Tag: ligand

‘Drug Proving With High Potency Drugs’- A ‘Belief’ Never Verified By Well-Organised Experiments

Homeopaths have many deep-rooted ‘beliefs’- most of them very irrational and unscientific. But I am sure, they cannot be convinced by talking logic or science that goes against such beliefs.

Homeopaths ‘believe’ that ‘highly potentized’ drugs can produce symptoms, and can be used for ‘drug proving’. They believe it is dangerous to use potentized drugs without indications.

One homeopath claimed: “I once took a dose of medhorrinum 1M, because I really wanted to know more about Homeopathy, and I got a date of symptoms for some time (a month or less), most corresponded well to the set of symptoms described in materia medica for medhorrinum… So you say that high dilutions is not good for experimentations…. I think it is not correct…”

Pure rubbish. If he wanted to “know more about homeopathy”, this is not the way he should do experiments. Taking oneself ‘single dose’ of a drug and waiting for ‘its symptoms’ to appear! And he got symptoms of that drug for one month! And he considers he has ‘proved’ that “high dilutions are good for experimentation” beyond any doubt!

If he really wanted to ‘prove’ that potentized drugs can produce symptoms, he should conduct the experiments according to scientific method. Person who is subjected to experiment should not know which medicine he is taking. Person conducting the experiment should not know which drug is given to which individual. There should be enough controls also. Then we should try to identify the drugs from comparing the symptoms produced with symptoms in materia medica. Only when we succeed in identifying drugs from symptoms in such a well controlled blinded experiment, we can say we ‘proved’ that high potency drugs could produce symptoms.

Taking a dose of ‘known’ drug oneself, waiting for its symptoms for one month, and ascribing all symptoms you produced during one month to that single drug- it is a joke. After taking that ‘single dose’, he will be ‘taking’ diverse types of exogenous molecules into your body- through food, water, drinks, air and many many other environmental factors. All those molecules can produce symptoms in him. How can he say all symptoms produced for one month ‘after’ a ‘single dose of medorrhinum 1m’ were due that ‘single dose’?

Only homeopaths, blinded by ‘beliefs’ can make such claims. For them, everything that happens ‘after’ their dose is the ‘effect’ of that dose! They never bother to consider the variables involved! I know it is a waste of time arguing to convince them. They cannot be convinced by logic or science. They are ‘believers’.

Homeopathic drugs potentized above avogadro limit (12c) contain only ‘molecular imprints’. Molecular imprints are supramolecular nanostructures formed by hydrogen bonding of ethyl alcohol-water molecules, into which the 3-dimensional configuration of drug molecules are imprinted as nano-cavities. These nano-cavities can act as artificial binding sites for endogenous or exogenous molecules having configurational similarity to the molecules used for imprinting. We can say, molecular imprints are ‘artificial key-holes’ for pathogenic molecular keys.

Biochemical processes involves two aspects: 1.Binding of ligands to targets, which is determined by configurational affinity.2. Chemical transformation, which is determined by charge affinity of ligands and targets. Since ‘molecular imprints’ have only ‘configurational affinity’, without any ‘charge affinity’ towards biological molecules, potentized drugs cannot interfere in normal biological processes.

Molecular imprints contained in the potentized homeopathic preparations bind to ligands or biological molecules merely due to their complementary cofigurations without any charge affinity, whereas natural ligands bind to their biological target molecules in capacity of their appropriate spacial configurations as well as charge affinities. So, the bindings of molecular imprints with biological molecules or their ligands will be very temporary and cannot stay long. Such bindings of molecular imprints cannot replace the natural ligand-target interactions happening as part of vital processes. Molecular imprints can not compete with natural ligands in binding to their natural biological targets. Hence it is obvious that potentized homeopathic preparations cannot interfere in biological ‘ligand-target’ processes such as ‘substrate-enzyme’, ‘antigens-antibodies’, ‘signal-receptor’ etc. As such, chances of potentized homeopathic medicines acting as pathological agents are very rare even if used indiscriminately. Molecular imprints can interfere only in interactions between pathogenic molecules and biological molecules, as well as off-target bindings of ligands with biological molecules, where only configurational affinity is involved. Obviously, molecular imprints can act upon only the molecular blocks created by exogenous or endogenous foreign pathological molecules.

Molecular imprints contained in the potentized homeopathic preparations cannot successfully compete with natural ligands in binding with their biological target molecules, and hence, cannot interfere in the interactions between biological molecules and their natural ligands. Obviously, potentized drugs cannot produce any pathological molecular inhibitions in the organism or produce symptoms.

According to scientific view, ‘Similia Similibus Curentur’ means: ‘diseases caused by specific molecular inhibitions and expressed through specific groups of subjective and objective symptoms can be cured by potentized forms of drugs that could create similar pathologic molecular inhibitions and symptoms in healthy individuals if applied in crude form’. Same can be stated in a different way as: “pathological molecular inhibitions can be rectified using ‘molecular imprints’ of drug molecules that can create similar molecular inhibitions if applied in molecular form”.

Homeopathy utilizes ‘drug proving’ for studying the pathogenic properties of drug substances by observing their capacity to produce various pathological symptoms in healthy organisms. Homeopathy is based on the principle that a substance becomes a medicinal agent only because it has some disease-producing properties. In other words, if we could know what pathological inhibitions and symptoms a drug can create in healthy organism, we can decide in what disease states that drug could be used as a therapeutic agent in potentized form. Drug proving is unique to homeopathy. Whereas modern medicine studies the disease-curing properties of drugs, homeopathy studies the disease-producing properties of drugs. That makes a great difference.

Drug proving is done by administering small quantities of a particular drug to controlled volunteer groups of apparently healthy individuals. The subjective and objective symptoms, representing the diverse molecular deviations caused in the organism by the drug substance are carefully observed and recorded. These symptoms are systematically arranged compiled as materia medica of the substance used.

