Re: fructose

[Guest guest]

Forgot to add, I avoid all processed foods as much as possible. Don' t wish

Mamon tinkering with my health. But once off the sweet wagon, it becomes

really unpleasant to the tongue. I avoid all sweet tasting substances out of

preference, be it non glucose jam to stevia, which I find ghastly. (my next

project is to get off salt tho the BP is very low) Yoghurt is delicious

without any sweetener, and same for the wonderful varieties of gorgeous

real-leaf teas.

On that last, we should make the effort to drink eco tea as otherwise the

drink becomes " Infusion of DDT " or those parkinsons-causing insecticides

they've just identified. And IMHO, bag tea isn't tea. Bags are tea droppings

( ; -} ) that in the trade are called 'dust'. In fact, it is swept from the

floor (with what else?) of the tea factories after the more prestigious tea,

is sifted through large strainers. Were it only dust! The big leaf tea is

the best and the taste is a quantum leap above the 'dust'. Most people

haven't tried 'real' green tea, that is, fresh from the last season,

properly stored in cool dark places without contact to air. It is a great

delicacy and is worth the expense! There are several wonderful sources on

the internet where gourmet eco tea can be found- uptontea.com, stashtea.com

(or was that stash.com?) and many many other sites found by punching in

'green tea' in a search engine. For Japanese tea, Ippodo company is one of

the very best to be found. Expensive though...

As you can see, I am a quasi-fanatic, but then, I enjoy the best the world

has to offer

MM (as in mmmmm)

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[Guest guest]

> >>>>Do keep in mind that the current dogma is that oxidized LDL

> cholesterol is what makes arterial plaque inflammed.

>

> ***, by referring to the current line of thinking as " dogma "

are you

> indicating that you think it's incorrect? If so, do you have an

alternate

> theory? I've read the 'oxidized LDL' research and it seems to make

sense to

> me. But it's not like I'm really capable of seeing flaws in studies

like

> this because I don't yet have a solid enough foundation in

biochemistry to

> view it critically, or identify flaws.

hmm, my rhetorical techniques exposed!

The thing to keep in mind about the oxidized LDL theory is that

regardless of whether or not it pans out, we know one way not to

treat it: lowering cholesterol. We've tested lowering cholesterol

clinically many times and it has failed every time(except for the

statin drugs, which are also ant-oxidants, anti-inflammatories, anti-

thrombotic (technical word for anti-clotting), and restore

endothelial function). At this point the research is unequivicable:

lowering cholesterol neither lowers the rate of heart disease or

overall mortality.

So with that in mind, oxidized LDL is still very theoretical. All the

research so far is in-vitro. In-vitro, when you oxidize LDL by

exposing it to metal ions, it causes atherosclerosis to progress in

the bad way (become inflammed etc...). But when you add anti-

oxidants, this doesn't happen. This is why people are now advised to

eat brightly colored veggies (is Dr. Byrnes or anyone else who knows

more about the meat based anti-oxidants like glutathione around to

comment on that?).

However, no one knows the source of the oxidation. Its actually a hot

topic in research right now. Google " source oxidized LDL in-vivo " and

you'll get a lot of web pages of scientists with a lot of differant

pet theories with preliminary research. If the theory holds up, then

it would be this source that causes heart disease, and its very

unlikely that this source is dietary saturated fat - saturated fat is

harder to oxidize than unsaturated fat! If anything saturated fat

should be protective because it won't draw as much on the bodies anti-

oxidant stores as other types of fat.

So really all that oxidized-LDL does is keep the focus on

cholesterol, and the clinically unsound advice to lower your

cholesterol can be uncritically accepted.

[Guest guest]

>>>>hmm, my rhetorical techniques exposed!

***Well, someone had to do it!

>>>>So really all that oxidized-LDL does is keep the focus on

cholesterol, and the clinically unsound advice to lower your

cholesterol can be uncritically accepted.

***OK, I guess I've been reading the 'wrong' stuff on this. My understanding

is that PUFAs are in large part responsible for oxidized LDL. I guess I

don't read enough mainstream lit, and read too much alteranative

literature - which is where I get such wacky ideas

Suze Fisher

Web Design & Development

http://members.bellatlantic.net/~vze3shjg/

mailto:s.fisher22@...

[Guest guest]

> >>>>hmm, my rhetorical techniques exposed!

>

> ***Well, someone had to do it!

*sulks unhappily*

> >>>>So really all that oxidized-LDL does is keep the focus on

> cholesterol, and the clinically unsound advice to lower your

> cholesterol can be uncritically accepted.

