Problems of Natural Selection from Humans to Bacteria
By Wolfgang G. Gasser
Essay "Problems with the Theory of Natural Selection" – 2000-11-20
david ford:
> Koestler, Arthur. 1978. _Janus: A Summing Up_ (NY: Vintage
> Books), 354pp. On 175-176:
>
> To
conclude this section, here is a less dramatic example of
> an evolutionary advance-- the
seemingly modest step which
> led to the transformation of the
amphibian egg into the
> reptilian egg. I have
described this process in _The Ghost
> in the Machine_, and am quoting
it again, because its
> explanation by the Darwinian schema
is not only vastly
> improbable, but logically
impossible.
>
> The
vertebrates' conquest of dry land started with the
>
evolution of reptiles from some primitive amphibian form.
> The
amphibians reproduced in the water, and their young
> were
aquatic. The decisive novelty of the reptiles was
> that,
unlike amphibians, they laid their eggs on dry
> land;
they no longer depended on the water and were free
> to roam
over the continents. But the unborn reptile
> inside
the egg still needed an aquatic environment: it
> had to
have water or else it would dry up at an early
>
stage. It also needed a lot of food: amphibians hatch
> as
larvae who fend for themselves, whereas reptiles hatch
> fully
developed. So the reptilian egg had to be provided
> with a
large mass of yolk for food, and also with
>
albumen-- the white of egg-- to provide the water.
> Neither
the yolk by itself, nor the egg-white itself,
> would
have had any selective value. Moreover, the
>
egg-white needed a vessel to contain it, otherwise its
> moisture
would have evaporated. So there had to be a
> shell
made of a leathery or limey material, as part of
> the
evolutionary package-deal. But that is not the end
> of the
story. The reptilian embryo, because of this
> shell,
could not get rid of its waste products. The
>
soft-shelled amphibian embryo had the whole pond as a
>
lavatory; the reptilian embryo had to be provided with a
> kind of
bladder. It is called the allantois, and is in
> some
respects the forerunner of the mammalian placenta.
> But this
problem having been solved, the embryo would
> still
remain trapped inside its tough shell; it needed a
> tool to
get out. The embryos of some fishes and
> amphibians,
whose eggs are surrounded by a gelatinous
>
membrane, have glands on their snouts: when the time is
> ripe,
they secrete a chemical which dissolves the
>
membrane. But embryos surrounded by a hard shell need a
>
mechanical tool: thus snakes and lizards have a tooth
>
transformed into a kind of tin-opener, while birds have a
>
caruncle-- a hard outgrowth near the tip of their beaks
> which
serves the same purpose, and is later shed by the
> adult
animal.
>
> Now according to the Darwinian
schema, all these changes
> must have been gradual, each
small step caused by a chance
> mutation. But it is
obvious that each step, however small,
> required simultaneous,
interdependent changes affecting
> _all_ the factors involved in
the story. Thus the liquid
> store in the albumen could not
be kept in the egg without
> the hard shell. But the
shell would be useless, in fact
> murderous, without the allantois
and without the tin-opener.
> Each of these changes, if they
had occurred alone, would
> have been harmful, and the
organisms thus affected would
> have been weeded out by natural
selection (or rather, as
> suggested above, by 'natural
elimination'). You cannot have
> an isolated mutation A, preserve
it over an incalculable
> number of generations until
mutation B occurs in the same
> lineage and so on to C and
D. Each single mutation would be
> wiped off the slate before it
could be combined with all the
> others. They are all
interdependent within the organism--
> which is a functional whole, and
not a mosaic. The doctrine
> that the coming together of all
requisite changes was due to
> a series of coincidences is an
affront not only to common
> sense but to the basic
principles of scientific explanation.
This is only one of some counterarguments, each alone strong
enough to refute neo-Darwinism. Here another variant of the
same argument:
Many animals hibernate. Hibernation is a
complex phenomenon
consisting of various components, from cellular metabolic
processes to several behavior patterns. These components are
linked together only insofar as they serve to the same purpose.