Let us examine what actually happens at molecular level during drug proving:

First point we have to note is that most drug substances, especially of vegetable or animal origin, are not ‘simple’ substance. Even if we use them as a ‘single’ substance, actually they consist of diverse types of individual molecules. A substance can interact with biological molecules only as individual molecules. If we really want to understand homeopathy and drug proving scientifically, we should first of all learn to perceive drug substance in terms of its diverse constituent molecules. Once we introduce a sample of drug substance into the living organism for ‘proving’, its constituent molecules are instantly subjected to various processes such as disintegration, ionization, hydration and certain chemical transformations.
Individual constituent molecules are carried and conveyed through blood and other internal transport systems into the cells and body fluids in different parts of the body. They can interact with various enzymes, receptors, and other biological molecules inside the organism. Individual drug molecules, in capacities of their molecular affinities, get themselves bound to various bio-molecules which participate in the essential biochemical activities in the organism. These interactions are decided and directed by the specific properties such as configurations and charges of active groups of individual drug molecules, and their specific affinity towards biological target molecules.

The three dimensional structure of the individual drug molecules, and that of the concerned bio-molecules are the decisive factors in this process of formation of molecular binding between them. This peculiarity is called molecular affinity. It is very important to note that drug substances interact with different biological molecules, not as a singular entity, but as individual constituent molecules and ions. These individual drug molecules and ions are capable of competing with natural ligands and substrates in binding to their biological targets, thereby inhibiting the essential bio-chemical processes which can take place only with their presence and mediation. Such molecular inhibitions in various bio-chemical pathways result in a condition of pathology, expressed in the form of a train of subjective and objective symptoms, due to the involvement of various neuro-mediator, neuro-transmitter and cellular signalling systems.

From this point of view, drug proving has to be done using molecular forms of drugs, since only they can produce real pathological molecular inhibitions in the organism.

Let us examine what actually happens when potentized drugs are administered into ‘apparently’ healthy individual individuals for drug proving. First point we need to remember is that ‘apparently’ healthy people will not be totally free from pathological molecular inhibitions. There will be diverse types of hidden molecular errors existing in them, arising from diverse types of factors such as nutritional, environmental, miasmatic, genetic, emotional, metabolic, infectious and others. When potentized drugs are introduced into the body, some or other molecular imprints contained in them may act upon these existing molecular inhibitions, which may be reflected as some transient symptoms. Actually, those symptoms are not indicating the ‘disease producing’ properties, but ‘diseases curing’ properties of concerned drugs. As such, symptoms obtained from drug proving using high potencies may confuse our materia medica.

Potentized drugs may act on ‘healthy’ organism by a different mechanism. Molecular imprints may bind to the natural ligands in the body, if they have any configurational affinity. But, such bindings will not lead to a state of pathology since molecular imprints cannot interfere in the interaction between natural ligands and targets which will have stronger affinity to each other. As such, symptoms appearing from such interactions will be very much temporary, and cannot be considered ‘pathological symptoms’.

Drugs potentized above 12c cannot cause pathological molecular inhibitions or produce symptoms. As such ‘drug proving’ with ‘high potencies’ is only a myth- ab false belief that is deep-rooted in the minds of homeopaths.

Confusions Created By Proponents Of Energy Medicine Over The Concept Of ‘Molecular Imprints’

The term ‘molecular imprints’ is now almost hijacked by the proponents of all diverse shades of unscientific ‘energy medicine’ and ‘spiritual’ theories about homeopathy. It makes distinguishing between scientific and unscientific approaches very hard.

The term ‘molecular imprinting’ and ‘molecular imprints’ originally comes from polymer chemistry, where these terms are used to describe a technique of creating template-shaped cavities in polymer matrices with memory of the template molecules, to be used as artificial molecular recognition sites.

This technique is based on the system used by enzymes for substrate recognition, which is called the “lock and key” model. The active binding site of an enzyme has a unique geometric structure that is particularly suitable for a substrate. A substrate that has a corresponding shape to the site is recognized by selectively binding to the enzyme, while an incorrectly shaped molecule that does not fit the binding site is not recognized.

In a similar way, molecularly imprinted materials are prepared using a template molecule and functional monomers that assemble around the template and subsequently get crosslinked to each other. The functional monomers, which are self-assembled around the template molecule by interaction between functional groups on both the template and monomers, are polymerized to form an imprinted matrix. They are known in the scientific community as a molecular imprinted polymer (MIP). Then the template molecule is removed from the matrix under certain conditions, leaving behind a cavity compl ementary in size and shape to the template. The obtained cavity can work as a selective binding site for a specific template molecule.

I have been using the concepts of ‘molecular imprinting’ and ‘molecular imprints’ to explain homeopathic potentization in this scientific perspective. My contention is that water has polymer-like properties at supramolecular level, and as such, water can be used as molecular imprinting medium exactly similar to other polymer substances. During potentization, three dimensional configuration of drug molecules are imprinted as nanocavities into the hydrogen-bonded supra-molecular networks of ethyl alcohol-water matrix. These ‘molecular imprints’ or ‘hydrosomes’ can act as ‘artificial binding sites’ for the drug molecules used for imprinting, as well as to pathogenic molecules having similar configurations. Active principles of potentized drugs are these ‘molecular imprints’.

This is the scientific understanding of ‘molecular imprinting’ and ‘molecular imprints’.

Now, the proponents of ‘energy medicine’ theories are trying to hijack this scientific concept to promote their pseudo-scientific theories. They talk about ‘molecular imprints’ of ‘drug energy’ and even ‘spiritual energy’. They talk about ‘molecular imprinting’ of ‘thoughts’ into water. According to them, ‘molecular imprints’ act by ‘emitting’ ‘radiations’, ‘waves’, ‘resonance’ and such things. They mix up ‘molecular imprinting’ with ‘water memory’ theories of people like Emotto, Chaplin and Rustum Roy. Their theories have nothing in common with the scientific concepts of ‘molecular imprinting’.

