EFAD protects kidneys
Taka
Essential fatty acid deficiency normalizes function and histology in
rat nephrotoxic nephritis
Kihito Takahashi, Tetsuo Kato, George F Schreiner, Joan Ebert and
Kamal F Badr
Essential fatty acid deficiency normalizes function and histology in
rat nephrotoxic nephritis. The central lipid abnormality in essential
fatty acid deficiency (EFAD) is the lack of availability of
arachidonic acid. To examine the role of total eicosanoid's
biosyntheses in the pathology and pathophysiology of
glomerulonephritis, EFAD was induced in weanling rats, which were then
subjected to antiglomerular basement membrane antibody (NTS)-induced
injury in adulthood. Glomerular dynamics (as assessed by
micropuncture), quantitative histology, and eicosanoid generation
rates were measured at two hours and two weeks post-NTS, and compared
to those of standard diet-fed (STD) controls. Two hours post-NTS, and
despite the occurrence of proteinuria in both EFAD and STD animals,
glomerular dynamics were essentially normal in EFAD rats, whereas STD
animals had reduced values for glomerular filtration rate (GFR) and
renal plasma flow rate (RPF). At two weeks, severe histologic changes
were observed in STD animals including mesangial and stalk
hypercellularity, moderate sclerosis, and interstitial nephritis,
coupled with heavy proteinuria and reduced GFR and RPF. In dramatic
contrast, EFAD rats displayed totally normal glomerular structures and
functions. In parallel, glomerular generation rates of prostaglandin
E2 and thromboxane A2 were suppressed markedly in EFAD rats. Thus,
EFAD confers complete protection against the histopathologic and
functional sequelae of immune-initiated injury in the glomerulus. The
data suggest that the initial wave of complement-induced neutrophil
infiltration (with resultant proteinuria) is not sufficient to
perpetuate injury into the more destructive chronic phases. The
results provide strong impetus for the design of more specific
interventional therapies targeting the various enzymes and products of
arachidonic acid metabolism in the attempts to control glomerular
inflammation.
SOURCE: http://www.nature.com/ki/journal/v41/n5/abs/ki1992186a.html
Essential Fatty Acid Deficiency Ameliorates Acute Renal Dysfunction in
the Rat
after the Administration of the Aminonucleoside of Puromycin
The administration of the aminonucleoside of puromycin
(PAN) to rats causes the nephrotic syndrome that is associated
with an acute decline in renal function, and an interstitial
infiltrate.
We examined whether essential fatty acid deficiency
(EFAD), which inhibits macrophage infiltration in glomerulonephritis,
affects PAN-induced renal dysfunction.
Both control and EFAD rats developed proteinuria that
resolved over 28 d. After PAN administration, there was a
prominent infiltration of macrophages in rats fed a normal diet.
The infiltrate was prevented by the EFAD diet. The absence of
a macrophage interstitial infiltrate was associated with a
significantly
higher C,, in the EFAD rats than in controls at 7 d
(5.21±1.19 versus 0.39±0.08, P < 0.002 ml/min/kg BW). In
addition, CPAH fell to < 10 ml/min/kg BW by day 7 in controls,
but remained the same as normal in the EFAD. After administration
of PAN to control rats, there was no increase in urinary
thromboxane excretion or an increase in glomerular thromboxane
production. Furthermore, the effect of EFAD could not
be mimicked by the administration of a thromboxane synthase
inhibitor. Irradiation-induced leukopenia in rats on a normal
diet markedly improved glomerular filtration and renal blood
flow in acutely nephrotic rats.
EFAD prevents the interstitial cellular infiltrate and the
renal ischemia associated with experimental nephrosis. The
recruitment of mononuclear cells into the kidney following
PAN directly contributes to the decline in renal function. (J.
Clin. Invest. 1990. 86:1115-1123.)
