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Neurotransmitter Acetylcholine

11 Feb 2018

The neurotransmitter acetylcholine improves memory and concentration of attention.

Acetylcholine can be considered the most important neurotransmitter involved in the process of remembering information. This highly chemically active substance is an ester of choline and acetic acid. It contributes to the fact that information is quickly and unhindered transmitted from the senses to the main control center - the brain.

Unfortunately, with age, less acetylcholine is synthesized in the human brain. As a result of this, scientists believe, forgetfulness, problems with concentration of attention, difficulties in the selection of necessary words.

Meclofenoxate and choline serve as a basis for good brain activity. In order to improve memory in a short time and keep it clear for a long time, the famous researcher of brain activity, professor of the University of Hyssin, Wilfried Dimpfel, recommends that the concentration of the main neurotransmitter, acetylcholine, be purposefully stabilized. This can be achieved by taking choline preparations. Choline is a natural building block for the synthesis of acetylcholine molecules.

It is even better to build your own food in such a way as to ensure sufficient natural intake of choline in the body with natural food. A large amount of choline contains cabbage (especially cauliflower and broccoli), eggs, peanuts, fish, meat, hard cheese varieties, liver, milk and wheat sprouts. In addition to choline for the synthesis of acetylcholine, vitamins such as pantothenic acid (vitamin B3), folic acid, vitamins B12 and B1 are needed. Just in the elderly, as well as in people suffering from bowel disease, there is a shortage of B vitamins.

The scientists also place great hopes on deanol (meclofenoxate) - in a scientific environment known as dimethylaminoethanol (Dimethylaminoethanol) or abbreviated DMAE. With a lack of acetylcholine in the body, it can be re-synthesized in the required amount from deanol. Some medical research has proved the positive effect of this substance on brain function.

In one experiment, conducted over a period of 3 months, a group of people with memory problems and concentration of attention took medications containing deanol and choline. At the end of the experiment, problems with concentration disappeared in 84% of the subjects, memory improved in 75% of the participants in the experiment.

In addition, supplying your body with all the necessary substances for building neurotransmitter molecules by substances, do not forget that the synthesis of acetylcholine (and hence memory improvement) will occur only if the brain is actively involved, receiving sufficient information for thought and memorization. Do not be lazy to load your memory, giving it food for thought.

And one more aspect of the problem of memorization. For intensive activity, brain cells require continuous intake of energy and nutrients, which is ensured by the flow of blood. Poor blood supply leads to rapid fatigue, headache and drowsiness. So do not be lazy at least 30 minutes a day to devote to intense physical training. Only all three factors - proper nutrition, physical and intellectual loads, - in aggregate will help to significantly improve memory and keep it to a very old age.



10 Feb 2018

At once it is necessary to make a reservation that it is possible to put so a question when it comes to mental disorders and psychological problems in which psychotherapy is shown. With problems related to the competence of psychiatry (psychotic states, schizophrenia, manic-depressive psychosis, etc.), without taking psychotropic drugs, alas, usually can not do.

xanax phenazepam

Psychotherapy in general and psychoanalysis, in particular - drug-free types of treatment of mental disorders, but sometimes the use of light antidepressants and tranquilizers can be combined with psychotherapy.

If we talk about the medical treatment of mental disorders, it should be noted that the use of psychotropic drugs can only alleviate the current mental state, to improve the condition in the long run, drugs are not invented. Self-administration is not recommended, as much depends on the dosage and frequent side effects; also psychotropic drugs cause dependence quickly enough, to obtain an effect, more and more dosage is required, and if they fail, the mental state is aggravated.

