Omega-3 fatty acids: cancer promoter or preventer?
Michael H.
in flaxseed oil). Some say that they are essential to good health and
help to prevent cancer, and possibly slow existing cancers, whereas I
recently saw a site in which it was claimed that omega-3's increase the
risk of cancer, particularly of the prostate, and promote faster growth
of existing cancers. Flat contradiction.
Does anybody know the real facts on omega-3 fatty acids?
Michael H.
Michael H.
e.g. check out
http://home1.inet.tele.dk/danital/n_3Effects.htm
as versus
http://www.prostatecancer.com/pcdc.html
Michael H.
Michael H.
>
> In a moment of clarity, "Michael H." <zol...@netcom.ca> mentioned:
> prostrate cancer site, and then post the exact URL? Unfortunately, there is no
> search function on that site...
>
I did cut and paste the url, but I forgot the fact that with frames the
url doesn't change, so I'll just cut and paste the part:
(you get there by clicking for the cookbook, which leads to a page with
three choices, and you pick the bottom one, "CLICK HERE for helpful
hints")...here it is:
------------------------------------------------------------------------------------------
Consider fatty acids. Certain fatty acids like alpha-linolenic acid
(ALA) and arachidonic acid make PC cells thrive and
reproduce at a greater rate. But the same cells are killed when
stearic acid is added to the lab dish. What does this
mean for patients concerned about their daily diet? All
polyunsaturated oils are high in ALA or arachidonate
precursors. Avoid flax seed, canola, soybean, safflower, corn,
cottonseed and peanut oil, as well as margarine and
mayonnaise. The monounsaturated coconut, palm and olive oils are low
in "bad" ALA & arachidonate precursors, but
only olive oil is not considered bad for the heart. That makes olive
oil the least of all evils. Try to reduce fat to
10-20% of your calories, but if you need to use fat, olive oil is
considered to be the safest.
Arachidonic acid is found in meat and dairy products. Prostate cancer
patients should avoid red meat, pork and fatty
white meat, cheese, butter, egg yolks, and all milk, yogurt and sour
cream containing fat. And don't be fooled by
"reduced fat" items. Frequently, all of the calories in such items
still come from fat. Read labels! Only "Fat Free"
means what it says.
Now, about the fatty acid that kills PC cells but doesn't increase the
risk of heart disease. Cocoa butter contains
stearic acid, but fat free cocoa does not. It is imperative to use
only chocolate made without milk. The squares of
"bakers chocolate" contain cocoa butter, and therefore stearic acid.
Several companies, like Giradelli and Lindt, make a
dark chocolate candy bar that contains cocoa butter but no milk. Also,
use only dairy free chocolate chips, such as
Chatfield's.
Soy, green tea and lycopenes are also believed to be beneficial for PC
patients and deserve serious attention.
Substitute soy milk for cow's milk, use tofu as a base for milkshakes,
dips, dressings, sauces, puddings and even for
cheese in lasagna recipes. Add tempeh and tofu to casseroles and
chilis, and snack on roasted "soynuts" (which are
soybeans.). Drink tea instead of coffee and green tea is best. Eat
tomatoes for lycopene but be advised that the
lycopene is more easily absorbed when the tomatoes are cooked and a
small amount of olive oil is added to increase
solubility.
With this new knowledge, you can start making dishes that do less or
no harm, and may possibly help. These simple
hints and substitutions are an exciting guide to tasteful eating for
prostate cancer patients.
-------------------------------------------------------------------------------------------
I don't have prostate cancer (that I know of), but being a middle-aged
male looking for an optimal diet, preventing prostate cancer is
obviously a high priority, and I came across this while doing a search
on omega-3 fatty acids. The first url seems more credible just by the
tone of it, but the other tips in the above quoted passage are valid -
green tea, lycopene and soy are health-promoting. Olive oil is reputed
to be the best oil (although generally all fat/oil consumption should be
minimal), but canola oil is also quite high in monounsaturates (but not
as high as olive oil), so I disagree with rejecting canola oil as
unhealthy. I prefer to vary my diet, and not have the same things every
day, and alternate every few days between olive and canola oils, and
sometimes sesame oil.
Omega-3 fatty acids are widely reputed to be good for circulatory
health, prevention of hypertension and heart disease, which is also a
concern.
I take flaxseed oil, and I don't want to stop taking it unless it
definitely poses an increased risk of prostate cancer. It would be
unpleasant to have to choose between protecting your prostate and
protecting your circulatory health. Surely there must be a way to
protect both.
I must say that I DO like the idea of eating chocolate as a health
supplement! :)
Michael H.
Michael H.
>
> "Michael H." <zol...@netcom.ca> wrote:
>
> >> Since you've already seen it, can you find the particular reference in the
> >> prostrate cancer site, and then post the exact URL? Unfortunately, there is no
> >> search function on that site...
> >>
> >(ALA) and arachidonic acid make PC cells thrive and
> > reproduce at a greater rate. But the same cells are killed when
>
> believe. Most possible they menat linoleic acid, not alpha-linoleic
> acid.
>
> EPA on the other hand is an inhibitor of the synthesize of arachidonic
> acid based signals (eicosanoids) and a very good inhibitor with a Km for
> COX II around 1/10 (bind 10 times more tight) and with a Vm around 1/10,
> that is, when COX use EPA as source, they may produce only 1/10 of
> eicosanoids pr time unit as when it use arachidonic acid.
> Since I don't have the enzymic data when using EPA as an inhibitor (the
> figures are when EPA is producing eicosanoids of 3-series where several
> of the products have no biological function, where the 2-series analogue
> has tremendous physiological effects (TXA-3 which is not formed at all
> versus TXA-2 which is making clots) Also DHGLA is a good inhibitor of
> the series-2 eicosanoid synthesis which also form a lot of inactive
> molecules compared to the 2-series.. I have seen many reports who are
> based on the belief that the 1-series eicosanoids has special functions.
> But the most important function is just by giving the COX-enzymes lot of
> work without making any active signals at all
Thanks for the info, although it's way over my head. I've never studied
biochemistry or molecular biology to that extent, so I am still not sure
whether I should be taking flaxseed oil or not. It sounds like a "yes"
to me.
Michael H.
Alf Christophersen
>> Since you've already seen it, can you find the particular reference in the
>> prostrate cancer site, and then post the exact URL? Unfortunately, there is no
>> search function on that site...
>>
>Consider fatty acids. Certain fatty acids like alpha-linolenic acid
>(ALA) and arachidonic acid make PC cells thrive and
> reproduce at a greater rate. But the same cells are killed when
I have a feeling that the explanation is mor esimple than what you
believe. Most possible they menat linoleic acid, not alpha-linoleic
acid.
EPA on the other hand is an inhibitor of the synthesize of arachidonic
acid based signals (eicosanoids) and a very good inhibitor with a Km for
COX II around 1/10 (bind 10 times more tight) and with a Vm around 1/10,
that is, when COX use EPA as source, they may produce only 1/10 of
eicosanoids pr time unit as when it use arachidonic acid.
Since I don't have the enzymic data when using EPA as an inhibitor (the
figures are when EPA is producing eicosanoids of 3-series where several
of the products have no biological function, where the 2-series analogue
has tremendous physiological effects (TXA-3 which is not formed at all
versus TXA-2 which is making clots) Also DHGLA is a good inhibitor of
the series-2 eicosanoid synthesis which also form a lot of inactive
molecules compared to the 2-series.. I have seen many reports who are
based on the belief that the 1-series eicosanoids has special functions.
But the most important function is just by giving the COX-enzymes lot of
work without making any active signals at all (like the Austrian
sabotages with german V1 and V2 bombs that just killed a few people just
by hitting them, but did not kill any people because they had no
ignition systems, just being defective. If they hadn't, most London
would have been erradicated and also lots of other towns, plus maybe we
still would have a Nazi system in Europe today. Just meant as an
examplification, not a start of a new thread)
---------------------------------
Alf Christophersen, Computer engineer
University of Oslo
Tel. +47 22 85 13 27, Fax: 22 85 15 32
URL: http://www.uio.no/~achristo
Alf Christophersen
>(1) Ingesting omega-3 fatty acids in the form of "EPA", which inhibits the
>activity of the D5D enzyme which creates AA.
From where do you have that EPA inhibits D5D enzyme ?
It inhibits the COX'es and the lipoxygenases, though. It is the
C20:4(n-3) that competes with C20:3(n-6) for the desaturase (D5D), so it
is the biosynthesis of EPA that concur. (If not there ahs been published
some works that EPA function as a feedback inhibitor, I have not seen
anyone)
Arnold Gold
a time, and put 1 tbls.on my cereal each day.Read the positive benifits
of flax at:
http://www.flaxcouncil.ca/flaxnut1.html
Arnold
arnol...@webtv.net
http://www.healthchecksystems.com/success.htm
Alf Christophersen
>No, what is being said is that "EPA" (as found in fish oil capsules) is
>preferable, because it is an Omega-3 fatty acid. Flax Oil should not be taken
>in quantities over one tablespoon per day, otherwise it competes with your
>body's production of DGLA.
I have not seen clearcut reports that state that DGLA has unique
products except those that are defunct in physiological regulation or is
just a big concurrent with AA for the enzymes converting AA to different
eicosanoids. So whether the body has DGLA or EPA (and linoleic acid
which has unique lipoxygenase products and lipoxygenase products that
has unique properties in itself) as a concurrent to inhibit AA to bind
to the cyclooxygenases and lipoxygenases are probably just the same.
There exists also other unique oils in fish, though, that has the same
properties as a concurrent with AA and which inactivate COX II as
quickly as any of the other substrates (COX should be turned on and then
off to stop making signal molecules, otherwise they are not anymore a
signal molecule (in a regulatory sense)). There is a C21:4 acid that
binds well to cyclooxygenase but has a very low Vm, that is a bad
substrate, but a very good inhibitor.
Michael H.
