Study finds that omega-3 PUFAs reduced (!) oxidative stress in vivo
Matti Narkia
I just happened to find a Medline abstract of a ne study which found that
daily fish meals together with either EPA or DHA _reduced_ oxidative
stress in vivo.
Effect of omega3 fatty acids on oxidative stress in humans: GC-MS
measurement of urinary F2-isoprostane excretion.
Redox Rep. 2000;5(1):45-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10905544&dopt=Abstract
Abstract:
"Despite the reported benefits associated with omega3 fatty acids for
cardiovascular disease, there remains concern that increased intake may
lead to increased lipid peroxidation. To date, however, the data,
particularly in vivo, are inconclusive. This report describes two
interventions, one providing daily fish meals and the other
eicosapentaenoic acid (EPA, 20:5 omega3) or docosahexaenoic acid (DHA,
22:6 omega3), the two principal omega3 fatty acids in marine oils, in
which in vivo lipid peroxidation was assessed by measurement of urinary
excretion of F2-isoprostanes. In both trials, urinary F2-isoprostanes
were significantly reduced by 20-27%. Therefore, in contrast with
previous reports in the literature, these results demonstrate that
omega3 fatty acids reduce in vivo oxidant stress in humans."
--
Matti Narkia
Matti Narkia
Matti Narkia
Quentin Grady
On Sun, 20 Aug 2000 20:09:45 +0300, Matti Narkia <mn...@iname.com>
wrote:
G'day G'day Matti,
OK so this good news for people taking fish or fish oil capsules.
What I am wondering is,
"How does fish or fish oil reduce oxidative stress?"
It is easy to imagine that unnamed compounds present in fish could be
antioxidants but with fish oil the possibilities seem limited.
Whatever the outcome of the question, thank you for posting the
abstract. It is important in a world where disturbing possibilities
become disseminated widely and take root in the beliefs of many people
that reassuring outcomes should get equal publicity even if it takes
more effort.
Thanks again,
--
Quentin Grady ^ ^ /
New Zealand, >#,#< [
/ \ /\
"... and the blind dog was leading."
http://homepages.paradise.net.nz/quentin
http://linux.inhb.co.nz/blind-dog
jwwright
regards.
Matti Narkia
<39A16378...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>Quentin, it says "oxidant" stress. I don't see how oxidative stress is lowered with increased PUFA's.
>That's why the CR'ers use vit e with there fish oil.
>
Well, in the title it reads "Effect of omega3 fatty acids on oxidative
stress in humans". And what is the difference? Oxidants cause oxidative
stress.
Assuming that there is nothing wrong with the study, which of course is
far from sure, the result admittedly seems illogical. The only explanation
I can come up at the moment is that omega-3 fatty acids somehow increase
body's own antioxidant production so that the net result is reduced
oxidative stress regardless of the vulnerability of omega-3 PUFAs to
oxidation.
--
Matti Narkia
jwwright
This report compares eating fish with eating fish oil, right?
Despite the reported benefits associated with omega3 fatty acids for
cardiovascular disease, there remains concern that increased intake
may lead to
increased lipid peroxidation. To date, however, the data,
particularly in vivo,
are inconclusive. This report describes two interventions, one
providing daily
fish meals and the other eicosapentaenoic acid (EPA, 20:5
omega3) or
docosahexaenoic acid (DHA, 22:6 omega3), the two principal omega3
fatty acids in
marine oils, in which in vivo lipid peroxidation was assessed by measurement
of
urinary excretion of F2-isoprostanes. In both trials, urinary F2-isoprostanes
were significantly reduced by 20-27%. Therefore, in contrast with previous
reports in the literature, these results demonstrate that omega3 fatty
acids
reduce in vivo oxidant stress in humans.
The term oxidant must not be the same as oxidative.
Since i can't get the medline text yet, i can't be sure of their conclusion, but it doesn't make common sense that eating PUFA's won't cause increased oxidation of those in the blood and in fact there are reports which have shown that oxidation of LDL is increased. That's why the vit e with pufa's.
Regards.
Matti Narkia wrote:
Mon, 21 Aug 2000 12:14:32 -0500 in article
<39A16378...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>Quentin, it says "oxidant" stress. I don't see how oxidative stress is lowered with increased PUFA's.
>That's why the CR'ers use vit e with there fish oil.
>
Well, in the title it reads "Effect of omega3 fatty acids on oxidative
John 'the Man'
>The term oxidant must not be the same as oxidative.
>Since i can't get the medline text yet, i can't be sure of their
conclusion,
>but it doesn't make common sense that eating PUFA's won't cause increased
>oxidation of those in the blood and in fact there are reports which have
>shown that oxidation of LDL is increased. That's why the vit e with pufa's.
Allopaths like to play word games.
With them, it is NOT what you say, but HOW you say it that counts.
That word play between "oxidant" versus "oxidative" changes the entire
meaning of the abstract.
Just like that recent study that knocked Vitamin C, ... I simply do NOT
believe any study that defyies simple COMMON SENSE. Science hath already
determined the physical properties of ALL PUFA's. It is about time, Matti
figured that out.
Furthermore, no one should give the time of day, to any study that ain't "in
vivo."
--
P.S.: I post comments, I NEVER answer questions on ngs.
John Gohde,
Natural Health Advocate of the Healing Power of Nature.
http://home.att.net/~johngohde/
Eat your Fruits & Vegetables. Drink your tea. And, be
sure to cook your food with Spice.
Matti Narkia
<39A16D6D...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>
>The term oxidant must not be the same as oxidative.
>
in several contexts elsewere as if they were interchangeable, or so it
seems. Below some excerpts from the web pages where these terms as well as
terms isoprostanes and F2-isoprostanes are discussed:
Generating New Medical Knowledge
http://www.bwfund.org/1999_annual_report/99_generating_new_medical.htm
"“Oxidant stress, or oxidative injury, is a term that refers to the
presence in the body of too many free radicals--that is, a kind of
molecule that is derived from oxygen and is very unstable,” says Jason
Morrow, M.D. Free radicals have the potential to damage important
biomolecules, including proteins, lipids, and DNA, by modifying them
chemically, destroying their ability to function.
“The human body has developed an inordinate number of mechanisms to
repair or control oxidative stress,” continues Dr. Morrow, who
specializes in this field as a professor of medicine and pharmacology at
Vanderbilt University Medical Center. His research focuses on a family
of molecules called the isoprostanes, which form spontaneously in the
body in response to oxidative stress. “The chemical reaction of oxygen
with arachidonic acid [a major component of all cell membranes] gives
rise to a number of prostaglandin-like molecules, one of which is the
isoprostanes,” Dr. Morrow explains. He has been able to determine that
isoprostane formation occurs very predictably and consistently in this
way--so much so that spectrometric measurements of isoprostane formation
have become the “gold standard” for assessing oxidative injury in vivo.
Previous methods had performed well in the test tube but fallen short in
their application to living humans. “There had been a translational gap
there, no doubt about it,” says Dr. Morrow, who has received three
patents for this new means of assessing oxidative injury. "
Functional food science and defence against reactive oxidative species
http://nutrition.cabweb.org/BJN/journals/FULLTEXT/AUG_SUPP/Bj80s077.asp
"Quantification of F2-isoprostanes represents a reliable and useful
approach to assessment of lipid peroxidation and oxidant stress in vivo
(Morrow & Roberts, 1994).
