Taka wrote:
- quote -

You guys talking about lipolysis, lipogenesis, adipose tissue, type 2
diabetes, etc.?

I can contribute some paragraphs from /Metabolism at a Glance, ed3/,
if you like.

--
Marshall Price of Miami
Known to Yahoo as d021317c

On May 17, 6:45 am, Marshall Price <d0213...[at]yahoo.com> wrote:
- quote -

http://tinyurl.com/47fuhv

http://tinyurl.com/6cpdnp

Taka wrote:
- quote -

Could you provide a link to that, Taka?

--
Marshall Price of Miami
Known to Yahoo as d021317c

On May 7, 11:56 pm, "John Hasenkam" <jo...[at]goawayplease.com> wrote:
- quote -

Looking at Medline the NPD1/LXA4 lipoxins, resolvins and protectins
(e.g. PMID: 18233953,18437155,15912889,15152078,17965751,18060 755)
stories look appealing (finally some sensible function for Omega-3s!)
but they are needed only in the presence of AA and its proinflammatory
metabolites such as LTB4. So much research effort and money is being
invested into finding different ways to counteract the AA-mediated
"oxidative stress" while no one looks at the simplest solution to
reduce or eliminate AA/LA from the body. If AA is so essential why do
we need to counteract it with drugs like aspirin or NSAIDs all the
time? If you catch cold or get injured why do you need to take
substances inhibiting AA metabolization???

Taka

"MattLB" <mattlb[at]angelfire.com> wrote in message
news:ebe51aa4-63d5-4b9f-a41e-f7e65b0d6f14[at]d45g2000hsc.googlegroups.com...
- quote -

The mammalian brain likes to preserve DHA and EPA, particularly the former.
DHA is a substrate for NPD1, a neuroprotectant. Studies on omega 3
supplementation in relation to depression, bipolar, and schizophrenia are
conflicting but in relation to depression at least if the diet is low in
omega 3's increasing intake of the same is a reasonable safeguard. Omega 3
intake also correlates with retinal health, obviously because NPD 1 is very
important for retinal neurons. Ironically studies indicate that it is omega
3's that are very easily oxidised here, hence it is good to maintain the key
carotenes that facilitate retinal health, lutein and zeaxanthin, because
without omega 3's your vision is going to deteriorate anyway. Catch 22, as
it so often bloody well is. Supplementing pregnant women with omega 3's did
lead to measurable increases in visual acuity in their newborn infants.
Deficiencies in omega 3's during pregnancy may result in the mother
experiencing omega 3's deficiencies because the fetus wills strip these fats
from the mother. I sometimes wonder if this serves as a partial basis for
post partum depression.

On May 6, 10:25 pm, MattLB <mat...[at]angelfire.com> wrote:
- quote -

Perhaps the body knows what is dangerous molecule and tends to get rid
of it first. This could also explain no ill effects of high Omega-3
intake in the "paleo low carb people" who run mostly on fat (ketosis)
but deleterious effects (such as the metabolic syndrome) in the high
carb + PUFA sedentary crowd.

- quote -

Prostaglandins can be only made by the inducible COX enzymes but the
more dangerous and destructive leukotrienes are made at least
partially by spontaneous oxidation. So if AA gets loose in the
tissues it would be primarily converted to leukotienes. I think he
means that coconut oil somehow stimulates the phospholipase (PLA-2).
In any case there is a spontaneous turnover of AA leading to its
continuous release which is higher in people with high AA content in
membranes or under different stress conditions. I don't think the
triglyceride-bound form of AA as a transport vehicle in the blood is
dangerous in terms of forming the signaling molecules.

- quote -

But this is enough to completely block the Mead acid production. It
is interesting to read what the people supplementing with AA on
purpose say, no systemic inflammation but much stronger responses to
stimuli such as exercise. I wonder whether the body has a mechanism
to stop producing AA when the cell membranes are "charged" with it
enough ...

- quote -

Yes, they probably end up sticking to/oxidizing nearby macromolecules
forming AGEs and other nasty stuff such as DNA adducts.

- quote -

I have seen some studies suggesting that the Inuits have low
activities of desaturases so that they must be getting the long chain
PUFAs directly e.g. from meat like the cat. Also atopic dermatitis
has been blamed on insufficient AA in one paper. But one must
consider that if there is a problem with the LC-PUFA synthesis the
body cannot also make the Mead acid. This is, however, rarely taken
into account. With every EPA/DHA or AA supplementation experiment
there should be a proper Mead acid control.

