Metabolic therapy with amino acids

 

The patients often ask: What is the metabolic therapy, how do drugs work, what is the peculiarity of this treatment?. This section attempts to answer the questions posed. Unfortunately, it is very difficult to present the subject in popular language due to the danger of oversimplifying the essence of the matter.

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The "Primavera Medica" Scientific Medical Center has been operating since 1993. At the beginning of our activity, we started from the fact that nerve cells can be restored. In the early 90's this was revolutionary. 

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In the following years, the efforts of scientists from different countries have convincingly shown that neurogenesis (the formation of nerve cells) continues after birth and gradually slows down, possibly also in old age. 

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Obviously, any problem during pregnancy (maternal diseases, fetal placental insufficiency, viral lesions), which leads to hypoxia and, as a consequence, to a free radical process, disrupts the formation of a particular structure of the fetal brain, which means pluripotent cells migrate in this period to this area from periventricular and subventricular zones, and do not differentiate into neuronal or glial elements, but on the contrary die by apoptosis or aponecrosis as a result of the "fire" of free radicals. As a result, after birth, for example, underdevelopment of the cerebral cortex, corpus callosum or cerebellar structures is revealed. 

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Therefore, in the brain of a child with these types of problems there is a lack of brain tissue, which is often combined with the expansion of the ventricular system. It is clear that an insufficient number of neuronal and glial cells cannot provide the normal function of this structure and, of course, they work in a more than intensive way, that is to say they are constantly in a situation of stress. As a result, in this area of Reduction – Oxidation the homeostasis is altered. Figuratively speaking, a "free radical fire" is burning in the context of an excess of excitatory dicarboxylic neurotransmitters and a lack of inhibitors. And the stem cells that migrate from the herment area are doomed to death. 

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The existing world medical science identifies the following nosological forms that arise from perinatal pathology: cerebral palsy of one form or another (spastic, hyperkinetic, atonic-static), oligophrenia, autism. It should be noted that, in the literature available to us, we did not find a clear molecular, biochemical, or neurophysiological explanation for these conditions. There are only general references to the violation of the formation of the pyramidal tract in spastic conditions, suffering from subcortical structures in hyperkinetic form, ... On the other hand, many clinicians know that some antiepileptic drugs reduce the degree of pyramidal spasticity, and a decrease in epileptic equivalents may be observed in the treatment of hyperkinesis. 

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It should be emphasized that we should not treat spasticity and the atonic-ataxic form of cerebral palsy in different ways. The same applies to the treatment of delayed psycho-verbal development of both hereditary and non-hereditary nature. So how should brain damage be treated?   

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In our work, we start from the following premises: 

 

1) Establish a poly-antioxidant therapy as a basic condition. Using several groups of drugs of appropriate action, which affect:   

  

a) superoxide dismutase with its histidine component, as well as copper and zinc - containing an active center, in combination with catalase 

 

b) an increase in the store of glutathione, a tripeptide considered the most powerful antioxidant intracellular substance, and its main component the “thiol”  

 

c) increases of the reserve of carnosine in the brain, one single dipeptide due especially to its damping properties 

 

d) free radical chain breakage during lipid peroxidation of cell membranes due to the use of aliphatic compounds with high carbon content and a large number of double bonds. 

 

2) Restore the energy function of cells. Among the drugs used we find "Dehol" which includes oxalate and citrate, the key substrates that determine the speed of the tricarboxylic acid cycle. It should be noted that normalization of Reduction-Oxidation homeostasis stops output of reducing equivalents of mitochondria into the cytoplasm, which ensures a repair transport system mitochondrial electron conjugation with oxidative phosphorylation. 

 

3) Elimination of the neuronal cells stress, blocking the transmission of NMDA and non-NMDA. This makes it possible to transfer the excessively stressed functioning of neurons to a smoother mode. For this, we use "Glucaprim-MG" and "Cerebron" - drugs containing aspartate or glycine associated with Mg ++, which allows non-competitive inhibition of the corresponding cellular receptors. With a deficit or more pronounced damage in neuronal tissue, accompanied by epileptic manifestations, an AMPA receptor blocker is also used due to competitive inhibition: "Cerebron-R".    

 

4) It is impossible to achieve a greater harmonization of the work of the neuronal and glial components of the brain under conditions of cellular deficit of overloaded functioning without the use of agents that enhance GABA and glycinergic inhibition. For this, we use drugs that increase the pool of amino acids: GLYCINE, GABA, TAURINE. It is known that the oral intake of TAURINE or GABA does not lead to the desired results; since for example the TAURINA not cross the blood brain barrier. Therefore, it is necessary to use precursor substrates that are metabolized into the necessary ligands. These medications include Aminovil-P, Aldarin, Glucaprim-P. It should be noted that some drugs, due to their composition, can serve a dual purpose. These drugs include "Aldarin " and "Aminovil-P" (antioxidant action and inhibitory neurotransmitter).  