>
> kst...@jps.net (Ken Stuart) wrote:
>
> >(1) Ingesting omega-3 fatty acids in the form of "EPA", which inhibits the
> >activity of the D5D enzyme which creates AA.
>
> From where do you have that EPA inhibits D5D enzyme ?
>
> It inhibits the COX'es and the lipoxygenases, though. It is the
> C20:4(n-3) that competes with C20:3(n-6) for the desaturase (D5D), so it
> is the biosynthesis of EPA that concur. (If not there ahs been published
> some works that EPA function as a feedback inhibitor, I have not seen
> anyone)
>
Let me just ask two questions, putting aside the issue of fish oils vs
flaxseed oil.
1. Re circulatory health: are omega-3 fatty acids helpful, detremental
or neutral?
2. Re prostate cancer and cancer in general: do omega-3 fatty acids tend
to prevent it, promote it, or have no effect one way or the other?
I would like to know this because I currently take flaxseed oil three
times a week and salmon oil once a week. I am half-way between taking
full supplementation and giving it up completely. I don't want a
deficiency that might cause problems, but I do not want to take an
excess of something that promotes cancer, so it is important for me to
get these questions settled.
I appreciate the discussion, and have learned a lot, but I'd like to
know what fatty acid supplements to take or not take for optimum health.
Michael H.
Pete Beyer
Michael H. wrote:
Michael et al-- You can see from all these talented people you are having
difficulty getting a nice clean answer-- the problem is that the picture is not
perfectly clear-- See the abstracts as an example: None are conclusive, but the
studies give hints as to what is happening.
More work in the future will help. For what its worth Pete
Prediagnostic level of fatty acids in serum phospholipids: omega-3 and omega-6
fatty acids and the risk of prostate cancer.
AU: Harvei-S; Bjerve-KS; Tretli-S; Jellum-E; Robsahm-TE; Vatten-L
SO: Int-J-Cancer. 1997 May 16; 71(4): 545-51
JN: INTERNATIONAL-JOURNAL-OF-CANCER
Ecological and case-control studies have demonstrated a positive correlation
between consumption of fat and the risk of prostate cancer. Two recent human
studies have focused on alpha-linolenic acid as a risk factor for prostate cancer.
Animal experiments have shown that dietary omega-6 polyunsaturated fatty acids
have generally stimulated tumour development, whereas omega-3 polyunsaturated
fatty acids have diminished it. The aim of our study was to investigate the
association between these fatty acids and the subsequent risk of prostate cancer.
Blood donors to the Janus serum data bank in Norway, who later developed prostate
cancer, were matched to blood donors without prostate cancer (141 matched sets);
the proportional level of fatty acids measured before diagnosis in the donors'
serum was examined. The risk of later prostate cancer was analysed by conditional
logistic regression. Increasing risk for prostate cancer was found with increasing
quartiles of palmitoleic, palmitic and alpha-linolenic acid. An inverse risk
association was found with increasing levels of tetracosanoic acid, for the ratios
of linoleic to alpha-linolenic acid and arachidonic to eicosapentaenoic acid.
There was no clear association between the risk effect of total omega-3 and total
omega-6 fatty acids. There were no indications of a relationship between fatty
acids and more aggressive cancers. Our results verify recent findings of a
positive association between alpha-linolenic acid and a negative association
between the ratio of linoleic to alpha-linolenic acid and the risk of prostate
cancer.
The effect of essential fatty acids on growth and urokinase-type plasminogen
activator production in human prostate DU-145 cells.
AU: du-Toit-PJ; van-Aswegen-CH; du-Plessis-DJ
SO: Prostaglandins-Leukot-Essent-Fatty-Acids. 1996 Sep; 55(3): 173-7
JN: PROSTAGLANDINS-LEUKOTRIENES-AND-ESSENTIAL-FATTY-ACIDS
AB: Urokinase-type plasminogen activator (uPA) is an important protease enzyme in
carcinogenesis, and is involved in both invasion and metastasis of cancer.
Increased uPA activity and decreased essential fatty acid (EFA) levels have been
reported in cancer. This phenomenon may be explained by the fact that certain
EFAs, such as gamma-linolenic acid (GLA) and eicosapentaenoic acid (EPA), inhibit
uPA activity. The effect of EFA on human prostate DU-145 cell growth and uPA
production is still unknown and was investigated in this study. Data obtained from
the different unsaturated fatty acids showed that oleic acid (OA) and EPA enhanced
DU-145 cell proliferation at 0.004 and 0.04 mM for up to 4 days. However,
alpha-linolenic acid (ALA), linoleic acid (LA), GLA and arachidonic acid (AA)
suppressed cell proliferation under the same conditions, possibly as a result of
inhibition of DNA and protein synthesis as measured using labelled thymidine and
glycine incorporation. In contrast to the cell proliferation, uPA production was
inhibited by all the unsaturated fatty acids under investigation. Therefore, the
absence of EFAs, as reported, may affect invasion and metastasis of cancer.
TI: The effects of omega-3 and omega-6 fatty acids on in vitro prostate cancer
growth.
AU: Pandalai-PK; Pilat-MJ; Yamazaki-K; Naik-H; Pienta-KJ
SO: Anticancer-Res. 1996 Mar-Apr; 16(2): 815-20
JN: ANTICANCER-RESEARCH
AB: Dietary intake of essential fatty acids (EFA) may play a role in prostate
cancer cell proliferation. Epidemiological studies have demonstrated that men
whose dietary intake is high in omega-3 fatty acid (FA) composition have a lower
incidence of clinical prostate cancer, suggesting that external factors such as
diet may play an important role in development and growth of prostate cancer.
Furthermore, in prostate cancer cell lines, omega-6 and omega-3 FAs have
demonstrated promotional and inhibitory effects respectively. To investigate the
effects of dietary fats on nontumorigenic prostate cell growth we conducted in
vitro studies with human metastatic PC-3, LNCaP and TSU prostate cell lines, the
rat metastatic Mat-Ly-Lu cell line and rat non-metastatic epithelial cell lines
EPYP1, EPYP2 and EPYP3. Cell lines were treated with linoleic acid (LA), an
omega-6 FA (n-6), as well as linolenic (LLA) and eicosapentaenoic (EPA) acids,
which are both omega-3 FAs (n-3). All cell lines were treated with 10% and 0.5%
serum supplemented media plus fatty acid for comparison. Our results demonstrate
that linoleic acid(n-6) has promotional effects at doses of 1-100ng/ml in all cell
lines with the exception of EPYPl. Experiments with linolenic acid (n-3)
demonstrated consistent growth promotion in all cell lines examined with the
exception of the EPYP2 cell line in which there was no significant effect. EPA had
no effect in culture media supplemented with 10% serum, while in media containing
0.5% serum this FA demonstrated significant promotion in all human lines. Previous
studies have indicated that EPA should inhibit human prostate cancer growth in
vitro, however our results demonstrated promotion at low concentrations (lng/ml).
At higher concentrations, EPA did inhibit prostate cell growth. These data
indicate low levels of dietary fat, regardless of composition, may play a role in
prostate cancer proliferation and could be an avenue for therapeutic intervention.
pb
Alf Christophersen
>I think some of the problems come from looking at these things as if they were
>totally isolated, instead of interacting parts that are affected for other
>factors.
>
>Dr. Barry Sears spent years developing a system to stimulate PGE1 synthesis by
>supplementing with GLA and EPA. He tested this system on elite athletes and it
>would work for awhile, then all of a sudden it would stop working with some
>athletes. Eventually, he discovered that it stopped working when those
>particular athletes would carbo load before a competition, thus dramatically
>increasing their insulin levels.
>
>This led him to investigate the effects of insulin on all these processes, and
>his research led him to conclude that elevated levels affected these fatty acid
>and prostaglandin syntheses in such a way as to facilitate most of the modern
>maladies, ie heart disease, cancer, etc.
>
>So, the short answer is to supplement with EPA and not with flax. But, your
>dietary habits may prevent any benefit from these. Read "The Anti-Aging Zone"
>for an in-depth technical discussion of these issues.
There is possibly also another explanation.
Most measurement technics are based on what you observe is a static
system, using methods and evt. equations for static systems, while the
system is dynamic.
When you put something into the system and look at it's conversion fra A
to B to C to D to E, all conversions are affected, not only from the
other stuffs mentioned, but also many other which is present as a
remains from previous feedings. These remains inhibit (hinder) the
different conversions, but the effect of inhibition is highly dependent
both on what stuff does inhibit, but also the mix ratio for the
different lipids (and some other factors, like mentioned, insulin and
other). As long as you do a change in composition, you will get dramatic
effect on the other systems, but when stabilized after a period, the
effect of inhibition is outlined and the system is just as bad as it
was. When there is a uniform mix, then nothing will disturb the
conversion and you will produce arachidonate at maximum speed, that is
DGLA will immediately be converted in AA because AA is missing. While AA
is high, DGLA will not be converted and it will give rise to PGE1
instead and the DGLA->PGE1 conversion would block the AA->PGE2
conversion. When AA get low in tissue because the change has worked,
then nothing is any more blocking the conversion from DGLA to AA, and
now lot of AA is produced by liver, DGLA disappears from the system and
now COX I and COX II in particular has nothing to inhibit AA to PGE2
conversion.
Ever tried to simulate the seemingly very simple system of rabbit eating
greens on an island and foxes eating rabbits ? Try running it with
different coupling parameters (how good are rabbits to feed on greens on
the island is the coupling btw. rabbit and greens, and how easy is it
for the fox to catch lazy rabbits. Varying these parameters and
backcoupling time you will get very oscillating systems. With even more
couples (A to B etc), the more chances are the system will oscillate and
when AA -> PGE2 goes up, the more hell the patient would have!
Alf Christophersen
>
>DGLA is converted to PGE1 and others in the same series.
Yes. And they are either without any physiological function or has much
weaker effects than the same in the 2-series. They function like water
with etanol. PG of the 2-series are the analogue to the ethanol,
1-series and 3-series are analogues to water.