SOURCE: http://www.jci.org/articles/view/114816/files/pdf
Essential fatty acid deficiency reduces the inflammatory cell invasion
in rabbit hydronephrosis resulting in suppression of the exaggerated
eicosanoid production.
S M Spaethe, M S Freed, K De Schryver-Kecskemeti, J B Lefkowith and P
Needleman
The rabbit hydronephrotic kidney (HNK) is a model of renal
inflammation characterized by a marked increase in arachidonic acid
metabolism which is temporally associated with an inflammatory cell
influx into the injured tissue. The HNK exhibits an exaggerated
elaboration of eicosanoids ex vivo in response to inflammatory
agonists (bradykinin and the chemotactic peptide, n-formyl-methionyl-
leucyl-phenylalanine). Essential fatty acid (EFA) deficiency [i.e.,
deprivation of (n-6) fatty acids] attenuated markedly the ex vivo
elaboration of eicosanoids and prevented the enhancement of the
microsomal cyclooxygenase and thromboxane synthase activity associated
with 3 days of ureter occlusion. In contrast, postobstructive release
prevented the ex vivo elaboration of eicosanoids by the HNK. When the
HNK was assessed morphologically by electron microscopy, both EFA
deficiency and postobstructive release markedly reduced the population
of interstitial macrophages normally seen in the HNK. Apparently, EFA
deficiency blocked the influx of macrophages whereas postobstructive
release resulted in the efflux of macrophages from the HNK. Because
EFA deficiency has been shown to inhibit the synthesis of leukotriene
B4, a potential chemotaxin, it was hypothesized that EFA deficiency
might prevent the influx of macrophages due to an inhibition of
leukotriene B4 synthesis. Indeed, EFA deficiency suppressed the
synthesis of this eicosanoid in blood whereas prostaglandin E2 and
thromboxane A2 production were unaffected. In summary, this study
demonstrates that EFA deficiency prevents the influx of macrophages
into the HNK and prevents the enhanced arachidonate metabolism which
normally occurs after ureter obstruction. A potential role for
leukotriene B4 as a chemotactic agent in this model of renal
inflammation also is suggested.
SOURCE: http://jpet.aspetjournals.org/content/245/3/1088.abstract
J. Clin. Invest. 80(4): 947-956 (1987). doi:10.1172/JCI113187.
Essential fatty acid deficiency depletes rat glomeruli of resident
macrophages and inhibits angiotensin II-induced eicosanoid synthesis.
J B Lefkowith and G Schreiner
Essential fatty acid (EFA) deficiency exerts a beneficial effect on
immune-mediated glomerulonephritis, preventing both the tissue injury
and consequent mortality. Because both macrophages and eicosanoids are
thought to play pathogenic roles in glomerulonephritis, and because
macrophages play an important role in modulating arachidonate
metabolism at sites of renal injury, the effects of EFA deficiency on
the population of resident glomerular macrophages and on glomerular
eicosanoid generation were examined. EFA deficiency led to a striking
reduction in the number of resident glomerular macrophages and a
corresponding reduction in the number of resident glomerular Ia+
cells. This phenomenon was not strain-specific, was not due to a
decrease in circulating monocytes, was not a function of changes in
cell surface labeling characteristics, and was not restricted to a
specific subset of glomeruli. In addition, EFA deficiency affected
other areas of the renal cortex: a comparable depletion of
interstitial macrophages and Ia+ cells was also observed. In
conjunction with the decrease in glomerular macrophages seen with the
deficiency state, a marked decrease in both basal and angiotensin II-
stimulated glomerular eicosanoid production was noted. In contrast to
angiotensin II, platelet-activating factor-induced eicosanoid
production was not significantly affected by the deficiency state.
