Joined: Oct. 2005
December 6, 2019 at 7:08 am
Bob O’Hara is Professor in the Department of Mathematical Sciences at Norwegian University of Science and Technology.
He jokes that,
“My career has been dedicated to discovering whether I am a biologist or a statistician – I intend to retire once I come to a definite answer.”
Thus, obviously Bob should have a fairly descent idea about what the mathematics behind Darwinian evolution actually entail.
And in post 171 (Professor) Bob O’Hara’s claims that,
“Fisher showed that the response to (directional) selection is determined by the additive genetic variance.”
Yet, besides the fact that, (as was shown in post 174), “When the realistic rate of detrimental mutations are taken into account, then it mathematically falsifies “Fisher’s belief that he had developed a mathematical proof that fitness must always increase”, besides that little inconvenient ‘correction’ to Fisher’s theorem that falsifies it, it is also now empirically shown, via Lenski’s “Long Term Evolution Experiment” (LTEE), that Fisher’s belief that beneficial mutations will be “additive” was also another false presupposition on Fisher’s part (and thus, is also currently a false presupposition on Bob’s part).
Specifically, “antagonistic epistasis” between beneficial mutations shows that beneficial mutations are not “additive”. As the following study found, “the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.”
Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
As Casey Luskin explained, The title of a summary piece in Science tells the whole story: “In Evolution, the Sum Is Less than Its Parts.”
New Research on Epistatic Interactions Shows “Overwhelmingly Negative” Fitness Costs and Limits to Evolution – Casey Luskin June 8, 2011
Excerpt: The title of a summary piece in Science tells the whole story: “In Evolution, the Sum Is Less than Its Parts.” It notes that these studies encountered “antagonistic epistasis,” where negative effects arise from epistatic interactions:
“Both studies found a predominance of antagonistic epistasis, which impeded the rate of ongoing adaptation relative to a null model of independent mutational effects.”
In essence, these studies found that there is a fitness cost to becoming more fit. As mutations increase, bacteria faced barriers to the amount they could continue to evolve. If this kind of evidence doesn’t run counter to claims that neo-Darwinian evolution can evolve fundamentally new types of organisms and produce the astonishing diversity we observe in life, what does?
That these findings falsify Darwinian expectations that beneficial mutations should be additive, these findings also reveal that Darwinists don’t even have a coherent explanation why “antagonistic epistasis” between beneficial mutations should even exist.
On the other hand, Intelligent Design advocates readily understand why “antagonistic epistasis” between beneficial mutations are as they are.
As was mentioned previously in this thread, instead of the genome being dominated by ‘genes for’ something, as is presupposed in Darwinian thought,
Gene previously linked to obesity is unrelated – June 29, 2015
Excerpt: … in the real world of careful analysis, scientists are just not finding the “genes” that the headline writers need. British geneticist Steve Jones points out that most human traits are influenced by so many genes that there is no likely systematic cause and effect:
“We know of more than 50 different genes associated with height … That has not percolated into the public mind, as the Google search for “scientists find the gene for” shows. The three letter word for — the gene FOR something — is the most dangerous word in genetics.”
And the craze is not harmless, he warns. …
,,, instead of the genome being dominated by ‘genes for’ something, as is presupposed in Darwinian thought, the ‘genes’ in a genome are instead now found to be existing in a holistic web of mutual interdependence and cooperation, wherein, “such traits are the work of thousands of genetic variants, working in concert.”
What If (Almost) Every Gene Affects (Almost) Everything? – JUN 16, 2017
Excerpt: If you told a modern geneticist that a complex trait—whether a physical characteristic like height or weight, or the risk of a disease like cancer or schizophrenia—was the work of just 15 genes, they’d probably laugh. It’s now thought that such traits are the work of thousands of genetic variants, working in concert. The vast majority of them have only tiny effects, but together, they can dramatically shape our bodies and our health. They’re weak individually, but powerful en masse.
This ‘holistic web of mutual interdependence and cooperation’ places severe constraints on Darwinian evolution.
As Dr. Sanford explained in his book “Genetic Entropy and the Mystery of the Genome”, if we were to actually get a proper “beneficial mutation’ in a polyfunctional genome of say 500 mutually interdependent genes, then instead of the infamous “Methinks it is like a weasel” single element of functional information that Darwinists pretend they are facing in any evolutionary search, we would instead be encountering something much more akin to this illustration found on page 141 of the book ‘Genetic Entropy’ by Dr. Sanford.