The main effect is to hinder a very dramatic feedback signal with very
large amplitudes from a cybernetic viewpoint.
Michael H.
supplements causes cancer. Great. That will save me a lot of money I
have been wasting on supplements.
Michael H.
Alf Christophersen
> It seems that taking supplements causes cancer, and not taking
>supplements causes cancer. Great. That will save me a lot of money I
>have been wasting on supplements.
Which supplements did you have in mind and on what grounds from what I
wrote are you able to make that conclusion ?
Sounds rather what like what we call "GMØ", "Goddag Mann - Økseskaft"
Tom Matthews
> > Thanks for the info, although it's way over my head. I've never studied
> >biochemistry or molecular biology to that extent, so I am still not sure
> >whether I should be taking flaxseed oil or not. It sounds like a "yes"
> >to me.
>
> No, what is being said is that "EPA" (as found in fish oil capsules) is
> preferable, because it is an Omega-3 fatty acid. Flax Oil should not be taken
> in quantities over one tablespoon per day, otherwise it competes with your
> body's production of DGLA.
>
> EPA also prevents both formation and release of Arachidonic Acid, which is - for
> modern man - a relatively harmful fatty acid.
>
> So, fish oil is the best Omega-3 fatty acid. Look for a molecularly distilled
> or "chlorestorol-free" fish oil that is preserved with Vitamin-E or similar
> oxidation-preventing additive. 300-500mg of EPA per day is probably sufficient.
Which is, of course, exactly what I said vegetarians should do on the
other thread!
--Tom
Tom Matthews
The LIFE EXTENSION FOUNDATION - http://www.lef.org - 800-544-4440
A non-profit membership organization dedicated to the extension
of the healthy human lifespan through ground breaking research,
innovative ideas and practical methods.
LIFE EXTENSION MAGAZINE - The ultimate source for new
health and medical findings from around the world.
Tom Matthews
>
> I do as Dr.Weil recommends. I buy Flax seed and grind a weeks supply at
> a time, and put 1 tbls.on my cereal each day.Read the positive benifits
> of flax at:
> http://www.flaxcouncil.ca/flaxnut1.html
A very important point here, is that consuming whole (ground) flax is
not equivalent to taking flax seed oil!
Ground whole flax contains potent anti-cancer lignans.
Tom Matthews
> >preferable, because it is an Omega-3 fatty acid. Flax Oil should not be taken
> >in quantities over one tablespoon per day, otherwise it competes with your
> >body's production of DGLA.
>
> products except those that are defunct in physiological regulation or is
> just a big concurrent with AA for the enzymes converting AA to different
> eicosanoids. So whether the body has DGLA or EPA
Hi Alf,
Please elaborate more on the following parenthetical remark
> (and linoleic acid which has unique lipoxygenase products and
> lipoxygenase products that has unique properties in itself)
What are these products and properties of the shortest omega-6 fat,
C18:2n6 that its derivatives fats or others do not possess?
> as a concurrent to inhibit AA to bind
> to the cyclooxygenases and lipoxygenases are probably just the same.
> There exists also other unique oils in fish, though, that has the same
> properties as a concurrent with AA and which inactivate COX II as
> quickly as any of the other substrates (COX should be turned on and then
> off to stop making signal molecules, otherwise they are not anymore a
> signal molecule (in a regulatory sense)). There is a C21:4 acid that
> binds well to cyclooxygenase but has a very low Vm, that is a bad
> substrate, but a very good inhibitor.
Thanks for this additional tid bit re C21:4, once again showing the
importance of eating the whole oil or food instead of relying on the
EPA/DHA concentrate which may have lost some of the other valuable
components.
Tom Matthews
> It seems that taking supplements causes cancer, and not taking
> supplements causes cancer. Great. That will save me a lot of money I
> have been wasting on supplements.
Michael, you need to be clear that *none* of these oils are likely
*causing* prostate cancer. The promotion or inhibition of existing
cancer is very different from the *initiation* of cancer.
Things like lycopene (tomatoes), soy, and green tea (and other
antioxidants which get into the cells should greatly help prevent the
initiation of the cancer in the first place.
Until/unless you *know* that you have prostate cancer already initiated,
you should concentrate on the benefits of the oils (and other
supplements too) for cancer, heart disease, stroke diabetes, and
arthritis disease *prevention*.
Michael Sierchio
> A very important point here, is that consuming whole (ground) flax is
> not equivalent to taking flax seed oil!
> Ground whole flax contains potent anti-cancer lignans.
Tom --
the proper spelling is "lignin" -- although alternative health sites
seem to prefer "lignan." But then again, these sites are run by
people whose VCRs are blinking "12:00" If you do a web search on
"flax AND lignin" you get a lot of good science stuff, and if you
do a web search on "flax AND lignan" you get tofu and sprouts, too.
Better change those LEF pages, or get lumped with the aspartame
loonies!
http://www.nal.usda.gov/ttic/tektran/data/000008/66/0000086680.html
http://www.olywa.net/when/sect07.html
http://www.unige.ch/LABPV/newsletters/newslet2.html
http://fisher.bio.umb.edu/pages/jfgenus/Jfgenus5.htm
Tom Matthews
Thanks for the help, and it is true that the LEF website only refers to
"lignans", but I think they are different things.
"flax lignans" gave 15 hits on medline. "flax lignins" only 1 hit.
"lignin lignan" gave 32 hits among them the following:
Science 1997 Jan 17;275(5298):362-6
Stereoselective bimolecular phenoxy radical coupling by an auxiliary
(dirigent) protein without an active center.
Davin LB, Wang HB, Crowell AL, Bedgar DL, Martin DM, Sarkanen S, Lewis
NG
Institute of Biological Chemistry, Washington State University, Pullman,
WA 99164-6340, USA.
The regio- and stereospecificity of bimolecular phenoxy radical coupling
reactions, of especial importance in lignin and lignan biosynthesis, are
clearly controlled in some manner in vivo; yet in vitro coupling by
oxidases, such as laccases, only produce racemic products. In other
words, laccases, peroxidases, and comparable oxidases are unable to
control regio- or stereospecificity by themselves and thus some other
agent must exist. A 78-kilodalton protein has been isolated that, in the
presence of an oxidase or one electron oxidant, effects stereoselective
bimolecular phenoxy radical coupling in vitro. Itself lacking a
catalytically active (oxidative) center, its mechanism of action is
presumed to involve capture of E-coniferyl
alcohol-derived free-radical intermediates, with consequent
stereoselective coupling to give (+)-pinoresinol.
Which clearly shows they are scientifically considered to be distinct.
Thanks for noting this, however. I will continue to look for a
definition and it may well be the case that some of the LEF uses of
'lignan' should be 'lignin' instead.
Michael Sierchio
> Thanks for noting this, however. I will continue to look for a
> definition and it may well be the case that some of the LEF uses of
> 'lignan' should be 'lignin' instead.
Normally, I just assume the Encyclopaedia Brittanica to be correct,
unless
it's a topic I wouldn't consult it on. Lignans must be new? ;-)
Tom Matthews
> Normally, I just assume the Encyclopaedia Brittanica to be correct,
> unless
> it's a topic I wouldn't consult it on. Lignans must be new? ;-)
I did not consult my Merck Index before because I thought these terms
were too generic, and not specific chemicals that would be in there.
However, Merck makes a clear distinction between them, as I already
determined was the case. In fact, they have no relationship to one
another at all!
Lignin:
"The most abundant natural aromatic organic polymer found in all
vascular plants. Lignin together with cellulose and hemicellulose are
the major wall components of the fibers of all wood and grass species.
Lignin is composed of coniferyl, p-coumaryl adn sinapyl alcohols in
varying ratios in different plant species."
Lignans:
"Plant products of low molecular weight formed primarily by the
oxidative coupling of p-hydroxyphenylpropene units in which the two
units may be linked by an oxygen bridge. The monomeric precursor units
are cinnamic acid, cinnamyl alcohol, propenylbenzene and allylbenzene.
-- Lignans occur widely and have been obtained from roots, heartwood,
foliage, fruit, and resinous exudates of plants.
Michael H.
Unfortunately, none of this resolves the dispute between those who think
that flaxseed oil causes cancer, versus those who allege that flaxseed
oil prevents cancer.
Michael H.
i.e. the univeral answer is, "I don't know." Well that is honest, and
rare among the scientifically obsessed, paradoxically.
>See the abstracts as an example: None are conclusive, but the
> studies give hints as to what is happening.
> More work in the future will help. For what its worth Pete
>
> Prediagnostic level of fatty acids in serum phospholipids: omega-3 and omega-6
> fatty acids and the risk of prostate cancer.
> AU: Harvei-S; Bjerve-KS; Tretli-S; Jellum-E; Robsahm-TE; Vatten-L
> SO: Int-J-Cancer. 1997 May 16; 71(4): 545-51
> JN: INTERNATIONAL-JOURNAL-OF-CANCER
> Ecological and case-control studies have demonstrated a positive correlation
> between consumption of fat and the risk of prostate cancer. Two recent human
> studies have focused on alpha-linolenic acid as a risk factor for prostate cancer.
> Animal experiments have shown that dietary omega-6 polyunsaturated fatty acids
> have generally stimulated tumour development, whereas omega-3 polyunsaturated
> fatty acids have diminished it. The aim of our study was to investigate the
> association between these fatty acids and the subsequent risk of prostate cancer.
Omega-6 fatty acids (evening primrose oil & borage) are normally touted
as cancer preventers, with sheafs of supporting documentation. Geez, it
gets harder and harder to answer a simple question. Maybe, as you
suggest, it is not a simple question.
> Blood donors to the Janus serum data bank in Norway, who later developed prostate
> cancer, were matched to blood donors without prostate cancer (141 matched sets);
> the proportional level of fatty acids measured before diagnosis in the donors'
> serum was examined.