These changes in glomerular eicosanoid production could not be
attributed to changes in glomerular cyclooxygenase or reacylation
capacity. Dietary (n-6) fatty acid supplementation, but not (n-3)
fatty acid supplementation, reversed both the decrease in glomerular
macrophages and the diminished eicosanoid metabolism seen with the
deficiency state. Understanding the mechanisms behind the changes in
the glomerular microenvironment induced by EFA deficiency may provide
a basis for elucidating the protective effect of dietary fatty acid
manipulation on immune-mediated glomerulonephritis.
Taka
ignored and patients are fed the life-shortening Omega-3s
instead ... Taka
-------------------------
Essential Fatty Acid Deficiency in Renal Failure: Can Supplements
Really Help?
LOUISE W PECK, PhD, RD
Abnormal fatty acid metabolism may contribute to clinical problems
such as itching, abnormal perspiration, susceptibility to infection,
delayed wound healing, anemia, and increased hemolysis, as seen in
patients with chronic renal failure. A double-blind study of patients
on hemodialysis who received either fish oil, olive oil, or safflower
oil documented that patients may have increased levels of the
proinflammatory prostaglandin PGE2 and that fish oil intervention may
decrease these levels, change the fatty acid profile, improve
hematocrit levels, and improve patient perception of symptoms of
pruritus. J Am Diet Assoc. 1997;97(suppl 2): S150–S153.
SOURCE: http://www.adajournal.org/article/S0002-8223(97)00753-0/abstract
-------------------------------
Omega 3 Fatty Acids and Canine Renal Failure
Omega 3 fatty acids and canine renal failure have been the focus of
recent research into nutritional therapy for dogs. The research
indicates that a diet that is high in omega 3’s benefits dogs with
chronic renal failure in several ways.
Nephrons are the functional unit in the dog’s kidneys. Each kidney
contains hundreds of tiny nephrons, and together they filter the
blood, control the balance between acids and bases and perform other
functions.
At any given time, in a normal kidney, some of the nephrons are
working and some are resting. That gives the dog—or the person—a
functional reserve. Many nephrons must be damaged before the kidney
loses its ability to function well. In most cases, when kidneys fail,
they gradually lose their ability to work. This is chronic renal
failure.
Decreasing Inflammation
The goal of treatment in chronic renal failure is to maximize the
functional ability of the remaining nephrons. Omega 3 fatty acids do
this by decreasing the inflammation in damaged nephrons, enabling them
to work better.
Lowering Blood Pressure
One of the kidney’s functions is to help control blood pressure. The
kidneys do this by secreting powerful hormones that cause the arteries
to constrict, raising the pressure within them. This is adaptive to a
point, because it forces more blood through the kidneys. If it goes
on too long, however, it causes the arteries to become so constricted
that blood cannot get through them.
Omega 3 fatty acids have a counteracting relaxing effect on arteries,
which helps more blood flow through the kidneys.
Opposing Omega 6
One recent study demonstrated that when a dog has chronic renal
failure, excessive amounts of omega 6 fatty acids make it worse.
Omega 3 fatty acids compete with, or oppose, omega 6 fatty acids.
This prevents additional damage from excessive omega 6’s.
Omega 3 fatty acids and canine renal failure are the subject of
ongoing research. Currently, most veterinarians recommend a diet that
is moderately restricted in protein and salt for dogs with chronic
renal failure. An omega-balanced diet, with sufficient omega 3’s, is
also important.
-----------------------------------
Immunoglobulin A Nephropathy
Immunoglobulin A (IgA) nephropathy is a kidney disorder that results
from the deposition of IgA in the glomeruli of the kidney. The cause
of IgA nephropathy is not clear, but progressive renal failure may
eventually develop in 15-40% of patients (171). Since glomerular IgA
deposition results in increased production of inflammatory mediators,
omega-3 fatty acid supplementation could potentially modulate the
inflammatory response and preserve renal function. In a multicenter,
randomized controlled trial, supplementing IgA nephropathy patients
with fish oil (1.8 g/day of EPA + 1.2 g/day of DHA) for two years
significantly slowed declines in renal function (172). Over the 2-year
treatment period, 33% of the placebo group experienced a 50% increase
in serum creatinine (i.e., evidence of declining renal function)
compared to only 6% in the fish oil supplemented group. These results
were sustained over an average of six years of follow-up (173), but
improvements were not observed with higher doses of fish oil (174). A
much smaller 2-year trial found that a low dose of omega-3 fatty acids
(0.85 g/day of EPA + 0.57 g/day of DHA) slowed the progression of
renal disease in high-risk IgA nephropathy patients (175). In
contrast, several studies have failed to find a significant benefit of
omega-3 PUFA supplementation in IgA nephropathy patients (176-179).