Therefore we can exclude that mutations responsible for one
component of hibernation enable all the other components
besides. (That a single mutation may switch on or off all the
components is a different problem.) DNA mutations which cause
animals to build a usable nest just at the right time must have
some complexity. Even under the completely unrealistic
assumption that four point mutations are enough to cause such
a behavior, the appearance of exactly these mutations is
extremely improbable. If yet the appearance of one single
component of hibernation is extremely improbable, then we can
exclude that all components might have evolved only by genetic
mutations. Nevertheless, hibernation evolved independently in
many species. (Source)
So because neo-Darwinism represents no longer a theory which
can be taken seriously as THE explanation of evolution, we must
either create more realistic and consistent evolution theories
or we accept some form of creationism.
---
Materialistic evolution theories are essentially SUPER-CREATION
or HYPER-DESIGN theories: the universe was hyper-designed and
super-created in such a complex way that blind downhill processes
can design and create whole ecosystems.
Essay "Problems with the Theory of Natural Selection" – 2000-11-21
Duncan:
| Also, hibernation time is continuous. All animals find a warm
place
| to sleep at night if they can. As hibernation length GRADUALLY
| increases, it is natural that preparation for such a sleep would be
| more cost-effective. This would gradually lead to more elaborate
| nest-building, and these two variables could simply increase in
| tandem without any need for an evolutionary leap.
|
| This is only an attempt at an answer. I welcome any criticism or
| outright denials, but I think the best explanation here is that all
| the variables mentioned here - protein supply, water supply, shell
| thickness, beak strength, hibernation length, preparation time -
| they are all continuous. None are useless without the others, but
| they complement each other, so it is natural that they evolve
| together.
|
| Concluding that these two rather dodgy examples invalidate
| Darwinism is just silly. Concluding that they validate Creationism
| is even sillier.
The question at issue is not whether gradual
transitions are
conceivable (and existent), but whether they can be explained
by the assumption that they are caused by random mutations.
Take the case of humans after their separation from
chimps some
million years ago. An upper limit to the number of individuals
having been born since then is 10^16 (i.e. 10^9 newborns per
year for 10^7 years).
10^16 is an extremely small number when compared with the number
of possible mutations in the genetic code. Let us assume that
the number of relevant base pairs (i.e. without junk DNA) is
100'000'000 pairs per chromosome set. This results in three
hundred million possible point-replacement mutations (because
every base pair can be replaced by three alternatives).
The number of possible combinations of two such point mutations
is already 10^17, i.e. higher than the number of all "humans"
ever born since our separation from chimps. The number of
all possible single-step mutations is even much higher than
the number of point-replacement mutations.
So, evolutionary advantages depending on two or more single-step
mutations cannot have had a relevant impact (at least for human
evolution). If we believe in neo-Darwinism we must assume that
every innovation is produced by a sequence of single-step
mutations, each of which alone responsible for a relevant
increase in fitness.
Once again Arthur Koestler:
'
You cannot have
' an isolated mutation A, preserve it over an incalculable
' number of generations until mutation B occurs in the same
' lineage and so on to C and D. Each single mutation
would be
' wiped off the slate before it could be combined with all
the
' others. They are all interdependent within the
organism--
' which is a functional whole, and not a mosaic. The
doctrine
' that the coming together of all requisite changes was due
to
' a series of coincidences is an affront not only to common
' sense but to the basic principles of scientific explanation.
A further quote from the The Psychon Theory:
Living beings never could adapt so promptly
to new conditions
(e.g. climatic changes), if corresponding (dominant) mutations
had to appear at first. The spread of the ability of adults to
make use of lactose has paralleled the spread of dairy farming.
The advantage of this ability is certainly not big enough to
explain its wide spread in only a few thousand years by
selection.