S A T O R
A R E P O
T E N E T
O P E R A
R O T A S
That five-word palindrome translates as,
THE SOWER NAMED AREPO HOLDS THE WORKING OF THE WHEELS.
This ancient palindrome, which dates back to at least 79 AD, reads the same four different ways, Thus, if we change (mutate) any letter we may get a new (beneficial) meaning for a single reading read any one way, but we will consistently destroy the other 3 readings of the message with the new mutation (save for the center letter). Moreover, mutating any subsequent letter in the palindrome will obviously induce “antagonistic epistasis” towards the first mutated letter, wherein any benefit that the first mutated letter may have conferred will be compromised by any subsequent change, with the benefit being compromised even further as even more letters are changed in the palindrome.
As John Sanford and company explained in the following paper, “As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero.”
Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 – May 2013
Conclusions: Our analysis confirms mathematically what would seem intuitively obvious – multiple overlapping codes within the genome must radically change our expectations regarding the rate of beneficial mutations. As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero. Therefore the new evidence for ubiquitous overlapping codes in higher genomes strongly indicates that beneficial mutations should be extremely rare. This evidence combined with increasing evidence that biological systems are highly optimized, and evidence that only relatively high-impact beneficial mutations can be effectively amplified by natural selection, lead us to conclude that mutations which are both selectable and unambiguously beneficial must be vanishingly rare. This conclusion raises serious questions. How might such vanishingly rare beneficial mutations ever be sufficient for genome building? How might genetic degeneration ever be averted, given the continuous accumulation of low impact deleterious mutations?
And the genome is indeed found to be severely poly-functional
38. Sanford J (2008) Genetic Entropy and the Mystery of the Genome. FMS Publications, NY. Pages 131–142.
39. Trifonov EN (1989) Multiple codes of nucleotide sequences. Bull of Mathematical Biology 51:417–432.
40. Trifanov EN (1997) Genetic sequences as products of compression by inclusive superposition of many codes. Mol Biol 31:647–654.
41. Kapranov P, et al (2005) Examples of complex architecture of the human transcriptome revealed by RACE and high density tiling arrays. Genome Res 15:987–997.
42. Birney E, et al (2007) Encode Project Consortium: Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project. Nature 447:799–816.
43. Itzkovitz S, Hodis E, Sega E (2010) Overlapping codes within protein-coding sequences. Genome Res. 20:1582–1589.
For one particularly crystal clear example of the staggering level of poly-functionality now being found in genomes, “there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins!”
Time to Redefine the Concept of a Gene? – Sept. 10, 2012
Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins!
While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25.
Thus in conclusion, “antagonistic epistasis” between beneficial mutations falsifies Fisher’s belief that beneficial mutations should be additive, and also reveals that Darwinists, (with their reductive materialistic framework), don’t even have a coherent explanation why “antagonistic epistasis” between beneficial mutations should even exist,
Whereas on the other hand, Intelligent Design advocates readily do understand why “antagonistic epistasis” between beneficial mutations are as they are. Moreover, the staggering levels of overlapping poly-functional complexity now being found in genomes, renders the Darwinian belief in ‘additive beneficial mutations’ to be a patently absurd belief. And, on the other hand, renders the belief that the genome was Intelligently Designed to be glaringly obvious.
If Bob O’Hara has an ounce of integrity in his responsibility as a professor, he should take all this falsifying evidence into account and adjust his teaching accordingly. Simply put, Darwinian evolution is empirically and mathematically shown to be false and Bob should, as a responsible educator, accept what the science is actually saying no matter how he may personally feel about it.
But as for me, I will walk in mine integrity. Redeem me, and be gracious unto me.
O come, O come, Emmanuel – (Piano/Cello) – The Piano Guys
Lol edited this to fix this link, but look at this shit.
December 6, 2019 at 8:43 am
ba77 – additive genetic variance is not an easy concept to understand: it doesn’t mean (for example) that mutations have to be additive. Epistasis will also include an additive component: the additive effect of an allele is the average effect of changing that allele (i.e. averaged over the different genetic backgrounds it could appear in).
As you might guess, I don’t feel inclined to change my views if I’m being lectured by someone who clearly doesn’t understand the topic.
|Code Sample |
Who wrote that link? An eighth-grader who still has to sound out words?
Edited by stevestory on Dec. 06 2019,10:12