Science and Technology news... :: View topic - The New Generation of Physicians are Frauds!

Matti Narkia · Guest

ironjustice@aol.com wrote:

[quote]On Nov 27, 9:59 am, Matti Narkia <m...@mbnet.fi> wrote:But it is these
"other fatty acids" (mainly EPA and DHA) that ALA is being converted
to.

I don>t really think you have gotten the whole **GIST** of the
thread ..

The thread IS .. too much EPA causes a lack of ALA conversion ..

The thread is .. ALA ..

It seems what you seem to be saying is .. ALA is not that important ..

It probably isn>t. It>s main function is to serve as a precursor to EPA,[/quote]
which is a precursor of DPA, which is a precursor of DHA. If you
get enough EPA directly from food or supplements, there is no need
to convert ALA to EPA. That is not so hard to understand, is it?
ALA still possibly can have some other functions, which we are not
aware yet, but if you get enough EPA directly, ALA conversion is
not needed.

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

Matti Narkia · Guest

monty1945@lycos.com wrote:

[quote]It>s not about omega 3s, but about avoiding omega 6s. I avoid both,
and "cured" myself.
[/quote]
Really? I wouldn>t be so sure. How is your mental health?

[quote]No need to ingest highly oxidizable molecules.
The native Greenlanders did this and were lucky to live to reach their
40s.

You know very well that you cannot compare life expectancy of old days[/quote]
eskimos living very hazardous accindent prone life without proper
medical care with modern people living in safe environments and getting
the best medical care available. The right groups to compare with
are Japanese and Icelandic, who get more omega-3 PUFAs that others
and live longer than others.

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

RF · Guest

Has anyone seen this:

Preventing Cardiovascular Disease Naturally

By Julius Goepp, MD

In our war against heart disease,1 too many
Americans sadly continue to rely purely on risky
surgical treatments that can only be effective
after the fact—after years of neglect and even
abuse of their naturally resilient bodies.2-6 And
while our pharmacopoeia of drugs is indeed large
and powerful, it is only a small part of an
integrated solution to this global problem.7-9

The good news is that experts are now increasingly
recognizing the value of nutritional, dietary, and
lifestyle therapies for cardiovascular disease
prevention and management.1 In particular, an
apparently simple combination of nutrients (from a
berry and vegetable sprouts) has shown remarkable
clinical effectiveness in lowering dangerous
low-density lipoprotein (LDL) and triglycerides,
raising protective high-density lipoprotein (HDL),
reducing inflammation, and reversing visible
atherosclerotic changes in damaged blood vessels.
This unique formulation offers a broad-spectrum
nutritional approach to preventing and treating
arterial occlusion as we age.

http://www.lef.org/magazine/mag2008/nov2008_Preventing-Cardiovascular-Disease-Naturally_01.htm

Matti Narkia · Guest

ironjustice@aol.com wrote:

[quote]On Nov 27, 4:37 pm, Matti Narkia <m...@mbnet.fi> wrote:
It probably isn>t. It>s main function is to serve as a precursor to
EPA,
which is a precursor of DPA, which is a precursor of DHA. If you
get enough EPA directly from food or supplements, there is no need
to convert ALA to EPA. That is not so hard to understand, is it?
ALA still possibly can have some other functions, which we are not
aware yet, but if you get enough EPA directly, ALA conversion is
not needed.

This ALA conversion is what produces THE acetylcholine / choline which
you fail to mention ..

No, its' not. The ALA conversion you were talking about converts ALA[/quote]
to EPA through some intermediate steps. There is no choline involvement
in this particular conversion.
[quote]
Is it somehow hard to understand you CANNOT get your choline from fish
oil .. ?

As far as I know you don>t get it fom ALA either. But you get it from[/quote]
fish, among other things, see

Functions of Vitamin Choline - Food Sources and Deficiency Symptoms
<http://www.bodybuilding4u.com/vitamins/vitamin-choline.htm>

"The main sources of choline vitamin are as:-

It is mainly found in whole grains, liver, eggs, beans,
chicken, fish and vegetable foods."

Natural Mind and Memory Boosters - FamilyEducation.com
<http://life.familyeducation.com/mental-health/social-emotional/35987.html>

"Choline: The Building Block Of Memory

The key brain chemical for memory is acetylcholine. A deficiency
in this chemical is probably the single most common cause for
declining memory. Acetylcholine is derived from the nutrient
choline. Fish, especially sardines, are rich in it, hence the old
wives' tale of fish being good for the brain. Eggs are also a
major source of choline, followed by liver, soy beans, peanuts,
and other nuts. Ever since egg phobia set in, the average intake
of choline from the diet has dropped dramatically. From the point
of view of memory enhancement, it is certainly worth eating more
eggs. But just eating choline-rich foods won>t do it. You also
need vitamins B5 (pantothenic acid), B1, B12, and C to form
acetylcholine in your body."

Choline content of fish meals from various origins
Stuart M. Barlow, Ian H. Pike, Frederick Nixon
Journal of the Science of Food and Agriculture, 11 May 2006, Volume 30
Issue 1, Pages 89 - 92.
doi: 10.1002/jsfa.2740300114
<http://www3.interscience.wiley.com/journal/112611147/abstract>

"The choline content of 45 samples of fish meal from nine different
origins has been determined. The overall average was 4396 with a
standard error of a single sample of ± 995 mg kg-1. No significant
differences were found between meals of different origins,
different species of fish, or different processing conditions."

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

Jack Campin - bogus addre · Guest

[quote] Isn>t MSG a natural component of many foods, especially such
protein-rich ones as chicken?
Per wiki, Glutamate itself is a widespread amino acid. It is found
naturally in all living cells, primarily in the bound form as part of
proteins. Only a fraction of the glutamate in foods is in its "free"
form, and only free glutamate can enhance the flavor of foods...
For instance, wiki table shows that 100 grams of chicken has
3309 mg of bound glutamate and only 44mg of free glutamate.
[/quote]
Free glutamate is a product of protein hydrolysis, which can occur
with many cooking processes. Look up a food composition database
for the amount there is in pea soup, for example.

If that wiki page doesn>t distinguish raw chicken from its cooked
forms it isn>t worth bothering with.

