NUTRITION AND BEHAVIOUR

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NUTRITION AND BEHAVIOUR
Andrée G. Roberge, Ph.D.
President and CEO
Brain is Highly Susceptible to Nutritional Environment
It is commonly known that the brain is like a computer – it receives, integrates,
programs and transmits all sensory-motor information. We also know that it
manages all physiological and psycho-affective behaviour. Many studies have,
in fact, demonstrated the importance of nutrition during children’s physical growth
and mental development1,2,3.
More recently, however, we have begun to realize that the developed brain too,
is highly susceptible to its nutritional environments. For example, although still in
its preliminary stages, a role for nutrition is currently being developed in the
etiology and treatment of neurological and psychiatric behaviour.
It is now known that the activity of neurons is influenced by different rhythms
(circadian, monthly and seasonal) and is influenced by factors as variable as
meal times, choice of food and chemical constituents of foods 4. Not surprisingly,
then, nutrients can be instrumental in determining: physiological and psychoaffective behaviour; the organism’s capacity to adapt to different environmental
situations; and hunger and satiety.
CONTROL OF NEUROTRANSMITTER SYNTHESIS
The key link between brain function and diet lies in the neurotransmitters. Since
the 1959’s, it has been demonstrated that catecholamines and serotonin play an
important role in both humans and animals in several physiological states.
Serotonin, for example, has been associated with the sleep cycle and
noradrenaline with awake and vigilance states. These neurotransmitters are also
involved in thermoregulation, mechanism of hunger and satiation, and in the
process of learning and memory.
Neurotransmitters exert their action in nerve endings after release into the
spaces or synapses, between cells. The pre-synaptic cell which releases the
neurotransmitter, thus communicates with receptors on the post-synaptic cell. As
a result, pathways throughout the brain serve as communication lines controlling
brain function. A neurotransmitter never acts alone, it is always in metabolic or
physiological relation with one or many neurotransmitters5.
The neuroanatomical systems (motor or limbic systems) serve as supports and
intermediaries for the transmission of information.
Serotonin and catecholamines are readily affected by diet. Synthesized in the
brain, they are formed when tryptophan and tyrosine undergo an initial
transformation (hydroxylation) by two different enzymes sharing the same
nutrient cofactors (pteridine, vitamin C and iron). After hydroxylation both amino
acids are then decarboxylated by a vitamin B6 dependent enzyme to form the
neurotransmitters dopamine and serotonin.
This step in the conversion of the amino acids to the neurotransmitters is
metabolically significant because it appears to assure a biochemical balance
between the synthesis of the dopamine (DA) and that of serotonin (5-HT)6,7. An
administration of tryptophan, therefore, will provoke an increase of serotonin and
a decrease of dopamine, whereas an administration of L-DOPA8, used in the
control of Parkinson’s disease will generate an increase of dopamine and a
decrease of serotonin. This is only one example of biochemical balance
generated in the brain to allow neurotransmitters to receive and organize
information.
Under normal concentrations of brain tryptophan and tyrosine, the hydroxylases,
which are the rate limiting enzymes in both pathways, are not saturated by
substrate.
This means that diet induced changes in blood amino acid
concentrations, and as a result in the brain, will influence the brain synthesis of
these two important neurotransmitters.
It is probable that these simple
relationships between the diet plasma and brain neuro-chemistry allow the brain
to gather information on diet composition and the metabolic state of the body and
to use this information in the regulation of many of its functions.
BRAIN DISTINGUISHES BETWEEN NUTRIENTS
It is through this system that the brain can distinguish a carbohydrate meal from
a protein meal. Carbohydrate consumption increases plasma tryptophan relative
to the competing neutral amino acids. This happens because the release of
insulin which occurs after carbohydrate is consumed causes rapid uptake of
amino acids, except tryptophan, by tissues9. When the amino acids pass
through the brain capillaries, tryptophan has an advantage for uptake. As a
result, brain tryptophan and serotonin levels increase.
The opposite happens to brain serotonin when proteins consumed. Proteins are
relatively low in tryptophan, but high in the amino acids which compete for its
uptake by the brain. Thus a meal of protein decreases the plasma tryptophan to
competing neutral amino acid ratio, and the brain is informed that protein is
consumed.
Dopamine, the immediate precursor of noradrenaline (NA), is derived from the
amino acid tyrosine. However, its synthesis is not directly influenced by plasma
and brain concentration of tyrosine, as is the saturation describing the
relationship between tryptophan and serotonin. The synthesis of noradrenaline,
from dopamine is limited by the biochemical properties of the synthesis enzyme
(dopamine-B-hydroxylase) and by the location of this enzyme in the nerve cell.