Anyhow, these people create a lot of confusions during our discussions about scientific homeopathy. To avoid confusions, now I prefer to use the term ‘hydrosomes’ instead of ‘molecular imprints’, to indicate ‘molecular imprinted nanocavities of water acting as artificial molecular binding sites’.

Modern biochemistry explains molecular mechanisms of disease and cure in terms of ‘key-lock’ relationship between ligands and their target molecules. This ‘key-lock’ concept has been proved right by the preparation and use of target specific designer drugs. Any scientific explanation we provide for molecular mechanism of homeopathic therapeutics involved in ‘similia similibus curentur’ should be fitting to this ‘key-lock’ concept of molecular interactions. My explanation of of homeopathy on the basis of ‘molecular imprints’ or ‘hydrosomes’ acting as ‘artificial binding sites for pathogenic molecules’ perfectly meets this fundamental condition.

Similarity Of ‘Functional Groups’ Of Drug Molecules And Pathogenic Molecules Determines ‘Similimum”

To understand the real science behind the phenomena of ‘similia similibus curentur’, ‘drug proving’ and ‘potntization’, we should study drug substances in terms of not only their ‘constituent molecules’, but in terms of ‘functional groups’ and ‘moieties’ of those drug molecules. A drug substance is composed of diverse types of drug molecules. A drug molecule interacts with ‘active groups’ of biological target molecules such as enzymes and receptors using their ‘functional groups’ or ‘moieties’. It is the ‘functional groups’ and ‘moieties’ on the individual drug molecules that decide to which biological molecules they can bind to and produce molecular inhibitions. Different drug molecules with different size and structures, but having same ‘functional group’ or ‘moiety’ can bind to same biological molecules and produce similar molecular errors and similar groups of symptoms. A drug molecule become similimum to a disease when the drug molecule and disease-producing molecule have same functional groups, so that they could bind to same biological targets producing same molecular errors and same symptom groups.

Drug molecules act upon the biological molecules in the organism by binding their ‘functional groups’ to the active groups on the complex biological molecules such as receptors and enzymes. These molecular interactions are determined by the affinity between functional groups or moieties of drug molecules and active sites of biological molecules. Here, the functional groups of drug molecules are called ‘ligands’, and the biological molecules are called ‘targets’. Ligand-target interaction is  determined by a peculiar ‘key-lock’ relationship due to complementary configurational affinities.

It is to be specifically noted that same functional group will undergo the same or similar chemical reactions regardless of the size or configuration of of the molecule it is a part of. However, its relative reactivity can be modified by nearby functional groups known as facilitating groups. That means, different types of drug molecules or pathogenic molecules having same functional groups and facilitating groups can bind to same biological molecules, and produce similar molecular inhibitions and symptoms. Homeopathic principle of ‘similimum’ is well explained by this understanding. If a drug molecule can produce symptoms similar to symptoms of a particular disease, it means that the drug molecules and disease-causing molecules have same functional groups on them, by which they bind to same biological molecules. Obviously, similarity of symptoms means similarity of functional groups of pathogenic molecules and drug molecules. To be similimum, the whole molecules need not be similar, but similarity of functional groups is enough.

Potentized drugs would contain the molecular imprints of drug molecules, along with molecular imprints of their functional groups. These molecular imprints will have specific configurational affinity towards any molecule having same functional groups, and can bind and deactivate them.

According to the scientific definition proposed by Dialectical Homeopathy, ‘Similia Similibus Curentur’ means:

“If a drug substance in crude form is capable of producing certain groups of symptoms in a healthy human organism, that drug substance in potentized form can cure diseases having similar symptoms”.

Potentization is explained in terms of molecular imprinting. As per this concept, potentized drugs contains diverse types of molecular imprints representing diverse types of constituent molecules contained in the drug substances used for potentization.

In other words, “potentized drugs can cure diseases having symptoms similar to those produced by that drug in healthy organism if applied in crude forms”.

Homeopathy is based on the therapeutic principle of ‘similia similibus curentur’, which scientifically means “endogenous or exogenous pathogenic molecules that cause diseases by binding to the biological molecules can be entrapped and removed using molecular imprints of drug molecules which in molecular form can bind to the same biological molecules, utilizing the complementary configurational affinity between molecular imprints and pathogenic molecules”.

So far, we understood ‘Similia Similibus Curentur’ as ‘similarity of symptoms produced by drugs as well as diseases’. According to modern scientific understanding, we can explain it as ‘similarity of molecular errors produced by drug molecules and pathogenic molecules’ in the organism.

To be more exact, that means ‘similarity of molecular configurations of pathogenic molecules and drug molecules’. Potentized drugs contains ‘molecular imprints’ of constituent molecules of drug used for potentization. ‘Molecular imprints’ are three-dimensional negatives of molecules, and hence they would have a peculiar affinity towards those molecules, due to their complementary configuration. ‘Molecular imprints’ would show this complementary affinity not only towards the molecules used for imprinting, but also towards all molecules that have configurations similar to those molecules. Homeopathy utilizes this phenomenon, and uses molecular imprints of drug molecules to bind and entrap pathogenic molecules having configurations similar to them. Similarity of configurations of drug molecules and pathogenic molecules are identified by evaluating the ‘similarity of symptoms’ they produce in organism during drug proving and disease. This realization is the the basis of scientific understanding of homeopathy I propose.

To be ‘similar’ does not mean pathological molecule and drug molecules should  be similar in their ‘whole’ molecular structure. To bind to same targets, similarity of ‘functional groups’ or even a ‘moeity’ is enough. If the adjacent groups that facilitate binding with targets are also same, similarity becomes more perfect. If a drug molecule could produce symptoms similar to a disease, that means the drug molecules contains some functional groups simialr to those of pathogenic molecules that caused the disease. By virtue of these similar functional groups, both pathogenic molecules and drug molecules could bind to same biological targets, producing similar molecular errors and symptoms in the organism.

Molecular imprints of similar functional groups will also be similar. As such, potentized forms of a drug substance can bind and deactivate the pathogenic molecules having similar functional groups. This is the real molecular mechanism of ‘similia similibus curentur’.

