BRAIN FOOD: HOW NUTRITION ALTERS OUR MOOD AND BEHAVIOUR

Abstract

Studies have been showing the food we eat affects chemical composition of our brain and alters our mood. Nutrition affects cognitive possibilities, including alertness and the production or release of neurotransmitters, the chemical messengers that carry information from one nerve cell to another. Foods are made up of more than one nutrient, and their interaction is going to affect the production and release of neurotransmitters. Neural impulses are largely resulting from sodium-potassium exchange, but numerous others such as complex carbohydrates, amino acids (tryptophan and tyrosine), fatty acids, particularly omega-3 fatty acids, affect permeability of cell membrane, neurotransmitter metabolism and glial cells. The delicate brain chemical balance is somewhat controlled by the blood – brain barrier. Still, brain remains, highly susceptible to changes in body chemistry resulting from nutrient intake and deficiency. The direct connection between nutrition, brain function and behaviour exists, without any doubt. It can be seen through brain’s capability of receiving, storing and integrating sensory information, while initiating and controlling motor responses. These functions correspond to mental activities and form the basis for our behaviour. Constant rise in number of evidence from epigenetic studies confirms that specific nutrients alter our brain development and susceptibility to diseases. Still, specific combination of foods can be extrapolated to a dietary regime, like the Mediterranean diet which has shown its positive impact on maintaining brain function and lower incidence of neurodegenerative diseases. This is of special importance since elderly population (people of 65 years and older) is on the rise all over the world, and the quality of life becomes a priority.

Full text

Hrana u zdravlju i bolesti, znanstveno-stručni časopis za nutricionizam i dijetetiku (2014) 3 (1)
*Corresponding author: ines.banjari@ptfos.hr
BRAIN FOOD: HOW NUTRITION ALTERS OUR MOOD AND BEHAVIOUR
Ines Banjari*, Ivana Vukoje, Milena L. Mandić
Josip Juraj Strossmayer University of Osijek, Faculty of Food Technology Osijek, Department of Food and
Nutrition Research, Franje Kuhača 20, HR-31000 Osijek, Croatia
review
Summary
Studies have been showing the food we eat affects chemical composition of our brain and alters
our mood. Nutrition affects cognitive possibilities, including alertness and the production or
release of neurotransmitters, the chemical messengers that carry information from one nerve cell
to another. Foods are made up of more than one nutrient, and their interaction is going to affect
the production and release of neurotransmitters. Neural impulses are largely resulting from
sodium-potassium exchange, but numerous others such as complex carbohydrates, amino acids
(tryptophan and tyrosine), fatty acids, particularly omega-3 fatty acids, affect permeability of cell
membrane, neurotransmitter metabolism and glial cells. The delicate brain chemical balance is
somewhat controlled by the blood – brain barrier. Still, brain remains highly susceptible to
changes in body chemistry resulting from nutrient intake and deficiency. The direct connection
between nutrition, brain function and behaviour exists, without any doubt. It can be seen through
brain’s capability of receiving, storing and integrating sensory information, while initiating and
controlling motor responses. These functions correspond to mental activities and form the basis
for our behaviour. Constant rise in number of evidence from epigenetic studies confirms that
specific nutrients alter our brain development and susceptibility to diseases. Still, specific
combination of foods can be extrapolated to a dietary regime, like the Mediterranean diet which
has shown its positive impact on maintaining brain function and lower incidence of
neurodegenerative diseases. This is of special importance since elderly population (people of 65
years and older) is on the rise all over the world, and the quality of life becomes a priority.
Keywords: nutrition, food composition, neurotransmitters, mood, behaviour
Nutrition and cognitive performance
All that we experience affects synapses
(junctions of neurons), and these changes are
responsible for memory and other mental
abilities. According to Thurston primary
mental abilities are (set in 1938): verbal
fluency (eloquence), verbal comprehension,
visual and spatial (physical) abilities,
memory, numerical ability, perceptual speed
spotting, inductive reasoning (from individual
to general) and deductive reasoning (from
general to specific). Practically, when
something that we are going to remember
happens electric signal occurs, causing
chemical and structural changes in the
neurons. These changes are possible due to a
series of reactions involving various
molecules, including calcium, some enzymes
and neurotrophins, aiming for synapses
activation. Healthier brain produces more
neurotrophins, which reinforce links between
neurons in the part of the brain responsible for
learning and memory. Parts of the brain
where specific memory is stored have been
discovered. For semantic memory, which
concerns facts are responsible multiple
cortical areas, while procedural memory
involved in motor learning depends on the
other parts of the brain, including basal
ganglia (Fig. 1). Nutrition in the first years of
life can have a significant impact on
development; the ability to learn,
communication, analytical thinking,
successful socialization and adaptation to new
situations (Isaacs and Oates, 2008; Budson
and Price, 2005).