>

> ***OK, I guess I've been reading the 'wrong' stuff on this. My

understanding

> is that PUFAs are in large part responsible for oxidized LDL. I

guess I

> don't read enough mainstream lit, and read too much alteranative

> literature - which is where I get such wacky ideas

Considering that we're advised to take anti-oxidants for that reason,

I think it would be a very logical conclusion to also try to reduce

the total oxidative stress put on the system. I've even come across a

study that promoted olive oil because it reduced the levels of

oxidation. Where are the studies promoting animal fats and tropical

oils as doing an even better job than olive oil?

But now that you mention it, I'd love to see an experiment in which

in-vitro LDL cholesterol is exposed to polyunsatured fats to see how

readily it oxidizes. The lipid cores of atherosclerotic plaques are

primarily polyunsaturates.

[Guest guest]

>>>>>*sulks unhappily*

***stop sulking...you are too much fun to tease, but not if you sulk and not

if it makes you unhappy ;->

Me:

OK, I guess I've been reading the 'wrong' stuff on this. My

understanding is that PUFAs are in large part responsible for oxidized LDL.

I

guess I don't read enough mainstream lit, and read too much alteranative

literature - which is where I get such wacky ideas

J:

Considering that we're advised to take anti-oxidants for that reason,

I think it would be a very logical conclusion to also try to reduce

the total oxidative stress put on the system.

***For any number of reasons, I'm sure. When you think about it, everything

we are doing nutritionally as a society is absurd. Which I'm sure everyone

here is already aware of. We cosume way too much refined carbs (that may

result in glycation), way too much factory-farmed meat (which no longer

resembles anything natural thanks to bizarre farming practices as clearly

outlined in the NY Times article posted today, and has a *very high* n-6:n-3

ratio), and we are now consuming fish and flax oils in relatively large

quanitity to counteract the high n-6 content of our diet resulting from

eating too much grain and factory farmed meats...thus creating an oxidative

burden likely unknown to our ancestors.

Nice.

>>>I've even come across a

study that promoted olive oil because it reduced the levels of

oxidation. Where are the studies promoting animal fats and tropical

oils as doing an even better job than olive oil?

***Assuming that the reason mono and saturated lipids *reduce* oxidation

levels due to the fact that they *replace* PUFAs?

>>>>But now that you mention it, I'd love to see an experiment in which

in-vitro LDL cholesterol is exposed to polyunsatured fats to see how

readily it oxidizes. The lipid cores of atherosclerotic plaques are

primarily polyunsaturates.

***Would something like this help?

----------

Effect of the fat composition of a single meal on the composition and

cytotoxic potencies of lipolytically-releasable free fatty acids in

postprandial plasma.

Chung BH, Hennig B, Cho BH, Darnell BE

Atherosclerosis 1998 Dec 141:321-32

Abstract

Ingestion of a meal increases plasma levels of triglyceride (TG)-rich

lipoproteins through the secretion of intestine-derived chylomcirons and

liver-derived very low density lipoproteins (VLDL). We have determined the

effects of the fat composition of a single meal on the composition of TG in

TG-rich lipoproteins (VLDL + chylomicrons) and circulating and

lipolytically-releasable free fatty acids (FFA) in postprandial (PP) plasma

and on the cytotoxic potencies of the lipolytically-released FFA to cultured

arterial wall cells. PP lipemia was induced by feeding fasted normolipidemic

human subjects with a meal rich in saturated fat (SF) and another meal rich

in polyunsaturated fat (PUF), or vice versa; each meal provided 65% of

energy as fat, and polyunsaturated to saturated fatty acid ratios (P/S) of

the SF and PUF in the meals were 0.40 and 2.49, respectively. The mean P/S

of TG in TG-rich lipoproteins (1.43) and circulating FFA (1.46) in 4 h PP

plasma of PUF were significantly higher than those in PP plasma of SF (0.44

and 0.59, respectively) in fasting plasma (0.52 and 0.53, respectively). In

vitro lipolysis of fasting and PP serum by purified bovine milk lipoprotein

lipase (LpL) resulted in a marked (8.8-12.3-fold) increase in the serum FFA

level. The P/S of serum FFA in postlipolysis fasting and PP serum were

consistently higher than that of FFA or that of TG associated with TG-rich

lipoproteins in prelipolysis fasting and PP serum, indicating that

polyunsaturated TG in VLDL and/or chylomicrons is more susceptible than

saturated TG to lipolysis. When postlipolysis serum was interacted with

cultured endothelial cells and mouse peritoneal macrophages (MPM), the

lipolytically-released FFA in PP serum of SF and PUF disrupted the barrier

function of endothelial cells and were cytotoxic to cultured MPM; FFA in

postlipolysis fasting serum was not cytotoxic. FFA in postlipolysis PP serum

of PUF were consistently more potent than that in postlipolysis PP serum of

SF. Further study showed that all long-chain monounsaturated FFA and

polyunsaturated FFA, but not saturated FFA, incorporated into lipoproteins

(LDL) were cytotoxic to cultured MPM. In conclusion, despite the generally

well-accepted belief that SF is more atherogenic than PUF, the present study

provides in vitro evidence that the lipolytic remnant products of TG-rich

lipoproteins produced after a meal rich in PUF are more injurious to

arterial wall cells than those produced after a meal rich in SF.

