Pekka Ala-Mäyry kiisti muistikuvani aikaisemmasta keskustelusta, jossa hän
natkutti pitkään Kimuran käppyrästä ja syytti Sanfordia vääristelystä, ja
toisti nyt samoja syytöksiä haasteketjussa. Kommentoin siellä vain lyhyesti,
kun oli kiire ja viestissä oli paljon muitakin kommentoitavia kohtia, joten
tässä nyt pitempi versio:
Pekka Ala-Mäyry toisteli ihan samaa kritiikkiä, jota eräs Scott suolsi
nettiin noin 10 vuotta sitten, Pekka ei selvästikään ole itse löytänyt
mitään vikaa vaan lähinnä copypastaa evotovereittensa harhoja. Joihin
Sanford on vastannut jo lähes 10 vuotta sitten:
2. Kimura's Figure:
Scott makes a huge deal about my reference to a figure in Kimura's work. He
misrepresents me by arguing I misrepresented Kimura (I did not claim Kimura
agrees with me). But this is a rabbit trail; the argument is not about
Kimura. The crucial issue is about defining the correct distribution of
mutation effects. For deleterious mutations, Kimura and most other
population geneticists agree the distribution is essentially exponential.
Figure 3c in my book (based upon Kimura) shows an exponential-type
distribution of deleterious mutations, with most deleterious mutations being
'nearly-neutral' and hence un-selectable (effectively neutral).
But, as I point out, Kimura's picture is not complete, because degeneration
is all about the ratio of good to bad 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
(Figure 3d).
Scott does not appear to contest my representation of the mutational effect
distribution, which is the main issue here. Scott should easily be able to
see that most mutations fall within the 'no-selection zone' and that almost
all of them are deleterious. So even with strong selection, this entire zone
can only undergo degeneration. Outside this zone, the substantially bad
mutations will be selected away, and an occasional rare high-impact
beneficial will be amplified (which can explain isolated events such as
antibiotic resistance).
ja sitten myöhemmin, käytyään läpi kaikki 10 kohtaa, Sanford kertoo:
Scott and I corresponded briefly before his posting, and I tried to explain
to him why his criticisms were not correct. I did not find him to be a very
good listener as I tried to explain how he was misrepresenting me. I then
sent him a series of preprints (in press), which extensively and
conclusively addressed all his objections. Upon reading his essay now, I can
see he did not bother reading those preprints, which are very rigorously
written scientific research papers. I also see from his current arguments,
that he really did not give my book a fair read. If Scott has misrepresented
both the book and myself, then which of us is lacking in integrity?
Ja myös sitä Pekka Ala-Mäyrynkin vinkumaa aidosti hyödyllisten mutaatioiden
määrää on kommentoitu
3. Just how rare are beneficial mutations?
Scott speaks as if I do not acknowledge there are beneficial mutations. I
acknowledge them very openly in the book, but I also insist that beneficials
must be very rare compared to deleterious mutations (as do nearly all
geneticists). The critical question is "how rare?"
Genomes are the genetic specifications that allow life to exist.
Specifications are obviously inherently SPECIFIC. This means that random
changes in specifications will disrupt information with a very high degree
of certainty. This has become especially clear ever since the publication of
the ENCODE results, which show that very little of our genome is actually
'junk DNA'.10 The ENCODE project also shows that most nucleotides play a
role in multiple overlapping codes, making any beneficial mutations which
are not deleterious at some level vanishingly rare
(
https://doi.org/10.1142/9789814508728_0006). Our own numerical simulations
(in press) show that that unless beneficial mutations are extremely common,
they are not sufficient to compensate for accumulating deleterious
mutations.
The bottom line is that selection removes only the worst deleterious
mutations and amplifies only the best beneficial mutations. This means that
the accumulating damage is largely invisible (like rust on a car), while
adaptations tend to be highly visible (e.g., antibiotic resistance). This
means that even if Scott presents us with 1000 examples of adaptation via
beneficial point mutation, he has still failed to address the key issue-net
gain versus net loss. Adaptation explains fine-tuning to an environment; it
does not explain the astounding internal workings of life. It does not begin
to explain the mystery of the genome.
Where are the beneficial mutations in man? It is very well documented that
there are thousands of deleterious Mendelian mutations accumulating in the
human gene pool, even though there is strong selection against such
mutations. Yet such easily recognized deleterious mutations are just the tip
of the iceberg. The vast majority of deleterious mutations will not display
any clear phenotype at all. There is a very high rate of visible birth
defects, all of which appear deleterious. Again, this is just the tip of the
iceberg.
Why are no beneficial birth anomalies being seen? This is not just a matter
of identifying positive changes. If there are so many beneficial mutations
happening in the human population, selection should very effectively amplify
them. They should be popping up virtually everywhere. They should be much
more common than genetic pathologies. Where are they? European adult lactose
tolerance appears to be due to a broken lactase promoter [see Can't drink
milk? You're 'normal'! Ed.]. African resistance to malaria is due to a
broken hemoglobin protein [see Sickle-cell disease. Also, immunity of an
estimated 20% of western Europeans to HIV infection is due to a broken
chemokine receptor-see CCR5-delta32: a very beneficial mutation. Ed.]
Beneficials happen, but generally they are loss-of-function mutations, and
even then they are very rare!
Huomatkaa merkkijono "as do nearly all geneticists". Sanford ei todellakaan
keksi omasta päästään perättömiä väitteitä, vaan lähinnä toistaa teidän
evolutionistien omien tiedemiesten esittämiä faktoja, ainoa ero että hän
sitten vetää niistä faktoista loogiset johtopäätökset ja nöyrtyy niiden
edessä, kun taas evotieteessä aletaan heilutella käsiä uskonkiihkossa nenä
pystyssä ja suu vaahdossa...
Vaan mitäs Kaj Stenberg tuohon allaolevaan sanoo??
Kondrashov, an evolutionist who is an expert on this subject, has advised me
that virtually all the human geneticists he knows agree that man is
degenerating genetically. The most definitive findings were published in
2010 in the Proceedings of the National Academy of Science by Lynch.4 That
paper indicates human fitness is declining at 3-5% per generation. I
personally feel the average mutational effect on fitness is much more subtle
than Lynch does-so I think the rate of human degeneration is much slower
than he suggests-but we at least agree that fitness is going down, not up.
Can Scott find any qualified geneticist who asserts man is NOT now
degenerating genetically?
Löydätkö sinä, Stenberg, yhtään pätevää geneetikkoa joka väittää että
ihmiskunta ei rappeudu geneettisesti?? Tai pystytkö peräti osoittamaan, että
Kondrashovin tuntemat geneetikot ovatkin vähemmistö???
https://creation.com/genetic-entropy
--
--TJT--
Kondrashov, an evolutionist, ... virtually all the human geneticists he
knows agree that man is degenerating genetically.