so, in essence you have people concluding things about
this so-called 'fossil record' with a very key bit of
information not only missing, but unattainable.

so, for instance, someone concludes that two sets
of boney fragments that look somehwhat alike in form

constitute a similar organism, and that two fragments
that look quite dissimilar, constitute variant organisms

all without any way of establishing absolute breeding population.

meaning, -if- you were to dig up something that looked
like a pekinese, and some other thing that looked like
a great dane, you -could- argue about them as if they
were different 'species' to the exclusion of any opinion
that would suggest that they are the same "species",

by "convention" all without any way of determining if
the two fragments were ever able to mate and produce
viable offspring, which, as it turns out, they can.

and, it's also, quite possible, that two bugs,
that look nearly identical may not be able to have
ever produced viable offspring, and, were therefore,
never part of a single contiguous breeding population
and, therefore, not the same 'species' and yet, be
classified -as- the same species with no chnace of
fully demonstrating breeding population, based
on outward appearance alone.

now, you find a variety of bugs, and start
trying to hang "extinct" labels on them all
without any idea as to whether one of -them-
could reproduce viable offspring with a bug that
is wandering about today, even if, it's appearance
has changed somewhat and it looks different as
far as one can tell from a 'fossil'

so, you start making up all these stories about
"extinct" species that you have zero method of
determining relationship with present day finds
with regards to breeding potential.

and then we have the problem of what appears
to be a genetic poverty developing as opposed
to a genetic richness.

take, for instance, the cheetahs and their potential
for extinction because they have had loss in populations
which can not be replenished because much genetic
information has been lost to the population losses

and gentic lethalities are prevalent and the
same sort of situation is occuring
in human beings.

it looks as though genetic poverties are on the rise
and not genetic richness, and this -because- of divergences.
and so, the model from creation would posit prototype models
with a genetic -richness- which included an array of potential
outward expressions of traits  many of which are now classified
as variant -species- by taxonomers but which are, in reality,
simply variant expressions of trait structures that were already
present in the initial prototypes from square one.

and bones, being what they are, there is little opportunity
of demonstrating absolute breeding populations from bones alone,
and so, the models rise to an impassive ambiguity which
cannot be broken based on that boney evidence.

there simply is no contiguous breeding population to latch on to
to demonstrate any sort of 'interspecies' transformation.

it's inconclusive...

meaning, it's not possible to conclude either of these;

"it is possible that a fossil find could have bred
with a contemporary living organism and produce
viable offspring"

or

"it is not possible that a fossil find could have
bred with a contemporary living organism and produce
viable offspring"

or, "it is possible that a fossil find could have
bred with another fossil find to produce viable offspring"

or, "it is not possible that a fossil find could have
bred with another fossil find and produced viable offspring"

and without that very key information,
all statements concerning fossil relationships to
contemporary organisms are rather meaningless.

there's just no way of establishing
a contiguous breeding population

and so, positting that such a contiguous
breeding population exists is speculation.

not fact...

there is no physical record of any contiguous breeding population
which includes any non-human organism [X] and humans.

it is only speculation that such a
contiguous breeding population exists.
such a contiguous breeding population
is not a fact.

the speculation on the existance of
a contiguous breeding population which
includes a non-human organism and humans
certainly seems to be non-verifiable with
any sort of physical observation.

such speculation is a bad 'theory'...

you -guess- that these species
diverged 10 million years ago.

you compare the genotypes in
the foot prints you have.

you guess that each difference in
sequence represents 'x' million years.

you juggle the guesses until you can draw
a straight line thru this guessed
at correspondence.

stopping there, you'd be trying to do
something like ascertain the average
height of human beings based on the
height of a single person, which is unuseful,

meaning, you don't have any average,
you have what may loosely described
as a single point., with huge error bars.

so, you must use more specific trait sequences
and compile an average set of lineages.

what you find is that there is no neat
one to one correspondence in the slopes
of the lines gathered up for a specific
guess at divergence coupled with sets
of sequence variation of multiple traits.

meaning, you get -different- numbers for the
'x' millions of years per sequence variation
for two identical data sets.

meaning, trait A allegedly alters
at 1.5 million years per difference,
and trait B alters at 0.75 million years
and trait C alters at 35 million years
per change, [outside of the proposed date of divergence]

so, you erect -larger- error bars which will
cull a multiplicity of lines into
a single averaging

and then, you remove the error bars and
claim you arrived at a reasonabe
correlation to your initial -guess-.

which is to say,

you get a happhazzard array of scattered slopes
with weighted averaging techniques employed
so as to -broaden- the error bars,

and then make an attempt at drawing a
single average from all these
scattered slopes,

and then simply remove the error bars
because they tend to clutter up the graph.

that, and this assumes the differences in
genotypes are solely attributable to one
species changing from the other.

these 'rules' are considered -by-
scientists as not very useful.

well, in order to even try employing "gene clocks"

you'd have to suggest that one remained static
while the other moved away from the static one,

and, if you suggest that both moved away
from the center, which you -do not- have,

then, the standard "species X" is an unknown

and you're juggling one equation with two unknowns,

and, there would be many non-unique solutions.

which you'd claim is 20 million amino acid or
somesuch different from both humans and chimps,

the prospect of reproducing -the- genetics

of "species X' in this situation is not very good.

so, you generally see that they take the
differences between modern chimps and modern humans

and constructing a timeline, based
on no actual record of "species X"

chimps and human beings are said to
have 40 million genetic differences.

there is no "species X' to which we may trace chimps
and humans and for which, there is any dna evidence.

no presumed "mutation rate" has ever been
established to progress at some regular pace,
and the 200 per generation is highly theoretical
based on a number of assumptions. and any presumed

"divergence date" from some unknown
"species X" is unknown,

and so, neither stand as independant fact
but both would be dependant upon the other.

so, it's one equation and two unknowns
which results in a circular statement.

the 'divergence date' of unknown "species x" is
dependant upon the presumed mutation rate,
and the presumed mutation rate is dependant
upon the divergence date, and neither are known.

any so-called 'fossil' cannot be used to establish
breeding population, and so, is not useful
in describing "species X"

so, it's fairly circular and
based on many conjectures.

