Relevant extracts from my posts of July 1999
By Wolfgang G. Gasser
Despite many contradicting claims, it is a (logical) fact that
abiogenesis is a prerequisite for neo-Darwinism. If abiogenesis can
be proven impossible, the whole neo-Darwinian house of cards folds
up, leaving a lot of valuable stuff for alternative paradigms.
The difficulty to refute reductionist abiogenesis lies in the lack
of concrete knowledge. The more concrete facts and explanations are
brought forward, the more difficult it becomes for neo-Darwinism to
Everybody should agree that the common ancestor of terrestrial life
must have had the capacity of reproducing and the potential of further
evolving by selection. In order to refute neo-Darwinism, I have to
replace the gaps in knowledge by concrete assumptions concerning the
1) Adam was a bacteria-like creature with a cell wall.
2) Adam contained 10 different enzymes consisting of each 100
3) The genome of Adam consisted of 10 x 100 x 3 = 3000 nucleotides.
4) There were 100 copies of each enzyme within Adam.
5) Adam lived in a primordial pond with high proportions of
prefabricated amino acids, nucleotides and high energy molecules.
6) These nutrient molecules and waste molecules could easily cross
the cell wall.
7) The cell wall protected Adam from harmful molecules.
8) The replication of Adam occurred by
a) doubling the number of each enzyme from 100 to 200,
b) doubling the genome molecule(s),
c) splitting the cell into two equal parts by randomly
distributing enzymes and genome molecules to the parts.
If we ignore the cell wall, we conclude that 103'000 chemical uphill
reactions had to be carried out for Adam to replicate. It is perfectly
natural that the enzymes of very early life on earth could not have
worked as efficiently as the enzymes of modern bacteria. Error
correcting mechanisms did not yet exist.
So I think it is reasonable to assume that the error rate in building
chemical bonds was not lower than 1 percent. The task of chaining
building blocks correctly by using templates and energy from other
molecules is certainly not trivial. An error rate of 1 percent leads
on average to 1'030 errors per replication, 30 of them in the
The assumption that the majority of these errors have no or even
have positive effects is not reasonable. So even without fatal errors
or dangers from the environment, Adam and his descendants would have
degenerated during every cell division and certainly would have
become extinct after some generations, unless ...
What can be accepted as evidence depends on one's own world view.
The evidence of the existence of a first human couple from which
we all descend seemed overwhelming to most European scientists
(theologians) some centuries ago. The evidence that a single
living organism could have survived by replicating in a hostile
environment of only dead matter is in some respect even more
questionable than the evidence for a first human couple in a
Simple bacteria turned out to be (almost) as complex as Darwin
and his contemporaries thought animals and plants are. One must
not forget that the complexity of life was once considered so low
that even spontaneous generation of simple macroscopic organisms
Autotroph bacteria must be able to carry out a huge number
of different tasks in order to build up functioning copies of
themselves. The spontaneous generation of one autotroph first
progenote based on the chemistry of modern bacteria (amino
acids, nucleotides, etc.) or on a related one is virtually
zero. There must have been some kind of a continuous emergence
of a 'primitive ecosystem' which provided 'food' and made
possible innumerous attempts for the creation of more and more
autonomous cells by enzymes, ribozymes and other molecules.
One can compare the formation of cells by enzymes with the
formation of complex cities by humans. There never has existed
a first city all other cities derive from. There has been a lot
of horizontal technological transfer between villages and cities
(of different cultures).
John Wilkins writes:
"Even geneticists sometimes hold the sneaking suspicion that
evolution is not genetically based, because they observe in
small scale a general resistance of organic development to
change from the 'norm' or 'wild type'. If any biologist is
going to be anti-evolutionist, it will be one who works at the
molecular level, such as a molecular geneticist or biochemist."
Can anybody provide me with more information on this "general
resistance of organic development to change from the 'norm'
or 'wild type'".
By the way, last week I read that bacteria have been detected
below hundreds of meters of sediments on the seabed. This finding
was so unexpected that at first it was explained by bacterial
contamination. It was written in the article that the replication
cycle of these bacteria is assumed to be many decades or maybe
even hundreds of years, but no explanation was given for this
assumption. I suppose it is because of 'food'. If bacteria can
only survive by increasing entropy, survival becomes impossible
the sooner, the shorter their replication cycles.
Is there any scientific work having predicted antibiotic-resistant
bacteria before the fact? I was rather under the impression that
scientists had been surprised by the emergence of multiple-
antibiotic-resistant bacteria in such a short time.