Human body fluids also contain low levels of F2-isoprostanes, compounds
isomeric to prostaglandins that appear to arise by free-radical
oxidation of phospholipids containing arachidonic acid (Morrow &
Roberts, 1994; Morrow et al. 1995). Isoprostanes appear to exist in
human plasma largely esterified to phospholipids rather than ‘free’, and
sensitive assays to measure them have been described (Morrow & Roberts,
1994; Wang et al. 1995). Isoprostanes and their metabolites can be
measured in human urine (Morrow & Roberts, 1994; Morrow et al. 1995) by
GC–MS and this may prove a valuable assay of whole-body lipid
peroxidation if a confounding effect of diet can be ruled out. These
compounds are useful ‘markers’ of lipid peroxidation and can be measured
in plasma (35 (sd 6) pg/ml) and urine (1600 (sd 600) pg/mg creatinine)
of healthy volunteers, indicative of ongoing lipid peroxidation even in
healthy human subjects (Halliwell, 1996)."
OXIDATIVE STRESS
http://molebio.iastate.edu/~jat/glutchp.htm
"Oxidative stress results from the metabolic reactions that use oxygen,
and it has been defined as a disturbance in the equilibrium status of
pro-oxidant/anti-oxidant systems in intact cells. This definition of
oxidative stress implies that cells have intact pro-oxidant/anti-oxidant
systems that continuously generate and detoxify oxidants during normal
aerobic metabolism. When additional oxidative events occur, the
pro-oxidant systems outbalance the anti-oxidant, potentially producing
oxidative damage to lipids, proteins, carbohydrates, and nucleic acids,
ultimately leading to cell death in severe oxidative stress. Mild,
chronic oxidative stress may alter the anti-oxidant systems by inducing
or repressing proteins that participate in these systems, and by
depleting cellular stores of anti-oxidant materials such as glutathione
and vitamin E."
To summarise, definitions from above excerpts:
"Oxidant stress, or oxidative injury, is a term that refers to the
presence in the body of too many free radicals"
"Oxidative stress results from the metabolic reactions that use oxygen,
and it has been defined as a disturbance in the equilibrium status of
pro-oxidant/anti-oxidant systems in intact cells."
Another definition for _oxidative stress_ from the web page
http://www.cwu.edu/~chem/seminars/Dehen/sld003.htm :
"Oxidative stress is a situation of a serious imbalance between
production of reactive oxygen species (ROS) and the levels of
antioxidant defenses."
>Since i can't get the medline text yet, i can't be sure of their conclusion, but it doesn't make common
>sense that eating PUFA's won't cause increased oxidation of those in the blood and in fact there are
>reports which have shown that oxidation of LDL is increased. That's why the vit e with pufa's.
>
I made a brief search in Medline. As the abstract of the study by Mori et
al. suggested, the evidence in vivo with humans seems to be inconclusive.
Below some references I found:
Bechoua S, Dubois M, Dominguez Z, Goncalves A, Nemoz G, Lagarde M, Prigent
AF.
Protective effect of docosahexaenoic acid against hydrogen
peroxide-induced oxidative stress in human lymphocytes.
Biochem Pharmacol. 1999 May 1;57(9):1021-30.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10796072&dopt=Abstract
"Collectively, these results suggest that lymphocytes are relatively
resistant to H2O2-induced lipid peroxidation due to their high GSH-Px
content, and that low doses of 22:6n-3 are able to prevent some of the
H2O2-induced alterations such as lipid peroxidation and PDE inhibition.
Docosahexaenoic acid might thus offer some protection against
oxidant-induced lymphocyte suppression."
Pogozheva AV, Rozanova IA, Sorokovoi KV, Karagodina ZV, Levachev MM.
[Lipid peroxidation in patients with ischemic heart disease,
hyperlipidemia and/or hypertension while polyunsaturated omega-3 fatty
acids of plant and animal origin were in their diet].
Vopr Pitan. 1997;(4):32-5. Russian
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9412077&dopt=Abstract
"Usage of antisclerotic diet with PUFA n-3 from vegetable or animal
source in 326 patients with IHD, HL and HBP resulted in positive dynamic
of clinical manifestation, blood lipids and coagulogramms of the
patients. The favorable changes of membrane lipids and the decrease of
intensity of lipid peroxidation was also revealed. The decrease of
primary and secondary metabolites of lipid peroxidation could be a
result of hypolipidemic effect of the diets and sufficient level of
vitamin E."
Brude IR, Drevon CA, Hjermann I, Seljeflot I, Lund-Katz S, Saarem K,
Sandstad B, Solvoll K, Halvorsen B, Arnesen H, Nenseter MS.
Peroxidation of LDL from combined-hyperlipidemic male smokers supplied
with omega-3 fatty acids and antioxidants.
Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2576-88.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9409230&dopt=Abstract
"In conclusion, omega-3 FAs neither rendered the LDL particles more
susceptible to undergo in vitro oxidation nor influenced mononuclear
cells' ability to oxidize autologous LDL"
Allard JP, Kurian R, Aghdassi E, Muggli R, Royall D.
Lipid peroxidation during n-3 fatty acid and vitamin E supplementation in
humans.
Lipids. 1997 May;32(5):535-41.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9168460&dopt=Abstract
"The results demonstrate that supplementing the diet with n-3 fatty
acids resulted in an increase in lipid peroxidation, as measured by
plasma MDA release and lipid peroxide products, which was not suppressed
by vitamin E supplementation."
--
Matti Narkia
Matti Narkia
Metabolism 1999 Nov;48(11):1402-8 Related Articles, Books, LinkOut
Effect of dietary fish and exercise training on urinary F2-isoprostane
excretion in non-insulin-dependent diabetic patients.
Mori TA, Dunstan DW, Burke V, Croft KD, Rivera JH, Beilin LJ, Puddey IB
Department of Medicine, University of Western Australia, Perth, Australia.
Despite the potential benefits of dietary treatment with marine omega3
fatty acids in cardiovascular disease, there remains concern with respect
to their potential for increased lipid peroxidation. Thus far, data from
in vivo studies are inconclusive. Increased lipid peroxidation has also
been associated with acute exercise in some studies, but the methods have
been nonspecific. The quantitation of F2-isoprostanes provides a more
reliable and useful assessment of in vivo lipid peroxidation. We therefore
aimed to assess the independent and combined effects of dietary omega3
fatty acids and aerobic exercise training on urinary F2-isoprostane levels
in dyslipidemic non-insulin-dependent diabetic (NIDDM) patients. In a
randomized controlled trial, 55 untrained, sedentary, dyslipidemic NIDDM
patients were randomly assigned to a low-fat diet (30% of daily energy)
with or without one daily fish meal (3.6 g omega3 fatty acids per day) and
further randomized to either a moderate (55% to 65% maximal oxygen
consumption [VO2max]) or light (heart rate <100 bpm) exercise training
program for 8 weeks. Twenty-four-hour urine samples from 49 subjects were
collected for measurement of urinary F2-isoprostanes by gas
chromatography-mass spectrometry before and after intervention. The fish
diets reduced urinary F2-isoprostanes by 830+/-321 pmol/24 h (20%, P =
.013) relative to the low-fat diet alone. This effect was independent of
age, gender, and body weight change. Moderate exercise training did not
alter F2-isoprostanes. These findings show that, at least in the
short-term, exercise had no effect, whereas the inclusion of regular fish
meals as part of a low-fat diet reduced in vivo lipid peroxidation in
dyslipidemic NIDDM patients. This response could further complement the
known benefits of omega3 fatty acids and exercise favoring a reduced
cardiovascular risk in diabetic patients.
URL:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10582548&dopt=Abstract
--
Matti Narkia
jwwright
I'll be looking for the whole article to see how they performed the
test.
BTW, what engine did you use to get your refs so fast?
Regards.
Alf Christophersen
wrote:
>Mon, 21 Aug 2000 12:57:01 -0500 in article
><39A16D6D...@livingston.net> jwwright <jwwr...@livingston.net>
>wrote:
>>
>>The term oxidant must not be the same as oxidative.