See also (especially the last two contributions)
Simple refutation of neo-Darwinism (was: Essay ...) – 2000-11-23
lenny:
> Why on earth would you limit the number of mutations to the number
> of individuals born? A great many (possibly most) mutations are
> likely so devastating that they lead to spontaneous abortion of
> the fetus. The number of individuals born places a limit only
> on the number of mutations that were not so traumatic that they
> prevented development to parturition, and that screws up your
> math.
We are dealing with the frequent case where evolutionary progress
requires simultaneous, interdependent changes of more than one
single genetic factor.
Let us assume that three factors must be affected for an increase
in fitness to emerge. So even if the probability of a beneficial
mutation in a newborn were as high as 10^-5 for each factor,
the probability that beneficial mutations occur for all three
factors is 10^-15, i.e. extremely improbable.
So neo-Darwinism requires essentially this hypothesis:
Every evolutionary innovation can be produced by a sequence
of single-step mutations, each of which alone responsible
for a relevant increase in fitness.
Because this hypothesis is obviously wrong, neo-Darwinism
is refuted.
If we take into account that many properties depending each
on more than one single genetic factor must evolve at the
same time, it becomes even more obvious that the neo-Darwinian
explanation of evolution is simply untenable.
Simple refutation of neo-Darwinism (Upright gait) – 2000-11-27
Wolfgang:
|| We are dealing with the frequent case where evolutionary progress
|| requires simultaneous, interdependent changes of more than one
|| single genetic factor.
Al Klein:
| There's no such case. A single change may lie dormant for
| generations, until joined by a second and, later, a third. Then,
| when the environment changes, the individuals with the 3 changes
| are the ones most fit.
The upright gait was only one of many traits which had to evolve
in us after our separation from chimps. For that to happen, the
structures of bones, of muscles and of tendons had to gradually
change. Let us ignore that in fact the bone structure (involved
in the upright-gait evolution) alone consists of several bones
with each several traits.
So let us make the completely unrealistic assumption that one
'progressive' single-step mutation in the genetic factor of each
(i.e. bone, muscle and tendon) structure is enough to entail
a relevant increase in fitness.
Let us further assume that the probability of such progressive
mutations in newborns is each as high as 10^-5. So we conclude
that among 10^15 newborns (i.e. a billion newborns of a million
generations), only one individual will carry all three
necessary mutations.
Because a change in only one or two of the three involved
structures cannot lead to a relevant increase in fitness (rather
the contrary), it becomes obvious that the upright gait cannot
have evolved in a neo-Darwinian way.
Confusing the origin of HIV: http://www.deja.com/=dnc/getdoc.xp?AN=686210184
Human vs. bacteria evolution (was: Simple refutation of neo-Darwinism) – 2000-11-30
Wolfgang:
||| So even if the probability of a beneficial
||| mutation in a newborn were as high as 10^-5 for each factor,
||| the probability that beneficial mutations occur for all three
||| factors is 10^-15, i.e. extremely improbable.
Mike Syvanen:
| It is an extremely subtle point of which
| many are unaware. To give an example in bacterial genetics. The
| mutation frequency for resistance to say antibiotic 1 is 10^-7
| and to antibiotic 2 is 10^-7 (these are in units of mutants arising
| per generation and are usually a little less than the frequency
| of mutants that would be found in a typical population).
| According to the reasoning given above the frequency of mutants with
| resistance to both antibiotics in the population should be 10^-14.
| In fact, it is usually about 1000 higher than that. This apparent
| dilemma can be explained by the same process that gives rise to
| the Luria-Delbruck fluctuation phenomena. This fact, coupled to
| the recombination that Lenny mentions, (especially if there is
| positive s on any of the mutations) makes the chances of encountering
| multiple mutations many orders of magnitude higher that would
| be expected from the random assortment model.
It is a logical fact: if two mutations in the genome have each
a probability of 10^-7 then the probability of both mutations
is 10^-14. This has at least in the general case nothing to do
with "the Luria-Delbruck fluctuation phenomena" or with
recombination. That the combination of both mutations actually
occurs with a probability of 10^-11 instead of 10^-14 is simply
further evidence for the rather obvious fact that mutations are
not completely random.