If (the enzymes of) bacteria or viruses become resistant to toxins
or drugs then it is explained by the appearance of mutations. But
also long-living organisms such as animals and plants can get
accustomed to toxins and drugs. Take the case of anti-HIV-drugs.
In many cases, HIV positive people develop side effects when they
first start taking a new anti-HIV drug, but with time, the side
effects lessen or even disappear. But when this happens, also HIV
often has become resistant to the drugs.
(According to the psychon theory, enzymes of long-living organisms
can become resistant to toxins and drugs even without mutations.
That's a testable prediction!)
If the rate of RANDOM point mutations can vary between 10^-4 and 10^-12
(a range over eight orders of magnitude) then almost in every case a
beneficial mutation in bacteria and viruses can be called RANDOM.
Suppose the case that under certain repeatable conditions a helpful
mutation regularly occurs and is selected for. Suppose further that
this mutation actually has a substantially higher probability than a
random one. Can such a case refute neo-Darwinism? No. Neo-Darwinists
only conclude that the region where the mutation occurs has for some
unexplained reason an exceptionally high mutation rate.
Darwins theory, also called the theory of natural selection, is
only one possible theory of evolution (or continuous creation) and
certainly not THE theory of evolution of the third millennium.
And take into account that selection implies reproduction with
random mutations (and recombination), and that genetic drift
(to-FAQ: "a random change in allele frequencies") is essentially
the same as selection. Whereas natural selection is based on a
higher reproductive success, genetic drift is based on random
It is generally acknowledged that mutation rates are very different
within a single genome. There are genes such as cytochrome-c and
ubiquitin with a mutation rate of almost zero. Also within genes,
regions with high mutation rates are confronted with highly
Around 70 percent of the mutations of the third position of a DNA
triplet are silent. According to Motoo Kimura (Scientific American,
11/1979) such positions seem to be especially variable. If they
actually have a higher mutation rate than the first two positions
of triples then neo-Darwinism has a big problem.
There are cases where bacterial resistance to an antibiotic depends
on one single point mutation. It is very surprising how easy it is for
an enzyme that is inhibited by an antibiotic to become an enzyme that
hydrolyzes that antibiotic.
One single point mutation and the enzymes defends itself by attacking
One single point mutation, and the enzyme carries out in addition to
its normal tasks the task of hydrolyzing its own aggressor!
One single point mutation resolving all biochemical problems involved
in adding such a complex function to a protein without spoiling its
To explain all this by a lucky conformational change resulting from
the substitution of one amino acid by another defies common sense,
logical reasoning and simple probability estimates.
One cannot refute the possibility of directed mutations by a few
experiments whose results allow a random mutation interpretation.
That all or most possible point mutations are regularly tried
out with more or less the same probability seems to me merely an
In a genome consisting of 10^7 base pairs there are each 10^7
possibilities to cut out one, two, three or more base pairs. There
are 4 x 10^7 possibilities to insert one base pair, 4^2 x 10^7 to
insert two and 4^n x 10^7 possibilities to insert n base pairs.
20^10 x 10^7 = 10^20 possibilities exist for the insertion of a
sequence of ten amino-acids.
"Hall began working with a system that required two mutations to
occur before E. coli could use the sugar salicin. One of the
mutations, he documented in a 1988 Genetics article, is so rare in
growing cells that he failed to detect it. But plated on salicin,
Sal+ revertants appeared after a delay of about 12 days. Their
frequency was orders of magnitude greater than expected if the two
mutations were occurring independently and spontaneously.
Furthermore, the rarer spontaneous mutation happened first. This
mutation was excision of an insertion sequence. It was followed
relatively quickly by the second mutation, which only then permitted
transcription. When salicin was absent, Sal+ revertants had no
advantage, and Hall was unable to detect excision mutants."
It is always possible to explain away the "apparent" increased
probability of advantageous mutations by some ad-hoc-hypothesis.
"Hall wrote that the problem 'is to explain how selective
conditions could increase the frequency of useful mutations
without increasing the frequency of mutations at other loci.'"
The psychon theory also can explain why genes, even in the case of
large populations, do not drift apart into uncountable alleles but
rather converge to a few or even to one single allele. It's not
selection, it's MUTATION!
Because of the huge number of animals it is impossible to explain
by genetic drift the fact that there is only one single allele of
ubiquitin in all animals. Drift only works for little populations,
but certainly not for all animals if considered as one species.
