This post is in response to MattLB and Mr. Carter, but it is for those
with an open mind.  Mr. Carter’s mind is not entirely closed,
but MattLB’s appears to be.  All I ask is to supply evidence to
support one’s claim.  If there is solid contradictory evidence
against it, a hypothesis must be abandoned or reworked significantly.
I’m not sure what MattLB’s “angle” is, but he
appears unwilling to face overwhelming evidence against his notions
(just a small part of this evidence is presented below).  The health
implications are enormous, however, and should be of interest to
anyone reading posts in this newsgroup.

I have investigated the history of the “lipid membrane”
claims, and they appear in books first as one of several
possibilities, then as a likelihood, then as “fact,” and
yet no experiments were done to verify it.  In the first
“modern” text on this subject (in English),  Setlow and
Pollard’s “Molecular Biophysics” (1962),
Danielli’s model of a “cell membrane” consisting of
banded proteins and fatty acids, is presented, for example.  While
this model is no longer accepted by any scientist, it was a reasonable
idea at the time, but it just did not account for all of the data.
That same year Gillbert Ling presented a hypothesis that does account
for all the data in his book, “A physical theory of the living
state.”  Since then, he has refined his hypothesis and examined
new evidence (see his latest “Life at the cell and below-cell
level,” for example).  No only can the “lipid
bilayer” claim not account for all the data, but those who write
textbooks cannot account for the data in a way that makes any sense
even in a simplified form.  For example, textbooks claim that many
cells are subject to tremendous shearing forces, and yet they also
claim that the cytoskeleton provides structure to the cell (which is
why it got the “skeleton” name).  Some books even say the
“cell membrane” is “delicate.”

MattLB expresses concern about my motivations, but he appears much
less interested in actual science.  I cite evidence in abundance (see
below), but he rarely cites anything of use (though he did cite a
study that actually contradicts his claims, which I discuss below).  A
textbook statement that does not cite a source is not science, it is
an educational model, at best.  Interestingly, he criticized my
interest in the HIV=AIDS claims.  Viruses do not posses a “lipid
bilayer,” yet have survived for millions of years:
“Chemical analysis of viruses reveals a nucleic acid content
varying from 1 per cent to 50 per cent according to the virus, the
remainder being almost entirely protein…”  Page 139 of
“Davidson’s The Biochemistry of the Nucleic Acids”
(8th edition, 1976).  Moreover, in the nucleus of cells, proteins are
the structural element: “These major proteins [actin and myosin,
amongst others]… are stable which suggests that they may play a
structural role” (page 17).  Now if you’ve got a
“lipid bilayer” (or just phospholipds curled up into balls
and stuck into the groove in structural proteins, as the evidence
suggests) packed with unstable polyunsaturated fatty acids,
you’ve got something worse than a recipe for disaster.

If viruses broke down “lipid bilayer cell membranes,” as
is claimed by HIV=AIDS people, then it would irresponsible to use
protease inhibitors because lipase breaks down fatty acids.  A lipase
inhibitor should be used.  But the protease inhibitors do work (too
well, in the sense of toxic side-effects) – unfortunately, HIV
is a weak virus, and blaming it for pathological conditions is like
blaming plankton because it came in on the tidal wave that knocked
your house down.

Science is supposed to debunk dogma, not create and propagate it, but
today we see “experts” making all kinds of claims, yet not
citing evidence, and worse still, not solving any of the problems for
which they are being paid to solve.  This may be more of a
psycho-social issue, and is clearly not a topic for the
sci.med.nutrition newsgroup.  Anyone who reads a web site like
www.sciencedaily.com on a regular basis can see for themselves how
existing notions are modified or abandoned quite often.  This is what
is known as the “scientific process,” though MattLB seems
to be unaware of it.  In fact, today in the local newspaper, New York
state’s “Newsday,” page A28, there is a story about
scientists who study Huntington’s disease.  They claim that
their experiments show that the protein that clumps up in the brains
of these patients is a protective mechanism, which is consistent with
the idea that it is oxidative stress that is the primary cause, and
that the clumped protein is further down the pathway, just as
cholesterol buildup in arteries is not due to having “high
cholesterol” (though high amounts of serum oxysterols is likely
worse for most people than lower levels).  For one example, see:
“Cerebrospinal fluid F2-isoprostanes are elevated in
Huntington’s disease.” Montine et. al., in Neurology.1999;
52: 1104.  However, the following presents a great review, and
supports my claims about the dangers of dietary polyunsaturates:

“Neurochem Res. 2000 Oct;25(9-10):1357-64.       

Isoprostanes, novel markers of oxidative injury, help understanding
the pathogenesis of neurodegenerative diseases.

Greco A, Minghetti L, Levi G.

Laboratory of Pathophysiology, Istituto Superiore di Sanita, Rome,
Italy.

Isoprostanes are prostaglandin-like compounds which are formed by free
radical catalysed peroxidation of arachidonic acid esterified in
membrane phospholipids. They are emerging as a new class of sensitive,
specific and reliable markers of in vivo lipid peroxidation and
oxidative damage. Since their initial description of in 1990, the
rapid development of analytical methods for isoprostane measurement
has allowed to overcome some of the pitfalls of the previous and most
widely used methods of assessing free radical injury. Here, we
summarise the current knowledge on these novel class lipid
peroxidation products and the advantages of monitoring their formation
to better define the involvement of oxidative stress in neurological
diseases. Although the literature data are still not abundant, they
indicate that in vivo or post mortem cerebrospinal fluid and brain
tissue levels of isoprostane are increased in some diseases such as
multiple sclerosis, Alzheimer's disease, Huntington's disease, and
Creutzfeldt-Jakob disease.”

In terms of both biophysics and biochemistry, the “lipid
bilayer” claim is ridiculous.  For example, if you put a paper
mache shirt on a mannequin, then hit the shirt with a hammer, the
shirt is going to rip.  That’s what would happen to this
“lipid bilayer membrane” if it were some sort of
structural wall.  Chemically, there are no bonds holding this alleged
structure together, only its hydrophobic qualities.  What is the
mechanism by which cells are directed to build “lipid
bilyaers?”  Euphemistically, I’ve seen claims that this
alleged structure “forms spontaneously,” meaning they
haven’t got a clue.  Cells are highly ordered and directed.  A
cellular signal would be required.  But there is no evidence
whatsoever here, and the reason is that the fatty acids are just being
pushed out by the water molecules bound to the structural/cytoskeletal
proteins.  If you drink something and have some fat on your lip, you
might see a little oil slick in your cup, on top of whatever the
water-based liquid is, and this is because the water is pushing the
fat up there, and this is due to the non-polar quality of the fat and
the polar quality of the water.  Basic science, no mystery.

I don’t know what kind of education MattLB received, though I
don’t have any doubt he does well on multiple-choice tests,
because he seems entirely bereft of critical thinking skills.  He
claims that the EM photos that took years to create (in order to
illustrate a “lipid bilayer”) are the
“reality,” and yet they don’t show hydrophobic tails
or embedded “channel proteins” – they are undeniably
artifacts.  Furthermore, these photos could represent proteins as well
as just about anything else that one would find at this interfacial
site.  Keep in mind, I am not suggesting that plenty of phospholipids
are not present, just that they do not play a structural role, and
that is because I have not seen the evidence that would support such
an outrageous claim.  There is no such biological entity held together
without one of the known bond types.  Here’s a good quotation
about these molecules:

“We could not envision a cell without these split-personality
molecules, which, being unable to decide between oil and water, are
consigned to exist permanently at interfaces.”  Page 29.
Harold J. Morowitz (Professor of Molecular Biophysics and Biochemistry
at Yale) “Mayonnaise and the Origin of Life: Thoughts of Minds
and Molecules,” (1985).

These phospholipids just curl up and get stuck in grooves in the
structural proteins (more evidence presented below).  I have a
question for MattLB.  Do you or do you not understand that water
molecules can adsorb to protein molecules?  This is as basic as it
gets, as there is no other explanation for gelatin, as well as many
biological molecules.  And if the answer is yes (and if it
isn’t, you are dealing in religion not  science, whatever your
credentials happen to be), then why is it so difficult for you to
consider the possibility that ATP allows H2O molecules to adsorb to
the structural proteins, with phospholipids , as Morowitz says, just
getting tossed around at interfaces, with some finding their way into
the grooves in the cytoskeletal proteins?

You are the “flat-earther,” not me.  I’ve spent
considerable time investigating this issue, and like the HIV=AIDS
issue, it makes no difference to me what the “reality” is,
but I don’t want fairy tales, I want science, and science makes
certain demands.  If you want to name call, like your new friend Mr.
Carter, that’s fine, but I want to see the scientific evidence
as well.  And that, you just do not have.  What’s worse, you
don’t even have common sense on your side on this issue.  Just
because something is in a textbook does not mean it is accurate.  The
science textbooks I own that have been published over the last few
years are filled with phrases like “it is believed,”
“this may be,” and “it is assumed.”  If
assumptions such as HIV causing “AIDS,” “cell
membranes” being structural, or dietary polyunsaturated fatty
acids being “essential” were true, there would have been
much more progress in numerous areas of medicine, but these faulty
notions are holding back progress and making people ill.  And just as
I said to Mr. Carter, if you can get a Ph.D. in cellular biology to
agree to a standard debate format with full public and media access,
I’ll get a Ph.D., if not Gilbert Ling himself, to agree to take
the side I am espousing in this post (actual traveling expenses will
be required, if travel is necessary).  The ball’s in your court,
MattLB:  supply the evidence or set up the debate.  But no,
you’ll just keep tossing around non-evidence (or evidence that
contradicts your own arguments) and textbook statements as if you were
some sort of cult leader trying to indoctrinate followers with
“the right way,” instead of doing the proper
investigation, research, and questioning.

