Re: Will the "MattLB" types now admit they are wrong?
- From: "mike V" <mikev@xxxxxxxxxxxxxxxx>
- Date: Wed, 14 Nov 2007 11:58:10 -0500
"MattLB" <mattlb@xxxxxxxxxxxxx> wrote in message
news:1195049286.975513.281700@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
On Nov 14, 2:01 am, Taka <taka0...@xxxxxxxxx> wrote:
On Nov 14, 2:51 am, MattLB <mat...@xxxxxxxxxxxxx> wrote:
J Lipid Res. 1992 Nov;33(11):1719-26.
An in vitro model for essential fatty acid deficiency: HepG2 cells
permanently maintained in lipid-free medium.
These are cancer cells. Cancer cells by definition are abnormal cells
that stay alive when they shouldn't.
Do you mean that cancer cells are some sorts of zombies and stay alive
even if you deprive them from the "essential" nutrients they cannot
synthesize?
Pretty much, yes. Cancer cells ignore all the signals to die that
other cells obey. Cancer cells have an altered metabolism and altered
requirements. The major function of AA and its eicosanoid
derivatives is as a signalling molecule. Cancer cells don't respond
to signals in the same way, or at all, so whether or not they can make
eicosanoids is irrelevant to their continued growth, because it's
unregulated.
Or aren't the "essential" nutrients in fact that much
essential, are they?
Like monty1945 you seem to be equating "required for normal function"
with "will die horribly and quickly in their absence". Essential in
the context of EFA refers to the ability to synthesize them, not how
important they are to staying alive.
In vitro model of essential fatty acid deficiency.
The polyunsaturated fatty acids linoleic acid (18:2, n-6) and
arachidonic acid (20:4, n-6) are essential for normal skin function
and structure, both as eicosanoid precursors and as components of
lipids forming cell membranes.
They say they're essential right there! How is this paper supporting
your claim that the other one is absurd?
The cells are doing just fine even in the absence of the "essential"
factor, that's the point here. Previously you were pointing out that
the cells in culture would die quickly without EFAs.
Not all cells, because not all cells have the same requirements. Those
that need to respond to the "stay alive" signals from their neighbours
will die when they stop getting that signal. Those that don't need to
be told to stay alive (like cancer cells) will carry on living. Skin
cells may not need feedback from the cells around them to carry on
growing. Although the paper says they are normal once grafted into
living bodies it doesn't mean they would carry on being normal if left
in culture and allowed to become confluent.
Saying something is "essential" has apparently dubious meaning here
Monty1945 uses the layman's term rather than the scientific one.
and the modern studies are just parroting this phrase. I would
question even the essentialness for skin health if the dry skin can be
prevented with other factors such as VitB6.
Prevented or attenuated? Masking one deficiency with another nutrient
is a known phenomenon. Folic acid and B12 have a similar relationship.
It would be more constructive MattLB if you can come up with some
studies showing directly severe damage from the EFAD state such as
organ failure or severe infections and compromised immunity.
Again, you're anticipating far more of a dramatic consequence than is
warranted. You can knock out whole genes and still see only minor or
apparently non-existent consequences. It takes a long time to get to
death from essential amino acid deficiency and they're far more than
just signalling molecules.
So far I
am only seeing Monty walking around infected people not catching a
cold in 4 years
He's telling you that and you're believing him, that's not proof. I go
for years without a cold too, yet I make no effort to deprive myself
of EFA. Until he has a blood test that shows he's clinically EFAD
anything he says is pure propaganda.
In the following study you can see that even the fish is not dying
from EFAD:
Well, apart from anything else, they still have EFA in their bodies:
The content of DHA in
phosphatidylserine (PS) was high in control animals (40% in skin and
35% in opercular membrane) and was mostly retained in EFA deficient
animals.
So whatever negative effects might be seen from DHA deficiency, won't
be seen if it's not deficient.
Arachidonic acid (AA) was the most abundant PUFA esterified
to phosphatidylinositol (PI) and was significantly reduced in EFA
deficient animals (from 31% to 13% in skin),
Reduction isn't elimination, and it may be that 13% is still enough to
maintain normal signalling or at least normal enough to avoid seeing a
clear deficit.
MattLB
Hi MattLB:
To me whether or not PUFA are technically "essential", conditionally
essential, or merely highly important to human health has very little
relevance in the real world.
I am satisfied to know that PUFA have been in the human diet since our
prefarming days while our metabolism was evolving.
The following review does an excellent job of summarizing the needs and
benefits of PUFA in human health.
I did notice it suggested the presence of mead acid as merely an indicator
of low general PUFA status! Does it have any importance in it's own right,
do you think?
Quotation from: http://www.jacn.org/cgi/reprint/23/4/281
"Polyunsaturated Fatty Acids: Biochemical, Nutritional and Epigenetic
Properties"
Paola Benatti, MC, Gianfranco Peluso, MD, Raffaella Nicolai, PhD, and
Menotti Calvani, MD Scientific Department, Sigma Tau S.p.A. Pomezia, Rome
(P.B., R.N., M.C.), Department of Experimental Oncology, National Cancer
Institute, Naples (G.P.), Italy
"Guidelines for the Assesment of PUFA Status.
For the assessment of the essential PUFA status of an individual, the total
amount of the various EFA and PUFA in plasma or erythrocyte phospholipids is
a useful It should be realized that the plasma content of essential PUFA
does not necessarily guarantee the proper use of these fatty acids by cells
and tissues. Therefore, additional status markers are required to reliably
assess the functional PUFA status of a given individual.
In general, if insufficient essential PUFA are available to meet PUFA
requirements, the body starts to synthesize certain fatty acids that are
hardly present if the EFA and PUFA status is adequate. Therefore, these
fatty acids can be essential PUFA status markers.
The best known marker is Mead acid (C20:3 n-9). The synthesis of this fatty
acid is promoted if there are insufficient concentrations of LA and LNA to
meet the need for the synthesis of long-chain PUFA. EPA and DHA inhibit Mead
acid synthesis, the presence of Mead acid indicates a general shortage of
all essential PUFA.
Another suitable indicator of essential PUFA status is the essential PUFA
status index, which is the ratio between all essential PUFA (the sum of all
n-3 and n-6 fatty acids) and all nonessential unsaturated fatty acids (the
sum of all n-7 and n-9 fatty acids). The higher the essential PUFA status
index, the better the essential PUFA status.
Finally, if there is a functional shortage of DHA, the body starts to
synthesize the most comparable long-chain PUFA of the n-6 family, osbond
acid (22:5n-6). Therefore, under steady state conditions, the ratio between
DHA and osbond acid is a reliable indicator of the functional DHA status
(226)".<<<<<<
I am a retired engineer, and therefore claim no knowledge of biochemistry
beyond what I can read and only partially understand from other people's
work.
I do find it interesting that monty's (nicks') ideas have been the subject
of endless raypeatition at least since you and Larry Hoover were taking
issue with him in the Fall of 2002.
http://groups.google.com/group/sci.med.nutrition/search?hl=en&group=sci.med.nutrition&q=nick+2002&qt_g=Search+this+group
Five years of Mental Masturbation at it's finest!
I salute you as a man of considerable stamina!
MikeV
.
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