Re: Cold-water fish, hot questions ;)

"montygram" <[email hidden]> schrieb im Newsbeitrag
news:[email hidden]...

Quoted message said:

Long chain omega 3 PUFAs, such as EPA and DHA, are only "beneficial"
for a short period of time

Citation please.

Quoted message said:

due to their inhbition of the metabolization
of the long chain and very dangerous omega 6 PUFA, arachidonic acid.
Because it is assumed that your diet is high in omega 6s, as almost all
Americans' diets are these days, you are being told to "supplement"
with toxic substances with EPA/DHA.

Told to supplement by whom is the question.
The current official recommendations do not suggest supplementation.

Quoted message said:

A recent study, for example, found
substantial immune system suppression from "moderate" amounts of EPA.
You need to worry at least as much about toxicity from the EPA/DHA as
you do metals/pollutants. In fact, these fatty acids make your body
much less resistant against various metals/pollutants. A recent study
did not find the iron overload "diseases" among Asians on coconut oil
diets, for example. Search this group for montygram and read through
some of my posts for mor details. If you have any questions, feel free
to ask.

On 8 Dec 2005 17:58:10 -0800, montygram wrote in
<news:[email hidden]> on
sci.med.nutrition :

Quoted message said:

Long chain omega 3 PUFAs, such as EPA and DHA, are only "beneficial"

So, they are "beneficial". That's something... 😉

Quoted message said:

for a short period of time due to their inhbition of the metabolization
of the long chain and very dangerous omega 6 PUFA, arachidonic acid.

If long chain omega 3 PUFAs counterbalance omega 6 PUFAs (I read of
some 1:5 / 1:6 ratio recommendations, by the way), why is it a "short
period" effect?

Quoted message said:

Because it is assumed that your diet is high in omega 6s, as almost all
Americans'

Well, a few of us in this newsgroup are not from the States. 🙂
Anyway, I gather that a typical today's Western diet is high in omega
6s, not just in the USA.
Even if you were right, and the "beneficial" effect of LC n-3s was
just that, i.e. making up for the omega 6s in a typical Western diet,
would that be a Good thing or a Bad thing? 😉

Quoted message said:

diets are these days, you are being told to "supplement"

In fact, the ISSFAL statement states quite the contrary: "This intake
[500mg EPA+DHA] is both safe and achievable by diet alone".
They say "by diet", not supplements.

Here is a bunch of other national and international recommendations:
ISTM they don't exceed 500 mg per day, for healthy people.
http://www.issfal.org.uk/welcome/GlobalRecomendations.asp

Quoted message said:

with toxic substances with EPA/DHA.

A report from AFSSA (Agence française de sécurité sanitaire des
aliments, the French equivalent of the US FDA) states that no
remarkable side effects were observed in diets with up to 2 grams per
day of EPA+DHA, even on a long term basis ("en administration
prolongée et sans que des effets latéraux notables ne soient
signalés"😉.

(in French, sorry)

http://www.afssa.fr/ftp/afssa/basedoc/rapportomega3.pdf
http://www.afssa.fr/ftp/afssa/basedoc/Dossier.pdf

