While introducing the concept of MIASMS of ‘infectious diseases’ as the causative factor of CHRONIC DISEASES, HAHNEMANN was actually thinking far ahead of his contemporary science. Both the scientific community, as well as his own followers failed in understanding the real meaning and implications of this epoch making revelation.

Modern science has only just started to realize the role of ANTIBODIES as a major class of disease-producing molecules, which were so far considered only as ‘defense molecules’ of our body.

Recent studies of ‘off target’ inhibitions produced by antibodies as a major causative factor in chronic diseases so far called as ‘auto-immune’ diseases shows that hahnemann was thinking 200 years ahead of his time while introducing the concept of miasms.

Let us bow our heads in memory of that great genius, whose observational and reasoning skills transcended the limitations of not only his time and knowledge available to him, but even coming centuries.

Fundamental error ‘classical miasmatic analysts’ make is, they have turned hahnemann’s concept of miasms upside down. According to those people, ‘gonorrhoea is CAUSED BY sycosis’, itch infection is CAUSED BY psora’, and ‘syphilis disease is CAUSED BY miasm of syphilis’. And these ‘miasms are caused by original sins of humanity’!

They interpret hahnemann in a very wrong way. Kindly read CHRONIC DISEASES once again carefully, avoiding ‘interpreters’. Hahnemann actually said, these three miasms were CAUSED BY these infectious diseases. And, these three miasms in turn CAUSE other diverse types of CHRONIC DISEASES.

According to hahnemann, PSORA is never acquired unless the person is ONCE infected by itch disease, SYCOSIS is never acquired unless the person is ONCE infected by gonoorhoea, SYPHILIS is never acquired unless the the person is ONCE infected with syphilis disease.

All confusions regarding miasms could be resolved only by first resolving the confusion whether hahnemann considered PSORA, SYPHILIS and SYCOSIS are CAUSED by infectious diseases, or those infectious diseases are CAUSED by already existing miasms of ORIGINAL SINS OF HUMANITY.

If anybody has least doubt whether or not hahnemann was talking about the ‘miasm of psora’ as originating from ‘infection of itch disease’, kindly read this part from ‘Chronic Diseases’-Para 37:

“Psora (itch disease), like syphilis, is a miasmatic chronic disease, and its original development is similar. The itch disease is, however, also the most contagious of all chronic miasmata, far more infectious than the other two chronic miasmata, the venereal chancre disease and the figwart disease”.

“But the miasma of the itch needs only to touch the general skin, especially with tender children”.

“No other chronic miasma infects more generally, more surely, more easily and more absolutely than the miasma of itch; as already stated, it is the most contagious of all. It is communicated so easily, that even the physician, hurrying from one patient to another, in feeling the pulse has unconsciously inoculated other patients with it; wash which is washed with wash infected with the itch; new gloves which had been tried on by an itch patient, a strange lodging place, a strange towel used for drying oneself have communicated this tinder of contagion; yea, often a babe, when being born, is infected while passing through the organs of the mother, who may be infected (as is not infrequently the case) with this disease; or the babe receives this unlucky infection through the hand of the midwife, which has been infected by another parturient woman (or previously); or, again, a suckling may be infected by its nurse, or, while on her arm, by her caresses or the caresses of a strange person with unclean hands; not to mention the thousands of other possible ways in which things polluted with this invisible miasma may touch a man in the course of his life, and which often can in no way be anticipated or guarded against, so that men who have never been infected by the psora are the exception. We need not to hunt for the causes of infection in crowded hospitals, factories, prisons, or in orphan houses, or in the filthy huts of paupers; even in active life, in retirement, and in the rich classes, the itch creeps in”.

It is obvious that hahnemann considered human beings aquiring ‘miasm of psora’ only by getting ‘infected’ with ‘itch’ disease.

But our ‘miasmatic experts’ make theories about even ‘genetic inheritance’ of ‘psora’! I would request young homeopaths to carefully read the original works of hahnemann with a logical and scientific mindset, instead of ‘learning miasms’ from modern interpreters.

Listen to hahnemann saying: “not to mention the thousands of other possible ways in which things polluted with this invisible miasma may touch a man in the course of his life, and which often can in no way be anticipated or guarded against, so that men who have never been infected by the psora are the exception”.

Hahnemann explains the diverse ways of getting infected by itch to show why “men who have never been infected by psora are the exception”. But our miasmatic experts would say that it is due to ‘genetic inheritance’!

Kindly read CHRONIC DISEASES carefully once again. You will realize, while introducing the concepts of MIASMS, hahnemann was actually talking about the life long ‘chronic disease dispositions’ resulting from infectious diseases.

He limited his discussions to ‘three’ miasms, since according to him, itch-leprosy, syphilis and figwart-gonorrhoea disease were the most widely distributed infectious diseases during his time.

How an ‘infectious agent’ can produce a ‘chronic disposition’ even after the infectious disease is cured, is the subject of my inquiries. According to me, it can happen only through the antibodies generated in the organism against those infectious substances, which contain protein molecules alien to the organism. These antibodies remain lifelong, and can bind to ‘off-target’ biological molecules, thereby producing diverse types of chronic diseases.

ANTIBODIES are the carriers of miasms- this is what I try to make out. Antibodies and misformed proteins generated in the body against diverse types of infectious agents and other ‘alien’ proteins constitute a major class of pathogenic agents that cause diverse types of CHRONIC DISEASES, including even auto-immune diseases and proteinopathies.

Hahnemann called this pathogenic factors as ‘miasms’, as he was not much aware of antibodies and immunology during his period.

Did Homeopathy Community Actually Do Justice to Samuel Hahnemann?

Samuel Hahnemann was such a wonderful genius that he could introduce a set of ideas and therapeutic tools that were naturally unimaginable and inconceivable to anybody belonging to the scientific community in the contemporary primitive knowlege context he lived in 200+ years ago!

As per modern scientific pardigms, hahnemann’s revolutionary ideas included ‘studying drug pathology’ by observing symptoms drug substances produced when applied in healthy individuals (DRUG PROVING), ‘studying disease pathology’ by observing symptoms produced in disease conditions (TOTALITY OF SYMPTOMS), removal of molecular inhibitions utilizing ‘molecular mimicry’ and ‘molecular competitions’ (SIMILIA SIMILIBUS CURENTUR), ‘molecular imprinted drug designing’ using azeotropic water-ethanol mixtures (HOMEOPATHIC POTENTIZATION) etc.

Is it not really amazing that during a period when modern biochemistry did not even emerge, hahnemann could observe the phenomenon of “competitive relationship of similar chemical molecules in binding to the biological targets”, and develop it into the foundation of a therapeutic principle he called SIMILIA SIMILIBUS CURENTUR?

Is it not equally amazing that Hahnemann could utilize the natural phenomenon of MOLECULAR IMPRINTING and develop it into a technology of preparing a new class of therapeutic agents, during a period when modern polymer technology or supra-molecular chemistry did not even emerge?

Did we actually do justice to Samuel Hahnemann?

Did we, his “followers” and “disciples”, actually do anything all these two hundred years to take forward and update his contributions?

Did we do anything seriously to study and scientifically explain his ideas, and present them to the modern scientific community so as to get the due recognition and place he deserved in the human knowledge history?

What his “blind” followers did all these years was to make him an idol of worship, without recognizing the great scientist in him. They converted his words into mere dogmas, to be learned and recited just like religious preachings!

Hahnemann failed to get the due respect and recognition in the history of medical science, only due to his unscientific and shortsighted followers and disciples who made his ideas and its practices more and more superstitious, spiritualistic and irrational.


MIT concepts explains MIASMS in terms of chronic disease dispositions caused by ANTIBODIES or DEFORMED PROTEINS. This explanation helps us to approach those so-called AUTO IMMUNE DISEASES from a new angle.

