Re: Coconuts in the context of tradiitional diets reduce the risk of CHD

From: montygram (nazztrader_at_lycos.com)
Date: 03/20/05

  • Next message: Laurie: "% cal from xxx..." 
    Date: 19 Mar 2005 20:20:08 -0800

    I've been posting about this for years here. Welcome to the club! The
    statistics are incredible, and the problem is that the phrase
    "saturated fat" has no scientific meaning as it is used by most people,
    including scientists. Here's a study that talks about fat and "red
    meat" causing cancer, and when they go into specifics about the fat,
    notice that they are talking about polyunsaturated faffy acids, not
    saturated ones. It's all about oxidative stress, and saturated fatty
    acids actually act as a buffer against this form of stress, while the
    other fatty acids are potentially very bad news (if eaten in more than
    small amounts).

    Ann N Y Acad Sci. 2004 Dec;1031:169-83.
    Effect of vitamin e on gene expression changes in diet-related
    carcinogenesis.
    Lunec J, Halligan E, Mistry N, Karakoula K.
    Genome Instability Group, University of Leicester, Genome Instability
    Group, Department of Cancer & Molecular Medicine, Level 0, RKCSB, LRI,
    Leicester, LE2 7LX, U.K. jl20@le.ac.uk.
    Colorectal cancer (CRC) is responsible for the second highest
    associated mortality in Western Europe and the United States.
    Approximately 95% of CRC is sporadic and believed to involve
    environmental agents and chronic inflammation as causal elements.
    Several recent studies have suggested a link with diet, in particular,
    red meat, dietary fats, and low consumption of vegetables. Lipid
    peroxidation and arachidonic acid metabolism have specifically been
    implicated in genotoxicity, tumor initiation, and promotion. We have
    examined the global gene expression profiles (Affymetrix; HU133A) of
    differentiated vs. undifferentiated colonocytes (CRL-1807), with and
    without vitamin E supplementation, while undergoing a lipid
    peroxidative stress. Malondialdehyde and hydroxynonenal, generated by
    heating a mixture of linoleic and linolenic acid, caused DNA adduct
    formation identified by immunofluoresence. We also observed a decreased
    ability for vitamin E to upregulate detoxifying enzymes against
    free-radical peroxidation, with the exception of mitochondrial
    superoxide dismutase in undifferentiated cells. However, there was an
    increased ability in undifferentiated, rather than in differentiated,
    colonic cells to detect DNA damage, initiate cytostasis, and then
    effect subsequent DNA repair and apoptosis, in the presence of vitamin
    E. The expression profile implies less genotoxic stress is experienced
    in vitamin E-supplemented colonocytes, particularly undifferentiated
    cells, and points to a mechanism by which dietary supplementation may
    prevent genotoxic damage and subsequent carcinogenic events in the
    colon, by both antioxidant and non-antioxidant-related mechanisms.

  • Next message: Laurie: "% cal from xxx..."

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