The Matrix Method with Tetractys Model

Dr Mirjana Zivanov, Dr Stojan Primovic, Dr Andreas Kelemen discuss The Matrix Method with Tetractys Model.

Dr Mirjana Zivanov, Dr Stojan Primovic, Dr Andreas Kelemen

Classical case taking and case analysis are irreplaceable tools of every homeopath, but there are some critical points in this process that could be improved. We have focused on the following three in the creation of the Matrix method:

  • In the process of case taking one of the key difficulties is to get a complete and accurate picture of the patient’s mental, emotional and physical state. Because a patient forgets or avoids providing information that may prove to be crucial for the entire process, a homeopath needs to find a way to get past all of these conscious and unconscious barriers. Therefore it may take a long time for the patient to open up. The patient may sometimes get tired of waiting and move on.
  • In the process of case analysis a number of symptoms are chosen by a homeopath as most significant and key to the case. This step depends very much on skill, experience and talent that is not equal in all homeopaths, meaning that we may expect that many mistakes are made at this point, in everyday homeopathic practice.
  • In a case a homeopath gets, or more precisely chooses, there are a number of symptoms and themes, and she needs to associate all of them with a single homeopathic remedy – Simillimum. Since there are a great number of homeopathic remedies, finding the right remedy for a chosen set of symptoms may be quite challenging, especially because both of the previously defined critical points of case taking and case analysis may influence the choice of symptoms. There are many similarities and differences of homeopathic remedies that we may find described in great detail in a repertory. There is still a question of a point, a missing link, between a symptom and a remedy, a small number of general categories, defined by many symptoms and shared by many remedies. Also, by defining the relations between these general categories we would get an insight into the relations of symptoms and remedies.

Much of homeopathic education is focused on preparing a homeopath to recognize the key symptoms and themes in a case-taking, but we shouldn’t forget there is another person there as well – the patient, with truthful unconscious information usually hidden under the mask, sometimes quite deeply. The issues, contents of unconscious, most important for the person, are associated with intense, highly charged, emotions and behaviors. Some psychological techniques may be of great help in unlocking the contents of the patients unconscious, so we were looking for a fast and accurate technique that could provide the most intense emotions and sensations of a patient, and simple enough to be used by a homeopath with no psychological training. We have found that the best suited technique for this purpose, to our knowledge, is the Deep PEAT technique by Z. Mihalovic – Slavinski. This technique may be included in a group of psychological techniques known as Meridian therapies, because the subject taps certain points on his/her face, body or fingers that are placed along meridians (path through which the life-energy known as “qi” flows in traditional Chinese medicine), hence the name. There has been an almost three decades long discussion in psychology on the effectiveness of meridian therapies, but even the results of their most vocal critics have found that these techniques are effective only not because of use of the meridians.

Meridian therapies are based on the idea of using tapping or pressing on a sequence of acupuncture points, located on main meridians, during the psychological treatment, basically using distraction and desensitization paired with exposure[1] – a well established psychological treatment technique[2],[3]. While it was shown that “tapping (or pressing) of meridians” was not a critical mechanism, the tapping and pressing of any points, as instructed by the therapist, has shown significant reductions in fear for all 3 groups that used tapping variations[4] but not for the control group[5]. It is important to point out that two of these three groups were also control groups regarding the use of points on meridians[6]. The other key element of this treatment technique is exposure, and since it is often difficult to achieve in clinical settings[7], the imaginary exposure is commonly used. Since these findings didn’t show these techniques to be ineffective, just that there is no connection to meridians, we’ve had pursued this path.

The Deep PEAT technique, is a process that usually lasts up to half an hour and gets us the deepest pair of opposites of a person, called the Primes, and a line of content that leads to it. Originally in the technique, the prime goal was to get and integrate this deepest pair of opposites – the Primes, while the other contents are a byproduct. But for a homeopath trying to find the patient’s Simillimum, the chain of these other contents are usually just as important, and often even more so. These contents highlight the most important issues in the case-taking, and often open up a number of issues that didn’t even come up in the case taking. This gives a much more complete picture necessary for finding the Simillimum. So, while in the Deep PEAT process the aim is to get to the Primes as fast as possible, in as few steps as possible, for a homeopath using this technique the aim is to get as much content as possible.