In general, there are the following groups of the most commonly used psychotropic drugs:

- tranquilizers (soothing, with anxiety and insomnia) - glycine, phenazepam, tazepam, elenium (librium), relanium (seduxen), nosepam,

- Neuroleptics (for the relief of psychotic disorders, in small doses for neurotic) - sonapaks, etaperazine, chloroprotexen, aminazine, haloperidol, respolept (the last three are for psychotic disorders only),

- antidepressants (increasing mood) - with all neurotic depressions and anxiety - Prozac (fluoxetine, portal, profluzak), tsipramil; at dreary and asthenic depressions - pyrazidol, eglonil; with anxious depression - ludiomil, coaxil, zoloft,

- nootropics (to improve memory and attention) - nootropil, pyracetam, coguitum, centedrine,

- Atarapticks (anti-anxiety preparations of selective action (before flight, examination) - Xanax.

The most common side effects of psychotropic drugs - drowsiness, decreased potency and sexual desire, decreased appetite, nootropics stimulate anxiety. All psychotropic drugs are incompatible with alcohol.

The use of psychotropic drugs can be recognized as justified when, for example, it is a question of quickly arresting severe emotional experiences, depressive episodes (antidepressants of the last generation), restoring the sleep regimen (tranquilizers) - that is, to help a person return to a workable state. The course should not exceed one to two months. Thus, it is necessary to understand that antidepressants relieve the condition, and do not treat. Although the availability of drugs in the treatment scheme is sometimes justified. But it is one thing - to conduct a course of antidepressant medication, to start to function normally, to fix the improved condition and to search for the causes of the emergence of psychic problems with the help of psychotherapy, it's another thing to see an antidepressant as a panacea for mental problems and come into dependence on it.


Pyrithinol - Pyriditolum

06 Feb 2018

Pyrithinol (Pyriditolum)

Bis- (2-methyl-3-hydroxy-4-hydroxymethylpyridyl-5-methyl) -disulfide dihydrochloride.

Synonyms: Pyrithinol, Cerebol, Energol, Encephabol.

The structure of pyriditol differs from nootropic drugs GABAergicheskoy nature. It can be considered as a doubled pyridoxine molecule containing a disulfide "bridge" (pyridoxine polysulphide).


Pharmacologically, the drug is characterized by nootropic activity with a complex spectrum of psychotropic activity. It enhances the effects of phenamine, but also reduces spontaneous motor activity, prolongs the hypnotic effect of barbiturates, enhances the anticonvulsant effect of phenobarbital. The drug activates metabolic processes in the central nervous system, promotes the acceleration of the penetration of glucose through the blood-brain barrier, reduces the excessive formation of lactic acid, increases the resistance of brain tissue to hypoxia. There is evidence of a decrease in the content of GABA in the nervous tissue under the influence of pyriditol. B6-vitamin activity does not.

According to clinical effects, pyriditol is similar to antidepressants, which have sedative properties, but in the aggregate, its action is classified as nootropic drugs.

Piriditol is used for complex therapy in shallow depressions with retardation phenomena in asthenic conditions, adynamia, neurosis-like disorders, traumatic and vascular encephalopathy, residual phenomena after neuroinfections and cerebral circulatory disorders, cerebral atherosclerosis, migraine. Children are used to delay mental development, cerebrosthenic syndrome, oligophrenia, encephalopathy.

Contraindicated in severe psychomotor agitation, epilepsy, increased convulsive readiness.



01 Feb 2018

Continuing the topic of medicine, I want to say about Kogituma. Piracetam, encephabol, pantogam, ceraxon, glycine - give noticeable progress. But for many people it is Cogitum that becomes a real breakthrough.

Cogitum contains acetylamino-succinic acid, a biologically active substance, which:

  • stimulates the work of the central nervous system - all electrochemical processes in the brain are faster;
  • normalizes the processes of regulation - the tasks assigned to the brain are more clearly and harmoniously performed;
  • increases the plasticity of the nervous system - the child, like a sponge, absorbs the knowledge gained and easily applies them in practice;
  • Accelerates the child's mental and speech development;
  • has general toning properties, helps to cope more quickly with stress, increases stamina;
  • stimulates the production of interferon and antibodies, strengthens the immune system

Cogitumum to children is appointed at:

  • speech development delay
  • delay in psychomotor development
  • head injuries, including birth trauma
  • severe adaptation in school or kindergarten
  • asthenic syndrome, and also in the recovery period after a long protracted illness.