>>
>No, but IMHO terms _oxidant stress_ and _oxidative stress_ seem to be used
>in several contexts elsewere as if they were interchangeable, or so it
>seems. Below some excerpts from the web pages where these terms as well as
>terms isoprostanes and F2-isoprostanes are discussed:
If you have read the articles (not only tjhe abstracts), can you tell
me if they have measured all metabolites of ALL substrates for the COX
enzymes, that is, not only F2-prostanes and other arachidonic acid
metabolites, but also the F3-prostanes and/or F1-prostanes and other
metabolites of primarily DHGLA and EPA. F2-prostanes are the
metabolites of arachidonic acid and feeding EPA of course out concure
arachidonic acid from being converted. But it is not a proof of
reduced oxidative stress, just that less AA is converted into
prostaglandines, but that isn not any novelty.
Only if all metabolites of all eicosanoids in sum is decreased by
increasing EPA intake, you may perhaps conclude that oxidative stress
is reduced (also malone dialdehyde production in total should also
decrease!)
Telling oxidative stress is decreased in total just by measuring the
metabolite of just one of many eicosanoids, is more or less
falsifying.
Matti Narkia
<39A19014...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>So i checked the med refs and oxidant stress seems to be used the same as oxidative stress, i.e., stress on
>cells. What do you conclude from the articles you posted? Do you think ingestion of PUFA's increase
>oxidant/oxidative stress? I do, so i limit all fat intake. I'll take the chance that no excess fat is better
>than taking antioxidants above rda's.
>
I don't think that one should take too much fats, but around 30% of
calories may be ok. I don't believe in low fat diets, they may do more
harm than good. IMHO it's perhaps a good idea to limit all visible fats to
extra virgin olive oil and omega-3 PUFAs. According to some evidence I've
recently found, it could make sense to get part of omega-3 from marine
sources and part from terrestrial sources such as flaxseeds.
I don't know if ingestion of PUFAs increases oxidative stress. Anyway, I
wouldn't ingest visible omega-6 PUFAs such as most refined vegetable oils.
As for omega-3, the evidence about oxidative stress in vivo with humans
seems to be inconclusive and somewhat contradictory. However, I do eat my
fish, mostly salmon and canned sardines, have started again to grind
flaxseeds and throw in some fish oil. I do have a fairly extensive
antioxidant supplement program. My program is mainly geared towards
treatment of a disease and may not be suitable for healthy individuals.
BTW I found some additional studies by Mori's team:
Mori TA, Dunstan DW, Burke V, Croft KD, Rivera JH, Beilin LJ, Puddey IB.
Effect of dietary fish and exercise training on urinary F2-isoprostane
excretion in non-insulin-dependent diabetic patients.
Metabolism. 1999 Nov;48(11):1402-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10582548&dopt=Abstract
Mori TA, Bao DQ, Burke V, Puddey IB, Watts GF, Beilin LJ.
Dietary fish as a major component of a weight-loss diet: effect on serum
lipids, glucose, and insulin metabolism in overweight hypertensive
subjects.
Am J Clin Nutr. 1999 Nov;70(5):817-25.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10539741&dopt=Abstract
"CONCLUSIONS: Incorporating a daily fish meal into a weight-loss regimen
was more effective than either measure alone at improving
glucose-insulin metabolism and dyslipidemia. Cardiovascular risk is
likely to be substantially reduced in overweight hypertensive patients
with a weight-loss program incorporating fish meals rich in n-3 fatty
acids."
Mori TA, Bao DQ, Burke V, Puddey IB, Beilin LJ.
Docosahexaenoic acid but not eicosapentaenoic acid lowers ambulatory blood
pressure and heart rate in humans.
Hypertension. 1999 Aug;34(2):253-60.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10454450&dopt=Abstract
"Only DHA reduced 24-hour and daytime (awake) ambulatory BP (P<0.05).
Relative to the placebo group, 24-hour BP fell 5.8/3.3
(systolic/diastolic) mm Hg and daytime BP fell 3.5/2.0 mm Hg with DHA.
DHA also significantly reduced 24-hour, daytime, and nighttime (asleep)
ambulatory HRs (P=0. 001). Relative to the placebo group, DHA reduced
24-hour HR by 3. 5+/-0.8 bpm, daytime HR by 3.7+/-1.2 bpm, and nighttime
HR by 2. 8+/-1.2. EPA had no significant effect on ambulatory BP or HR."
[...]
Purified DHA but not EPA reduced ambulatory BP and HR in mildly
hyperlipidemic men. The results of this study suggest that DHA is the
principal omega3 fatty acid in fish and fish oils that is responsible
for their BP- and HR-lowering effects in humans. These results have
important implications for human nutrition and the food industry."
Bao DQ, Mori TA, Burke V, Puddey IB, Beilin LJ.
Effects of dietary fish and weight reduction on ambulatory blood pressure
in overweight hypertensives.
Hypertension. 1998 Oct;32(4):710-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9774368&dopt=Abstract
"Combining a daily fish meal with a weight-reducing regimen led to
additive effects on ambulatory BP and decreased heart rate. The effects
were large, suggesting that cardiovascular risk and antihypertensive
drug requirements are likely to be reduced substantially by combining
dietary fish meals rich in omega3 fatty acids with weight-loss regimens
in overweight medication-treated hypertensives. The reduction in heart
rate seen with dietary fish suggests a cardiac/autonomic component, as
well as vascular effects, of increased consumption of omega3 fatty acid
from fish."
>I'll be looking for the whole article to see how they performed the test.
>BTW, what engine did you use to get your refs so fast?
>
For Medline searches I use PubMed
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
and for web searches Google
http://www.google.com/
--
Matti Narkia
Quentin Grady
<jwwr...@livingston.net> wrote:
>Quentin, it says "oxidant" stress.
Is there some double talk going on?
>I don't see how oxidative stress is lowered with increased PUFA's.
Me neither.
>That's why the CR'ers use vit e with there fish oil.
Also true.
>regards.
G'day G'day Jim,
Don't ya just love a mystery!
Michael Sherman
> "The chemical reaction of oxygen
> rise to a number of prostaglandin-like molecules, one of which is the
Uh-oh. If isoprostanes are from AA (a long-chain omega 6),
then the fact that isoprostanes were reduced by EPA & DHA
(competing long-chain omega 3s) might just signal replacement
of AA by EPA or DHA in the membranes. They might be oxidizing
worse than the AA was, but if only AA byproducts are measured
the apparent effect might be the one observed.
To me that would only justify the conclusion that AA oxidation
was reduced, not that lipid oxidation in general was reduced.
Specifically the abstract said F2-isoprostane production
was reduced. Would oxidation of EPA or DHA produce F2-isoprostane?
sherm
Matti Narkia
alf.chris...@basalmed.uio.no (Alf Christophersen) wrote:
>
>If you have read the articles (not only tjhe abstracts), can you tell
>me if they have measured all metabolites of ALL substrates for the COX
>enzymes, that is, not only F2-prostanes and other arachidonic acid
>metabolites, but also the F3-prostanes and/or F1-prostanes and other
>metabolites of primarily DHGLA and EPA. F2-prostanes are the
>metabolites of arachidonic acid and feeding EPA of course out concure
>arachidonic acid from being converted. But it is not a proof of
>reduced oxidative stress, just that less AA is converted into
>prostaglandines, but that isn not any novelty.
>
>Only if all metabolites of all eicosanoids in sum is decreased by
>increasing EPA intake, you may perhaps conclude that oxidative stress
>is reduced (also malone dialdehyde production in total should also
>decrease!)
>
>Telling oxidative stress is decreased in total just by measuring the
>metabolite of just one of many eicosanoids, is more or less
>falsifying.
That seems to make sense. What still puzzles me is how apparently a rather
experienced research team could have made this kind of error in conclusion
_twice_, and how this error could have escaped from the reviewers of _two_
peer reviewed Medline publications? The full texts of the studies might
shed some light to this mystery, perhaps I should try to get hold of them
:-).