Except those substances of simple chemical formula belonging to mineral groups, most of the pathogenic agents as well as drug substances consist of complex organic molecules. In the study of chemical interactions involving these organic molecules, understanding the concept of ‘functional groups’ is very important.  ‘Functional groups’ are specific groups of atoms within large organic molecules that are responsible for their characteristic chemical reactions.  Different organic molecules having same functional group will undergo the same or similar chemical reactions regardless of the size of the molecule it is a part of.  However, its relative reactivity can be modified or influenced to an extent by nearby functional groups.

Even though the word moiety is often used synonymously to “functional group”, according to the IUPAC definition,a moiety is a part of a molecule that may include either whole functional groups or a parts of functional groups as substructures.

The atoms of functional groups are linked to each other and to the rest of the molecule by covalent bonds. When the group of covalently bound atoms bears a net charge, the group is referred to more properly as a polyatomic ion or a complex ion. Any subgroup of atoms of a compound also may be called a radical, and if a covalent bond is broken homolytically, the resulting fragment radicals are referred as free radicals.

Organic reactions are facilitated and controlled by the functional groups of the reactants.

A ‘moeity’ represents discrete non-bonded components. Thus, Na2SO4 would contain 3 moieties (2 Na+ and one SO42-). A “chemical formula moiety” is defined as “formula with each discrete bonded residue or ion shown as a separate moiety”.

We should learn different types of ‘functional groups’ and ‘moieties’ of constituent molecules of our drug substances, as well as diverse types of pathogenic molecules. We have to study our materia medica from this viewpoint, comparing symptoms of different drug molecules having same functional moieties.  Then we can logically  explain the phenomenon of ‘drug relationships’. We can explain the similarity of drugs belonging to different groups such as ‘calcarea’, ‘merc’, ‘kali’, ‘acid’, ‘sulph’, ‘mur’ etc. Such an approach will make our understanding of homeopathy more scientific and accurate.

Learn ‘Functional Groups’ from Wikipedia:

The following is a list of common functional groups. In the formulas, the symbols R and R’ usually denote an attached hydrogen, or a hydrocarbon side chain of any length, but may sometimes refer to any group of atoms.

Functional Groups containing Hydrocarbons

Functional groups, called hydrocarbyls, that contain only carbon and hydrogen, but vary in the number and order of π bonds. Each one differs in type (and scope) of reactivity.

Chemical class

Group

Formula

Structural Formula

Prefix

Suffix

Example

Alkane

Alkyl

RH

alkyl-

-ane

Ethane

Alkene

Alkenyl

R2C=CR2

alkenyl-

-ene

Ethylene
(Ethene)

Alkyne

Alkynyl

RC≡CR’

alkynyl-

-yne

Acetylene
(Ethyne)

Benzene derivative

Phenyl

RC6H5
RPh

phenyl-

-benzene

Cumene
(2-phenylpropane)

Toluene derivative

Benzyl

RCH2C6H5
RBn

benzyl-

1-(substituent)toluene

Benzyl bromide
(α-Bromotoluene)

There are also a large number of branched or ring alkanes that have specific names, e.g., tert-butyl, bornyl, cyclohexyl, etc.

Hydrocarbons may form charged structures: positively charged carbocations or negative carbanions. Carbocations are often named -um. Examples are tropylium and triphenylmethyl cations and the cyclopentadienyl anion.

Functional Groups containing halogens

Haloalkanes are a class of molecule that is defined by a carbon-halogen bond. This bond can be relatively weak (in the case of an iodoalkane) or quite stable (as in the case of a fluoroalkane). In general, with the exception of fluorinated compounds, haloalkanes readily undergo nucleophilic substitution reactions or elimination reactions. The substitution on the carbon, the acidity of an adjacent proton, the solvent conditions, etc. all can influence the outcome of the reactivity.

Chemical class

Group

Formula

Structural Formula

Prefix

Suffix

Example

haloalkane

halo

RX

halo-

alkyl halide

Chloroethane
(Ethyl chloride)

fluoroalkane

fluoro

RF

fluoro-

alkyl fluoride

Fluoromethane
(Methyl fluoride)

chloroalkane

chloro

RCl

chloro-

alkyl chloride

Chloromethane
(Methyl chloride)

bromoalkane

bromo

RBr

bromo-

alkyl bromide

Bromomethane
(Methyl bromide)

iodoalkane

iodo

RI

iodo-

alkyl iodide

Iodomethane
(Methyl iodide)

Functional Groups containing oxygen

Compounds that contain C-O bonds each possess differing reactivity based upon the location and hybridization of the C-O bond, owing to the electron-withdrawing effect of sp hybridized oxygen (carbonyl groups) and the donating effects of sp2 hybridized oxygen (alcohol groups).

Chemical class

Group

Formula

Structural Formula

Prefix

Suffix

Example

Alcohol

Hydroxyl

ROH

hydroxy-

-ol

Methanol

Ketone

Carbonyl

RCOR’

-oyl- (-COR’)
or
oxo- (=O)

-one

Butanone
(Methyl ethyl ketone

Aldehyde

Aldehyde

RCHO

formyl- (-COH)
or
oxo- (=O)

-al

Ethanal
(Acetaldehyde)

Acyl halide

Haloformyl

RCOX

carbonofluoridoyl-
carbonochloridoyl-
carbonobromidoyl-
carbonoiodidoyl-

-oyl halide

Acetyl chloride
(Ethanoyl chloride)

Carbonate

Carbonate ester

ROCOOR

(alkoxycarbonyl)oxy-

alkyl carbonate

Triphosgene
(Di(trichloromethyl) carbonate)

Carboxylate

Carboxylate

RCOO−

carboxy-

-oate

Sodium acetate
(Sodium ethanoate)

Carboxylic acid

Carboxyl

RCOOH

carboxy-

-oic acid

Acetic acid
(Ethanoic acid)