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
Fig. 1. Memory systems and parts of the brain (Budson and Price, 2005)
Proper nutrition and health are closely
interrelated throughout life, but probably
the highest importance is expressed in the
first years of life. Inadequate nutrition
causes lower cognitive development,
reduced attention and concentration and
reduces performance in later life. Also,
foetal programming in utero should not be
neglected, for its proven influence on the
later development of a child (Langley-
Evans, 2008). As nicely illustrated by
Vanhees et al. (2014) we are what we eat,
and so are our children. Their extensive
review on epigenetic studies clearly
illustrates the importance of balanced diet
of both, mother and father. Besides
macronutrient composition of the diet
(high-fat diets, protein restricted diet, diet
high in carbohydrates), intake of specific
micronutrients, especially those involved
in one-carbon metabolism (folic acid,
vitamin B2, B6 and B12) day by day shows
more potential in programming offspring’s
epigenome (Vanhees et al., 2014).
At birth, the brain reaches 70 % size and
25 % weight of an adult brain. In the
subsequent period, are created new nerve
cells (neurons) that travel to their final
destination. Brain changes throughout life.
It normally makes fiftieth part of human
body weight (average weighs between
1000-1500 grams), in adolescence reaches
its definite size (Benton, 2008). Brain is a
very dynamic organ, showing high
plasticity. Due to this characteristic,
altering our diet in terms of having a
balanced nutrition without any deficiency
or over-nutrition can preserve our brain
from deterioration. For example, one study
showed that high-dose supplementation
with folic acid during early pregnancy
shows association with increased
neurodevelopment, resulting in enhanced
vocabulary development, communicational
skills and verbal comprehension at 18
months of age (Chatzi et al., 2012). Similar
findings have been shown for boosting
cognitive performance and intake of iron
(after correcting iron deficiency anaemia)
(McCann and Ames, 2007; Black et al.,
2011; Goergieff, 2011).
Food and neurotransmitters
Neurotransmitters are produced in our brain
from numerous nutrients originating from

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
our diet by means of a many-step process.
First, nutrients (marked as 1 in Fig. 2), such
as amino acids, carbohydrates, fats, and
peptides, are extracted and absorbed from
the food we eat and transported out of the
arterial blood supply to the brain. They are
actively carried through the blood–brain
barrier and transported into neurons.
Enzymes (2) convert these nutrients into
different neurotransmitters. Neurotransmitter
molecules are actively transported into
synaptic vesicles (3). The arrival of an action
potential (4) at an end of the axon induces
entry of calcium ions, which initiate release
of neurotransmitters (5) into synaptic cleft.
The neurotransmitter molecule briefly
interacts or binds with a protein, i.e. receptor
(6), on the neuron surface on the other side
of the synapse. Consequence of this binding
action is that some ions, such as calcium or
sodium, move into the downstream neuron
to induce secondary biochemical processes
(7), which may have long-term
consequences on the neuron’s behaviour.
Meanwhile, after interacting with the
receptor, neurotransmitter’s actions must be
terminated by reabsorption (8) back into the
neuron that originally released it, which is
called reuptake. A secondary method of
neurotransmitter inactivation is by enzymatic
conversion (9) into a chemical that can no
longer interact with brain. Once inactivated
by enzyme, neurotransmitter is removed
from the brain into the bloodstream (10).
Such byproducts can be easily monitored in
body fluids, and used to determine whether
our brain functions normally. Nutritional
composition of our diet can interact with any
of these previously described processes and
impair, or even enhance, the production of
neurotransmitters, as well as impair their
storage into synaptic vesicles, alter their
release from neurons, modify their
interaction with receptor proteins (11), slow
their reuptake, and possibly even stop their
enzymatic inactivation (Wenk, 2010).
Fig. 2. The absorption of nutrients and their effect on neurotransmitters (Wenk, 2010)

