had a higher mutation rate. This rescuing device doesn't impress me at all.

Furthermore, even according to the creationist model, chimpanzees would be the proper out group since they are the ones that are the most similarly created to humans. It’s rather odd to ignore this, because if you root the tree in the way that Standing wants to root it, you end up having chimpanzees nested WITHIN the African haplogroups. Furthermore, you don’t even have to use chimpanzees as the out group. You could also use Neanderthal mt-DNA and creationists usually have no problem with the idea that we are related to them, but if you do this, you end up with the same root as you get with chimps.
The complete mitochondrial DNA genome of an unknown hominin from southern Siberia wrote:Image
Figure 3: Phylogenetic tree of complete mtDNAs.
A mitochondrial genome sequence of a hominin from Sima de los Huesos wrote:Image
Figure 4: Bayesian phylogenetic tree of hominin mitochondrial relationships based on the Sima de los Huesos mtDNA sequence determined using the inclusive filtering criteria.
Image
Extended Data Figure 6: Complete view of the mid-point rooted phylogenetic tree constructed with a Bayesian approach under a GTR + I + Γ model of sequence evolution using the Sima de los Huesos consensus sequence generated with inclusive filters as well as 54 present-day humans, 9 ancient humans, 7 Neanderthals, 2 Denosivans, 22 bonobos and 24 chimpanzees.


26:15 - 29:47
The very first time Standing is actually reading from what I said. There is also this other guy, I believe his name is Jeremy, who decides to call “atheist evolutionists” apes just to be disrespectful…as if that would be an insult. I don’t find that insulting at all considering the fact that we humans are apes in the same way that dogs are canines. He may as well call me a vertebrate as an insult. Moving on…

Standing reads my first problem that I had with Jeanson. He picks 3 haplogroups from an unrooted three and calls those the 3 main haplogroups. He doesn’t give any reason for why there aren’t 4 or 2 haplogroups. He completely disregards haplogroup R for example, dismissing it as merely a subset of N, while omitting that both M and N are subset of L3 which in turn is a subset of L since that is the root.

Jeremy is the first to respond and…oh boy…. He drops the “hitler and Stalin” thing out of nowhere, which produced an awkward moment of silence. After blabbering on about how atheists are the most biased people on earth, he finally gets to the damn point. He stated that the L, M and N haplogroups are unique and thus SEPARATED from the others from Africa? I think he didn’t want to say this, but by using that specific word “separated” makes it sound like he is claiming that the other haplogroups are not descended from L, M or N? It sounds like he is saying that these three are in fact haplogroups L3, N and M which are distinct from all the other L haplogroups, just as I explained before. But I give him the benefit of the doubt that he just misspoke there. (spoilers: I will retract this later).

He says that the first evidence for why there are just three main haplogroups, specifically L M and N and why the are so unique is because…..they are in the literature….and they show genetic differences from each other…. Not very impressive. Newsflash doofus, EVERY single haplogroup that we know about is in the literature and everyone of them is genetically different from each other (otherwise we wouldn’t be able to tell them apart). None of this make these specific three unique at all. He also mentions that the M and N haplogroups demonstrates the out of Africa migration of humans, which is correct! But how does this support Jeanson’s claims? I thought Jeanson is arguing against that scenario.....Anyway, even though he is right about it showing the out of Africa migration, Jeremy is still wrong when he said that L M and N are the closest to the North East of Africa. No, both N and M are indigenous OUTSIDE of Africa. The L haplogroup is centred within Subsaharan Africa, concordant with the evolutionary out of Africa scenario.
Reconstructing ancient mitochondrial DNA links between Africa and Europe wrote: Mitochondrial DNA (mtDNA) lineages of macro-haplogroup L (excluding the derived L3 branches M and N) represent the majority of the typical sub-Saharan mtDNA variability.
Image
Figure 1. Spatial haplogroup distribution of sub-Saharan African lineages in Europe based on control-region data. (A) Macro-haplogroup L; (B) haplogroup L1b. Green crosses in A indicate the sampled regions (see also Supplemental Data S1).


