May 2003: (II)S61–S67
Carbohydrate, Memory, and Mood
David Benton, Ph.D., and Samantha Nabb, B.Sc.
From a physiologic perspective, the role of glu-
cose in brain functioning is reviewed and the
effect of diet-induced changes in blood glucose
on mood and cognition are outlined. Many stud-
ies have used a glucose drink or a meal com-
posed almost entirely of carbohydrate as an ex-
perimental tool. Because pure sources of
carbohydrate will be rarely consumed, the possi-
bility that foods of different glycemic indices will
modify mood and memory is briey considered.
Key words: carbohydrate, glucose, glycemic in-
dex, memory, mood
© 2003 International Life Sciences Institute
doi: 10.131/nr.2003.may.S61–S67
Glucose and the Brain
Unlike other organs, the energy requirement of the brain
is met almost exclusively by aerobic glucose degrada-
tion. The use of C14-labeled glucose shows that in the
perfused brain, only 30% is oxidized directly to CO2 and
water; much of the remainder is used for the synthesis of
amino acids, peptides, lipids, and nucleic acids.1 Specif-
ically, acetyl-CoA, a metabolite of glucose, is essential
for the synthesis of the neurotransmitter acetylcholine,
that plays a role in the modulation of memory.
The energy requirement of the brain is dispropor-
tionately large. When the body is at rest it accounts for
approximately 20% of energy consumption, although it
comprises only 2% of body weight. The energy stores in
the brain are extremely small when compared with the
high rate of glucose utilization, and the brain therefore
relies on a continuous glucose supply. At the basal rate of
consumption the glucose content of the brain would be
exhausted in 10 to 15 minutes.2
Traditionally, the concentration of glucose is
thought to be the same throughout the brain. Consensus
was that the ability to transport glucose exceeded the
demand for fuel, ensuring that levels do not vary.3,4 This
perspective views the uptake of glucose by the brain as
Drs. Benton and Nabb are with the Department of
Psychology, University of Wales Swansea, Singleton
Park, Swansea SA2 8PP, Wales, United Kingdom.
Nutrition Reviews , Vol. 61, No. 5
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largely independent of the level of blood glucose, al-
though abnormally low blood glucose levels would limit
transport across the blood-brain barrier. An equilibrium
forms between the levels of glucose in the plasma and the
brain’s extracellular  uid (ECF) such that higher levels
of blood glucose are associated with higher levels of
glucose in the brain.3,5,6
Positron emission tomography (PET scan) involves
an injection of glucose, usually with a radioactive label
of F18. Because glucose goes to the most active areas of
the brain PET establishes those areas important for a
particular type of functioning. Such studies demonstrate
that mental inactivity requires a lower rate of brain
metabolism than when processing information. For ex-
ample, light stimulation increases cerebral glucose me-
tabolism in the occipital cortex, which processes visual
information; similar changes can be measured in other
areas of the brain after particular cognitive tasks.7,8 Thus,
increased mental activity is associated with increased
glucose metabolism. The use of PET scans illustrates that
glucose in the blood enters the brain in a matter of
minutes and is directed to those areas that are metabol-
ically active. The major mechanism is thought to be
capillary recruitment, that allows increased blood  ow,
and hence the provision of glucose to metabolically
active areas.
