A specific sympathetic nerve channel between the vegetative centers and the adrenals directly stimulates the release of noradrenaline and adrenaline from cells of the adrenal marrow into the blood stream when under stress. This vital cell system, influenced by amphetamines and under stress from the hormones adrenaline and noradrenaline, together with the whole metabolism and hormone and immune systems, are compromised. The adrenergic cells of the adrenal marrow are stimulated simultaneously by cortisol that formed in the adrenal cortex. Cortisol is the final hormone from the stress cycle of the hypothalamus-pituitary-adrenal axis. This axis is also influenced by the amphetamine over activation, via the noradrenagic, dopamine and serotonin agitation of the limbic system. In this scenario the frontal pituitary excretes cortisol stimulating ACTH hormone into the blood stream, which stimulates cortisol synthesis in the adrenals. The elevated cortisol table has a stress reducing effect on the hypothalamus which acts like a control valve to prevent backflow (graphic 10). This negative backward coupling can be disturbed by permanent stress. It is the opinion of today's psychiatrists that nearly all depressive episodes are caused by stress, which blocks the cortisol. Since most of the anti -depression drugs, like amphetamine, elevate noradrenaline and serotonin in the brain synapses, the hyper kinetic syndrome and the attention deficit can be seen as stressors and the positive amphetamine effect in the beginning can be seen as a stress reducing factor. The relationship between the cortisol hormone and the adrenal receptors in the brain or between the inner organs in the periphery of the brain is, in any case, much more complicated. Since there are different adrenal receptors (alpha and beta receptors) and a constantly elevated cortisol level mainly sensitizes the beta receptors and increases their numbers, the signaling path of the beta receptors is more strongly activated within the cell.
As with all amphetamines, there is a reduction in effectiveness over time, because the effective dosage has to overcome the threshold value for the activation of the adrenal alpha-receptors. The permanent stimulation of these receptors, caused by Ritalin, also activates a desensitizing effect, as a counter regulation of the receptors. The therapeutic dose has to be increased and the dependency potential develops which involves the noradrenaline, dopamine, and serotonin receptors as well as their coupled intracellular signal pathways and the synthesis of the cell energy. Besides that, the danger exists with higher Ritalin doses that the neurotransmitter reservoirs don't replenish fast enough because Ritalin forces a sudden drainage. The result can be unexpected psycho-social and organic slips .
Ritalin is a Doping Medication Not a Healing Medication.
Inevitably the question arises whether the cause of ADD is indeed a deficit of the noradrenalin or due to the different sensitivities of the noradrenergic sub-receptors when under normal noradrenalin release. The fact is that when an increase of noradrenalin, induced by Ritalin, takes place, enough noradrenalin is at hand and the noradrenalin receptors are quickly and lastingly agitated; this underlines the fact that with hyperactive children, the alpha receptors, under stress with normal noradrenalin output, are not sufficiently stimulated and the dopamine psycho-motor synapses are not sufficiently counter stimulated. The central stimulation of the noradrenergic alpha receptors seem to be, at first glance, the means for stimulating the wakefulness and attention controlling brain area during therapeutic practice. Long tern Ritalin therapy proves to interfere enormously with personality development and physical maturity during childhood and teen years, with highly risky long-term consequences.
From the experience with simple tyrosine stimulation instead of long-term Ritalin stimulation, the alternative therapy principle for children and teens with ADD and ADHD can be derived from an orthomolecular therapy principle. In clinical studies, tyrosine applications have shown to produce stress-reducing effects.
Tyrosine is also the starter molecule for the synthesis of the thyroid hormone (thyromine). Under stress conditions the free thyronine (T3), in relationship to the inactive reverse thyronine (rT3), respectively to the thyronine which is tied to a protein, is decreased. The T3 content is nonetheless essential for the synthesis of the universal energy carrying molecule adensintriphosphate (ATP) within the breathing cells of the mitochondria. The adrenergic stimulated neurons the ATP requirement is increased, since the ionic in and out flow, plus the secondary signal pathways, are energy dependent.
T3-thyronine deficiency can also produce psycho-motor unrest and lack of concentration.