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Anorexia Nervosa Versus Hyperinsulinism: The Two Opposite Faces of the Coin——Therapeutic Effects of Neuropharmacological Manipulations

Author(s): Fuad Lechin | Bertha van der Dijs | Betty Pardey-Maldonado | Scarlet Baez | Marcel E. Lechin

Journal: Neuroscience & Medicine
ISSN 2158-2912

Volume: 03;
Issue: 01;
Start page: 1;
Date: 2012;
Original page

Keywords: Amantadine | Anorexia Nervosa | Adrenal Sympathetic Activity | Hyperglycemia | Hyperinsulinism | Neural Sympathetic Activity

We demonstrated that anorexia nervosa (AN) was underlain by overwhelming adrenal sympathetic activity which annuls neural sympathetic branch of the peripheral autonomic system (ANS). This physiological disorder is responsible for the gastrointestinal hypomotility + hyperglycemia + raised systolic blood pressure + raised heart rate and other neuroendocrine disorders. Thus we prescribed neuropharmaclogical therapy addressed to revert central nervous system + ANS disorder, in order to normalize both clinical + neuroendocrine profiles. We measured blood pressure, heart rate, circulating neurotransmitters, (noradrenaline, adrenaline, dopamine, platelet serotonin, plasma serotonin during supine resting + one-minute orthostasis + five min exercise test before and after 1, 2 and 3 months of treatment with amantadine, a drug which abrogate adrenal sympathetic activity by acting at the C1(Ad) medullary nuclei, responsible for this peripheral sympathetic activity. We found that the drug eliminated AN symptoms since the first oral dose. Normalization of ANS plus cardiovascular parameters was registered within the first days of therapy. Abrupt and sustained increases of the noradrenaline/adrenaline plasma ratio + disappearance of abnormal plasma glucose rises were registered throughout the 3 months lasted the trial. Significant and sustained body weight increases were registered in all the cases. No relapses were observed in any case. We ratified our previous findings showing that the anorexia syndrome depends on hypomotility of the gastrointestinal tract plus de hyperglycemia associated with the hyperactivity of the adrenal sympathetic activity. In addition, we afford exhaustive evidence showing that the hyperglycemia + adrenal sympathetic overactivity syndrome and the hypoglycemia + the neural sympathetic overactivity disorder depend on the predominance of the C1(Ad) medullary + adrenal glands axis and the A5(NA) + neural sympathetic axis, respectively. Both syndromes are successfully treated with neuropharmacological manipulations.
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