Interestingly, fish oil treatment (3 g/day of EPA + DHA) for six
months did not decrease the urinary excretion of inflammatory
mediators in IgA nephropathy patients (180). Two meta-analyses of
randomized controlled trials of fish oil supplementation did not find
evidence of a statistically significant benefit in IgA nephropathy
patients overall (181, 182). Due to the inconsistent results of
available randomized controlled trials, it is not clear whether fish
oil supplementation will prevent the progression of IgA nephropathy in
children or adults (147).
SOURCE: http://lpi.oregonstate.edu/infocenter/othernuts/omega3fa/
montygraham
"infectious" and "non-infectious" disease, because it's the
inflammatory/immune response that having AA in your body makes too
powerful, and hence dangerous.
Taka
actually the organs which truly need the EFAs will retain them despite
of the rest of the body being clinically "deficient". At worst, the
EFAD tissues go into a state of arrest (including the aging program
put on hold!) which is quickly reversible by mild EFA supplementation
such as by introducing the olive oil in the diet. Taka
--------------------------------
Paradoxical conservation of cardiac and renal arachidonate content in
essential fatty acid deficiency.
J B Lefkowith, V Flippo, H Sprecher and P Needleman
The effects of essential fatty acid (EFA) deprivation on the
arachidonate content and phospholipid composition of different tissues
are quite diverse. When C57B1 mice were placed on a fat-free diet,
hepatic liquids were readily depleted of arachidonate. In contrast,
the renal cortex tenaciously retained arachidonate, whereas
surprisingly the heart showed a doubling of its content of
arachidonate. This increase in cardiac arachidonate was due to a four-
fold increase in arachidonylphosphatidylethanolamine (PE). The renal
cortex showed preservation of its arachidonate content in PE,
phosphatidylserine, and phosphatidylcholine. Only phosphatidylinositol
was depleted of arachidonate in heart or renal cortex. Using an in
vivo labeling technique, it was shown that the liver incorporated most
of the [1-14C]arachidonate initially following intraperitoneal
injection. Over 11 days, as levels of labeled arachidonate fell in
liver, the EFA-deficient heart accumulated arachidonate selectively in
PE (8-fold greater than control), and the EFA-deficient renal cortex
accumulated arachidonate in PE, phosphatidylserine, and
phosphatidylcholine (2-3-fold greater than control). This uptake was
shown to be specific for arachidonate over 20:3(n-9). Despite the
conservation of cardiac and renal arachidonate seen with EFA
deficiency, prostaglandin production by the isolated perfused EFA-
deficient heart and kidney was markedly decreased relative to control
in response to specific agonist stimulation with angiotensin II,
although it was equivalent to control in response to nonspecific
stimulation by ischemia. These data suggest that the liver serves to
supply other tissues with arachidonate in EFA deficiency, and that the
heart and renal cortex both contain mechanisms to accumulate
arachidonate selectively in certain phospholipids. However,
phosphatidylinositol, which is uniquely depleted of arachidonate in
heart and renal cortex with EFA deficiency, appears to be the
principal source of arachidonate in response to receptor-mediated
agonists.
SOURCE: http://www.jbc.org/content/260/29/15736.abstract
J Nutr. 1996 Dec;126(12):3040-5.
