The question is can the brain run without glucose or not,simple!!!
If only it were!
As a type one it is very clear that hypoglycemia requires the fast action of glucose to reverse it (and its effect on brain function) This has been found to be the case in a small study.
Post-hypoglycaemic hyperketonaemia does not contribute to brain metabolism during insulin-induced hypoglycaemia in humans Diabtologia 1993 Fanelli C, et al
Human breast milk has about 35/45% carb content so one would imagine that this is the optimal proportion of carbs for development... including that of the brain which develops rapidly in early life, but the energy requirement is high and babies also use lactate and ketones.
There is increasing evidence that glucose and /or carbohydrate ingestion has an effect on cognitive functioning. This is a relatively new area of research and much of it contradictory.
It may be that some functions, particularly some memory functions require rapid replacement of fuel therefore glucose is optimal. (See research by Gold and McNay, C. Greenwood, Kaplan )
On the other hand there is for example evidence that adults with poor glycemic control have some memory impairment and that the ingestion of high gi carbs compounds the problem.(Greenwood et al [ Carbohydrate-Induced Memory Impairment in Adults With Type 2 Diabetes
:!: :!:
For those who
really want to investigate further, or are doing a literature search for a post grad degree! (ignore otherwise)
This extract from
METABOLIC ADAPTATIONS
JR Skoyles - precedings.nature.com
. Skoyles 1 Human metabolic adaptations and prolonged expensive
neurodevelopment: A review John R. Skoyles
discusses the matter, (but not always clearly) I've put in some underlining. The references are in the original text.
Ketone bodies. Ketone bodies (β-hydroxybutyrate and acetoacetate) are the major energy
supply to the brain during lactation being created from blood brain boundary impenetrable
free fatty acids (Nehlig, 2004).
During famine, the brain can subsist with 60% of its energy
needs being supplied by their hepatic conversion via lipid mobilization from adipose tissue
(Bougneres, Lemmel, Ferre, & Bier, 1986). It has recently been suggested that when the
equivalent of two alcoholic drinks (0.5 g kg-1) of alcohol depresses glucose measured brain
metabolism by 23%, acetoacetate makes up the deficit (Volkow et al., 2006)20. However,
ketone bodies have pharmacokinetic properties that are distinct from those of glucose. This is
most evident in the ketogenic diet treatment of epilepsy for which these differences provide
its neurological effectiveness. The specific effects of the ketogenic diet and a high use of
ketone bodies by the brain are not well understood but seem to link to alterations in the
metabolism of the major excitatory neurotransmitter, glutamic acid (Yudkoff, Daikhin,
Nissim, & Lazarow, 2001). Such alternations could have a potentially disruptive role in
neurodevelopment since key glutamate receptors, such as AMPA and NMDA are closely
involved with the regulation of the stability of synapses (Adesnik et al., 2008; De Paola,
Arber, & Caroni, 2003).
There is evidence from hippocampal slices that ketone bodies cannot maintain neural activity
comparably to that of glucose (Arakawa, Goto, & Okada, 1991). Consistent with this,
weaning rats fed a ketogenic diet grew up to have impaired visual-spatial learning and
memory defects and reduced brain size (Zhao, Stafstrom, Fu, Hu, & Holmes, 2004). In one
study, the production of ketone bodies that are produced in hypoglycemia were inhibited by
the drug acipimox: the absence, however, of hypoglycemia induced ketone bodies due to
acipimox did not increase the cognitive and effects of hypoglycemia (Fanelli et al., 1993).
This suggest that ketone bodies do not compensate the brain for the plasma glucose deficit in
hypoglycemia (Fanelli et al., 1993). It has been suggested that ketone bodies “spare glucose
for the emergence of various functions such as audition and vision as well as more integrated
and adapted behaviors whose appearance during brain maturation seems to critically related
upon active glucose supply and specific regional increased use” (Nehlig, 2004, p. 265).
Thus,
ketone bodies and glucose are not equivalent in their effects upon the brain, particularly
during its development, and this might, if high in percentage contribution, make it a
suboptimal replacement.
A second place to find multiple references to follow up is
http://www.fao.org/docrep/W8079E/w8079e08.htm#carbohydrate and behaviour