(See http://www.deja.com/=dnc/getdoc.xp?AN=500641694)
The increased probability of the combination of both mutations
can simply result from the genetic variability of the concerned
bacteria strain. If 10^-6 is the proportion resistant to
antibiotic 1, 10^-8 to antibiotic 2, and 10^-11 the proportion
of bacteria resistant to both antibiotics, then the probability
of the emergence of antibiotic resistant bacteria from
sensitive ones lies in the order of 10^-6 for antibiotic 1,
of 10^-8 for antibiotic 2 and of 10^-11 for both antibiotics.
(See http://www.deja.com/=dnc/getdoc.xp?AN=517092818)
The panpsychistic explanation further leads to this
prediction: if you start with a bacterium resistant to both
antibiotics then in the absence of the antibiotics the
proportions of resistant bacteria will decrease until
reaching the original values. That simply means that a
substantial part of the genetic variability of a strain
can easily reemerge from one single bacterium.
Whereas in the case of bacteria evolution, adaptations
resulting from mutations with probabilities of 10^-11 or
even less can have a relevant impact, such adaptions cannot
explain the evolution from monkeys to humans over a few
millions of years.
And take into account that (within neo-Darwinism) coherent
changes of the involved structures in upright-gait direction
are not more likely than coherent changes in the inverse
direction. The probability of incoherent changes however is
much higher, because the many parts which must work together
can evolve in very different directions.
Human vs. bacteria evolution (was: Simple refutation of neo-Darwinism) – 2000-12-01
Wolfgang:
|| I don't see why the distinction between "mutation
frequency"
|| and "frequency of mutants" should be relevant to my argument.
Mike Syvanen:
| Because mutation frequency (in terms of new
mutants formed per
| cell generation) is not the same as frequency of mutants (number
| of mutants found in a given population). This is not a
| distinction between frequencism and Bayesian logic. It shows
| up in experiment. About one streptomycin resistance mutant
| will appear in a population of 10^9 cells and there will be
| about 1000 nalidixic acid resistant mutants. One might think
| that one would have to screen 10^15 cells to find a double
| mutant. But no, one will likely occur in 10^12 cells. These
| mutations are completely independent of each other. They are
| also, under the conditions of the experiment, entirely neutral.
If I understand correctly then the experimental facts are the
following:
1) the first nalidixic acid resistant bacterium (mutant-1)
appears when a population reaches around 10^6 cells
(by
mutation 1)
2) the first streptomycin resistant (mutant-2) bacterium
appears when a population reaches around 10^9 cells
(by
mutation 2)
3) the first doubly resistent bacterium (mutant-1-2) appears
when a population reaches around 10^12 cells.
Nevertheless you claim that these experimental facts are
consistent with the following assumptions:
4) both mutations are under the conditions of the experiment
entirely neutral
5) mutations 1 and 2 are completely independent of each other
You consider the obvious contradiction between 1,2,3 and 4,5
as an "apparent dilemma [which] can be explained by the same
process that gives rise to the Luria-Delbruck fluctuation
phenomena".
Nevertheless, if we can exclude a selection effect then simple
logic leads to the conclusion that (at least) one of the
following statements must be true:
5a) the rate of mutation 1 in mutant-2 is around 10^-3
(instead of 10^-6)
5b) the rate of mutation 2 in mutant-1 is around 10^-6
(instead of 10^-9)
5c) the rate of a combined mutation in the original form
is around 10^-12 (instead of 10^-15)
All three possibilities refute your assumption 5.
If the "Luria Delbruck fluctuation" should have been invented
in order to remove such inconsistencies from the neo-Darwinian
belief system, then it would represent rather something like
a religious immunization strategy than scientific knowledge.
The evidence against neo-Darwinian 'randomism' is overwhelming
(at least for fully unprejudiced persons with common sense,
see for
instance).