Wait a minute now. "Serum" levels? Given that a gobbler of iron
supplements can have iron-deficiency anemia, and given that an alcoholic
on a low-cholesterol diet can have high serum cholesterol levels, and
given that a diabetic on a sugar-free diet can have high serum sugar
levels, it is clear that data concerning blood levels cannot be
generally relevant to supplementation. Serum levels of omega-3 and
omega-6 fatty acids depend on metabolism, not on supplementation, so
serum data, while interesting, is inapplicable in recommending
supplementation.
>The risk of later prostate cancer was analysed by conditional
> logistic regression. Increasing risk for prostate cancer was found with increasing
> quartiles of palmitoleic, palmitic and alpha-linolenic acid. An inverse risk
> association was found with increasing levels of tetracosanoic acid, for the ratios
> of linoleic to alpha-linolenic acid and arachidonic to eicosapentaenoic acid.
> There was no clear association between the risk effect of total omega-3 and total
> omega-6 fatty acids. There were no indications of a relationship between fatty
> acids and more aggressive cancers. Our results verify recent findings of a
> positive association between alpha-linolenic acid and a negative association
> between the ratio of linoleic to alpha-linolenic acid and the risk of prostate
> cancer.
That is interesting. All I have to do now is translate that into the
language of supplements.
That is what one of the sites I alluded to maintained. Omega-3 fights
prostate cancer.
>suggesting that external factors such as
> diet may play an important role in development and growth of prostate cancer.
> Furthermore, in prostate cancer cell lines, omega-6 and omega-3 FAs have
> demonstrated promotional and inhibitory effects respectively.
That is so crazy. One of the main selling points of omega-6 fatty acids
is that it prevents prostate and breast cancer. Where is the truth among
all of the smoke and mirrors?
>To investigate the
> effects of dietary fats on nontumorigenic prostate cell growth we conducted in
> vitro studies with human metastatic PC-3, LNCaP and TSU prostate cell lines, the
> rat metastatic Mat-Ly-Lu cell line and rat non-metastatic epithelial cell lines
> EPYP1, EPYP2 and EPYP3.
Some people might call me a rat, but I don't think that these
experiments necessarily apply.
>Cell lines were treated with linoleic acid (LA), an
> omega-6 FA (n-6), as well as linolenic (LLA) and eicosapentaenoic (EPA) acids,
> which are both omega-3 FAs (n-3). All cell lines were treated with 10% and 0.5%
> serum supplemented media plus fatty acid for comparison. Our results demonstrate
> that linoleic acid(n-6) has promotional effects at doses of 1-100ng/ml in all cell
> lines with the exception of EPYPl. Experiments with linolenic acid (n-3)
> demonstrated consistent growth promotion in all cell lines examined with the
> exception of the EPYP2 cell line in which there was no significant effect. EPA had
> no effect in culture media supplemented with 10% serum, while in media containing
> 0.5% serum this FA demonstrated significant promotion in all human lines. Previous
> studies have indicated that EPA should inhibit human prostate cancer growth in
> vitro, however our results demonstrated promotion at low concentrations (lng/ml).
> At higher concentrations, EPA did inhibit prostate cell growth. These data
> indicate low levels of dietary fat, regardless of composition, may play a role in
> prostate cancer proliferation and could be an avenue for therapeutic intervention.
>
That is so freaking ambiguous. What are they saying? Are they saying
that low levels of dietary fat cause prostrate cancer proliferation, or
prevent it.
I have accepted a low-fat vegetarian diet as health-promoting, but the
above quoted seems to be saying that limiting dietary fat promotes
cancer, or was the author perhaps literacy-challenged, in the last
sentence?
Michael H.
>
> "Michael H." <zol...@netcom.ca> wrote:
>
> > It seems that taking supplements causes cancer, and not taking
> >supplements causes cancer. Great. That will save me a lot of money I
> >have been wasting on supplements.
>
> wrote are you able to make that conclusion ?
>
>
Sounds cool, whatever it means. All I meant is that the cumulative
commentary, (yours plus others) seemed to suggest that taking flaxseed
oil supplements is simulataneously suicidal and the fountain of eternal
life. In other words, my hopes for a straightforward answer have been
shipwrecked.
Michael H.
Michael H.
> But .... the number one cause of death is not cancer, but heart disease....
>
That doesn't run in my family. Cancer does. That is why I am so
specific in my questions. It would probably be funny if I had a heart
attack from worrying about getting cancer (well, maybe not), but I think
that many people, such as myself, with pro-cancer genetics, are looking
for the optimal cancer-prevention diet, and not having a hell of a lot
of success with all of the totally ambiguous responses to precise
questions. Let me make it simple:
Omega-3 acids!!! Cancer-promoter or cancer-preventative? Is that so
complicated to understand? (Notice how many "experts" run and hide). Who
knows, really? I would like an answer, though, and it is too bad that I,
and everyone in my position, is not getting one.
Michael H.
Michael H.
>
> Michael H. wrote:
>
> > It seems that taking supplements causes cancer, and not taking
> > supplements causes cancer. Great. That will save me a lot of money I
> > have been wasting on supplements.
>
> *causing* prostate cancer. The promotion or inhibition of existing
> cancer is very different from the *initiation* of cancer.
> Things like lycopene (tomatoes), soy, and green tea (and other
> antioxidants which get into the cells should greatly help prevent the
> initiation of the cancer in the first place.
I am just going on the family record. I assume I don't have prostate
cancer (although I realize that it is not uncommon in a dormant state in
my age group). I make a great tomato soup with tomato juice and soy milk
plus spices, and actually enjoy it more than most meals.
>
> Until/unless you *know* that you have prostate cancer already initiated,
> you should concentrate on the benefits of the oils (and other
> supplements too) for cancer, heart disease, stroke diabetes, and
> arthritis disease *prevention*.
You say "concentrate on the benefits of oils," which is my problem. I
don't care about what happens to cancer cells in a Petrie dish when
doused in oil; often the immune-system boost from nutrients counteracts
Petrie-dish dousings, making such data irrelevant. I want the optimal
blend of fatty acids for a non-cancer case who is trying to prevent
cancer, but I am having a very difficult time finding out the facts on
which oils are good and which are bad.
Michael H.
Alf Christophersen
> Omega-3 acids!!! Cancer-promoter or cancer-preventative? Is that so
>complicated to understand? (Notice how many "experts" run and hide). Who
>knows, really? I would like an answer, though, and it is too bad that I,
>and everyone in my position, is not getting one.
The question is to general. You must define what you mean by cancer,
prostate cancer, colon concer etc.
It is supposed that n-3 acids are either neutral or inhibitory with some
cancers, others has not been tested. Arachidonic acid seems to be
pro-cancerogenic in several cancer types, but has not been proven to be
general. To be more specific, it is the enzymes that converts AA to
signal products like prostaglandines and lipoxides that is out of
control in several cell lines of cancer. Since n-3 oils are inhibiting
the production of PG-2 series, but also form their own metabolites who
may have or may not have the same effect, using different oils may have
very different effects.
On the other side is specific inhibitors of the enzymes that are out of
control more promising. Eg. specific COX II inhibitors seems to have
good effect on colon cancer where it is speculated that COX II out of
control is an important factor for cell division and metastasis.
Likewise is inactivators of 5-lipoxygenase promising with prostate
cancer cell lines where inactivation of the enzyme in vitro activates
apoptosis within very short time. 5-HETE seem to be the stuff produced
in excess protecting the cancer cells from programmed death.
It is really a sin that a very promicing stuff like the film developer
phenidone cannot be tested as an anti-cancerogenic stuff since it is not
patentable anymore and thus has no more economic interest for
pharmaceutical industry. It is a broad specter inactivator of both COX
II and diverse lipoxygenases and thus should be more general in effect
on a wide specter of cancer cell lines. From film industry it has been
documented to have generally low toxicoty too. (Just make a search on
phenidone and see the effects it has on prostaglandine and lipoxide
generation)
Alf Christophersen
>omega-6 fatty acids depend on metabolism, not on supplementation, so
>serum data, while interesting, is inapplicable in recommending
>supplementation.
Serum levels of n-3 and n-6 are solely dependent on nutrition, not
metabolism. They are broken down (by burning in cells) at the same rate,
so composition at input is the critical stage. Since they can't
interconvert (n-3 -> n-6 or vice versa) then if a linoleic acid molecule
ingested is converted to EPA or DHA doesn't change the ratio n-6 to n-3
oil.
Tom Matthews
>
> Thank goodness someone has cleared up "lignins" vs "lignans."
> Unfortunately, none of this resolves the dispute between those who think
> that flaxseed oil causes cancer, versus those who allege that flaxseed
> oil prevents cancer.
I think the answer, as with most things, is that it can do both and the
whole spectrum between those extremes, depending on many other
variables.
Tom Matthews
>
> Tom Matthews wrote:
> >
> > Michael H. wrote:
> >
> > > It seems that taking supplements causes cancer, and not taking
> > > supplements causes cancer. Great. That will save me a lot of money I
> > > have been wasting on supplements.
> >
> > Michael, you need to be clear that *none* of these oils are likely
> > *causing* prostate cancer. The promotion or inhibition of existing
> > cancer is very different from the *initiation* of cancer.
> > Things like lycopene (tomatoes), soy, and green tea (and other
> > antioxidants which get into the cells should greatly help prevent the
> > initiation of the cancer in the first place.
>
> I am just going on the family record. I assume I don't have prostate
> cancer (although I realize that it is not uncommon in a dormant state in
> my age group). I make a great tomato soup with tomato juice and soy milk
> plus spices, and actually enjoy it more than most meals.
Great! Don't forget to put in a little olive oil to make the lycopene
more bioavailable.
> > Until/unless you *know* that you have prostate cancer already initiated,
> > you should concentrate on the benefits of the oils (and other
> > supplements too) for cancer, heart disease, stroke diabetes, and
> > arthritis disease *prevention*.