-----------------------------

Also of interest:

crsociety/files/VCO/OilAnalysis291201.gif

(check out the plaque formation index)

Is this the olive oil study you mentioned?

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=8\

406127 & dopt=Abstract

Free Radic Biol Med 1993 Sep;15(3):273-80 Related Articles, Books

Oxidation resistance, oxidation rate, and extent of oxidation of human

low-density lipoprotein depend on the ratio of

oleic acid content to linoleic acid content: studies in vitamin E deficient

subjects.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN.

Department of General Internal Medicine, University Hospital, Nijmegen, The

Netherlands.

The purpose of this study was to understand better the factors providing

oxidation resistance to human low-density

lipoprotein (LDL). Therefore, the susceptibility to copper-induced in vitro

oxidation of LDL from vitamin E deficient

patients and normal healthy subjects was studied. Surprisingly, the LDL of

vitamin E deficient patients appeared less

susceptible to oxidation than control LDL. Both oxidation rate and extent of

oxidation, measured as diene production,

were reduced when compared to control LDL. The lag time, a measure of

resistance to oxidation, was not different from

the lag time of LDL from healthy subjects. No relation was found between

vitamin E content and resistance against

oxidation. LDL from vitamin E deficient patients contained lower amounts of

vitamin E, less cholesteryl esters, and

increased amounts of triglycerides. Furthermore, its oleic acid content was

increased and its linoleic acid content

decreased. Linear regression analyses revealed that the ratio of oleic acid

content to linoleic acid content was

strongly correlated with the lag time, and inversely correlated with

oxidation

rate and extent of oxidation. Thus, LDL

rich in oleic acid and poor in linoleic acid was less easily oxidized.

It is concluded that the susceptibility of LDL to oxidation is determined

not

only by its antioxidant content, but also

by other compositional factors, and more specifically by the ratio of oleic

acid content to linoleic acid content.

PMID: 8406127 [PubMed - indexed for MEDLINE]

Suze Fisher

Web Design & Development

http://members.bellatlantic.net/~vze3shjg/

mailto:s.fisher22@...

[Guest guest]

> >>>>>*sulks unhappily*

>

> ***stop sulking...you are too much fun to tease, but not if you

sulk and not

> if it makes you unhappy ;->

> Me:

> OK, I guess I've been reading the 'wrong' stuff on this. My

> understanding is that PUFAs are in large part responsible for

oxidized LDL.

> I

> guess I don't read enough mainstream lit, and read too much

alteranative

> literature - which is where I get such wacky ideas

I had the same problem for a long time. Everything I'd read came from

Ravnskov, etc... I participated on general nutrition groups and

although I made some good points I also got into trouble. That may be

why I try not to be *too* dismissive of the cholesterol research even

if I don't agree with the conclusions. We are all subject to bias and

selective citation! Reading the mainstream research has been a big

help, and I think it makes me a better debater!

> J:

> Considering that we're advised to take anti-oxidants for that

reason,

> I think it would be a very logical conclusion to also try to reduce

> the total oxidative stress put on the system.

>

> ***For any number of reasons, I'm sure. When you think about it,

everything

> we are doing nutritionally as a society is absurd. Which I'm sure

everyone

> here is already aware of. We cosume way too much refined carbs

(that may

> result in glycation), way too much factory-farmed meat (which no

longer

> resembles anything natural thanks to bizarre farming practices as

clearly

> outlined in the NY Times article posted today, and has a *very

high* n-6:n-3

> ratio), and we are now consuming fish and flax oils in relatively

large

> quanitity to counteract the high n-6 content of our diet resulting

from

> eating too much grain and factory farmed meats...thus creating an

oxidative

> burden likely unknown to our ancestors.

> Nice.

It's a mess. I think that's why I clicked with WAP. Everything else

had such easy answers to poor health. It was only WAP that took the

full measure of how bad our diet has deteriorated, but it also shows

what you can do to get healtheir.

> >>>I've even come across a

> study that promoted olive oil because it reduced the levels of

> oxidation. Where are the studies promoting animal fats and tropical

> oils as doing an even better job than olive oil?