Ester

Ester

RCOOR’

alkanoyloxy-
or
alkoxycarbonyl

alkyl alkanoate

Ethyl butyrate
(Ethyl butanoate)

Hydroperoxide

Hydroperoxy

ROOH

hydroperoxy-

alkylhydroperoxide

Methyl ethyl ketone peroxide

Peroxide

Peroxy

ROOR

peroxy-

alkyl peroxide

Di-tert-butyl peroxide

Ether

Ether

ROR’

alkoxy-

alkyl ether

Diethyl ether
(Ethoxyethane)

Hemiacetal

Hemiacetal

RCH(OR’)(OH)

alkoxy -ol

-al alkylhemiacetal

Hemiketal

Hemiketal

RC(ORʺ)(OH)R’

alkoxy -ol

-one alkylhemiketal

Acetal

Acetal

RCH(OR’)(OR”)

dialkoxy-

-al dialkyl acetal

Ketal (orAcetal)

Ketal (orAcetal)

RC(ORʺ)(OR‴)R’

dialkoxy-

-one dialkyl ketal

Orthoester

Orthoester

RC(OR’)(ORʺ)(OR‴)

trialkoxy-

Orthocarbonate ester

Orthocarbonate ester

C(OR)(OR’)(ORʺ)(OR″)

tetralkoxy-

tetraalkylorthocarbonate

Functional Groups containing nitrogen

Compounds that contain nitrogen in this category may contain C-O bonds, such as in the case of amides.

Chemical class

Group

Formula

Structural Formula

Prefix

Suffix

Example

Amide

Carboxamide

RCONR2

carboxamido-
or
carbamoyl-

-amide

Acetamide
(Ethanamide)

Amines

Primary amine

RNH2

amino-

-amine

Methylamine
(Methanamine)

Secondary amine

R2NH

amino-

-amine

Dimethylamine

Tertiary amine

R3N

amino-

-amine

Trimethylamine

4° ammonium ion

R4N+

ammonio-

-ammonium

Choline

Imine

Primary ketimine

RC(=NH)R’

imino-

-imine

Secondary ketimine

RC(=NR)R’

imino-

-imine

Primary aldimine

RC(=NH)H

imino-

-imine

Secondary aldimine

RC(=NR’)H

imino-

-imine

Imide

Imide

(RCO)2NR’

imido-

-imide

Azide

Azide

RN3

azido-

alkyl azide

Phenyl azide (Azidobenzene)

Azo compound

Azo
(Diimide)

RN2R’

azo-

-diazene

Methyl orange
(p-dimethylamino-azobenzenesulfonic acid)

Cyanates

Cyanate

ROCN

cyanato-

alkyl cyanate

Methyl cyanate

Isocyanate

RNCO

isocyanato-

alkyl isocyanate

Methyl isocyanate

Nitrate

Nitrate

RONO2

nitrooxy-, nitroxy-

alkyl nitrate

Amyl nitrate
(1-nitrooxypentane)

Nitrile

Nitrile

RCN

cyano-

alkanenitrile
alkyl cyanide

Benzonitrile
(Phenyl cyanide)

Isonitrile

RNC

isocyano-

alkaneisonitrile
alkyl isocyanide

Methyl isocyanide

Nitrite

Nitrosooxy

RONO

nitrosooxy-

alkyl nitrite

Isoamyl nitrite
(3-methyl-1-nitrosooxybutane)

Nitro compound

Nitro

RNO2

nitro-

Nitromethane

Nitroso compound

Nitroso

RNO

nitroso-

Nitrosobenzene

Pyridine derivative

Pyridyl

RC5H4N

4-pyridyl
(pyridin-4-yl)

3-pyridyl
(pyridin-3-yl)

2-pyridyl
(pyridin-2-yl)

-pyridine

Nicotine

Functional Groups containing sulphur

Compounds that contain sulfur exhibit unique chemistry due to their ability to form more bonds than oxygen, their lighter analogue on the periodic table. Substitutive nomenclature (marked as prefix in table) is preferred over functional class nomenclature (marked as suffix in table) for sulfides, disulfides, sulfoxides and sulfones.

Chemical class

Group

Formula

Structural Formula

Prefix

Suffix

Example

Thiol

Sulfhydryl

RSH

sulfanyl-
(-SH)

–thiol

Ethanethiol

Sulfide
(Thioether)

Sulfide

RSR’

substituent sulfanyl-
(-SR’)

di(substituent) sulfide

 (Methylsulfanyl)methane (prefix) or
Dimethyl sulfide (suffix)

Disulfide

Disulfide

RSSR’

substituent disulfanyl-
(-SSR’)

di(substituent) disulfide

 (Methyldisulfanyl)methane (prefix) or
Dimethyl disulfide (suffix)

Sulfoxide

Sulfinyl

RSOR’

-sulfinyl-
(-SOR’)

di(substituent) sulfoxide

(Methanesulfinyl)methane (prefix) or
Dimethyl sulfoxide (suffix)

Sulfone

Sulfonyl

RSO2R’

-sulfonyl-
(-SO2R’)

di(substituent) sulfone

(Methanesulfonyl)methane (prefix) or
Dimethyl sulfone (suffix)

Sulfinic acid

Sulfino

RSO2H

sulfino-
(-SO2H)

–sulfinic acid

2-Aminoethanesulfinic acid

Sulfonic acid

Sulfo

RSO3H

sulfo-
(-SO3H)

–sulfonic acid

Benzenesulfonic acid

Thiocyanate

Thiocyanate

RSCN

thiocyanato-
(-SCN)

substituent thiocyanate

Phenyl thiocyanate

Isothiocyanate

RNCS

isothiocyanato-
(-NCS)

substituent isothiocyanate

Allyl isothiocyanate

Thione

Carbonothioyl

RCSR’

-thioyl-
(-CSR’)
or
sulfanylidene-
(=S)

–thione

Diphenylmethanethione
(Thiobenzophenone)

Thial

Carbonothioyl

RCSH

methanethioyl-
(-CSH)
or
sulfanylidene-
(=S)

–thial

Groups containing phosphorus

Compounds that contain phosphorus exhibit unique chemistry due to their ability to form more bonds than nitrogen, their lighter analogues on the periodic table.