==== j a c k at c a m p i n . m e . u k === <http://www.campin.me.uk> ====
Jack Campin, 11 Third St, Newtongrange EH22 4PU, Scotland == mob 07800 739 557
CD-ROMs and free stuff: Scottish music, food intolerance, and Mac logic fonts

Guest

Don>t know what you have against Taka, except that he seems to
contradict previous posts from time to time. At least he seems to be
trying to understand the literature, which of course often contradicts
itself (if one views it as a whole). The "bottom line" is that there
is no "chronic inflammation" if you have no or the tiniest trace
amounts of PUFAs in your diet, so all this talk of essentially
ingesting a "monster" to kill one is just ridiculous. And it is now
known that "chronic inflammation" is what causes just about all
"chronic diseases." This does not take a "genius" level intellect to
understand it.

Matti Narkia · Guest

vauxall wrote:
[quote]
http://en.wikipedia.org/wiki/Essential_fatty_acid_interactions#The_paradox_of_dietary_GLA

The paradox of dietary GLA
Dietary linoleic acid (LA, 18:2 Ï‰-6) is inflammatory. In the body, LA
is desaturated to form GLA (18:3 Ï‰-6), yet dietary GLA is anti-
inflammatory. Some observations partially explain this paradox: LA
competes with Î±-linolenic acid, (ALA, 18:3 Ï‰-3) for Î”6-desaturase, and
thereby eventually inhibits formation of anti-inflammatory EPA (20:5
Ï‰-3). In contrast, GLA does not compete for Î”6-desaturase. GLA>s
elongation product DGLA (20:3 Ï‰-6) competes with 20:4 Ï‰-3 for the Î”5-
desaturase, and it might be expected that this would make GLA
inflammatory, but it is not, perhaps because this step isn>t rate-
determining. Î”6-desaturase does appear to be the rate-limiting step;
20:4 Ï‰-3 does not significantly accumulate in bodily lipids.

DGLA inhibits inflammation through both competitive inhibition and
direct counteraction (see above.) Dietary GLA leads to sharply
increased DGLA in the white blood cells' membranes, where LA does not.
This may reflect white blood cells' lack of desaturase.Supplementing
dietary GLA increases serum DGLA without increasing serum AA.

It is likely that some dietary GLA eventually forms AA and contributes
to inflammation. Animal studies indicate the effect is small. The
empirical observation of GLA>s actual effects argues that DGLA>s anti-
inflammatory effects dominate.

Thanks vauxall![/quote]

GLA is elongated to DGLA. DGLA>s three direct metabolitess
are prostaglandin PGE1 via the cyclooxygenase pathway, 15-HETrE
via the 15-lipoxygenase pathway, and arachidonic acid (AA) via
the delta 5 desaturase pathway. Of these conversions, the conversion
to the AA is the most inefficent, delta 5 desaturase is rate-limiting.
The AA pathway can be further blocked by taking EPA or fish oil
including EPA with GLA, because EPA inhibits delta 5 desaturase. The
metabolite PGE1 is anti-inflammatory and therefore adds to the
anti-inflammatory effect of GLA. The metabolite 15-HETrE inihibits
5-LOX nand therefore helps in ihibiting the production of series 4
leukotrienes including LTB4 from AA, Thus also the matabolite 15-HETrE
adds to the anti-inflammatory effect of GLA.

IMHO a good article about GLA is the review article

Fan YY, Chapkin RS.
Importance of dietary gamma-linolenic acid in human health and nutrition.
J Nutr. 1998 Sep;128(9):1411-4. Review.
PMID: 9732298
<http://jn.nutrition.org/cgi/content/full/128/9/1411>

Abstract:

"Considerable debate remains regarding the distinct biological
activities of individual polyunsaturated fatty acids (PUFA).
One of the most interesting yet controversial dietary
approaches has been the possible prophylactic role of dietary
gamma-linolenic acid (GLA) in treating various chronic disease
states. This strategy is based on the ability of diet to modify
cellular lipid composition and eicosanoid (cyclooxygenase and
lipoxygenase) biosynthesis. Recent studies demonstrate that
dietary GLA increases the content of its elongase product,
dihomo-gamma-linolenic acid (DGLA), within cell membranes
without concomitant changes in arachidonic acid (AA).
Subsequently, upon stimulation, DGLA can be converted by
inflammatory cells to 15-(S)-hydroxy-8,11,13-eicosatrienoic
acid and prostaglandin E1. This is noteworthy because these
compounds possess both anti-inflammatory and antiproliferative
properties. Although an optimal feeding regimen to maximize the
potential benefits of dietary GLA has not yet been determined,
it is the purpose of this review to summarize the most recent
research that has focused on objectively and reproducibly
determining the mechanism(s) by which GLA may ameliorate health
problems."

The Figure 1 in this article is very enlightening:

Figure 1. Metabolism of gamma-linolenic acid.
<http://jn.nutrition.org/cgi/content/full/128/9/1411/F1>
<http://jn.nutrition.org/content/vol128/issue9/images/large/jn.5222f1.jpeg>

Here the explanatonary text attached to the Figure 1:

"In many animal tissues and cells, LA is converted to AA by an
alternating sequence of delta 6 desaturation, chain elongation
and delta 5 desaturation, in which hydrogen atoms are
selectively removed to create new double bonds and then two
carbon atoms are added to lengthen the fatty acid chain.
Dietary GLA bypasses the rate-limited delta 6 desaturation
step and is quickly elongated to DGLA by elongase, with only a
very limited amount being desaturated to AA by delta 5
desaturase. DGLA can be converted to PGE1 via the
cyclooxygenase pathway and/or converted to 15-HETrE via the 15-
lipoxygenase pathway. 15-HETrE is capable of inhibiting the
formation of AA-derived 5-lipoxygenase (proinflammatory)
metabolites."

Other excerpts form this article:

"The increase in DGLA relative to AA is capable of attenuating
the biosynthesis of AA metabolites, i.e., 2-series
prostaglandins, 4-series leukotrienes and platelet-activating
factor (PAF), and exerts an anti-inflammatory effect in human
subjects (Johnson et al. 1997). In addition, because GLA
bypasses a key regulatory rate-limiting enzymatic step (6
desaturase) that controls the formation of long-chain PUFA of
the (n-6) series, it may serve to alleviate a systemic decline
in 6 desaturation. Such a reduced capacity to convert LA to GLA
has been associated with various physiologic/pathophysiologic
states, including aging, diabetes, alcoholism, atopic
dermatitis, premenstrual syndrome, rheumatoid arthritis, cancer
and cardiovascular disease (Bolton-Smith et al. 1997, Horrobin
1990, Leventhal et al. 1993). Therefore, supplementation of GLA
may be of value in alleviating some of the symptoms of these
various diseases (discussed below)."