>

> ***Assuming that the reason mono and saturated lipids *reduce*

oxidation

> levels due to the fact that they *replace* PUFAs?

I'd say that, also it may be that carbs can increase oxidation via

glycation, although I'd guess that it would be a minor or non-

existant factor in a healthy person.

> >>>>But now that you mention it, I'd love to see an experiment in

which

> in-vitro LDL cholesterol is exposed to polyunsatured fats to see how

> readily it oxidizes. The lipid cores of atherosclerotic plaques are

> primarily polyunsaturates.

>

> ***Would something like this help?

>

<snip abstracts>

Wow! That in-vitro one about SF v. PUFA is a great find! Thanks for

that abstract, I'm definitely hanging on to that. I'll have to check

out 'related articles' as well as other works by the authors to see

what else they've done.

I think that I came across a differant olive oil study, but I didn't

pay too much attention to it so I was looking for other things at the

time. But it makes the same point.

[Guest guest]

Hi folks:

I am NOT recommending fructose. It is after all empty calories like

glucose and sucrose.

But, unlike other natural sweeteners, it has an extraordinarily low

glycemic index of 20. It is also much sweeter than other natural

sweeteners per gram, about 2.5 times sweeter than glucose IIRC.

So it has some things going in its favor. At least relative to

sucrose and glucose.

Here is one source listing glycemic indexes of foods, including

fructose.

http://www.sportfit.com/tips/nutrition/glycemic_index.html

Rodney.

> > > Hi All,

> > >

> > > It seems from the pdf- but not Medline abstract-available below

> > excerpts of a paper

> > > that fructose in our diets is bad. Fructose is part of

sucrose,

> > but now it seems

> > > that they add fructose to many drinks.

> > >

> > > Dietary Fructose: Implications for Dysregulation of Energy

> > Homeostasis and

> > > Lipid/Carbohydrate Metabolism.

> > > Havel, J..

> > > Nutrition Reviews, May2005, Vol. 63 Issue 5, p133, 25p

> > >

> > > Abstract: Fructose intake and the prevalence of obesity have

both

> > increased over the

> > > past two to three decades. Compared with glucose, the hepatic

> > metabolism of fructose

> > > favors lipogenesis, which may contribute to hyperlipidemia and

> > obesity. Fructose

> > > does not increase insulin and leptin or suppress ghrelin, which

> > suggests an

> > > endocrine mechanism by which it induces a positive energy

balance.

> > This review

> > > examines the available data on the effects of dietary fructose

on

> > energy homeostasis

> > > and lipid/carbohydrate metabolism. Recent publications, studies

in

> > human subjects,

> > > and areas in which additional research is needed are emphasized.

> > >

> > > ... SOURCES AND INTAKE OF DIETARY CARBOHYDRATE

> > > Dietary Carbohydrate Intake

> > > The National Academy of Sciences has recommended

> > > that between 45% and 65% of energy be derived from

> > > carbohydrates, 20% to 35% from fat, and 10% to 35%

> > > from protein, with no more than 25% of total energy

> > > from added sugars.5 Recommendations by the American

> > > Heart Association 6 and the American Diabetes Associa-tion

> > > 7 fall well within these broad guidelines: approxi-mately

> > > 50% of energy from carbohydrate, 30% from fat,

> > > and 20% from protein. There are two major, population-based

> > > methodological approaches for estimating energy

> > > and nutrient intakes. Food disappearance data reflect the

> > > nationwide availability of foods and thus tend to over-estimate

> > > consumption. In contrast, survey-based ap-proaches

> > > that rely primarily on the ability of respondents

> > > to recall categories and amounts of previous intake tend

> > > to underestimate consumption but have the advantage of

> > > estimating intake characteristics in distinct subsets of the

> > > population. Results from the US Department of Agricul-ture

> > > Continuing Survey of Food Intakes by Individuals

> > > (CSFII) suggest that from 1994 to 1996, non-vegetarians

> > > consumed 50% of energy from carbohydrate, 33% from

> > > fat, and 16% from protein, with 15% to 16% of energy

> > > provided by added sugars. Data from the National Health

> > > and Nutrition Survey (NHANES) as reported by the

> > > Centers for Disease Control and Prevention (CDC)8

> > > indicate that carbohydrate intake increased by about 62

> > > g/d in women and by about 69 g/d in men between 1971

> > > and 2000.

> > >

> > > ... ACKNOWLEDGMENTS

> > > This work was supported by Academic Network,

> > > Portland, Oregon. Academic Network receives grant

> > > funding from the Sugar Association, the Salt Institute,

> > > and Dairy Management, Inc. ...

>

> Al Pater, PhD; email: old542000@y...

>

>

>

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