--
Matti Narkia
Matti Narkia
http://www.orst.edu/dept/IIFET/2000/abstracts/wander.html
I found the following rather interesting abstract which seems to confirm
the results of the study which started this thread:
"Do We Go Rancid after Eating Fish?
By Rosemary C. Wander
ABSTRACT
Fish off-flavor and odor develops, in part, through oxidation of the
long-chain, highly unsaturated fatty acids, eicosapentaenoic acid (EPA)
and docosahexaenoic acid (DHA), fish contain, a condition referred to as
rancidity. This deterioration proceeds through a free-radical mediated,
chain reaction. Even though numerous epidemiologic studies have shown that
fish consumption decreases cardiovascular mortality, there is concern that
its consumption could increase in vivo lipid oxidation, contributing to
the development of such diseases as cardiovascular disease, cancer, and
diabetes. In the past, a limitation to measuring in vivo oxidation was the
lack of appropriate tools. Recently, more sensitive measures have been
developed, e.g., the adduct formed by the reaction of malondialdehyde with
thiobarbituric acid using high pressure liquid chromatography,
F2-isoprostanes, malondialdehyde by gas chromatography/mass spectrometry,
and protein oxidation. Using these techniques, we measured lipid oxidation
in plasma of post menopausal women after they consumed a supplement of
fish oil containing an amount of EPA/DHA equivalent to two servings of
Chinook salmon. In vivo oxidation was either similar to or lower than that
which occurred when the women were not consuming the fish oil. On the
other hand, plasma concentrations of thiobarbituric acid reactive
substances (TBARS), a much older method for measuring lipid oxidation,
consistently increased. Using low-density lipoprotein (LDL)obtained from
the same subjects, we determined that the ex vivo rate of oxidation of LDL
enriched with EPA and DHA was slower than LDL not enriched. These data
suggest that oxidative stress is not increased but may actually be lowered
by fish consumption.
KEYWORDS: oxidation, cardiovascular disease, F2-isoprostanes, TBARS,
malondialdehyde"
--
Matti Narkia
John 'the Man'
news:miq2qs8bep3fmtipq...@4ax.com...
> Don't ya just love a mystery!
If you mean .... How can fish oil be an antioxidant?
It is NOT! Matti is just confused, .... once again. :-)
Alf Christophersen
wrote:
>That seems to make sense. What still puzzles me is how apparently a rather
>experienced research team could have made this kind of error in conclusion
>_twice_, and how this error could have escaped from the reviewers of _two_
>peer reviewed Medline publications? The full texts of the studies might
>shed some light to this mystery, perhaps I should try to get hold of them
Unfortunately they have no training in thinking about dynamic systems,
just static systems.
I myself has a very strange background for my biochemistry degree.
Previously I came from mechanical engineering and computer science,
not from biology where you learn next to nothing about dynamic
systems. As mechanical engineer you are trained and drilled in dynamic
thinking. It is very difficult for most people in the beginning, but
in next turn, you will have lot of use of the knowledge about eg.
hydromechanics which is a very good analogy to how biological systems
are regulated. Try to remember that steady state level can be
regulated by two ways, either change input or change output. Most
biological researcher do only think about input :-(
jwwright
we totally understood the bio pathways. The article seems to say some
fish oil is good, but then how much? I can only judge but my reaction to
DHA, EPA, fish oil caps, which is that it raises my blood pressure.
regards.
John 'the Man' wrote:
> "Quentin Grady" <que...@paradise.net.nz> wrote in message
> news:miq2qs8bep3fmtipq...@4ax.com...
>
> > Don't ya just love a mystery!
>
John 'the Man'
> Of course, fish oil is not an antiox per se, but the effect could be, if
> we totally understood the bio pathways.
Tell me something I don't know, ... Please.
It is really very simple.
Eat fish, take Flaxseed or Fish Oil supplements and you have to take it with
anitoxidants,, ... period. How much do you really need, ... Who knows?
What I do know is that consuming excessive abouts of PUFAs are counter
productive to your Antioxidant program. Anybody who doesn't see the
implications of this is a real dumb, dumb.
Personally, I spend money on antioxidants to protect me from my environment,
.... NOT to protect me from my supplements!!!!
Is the brave Matti, ... Now saying that everyone should eat all the Fish
they want ... With NO Vitamin E, .... at all? If NOT, then please shut up
Matti!
You are making a fool of yourself, Matti, as usually by repeatedly
demonstrating that you have absolutely NO Common Sense.
I personally eat food and take ALL my supplements because the overall effect
is positive. Gee, are you really saying that consuming Omega-3 in the
correct amount gives an overall positive effect? Please, ... tell me
something that I don't know!!!
And, remember your body needs only ONE tiny tiny tiny gram a day.
MegaDosing on Omega-3s is even dumber than MegaDosing on Vitamin C.
-- P.S.: I post comments, I NEVER answer questions on ngs.
John Gohde,
Natural Health Advocate of the Healing Power of Nature.
http://home.att.net/~johngohde/
Eat your Fruits & Vegetables. Drink your tea. And, be
sure to cook your food with Spice.
> John 'the Man' wrote:
>
> > "Quentin Grady" <que...@paradise.net.nz> wrote in message
> > news:miq2qs8bep3fmtipq...@4ax.com...
> >
> > > Don't ya just love a mystery!
> >
jwwright
Regards.
John 'the Man' wrote:
> > > > Don't ya just love a mystery!
> > >
jwwright
So DHA maybe lowered me 5.8 and i just couldn't SEE it. who cares?
BP measurement is the most complex and least understood item in medicine. BP changes during the day are equally complex.
Regards.
Matti Narkia wrote:
Tue, 22 Aug 2000 11:02:09 -0500 in article
<39A2A401...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>Of course, fish oil is not an antiox per se, but the effect could be, if
>we totally understood the bio pathways. The article seems to say some
>fish oil is good, but then how much? I can only judge but my reaction to
>DHA, EPA, fish oil caps, which is that it raises my blood pressure.
>
The result of the study
Mori TA, Bao DQ, Burke V, Puddey IB, Beilin LJ.
Docosahexaenoic acid but not eicosapentaenoic acid lowers ambulatory blood
pressure and heart rate in humans.
Hypertension. 1999 Aug;34(2):253-60.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10454450&dopt=Abstract
was that 4 g/d of purified DHA reduced 24-hour BP 5.8/3.3
(systolic/diastolic) mm Hg and daytime BP 3.5/2.0 mm Hg
compared with placebo (olive oil) group. Purified EPA didn't have
significant effect on BP. 4 grams of purified DHA is a lot, to get it from
fish oil one would need to take about 13 g concentrated (70% EPA+DHA) fish
oil or 31 - 62 g regular (15 - 30% EPA+DHA) fish oil! Martek manufactures
algae derived DHA:--
Matti Narkia
Matti Narkia
alf.chris...@basalmed.uio.no (Alf Christophersen) wrote:
>On Tue, 22 Aug 2000 09:53:28 +0300, Matti Narkia <mn...@iname.com>
>wrote:
>
>>That seems to make sense. What still puzzles me is how apparently a rather
>>experienced research team could have made this kind of error in conclusion
>>_twice_, and how this error could have escaped from the reviewers of _two_
>>peer reviewed Medline publications? The full texts of the studies might
>>shed some light to this mystery, perhaps I should try to get hold of them
>
>Unfortunately they have no training in thinking about dynamic systems,
>just static systems.
