Re: Atkins vs South Beach vs Ornish

Jackie Patti wrote:

Michael Sand wrote:
I'm very optimistic in this respect. But why not using cheap oils
(rapeseed / canola for hot cooking and additionally flaxseed aka
linseed for salads etc.) a canister for at most a few $s instead of
buying it extravagantly packed in capsules or even following the
expensive fish oil hype. No problem for your body to build
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the most
important fish oil ingredients, from ALA. Or are there any advantages
I'm not aware of?

I understand that commonly-available canola oil is processed and
therefore contains trans fats, just at a low enough level to round to 0g
per serving on the label.

Are you sure? Why hydrogenate it? Moderate heat shouldn't harm.

As for the EPA/DHA thing, apparently ALA converts at a very low rate.
I'm not sure if this is true for everyone or a subset of folks. I know
Davis uses fish oil and is successful at reducing heart scan scores with
it and has had difficulty finding anything as successful for
vegetarians, except some expensive DHA stuff available a few places that
doesn't come from fish.

I never read about such an unavoidable bottleneck.
http://www.canolainfo.org/pdf/BRIO_01.PDF says

| ALA is converted in the body to to the omega 3 long chain,
| polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA)
| and docosohexaenoic acid (DHA) at a rate of approximately 20%.

but 'The Scientific Evidence for a Beneficial Health Relationship
Between Walnuts and Coronary Heart Disease'
http://jn.nutrition.org/cgi/reprint/132/5/1062S.pdf reports

| Addition of walnuts to either the HD [habitual] or LF [20% fat] diet
| increased plasma concentrations of linoleic and alpha-linolenic
| acids and decreased palmitic (16:0), oleic, and arachidonic acids
| without changing concentrations of EPA and DHA.

and in 'Dose-response effects of dietary gamma-Iinolenic acid-enriched
oils on human polymorphonuclear-neutrophil biosynthesis of leukotriene
B4' http://www.ajcn.org/cgi/reprint/55/1/39.pdf I read on p. 41

| Although the PMN concentration of alpha-linolenic acid, a
| constituent of BCO, was increased in PMNs of the BCO group,
| interestingly, this increase did not significantly influence
| the PMN concentrations of EPA and docosahexaenoic acid (DHA,
| 22:6n-3), which are both desaturation and elongation
| metabolites of alpha-linolenic acid.

Weird, increase in ALA, but no change in EPA / DHA levels.

I found the most profound statement on page 6 of 'Polyunsaturated
fatty acids in the food chain in the United States'
(http://www.ajcn.org/cgi/reprint/71/1/179S.pdf):

| The recommended ratio of n-6 to n-3 fatty acids is 2.3:1 and has
| been made to maximize the conversion of ALA to DHA (40). Because
| of competition between n-6 and n-3 fatty acids for desaturase and
| elongase enzymes, the quantity of linoleic acid in the diet can
| affect the extent to which ALA is converted to EPA and DHA in vivo.
| Kinetic studies conducted in vivo (41) have shown that ~15% of
| dietary ALA is converted to the long chain n-3 fatty acids [which
| include 5 fatty acids of which 3 predominate: 20:5, 22:5, and 22:6
| at typical intakes of both linoleic acid (15 g/d; 5% of energy)
| and ALA (2 g/d; 0.6% of energy)]. Quantitatively, this conversion
| results in ~300 mg of n-3 long-chain fatty acids being derived via
| conversion from ALA. When dietary linoleic acid is increased to
| 30 g/d, conversion of ALA to the long-chain n-3 fatty acids is
| reduced by ~40% (41). Thus, the conditions that favor maximal
| conversion of ALA to EPA and DHA are critically dependent on the
| amount of linoleic acid in the diet.

In consequence, when continuing the 'western' dietary style, a
supplement of EPA and DHA seems to be favourable. But one primarily
ought to focus on improving the omega-6:omega-3 ratio, which promotes
the building of EPA/DHA (highly unsaturated fatty acids, HUFA) as
well. I won't doubt, that with our ancestors' n-6:n-3 ratio of about 1
sufficient quantities were attainable:

In the example above with an n-6:n-3 ratio of 15 g/d : 2 g/d = 7,5,
which is a bit better than the current US average, you get 15% of ALA
= 300 mg converted, whereas the goal is about 650 mg EPA + DHA per
day. The question is, by how much the conversion rate increases when
cutting the ratio in half (to realistic 3, half the way to
physiological conditions) with the knowledge of a 40% reduction when
doubling the ratio. Not unlikely, that even such a little move may be
enough to cover the daily need in HUFA. An ALA intake of 2 g/d is
equivalent to 4 ml flaxseed oil (inherent ratio of 0,3) or 20 ml
canola oil (inherent ratio of 2), the latter less qualified to correct
the overall ratio as long as unfavourable n-6 fatty acids from other
sources are involved in relevant quantities and have to be countered.