Although the blood-brain barrier does not limit the
supply of glucose, the model of the brain as being
virtually always well supplied with glucose has come
under question. The many reports that glucose adminis-
tration improves the memory of both animals9,10 and
humans,11–14 particularly the elderly,15–17 need to be
explained. That memory is enhanced when glucose is
administered directly into the brain18 indicates that an
increased central supply enhances functioning. The ob-
servation that increased provision of glucose enhances
acetylcholine synthesis is additional evidence that the
brain is sensitive to the provision of glucose.19
The Supply and Demand for Glucose
The essential question that arises is whether the direction
of blood  ow to active areas of the brain is always
sufŽ cient to meet the demands for glucose. Partridge20
speculated that when the demand for glucose is very
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high, there is a tendency for metabolically active regions
of the brain to become locally neuroglycopenic, that is,
they develop low intracellular levels of glucose. In freely
moving rats, during a spatial working memory task, a
decrease in hippocampal extracellular glucose has been
reported. An injection of glucose, but not a placebo,
prevented this decline in the level of glucose in the
hippocampus and improved learning.21 Consistent with
the decline in extracellular glucose re ecting an inability
to locally maintain glucose concentrations, extracellular
glucose levels in the hippocampus decreased by 32%
when a complex maze was performed. By contrast, when
a less complex maze was run, glucose levels fell by only
11%. The authors concluded that their data “strongly
suggest that the observed decreases in hippocampal ECF
glucose are associated with cognitive demand . . . it
seems that memory processing by the hippocampus may
be limited by the availability of glucose.”21
It is not possible to measure glucose concentrations
in the human brain; nevertheless it has also been sug-
gested that enhanced provision of glucose selectively
beneŽ ts tasks that are cognitively demanding.13 Al-
though it is difŽ cult to quantify “cognitive demand,” the
duration of the demand and its complexity can be con-
sidered. The provision of blood glucose has been found
to in uence the difŽ cult rather than the easier trials of the
Stroop test11 and to improve choice rather than simple
reaction times.12 A glucose drink selectively in uenced
the more difŽ cult tests of the Porteus Maze.13 In all of
these instances it was the more demanding tasks that
were susceptible to changes in blood glucose levels.
When the duration of a task has been considered, blood
glucose has been found to in uence a vigilance task, but
only towards the end of the test session.22,23 In a driving
simulator glucose only in uenced performance after
driving 70 kilometres.23 Thus it is only the later stages
of prolonged tasks that are susceptible to the provision of
glucose. A Ž nal line of evidence that the provision of
glucose may on occasion limit neural functioning comes
from a study that made the assumption that when per-
forming verbal tasks, the more metabolically active left
hemisphere would be partially depleted of glucose. The
prediction was conŽ rmed that increased levels of blood
glucose would speciŽ cally beneŽ t memory for informa-
tion directed to the left rather than right hemisphere.24
Glucose and Memory
The mechanism by which an increased supply of glucose
enhances memory is poorly understood. One possibility
is that the synthesis of the neurotransmitter acetylcholine
is increased. The role played by acetylcholine in the
modulation of memory has been frequently consid-
ered.25,26 The evidence is of various types. Firstly, there
are consistent reports that Alzheimer’s disease, which is
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characterised by a profound failure of memory, is asso-
ciated with a depletion of cholinergic neurons. Secondly,
drugs that block the action of acetylcholine disrupt the
memory of both animals and humans. Thirdly, therapeu-
tic drugs prescribed to improve the memory of Alzhei-
mer’s patients often act by increasing cholinergic
activity.
The enyzme choline acetyl transferase, found in the
presynaptic nerve terminal, converts the precursors cho-
line and acetyl CoA to acetylcholine. Glucose is the main
source of the acetyl groups of acetyl CoA.27 Glycolysis
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converts glucose by a series of steps to pyruvate, that in
turn is broken down by the pyruvate oxidase system to
form acetyl CoA. Choline acetyltransferase is not a
saturated enzyme, thus an increased supply of acetyl
CoA, resulting from increased glucose metabolism, is
associated with increased production of acetylcholine.
In rats that have not eaten for 24 hours brain ace-
tylcholine levels are lower, something that can be re-
stored by feeding normal food or by administering glu-
cose and choline.28 A review concluded that under
resting conditions increased glucose availability has little
effect on acetylcholine levels in continuously fed ani-
mals.19 When there is a high demand for acetylcholine,
however, a high availability of glucose increases the rate
of the synthesis of the transmitter by increasing the
production of acetyl CoA. Using the uptake of choline as
an index of cholinergic activity, investigators found that
a glucose injection increased acetylcholine synthesis in
mice.19 Raising glucose levels reportedly increases the
release of acetylcholine from the rat hippocampus, an
area of the brain important in modulating memory.29 In
mice, increasing glucose levels attenuated the amnesia
induced by the anticholinergic drug scopolamine.19,30
Taken together these animal studies provide strong evi-
dence that, under periods of neuronal activity, raising the
glucose supply is associated with an increased synthesis
of acetylcholine, which beneŽ ts memory.