Dietary essential fatty acid deficiency differentially affects tissues
of rats.
Moussa M, Garcia J, Ghisolfi J, Périquet B, Thouvenot JP.
Groupe d'Etudes en Nutrition Infantile, CHU Purpan, Toulouse, France.
Abstract
Quantitative variations of polyunsaturated fatty acids (PUFA) were
studied in various tissues: red blood cells (RBC), hepatic microsomes,
kidney, skeletal muscle and heart of young rats fed either a control
diet (n = 7) or an essential fatty acid (EFA)-deficient diet (n = 7).
After 4 wk, the EFA-[deficient rats had significantly lower
proportions of (n-6) and (n-3) fatty acids in RBC, hepatic microsomes
and kidney than the control group. Paradoxically, normal proportions
of arachidonic acid [20:4(n-6)] and 5,8,11,14,17-eicosapentaenoic acid
[20:5(n-3)] were retained in heart and skeletal muscle despite
generally lower proportions of the precursors, 18:2(n-6) and
18:3(n-3). Moreover, absolute levels of 20:4(n-6) and 20:5(n-3) in
skeletal muscle of the EFA deficient group were significantly higher
than in controls and 22:5(n-3) and 22:6(n-3) levels were comparable.
This suggests that fatty acid proportions alone, without any
consideration of long-chain polyunsaturated fatty acid quantities, may
not reflect the (n-6) and (n-3) PUFA status of individual tissues.
This study indicates that diet-[induced changes in the PUFA
composition of RBC, which are often used in clinical investigations,
do not fully reflect the changes in the fatty acid composition of
organs, and that individual tissues respond differently to EFA
deficiency. The conservation of proportional and absolute levels of
20:5(n-3) and 20:4(n-6), and the decrease in the more unsaturated
homologues in the heart, suggest that this organ may avidly retain
20:5(n-3) and 20:4(n-6) in order to maintain eicosanoid production.
PMID: 9001372
Taka
-----------------------------
Saturated Fats and the Kidneys
One of the body's most important organs is the kidney. Properly
functioning kidneys are essential for maintaining proper blood volume
and composition; for filtering and excreting or saving various
chemical metabolites; and for helping to maintain proper blood
pressure. Hypertension (high blood pressure) is known to result from
improperly functioning kidneys. Research carried out during the last
few years indicates that both saturated fat and cholesterol play
important roles in maintaining kidney function, as do the omega-3
fatty acids.
The kidneys need stable fats both for their cushioning and as their
energy source. We know that the kidney fat normally has a higher
concentration of the important saturated fatty acids than are found in
any of the other fat depots. These saturated fatty acids are myristic
acid (the 14-carbon saturate), palmitic acid (the 16-carbon saturate),
and stearic acid (the 18-carbon saturate). When we consume various
polyunsaturated fatty acids in large amounts, they are incorporated
into kidney tissues, usually at the expense of oleic acid, because the
normal high level of saturated fatty acids in the kidney fat does not
change.1
A species of rat known to be prone to strokes and to spontaneously
develop hypertension (high blood pressure) has been used to evaluate
effects of different lipids such as plant sterols or cholesterol, and
also fatty acids such as omega-3 or omega-6 fatty acids in the finely
tuned functions of the kidney. These animals are very sensitive to
dietary cholesterol manipulations and a deficiency of cholesterol in
their membranes makes their membranes weak and fragile. When plant
sterols found in vegetable oils are substituted for cholesterol in
their diets, these animals have a shortened life span.2 Also, these
animals are reported to need a proper omega-6 to omega-3 ratio in the
kidney phospholipids. It was further reported that feeding oils high
in omega-6 fatty acids without omega-3 fatty acids resulted in renal
injury, and that feeding oils rich in the omega-3 fatty acids such as
fish oil, perilla oil, and flaxseed oil prolonged the survival time of
this animal.3
The omega-3 fatty acids are recognized as being important, and the
conversion of the flax oil-type omega-3 fatty acid (alpha-linolenic
acid) to the fish oil-type omega-3 fatty acids (EPA and DHA) is
enhanced when the diet contains saturated fat such as coconut oil.