Consequently, an increase in the dopamine content does not necessarily
correspond to an increase in noradrenaline content on the neuroanatomical and
neuro-physiological levels. It is interesting to note that in certain regions of the
brain such as the cortical regions, the synthesis of dopamine is to serve almost
exclusively for the synthesis of noradrenaline, whose role as a neurotransmitter
is dominant.
REGULATION OF FOOD INTAKE: RECENT THEORIES
Food intake regulation is a good example of behavioural response. Many
theories have tried to explain how the brain controls food intake and is
responsible for hunger and satiation mechanisms. The theories of the control of
blood glucose and of lipid reserves are described as the glucostatic and lipostatic
hypotheses.
According to the glucostatic hypothesis, appetite control is
determined by the use of glucose by brain cells. If utilization is low, neurons
would be activated and hunger increases. Conversely, when the rate of glucose
utilization is high, the activity of the brain cells sensitive to glucose would be
diminished, and the sensation of satiation attained. Unlike peripheral tissues,
such as muscle, the brain does not need insulin to metabolize glucose and
cannot store the glucose, suggesting further that the metabolism of glucose may
have a unique place in the regulation appetite.
The lipostatic hypothesis suggests that the size of fat deposit in the organism is
connected to the neuronal or hormonal control of appetite. Temperature
changes affect degree of appetite, possibly by affecting energy storage. Thus in
humans, a cold environment stimulates appetite, whereas a warmer environment
diminishes appetite.
An hypothesis suggests that changes in plasma amino acids patterns and brain
uptake of amino acids after food ingestion provide signals which allow the
regulation of appetite10,11.
Both the catecholamines and serotonin
neurotransmitters systems are known to be involved in appetite regulatory
mechanisms. The control of their synthesis by the availability of their amino acid
precursors, therefore, suggests that appetite regulation may be achieved by this
mechanism.
Other hypothesis exist for the regulation of appetite, but their physiological and
biochemical significance are yet to be specified. The brain may possess many
mechanisms capable of modulating the functional use of nutrients.
PSYCHO-AFFECTIVE BEHAVIOURS
The importance of macro-and micro-nutrients in psycho-affective disorders is
recognized more and more. For example, it has been demonstrated that the
circadian rhythm of free tryptophan but not that of tyrosine in plasma was
perturbed in depressive subjects maintained on a controlled diet 12. Furthermore,
an abnormality in the metabolism of tryptophan has also been described to
cause emotional instability, irritability, fatigue, perturbed sleep, loss of libido and
relatively depressive state. In subjects using oral contraceptives, a disturbance
in the metabolism of tryptophan was corrected using a vitamin B 6 supplement13.
PSYCHO-AFFECTIVE FOOD-INTAKE BEHAVIOUR
Anexoria nervosa is a disease primarily of young women characterized by the
pursuit of a thin body and a dread of weight-gain. It is an example of food-intake
behaviour thought to be of psycho-affective origin, and may be reflected in a diet
which shows a selective privation of certain macro-nutrients and a very restrictive
energy intake, significantly lower than the norm causing excessive weight loss 11.
Anorexic14,15 subjects select their food according to mood, expectations or
deceptions and generally eat in a disorderly fashion. Often the preferred
hypocaloric diet is relatively high in proteins, low in carbohydrate and lipids and
rich in fibber. Consequently, the individual’s nutritional state deteriorates and the
subject will show man symptoms of nutrient deficiency including lack of
menstruation, hypothermia, bradycardia, hypertension, constipation, anxiety, and
depression. In all these cases, a biochemical imbalance appears to exist
between the brain’s neurotransmitters and the limbic system’s functions.
Therefore, the first nutritional step to be undertaken in the treatment of affected
individuals should be aimed at weight gain as well as at stabilizing the psychoaffective state.
As discussed earlier the brain can distinguish a carbohydrate meal from a protein
meal. An increase in brain serotonin after a glucose carbohydrate meal reduces
mental activity and provokes drowsiness, both well known responses after a
meal. Similarly, it has been demonstrated in rats that a carbohydrate and lipidrich diet increases serotonin synthesis but decreases activity in the noradrenergic
system16,17. Although it is a difficult task to change the anorexic sufferer’s
protein-rich diet to a relatively carbohydrate-rich diet, these effects of protein ad
carbohydrate on the brain suggest that anorexic individual might benefit from a
dietary increase in carbohydrate to reverse the the neuro-chemical effects of the
high protein diet. This is only one example of psycho-affective food-intake
behaviour. Possibly obesity treatment by diet may be enhanced by appropriate
manipulation of neurochemical systems through food composition.