Let us look into the exhaustive list of diseases included in the class of AUTO-IMMUNE DISEASES, which are actually ‘chronic diseases caused by off-target actions of antibodies’. Kindly go through this list to realize the real magnitude of ‘anti-body’ mediated diseases or ‘miasmatic’ diseases in our day today medical practice:

” Acute disseminated encephalomyelitis, Acute hemorrhagic leukoencephalitis, Addison’s Disease, Agammaglobulinemia, Alopecia areata, Amyotrophic Lateral Sclerosis, Ankylosing Spondylitis, Anti-GBM/TBM Nephritis, Antiphospholipid syndrome, Antisynthetase syndrome, Atopic allergy, Atopic allergy, Atopic dermatitis, Autoimmune aplastic anemia, Autoimmune cardiomyopathy, Autoimmune enteropathy, Autoimmune hemolytic anemia, Autoimmune hepatitis, Autoimmune inner ear disease, Autoimmune lymphoproliferative syndrome, Autoimmune peripheral neuropathy, Autoimmune pancreatitis, Autoimmune polyendocrine syndrome, Autoimmune thrombocytopenic purpura, Autoimmune progesterone dermatitis, Autoimmune urticaria, Autoimmune uveitis, Balo disease/Balo concentric sclerosis, Bechets Syndrome, Berger’s disease, Bickerstaff’s encephalitis, Blau syndrome, Bullous pemphigoid, Cancer, Celiac disease, Castleman’s disease, Chronic inflammatory demyelinating polyneuropathy, Chronic recurrent multifocal osteomyelitis, Churg-Strauss syndrome, Cicatricial pemphigoid, Cogan syndrome, Cold agglutinin disease, Complement component 2 deficiency, Cranial arteritis, CREST syndrome, Crohns Disease, Cushing’s Syndrome, Cutaneous leukocytoclastic angiitis, Dego’s disease, Dercum’s disease, Dermatitis herpetiformis, Dermatomyositis, Diabetes mellitus type 1, Discoid lupus erythematosus, Eczema, Erythema nodosum, Diffuse cutaneous systemic sclerosis, Enthesitis-related arthritis, Epidermolysis bullosa acquisita, Eosinophilic gastroenteritis, Eosinophilic fasciitis, Dressler’s syndrome, Diffuse cutaneous systemic sclerosis, Essential mixed cryoglobulinemia, Evan’s syndrome, Fibrodysplasia ossificans progressive, Fibrosing aveolitis, Gastritis, Gastrointestinal pemphigoid, Giant cell arteritis, Glomerulonephritis, Goodpasture’s syndrome, Graves’ disease, Henoch-Schonlein purpura, Guillain-Barré syndrome, Hashimoto’s encephalitis, Hashimoto’s thyroiditis, Haemolytic anaemia, Herpes gestationis, Hypogammaglobulinemia, Idiopathic Inflammatory Demyelinating Diseases, Idiopathic pulmonary fibrosis, Idiopathic thrombocytopenic purpura, IgA nephropathy, Inclusion body myositis, Inflammatory demyelinating polyneuopathy, Interstitial cystitis, Juvenile idiopathic arthritis, Juvenile rheumatoid arthritis, Kawasaki’s Disease, Lambert-Eaton myasthenic syndrome, Leukocytoclastic vasculitis, Lichen planus, Linear IgA disease, Lichen sclerosus, Lou Gehrig’s disease, Lupoid hepatitis, Lupus erythematosus, Majeed syndrome, Ménière’s disease, Microscopic polyangiitis, Miller-Fisher syndrome, Mixed Connective Tissue Disease, Morphea, Mucha-Habermann disease, Multiple sclerosis, Myasthenia gravis, Myositis, Neuromyelitis optica, Neuromyotonia, Occular cicatricial pemphigoid, Opsoclonus myoclonus syndrome, Ord thyroiditis, Palindromic rheumatism, pediatric autoimmune neuropsychiatric disorders associated with streptococcus, Paraneoplastic cerebellar degeneration, Paroxysmal nocturnal hemoglobinuria, Parry Romberg syndrome, Parsonnage-Turner syndrome, Pars planitis, Pemphigus vulgaris, Pernicious anaemia, Perivenous encephalomyelitis, POEMS syndrome, Polyarteritis nodosa, Rheumatoid fever, Psoriasis, Polymyalgia rheumatica, Polymyositis, Primary biliary cirrhosis, Primary sclerosing cholangitis, Progressive inflammatory neuropathy, Psoriatic arthritis, Pyoderma gangrenosum, Pure red cell aplasia, Rasmussen’s encephalitis, Raynaud phenomenon, Relapsing polychondritis, Reiter’s syndrome, Restless leg syndrome, Retroperitoneal fibrosis, Rheumatoid arthritis, Sarcoidosis, Schmidt syndrome, Schnitzler syndrome, Scleritis, Scleroderma, Sjögren’s syndrome, Spondyloarthropathy, Still’s disease, Undifferentiated spondyloarthropathy, Stiff person syndrome, Subacute bacterial endocarditis, Susac’s syndrome, Sweet’s syndrome, Sydenham chorea, Sympathetic ophthalmia, Takayasu’s arteritis, Temporal arteritis, Tolosa-Hunt syndrome, Transverse myelitis, Ulcerative colitis, Undifferentiated connective tissue disease, Vasculitis, Vitiligo, Wegener’s granulomatosis”

I have been trying to explain concept of ‘miasms’ as ‘chronic disease dispositions’ due to the ‘off-target’ molecular inhibitions caused by ‘antibodies’ formed against ‘infectious agents’ and ‘exogenous’ proteins. As per this view, antibodies are the causative agents of ‘miasms’.MI

All of us know, so-called ‘autoimmune diseases’ are caused by ‘antibodies’. But, those ‘antibodies’ are considered to be formed not against ‘exogenous antigens’, but ‘endogenous or host antigens’. If we explain ‘miasms’ as ‘antibodies’ formed against ‘exogenous’ proteins, should we exclude ‘autoimmune diseases’ from ‘miasms’, since they are considered to be formed against ‘endogenous antigens’, not ‘exogenous proteins’?

Here, we have to undertake a serious study of the phenomena of ‘autoimmunity’ and ‘autoimmune diseases.

According to immunologists, ‘autoimmune diseases’ arise from an overactive immune response of the body against substances and tissues normally present in the body. In other words, the body actually attacks its own cells. The immune system mistakes some part of the body as a pathogen and attacks it. This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture’s disease which may affect the basement membrane in both the lung and the kidney).

Hundreds of chronic systemic diseases are now classified as ‘autoimmune diseases’. This group include Coeliac disease, diabetes mellitus type 1, systemic lupus erythematosus (SLE), Sjögren’s syndrome, Churg-Strauss Syndrome, Hashimoto’s thyroiditis, Graves’ disease, idiopathic thrombocytopenic purpura, rheumatoid arthritis (RA), lupus and allergies. This group is expanding every day.

Autoimmune diseases are broadly divided into systemic and organ-specific or localised autoimmune disorders, depending on the principal clinico-pathologic features of each disease.

Systemic autoimmune diseases- include SLE, Sjögren’s syndrome, scleroderma, rheumatoid arthritis, and dermatomyositis. These conditions tend to be associated with antibodies to antigens which are not tissue specific. Thus although polymyositis is more or less tissue specific in presentation, it may be included in this group because the autoantigens are often ubiquitous t-RNA synthetases.