29:48 - 31:33
Here something weird happens. Jeremy is now INDEED saying that the L, M and N haplogroups are more similar to each other than the other L haplogroups, which shows larger genetic differences….the differences between L, M and N are distinctly fewer (as he puts it) than the NEXT closest haplogroup….another L something….eventually he pick L2 as the next closest haplogroup to the L, M and N cluster.

This basically confirms what my previous suspicion about him saying that the L, M and N haplogroups are unique and thus SEPARATED from the others from Africa. He is saying that the L (or rather L3), M and N haplogroups are all more closely related to each other than the next closest related lineages, L2…..well the next closest is actually L4, but L2 is still pretty close.
Updated Comprehensive Phylogenetic Tree of Global Human Mitochondrial DNA Variation wrote:Image
Figure 1. Simplified mtDNA phylogeny illustrating the use of alphabetical letters for haplogroup designation. All letters of the alphabet, except O (Palanichamy et al. [2004] proposed this label for a haplogroup that was later relabeled N12 by Hudjashov et al. [2007]), have been used so far. The root of the tree is indicated by a star representing the most recent common matrilineal ancestor of all humans. The L haplogroups are the most deep-rooting lineages and are African specific indicating the African origin of modern humans as well as the out-of-Africa exodus as also found based on other genetic as well as fossil data. Haplogroup L3 gave rise to macrohaplogroups M, N and R (the latter itself a subclade of N), which encompass all variation observed outside Africa. Nomenclature evolved in such a way that letters C, D, E, G, Q, and Z designate lineages belonging to M; letters A, I, S, W, X, and Y lineages within N; and B, F, HV, H, J, K, P, T, U, and V lineages within R. Haplogroup symbols followed by a star represent allother descendant lineages (besides the ones shown) of a particular clade, for which no unique alphabetical letters were reserved; e.g. N* stands for N5, N12, N13, N14, N21 and N22. Note that this tree should not be seen as a summary of global mtDNA variation (for this see the tree in the supporting information or at http://www.phylotree.org); it is merely meant to show the topology of alphabetically named haplogroups
And notice that near the very end of this time frame (around 31:20) he says that it’s the L3 Haplogroup that connects the N and M haplogroups to each other in the phylogenetic tree, just as I repeatedly pointed out to Standing.

So Jermy is actually arguing against the root that Standing is favouring without realising this. Why did nobody jump in and try to stop him from shooting bullets in their own feet? I guess they didn’t even listen carefully to what he was saying here.

I am skipping the rest of this hangout, since it is getting too long and I want to address some things in the next hangout.


00:00 - 3:02
Standing doesn’t realise that linkage group is a very old term for chromosomes, or rather it referred to the observation that some genes were inherited together contradicting independent assortment. Later we realised that this was due to the existence of chromosomes. Also, chromosomes do a nifty little thing called recombination, so his problem of linkage or rather “genetic drag” since that supposedly makes genetic entropy even worse is completely behind the science. And even if you have a situation where you don’t have recombination, let’s take asexual organisms that are subject to Muller’s ratchet, wherein the whole genome is linked. Well, I already cited this specific paper before.


4:36 - 4:50
Standing for Truth wrote:“It just goes to show…how the best these evolutionists like nesslig can do…is find their rebuttals on a blog or a review on amazon..”


That’s not all I did. I cited numerous studies directly here. For example, before I mention the amazon review, I explained that Sanford misrepresented the figures from Simonsen et al about the H1N1 virus (see first post in this thread), where I cited the literature. After this, I mentioned that this was already pointed out by a reviewer on Amazon. That was NOT my primary source!! Standing is being very dishonest when he states that I am only quoted blogs and reviews on Amazon. This is Standing’s head-up-his-ass way of avoiding the actual point, which was Sanford misusing the data of the H1N1 virus from the Simonsen et al paper.

7:40 - 11:24
Here Standing brings up Sanford’s rebuttal to the Amazon review. I thought, okay, this should be good. Standing is about to go into the details, explaining some of Sanford's points to me where the amazon reviewer went wrong. But that’s not what Standing did. He basically kissed Sanford’s ass for about a minute or so, praising his work and academic status, while screen sharing what he wrote. He also read Sanford’s piece on his persecution complex. Creationists are as persecuted in academia as flat earthers are. You won’t get in any trouble if you stated that you had a personal belief in a flat earth, but you should expect to see some raising eyebrows. However, if you are for example a teacher teaching flat earth geology in a classroom, you should be fired for it. So, I highly doubt that there is this grand conspiracy that Sanford’s claims there is, however this is totally irrelevant to whether he is right or wrong about his claims on genetic entropy.

