Re: Ernst Mayr: Where Are We (1976)



"Malcolm" regniztar@xxxxxxxxxxxxxx

> > JM:-
> > Because it is an "empirically true fact" that epistatic gene
fitnesses
> > (as you seem to use this term) are not heritable.

> M:-
> "Empirical" means "of experience". It is difficult to measure fitness,
or
> the contribution of any one gene to fitness, directly.

JE:-
Empirical means: a valid observation of nature which limits "experience"
to only _verified objective observations_ of nature, i.e. it excludes
the "experience" of subjective "witches" as a valid observation of a
science.

> M:-
> John Edser's argument goes; we know that it is unlikely that a a gene
> could
> produce something as complex as altruistic behaviour all on its own.

JE:-
My argument was and remains: organism fitness altruism is not, and never
has been, empirically based. All biological events so far classified
within Neo Darwinism as organism fitness altruism (OFA) have never
actually excluded organism fitness mutualism (OFM) as equally possible.

I have proven that Hamilton's Rule does not include any reference to
OFM. If you multiply the rule by -1 the magnitude of the rule remains
exactly the same so this mirror image rule does remain mathematically
equal but it is NOT biologically identical because fitness largess moves
in exactly the opposite direction: from Hamilton's recipient to the
donor as the diagnostic sign of c changes from positive to negative.
Hamilton et al have incorrectly argued that the sign of c can separate
altruism form mutualism within Hamilton's Rule. It will never be able to
do so until the total fitness of the actor is actually included and not
just deleted from the rule. All it can do as just a 100% relative
premise is separate selfishness from altruism as just relative opposite
propositions where only zero mutualism is represented.

Hamilton et al error of the misuse of just a relative proposition is
exactly the sort of error you can expect when biologically ignorant
mathematicians fail to correct (therefore misuse) an _oversimplified_
model of a theory of nature. The oversimplification within Hamilton's
Rule remains the artificial deletion by Hamilton et al of a mathematical
constant: the total fitness of the actor. This represents the
_empirical_ total (Darwinian) fitness of the actor.

Only as just a heuristic exercise is it valid to argue that "we know
that it is unlikely that a gene could produce something as complex as
altruistic behaviour all on its own" simply because not one single OFA
event (normally referred to as just "altruism") has ever been documented
in nature. OTOH many documentations of mutual fitness events exist. One
of the most important is the solution to the slime mould puzzle. I would
like to thank Dr Guy Hoelzer for supplying the reference. It has finally
been proven after many years of intense debate that _empirically_ the
supposed sacrifice of the cells that will form the stalk within the
slime mould slug aggregate is in fact an investment by parent cells in
their own reproductive fitness gain. The risk of non reproduction is
actually an investment cost that provides a mean fitness gain for each
slime mould cell within the aggregate, i.e. this selective event has
been proven fitness mutualistic per cell and not fitness altruistic. The
cells that fail to take the risk of forming the stalk and therefore not
reproducing at all will leave less total replicates of themselves on
average in the same population than those that do take this risk. Thus
the risk is well worth taking. This sort of scenario is obvious to
anybody who runs a business because risk is always unavoidable and at a
premium. Insurance sells risk reduction as a profitable resource and I
argue nature does the same. However it appears Neo Darwinists
cannot/refuse to see the argument. They always prefer to see altruism
instead.

> M:-
> If
> several genes are involved it is likely that mutations affecting the
trait
> are present on more than one gene within the population. So let's
assume
> we
> have three loci, a, b, and c, with alternate allele A, B, C, such
that
> the
> combination ABC gives a certain level of altruism. Now the chance of a
> relative also having the combination ABC is r^3 (skating over
Washburne's
> fallacy here).

JE:-
The above model that I supplied would assume that no linkage exists
between the 3 loci involved, i.e. each of the 3 loci are heuristically
supposed to exist on 3 separate chromosomes. Therefore this model
maximises and does not minimise the impact of epistasis. To minimise the
impact you must assume that these 3 loci are next to each other on
exactly the same chromosome. My model calculation of relatedness (r^e)
is indeed a model simplification which is better and more accurate than
the massive oversimplification that Hamilton et al assume where e
remains FIXED for all time to just 1, i.e. e is deleted and just
forgotten. Unlike the Neo Darwinists I _insist_ that my model (and any
other model) be corrected by the theory it was simplified/oversimplified
from BEFORE it is allowed as any valid proposition of science.


> M:-
> Therefore, and here is where I beleive he goes wrong, the
> combination will only spread if benefit exceeds cost by a ratio of
r^3.