[...]

A growing number of studies suggest that GLA is unique among
the (n-6) PUFA family members (LA, GLA and AA) in its potential
to suppress tumor growth and metastasis. GLA has the ability to
inhibit both motility and invasiveness of human colon cancer
cells by increasing the expression of E-cadherin, a cell-to-
cell adhesion molecule that acts as a suppressor of metastasis (
Jiang et al. 1995). In addition, GLA reduces tumor-endothelium
adhesion, a key factor in the establishment of distant
metastases, partly by improving gap junction communication
within the endothelium (Jiang et al 1997). These observations
have been corroborated by Kokura et al (1997) who demonstrated
that dietary GLA is effective in suppressing tumor growth in
vivo. Whether oxidative metabolites of GLA are involved remains
to be determined. These encouraging results indicate that
further investigations should be given priority.

Because complications of diabetic neuropathy may be related to
abnormal delta 6 desaturase activity and therefore membrane
function ( Horrobin 1990), the effect of GLA on neurovascular
deficits in experimental diabetes has been investigated.
Triacylglycerols containing GLA have been shown to normalize
nerve conduction velocity and sciatic endoneurial blood flow (
Dines et al. 1995). Although the mechanism of action has not
been elucidated, GLA may correct nerve conduction abnormalities
by enhancing the synthesis of the cyclooxygenase-derived
vasodilator prostanoid, PGE1, which is capable of increasing
vasa nervorum perfusion ( Cameron and Cotter 1996).
Interestingly, the combination of GLA and ascorbate could have
therapeutic advantage over GLA alone in correcting
neurovascular deficits in diabetic rats (Cameron and Cotter
1996). It is possible that ascorbate may act by suppressing
tissue oxidative damage associated with diabetes mellitus.
Therefore, ascorbyl GLA may be a suitable candidate for
clinical trials of diabetic neuropathy.

In summary, manipulation of dietary PUFA intake may have
biological significance because many disease states are
associated with an overproduction of eicosanoids derived from
AA. Somewhat paradoxically, intracellular AA pools in humans
and rodent species do not appear to be influenced by dietary
GLA (Johnson et al. 1997, Zurier et al. 1996). Nevertheless,
GLA alimentation reduces AA-derived LTB4, LTC4 and PAF
synthesis, while increasing DGLA, PGE1 and 15-HETrE synthesis (
DeLuca et al. 1995, Johnson et al. 1997, Miller et al. 1991,
Zurier et al. 1996). The data reported in the past few years
have confirmed that although the average intake of GLA in the
diet is more than 100 times lower than that of LA, its
consumption may have physiologic relevance. Therefore, even
though North Americans consume on average more than 10 times
the amount of (n-6) PUFA required to meet minimal essential
fatty acid requirements ( Okuyama et al. 1997), the consumption
of GLA may offer new strategies for treatment and prevention of
certain chronic diseases. Potential candidates, e.g.,
rheumatoid arthritis patients, will have to take GLA
supplements in order to mimic clinical dosages, because GLA is
not readily found in common foods."

An article showing that taking EPA with GLA prevents the accumulation
of AA in serum:

Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented
diets prevents serum arachidonic acid accumulation in humans.
Barham JB, Edens MB, Fonteh AN, Johnson MM, Easter L, Chilton FH.
J Nutr. 2000 Aug;130(8):1925-31.
PMID: 10917903
<http://jn.nutrition.org/cgi/content/full/130/8/1925>

Abstract:

"Previous studies reveal that supplementation of human diets
with gamma-linolenic acid (GLA) reduces the generation of lipid
mediators of inflammation and attenuates clinical symptoms of
chronic inflammatory disorders such as rheumatoid arthritis.
However, we have shown that supplementation with this same
fatty acid also causes a marked increase in serum arachidonate (
AA) levels, a potentially harmful side effect. The objective of
this study was to design a supplementation strategy that
maintained the capacity of GLA to reduce lipid mediators
without causing elevations in serum AA levels. Initial in vitro
studies utilizing HEP-G2 liver cells revealed that addition of
eicosapentaenoic acid (EPA) blocked Delta-5-desaturase activity,
the terminal enzymatic step in AA synthesis. To test the in
vivo effects of a GLA and EPA combination in humans, adult
volunteers consuming controlled diets supplemented these diets
with 3.0 g/d of GLA and EPA. This supplementation strategy
significantly increased serum levels of EPA, but did not
increase AA levels. EPA and the elongation product of GLA,
dihomo-gamma-linolenic acid (DGLA) levels in neutrophil
glycerolipids increased significantly during the 3-wk
supplementation period. Neutrophils isolated from volunteers
fed diets supplemented with GLA and EPA released similar
quantities of AA, but synthesized significantly lower
quantities of leukotrienes compared with their neutrophils
before supplementation. This study revealed that a GLA and EPA
supplement combination may be utilized to reduce the synthesis
of proinflammatory AA metabolites, and importantly, not induce
potentially harmful increases in serum AA levels."

Figure 5. Effects of gamma-linolenic acid (GLA) and eicospentaenoic acid
(EPA) supplementation on the biosynthesis of leukotriene B4 (LTB4),
20-hydroxy (20-OH)-LTB4 and 6-trans-isomers-LTB4 by A23187-stimulated
neutrophils. Neutrophils, isolated before (wk 0) and 3 wk after
supplementation were stimulated with 1 Âµmol/L A23187. The lines
represent the percentage of control values for each subject that
participated in study and (â€¢) represents the mean Â± SEM, n = 10.
*Significantly different from wk 0, P < 0.05. Abbreviation, PMN,
polymorphonuclear leukocytes.
<http://jn.nutrition.org/cgi/content/full/130/8/1925/F5>
<http://jn.nutrition.org/content/vol130/issue8/images/large/4w0801027005.jpeg>