Local syndromes which affect a specific organ or tissue:

Endocrinologic: Diabetes mellitus type 1, Hashimoto’s thyroiditis, Addison’s diseaseGastrointestinal: Coeliac disease, Crohn’s Disease, Pernicious anaemia

Dermatologic: Pemphigus vulgaris, Vitiligo

Haematologic: Autoimmune haemolytic anaemia, Idiopathic thrombocytopenic purpura

Neurological: Myasthenia gravis

Autoimmunity is defined as “the failure of an organism to recognize its own constituent parts as self, which allows an immune response against its own cells and tissues. Any disease that results from such an aberrant immune response is termed an autoimmune disease”.

This definition does not answer the question we are interested. Are the antibodies ‘formed against’ native targets, or ‘antibodies formed against’ exogenous antigens mistaking native targets as the ‘exogenous antigens’?

Actually, are the antibodies considered to be the causative agents of ‘autoimmune diseases’ really formed against ‘host antigens’? Or, are they ‘antibodies’ formed against ‘exogenous proteins’ attacking ‘off-target’ sites in the organism?

This topic is still a controversial subject in immunology. We should remember that ‘immune’ mechanism is basically a defense mechanism of our organism to identify and destroy ‘exogenous proteins’ which are alien to our genetic blueprint. Several mechanisms are thought to be operative in the pathogenesis of autoimmune diseases, against a backdrop of genetic predisposition and environmental modulation. It is beyond the scope of this article to discuss each of these mechanisms exhaustively, but a summary of some of the important mechanisms suggested by various hypotheses may be examined.

  1. T-Cell Bypass – A normal immune system requires the activation of B-cells by T-cells before the former can produce antibodies in large quantities. This requirement of a T-cell can be bypassed in rare instances, such as infection by organisms producing super-antigens, which are capable of initiating polyclonal activation of B-cells, or even of T-cells, by directly binding to the β-subunit of T-cell receptors in a non-specific fashion.
  2. Molecular Mimicry – An exogenous antigen may share structural similarities with certain host antigens; thus, any antibody produced against this antigen (which mimics the self-antigens) can also, in theory, bind to the host antigens, and amplify the immune response. The idea of molecular mimicry arose in the context of Rheumatic Fever, which follows infection with Group A beta-haemolytic streptococci. Although rheumatic fever has been attributed to molecular mimicry for half a century no antigen has been formally identified (if anything too many have been proposed). Moreover, the complex tissue distribution of the disease (heart, joint, skin, basal ganglia) argues against a cardiac specific antigen. It remains entirely possible that the disease is due to e.g. an unusual interaction between immune complexes, complement components and endothelium.
  3. Idiotype Cross-Reaction – Idiotypes are antigenic epitopes found in the antigen-binding portion (Fab) of the immunoglobulin molecule. Plotz and Oldstone presented evidence that autoimmunity can arise as a result of a cross-reaction between the idiotype on an antiviral antibody and a host cell receptor for the virus in question. In this case, the host-cell receptor is envisioned as an internal image of the virus, and the anti-idiotype antibodies can react with the host cells.
  4. Epitope spreading or epitope drift – when the immune reaction changes from targeting the primary epitope to also targeting other epitopes. In contrast to molecular mimicry, the other epitopes need not be structurally similar to the primary one.

If we carefully study the above hypotheses proposed by modern immunology, you will find that all these hypotheses indirectly agree with our contention that so called autoimmune diseases are actually caused by ‘off-target’ inhibitions created by ‘antibodies’ formed against ‘exogenous antigens’

A recent observation regarding relationship of autoimmune diseases and infectious diseases is found to be very important from our ‘miasmatic’ angle. Studies revealed strong association of certain microbial organisms with autoimmune diseases. For example, Klebsiella pneumoniae and coxsackievirus B have been strongly correlated with ankylosing spondylitis and diabetes mellitus type 1, respectively. This has been explained by the tendency of the infecting organism to produce ‘super-antigens’ that are capable of polyclonal activation of B-lymphocytes, and production of large amounts of antibodies of varying specificities, some of which may be self-reactive.

This ‘polyclonal’ ‘super-antigen’ theory goes very close to our explanation of ‘miasms’ as antibody-mediated.

There is a recent proposal among immunologist that the spectrum of autoimmunity should be viewed along an “immunological disease continuum,” with classical autoimmune diseases at one extreme and diseases driven by the innate immune system at the other extreme. Within this scheme, the full spectrum of autoimmunity can be included. Many common human autoimmune diseases can be seen to have a substantial innate immune mediated immunopathology using this new scheme.


Thanks to the compulsions of corona epidemic, the term Homeopathic PROPHYLAXIS is now displaced by a new term IMMUNE BOOSTER in the vocabulary of of homeopaths. Homeopaths themselves have already accepted the new term very enthusiastically, as if they consider it gives to a new higher STATUS to homeopathy! They are not much bothered about the meaning of “immune boosting”, what is the biological mechanism of immune boosting, or HOW homeopathic medicines boost immunity. It is a nice and appealing term, that is enough for them to rejoice!

Now comes another term and another STATUS for homeopathy – ANCILLARY MEDICINE. Homeopathy is now raised to a NEW status of ANCILLARY MEDICINE, instead of the erstwhile status of ALTERNATIVE MEDICINE! This new status is the contribution of OUR HOMEOPATHIC CORONA RESEARCHERS.

The title given to a “homeopathic drug trial” conducted by a team of leading homeopaths was
“Effectiveness of Homeopathy as an ancillary mode of treatment and management in combating corona virus infection”.

Going to the details of that “RESEARCH” it is found that homeopathic medicines were used along with “drugs of modern medicine according to standard treatment protocol”!

In modern medicine, the word ANCILLARY is clearly defined.

Ancillary services in modern medicine is classified into three categories:
Diagnostic services include laboratory tests, radiology, genetic testing, diagnostic imaging, and more.

Therapeutic services range from rehabilitation to physical and occupational therapy, as well as massage, chiropractic services, and speech therapy.

Custodial services include everything from hospice care and long-term acute care to nursing facilities and urgent care.

Ancillary services are medical services or supplies that are not provided by acute care hospitals, doctors or health care professionals. Examples of ancillary services include:
Ambulance services
Ambulatory surgery center (ASC) services
Audiology services
Behavioral health services (inpatient and outpatient)
Cardiac monitoring
Dialysis services
Durable medical equipment (DME)
Hearing services
Home health care services
Home infusion therapy services
Hospice care services
Laboratory services
Medical day care (adult and pediatric)
Mobile diagnostic services
Orthotics and prosthetics
Personal care assistant services
Private duty nursing
Radiology/diagnostic imaging
Rehabilitation services (inpatient and outpatient)
Skilled nursing services
Sleep laboratory services
Speech services
Substance-abuse services (inpatient and outpatient)
Ventilator services
Wound-care services

By earning a status that is ANCILLARY to modern medicine, what advancement we have to expect for homeopathy? By REDEFINING HOMEOPATHY as Molecular Imprints Therapeutics, we were trying to establish that homeopathy is actually a scientifically more advanced stage of modern medicine. Using the corona researchers, modern medicine has very successfully pulled down homeopathy to the status of their ANCILLARY system, even from the current status of ALTERNATIVE MEDICINE ! Do homeopaths think ANCILLARY status is more desirable and prestigious that ALTERNATIVE status? Why do you fail to think about at least a PARALLEL status?

Why should homeopaths do research to establish homeopathy as an ANCILLARY of modern medicine? What you are actually trying to prove by giving homeopathy medicines along with “drugs of modern medicine according to standard treatment protocol”! Is it not the real MIXOPATHY or MIXING OF MEDICAL SYSTEMS you are so MUCH abhorrent about? Even if our medicines acted in such cases, do you expect scientific will accept your research as a proof for effectiveness of homeopathy?

