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Brain Foods- The Effects of Nutrients on Brain Function

Brain Foods- The Effects of Nutrients on Brain Function

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 Acknowledgements
The authors are grateful to funding agencies in their respec-tive countries for supporting this work. The Gobierno deNavarra/Nafarroako Gobernua and the town and people of Petilla are acknowledged for graciously hosting the meetingthat originated this document. Special thanks are due to A. Rowan, who attended the Petilla meeting and greatlycontributed to establishing the initial vision for this report.
FURTHER INFORMATION
Petilla Terminology:
Neuroscience Information Framework:
Neurogateway:
SenseLab:
NeuroMorpho:
SUPPLEMENTARY INFORMATION
See online article:
 
ALL LINKS ARE ACTIVE IN THE ONLINE PDF
Although food has classically been perceivedas a means to provide energy and buildingmaterial to the body, its ability to preventand protect against diseases is starting to berecognized. In particular, research over thepast 5 years has provided exciting evidence
SCIENCE AND SOCIETY
Brain foods: the effects of nutrientson brain function
Fernando Gómez-Pinilla
Abstract | It has long been suspected that the relative abundance of specificnutrients can affect cognitive processes and emotions. Newly described influencesof dietary factors on neuronal function and synaptic plasticity have revealedsome of the vital mechanisms that are responsible for the action of diet on brainhealth and mental function. Several gut hormones that can enter the brain, or thatare produced in the brain itself, influence cognitive ability. In addition, well-established regulators of synaptic plasticity, such as brain-derived neurotrophicfactor, can function as metabolic modulators, responding to peripheral signals suchas food intake. Understanding the molecular basis of the effects of food oncognition will help us to determine how best to manipulate diet in order to increasethe resistance of neurons to insults and promote mental fitness.
for the influence of dietary factors onspecific molecular systems and mechanismsthat maintain mental function. For instance,a diet that is rich in omega-3 fatty acids isgarnering appreciation for supporting cogni-tive processes in humans
1
and upregulating
PERSPECTIVES
568
|
JULY 2008
|
VOLUME 9
www.nature.com/reviews/neuro
 
 
ab
Contemporary fish consumptionversus major depression
6543210
   M  a   j   o  r   d  e  p  r  e  s  s   i  o  n  a  n  n  u  a   l  p  r  e  v  a   l  e  n  c  e   (  r  a   t  e  p  e  r   1   0   0  p  e  r  s  o  n  s   )
New ZealandCanadaFrancer = –0.84p < 0.005Korea JapanTaiwanPuertoRicoUnitedStatesApparent fish consumption(Ibs per person per year)WestGermany
20406080100120130150
   C  o  g  n   i   t   i  v  e  s   k   i   l   l  s   D   H   A
of digestion, such as the release of enzymesand food absorption. The use of VNS hasbecome a routinely approved procedurefor the treatment of refractory partial-onsetseizures. Based on observations that theapplication of VNS to patients with epilepsy was associated with improved mood, VNSwas perceived as a potential treatment fordepression. In humans, VNS failed to pro-duce improvements in depression patientswho participated in a short-term open trial(lasting 10 weeks)
6
; however, in a longer-termstudy (lasting 12 months), VNS producedbeneficial effects that were sustained after2 years
7
. Specifically, patients treated withVNS doubled their improvement per monthin the Inventory of Depressive Symptomsself report relative to patients receivingtreatment as usual (TAU) by itself. TAUconsisted of managing treatment-resistantdepression with medication or with anothertherapy that was deemed appropriate by genes that are important for maintainingsynaptic function and plasticity in rodents
2
.In turn, diets that are high in saturatedfat are becoming notorious for reducingmolecular substrates that support cognitiveprocessing and increasing the risk of neuro-logical dysfunction in both humans
3
andanimals
4
. Although these studies emphasizean important effect of food on the brain,further work is necessary to determine themechanisms of action and the conditions fortherapeutic applications in humans.Over thousands of years, diet, in conjunc-tion with other aspects of daily living, suchas exercise, has had a crucial role in shapingcognitive capacity and brain evolution
(BOX 1)
.Advances in molecular biology have revealedthe ability of food-derived signals to influenceenergy metabolism and synaptic plasticity and, thus, mediate the effects of food oncognitive function, which is likely to havebeen crucial for the evolution of the modernbrain. Feeding habits have been intrinsically associated with the development of humancivilization, as people’s choice of what to eatis influenced by culture, religion and society.The newly discovered effects of food on cog-nition are intriguing for the general public,as they might challenge preconceptions,and they attract substantial interest from themedia. The fact that feeding is an intrinsichuman routine emphasizes the power of dietary factors to modulate mental health notonly at the individual level, but also at thecollective, population-wide level. Here Idiscuss the effects of both internal signalsthat are associated with feeding and dietary factors on cell metabolism, synaptic plasticity and mental function
(FIG. 1)
. Throughout Iuse the term cognition from a neurobiologicalperspective, to refer to the mental processesthat are involved in acquiring knowledgeand to the integration of these processes
 
