From: gts (gts_2000@yahoo.com)
Date: Mon Apr 14 2003 - 21:29:37 MDT
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.
This archive was generated by hypermail 2.1.5 : Mon Apr 14 2003 - 21:36:55 MDT