>
> You say "concentrate on the benefits of oils," which is my problem. I
> don't care about what happens to cancer cells in a Petrie dish when
> doused in oil; often the immune-system boost from nutrients counteracts
> Petrie-dish dousings, making such data irrelevant. I want the optimal
> blend of fatty acids for a non-cancer case who is trying to prevent
> cancer, but I am having a very difficult time finding out the facts on
> which oils are good and which are bad.
As long as they do not get oxidized (and consuming lots of vitamin E,
lycopene, etc should largely prevent that), I don't think there is any
good evidence that any of them are going to initiate cancer.
That is what I meant by concentrating on their other benefits and
ignoring their relevance to cancer (by *you* preventing that
possibility).
Alf Christophersen
>This terminology is mainly used by companies in marketing. The eggs I buy now
>say "Omega-3 enriched" on the box, I kid you not.
>
>In reality, the body does not do the same thing with all "Omega-3 fatty acids",
>they are not interchangeable.
Not completely right, rather wrong. From EPA you may go back to ALA
through the intermediates since all the ela\ongases and desaturases are
working in both directions. From EPA you may also elongate and
desaturate to DHA. But, each enzymes also works with the n-6 acids, so
there is alsways a concurrence btw. substrates and products for the
catalytic site.
BL 1204
preventive oil, and it is found in meat and dairy products-- go figure.
Anticancer Res 1998 May-Jun;18(3A):1429-34
Opposite effects of linoleic acid and conjugated linoleic acid on human
prostatic cancer in SCID mice.
Cesano A, Visonneau S, Scimeca JA, Kritchevsky D, Santoli D
Wistar Institute, Philadelphia, PA 19104, USA.
The relationship between dietary fat intake (level and type) and cancer
development is a matter of concern in Western society. The purpose of this
study was to determine the effect of three different diets on the local growth
and metastatic properties of DU-145 human prostatic carcinoma cells in severe
combined immunodeficient (SCID) mice. Animals were fed a standard diet or diets
supplemented with 1% LA or 1% CLA for 2 weeks prior to subcutaneous (s.c.)
inoculation of DU-145 cells and throughout the study (total of 14 weeks). Mice
receiving LA-supplemented diet displayed significantly higher body weight,
lower food intake and increased local tumor load as compared to the other two
groups of mice. Mice fed the CLA-supplemented diet displayed not only smaller
local tumors than the regular diet-fed group, but also a drastic reduction in
lung metastases. These results support the view that dietary polyunsaturated
fatty acids may influence the prognosis of prostatic cancer patients, thus
opening the possibility of new therapeutic options.
PMID: 9673351, UI: 98338068
Cancer Lett 1998 May 15;127(1-2):15-22
Conjugated linoleic acid reduces arachidonic acid content and PGE2 synthesis in
murine keratinocytes.
Liu KL, Belury MA
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907,
USA.
Dietary conjugated linoleic acid (CLA) is associated with decreased
12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced tumor promotion in mouse
skin. In addition, CLA decreases TPA-induced prostaglandin E synthesis and
ornithine decarboxylase activity in cultured keratinocytes compared with
linoleic acid (LA) and arachidonic acid (AA). When LA or CLA was added to
keratinocyte cell cultures, the amounts of each of these cellular fatty acids
increased significantly in a dose-dependent manner. Furthermore, LA treatment
was associated with increased cellular AA while the AA content of keratinocytes
was reduced when cultures were treated with CLA. Moreover, CLA (16 microg/ml)
was more potent than LA at decreasing the level of 14C-AA incorporated into
cellular phosphatidylcholine. In order to determine the effect of CLA on
arachidonate-derived PGE2, the release of 14C-AA and 14C-PGE2 synthesis was
measured in cultures pre-treated with LA/14C-AA or CLA/14C-AA for 12 h. The
amount of 14C-AA release induced by TPA in CLA/14C-AA pre-treated cultures was
significantly lower than cultures pre-treated with LA/14C-AA. Furthermore,
TPA-induced 14C-PGE2 was significantly lower in cultures pre-treated with
CLA/14C-AA compared with cultures pre-treated with LA/14C-AA. The effects of LA
and CLA on AA composition of phospholipids and subsequent arachidonate-derived
PGE2 synthesis will provide insight into the anti-promoter mechanisms of CLA.
PMID: 9619853, UI: 98281152
Amer J Clin Nutr 1997 Dec;66(6 Suppl):1523S-1529S
Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated
fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals.
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY
14263, USA. c...@sc3101.med.buffalo.edu
I review the effects of trans fatty acids, oleic acid, n-3 polyunsaturated
fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals.
The goal is not to provide an exhaustive survey of all the publications on
these topics; such a Herculean effort has been accomplished by previous
reviews, which are cited in the text. Instead, the emphasis is on the
consistency or lack of consistency of information regarding each of the above
fatty acids, confounding factors that may help to reconcile discrepancies in
the database, a perspective of the history of the research, and certain unique
or exciting opportunities that are worthy of special attention in evaluations
of the relations between specific fatty acids and cancer. This review arrives
at four conclusions: 1) There is little evidence that trans fatty acids have an
adverse effect on carcinogenesis. 2) The data on cancer protection by oleic
acid are not convincing. An inhibitory effect attributed to an increased intake
of oleic acid could be due to an inadequate supply of linoleic acid. 3)
Although a suppressive response to n-3 polyunsaturated fatty acids is observed
in most cases, the availability of linoleic acid is likely to be a confounding
factor in determining the final outcome. 4) Conjugated linoleic acid is unique
in the sense that concentrations < or = 1% are sufficient for producing
significant cancer protection and that this effect seems to be independent of
the other fatty acids.
Publication Types:
•Review •Review, tutorial
PMID: 9394710, UI: 98056692
Cancer Res 1997 Nov 15;57(22):5067-72
Morphological and biochemical status of the mammary gland as influenced by
conjugated linoleic acid: implication for a reduction in mammary cancer risk.
Thompson H, Zhu Z, Banni S, Darcy K, Loftus T, Ip C
Division of Laboratory Research, AMC Cancer Research Center, Denver, Colorado
80214, USA.
Previous research showed that treatment with conjugated linoleic acid (CLA)
during the period of active mammary gland morphogenesis was sufficient to
confer a lasting protection against subsequent mammary tumorigenesis induced by
methylnitrosourea. The present study was designed to characterize certain
morphological and biochemical changes of the mammary gland that might
potentially render it less susceptible to cancer induction. Female Sprague
Dawley rats were fed a 1% CLA diet from weaning until about 50 days of age. The
mammary gland parameters under investigation included (a) the deposition of
neutral lipid, (b) the identification and quantification of CLA and its
metabolites, (c) the density of the epithelium, and (d) the proliferative
activity of various structural components. Our results showed that CLA
treatment did not affect total fat deposition in the mammary tissue nor the
extent of epithelial invasion into the surrounding fat pad but was able to
cause a 20% reduction in the density of the ductal-lobular tree as determined
by digitized image analysis of the whole mounts. This was accompanied by a
suppression of bromodeoxyuridine labeling in the terminal end buds and
lobuloalveolar buds. The recovery of desaturation and elongation products of
CLA in the mammary gland confirmed our prior suggestion that the metabolism of
CLA might be critical to risk modulation. The significance of the above
findings was investigated in a mammary carcinogenesis bioassay with the use of
the dimethylbenz[a]anthracene model. When CLA was started at weaning and
continued for 6 months until the end of the experiment, this schedule of
supplementation produced essentially the same magnitude of mammary tumor
inhibition in the dimethylbenz[a]anthracene model as that produced by 1 month
of CLA feeding from weaning. The observation is consistent with the hypothesis
that exposure to CLA during the time of mammary gland maturation may modify the
developmental potential of a subset of target cells that are normally
susceptible to carcinogen-induced transformation.
PMID: 9371504, UI: 98037555
Lipids 1997 Jul;32(7):725-30
Conjugated linoleic acid modulation of phorbol ester-induced events in murine
keratinocytes.
Liu KL, Belury MA
Department of Foods and Nutrition, Purdue University, West Lafayette, Indiana
47906, USA.
Recent work in our lab has shown that the chemoprotective fatty acid,
conjugated linoleic acid (CLA), inhibits phorbol ester skin tumor promotion in
mice. Because little is known about the deposition of CLA into tissues as well
as its biological activity, this study compared the incorporation and
biological activity of CLA to linoleic acid (LA; 18:2, c9,c12) and arachidonic
acid (AA; 20:4 c5,c8,c11,c14) in cultured keratinocytes. When keratinocytes
(HEL-30) were grown in media containing 14C-CLA for various periods, more than
50% of the 14C-CLA was incorporated into cellular lipids by 9 h. The
distribution of CLA in phospholipid classes was similar to LA, Approximately
50% of 14C-LA and 14C-CLA were incorporated into phosphatidylcholine (PC),
while the remainder was taken up by phosphatidylethanolamine (PE) and
phosphatidylserine/phosphatidylinositol (PS/PI). In contrast, 14C-AA was more
equitably distributed into PC, PE, or PS/PI (27, 30, or 38%, respectively).
When keratinocytes were prelabeled with radiolabeled fatty acids, phorbol
ester-induced release of 14C-CLA was 1.5 times higher than 14C-LA and 14C-AA.
However, 14C-prostaglandin E (PGE) release in 14C-CLA prelabeled cultures was 6
and 13 times lower than cultures treated with 14C-LA and 14C-AA, respectively.
Moreover, the ability of non-radiolabeled CLA to support ornithine
decarboxylase activity, a hallmark event of tumor promotion, was significantly
lower than in LA- and AA-treated cultures. These studies suggest that CLA
inhibits skin tumor promotion, in part, through a PGE-dependent mechanism.
PMID: 9252960, UI: 97396796
Cancer Lett 1997 Jun 24;116(2):121-30
The growth inhibitory effect of conjugated linoleic acid on MCF-7 cells is
related to estrogen response system.
Durgam VR, Fernandes G
Department of Medicine/Clinical Immunology, The University of Texas Health
Science Center at San Antonio, 78284-7874, USA.