Homeopaths are averse to give TWO medicines together in potentized form, as it is against the “words of maser”! But they have no aversion to give homeopathic medicines ALONG WITH allopathic medicines to same patient, if it is given by another doctor! Is it not ridiculous? Where did master permit you to use potentized homeopathic medicines to a patient along with allopathic medicines?


One of the accusations we hear against homeopathy from its critics is that homeopathy treat only symptoms, without diagnosing the disease. This criticism comes from the idea that diagnosis means fitting the sufferings of the patient into a ‘disease name’ given in the textbooks.

It is wrong to say “homeopathy treats symptoms”.

Actually, homeopathy uses “totality of symptoms” as an indirect means for identifying the biomolecular errors underlyning the disease conditions, as symptoms are nothing but subjective and objective expressions of underlying molecular level pathology.

Homeopathy uses ‘similarity of disease symptoms and drug symptoms’ as a means to identify the appropriate therapeutic agent, based on the knowledge of biochemistry that molecules with ‘similar’ functional groups can bind to ‘similar’ biological targets and produce ‘similar’ molecular inhibitions that are expressed through ‘similar’ trains of symptoms, and that ‘similar’ molecules will compete each other for binding to same biological targets, leading to the removal of molecular inhibitions. This is the basis of therapeutic principle ‘similia similibus curentur’.

If we could identify the drug molecules that are ‘similar’ to particular disease-causing molecules, molecular imprints of those drug molecules can act as artificial binding pockets for those disease-causing molecules by their conformational affinity and deactivate them, thereby removing the pathological molecular inhibitions they had produced in the organism. This is the molecular mechanism of high dilution therapeutics involved in homeopathy.

When a homeopath selects a particular drug or a combination of drugs as ‘similimum’ for a particular patient on the basis of ‘totality’ of subjective and objective symptoms, he is actually making a ‘diagnosis’- a diagnosis that is more comprehensive, more minute, more deep, more subtle and more specific than what is commonly known as ‘diagnosis’ according to the paradigms of modern medicine.

Homeopathic diagnosis of identifying a ‘similimum’ actually goes much deeper level into the identification of exact ‘molecular level’ errors existing in the individual. These molecular level errors could not be accurately identified with any modern sophisticated techniques or bio-chemical studies with such a perfection, other than by the observation of subjective and objective symptoms expressed by the individual. Disease diagnosis of modern medicine is only a very superfluous part of this molecular level ‘total diagnosis’ done by homeopathy. That is why modern medicine find it difficult to treat without proper ‘disease diagnosis’, where as homeopathy can treat any complex case by it ‘symptom diagnosis’ methodology.

Derangement in a particular biochemical pathway resulting from a molecular level inhibition produces a specific train of subjective and objective symptoms in the organism. In other words, each specific group of symptoms exhibited by the organism indicates a particular error occurred in the molecular level.

Homeopathy actually chases these trains of symptoms to their minutest level, from periphery to interior, in order to identify the exact molecular errors underlying any particular state of pathology.Then, those pathological molecular inhibitions are removed by applying appropriate therapeutic agents, selected on the basis of ‘law of similars’ or ‘Similia Similibus Curentur’.

The subjective and objective symptoms presented by the organism are the only reliable indicators to help us correctly understand the minute molecular deviations underlying a state of pathology. Each group or trains of symptoms represent a specific molecular error that had occurred in a particular biochemical pathway. These symptoms invariably indicate the specific type and character of the endogenous or exogenous foreign molecules or ions responsible for the causation of particular molecular inhibition. By studying the train of symptoms carefully and systematically, homeopaths are actually observing these exact molecular inhibitions.

This symptom-based analytical method of diagnosing done in homeopathy is far more exact and superior to the multitude of expensive complex laboratory chemical tests and imaging technologies we consider to be ‘scientific’. Identifying the exact molecular errors in the organism of the patient by observing the expressed symptoms, and identifying the most appropriate therapeutic agents from the similarity of symptoms those drugs could produce in healthy organism- this is the scientific essence of “similia similibus curentur”.

This fundamental strategy underlying the homeopathic system of therapeutics evidently surpasses even the most ‘scientific’ methods of modern molecular medicine. It is high time that the modern medicine realize and recognize this great truth, and incorporate this wonderful tool of homeopathy into their armamentarium. Obviously, “similia similibus curentur” is the most effective technique of identifying and removing the pathological molecular inhibitions in the organism.

Why Biological Properties of Molecular Forms and Molecular Imprinted Forms of A Drug Substance Appear Mutually Opposite?

Homeopathy or Similia Similibus Curentur is actually a therapeutic method that utilise the mutually OPPOSITE actions of crude forms and potentized forms of drug substances. It is the fundamental of homeopathy. If a drug substance can produce a group of symptoms in a healthy individual that are similar to the symptoms of a disease, that disease can be cured by applying the potentized forms of that drug substance. Producing symptoms actually means producing certain molecular errors in the body. Similarity of symptoms indicates similarity of molecular errors. If a drug substance in its crude forms can produce certain molecular errors in the body, its potentized forms can remove that molecular errors.

In our everyday clinical practice, we have a lot of experiences with this OPPOSITE actions of crude drugs and their potentized forms. Many times we apply this knowledge also. Using APIS MEL 30 for bee stings, anacardium 30 for antidoting anacardium poisoning, tabaccum 30 for removing bad effects of tobacco, cannabis 30 for cannabis addiction – there are actually hundreds of such empirical uses which very successful.

Tautopathy is the use of potentized forms of allopathic drugs to remove the short-term or long-term bad effects of allopathic drugging. Potentized forms of almost all allopathic drugs are available in market. Many nosodes are successfully used by homeopaths on the basis of this knowledge of OPPOSITE actions of crude forms and potentized forms. The researches referred above regarding the use of Arsenic Alb 30 in arsenic toxicity, cadmium sulph 30 in cadmium toxicity etc also ratify the correctness of this observation.

When trying to find an answer to the question “what are the active principles of post-avogadro potentized drugs, it is very important that these ACTIVE PRINCIPLES should be something that can remove the molecular inhibitions caused by the molecular forms of that drug.

We have already found in earlier discussions that post-avogadro dilutions do not contain any molecule of original drug substance, and that they contain nothing but alcohol and water, along with some particles coming through contaminations. We have also found that chemical properties of post-avogadro dilutions and unpotentized water-alcohol mixture are similar. But all of us know, and it is well established that these post-avogadro dilutions without any drug molecule contained in them have specific biological actions and disease curing properties. It was also observed and proved through spectroscopic studies mentioned earlier that post-avogadro dilutions have some supra-molecular arrangements that make them different from the plain water-alcohol mixture. It is now obvious that the ACTIVE PRINCIPLES should be some supra-molecular water-ethyl alcohol structures formed during the process of potentization. And it is very much evident that these supra-molecular structures are not MIMICS of drug molecules, but something that can produce biological effects that are exactly OPPOSITE to those produced by original drug molecules.

Our inquiry for ACTIVE PRINCIPLES of post-avogadro diluted homeopathic drugs has now arrived at a very decisive point. Now we are very much sure that these active principles are some sort of supramolecular structures formed by water and alcohol, and these structures have retained the medicinal properties of original drug molecules in a REVERSE order.

It is already known to us that chemical molecules produce errors in biological processes by binding to and inhibiting biological molecules such as enzymes, receptors, transport molecules etc. Chemical molecules having some functional groups or moieties SIMILAR to those of natural ligands can compete with the natural ligands in binding to the biological targets. When a chemical molecule succeed in this competition, the biological molecules get inhibited, and the interactions between biological molecules and their natural ligands are blocked. This is the molecular mechanism involved in disease processes. Drug molecules as well as various pathogenic molecules can inhibit the actions of biological molecules by this mechanism, which result in diverse kinds of pathological conditions.