 

5) Also worth remembering interneurons and interneurons GABA-ergic (acting as the mechanism of action of the Renshaw cell type). So, we can deduce that if inadequate therapeutic measures are applied, they can cause unilateral enhancement of the inhibitory effect or an emphasis on reducing the transmission of excitatory glutamate (this leads to a decrease in the inhibitory effect of interneurons). Furthermore, this situation can cause an undesirable effect of inhibition of the inhibition and, as a result, disinhibition of neurophysiological processes. Apparently, the correct tactic (but not the only one) is the pharmacological increase in inhibitory innervation (with the help of a group of drugs) and, in this context, an increase in excitatory neurotransmission (also with the help of a group of medicines).     

 

6) Influence the neurotransmission of acetylcholine, by use of "Iminogel" "Iminol" and "Aminostimunol". In addition, “Iminogel" and “Iminol" weakens the action of acetylcholine, and "Aminostimunol" improves it. Thus, inhibition of acetylcholine neurotransmission is used for dystonia in young children, for hyperkinesia, to remove the pyramidal spasticity and for pain syndrome in Osteocondrosis. On the opposite, "Aminostimunol" enhances the action of acetylcholine, which is used successfully to improve memory and other intellectual functions.  

 

7) The combined use of the drugs "Vitorat" and "Aminopurinol" can reduce the degradation of hypoxanthine and at the same time increase the synthesis of purines and thus affect the purinergic transmission. This leads to the following physiological effects: sedative, anticonvulsant and hypotensive. 

  

8) For the regulation of neuronal processes, it is not enough to influence only the inhibitory and excitatory mechanisms. Other players also exert a powerful effect on this system, the so-called modulators, a great team that includes dopamine, serotonin, monoamines, substance P, etc. (Of course, these regulators, in addition to being modulators, have an independent meaning). 

  

9) Development of cognitive functions and improvement of learning capacity. The mechanism of action is a significant enhancement of NMDA-ergic transmission in combination with the ability to influence LTP (Long-Term Potentiation) or LTD (Long-Term Depression) processes. With drugs such as "Vitamikst-P", "Neoprim-P", "Glucaprim-P") which should be used when a certain result has been obtained in the previous stage of metabolic therapy.  

  

10) In its comprehensive approach to the problem, metabolic therapy also takes into account the possibility of influencing neuro-immunological mechanisms. Immunity disorders can result from an imbalance in the state of various neurotransmitter systems. The suppression of the functions of immune protection may occur with suppression of dopamine neurotransmission, acetylcholine and GABA-ergic and an increased activity of serotonergic transmission in certain brain structures that are part of the neuro immune regulatory apparatus. Therefore, the neurochemical correction of the nervous regulatory mechanisms leads to increased immunity. 

  

It should be noted that activation of NMDA neurotransmission (if this fails) determines not only the level of the cerebral cortex, but also other important brain structures, as for example the hypothalamicpituitary region. And through the normalization of the work of the hypothalamic-pituitary gland (which is the main regulator of the body's endocrine system), the function of the endocrine glands is normalized.   

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Therefore, children with cerebral palsy or ZPRD are usually small and thin. In such cases, the metabolic therapy provides not only the elimination of neurologic, intellectual, and immune deficiencies, but also accelerate physical development and growth.   

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We assume that the same regulation mechanism of hypothalamic-pituitary insufficiency by metabolic therapy may be successful in a completely different field of medicine, gynecology, in the treatment of infertility. 

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Therefore, the general strategy of therapy boils down to providing the conditions for full-blown neurogenesis with replenishment of the brain tissue deficit. Long-term experience shows that in the event of severe brain damage, the child's metabolic support is necessary for 2.5 to 4 years. In less difficult situations, we have satisfactory results in 2-5 months. It should be noted that the first clear signs of the effectiveness of therapy are determined in just 2-3 days from the start of treatment.    

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Another important observation: Even with very good clinical results, treatment can never be considered complete. The nervous system continues to form and develop, and at the same time critical periods arise due to recurring colds, stressful situations and, finally, puberty. This means that a compensated but initially damaged nervous system will periodically need metabolic support. We should emphasize particularly that the treatment should begin as soon as possible, preferably in the first days after birth, especially premature babies. In such cases, the plastic brain child and high intensity of neurogenesis are most grateful for metabolic assistance, and recovery is much faster.