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
Carbohydrates and the brain
Brain needs two times more energy than
other cells in our body, and glucose is the
only fuel that can be used directly by the
brain (Coimbra, 2014). Neurons are always
in a state of metabolic activity and have
constant demand for energy, even during
sleep. Most of the neuron's energy demand
goes on bioelectric signals responsible for
communication of neurons; they consume
one-half of the brain's energy which is
nearly 10 % of total human energy
requirements (Coimbra, 2014). Because
neurons cannot store glucose, they depend
on the bloodstream to deliver a constant
supply of this primary fuel. Different
sugars have different effects on the brain.
While glucose has an impact on regions
like insula and ventral striatum, controlling
appetite, motivation and reward
processing, fructose does not (Page, 2013;
Purnell and Fair, 2013).
Therefore, it is important to control the
amount of carbohydrate in our diet, as well
as the type of food we combine. This is
where we get to the glycaemic index (GI)
concept. GI is a ranking system
categorizing the food according to its
impact on blood glucose levels, so GI
indicates whether certain foods raise blood
sugar levels dramatically, moderately or
slightly. The intake of foods made from
white flour and white sugar should be
limited for the above reasons. Potatoes also
have a high GI value (Ek et al., 2012). The
best choices are fibre-rich foods. Complex
carbohydrates take longer to digest,
causing a slower and more gradual release
of glucose into bloodstream, leading to a
feeling of fullness for longer period of
time. A fibre-rich diet, besides its proven
effect in the prevention of type 2 diabetes
and cardiovascular diseases, probably
helps improving memory and cognition
(Kendall et al., 2010; Kaczmarczyk et al.,
2012). The glycemic response depends on
the combination of consumed food.
Complex, varied meal that contains
complex carbohydrates, proteins and
adequate types of fats, rich on dietary
fibers will provide a moderate GI and
supply the brain for a long time with
glucose. Combining foods with high GI
and those with a low GI balances the
response of the organism (Jenkins et al.,
2013).
Fats and the brain
Fatty acids are present in membranes of
every cell of our body and make 60 % of
the brain’s dry weight, half of which are
omega-6 fatty acids, while the other half
consists of omega-3 fatty acids. Dietary
fats alter the composition of nerve cell
membrane and myelin sheath, and that, in
turn, influences neuronal function. Fatty
acids are involved in the development and
growth of the brain, they affect cognitive
abilities (attention, reasoning, memory, and
learning), vocabulary and intelligence
(Gogus and Smith, 2010). Humans cannot
synthesize essential fatty acids from simple
carbon precursors so they must be acquired
through diet. There are two essential fatty
acids, both polyunsaturated fatty acids,
linoleic acid (LA) which is a precursor of
omega-6 fatty acids and alpha-linolenic
(ALA), which is a precursor of omega-3
fatty acids. Arachidonic acid (AA) is
synthesized from LA, while from ALA
eicosapentaenoic (EPA) and
docosahexaenoic (DHA) acids are
synthesized (Davis and Kris-Etherton,
2003; Vannice and Rasmussen, 2014).
Long-chain omega-3 and omega-6 fatty
acids compete for the same enzymes
cyclooxygenase and lipoxygenase and
therefore a diet is considered to be the best
way to maintain balance between omega-3
and omega-6 fatty acids. It is believed that
this ratio should not be greater than 5:1 in
favour of omega-6, and it is known that the
Western diet has a ratio of 12:1, or even
worse. The importance of this ratio is
supported by the fact that inflammatory
eicosanoids are formed by the metabolism

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
of omega-6 fatty acids, while EPA and
DHA products are thought to be relatively
anti-inflammatory (Gogus and Smith,
2010; Vannice and Rasmussen, 2014;
Kidd, 2007; Shaikh and Brown, 2013).
Omega-3 fatty acids are critical for foetal
and newborn neurodevelopment. During
the third trimester of pregnancy,
approximately 50-70 mg of DHA per day
is delivered to foetus via placental transfer.
DHA is accumulated in the central nervous
system (CNS) before birth, and therefore
considered to play a critical role in the
development of cognitive functions
(Langley-Evans, 2008; Greenberg et al.,
2008; Montgomery et al., 2013). Nutrient
deficiencies during development may have
long-lasting consequences on neurone
outgrowth (Greenberg et al., 2008;
Montgomery et al., 2013). A positive
correlation has been observed between
DHA in red blood cells and visual acuity,
as well as other indexes of brain
development in newborns (Jensen et al.,
2005). Nutritional guidelines during
pregnancy recommend an additional intake
of omega-3 fatty acids, i.e. 250 mg/day
EPA and DHA (Vannice and Rasmussen,
2014; WHO, 2008; EFSA, 2010; FAO,
2010). Essential fatty acids are necessary
for the child’s normal growth and
development, which is an approved health
claim by the European Food Safety
Authority. Beneficial effect has been
proven by taking 1 % of the total energy of
LA and 0.2 % ALA per day (EFSA, 2008).
DHA is essential for the growth and
functional neurodevelopment of newborns,
and required to maintain a normal function
of adult brain. Intake of DHA during
pregnancy and lactation of at least 200 mg
per day, contributes to the normal brain
development of foetus and infant (EFSA,
2009). Low brain DHA is associated with
age-related cognitive decline, as well as the
early development of Alzheimer's disease.
On the other hand, increased dietary intake
of DHA can result in improved cognitive
abilities due to the fact that a lack of
essential fatty acids has been linked to
deficits in learning and memory (Cunnane
et al., 2009; Yurko-Mauro et al., 2010;
Cunnane et al., 2013).
Interesting results shows a study by
Conklin et al. (2007). The study involved
fifty-five healthy adults who completed
two 24 h dietary recall interviews. Based
on an intake of EPA and DHA, the
respondents were divided into three
groups: low intake (0-20 mg/day, 16
respondents), medium intake (25-70
mg/day; 21 respondents) and high intake of
EPA and DHA (80-1600 mg/day, 18
respondents). Magnetic Resonance
Imaging (MRI) scans of respondent's
brains revealed a positive correlation
between increased intake of these two fatty
acids and the volume of gray matter in the
anterior cingulate cortex, the right
hippocampus and the right amygdala.
Since mentioned areas are responsible for
mood, scientists believe that increased
intake of EPA and DHA has a positive
effect on mood, but also on memory
functions (Conklin et al., 2007).
The best dietary sources of omega-3 fatty
acids are oily fish (sardines, mackerel,
tuna, anchovies), cold water fish (herring,
salmon), algae, zooplankton and seafood as
well as seeds and nuts. Nutritional
supplements containing purified and
concentrated fish oil are also a valuable
source of omega-3 fatty acids in the diet of
a modern man (Shaikh and Brown, 2013;
Bradbury, 2011). The amount of EPA and
DHA in fresh fish varies depending on a
species. Oily fish is particularly useful for
pregnant women, and it is recommended to
be consumed once a week. But the special
attention is needed with canned tuna for
possible intoxication with mercury.
Species of fish that are long-lived and high
on the food chain tend to have higher
levels of methylmercury which has
negative impact on the nervous system of a
foetus. A total amount of methylmercury in
fish remains relatively unchanged after
cooking (WHO, 2007; WHO, 2010;
Brown, 2010).