CURE involves removal of pathological inhibitions happened in biological molecules. If the post-avogadro diluted drugs can cure disease conditions produced by their molecular forms , it means, they contain some supra-molecular structures that can bind to those molecules, deactivate them, and remove the molecular inhibitions they produced. In order to bind to the chemical molecules, these supra-molecular structures should have some conformational properties that are just opposite to the concerned chemical molecules.

Now our answer for the question “what are ACTIVE PRINCIPLES of post-avogadro potentized drugs” is very much near to us. We can say, the ACTIVE PRINCIPLES are some “supra-molecular structures formed in water-ethyl alcohol medium during the process of potentization, which can act as artificial binding sites for pathogenic molecules having some sort of opposite conformations”.

Next question we have to answer is, HOW these “supra-molecular structures” are formed during the process of potentization. This question could be answered only if we study the supramolecular properties of water-ethyl alcohol mixture, phenomena of hydrogen bonding, formation of host-guest complexes, cavitation and a lot of such things, and also the molecular processes involved in the technology of MOLECULAR IMPRINTING.


I am not “trying to change fundamental laws of homeopathy” as some of our homeopath friends accuse. I am only trying to “explain fundamentals” of homeopathy in terms of modern science , and to prove them using scientific method. If you take some time to go through my articles on this topic, you would realize that I have “explained” ‘similia similibus curentur’ and ‘potentization’ “as per ‘already proved’ modern science”. I am not proposing any “new theory” or trying to “change fundamental laws”.

Please note, so far there is no any ‘fundamental law’ or any hypothesis in homeopathy which anybody proved or could be proved “as per modern science”. Not even “explained” as per modern science”. But we teach, learn and practice those “unproved” ideas as “fundamental  laws” without any hesitation. You never asked anybody to “prove” those theories before accepting them. 

One friend even asked me to “show molecular imprints present in potentized drugs”, as if he understands molecular imprints as something that could be picked by a forceps and shown to him! Can anybody ‘show’ him supra-molecular formations of water? It should be by indirect methods and ‘understood’, not ‘seen’. Either they did not read what I have written, or failed to follow the concepts due to poor back ground knowledge in the scientific topics I have discussed to ‘prove’ molecular imprints concept. Or, it may be that they do not want to understand on reasons known only to them!

How can I convince you something, if you hesitate to read anything? I regularly post at least one article everyday explaining my concept of ‘molecular imprints’ and their implication in homeopathy. Without reading what I write, you ask me to “prove”! I once again request you to take some time to read at least some of those articles.

How can I prove my scientific concepts of homeopathy to somebody who does not know or is not willing to learn supra-molecular properties of water? How can I prove my concepts to somebody who does not know or is not willing to learn the subject matter of molecular imprinting technology? How can I prove my concepts to somebody who does not know or is not willing to learn the modern biochemistry and molecular biology? How can I prove my concepts to somebody who does not know or is not willing to learn advanced concepts of enzyme kinetics and molecular level pathology?

My request to those who ask for ‘proof for my concepts’ is, kindly update your basic knowledge in the topics I discuss. Then only you can follow these concepts. Then only I can ‘prove’ molecular imprints concepts to you. Once you acquire the background knowledge and then read my articles, you will see that everything I say is simple ‘proved’ science, and only very little remains to be ‘proved’.

If you go through my articles and try to understand the ideas I am proposing, you will realize that I have successfully explained   SIMILIA SIMILIBUS CURENTUR and POTENTIZATION in a way fitting very well to modern biochemistry, molecular pathology,  pharmacodynamics and supramolecular chemistry. Nobody even from scientific community can question my explanation of SIMILIA concept in terms of competitive relationship between similar molecules in binding to biological targets, and the phenomenon of “molecular mimicry” well explained in modern biochemistry. You should understand, my studies of POTENTIZATION as a tecnique of preparing molecular imprints has paved the way for hectic research activities in modern medicine to produce a whole range of target-specific MOLECULAR IMPRINTED DRUGS. It is undeniable that my explanations of MIASMS as “chronic disease dispositions produced by off-target inhibitions of biological molecules caused by antibodies generated against alien proteins and infectious agents” has raised the status of homeopathy to a new level. 

I would like to make it clear that I did not produce any ‘theories’ artificially. All my proposals on various aspects homeopathic practice are logical extensions evolved naturally from the fundamental concept of ‘molecular imprinting’ as the process involved in potentization. Once we accept ‘molecular imprints’ as the active principles of potentizaed drugs, and that they act therapeutically upon the organism by selectively binding to the pathogenic molecules, we cannot perceive or resolve these practical issues from another angle.

How can I ‘modify’ or distort logical and obvious scientific truths to satisfy your erstwhile habits, deep-rooted beliefs and long continued comfortable ways of practicing?

I can understand the discomfort brewing among ‘settled’ homeopaths when hearing my concepts that they fear would ‘change their ‘fundamentals’. “Coming out of comfort zones” is not an easy task, especially for ‘seniors’. It is very difficult to get exposed to a new knowledge environment, which would demand a fundamental re-thinking and modifying of many things they ‘believed’, learned, taught and practiced in their whole life. That would be a very uneasy situation, very hard to cope with.


Metabolic Syndrome has become a major lifestyle related health issue of modern man, probably due to stressful life, lack of exercise and changed food habits. 

Metabolic syndrome or MetS is a cluster of common abnormalities arising from persistent high levels of cortisol in the blood. This Syndrome includes hyperglycemia, abdominal obesity, reduced high-density lipoprotein cholesterol levels, and elevated triglyceride and blood pressure. The common characteristics of MetS and hypercortisolemic conditions such as Cushing’s syndrome suggest that the pathogenesis of MetS and central obesity might involve prolonged and excessive exposure to cortisol.

Metabolic Syndrome was originally described as “insulin resistance syndrome”.

 The components of Metabolic Syndrome are associated with endothelial dysfunction and atherosclerosis and increase the risk for type 2 diabetes mellitus as well as vascular morbidity and mortality. It is estimated that about one fourth of the world’s adult population has Metabolic Syndrome.

Metabolic Syndrome is diagnosed when three or more of the following parameters are present: waist circumference greater than 102 cm in men and greater than 88 cm in women, triglycerides of at least 150 mg/dl, HDL cholesterol less than 40 mg/dl in men and less than 50 mg/dl in women, blood pressure of at least 130/85 mm Hg, and fasting glucose of at least 110 mg/dL.

It is unclear whether a single primary abnormality triggers a cascade of diverse events that lead to the manifestation of the components of MetS. Because the diagnostic features of MetS are shared by Cushing’s syndrome (CS), which results from endogenous or exogenous hypercortisolism, it was proposed that cortisol contributes to the pathogenesis of both states although only mild hypercortisolism occurs in MetS in contrast with CS. It was also suggested that inhibiting cortisol action could provide a novel therapeutic approach for MetS. 

Indeed, preliminary data suggest that circulating cortisol concentrations are higher in patients with MetS compared with healthy subjects, both in basal conditions and during dynamic stimulation. This difference is more evident in patients with MetS and hypertension or impaired glucose tolerance. Furthermore, weight loss normalizes cortisol levels and improves insulin resistance. Despite the fact that cortisol levels are within the normal range, there is evidence of increased activity of cortisol in the periphery and dysregulation of the hypothalamic-pituitary-adrenal axis. 

Differences between CS and MetS also need to be emphasized; in CS, once the tumor is removed, symptoms improve; in the MetS, weight loss reverses both hypercortisolism and phenotypic abnormalities.

