Taka wrote:
- quote -

Of course they're true cells, and the fact that they don't reproduce
is nothing unusual. Most cells don't reproduce.

I think you've got to review the Cori cycle to understand how
anaerobic metabolism in muscle and red blood cells relies on the
*liver's* ability to oxidize lactate into pyruvate, and look more
closely into how cancer interferes with apoptosis. Here's a passage
from /MBOC4/ p1010 on how important and normal apoptosis is:

-----
Programmed cell death (apoptosis)

The cells of a multicellular organism are members of a highly organized
community. The number of cells in this community is tightly regulated -
not simply by controlling the rate of cell division, but also by
controlling the rate of cell death. If cells are no longer needed, they
commit suicide by activating an intracellular death program. This
process is therefore called *programmed cell death,* although it is more
commonly called *apoptosis* (from a Greek word meaning "falling off," as
leaves from a tree).

The amount of apoptosis that occurs in developing and adult animal
tissues can be astonishing. In the developing vertebrate nervous system,
for example, up to half or more of the nerve cells normally die soon
after they are formed. In a healthy adult human, billions of cells die
in the bone marrow and intestine every hour. It seems remarkably
wasteful for so many cells to die, especially as the vast majority are
perfectly healthy at the time they kill themselves. What purposes does
this massive cell death serve?

In some cases, the answers are clear. Mouse paws, for example, are
sculpted by cell death during embryonic development: they start out as
spadelike structures, and the individual digits separate only as the
cells between them die (Figure 17-35). In many other cases, cell death
helps regulate cell numbers. In the developing nervous system, for
example, cell death adjusts the number of nerve cells to match the
number of target cells that require innervation. In all these cases, the
cells die by apoptosis.

In adult tissues, cell death exactly balances cell division. If this
were not so, the tissue would grow or shrink. If part of the liver is
removed in an adult rat, for example, liver cell proliferation increases
to make up for the loss. Conversely, if a rat is treated with the drug
phenobarbital - which stimulates liver cell division (and thereby liver
enlargement) - and then the phenobarbital treatment is stopped,
apoptosis in the liver greatly increases until the liver has returned to
its original size, usually within a week or so. Thus, the liver is kept
at a constant size through the regulation of both the cell death and the
cell birth rate.

....

The intracellular machinery responsible for apoptosis seems to be
similar in all animal cells. This machinery depends on a family of
proteases that have a cysteine at their active site and cleave their
target proteins at specific aspartic acids. They are therefore called
*caspases.* Caspases are synthesized in the cell as inactive precursors,
or /procaspases,/ which are usually activated by cleavage at aspartic
acids by other caspases (Figure 17-38A). Once activated, caspases
cleave, and thereby activate other procaspases, resulting in an
amplifying proteolytic cascade (Figure 17-38B). Some of the activated
caspases then cleave other key proteins in the cell. Some cleave the
nuclear lamins, for example, causing the irreversible breakdown of the
nuclear lamina; another cleaves a protein that normally holds a
DNA-degrading enzyme (a DNAse) in an inactive form, freeing the DNAse to
cut up the DNA in the cell nucleus. In this way, the cell dismantles
itself quickly and neatly, and its corpse is rapidly taken up and
digested by another cell.

Activation of the intracellular death pathway, like entry into a new
stage of the cell cycle, is usually triggered in a complete, all-or-none
fashion. The protease cascade is not only destructive and
self-amplifying but also irreversible, so that once a cell reaches a
critical point along the path to destruction, it cannot turn back.

....

In the best understood pathway, mitochondria are induced to release the
electron carrier protein /cytochrome c/ (see Figure 14-26) into the
cytosol, where it binds and activates an adaptor protein called *Apaf-1*
(Figure 17-39B). This mitochondrial pathway of procaspase activation is
recruited in most forms of apoptosis to initiate or to accelerate and
amplify the caspase cascade. DNA damage, for example, as discussed
earlier, can trigger apoptosis. This response usually requires p53,
which can activate the transcription of genes that encode proteins that
promote the release of cytochrome /c/ from mitochondria. These proteins
belong to the Bcl-2 family.
-----

So it's no coincidence that cancerous cells' mitochondria aren't
"healthy." Cancer thrives by interfering with mechanisms in the
mitochondrion which ordinarily would cause the orderly death and
disintegration of the cell, *but* it does so without interfering with
those cell functions it needs to survive and grow.