One point that should be made here is that establishment scientists,
in general, are highly specialized, and do not question claims made by
their colleagues in a related field.  Assumptions get tossed around,
and often find their way into textbooks, without any verification
through scientific experimentation.  However, if one looks at all the
“chronic disease” of today (as well as other phenomena,
such as “chronic fatigue syndrome,” “AIDS,”
etc.), and thoroughly investigates the actual evidence (not the
assumptions or textbook statements), one finds that the unifying
thread is that while excess iron, low stomach acid, vitamin/mineral
deficiency, etc., can all be major problems, dietary polyunsaturated
fatty acid consumption beyond a trace amount deserves to be called the
underlying cause.  Do your own research – go to www.pubmed.com
and search for arachidonic, lipid peroxidation, oxidative stress,
linoleic, and free radicals, for starters.

Below is a response to a post by MattLB about “cell
membranes” from a few months back, but because of computer
problems, I was unable to post it then, so I thought it best to save
it until the issue came up again.

Science is supposed to be the evidence that exists at a given time as
interpreted by those who are familiar with the material and willing to
keep an open mind.  If most of these “experts” agree, then
claims are called theories.  If the experts believe more work needs to
be done, claims are called hypotheses.  If a claim can be repudiated,
the claim must be abandoned or reworked substantially.  In the absence
of anything better, “models” are often cooked up to
explain something, but what’s happened over the years is that
models (or even worse, “markers,” such as “high
cholesterol,” have come to be presented by “experts”
almost as a disease in and of themselves) have come to be taken for
hard theories.  And, unfortunately, some disciplines, such as biology,
suffer from a general unwillingness to question assumptions that were
never even hypotheses, but were included in textbooks because they
were intuitive (and could not simply be ignored), just as sages once
believed the earth was flat (technically, they are called
“models,” which means that they’ve got to put
something in the textbook to cover an area that is poorly understood,
so they fabricate a story that sounds reasonable if you don’t
question it too closely, or at all).  This is the case for the
so-called lipid bilayer that, most textbook authors now claim, keeps
the inner contents of cells (which they claim is largely aqueous
water) enclosed and protected.  The scientific evidence against this
notion is overwhelming.  You can read one of Gilbert Ling’s
recent books and decide for yourself.  What is interesting is that you
can cook up a few common food items and disprove the lipid bilayer
claim very easily (also explained below).  Why this is important in
the diet and health context will be made clear below.
 
The following was composed over a number of days, whenever
I could spare the time, so I apologize in advance for any
“choppiness” in the presentation.

The quoted passages are mostly from one MattLB post,
unless otherwise stated.  MattLB claims to be an X-ray
crystallographer, which means he is dealing with artifacts, which are
often nothing more than mirages, and as will be made clear below, he
seems to value common sense and basic scientific methodology very
little.  For those of you who are interested, read “The
Billion-Dollar Molecule” (1994) by Werth, to get a sense of what
our great scientists are doing these days.  In this book, Mark Murko,
who also seeks to delineate a protein’s structure, states:
“…not all the equations we use to describe those
interactions are accurate.  Some of them are fudge factors.  Some of
them are thought to be correct even though the experimental data
they’re based on are wrong, only nobody knows that because
nobody’s gone back and double-checked the experiments.  Some are
pure guesses.  There are assumptions, biases.  There’s user
error.  There’s imprecision in the hardware and software.”
Page 303.  And on page 209, it is said that the great chemist Joshua
Boger thinks biology is “too mushy.”  Boger states:
“I mean, what are the basic concepts of biology and how sure are
we of them?  Well, there aren’t any, hardly.  It isn’t
that the people are stupid, it’s that the data isn’t
there.”  But some things are known, and then common sense can be
applied (explained below).

Photos of “lipid bilayer” membranes, taken by an electron
microscope after staining with a particular stain, produce two
continuous lines, like railroad tracks.  Where are the channels,
pumps, or pores?  Why don’t the fatty acid “tails”
ever show up?  They never have.  And why are the lines straight
– shouldn’t there be “bumps” (proteins, etc.)?
How could all the molecules that come in and out of a cell every
second (according to this “theory”) get through this
apparently continuous band?  One thing that is never said explicitly
is that kinds of other “membranes” can be created by using
different stains and methods (for instance, the freeze fracture
process).  None may accurately represent what the
“membrane” actually looks like, at least in terms of the
models that have been proposed, but under these conditions, scientists
need to be honest about what they actually know and what they
don’t.  Why doesn’t MattLB supply references for X ray
crystallography that purports to show this “lipid bilayer”
in enough detail for conclusive visual evidence of its existence?
Otherwise, why does he talk about this technique as if it can
“prove” his claims?

To get a little technical:

The osmic acid used for the “lipid bilayer” EM pictures
you find in many textbooks make no sense, because osmic acid
“reacts primarily w/ double bonds and sulfhydryl groups of
proteins, causing major conformational changes in the 1E and 2E
structure of proteins.”  Thus, these “lipid bilayer”
pictures are much more likely to be proteins, or mostly proteins, than
anything else.

Source:  www.uga.edu/~caur/lect4.ht

Also, osmic acid is a very strong oxidant and would be able to easily
penetrate a “lipid bilayer.”  After doing so, the double
bonds found in many of the “membrane lipids” would be
stained just as darkly as the two lines you see (due to oxidation), so
that the two lines that are seen should have dark spots between them
in many places.  The pictures do not show this.

“In the presence of osmic acid the fat is oxidized at the double
bonds…”
Source:  http://food.oregonstate.edu/ref/bake/jooste/test.html
When well-respected British scientist Harold Hillman looked into when
basic experiments were done to establish criteria for evaluating the
reliability of particular techniques, he discovered that no one could
answer: “…the questions of when these confirmatory tests
were ever done and where they were published.”  And when
“he was doing work on nerve cells with microscopist Peter
Sartory. To get the best images, they used transmission electron
microscopy (EM) and were astonished by what they saw.
“We noticed something so peculiar that we really
couldn’t’ believe it,” Hillman recalls. “About
80% of the membranes in the cell appeared end-on, [as if the cell had
been sliced through its center]. It took Sartory and myself several
weeks to realize that it simply wasn’t possible.” Yet that
is what virtually all electron micrographs and illustrations in papers
and textbooks show. “That was our first shock,” says
Hillman. That implied that every electron microscopist was cutting
virtually everything in the cell perfectly at right angles.”
“According to conventional thinking, cell membranes consist of
two layers. In stained EM sections the two layers show as two parallel
lines of dark stain, like railroad tracks. But, Hillman observes,
however you cut a cell, the two lines are always the same distance
apart in the EM image. He draws the analogy of a chef cutting an
orange. If he slices it clean through the center, the sliced surface
will show a thin rim of peel. If he cuts it with a glancing blow, so
that only a small slice is taken off, the peel won’t be cut at
right angles—it will show as a much “thicker” rim.
Hillman reasons that because the rim is always the same width in EM
sections, it cannot represent a thick two-layer membrane. Rather, he
believes, it is a single thin membrane stained on both sides.
“I have challenged electron microscopists to make a
three-dimensional model of any living cell in which this [a membrane
appearing to have identical thickness however it is cut] is so. It
simply isn’t possible. All the stains they examine them with are
heavy metals that deposit on both sides of the membrane, thus any real
membrane will appear as two lines.” “
Source: The Scientist 2[14]:5, Jul. 25, 1988  (written by Richard
Stevenson).

MattLB’s misunderstanding of the
physical structure of the cell most likely will cause
him problems in his endeavors.  His misunderstanding,
however, is not atypical.  Popular “health guru”
Dr. Nicholas Perricone, for example, correctly points out
that oxidized LDL, not normal (or “native”) LDL is the
problem in most cases of atherosclerosis.  He is also correct to
note that the inside of cells is like gelatin or
jelly, though the cytoplasm is usually “tougher”
towards the outside and “softer” towards the middle.
His big mistake is claiming that the “cell wall” is
composed of a “lipid bilayer,” which he claims has the
structural integrity of a soccer ball (he tells
readers to imagine cells as soccer balls filled with
jelly).  Please, do some independent thinking here.
How could fatty acids, only the thickness of two
molecules, have that kind of structural integrity? A thin layer of
grease is what is being claimed protects the entire cell contents.
Absurd is too kind a word for this nonsense.
The fact that there are fatty acids on the outside of
cells does not mean they are a “wall.”  The
“jelly”
will hold together just fine, because there are actual bonds there.  A
covalent bond is a bond, an ionic bond is a bond, etc., but the only
bond that can exist between the cytokeletal proteins and the
phospholipids is the so-called electric double layer, and not
hydrophobic “bonds,” due to the charges between groups on
the proteins and the “heads” of the phospholipids.

Why does this matter in terms of health?  Two reasons,
related to the “lipid bilayer theory.”  If the jelly
needs to be held in, and if fatty acids are doing it,
it is claimed that polyunsaturated fatty acids (PUFAs)
are needed for “flexibility.”  The second claim is
that PUFAs are “essential” because your body needs
them to make eicosanoids.  But the body will make its
own eicosanoids from common non-polyunsaturated fatty
acids, and this is one of the supposedly beneficial
effects of taking low doses of aspirin (via the way it
inhibits the COX-2 pathway).

A simple, very inexpensive experiment could be done to
validate or refute these claims.  Feed a few dogs
fresh coconut oil as their only source of fat, and be
sure to feed them very well in all other respects (dogs
are a good model to compare to humans in this
instance, and there are no ethical problems, as there
would be for human subjects).  If the dogs stiffen up
and die, then the claim that cells need “flexibility”
would seem to be correct, but of course could be
investigated further.  If the dogs cannot handle
simple stresses, such as cuts and bruises, without
bleeding to death or falling apart (literally), then the dogs needed
those
eicosanoids produced only by PUFAs.  That’s it.  And
if it turns out that the dogs do very well on the
coconut diet, then the recent textbooks MattLB and
others think so highly of will have to be rewritten,
and dietary guidelines will need extensive revision.
On some remote Asian islands, the pigs and chickens kept by the people
living there were fed coconut scraps, and no other major source of
fatty acids.  Theses animals, as well as the people (who also ate
coconuts as their primary fat source) were extremely healthy, even
though they had what in America would be called “high
cholesterol.”