Glucose in uences many neurotransmitter systems
and can modify the impact on memory of drugs that act
via opiate, GABAergic, glutaminergic, and cholinergic
sites.10 Peripheral injections of glucose have been shown
to suppress the Ž ring of nigrostriatal dopamine-contain-
ing neurons31 and to lower the level of dopaminergic
metabolites.32 When drugs are injected directly into the
brain, the action of glucose is more speciŽ c and the
nature of its action varies with brain site. For example,
the amygdala is an area of the brain that in uences
memory for emotional events. The opiate agonist mor-
phine, when injected into the amygdala, impairs the
avoidance learning of rats, an effect that is attenuated by
the injection of glucose into the same brain area.33 The
septohippocampal system is important for the learning of
spatial tasks. The injection of glucose into the medial
Nutrition Reviews , Vol. 61, No. 5
septum antagonized the behavioral in uence of mor-
phine but not the cholinergic drug scopolamine or the
adrenergic drug propranonol.34 These studies illustrated
that glucose acts in a selective manner, in particular,
in uencing opiate mechanisms. Data suggest that opiate
mechanisms in uence cholinergic functioning.35 Opiate
receptors in the septum inhibit the release of acetylcho-
line from the hippocampus; morphine injected into the
medial septum reduced the release of acetylcholine in the
hippocampus, an effect blocked by the co-injection of
glucose.35
The Type of Carbohydrate, Meals, and Memory
Various strands of evidence question the assumption that
the ability to transport glucose to particular areas of the
brain never in uences neural functioning. If the provi-
sion of glucose to the brain on occasion limits cognitive
performance, the question arises as to whether diet plays
a role. Do the pattern of meals and the glycemic load of
the diet modulate functioning? Although there have been
no studies of the association between glycemic load and
memory, there are good reasons to suggest that there
maybe an association. Given the suggested relationship
between glycemic load and type 2 diabetes,36 and the
association between poor glucose tolerance and cogni-
tive decline,37 the possibility that glycemic load will
in uence cognitive functioning should be explored
Meals may also have a shorter-term in uence. On a
number of occasions, memory and school performance
have been in uenced adversely by missing break-
fast.38–45 In an Israeli study,45 however, the effect was
short term, explained by the authors as a re ection of the
short-term increase in blood glucose that follows a meal.
There is evidence of a possible role for glucose in the
memory-enhancing effect of breakfast. In adults memory
performance two hours after breakfast was found to
correlate with blood glucose values,38 and the adverse
effect of missing breakfast was reversed by giving a
glucose-containing drink.42,43
A recent study provided breakfasts containing an
equal amount of carbohydrate; in one diet the carbohy-
drate source was mostly in the form of slowly (SAG)
rather than rapidly available glucose (RAG). The SAG
breakfast beneŽ ted memory later in the morning; RAG
had no effect.46
In a sample of elderly people, three types of carbo-
hydrate were consumed: glucose, instant potato, or bar-
ley.47 Although memory was better after the consump-
tion of both potato and barley, improvement was not
associated with the level of plasma glucose. The con-
sumption of the low– glycemic index barley improved
memory more than potato.
In summary, although increased glucose supply en-
hances memory in humans and animals, it is an effect
Nutrition Reviews , Vol. 61, No. 5
that appears to be stronger in the elderly and depends on
the nature of the test. There have been few attempts to
consider the effect of the glycemic index of carbohy-
drates on memory, although paradoxically the limited
data available suggest that a food with a low glycemic
index maybe beneŽ cial.46,47 Given the known effect of
low– glycemic index foods to improve glucose tolerance,
the possible role of this mechanism should be consid-
ered.