--
Marshall Price of Miami
Known to Yahoo as d021317c

On Jun 13, 9:39 pm, MattLB <mat...[at]angelfire.com> wrote:
- quote -

Perhaps depending on the chain length ... Energy (ATP) can be
produced from glucose anaerobically, i.e. without oxygen what means
without mitochondria. This is impossible with fatty acids so the
energy production from fat is more "mitochondria costly" and requires
complicated biochemistry (membrane bound enzymatic systems). You need
highly differentiated cells at least in terms of mitochondria to
efficiently produce energy from fat, these are not the malignant cells
which went back to the embryonic state in a sense.

- quote -

You caught me, but I would not consider these true cells because they
have no nuclear DNA/chromosomes either and cannot reproduce (at least
in primates).

Taka

On Jun 12, 4:34 pm, Taka <taka0...[at]gmail.com> wrote:
- quote -

Malignant cells dying via apoptosis is a good thing.

- quote -

There is no switch. Whether burning fat or glucose it's all in the
form of Acetyl CoA by the time the mitochondrion gets going on it.

- quote -

In what way? The energy output per molecule is much higher than
glucose.

- quote -

Red blood cells have no mitochondria.

MattLB

On Jun 12, 1:12 pm, Marshall Price <d0213...[at]yahoo.com> wrote:
- quote -

Yes, cells with defective or downregulated mitochondria cannot
reproduce well without sugar because they use its glycolysis (under
anaerobic conditions) to produce energy. Normal stem cells could be
such an example but they seem to survive by entering a quiescent state
and using the little glucose body provides even if you don't ingest
any carbohydrates (liver actually makes sugar from protein by
gluconeogenesis). But the malignant cells won't cease dividing easily
and overproduce ROS instead of preserving energy what is going to kill
them first under severe sugar deprivation conditions and Omega-3s can
facilitate this process by triggering apoptosis.

- quote -

Terminally differentiated cells easily switch their mitochondria from
burning sugar to burning fat if the former is unavailable. The
efficiency of burning fat is lower so the cells additionally amplify
their mitochondria to compensate for this. If they have defective
mitochondria like cancer cells and amplify them they also amplify the
production of ROS what kills them. There are no cells without
mitochondria and the brain or muscle cells contain them in large
numbers. Stem cells like the muscle satellite cells function like a
healthy mitochondria storage and they are injecting them into the
muscle fibers when needed. Also there is a wonderful process of
healthy mitochondria selection/injection during the oocyte
development. Defective mitochondria can be removed by the process of
autophagy which some people here like DZ are trying to accomplish by
intermittent fasting.

Taka

Taka wrote:
- quote -

But most cells can't live without mitochondria, right? So you're
saying the cells die on a low-carb diet? Including fat and muscle
cells? That makes no sense to me. Once gone, they're gone for good.

--
Marshall Price of Miami
Known to Yahoo as d021317c

On Jun 4, 9:09 am, jay <jaym1...[at]hotmail.com> wrote:
- quote -

The grain-fed cattle does the same. No wonder people in developed
countries are overloaded with Omega-6 AA. You are what you eat
especially in the case of the fatty acid types. For some very
physically active people, the extra AA may be a plus given that they
are "burning" it in muscles for the production of the "good"
prostaglandins and use all ingested carbohydrates for energy
production (like the birds do, flying is very physically demanding
activity). However, this may only work in younger subjects with
undamaged tissues/cells I believe.

Taka

For several years before my body went haywire, I ate farm-raised
salmon frequently, sometimes for lunch and dinner. According to one
book, at the top of the list, a 4oz serving of farm-raised salmon
delivered a whopping 1,300 mg of AA, an amount that could not be
authorized for human study. Apparently salmon, which normally feed on
vegetation, produce AA very efficiently from grain/soy-based diets.
Can anyone backup this info?


