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Fructose and heart disease

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01 / Original postFructose and heart diseasebigvince · 28 Jun 2007 02 / This pagePosts 1–7Page 1 of 1 · chronological order 03 / Latest replyPost #7bigvince · 30 Jun 2007

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General fitness, health and nutrition
Published
28 June 2007
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bigvince
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  1. Original post
    bigvince
    Archived post
    #1

    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/MeetingCoverage/ADAMeeting/tb/6021

    Report
  2. Email address hidden
    Archived post
    #2

    "...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.

    Report
  3. MattLB
    Archived post
    #3
    Quoted message said:

    "...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

    Report
  4. Email address hidden
    Archived post
    #4

    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.

    Report
  5. MattLB
    Archived post
    #5
    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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?

    Quoted message said:

    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.

    Quoted message said:

    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?

    Quoted message said:

    evidence is plentiful on this point.

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

    Quoted message said:

    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

    Report
  6. bigvince
    Archived post
    #6
    Quoted message said:

    "...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

    Report
  7. bigvince
    Archived post
    #7
    MattLB said:
    Quoted message said:

    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.

    Quoted message said:

    for example:

    Quoted message said:

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

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

    Quoted message said:

    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?

    Quoted message said:

    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.

    Quoted message said:

    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

    Report

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