The drug does not interfere directly in the work of the brain, but only directs the development of the central nervous system in the right direction, helping the kid quickly catch up undeveloped skills and catch up with peers in development.




31 Jan 2018

The NMDA antagonist used in the treatment of Alzheimer's disease, but also undergoing clinical trials as a possible therapy for a number of other conditions, including ADHD, HIV-associated dementia, nystagmus, multiple sclerosis.


Memantine is on the list of vital and essential medicines.

Memantine is a selective blocker of N-methyl-D-aspartate (NMDA) - glutamate receptors. The mechanism of action is associated with the modulation of glutamatergic transmission, which mediates cortico-cortical and cortico-subcortical relationships in the brain. In a series of controlled studies, the ability of memantine to improve and stabilize cognitive functions, daily activity, and reduce behavioral disorders in patients with asthma (both at an early stage and especially at the stage of moderate and severe dementia) has been proven. The positive effect of memantine on cognitive functions was also noted in vascular dementia. In open studies, the effectiveness of memantine in mixed dementia, dementia with Levy bodies, alcoholic dementia and Korsakov's amnestic syndrome, frontotemporal dementia is shown. Memantine is the first choice drug for moderate and severe dementia, but it can also be used in the stage of mild dementia as a monotherapy or in combination with cholinesterase inhibitors. The long-term effectiveness of memantine has been studied to a lesser extent.

Memantine has good tolerability, however, dizziness or confusion may occur in the titration phase, which, as a rule, are transient. Less often there are drowsiness, falls, headache. In the experiment it was shown that memantine is able to protect cells from the toxic effect of excitatory amino acids and inhibit the formation of neurofibrillary glomeruli, affecting the metabolism of t-protein, which is one of the key links in the pathogenesis of asthma.


Dopamine Receptors

30 Jan 2018

The class of transmembrane metabolotrophic G-protein-linked cellular receptors, which play an important role in the functioning of the central nervous system of vertebrates. The main endogenous ligand agonist of these receptors is dopamine. Dopamine receptors are involved in the processes of motivation, training, fine motor coordination, modulation of neuroendocrine signals. This class includes five types of receptors: D1, D2, D3, D4 and D5.

The change in dopaminergic function is noted in a number of neurological and psychiatric disorders, and the receptors themselves are targets for a variety of medications. The vast majority of antipsychotics are dopamine receptor antagonists, and psychostimulants often indirectly activate them.

Five human genes encoding dopamine receptors are known. According to the structural, biochemical and pharmacological characteristics, the corresponding receptors are subdivided into D1-like (D1, D5) and D2-like (D2, D3, D4). For the first time, these two classes of receptors were isolated in 1979 on the basis that only D1-like receptors activate adenylate cyclase. Receptors of group D2, on the contrary, inhibit it. It is assumed that there are D6 and D7 receptors, but their existence has not yet been proven.

The alternative classification proposed in 1983 divides the receptors according to their effects: activation of DA1 receptors causes muscle relaxation and vasodilation; for these receptors (R) -sulfyride is a strong antagonist, apomorphine is a weak agonist, and domperidone does not act on them. Activation of DA2 receptors inhibits the action of noradrenaline, apomorphine is their strong agonist, and the strong antagonists are (S) -sulpiride and domperidone. Dopamine receptors of the central nervous system seem to belong to this class.

D1-like receptors

As mentioned above, D1-like receptors include the D1 and D5 receptors. A characteristic feature of the receptors of this class is that they activate G-proteins of the Gαs / olf family, which in turn activate the adenylate cyclase. D1-like receptors are found only on postsynaptic membranes of dopamine sensitive cells. The receptor genes of this class do not contain introns, so D1 and D5 receptors exist in a single splice variant.