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
Amino acids and neurotransmitters
The most common neurotransmitters are:
acetylcholine, glutamate, gamma-
aminobutyric acid (GABA), glycine,
serotonin, dopamine, norepinephrine,
epinephrine and histamine produced by our
brain directly from nutritional components
of our diet. Activity and levels of these
neurotransmitters depend on food intake
and change in nutrient intake can
significantly affect behaviour, sleep and
energy levels (Sommer, 1995; Gustafson,
2008).
Serotonin is produced from the amino acid
tryptophan, which is found in protein-rich
food, such as chicken, dairy products, eggs
and legumes. Ironically, consumption of
high-protein foods decreases levels of
tryptophan and serotonin in the brain,
while the consumption of carbohydrate-
rich foods has the opposite effect. After
consumption of high-protein foods,
tryptophan competes with other amino
acids in order to pass the blood-brain
barrier, which results in a lower increase in
brain serotonin. When large amounts of
carbohydrates are eaten, insulin is released,
causing the absorption of the majority of
amino acids into the bloodstream while
giving advantage to tryptophan for brain
access, leading to increased level of brain
serotonin. The resulting increase in brain
serotonin promotes the feeling of
calmness, improves sleep, increases pain
tolerance and reduces food cravings
(Sommer, 1995; Fernstrom, 2013; Parker
and Brotchie, 2011).
Dopamine and norepinephrine are
synthesized from the amino acid called
tyrosine, with the assistance of folic acid,
magnesium and vitamin B12. Unlike
tryptophan, tyrosine level raises after
consuming a protein-rich foods which
leads to increased levels of dopamine and
norepinephrine, both affecting alertness
and mental energy (Sommer, 1995;
Fernstrom, 2013; Parker and Brotchie,
2011; Daubner et al., 2011). Acetylcholine
is synthesized from choline and unlike
other amino acids that have to compete for
brain access, choline does not need to. The
best source of choline is egg yolk.
Acetylcholine is important for memory and
general mental ability. Reduced levels of
acetylcholine are associated with memory
loss, decreased cognitive function and
Alzheimer's disease at old age. Choline
deficiency induces neuronal death and
mental fatigue, a person cannot think
clearly, is depressed and forgetful
(Sommer, 1995; Holmes et al., 2002;
McCann et al., 2006).
Mediterranean diet
When speaking about brain food we must
not forget about one specific dietary
regime which shows immense potential in
maintaining and boosting brain
functioning. This is the Mediterranean diet
(MD). Despite several differences between
Mediterranean regions, they all have
something in common. The specific
combination of foods make it so simple
and yet so complicated at the same time
(Banjari et al., 2013). Yet this is exactly
the perfect combination of macro and
micronutrients, making it a number one
choice for health and longevity. Health
benefits of the MD go well beyond
preventing cardiovascular diseases, lover
mortality and morbidity (Banjari et al.,
2013), as shown by the Lion Diet Heart
Study (De Lorgeril, 2013), study by
Trichopoulou et al. (2003) in Greece, or
the PREDIMED study conducted in Spain
(Estruch et al., 2013). Protective effect of
the MD has been determined for number of
degenerative diseases, like cancers
dementia, and the risk of Alzheimer’s
disease (Shah, 2013; Lourida et al., 2013;
Sofi et al., 2013). Furthermore, Skarupski
et al. (2013) showed its potential in
reducing depression among people of 65
years and older. Also, rising interest of the
non-Mediterranean countries, firstly
Scandinavian countries, resulted in vast
number of evidence showing the MD
potential in protecting from premature