Now, over to MattLB’s claims:

MattLB: “In order to form a
crystal that can be used to get an X-ray structure,
the molecules must
be arranged in a regular, ordered fashion. The fact
that membrane
proteins and phospholipids co-crystalise means they
are arranged in
such an ordered fashion. I'm saying that ordered
structure is as a
lipid bilayer, just as in the intact cell.”

He can say what he wants, but the issue is not whether proteins and
phospholipids are arranged in an “ordered fashion,” but
whether a two molecule thick layer of common fatty acids can hold a
cell together.  Though this claim is beyond absurd – at least to
those who know anything about the forces at work (the only one that
could be at work here is the hydrophobic force, which could never
withstand the stresses cells endure all the time), science dictates
that claims need to be addressed (at least those made by scientists).
Harold Hillman did experiments to get to the bottom of the issue, and
came to
the conclusion that he was dealing with a monolayer (or something that
behaved more like a monolayer than a bilayer.
The cells he cut at random almost always revealed what
looked like parallel lines in the area of the supposed
“lipid bilayer.”  This is impossible, unless there is
one layer that gets stained on both sides, which was
his, and other scientists’ conclusion – nothing else
makes any sense (though an electric double layer, which behaves like a
monolayer in certain respects, is possible).  How could cutting done
completely at random nearly always yield perfect parallel lines?
There simply can’t be a “bilayer” as is illustrated
in many current textbooks.

“It falls on you to suggest
an alternative explanation.”

Wish I could take credit for the work of Ling and many others, but I
don’t play that game.  In fact, a recent conference was held to
discuss the implications of the work of Ling and others.  For those
interested, here is the information:

“Interfacial Water In Cell Biology”

June 6-11, 2004
Mount Holyoke College
South Hadley, MA

Chairs: Gerald H Pollack & Chaim Frenkel

ABSTRACT:  A significant fraction of cellular water consists of
interfacial water, i.e., water that is confined by or in proximity to
macromolecular and other kinds of surfaces. Proximity to interfaces
appears to modify the structure and the physical properties of
interfacial water, apparently toward higher degree of complexity but
an understanding of the structure of interfacial water has, to date,
escaped a complete and accepted description.

Because interfacial water may govern many or perhaps all aspects of
cellular metabolism and because the physical properties of interfacial
water are believed to be different from those of free water, it is of
fundamental importance to understand how interfacial water mediates
cellular processes. Examples are the role of interfacial water in
macromolecular assembly and function, in allosteric regulation of
proteins and enzymes, in energy metabolism or selectivity of cellular
ion flux, in signal transmission, and in association of macromolecules
with one another

[for a complete list of the lectures and lecturers, go to the end of
this post – are all these scientists “wackos,”
MattLB?]

Source: http://www.grc.uri.edu/programs/2004/intwater.htm

“Fatty acids when in a phospholipid in a membrane
bilayer aren't
"doing" anything except providing a barrier to
molecules.”

Physically impossible, and demonstrating a total lack
of understanding of surfactant biochemistry.  These lipids are quite
“active” (see below).  Moreover, the closest to a
“lipid bilayer” in the human body is to be found in the
lungs, but: “…pulmonary surfactant is primarily a
monolayer in the alveolus, separating the minimal water phase from the
air and lying almost adjacent to the surface of cells. These
monolayers become double in the folds of underinflated alveoli.
Stabilisation or a predisposition to folding can be imparted by the
presence of proteins in biological surfactant layers.”  The
proteins are doing the work, and the lipids are not structural, for
example: “In the lung, the long-chain phosphatidylcholines are
combined with… four proteins… The proteins make roughly 10
percent of the mass and improve surfactant adsorption to the
saline-air interface and cells in the alveolus.”
Also noteworthy: “Surfactant has a high rate of turnover and is
replaced with a half life of about 10 hours.”
But because they are unfamiliar with Ling’s hypothesis, they
must admit that: “The discussion of Pulmonary Surfactant is
readily made complicated, because much remains to be
discovered.”

Source: myweb.lsbu.ac.uk/~dirt/museum/surfactant.html

However, interestingly, but not surprisingly, as lipid expert Mary
Enig notes, saturated fatty acids are the “essential fatty
acids” in lung surfactant: “When it comes to our lungs,
the very important phospholipid class called lung surfactant is a
special phospholipid with 100 percent saturated fatty acids. It is
called dipalmitoyl phosphatidylcholine and there are two saturated
palmitic acid molecules attached to it.”
http://www.westonaprice.org/know_your_fats/fats_lungs.html
All you have to do is look up this phospholipid in a chemistry catalog
to confirm her point – no mystery here.

As recently as 1999, in “The Colloidal Domain” by Evans
and Wennerstrom, the authors admit that they are making assumptions
about a “lipid bilayer:” “The biological membran is
a  complex structure containing lipids, proteins, and polysaccharides.
We adopt the point of view that the lipids provide the basic
structural unit.”  Page 327.  Also worthy or note: “In all
organisms except the most primitive ones, the plasma membrane of the
cell envelope only represents a small fraction of the total membrane
content.”  Page 328.  They do nothing to explain exactly how
this “structural unit” could withstand the stresses that
cells endure (and they cite no references).  And they note that
“lipid bilayer membranes” can be as much as 75% protein:
“A biological membrane consists of anywhere between25 and 75%
w/w lipid.  The remaining 75 to 25% is protein, glycoprotein, or
lipoprotein.”  Here again, claims that the lipids can
“hold the cell together” are RIDICULOUS – if a cell
membrane is composed of 75% non-lipids, how in the world could you
even imagine a two molecule thick layer of fatty acids in the other
25% being able to hold the aqueous water inside – do you realize
what kinds of pressure would be exerted on those fatty acids, even
when just “doing nothing?”  Considering the fact that some
sort of chemical bond is necessary to even begin to talk of a
structural role for something, and the phospholipids are not said to
be bonded to each other, how much sillier can this get?  The fatty
acids just get pushed out of the cell by the highly organized water
molecules, which are adsorbed to the cytoskeletal proteins.  There, an
electric double layer can be formed which can include the
phospholipids, as well as other molecules.  The study you cited, in
fact, supports this view.

What is interesting in “The Colloidal Domain” book is that
they talk about how important electron microscopy and other techniques
are for determining such structures: “Several microscopy
techniques provide direct visualization of bilayer structures.”
Page 313.  But then they say, “We cannot obtain direct
structural dimensions with such small objects because the images are
enlarged by diffraction.  However, we can see real-time behavior and
obtain some feeling for the dynamics of such structures.”  Also
page 313.  This would explain why some claims make sense (see below)
whereas others, especially the structural claim for “lipid
bilayers” are unbelievably absurd.  The authors provide a
video-enhanced microscopy  (VEM) image of a “double-chain ionic
surfactant sample” and note that it: “…confirms the
tendency of most bilayers to be curved back on themselves, eliminating
any exposed bilayer hydrocarbon edges.”  Page 313, illustration
on page 314.  No images of biological “lipid bilayers” are
provided by these authors, but what you see in the page 314
illustration are basically a bunch of soap bubbles.  Now they are very
pretty, but have no structural integrity in a “cell wall”
context.  The only structure known that is consistent with all the
data is an electric double layer, and in this case that would mean one
layer of lipids bound to the proteins on the outskirts of the cell
(this is the Stern layer), and then other substances beyond this layer
(outside the cell) can bind and detach depending upon exact conditions
(see the Myers book, mentioned below).

As for Gilbert Ling, he says he will take on all comers, so why
not present your claims against his hypothesis (you
can email him) – isn’t that what scientists are
supposed to do.  I don’t know what your credentials
are, but he, and many who support his hypothesis have
impressive scientific credentials (if you do a google
search on him, you will find several of these
scientists who support his hypothesis), and they are
willing to debate their claims, unlike those such as
yourself, who talk about what is in a textbook (or
quote useless or equivocal studies), instead of
explaining exactly how your notion works and providing
experimental data to support it.  Why not write a
paper against the A-I hypothesis?  Two of Ling’s grad
students did in the 1970s, and it turns out they were
wrong, so if it’s so easy, why not quickly type up a
few pages and submit it to a journal?  You’ll be
famous.  In the meantime, I would suggest instead that
you start with the basics – read the works of
Bungenberg de Jong and K. Mysels.

Scientists who are true to their calling look at what
the evidence as a whole suggests (and they quote an
establishing source if they claim that an issue is
settled, so that there is a base that can be built
upon, if it’s worthy – do you realize how flawed the
Burr and Burr experiment of 1929/1930 that supposedly
established the “essentiality” of PUFAs actually is?
It wasn’t even done on humans, for goodness sake!!).  
I’m not making the outstanding claim that Mead acid is
“essential.”  I’m pointing out what is known by all:
arachidonic acid and other HUFAs derived from PUFAs
are much more potent than the signaling molecules
derived from Mead acid.  Since the evidence for a
major, if not determining role, for COX 2 (PG E2
especially) and Leukotriene B4 in cancer, etc. is
overwhelming, one could just avoid this whole problem
by eliminating all but trace amounts of PUFAs from the
diet (as HUFAs from omega 3 PUFAs are similarly too
potent and toxic).  Since there is no overwhelming
body of evidence demonstrating anything derived from
Mead acid will do this kind of harm, and since it is
known by all that Mead acid is more stable and
produces less potent metabolites, basic,
non-scientific common sense tells one to follow up
this line of thought to see if being “essential fatty
acid deficient” is or is not the best state of affairs
for a human.  At this point it appears to be, and
since you have to eat something now, avoiding PUFAs in
large quantities, so that Mead acid is the dominant
stressor-induced fatty acid, seems the wisest course
of action by an order of magnitude.