Human vs. bacteria evolution (was: Simple refutation of neo-Darwinism) – 2000-12-06
Mike Syvanen:
> This problem does not have an exact or closed form
solution;
> it yields an unwieldy combinatoric if you try. Let's consider
> 100 independent clones each of which will be grown to a final
> population of 10^12 cells. The mutation frequency to nalR is
> 10^-6 per cell division and the frequency to stpR is 10-9 per cell
> division. In 50 % of the cultures, the first mutation to nalR
> will appear when the population reaches 10^6, this mutant will
> grow with the culture and after 20 generations will contribute
> 10^6 offspring to the final culture. New mutations arising
> elsewhere will also contribute to the final. Thus when the
> population reaches 10^12 there will be 2 x 10^7 nalR mutants.
> In that last generation when 2x10^7 cells divide there will
> 10^-9 times 2 x 10^7 = .02 or 1 % of the original cultures will
> have nalR stpR mutants created by this pathway. In one percent
> of the cultures the first nalR mutant will arise when the culture
> reaches 10^4, this culture will result in a jackpot of nalR
> mutants. There is a 2% chance that the first nalR mutant arises
> at 2 x 10^4 cell, and 4% chance that the first appears at 4 x 10^4
> and so on. This second 50 % of the culture will have a slightly
> higher chance of producing nalR stpR doubles ( about 2%).
>
> So there is ca a 3 % chance of the double mutants arising such that
> nalR is produced first and stpR is produced second. The chances of
> the double being formed by stpR first and nalR second is also about
> 3%. Thus we would expect to find 6 cultures out of the 100, with
> double mutants.
>
> So to conclude when we calculate the odds by multiplying 10^-9 to
> 10^-6 to obtain 10^-15 we are calculating the odds that the
> double mutant will arise in the same cell and the same generation.
>
> Population geneticists have recognized this problem for many
> years that is why they deal in terms of frequency of alleles
> in populations and make no effort to relate that to mutation
> frequency.
I've learned a lot a when trying to understand these
paragraphs, namely about the relation between mutation rate
and rate of mutants. Nevertheless what I've learned is not
consistent with your statement that mutation frequencies
"are usually a little less than the frequency of mutants
that would be found in a typical population".
Let us define a "mutation rate per replication cycle" of
10^-6 in such a way that both bacteria emerging by cell
division from a sensitive one have each a chance of 10^-6
of being resistant.
If we start with 10^12 sensitive bacteria we get 2 x 10^12
bacteria by every replication cycle. Let us keep the number
of bacteria constant at 10^12 by randomly destroying
bacteria after every replication cycle. Then we get this
result:
No mutants by definition in cycle-zero, 10^6 mutants in
cycle-1, 2x10^6 mutants in cycle-2, 3x10^6 mutants in
cycle-3, 10^7 mutants in cycle-10, 10^8 mutants in
cycle-100 and so on. Already after 100 replication cycles
we get a "frequency of mutants" (i.e. 10^-4) which is
substantially higher than the "frequency of mutation"
(i.e. 10^-6).
What are the implications for our above "experimental
facts"?
1) the first nalidixic acid resistant bacterium (mutant-1)
appears when a population reaches around 10^6 cells
(by
mutation-1)
We need 20 replication cycles in order to reach 10^6 cells
because 2^20 = 1.1 * 10^6. If the mutation rate were 10^-6
then we would expect on average not 1 but 20 resistant
bacteria when the population reaches 10^6 cells. So the
mutation rate must be only 10^-6 / 20 = 5 x 10^-8.
2) the first streptomycin resistant (mutant-2) bacterium
appears when a population reaches around 10^9 cells
(by
mutation 2)
Because 30 cycles are necessary in order to reach 10^9 cells
the mutation rate must be 10^-9 / 30 = 3 x 10^-11.
In this way it becomes even more obvious that there is a
HUGE "contradiction between 1,2,3 and 4,5". Nevertheless my
conclusions concerning 5a,5b,5c represent rather a case
of naive than of simple logic.