>
Ok, perhaps we better leave the study by Mori et al. alone at least until
we know more about it and F2-isoprostanes. But what about the abstract
(which I posted earlier) of the presentation given last month by Rosemary
C. Wander, Ph.D, Department of Nutrition, University of North Carolina,
USA ( http://www.uncg.edu/nfs/faculty/r_wander.html ) at the conference
IIFET 2000: Microbehavior and Macroresults July 10-15, 2000 in Corvallis,
Oregon USA
As a citation from the web page
Do We Go Rancid after Eating Fish?
http://www.orst.edu/dept/IIFET/2000/abstracts/wander.html
shows, several different tests were used in assessing the oxidative
stress:
"Recently, more sensitive measures have been developed, e.g., the adduct
formed by the reaction of malondialdehyde with thiobarbituric acid using
high pressure liquid chromatography, F2-isoprostanes, malondialdehyde by
gas chromatography/mass spectrometry, and protein oxidation. Using these
techniques, we measured lipid oxidation in plasma of post menopausal
women after they consumed a supplement of fish oil containing an amount
of EPA/DHA equivalent to two servings of Chinook salmon."
Still the conclusion was:
"These data suggest that oxidative stress is not increased but may
actually be lowered by fish consumption."
One of Wander's earlier studies concluded that "EPA/DHA-enriched LDL have
decreased oxidative susceptibility". Below its abstract:
Wander RC, Du SH, Thomas DR.
Influence of long-chain polyunsaturated fatty acids on oxidation of low
density lipoprotein.
Prostaglandins Leukot Essent Fatty Acids. 1998 Aug;59(2):143-51.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9774178&dopt=Abstract
"Enrichment of low density lipoprotein (LDL) with long-chain fatty
acids, such as eicosapentaenoic acid (EPA; 20:5 n-3) and docosahexaenoic
acid (DHA; 22:6 n-3) found in fish oil, is thought to increase its
oxidative susceptibility although such an increase has not been clearly
demonstrated. The purpose of this study was to determine the composition
and fatty acid concentration of LDL obtained from postmenopausal women
given a supplement of fish oil and relate these values to its oxidative
susceptibility. Fish oil supplementation significantly increased LDL
concentration of EPA (P = 0.0001) and DHA (P = 0.0001) and decreased
that of linoleic acid P = 0.006). The concentration of free cholesterol,
cholesterol ester, phospholipids and protein was unchanged while
triglyceride concentration increased 8% (P = 0.02). Cu2+-mediated
oxidation resulted in a shorter lag time, slower oxidation rate and
similar concentrations of conjugated dienes of EPA/DHA-enriched LDL than
EPA/DHA-unenriched LDL. Stepwise multiple regression indicated that the
primary predictor of oxidative susceptibility of LDL was linoleic acid,
even after enrichment with EPA and DHA. The oxidation rate of
EPA/DHA-unenriched LDL correlated with the cholesteryl ester
concentration (P = 0.003) while that of EPA/DHA-enriched correlated with
the concentration of phospholipids (P = 0.03). These data suggest that
EPA/DHA-enriched LDL have decreased oxidative susceptibility and that
surface lipids may mediate its rate of oxidation."
--
Matti Narkia
Matti Narkia
Matti Narkia
<39A30A95...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>AND, I think that 1 gram is 18:03 not pure EPA.
>
No, according to John's earlier post it was EPA+DHA. I assume that it was
a kind of minimum daily dose in ideal conditions. If omega-6 intake is
large, one probably needs to increase EPA+DHA intake to retain a useful
omega-6/omega-3 ratio.
--
Matti Narkia
joe record
world of CR society list. cheers joe.
Matti Narkia wrote:
I just happened to find a Medline abstract of a new study which found that
daily fish meals together with either EPA or DHA _reduced_ oxidative
stress in vivo.
Mori TA, Puddey IB, Burke V, Croft KD, Dunstan DW, Rivera JH, Beilin LJ.
Effect of omega3 fatty acids on oxidative stress in humans: GC-MS
measurement of urinary F2-isoprostane excretion.
Redox Rep. 2000;5(1):45-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10905544&dopt=Abstract
Abstract:
"Despite the reported benefits associated with omega3 fatty acids for
cardiovascular disease, there remains concern that increased intake may
lead to increased lipid peroxidation. To date, however, the data,
particularly in vivo, are inconclusive. This report describes two
interventions, one providing daily fish meals and the other
eicosapentaenoic acid (EPA, 20:5 omega3) or docosahexaenoic acid (DHA,
22:6 omega3), the two principal omega3 fatty acids in marine oils, in
which in vivo lipid peroxidation was assessed by measurement of urinary
excretion of F2-isoprostanes. In both trials, urinary F2-isoprostanes
were significantly reduced by 20-27%. Therefore, in contrast with
previous reports in the literature, these results demonstrate that
omega3 fatty acids reduce in vivo oxidant stress in humans."
--
Matti Narkia
Matti Narkia
<39A30D82...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>Well first of all, anyone who claims anything from a 5.8/3.3 change in BP is dealing in mystical crap,
>because that's in the noise of the measurement.
Well, the reduction was not big, but it definitely was not noise, because
it was statistically significant (P<0.05).
--
Matti Narkia
John 'the Man'
> AND, I think that 1 gram is 18:03 not pure EPA.
Actually it is both DHA/EPA. That is to say it refers to Fish Oil, NOT
Flaxseed Oil. For flaxseed, it would be one tablespoon full or 8 or 9
grams.
I eat fish three times a week, and take one tablespoon full of flaxseed oil
a day to boot. Previously, I was also taking about 3 grams of fish oil a
day, back when my fish intake was a bit less routine.
--
P.S.: I post comments, I NEVER answer questions on ngs.
John Gohde,
Natural Health Advocate of the Healing Power of Nature.
http://home.att.net/~johngohde/
Eat your Fruits & Vegetables. Drink your tea. And, be
sure to cook your food with Spice.
>
> Regards.
>
> John 'the Man' wrote:
>
> > "jwwright" <jwwr...@livingston.net> wrote in message
> > news:39A2A401...@livingston.net...
> >
> > > Of course, fish oil is not an antiox per se, but the effect could be,
if
> > > we totally understood the bio pathways.
> >
> > > > > Don't ya just love a mystery!
> > > >
Alf Christophersen
wrote:
>Ok, perhaps we better leave the study by Mori et al. alone at least until
>we know more about it and F2-isoprostanes. But what about the abstract
>(which I posted earlier) of the presentation given last month by Rosemary
There is one thing that is important to remember.
1 mol of EPA do not form the same amount of PG and other eicosanoids
as 1 mol of AA. I do not know exactly the kinetic parameters for the
lipoxygenases, but kinetic data reported for COX I show that Vm for
EPA is much less (about 1/10) while the Km also is much less. That is,
1/2 Vm is reached at much lower concentrations for EPA than for AA,
while about 10 times more PG pr second is formed at Km concentration.
That might be the explanation for the decreased amounts of PG's.
Whether the same also applies for other enzyme directed reactions
involving free radical formation using EPA or AA as substrate, I do
not know.
On the other hand, non-enzymatically peroxidations are most possibly
faster with EPA and DHA because the more amount of double bonds which
could be peroxidized.
But all of it is also dependent on the presence of oxidizing and
reducing agents, not only oxygen are able to peroxidize lipid
molecules.
There are also reports on chemical agents that might pick up the free
radical formed by COX under conversion from AA to PGH (via PGG).
Normally the free radical might attack Tyrosine at the active site of
COX and inactivate the enzyme, socalled suicide inactivation. It seems
to be a ___VERY___ important way of controlling the overall activity
of COX. It should most probably only make a shoot and then cease
producing PG's. That is, when activated by oxidative stress, it will
activate more enzyme molecules by adding more free radicals of
different kinds and when doing so, it will increase the chance both to
activate even more enzyme molecules, but also the chance of being hit
by a free radical that destroy it. Concentration plotted against time
will show first a weak increase and then suddenly it rise sharply, get
to a maximum and then decease even more rapid because all enzyme
molecules are destroyed.
