Text 1236, 201 rader
Skriven 2004-12-29 14:54:00 av Jim McGinn (1:278/230)
Ärende: Re: Hamilton's Nonsense
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Perplexed in Peoria wrote:
> "Tim Tyler" <tim@tt1lock.org> wrote in message
news:cqs2lm$31ht$1@darwin.ediacara.org...
> > Jim McGinn <jimmcginn@yahoo.com> wrote or quoted:
> > > Perplexed in Peoria wrote:
> > > > "Jim McGinn" <jimmcginn@yahoo.com> wrote
> >
> > > > > Does IBD actually measure relatedness
> > > > > or is it, as I indicate, a vague abstraction that
> > > > > is only peripherally indicative of relatedness?
> > > > > [snip]
> > > >
> > > > This question seems to be at the heart of your
misunderstanding,
> > > > so I will try to address it.
> > > >
> > > > Short answer:
> > > > What "really" matters is how frequently the recipient of
altruism
> > > > carries the gene for altruism, as compared to non-recipients.
> > >
> > > There is no one gene for altruism.  As with any and all
> > > traits/behaviors there are many genes that determine their
phenotype.
> > > All members of any population will share over 99% of an such
genes.
> > > Consequently this notion that there is one gene for altruism is
an
> > > idiotic notion that has nothing to do with biological reality.
> >
> > Before jumping to the conclusion that "Perplexed in Peoria" is
spouting
> > idiocy, you might want to re-examine the possibility that you
didn't
> > properly understand what he meant.
> >
> > The accusation that "no one gene codes for any particular trait" is
one I
> > frequently encounter.  However - AFAICS - it is almost never
justified.
> > In fact it is usually pretty patronising.
>
> In fact, "Perplexed in Peoria" quite clearly IS an idiot, as
> evidenced by the fact that he keeps trying to communicate with
> McGinn.  A wise man would tell McGinn to read a textbook and then
> would keep his mouth shut thereafter.
>
> One of the advantages of a textbook

In this forum people refer to textbooks when they've
lost the argument and want to save face.  Imagine how
comical it would appear if you were reading a journal
paper or a doctoral thesis if just when the author
was about to make his point he declared, "GO READ A
TEXTBOOK!"  Obviously this tactic has everything to
do with politics and nothing to do with honest
scholarship.


> . . . is that shorthand language such
> as "gene for ..." is either avoided or justified.  And the language
> can be justified - it just takes some effort - effort that is not
> usually taken in sbe.
>
> Naively (I like that word, "naive"!), there are three problems with
> "gene for ..." language.
> 1.  "Gene" is ambiguous.  Properly, one should talk of alleles or
loci.
> 2.  Epistasis.  There may be many "genes" contributing to a trait.
>     Hence, as McGinn indicates, there are many "genes for altruism".
> 3.  Pleiotropy.  Any "gene" contributes to many traits.  Hence, no
>     gene is exclusively "for" altruism.

Right.  Another problem with silly "gene for ..." notion
involves the nature of adaptation.   As you all know (or
should know) new adaptations do no emerge independently.
Rather they involve relatively modest alterations of
existing morphologies/behaviors.  These existing
morphologies/behaviors are commonly referred to as
preadaptations.

What are the preadaptations for altruism?  Well, let's
think about it.  Altruism involves one organism taking
actions to assist another organism.  Are situations that
involve altruism the only situations that we might
witness this behavior?  Obviously not.  A good example
is parental nurturing.  All mammals are have parental
nurturing as part of their survival/reproductive
strategy.  It is concievable that altruism for mammals
involves a very slight modification of their parental
nurturing behaviors/morphologies.  IOW, we might say
(for purposes of argument herein) that 99% of the
behaviors/morphologies that are involved with altruism
of an un-named) newly emerged altruistic species are THE
SAME as the behaviors/morphologies involved with parental
nurturing.

Now, with this more sophisticated understanding of
adaptation in mind let's apply it to something that you
(perplexed in Peoria) stated previously:

"What we are interested in is under what circumstances a "gene for"
altruism can increase in frequency in the population. Naively, it
would seem that this is impossible, since the carrier of the gene
indulges in altruistic behavior, which is by definition detrimental
to its fitness, which means that it will pass on fewer copies of the
gene to the next generation."

The premise that you (perplexed in Peoria) presented
here is that there is something detrimental about
having behaviors/morphologies that are altruistic.
However if we were to take what you're saying literally
then we'd also have to assume that there is something
detrimental about parental nurturing because, like I
stated above, 99% of the behaviors and morphologies
associated with parental nurturing are the same as those
associated with altruism.  Obviously you do not intend
to suggest that parental nurturing is detrimental.

There is a way out of this problem.  And its a way
that, I think, does result in an understanding  that
may be acceptable to both of us.  If when you are
referring to "the" gene for altruism you are not
referring to all of the behaviors/morphologies that
comprise altruism (and parental nurturing) you are
only referring to the very small percentage of these
genes (what might, in actuality, be an absence of
genes) that differentiate altruism from parental
nurturing.  IOW, in the context of the example I
discussed above, when you refer to the gene for
altruism you could be referring to the 1% difference.
This is acceptable to me.  (And I suppose you could
even claim that this is what you intended all along.)
But this raises other issues with respect to another
assumptions of Hamilton's rule, the rarity of "the"
gene for altruism.


> Nevertheless, in order to get to the situation that McGinn describes,
> in which "all members of any population will share over 99% of any
> such genes", those genes had to increase in frequency at some point.

Yes, they were preadaptations that served other
purposes.

> Each and every one of those genes had to increase in frequency.  So
> let us focus on just one of those genes and inquire why it increased
> in frequency.  That gene is arguably "a gene for altruism", and after
> we have selected it as the focal gene, we can call it "the gene for
> altruism".
>
> In principle, thinking of this sort - ignoring epistasis and
pleiotropy -
> can be traced back to Fisher.  The arguments justifying this kind
> of thinking are completely spelled out in the textbooks.

Okay, as long as it's understood that "the" gene
for altruism involves relatively slight modifications
of existing behaviors/morphologies then I don't see
that we have a dispute on this part of Hamilton's
rule.  Fair enough?

Now tell us why we should assume that such a slight
modification should necessarily be rare in a
population.  Will it's rarity be the same
regardless of the level of adaptation that the
population is and has been experiencing?  (Let me
explain.  By the phrase "level of adaptation" I'm
referring to whether or not and to what degree the
population is experiencing group selection vs.
individual selection.)  Think about it.

> Those of
> us who have read the textbooks sometimes forget that not everybody
> has had our advantages.
>
> Of course, you can avoid all of the arguments regarding the
justification
> of genetic models by taking the high road of a direct proof of
> Hamilton's rule at the quantitative trait level - starting perhaps
> from the Price equation.  Unfortunately, though, this doesn't answer
> McGinn's questions regarding the relationship between IBD and
> "relatedness".

Yes, Hamilton's rule is a chain with a number
of broken links (3 to 5 depending on how you count
them) fixing any one of these links (as it seems
you've done here) is not going to make the chain 
usable.

Jim
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