In order for a claim to be a “scientific theory” there
must be no strong evidence against it.  Ling points to
several problems one finds in the textbook claims
about the lipid bilayer that cannot be resolved, and I
notice that you, apparently not wanting to do science,
feel you must attack his notions, without looking at
it from the other side.
For example, Ling notes that: “…a cell assembly
without functional cell membrane (and postulated
sodium pump) maintains a steady low sodium-ion
concentration like its normal intact counterpart.”
This is impossible according the pabulum being fed to
students these days.  And there are several other
examples.  It may be that no hypothesis is worthy of
being called a “theory” at this point in time, but at
least Ling calls his claim a hypothesis, not a theory.
THERE IS NO LIPID BILAYER THEORY at this point,
because there is credible experimental evidence (as
well as common sense, particularly from the structural
point of view) against it.  Until Ling’s hypothesis is
addressed in detail, one can’t say there is a “lipid
bilayer theory” and be true to the underlying
principles of science.

Towards my point, Ling notes: “Everybody knows what a
raw hamburger is like. From its rich water content, it
resembles a wet sponge. Yet it is also quite different
from a wet sponge. Squeeze a wet sponge, water comes
out. Squeeze harder, more water comes out until
finally the sponge becomes almost dry. If instead, you
take a raw hamburger and try to squeeze the water out
from this water-rich material, you will find that it
is well nigh impossible to squeeze any water out even
after the meat has been chopped into tiny pieces.
Indeed we carried on this line of inquiry in a more
rigorously controlled manner.
“Thus instead of squeezing the cut-up muscle by hand,
we utilized centrifugation. As you know, it is by
means of centrifugation, that water is extracted from
wet laundry in a washing machine. Only in the muscle
experiment, we made sure that every muscle cell had
been cut into short segments with both ends
open---which do not regenerate a new membrane, see
linked page, lp6a{3}--- and subjected them to a
centrifugal force of 1000 times gravity. Thus after
centrifuging for 4 minutes, all the water found in
between the muscle cells are completely extracted. Yet
water from the inside the broken cells remains inside
the cells (See Ling and Walton in Science, Volume 191,
pp.293-295, 1976).
“So this exceedingly simple experiment adds yet
another set of evidence showing without ambiguity that
the basic tenet of free water in membrane-pump theory
is wrong. The cell water cannot be normal liquid
water. Were the cell water truly normal liquid water,
it would have been extracted along with the
indisputably normal liquid water (held in between the
muscle cells), which is quantitatively squeezed out.
What remains would be nothing more than dried proteins
like a fully-squeezed out sponge. But that does not
happen while the cells are still alive or close to
being alive.”

If a living human cell is physically equivalent to a
bag of water enclosed by a two molecule thick wall of
fatty acids (with a few proteins sticking out here and
there), it would not have this kind of structural
integrity.  Period, there is no way around this point,
unless you want to be fitted with that strange white
suit that ties up your arms behind your the back.  And
that means that PUFAs have no place in the “cell
membrane” (with the Mead acid exception – this the
body does naturally, because it is necessary to deal
with certain stresses) because they are too
susceptible to lipid peroxidation under common in vivo
conditions, and their metabolites are cytotoxic.
Fatty acids simply cannot have a structural role, as the “lipid
bilayer theory”
posits, holding the aqueous cytoplasm inside the
cell (much of the water is in the form of polarized
multilayers that do not need to be held in by an outer
wall because they are bound to the cytoskeletal
proteins, as the hamburger example demonstrates – some
“free water” exists in a central vacuole).  Other
points concerning his hypothesis are not of as much
interest to me, as they don’t have a role in the
diet/health connection, at least not to the degree
that this point does, but to answer:

“Why would hydrophobic properties push them to the
cell's surface when
there is far more free water outside the cell than
inside?”

It’s called adsorption of surfactants at interfaces.
You need to read
http://216.239.41.104/search?q=cache:cXi3YZhC_OAJ:www.chm.bris.ac.uk/pt/eastoe/c
hapters%2520oct%25202003/2%2520Aggregation%2520and%2520adsorption%2520at%2520int
erfaces.pdf+Adsorption+at+interfaces&hl=en

The hydrophobic effect is spontaneous, as is
described on this web site.  There is a net inward
pull by the water, which is in polarized multilayers,
so the phospholipids stay bound to the cell, packed
tightly, actually (though if there were “pumps” the
phospholipids would interfere with them).  If you take
some time and read it, you’ll realize that the water
is, in a sense, holding the phospholipids to it, not
the other way around (i.e., the water molecules are
not being “held in” by the phospholipids).  As they
say, “…adsorption is a dynamic equilibrium with
surfactant molecules perpetually arriving at, and
leaving, the surface.”  This is consistent with the
study you cited, which states: “An individual lipid
molecule will remain in the annular shell around a
protein for only a short period of time…” (Biochim
Biophys Acta. 2003 May 2;1612(1):1-40).  So again, the
common textbook model is a total joke, especially in
the structural sense.  You yourself mentioned the role
of the cytoskeletal proteins, and the only thing you
seem unaware of (and unwilling to accept) is the
polarized water, which makes a “lipid bilayer”
unnecessary (and actually impossible) structurally.
And even Perricone, no intellectual heavyweight as far as I can tell,
knows
this.

The health implications are: Outside the cell, if the
outer shell, or “membrane,” is packed with
phospholipids high in SFAs and MUFAs, they will be
very resistant to free radical damage, whereas PUFAs
here will often get peroxidized (doing damage to crucial cellular
components – mitochondria, DNA, etc.), especially as
people age and in the
absence of plenty of the right dietary antioxidants.

And when one discounts completely the energy needs of
“pumps,” as you have done with the statement: “The
differences between potassium and sodium channels are
due to
differences in free energy change in losing their
solvation shell i.e.
potassium does, sodium doesn't, when faced with a
potassium channel. [Once again, where is your evidence for this, or
are you some sort of science god who demands not to be questioned?]
Ergo, discrete channels *are* possible (and other
examples exist)…” the problem is that the cell
membrane would be covered in these discrete pumps,
because of so many different molecules that need to be
pumped in and out every minute, and there would be no
room for much of a “lipid bilayer” then, so the
“theory,” in a way, violates itself (because what would be
the point in arguing that a few phospholipids here and there are
holding the cell together – that clearly makes no sense).  Cells
could not look as they actually do.  And as Ling notes, this
does not explain how pumps could exist for molecules
that have been recently synthesized by humankind in a
lab.  

You conveniently omitted Ling’s statement that your
point does “makes the dog hole-cat hole criticism less
pressing” (http://www.gilbertling.org/lp16.htm).  As
he points out there: “In 1953 I introduced the idea
that fixed ionic sites on the cell surface could offer
a basic mechanism for the selective permeability of
one ion (e.g., potassium ion) over another (e.g.,
sodium ion). This seminal idea was further elaborated
in years following as part of the AI Hypothesis (for
details see linked page lp16a): The selective
permeability of potassium/sodium ion through cell
membranes is achieved here not by diameters of
membrane pores, but by the presence of fixed
negatively charged groups on which the potassium or
sodium ion must first adsorb before entering or
leaving the cell. If the fixed negatively charged
group selectively adsorbs potassium ion, that passage
will admit mostly potassium and less sodium. On the
other hand, if the charged group selectively adsorbs
sodium ion, that passage will be admitting mostly
sodium ion and less potassium ion (see Ling, J. Gen.
Physiol.43:149, 1960). In this model, neither path is
allowing only one kind of ion to go through. Only the
relative probability of going through differs. This is
in harmony with the finding of Chandler and Meves
cited above.”

So you chose one element that works in both
hypotheses, and claim that it refutes all the other
points that Ling makes, even though it is the “lipid
bilayer theory” that is actually full of holes
(couldn’t resist that pun).  Anyone who knows a
modicum about science knows that two hypotheses often
account for some overlapping phenomena.  What you have
done demonstrates a lack of integrity, or a gross
ignorance of science, though it does seem that most
“scientists” these days lack an understanding of
scientific methodology, at least in some ways.
Perhaps you are just part of this unfortunate
historical development.  Poor you.

A common claim made in textbooks: “Cells are basically
sacs of water surrounded by an oil membrane…” is
beyond ridiculous, and Ling demonstrates this,
regardless of the fate of his A-I hypothesis in all
its detail.  The sack would not allow enough molecules
in and out, as is required, nor does it have the
structural integrity (and of course it is refuted by
simple experiments).  On the other hand, having pumps
that could get the job done would mean a cell with so
many pumps that there would be little room for the
fatty acids that are supposedly holding the aqueous
water inside.  And what is supplying the energy for all this
“pumping?”  You make cells sound like sets for
pornographic films.

An interesting experiment (that has been done – see “Life
at the cell and below-cell level for details) involves cutting open a
cell and letting the contents drain into a water solution.  What you
see are a bunch of spherical objects form out of the cytoplasm as it
slides into the water.  According to the lipid bilayer theory, the
cytoplasm is regenerating a cell membrane, which is supposed to
consist of the phospholipids.  However, so many small objects are
formed that the number of phospholipids needed to cover all the
surface area of the new “membranes” was never present in
the original cell!  And it goes on and on – the number of
obvious reasons why the “lipid bilayer theory” is nothing
but a bad joke seems endless at times.