Chemical class

Group

Formula

Structural Formula

Prefix

Suffix

Example

Phosphine
(Phosphane)

Phosphino

R3P

phosphanyl-

-phosphane

Methylpropylphosphane

Phosphonic acid

Phosphono

RP(=O)(OH)2

phosphono-

substituent phosphonic acid

Benzylphosphonic acid

Phosphate

Phosphate

ROP(=O)(OH)2

phosphonooxy-
or
O-phosphono- (phospho-)

substituent phosphate

Glyceraldehyde 3-phosphate (suffix)

O-Phosphonocholine (prefix)
(Phosphocholine)

Phosphodiester

Phosphate

HOPO(OR)2

[(alkoxy)hydroxyphosphoryl]oxy-
or
O-[(alkoxy)hydroxyphosphoryl]-

di(substituent) hydrogen phosphate
or
phosphoric acid di(substituent) ester

DNA

O‑[(2‑Guanidinoethoxy)hydroxyphosphoryl]‑l‑serine (prefix)
(Lombricine)

Learn Dynamics Of ‘Target-Ligand’ Interactions To Understand ‘Similia Similibus Curentur’

To understand the scientific interpretation of ‘similia similibus curentur’ in its real perspective, one should know the fundamentals of ‘target-ligand’ relationships and  dynamics of ‘bio-molecular inhibitions’.

There are diverse types of molecular ‘targets’  such as receptors, enzymes and antibodies which interact with appropriate ‘ligands’, so that the biochemical pathways underlying vital processes are maintained unhindered. Knowledge of the real molecular dynamics involved in ‘ligand-target’, ‘signals-receptors’, ‘substrates-enzymes’ and ‘antigen-antibody’ interactions is essential for understanding the science behind ‘similia similibus curentur’.

A receptor is a molecule found on the surface of a cell, which receives specific chemical signals from neighbouring cells or the wider environment within an organism. These signals tell a cell to do something—for example to divide or die, or to allow certain molecules to enter or exit the cell.

In biochemistry, a receptor is a protein molecule, embedded in either the plasma membrane or the cytoplasm of a cell, to which one or more specific kinds of signaling molecules may attach. A molecule which binds (attaches) to a receptor is called a ligand or ‘signal’, and may be a peptide (short protein) or other small molecule, such as a neurotransmitter, a hormone, a pharmaceutical drug, or a toxin. Each kind of receptor can bind only certain ligand shapes. Each cell typically has many receptors, of many different kinds. Simply put, a receptor functions as a keyhole that opens a neural path when the proper ligand is inserted.

A ligand  may be a whole molecule, a functional group, a moiety or even a radical or free ion.

Ligand binding stabilizes a certain target conformation (the three-dimensional shape of the target protein, with no change in sequence). This is often associated with gain of or loss of protein activity, ordinarily leading to some sort of cellular response. However, some ligands (e.g. antagonists) merely block target molecules, without inducing any response. Ligand-induced changes in targets result in cellular changes which constitute the biological activity of the ligands. Many functions of the human body are regulated by these diverse types of biological target molecules responding uniquely to specific ligand molecules like this.

Studies on the the shapes and actions of target molecules, especially receptors and enzymes have advanced the understanding of drug action at the binding sites of biological molecules.

Depending on their functions and ligands or signalling molecules, several types of receptors may be identified:

Some receptor proteins are peripheral membrane proteins.

Many hormone and neurotransmitter receptors are transmembrane proteins: transmembrane receptors are embedded in the phospholipid bilayer of cell membranes, that allow the activation of signal transduction pathways in response to the activation by the binding molecule, or ligand.

Metabotropic receptors are coupled to G proteins and affect the cell indirectly through enzymes which control ion channels.

Ionotropic receptors (also known as ligand-gated ion channels) contain a central pore which opens in response to the binding of signalling molecule.

Another major class of receptors are intracellular proteins such as those for steroid and intracrine peptide hormone receptors. These receptors often can enter the cell nucleus and modulate gene expression in response to the activation by the ligand.

One measure of how well a molecule fits a receptor is the binding affinity, which is inversely related to the dissociation constant. A good fit corresponds with high affinity and low dissociation constant. The final biological response (e.g. second messenger cascade, muscle contraction), is only achieved after a significant number of receptors are activated.

The receptor-ligand affinity is greater than enzyme-substrate affinity.  Whilst both interactions are specific and reversible, there is no chemical modification of the ligand as seen with the substrate upon binding to its enzyme.

Many pathological molecular errors are caused by inhibitions of these target molecules such as receptors and enzymes by binding of exogenous or endogenous molecules or ions on them. Bacterial toxins, drugs and such pathological agents act this way.

Dynamcs of ‘ligand-target’ interactions can be understood only if we have a working knowledge of protein chemistry, especially enzyme chemistry.

There exist millions of protein molecules belonging to thousands of protein types in a living organism. Each protein molecule is formed by the polymerization of monomers called amino acids, in different proportions and sequences. Each protein type has its own specific role in the bio-chemic interactions in an organism. Most of the amino acids necessary for the synthesis of proteins are themselves synthesized from their molecular precursers inside the body.  A few types of  amino acids cannot be synthesized inside the body, and have to be made available through food. These are called essential aminoacids. There are specific protein molecules assigned for each bio-chemic process that take place in the body. Various proteins play different types of roles, like biological catalysts or  enzymes, molecular receptors, transport molecules, hormones  and antibodies. Some proteins function as specialized molecular switches, systematically switching on and off of specific bio-chemic pathways. Proteins are synthesized from amino acids, in conformity with the neucleotide sequences of concerned genes, with the help of enzymes, which are themselves proteins. ‘Protein synthesis’ and ‘genetic expression’ are very important part of vital process. It may be said that genes are molecular moulds for synthesizing proteins. There are specific genes, bearing appropriate molecular codes of information necessary for synthesizing each type of protein molecule. Even the synthesis of these genes happens with the help of various enzymes, which are protein molecules. There is no any single bio-molecular process in the living organism, which does not require an active participation of a protein molecule of any kind.