But let me state it clearly, it's a different story, if you not only
aim at a healthy nutrition, but try to shape your dietary components
in a way to positively influence a specific medical condition. One
example:

You may have read my comments on gamma-linolenic acid (GLA) as a
component of Atkins' 'essential' oil capsules, which I don't think is
indispensable for healthy people. OTOH supplementing GLA may make
sense under certain conditions like acute or chronic inflammatory
processes (psoriasis vulgaris, rheumatoid arthritis, other autoimmune
diseases etc.), where some immunomodulatory effect has been shown.
Vincent A. Ziboh worked on this topic and demonstrated an inhibition
of the transformation from arachidonic acid to leukotriene B4 by the
metabolites of GLA, though I'm not able to duplicate his explanation
(competitive inhibition, PGE1 production etc.). In
http://www.ajcn.org/cgi/reprint/71/1/361S.pdf the diagram on page 365S
lacks the important fact, that the classical desaturation & elongation
pathway from linoleic acid (LA; 18:2n-6) to arachidonic acid (AA;
20:4n-6) also leads via gamma-linolenic acid (GLA; 18:3n-6) and
dihomo-gamma-linolenic acid (DGLA; 20:3n-6), e.g. described in
http://www.jlr.org/cgi/reprint/28/11/1342.pdf. Now, why in the world
should the dietary GLA behave differently from GLA produced internally
from dietary LA? Maybe someone else has a plausible explanation to
bring me round. But as long as this uncertainty continues I see GLA as
an ordinary omega-6 fatty acid, which I personally won't deliberately
add to my diet, though in case of an immunologic disorder it may be
beneficial.

I am not clear on the saturated fat vs. polyunsaturated fat question;
research seems contradictory to me.

In which respect? Replacing saturated fat by omega-6 rich vegetable
oils, as proclaimed by the anti-cholesterol campaign throughout
previous decades, obviously was a washout. But what against taking the
chance to shift to the advantageous omega-3 fatty acids instead?

The proinflammatory effects of LA also raise some further questions,
e.g. whether VAT is dangerous in principle or only with a PUFA
dysbalance high in unhealthy n-6 fatty acids. There's a study, which
shows a dependency of the blood pressure from the alpha-linolenic acid
contents of fatty tissue. Allow me another citation from 'The
Scientific Evidence for a Beneficial Health Relationship Between
Walnuts and Coronary Heart Disease'
(http://jn.nutrition.org/cgi/reprint/132/5/1062S.pdf):

| Another study, by Berry et al. (68), investigated the
| relationship of the fatty acid concentration in adipose tissue
| and BP in 399 free-living males in New York City. The
| investigators concluded that alpha-linolenic acid had a
| disproportionate association with BP, ie, a 1% increase in
| alpha-linolenic acid reduced BP 5 mm Hg.

Moreover, it's no secret, that LA also induces insulin resistance.
What if our metabolic disaster as a whole is mainly driven by the PUFA
problematic, and you see a major improvement of all aspects of this
syndrome with nothing but a normalized omega-3 FA concentration in
your fatty tissue regardless of your BMI? Should we simply turn our
bad VAT into good VAT instead of getting rid of it, which anyway we
rarely succeed in?

I eat flax meal as a basic cereal ingredient and to make bread-like and
muffin-like concoctions (often with almond meal).

Is that grinded resp. pulverized linseed / almonds? And what do you
use to bind the dough? Eggs?

I replaced cocoa butter in chocolate with coconut oil via a homemade
bark I make. Net increase in saturated fat is zero with whatever
advantages coconut oil adds.

You replace it? Or do you make chocolate from scratch using
(hardened?) coconut oil and cocoa? Some time ago I came across
http://www.level1diet.com/coconut-oil-supplement-medium-chain-triglycerides-health-benefits.html
but think that's nonsense, though I appreciate the beneficial effects
of coconut oil ... to my skin in the form of suntan oil. ;-)

I use lecithin as the main emulsifier in cooking. It's dead cheap when
bought as a baking ingredient and only gets expensive if packaged as a
supplement. A completly painless change in my diet.

It seems to me that eating better is a lot easier, cheaper and more
pleasant than taking pills. It also seems my strategy maximizes my
health no matter what turns out to be the ultimate truth about fats.

Right. We have to be content with a healthy approach, as the
theoretical optimum is out of reach.

Were you aware of the subversive tendencies described below (once
again http://www.ajcn.org/cgi/reprint/71/1/179S.pdf, p. 3):

| Factors such as cultivar, variety, growing region, and climatic
| conditions have marked influences on the ALA content of soybean
| and canola oil. For example, there have been substantial efforts
| over the years to reduce the ALA content of soybean oil through
| classic plant-breeding techniques and, more recently, by genetic
| manipulation. This is attractive to the edible-oil industry for
| use in a nonhydrogenated liquid salad oil and in deep-frying
| applications because of the increased oxidative stability.
| Low-ALA soybean varieties with much lower ALA contents, in the
| range of 3-4%, than the common williams variety (ie, ~7.8%) are
| now becoming commercially available.

That means, for a better keeping 'quality' the food industry
deliberately further weakens our already impaired health, and the
consumer isn't even aware of the lousy ingredients, reads 'soybean'
and thinks 'wow, great'. Looks like premeditated grievous bodily harm.

Kind regards

Mike

BTW: You got my mail?

.

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