Conjugated linoleic acid (CLA) has been shown to have a direct oncostatic
action on MCF-7 human breast cancer cells in culture. However, the mechanism
involved is not fully elucidated. In this study we have examined whether the
inhibitor action is related to the estrogen responsiveness of MCF-7 cells. Our
results demonstrate that CLA selectively inhibits proliferation of ER positive
MCF-7 cells as compared with ER negative MDA-MB-231 cells. Cell cycle studies
indicated that a higher percentage of CLA treated MCF-7 cells remained in the
G0/G1 phase as compared to control and those treated with linoleic acid (LA).
CLA also inhibited expression of c-myc in MCF-7 cells. These results
demonstrate that CLA may inhibit MCF-7 cell growth by interfering with the
hormone regulated mitogenic pathway. We are reporting for the first time the
involvement of CLA, a dietary factor, in the regulation of hormone mediated
mitogenic pathways in ER positive breast cancer cell proliferation in vitro.
PMID: 9215854, UI: 97358758
J Nutr 1997 Jun;127(6):1055-60
Cows' milk fat components as potential anticarcinogenic agents.
Parodi PW
Human Nutrition Program, Dairy Research & Development Corporation, Glen Iris,
Victoria, Australia.
The optimum approach to conquering cancer is prevention. Although the human
diet contains components which promote cancer, it also contains components with
the potential to prevent it. Recent research shows that milk fat contains a
number of potential anticarcinogenic components including conjugated linoleic
acid, sphingomyelin, butyric acid and ether lipids. Conjugated linoleic acid
inhibited proliferation of human malignant melanoma, colorectal, breast and
lung cancer cell lines. In animals, it reduced the incidence of chemically
induced mouse epidermal tumors, mouse forestomach neoplasia and aberrant crypt
foci in the rat colon. In a number of studies, conjugated linoleic acid, at
near-physiological concentrations, inhibited mammary tumorigenesis
independently of the amount and type of fat in the diet. In vitro studies
showed that the milk phospholipid, sphingomyelin, through its biologically
active metabolites ceramide and sphingosine, participates in three major
antiproliferative pathways influencing oncogenesis, namely, inhibition of cell
growth, and induction of differentiation and apoptosis. Mice fed sphingomyelin
had fewer colon tumors and aberrant crypt foci than control animals. About one
third of all milk triacylglycerols contain one molecule of butyric acid, a
potent inhibitor of proliferation and inducer of differentiation and apoptosis
in a wide range of neoplastic cell lines. Although butyrate produced by colonic
fermentation is considered important for colon cancer protection, an animal
study suggests dietary butyrate may inhibit mammary tumorigenesis. The dairy
cow also has the ability to extract other potential anticarcinogenic agents
such as beta-carotene, beta-ionone and gossypol from its feed and transfer them
to milk. Animal studies comparing the tumorigenic potential of milk fat or
butter with linoleic acid-rich vegetable oils or margarines are reviewed. They
clearly show less tumor development with dairy products.
Publication Types:
PMID: 9187617, UI: 97331285
Michael H.
> >serum data, while interesting, is inapplicable in recommending
> >supplementation.
>
> metabolism. They are broken down (by burning in cells) at the same rate,
> so composition at input is the critical stage. Since they can't
> interconvert (n-3 -> n-6 or vice versa) then if a linoleic acid molecule
> ingested is converted to EPA or DHA doesn't change the ratio n-6 to n-3
> oil.
Oh. Thanks for clearing that up. I do appreciate your comments and
references on this topic. I am tending away from the flaxseed
supplements.
Michael H.
Michael H.
>
> Michael H. wrote:
> > I make a great tomato soup with tomato juice and soy milk
> > plus spices, and actually enjoy it more than most meals.
>
> Great! Don't forget to put in a little olive oil to make the lycopene
> more bioavailable.
I generally do that. I know that the lycopene is fat-soluble. I was
thinking that the soymilk has a non-zero fat content and maybe that
might be good enough in itself.
What is your opinion on this question: does the tomato actually have to
simmer in the oil, i.e. to benefit from the lycopene content, or could
one, for example, simply stir a small amount of oil into a glass of
tomato juice and get the lycopene that way?
I know that my questions lately have not been easy ones, partly because
some of these nutrients have not been identified as health-promoting for
a sufficiently long time for extensive research to have been done.
> > > Until/unless you *know* that you have prostate cancer already initiated,
> > > you should concentrate on the benefits of the oils (and other
> > > supplements too) for cancer, heart disease, stroke diabetes, and
> > > arthritis disease *prevention*.
> >
> > You say "concentrate on the benefits of oils," which is my problem. I
> > don't care about what happens to cancer cells in a Petrie dish when
> > doused in oil; often the immune-system boost from nutrients counteracts
> > Petrie-dish dousings, making such data irrelevant. I want the optimal
> > blend of fatty acids for a non-cancer case who is trying to prevent
> > cancer, but I am having a very difficult time finding out the facts on
> > which oils are good and which are bad.
>
> As long as they do not get oxidized (and consuming lots of vitamin E,
> lycopene, etc should largely prevent that), I don't think there is any
> good evidence that any of them are going to initiate cancer.
> That is what I meant by concentrating on their other benefits and
> ignoring their relevance to cancer (by *you* preventing that
> possibility).
>
You mean through anti-oxidants etc., I presume?
Michael H.
Tom Matthews
>
> Well, there is some evidence that conjugated linoleic acid may be a cancer
> preventive oil, and it is found in meat and dairy products-- go figure.
It is virtually impossible to distinguish between prevention of
*initiation*, rather than of promotion, and in practical terms the
difference may not be important, unless the initiation occurs at a young
age and you are trying to live forever.
Tom Matthews
>
> Tom Matthews wrote:
> >
> > Michael H. wrote:
>
> > > I make a great tomato soup with tomato juice and soy milk
> > > plus spices, and actually enjoy it more than most meals.
> >
> > Great! Don't forget to put in a little olive oil to make the lycopene
> > more bioavailable.
>
> I generally do that. I know that the lycopene is fat-soluble. I was
> thinking that the soymilk has a non-zero fat content and maybe that
> might be good enough in itself.
> What is your opinion on this question: does the tomato actually have to
> simmer in the oil, i.e. to benefit from the lycopene content, or could
> one, for example, simply stir a small amount of oil into a glass of
> tomato juice and get the lycopene that way?
There are studies that have been posted here, showing thay long
simmering of the tomato in oil increases its bioavailability. That is
why my favorite tomato product is olive oil based pasta sauce. Still, I
do eat sliced tomatoes on almond butter spread, or sardine covered whole
rye bread (I feel hungry :-)
> > As long as they do not get oxidized (and consuming lots of vitamin E,
> > lycopene, etc should largely prevent that), I don't think there is any
> > good evidence that any [fats] are going to initiate cancer.
> > That is what I meant by concentrating on their other benefits and
> > ignoring their relevance to cancer (by *you* preventing that
> > possibility).
> You mean through anti-oxidants etc., I presume?
Yes, especially fat soluble ones.
Alf Christophersen
>However, if I ingest ALA and EPA and DHA, they don't all do the same thing, they
>are not interchangeable, there are different effects from ingesting them.
But you didn't get my point.
If you eat only EPA, your body will immediately convert some of it to
DHA and some of it to the immediate precursor of EPA from ALA side, and
some of that precursor back to that one's precursor and so on back to
ALA. But there will be lesser and lesser of those where the skeleton
comes from your EPA drink. From there they the skeleton will have
different fates depending if the skeleton was converted to DHA, ALA or
other n-3 acids.
But you will never find any EPA skeletons converted to any n-6 acids in
your body, at least not from liver conversion. (I cannot guarantee that
you don't have bacterias in your gut who may saturate the correct
position and convert a n-3 into a n-6 acid or the opposite, from n-6 to
n-3)
Michael H.
>
> "low-fat" and "low-fat vegetarian". (There is nothing unhealthy about a
> vegetarian diet per se IF it is very carefully constructed to have adequate
> intake of protein and micronutrients, which is harder to do than it originally
> looked, since many highly refined and processed soy products - that are
> otherwise the most convenient forms of vegetarian protein - actually have other
> health problems, such as affecting the absorption of minerals).
>
Protein is over-rated, especially in the US due to rancher propaganda.
If anything, the nitrogenous wastes produced by excess protein are more
of a health hazard than any hypothetical protein deficiency. It is
virtually impossible to have a protein deficiency unless one eats
nothing but Twinkies. Any whole grain bread contains a higher percentage
of complete protein (i.e. essential amino acid blend) than is required
for good health. I suppose that a chopped-up worm trying to grow a new
head could use some protein, but for the average person, excess protein
is the big problem. Breaking down excess protein is not healthy. People
should stay away from killer protein as much as possible and stick to a
low-protein diet for optimal health.
Michael H.
Michael H.
>
> kst...@jps.net (Ken Stuart) mentioned:
>
> >In a moment of clarity, "Michael H." <zol...@netcom.ca> mentioned:
> >
> >>Ken Stuart wrote:
> >>>
> >>> In a moment of clarity, "Michael H." <zol...@netcom.ca> mentioned:
> >>>
<snipped exchange re my criticism of a high-protein diet>
> >Vegan propaganda.
> >
> >None of those statements are accurate.
> >
> >A couple of good websites in rebuttal:
> >
> >http://www.beyondveg.com/
> >
> >http://www.acsh.org/publications/priorities/0902/vegetarian.html
>
> And here a couple of article specifically about protein requirements:
>
> http://www.zonehome.com/zlib0001.htm
>
> http://www.brinkzone.com/protein.html
>
I've looked at a Zone Diet book and reject that diet completely because
it contradicts every reputable opinion about protein that I have ever
read, but I don't care to get into a debate about that. I would if I had
more time, but I don't.