intothe conscious aspect of emotions, whichinfluences mood and has psychiatricmanifestations
5
.
Internal signals and cognition
The influence of visceral signals on mentalfunction has been appreciated since ancienttimes, and to this day lifestyle factors, suchas diet and exercise, are used as part of thera-pies to reduce depression, schizophrenia andbipolar disorders. In this section I discussthe influence of vagal nerve stimulation(VNS) and gut hormones on cognition andemotion
(FIG. 1)
.
Effects of vagal nerve stimulation on cognition.
 Vagal afferents from the gastrointestinal tractare critical for monitoring various aspects
Box 1 |
Feeding as an adaptive mechanism for the development of cognitive skills
Adaptations that facilitated food acquisitionand energy efficiency exerted strongevolutionary pressures on the formation ofthe modern brain and the energy-demanding development of cognitive skills.For example, the wildebeest annually travelshundreds of miles to find feeding grounds inthe savannah, a behaviour that requires fullyoperational and complex navigational,defensive and cognitive conducts forsurvival. The function of brain centres thatcontrol eating behaviour is integrated withthose of centres that control cognition
(FIG. 1)
.For instance, animals that eat a potentiallypoisonous meal develop a perpetualaversion to its flavour through complexmechanisms of learning and memory thatinvolve the hypothalamus, the hippocampusand the amygdala
133
. In turn, pleasantmemories of foods have been related tobrain pathways that are associated withreward
134
.Abundant paleontological evidencesuggests that there is a direct relationshipbetween access to food and brain size, andthat even small differences in diet can havelarge effects on survival and reproductivesuccess
135
. Larger brains in humanoids areassociated with the development ofcooking skills, access to food, energysavings and upright walking and running
136
;all of these features require coordinationwith cognitive strategies that are centredin successful feeding. Dietary consumptionof omega-3 fatty acids is one of the best-studied interactions between food and brain evolution. Docosahexaenoic acid (DHA) is themost abundant omega-3 fatty acid in cell membranes in the brain
137
; however, the human bodyis not efficient at synthesizing DHA, so we are largely dependent on dietary DHA
138
. It has beenproposed that access to DHA during hominid evolution had a key role in increasing the brain/body-mass ratio (also known as encephalization)
138
(see figure, part
a
). The fact that DHA is animportant brain constituent supports the hypothesis that a shore-based diet high in DHA wasindispensable for hominid encephalization. Indeed, archeological evidence shows that earlyhominids adapted to consuming fish and thus gained access to DHA before extensiveencephalization occurred. The interplay between brain and environment is ongoing. Over thepast 100 years, the intake of saturated fatty acids, linoleic acid and
trans
fatty acids hasincreased dramatically in Western civilizations, whereas the consumption of omega-3 fattyacids has decreased. This might explain the elevated incidence of major depression in countriessuch as the United States and Germany (see figure, part
b
)
78
. Both photographs in part
a
 
Jeffrey H. Schwartz. Part
b
of the figure reproduced, with permission, from
REF. 78
 
