The Brain is Highly Susceptible to its 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 behavior. Many studies have demonstrated the importance of nutrition during children’s physical growth and mental development.

We have begun to realize that the developed brain is highly susceptible to its nutritional environment. For example, although still in its preliminary stages, a role for nutrition is currently being developed in the causes and treatment of neurological and psychiatric behavior.

It is now known that the activity of neurons is influenced by different rhythms (circadian, monthly and seasonal) and by factors such as meal times, choice of food, and the chemical components of food. Not surprisingly, nutrients can be instrumental in determining: physiological behavior, the organism’s capacity to adapt to different environmental situations, hunger, and satiety.

The Key Link Between Brain Function and Diet Lies in Neurotransmitters

Since the 1950’s, it has been demonstrated that neurotransmitters such as catecholamines and serotonin play an important role in several physiological states. Serotonin has been associated with the sleep cycle and noradrenaline with awake and vigilant states. Neurotransmitters are also involved in thermoregulation (maintenance of body temperature), the mechanism of hunger and satiation, and the process of learning and memory.

Neurotransmitters exert their actions in nerve endings after being released into the synapses - the spaces between cells. The pre-synaptic cell, which releases neurotransmitters, 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 a metabolic or physiological relation with other neurotransmitters. The neuro-anatomical systems (motor or limbic systems) serve as support and as intermediaries for the transmission of information.

Serotonin and catecholamines are affected by food intake. Synthesized in the brain, they are formed when the amino acids, 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 amino acids into neurotransmitters is metabolically significant because it assures a biochemical balance between the synthesis of dopamine (DA) and serotonin (5-HT). Tryptophan will provoke an increase of serotonin and a decrease of dopamine, whereas dihydroxyphenylalanine (used, for example, in the control of Parkinson’s disease) will generate an increase of dopamine, and a decrease of serotonin. This is only one example of a biochemical balance generated in the brain that allow neurotransmitters to receive and organize information.

Under normal concentrations of tryptophan and tyrosine in the brain, the hydroxylases, which are the rate limiting enzymes in both pathways, are not saturated by the substrates, tryptophan and tyrosine. This means that diet induced changes in blood amino acid concentrations will influence the brain’s synthesis of these two important neurotransmitters. This simple relationship between the diet plasma and brain neurochemistry allow the brain to gather information on diet composition and the metabolic state of the body and use this information to regulate many of its functions.

The 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 competing neutral amino acids. This happens because the release of insulin, which occurs after carbohydrates are consumed, causes the rapid uptake of amino acids by tissues, except tryptophan. When amino acids pass through the brain capillaries, tryptophan has an uptake advantage. As a result, tryptophan and serotonin levels increase in the brain.

The opposite happens to serotonin in the brain when proteins are consumed. Proteins are relatively low in tryptophan, but are high in the amino acids that compete for their uptake into the brain. Thus a protein rich meal decreases the plasma tryptophan and the brain is informed that protein is consumed.

Another neurotransmitter, dopamine, the immediate precursor of noradrenaline, is derived from the amino acid, tyrosine. However, its synthesis is not directly influenced by plasma and brain concentrations of tyrosine, as it is for 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 cells. Consequently, an increase in the dopamine content does not necessarily correspond to an increase in the noradrenaline content on a neuroanatomical and neurophysiological basis. In certain regions of the brain such as the cortical areas, the synthesis of dopamine is almost exclusively used for the synthesis of noradrenaline whose role as a neurotransmitter is dominant.

Regulation of Food Intake

Food intake regulation is a good example of a behavioral response. Many theories have tried to explain how the brain controls food intake and is responsible for hunger and satiation mechanisms. The theories on the control of blood glucose and 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 glucose is low, neurons are activated and hunger increases. Conversely, when the rate of glucose is high, the activity of the brain cells sensitive to glucose is diminished, and the sensation of satiation is attained. Unlike peripheral tissues, such as muscles, the brain does not need insulin to metabolize glucose, suggesting further that the metabolism of glucose may have a unique place in controlling one’s appetite.

The lipostatic hypothesis suggests that the size of fat deposits 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.

Changes in plasma amino acid patterns and the uptake of amino acids into the brain after food ingestion provide signals that allow for the regulation of appetite. Both the catecholamines and serotonin neurotransmitter systems are known to be involved in appetite regulatory mechanisms. The control of their synthesis by the availability of their amino acid precursors suggests that appetite regulation may be achieved by this mechanism.

The effects of nutrition on behaviors linked to human mental and psycho-affective activity are numerous and complex. It is important to remember that macronutrients and micronutrients are essential to the brain’s good functioning. Moreover, as amino acids play an obvious role as precursors of neurotransmitters, it must not be overlooked that they are closely tied to vitamins and minerals. It is clear that a healthy and balanced diet contributes to the stable maintenance of the brain’s vital functions.

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