[...]
Limite maximale d'apport

La rareté des données disponibles sur les effets d'une ingestion
chronique de quantités massives d'acides gras oméga 3 n'a pas permis
de déterminer avec certitude une limite de sécurité pour ces
nutriments. Dans les études répertoriées, un allongement du temps de
saignement (critère intermédiaire) est observé dans des situations
d'apports en acides gras oméga 3 élevés (jusqu'à 9 g de EPA et DHA
par jour), sans toutefois qu'une influence substantielle sur le
risque hémorragique n'ait été mise en évidence dans la population
générale. Toutefois, dans une optique de précaution maximale et afin
de ne pas encourager un enrichissement massif et généralisé des
aliments en acides gras oméga 3, le groupe de travail a opté pour
l'établissement d'une limite maximale d'apport, qui devra être
considérée comme un niveau d'apport quotidien au delà duquel
l'intérêt nutritionnel des acides gras oméga 3 n'est plus avéré. Il
ne s'agit pas d'une limite de sécurité c'est à dire d'un apport au
delà duquel un risque sanitaire apparaît. En raison des capacités
d'élongation limitées de l'acide alpha-linolénique (rendement de
conversion en EPA et DHA faible), une limitation des apports en acide
alpha-linolénique ne saurait être recommandée dans les conditions
habituelles de consommation. En ce qui concerne les AGPI-LC (EPA et
DHA), une limite maximale d'apport a donc été établie à environ 2
g/jour. Cette valeur est proche des apports moyens mis en oeuvre dans
les études épidémiologiques, en administration prolongée et sans que
des effets latéraux notables ne soient signalés (valeur proche de
celles observées dans les populations ayant d'importants niveaux de
consommation de produits marins). Il faut noter qu'aux USA (Food and
Drug Administration), le statut GRAS (Generally recognized as safe)
est accordé aux huiles pour lesquelles les apports journaliers en EPA
et DHA sont estimés à moins 3 g/jour. En outre, le groupe de travail
préconise que la teneur en AGPI-LC par unité de consommation
journalière de l'aliment enrichi soit inférieur à 100 % de l'ANC pour
l'homme adulte, des teneurs supérieures étant considérées comme
hasardeuses. Le dossier justificatif du pétitionnaire devra donc
intégrer des données de simulation relatives au respect de la limite
maximale d'apport.

Quoted message said:

A recent study, for example, found
substantial immune system suppression from "moderate" amounts of EPA.

What amount is a "moderate" amount?

Quoted message said:

You need to worry at least as much about toxicity from the EPA/DHA as
you do metals/pollutants. In fact, these fatty acids make your body
much less resistant against various metals/pollutants. A recent study
did not find the iron overload "diseases" among Asians on coconut oil
diets, for example. Search this group for montygram and read through
some of my posts for mor details. If you have any questions, feel free
to ask.

It would surprise me that the omega 3 fatty acids found in so many
foods (vegetables have no long chain omega 3s but contain short chain
omega 3s, and from those our body can make some long chain ones,
right?), were to reveal toxic for a species that has been consuming
them since ever, AFAIK.

--
Enrico C

"Spock, beam him up!"

I have cited the studies before, which is why I said to search the
group for montygram. The same people say the same things, over and
over again. Many of them are likely industry shills, who want you to
buy their "supplements," even though the evidence points to avoiding
these toxic substances. If you choose to listen to them, you will be
the one who suffers, not me.

Keep this in mind: they never answer my questions, they fail to cite
experiments that are on point, and most significantly, they
misinterpret the evidence. I have put forth an explanation of the
data, along with proposals for experiments that would demonstrate
whether my explanation is accurate or not, but they will not even
explain why they don't want to take me up on any of these offers. We
generally agree on the data, but differ on the interpretation. If you
want, you can do your own experiment: get a couple dozen feeder mice
and feed half a diet of 30 percent canola and fish oil, and the other
half fresh coconut oil. Give them the same protein/carb sources and
just a basic vitamin/mineral supplement, and then see which group lives
longer. It's as simple as that. Before you go spending a lot of money
on supplements that will damage your body severely, do the experiment
and see the cancer and the terrible mortality rates among the canola
and fish oil group.

I will cite a couple of relevant studies here, but it's interesting
that when I post a bunch of studies, I get attacked for posts that are
"too long." And when I ask the attackers/shills to post evidence, they
ignore me or post a study that usually demonstrates the opposite of
what they content.

In this study, you see that olive oil, by itself, will not help. You
need to avoid omega 6s. You can use the omega 3s to inhibit LTB4
production, but then other toxic metabolites will be produced. The
evidence can be found at www.pubmed.com Search for neuroprostanes DHA
for example, and you will find, for example:

Chem Phys Lipids. 2004 Mar;128(1-2):117-24.

Isoprostanes and related products of lipid peroxidation in
neurodegenerative diseases.

Montine KS, Quinn JF, Zhang J, Fessel JP, Roberts LJ 2nd, Morrow JD,
Montine TJ.

Department of Pathology, University of Washington, Harborview Medical
Center, Box 359791, 325 9th Ave., Seattle, WA 98104, USA.