===
Bruder speculates that such variation is a natural occurrence
that accumulates with age in everyone. "I believe that the
genome that you're born with is not the genome that you
die with—at least not for all the cells in your body," he says.

Charles Lee, a geneticist at Brigham and Women’s Hospital
in Boston, agrees. Genetic variations can arise after a
double strand of DNA breaks when exposed to ionizing
radiation or carcinogens. "It reminds us to be careful
about our environment because our environment can help
to change our genome," he says.

Plus, these variations may predict age-related diseases.
Lee adds: "As you age … your chances for having a genomic
rearrangement that causes a certain disease increases all the time."

The differences between identical twins increase as they age,
because environmentally triggered changes accumulate. But twins
can also begin their lives with differences, according
to Bruder's study, and that calls into question their very name.
===

this is an interesting bit;

Bruder suggests that variations
pile up over time, -after birth-,

and this can also suggest that such variations
may begin to pile up, directly from -conception-,
and these twins were all adults when compared.

the notion of variations piling up -after birth-
and possibly as soon as -after conception- does
not bode well for establishing a "mutation rate"
at all.

this calls in to question the entire scheme,
as variations of this sort may resemble things
like getting plastic surgery after birth, and
not passing these variations on to anyone.

===
http://www.genetherapy.me/spermatogenesis/

Spermatogenesis, which begins at puberty, includes all
of the events by which spermatogonia are transformed
into spermatozoa.

At birth, germ cells in the male can be recognized in the
sex cords of the testis as large, pale cells surrounded
by supporting cells (Fig. 1.21A). Supporting cells, which
are derived from the surface epithelium of the gland in
the same manner as follicular cells, become sustentacular cells,
or Sertoli cells (Fig. 1.21C ). Shortly before puberty, the
sex cords acquire a lumen and become the seminiferous tubules.

At about the same time, primordial germ cells give rise
to spermatogonial stem cells. At regular intervals, cells
emerge from this stem cell population to form type A spermatogonia,
and their production marks the initiation of spermatogenesis.

Type A cells undergo a limited number of mitotic divisions
to form a clone of cells. The last cell division produces
type B spermatogonia, which then divide to form primary spermatocytes
(Figs. 1.21 and 1.22). Primary spermatocytes then enter
a prolongedprophase (22 days) followed by rapid completion
of meiosis I and formation of secondary spermatocytes. During

the second meiotic division, these cells immediately begin
to form haploid spermatids (Figs. 1.21–1.23). Throughout this
series of events, from the time type A cells leave the stem
cell population to formation of spermatids, cytokinesis is incomplete,
so that successive cell generations are joined by cytoplasmic bridges.
Thus, the progeny of a single type A spermatogonium form a clone
of germ cells that maintain contact throughout differentiation
===\\

the germ cells are very well insulated from the
envirnomental 'hazzard' sort of thing which will
tend to cause disruptions in the dna -after- birth
and pile up incorrect copies in =adult= samplings.

environmental disruptions, which constitute
the larger portion of total disruptions,
are taking place -after- birth,
and are not passed on.

we have no set predetermined 'mutation rate'

being passed along in the germ cells.

dubious consequences for 'gene clock'

but, it's really quite beautiful, in that
the germ cells are so very well insulated
from envirnmental exposure,

the germ cells are sheathed and encased in layers
of cells that =filter= water and nutrients that
would be passed on as nutrients for
the primordial germ cells.

wheras, liver and kidney and heart and blood cells, etc.
may take a direct 'hit' from any passing environmental
'bullet' and see disruptions in their sequencing,
because they have water and nutrients passing
directly to and through them

these germ cells are fed on filtered and purified
water and nutrients that -first- pass through the
surrounding 'sertoli' and/or 'sustenacular' cells.

like as if, -these- cells are little nannies

and an elaborate police force

for the germ cells.

it's layers of protection.

the germ cells are not directly exposed
to the environment in the ways all other
cells are exposed.

and much disruption occurs after birth

in the cells which are so exposed,

heart liver blood etc...

of course, things like X-rays can still
penetrate this protective screen,

but, remember to wear your little
lead sheath when you go to the
dentist for X-rays.

if the dentist forgets, you remember.

"ay, put the lead sheath on"

because, in real life,

this sort of 'hazzard' is deleterious.

persons who stood in front of an X-ray machine
for too long never passed on 'super-human' powers
to their offspring.

in all likelihood, they became sterile.

as it stands, "mutation theory" is rather dubious

the germ cells are very well protected from environmental damage

damage that would show up as 'mutations' in genetic
samplings of human beings in a genomic project,

the genetic samples that -are- used are generally the
more environmentally damaged cells found in blood
and spittle etc.

so, to suggest that -these- alterations which are
found in damaged cells make up a degree of 'mutation'
that is at all relevnat is somewhat misguided in that
these damaged cell lines do not get passed onto subsequent
 generations and only the germ cells which are more
insulated and protected get passed on.

see, they're positting a 'mutation rate' based on
 cell lines that donot participate in procreation.

so,any -number- derived from these are unreliably unreliable.