(1998)Lancet Publishing Group.
PERSPECTIVES
NATURE REVIEWS
|
 
NEUROSCIENCE 
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569
 
 
Sensory inputCognitionand emotionVagus nerveFood intakeBodyphysiologyLeptinIGF
 
1, insulin,ghrelin and GLP1
Limbic systemHypothalamusCaudal brainstemHPA, immune system
the treating physician. Based on the resultsof the long-term studies, the US Food andDrug Administration recently approved theuse of VNS for the treatment of chronic (notacute) resistant depression (see
REF. 8
fora review). Although the mechanisms thatunderlie the effects of VNS on depressionare not well-understood, a recent study demonstrated that VNS increases the levelsof the mRNAs for brain-derived neuro-trophic factor (BDNF) and fibroblast growthfactor 2 (FGF2) in the rat hippocampusand cerebral cortex, as well as the level of noradrenaline in the prefrontal cortex
9
. Aselevations of BDNF
10
and noradrenalinehave been associated with the effects of antidepressant treatments, these findingsprovide insights into how signals derivedfrom the gut can affect mood. Furthermore,on the basis that neurons of the dorsal motornucleus of the vagus nerve retrogradely transport BDNF and other neurotrophins
11
,it is likely that neurotrophins are involvedin sensory and motor signalling from the viscera. Interestingly, a separate line of investigations indicated that the applicationof VNS to humans
12
or rodents
12
enhancedmemory performance, suggesting that theinformation that is signalled to the brainby the vagus nerve might serve to influencehigher-order cognitive processing.
Gut hormones associated with cognition.
 In addition to the capacity of the gut todirectly stimulate molecular systems that areassociated with synaptic plasticity and learn-ing, several gut hormones or peptides, suchasleptin,ghrelin
,
glucagon-like peptide 1(GLP1) and insulin have been found to influ-ence emotions and cognitive processes
(FIG. 1)
.Leptin is synthesized in adipose tissueand sends signals to the brain to reduceappetite (see
REF. 13
for a review). Leptinreceptors have been identified in severalbrain areas, including the hypothalamus, thecerebral cortex and the hippocampus. Thefact that leptin elevates BDNF expressionin the hypothalamus suggests that BDNFmight mediate the effects of leptin on foodintake and energy homeostasis
14
. Like BDNF,leptin facilitates synaptic plasticity in thehippocampus
15
. Genetically obese rodentswith dysfunctional leptin receptors showimpairments in long-term potentiation(LTP) and long-term depression and dif-ficulties in spatial learning
16
. These effectswere rescued by administrating leptin intothe hippocampus
15,17
. New studies showingthat leptin promotes rapid changes in hippo-campal dendritic morphology 
 
suggest thatleptin exerts a direct action on hippocampalplasticity 
18
.Ghrelin is an adipogenic hormone thatis secreted by an empty stomach (see
REF. 19
 for a review); it acts as an appetite stimulantin mice
20
and humans
21
. Ghrelin is theendogenous ligand of the growth hormonesecretagogue receptor, which is expressed inthe arcuate nucleus in the hypothalamus
22
 and in the hippocampus
23
. Peripheraladministration of ghrelin increases foodintake in normal rodents
24,25
and humans
26,27
,whereas chronic administration can lead toadiposity 
24,25
. Ghrelin also promotes rapidreorganization of synaptic terminals in thehypothalamus
28
, and in the hippocampusit promotes synapse formation in dendriticspines and LTP, which are paralleled by enhanced spatial learning and memory formation
29
.GLP1, which is synthesized by intestinalcells, regulates energy metabolism by stimulating pancreatic insulin secretion and
Figure 1 |
Effects of feeding on cognition.
Neural circuits that are involved in feeding behaviourshow precise coordination with brain centres that modulate energy homeostasis and cognitive func-tion. The effects of food on cognition and emotions can start before the act of feeding itself, as therecollection of foods through olfactory and visual sensory inputs alters the emotional status ofthe brain. The ingestion of foods triggers the release of hormones or peptides, such as insulin andglucagon-like peptide 1 (GLP1)
31
, into the circulation (see
REF. 31
for a review); these substances canthen reach centres such as the hypothalamus and the hippocampus and activate signal-transductionpathways that promote synaptic activity and contribute to learning and memory. In turn, the lack offood that is signalled by an empty stomach can elicit the release of ghrelin, which can also supportsynaptic plasticity and cognitive function. Chemical messages derived from adipose tissue throughleptin can activate specific receptors in the hippocampus and the hypothalamus, and influence learningand memory. The positive actions of leptin on hippocampus-dependent synaptic plasticity — that is,its actions on NMDA (
N
-methyl-
-aspartate) receptor function and long-term potentiation facilitation— are well characterized (see
REF. 13
for a review). Insulin-like growth factor 1 (IGF1) is produced bythe liver and by skeletal muscle in response to signals derived from metabolism and exercise. IGF1 cansignal to neurons in the hypothalamus and the hippocampus, with resulting effects on learning andmemory performance. In addition to regulating appetite, the hypothalamus coordinates activity in thegut and integrates visceral function with limbic-system structures such as the hippocampus, the amyg-dala and the cerebral cortex. Visceral signals can also modulate cognition and body physiologythrough the hypothalamic–pituitary axis (HPA). The effects of the
 
hypothalamus can also involve theimmune system, as it heavily innervates the thymus and several immune-system
 
molecules can affectsynaptic plasticity and cognition. The parasympathetic innervation of the gut by the vagus nerveprovides sensory information to the brain, enabling gut activity to influence emotions. In turn, emo-tions can also influence the viscera through parasympathetic efferents in the vagus nerve. Vagal nervestimulation is being used therapeutically to treat chronic depression
.
PERSPECTIVES
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www.nature.com/reviews/neuro

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