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
death (Hodge et al., 2011; Gardener et al.,
2011; Hoevenaar-Blom et al., 2012;
Martínez-González et al., 2012; Hoffman
and Gerber, 2013; Tognon et al., 2013),
and cerebrovascular diseases (Misirli et al.,
2012).
Food and mood
We can boost our mood by retaining
available neurotransmitters in the gap
between nerve cells as long as possible and
it seems possible, but yet-to-be-tested, that
expressions of foods in art can also serve
to improve mood. Regulation of three key
neurotransmitters responsible for mood
(dopamine, noradrenaline and serotonin)
by modulating food intake impacts
durability of their stimulation of nerve
cells, thus impacts mood and behaviour
(Privitera et al., 2013; Hamburg et al.,
2014).
Chocolate and caffeine
A study of 8000 people has shown that
people who consume chocolate live longer
compared to those who never eat chocolate.
Positive effect of a chocolate lies in its
flavonoid content. Chocolate flavonoids
reduce the amount of low-density lipoprotein
(LDL) cholesterol and reduce blood
pressure. They also show the potential to
slowdown growth of cancer cells (Engler
and Engler, 2004; Paoletti et al., 2012). Due
to chocolate production processes, it is
believed that only dark chocolate products
with a cocoa content of approximately 70 %
or higher truly offer a significant benefit of
flavonoids (Goldoni, 2004; Rawel and
Kulling, 2007). Cocoa beans contain 61 % of
cocoa butter, tannin, catechin and alkaloids
theobromine and caffeine, which have
different effects on our brain and emotions.
Cocoa beans are also rich in hydrolysis
products of polyhydric phenols such as
quercetin, caffeic and p-hydroxycinnamic
acid (Jalil and Ismail, 2008; Smit et al.,
2004; Parker et al., 2006). It is known that
chocolate contains over 300 substances, but
the key ingredient is phenylethylamine. Most
phenylethylamine is metabolized in the
body, but some reaches the brain where it
leads to dopamine increase. After
consumption of chocolate, phenylethylamine
is released into the human system producing
the arousing effects of an intense emotional
stimulus leading to euphoria. Some
antidepressants have a similar effect, because
they inhibit monoamine oxidase (MAO
inhibitors) and prevent the degradation of
phenylethylamine. Therefore, chocolate can
have antidepressant effect. Chocolate
contains anandamide, a substance that is an
endogenous cannabinoid and occurs
naturally in the brain where stimulates
positive feelings. Anandamide targets the
same brain structure as tetrahydrocannabinol
(THC), the active ingredient in cannabis.
Chocolate also contains tryptophan. The
release of endorphins is stimulated with
chocolate generating feeling of pleasure and
promoting a sense of well-being. Alkaloids
in chocolate, as well as in wine and beer
improve mood (Smit et al., 2004; Parker et
al., 2006).
Some researchers believe that women
crave chocolate prior to menstruation
because it contains high levels of
magnesium. Magnesium deficiency
increases the intensity of premenstrual
syndrome. Even 91 % of women have
cravings for chocolate in the second half of
their menstrual cycle, with greater desire in
the afternoon and early evening, and
magnesium intake could significantly
improve premenstrual mood changes
(Ghalwa et al., 2014).
Another CNS stimulant is caffeine, which
shows positive and adverse effects
depending on a dose and frequency of
administration. Caffeine is a chemical
methylxanthine, first isolated from coffee
beans, which is the major source of caffeine,
but is also found in other drinks such as
green and black tea, Guaraní, cocoa and soft
drinks, especially Cola and energy drinks
(Persad, 2011). The amount of caffeine
present in products depends on the type of a
product, serving size and preparation

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
method. Chocolate also contains small
amounts of caffeine, but for the sake of
comparison it can be said that a cup of cocoa
contains 20 mg of caffeine, while a cup of
tea contains 40 mg on average, and a cup of
coffee contains 155 mg of caffeine
(Heckman et al., 2010).
Caffeine acts as an antagonist to adenosine
receptors. Adenosine is a substance
produced in the body as a product of
increased metabolism and signals fatigue and
the need for rest (Higgins et al., 2010).
Caffeine therefore acts as a psychostimulant
in the brain: enhances attention, causes
alertness, improves memory and increases
the ability to process degraded stimuli. At
the same time also raises heart rate, increases
force of myocardial contraction, secretion of
urine and secretion of gastric juice. The most
notable behavioural effects of caffeine occur
15 minutes after drinking caffeinated
beverage (Persad, 2011).
Due to caffeine effects, including increased
alertness, energy, ability to concentrate and
wakefulness, it is primarily used as a
stimulant in fatigue and somnolence.
Consumption of caffeinated coffee in a
dose-dependent was found to reduce the
incidence of dementia, particularly
Parkinson's disease (Fredholm, 2011).
Scientists believe that caffeine consumption
is safe up to 200 mg per day and has
beneficial effects on the body even in people
with hypertension (Cano-Marquinaa et al.,
2013).
Ingestion higher than 400 mg of caffeine,
especially in caffeine-sensitive individuals,
pregnant women and children, may have
adverse effects like insomnia, excessive
excitement, nervousness, increased heart
rate and increased gastric acid secretion
(Persad, 2011; Higgins et al., 2010; Nehlig
et al., 1992; Snel and Lorist, 2011).
Conclusions
Studies have shown that food can promote
proper functioning of the brain. In order to
improve our mental abilities, concentration,
memory and vigilance, proper nutrition is of
great importance. By affecting
neurotransmitters, substances that activate
different regions of the brain, actively
participate in the creation of nerve impulses
and thereby regulate our mental abilities,
emotions and mood. Cognitive performance
and maintenance of mental health, especially
among elderly may be improved with proper
diet consisting of complex carbohydrates,
polyunsaturated fatty acids, especially
omega-3 fatty acids, proteins and specific
foods containing specific nutrients, like
flavonoids. In addition, mood and
concentration as well as alertness can be
affected by moderate consumption of
chocolate and caffeinated beverages.
Keeping in mind the risk factors for loss of
mental abilities, by proper nutrition we can
potentially prevent or delay
neurodegenerative changes in the brain
including Parkinson's and Alzheimer's
disease. The conclusion arising from the
compiling evidence elaborated in the text
says that in order to improve cognitive
performance and maintain brain vitality the
Mediterranean diet should be chosen. The
Mediterranean diet poses itself as a
possible solution via its specific
combination of foods which are, if
separately analysed for nutrient
composition, the ideal combination to
maintain and keep proper brain function
through old age.
References
Banjari I, Bajraktarović-Labović S, Misir
A et al. (2013) Mediterranean diet and
cardiovascular diseases. Timočki
medicinski glasnik 38(4), 188-202.
Benton D (2008) The influence of
children’s diet on their cognition and
behaviour. Eur J Nutr 47(3), 25-37.
Black MM, Quigg AM, Hurley KM et al.
(2011) Iron deficiency and iron-deficiency
anemia in the first two years of life:
strategies to prevent loss of developmental
potential. Nutr Rev 69(Suppl 1), S64-S70.