The First Step

The first step of the Matrix method is doing the Deep PEAT process, after the classical homeopathic case-taking, but aiming to get as much content as possible before getting to the Primes, because these are the emotions, sensations and behaviors with highest emotional charge – the key symptoms and themes we need for repertorisation. This may reduce the risk for the homeopath of choosing an inadequate set of key symptoms and themes from the case taking.

By using the Deep PEAT technique after the case taking, we may significantly improve the first critical point we have listed at the beginning, because it can assist the patient in opening up. Also by modifying the aim of the technique for use in homeopathy, we may get a longer chain of contents, for the case analysis.


The Design of the Matrix Model of Behavioral States

The relations of the contents we have got in the previous step, are parts of the bigger picture of the general behavior and emotional states. For better understanding of the relations between the contents we have got from the patient, as well as their effect on the complete picture of a patient, and understanding the patient’s miasm, we have created a three-dimensional model of general behavioral states in relation to the three monoamines (serotonin, dopamine and noradrenaline) – the Matrix model, and it’s flattened two-dimensional version, the Tetractys model, named after the ancient Pythagorean symbol of tetractys, that turned out to be very similar to this flattened model. The chain of contents we get from the Deep PEAT technique basically consists of emotions, as well as sensations and thoughts that express the underlying emotion.

People are expressing many different emotions, using even more words, but are all those emotions completely different from each other, or are there significant similarities that allow us to group all emotions in just a few clusters?

Charles Darwin in The Expression of the Emotions in Man and Animals listed over thirty emotions, classified into seven clusters. Ever since this groundbreaking work scientists have argued over whether or not there is a finite number of basic emotions at all[8]. Certain emotions may be grouped in clusters because they share an underlying pattern of behavioral-neuro-endocrine control, in which monoamines play a vital role.

Monoamines are phylogenetically ancient signaling molecules and it has been found that they are involved in behavioral control in a wide range of species from humans to structurally simple organisms such as nematodes[9],[10] . The fact that many allopathic psychotropic drugs, like antidepressants and antipsychotics act by interfering with the monoamine system, may illustrate the importance of monoamine systems in human beings[11].

The three monoamines essential to behavioural-neuroendocrine response patterns are serotonin, dopamine and noradrenaline[12]. A certain relation of quantities of these three monoamines, creates a basic pattern that corresponds to a type of emotional response or behavior, such as “fight or flight”, imprinted in the limbic-amygdala hippocampus section of the mammalian brain (paleocortex), as well as in the subordinate hypothalamic and brainstem centres[13]. Since the phylogenetically ancient monoamines are crucial for behavioral control throughout evolution, these systems give a great advantage for survival because they enable an organism to modify its behavior. Monoamine systems are very dynamic, probably in relation to the need for quite rapid modifications in behaviors and emotion in order to adjust to changes of environment. We can only imagine the huge diversity of situations that monoamine systems had to deal with successfully in order to survive, therefore, a system of behavioral control cannot be specific to every possible situation. It has to activate a number of general emotional and behavioral patterns[14].

The effects of dopamine and serotonin are still not completely understood, because the brain may use a particular neurotransmitter for different purposes in different parts of the body. Some forms of dopamine are related to reward, or more precisely to reward prediction[15], and some forms of serotonin are related to aversion and punishment[16].

In order to better understand the complex relations between the three essential monoamines and the general behavioral and emotional patterns, we will focus on eleven characteristic ratios of these monoamines and try to associate them with certain characteristic emotional states.

A plasma dopamine and noradrenaline variations research, in response to stress, has shown that both monoamines are not high or low at the same time, so if either one of these two is high in response to stress, the values of the other monoamine are small[17] – high negative correlation has been found.

Negative correlation is a relationship between two variables in which one variable increases as the other decreases, and vice versa[18].



A research on serotonin and dopamine system interactions in the neurobiology of impulsive aggression, has shown that serotonin hypofunction may represent a biochemical trait that predisposes individuals to impulsive aggression, with dopamine hyperfunction[19], so between these two monoamines has also been found negative correlation.

Anatomical and pharmacological data also suggest that serotonin and dopamine may act as mutual opponents[20], meaning in negative correlation.