An early experiment in attempting to determine the age
of the earth was heating up a spherical rock and
noting how long it took to cool down, then
extrapolating for the size difference.  Why not do the
same thing for your cell model.  Try to create a bag
of water enclosed by a wall of fatty acids – use as
many fatty acids as you like – don’t worry about those
precious pumps – use a scaffolding material of your
choice to mimic the cytoskeletal proteins.  Of course,
you’ve got to use the fatty acids commonly found in
human cells, in a mostly non-oxidized form.  See what
happens.  Your hands will be quite greasy, and there
will be a large puddle of water on your floor (Bungenberg de Jong
makes a similar point in his book).  Beyond that, you will have
accomplished nothing, aside from
demonstrating how ABSURD this “theory” is.

As biochemist Ray Peat has noted: “The standard doctrine about
the structure of the membrane is that it is a lipid bilayer, meaning
that an outer layer of fat (phospholipid) is arranged with its acidic
water-soluble end turned outward toward the watery environment, and
its fatty water-repellent tail turned inward, against the fatty tail
of another layer of molecules, which has its acidic end turned inward,
toward the supposedly watery cytoplasm. In support of this
arrangement, an "oil loving" stain is applied to hardened cells
(otherwise no membrane can be seen under the electron microscope), and
a double line appears near the cell's surface. This is called the
"lipid bilayer." However, since the theory says that the fatty parts
of the two layers are pressed against each other, there is in the
theory a continuous band of fat, separating two layers made up of the
acidic heads of the molecules, and the theoretical structure of the
"lipid bilayer" has no resemblance to the double line that is created
by the stain. The material generally used to produce the image of a
bilayer membrane is osmic acid, an oxidant; it wouldn't be expected to
stain the layers of acidic heads of fat molecules. This might seem to
be an embarrassing inconsistency, but apparently not to most
scientists. After the electron microscope began making pictures of
cells, it took some time to find the stain that would produce any
membrane at all, and then it took about thirty years to learn to
produce a "membrane" image that had a thickness that seemed
appropriate for the theory. Considering the great effort required to
produce a "membrane" image of the right size in the right location,
they are willing to overlook the fact that the fat-loving stain hasn't
quite found its way to the single band of fat between the acidic
layers which their theory describes. Gilbert Ling described the
boundary at the cell surface as a phase bouundary, of the sort that
exists where two different materials meet, for example at an oil-water
interface. When the two substances have different electrical-chemical
properties, the forces between the phases move electrons and/or
molecules near the surface into what is called an electric
double-layer. Since stains have their own electrical and chemical
properties, the stain molecules would be affected by the fields that
produce an electric double-layer. Osmic acid would be expected to
stain certain protein groups, including sulfhydryls and amines, which
could be exposed in such an area of strong fields. (Brain tissue that
is deprived of oxygen stains diffusely with these "membrane" stains,
suggesting that proteins are changing shape sufficiently to expose
groups of this sort.) The forces between fat molecules, that allow
them to form "hydrophobic bonds," are actually so weak that they
should hardly be called "bonds," at least at normal temperatures.
Fatty surfaces seem to seek each other out in a watery environment
because water molecules bind so powerfully to each other that they
tend to force out anything that doesn't bind to them. So, if we even
consider the association between fat molecules as a "bond," it is the
weakest bond that exists between any biological molecules. When a cell
is attached to a surface, it can be torn to bits in trying to move it,
without breaking its attachment to the surface. Obviously, it isn't
attached to the surface by its "lipid bilayer membrane." The strength
of a lipid bilayer would be limited by the extremely weak affinity of
fat for fat; if you step on a sticky floor wearing tissue-paper
slippers, your foot won't be ripped from your leg. A lipid bilayer has
no more strength than the rainbow that forms on a puddle of water when
a microscopic film of oil spreads over its surface. And the rainbow on
the puddle is something that really exists.”

In “Surfaces, Interfaces, and Colloids” (1990), a good
explanation of what is likely happening in the “membrane”
area is given by Drew Myers (page 81): “When a charged particle
(or surface) moves relative to an electrolyte solution, viscosity
effects dictate that only that portion of the electric double layer up
to (approximately) the Stern layer will move.  The ions in the Stern
layer will remain with the surface.”  Furthermore: “If the
film pressure is increased (ie, more molecules per unit area of
surface), at some point the particles become fixed in place… and
the film behaves as if it is in a condensed state (liquid or
solid).”  Page 161.  And: “…the protein monolayer
may even form a substantially rigid and strong gel or
‘skin’ which can be physically removed from the surface as
a unit.”  Page 171.  In this kind of model, PUFAs don’t
work: “…cis isomers, due to the inherent curve of the
molecule, prevent close packing and produce much more expanded
films.”  Page 168.  The expanded films would never protect
cells, and this therefore contradicts MattLB’s claim about
“loose packing” (which also was contradicted by the
scientific paper he provided that supposedly supported his case
– to be addressed below).  In general, it seems best to eat fats
highest in saturated fatty acids, then your body will make MUFAs and
PUFAs when it needs to do so.  None of this, of course, is relevant to
the fact that “cytoplasm” is mostly water bound the
cytoskeletal proteins.  If you heat an egg white, at some point a
rubbery substance is formed.  There is still plenty of water, along
with the protein, but no fatty acids.  That’s how a cell holds
together, regardless of how the lipids on the outer shell of cells are
held in place, or what kind of formation possess.  Take that rubbery
egg white and spread a thin layer of grease on it – is it any
stronger?  Is it necessary for anything, structurally?

The electron micrographs of cells, supposedly showing the “lipid
bilayer” are just one form of artefact (other kinds can be
produced), and there is no way to know exactly what interpretation one
should come to by looking at it.  As Myers states clearly:
“While it is reasonably easy to determine the constituents of
the biological membrane, elucidating just how the various components
are put together, how they interact, and their function within the
membrane represents a decidedly more difficult task.”  Page 330.
The title of chapter three of “Biochemistry and Molecular
Biology” by Elliott and Elliott (1997), is: “The cell
membrane – a structure depending only on weak forces.”
Page 39.  How could such a structure withstand incredible shearing
forces?  That’s impossible in this universe.  But Elliott and
Elliott provide the answer to how the “membrane” can be
structurally sound, when they discuss proteins called mucins:
“The mucins form a network of fibres, interacting by noncovalent
bonds and resulting in a gel containing more than 90% water that
protects intestinal cells [from stomach acid].”  Page 63.  There
it is – a structure that protects, can “keep water
out” (since the gel can be very strong and impervious, depending
upon the proteins involved), and don’t have various
“pumping” problems (as the “lipid bilayer
theory” does).  I guess using common sense is just too difficult
for some “scientists.”

It is undeniable that the textbook model cannot be correct because:
“Biological membranes are, like micelles and vesicles, dynamic
structure in which lipids and proteins can move about relatively
freely…”  Page 332, Myers.  This is only possible if the
water inside the living cell is mostly adsorbed to the cytoskeletal
proteins, otherwise the water would “leak out,” though as
I have been pointing out, there is no way a two molecule thick layer
of common fatty acids could “hold” aqueous water inside a
cell in the first place.  Also interesting in this book is that if
scientists can develop artificial “membranes” similar to
biological ones, Myers notes that: “…adding the structural
integrity and increased stability of a crosslinked polymeric
structure” would be required.  Page 330.  This is not something
that the textbook model of the “lipid bilayer” possesses.

Even the textbooks that talk about the “lipid bilayer”
invalidate their own “theory.”  For example, in
“Biochemistry and Molecular Biology” by Elliott and
Elliott (1997), the authors talk of a cell’s cytoskeleton as:
“an internal scaffolding that maintains the shape of the cell
and is involved in amoeboid motility.”  They describe red blood
cells as being “always on the move and therefore subject to
shearing forces… demanding a robust but flexible cell
membrane.”  Pages 52 to 53.  Yet they show the “lipid
bilayer” as essentially a soap bubble (in terms of structural
integrity), which we all know has little strength to withstand such
forces.  Indeed, there is nothing known in nature that suggests that
this kind of structure could withstand the forces discussed on pages
52 to 53.  If the “lipid bilayer theory” is correct, red
blood cells’ “lipid bilayer membranes” would be
easily pushed aside by such forces, the supposedly aqueous cytoplasm
would spill out, and the cell would cease to exist.  As Booij and
Bungenberg de Jong pointed out a long time ago in “Biocolloids
and their Interactions” (1956): “…water molecules
(and ions) would pass the protein structure rapidly; in other words
the cell would be like a leaky ship.”  Page 139.  Only if the
elaborate cytoskeleton of the RBCs has water molecules adsorbed to it
could such forces be withstood without such leaking.  Booij and
Bungenberg de Jong did not consider water adsorption, so they were
confounded, though they realized that: “The only possibility
which is not seriously in conflict with physico-chemical laws seems to
be that the lipids are embedded in a rigid framework of
proteins.”  So take a cue from them, and JUST USE A LITTLE
COMMON SENSE HERE, PLEASE!

Not that it would matter, but: “This was known in the
early 90s…”

My point here is that you asked for references – where
are yours on this point?  There are other issues as
well, but Ling covers them, and I won’t reiterate them
all here, as he addresses them with no problems (his
paper on PDF that you can download was written in 1997
– the studies before that do not refute his
hypothesis, though I’d like to see you try - if you
do, I’d expect the same level of depth and clarity
that his claims possess).

“I'm glad you added the ? as I don't know what you
mean by that either.”

The question marks in my last post were due to text
conversion factors that were out of my control.  I’m
surprised you could not discern that whenever there
was a “?” there should have been an apostrophe – it
was
fairly obvious.  You yourself made numerous typos, as
well as errors more egregious than mine – this happens
when one is just trying to get it done quickly do to
time constraints (for example, I may
have said Mead acid was a MUFA, instead of being
derived from a MUFA, but I’m always the first to point
out my typos in the next
posting if I notice them - your error, apparently in
reading the study
you quoted to support your argument, when in fact it
does the opposite, is difficult to understand – see
below).