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
Bradbury J (2011) Docosahexaenoic Acid
(DHA): an ancient nutrient for the modern
human brain. Nutrients 3, 529-554.
Brown LS (2010) Life cycle nutrition: An
evidence-based approach. In: Edelstein S,
Sharlin J (ed) Nutritional requirements
during pregnancy and lactation. Jones and
Bartlett Publishers, London.
Budson AE, Price BH (2005) Memory
dysfunction. N Engl J Med 352:692–699.
Cano-Marquinaa A, Tarínb JJ, Canoc A
(2013) The impact of coffee on health.
Maturitas 75, 7-21.
Chatzi L, Papadopoulou E, Koutra K et al.
(2012) Effect of high doses of folic acid
supplementation in early pregnancy on
child neurodevelopment at 18 months of
age: the mother-child cohort ‘Rhea’ study
in Crete, Greece. Public Health Nutr 15(9),
1728-1736.
Coimbra NC (2014) Nourish -
Carbohydrates Fuel Your Brain. The
Franklin Institute Online.
http://www.fi.edu/learn/brain/carbs.html.
Accessed 15 February 2014
Conklin SM, Gianaros PJ, Brown SM et al.
(2007) Long-chain omega-3 fatty acid
intake is associated positively with
corticolimbic gray matter volume in
healthy adults. Neurosci Lett 421(3), 209-
212.
Cunnane SC, Plourde M, Pifferi F et al.
(2009) Fish, docosahexanoic acid and
Alzheimer’s disease. Prog Lipid Res 48,
239-256.
Cunnane SC, Chouinard-Watkins R,
Castellano CA et al. (2013)
Docosahexaenoic acid homeostasis, brain
aging and Alzheimer’s disease: Can we
reconcile the evidence? Prostaglandins
Leukot Essent Fatty Acids 88, 61-70.
Daubner SC, Le T, Wang S (2011)
Tyrosine hydroxylase and regulation of
dopamine synthesis. Arch Biochem
Biophys 508(1), 1-12.
Davis BC, Kris-Etherton PM (2003)
Achieving Optimal Essential Fatty Acid
Status in Vegetarians: Current Knowledge
and Practical Implications. Am J Clin Nutr
78(3), 640S-646S.
De Lorgeril M (2013) Mediterranean diet
and cardiovascular disease: historical
perspective and latest evidence. Curr
Atheroscler Rep 15:370. DOI:
10.1007/s11883-013-0370-4.
EFSA, European Food Safety Authority
(2008) ALA and LA and growth and
development of children. The EFSA
Journal 783, 1-9.
EFSA, European Food Safety Authority
(2009) DHA and support of the cognitive
development of the unborn child and
breastfed infant. The EFSA Journal 1007,
1-14.
EFSA, European Food Safety Authority
(2010) Scientific Opinion on Dietary
Reference Values for fats, including
saturated fatty acids, polyunsaturated fatty
acids, monounsaturated fatty acids, trans
fatty acids, and cholesterol. EFSA Journal
8(3), 1461.
Ek KL, Brand-Miller J, Copeland L (2012)
Glycemic effect of potatoes. Food Chem
133(4), 1230-1240.
Engler MB, Engler MM (2004) The
vasculoprotective effects of flavonoid-rich
cocoa and chocolate. Nutr Res 24(9), 695-
706.
Estruch R, Ros E, Salas-Salvadó J et al.
(2013) Primary prevention of
cardiovascular disease with a
Mediterranean diet. N Engl J Med 368(14),
1279-1290.