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Carbohydrate Intake, Serotonin, and Mood
A related suggestion is that the level of blood glucose
in uences mood. Many people consume sugary snacks
when they are feeling low or in need of energy. The
opposite suggestion has also been proposed, that the
intake of carbohydrate is calming because it increases the
synthesis of serotonin in the brain.48,49 Some have sug-
gested that individuals eat high-carbohydrate foods for a
psychopharmacologic effect, to improve mood, for ex-
ample, those suffering with Seasonal Affective Disorder
(SAD) and premenstrual syndrome (PMS).49
The increase in blood glucose following the con-
sumption of carbohydrate is associated with the release
of insulin. Insulin causes the large neutral amino acids
(LNAA: tyrosine, phenylalanine, leucine, isoleucine, va-
line) to be taken up into muscle although tryptophan is
bound to albumin in the blood. A meal comprising
almost totally carbohydrate thus increases the ratio of
tryptophan to LNAA in plasma. The LNAA and trypto-
phan compete for a transporter molecule. When a high-
carbohydrate meal increases the tryptophan-to-LNAA
ratio, therefore, relatively more tryptophan is transported
into the brain where it is metabolized into the neurotrans-
mitter serotonin. Although in animals the intake of pure
carbohydrate is associated with increased serotonin syn-
thesis,50 in humans, even when the level of tryptophan
increases, there is no evidence of an increased release of
serotonin.48,51 When 30 human studies were summa-
rized, meals that were almost totally carbohydrate were
found to have increased the tryptophan-to-LNAA ratio in
the blood. However, although when protein comprises
less than 2% of total calories, there was more tryptophan
available, as little as 5% of the calories in the form of
protein was enough to ensure that this phenomenon did
not occur.52 The improbability of eating meals that
contain such a low level of protein raises considerable
doubt as to importance of this mechanism as a part of
normal diet. In foods that many would classify as high in
carbohydrate, such as bread, rice, or chocolate, there are
levels of protein sufŽ cient to prevent an increase in the
availability of tryptophan.
In many women at the end of the monthly cycle
there is an increase in appetite and food consumption. It
has been concluded that “individuals with PMS increase
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their carbohydrate consumption in the pre-menstrual
stage.”53 A study providing an experimental meal that
contained no protein decreased the depression, anger,
and confusion of those with PMS.54 Reviews of the topic
Ž nd a signiŽ cant increase in energy intake during the
luteal phase,55 and there is evidence of increased basal
metabolic rate.56 However, one must distinguish in-
creased carbohydrate intake from increased intake of all
macronutrients. The question arises as to whether the
anecdotal observation of increased craving for sugary
items results in characteristic changes in macronutrient
intake. An isolated study found that there was an in-
creased intake of carbohydrate but not other macronutri-
ents;57 however, the vast majority of studies do not share
these observations.55 The weight of evidence is that
carbohydrate intake is not selectively increased in the
premenstrual stage. Although there is support for anec-
dotal statements that cravings for sweet, pleasant-tasting
foods increase,58,59 the driving force is likely to be an
increased consumption of food items containing carbo-
hydrate and fat rather than an increased appetite for
carbohydrate.
Similarly, investigators have suggested that those
suffering with SAD have a speciŽ c hunger for carbohy-
drate, a mechanism suggested to improve mood.60,61 A
review of the topic, however, concluded that that there
was little evidence to support a speciŽ c hunger for
carbohydrate although there may be a preference for
pleasant-tasting foods.48
Long-term Carbohydrate Intake and Mood
Although the modulation of serotonin levels is not a
credible mechanism, there are several studies that have
reported that the cumulative intake of carbohydrate was
associated with better mood. Based on food diaries kept
over nine days, a negative relationship was found be-
tween the proportion of energy consumed as carbohy-
drate and depression.62 The association was not between
meals and mood around the time of eating, but over
several days there was a cumulative impact. More re-
cently, 686 individuals were asked at midday to report
their mood and what they had eaten that morning (Ben-
ton, unpublished Ž nding,). The more carbohydrate that
people had consumed, the happier male subjects reported
they had been during the morning. In both of these
studies the intake of protein was sufŽ cient to prevent an
increase in the plasma tryptophan-to-LNAA ratio. When
experimental diets containing low, medium, or high
levels of carbohydrate were consumed for a week, the
low-carbohydrate diet was associated with increased an-
ger, depression, and tension.63 This report supported the
Ž nding that eating a low-carbohydrate, high-protein
breakfast for three weeks resulted in increased levels of
anger.64 When a group of young German women dieted
S64
for six weeks, those whose meals were based on cereals
and vegetables, rather than meat and Ž sh, reported better
mood.65 Eating experimental diets that are higher in
carbohydrate are therefore associated with better mood.