Taka

On May 2, 4:37 pm, Taka <taka0...[at]gmail.com> wrote:
- quote -

Not deliberately, but if there's as much in the diet as monty1945
*suggests* then it will end up in adipose stores because I don't think
the intestinal acyltransferases that attach FA to glycerol are all
that fussy.

- quote -

I think *most* storage fat comes from the diet, although that
obviously depends on what the diet is.

In terms of burning FA, radiolabelling experiments have shown that the
order is LNA > LA > oleic > saturated i.e. LNA is the preferred
substrate for beta oxidation enzymes. AA wasn't included in the
experiment so I don't know to what extent it is used as energy rather
than for signalling.

- quote -

I doubt it's significant too, but monty1945 always talks about release
of AA when switching to his diet and in the absence of a clear
explanation of what he means I'm assuming he means release from tissue
stores into the blood to cause systemic inflammation. If what he
really means is release of prostaglandins from cells then he should
say so.

- quote -

No, it's a very low conversion rate. For a typical 10g daily
consumption of LA, only 0.06g grams ends up as AA.

- quote -

They have to have a limited lifespan/reach or they wouldn't be any use
as a localized targeting aid.

- quote -

Low EPA is associated with depression, I believe, but in general I'd
suspect that the brain did indeed hold on to FA better than (or at the
expense of) other tissues. A gradual brain-wide decline in efficiency
may not be so noticeable as areas of scaly skin.

MattLB

On May 4, 10:53 am, Marshall Price <d0213...[at]yahoo.com> wrote:
- quote -

I recommend you have a look at my previous post about the Mead acid
eicosanoid family which seems to be complete in terms it can supply
all the "essential" functions of the AA metabolites such as
prostaglandins. It isn't just being actively investigated because it
is so rare in novadays people and experimental animals which are fed
vegetable oils. I have also tried to summarize the available evidence
in the thread "Mead acid studies" on Monty's site. Without the
Omega-6/AA and refined carbohydrate overload (combined with artificial
lighting) the human population wouldn't expand so much but people will
live healthier without degenerative diseases caused by chronic
inflammation and the Earth would be cleaner without industrial
pollutions caused by overpopulation.

Taka

- quote -

Taka wrote:
- quote -

From /Metabolism at a Glance/, 3rd edition, Chapter 11 ("Metabolism
of glucose to fatty acids and triacylglycerol"), p. 30:

-----
*The pentose phosphate pathway generates NADPH for fatty acid synthesis*

To reiterate, once the immediate energy demands of the animal have
been satisfied, surplus glucose will be stored in the liver as glycogen.
When the glycogen stores are full, any surplus glucose molecules will
find the glycolytic pathway restricted at the level of
phosphofructokinase. Under these circumstances, metabolic flux via the
*pentose phosphate pathway* is stimulated. This is a complex pathway
generating *glyceraldehyde 3-phosphate,* which then re-enters
glycolysis, thus bypassing the restriction at phosphofructokinase-1.
Because of this bypass, the pathway is sometimes referred to as the
'hexose monophosphate shunt' pathway.

One very important feature of the pentose phosphate pathway is that
it produces NADPH from NADP+. NADPH is a hydrogen carrier derived from
the vitamin niacin, and as such is a phosphorylated form of NAD+, the
important functional difference being that, whereas NADH is used for ATP
production, NADPH is used for fatty acid synthesis and other
biosynthetic reactions.

*Fatty acid synthesis and esterification*

Starting from glucose, the chart shows the metabolic flux via the
pentose phosphate pathway and glycolysis to mitochondrial acetyl CoA,
and hence via citrate to acetyl CoA in the cytosol. Fatty acid
synthesis is catalysed by the fatty acid synthase complex, which
requires malonyl CoA. The latter combines with the *acyl carrier
protein (ACP)* to form *malonyl ACP.* Fatty acid synthesis proceeds via
the cyclical series of reactions as shown in the chart to form
*palmitate* (and also stearate, which is not shown). However, fat is
stored not as fatty acids but as *triacylglycerols* (triglycerides).
These are made by a series of esterification reactions that combine
three fatty acid molecules with *glycerol 3-phosphate* (see Chapter 25).
-----

Note that this is only about the synthesis of fatty acids (palmitate
and stearate) from glucose. The incorporation into adipose tissue of
fatty acids from the diet is a different subject entirely.


--
Marshall Price of Miami
Known to Yahoo as d021317c

MattLB wrote:
- quote -

(Let's reserve "AA" for "amino acid.") Nobody would ever have
thought of adding MSG to food if it weren't already found in food. Some
of that glutamate, at least, goes into muscles and other tissues, and
enzymes, and it spares the energy and niacin required to make it from
alpha-ketoglutarate, a Krebs cycle intermediate.