The most important factor we have to understand while discussing proteins is the role of their three-dimensional spacial organization evolving from peculiar di-sulphide bonds and hydrogen bonds. Water plays a vital role in maintaining the three dimensional organization of proteins intact, thereby keeping them efficient to participate in the diverse biochemical processes.  Proteins exhibits different levels of molecular organization- primary, secondary, tertiary  and quaternary. It is this peculiar three dimensional structure that decides the specific bio-chemical role of a given protein molecule. More over, co-enzymes and co-factors such as metal ions and vitamins play an important role in keeping up this three-dimensional structure of protein molecules  intact, thereby activating them for their specific functions.

Whenever any kind of error occurs in the particular three-dimensional structure of a given protein molecule, it obviously fails to interact with other bio-molecules to accomplish the specific functions it is intended to play in the concerned bio-chemical processes. Such a failure leads to harmful deviations in several bio-chemical processes in the organism that require the participation of this particular protein, ultimately resulting in a cascading of multitude of molecular errors. This is the fundamental molecular mechanism of pathology, which we perceive as disease of some or other category.  These deviations in bio-chemical pathways are expressed as various groups of subjective and objective symptoms of disease. The organic system exhibits a certain degree of ability and flexibility to overcome or self repair such molecular deviations and preserve the state of homeostasis required to maintain life. Anyhow, if these deviations happen in any of the vitally decisive bio-chemical pathways, or, if these are beyond self repair, the bio-chemical processes ultimately stop and death happens.

Almost all conditions of pathology we normally confront, including those resulting from genetic origin, are involved with some or other errors or absence of some protein molecules that are essential for concerned bio-chemical processes. Moreover, most of such molecular errors other than genetic origin, arise due to binding of some exogenous or endogenous foreign molecules or ions on the active, binding or allosteric sites of protein molecules, effecting changes in the three-dimensional configurations of protein molecules. A host of diseases originating from viral-bacterial infections, allergies, miasms, poisoning, drugs, food etc, belong to this category.

The most important factor we have to bear in mind when talking about kinetics of proteins in general and enzymes in particular is their highly defined, peculiar specificity. Each type of protein molecules,  or some times even some part of a single protein molecule, is designed in such a way that it can bind only with a specific class of molecules, and hence participate in a specific type of bio-chemical interaction only. This functional specificity is ensured through the peculiar three-dimensional configuration of the protein molecules, exhibited through their characteristic folding and spacial arrangement. Reactive chemical groups known as active sites, binding sites, and regulatory sites are distributed at specific locations on this three dimensional formations of protein molecules. These chemical groups can interact only with molecules and ions having appropriate configurations that fit to their shape. This phenomenon can be compared with the relationship existing between a lock and its appropriate key. Just as a key with an exactly fitting three dimensional shape alone can enter the key hole of a lock and open it, molecules with exactly fitting three dimensional structures alone can establish contact and indulge in chemical activities with specific protein molecules. This key-lock relationship with substrates defines all biochemical interactions involving proteins, ensuring their optimum specificity. Obviously, any deviation in the three dimensional configuration of either lock or key makes their interaction impossible.

It has been already explained that the primary basis of any state of pathology is some deviations occurring in the biochemical processes at the molecular level. Endogenous or exogenous foreign molecules or ions having any functional moieties with configurational similarity to certain biochemical substrates can mimic as original substrates to attach themselves on the regulatory or the active sites of proteins, effecting changes in their native 3-D configuration, thereby making them unable to discharge their specific biochemical role. This situation is called a molecular inhibition, which leads to pathological molecular errors. It is comparable with the ability of objects having some similarity in shape with that of key, to enter the key hole of a lock and obstructing its function. As a result of this inhibition, the real substrates are prevented from interacting with the appropriate protein molecules, leading to a break in the normal biochemical channels. These types of molecular errors are called competitive inhibitions. It is in this way that many types of drugs, pesticides and poisons interfere in the biochemical processes, creating pathological situations. Such substances are known as anti-melabolities.

When we prove our drugs in healthy people, the constituent molecules contained in the drug substances may bind to diverse types of ‘receptors’ and enzymes’ due to the similarity of configurations between functional groups of original ligands and drug molecules. Molecules having functional moieties with ‘similar’ configuration can bind to similar target molecules, causing similar pathological molecular errors expressed through ‘similar’ subjective and objective symptoms. The concept of ‘similarity of symptoms’ can be scientifically understood if we know the dynamics of ‘ligand-receptor’ and ‘substrate-enzyme’ relationships. Without this fundamental understanding one cannot follow my concepts regarding ‘potentization’ and ‘similia similibus curentur’.

Infectious Agents Of ‘Itch’- The Causative Factors Of Miasm Of ‘Psora’

According to samuel Hahnemann, the “miasm” of PSORA is the cause of a wide range of chronic diseases. He explained PSORA as the residual chronic effects of INFECTIOUS AGENTS OF ITCH.

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.”

I think we have to study the INFECTIOUS AGENTS OF ITCH in detail, in order to understand the MIASM OF PSORA. Then only we can realize why Hahnemann considered PSORA as the mother of CHRONIC DISEASES

Scabies (from Latin: scabere, “to scratch”), known colloquially as the seven-year itch, is a contagious skin infection that occurs among humans and other animals. It is caused by a tiny and usually not directly visible parasite, the mite Sarcoptes scabiei, which burrows under the host’s skin, causing intense allergic itching. The infection in animals (caused by different but related mite species) is called sarcoptic mange.