D2-like receptors

D2-like receptors include the D2, D3, and D4 receptors. These receptors bind to G-proteins of the Gαi / o family and therefore inhibit adenylate cyclase. Unlike D1-like, D2 and D3 receptors are present not only on postsynaptic membranes of dopamine sensitive cells, but also on presynaptic membranes of dopaminergic neurons. The genes of D2-like receptors contain introns: 7 introns in the D2 receptor gene, D3 - 5 in the gene, and 3 (human genes) in the D4 gene. It is known that the D2 and D3 receptors exist in several forms, which is the result of an alternative splicing of their pre-mRNA. Structurally, D2-like receptors differ in that their C-terminal domains are 7 times shorter than in D1-like receptors.

Dopamine receptors are present in both the central nervous system and in peripheral organs. The relative proportion of dopaminergic neurons in the brain is low (less than 1 / 100,000 of all neurons). These neurons form several basic dopaminergic pathways: nigrostrioral, mesolimbic, mesocortical and tuberin-fibundibular.

The dopamine receptor D1 is the most widely distributed dopamine receptor in the brain, it is synthesized in greater numbers than other receptors. It is found in a high concentration in the nigrostriral, mesolimbic and mesocortical ways, namely in the frontal lobes, striatum, black substance, contiguous nucleus, olfactory tubercle and amygdala. Also in a lesser concentration, it is present in the hippocampus, cerebellum, thalamic and hypothalamic regions.

The high-concentration D2 receptor is present in the striatum, the olfactory tubercle, the contiguous nucleus, the black substance, the hypothalamus, the ventral region of the tire and the amygdala, that is, approximately in the same regions of the brain where the D1 receptor is also found. However, additional studies have helped to establish that only 5-15% of the projection neurons of the dorsal part of the striatum express both receptors simultaneously. The remaining neurons can be divided into two groups, depending on which of the receptors they contain.

The D3 receptor has a narrower distribution profile than the receptors described above. In the highest concentration, it is present in the nucleus accumbens, the olfactory tubercle and the islets of Kaleha. At substantially lower concentrations, the D3 receptor is found in a compact portion of the black substance, the ventral region of the tire, and the cerebellum.

The expression level of the D4 receptor in the brain is significantly lower than that of the D2 receptor. It is proved that the D4 receptor is present in the cortex of the large hemispheres, the hippocampus, the striped and amygdala-shaped bodies.

The D5 receptor is synthesized in small numbers in different parts of the brain: in pyramidal neurons of the prefrontal cortex, cingulate cortex, entorhinal cortex, black substance, dentate gyrus, hippocampus and hypothalamus.

All five types of dopamine receptors are found outside the brain. So the receptors D1, D2 and D4 were found in the retina, and the receptor D2 - in the pituitary. Dopamine receptors are synthesized in different proportions in the cells of the kidneys, adrenal glands, sympathetic ganglia, blood vessels, heart and digestive tract.



29 Jan 2018

We had 2 packages of caffeine, 75 tablets of modafinil, 5 packages of prairiatsetam, half an amputation of agmatin and a whole host of stimulants of all sorts and colors, as well as theanine, idebenon, a box of Vitamins, a pint of pure Semax and DMAA. Not that it was a necessary supply, but if it began collecting nootropics, it becomes difficult to stop. The only thing that aroused my fear was Memantine. Nothing in the world is more helpless, irresponsible and vicious than dissociative zombies. I knew that sooner or later we will move on to this rubbish.



GABA - Gamma-aminobutyric acid

25 Jan 2018

GABA - an organic compound, a non-proteinogenic amino acid, the most important inhibitory neurotransmitter of the central nervous system (CNS) of humans and other mammals. Aminobutyric acid is a biogenic substance. Contained in the central nervous system and takes part in the neurotransmitter and metabolic processes in the brain.