Given the negative correlation between the monoamines, to present it in the theoretical model, we will use the perfect negative correlation of dopamine (DA) and noradrenaline (NA), in an orthogonal coordinate system with two axes, with each end of the arrows represents low and high levels of signaling respectively, with five representative positions marked with circles: zero-point (NA=0; DA=0), high noradrenaline point (NA=1; DA=0), high dopamine point (NA=1; DA=0), noradrenaline/dopamine point (2/3 NA; 1/3 DA) and dopamine/noradrenaline point (1/3 NA; 2/3 DA). Because of this negative correlation the area is triangular instead of square (it would be square in positive correlation). The zero-point and the high points of both monoamines are the three points that define this coordinate system, as the points of low and high signaling. All possible ratios of the two monoamines in negative correlation are inside the gray triangular area marked on the diagram, half of which have predominance of one monoamine over the other and vice versa for the other half. Both circles placed on the negative correlation borderline, between the points of arrows on the two axes, represent the areas where both monoamines are present in a significant percent with one dominating over the other. For illustration of these two states in this theoretical model we have marked with circles the positions with 2/3 of one monoamine and 1/3 of the other – in this example the Noradrenaline/Dopamine point (2/3 NA; 1/3 DA) and the Dopamine/Noradrenaline point (1/3 NA; 2/3 DA) representing all ratios with predominance of noradrenaline over dopamine in former, and vice versa in the later. This is the diagram representing the theoretical model of two monoamines correlation with five typical ratios marked:


On the following pages we will try to associate each of these typical ratios to a behavioral or emotional state.

In a study of rats that have been conditioned to fight at a specific time each day over a 10-day period, with serotonin levels decreased in the nucleus accumbens, heart rate and dopamine release were concurrently measured and both were raised in anticipation of the fight[21]. This study shows us that lowering of serotonin, raises the other two monoamines, but not in what ratio. Another study of aggressive behaviour shows that when noradrenaline is in excess (i.e., release is stimulated or reuptake is blocked by pharmacologic manipulations) it influences aggression biphasically: a slight activation increases aggression, while a strong activation decreases it[22]. Putting these two studies together may lead us to conclusion that aggressive behavior is connected to low serotonin, high dopamine and moderately elevated noradrenaline, meaning that all three monoamine systems are negatively correlated to each other. Only in a theoretical situations that one monoamine is at minimum, a 2D diagram, such as the previous one presenting a correlation between only two monoamines, has sense.

Much closer to reality, would be to use a 3D model of the all three monoamines in negative correlation. Because of this negative correlation of all three monoamines, the area of the diagram is limited to the tetrahedron presented in the image below, instead of a cubic area of positive correlation.


If we mark the five points of typical ratios of each monoamine pair on the three triangular faces which meet at the zero-point corner, of the tetrahedron like 3D model of the all three monoamines in negative correlation, we will get ten marked points of typical ratios on it, since five points are overlapped on the 3D model. We will add to these 10 points one more, the point of highest equal parts of all three monoamines, placed in the center of the fourth triangle tetrahedron – the darker gray one on the previous image, and the following one. This is the Theoretical 3D model of three monoamines correlation with eleven typical ratios of monoamines marked with circles and labeled based on their predominance:

The three monoamines are placed on the three orthogonal axes creating a tetrahedral space, since monoamines are supposed to be mutually orthogonal in a 3D model of monoamines as this maximizes the amount of information that can be transmitted, making it evolutionarily rational[23].

Associating these eleven typical ratios of the three monoamines, is may lead to better understanding of relations between a number of emotional and behavioral states.

Humans, unlike other species, have the sophisticated neocortex, that allows us to learn, at least to certain extent, to voluntarily suppress or modify the somatomotor-behavioural responses, while the autonomic and hormonal expressions cannot be suppressed voluntarily in the same manner. Voluntary suppression or modification of somatomotor-behavioural responses, if often repeated, may even permanently change them if often repeated, disturbing the balance in our physiological systems – “homeostasis”, consequently making changes in organic systems and tissues, including the immune system[24].

The sophisticated psychosocial challenges of today’s modern life may evoke a modified pattern of emotional response, and to understand these partially suppressed emotions and behaviors, we sometimes have to observe the autonomic and hormonal expressions that cannot be suppressed voluntarily.

To truly understand these modifications and suppressions it is necessary learn more about the general, unmodified and unsuppressed, emotional and behavioral states and to connect them to specific ratios of the three monoamines. Thanks to a huge number of studies on monoamine systems conducted through decades, there is an abundance of data available on these issues, and we will use some of these studies to propose the associations between the 11 typical ratios of the three monoamines with emotional and behavioral states.

We will start with the zero-point, as the point of origin.