Cortisol appears to play a role in adiposity in Metabolic Syndrome. Elevated serum uric acid levels are shared by MetS and CS Syndome. Increased exposure to cortisol contributes to increased fat accumulation in visceral deposits of fat. Increased cortisol serum overnight levels are also associated with insulin resistance.

Some studies showed elevated cortisol levels in situations such as work stress and unemployment. Others reported that chronic life stress results in subtle hyperactivity of HPA axis leading to intraabdominal adiposity and development of Metabolic Syndrome. Patients with Metabolic Syndrome appear to have higher urinary excretion of cortisol metabolites compared with healthy subjects. In vitro, cortisol appears to increase lipoprotein lipase or fat-storing enzyme levels in adipose tissue and particularly in visceral fat.

Cortisol, also known as “stress hormone”, is a very important hormone produced mainly by the zona fasciculata of the adrenal cortex in the adrenal gland. It is produced in other tissues also in smaller quantities. It is released with a diurnal cycle and its release is increased in response to stress and low blood-glucose concentration. It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates. It also decreases bone formation.

In general, cortisol stimulates the synthesis of ‘new’ glucose from non-carbohydrate sources. This is known as gluconeogenesis, mainly in the liver, and also in the kidneys and small intestine under certain circumstances. The net effect of cortisol is an increase in the concentration of glucose in the blood, further complemented by a decrease in the sensitivity of peripheral tissue to insulin, thus preventing this tissue from taking the glucose from the blood. Moreover, cortisol has a permissive effect on the actions of hormones that increase glucose production, such as glucagon and adrenaline.

Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis, the breaking down of glycogen to glucose.

Elevated levels of cortisol, if prolonged, can lead to proteolysis or breakdown of proteins, and muscle wasting. The reason for proteolysis is to provide the relevant tissue with ‘building blocks’ for gluconeogenesis. The effects of cortisol on lipid metabolism are more complicated since lipogenesis is observed in patients with chronic, raised circulating cortisol levels, although an acute increase in circulating cortisol promotes lipolysis. The usual explanation to account for this apparent discrepancy is that the raised blood glucose concentration through the action of cortisol will stimulate insulin release. Insulin stimulates lipogenesis, so this is an indirect consequence of the raised cortisol concentration in the blood but it will only occur over a longer time scale.

Experimental studies with cortisol inhibitors further support the role cortisol in the pathogenesis of Metabolic Syndrome, and might provide novel therapeutic approaches in patients with metabolic syndrome or obesity.

The components of Metabolic Syndrome are associated with endothelial dysfunction and atherosclerosis, and increase the risk for type 2 diabetes mellitus as well as vascular morbidity and mortality.

It was also suggested that inhibiting cortisol action could provide a novel therapeutic approach for Metabolic Syndrome. Indeed, preliminary data suggest that circulating cortisol concentrations are higher in patients with Metabolic Syndrome compared with healthy subjects, both in basal conditions and during dynamic stimulation. It was also proved that
reduction of body weight normalizes cortisol levels and improves insulin resistance.

Emerging data suggest that patients with MetS show hyperactivity of the hypothalamic-pituitary-adrenal axis, which leads to a state of “functional hypercortisolism”. The cause for this activation of the HPA axis remains uncertain but may be associated with chronic stress, which is associated with increased circulating cortisol levels and greater responsiveness of the HPA axis. Increased exposure to cortisol contributes to increased fat accumulation in visceral depots. Increased enzyme activity in adipose tissue and liver might contribute to the development of several features of the MetS.

Central abdominal obesity is one of the main components of the MetS. Cortisol appears to play a role in adiposity in MetS. Increased urinary cortisone/cortisol ratio in women with increased abdominal fat compared with those with peripheral fat distribution was observed by researchers, suggesting an increase in the peripheral metabolism of cortisol. Interestingly, cortisol clearance seems to be inversely correlated with insulin sensitivity, and this correlation is independent of body fat. It is also well documented that glucocorticoids promote the differentiation and proliferation of human adipocytes and that their receptors are more abundant in visceral than in subcutaneous adipose tissue. They also redistribute adiposity from peripheral to central depots, increase the size and number of fat cells, and activate lipolysis and the release of free fatty acids into the circulation.

Increased cortisol levels are also associated with insulin resistance. Higher cortisol concentrations were related to a reduced insulin secretion.

Hypertension is one of the most distinguishing features of Metabolic Syndrome as well as hypercortisolism. Many studies reported an association between cortisol and systolic and diastolic BP levels. This correlation might be attributed to the effect of stress, which is associated with the activation of the HPA axis and sympathetic nervous system. Indeed, patients with Metabolic Syndrome and hypertension appear to have higher urine levels of both cortisol and catecholamine metabolites than healthy individuals. A possible mechanism by which cortisol elevate BP seems to be an increased responsiveness to vasoconstrictors along with a decreased vasodilator production.

Obesity , a common finding in both CS and MetS, is also associated with hypertension. The possible underlying mechanisms include volume expansion, increased cardiac output and systemic vascular resistance, increased sodium reabsorption, increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, high leptin levels and concurrent leptin resistance.

Patients with Metabolic Syndrome as well as hypercortisolism frequently have elevated blood glucose levels. In patients with MetS, serum cortisol levels are significantly associated with fasting glucose concentration. The relationship between fasting hyperglycemia and cortisol is due to the glucocorticoid effects on hepatic gluconeogenesis and insulin secretion.

Metabolic Syndrome is associated with endothelial dysfunction that significantly predisposes to an increased risk for cardiovascular diseases. Endothelial dysfunction is also observed in patients with hypercortisolism. Hypercoagulability of blood is also present in MetS. Indeed, elevated fibrinogen and homocysteine concentrations have been observed in MetS patients compared with healthy controls. Hyperfibrinogenemia and homocysteinemia seem to be independent risk factors for cardiovascular diseases and venous thrombosis.

Elevated serum uric acid levels are seen both in Metabolic Syndrome and Hypercortisolism. High uric acid levels are regarded as a predictor of cardiac and overall mortality in patients with cardiovascular diseases or stroke. Elevated uric acid is also associated with higher risk of stroke in patients with or without cardiovascular disease. It was demonstrated that statin atorvastatin therapy is associated with a reduction in uric acid levels, along with an increase in estimated glomerular filtration rate in CKD patients with MetS. This effect on renal function is perhaps due to an amelioration of endothelial function and renal blood flow. 

Adipose tissue is recognized as an important endocrine organ that secretes a variety of bioactive peptides, termed adipokines. These adipokines exert multiple effects and play a key role in glucose and lipid metabolism, insulin sensitivity, BP, and angiogenesis. The major components of this family of adipokines are adiponectin and leptin, which are mainly produced by adipose tissue. Both these proteins exert an insulin-sensitizing effect through fatty-acid oxidation and, in addition, adiponectin is associated with antiatherogenic, antidiabetic, and antiinflammatory properties. In obesity, insulin resistance has been linked to leptin resistance, elevated leptin, and low adiponectin levels, which are associated with higher cardiovascular risk. Resistin is expressed in abdominal fat and is also associated with increased risk of central obesity-related diabetes. However, resistin may not be an “adipokine” because in humans it is mainly produced by monocytes, and its link with central obesity is debated. Excess adiposity leads to dysregulation of adipokine production, which in turn promotes a state of low-level systemic chronic inflammation predisposing to atherosclerosis.

According to MIT approach, since molecular imprints of cortisol can act as artificial binding pockets for cortisol, it can antidote the adverse biological effects of excess cortisol circulated in the body. 