Figure 6. Effects of gamma-linolenic acid (GLA) and eicospentaenoic acid
(EPA) supplementation on the biosynthesis of leukotriene B5 (LTB5) by
A23187-stimulated neutrophils. Neutrophils were isolated before
supplementation (wk 0) and after 3 wk. After supplementation neutrophils
were stimulated with 1 Âµmol/L A23187. Values are means Â± SEM, n = 12.
*Significantly different from wk 0, P < 0.05. Abbreviation: PMN,
polymorphonuclear leukocytes.
http://jn.nutrition.org/cgi/content/full/130/8/1925/F6
<http://jn.nutrition.org/content/vol130/issue8/images/large/4w0801027006.jpeg>

Figure 7. Mechanism of inhibition of delta-5-desaturase by dietary
eicospentaenoic acid (EPA). Abbreviations: GLA, gamma-linolenic acid;
DGLA, dihomo--linolenic acid; AA, arachidonic acid.
<http://jn.nutrition.org/cgi/content/full/130/8/1925/F7>
<http://jn.nutrition.org/content/vol130/issue8/images/large/4w0801027007.jpeg>

Excerpt from the Discussion chapter:

"Studies by several investigators have demonstrated that
dietary supplementation with GLA has the potential to reduce
inflammation. This reduction in inflammation has been
attributed to the capacity of the elongation product of GLA,
DGLA, to block the synthesis of AA products and the capacity of
DGLA to be converted to oxidized products that have anti-
inflammatory activities (Billah et al. 1985 , Chilton-Lopez et
al. 1996 , DeLuca et al. 1999 , Iversen et al. 1991 and 1992 ,
Vanderhoek et al. 1980 ). Our previous studies (Chilton et al.
1993, Chilton-Lopez et al. 1996 , Johnson et al.1996) and those
of Ziboh and Fletcher (1992) have demonstrated that
supplementation of low-to-moderate fat diets with GLA markedly
decreases the capacity of inflammatory cells such as human
neutrophils to produce leukotrienes (Johnson et al.1997 ). We
further demonstrated that the likely mechanism of inhibition by
GLA stems from its capacity to be elongated by an endogenous
elongase activity within the neutrophil to a close structural
analog of AA, DGLA (Fig. 7 ). However, neutrophils cannot
further desaturate DGLA to AA because they lack -5-desaturase
activity (Chilton-Lopez et al.1996 ). Thus, the endogenous
elongase activity within inflammatory cells can be utilized to
synthesize close structural analogs of AA (i.e., DGLA) from
appropriate dietary precursors. It is postulated that these
analogs affect AA metabolism, thereby mitigating clinical
manifestations induced by AA metabolites.

A potentially important side effect of GLA supplementation is
elongation of GLA to DGLA and further desaturation via -5-
desaturase to AA by enzymes in the liver. This causes a marked
increase in serum AA levels. In a previous study of AA
supplementation in humans, similar increases in serum AA levels
were associated with an increase in the in vivo aggregation of
platelets (Seyberth et al.1975 ). This increase in platelet
sensitivity raised concerns about potentially harmful
cardiovascular side effects and the long-term safety of any
dietary strategy that increases serum AA levels, including
those current formulations being sold in nutraceutical markets.

The current study was designed to determine whether dietary
strategies could be designed that have the anti-inflammatory
potential of GLA without leading to increases in serum AA. This
was accomplished by the addition of the delta-5-desaturase
product of the (n-3) pathway, EPA. Initial in vitro experiments
demonstrated that EPA had the capacity to block delta-5-desaturase
activity in an isolated hepatocarcinoma cell line. These
experiments were followed by in vivo studies that showed EPA
supplementation of human diets prevented the accumulation of
serum AA in response to GLA without inhibiting accumulation of
DGLA in neutrophils. Thus, both in vivo and in vitro studies
revealed that EPA may act as an end product inhibitor of the
delta-5-desaturase.

We further examined the influence of the GLA + EPA combination
on leukotriene generation. The capacity of human neutrophils to
release AA was not influenced by the GLA + EPA supplementation.
In contrast, their capacity to generate leukotrienes (LTB4, 20-
OH-LTB4 and related isomers) was inhibited significantly (~40%)
compared with neutrophils from these same volunteers before
supplementation. The inhibition observed in this study was
greater than what has been observed before for EPA alone (
Chilton et al.1993 ). In contrast, the inhibition with EPA/GLA
was somewhat less than that seen in a previous study in our
laboratory with GLA alone (Johnson et al. 1997). However, the
differences in leukotriene generation in these studies were not
powered sufficiently to detect statistically significant
differences and may be a function of biologic variability among
the volunteers.

Clinicians, patients, pharmaceutical and nutraceutical
companies are all increasingly utilizing natural products for
the treatment of clinical disorders. As this trend continues,
it is important that these products be both safe and effective.
Overall, little attention has been paid to the potentially
adverse effects of dietary supplements and specifically,
dietary fatty acid supplementation strategies. This study shows
how a potentially important complication, arising from
supplementation with a simple fatty acid, can be avoided by
using appropriate fatty acid combinations. As the nutraceutical
industry continues to experience explosive growth, it will be
increasingly important to understand the safety profiles of
dietary supplements and avoid complications that arise from
such supplements."

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

Taka · Guest

On Nov 30, 3:01 am, Matti Narkia <m...@mbnet.fi> wrote:
[quote]vauxall wrote:

http://en.wikipedia.org/wiki/Essential_fatty_acid_interactions#The_pa...

The paradox of dietary GLA
Dietary linoleic acid (LA, 18:2 ù-6) is inflammatory. In the body, LA
is desaturated to form GLA (18:3 ù-6), yet dietary GLA is anti-
inflammatory. Some observations partially explain this paradox: LA
competes with á-linolenic acid, (ALA, 18:3 ù-3) for Ä6-desaturase, and
thereby eventually inhibits formation of anti-inflammatory EPA (20:5
ù-3). In contrast, GLA does not compete for Ä6-desaturase. GLA>s
elongation product DGLA (20:3 ù-6) competes with 20:4 ù-3 for the Ä5-
desaturase, and it might be expected that this would make GLA
inflammatory, but it is not, perhaps because this step isn>t rate-
determining. Ä6-desaturase does appear to be the rate-limiting step;
20:4 ù-3 does not significantly accumulate in bodily lipids.