The zero-point (Low 5-HT; Low NA; Low DA)

The zero-point of orthogonal coordinate system, should be understood as a point where all three monoamines are at the their lowest values, lower then normal basal level, a depressed state in the range from dysthymia to major depression disorder.

Dysthymia form of subthreshold depressive pathology, that may last for decades, neither getting better nor developing a full blown psychological disorder, such as major depression disorder, bipolar disorder etc. Therefore, this state wasn’t conidered to be a pathologycal condition, but a constitutional personality type. In dysthimia(old diagnose was melancholy) a person is in a long-lasting state of gloominess, anhedonia, low drive and energy, low self-esteem and pessimistic outlook[25].

The association between low values of all three monoamines and depression[26], was the leading concept in 1960s, that regains its importance in recent years, with new research on triple monoaminergic reuptake inhibitors (TRIs), as next generation antidepressants[27]. When patients talk about this state, they often associate it with the sensations of darkness, cold and heaviness, feeling sadness, some of the patients start to cry etc. In the homeopathic Repertory, the big Mind rubric we could associate to this state is SADNESS or MELANCHOLY, so we will use this therm for the zero-point.


High Dopamine point (High DA; Low 5-HT; Low NA)

Dopamine is considered to have rewarding, motivating and reinforcing effects, and it is associated with impulsive and addictive behavior.[28] Dopamine system also signals a large class of stimuli that are intrinsically appetitive (e.g., pleasure or sweet)[29], and react to them with the anticipation of appetitive stimuli – reward. The key theme for dopamine could be ANTICIPATION OF REWARD, that may be motivating, cause of addiction and/or impulsive behavior.


Dopamine/ Serotonin point (High DA; Moderate 5-HT; Low NA)

Noradrenergic neurotoxin DSP-4, preceded by zimelidine to prevent serotonin depletion, was administered IP to rats behaving in a defensive-submissive manner in a resident-intruder paradigm, resulting in decrease of frequency and duration of defensive episodes and marked increase of offensive aggression. This might suggest an increase of aggressiveness and therefore support the notion of an inhibitory role of the noradrenergic system in aggressive behavior[30].

As a result of selective lesions of dorsal (DB) noradrenergic (NA) system it was observed that it doesn’t simply decrease noradrenergic metabolism, but also violates its balance with the serotonergic (5-HT) system, because of the lack of noradrenergic tonic excitatory effect on serotoninergic system it decreases[31]. Since both noradernergic and serotonergic systems are lowered in this research the increase in affective aggression may be associated with the dopaminergic system. The increase in aggression is caused by changes in dopamine and serotonin levels, after noradrenaline depletion[32]. OFFENSIVE or predatory AGGRESSION is characterized by planned, goal-directed, emotionless, hidden and not preceded by autonomic arousal[33]. We could also say it is cold in nature, since one of is characteristics is low NA.

Individuals seek out the opportunity to engage in certain aggressive acts, since the performance of aggressive behavior can serve as a potent positive reinforcing event, therefore high dopaminergic.

Study shows that primates with lowered serotonin levels show behaviors similar to type II alcohol abuse: poor impulse control, risky behavior, and consumption of alcohol in huge amounts[34], while another study finds that high dopamine levels have been observed in some populations of substance users such as type II alcoholics[35] – leading to conclussion that type II alcoholic addiction could be associated with this dopamine/serotonin point. Cocaine, unlike MDMA, shows consistent rewarding effects, due to the high dopamine level – significantly contributing to cocaine addiction. The other two monoamines are moderately elevated, so the cocaine abuse may be placed close to this point. It may be placed here also because a study of repeated low-dose cocaine treatment (0.5 mg/kg/day) during adolescence facilitates offensive aggression in male Syrian hamsters, while treatment with fluoxetine (SSRI), resulting in elevated serotonin, inhibited the cocaine-facilitated aggressive response[36].

Therefore, we may associate this point with ADDICTION and OFFENSIVE AGGRESSION.

Serotonin/Dopamine point (High 5-HT; Moderate DA; Low NA)

The dopaminergic system together with oxytocin and vasopressin are crucial in the formation of pair-bonds[37], and dopamine reward system makes love a rewarding experience[38]. Infusions of moderate doses of dopamine into the nucleus accumbens facilitate pair-bonding, whereas infusion of high doses does not generate this effect. Love can feel like an addiction, and the dopaminergic pathways that are involved in love and pair-bond formation are largely similar to those that are involved in addictive behavior[39]. Since it is suggested that serotonin and dopamine act as mutual opponents[40], we may assume that lower dopamine levels result in higher serotonin levels.