This conversion is hindered when there is extra omega-6 oils in the
diet.4 Injury to the kidney from immune dysfunction (IgA nephropathy)
responds to omega-3 fats (both flax oil-type omega-3 and fish oil-type
omega-3).5 As noted, adding the saturated fats, especially coconut
oil, improves the body's use of omega-3 fatty acids.
Another reason that coconut oil enhances kidney function is because it
supplies myristic acid, the 14-carbon saturated fatty acid.6 Myristic
acid is involved in the signalling from cell membrane receptors
through G proteins and their attachment to membranes. These signalling
proteins require a lipid such as myristic acid to be added to one end
of the protein, a process called myristolation.7
Thus, the fats that we recommend for general good health, namely
various saturated animal fats and tropical oils, along with a
supplement of flax oil, are also specifically helpful for kidney
function. Products containing high omega-6 oils and trans fatty acids
should be avoided.
REFERENCES
1.Suarez et al, Lipids 1996;31:345; Taugbol and Saarem, Acta Vet Scand
1995;36:93
2.Ratnayake, et al, J Nutrition 2000;130:1166
3.Miyazaki et al, Biochim Biophys Acta 2000;1483:101
4.Gerster, Int J Vitam Nutr Res 1998;68:159
5.Kelley, ISSFAL, 2000;7:6
6.Monserrat et al, Res Exp Med (Berl) 2000;199:195
7.Busconi and Denker, Biochem J 1997;328:23
SOURCE: https://www.westonaprice.org/Saturated-Fats-and-the-Kidneys.html
Kofi
> ignored and patients are fed the life-shortening Omega-3s
> instead ... Taka
Is Fox paying you to be an anchor now?
If you're going to lie, at least bother to doctor the evidence. Every
shred of data you cite in your posts points to omega-3's being either
helpful or not harmful to the various conditions under discussion.
Yet you draw the opposite conclusion.
> patients with chronic renal failure. A double-blind study of patients
> on hemodialysis who received either fish oil, olive oil, or safflower
> oil documented that patients may have increased levels of the
> proinflammatory prostaglandin PGE2 and that FISH OIL INTERVENTION
> MAY DECREASE THESE LEVELS, CHANGE THE FATTY ACID PROFILE,
> IMPROVE HEMATOCRIT LEVELS, AND IMPROVE PATIENT PERCEPTION
> OF SYMPTOMS OF PRURITUS
>
> ...
>
> Omega 3 Fatty Acids and Canine Renal Failure
>
> Omega 3 fatty acids and canine renal failure have been the focus of
> recent research into nutritional therapy for dogs. The research
> indicates that a diet that is high in omega 3�s BENEFITS dogs with
> chronic renal failure in several ways.
>
> ...
>
> inflammatory response and preserve renal function. In a multicenter,
> randomized controlled trial, supplementing IgA nephropathy patients
> with fish oil (1.8 g/day of EPA + 1.2 g/day of DHA) for two years
> significantly SLOWED declines in renal function (172).
These people are benefiting from EFAD because of the drop in arachidonic
acid, NOT omega-3's. This is the old prostaglandin 2 vs. prostaglandin
1 pathway argument we always have.
Seriously. You do know that omega-3 fatty acid deficiency in the brain
is associated with schizophrenia and one of the signs of schizophrenia
is the inability to see reality for what it really is? These people
hallucinate, cling to delusions and, in extreme cases, have even been
know to - *gasp* - vote Republican.
