Fructose and heart disease

[Bigvince]

More about the association of sugar and heart disease. From
the ADA meeting

" ADA: Cheap Fructose May Exact High Metabolic Price
;Medpage today;
6/26/07"

"CHICAGO, June 25 -- Fructose in sodas and other beverages --
but not glucose -- can set patients on the fast track to
atherosclerosis, investigators here reported.

These data were presented at a conference and the data and
conclusions should be considered preliminary until published
in a peer-reviewed journal. Overweight men and women assigned
to drink fructose-sweetened beverages as 25% of their energy
intake developed atherogenic lipid profiles in just two weeks,
whereas those who drank glucose-sweetened drinks did not, said
Kimber Stanhope, M.S., of the University of California at
Davis, and colleagues.

"Compared with consumption of glucose, 10 weeks of
fructose consumption as 25% of energy requirements
promoted the development of an atherogenic lioproprotein
phenotype and glucose intolerance/insulin resistance in
older, overweight and obese men and women," Stanhope said
at the American Diabetes Association meeting"........ the
article further notes

" In addition, patients who took fructose had increases in
fasting plasma concentrations of LDL (up 17% + 4%),
Apolipoprotein B (up 28% 7%), small dense LDL (up 27% + 11%),
postprandial concentrations of remnant lipoprotein (up 77% +
19%) and of remnant-like particle cholesterol (up 53% + 12%; P
for each < 0.01). None of these parameters was unchanged in
patients who drank glucose.

"These effects appear to be exacerbated when fructose
sweetened- beverages are consumed with a typical ad labium
western diet compared with an energy-balanced moderate fat
diet," she said."

I expect this may contribute to the ADA reconsidering thier
dietary advice Thanks Vince http://www.medpagetoday.com/Meet-
ingCoverage/ADAMeeting/tb/6021

[monty1945]

"...developed atherogenic lipid profiles..."

These are just indirect markers. It is now known that only LDL
with PUFAs in it can lead to atherosclerosis, so if you know
what to do to avoid this situation, you don't need to fear
indirect markers. That said, I only drink unsweetened, organic
white tea or filtered water. On very rare occasions I drink
unsweetened fruit juice (usually pineapple or orange). The
problem with most soft drinks is that they are just excess
calories, often consumed in between meals, and some contain
phosphoric acid, which should be avoided. You don't want to
keep raising your insulin every hour or so - you just want an
insulin spike three times a day, with each meal.
Calorie-restricted animals which live longer have an intense
insulin spike with each meal, which
Dr. Spindler believes is useful for ridding the body of
damaged biomolecules and creating new, functional ones.
However, the spike doesn't last long. If you drink the
usual soft drinks between meals, you keep your high
insulin levels raised, which can lead to insulin
desensitization.

http://groups.msn.com/TheScientificDebateForum-

I am not selling anything and am not affiliated with anyone or
any company that is. What you will find are the results of my
investigations over the last several years, along with a great
deal of evidence citation from the professional literature.

[Mattlb]

On Jun 28, 3:55 am, monty1...@lycos.com wrote:
> "...developed atherogenic lipid profiles..."
>
> These are just indirect markers. It is now known that only
> LDL with PUFAs in it can lead to atherosclerosis,

That's all LDL then. Even yours. As the article points out,
small dense LDL was increased and this is more atherogenic
(and contains less PUFA) than other types of LDL. LDL
type/level isn't even a marker (indirect or otherwise), it's a
risk factor.

MattLB

[monty1945]

Risk factor and marker (indirect) are used to mean the exact
same thing, for example:

[Fibrinogen as a cardiovascular risk factor--marker or
causal factor?]

Source: Tidsskr Nor Laegeforen. 1999 Aug 20;119(19):2829-32.

However, the more important point is that it's not that a
person has some LDL molecules with PUFAs in them, but the
amount of PUFAs. The more PUFAs, the more likely the LDL is to
become dsyfunctional. Obviously, an antioxidant-rich diet
might also play a major role, relative to an antioxidant-poor
diet. Similarly, a diet rich in meat cooked while exposed to
air is likely to cause more problems than a diet that contains
no such items (or very small amounts).

As many scientists have pointed out: ..."small dense LDL is
more readily available to be oxidized. In addition, small
dense LDL particles are themselves more susceptible to
oxidation..."

Source:
http://jcem.endojournals.org/cgi/content/full/84/9/3212

The key is to avoid oxidative stress, which is something that
is very difficult to do if you have arachidonic acid in your
cells. The evidence is plentiful on this point. If you find
that it causes you cognitive dissonance for some reason, that
is another matter - one that is of little interest to me.

[Mattlb]

On Jun 28, 9:53 pm, monty1...@lycos.com wrote:
> Risk factor and marker (indirect) are used to mean the exact
> same thing,

No they aren't. You're using muddled terminology again. A risk
factor is something that causes (directly or indirectly) a
problem and the more of it you have the greater the risk of
the problem occurring. A marker is something that indicates a
problem is already present i.e. it's a recognisable
consequence of the problem, not a cause.