Arachidonic acid-induced hind limb gangrene: a new experimental rat
model of peripheral vascular disease.

The purpose of this study was to investigate the characteristics of
arachidonic acid-induced peripheral vascular disease in rats.
Injecting arachidonic acid (2 mg/leg) into the femoral artery caused
hind limb gangrene. Histopathological examination revealed occlusive
thrombi and marked vascular injury, including denudation of the
endothelium and degeneration of the media in the paw arteries.
Arachidonic acid injection markedly enhanced the platelet response to
both U-46619 and collagen. Although the number of circulating
platelets did not differ between sham-operation rats and arachidonic
acid-injected rats, the numbers of circulating white blood cells and
red blood cells were raised 10 d after arachidonic acid injection.
Thrombocytopenia, induced before arachidonic acid injection, markedly
suppressed arachidonic acid-induced hind limb gangrene in rats. In
addition, the combined administration of aspirin (100 mg/kg/d, p.o.)
and ticlopidine (300 mg/kg/d, p.o.) prevented the progression of
arachidonic acid-induced hind limb gangrene. These results suggest
that platelets are involved in the progression of arachidonic acid-
induced hind limb gangrene. This experimental rat model may be
suitable for developing novel drugs for the treatment of peripheral
vascular disease. PMID: 10220280


Assessment of the arachidonic acid content in foods commonly consumed
in the American diet.
Arachidonic acid (AA) is an extremely important fatty acid involved in
cell regulation. When provided in the diet, it is cogently
incorporated in membrane phospholipids and enhances eicosanoid
biosynthesis in vivo and in vitro; however, controversy exists as to
the levels of AA in food and in the diet. This study determined the
amount of AA in cooked and raw portions of beef (rib eye), chicken
(breast and thigh), eggs, pork (loin), turkey (breast), and tuna; it
compared these results to values published in Agriculture Handbook No.
8 (HB-8). The cooked portions were prepared as described in HB-8. With
the exception of chicken thigh and tuna, the levels of AA (w/w) in the
selected foods analyzed were significantly higher, in general, than
those values published in HB-8. The greatest differences were observed
in beef (raw and cooked), turkey breast (raw and cooked), and pork
(cooked) where AA levels were twice that of the values in HB-8. In
contrast, the AA and n-3 fatty acid contents in tuna were almost half
the HB-8 values. The present data indicate that HB-8 tends to
underreport the amounts of AA in a number of foods commonly consumed
in the American diet, and new initiatives should be considered to
validate and update the current database for fatty acid composition of
foods.


By the way according to nutritiondata.com, which gets it data from
USDA, butter has 0mg of AA

Arachidonic acid supplementation dose-dependently reverses the effects
of a butter-enriched diet in rats.

Male Sprague Dawley rats were fed a butter-enriched diet (50% fat) for
2 weeks which was supplemented orally with 9, 18, 36, or 72 mg/day of
ethyl arachidonate for a further 2 weeks. The control group of animals
were fed a 5% fat diet for 4 weeks. Aortic prostacyclin (PGI2)
production, platelet aggregation and thromboxane A2 (TXA2) production
and plasma and aortic phospholipid (PL) fatty acids were measured. 50%
butter-feeding resulted in a significant reduction in aortic PGI2
production and collagen-induced platelet aggregation and TXA2
production. These changes were accompanied by a reduction in plasma
and aortic PL arachidonic acid levels and an increase in
eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), 5,8,11-
eicosatrienoic acid (ETA) and dihomo-gamma-linolenic acid (DGLA).
These changes in prostanoid production, platelet aggregation and PL
fatty acid composition were dose-dependently reversed by the daily
oral administration of ethyl arachidonate (9, 18, 36, or 72 mg). The
threshold dose being as little as 9 mg of ethyl arachidonate/rat/day
for reversal of PL fatty acid composition, collagen-induced platelet
aggregation and TXA2 production, and 18 mg of ethyl arachidonate/rat/
day for reversal of aortic PGI2 production. Full reversal was seen
generally with 36 or 72 mg of ethyl arachidonate/rat/day. The data
highlight the responsiveness of tissue eicosanoid production to small
quantities (ppm) of dietary eicosanoid precursors. PMID: 8469684