The repeated Ž nding that carbohydrate intake has a
cumulative in uence suggests the need to examine the
impact of glycemic load on mood.
The Short-term Effect of Carbohydrate on
Mood
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Studies of the short-term impact of carbohydrate on
mood have either compared sugar- or starch-based foods
with those offering high levels of protein; alternatively,
they have provided a sucrose- or glucose-containing
drink. When a protein-rich meal such as turkey breast
was compared with a carbohydrate-rich meal, the latter
tended to result in subjects feeling less energetic.66–70
Studies comparing the consumption of a sugar-contain-
ing drink and a calorie-free drink have produced equiv-
ocal Ž ndings; two found increased subjective energy71,72
and three others reported nonsigniŽ cant Ž ndings.73–75
A major variable appears to be the time after con-
sumption when mood was assessed. The studies report-
ing decreased subjective energy after a carbohydrate-
containing meal measured mood approximately two
hours after consuming the drink or meal. By contrast,
when subjective energy was found to increase after a
sugar-containing drink, this occurred after 15, 30,71 or 60
minutes.72 Benton and Owens,71 who used by far the
largest sample sizes in this area, commented that the
short-term increase in reported energy seemed to be a
robust phenomenon as they replicated the Ž nding. It was,
however, a small effect that would likely not be repro-
duced in a small sample size. The report that people
consuming a sugary snack experienced a short-term
increase in energy followed by a longer-term fall in
subjective energy76 is consistent with a two-stage effect.
Although many of these studies used a source of pure
glucose and hence had the potential to increase the
tryptophan-to-LNAA ratio, at least some of the effects on
mood were too rapid for increased serotonin synthesis to
have occurred.
Mood Under Demanding Conditions
The possibility that increasing blood glucose maintains
mood when sustained demands are placed on an individ-
ual has been little considered. When mood was assessed
before and after performing three cognitively demanding
tasks, falling levels of blood glucose were associated
with lower self-reported energy.77 That the tasks in this
series placed greater cognitive demands on subjects than
in previous studies may be an important factor in the
association between falling blood glucose and falling
Nutrition Reviews , Vol. 61, No. 5
levels of subjective energy. One can speculate that the
association between falling blood glucose and falling
subjective energy may be the consequence of localized
neuroglycopenia, a result of the demanding cognitive
tasks that had been performed. Previously investigators
reported that subjects whose blood glucose remained low
reported greater tension than those whose blood glucose
levels were higher.71
Individual Differences in the Control of Blood
Glucose
Finally, when considering the association between diet,
blood glucose levels, and psychological functioning, it is
essential to take into account individual differences in
physiology. In Peruvian Indians known for their aggres-
siveness,78 violent offenders,79,80 and undergraduates
who report themselves as irritable,81,82 a greater degree
of aggressiveness has been associated with a tendency
for rapidly falling blood glucose levels during a glucose
tolerance test. The possibility of a causal relationship
between blood glucose levels and aggressiveness was
supported by reports in both children83 and adults,71 in
which raising blood glucose levels with a sugar-contain-
ing drink led to less irritable behavior.
One must also take into consideration individual
differences in the ability to regulate blood glucose when
considering cognitive functioning. Better glucose toler-
ance was associated with better cognition in rats,84
young humans,12 the healthy elderly,15,17 and those suf-
fering with Alzheimer’s disease.16 Better glucose toler-
ance is displayed when blood glucose levels fall rapidly,
following a rise after a glucose drink. Because meals
with a low glycemic load improve glucose tolerance,85
the above data suggest a differential impact of foods with
a different glycemic index on mood and cognition, al-
though the question has not yet been addressed system-
atically.
Conclusion
There is growing evidence that the provision of glucose
may in uence both memory and mood, particularly when
intense metabolic demands are placed on the brain.
Individual differences are important: those with better
glucose tolerance have better mood and memory. In the
future, investigators should consider the possibility that
the nature and schedule of meals and snacks can in u-
ence psychological functioning. Diets of different glyce-
mic load have the potential to in uence the pattern of
glucose supply and to modify glucose tolerance; both of
these have the potential to in uence the way the brain
functions.
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