By this time function, it can fullfill a role as a pulse producer that
might have a signal function, like a fire match hold against a fire
sensor, trigging a chain of events.
Inhibiting the attack of free radicals will stop the fall of activity
and the time function will show a very different trend by not falling
back to low level again, being an analogy to a fire that keep the fire
sensors busy for long time or a feedback controller going mad :-)
The regulated system is thus out of control because a pulse generator
do not cease of giving pulses when it should not give pulses. Eg.
growth signals.
COX II out of control thus has a very special role in cancer
development.
jwwright
regards.
jwwright
understand why i need them. Or maybe i get enough in the little bit of soy oil i
eat?
Regards.
John 'the Man' wrote:
> "jwwright" <jwwr...@livingston.net> wrote in message
> news:39A30A95...@livingston.net...
>
> > AND, I think that 1 gram is 18:03 not pure EPA.
>
> > > > > > Don't ya just love a mystery!
> > > > >
Matti Narkia
<39A43CDB...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>what's the symptoms of having the wrong ratio?
>
Too high omega-6/omega-3 ratio results in excessive production of
arachidonic acid and its eicosanoid products which can lead to increased
vulnerability to many chronic diseases including cancer.
--
Matti Narkia
John 'the Man'
> Well, i guess one of the symptoms of a deficiency in w3's is not being
able to
> understand why i need them. Or maybe i get enough in the little bit of soy
oil
Actually I got the ANSWER on my web site. You mean Matti in all his
bablings has NOT told you yet?
http://home.att.net/~johngohde/Prevention.html
Prevent Specific Health Conditions
Read the section labeled: High rates of Prostanoid Synthesis. Gee, I guess
that is how you avoid high rates of Prostanoid Synthesis?
> > > > > > > Don't ya just love a mystery!
> > > > > >
jwwright
of the data. If i have a person with a bad "ear" or instruments that react to sounds diff, or patients who
vary the salt in their dietary intake, the BP can change dramatically like 25/15 mmhg.
Even if i can hold all those things constant there is still the individual reaction to the taking of the
BP.
Regards.
jwwright
There's not enough fiber and no carbos to hold the water in the gut. Clear now?
Regards,
Howard Lee Harkness wrote:
> jwwright <jwwr...@livingston.net> wrote:
>
> >If you have HTN, the best thing is stop eating anything that contains sodium. And follow a
> >low fat diet (ornish).
>
> I had much better bp reduction on a high-fat, low-carb diet than I had
> with Ornish/McDougal.
>
> Howard 330/270/220 started LC Dec 1999
> 50/42/38 (pants size)
> Grossly obese/Chubby but muscular/Nothing jiggles
> 1951(4 lbs, 2oz)/2000/2101
jwwright
Why not just avoid excess fat?
Regards
John 'the Man' wrote:
> > > > > > > > Don't ya just love a mystery!
> > > > > > >
Michael Sherman
Alf Christophersen wrote:
> If you have read the articles (not only tjhe abstracts), can you tell
> me if they have measured all metabolites of ALL substrates for the COX
> enzymes, that is, not only F2-prostanes and other arachidonic acid
> metabolites, but also the F3-prostanes and/or F1-prostanes and other
> metabolites of primarily DHGLA and EPA. F2-prostanes are the
> metabolites of arachidonic acid and feeding EPA of course out concure
> arachidonic acid from being converted. But it is not a proof of
> reduced oxidative stress, just that less AA is converted into
> prostaglandines, but that isn not any novelty.
Regarding Mori's paper, I sent him the following question
and got the reply below. Can anyone figure out what he is saying?
Anyone have a follow-up question for him -- if so I'll send it.
sherm
>Aren't F2-isoprostanes arachidonic acid metabolites? Could
>their reduction simply reflect substitution of DHA and EPA for AA
>in the test subjects rather than an actual reduction in oxidation?
>Could you have detected oxidation of DHA or EPA in that case?
> From: Trevor Mori [mailto:tm...@cyllene.uwa.edu.au]
> Sent: Thursday, August 24, 2000 2:13 AM
> To: Michael Sherman
> Subject: Re: Question regarding: Redox Rep 2000;5(1):45-6
>
> Dear Michael,
>
> You are correct in that the F2-isoprostanes are
> oxidation metabolites of arachidonic acid. However,
> we found no statistical relationship
> between the changes in urinary isoprostanes
> and changes in plasma, platelet and red
> blood cell fatty acid composition. In particular we
> found no relationship with any w6 or w3 fatty acid
> changes. We detected very small amounts of the
> EPA-derived isoprostanes in a small number of samples.
>
> I hope this claries your queries.
>
> Yours sincerely
>
> Trevor Mori
>
>
> ---------------------------------------------------------------------
> Dr Trevor A Mori
>
> Department of Medicine Phone: 61 8 9224 0273
> University of Western Australia Fax: 61 8 9224 0246
> C/- GPO Box X2213
> Perth WA 6847 AUSTRALIA
>
> ---------------------------------------------------------------------
John 'the Man'
Global effects are global, and can not be explained in two words. Hence,
the 1,000 citations from Matti. :-(
If you do NOT like my answer, then research the question yourself.
"jwwright" <jwwr...@livingston.net> wrote in message
news:39A559E3...@livingston.net...
> > > > > > > > > Don't ya just love a mystery!
> > > > > > > >
Will Brink
<mn...@iname.com> wrote:
> Mori TA, Puddey IB, Burke V, Croft KD, Dunstan DW, Rivera JH, Beilin LJ.
> I just happened to find a Medline abstract of a ne study which found that
> daily fish meals together with either EPA or DHA _reduced_ oxidative
> stress in vivo.
>
Interesting study. There is other data to support that n-3 lipids actualy
reduce oxidative stress. Its been assumed that the simple stucture of n-3
lipids, being PUFS, gave them the potential to increase oxidative stress.
However, as always, it turns out to be far more comlex than that. n-3
lipids having effects on anti inflam. PGEs, reducing TNF, etc, makes it
acualy reduce whole body oxidative stress while n-6 lipids increase
oxidatibe stress.
This information has to be taken in context however and does not really
tell us that we should not worry about taking additional anti oxidants. It
just appears than n-3 lipids dont increase oxidative stress as one would
expect, the effects are far more complicated than simple PUF status, and
anti oxidants shuold always be taken with PUFS.
>
>
>
> --
> Matti Narkia
--
Will Brink
__________________
http://www.brinkzone.com/
http://www.healthandmuscle.com/
Will Brink
"John 'the Man'" <DeMan[5]@hotmail.com> wrote:
>
> Furthermore, no one should give the time of day, to any study that ain't "in
> vivo."
It was in vivo nim rod.
Will Brink
<jwwr...@livingston.net> wrote:
> --------------2359342AB63BEA41D85FC6D1
> Content-Type: text/plain; charset=x-user-defined
> Content-Transfer-Encoding: 8bit
>
> So i checked the med refs and oxidant stress seems to be used the same
as oxidative stress,
It is.
> i.e., stress on
> cells. What do you conclude from the articles you posted? Do you think
ingestion of PUFA's increase
> oxidant/oxidative stress? I do,
No. It tells us n-3 lipids reduce it while n-6 increase it. So far, thats
what the modern data is pointing to.
> so i limit all fat intake.
Wrong. Limit n-6 in favor of n-3 and take your anti oxidants.
>I'll take the chance that no excess fat is better
> than taking antioxidants above rda's.
Oh, nothing like those rda's to protect our health. Geez.
John 'the Man'
news:wbrink-2408...@user-2ive1h6.dialup.mindspring.com...
> In article <ov30qskrkvr3r4fpd...@4ax.com>, Matti Narkia
> <mn...@iname.com> wrote:
> > Mori TA, Puddey IB, Burke V, Croft KD, Dunstan DW, Rivera JH, Beilin LJ.