On Jun 3, 7:42 am, jay <jaym1...[at]hotmail.com> wrote:
- quote -

What I think the low carb diet does is to fully turn on the
mitochondria and probably eliminate the defective ones because the
cells which cannot properly oxidize fat to produce energy (if they
just make the free radicals) cannot get enough energy (in the absence
of sugar and the glycolytic pathway) and die. This can be taken
advantage of in the case of killing cancers which have almost always
mitochondrial defects, overproduce free radicals and thrive on sugar.
On the other hand be warned that you need certain level of oxidative
stress and sugar to produce enough sex hormones to reproduce. I agree
that AA on its own (if not turned into the inflammatory mediators) is
far less dangerous than the more unstable Omega-3 fatty acids - just
look at how different species increase their maximal lifespan - they
reduce Omega-3s in the membranes while leaving Omega-6 mostly
"untouched".

Taka

On Jun 3, 8:16 am, jay <jaym1...[at]hotmail.com> wrote:
- quote -

I would say you hit the nail on its head with this study, thanks. 5-
LOX produces the destructive eicosanoids Leukotrienes which are
directly responsible for all the chronic degenerative diseases. They
are produced in the first "immediate" phase of inflammation.
Originally, it was intended to last just for a short time to help
tissue remodeling or to "melt" the parasites but for different reasons
it is overactivated in the "modern" diseases. I suspect the
metastatic cancers are also making their ways throughout the body by
melting the tissue collagen with these signaling molecules. Genetic
predisposition is one way 5-LOX is overactivated, the other may be AA
overload or irritants which constantly stimulate its production. The
effect of sugar/carbohydrates/insulin well may be to disturb the
balance between 5-LOX and COX-1,2 in the favor of the former, but this
is just my speculation. It may be good to melt out the old damaged
tissues some times and in spikes, not constantly. Why exercise is not
proinflammatory may have the same reasons as to why the low carb diet
is not proinflammatory despite of AA release - it is made into the
Prostaglandins rather than Leukotrienes (see my other post about the
"Spaceflight muscle wasting"). That AA increases while you restrict
the carbohydrates is because your body starts mobilizing its fat
stores which are overloaded with linoleic acid (Omega-6, LA) in
novadays people and there is not enough sugar to inhibit the
desaturases and elongases which make it into the longer AA. It's
foolish to think Omega-3/fish oil will protect you from the AA-
Leukotriene production because it will do more harm in other ways -
first your GI tract goes ... 2.5% of LA in the diet is not low enough
to lower AA, there is a threshold. You need to go to about 1% (the
sweet spot, also depends on the level or your physical activity) and
keep it for long enough (2 years!) to deplete the excessive Omega-6
stores in your body. The appearance of Mead acid is a good marker and
should be measured by all these "expert" researchers in addition to
the Omega-6 and Omega-3 series.

Taka

Taka or Monty, please comment on below abstract which seems to say
that the amount of dietary LA from 2.5 to 17.5% of energy had little
affect on the amount of AA in neutrophil and plasma lipids, but was
decreased by 4g of fish oil.

Simple relationships exist between dietary linoleate and the n-6 fatty
acids of human neutrophils and plasma.

Eicosanoids, the enzymatically oxygenated products of arachidonic acid
(AA), appear to be overproduced in some disorders of inflammation.
Dietary strategies for decreasing tissue AA require information on the
relationships between dietary linoleic acid (LA) and tissue
concentrations of AA. The use of either high- or low-LA spreads and
cooking oils by healthy male volunteers resulted in a range of LA
intakes of 2.5-17.5% of energy, as estimated by diet-diary analysis.
Analysis of LA and AA concentrations in neutrophils and plasma lipid
fractions from these subjects indicated that there were positive
linear relationships between dietary LA and the LA concentrations in
neutrophil phospholipids, plasma triglycerides, and plasma cholesteryl
esters. By contrast, differences in dietary LA within a broad range
were not associated with differences in concentrations of AA in these
same neutrophil and plasma fractions. AA concentrations were decreased
by supplementation of the diet with 4 g fish oil (1.6 g
eicosapentaenoic acid, 0.3 g docosahexaenoic acid). The results
suggest that the LA content of tissue lipids may be used to estimate
LA intake, and the reduction of dietary LA by using standard dietary
strategies is not likely to lead to reduction in tissue AA whereas
this can be accomplished by fish-oil supplementation. PMID: 8379505

Taka and Monty, following abstract seems to support your points.

Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic
acid, and atherosclerosis.

BACKGROUND: Leukotrienes are inflammatory mediators generated from
arachidonic acid (polyunsaturated n-6 fatty acid) by the enzyme 5-
lipoxygenase. Since atherosclerosis involves arterial inflammation, we
hypothesized that a polymorphism in the 5-lipoxygenase gene promoter
could relate to atherosclerosis in humans and that this effect could
interact with the dietary intake of competing 5-lipoxygenase
substrates. METHODS: We determined 5-lipoxygenase genotypes, carotid-
artery intima-media thickness, and markers of inflammation in a
randomly sampled cohort of 470 healthy, middle-aged women and men from
the Los Angeles Atherosclerosis Study. Dietary arachidonic acid and
marine n-3 fatty acids (including a competing 5-lipoxygenase substrate
that reduces the production of inflammatory leukotrienes) were
measured with the use of six 24-hour recalls of food intake. RESULTS:
Variant 5-lipoxygenase genotypes (lacking the common allele) were
found in 6.0 percent of the cohort. Mean (+/-SE) intima-media
thickness adjusted for age, sex, height, and racial or ethnic group
was increased by 80+/-19 microm (95 percent confidence interval, 43 to
116; P<0.001) among carriers of two variant alleles, as compared with
carriers of the common (wild-type) allele. In multivariate analysis,
the increase in intima-media thickness among carriers of two variant
alleles (62 microm, P<0.001) was similar in this cohort to that
associated with diabetes (64 microm, P=0.01), the strongest common
cardiovascular risk factor. Increased dietary arachidonic acid
significantly enhanced the apparent atherogenic effect of genotype,
whereas increased dietary intake of n-3 fatty acids blunted the
effect. Finally, the plasma level of C-reactive protein, a marker of
inflammation, was increased by a factor of 2 among carriers of two
variant alleles as compared with that among carriers of the common
allele. CONCLUSIONS: Variant 5-lipoxygenase genotypes identify a
subpopulation with increased atherosclerosis. The observed diet-gene
interactions further suggest that dietary n-6 polyunsaturated fatty
acids promote, whereas marine n-3 fatty acids inhibit, leukotriene-
mediated inflammation that leads to atherosclerosis in this
subpopulation. PMID: 14702425

Taka and Monty: Could you comment on below abstract?

An arachidonic acid-enriched diet does not result in more colonic
inflammation as compared with fish oil- or oleic acid-enriched diets
in mice with experimental colitis.

Fish oils (FO) - rich in EPA and DHA - may protect against colitis
development. Moreover, inflammatory bowel disease patients have
elevated colonic arachidonic acid (AA) proportions. So far, effects of
dietary AA v. FO on colitis have never been examined. We therefore
designed three isoenergetic diets, which were fed to mice for 6 weeks
preceding and during 7 d dextran sodium sulfate colitis induction. The
control diet was rich in oleic acid (OA). For the other two diets, 1.0
% (w/w) OA was exchanged for EPA+DHA (FO group) or AA. At 7 d after
colitis induction, the AA group had gained weight (0.46 (sem 0.54) g),
whereas the FO and OA groups had lost weight ( - 0.98 (sem 0.81) g and
- 0.79 (sem 1.05) g, respectively; P < 0.01 v. AA). The AA group had
less diarrhoea than the FO and OA groups (P < 0.05). Weight and length
of the colon, histological scores and cytokine concentrations in colon
homogenates showed no differences. Myeloperoxidase concentrations in
plasma and polymorphonuclear cell infiltration in colon were decreased
in the FO group as compared with the OA group. We conclude that in
this mice model an AA-enriched diet increased colonic AA content, but
did not result in more colonic inflammation as compared with FO- and
OA-enriched diets. As we only examined effects after 7 d and because
the time point for evaluating effects seems to be important, the
present results should be regarded as preliminary. Future studies
should further elucidate differential effects of fatty acids on
colitis development in time. PMID: 18205994

Taka or Monty, I would be interested in your interpretation of below
abstract:

Comparison of low fat and low carbohydrate diets on circulating fatty
acid composition and markers of inflammation.