MattLB: “What do mean structural? Is the fat in a
doughnut structural?”

This is exactly my point – would you use donuts as
foundation bricks for a house?  The stresses to which
cells are subject are too great to be held together
by a think layer of fatty acids, though a paste-like
layer of fatty acids and other lipids on the outside
of the cell can be excellent protection against lipid peroxidation
that can lead to damage to mitochondria, proteins, DNA, etc., as
Parassasi and
others have shown, which is why saturated fatty acids are best suited
for
this purpose.  I make all kinds of breads from
scratch.  If I want a tough bread, like an
Italian/French bread, I use high-gluten wheat (the protein holds it
together), whereas if I want a bread that crumbles
easily, I use rice flour (no gluten), but I still use butter and/or
coconut oil.  I can use eggs
to hold bread together (due to the egg protein), and a banana helps a
bit (no fat there), but I use fat for the moist, heavy quality it
imparts (and because it is much more satisfying than eating a bread
high in carbs), not to hold the bread together structurally.  Use any
common oil with rice flour, water, and baking
powder/soda, and see how crumbly it is.  This is what
I mean by common sense.  But if you don’t believe me,
let’s go to chemist Arthur E. Grosser’s book “The
Cookbook Decoder or Culinary Alchemy Explained” (1981).  In it,
Grosser explains: “…eggs must be included [in the pound
cake] to assume the structure-forming function.”  Fat actually
can be considered anti-structural: “In Recipe 98, Pie Pastry,
fat tenderized the dough by interfering with gluten formation [the
union of two different proteins], and so broke down the dough’s
cohesiveness.”  Both quotes, page 226.  So let’s be clear
on this point: YOU WERE COMPLETELY, 100% WRONG HERE!  But talking food
is actually a good idea because, as Grosser explains, water molecules
can bind to proteins, or proteins can bind to other proteins, in many
common recipes, providing structure.  Why not read Grosser’s
book with Ling’s hypothesis in mind, and without the
preconceptions?  If you do, you might actually do some good for
humanity at some point with your crystallography work.  Otherwise,
you’ll just be chasing ghosts thinking that a “lipid
bilayer” has structural integrity in the context of “cell
membranes.”  I’m not questioning whether you were the
smartest kid in your High School, but this is about interpreting
evidence, not just repeating what the teacher says, as a parrot would
do.  It’s time for you to think independently and question
assumptions.  Otherwise, you’ll be like the
“experts” we hear all the time telling us how
“puzzling” some “disease” is, when the
biophysics or the biochemistry is not all that difficult.  For
example, we hear about how bad “processed food” is, and
while there may be several reasons, one appears to be that necessary
“primer” molecules, as Ling calls them, are needed for the
“turning” mechanism in the present receptor notions.  Most
people have by now heard of cellular receptors described as a lock and
key mechanism, but with such a mechanism, the key must be turned,
though there is no explanation for that with mainstream notions.  It
is truly amazing that not only can’t they generate a simple
model that fits the evidence, but they posit a model that actually
contradicts it!  Ling’s priming molecules explain a great deal
of phenomena that are at this point inexplicable with the present
notion of receptors and “lipid bilayer membranes.”  Buy
one of his books and see the tremendous amount of evidence he has
amassed to support his claims.

And then you’ve got this:
“Unsaturated fatty acid tails prevent extremely close
packing of the
phopholipids. This makes it easier for membrane
proteins to move
around through them - compare a hedge to a row of
bushes. The even
distribution of proteins over the cell surface can be
very important
and is assured by allowing the free movement of them
laterally through
the membrane.”

You are assuming the point that is in contention – one
of the worst mistakes a scientist can make.  The only
good thing that can be said for having lots of PUFAs
in the “cell membrane” is that if you inhabit very
cold waters, the body will be kept from stiffening up,
but this would only be of value if you were a salmon,
seal, etc., not a human, who would die in a short
period of time regardless of how many PUFAs they ate
if they were thrown in water below a certain
temperature.  Do you even know the melt point temperature for SFAs
commonly found in humans (palmitic, stearic, or shorter chain)?
Perhaps most interestingly, the study
you cited in your previous response post contradicts
this “loose-packing point” of yours – do you even
read
the studies you cite?  Here is their statement:

“The surface of a membrane protein contains many
shallow grooves and protrusions to which the fatty
acyl chains of the surrounding lipids conform to
provide tight packing into the membrane.”
From: Biochim Biophys Acta. 2003 May 2;1612(1):1-40.
Lipid-protein interactions in biological membranes: a
structural perspective.
Lee AG.
Division of Biochemistry and Molecular Biology, School
of Biological Sciences, University of Southampton,
Bassett Crescent East, SO16 7PX, Southampton, UK.
agl@soton.ac.uk

It’s clear that fatty acids adhere to cells tightly,
but don’t stay bound for long, due to forces and
conditions that are difficult for the human mind to
imagine.  This is why experiments are done, otherwise we would just
assume what appears to be the case, such as the long-held belief that
the
world is “flat.”

“Membranes that have been exposed to free radical
attack are *less*
flexible as the proteins and lipids within them become
cross-linked.
Joints, muscles and skin get stiff with age for the
same reasons.”

True enough, but the evidence suggests that Mead acid
was meant to be in these important tissues:
“FASEB J. 1991 Mar 1;5(3):344-53.
Unique fatty acid composition of normal cartilage:
discovery of high levels of n-9 eicosatrienoic acid
and low levels of n-6 polyunsaturated fatty acids.

Adkisson HD 4th, Risener FS Jr, Zarrinkar PP, Walla
MD, Christie WW, Wuthier RE.

Department of Chemistry, University of South Carolina,
Columbia 29208.

We report here the finding that normal, young
cartilages, in distinction from all other tissues
examined, have unusually high levels of n-9
eicosatrienoic (20:3 cis-delta 5,8,11) acid and low
levels of n-6 polyunsaturated fatty acids (n-6 PUFA).
This pattern is identical to that found in tissues of
animals subjected to prolonged depletion of
nutritionally essential n-6 polyunsaturated fatty
acids (EFA). This apparent deficiency is consistently
observed in cartilage of all species so far studied
(young chicken, fetal calf, newborn pig, rabbit, and
human), even though levels of n-6 PUFA in blood and
all other tissues is normal. The n-9 20:3 acid is
particularly abundant in phosphatidylethanolamine,
phosphatidylinositol, and the free fatty acid
fractions from the young cartilage. Several factors
appear to contribute to the reduction in n-6 PUFA and
the appearance of high levels of the n-9 20:3 acid in
cartilage: 1) limited access to nutritional sources of
EFA due to the impermeability and avascularity of
cartilage, 2) rapid metabolism of n-6 PUFA to
prostanoids by chondrocytes, and 3) a unique fatty
acid metabolism by cartilage. Evidence is presented
that each of these factors contributes. Previously,
EFA deficiency has been shown to greatly suppress the
inflammatory response of leukocytes and rejection of
tissues transplanted into allogeneic recipients.
Because eicosanoids, which are derived from EFA, have
been implicated in the inflammatory responses
associated with arthritic disease, reduction of n-6
PUFA and accumulation of the n-9 20:3 acid in
cartilage may be important for maintaining normal
cartilage structure.

PMID: 2001795 [PubMed - indexed for MEDLINE]”

So the body is protecting this vital tissue by trying
not to allow the Mead acid to be replaced by HUFAs
derived from PUFAs, almost always arachidonic acid in
the Western diet context, of course, which can cause
the “inflammatory disorders” that are so common in
countries like the USA these days.

And then you’ve got: “There'd be no inflammatory
prostaglandins and the respose to
injury/infection would be greatly reduced.”

There would be inflammatory molecules that perform the
same function, but not as quickly or as dangerously.
You just wouldn’t have the cancer, coronary heart
disease, diabetes, etc.  Find a study of a few hundred
EFAD people who die of cuts.  In myself, I’ve seen a
drastic difference in the last several months.  My
cuts heal up so well it’s incredible.  No pain, quick
healing, no infections.  And as I’ve mentioned before,
the nosebleeds that occur when I get a head cold don’t
have
that gushing quality they used to, the bleeding stops
quickly, and the scab is rubbery, not like the hard
plastic quality they used to have.  I’ve had several
CBCs done over the last few years (as well as an
eco-cardiogram a month ago) and everything is fine.  I
have not seen any effects of the horrible
“essential fatty acid deficiency” nonsense.

And yes, I sometimes use strong language, and the
reason is:  THAT IS WHAT THE
EVIDENCE SUGGESTS.  Not because I give a rat’s
butt whether Mead acid is better for humans than
arachidonic acid or some other HUFA as the dominant
stressor-induced fatty acid.   Ludicrous, silly,
naïve, ridiculous, etc. work well to describe
ideas that just don’t meet scientific standards AND
also don’t make any sense when the evidence that does
exist is viewed as a whole.

“If AA build up due to lack of conversion to
prostaglandins it can be
cell toxic, yes, but adding exogenous arachidonic acid
is not very
representative of what happens in the body.”

