RE: FITNESS: Diet and Exercise

From: gts (gts_2000@yahoo.com)
Date: Mon Apr 14 2003 - 21:29:37 MDT

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    Anders Sandberg wrote:

    > On Sat, Apr 12, 2003 at 04:44:08PM -0400, gts wrote:
    >>
    >> A huge theoretical problem I have with Atkins is that the brain
    >> subsists almost entirely on glucose. It uses something like 25% of
    >> available glucose while representing only something like 5% of total
    >> body weight.
    >
    > A related issue which would be interesting to examine is the
    > memory effects. Glucose is a memory enhancer, and seems to
    > act by stimulating the basal forebrain/septal area to sent
    > acetylcholine to the hippocampus. Giving it glucose-like
    > chemicals produces the same effect, and has the same
    > inverted-u dose response curve. But what about ketones?

    Sorry it took so long for me to get back to you on this, Anders. Your
    question "But what about ketones?" was too interesting to answer without
    doing some research.

    The abstract below indicates that in whole animals ketones enhance the
    synthesis of GABA at the expense of NMDA receptor agonists like aspartate.
    This is not surprising to me. My own experience of the Atkins ketogenic diet
    is that, over time, it tends to dull the mind. This is just exactly what the
    up-regulation of GABA and down-regulation of aspartate should do. On the
    positive side, the down-regulation of NMDA agonists might inhibit
    excitotoxic damage. -gts

    ABSTRACT:
    Ketone bodies and brain glutamate and GABA metabolism.
    Dev Neurosci 1998;20(4-5):358-64 (ISSN: 0378-5866)
    Daikhin Y; Yudkoff M
    Department of Pediatrics, University of Pennsylvania School of Medicine,
    Children's Hospital of Philadelphia and Children's Seashore House,
    Philadelphia, PA, USA.
    The effects of ketone bodies on brain metabolism of glutamate and GABA were
    studied in three different systems: synaptosomes, cultured astrocytes and
    the whole animal. In synaptosomes the addition of either acetoacetate or
    3-OH-butyrate was associated with diminished consumption of glutamate via
    transamination to aspartate and increased formation of labelled GABA from
    either L-[2H5-2,3,3,4, 4]glutamine or L-[15N]glutamine. There was no effect
    of ketone bodies on synaptosomal GABA transamination. An increase of total
    forebrain GABA and a diminution of aspartate was noted when mice were
    injected intraperitoneally with 3-OH-butyrate. In cultured astrocytes the
    addition of acetoacetate to the medium was associated with a significantly
    enhanced rate of citrate production and with a diminution in the rate of
    conversion of [15N]glutamate to [15N]aspartate. These data are consistent
    with the hypothesis that the metabolism of ketone bodies to acetyl-CoA
    results in a diminution of the pool of brain oxaloacetate, which is consumed
    in the citrate synthetase reaction (oxaloacetate + acetyl-CoA --> citrate).
    As less oxaloacetate is available to the aspartate aminotransferase
    reaction, thereby lowering the rate of glutamate transamination, more
    glutamate becomes accessible to the glutamate decarboxylase pathway, thereby
    favoring the synthesis of GABA.



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