RELATIONSHIPS SHOULD NOT BE OVERSIMPLIFIED
The effects of nutrition on behaviours linked to human mental and
psychoaffective activity are numerous and complex. It is important to remember
that macro and micro-nutrients are essential to the good functioning of the brain
even though it is presently difficult to evaluate fully their role in origin of a
cerebral malfunction. Moreover, as amino acids play an obvious role as
precursors of neurotransmitters, it must no be overlooked that they are closely
tied to vitamins and minerals in all their metabolic progress.
It is clear that a healthy and balance diet contributes to the stable maintenance of
the brain’s vital function. These relationships should not be oversimplified,
however, because the link between nutrition and human behaviour constitutes a
continuum of multiple well-integrated sequences capable of maintaining a
homeostatic state for as long as the organism’s physiological limits have not
been excessively distorted by disease or more frequently, by various stressful
situation.
References :
1. Roberge, A.G.O2K NEURO NUTRITION CONCEPT. Conférence présentée
le 8 février 2002 à Nassau, Bahamas pour Matol Botanical International.
2. Roberge, A.G. Nutrition and Behaviour. Perspectives, Vol. 3, No 1/Spring
1985.
3. Himwich, H.E. Early studies of the developing brain. Biochemistry of
Developing Brain. Ed. W. Himwich, Marcel Dekker Inc., 1973. Vol.1:1-50.
4. Moore-Ede, M.C., Sulzman, F.M. and Fuller, C.H.The Clocks That Time Us.
Physiology of the Circadian Timing System. Harvard University Press, 1982.
5. Roberge, A.G., Parent, A. et Boulay, M. Démonstration d’une relation
inversement proportionnelle entre la dopamine et la sérotonine dans
certaines structures cérébrales :aspects neurochimique et morphologiques. J.
Neurochem., 1976. 26:591-595.
6. Erickson, C.K. Functional relationship among central neurotransmitters.
Review of Neuroscience, Ed. Ehrenpreis & Kopin, Raven Press, 1978. Vol.
3:1-34.
7. Roberge, A.G. A morphological and biochemical dissociation between
dopamine and serotonin in cat brain. Catecholamines: Basic and Clinical
Frontiers, 1978. 2:1110-1113.
8. Bouchard, S. & Roberge, A.G. Biochemical properties and kinetic parameters
of DOPA/5-HTP Decarboxylase in brain, liver and adrenals of cat. Can.J.
Biochem., 57(7): 1014-1018.
9. Héroux, O. and Roberge, A.G. Different influences of two types of diets
commonly used for a rats on a series of parameters related to the metabolism
of central serotonin and noradrenaline. Can. J. Physiol. And Pharmacol.,
1981, 59(2): 108-112.
10. Altern, H., Dudel, J., Grusser, O.J., Griieser-Cornehls, U., Klinke, R., Schmidt,
R.F. and Zimmerman, M. Fundamentals of sensory physiology. Ed. Schmidt,
R.F., Springer-Verlag, New York, 1981.
11. Blackburn, H., Roberge, C. et Roberge, A.G. Effets d’un régime
hyperlipidique et hyperglucidique et d’un régime hypocalorique sur la teneur
des amines biogènes du cerveau de rat. ACFAS, Univ. du Québec à TroisRivières, 25-27 mai 1983.
12. Anderson, G.H. and Johnston, J.L. Nutrition control of brain neurotransmitter
synthesis and function. Can. J. Physio. Pharmacol., 1983. 61:271-281.
13. Adams, P.W., Rose, D.P., Folkard, J., Wyne, U., Seid, M. and Strong, R.
Effect of pyridoxine hydrochloride (vitamin B6) upon depression associated
with oral contraception. Lancet, 1973, 897-904.
14. Thibault, L. et Roberge, A.G. The Nutritional Status of Subjects with Anorexia
Nervosa. Intern. J. Vit. Nutr. Res., 57 :447-452.
15. Gillberg, C. Low dopamine and serotonin levels in anorexia nervosa. Am. J.
Psychiat., 1983, 140(7): 948.
16. Pouliot, T., De la Noüe, J. & Roberge, A.G. Influence of Social Interaction on
Physiological and Neurochemical Responses of Rainbow trout under Hypoxia
Stress. Nanjing – The third International Symposium on Antennas and
Electromagnetic Theory (ISAE’93), China, September 6-9, 1993.
17. Pouliot, T., Roberge, A.G. & De la Noüe, J. Impact of Dietary Protein Quality
on the Resistance of Rainbow Trout to Chronic Hypoxia Stress. Hobart – 6th
International Symposium on Fish Nutrition and Feeding, Australia, Oct. 4-7.
1993.
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