The alternative that every mutation in animal ubiquitin is lethal
or harmful enough to disappear by selection seems much more
unreasonable to me than the assumption that (non-silent) mutations
are almost inexistent in ubiquitin. Also the existence of 'hot
spots' could suggest the existence of 'cold spots'.
Think about the evolution of mankind during the last Million of
years. The mean age at death was certainly lower than today. So
we can assume that the average number of children per couple was
ten (the less, the better for my argument). We can further assume
that children had on average three mutations actually influencing
the phenotype and that fifty percent of the children died
independently of their genetic constitution.
If the probability that a mutation is harmful is 80 percent, then
it is very improbable that mankind could have further evolved,
because genetic selection could only act on five children two of
which had to survive.
If one takes into account all facts and tries to be consistent,
then one concludes that the many highly conserved regions of
genomes cannot be the result of continuous selection, but must
be the result of low rates of mutations.
According to Wesley's page  the human cytochrome-c does not
differ from the one of chimps and according to my biochemistry
encyclopedia pigs differ neither from cows nor from sheep.
Your six-substitution-rule would result in around 100^6 or 10^80
possible selectively neutral alleles of cytochrome-c. You even
claim that "for the vast majority of proteins, such as cytochrome C,
trypsin, haemoglobin, barnase and lactate dehydrogenase it is an
In any case, the fact that pigs, cows and sheep all have the same
cytochrome-c is a huge ENIGMA within neo-Darwinism, I even dare to
say that it's a further knockout blow to pure materialism. Think
about the odds!
1444 different alleles can emerge from animal ubiquitin by a single
point mutation. The fact that none of these alleles actually can be
found (with a reasonable frequency?) in animals must be explained
The claim that "drift works in arbitarily large populations" is
simply wrong. That genes have converged to only very few or even
one single allele during evolution is an empirical fact. Its
explanation by genetic drift, however, is rather a typical case
of the "ordinary unintentional scientific dishonesty".
| However, with DNA sequences there is an extra level of redundancy. The
| genetic code itself is redundant; on average there are 3 different
| codons (a codon is a triplet of DNA bases) that can specify the exact
| same amino acid.
| Thus, for cytochrome c there are 3^104, or over 10^49, different DNA
| sequences (and, hence, 10^49 different possible genes) that can specify
| the very exact same protein sequence.
| As mentioned above, the cytochrome c proteins in chimps and humans are
| exactly the same. The clincher is that the two DNA sequences that code
| for cytochrome c in humans and chimps differ by only one codon, even
| though there are over 10^49 different sequences that could code for
| these two proteins.
Because neither selection nor genetic drift can explain that human
and chimp [cytochrome c] DNA-sequences did not drift apart by random
mutations, neo-Darwinism is definitively dead !!!
That the achondroplasia mutation occurs at a rate of about 10^-6
and "with a couple of exceptions, always involves a particular
nucleotide change and amino acid change" is certainly not
consistent with the principle of random mutations. In a similar
way also mutations leading to cancer are far from being totally
The psychon theory explains substantially increased mutation
probabilities by the existence of psychons corresponding to
alternative alleles. In such a way, alleles can survive even
if they lead to death before reproduction.
What I write here may seem strange to someone who believes in
orthodox materialism, but the psychon thesis leads to lots of
testable predictions (and even to completely new medical methods).
For instance it predicts that artificially induced mutations
will mutate back to the original sequence with a substantially
Assume that the probability for a selectively neutral random
mutation in a certain protein is 10^6. If we assume a constant
population of 10^9 with one single allele at the respective
locus in the first generation, we get 10^3 alleles differing
from the original form in the second generation. After a million
generations a huge number of different selectively neutral
alleles have appeared and the frequency of the original allele
is reduced to around 37 percent.
That's simplest probability theory and cannot be denied in a
And what about domesticated species becoming wild. After a few
generations individuals with reduced domestication traits can appear.
How can this happen in a few generations if the necessary mutations
do not occur? Also in the case of extremely inbred rats, having
undergone prolonged gene purgation, genetic variability can reemerge
In my (homozygous) example above, in the second generation 1000
new alleles have appeared. Every of these alleles would have a
theoretical probability of 10^-9 (inverse of the population size)
to reach 'fixation' by drift after a huge amount of generations,
only if no more mutations occurred. But in every new generation
around 1000 alleles differing from the most frequent allele do
| My point was that the hypothesis of common descent predicts that
| chimps and humans should have similar DNA sequences, and they do
| despite incredible odds.