Abnormal distribution of plasma fatty acids and increased inflammation
are prominent features of metabolic syndrome. We tested whether these
components of metabolic syndrome, like dyslipidemia and glycemia, are
responsive to carbohydrate restriction. Overweight men and women with
atherogenic dyslipidemia consumed ad libitum diets very low in
carbohydrate (VLCKD) (1504 kcal:%CHO:fatrotein = 12:59:28) or low in
fat (LFD) (1478 kcal:%CHO:fatrotein = 56:24:20) for 12 weeks. In
comparison to the LFD, the VLCKD resulted in an increased proportion
of serum total n-6 PUFA, mainly attributed to a marked increase in
arachidonate (20:4n-6), while its biosynthetic metabolic intermediates
were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid
ratio also increased sharply. Total saturated fatty acids and 16:1n-7
were consistently decreased following the VLCKD. Both diets
significantly decreased the concentration of several serum
inflammatory markers, but there was an overall greater anti-
inflammatory effect associated with the VLCKD, as evidenced by greater
decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and
PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3
are commonly viewed as pro-inflammatory, but unexpectedly were
consistently inversely associated with responses in inflammatory
proteins. In summary, a very low carbohydrate diet resulted in
profound alterations in fatty acid composition and reduced
inflammation compared to a low fat diet. PMID: 18046594

- quote -

Would the following three foods be approx equivalent in term of AA?

100g (3.5 oz) of hazelnut
6 eggs yolks
1.44 kg (3.2 lb) of beef

based on data from nutritiondata.com
100 g hazelnut x 7.8g LA/100g x 0.06gAA/10g LA = 468mg of AA
75mg AA + 3.6mg AA from 601mg LA / large egg
30mg AA + 2.6mg AA from 440mg LA / 100g beef, chuck, arm roast

Taka wrote:
- quote -

Can you point me to more information on both these subjects -- AA in
muscle fibers and DHA in neurons?

Omega-3 supplements generally contribute small amounts of omega-3s
compared to fatty fish, don't they? Isn't it likely that humans
consumed much larger amounts of them in other times and places?

- quote -

Is it fair to say that most scientists consider the accumulation of
Mead acid in adipose tissue to indicate a pathological condition, but
Ray Peat disagrees, and that you are open-minded towards his position?

- quote -


--
Marshall Price of Miami
Known to Yahoo as d021317c

On May 20, 8:50 pm, Marshall Price <d0213...[at]yahoo.com> wrote:
- quote -

Muscle fibers are highly differentiated cells and AA may tend to
accumulate in them like DHA accumulates in the neurons. There is a
possibility that in small amounts the "EFAs" are truly essential for
the function of such differentiated tissues, they have been available
in human food all the time but nothing close to the amounts since the
introduction of the refined vegetable oils and Omega-3
supplements ... Undifferentiated cells and the connective tissues may
be better off with Mead acid.

- quote -

The problem is that you don't get large amounts of Mead acid
synthesized when you feed the experimental subjects Omega-6/3 fats.
And all people as well as experimental animals are ingesting large
amounts of these fatty acids even in the womb. The only thing which
can lead to measurable Mead acid accumulation is a fast growth or poor
blood supply so the conversion of ingested Omega-6 fats to AA doesn't
catchup with its incorporation in newly made cell membranes. Another
way to deplete AA is chronic inflammation when its needs for the
synthesis of the inflammatory mediators exceed its supply such as in
the active stage of celiac disease. Someone should really go to the
mountains and try measuring Mead acid and its metabolites in the wild
animals which are not fed vegetable oils or grains.

- quote -

Right, there is no need for "significant" amounts of dangerous
metabolites such as LTB4 especially in aging people.

