non è detto che io abbia ragione eh! non avendo la possibilità di fare continue analisi ormonali (tra l'altro i valori dei tiroidei liberi lascia il tempo che trova..) mi rifaccio ai dati disponibili su pubmed.
tempo fa avevo fatto una ricerca sugli effetti dei vari amminoacidi assunti singolarmente (volevo scrivere un articolo ma non avendo la certezza delle conclusioni ho preferito evitare di dire minchiate)
se ti può interessare ti incollo alcuni abstract che ritengo interessanti:
When--and why--should nutritional state control neurotransmitter synthesis?
The rates at which neurons synthesize such Group I neurotransmitters as serotonin, acetylcholine, and the catecholamines norepinephrine and dopamine depend physiologicall on the availability to them of the circulating precursors for these compounds (tryptophan, choline and tyrosine, respectively). The concentrations of precursor in the circulation and in neurons change rapidly after food consumption, depending upon what is eaten. Nutrient intake thus normally influences the synthesis of these neurotransmitters. Neurons that emit signals by releasing serotonin, acetylcholine, dopamine, or norepinephrine participate in the control of a number of bodily functions and behaviors (e.g., hunger, food choice, sleep, alertness, sensitivity to environmental stimuli and disease states). Dietary manipulations (or the consumption of individual nutrients) can thus be used as tools for the experimental analysis of functions mediated by monoaminergic or cholinergic neurons, and as adjuncts in the treatment of some diseases of these neurons. It is unclear "why" the evolutionary process should have "allowed" the neurotransmission mediated by acetylcholine or the monoamine transmitters to be influenced by the vagaries of food choice. One possible benefit that might accrue to the organism as a result of this dependency would be the use of cholinergic or monoaminergic neurons as "sensors", providing the brain with information about peripheral metabolic state. Thus carbohydrate consumption, which--by altering plasma amino acid levels accelerates brain serotonin synthesis--enhances the release of a transmitter (serotonin) that tends to diminish the animal's desire to consume carbohydrates.
Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain.
Fernstrom JD, Fernstrom MH.
Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. firstname.lastname@example.org
Aromatic amino acids in the brain function as precursors for the monoamine neurotransmitters serotonin (substrate tryptophan) and the catecholamines [dopamine, norepinephrine, epinephrine; substrate tyrosine (Tyr)]. Unlike almost all other neurotransmitter biosynthetic pathways, the rates of synthesis of serotonin and catecholamines in the brain are sensitive to local substrate concentrations, particularly in the ranges normally found in vivo. As a consequence, physiologic factors that influence brain pools of these amino acids, notably diet, influence their rates of conversion to neurotransmitter products, with functional consequences. This review focuses on Tyr and phenylalanine (Phe). Elevating brain Tyr concentrations stimulates catecholamine production, an effect exclusive to actively firing neurons. Increasing the amount of protein ingested, acutely (single meal) or chronically (intake over several days), raises brain Tyr concentrations and stimulates catecholamine synthesis. Phe, like Tyr, is a substrate for Tyr hydroxylase, the enzyme catalyzing the rate-limiting step in catecholamine synthesis. Tyr is the preferred substrate; consequently, unless Tyr concentrations are abnormally low, variations in Phe concentration do not affect catecholamine synthesis. Unlike Tyr, Phe does not demonstrate substrate inhibition. Hence, high concentrations of Phe do not inhibit catecholamine synthesis and probably are not responsible for the low production of catecholamines in subjects with phenylketonuria. Whereas neuronal catecholamine release varies directly with Tyr-induced changes in catecholamine synthesis, and brain functions linked pharmacologically to catecholamine neurons are predictably altered, the physiologic functions that utilize the link between Tyr supply and catecholamine synthesis/release are presently unknown. An attractive candidate is the passive monitoring of protein intake to influence protein-seeking behavior.
Food consumption, neurotransmitter synthesis, and human behaviour.
Fluctuations in the availability to the brain of tryptophan and tyrosine cause major changes in the rates at which neurons synthesize serotonin and the catecholamines respectively. Such changes occur when the pattern of neutral amino acids in the plasma is altered by what has been eaten, the plasma changes inducing parallel changes in the amounts of tryptophan or tyrosine that are transported from blood to brain. Diet-induced changes in plasma choline levels can produce similar changes in acetylcholine synthesis. The three nutrients, tryptophan, tyrosine and choline, when administered in the pure form or simply ingested in food, can thus act like drugs giving rise to important changes in the chemical composition of structures in the brain. The interactions that relate the amount of a nutrient administered or ingested to its level in the blood plasma, its level in the brain and its effect on nerve neurotransmission, are not simple. The conversion of tryptophan into serotonin is influenced by the proportion of carbohydrate in the diet; the synthesis of serotonin in turn affects the proportion of carbohydrate an individual subsequently chooses to eat. In the case of choline and tyrosine the effect on a neuron of an increased supply of the nutrient varies with the neuron's firing frequency and can lead to changes in that frequency. Choline and tyrosine can hence amplify neurotransmission selectively, increasing it at some synapses but not at others. Taken together, these findings illustrate a novel and hitherto unsuspected aspect of nutrition's effects on the brain and provide the basis for new modes of therapy for patients with some metabolic, neurologic or psychiatric brain diseases.