Parkinson’s disease (PD) is a degenerative disorder of the central nervous system related to loss of dopamine-generating cells, and consequent low dopamine levels, and again we may assume that in turn serotonin levels may be elevated[41]. Study has shown that young Parkinson’s disease (PD) patients, with early disease onset, have significantly higher incidence of hypomania and mania related to dopamine replacement therapy (DRT)[42], so in these cases to assumingly already elevated serotonin levels, dopamine levels are also increased. Therefore, we are going to associate hypomanic behavior with this point.

A hypomanic person is described as cheerful, optimistic, extroverted, self-confident, energetic and needing habitually less sleep than other people. They can also be irritable, rude, reckless and irresponsible[43]. Hypomanic people are also focused, productive and generally successful at work, Hypomania may be an evolutionary advantage, since hypomanic behavior is generally perceived as being energetic, euphoric, visionary, overflowing with new ideas, and sometimes overconfident and very charismatic, but coherent enough in thought and action to participate in everyday activities[44]. Therefore, a hypomanic person will rarely think of changing this state – going to treatment of this condition. Low dopamine levels have been found to contribute drug- and alcohol-seeking behavior[45], so basically attracted to addictive behavior, while the next point whit inverse serotonin/ dopamin ratio, is associated with addictions.

Since moderate doses of dopamine facilitate pair-bonding, so we may call this one the point of LEADERSHIP AND ATTRACTION.


Serotonin/Noradrenaline point (High 5-HT; Moderate NA; Low DA)

Very close to serotonin/noradrenaline point may be placed abused psychostimulant MDMA (Ectasy), has affinity for serotonin (5-HT), noradrenaline (NE) and dopamine (DA) transporters ( SERT, NET and DAT respectively)[46], but predominantly for SERT with 10-fold higher affinity at SERT compared to DAT, leading to lower rewarding strength, and consequently addictive, effect compared to cocaine, for example.

MDMA abuse is associated with euphoria, exhilaration, an increased perception and feeling of closeness to others – emapthy, mood-enhancement, increased energy and heightened senses, but also hyperthermia that, esspecially in warm environments may develop acute complications with potential fatal consequences, as well as tachycardia, hypertension, seizures etc.[47],[48] Most frequent acute somatic complaints of MDMA were jaw clenching, lack of appetite, impaired gait, and restless legs[49]. It affects mnemonic processes including spatial, working and episodic memory domains, but without affecting simpler aspects such as vigilance, reaction time, selective attention, and response inhibition. MDMA affecting response inhibition may be connected to serotoninergic inhibitory effect, while high dopaminergic effect of impulsiveness is found in cocaine impaired performance on response inhibition[50].

Single low dose of MDMA produces cognitive impairments lasting up to 72 h post-administration, whereas acute low doses of cocaine produced cognitive enhancement[51].

Although it was expected that drugs of abuse that increase sleepiness and sedation (e.g., cannabis) are more likely to induce dissociative symptoms than stimulant drugs (e.g., MDMA, cocaine), a study has demonstrated that MDMA and cannabis can induce dissociative symptoms, unlike cocaine. While cannabis significantly increased subjective ratings of depersonalization, derealization, and amnesia during intoxication, and MDMA primarily increased feelings of derealization, their magnitude of total dissociation was comparable[52].

Exhilaration with EMPATHY could be the most adequate terms to describe this behavioral state.


Noradrenaline/Serotonin point (High NA; Moderate 5-HT; Low DA)

In early stages of romantic love, there is a depletion of serotonin levels[53],[54].

In the classical experiment by Dutton and Aron the influence of an elevated noradrenergic state on the sexual attraction was shown, when the sexual attraction to an attractive interviewer was increased by locating the interview on a anxiety-arousing, high suspension bridge, as compared to a low bridge[55].

Depletion of central serotonin is also found in obsessive-compulsive disorder (OCD)[56]. Early stages of romantic love show similarities to OCD, like a mild serotonin-depletion-related form of obsessive behavior, including symptoms of anxiety, stress, and obtrusive thinking. Of course love is not a mental disorder, so 12–18 months after the start of the relationship, subjects do not have any obsessive ideation regarding the partner anymore[57]. The high levels of anxiety and stress indicates high noradrenaline content, so the obsessive component maybe related to serotonin.