But if the odds are too incredible, then some kind of order-creating
principles apart from random mutation and selection must be assumed.
| When considering your cyt c sequence and your mother's, the exact same
| incredible odds are involved - yet we don't "assume" any order-creating
| principles, aside from heredity.
Over one generation it is certainly not astonishing that DNA sequences
remain unchanged. But if sequences do not change over 100'000, 1'000'000,
10'000'000, 100'000'000 or even more generations, your objection becomes
It is a logical consequence of neo-Darwinism that all possible DNA
sequences coding for a given amino acid sequence are equivalent.
Therefore this theory predicts the existence of lots of different DNA
sequences for a given amino acid sequence (and in addition to that also
the existence of lots of more or less functionally equivalent alleles
for all gene loci).
| The catch is that there aren't enough genes. The human genome has
| approximately 70,000 genes. If genes are to determine traits
| quasi-continuously it will take 10-20 genes to control one trait which
| means that the number of traits controlled by the genome is on the order
| of 5,000 traits OR LESS.
| The observation that genes affect many traits and vice versa is not
| cogent; the issue is one of degrees of freedom. Likewise appeals to
| self-organization are not to the point; self-organization can elaborate
| the effects of genes but the variation must be supplied by the genome.
| It is relevant to point out that a gene on average consists of a
| thousand base pairs, thereby supplying many bits of information.
| However most of this supply of information is a mirage. The vast bulk
| of a protein is devoted to folding up into the right shape. The region
| of interest is the hot spot which only consists of a handful of amino
| acids. It should also be noted that a fair percentage of the genome is
| devoted to house-keeping machinery for the eukaryote cell.
| The problem then is that a few thousand (or less) evolvable traits is
| not enough to account for the evolution of the morphology of human
| beings and our fellow vertebrates. It does seem to be true that the
| synthesis accounts for the evolution of bacteria (and presumably the
| monera) - the number of traits to be governed is much smaller and the
| effects of the genome are strictly localized. However the synthesis was
| developed to account for the evolution of the metazoa and the metaphyta*
| in terms of population genetics and this, manifestly, is what it does
| not do.
| Look at beak size in those finches, for instance -- it's variation that
| can be quantified with a few simple parameters, but all the underlying
| biology is a total mystery.
There have been a lot of innovations in humans after their separation
from chimps several hundred thousand generations ago. If all what makes
us different from chimps depends on random mutations and selection then
mutations must occur with a certain frequency. But if not even the
many possible neutral mutations leaving amino acid chains unchanged
occur then it becomes highly improbable that mutations are the primary
cause of evolution or at least that mutations are random.
We cannot explain the evolution of humans after their separation
from chimps by the same means as the evolution of bacteria. As I
have already stated in another post, it is not very likely that
natural selection could have acted on more than five births per
couple per generation, because many deaths are unrelated to
Neo-Darwinism states that random mutations are the primary cause
of human evolution. So almost all deleterious mutations must be so
harmful that concerned gametes do not lead to pregnancy (or result
in early spontaneous abortion), and the remaining (slightly)
harmful mutations in new-born must not be substantially more
frequent than (slightly) beneficial mutations.
Two beneficial point mutations per generation affect 4 bits and
after 300'000 generations 150'000 bytes have been beneficially
changed. Can this account for all the differences between chimps
and child prodigies (e.g. chess, piano)? I don't think so.
In addition to that, the two beneficial mutations per generation
must spread over the whole population by selection whereas at
the same time deleterious mutations must disappear by selection.
Is this a realistic scenario? I don't think so.
Remember, all biological innovations of human evolution are said
to derive from random mutations. The proportion of beneficial to
deleterious mutations is therefore a crucial factor.
If "there are still 10^45 genuinely functionally and phenotypically
equivalent DNA coding sequences" [for cytochrome c] then one must
not take it for granted that the common ancestors of chimps and
humans used only one single version of more than 10^40 possibilities.
There is also no obvious reason within neo-Darwinism why most (all?)
humans share one version and most (all?) chimps share another one.
NEO-DARWINISM DOES REMAIN DEAD because it predicts either huge
numbers of functionally equivalent alleles and coding sequences or so
many constraints on non-deleterious mutations that evolution becomes
impossible (at least in the case of species having long replication