General fitness, health and nutrition · Public discussion

New theory on atherogenesis.

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General fitness, health and nutrition
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5 January 2006
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  1. Mol Nutr Food Res. 2005 Nov;49(11):999-1013. Related Articles, Links

    The relation of lipid peroxidation processes with atherogenesis: a new
    theory on atherogenesis.

    Spiteller G.

    Department of Organic Chemistry, University of Bayreuth, Bayreuth,
    Germany. [email hidden]

    The extremely high sensitivity of polyunsaturated fatty acids (PUFAs)
    to oxygen is apparently used by nature to induce stepwise appropriate
    cell responses. It is hypothesized that any alteration in the cell
    membrane structure induces influx of Ca2+ ions. Ca2+ ions are required
    to activate degrading enzymes, such as phospholipases and lipoxygenases
    (LOX) that transform PUFAs bound to membrane phospholipids to
    lipidhydroperoxides (LOOHs). Enzymatic reduction products of LOOHs seem
    to serve as ligands of proteins, which induce gene activation to
    initiate a physiological response. Increasing external impact on cells
    is connected with deactivation of LOX, liberation of the iron ion in
    its active center followed by cleavage of LOOH molecules to LO *
    radicals. LO * radicals induce a second set of responses leading to
    generation of unsaturated aldehydic phospholipids and unsaturated
    epoxyhydroxy acids that contribute to induction of apoptosis. Finally
    peroxyl radicals are generated by attack of LO * radicals on
    phospholipids. The latter attack nearly all types of cell constituents:
    Amino- and hydroxyl groups are oxidized to carbonyl functions, sugars
    and proteins are cleaved, molecules containing double bonds such as
    unsaturated fatty acids or cholesterol suffer epoxidation. LOOH
    molecules and iron ions at the cell wall of an injured cell are in
    tight contact with phospholipids of neighboring cells and transfer to
    these reactive radicals. Thus, the damaging processes proceed and cause
    finally necrosis except the chain reaction is stopped by scavengers,
    such as glutathione. Consequently, PUFAs incorporated into
    phospholipids of the cell wall are apparently equally important for the
    fate of a single organism as the DNA in the nucleus for conservation of
    the species. This review intends to demonstrate the connection of cell
    alteration reactions with induction of lipid peroxidation (LPO)
    processes and their relation to inflammatory diseases, especially
    atherosclerosis and a possible involvement of food. Previously it was
    deduced that food rich in cholesterol and saturated fatty acids is
    atherogenic, while food rich in n-3 PUFAs was recognized to be
    protective against vascular diseases. These deductions are in
    contradiction to the fact that saturated fatty acids withstand
    oxidation while n-3 PUFAs are subjected to LPO like all other PUFAs.
    Considering the influence of minor food constituents a new theory about
    atherogenesis and the influence of n-3 PUFAs is represented that might
    resolve the contradictory results of feeding experiments and chemical
    experiences. Cholesterol-PUFA esters are minor constituents of
    mammalian derived food, but main components of low density lipoprotein
    (LDL). The PUFA part of these esters occasionally suffers oxidation by
    heating or storage of mammalian derived food. There are indications
    that these oxidized cholesterol esters are directly incorporated into
    lipoproteins and transferred via the LDL into endothelial cells where
    they induce damage and start the sequence of events outlined above. The
    deduction that consumption of n-3 PUFAs protects against vascular
    diseases is based on the observation that people living on a fish diet
    have a low incidence to be affected by vascular diseases. Fish are rich
    in n-3 PUFAs; thus, it was deduced that the protective properties of a
    fish diet are due to n-3 PUFAs. Fish, fish oils, and vegetables contain
    besides n-3 PUFAs as minor constituents furan fatty acids (F-acids).
    These are radical scavengers and are incorporated after consumption of
    these nutrients into human phospholipids, leading to the assumption
    that not n-3 PUFAs, but F-acids are responsible for the beneficial
    efficiency of a fish diet.

    PMID: 16270286 [PubMed - in process]

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

    Who loves ya.
    Tom

    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com

    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore

    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking

  2. Yes, this is what I have been saying here for some time. When in
    doubt, you do not go against what is basic science, and instead rely
    upon the "epidemiological" studies that you want to "believe" in - that
    is just dangerous. There are other things in fish too, and many people
    mistakenly believe that scientists know about every kind of molecule in
    all food, which is far from the reality. The only hypothesis that
    accounts for "chronic disesease"/ "aging" at this point is the one
    involving free radical damage, so it only makes sense to avoid food
    that is likely to contribute to dangerous reactions of this sort. The
    "jury is still out" on fish, especially the oily kinds, and also in
    terms of pollution, processing, and cooking techniques, for example the
    study showing that steaming salmon results in massive amounts of
    oxidized cholesterol. Even the "experts" who advise eating fish say to
    limit the amount, due to pollution, etc. There are much better food
    choices, but because "saturated fat" got blamed for "heart disease,"
    when in fact the unsaturated fatty acids were to blame (especially
    considering the processing, cooking techniques, etc.), the "experts"
    look at oily fish as something "healthy," even though peoples who ate
    such diets died around age 40, if they were fortunate to live that
    long..

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