> > I just happened to find a Medline abstract of a ne study which found
that
> > daily fish meals together with either EPA or DHA _reduced_ oxidative
> > stress in vivo.
> Interesting study. There is other data to support that n-3 lipids actualy
> reduce oxidative stress. Its been assumed that the simple stucture of n-3
> lipids, being PUFS, gave them the potential to increase oxidative stress.
> However, as always, it turns out to be far more comlex than that. n-3
> lipids having effects on anti inflam. PGEs, reducing TNF, etc, makes it
> acualy reduce whole body oxidative stress while n-6 lipids increase
> oxidatibe stress.
So nim rod, Do you take your Omega-3 without any Vitamin E?
If NOT, then shut up!
> This information has to be taken in context however and does not really
> tell us that we should not worry about taking additional anti oxidants. It
> just appears than n-3 lipids dont increase oxidative stress as one would
> expect, the effects are far more complicated than simple PUF status, and
> anti oxidants shuold always be taken with PUFS.
So nim rod, n-3 lipids incresase antioxidant stress to the point where they
require additional antioxidants? They just do NOT do as much damage as
Trans Fatty Acids PUFA, do? Tell me something that I don't know!
So nim rod, "anti oxidants should always be taken with PUFS?" Tell me
something that I have NOT already stated!
Gee, that is what I stated from Day-One. You dumb Ass Twits can play all
the word games that you want to. And, Matti can continue to post 1,000's of
irrelevant abstracts.
Nothing will change the fact, that consuming accessive amounts of Omega-3
EFAs is counter productive to your antioxidant program, because they are
PUFS.
Nothing will change the fact, that this amateur has once again again, proven
the Scientific Want-a-Bees to be total fools without a lick of common sense.
Martin E. Lewitt
jwwright <jwwr...@livingston.net> wrote:
>Good for you. I think i said that i tried the atkin's diet and i can't shit with the atkins.
>There's not enough fiber and no carbos to hold the water in the gut. Clear now?
It probably was difficult for people to to guess that you were
operating under this misunderstanding until you shared it.
Fibre is not limited on low carb, only the non-fibre carbs
count. For example, almonds rate as almost zero carbs because
of this. Also if by "gut" you mean "stomach" there is no
need to hold a low carb meal in the stomach. The glucose/amylin
axis that delays stomach emptying is part of the body's
attempt to keep glucose in the blood below damaging
levels. While that sloshing feeling is admittedly
exciting, you must admit that it is probably not worth
risking ones health, and after experiencing it a few times
it starts to get old. Though this is a subjective
judgement, perhaps for you, each time is as the first.
-- Martin
--
Personal, not work info: Martin E. Lewitt My opinions are
Domain: lew...@swcp.com P.O. Box 729 my own, not my
Hm phone: (505) 281-3248 Sandia Park, NM 87047-0729 employer's.
Matti Narkia
<s7p8qscftvi1qdkhu...@4ax.com> Matti Narkia <mn...@iname.com>
wrote:
Deficiencies of omega 3 fatty acids in general may result in
hypertriglyceridemia, high blood pressure, a tendency to form blood clots
due to platelet stickiness, inflammation in a variety of body tissues,
cutaneous disorders, (especially dry skin), tissue swelling (edema),
deterioration in mental function, general disorders of immune function and
changes with a tendency to reductions in the metabolic rate of the body.
Alpha-linolenic acid deficiency has been associated with central nervous
system changes, including behavioral problems, paraesthesia (pins and
needles in the arms and legs), motor incoordination, muscle weakness,
impairment in learning ability, visual loss, and growth retardation.
--
Matti Narkia
Matti Narkia
<39A549E9...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>I don't think that indicates the noise of the measurement, but rather the accuracy of the math comparison
>of the data.
Well, if we have significant difference with P<0.05, it means that with
95 % probability the difference is real and not due to chance.
Calculations of the significance test values include in one way or other
the calculation of the variation in measurements, i.e. noise. When noise
increases relative to the size of the difference it becomes more and more
difficult to achieve significance, and vice versa, when the difference is
large enough compared with noise, it becomes significant.
--
Matti Narkia
Matti Narkia
<39A43D7F...@livingston.net> jwwright <jwwr...@livingston.net>
wrote:
>Well, i guess one of the symptoms of a deficiency in w3's is not being able to
>understand why i need them. Or maybe i get enough in the little bit of soy oil i
>eat?
>
If you take 14 g of soy oil/day that gives you 0.95 g of alpha-linolenic
acid (LNA), but no other omega-3 fatty acids. Recommended (by A Simopoulos
et al.) adequate intake of LNA is 2.22 g/day.
--
Matti Narkia
jwwright
over long time, that you can't see. And that fat is the thing that shortens life.
Regards.
Susan Fein wrote:
> x-no-archive:yes
>
> In article <39A54A79...@livingston.net>, jwwright
> <jwwr...@livingston.net> writes:
>
> >Good for you. I think i said that i tried the atkin's diet and i can't shit
> >with the atkins.
> >There's not enough fiber and no carbos to hold the water in the gut. Clear
> >now?
> >
>
> I became increasingly IR on Ornish, with worsening labile HTN, and developed
> PCOS, too. Restricting carbs is the only dietary measure to help *me* with
> HTN, but YMMV.
>
> FWIW, Atkins induction diet is not the only way to low carb, and clearly, it's
> not good for you in particular.
>
> Susan
jwwright
what seems to be the req'd amount, like Matti showed? ~i Tbls soy, 1/2 tsp Cod
liver oil?
Regards.
Will Brink wrote:
> In article <ov30qskrkvr3r4fpd...@4ax.com>, Matti Narkia
> <mn...@iname.com> wrote:
>
> > Mori TA, Puddey IB, Burke V, Croft KD, Dunstan DW, Rivera JH, Beilin LJ.
> > I just happened to find a Medline abstract of a ne study which found that
> > daily fish meals together with either EPA or DHA _reduced_ oxidative
> > stress in vivo.
> >
>
> Interesting study. There is other data to support that n-3 lipids actualy
> reduce oxidative stress. Its been assumed that the simple stucture of n-3
> lipids, being PUFS, gave them the potential to increase oxidative stress.
> However, as always, it turns out to be far more comlex than that. n-3
> lipids having effects on anti inflam. PGEs, reducing TNF, etc, makes it
> acualy reduce whole body oxidative stress while n-6 lipids increase
> oxidatibe stress.
>
> This information has to be taken in context however and does not really
> tell us that we should not worry about taking additional anti oxidants. It
> just appears than n-3 lipids dont increase oxidative stress as one would
> expect, the effects are far more complicated than simple PUF status, and
> anti oxidants shuold always be taken with PUFS.
>
> >
> >
> >
> > --
> > Matti Narkia
jwwright
cod-liver oil?
regards.
Will Brink wrote:
jwwright
measurement. Do you use the resting value from this morning, this afternoon, after exercise, after eating
Chinese food, or what. These are all diff and can vary as much as 20 mmhg. There is no such thing as a
controlled measurement of BP, period.
Regards.
jwwright
lived in caves, mine in trees.
Regards.
"Martin E. Lewitt" wrote:
> In article <39A54A79...@livingston.net>,
> jwwright <jwwr...@livingston.net> wrote:
> >Good for you. I think i said that i tried the atkin's diet and i can't shit with the atkins.
> >There's not enough fiber and no carbos to hold the water in the gut. Clear now?
>
Will Brink
"John 'the Man'" <DeMan[5]@hotmail.com> wrote:
> "Will Brink" <wbr...@earthlink.net/NOSPAM> wrote in message
> news:wbrink-2408...@user-2ive1h6.dialup.mindspring.com...