--
Marshall Price of Miami
Known to Yahoo as d021317c

Taka wrote:
- quote -

Wait a minute, Taka, what about wound healing? You want to do
without that?

Take a look at slide 19. Is protecting gastric mucosa a bad thing?
How about promoting and inhibiting platelet aggregation (think
"strokes"), relaxing vascular smooth muscle ("erections"), relaxing
bronchial smooth muscle ("breathing"), increasing renal blood flow
("peeing"), and regulating uterine smooth muscle ("childbearing")?

--
Marshall Price of Miami
Known to Yahoo as d021317c

MattLB wrote:
- quote -

Right on, MattLB.

And the whole presentation is about *chronic* (not acute)
inflammation and *cancer.* Who knew we were discussing cancer, of all
things?

I note that Taka rarely mentions the role of arachidonic acid in
normal human physiology. Why is that?

I get the distinct impression that arachidonic acid is an absolutely
necessary constituent of all prostaglandins ("biologically active
phospholipid molecules that regulate many physiological functions"), so
how can we live without it?

Could Taka be confusing arachidonic acid in physiology with
arachidonic acid in food, the way the establishment did for many years
with cholesterol?

Now that HDL (high-density lipoprotein) cholesterol is called "the
good cholesterol," you don't hear so many people saying they've "got to
cut down on cholesterol." Butter, eggs, and bacon are getting expensive
again, just as oatmeal did earlier. I wonder whether corporate buy-outs
had anything to do with that.

Have you ever called Kretschmer's 800 line and asked about whether
phytic acid was a good thing to eat with dairy products? If so, you
probably got the old "What? Never heard of it!" routine.

Quaker bought Kretschmer, and both their wheat germ and oat bran
products make *strong* health claims on their packaging, which IIRC, is
illegal.

Let's just fire all those air traffic controllers. Who needs them
and their lousy union anyway? (Reagan was the president of one union
while my father was the president of a rival one. Dad came out of a
meeting with him and said, "that guy ought to go into politics."
Thanks, Dad!)


--
Marshall Price of Miami
Known to Yahoo as d021317c

Taka wrote:
- quote -

Thanks, Taka! (I'm taking a break while it arrives.)

--
Marshall Price of Miami
Known to Yahoo as d021317c

On May 2, 10:24 pm, MattLB <mat...[at]angelfire.com> wrote:
- quote -

Now this is an interesting point I would like to know more about. I
had the feeling that AA is not used for energy storage in the adipose
tissues. The shorter Omega-6 version linoleic acid (LA) is used
instead and reflects its dietary intake (this may turn quite dangerous
if you get cancer and start "burning" such LA-rich fat). Most storage
fat would be normally made from carbohydrates and would be therefore
SFA or MUFA (oleic acid) like the animal lard. I don't think there is
enough AA in meat to be put into the adipose tissue storage? Or are
you suggesting that the adipocytes or liver have so robust
desaturation and elongation pathways that a significant amount of
ingested LA is converted into AA for storage? In my current view most
AA is put into cell and mitochondrial membranes to be used for local
signaling when the cells are mechanically or chemically stressed (e.g.
by nitric oxide or high dose of VitB3). And it is not only
intracellular matter but the prostaglandins and leukotrienes can
diffuse in tissues some distance (e.g. LTB4 acts as powerful
chemoattractant for the destructive leukocytes).

- quote -

Also interesting that nothing has been reported about the EFAD effects
on brain (in adults). No neurodegeneration from AA insufficiency but
rather the other way around. Either the brain has a very good
mechanism holding on to the "EFA" stores or it doesn't need them.
AFAIK EFAD has only effects on skin and this may not even be related
to AA but LA.

Taka

On May 2, 9:42 am, Taka <taka0...[at]gmail.com> wrote:
- quote -

Thankyou for supporting the point that it is deliberately released in
response to physiological stimuli. Monty1945's claims about AA being
released probably reflect confusion about the difference between
intra- and extracellular release. Release of AA from triglycerides in
adipose tissue into the blood is completely different from AA being
released from phospholipids in the cell membrane into the cytoplasm of
a cell.

- quote -

It's bit of a myth. The liver will soak up the majority of the
consumed glutamate and turn it into urea and energy.

- quote -

The brain has a precise and unusual fatty acid composition which
includes AA and DHA by design. It's not simply a reflection of dietary
intake like adipose tissue or blood cells.

MattLB

On May 1, 10:44 pm, MattLB <mat...[at]angelfire.com> wrote:
- quote -

Other factors releasing AA from the membranes are e.g. sugar and
saturated fatty acids as I have posted on these groups previously
(Monty also mentions AA release while starting the SFA/coconut oil
diet). It is also released for the signaling purposes during
development and by certain hormones like estrogen.