DGLA inhibits inflammation through both competitive inhibition and
direct counteraction (see above.) Dietary GLA leads to sharply
increased DGLA in the white blood cells' membranes, where LA does not.
This may reflect white blood cells' lack of desaturase.Supplementing
dietary GLA increases serum DGLA without increasing serum AA.

It is likely that some dietary GLA eventually forms AA and contributes
to inflammation. Animal studies indicate the effect is small. The
empirical observation of GLA>s actual effects argues that DGLA>s anti-
inflammatory effects dominate.

Thanks vauxall!

GLA is elongated to DGLA. DGLA>s three direct metabolitess
are prostaglandin PGE1 via the cyclooxygenase pathway, 15-HETrE
via the 15-lipoxygenase pathway, and arachidonic acid (AA) via
the delta 5 desaturase pathway. Of these conversions, the conversion
to the AA is the most inefficent, delta 5 desaturase is rate-limiting.
The AA pathway can be further blocked by taking EPA or fish oil
including EPA with GLA, because EPA inhibits delta 5 desaturase. The
metabolite PGE1 is anti-inflammatory and therefore adds to the
anti-inflammatory effect of GLA. The metabolite 15-HETrE inihibits
5-LOX nand therefore helps in ihibiting the production of series 4
leukotrienes including LTB4 from AA, Thus also the matabolite 15-HETrE
adds to the anti-inflammatory effect of GLA.

IMHO a good article about GLA is the review article

Fan YY, Chapkin RS.
Importance of dietary gamma-linolenic acid in human health and nutrition.
J Nutr. 1998 Sep;128(9):1411-4. Review.
PMID: 9732298
http://jn.nutrition.org/cgi/content/full/128/9/1411

Abstract:

"Considerable debate remains regarding the distinct biological
activities of individual polyunsaturated fatty acids (PUFA).
One of the most interesting yet controversial dietary
approaches has been the possible prophylactic role of dietary
gamma-linolenic acid (GLA) in treating various chronic disease
states. This strategy is based on the ability of diet to modify
cellular lipid composition and eicosanoid (cyclooxygenase and
lipoxygenase) biosynthesis. Recent studies demonstrate that
dietary GLA increases the content of its elongase product,
dihomo-gamma-linolenic acid (DGLA), within cell membranes
without concomitant changes in arachidonic acid (AA).
Subsequently, upon stimulation, DGLA can be converted by
inflammatory cells to 15-(S)-hydroxy-8,11,13-eicosatrienoic
acid and prostaglandin E1. This is noteworthy because these
compounds possess both anti-inflammatory and antiproliferative
properties. Although an optimal feeding regimen to maximize the
potential benefits of dietary GLA has not yet been determined,
it is the purpose of this review to summarize the most recent
research that has focused on objectively and reproducibly
determining the mechanism(s) by which GLA may ameliorate health
problems."

The Figure 1 in this article is very enlightening:

Figure 1. Metabolism of gamma-linolenic acid.
http://jn.nutrition.org/cgi/content/full/128/9/1411/F1
http://jn.nutrition.org/content/vol128/issue9/images/large/jn.5222f1....

Here the explanatonary text attached to the Figure 1:

"In many animal tissues and cells, LA is converted to AA by an
alternating sequence of delta 6 desaturation, chain elongation
and delta 5 desaturation, in which hydrogen atoms are
selectively removed to create new double bonds and then two
carbon atoms are added to lengthen the fatty acid chain.
Dietary GLA bypasses the rate-limited delta 6 desaturation
step and is quickly elongated to DGLA by elongase, with only a
very limited amount being desaturated to AA by delta 5
desaturase. DGLA can be converted to PGE1 via the
cyclooxygenase pathway and/or converted to 15-HETrE via the 15-
lipoxygenase pathway. 15-HETrE is capable of inhibiting the
formation of AA-derived 5-lipoxygenase (proinflammatory)
metabolites."

Other excerpts form this article:

"The increase in DGLA relative to AA is capable of attenuating
the biosynthesis of AA metabolites, i.e., 2-series
prostaglandins, 4-series leukotrienes and platelet-activating
factor (PAF), and exerts an anti-inflammatory effect in human
subjects (Johnson et al. 1997). In addition, because GLA
bypasses a key regulatory rate-limiting enzymatic step (6
desaturase) that controls the formation of long-chain PUFA of
the (n-6) series, it may serve to alleviate a systemic decline
in 6 desaturation. Such a reduced capacity to convert LA to GLA
has been associated with various physiologic/pathophysiologic
states, including aging, diabetes, alcoholism, atopic
dermatitis, premenstrual syndrome, rheumatoid arthritis, cancer
and cardiovascular disease (Bolton-Smith et al. 1997, Horrobin
1990, Leventhal et al. 1993). Therefore, supplementation of GLA
may be of value in alleviating some of the symptoms of these
various diseases (discussed below)."

[...]

A growing number of studies suggest that GLA is unique among
the (n-6) PUFA family members (LA, GLA and AA) in its potential
to suppress tumor growth and metastasis. GLA has the ability to
inhibit both motility and invasiveness of human colon cancer
cells by increasing the expression of E-cadherin, a cell-to-
cell adhesion molecule that acts as a suppressor of metastasis (
Jiang et al. 1995). In addition, GLA reduces tumor-endothelium
adhesion, a key factor in the establishment of distant
metastases, partly by improving gap junction communication
within the endothelium (Jiang et al 1997). These observations
have been corroborated by Kokura et al (1997) who demonstrated
that dietary GLA is effective in suppressing tumor growth in
vivo. Whether oxidative metabolites of GLA are involved remains
to be determined. These encouraging results indicate that
further investigations should be given priority.

Because complications of diabetic neuropathy may be related to
abnormal delta 6 desaturase activity and therefore membrane
function ( Horrobin 1990), the effect of GLA on neurovascular
deficits in experimental diabetes has been investigated.
Triacylglycerols containing GLA have been shown to normalize
nerve conduction velocity and sciatic endoneurial blood flow (
Dines et al. 1995). Although the mechanism of action has not
been elucidated, GLA may correct nerve conduction abnormalities
by enhancing the synthesis of the cyclooxygenase-derived
vasodilator prostanoid, PGE1, which is capable of increasing
vasa nervorum perfusion ( Cameron and Cotter 1996).
Interestingly, the combination of GLA and ascorbate could have
therapeutic advantage over GLA alone in correcting
neurovascular deficits in diabetic rats (Cameron and Cotter
1996). It is possible that ascorbate may act by suppressing
tissue oxidative damage associated with diabetes mellitus.
Therefore, ascorbyl GLA may be a suitable candidate for
clinical trials of diabetic neuropathy.