The problem, as a recent EJCN study points out, is
that whether the AA is bound in phospholipids or are
converted quickly to metabolite, there is no escaping
its extreme cytotoxic qualities.  It’s true that in
certain conditions, the metabolites of AA are the
problem (though they are so readily produced it may
not matter much in practice, especially as we age).  
Interestingly, you don’t seem to realize that your
claim can also be said about the study
you cited on Mead acid.  However, the “reduction in
the expression of the cell-cell adhesion molecule,
E-cadherin” [from that study] may be totally
irrelevant, because if you had Mead acid in you
instead of AA, the COX 2 activity that causes cancers
related to this effect would not be there.  On the
other hand, your point is problematic because people
are taking inhibitors could lead to its conversion to
LOX or other metabolites that
may be more dangerous.  And then there’s the ease with
which AA is converted to metabolites relative to the
much less reactive Mead acid.  This, along with the
overpowering nature of AA’s metabolites, makes it the
choice of those who seek punishment.  Thank you sir,
may I have more arachidonic acid!  When you read the scientific
literature
on AA, one things becomes clear: no matter what your body does with AA
does not matter – it is dangerous.  Yes, it matters in terms of
whether you get
cancer, diabetes, heart disease, or whatever but my point is that it
is so unstable
chemically that it is just a matter of what negative effect it will
have on you, not
whether or not it will have a dangerous effect.  As I’ve posted
many times
before, just go to www.pubmed.com and do an “arachidonic”
search and see
what I mean.  Make sure you are sitting down when you do it.  Note
that I’m doing
a follow-up post that contains just a small number of
studies demonstrating the harm PUFAs derived from diet
do (for the most part, not all may be on point, but
it’s what I was working on with a lipid peroxidation
products research paper).

“How do you know [if Mead acid would be as effective
as AA – this is about the kid who supposedly got
better with AA supplementation]?”

Nobody does, and I made that point.  The experiments
that would demonstrate what actually is in the best
interests of human physiology have not been done, so
we can only go by the evidence available – that’s what
science is.  You can’t just pull one clinical study
about one individual [who has a genetic defect, no
less] out and say that it’s all settled.  That, again,
is LUDICROUS.  But the key point is that when viewed
as a whole, the evidence supports my point better than
any of the alternatives.

The last anti-Mead acid study you cite (and I guess
these are the only pieces of evidence you could find,
compared to the ones on AA, which could fill up a set
of Encyclopedias), begins the abstract with an
assumption for which these is no good evidence (one
could say, no real evidence at all):
“The essential fatty acid deficiency (EFAD) is a
metabolic condition related to cancer development.”
They must have been smoking something other than
tobacco when they pulled that one out of thin air, and
where are their references (you asked for mine).  Then
they talk about: “The possible riskiness of
EFA-deprivation…” but where is the evidence.  There
are all kinds of deprivation syndromes that can
produce nasty symptoms, for example, vitamin B 12,
that have been well documented.  But in this context,
the evidence against Mead acid just does not exist,
but again, AA comes out looking like an absolute
monster under conditions in vivo that will occur,
usually by age 40 or so (and often occur earlier).
Interestingly, their conclusion could be correct,
because if a Mead acid person doesn’t get cancer to
begin with, then dousing cancer cells in Mead acid as
an in vitro experiment is RIDICULOUS – the results
don’t mean anything to actual people, and are just a
waste of time and money.  The omega 3 HUFA they
compared Mead acid to was anti-cancer because it is
TOXIC to cancer cells, as it is to normal cells (those
extra double carbon bonds).  They could have obtained
similar results with many other fatty acids that are
not considered dangerous by these people, such as the
“essential” linoleic acid, which dozens of scientists
have pointed out appears to be the cause (in amounts
consumed by many if not most Westerners) of the common
cancers (except lung).

“Maybe it's the high level of Mead PUFA [in some
Eskimos] that's the problem.”

First, which problem are we talking about?, and
second, this is certainly possible, though they have
diets that are very restricted, as you yourself
mentioned, so in and of themselves, they are not
definitive evidence in this context, only one area
that should be explored further.  In the meantime, we
all have to eat, so if we want to eat the healthiest
foods, we have to look at the evidence in total and
make a decision.

Now back to that study: “Levels of linoleic- and
dihomo-gamma-linolenic acids were higher in Inuit as
compared to Caucasian neonates…” and “Within the
Inuit
group, a higher intake of marine food was associated
with a better neonatal (n-3) status [meaning more
omega 3s].”  So who knows what is going on here?
There may be more lipid peroxidation due to the high
linoleic and linolenic levels.  It even mentions
genetic factors as a possible explanation.  And are
these particular people especially unhealthy?  It was
done in 1992, so what kind of diet were they on then?
They may have not have been on the diet their
ancestors (the ones who bled to death of minor bumps)
were consuming.  If the majority of our “scientists”
were investigating this undeniably promising area,
instead of trying to develop drugs that only prolong
agony, we would have this all resolved by now.

No more on “trans fat,” except that if it is changed
into an SFA, then it will act like an SFA, obviously.
But my point about semantics is valid: what you say
are saturated fatty acid molecules (derived from oleic
acid) are called “trans monounsaturated fatty acids”
in a study in the July edition of the European Journal
of Clinical Nutirition (vol. 56, # 7).  No need to
fear this molecule as some sort of Trojan horse
molecule – it’s among the healthiest things you can
eat!  The partially hydrogenated foods are unhealthy
because they are like lard, plenty of double bonded
carbons on fatty acids and little or no antioxidant
protection.  Very dangerous, obviously.  End of
semantics.  Experiments attempting to determine how effective herbs
and
spices are as antioxidants use pork and lard because they are so
easily degraded
by free radicals.  You can’t do this with fresh coconut oil
– the experiment would
take years instead of hours because it is so saturated.  That’s
why it is healthy, but
because lard, with 39% or so saturated fatty acids, is considered a
“saturated fat,”
saturated fatty acids get a blanket condemnation.  FOOLISH BEYOND
BELIEF.

“Familial anecdotes aren't science.”

Certainly true, but we are being told by 99.99% of the
“experts” out there (correctly for one of the few
times) that Westerners are getting almost no, or no
omega 3 PUFAs from their diets (as I said about plenty
of people I know), yet they also say that they are
“essential,” and this obvious logical inconsistency
should be brought to light.  Exactly how does one
define “essential,” in other words?  Notice that it is
never defined, or else they say one will get dandruff
or dry skin, which, even if true (my hair and skin is
better than ever these days, so that seems to be more
nonsense), does not compare to what AA does, which is supposedly
“essential.”  PREPOSTEROUS!!!!

“More unscientific hyperbole. As I said in the last
post: essential
means "can't be made by the body from scratch", not
"you'll rapidly
die without it".”

Again, a logical inconsistency.  Just because you’re
body can’t make something doesn’t mean your body needs
it.  Can your body make aluminum?  Or terpenes?  Or
squalene?  Something like squalene may be helpful, and
for some people it may be essential (once they develop
a particular “chronic disease”), again depending upon
how it is defined, but a claim of absolute
essentiality needs strong evidence to support it.  Why
don’t they just say what the evidence actually
suggests?
The media may be partly to blame, but then scientists
should get together a put out a press release
condemning the media’s overstatements.  

Your claim that more omega 3s and less omega 6s in the
diet is the solution is contradicted by many papers,
such as the following:

“Eur J Clin Nutr. 2004 Jul;58(7):1083-1089.
Increased alpha-linolenic acid intake lowers
C-reactive protein, but has no effect on markers of
atherosclerosis.

Bemelmans WJ, Lefrandt JD, Feskens EJ, Haelst Pv P,
Broer J, Meyboom-De Jong B, May JF, Tervaert JC, Smit
AJ.

[1] 1Department of General Practice, University of
Groningen, Groningen, The Netherlands [2] 3Centre for
Nutrition and Health, National Institute for Public
Health and the Environment, Bilthoven, The
Netherlands.

OBJECTIVE:: To investigate the effects of increased
alpha-linolenic acid (ALA)-intake on intima-media
thickness (IMT), oxidized low-density lipoprotein
(LDL) antibodies, soluble intercellular adhesion
molecule-1 (sICAM-1), C-reactive protein (CRP), and
interleukins 6 and 10. DESIGN:: Randomized
double-blind placebo-controlled trial. SUBJECTS::
Moderately hypercholesterolaemic men and women
(55+/-10 y) with two other cardiovascular risk factors
(n=103). INTERVENTION:: Participants were assigned to
a margarine enriched with ALA (fatty acid composition
46% LA, 15% ALA) or linoleic acid (LA) (58% LA, 0.3%
ALA) for 2 y. RESULTS:: Dietary ALA intake was 2.3 en%
among ALA users, and 0.4 en% among LA users. The 2-y
progression rate of the mean carotid IMT (ALA and LA:
+0.05 mm) and femoral IMT (ALA:+0.05 mm; LA:+0.04 mm)
was similar, when adjusted for confounding variables.
After 1 and 2 y, ALA users had a lower CRP level than
LA users (net differences -0.53 and -0.56 mg/l,
respectively, P<0.05). No significant effects were
observed in oxidized LDL antibodies, and levels of
sICAM-1, interleukins 6 and 10. CONCLUSIONS:: A
six-fold increased ALA intake lowers CRP, when
compared to a control diet high in LA. The present
study found no effects on markers for atherosclerosis.
SPONSORSHIP:: The Dutch 'Praeventiefonds'.European
Journal of Clinical Nutrition (2004) 58, 1083-1089.
doi:10.1038/sj.ejcn.1601938&#8221;

In EJCN&#8217;s volume 56, supplement 3 (August, 2004), page
S-17, there is the following:
&#8221;The eicosanoids produced from EPA are often less
biologically potent than the analogues synthesized
from arachidonic acid (eg LTB5 is only about 10% as
potent as LTB4&#8230;&#8221;

And this is also UNDENIABLY true about Mead acid
(i.e., it is even less biologically potent than
arachidonic acid than EPA is) except that you can eat
a
very high SFAs diet (with some MUFAs like oleic, and
traces of PUFAs because they are practically
unavoidable) and then lipid peroxidation is not a
problem.  Also, they and many others scientists are on
board with my point that a much less potent fatty acid
is much healthier, so why do you find the Mead acid so
unappealing for this purpose?  It would be nice to
have more evidence, but the evidence at this point is
clear: everything in favor except for a few
unrealistic studies (which can be found for just about
any substance in the scientific literature).  In the
study above (Eur J Clin Nutr. 2004
Jul;58(7):1083-1089.), of which there are many others
that are similar, demonstrates that omega 3s are not
the answer, though a &#8220;balance&#8221; between omega 3s and
omega 6s does seem better than a high omega 6 diet
with trace amounts of omega 3s.  Why choose between
bad and worse, though, when you can have optimal with
Mead acid?