JE:-
Your argument remains incomplete so I can't make any sense of it. What
exactly is the "benefit" and "cost" you refer to?

> M:-
> However the argument is not empirical, but mathematical.

JE:-
My argument was that r^e must be set minimally to the simplification of
e=2 and NOT JUST FIXED at the massive oversimplification of e=1 within
Hamilton's Rule. I specifically stated that gene fitnesses are either
epistatic and dependent or non epistatic and independent. If you have a
3 rd alternative please supply it. I referr to the _empirical fact_ that
all gene fitnesses remain epistatic and thus dependent, no exceptions.
If you can provide just one example of a non epistatic independent
genomic gene fitness that has actually been documented to exist in
nature then please supply it.


> M:-
> Joe Felsenstein
> posted a model a while back. Unfortunately he is not on speaking terms
> with
> John Edser so other sbem denizens never got to find out who was right.

JE:-
I called Felsenstein the "Pope of Neo Darwinism" in good humour and I
also suggested that his thinking remains entirely 100% relatively based
as was the Enron accounting fraud. I do NOT accuse him of a similar a
fraud but I do accuse him of chronic model misuse. He will not discuss
the correct/incorrect use of any model. He appears to be using all of
this as a pretence to never answer any of the questions I have put to
him. I remain on speaking terms with him but he refuses to be on
speaking terms with me until I apologise. Apparently, he has no sense of
humour and you are not allowed to accuse him of model misuse. I will
always refuse to apologise simply because Felsenstein has admitted that
none of the common Neo Darwinistic models are even testable. IMHO all
scientific propositions must be testable otherwise we are back to witch
hunting. It seems to me that Felsenstein is as much about the politics
of any situation as the science. I assume that this is a survival skill
acquired by the reality of his employment.

I have no other choice but to conclude that Felsenstein has no answers
to the questions I have asked of him so this must be the real reason he
refuses to reply. I can see no reason why anybody can refuse to answer a
simple question unless they were attempting to evade something. I am
happy to just to ask him questions and he answer them but he will
refuse. He also refuses to even name the theory Neo Darwinistic models
were simplified/over simplified from. More importantly he refuses to
correct any heuristic model results via their parent theory BEFORE they
are argued as valid propositions of science. He also appears be very
happy to allow popular simplified/oversimplified models to contest and
replace their parent theory, which of course is an absurdity.

> > JM:-
> > JM:-
> > snip<
> > Models exist for the cases of close (but not too close) linkage, but
> > they
> > are not exactly *simple* models. Models also exist which relax the
> > assumption of random mating, and which thereby make the epistasis
> > somewhat
> > "heritable" in that way. These models are definitely NOT simple.
> > snip<

> M:-
> It not obvious to me that epistatic interactions, if we relax
assumptions
> such as random mating or random meiosis, won't also lead to some
rethink
> of
> Hamilton's rule.

JE:-
Fixing e minimally 1 is just a massive oversimplification whereas
setting e to 2 is only a simplification. My proposed simplification
approaches empirical reality much more closely than Hamilton's massive
oversimplification. No valid argument exists that can sustain the common
misused oversimplification yet it still remains within Hamilton's Rule.

> M:-
> Also the "green beard effect", implausible for single
> genes, becomes less implausible if we start talking about groups of
genes.
> Maybe someone will post a model. However I cannot see how b > c r^e
will
> come out of any such model.

JE:-
The "green beard effect" fails when e=2 as does Hamilton's Rule because
the _minimal_ cost of 1 proxy reproduction blows out to at least 16 and
not just 2 normal reproductions, forgone. This is partly due to an
uncorrected error that Neo Darwinists keep on making which they
steadfastly refuse to correct. They wrongly allocate the donated fitness
b to the recipient and not the offspring of the recipient which is one
more generation removed. Therefore the maximal IBD relatedness any
recipient can have with normal sex within Hamilton's Rule is 0.25 and
not 0.5. Only Haldane's Pub Rule allocates largess to the recipient
itself allowing the maximal IBD relatedness to the commonly mooted
higher figure of 0.5. The minimal cost of one proxy reproduction within
the rule where e=2 is 0.25^2 = 0.0625 which represents 16 normal
reproductions. The rule fails even on just a 100% relative basis simply
because Hamilton's proposal of proxy reproduction replacing normal
reproduction is too expensive.

Give the fact that chromosomes exist but not one chromosome has been
proven to have an independent fitness to any of the others within the
same genome then it is fair and correct to assume a _minimal_ epistatic
model of two non linked loci with four alleles that code for the one
selectable trait. Anything smaller than this can reduce to just a
massive oversimplification allowing each allele to now have an
INDEPENDENT and not just a dependent fitness, i.e. Hamilton's over
simplification throws open an entirely heuristic 2nd level of selection
which is not required using my simplification of e = 2 within r^e.