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
FAO, Food and Agriculture Organization
of the United Nations (2010) Fats and fatty
acids in human nutrition: Report of an
expert consultation. FAO, Rome.
Fernstrom JD (2013) Large neutral amino
acids: dietary effects on brain
neurochemistry and function. Amino Acids
45(3), 419-430.
Fredholm BB (2011) Methylxanthines.
Handbook of Experimental Pharmacology
200. Springer, Berlin.
Gardener H, Wright CB, Gu Y et al. (2011)
Mediterranean-style diet and risk of
ischemic stroke, myocardial infarction, and
vascular death: the Northern Manhattan
Study. Am J Clin Nutr 94(6), 1458-1464.
Georgieff MK (2011) Long-term brain and
behavioral consequences of early iron
deficiency. Nutr Rev 69(Suppl 1), S43-
S48.
Ghalwa NA, Qedra RA, Wahedy K (2014)
Impact of calcium and magnesium dietary
changes on women pain and discomfort
from premenstrual syndrome at the Faculty
of Pharmacy-Gaza Strip. WJPPS 3(2), 981-
1005.
Gogus U, Smith C (2010) n-3 omega fatty
acids: a review of current knowledge. Int J
Food Sci Technol 45, 417-436.
Goldoni L (2004) Kakao zrna i kakao
proizvodi. In: Tehnologija konditorskih
proizvoda: Kakao i čokolada. Kugler,
Zagreb.
Greenberg JA, Bell SJ, Van Ausdal W
(2008) Omega-3 fatty acid
supplementation during pregnancy. Rev
Obstet Gynecol 1(4), 162-169.
Gustafson E (2008) Nutrition and mental
health. In: Fundukian LJ, Wilson J (ed)
Gale encyclopedia of mental health. 2nd
ed. Thompson Gale, Detroit.
Hamburg ME, Finkenauer C, Schuengel C
(2014) Food for love: the role of food
offering in empathic emotion regulation.
Front Psychol 5:32. DOI:
10.3389/fpsyg.2014.00032.
Heckman MA, Weil J, Gonzalez de Mejia
E (2010) Caffeine (1, 3, 7-
trimethylxanthine) in foods: A
comprehensive review on consumption,
functionality, safety, and regulatory
matters. J Food Sci 75(3), R77-R87.
Higgins JP, Tuttle DT, Higgins HL (2010)
Energy beverages: content and safety.
Mayo Clin Proc 85(11), 1033-1041.
Hodge AM, English DR, Itsiopoulos C et
al. (2011) Does a Mediterranean diet
reduce the mortality risk associated with
diabetes: evidence from the Melbourne
Collaborative Cohort Study. Nutr Metab
Cardiovasc Dis 21(9), 733-739.
Hoevenaar-Blom MP, Nooyens AC,
Kromhout D et al. (2012) Mediterranean
style diet and 12-year incidence of
cardiovascular diseases: the EPICNL
cohort study. PLoS One 7(9):e45458.
Hoffman R, Gerber M (2013) Evaluating
and adapting the Mediterranean diet for
non-Mediterranean populations: A critical
appraisal. Nutr Rev 71(9), 573-584.
Holmes GL, Yang Y, Liu Z et al. (2002)
Seizure-induced memory impairment is
reduced by choline supplementation before
or after status epilepticus. Epilepsy Res
48(1-2), 3-13.
Isaacs E, Oates J (2008) Nutrition and
cognition: assessing cognitive abilities in
children and young people. Eur J Nutr
47(3), 4-24.
Jalil AMM, Ismail A (2008) Polyphenols
in cocoa and cocoa products: Is there a link
between antioxidant properties and health?
Molecules 13:2190-2219.

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
Jenkins DJA, Augustin LSA, Malick A et
al. (2013) Glucose: Chemistry and Dietary
Sources. In: Encyclopedia of Human
Nutrition. 3th ed. University of Toronto,
Toronto.
Jensen CL, Voigt RG, Prager TC et al.
(2005) Effects of docosahexaenoic acid
intake on visual function and
neurodevelopment in breastfed term
infants. Am J Clin Nutr 82(1). 125-132.
Kaczmarczyk MM, Miller MJ, Freund GG
(2012) The health benefits of dietary fiber:
Beyond the usual suspects of type 2
diabetes mellitus, cardiovascular disease
and colon cancer. Metab Clin Exp 61,
1058-1066.
Kendall CWC, Esfahani A, Jenkins DJA
(2010) The link between dietary fiber and
human health. Food Hydrocolloid 24(1),
42-48.
Kidd PM (2007) Omega-3 DHA and EPA
for cognition, behavior, and mood: clinical
findings and structural-functional synergies
with cell membrane phospholipids. Altern
Med Rev 12(3), 207-27.
Langley-Evans SC (2008) Metabolic
programming during pregnancy:
Implications for personalized nutrition. In:
Kok F, Bouwman L, Desire F (ed)
Personalized Nutrition. Principles and
Applications. CRC Press, Routledge.
Lourida I, Soni M, Thompson-Coon J et al.
(2013) Mediterranean diet, cognitive
function, and dementia: a systematic
review. Epidemiology 24(4), 479-489.
Martínez-González MA, Guillén-Grima F,
De Irala J et al. (2012) The Mediterranean
diet is associated with a reduction in
premature mortality among middle-aged
adults. J Nutr 142(9), 1672-1678.
McCann JC, Ames BN (2007) An
overview of evidence for a causal relation
between iron deficiency during
development and deficits in cognitive or
behavioral function. Am J Clin Nutr 85,
931-945.
McCann JC, Hudes M, Ames BN (2006)
An overview of evidence for a causal
relationship between dietary availability of
choline during development and cognitive
function in offspring. Neurosci Biobehav
Rev 30, 696-712.
Misirli G, Benetou V, Lagiou P et al.
(2012) Relation of the traditional
Mediterranean diet to cerebrovascular
disease in a Mediterranean population. Am
J Epidemiol 176(12), 1185-1192.
Montgomery P, Burton JR, Sewell RP et
al. (2013) Low blood long chain omega-3
fatty acids in UK children are associated
with poor cognitive performance and
behaviour: A cross-sectional analysis from
the DOLAB study. PLoS ONE
8(6):e66697.
Nehlig A, Daval JL, Debry G (1992)
Caffeine and the central nervous system:
mechanisms of action, biochemical,
metabolic and psychostimulant effects.
Brain Res Rev 17(2), 139-170.
Page KA, Chan O, Arora J et al. (2013)
Effects of fructose versus glucose on
regional cerebral blood flow in brain
regions involved with appetite and reward
pathways. JAMA 309(1), 63-70.
Parker G, Brotchie H (2011) Mood effects
of the amino acids tryptophan and tyrosine.
Acta Psychiatr Scand 124, 417-426.
Parker G, Parker I, Brotchie H (2006)
Mood state effects of chocolate. J Affect
Disord 92, 149-159.
Paoletti R, Poli A, Conti A, et al. (2012)
Chocolate and Health. Springer, Milan.