I am more concerned about the issue of using fish oils to obtain EPA. I
have read that a healthy person makes EPA from ALA (as found in, say,
flaxseed oil), but that the conversion can be reduced as part of aging,
etc.
Salmon oil, for example, is reputed to be high in pre-formed EPA, but
my concerns with it are: (a) a build-up of vit A and D; and (b)
pollutants that are concentrated in the fish livers from which the oils
are extracted. I was advised earlier to get molecularly filtered fish
oils, but I don't know if these are available here, or if they are
affordable. So my questions are:
Q1: Is salmon oil also a hidden vit A/D supplement that should cause one
to reduce one's intake of fish-oil A/D supplements such as halibut oil
caps? Is there a real danger of vit A/D toxic build-up with salmon oil?
Q2: Given the small sizes of these fish-oil supplements, it seems to me
that even a moderately high concentration of pollutants would give a
fairly small absolute dosage of pollutants, perhaps even less than one
might get from a glass of tap water. Or is the concentration of
pollutants so very high (in the standard unfiltered fish-oils) that it
is like taking poison?
Q3: Although I am not that concerned about cholesterol, because my
levels have always been good, this is an appropriate place to wonder
aloud about the often-mentioned high levels of cholesterol in fish oils.
Q4: Is salmon oil the best source of EPA, or is there a better one?
Q5: Comparing salmon and halibut liver oils in reverse, do halibut-liver
oil A/D supplements contain useful quantities of EPA?
Michael H.
Tom Matthews
> Salmon oil, for example, is reputed to be high in pre-formed EPA, but
> my concerns with it are: (a) a build-up of vit A and D; and (b)
> pollutants that are concentrated in the fish livers from which the oils
> are extracted.
You are mixed up or have been mislead.
The EPA/DHA fish oil concentrate supplements are derived from only the
*body* of the fish, not its liver. The body has no A or D and less
pollutants.
When you eat a salmon steak of fillet, you are getting EPA and DHA, but
no A or D at all.
Fish liver oil is a totally separate product used for the A and D
content, eg cod or halibut liver oil.
> I was advised earlier to get molecularly filtered fish
> oils, but I don't know if these are available here, or if they are
> affordable.
TwinLab (also sold by LEF) makes an excellent highly filtered and
assayed pure product.
> So my questions are:
>
> Q1: Is salmon oil also a hidden vit A/D supplement that should cause one
> to reduce one's intake of fish-oil A/D supplements such as halibut oil
> caps? Is there a real danger of vit A/D toxic build-up with salmon oil?
No. As explained above it is only the body oil and contains no A and D.
> Q2: Given the small sizes of these fish-oil supplements, it seems to me
> that even a moderately high concentration of pollutants would give a
> fairly small absolute dosage of pollutants, perhaps even less than one
> might get from a glass of tap water. Or is the concentration of
> pollutants so very high (in the standard unfiltered fish-oils) that it
> is like taking poison?
The ocean is not that polluted yet that salmon meat (and the oil it
contains) is inedible. A capsule supplement is giving you no more than
you could get be eating salmon regularly with lots of healthy people do.
> Q3: Although I am not that concerned about cholesterol, because my
> levels have always been good, this is an appropriate place to wonder
> aloud about the often-mentioned high levels of cholesterol in fish oils.
There is very little in refined fish oil, although there is some
cholesterol in the salmon flesh although less than in meats. However,
this whole cholesterol business is completely warpped. Only a very small
portion of people need to be concerned about how much cholesterol they
eat. The rest need to be more concerned about how much their body
*produces* as the amount that gets into their blood from what they eat
is miniscule contain with what they can produce if the are eating a high
saturated fat and otherwise bad diet.
> Q4: Is salmon oil the best source of EPA, or is there a better one?
Salmon, tuna, mackerel, herring and sardines are all very high and
roughly the same.
>
> Q5: Comparing salmon and halibut liver oils in reverse, do halibut-liver
> oil A/D supplements contain useful quantities of EPA?
I have never seen salmon liver oil available, only cod and halibut.
You cannot get significant EPA from the liver oils without overdosing on
A and D.
Brian Manning Delaney
Tom Matthews wrote:
> Michael H. wrote:
[....]
>> So my questions are:
[....]
>> Q2: Given the small sizes of these fish-oil
>> supplements, it seems to me that even a
>> moderately high concentration of pollutants
>> would give a fairly small absolute dosage of
>> pollutants, perhaps even less than one might get
>> from a glass of tap water. Or is the
>> concentration of pollutants so very high (in the
>> standard unfiltered fish-oils) that it is like
>> taking poison?
> The ocean is not that polluted yet that salmon
> meat (and the oil it contains) is inedible.
How do you know that? Some studies indicate just the opposite,
though it depends on what you mean by "inedible." Virtually no
salmon will kill you right after you eat them. But eating
certain fish on a regular basis may be indeed by like "taking
poison," as Michael put it. I don't think we know for certain
yet. If you disagree, why do you?
>> I was advised earlier to get molecularly filtered
>> fish oils, but I don't know if these are available
>> here, or if they are affordable.
> TwinLab (also sold by LEF) makes an excellent
> highly filtered and assayed pure product.
Is it assayed for presence of the n-3 fatty acids, or for
toxins as well? If for toxins, is it assayed for both heavy
metals as well as organic toxins?
Thanks,
Brian.
--
Brian Manning Delaney
email = first initial + hyphen + last na...@uchicago.edu
I still have to live, for I still have to think.
Sum, ergo cogito: cogito, ergo sum. -Nietzsche.
Help me .. tear down my reason. -Trent Reznor, Nine Inch
Nails.
Michael H.
that one seldoms sees in print.
Tom Matthews wrote:
>
> Michael H. wrote:
>
> > Salmon oil, for example, is reputed to be high in pre-formed EPA, but
> > my concerns with it are: (a) a build-up of vit A and D; and (b)
> > pollutants that are concentrated in the fish livers from which the oils
> > are extracted.
>
> You are mixed up or have been mislead.
> The EPA/DHA fish oil concentrate supplements are derived from only the
> *body* of the fish, not its liver. The body has no A or D and less
> pollutants.
> When you eat a salmon steak of fillet, you are getting EPA and DHA, but
> no A or D at all.
>
> Fish liver oil is a totally separate product used for the A and D
> content, eg cod or halibut liver oil.
>
> > I was advised earlier to get molecularly filtered fish
> > oils, but I don't know if these are available here, or if they are
> > affordable.
>
> TwinLab (also sold by LEF) makes an excellent highly filtered and
> assayed pure product.
>
> > So my questions are:
> >
> > Q1: Is salmon oil also a hidden vit A/D supplement that should cause one
> > to reduce one's intake of fish-oil A/D supplements such as halibut oil
> > caps? Is there a real danger of vit A/D toxic build-up with salmon oil?
>
> No. As explained above it is only the body oil and contains no A and D.
>
> > Q2: Given the small sizes of these fish-oil supplements, it seems to me
> > that even a moderately high concentration of pollutants would give a
> > fairly small absolute dosage of pollutants, perhaps even less than one
> > might get from a glass of tap water. Or is the concentration of
> > pollutants so very high (in the standard unfiltered fish-oils) that it
> > is like taking poison?
>
> The ocean is not that polluted yet that salmon meat (and the oil it
Tom Matthews
>
> The issue of epa is a component of the zone diet. What are LEF's opinions
> with regard to the zone diet philosophy?
LEF is not a "one-voice" organization. Difference people involved with
them (including me) sometimes have different opinions on particular
issues.
That having been said, I have never seen anything yet appear in LE
Magazine about the Zone diet.
physical (Droll Troll)
>
The solution to this would appear to be fish farms.
HPLC-mass spec would answer this definitively. There should be articles
on this, as well as the stability of these oils on storage. Gel caps
make me sick to my stomach, even with food. I suspect that color is a
good indicator of freshness, but I could be wrong.
Oh, and just a reminder, Brian, that Arachidonic acid is linoleic
_sparing_, not strictly substitutive. :)
--
Futilely Espousing God's Word on Pre-Purchase Epiphany,
---------------------------------------------------------------------
Kristofer Hogg, ms rd, Who can't safely boil water, much less cook!
More inciteful ravings, but with a plumb, at http://www.holobarre.com
HoloBarre Fitness/Stretching Systems, NY phys...@erols.com
Nice Bodies are, well, nice, but still largely irrelevant.
---------------------------------------------------------------------
> Tom Matthews wrote:
> > Michael H. wrote:
>
> [....]
>
> >> So my questions are:
> [....]
> >> Q2: Given the small sizes of these fish-oil
> >> supplements, it seems to me that even a
> >> moderately high concentration of pollutants
> >> would give a fairly small absolute dosage of
> >> pollutants, perhaps even less than one might get
> >> from a glass of tap water. Or is the
> >> concentration of pollutants so very high (in the
> >> standard unfiltered fish-oils) that it is like
> >> taking poison?
>
> > The ocean is not that polluted yet that salmon
> > meat (and the oil it contains) is inedible.
>
> How do you know that? Some studies indicate just the opposite,
> though it depends on what you mean by "inedible." Virtually no
> salmon will kill you right after you eat them. But eating
> certain fish on a regular basis may be indeed by like "taking
> poison," as Michael put it. I don't think we know for certain
> yet. If you disagree, why do you?
>
> >> I was advised earlier to get molecularly filtered
> >> fish oils, but I don't know if these are available
> >> here, or if they are affordable.
>
> > TwinLab (also sold by LEF) makes an excellent
> > highly filtered and assayed pure product.
>
Brian Manning Delaney
"physical (Droll Troll)" wrote:
> Brian Manning Delaney wrote:
>> The solution to this would appear to be
>> fish farms. HPLC-mass spec would answer this
>> definitively. There should be articles
>> on this,
One would think. Strangely, they are hard to come by. I
haven't dug too hard yet, though. Regulations would require
studies, I would think, so there've got to be at least a few.
(Though the government[s] may just do spot-testing -- maybe no
one's compiled the tests into a published report?)