> > JM:-
> > You also demand that the models work at the "fertile organism level
of
> > selection" rather than just at the "organism level". I understand
this
> > to mean that the selective fate of an immature organism is taken to
be
> > a function of its parents' genomes, rather than its own. But this
is
> also
> > empirically untrue, at least in part. While the parents' genomes
are
> > important (in plants and in animals with parental care, at least),
the
> > genome of the immature organism is different from that of its
parents
> > and it is very important in determining the fate of the immature
> organism.

> M:-
> Not really. Many organisms don't influence their own success
significantly
> until quite an advanced stage of development. A baby bird, unless it
has a
> serious defect, will hatch if the parents incubate and not if they
don't.

JE:-
Sterile immatures exist at the behest of their parents. It is incorrect
to assume sterile immatures are equal to fertile parents as Neo
Darwinists commonly assume within UNCORRECTED models. From a gene
centric point of view the genes in the parents use the genes in the
infertile offspring to help spread the genes in the parents. From a
minimal epistatic model view, an epistatic association between two loci
on two different chromosomes is using the genes in the sterile offspring
to promote the epistatic combination that exists within the _parents_.


> M:-
> As
> a chick, when huge mortality takes place, its fate will be determined
> largely by the parent's ability to bring food, parasites, and other
> nestmates. Only when it leaves the nest and begins to find food for
itself
> will its genetic make-up really begin to be very important in
determinig
> whether it reproduces or doesn't.
> I don't however see the relevance to models of altruism.

JE:-
These MODELS assume that the sterile immatures can donate 100% of their
fitness to their parents. In its extreme this produces eusocials. OTOH
refutable Darwinian THEORY states that no sterile form has any fitness
to donate because these forms all have just a zero heritable fitness. It
does not matter how well they survive or anything else because this
cannot be inherited until they become fertile. The Darwinian fitness
Rubicon is only crossed when sterile immatures become fertile adults,
i.e. Neo Darwinism and Darwinism ENTIRELY differ as to what fitness
actually is within nature.


> > JM:-
> > Models which make selection dependent upon two or three genomes are
> > definitely NOT simple. They are also unnecessary, since Hamilton
has
> > shown us how to work with a simple model in which the *inclusive*
> fitness
> > of an organism is taken to be dependent upon only its own genome.
> >
> You could have a relatively simple model in which fitness of A depends
on
> whether father is A or a. Let's say it is gene for alcohol
dehydrogenase
> and
> the organism in question, the beer monster, relies on sneaking some of
> dad's
> supplies in early development. If dad is A, then dad cannot drink, and
> baby
> beer monster may die of thirst. If dad is a, plenty of beers in the
> fridge,
> and he's away.
> >
> > I invite people who understand pop gen better than I do to comment
upon
> > my summary.

> M:-
> Is that a disinvitation to those of us who understand it worse?
> Seriously, once you understand maths it is yours. Given the
assumptions,
> it
> is no more possible that the chance of a new mutation being fixed by
drift
> is not1/(2N) than it is that 2+2 = 5.

JE:-
If the simple rules of epistemology were followed all this confusion
would just evaporate.

Here is a useful flow chart:-

1) Describe a theory just using words.

2) Describe at least one empirical refutation of the theory and one
verification of it. If not return to 1.

3) Form a simplified model of the theory (avoid oversimplified models if
possible because they are more difficult to correct and can be entirely
misleading).

I define a simplification as artificially deleting variables by setting
them to zero. They may also remain but may be reset to a known
artificial An example would be the assumption of an infinite population
within the HW model to provide a model of zero gene frequency change of
just two alleles at one locus using a binomial distribution. I define an
oversimplification as any artificial change or deletion of a defined
constant. An example would be letting c within E = Mc^2 equal a much
smaller number than its empirical value so the effect of time dilation
and mass increase with velocity can be grossly exaggerated within a
model for just illustrative purposes.

Heuristically "exercise" all these models to provide a useful indication
as to how well/badly the theory _appears_ to perform. In business you
play around with spread*** hypotheticals to provide an indication of
the apparent plausibility of any given scenario.

4) Correct and rework the any useful model results by the theory they
were simplified from as far as possible. This applies if only words are
employed to make these corrections.

5)Use the model to help create an empirical test to refutation of the
theory. If this is not possible return to 2.

Regards,

John Edser
Independent Researcher

PO Box 266
Church Pt
NSW 2105
Australia

edser@xxxxxxxxxx




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