In summary, manipulation of dietary PUFA intake may have
biological significance because many disease states are
associated with an overproduction of eicosanoids derived from
AA. Somewhat paradoxically, intracellular AA pools in humans
and rodent species do not appear to be influenced by dietary
GLA (Johnson et al. 1997, Zurier et al. 1996). Nevertheless,
GLA alimentation reduces AA-derived LTB4, LTC4 and PAF
synthesis, while increasing DGLA, PGE1 and 15-HETrE synthesis (
DeLuca et al. 1995, Johnson et al. 1997, Miller et al. 1991,
Zurier et al. 1996). The data reported in the past few years
have confirmed that although the average intake of GLA in the
diet is more than 100 times lower than that of LA, its
consumption may have physiologic relevance. Therefore, even
though North Americans consume on average more than 10 times
the amount of (n-6) PUFA required to meet minimal essential
fatty acid requirements ( Okuyama et al. 1997), the consumption
of GLA may offer new strategies for treatment and prevention of
certain chronic diseases. Potential candidates, e.g.,
rheumatoid arthritis patients, will have to take GLA
supplements in order to mimic clinical dosages, because GLA is
not readily found in common foods."

An article showing that taking EPA with GLA prevents the accumulation
of AA in serum:

Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented
diets prevents serum arachidonic acid accumulation in humans.
Barham JB, Edens MB, Fonteh AN, Johnson MM, Easter L, Chilton FH.
J Nutr. 2000 Aug;130(8):1925-31.
PMID: 10917903
http://jn.nutrition.org/cgi/content/full/130/8/1925

Abstract:

"Previous studies reveal that supplementation of human diets
with gamma-linolenic
...

read more »
[/quote]
I appreciate the mechanistic studies you are posting lately Matti but
don>t forget that GLA can make you sterile, at least if you were a
worm:

Dev Biol. 2006 Apr 15;292(2):381-92. Epub 2006 Feb 17.

Dietary manipulation implicates lipid signaling in the regulation of
germ cell maintenance in C. elegans.

Watts JL, Browse J.
Institute of Biological Chemistry, Washington State University,
Pullman, WA 99614-6340, USA.

Reproduction in C. elegans relies on continuously proliferating germ
cells which, during germline development, exit mitosis, undergo
meiosis and differentiate into gametes. Supplementing the diet of C.
elegans with dihommogamma-linolenic acid (20:3n-6, DGLA), a long chain
omega-6 polyunsaturated fatty acid, results in sterile worms that lack
germ cells. The effect is remarkably specific for DGLA, as
eicosapentaenoic acid (20:5n-3, EPA) and other long-chain
polyunsaturated fatty acids with similar physical properties have
little or no effect on fertility. Germ cells undergoing mitosis during
larval stages are especially sensitive to DGLA, but exposure to DGLA
during adulthood also reduces germ cells and brood size, in part by
inducing inappropriate apoptosis of meiotic germ cells. Mutant strains
with defects in fatty acid desaturation and elongation display altered
susceptibility to DGLA, indicating that the sterility effect of the
dietary lipid depends on the amount of DGLA present in membranes as
well as on the capacity to convert DGLA to other fatty acids. We
propose that DGLA produces a signal that interacts with one or more
pathways regulating germ cell survival. Our DGLA findings are the
first report of a role for a specific fatty acid affecting the
development and maintenance of germ cells in C. elegans.
PMID: 16487504

Taka · Guest

On Nov 30, 12:36 pm, Matti Narkia <m...@mbnet.fi> wrote:
[quote]Yet another animal study. Why are you afraid of human studies?
Don>t their results please you, so you have to cherry-pick some
weird animal studies, which better fit in with your opinions?
[/quote]
Better cherry picking than "research" garbage collecting as you do
Matti. You know well that real properly controlled human experiments
cannot be conducted for ethical reasons. Thus all the review/
statistical/meta-analysis/evolutionary speculation you are presenting
here is crap mostly based on dubious questionnaires.

The only real human experiments which can be conducted are those on
ourselves and this is exactly what Monty and I have been doing. How
would you explain that I am no longer catching any cold after 1 year
restriction of dietary PUFAs? And why all my colleagues consuming
vegetable oils on daily basis always catch cold after eating grilled
fatty fish? If the placebo effect were
so strong we should start building churches instead of hospitals ...

Sorry, no more time wasting on you.
Taka

Matti Narkia · Guest

Taka wrote:

[quote]On Nov 30, 3:01 am, Matti Narkia <m...@mbnet.fi> wrote:
vauxall wrote:

http://en.wikipedia.org/wiki/Essential_fatty_acid_interactions#The_pa...
The paradox of dietary GLA
Dietary linoleic acid (LA, 18:2 ù-6) is inflammatory. In the body, LA
is desaturated to form GLA (18:3 ù-6), yet dietary GLA is anti-
inflammatory. Some observations partially explain this paradox: LA
competes with á-linolenic acid, (ALA, 18:3 ù-3) for Ä6-desaturase, and
thereby eventually inhibits formation of anti-inflammatory EPA (20:5
ù-3). In contrast, GLA does not compete for Ä6-desaturase. GLA>s
elongation product DGLA (20:3 ù-6) competes with 20:4 ù-3 for the Ä5-
desaturase, and it might be expected that this would make GLA
inflammatory, but it is not, perhaps because this step isn>t rate-
determining. Ä6-desaturase does appear to be the rate-limiting step;
20:4 ù-3 does not significantly accumulate in bodily lipids.
DGLA inhibits inflammation through both competitive inhibition and
direct counteraction (see above.) Dietary GLA leads to sharply
increased DGLA in the white blood cells' membranes, where LA does not.
This may reflect white blood cells' lack of desaturase.Supplementing
dietary GLA increases serum DGLA without increasing serum AA.
It is likely that some dietary GLA eventually forms AA and contributes
to inflammation. Animal studies indicate the effect is small. The
empirical observation of GLA>s actual effects argues that DGLA>s anti-
inflammatory effects dominate.
Thanks vauxall!