Gamma-aminobutyric acid in the body is formed from another amino acid - glutamine with the enzyme glutamate decarboxylase.

γ-Aminobutyric acid performs in the body the function of an inhibitory mediator of the central nervous system. When GABA is released into the synaptic cleft, the activation of the ion channels of GABAA and GABAA receptors results in inhibition of the nerve impulse. GABA receptor ligands are considered as potential agents for the treatment of various disorders of the psyche and central nervous system, which include Parkinson's and Alzheimer's diseases, sleep disorders (insomnia, narcolepsy), epilepsy.

It is established that GABA is the main neurotransmitter involved in the processes of central inhibition.

Under the influence of GABA, the energy processes of the brain are activated, the respiratory activity of the tissues increases, the utilization of glucose by the brain improves, the blood supply improves.

The effect of GABA in the central nervous system is realized through its interaction with specific GABAergic receptors, which are recently divided into GABA- and GABAB receptors, etc. In the mechanism of action of a number of central neurotropic substances (hypnotics, anticonvulsants, convulsants, etc.), their agonistic or antagonistic interaction with GABA receptors. Benzodiazepines potentiate the action of GABA.

The presence of GABA in the central nervous system was discovered in the mid-1950s, and in 1963 it was synthesized. In the late 1960s, under the name "Gamalon", GABA was proposed for use as a medicinal product abroad, then - under the name "Aminalon" - in Russia.

According to experimental data, GABA penetrates badly through the blood-brain barrier when introduced into the body, but there is evidence that GABA is transported to the brain with the help of specific membrane transports GAT2 and BGT-1.

In 2007, the GABAergic system was first described in the epithelium of the respiratory tract. The system is activated under the influence of allergens and can play a role in the mechanisms of asthma.

Another GABAergic system is described in testicles, it can affect the work of Leydig cells.

Researchers at the St. Michael, Toronto, Canada, established in July 2011 that GABA plays a role in preventing and possibly reversing the development of diabetes in mice.

In pharmacology:

Gamma-aminobutyric acid removes excitement and has a calming effect, it can also be taken as a tranquilizer, but without the risk of addiction. This amino acid is used in the complex treatment of epilepsy and hypertension. Since it has a relaxing effect, it is used in the treatment of sexual dysfunction. Excess gamma-aminobutyric acid, however, can increase anxiety, dyspnea, trembling of the limbs.


Cholinergic receptors - acetylcholine receptors

24 Jan 2018

Transmembrane receptors, the endogenous ligand-agonist of which is acetylcholine.

Acetylcholine serves as a neurotransmitter both in pre- and postganglionic synapses of the parasympathetic system and in preganglionic sympathetic synapses, in a number of postganglionic sympathetic synapses, neuromuscular synapses (somatic nervous system), and in some parts of the central nervous system. Nerve fibers that release acetylcholine from their endings are called cholinergic.

Synthesis of acetylcholine occurs in the cytoplasm of nerve endings; its reserves are stored as bubbles in presynaptic terminals. The onset of the presynaptic action potential leads to the release of the contents of several hundred vesicles into the synaptic cleft. Acetylcholine, released from these vesicles, binds to specific receptors on the postsynaptic membrane, which increases its permeability for sodium, potassium and calcium ions and leads to the appearance of an exciting postsynaptic potential. The action of acetylcholine is limited by its hydrolysis with the enzyme acetylcholinesterase.

Specific cholinergic receptors from the pharmacological point of view are divided into nicotinic (H-receptors) and muscarinic (M-receptors).

Nicotinic cholinergic receptors

The effects of acetylcholine in the region of preganglionic synapses of the parasympathetic and sympathetic systems can be replicated with the introduction of a nicotine alkaloid, so all autonomous ganglia are called nicotine. Nicotine-like transmission of nerve impulses is also carried out in the neuromuscular synapse, CNS, adrenal medulla and in some sympathetic postganglionic regions.