Homeopathic drug CORTISOL 30 contains Molecular imprints of the hormone cortisol. CORTISOL 30 is a great remedy for many ailments that are associated with Metabolic Syndrome. As such, cortisol 30 will be a powerful ingredient of Homeopathic Prescriptions in the management of all complaints associated with Metabolic Syndrome. Incorporation of PITUTRINUM 30 as well as common anti-stress homeopathy remedies such as Arg Nit 30, Gesls 30, Adrenalin 30 also produces beneficial effects in reducing the bad effects of stress and increased cortisol levels, and thereby preventing and curing Metabolic Syndrome and the health risks arising from its complications.


According to MIT explanations of homeopathy. SIMILIMUM means a drug substance that can provide all the molecular imprints required to remove all the pathological molecular inhibitions underlying a disease existing in a patient. SIMILIA SIMILIBUS is only a practical way of identifying such a drug substance by observing the symptoms in a patient, and comparing them with the symptoms drug substances are known to have produced earlier in healthy idividuals. This therapeutic technique is actually based on the knowledge that chemical molecules having similar conformations can bind to similar molecular targets, produce similar molecular inhibitions, that are expressed through similar symptoms.

This scientific understanding will obviously lead homeopathy to a shift from symptom based prescriptions to molecular pathology based prescritions. The more we understand the molecular pathology of disease conditions as well as the details of ligands and targets involved in each pathological molecular inhibitions, and the more we study the molecular constitution of drug substances we use, the more we will be able to make perfect homeopathy prescriptions on the basis of that knowledge, and the more we can avoid symptom based approach.

The more we know about the molecular pathology of each disease, and the more we know the molecular constitutions of drug substances, the more homeopathy will shift away from “similarity of symptoms” to “conformational similarity of pathogenic molecules and drug molecules”.

Let us try to demonstrate this idea using the knowledge regarding molecular pathology of HYPERTENSION. Renin or angiotensinogenase, is the key enzyme produced in kidneys that modulates body’s renin-angiotensin-aldosterone system (RAAS) that mediates volume of extracellular fluids such as blood plasma, lymph and interstitial fluid, as well as arterial vasoconstriction. Thus, RENIN regulates the body’s mean arterial blood pressure.

The enzyme renin is secreted by the kidneys from specialized cells called granular cells of the juxtaglomerular apparatus in response to stimuli such as decrease in arterial blood pressure or decrease in blood volume detected by pressure-sensitive cells known as baroceptors, a decrease in sodium chloride levels in the ultrafiltrate of the nephrons, or sympathetic nervous system activity, acting through the beta1 adrenergic receptors.

The renin enzyme produced in kidneys circulates in the blood stream and breaks down angiotensinogen secreted from the liver into angiotensin I.

Angiotensin I is further converted in the lungs by angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II is a very potent constrictor of all blood vessels. It acts on the smooth muscle and, therefore, raises the resistance posed by these arteries to the heart. The heart, trying to overcome this increase in its ‘load’, works more vigorously, causing the blood pressure to rise. This is the essential dynamics involved in rise of blood pressure.

Angiotensin II also acts on the adrenal glands and releases Aldosterone, which stimulates the epithelial cells in the nephrotic tubules and collecting ducts of the kidneys to increase re-absorption of sodium and water, leading to raised blood volume and raised blood pressure.

Aldosterone also acts on the CNS to increase water intake by stimulating thirst, as well as conserving blood volume, by reducing urinary loss through the secretion of Vasopressin from the posterior pituitary gland, resulting in increased blood pressure.

In normal physiological conditions, once the reduced blood pressure is raised to the adequate level, production of RENIN in kidneys is stopped by a NEGATIVE FEEDBACK mechanism, where angiotensin II act upon the special ‘angiotensin II receptors’ on the cell membranes of juxtaglomerular apparatus of kidneys. By this process, level of RENIN in blood stream is maintained with in limits, thereby preventing hypertension. 

Same way, production of catecholamines such as adrenalin which also plays a role in inducing production of RENIN and maintaining blood pressure high, is stopped by negative feedback action of adrenalin upon adrenogenic receptors on cells of adrenal cortex.

A pathological state of RENIN-ANGIOTENSIN AXIS happens once the NEGATIVE FEED BACK mechanism controlling the production of RENIN is disturbed by inhibition of angiotensin II receptors and adrenergic receptors involved in FEEDBACK process. Such inhibitions may be caused by binding of some pathogenic molecules of exogenous or endogenous origin, having functional groups similar to angiotensin II or adrenalin, so that they can competitively bind to the receptors. This leads to elevated state of RENIN in the circulation, resulting in ESSENTIAL HYPERTENSION.

Modern allopathic drugs are targeted either to block the conversion of angiotensin I into angiotensin II by inhibiting the angiotensin converting enzymes, or blocking the angiotensin II receptors using potent drug molecules. Since such molecular inhibitions may necessarily lead to molecular errors in different essential biochemical pathways, modern antihypertension drugs are prone to produce harmful side effects.

According to MIT concepts, maintaining the plasma level of RENIN by controlling its production by facilitating unhindered NEGATIVE FEED BACK mechanism is the ideal way of treating hypertension without any harmful side effects. Inhibition of FEEDBACK mechanism should be removed by using MOLECULAR IMPRINTS of angiotensin II, adrenalin, or drug molecules having similar functional groups. Various drug substances such as RAUWOLFIA contains a number of bioactive chemicals like ajmaline, aricine, corynanthine, deserpidine lankanescine rauwolscine, rescinnamine, reserpine, reserpiline, isoreserpine, isoreserpiline, serpentinine, and yohimbine, which can inhibit the angiotensin and adrenogenic receptors. As such, POTENTIZED FORMS of such drugs will contain MOLECULAR IMPRINTS that can act as artificial binding sites for binding to the endogenous and exogenous pathogenic molecules which are the causative factors of HYPERTENSION.

According to MIT approach, potentized or MOLECULAR IMPRINT forms of ANGIOTENSIN II, ADRENALIN, CATECHOLAMINES and various DRUG SUBSTANCES that can produce hypertension in crude form will be ideal drugs for treating hypertension without any side effects.


One of the most difficult questions related with scientific understanding of homeopathy was , how the medicinal properties of a drug substance could be transmitted and preserved into a medium without any drug molecule remaining in it. This cardinal question could be rationally answered once it was realised that homeopathic potentization involves a process of MOLECULAR IMPRINTING in water-ethanol azeotropic supramolecular matrix, and that MOLECULAR IMPRINTS of drug molecules are the active principles of post-avogadro diluted homeopathic drugs.

As per this scientific explanation, conformational details of drug molecules or template molecules are imprinted into the water-alcohol medium in the form of three dimensional nanocavities during the pricess of serial dilution and agitation involved in homeopathic potentization. By their conformational properties, these molecular imprints can act as artificial binding sites for pathogenic molecules that are similar to the template molecules, thereby deactivating pathogenic molecules and removing the molecular inhibitions they produced in the living system. Similia Similibus Curentur, the fundamental principle of homeopathy , could be satisfactorily explained by this biological mechanism, which fits very well to the advanced knowledge of biochemistry and pharmacodynamics.

In order to evolve this scientific explanation for potentization as well as similia similibus curentur, we had to delve deep into diverse areas of knowledge such as supramolecular chemistry of water and ethyl alcohol, polymer structure of water, hydrogen bonding, azeotropism, host-guest molecular interactions, cavitation, molecular imprinting in polymers, etc etc.

A mixture of water and ethyl alcohol in an approximate ratio of 10:90 is used as the medium for homeopathic potentization. According to some references, “pure distilled spirit” could also be used for this purpose, but all of us know, what is called “pure distilled spirit” actually contains 5% water and 95% ethanol, since it is impossible to separate water and ethanol beyond that level by fractional distillation, due to a peculiar phenomenon known as AZEOTROPISM. Studying the molecular level mechanism underlying the phenomenon of azeotropism is essential for understanding how molecular imprinting happens during homeopathic potentization.