Dude. Get help before Obama death panels you.
montygraham
is associated with schizophrenia and one of the signs of
schizophrenia"
Yes, the good old "association." Note that it would be very easy to
do an experiment to determine if it is "AA overload" rather than too
little omega 3s. My great grandparents lived to advanced ages and did
not eat foods that contained more than the tiniest trace amounts of
omega 3s. My grandfather was over 100 and had no signs of any brain
dysfunction or mental impairment, but instead died of complications
from the flu that was going around at the time. I've avoided all
foods that contain more than the tiniest trace amounts of omega 3s
since 2001. Thus, I know that this claim is false, which is why I'm
willing to put my own money up to do a direct experiment on this
specific issue. I will pay if I am wrong, but you Kofi would have to
pay if I am correct. Why not take me up on this offer and we will
settle it once and for all? We can get a lab that is agreeable to
both of us to do the actual experiment after we agree on the design,
with a lawyer holding the money in escrow pending the results. If you
think this is so important, how could you not take me up on such an
offer?
Taka
> > Even if this is as obvious as it could be, the EFAD studies are
> > ignored and patients are fed the life-shortening Omega-3s
> > instead ... Taka
>
> Is Fox paying you to be an anchor now?
>
> If you're going to lie, at least bother to doctor the evidence. Every
> shred of data you cite in your posts points to omega-3's being either
> helpful or not harmful to the various conditions under discussion.
You are short sighted Kofi. I am not talking about any immediate
effects such as the inhibition of inflammation when I say Omega-3 is
harmful. I am talking about the maximal life span of species
(including humans) and the frailty in advanced age. I have presented
numerous evidence about this in my past postings, get e.g. the papers
by "Barja G" in PubMed. Also I have done my personal experiment like
Monty and learned from my injuries suffered in the Omega-6/Omega-3
battle. Now I know that these AA wars can be avoided altogether but I
admit this is difficult for a normal busy working man in a modern
world. You seem smarter, Kofi, then the rest of the herd using just
chemical weapons like fish oil, various antioxidants and NSAIDs. You
employ biological weaponry such as the intestinal parasites and
symbiotic bacteria producing immune suppressants like PGE2 and
saturated fatty acids like butyrate. Yet you are still suffering
injuries from the "reactivated viruses" (triggered by lipoxidative
stress) like the others are getting their gall bladders clogged and
thyroids burned. These are the winning warriors, the losers get
kicked out by cancer and strokes ...
> These people are benefiting from EFAD because of the drop in arachidonic
> acid, NOT omega-3's.
And if you drop arachidonic acid/Omega-6, for what do you need
Omega-3 ? Evidence please! AFAIK there is only 1 peer review paper
on this about an IV girl receiving Omega-3 free infusion having some
neurological problems relieved by adding LNA (but this is still in the
context of Omega-6 and not checked for the Mead acid production).
This paper is being blown out as an evidence that we need Omega-3
supplementation by the Holman et al. and associated gangs.
> This is the old prostaglandin 2 vs. prostaglandin
> 1 pathway argument we always have.
What argument, please specify. Both prostaglandins are nonessential
for life as the experiments with COX-1/2 knockout animals suggest ...
Taka
Taka
> > ignored and patients are fed the life-shortening Omega-3s
> > instead ... Taka
>
> Is Fox paying you to be an anchor now?
>
> If you're going to lie, at least bother to doctor the evidence. Every
> shred of data you cite in your posts points to omega-3's being either
> helpful or not harmful to the various conditions under discussion.
>
> Yet you draw the opposite conclusion.
I draw my conclusion based on what is best to bring me to the very old
age either to be able to benefit from the rejuvenation therapies
proposed e.g. by Aubrey de Grey or make enough money to be able to pay
for my dewar at Alcor. This is the next "evolutionary adaptation" or
going back to the vegetative reproduction if you like. If you prefer
to mutate and reproduce like the salmon dying from massive
lipoxidative stress just hours after mating just keep your right
Omega-6:3 ratios with the total levels set by the modern nutrition and
you will be "fine".
Taka