At the very best, Standing quoted what Sanford wrote verbatim, without explaining anything. Which would be normally fine to me. If he wants to quote Sanford’s response, if it is relevant to my rebuttals, he can do that. However, remember that he previously stated that I am only quoting blogs and amazon reviews….which is WRONG….and now he is now doing the exact same thing he accused me of doing! Stop being such a hypocrite Standing!!

11:25 - 11:35
All the other stuff was mildly annoying at best, but the following is the only moment (so far) that got me mad as hell. Right, after he read a piece from Sanford’s response, regarding the size of the “no-selection-zone”, Standing says this:
Standing For Truth wrote:Nesslig just responds and says:
Straw Nesslig wrote:“oh….you know….his his rebuttal to that….you know….no good….SAD…whatever”
No….no, he is projecting…
:x Standing is lying - he pulled this straight out of his ignorant ass. I can definitively say that he is lying here with sincerity, because at the time when he spouted this verbal diarrhoea, I hadn’t made even a response to what Standing just read from Sanford. So this is not even a parody that refers to an actual response that I made. There is no alternative way you could spin this around. Simple ignorance or innocent stupidity cannot be used as excuses for this. Standing completely made up this so called "Straw Nesslig"!!

Also, regarding his accusation of projection….notice that he put the word “sad” in his made-up response? Let me refresh some memories by quoting what Standing said directly to me AFTER I notified him about my rebuttals in this thread:
Standing For Truth wrote: You are grasping at STRAWS nesslig. All your arguments against GE are weak and sad.

Im not joining your blog Ive looked over it and the arguments are sad.
So, he did not simply made up that "Straw Nesslig" line out of thin air…with this he projected this half-backed, knee-jerk response onto me!!!.....So he is also projecting his projections onto me at the very end as well.
:facepalm: Standing has no sense of self-awareness. :roll: You can’t make this up!!

11:36 - 12:27
Right after that abysmal sentence, he is just screen sharing some of Sanford papers. All he does is reading the titles of them and simply calling them “rock solid papers”. That’s it. While he does this, he says that he is….quote
Standing For Truth wrote:I am just digging deep into these
If you think that just reading the titles of papers count as “digging deep” you have even less of a clue than I gave you credit for. This is not something anyone can address, since he didn’t really say anything of substance that you can talk about. This is also one reason why I favour written discussion since we can take the time to get into those scary details, which is important if we want to dissect the facts. So I won’t bother with these papers. That’s enough for now. As I said at the beginning, if Standing wants me to address another point that he made which I didn’t mention here, he can come join the forum to have a written conversation, just as we agreed to have.
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Last edited by Nesslig20 on Fri Jan 25, 2019 9:45 am, edited 4 times in total.
Wed Jan 23, 2019 12:07 am
Nesslig20User avatarPosts: 288Joined: Wed Mar 16, 2016 6:44 pm Gender: Male

Post Re: New information, Genetic entropy and Junk DNA blablabla

Apparently, Standing just ran away after the latest rebuttal

So after I posted my latest rebuttal to his TWO hangouts, I notified Standing on google hangouts. This was his response....the ENTIRE response VERBATIM....nothing left out.... and it is pretty hilarious.

Standing For Truth wrote:No, the videos debunked your nonsense sufficiently. You can do what you have to do but we are onto other things now. Of course Ration says the arguments were "terrible" when in reality your guys arguments were "terrible"
See ya.

[standing left the hangout]


:lol: Nothing, no rebuttals, no arguments....just:
"I am right, you're wrong" and scuttles away...
Image

He probably needs to recover from the massive butthurt.
Image
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, and not those who know much, who so positively assert that this or that problem will never be solved by science."
Charles Darwin
Wed Jan 23, 2019 8:31 am
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