- quote -

Ditto, that's only good, you don't need to supplement with 5-LOX
inhibitors such as AKBA then.

- quote -

I am disappointed too on how the scientific establishment cannot find
a way to validate the old flawed 1929/1940 EFAD experiments ...

Taka

Taka wrote:
- quote -

I was hoping you'd point me to your reasons for saying, "the Mead
acid eicosanoid family... seems to be complete [in that] it can supply
all the 'essential' functions of the AA metabolites...."

The Wikipedia article on Mead acid says that in "the physiological
literature, it is given the name 20:3(n-9)." It also gives the PubChem
identifier for it: 5312531 (
http://pubchem.ncbi.nlm.nih.gov/summ...gi?cid=5312531 ).

PubChem gives the following synonyms:

Mead acid
BSPBio_001412
E5888_SIGMA
5Z,8Z,11Z-eicosatrienoic acid
cis-5,8,11-Eicosatrienoic acid
ETrE(5Z, 8Z, 11Z)
LMFA01030381
IDI1_033882
NCGC00161346-01
NCGC00161346-02

.... and the IUPAC Name: (5Z,8Z,11Z)-icosa-5,8,11-trienoic acid.

At the first link you gave, the first abstract in Message 1 mentions
"n-9 eicosatrienoic acid (ETrA; 20:3n-9)." Is that Mead acid? Assuming
it is, the text seems to contradict your assertion (in the forum), "Mead
acid is the main component of membranes in young, growing and healthy
tissues." Instead, it says that in fetal human and sheep joint
cartilage, Mead acid content was higher than in mature subjects, and
that the same is true of muscle tissues in sheep, but *not* in humans.
To me, that implies the contrary: that Mead acid is less abundant in the
muscle tissue of human fetuses than in that of adults.

(The last sentence in that abstract is disappointingly ambiguous:
"ETrA appears to be a readily measurable component of some tissues at
certain stages of development when its presence in tissues does not
indicate EFA deficiency." That could mean (a) that it is such a
component only *if* it does not indicate a deficiency, or (b) that at
certain stages of development it *doesn't* indicate deficiency, and is
readily measurable. Do they know that a comma after "development" is
mandatory if they intend the latter?)

The second abstract discusses "n-9 eicosatrienoic (20:3 cis-delta
5,8,11) acid," which again I take to mean Mead acid. Rather than
indicating that it is "the main component," it says that "normal, young
cartilages, in distinction from all other tissues examined, have
unusually high levels of" Mead acid. So except for cartilage, young
tissues do not have high levels of Mead acid, and even in young
cartilage (although it is "unusually" abundant), that may still mean
that the concentration of it is very low compared to other fatty acids.
The quotation doesn't say.

The third abstract (appears to be irrelevant to the youth issue, but)
seems to contradict your assertion (in the newsgroup) that Mead acid is
an adequate substitute for arachidonic acid, since it says that "only
insignificant amounts of LTB3 were formed...." (I take it that Mead
acid lacks AA's "double bond at C-14".)

The fourth abstract also seems to contradict your assertion. In rats
fed EFA-deficient diets, Mead acid failed to establish normal levels of
leukotriene B4 ("a 87% reduction"), "even though the arachidonate
content was reduced by only 34%..., due to inhibition of leukotriene A
hydrolase by a lipoxygenase metabolite." Also, "little or no
leukotriene B3 was formed."

I realize that there are 71 more messages in that discussion
("Nutrition: Mead acid studies"), and I haven't even looked at "Mead
acid eicosanoids - the family is complete" (except to note that Monty
winds up saying, "a simple animal experiment could be done") but so far,
I'm disappointed.

Remember, I'm a novice, and dyslexic, and these are rather heavy
homework assignments! ;-)

--
Marshall Price of Miami
Known to Yahoo as d021317c

Taka wrote:
- quote -

Nope. All I've got is the third edition. Maybe the new fourth
edition mentions it.

--
Marshall Price of Miami
Known to Yahoo as d021317c

On May 17, 5:09 pm, Marshall Price <d0213...[at]yahoo.com> wrote:
- quote -

If that book says something about the Mead acid I would like to see
it, other is all well known agenda.

Taka