GLA is elongated to DGLA. DGLA>s three direct metabolitess
are prostaglandin PGE1 via the cyclooxygenase pathway, 15-HETrE
via the 15-lipoxygenase pathway, and arachidonic acid (AA) via
the delta 5 desaturase pathway. Of these conversions, the conversion
to the AA is the most inefficent, delta 5 desaturase is rate-limiting.
The AA pathway can be further blocked by taking EPA or fish oil
including EPA with GLA, because EPA inhibits delta 5 desaturase. The
metabolite PGE1 is anti-inflammatory and therefore adds to the
anti-inflammatory effect of GLA. The metabolite 15-HETrE inihibits
5-LOX nand therefore helps in ihibiting the production of series 4
leukotrienes including LTB4 from AA, Thus also the matabolite 15-HETrE
adds to the anti-inflammatory effect of GLA.

IMHO a good article about GLA is the review article

Fan YY, Chapkin RS.
Importance of dietary gamma-linolenic acid in human health and nutrition.
J Nutr. 1998 Sep;128(9):1411-4. Review.
PMID: 9732298
http://jn.nutrition.org/cgi/content/full/128/9/1411

Abstract:

"Considerable debate remains regarding the distinct biological
activities of individual polyunsaturated fatty acids (PUFA).
One of the most interesting yet controversial dietary
approaches has been the possible prophylactic role of dietary
gamma-linolenic acid (GLA) in treating various chronic disease
states. This strategy is based on the ability of diet to modify
cellular lipid composition and eicosanoid (cyclooxygenase and
lipoxygenase) biosynthesis. Recent studies demonstrate that
dietary GLA increases the content of its elongase product,
dihomo-gamma-linolenic acid (DGLA), within cell membranes
without concomitant changes in arachidonic acid (AA).
Subsequently, upon stimulation, DGLA can be converted by
inflammatory cells to 15-(S)-hydroxy-8,11,13-eicosatrienoic
acid and prostaglandin E1. This is noteworthy because these
compounds possess both anti-inflammatory and antiproliferative
properties. Although an optimal feeding regimen to maximize the
potential benefits of dietary GLA has not yet been determined,
it is the purpose of this review to summarize the most recent
research that has focused on objectively and reproducibly
determining the mechanism(s) by which GLA may ameliorate health
problems."

The Figure 1 in this article is very enlightening:

Figure 1. Metabolism of gamma-linolenic acid.
http://jn.nutrition.org/cgi/content/full/128/9/1411/F1
http://jn.nutrition.org/content/vol128/issue9/images/large/jn.5222f1....

Here the explanatonary text attached to the Figure 1:

"In many animal tissues and cells, LA is converted to AA by an
alternating sequence of delta 6 desaturation, chain elongation
and delta 5 desaturation, in which hydrogen atoms are
selectively removed to create new double bonds and then two
carbon atoms are added to lengthen the fatty acid chain.
Dietary GLA bypasses the rate-limited delta 6 desaturation
step and is quickly elongated to DGLA by elongase, with only a
very limited amount being desaturated to AA by delta 5
desaturase. DGLA can be converted to PGE1 via the
cyclooxygenase pathway and/or converted to 15-HETrE via the 15-
lipoxygenase pathway. 15-HETrE is capable of inhibiting the
formation of AA-derived 5-lipoxygenase (proinflammatory)
metabolites."

Other excerpts form this article:

"The increase in DGLA relative to AA is capable of attenuating
the biosynthesis of AA metabolites, i.e., 2-series
prostaglandins, 4-series leukotrienes and platelet-activating
factor (PAF), and exerts an anti-inflammatory effect in human
subjects (Johnson et al. 1997). In addition, because GLA
bypasses a key regulatory rate-limiting enzymatic step (6
desaturase) that controls the formation of long-chain PUFA of
the (n-6) series, it may serve to alleviate a systemic decline
in 6 desaturation. Such a reduced capacity to convert LA to GLA
has been associated with various physiologic/pathophysiologic
states, including aging, diabetes, alcoholism, atopic
dermatitis, premenstrual syndrome, rheumatoid arthritis, cancer
and cardiovascular disease (Bolton-Smith et al. 1997, Horrobin
1990, Leventhal et al. 1993). Therefore, supplementation of GLA
may be of value in alleviating some of the symptoms of these
various diseases (discussed below)."

[...]

A growing number of studies suggest that GLA is unique among
the (n-6) PUFA family members (LA, GLA and AA) in its potential
to suppress tumor growth and metastasis. GLA has the ability to
inhibit both motility and invasiveness of human colon cancer
cells by increasing the expression of E-cadherin, a cell-to-
cell adhesion molecule that acts as a suppressor of metastasis (
Jiang et al. 1995). In addition, GLA reduces tumor-endothelium
adhesion, a key factor in the establishment of distant
metastases, partly by improving gap junction communication
within the endothelium (Jiang et al 1997). These observations
have been corroborated by Kokura et al (1997) who demonstrated
that dietary GLA is effective in suppressing tumor growth in
vivo. Whether oxidative metabolites of GLA are involved remains
to be determined. These encouraging results indicate that
further investigations should be given priority.

Because complications of diabetic neuropathy may be related to
abnormal delta 6 desaturase activity and therefore membrane
function ( Horrobin 1990), the effect of GLA on neurovascular
deficits in experimental diabetes has been investigated.
Triacylglycerols containing GLA have been shown to normalize
nerve conduction velocity and sciatic endoneurial blood flow (
Dines et al. 1995). Although the mechanism of action has not
been elucidated, GLA may correct nerve conduction abnormalities
by enhancing the synthesis of the cyclooxygenase-derived
vasodilator prostanoid, PGE1, which is capable of increasing
vasa nervorum perfusion ( Cameron and Cotter 1996).
Interestingly, the combination of GLA and ascorbate could have
therapeutic advantage over GLA alone in correcting
neurovascular deficits in diabetic rats (Cameron and Cotter
1996). It is possible that ascorbate may act by suppressing
tissue oxidative damage associated with diabetes mellitus.
Therefore, ascorbyl GLA may be a suitable candidate for
clinical trials of diabetic neuropathy.