- quote -

Or you can consume the brain excitotoxin MSG directly and don't even
need the brain injury :-)

BTW Omega-3s are also said to induce the long-term potentiation of
neuronal circuits what certain people consider beneficial or even
essential for improved memory ... With healthy brain you don't need
to overstimulate it with such things such as AA, DHA or MSG.

Taka

On May 1, 10:44 pm, MattLB <mat...[at]angelfire.com> wrote:
- quote -

What is considered normal these days doesn't mean that it was normal
during our evolution. I am speaking about the refined vegetable PUFA-
rich oils which are present everywhere especially in fast foods. And
the ludicrous thinking that we need to balance it with even more
chemically unstable PUFAs of the Omega-3 series. In the old times you
would get your dietary fat from lard or butter (mostly MUFAs or SFAs)
while these days they give it to you in the crust of fried meat which
is basically refined carbohydrates soaked in PUFA-rich oil all
"AGEylated" and oxidized at high temperature. I agree with Monty that
the human diet in the preindustrial age some 100 years ago resulted in
the appearance of measurable amounts of Mead acid in a healthy human
body.

And I suspect that the aging "program" is driven by AA metabolites
similarly to the developmental program so we may slow down aging and
the damage at old age by reducing AA to the bare minimum if any.

- quote -

How about stress? Even mental stress which is abundant in the modern
society. Better walking without the bomb than trying to protect its
trigger from setting off ... There are different signals in different
tissues, e.g. simple muscle contraction starts the AA cascade.

- quote -

Injuries happen all the time ... with less glutamate you will have
less damage anyway. Can something else less "dangerous" provide the
function of glutamate - NO. Can something else provide the function
of AA - YES, Mead acid. Again comparing oranges to elephants ...

Taka

On Apr 30, 6:38 am, Taka <taka0...[at]gmail.com> wrote:
- quote -

This isn't in question, it's what's you call excessive that is.
Excessive glucose causes abnormal glycation of proteins and diabetic
complications, excessive vitamin A kills - and so on for lots of other
examples of molecules that are supposed to be in the body in a certain
amount and cause problems when they exceed it. Your and monty1945's
assertion that we need less (or no) omega3/6 than what is considered
normal is what is in question, not that having more will cause
problems.

- quote -

You still need something to cause hydrolysis of the ester bond holding
the AA in the membrane. It doesn't need to be a leukocyte-linked
process, but you need some signal to activate the phospholipase that
starts the AA signalling cascade.

- quote -

It wasn't supposed to be. The point was that something that is
normally present (stomach acid) can causes specific problems
(ulceration of the oesophagus) when something else triggers a change
in behaviour (reflux).

Maybe excitotoxicity would be a closer match. Brain injury causes
uncontrolled release of excitatory glutamate neurotransmitter that
then overstimulates surrounding neurons. Glutamate in itself isn't
dangerous, nor is AA. Change glutamate to arachidonic acid and
overstimulates to over-inflames if you like, but you still need the
analogue to brain injury to start the whole thing off.

- quote -

More shameless hyperbole.

MattLB

On Apr 29, 7:18*am, MattLB <mat...[at]angelfire.com> wrote:
- quote -

Sidebar point. GERD can exist in the context of suppressed
or non-existent stomach acid secretion. This is called
bile reflux or alkaline reflux and it can be every bit as dangerous
as acid reflux.

I grant this doesn't disprove your original point, just there is
a need of a better illustration.

I am not taking sides here guys just yet, please continue.

On Apr 29, 11:18 pm, MattLB <mat...[at]angelfire.com> wrote:
- quote -

Destructive phase of a healthy inflammation lasts for a short time and
doesn't cause excessive tissue damage. With (excessive)AA in your
cells there is inadequate too powerful inflammatory response to mild
stimuli. Sometimes you don't need any inflammatory response like in
the case of symbiotic intestinal bacteria but AA triggers it. This
stresses the symbionts so they start fighting back in a vicious cycle
which can be stopped only with antibiotics.

- quote -

This is not exact, comparing the effects of AA to the effects of Mead
acid is like comparing the acid reflux with Hydrofluoric Acid versus
Hydrochloric acid. Or like putting rocket fuel instead of gasoline
into your car tank ...

- quote -

It is all about the thresholds and the more AA you have the lower the
threshold is. As you age more irritants accumulate in the body and
they are triggering the long-term chronic inflammation with AA but not
with the Mead acid/low AA.

Taka