> for example:
>
> [Fibrinogen as a cardiovascular risk factor--marker or
> causal factor?]

Yes. Is it a marker or a causal factor? One or the other.

> However, the more important point is that it's not that a
> person has some LDL molecules with PUFAs in them, but the
> amount of PUFAs. The more PUFAs, the more likely the LDL is
> to become dsyfunctional.

How many PUFA in an LDL particle is required then?

> As many scientists have pointed out: ..."small dense LDL is
> more readily available to be oxidized. In addition, small
> dense LDL particles are themselves more susceptible to
> oxidation..."

So you've changed your tune about the lipid profile just
being indirect markers have you? That's good, because small
dense LDL is a causitive agent and therefore a risk factor.
The reason it's worse is the reason LDL is bad in the first
place - long survival time in the blood so a greater risk of
ending up in the artery wall. The amount of PUFA is a
side-issue since in the blood LDL causes no harm and doesn't
get oxidised.

> The key is to avoid oxidative stress, which is something
> that is very difficult to do if you have arachidonic acid in
> your cells.

You still can't grasp that AA is released as a deliberate
signal molecule can you?

> evidence is plentiful on this point.

So you say, but you can't provide reasons or mechanisms so
it's just a faith position.

> If you find that it causes you cognitive dissonance for
> some reason, that is another matter - one that is of little
> interest to me.

Anything beyond your own version of biology seems to have
little interest to you, partly because your world-view would
be shattered if you acknowledged it.

MattLB

[Bigvince]

On Jun 27, 10:55 pm, monty1...@lycos.com wrote:
> "...developed atherogenic lipid profiles..."
>
> These are just indirect markers. It is now known that only
> LDL with PUFAs in it can lead to atherosclerosis, so if you
> know what to do to avoid this situation, you don't need to
> fear indirect markers. That said, I only drink unsweetened,
> organic white tea or filtered water. On very rare occasions
> I drink unsweetened fruit juice (usually pineapple or
> orange). The problem with most soft drinks is that they are
> just excess calories, often consumed in between meals, and
> some contain phosphoric acid, which should be avoided. You
> don't want to keep raising your insulin every hour or so -
> you just want an insulin spike three times a day, with each
> meal. I expect the problem with most soft drinks ;for those
> people who are at the most serious risk; those with insulin
> resistance ;is in fact more related to the insulin levels
> caused by soft drinks and other foods. The effect of
> calories is not as important. Thanks Vince

[Bigvince]

On Jun 29, 8:55 am, MattLB <mat...@angelfire.com> wrote:
> On Jun 28, 9:53 pm, monty1...@lycos.com wrote:
>
> > Risk factor and marker (indirect) are used to mean the
> > exact same thing,
>
> No they aren't. You're using muddled terminology again. A
> risk factor is something that causes (directly or
> indirectly) a problem and the more of it you have the
> greater the risk of the problem occurring. A marker is
> something that indicates a problem is already present i.e.
> it's a recognisable consequence of the problem, not a cause.
>
> > for example:
>
> > [Fibrinogen as a cardiovascular risk factor--marker or
> > causal factor?]
>
> Yes. Is it a marker or a causal factor? One or the other.
>
> > However, the more important point is that it's not that a
> > person has some LDL molecules with PUFAs in them, but the
> > amount of PUFAs. The more PUFAs, the more likely the LDL
> > is to become dsyfunctional.
>
> How many PUFA in an LDL particle is required then?
>
> > As many scientists have pointed out: ..."small dense LDL
> > is more readily available to be oxidized. In addition,
> > small dense LDL particles are themselves more susceptible
> > to oxidation..."
>
> So you've changed your tune about the lipid profile just
> being indirect markers have you? That's good, because small
> dense LDL is a causitive agent and therefore a risk factor.
> The reason it's worse is the reason LDL is bad in the first
> place - long survival time in the blood so a greater risk of
> ending up in the artery wall. The amount of PUFA is a
> side-issue since in the blood LDL causes no harm and doesn't
> get oxidised.
>
> > The key is to avoid oxidative stress, which is something
> > that is very difficult to do if you have arachidonic acid
> > in your cells.
>
LDL is not a risk factor for nor a marker of atherosclerosis,
How can I say that?. Studies have shown no correlation between
the amount of LDL and the amount of atherosclerosis, Also
reducing LDL levels with drugs other than statins has not been
shown to prevent events. If LDL by itself was a true causative
agent one would expect a much greater correlation between
these variables. Nor is it a marker ; while these terms are
sometimes used interchangeably . LDL levels again do not
accurately indicate atherosclerosis, What is the culprit
oxidized LDL. What ever benefit statins produce is a result of
their anti inflammatory effect not LDL lowering. Thanks Vince