> Oh, and just a reminder, Brian, that Arachidonic
> acid is linoleic _sparing_, not strictly substitutive. :)
<Ho Ho>Please, spare me.</Ho Ho>
> Futilely Espousing God's Word on Pre-Purchase Epiphany,
Not ENTIRELY futilely. Those with ears hear.
Steven B. Harris
<phys...@erols.com> writes:
>
>Brian Manning Delaney wrote:
>>
> The solution to this would appear to be fish farms.
> HPLC-mass spec would answer this definitively. There should be
articles
The articles on fish farms are rather funny. I mentioned that cold
water fish get a lot of omega 3 fats from the fish they eat, which get
it in turn ultimately from cold water plankton. Plus, I suspect that
cold itself stimulates fish to make more omega-3's. In fish farms they
feed them corn meal in warmer water, and the result is much lower omega
3 levels than in wild fish.
> Gel caps
>make me sick to my stomach, even with food. I suspect that color is a
>good indicator of freshness, but I could be wrong.
Since I'm starting to see completely black flax capsules, that
would be a problem...
> Oh, and just a reminder, Brian, that Arachidonic acid is linoleic
>_sparing_, not strictly substitutive. :)
News to me. Is there something important that linoleic acid does
in the body besides make arachadonate?? So what if you can't make 1
series prostaglandins-- are there any you really need? And (provided
you're not a cat) doesn't the synthetic enzyme work "backwards" as well
to make linoleate from arachadonate anyway, so you can eat either one?
physical (Droll Troll)
Beats the hell out of me.
Does this mean that goddammed Delaney was right?? Oh, tell me it ain't
so, cuz the old scars still haven't fully healed...
My out of hand assumption in this is that whenever one bypasses a
regulatory step with a down-stream metabolite, the piper will be paid
eventually. But maybe not in this case. I personally wouldn't presume
to eliminate PG1's, even if I didn't quite approve of what they did.
Although nudging levels of this and that seems par for the course.
--
Futilely Espousing God's Word on Pre-Purchase Epiphany,
Alf Christophersen
>> Oh, and just a reminder, Brian, that Arachidonic acid is linoleic
>>_sparing_, not strictly substitutive. :)
>
>
>
> News to me. Is there something important that linoleic acid does
>in the body besides make arachadonate?? So what if you can't make 1
>series prostaglandins-- are there any you really need? And (provided
>you're not a cat) doesn't the synthetic enzyme work "backwards" as well
>to make linoleate from arachadonate anyway, so you can eat either one?
Linoleate makes their own variants by cyclooxygenases and lipoxygenases.
The cyclooxygenases has been reported to have the opposite effect as the
PG-2 series (the products are the C18-analogues of PG's)
About synthesis:
Hamberg M. Arch Biochem Biophys 1998 Jan 15;349(2):376-80,
Stereochemistry of oxygenation of linoleic acid catalyzed by
prostaglandin-endoperoxide H synthase-2.
Laneuville O, Breuer DK, Xu N, Huang ZH, Gage DA, Watson JT, Lagarde M,
DeWitt DL, Smith WL. J Biol Chem 1995 Aug 18;270(33):19330-6. Fatty acid
substrate specificities of human prostaglandin-endoperoxide H synthase-1
and -2. Formation of 12-hydroxy-(9Z, 13E/Z, 15Z)- octadecatrienoic acids
from alpha-linolenic acid.
Check on PubMed also for Isoprostanes, HPODE and HODE.
Found some interesting new articles about HPODE and nitrification by NO
derivates.
Brian Manning Delaney
"physical (Droll Troll)" wrote:
> Steven B. Harris wrote:
[....]
>> The articles on fish farms are rather funny. I
>> mentioned that cold water fish get a lot of
>> omega 3 fats from the fish they eat, which get
>> it in turn ultimately from cold water plankton.
>> Plus, I suspect that cold itself stimulates fish
>> to make more omega-3's. In fish farms they feed
>> them corn meal in warmer water, and the result
>> is much lower omega 3 levels than in wild fish.
Yes. I was actually thinking more about the articles dealing
with toxicity, but if you can't get the n-3's you want from
farm-raised fish, then toxicity is irrelevant (though I hear
there are reasons to eat food other than to meet nutritional
requirements).
But there is a wee bit of species-dependence in the degree of
n-3's produced, from what I understand. Perhaps small, though,
compared with the effects of 1) food FAs and 2) water
temperature (that you point out).
>> "physical (Droll Troll)" writes:
[....]
>>> Oh, and just a reminder, Brian, that
>>> Arachidonic acid is linoleic _sparing_, not
>>> strictly substitutive. :)
>> News to me. Is there something important that
>> linoleic acid does in the body besides make
>> arachadonate?? So what if you can't make 1
>> series prostaglandins-- are there any you really
>> need? And (provided you're not a cat) doesn't
>> the synthetic enzyme work "backwards" as well to
>> make linoleate from arachadonate anyway, so you
>> can eat either one?
> Beats the hell out of me.
> Does this mean that goddammed Delaney
> was right?? Oh, tell me it ain't so, cuz
> the old scars still haven't fully healed...
It hurts, I know. Kristofer, my ex-girlfriends are having
their annual healing retreat near Sante Fe this year. A
beautiful location -- you might consider attending. You'll be
in the best of company. (But don't get any ideas, they're all
lesbians now.)
By the way, I think a particular well-known member of the
Supplement Disinfomercialism Cartel, who will go unnamed, will
be making a surprise appearance, as a court jester or
something.
Steven B. Harris
(Alf Christophersen) writes:
>sbha...@ix.netcom.com(Steven B. Harris) wrote:
>
>>> Oh, and just a reminder, Brian, that Arachidonic acid is linoleic
>>>_sparing_, not strictly substitutive. :)
>>
>>
>>
>> News to me. Is there something important that linoleic acid does
>>in the body besides make arachadonate?? So what if you can't make 1
>>series prostaglandins-- are there any you really need? And (provided
>>you're not a cat) doesn't the synthetic enzyme work "backwards" as
well
>>to make linoleate from arachadonate anyway, so you can eat either
one?
>
lipoxygenases.
>The cyclooxygenases has been reported to have the opposite effect as
the
>PG-2 series (the products are the C18-analogues of PG's)
Yes. So what? Again-- if the effect big enough to see clinically?
And can't you make linoleic from arachadonate anyway?
Alf Christophersen
> Yes. So what? Again-- if the effect big enough to see clinically?
> And can't you make linoleic from arachadonate anyway?
Arachidonate are probably made more to C22:5(n-6) and C22:6(n-6) than
backwards to linoleate via all shortening and saturations.
But first of all, most arachidonate are incorporated into a greater
portion of the phospholipids than otherwise. C22:1(n-9) is maybe the
most important concurrent for incorporation. But it depends highly on
what part of body we are talking about.
Steven B. Harris
(Alf Christophersen) writes:
>
>sbha...@ix.netcom.com(Steven B. Harris) wrote:
>
>> Yes. So what? Again-- if the effect big enough to see
clinically?
>> And can't you make linoleic from arachadonate anyway?
>
>Arachidonate are probably made more to C22:5(n-6) and C22:6(n-6) than
>backwards to linoleate via all shortening and saturations.
Yes, but so WHAT? We seem to be having a failure to communicate.
What evidence do you have that humans need series 1 prostagladins AT
ALL? Any more than cats do? Even if the worst scenario were true and
we can't convert arachadonate to linoleate at all (which cats can't,
but I suspect humans can, since they have the enzyme for the forward
process)? If you want to argue that some dietary linoleate is
absolutely necessary for humans, you've got to provide evidence for
both claims. I frankly don't believe it. We know it's perfectly
possible for humans to get along, reproduce, live normally, on a diet
of almost nothing but meat (Esquimos), very much like cats. If
linoleate were absolutely essential for people, that would be a pretty
difficult trick.
Nimrod Gil-Ad
>Arachidonate are probably made more to C22:5(n-6) and C22:6(n-6) than
>backwards to linoleate via all shortening and saturations.
C22:6(n-6)? I.e. 6,9,12,15,18,21cisC22:6??
I thought the delta-21 bond is the one that connects to the carboxyl,
which means it can't be desaturated. Am I wrong?
Nimrod
Alf Christophersen
>C22:6(n-6)? I.e. 6,9,12,15,18,21cisC22:6??
>I thought the delta-21 bond is the one that connects to the carboxyl,
>which means it can't be desaturated. Am I wrong?
No. I did a mistake here. I was thinking about C22:4 and C22:5 :-)
Alf Christophersen
> Yes, but so WHAT? We seem to be having a failure to communicate.
Maybe.
>What evidence do you have that humans need series 1 prostagladins AT
>ALL? Any more than cats do? Even if the worst scenario were true and
Very little. DGLA is probably more an inhibitor of PG-2 productions than
having special effects per se that is needed.
>we can't convert arachadonate to linoleate at all (which cats can't,
>but I suspect humans can, since they have the enzyme for the forward
Since the balance seems to be towards Arachidonate from DGLA rather than
the converse, you should have a very severe deficiency of linoleate to
get a convertion from AA via DGLA etc. to linoleate.
Since the dangerous guy is AA, getting all n-6 avids as AA may be equal
to lighten your bulbs with 60 kV power.
But, there are special products from lineoleate that cannot be exchanged
by another analogue from eg. AA or DGLA or other acids. Isoprostanoids
seems to have other physiological effects than the prostanoid analogue.
In fact, all PG's and LT, TX etc. have specific effects and effect of
PGE1 <> PGE2 <> PGE3 etc.
Steven B. Harris
writes:
>C22:6(n-6)? I.e. 6,9,12,15,18,21cisC22:6??
>I thought the delta-21 bond is the one that connects to the carboxyl,
>which means it can't be desaturated. Am I wrong?
>
>Nimrod
No, you're right. C22:6(n-3) is the familiar DHA. There is no
C22:6:n-6, for reasons you note.