In chemistry, AZEOTROPE is a mixture of liquids that has a constant boiling point, because the vapour has the same composition as the liquid mixture. The boiling point of an azeotropic mixture may be higher or lower than that of any of its components. The components of azeotropic mixtures of liquids cannot be separated by simple distillation.

An azeotropic mixture is a mixture of substances that has the same concentration at vapour and fluid phases. It is basically a mixture that contains two or more liquids. Azeotropic mixture basically has constant or the same boiling points and the mixtures’ vapour will also have the same composition as the liquid. Normally, we use distillation to isolate materials as the ideal solutions with one part normally more volatile than the other. However, in an azeotropic mixture, since the vapour and fluid concentrations will be the same this approach will prevent their separation.

Boiling a 95% solution of ethanol in water will produce a 95% ethanol vapour. It is not possible to obtain higher ethanol concentrations even by repeated distillations. Alcohol and water are miscible in any ratio, making it possible to combine any quantity of ethanol with any quantity of water to produce a homogeneous solution that could be separated by fractional distillation, but there will finally remain an azeotrope part in it containing 95% ethanol and 5% water that could not be separated by distllation.

I have been searching for a more biofriendly as well as stable substance that could be used as an ideal imprinting medium for preparing molecular imprinted drugs.

In an azeotropic mixture of two liquids, concentration of molecules will be such that each molecule of both compound will be strongly bound to each molecule of other compound, thereby restricting their freedom of movements. This mutual binding of molecules is retained even when they go to vapour phase. This is the reason why two liquids with different boiling points evaporate at a constant boiling point in azeotropic ratio. This unbreakable binding between molecules of constituent liquids in azeotropic mixture imparts peculiar physical and chemical properties to it.

Actually, it is this peculiar AZEOTROPIC properties that make water-ethanol mixture an ideal medium for homeopathic potentization and molecular imprinting. Even though pure water is a dynamic branched polymer, molecular imprints formed in it will be very transient and unstable due to the free movements of water molecules and the protonation-deprotonation process constantly taking place. But when ethanol is added to water in an azeotropic ratio, due to their mutual molecular binding, movements of molecules get restricted and protonation-deprotonation process reduced. Due to this mechanism, molecular imprints formed in an azeotropic mixture of alcohol and water remain stable and long standing. This phenomenon explains the importance of using water-ethanol mixture in a particular ratio as the medium for homeopathic potentization.

It is obvious that molecular imprints are actually formed by formation of hydrogen bonded networks of water molecules aroung drug molecules used as templates. It means, only the 5% water contained in the medium actually undergoes molecular imprining, and the remaining 90% alcohol plays only a preservative effects by stabilizing the molecular imprints formed in water. It means, potentized homeopathic drugs contain only 5% as their active principles. When we take 100 ml of potentized drug, only 5 ml of it actually carries molecular imprints. This is an important draw back of using water-ethanol mixture as potentizing medium, which also indicates the need for developing better alternatives.

Water-ethanol azeotropic mixture boils at 78.2 °C, even though boiling point of water is 100 degrees and that of ethanol is 78.4 degrees. It means potentized homeopathic drugs will evaporate in atmospheric temperature much easier than water or ethanol. It is a major problem encountered in homeopathy pharmacy.

I have been searching for long to find out an alternative imprinting medium for preparing molecular imprinted drugs and homeopathic potentization, that is more stable and more biofriendly than water-ethanol mixture.

After a lot of studies and research on this topic, an AZEOTROPIC mixture of water and propionic acid in the ratio 82.3: 17.7 is finally found to be a comparatively much better candidate as an ideal imprinting medium for preparing MOLECULAR IMPRINTED DRUGS, instead of water-ethanol azeotropic mixture conventionally used in homeopathic POTENTIZATION.

Propionic acid can hold much water than ethanol in an azeotropic mixture, it is a simple native fatty acid being a universal part of metabolic processes in living systems, it is hundred percent non toxic, and far much safer than ethanol.

PROPIONIC ACID is a simple fatty acid with chemical formula CH3CH2CO2H, belonging to the chemical group known as carboxylic acids. It is also known by different names, such as propanoic acid, ethylformic acid, methyacetic acid, carboxyethane, ethanecarboxylic acid, pseudoacetic acid, metacetonic acid etc.

Molecular mass of propionic acid is 74.079. It forms azeotropic mixture with water at a ratio 82.3 % water and 17.7% propionic acid. Boiling point of water-propionic acid azeotrope is 99.98 degree celsius, whereas boiling point of propionic acid is 141.1 degree celsius and boiling point of water is 100 degrees. As such, water-propionic acid azeotropic mixture cannot be separated by fractional distillation. Propionic acid consists of hydrogen bonded pairs of molecules in both the liquid and the vapor.

Propionic acid is a naturally occurring carboxylic acid with chemical formula CH3CH2CO2H. It is a liquid with a pungent and unpleasant smell somewhat resembling body odor.

Propionic acid has physical properties intermediate between those of the smaller carboxylic acids, formic and acetic acids, and the larger fatty acids. It is fairly miscible with water. As with acetic and formic acids, it consists of hydrogen bonded pairs of molecules in both the liquid and the vapor forms.

Propionic acid is a natural part of various biological processes and pathways. Propionic acid is produced biologically as its coenzyme A ester, propionyl-CoA, from the metabolicbreakdown of fatty acids containing odd numbers of carbonatoms, and also from the breakdown of some amino acids. The metabolism of propionic acid begins with its conversion to propionyl coenzyme A, the usual first step in the metabolism of carboxylic acids. Since propionic acid has three carbons, propionyl-CoA cannot directly enter either beta oxidationor the citric acid cycles. In most vertebrates, propionyl-CoA is carboxylated to D-methylmalonyl-CoA, which is isomerisedto L-methylmalonyl-CoA. A vitamin B12-dependent enzyme catalyzes rearrangement of L-methylmalonyl-CoA to succinyl-CoA, which is an intermediate of the citric acid cycle and can be readily incorporated there.
Propionic acid serves as a substrate for hepaticgluconeogenesis via conversion to succinyl-CoA.

Some propionic acid is used widely as a preservative for both animal feed and food for human consumption. Another major application is as a preservative in baked goods. As a food additive, it is approved for use in the EU, USA, Australia and New Zealand.

Designated as generally regarded as safe by the US Food and Drug Administration, propionic acid has shown little toxicity in humans and other organisms.

In the human body, however, propionic acid is generally metabolized with little ill effect and ultimately becomes a chemical intermediate in the citric acid cycle.

Some propionic acid is oxidized to lactic acid during absorption, but most passes to the liver, which removes nearly all of it from the portal blood. Propionic acid represents 20-25% of absorbed volatile fatty acids. Propionic acid is rapidly absorbed through the gastrointestinal tract.

Most absorbed propionic acid is passed to the liver, which removes nearly all of it from the portal blood.

As a compound that is typically found naturally in the body, little to no adverse cumulative health effects have been associated with exposure to propionic acid.

Designated as generally regarded as safe by the US Food and Drug Administration, propionic acid has shown little toxicity in humans and other organisms.

There are no known birth defects associated with the use of propionic acid in animals or humans.


I would request the authorities at CCRH to conduct studies regarding my proposal to use 18% azeotropic solution of propionic acid in water as a better alternative to alcohol water mixture as homeopathic imprinting medium. Since water-propionic acid azeotropic mixture contain 82% water, the resulting homeopathic products will contain very high percentage of active principles or molecular imprints, which is a big advantage over water-ethanol mixture which contain only 5% molecular imprints.

Chandran Nambiar KC