Nicotinic cholinergic receptors are ionotropic and are sodium channels. They consist of five protein subunits, usually two of them have binding sites for acetylcholine.

17 types of subunits of nicotinic receptors (α1-10, β1-4, γ, δ, ε) were revealed. Apparently, they can form a variety of different combinations, but some of them are most often encountered and are most important: (α1) 2β1δε (muscular type), (α3) 2 (β4) 3 (ganglionic type), (α4) 2 (β2) 3 (CNS-type) and (α7) 5 (another CNS-type).

Muscarinic cholinergic receptors

The action of acetylcholine in the region of postganglionic nerve endings is reproduced with the help of another alkaloid, muscarin. In addition to postganglionic synapses, muscarin-like transmission of nerve impulses is carried out in some parts of the central nervous system.

Muscarinic receptors are metabotropic and refer to receptors that are conjugated to G-proteins.

The effects of poisons and medications

Nicotinic receptors are blocked by such poisons as curare and α-bungarotoxin, and muscarinic receptors are blocked by atropine and scopolamine, which determines the symptoms of poisoning with appropriate poisons. Blockade of nicotinic receptors with the help of curare or curare-like drugs is used to immobilize patients during surgical operations.

Myasthenia gravis (Myasthenia gravis)

In this disease against the nicotinic cholinoreceptors of the muscle type, autoantibodies are produced, which leads to progressive muscle weakness.



23 Jan 2018

Olanzapine- antipsychotic drug (atypical antipsychotic), structurally and similarly to clozapine. It is used to treat schizophrenia and bipolar affective disorder. Has a wide range of psychopharmacological effects and has antidepressant effect.


Trade names: Olanzapine, Normiton, Olanex, Parnasan, Zalasta, Ziprexa, Egolansa

It is also produced in combination with fluoxetine called Symbiax for the treatment of bipolar depressive episodes and resistant depression.

In preclinical studies, the affinity of olanzapine for serotonin 5-HT2A, 5-HT2C, 5-HT3, 5-HT6, dopamine D1, D2, D3, D4 and D5, muscarinic (1..5), adrenergic α1 and histamine H1 receptors has been established. In experimental studies, the presence of antagonism of olanzapine with respect to serotonin receptors, dopamine and cholinergic receptors has been revealed. In vivo and in vitro, olanzapine has more pronounced affinity and activity with respect to 5-HT2 compared to D2 receptors.

According to electrophysiological studies, olanzapine selectively decreases the excitability of mesolimbic dopaminergic neurons, and at the same time has a negligible effect on the striatal neural pathways involved in the regulation of motor functions. Olanzapine reduces the conditioned protective reflex (a test characterizing antipsychotic activity) at doses lower than the doses causing catalepsy (a disorder reflecting a side effect on the motor function). In contrast to the "typical" antipsychotics, olanzapine enhances the anti-anxiety effect during the anxiolytic test.

Two placebo-controlled and two out of three comparative controlled trials involving 2,900 schizophrenic patients showed that olanzapine provides statistically significant reduction in the short term as productive (including delusions, hallucinations) and negative disorders. Data on the effect of different doses of olanzapine on negative symptoms are not completely consistent; perhaps the reduction in severity of negative disorders is explained by the action of olanzapine on secondary negative symptoms (eg, caused by drug parkinsonism or psychosis), rather than by direct action on primary negative symptoms.

According to the meta-analysis, olanzapine is superior to haloperidol in the likelihood of success of therapy, improvement in the severity of mental disorders, and a decrease in the severity of productive and negative disorders. According to some studies, olanzapine is superior to haloperidol in its effect on cognitive function, in other studies no difference was found. Studies show that relapses with olanzapine are significantly less frequent than when taking haloperidol.


~ treatment of exacerbations; supportive and long-term anti-relapse therapy for schizophrenia and other psychotic disorders with marked productive (including delirium, hallucinations, automatism) and / or negative symptoms (including emotional flattening, decreased social activity, impoverishment of speech) and symptomatic accompanying affective disorders;

~ Treatment of acute manic or mixed seizures in bipolar affective disorder. can be used to treat stimulant psychoses.

