Re: Most important paper in evolutionary biology
- From: "John Edser" <edser@xxxxxxxxxx>
- Date: Wed, 28 Sep 2005 16:11:48 -0400 (EDT)
"Jim McGinn" jimmcginn@xxxxxxxxx wrote:-
> > > Most of the problems of the current paradigm are
> > > the result of faulty semantics. Once the semantics
> > > are nailed down the validity of their arguments
> > > disappear.
> > Most of the confusion is confusion regarding semantics. Yes.
> > But it will come as no surprise that I disagree as to who is confused.
> > For McGinn, the key word is 'relatedness'. McGinn can see no sense
> > in using IBD as a measure of relatedness.
> Correct. It's a perfectly senseless notion. And this was repeatedly
> confirmed by the fact that nobody (yourself, Joe, etc.) was able to put
> together some words into a sentence that amounted to something more
> than, "take my word for it, it makes senses. Trust me.
JE:-
IBD remains a valid _probability_, that is all. It is just the probability
that a SINGLE allele from ONE parent ORGANISM has been reproduced in another
ORGANISM where the ORGANISM and NOT the allele provided the criterion of
"parent".
The big problem with IBD is what can it be validly used for? The first thing
to understand about IBD is that it has another critical, but _poorly
emphasized_ criteria: the parent gene and the related gene must remain
exactly the same gene. If the gene replicate mutates then the IBD
probability calculation must be restarted from ground zero i.e. you must
start the IBD calculation from the organism with the mutated gene all over
again and not from the parent with the non mutated gene.
Quite clearly, exactly the same genes need not have been replicated from the
same parent organism. If the hox gene within a snail and myself are exactly
the same gene this does not mean that the hox gene in my own daughter and
the hox gene in the snail, even if they are exactly the same gene, had
anywhere near the same probability of being replicated from myself. Jim
McGinn's argument that it does not matter at all where the gene has come
from because it what the gene does and not where it has come from that
matters is correct. However what JMcG has failed to realize is that the
Hamiltonian argument employs IBD within an inductive synthetic argument,
i.e. WHY the gene is selected and not within just a deductive analytic
argument of HOW it was selected. Thus correctly identifying the parent, even
as just a probability, is absolutely required because fitness units have to
be allocated to a parent and not just remain anonymous. IBD is and remains a
very useful probability for population genetic ANALYSIS (a study of where a
gene may have come from, i.e. HOW) but has been utterly misused within a
population genetics SYNTHESIS (a theory of what causes a gene to come from
somewhere, i.e. WHY), e.g. Hamilton's Rule.
If anybody starts arguing that genes are employing IBD to get themselves
selected (the popular gene level heuristic argument where IBD is quietly
switched from defining one ORGANISM as the parent to one GENE as the parent)
then they just end up comically reversing cause and effect within an
EMPIRICALLY BASED SYNTHESIS of WHY this is happening (the entirely fertile
organism centric Darwinian argument). The same error within an analytic HOW
does not matter as much because all you need to care about here is where the
gene may have come from and not why it may have come from anywhere or is
going somewhere. A reversal of cause and effect really matters within any
synthetic theory of WHY but not much within just an analytic argument of
HOW. Hamilton's rule remains based on this type of misuse, i.e. the IBD
relatedness probability r is misused to explain WHY a gene in selected
within Hamilton's inclusive fitness rationale. This misuse can be easily
proven by multiplying both sides of the rule by -1.
> > For Edser, the key word is 'altruism'. Edser can see no sense in
> > calling an action altruistic unless the actor is hurt by it. So far,
> > so good. But Edser insists that the measure of 'hurt' must take into
> > account not only the action itself, but the entire life cycle of the
> > actor.
JE:-
Yes, where only TDF is an EMPIRICALLY REFUTABLE measure of it. Unless A
MEASURE for the TOTAL fitness for the actor (who is alone proactive) is
included on just ONE side of Hamilton's Rule no fitness frame of reference
now exists for the rule to be able to do anything EMPIRICALLY. Therefore,
when the rule is misused to EMPIRICALLY argue that OFA (organism fitness
altruism) has ALONE allowed Hamilton's gene to spread because the sign of c
remains positive within rb>c it is SIMULTANEOUSLY arguing that exactly the
same gene is spreading via OFS (organism fitness selfishness) by exactly the
same actor within -rb<-c (a mathematically identical rule where both sides
of Hamilton's Rule have been multiplied by -1). This proves that the rule is
utterly misused to argue that ONLY actor OFA caused Hamilton's gene to
spread. Since actor OFA (any positive c) is CONTRARY to OFS (any negative c)
Hamilton's argument is proven to hoplessly be confounding and misleading,
i.e. an utter misuse of just an oversimplified model even when c>0.
> > As a result, he reasons that anything that hurts you cannot
> > be favored by selection. He is right, in his narrow sense, but he
> > just does not have the patience to sit through an explanation of
> > how the orthodox meaning of 'altruism' might also be useful and might
> > work in Hamilton's rule.
JE:-
No, I do not have the insincerity required to tell lies to myself or anybody
else here that a TDF gain can be politically spun into an "altruistic" act.
>snip<
Regards,
John Edser
Independent Researcher
edser@xxxxxxxxxx
.
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