>
> > In article <ov30qskrkvr3r4fpd...@4ax.com>, Matti Narkia
> > <mn...@iname.com> wrote:
>
> > > Mori TA, Puddey IB, Burke V, Croft KD, Dunstan DW, Rivera JH, Beilin LJ.
> > > I just happened to find a Medline abstract of a ne study which found
> that
> > > daily fish meals together with either EPA or DHA _reduced_ oxidative
> > > stress in vivo.
>
> > Interesting study. There is other data to support that n-3 lipids actualy
> > reduce oxidative stress. Its been assumed that the simple stucture of n-3
> > lipids, being PUFS, gave them the potential to increase oxidative stress.
> > However, as always, it turns out to be far more comlex than that. n-3
> > lipids having effects on anti inflam. PGEs, reducing TNF, etc, makes it
> > acualy reduce whole body oxidative stress while n-6 lipids increase
> > oxidatibe stress.
>
> So nim rod, Do you take your Omega-3 without any Vitamin E?\
You are too stupid for words. Guess they didnt teach reading skills in
those crummy schools you went to.
>
> If NOT, then shut up!
Blow me.
>
>
> > This information has to be taken in context however and does not really
> > tell us that we should not worry about taking additional anti oxidants. It
> > just appears than n-3 lipids dont increase oxidative stress as one would
> > expect, the effects are far more complicated than simple PUF status, and
> > anti oxidants shuold always be taken with PUFS.
>
> So nim rod, n-3 lipids incresase antioxidant stress to the point where they
> require additional antioxidants?
Nope. Sorry your reading skills and scientific knowledge are so poor you
cant follow me.
> They just do NOT do as much damage as
> Trans Fatty Acids PUFA, do? Tell me something that I don't know!
It appears everything I have said you didnt know and cant even follow.
>
> So nim rod, "anti oxidants should always be taken with PUFS?" Tell me
> something that I have NOT already stated!
>
> Gee, that is what I stated from Day-One. You dumb Ass Twits can play all
> the word games that you want to. And, Matti can continue to post 1,000's of
> irrelevant abstracts.
>
> Nothing will change the fact, that consuming accessive amounts of Omega-3
> EFAs is counter productive to your antioxidant program, because they are
> PUFS.
And nothing will change the fact that your knowledge is very limited and
you attempt to make up for it with an extra big mouth.
>
> Nothing will change the fact, that this amateur has once again again, proven
> the Scientific Want-a-Bees to be total fools without a lick of common sense.
Lick is the key word here and you can lick my nads all you want. If I am a
scientific wannabe be that makes you dog shit. Would you like to post
those journals you have published in for us here? The unversities you have
been asked to speak at? Pro athletes you have worked with? NON internet
publications you have been asked to write for? I Thought not.
> :-)
>
> --
> P.S.: I post comments, I NEVER answer questions on ngs.
Because you lack the knowledge to do so.
Will Brink
<jwwr...@livingston.net> wrote:
> Thanks Will. Can i assume that i don't need to overdose with PUFA's, just eat
> what seems to be the req'd amount, like Matti showed? ~i Tbls soy, 1/2 tsp Cod
> liver oil?
In my view no. Additional n-3 lipids only help with weight loss, health, etc.
jwwright
soy. And then i don't need any fish oil, since i don't have any desaturase problem.
Regards.
jwwright
right (i think) conclusions. We have done this about 3 times in the last 3
yrs. And i keep coming up with i don't have to eat fish (my body doesn't
like tyramines) and that i like. If i were to need more w3, i could just eat
more soy oil, but i get plenty as it is.
Regards.
Nancy HIll
> Would you like to post those journals you have published in for us here?
> The unversities you have been asked to speak at? Pro athletes you have
> worked with? NON internet publications you have been asked to write
> for? I Thought not.
<cheers>
Don't you know, a preposition is not something you're supposed to end
a sentence with, mullethead?
</cheers>
-Nancy
John 'the Man'
> Blow me.
Now, that is a quote that matches your picture on your website. :-)
You are a man who is "Plagued By Body Image Worries."
Check out:
http://www.healthcentral.com/drdean/DeanFullTextTopics.cfm?ID=38928&src=n31
And, Please get help now before it is too late.
You are just an allopathic snob, with absolutely no common sense. Let me
repeat, ... YOU GUYs are just a bunch of snobs. You start out attacking my
position. You make a lot noise. And, then YOU have the nerve to take my
originial position and try to pretend that you are holier than me. YOU GUYs
are really sick!
Furthermore, ... You can not even control your temper.
--
P.S.: I post comments, I NEVER answer questions on ngs.
John Gohde,
John 'the Man'
news:39A559E3...@livingston.net...
> That section does not say what the deficiency causes. Just more Bu-Sh
> (ha).
> Why not just avoid excess fat?
Now, that I had some free time I took a second look at my website and was
able to update my ANSWER, somewhat.
It is now as clear as this complex technical issue can get.
Your question was why is the Omega-3 to Omega-6 ratio important? Or, why is
it important to consume fish, fish oil, or flaxseed oil on a regular basis?
My ANSWER can be found at:
http://home.att.net/~johngohde/Prevention.html
Prevent Specific Health Conditions
Read the section labeled: High rates of Prostanoid / Eicosanoid Synthesis
I added Eicosanoid because that is the term most commonly used on smn.
> Why not just avoid excess fat?
Because excess fat is too general a term. Not all fat is bad for you. You
can consume a lot of fat and still be healthy provided you consume the RIGHT
kind of fat. My ANSWER points out an issue that has been ignored in this
thread.
The first thing that you have to do, is to cut back on your consumption of
saturated fat (i.e. SFA).
> That section does not say what the deficiency causes. Just more Bu-Sh
> (ha).
A short and precise answer would be:
If you are deficient in Omega-3 EFAs then you have an excess of Omega-6
EFAs. Thus, the end result of excess Eicosanoid Omega-6 hormones is an
restriction of blood flow (a factor that leads to hardening of the arteries,
heart disease, and strokes).
By promoting a favorable counter balance of Eicosanoid Omega-3 hormones you
end up promoting blood flow. In short, Omega-3's are blood thinners.
Once again, the specific health effects are global and can not be fully
answered in such a short answer.
jwwright
Regards.
Will Brink
<nch...@nospamcharter.net> wrote:
Wow, what a flame. How will I stand it?
>
> -Nancy
jwwright
eat what we need so we don't add weight, that's ideal. In my case, i added about
40 # over 21 yrs and i thought that wasn't too bad, because i accepted the fact
of aging. Now i know that was silly. I don't "need" to add any weight as i age.
Now i'm lower than oi was in 1973 when i thought i was in perfect shape. I'm
still have more fat than i want so i have to work out to remove it and the loose
skin. Possibly the reason i can get by with so little fat intake right now, is
that i still have 20# or so stored.
BTW, I appreciate your views.
Regards.
Susan Fein wrote:
> x-no-archive:yes
>
> In article <39A676CA...@livingston.net>, jwwright
> <jwwr...@livingston.net> writes:
>
> >As long as you don't eat more than you burn, ok. Otherwise you build up
> >fat/plaque
> >over long time, that you can't see. And that fat is the thing that shortens
> >life.
> >
>
> I don't think any of us want to eat any more of whatever our diet consists of
> than we need for good health, do we?
>
> Susan
Jay Tanzman
...
> oxidant/oxidative stress? I do, so i limit all fat intake. I'll take
the chance that no excess fat is better
> than taking antioxidants above rda's.
First of all, most antioxidants don't have RDAs. Secondly, for those
that do -- vitamins C and E -- the RDAs were not established with the
vitamins' antioxidant properties in mind. Rather, they are intended to
prevent frank nutritional deficiency diseases. Considering the
importance of vitamin C as an antioxidant, many nutritionists now
consider its RDA to be too low.
Jay
Sent via Deja.com http://www.deja.com/
Before you buy.
jwwright
Regards.