Lipid peroxidation is a major outcome of free radical-mediated injury
to brain, where it directly damages membranes and generates a number of
oxidized products. Some of the chemically and metabolically stable
oxidation products are useful in vivo biomarkers of lipid peroxidation.
These include the isoprostanes (IsoPs) and isofurans (IsoFs), derived
from arachidonic acid (AA), and neuroprostanes (NeuroPs), derived from
docosahexaenoic acid (DHA). We have shown increased levels of IsoPs,
NeuroPs, and IsoFs in diseased regions of brain from patients who died
from advanced Alzheimer's disease (AD) or Parkinson's disease (PD).
Increased cerebrospinal fluid (CSF) levels of IsoPs are present in
patients with AD or Huntington's disease (HD) early in the course of
their illness, and CSF IsoPs may improve the laboratory diagnostic
accuracy for AD. In contrast, quantification of IsoPs in plasma and
urine of AD patients has yielded inconsistent results. These results
indicate that brain lipid peroxidation is a potential therapeutic
target early in the course of AD and HD, that CSF IsoPs may aid in the
assessment of anti-oxidant experimental therapeutics and laboratory
diagnosis of AD.

Here's the study about olive oil not inhibiting AA metabolization:

Cleland, L.G.,

Clinical and Biochemical Effects of Dietary Fish Oil Supplements in
Rheumatoid Arthritis.

This paper reports the results of a double blind trial of fish oil
in RA. The investigators gave 18 Maxepa capsules per day for 3 months
to 60 RA patients. The Maxepa patients showed a significant drop in the
tender joint score, from 13 to 9.5, compared to a drop from 13 to 12 in
the placebo(olive oil) group. Grip strength was significantly increased
in the Maxepa group, but not in the olive oil group. Biochemical
measures showed a reduction in the generation of the inflammatory
leukotriene LTB4 in the Maxepa patients compared to the olive oil
group.

J.Rheumatol.,1988, 15;1471-5.

Here's a sense of what happens "long term:

Kremer, J.B., & Bigaouette,J.

Effects of manipulation of dietary fatty acids on clinical
manifestations of rheumatoid arthritis.

37 RA patients took part in a 12 week prospective, double blind study.
17 had a high pufa /low saturated fat diet with added MaxEPA (10g/d).
20 acted as controls,and had a normal diet with less pufa, together
with placebo capsules. At 12 weeks the trial group had less morning
stiffness, and fewer tender joints (6.4v9.0). At follow up 4-8 weeks
later,the MaxEPA group were significantly worse than the control group
for pain and overall condition. The control group was better for
morning stiffness & tender joints on follow up...

The Lancet,1985 Jan 26:i, 184-7.

Instead, if you avoid omega 3s and 6s, you don't have to worry about
any of this, nor about "chronic disease," for example:

Adkisson, H.D., Tranik,T.M., & Wuthier,R.E.

Relationship of cartilage Mead acid levels to aging and development of
osteoarthritis.

The authors studies the relationship of cartilage mead acid levels to
aging and development of osteoarthritis. They looked at the fatty acid
status of weight-bearing and non-weight bearing cartilage from autopsy
specimens, or from surgical procedures, in various ages and disease
states. Young cartilage is characterised by the presence of high levels
of 20:9 w-9, Mead acid, indicating a relative deficiency of EFA.
Skeletal muscle from the same subjects showed normal EFA levels, and no
Mead acid. Age decreases the Mead acid level and increases the EFA
level, with weight-bearing cartilage having more EFA and less Mead acid
than costal tissues. Cartilage from osteoarthritis affected joints
showed even lower Mead acid levels and even higher w-6 EFA levels,
leading the authors to speculate that accumulation of w-6 EFAs in
cartilage might predispose towards the development of OA, and that the
presence of Mead acid might somehow be protective. They also speculate
that weight-bearing cartilage might be better vascularised than costal
tissue.

Poster Presentation at the Third International Conference on Essential
Fatty Acids and Eicosanoids, Adelaide, Australia March 1 1992

Basically, what has happened over the last few decades is that
"nutritional science" became established, and they wanted a "turf" of
their own, so they ignored biochemistry, which is truly science, unlike
the nonsense that usually passes for science in the field of
"nutrition." One of the worst examples is the "essential fatty acid"
claim, derived from a rat study in 1930, and just about as flawed as an
experiment could be. You can read my other posts for all the details.
It was totally repudiated in 1948 - see the Britannica Book of the Year
for 1948 - but that doesn't stop all the major "nutritional science"
textbooks from citing it to this very day. And often, it is the only
study cited for the "EFA" claim.