In summary, manipulation of dietary PUFA intake may have
biological significance because many disease states are
associated with an overproduction of eicosanoids derived from
AA. Somewhat paradoxically, intracellular AA pools in humans
and rodent species do not appear to be influenced by dietary
GLA (Johnson et al. 1997, Zurier et al. 1996). Nevertheless,
GLA alimentation reduces AA-derived LTB4, LTC4 and PAF
synthesis, while increasing DGLA, PGE1 and 15-HETrE synthesis (
DeLuca et al. 1995, Johnson et al. 1997, Miller et al. 1991,
Zurier et al. 1996). The data reported in the past few years
have confirmed that although the average intake of GLA in the
diet is more than 100 times lower than that of LA, its
consumption may have physiologic relevance. Therefore, even
though North Americans consume on average more than 10 times
the amount of (n-6) PUFA required to meet minimal essential
fatty acid requirements ( Okuyama et al. 1997), the consumption
of GLA may offer new strategies for treatment and prevention of
certain chronic diseases. Potential candidates, e.g.,
rheumatoid arthritis patients, will have to take GLA
supplements in order to mimic clinical dosages, because GLA is
not readily found in common foods."

An article showing that taking EPA with GLA prevents the accumulation
of AA in serum:

Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented
diets prevents serum arachidonic acid accumulation in humans.
Barham JB, Edens MB, Fonteh AN, Johnson MM, Easter L, Chilton FH.
J Nutr. 2000 Aug;130(8):1925-31.
PMID: 10917903
http://jn.nutrition.org/cgi/content/full/130/8/1925

Abstract:

"Previous studies reveal that supplementation of human diets
with gamma-linolenic
...

read more »

I appreciate the mechanistic studies you are posting lately Matti but
don>t forget that GLA can make you sterile, at least if you were a
worm:

Dev Biol. 2006 Apr 15;292(2):381-92. Epub 2006 Feb 17.

Dietary manipulation implicates lipid signaling in the regulation of
germ cell maintenance in C. elegans.

Watts JL, Browse J.
Institute of Biological Chemistry, Washington State University,
Pullman, WA 99614-6340, USA.

snip[/quote]

Yet another animal study. Why are you afraid of human studies?
Don>t their results please you, so you have to cherry-pick some
weird animal studies, which better fit in with your opinions?

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

Matti Narkia · Guest

Taka wrote:

[quote]On Nov 30, 12:36 pm, Matti Narkia <m...@mbnet.fi> wrote:
Yet another animal study. Why are you afraid of human studies?
Don>t their results please you, so you have to cherry-pick some
weird animal studies, which better fit in with your opinions?

Better cherry picking than "research" garbage collecting as you do
Matti. You know well that real properly controlled human experiments
cannot be conducted for ethical reasons. Thus all the review/
statistical/meta-analysis/evolutionary speculation you are presenting
here is crap mostly based on dubious questionnaires.

The only real human experiments which can be conducted are those on
ourselves and this is exactly what Monty and I have been doing. How
would you explain that I am no longer catching any cold after 1 year
restriction of dietary PUFAs? And why all my colleagues consuming
vegetable oils on daily basis always catch cold after eating grilled
fatty fish? If the placebo effect were
so strong we should start building churches instead of hospitals ...

Taka, after I caught you tampering with evidence, .i.e. forging[/quote]
abstracts to suit your own purposes, I can no longer thrust anything
you write. Sadly, you seem to have an integrity of common criminal.

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

Guest

Matti:

This is a serious charge you have leveled against Taka. Please make a
case, citing specific passages that were fabricated. Otherwise, you
compel those with a strong academic background, like myself, to view
you as the one who is guilty of dishonesty. Taka>s point about human
studies is undeniably true, but I>m willing to volunteer myself for a
human study of those who avoid dietary PUFAs and eat large amounts of
SFAs, so just get the research money and let>s get the experiment
started! Also, I don>t think you>ve ever answered my question about
your ties to the fish oil industry. If you can>t answer that question
directly, you undermine your credibility. Or do you not understand
the concept of "conflict of interest?"

Guest

I read your first post to that thread. I>m not going to read them
all, so if there is something else, just copy and paste it on this
thread. In the meantime, I>ll address some of your claims in that
first post.

"For optimal health we need to get some EPA and DHA directly from
food (or supplements)."

"By definition an excessive amount of anything should be avoided.
But reducing AA is not enough, for optimal health you also need
to get a sufficient amount of EPA and DHA from the food or
supplements."

These are just notions. Properly controlled direct experiments have
never been conducted. However, the molecular-level evidence is clear,
and convinced me to avoid dietary PUFAs as much as is practically
possible for me, while not refraining from eating as much SFAs as I
like. I started doing this back in 2001 when I was in terrible shape
physically (after taking omega 3 supplements since 1998), and not only
am I well, but I recovered, "curing" myself with this kind of diet
(see my free web site for details; go to: http://thescientificdebateforum.aimoo.com).

You also claimed:

"There is no evidence of that. EPA and DHA are anti-inflammatory and
therefore help to reduce the harms of chronic low-grade
inflammation..."

Well, this is contradicted by plenty of evidence, down to the
molecular level. My problem with using omega 3s this way is that
omega 3s are so dangerous, and so the only intelligent thing to do is
to get the AA out of your cells, and then you will avoid "chronic
inflammation." There is no danger in doing this, as I learned from
first hand experience, though I suggest an antioxidant-rich diet for a
couple of years, while there is still some AA in your body. You
claims about what "nature intended" is what science is supposed to
determine. It>s not something you just know from birth, like some
sort of instinct. And who appointed you the spokesperson for "Mother
Nature?"

Guest

CORRECTION: Due to the way you worded that sentence, it sounded like
you were arguing against omega 3s as anti-inflammatory. However, it
should really be called anti-arichidonic acid. But just because
something stops a bad thing from happening doesn>t mean you want it
around all the time. You don>t douse your home interior with water,
for example, unless there is a fire. The point I>m making is that
without AA in your cells, there is no fire to put out, and you don>t
have to risk ruining furniture, carpet, etc. by dousing everything
with water.

Matti Narkia · Guest

monty1945@lycos.com wrote:

[quote]Matti:

This is a serious charge you have leveled against Taka. Please make a
case, citing specific passages that were fabricated.
[/quote]
I have documented it in my last message in the thread "Putting the wrong
oil in the beast".

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition


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