Another study has shown significant correlation between increased anxiety severity and decreased DAT availability in newly diagnosed, untreated PD patients[58], that may also indicate negative correlation between the three monoamines, by finding behavior associated with elevation of noradrenaline and serotonin as a result of lowering dopamine levels.

Serotonin agonists (5-MeODMT) raise pain thresholds dramatically, as well as very markedly facilitate male rat sexual behavior (male rats require fewer intromissions to reach ejaculatory threshold), but degeneration of central noradrenergic (NA) neurons by DSP4 abolished entirely the analgesic effect and most of the effects on male rats sexual behavior, of 5-MeODMT or serotonin (5-HT) itself [59],[60]. So, high serotonin levels loses both of these effects, without a moderate action of noradrenaline.

Since there is evidence to support association between low dopamine activity and social phobia, and increased dopamine transporter binding in generalized social anxiety disorder, making these conditions low dopaminergic, while high doses of caffeine with elevating noradrenergic effect might provoke panic attacks in patients with panic disorder or social phobia, and noradrenergic β-blockers are sometimes used to treat uncomplicated performance anxiety, so this might support that social anxiety/panic state is high-noradrenergic[61]. There is an increased serotonin transponder binding in generalized social anxiety disorder, therefor a lowered serotonine level[62], but since there are low dopamine levels in these conditions if we take into consideration the previosly mentioned negative correlation between serotonin and dopamine, the level of serotonin will be higher then dopamine levels, so we could say that we will have moderate serotonin level.

We could say this is the point of PASSIONATE, but also social anxiety/PANIC behavior.

High Serotonin point (High 5-HT; Low NA; Low DA)

In the previous study the serotonin component was linked to obsessive behavior, and also serotonin 5-HT2A receptor polymorphism has recently been linked to an obsessive romantic attachment behavior[63]. If there is a purpose to the obsessive behavior in OCD it is to avoid some potential or imaginary danger. Serotonin system signals a large class of stimuli that are intrinsically aversive (e.g., stress or pain)[64], and reacts to these stimuli with repulsion and withdrawal. Serotonin leads to behavior inhibition and aversion to punishment[65]. We may say that the key theme of serotonin could be avoiding danger, regulating the other two monoamines by inhibitory mechnisms, in other words CONTROL the system. Also, another study showed that systemic administration of the selective dopamine D2 receptor antagonist sulpiride caused proaversive effects in rats in the elevated maze[66], and since lowering dopamine may lead to elevated serotonin, this study also leads us to assumption of association between elevated serotonin and (pro)aversive behavior . Serotonin also has a well established anti-depressive effect, illustrated by the fact that serotonin synthesis in normal male was found to be 52% higher than in normal female, which might explain the lower incidence of major unipolar depression in males[67].It is also associated with nausea, and feeling disgust and CONTEMPT.

About the author

Mirjana Zivanov

Mirjana Zivanov

Dr. Mirjana Živanov DDS, Registered Homeopath, graduated from
Faculty of Medicine, University of Novi Sad (Serbia) and London International College of Homeopathy. She has 15 years of everyday clinical practice in Classical Homeopathy, at the Homeopathic clinic in Novi Sad, Serbia and is is the author of the books: “Homeopathy in Practice”, "Homeopathic medicine - Principles", "Homeopathic medicine - Invisible Influences", "Matrix method with Tetractys model", "Opening the Secret Door with Matrix &Tetractys" and many published articles in International Homeopathic magazines and web sites.
Dr. Mirjana is the creator of the new "Matrix theory" in Homeopathy. She presented her Matrix theory at the international homeopathic seminar London, UK Oct 2015, and at the International Homeopathic seminar London, UK Sept 2016, and at the international homoeopathic conference Bangalore, India Sept 2017, and in a state accredited lecture at Serbian Doctors Society Novi Sad, Serbia Dec 2017. Dr. Živanov is the International Vice-president of the Youth Homeopathic Association. More information is available on and Dr. Živanov may be ed at: [email protected]


  • Very Important Theory in Modern Homeopathy. It is new and excellent way to find perfect remedy.They explained it nicely. I already bought this book and reading day by day. I am learning many things from it. Great achievement by Dr Mirjana Zivanov and Her group. She is a Great Doctor.All the Best.

  • This is a very interesting and intriguing theory. A very original approach to get more in dept information about the patient. This theory may help to bridge the gap between homeopathy and modern science. Congratulations Dr Mirjana! Keep on the good work.

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