At the beginning of treatment, especially when choosing a dosage, it is necessary to observe: extrapyramidal side effects, orthostatic hypotension and reflex tachycardia, drowsiness, weight gain, hyperglycemia and hyperlipoproteinemia are possible. The risk of orthostatic hypotension increases with combined use of olanzapine with benzodiazepines. Drowsiness at the beginning of treatment develops often, so it is better to take the drug at night.

Caution should be given to patients with a reduced number of leukocytes and / or neutrophils, due to various causes; with signs of oppression / toxic damage to bone marrow function under the influence of drugs in the anamnesis; with oppression of bone marrow function due to concomitant disease, radiotherapy or chemotherapy in history; with hypereosinophilia or myeloproliferative disease. In clinical studies, the use of olanzapine in patients with clozapine-dependent neutropenia or agranulocytosis in a history was not accompanied by relapses of these disorders.

When olanzapine is prescribed for the first time, it is necessary to evaluate the probability of weight gain by the patient, taking into account his body mass index, anamnesis, the general clinical feeling of propensity to fullness - pastness, friability. Observing the patient taking olanzapine, it is important to consider the main principle of weight gain control: seven percent of the initial increase in body weight is an absolute contraindication to the further use of the drug.

For the prevention of obesity and its complications (in particular, diabetes mellitus) it is necessary:

~ Monitor before taking antipsychotics and during their intake of body weight and body mass index, fasting glucose (or hemoglobin A1c) and lipid levels in the blood plasma. The fasting glucose level should not exceed 126 mg / dl, hemoglobin A1c - not exceed 6.1%. To detect hyperglycemia, it is also desirable to measure not only the fasting glucose level, but also the level 2 hours after taking glucose. In patients with risk factors (family history, overweight), monitoring of glucose levels should be carried out every 2-4 months. All patients are also advised to measure blood pressure before starting therapy and during therapy.

~ Dose of antipsychotic to build up slowly, which allows you to partially prevent weight gain. In this case, the first weeks of neuroleptic therapy are especially important, since it is much easier to prevent weight gain than to decrease it in the future.

~ Treat attentively to the lifestyle and diet of the patient. It is necessary that food is as low as possible in terms of calories, and the way of life is much more active. In this diet and exercise require careful dosing. ~ It is recommended to reduce intake of saturated fats and cholesterol, increased consumption of fibrous food. Smoking is also recommended.

~ If significant weight gain is seen, refer the patient to a dietician and a physiotherapist.

~ When taking high doses of neuroleptic - a cautious approach to its combination with other diabetogenic drugs (beta-adrenoblockers, glucocorticoids, protease inhibitors, thiazide diuretics).

To prevent the development of life-threatening conditions associated with diabetes (acidosis and coma), it is necessary to recognize early and begin treatment of developing diabetes. Psychiatrists with olanzapine therapy should be wary of such symptoms of diabetes as weight loss, drowsiness, thirst, polyuria, if necessary, provide the patient with an endocrinologist's advice.

With the use of olanzapine, malignant neuroleptic syndrome, a potentially lethal symptom complex, whose clinical manifestations include a significant increase in body temperature, rigidity of the musculature, changes in mental status, and autonomic disorders (unstable pulse or arterial pressure, tachycardia, cardiac arrhythmia, increased sweating) may develop.

In comparative studies lasting more than 6 weeks, treatment with olanzapine was significantly less likely to be accompanied by the development of tardive dyskinesia (an irreversible neurological side effect) than the use of haloperidol. However, it is still necessary to consider the risk of this side effect with prolonged therapy with neuroleptics. When developing signs of tardive dyskinesia, it is recommended to reduce the dose or to cancel olanzapine. Symptoms of tardive dyskinesia may increase or manifest

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