&#8220;Prhaps you'd be better off recognising that the three
fatty acids are
precursors for unique sets of molecules. You can't
make the
prostaglandins that come from arachidonic acid from
Mead Acid, so by
definition a simple fatty substitution in position 2
will have a far
from simple biochemical effect.&#8221;

Totally agree &#8211; my point exactly (minus the typos).
No simple effect, if you consider the effect a virtual
elimination of the &#8220;chronic diseases&#8221; so common these
days.  You also can&#8217;t make AA metabolites from EPA,
but because EPA metabolite sometimes have opposing
effects, a notion of &#8220;balance&#8221; dawned on some idiot
who was writing a textbook, and now people are dousing
themselves in things like the highly dangerous
flaxseed oil or cod liver oil.  Again, my point is
that the evidence suggests, in the strongest possible
way, that the metabolites of AA and EPA are far too
dangerous for humans (and then there are the highly
toxic lipid peoxidation products of dietary PUFAs,
such as 4-HNE, which I haven&#8217;t even touched upon, but
for which there is an extensive scientific
literature).  There is no comparable body of evidence
against Mead acid as the stressor-induced fatty acid
in humans (though obviously, dousing cells in a dish
with it will create all kinds of irrelevant results &#8211;
you could call anything &#8220;bad&#8221; by doing that, even
water).  However, when you think of many &#8220;traditional
diets&#8221; high in coconut oil or palm kernel oil or olive
oil, it is obvious that most, if not almost all early
humans were &#8220;essential fatty acid deficient.&#8221;  There
were not enough PUFAs overall in those diets to move
Mead acid out of its role as dominant stressor-induced
fatty acid, and the study above about the crucial
tissues that preserve Mead acid are more evidence to
this point.  The claim made so often by the &#8220;experts&#8221; in
the
mainstream media, it should be noted, regarding endogenous
PUFA synthesis (in humans) is completely wrong, because Mead
acid is a PUFA, and can be made by humans.  It is a matter of
which of the three possible HUFAs is best as the predominant
stressor-induced
fatty acid in phopholipids.  We may never know for sure, because the
correct
experiments need to be done, but according
to the anthropologists, the kinds of diets early
humans consumed would lead to this &#8220;EFAD condition.&#8221;
We would not be here if Mead acid was so unhealthy!
And judging from the few people I know who have been
&#8220;essential fatty acid deficient&#8221; (including myself, of
course) for a while now the results are great.  When I
add this to everything known, it&#8217;s a &#8220;slam dunk&#8221; for
Mead acid, and an early shower for AA or EPA.

As a final point, www.newscientist.com had this posted
on their web site (&#8220;Hawking cracks black hole paradox&#8221;
on July 14, 2004):
&#8220;After nearly 30 years of arguing that a black hole
destroys everything that falls into it, Stephen
Hawking is saying he was wrong. It seems that black
holes may after all allow information within them to
escape.&#8221;

Why biologists and others involved with diet and
health issues don&#8217;t have the integrity Hawking does
(and he is almost worshipped by many as a new
Einstein) is another story, but less important for
those who understand what I have posted above, and are
willing to act upon it.

The above was written by the author of four books, the first two of
which were published in 2001, and only differed by two pages, the last
of the four (which was the only work of fiction published) being
published in 2004.

[Schedule of the conference mentioned above:
SUNDAY   
2:00 pm - 9:00 pm    Arrival and Check-in   
6:00 pm    Dinner   
7:30 pm - 9:30 pm    CONTROVERSIAL HISTORY OF BIOLOGICAL WATER: VOICE OF
THE PROTAGONISTS
Discussion Leader: Phillip Ball, Nature, London, UK    
Walter Drost-Hansen, University of Miami, Coral Gables, FL
"From vicinal hydration of biopolymers to cell function"   
Gilbert Ling, Damadian Foundation, Melville, NY
"The Polarized Multilayer (PM) theory of protoplasmic water in living
cells"
MONDAY   
7:30 am - 8:30 am    Breakfast   
8:45 am    Photo   
9:00 am - 12:30 pm    PHYSICAL CHEMISTRY OF WATER AT BIOLOGICAL
INTERFACES
Discussion Leader: Chaim Frenkel, Rutgers University   
Elaine Zhu, Harvard University, Cambridge MA
"How water meets a hydrophobic surface"   
Jacob Israelachvili, UC Santa Barbara
"Measurements of hydrophobic forces"   
Martin Chaplin, South Bank University, London, UK
"Does water clustering determine biological structure?"   
Gerald Pollack, Univ. of Washington, Seattle
"Solute behavior in the vicinity of hydrophilic surfaces"   
12:30 pm    Lunch   
6:00 pm    Dinner   
7:30 pm - 9:30 pm    INTERACTIONS BETWEEN MACROMOLECULES AND WATER   
Discussion Leader: Martin Chaplin, South Bank University, London   
Judith Herzfeld, Brandeis University, Waltham, Mass
"Crowding-induced order in cells"   
Daryl Eggers, San Jose State University, San Jose, CA
"Influence of interfacial water on protein folding equilibria in
crowded environments"
Teresa Head-Gordon, UC Berkeley, Berkeley, CA
"Hydration dynamics near a model protein surface: Implications for
protein function and protein- protein assembly"
TUESDAY   
7:30 am - 8:30 am    Breakfast   
9:00 am - 12:30 pm    BEHAVIOR OF WATER IN THE PRESENCE OF SOLUTES AT
EXTREMELY LOW CONCENTRATION
Discussion Leader: Pascale Mentre, Universite Pierre et Marie Curie,
Paris, France
Jacques Benveniste, DigiBio, Clamart, France
"Role of water in the transmission of molecular signals"   
Yolene Thomas, CNRS, Saint Cloud Cedex, France
"Activation of human neutrophils by electronically transmitted
phorbol-myristate acetate"
Mae-wan Ho, Director, Institute of Science in Society
"The cell as a liquid crystal"   
Shiimon Mizrahi, Technion Israel
"Water mediated cosolutes effects on gels swelling and osmotic
pressure of polymers"
12:30 pm    Lunch   
6:00 pm    Dinner   
7:30 pm - 9:30 pm    BASIC BIOPHYSICAL PROCESSES INVOLVING WATER   
Discussion leader: Miklos Kellermayer, Univ of Pecs, Hungary    
James Clegg, Univ of Cal., Davis, CA
Anhydrobiosis (life without water) reveals the essential functions of
intracellular water
Vladimir Voeikov, Moscow State University, Russia
"Self-organizing nature of oxygen radical-dependent processes in
aqueous systems"
Denys Wheatley, Univ. of Aberdeen, U. K.
"Metabolic control: diffusion, convection and encounter frequencies on
cytoplasmic surfaces"
WEDNESDAY   
7:30 am - 8:30 am    Breakfast   
9:00 am - 12:30 pm    BEHAVIOR OF SOLUTES IN INTERFACIAL WATER   
Discussion leader: John Sheehan, University of North Carolina   
Norio Ise, Kyoto University, Japan
"When does like like like? -- Structure formation of macro-ions in
solutions"
David Weitz, Harvard University, Cambridge MA
"Aqueous gels and networks: Mechano-properties and mechano-sensing"   
Guenter Albrecht-Buehler, Northwestern Univ., Chicago, IL
"Water structuring centers of mammalian cell surfaces"   
Ludwig Edelmann, Saarland University, Homburg/Saar, Germany
"Electron microscopic detection of potassium and water association at
cellular proteins"
12:30 pm    Lunch   
6:00 pm    Dinner   
7:30 pm - 9:30 pm    ROLE OF INTERFACIAL WATER IN CYTOSKELETAL PROCESSES   
Discussion leader: Carlton Hazlewood, President, PetroClean, L.L.C.,
and Research Consultants, International
Ivan Cameron, University of Texas, San Antonio, TX
"Water: Biology's forgotten molecule"   
Dan Urry, Univ. of Minnesota, Twin Cities, MN
"The fundamental role of differentiated water structure in protein
structure and function"
Frank Mayer, Univ. of Goettingen, Germany
"Interfacial Water: determinants for cell architecture and cell
function"
THURSDAY   
7:30 am - 8:30 am    Breakfast   
9:00 am - 12:30 pm    ROLE OF INTERFACIAL WATER IN BIOLOGICAL PROCESSES   
Discussion Leader: James Clegg, Univ. of California, Davis.   
Virginia Shepherd, University of New South Wales, Sydney, Australia
"Plant cells through the looking glass: Alternative interpretations of
cytoplasmic structure and electrophysiology"
Reuven Tirosh, Bar Ilan University, Ramat Gan, Israel
"Ballistic protons, water solitons, and bioenergetics"   
Sasha Safronov, Ural State University, Ekaterineburg, Russia
"Hydration in synthetic polyelectrolyte gels. Electrochemical
potential and enthalpy of swelling"
Fabio Bruni, University of Rome
"The glassy state of water in model and real systems: Is it
biologically useful?"
12:30 pm    Lunch   
6:00 pm    Dinner   
7:30 pm - 9:30 pm    ROLE OF WATER IN BIOMATERIALS AND GELS    
Discussion leader: Jacob Israelachvili, UC Santa Barbara   
Erwin Vogler, Pennsylvania State University, University Park, PA
"Role of water in protein adsorption/assembly at interfaces"   
Hans Griesser, University of South Australia, Adelaide, Australia
"Characterization of hydrated layers by colloid atomic force
microscopy"
Allan Hoffman, University of Washington, Seattle, WA
"The role of water in PEGylated 'non-fouling' surfaces"]