Other studies that have been done since 1948 have confirmed that omega
3s and 6s are not "esssential," yet people keep citing them. For
instance, in one experiment, healthy kittens were produced, even though
the mother cat received no "EFAs." I have proposed doing an on point
experiment, where pregnant cats are fed mice that have Mead acid in
them rather than omega 3s or 6s. The cats could pick apart the mice
and eat whatever they wish, as they would in the wild. I am willing to
"bet" my own money that almost all or all of the kittens would survive
and be in fine health. Of course, nobody is interested in taking me up
on any of my offers, apparently because they are industry shills,
formally or informally, and do not want to be "shown up" and lose money
at the same time. They would probably lose their jobs as well.

Now the "ball is in your court," my friend. I am here for you, but
it's time you started thinking for yourself and not make any
assumptions. I am providing you with a framework in which to
understand the data. If you take the time to research and think this
through, you will see that no other framework, if it exists, explains
the data nearly as well. I have challanged the attackers to put forth
a scientific hypothesis for the "EFA" claim, but they are not even able
to do that - a sure sign of a bogus notion.

montygram said:

If you
want, you can do your own experiment: get a couple dozen feeder mice
and feed half a diet of 30 percent canola and fish oil,

Why only these two? Seems a very artificial diet.

Quoted message said:

and the other
half fresh coconut oil. Give them the same protein/carb sources and
just a basic vitamin/mineral supplement, and then see which group lives
longer. It's as simple as that. Before you go spending a lot of money
on supplements that will damage your body severely, do the experiment
and see the cancer and the terrible mortality rates among the canola
and fish oil group.

Yes, that's the scientific method isn't it? Why do the experiment when
you already "know" the answer?

Quoted message said:

Lipid peroxidation is a major outcome of free radical-mediated injury
to brain, where it directly damages membranes and generates a number of
oxidized products. Some of the chemically and metabolically stable
oxidation products are useful in vivo biomarkers of lipid peroxidation.
These include the isoprostanes (IsoPs) and isofurans (IsoFs), derived
from arachidonic acid (AA), and neuroprostanes (NeuroPs), derived from
docosahexaenoic acid (DHA).

Well, once again you've posted something you think supports you but
actually contradicts you. The above paragraph says that AA is
chemically and metabolically stable, the exact opposite of your normal
tirade.

Quoted message said:

Other studies that have been done since 1948 have confirmed that omega
3s and 6s are not "esssential," yet people keep citing them.

How about you cite these studies (plural) you claim confirm
non-essentiality first?

Quoted message said:

instance, in one experiment, healthy kittens were produced, even though
the mother cat received no "EFAs."

If you looked at the kittens they'd have EFA in them. Also from what I
recall of the paper the majority of cats didn't have healthy kittens.

Quoted message said:

I have challanged the attackers to put forth
a scientific hypothesis for the "EFA" claim, but they are not even able
to do that - a sure sign of a bogus notion.

You've been told many times that the problem is you don't understand
what "essential" means in a biochemical context. Whatever procedure or
test would satisify you that vitamin C is essential could be done for
EFA as the "essential" is the same.

MattLB

On 12 Dec 2005 03:47:16 -0800, MattLB wrote in
<news:[email hidden]> on
sci.med.nutrition :

Quoted message said:

You've been told many times that the problem is you don't understand
what "essential" means in a biochemical context. Whatever procedure or
test would satisify you that vitamin C is essential could be done for
EFA as the "essential" is the same.

What is the "essential" minimum intake of omega 3s for adults?

In the "Dietary Reference Intakes 2002/2005" I read an Adequate Intake
for males of 1.6 g/d, and an AMDR-Acceptable Macronutrient
Distribution Range of 0.6 to 1.2% of total energy.

That DRI recommendation, though, refers to "n-3 polyunsaturated fatty
acids (alfa-linolenic acid)", from "selected food sources" like
"Vegetable oils such as soybean, canola, and flax seed oil, fish oils,
fatty fish, with smaller amounts in meats and eggs."

--
Enrico C

* cut the ending "cut-togli.invalid" string when replying by email *