Ines Banjari / Brain food: how nutrition ... / (2014) 3 (1)
Persad LAB (2011) Energy drinks and the
neurophysiological impact of caffeine.
Front Neurosci 5:116, PMC3198027.
Privitera G, Moshaty B, Marzullo F et al.
(2013) Expressing food through art:
evidence for a nutrient-specific effect on
mood. JBBS 3(2), 163-167.
Purnell JQ, Fair DA (2013) Fructose
ingestion and cerebral, metabolic, and
satiety responses. JAMA 309(1), 85-86.
Rawel HM, Kulling SE (2007) Nutritional
contribution of coffee, cacao and tea
phenolics to human health. J Verbr
Lebensm 2, 399-406.
Shah, R (2013) The role of nutrition and diet
in Alzheimer disease: a systematic review. J
Am Med Dir Assoc 14(6), 398-402.
Shaikh SR, Brown DA (2013) Models of
plasma membrane organization can be
applied to mitochondrial membranes to
target human health and disease with
polyunsaturated fatty acids. Prostag
Leukotr Ess 88(1), 21-25.
Skarupski KA, Tangley CC, Li H et al.
(2013) Mediterranean diet and depressive
symptoms among older adults over time.
The Journal of Nutrition, Health & Aging
17(5), 441-445.
Smit HJ, Gaffan EA, Rogers PJ (2004)
Methylxanthines are the psycho-
pharmacologically active constituents of
chocolate. Psychopharmacology 176, 412-
419.
Snel J, Lorist MM (2011) Effects of
caffeine on sleep and cognition. Prog Brain
Res 190, 105-117.
Sofi F, Macchi C, Casini A (2013)
Mediterranean diet and minimizing
neurodegeneration. Curr Nutr Rep 2, 75-
80.
Sommer E (1995) Food and mood. The
complete guide to eating well and feeling
your best. Henry Holt, New York.
Tognon G, Lissner L, Sæbye D et al.
(2013) The Mediterranean diet in relation
to mortality and CVD: a Danish cohort
study. Br J Nutr 111(1), 151-159.
Trichopoulou A, Costacou T, Bamia C et
al. (2003) Adherence to a Mediterranean
diet and survival in a Greek population. N
Engl J Med 348, 2599-608.
Vanhees K, Vonhögen IGC, van Schooten
FJ et al. (2014) You are what you eat, and
so are your children: the impact of
micronutrients on the epigenetic
programming of offspring. Cell Mol Life
Sci 71, 271-285.
Vannice G, Rasmussen H (2014) Position
of the Academy of Nutrition and Dietetics:
Dietary fatty acids for healthy adults. J
Acad Nutr Diet 114(1), 136-153.
Wenk GL (2010) Your brain on food. How
chemicals control your thoughts and feelings.
Oxford University Press, New York.
WHO, World Health Organization (2007)
Exposure to mercury: a major public health
concern. WHO, Geneva.
WHO, World Health Organization (2008)
Interim summary of conclusions and
dietary recommendations on total fat and
fatty acids: From the Joint FAO/WHO
Expert Consultation on fats and fatty acids
in human nutrition. WHO, Geneva.
WHO, World Health Organization (2010)
Children’s exposure to mercury
compounds. WHO, Geneva.
Yurko-Mauro K, McCarthy D, Rom D et
al. (2010) Beneficial effects of
docosahexaenoic acid on cognition in age-
related cognitive decline. Alzheimers
Dement 6(6), 456-464.