The disease may be transmitted from objects but is most often transmitted by direct skin-to-skin contact, with a higher risk with prolonged contact. Initial infections require four to six weeks to become symptomatic. Reinfection, however, may manifest symptoms within as little as 24 hours. Because the symptoms are allergic, their delay in onset is often mirrored by a significant delay in relief after the parasites have been eradicated. Crusted scabies, formerly known as Norwegian scabies, is a more severe form of the infection often associated with immunosuppression.

The characteristic symptoms of a scabies infection include intense itching and superficial burrows. The burrow tracks are often linear, to the point that a neat “line” of four or more closely-placed and equally-developed mosquito-like “bites,” is almost diagnostic of the disease.

In the classic scenario, the itch is made worse by warmth and is usually experienced as being worse at night, possibly because there are fewer distractions. As a symptom it is less common in the elderly.

The superficial burrows of scabies usually occur in the area of the hands, feet, wrists, elbows, back, buttocks, and external genitals. The burrows are created by excavation of the adult mite in the epidermis.

In most people, the trails of the burrowing mites show as linear or s-shaped tracks in the skin, often accompanied by what appear as rows of small pimple-like mosquito, or insect bites. These signs are often found in crevices of the body, such as on the webs of fingers and toes, around the genital area, and under the breasts of women.

Symptoms typically appear 2–6 weeks after infestation for individuals never before exposed to scabies. For those having been previously exposed, the symptoms can appear within several days after infestation. However, it is not unknown for symptoms to appear after several months or years. Acropustulosis, or blisters and pustules on the palms and soles of the feet, are characteristic symptoms of scabies in infants.

The elderly and people with an impaired immune system, such as HIV and cancer sufferers or transplant patients on immunosuppressive drugs, are susceptible to crusted scabies (formerly called “Norwegian scabies”). On those with a weaker immune system, the host becomes a more fertile breeding ground for the mites, which spread over the host’s body, except the face. Sufferers of crusted scabies exhibit scaly rashes, slight itching, and thick crusts of skin that contain thousands of mites. Such areas make eradication of mites particularly difficult, as the crusts protect the mites from topical miticides, necessitating prolonged treatment of these areas.

In the 18th century, Italian biologist Diacinto Cestoni (1637–1718) described the mite now called Sarcoptes scabiei, variety hominis, as the cause of scabies. Sarcoptes is a genus of skin parasites and part of the larger family of mites collectively known as “scab mites”. These organisms have 8 legs as adults, and are placed in the same phylogenetic class (Arachnida) as spiders and ticks.

Sarcoptes scabiei are microscopic, but sometimes are visible as pinpoints of white. Pregnant females tunnel into the stratum corneum of a host’s skin and deposit eggs in the burrows. The eggs hatch into larvae in 3–10 days. These young mites move about on the skin and molt into a “nymphal” stage, before maturing as adults, which live 3–4 weeks in the host’s skin. Males roam on top of the skin, occasionally burrowing into the skin. In general, there are usually few mites on a healthy hygienic person infested with non-crusted scabies; approximately 11 females in burrows can be found on such a person.

The movement of mites within and on the skin produces an intense itch, which has the characteristics of a delayed cell-mediated inflammatory response to allergens. IgE antibodies are present in the serum and the site of infection, which react to multiple protein allergens the body of the mite. Some of these cross-react to allergens from house-dust mites. Immediate antibody-mediated allergic reactions (wheals) have been elicited in infected persons, but not in healthy persons; immediate hypersensitivity of this type is thought to explain the observed far more rapid allergic skin response to reinfection seen in persons having been previously infected (especially having been infected within the previous year or two).  Because the host develops the symptoms as a reaction to the mites’ presence over time, there is usually a 4– to 6-week incubation period after the onset of infestation. As noted, those previously infected with scabies and cured may exhibit the symptoms of a new infection in a much shorter period, as little as 1–4 days.

Scabies is contagious, and can be spread by scratching an infected area, thereby picking up the mites under the fingernails, or through physical contact with a scabies-infected person for a prolonged period of time.  Scabies is usually transmitted by direct skin-to-skin physical contact. It can also be spread through contact with other objects, such as clothing, bedding, furniture, or surfaces with which a person infected with scabies might have come in contact, but these are uncommon ways to transmit scabies.  Scabies mites can survive without a human host for 24 to 36 hours.  As with lice, scabies can be transmitted through sexual intercourse even if a latex condom is used, because it is transmitted from skin-to-skin at sites other than sex organs.

The symptoms are caused by an allergic reaction of the host’s body to mite proteins, though exactly which proteins remains a topic of study. The mite proteins are also present from the gut, in mite feces, which are deposited under the skin. The allergic reaction is both of the delayed (cell-mediated) and immediate (antibody-mediated) type, and involves IgE (antibodies, it is presumed, mediate the very rapid symptoms on re-infection). The allergy-type symptoms (itching) continue for some days, and even several weeks, after all mites are killed. New lesions may appear for a few days after mites are eradicated. Nodular lesions from scabies may continue to be symptomatic for weeks after the mites have been killed.

Scabies may be diagnosed clinically in geographical areas where it is common when diffuse itching presents along with either lesions in two typical spots or there is itchiness of another household member. The classical sign of scabies is the burrows made by the mites within the skin. To detect the burrow the suspected area is rubbed with ink from a fountain pen or a topical tetracycline solution, which glows under a special light. The skin is then wiped with an alcohol pad. If the person is infected with scabies, the characteristic zigzag or “S” pattern of the burrow will appear across the skin; however, interpreting this test may be difficult, as the burrows are scarce and may be obscured by scratch marks.  A definitive diagnosis is made by finding either the scabies mites or their eggs and fecal pellets. Searches for these signs involve either scraping a suspected area, mounting the sample in potassium hydroxide, and examining it under a microscope, or using dermoscopy to examine the skin directly.

Symptoms of early scabies infestation mirror other skin diseases, including dermatitis, syphilis, various urticaria-related syndromes, allergic reactions, and other ectoparasites such as lice and fleas.

Mass treatment programs that use topical permethrin or oral ivermectin have been effective in reducing the prevalence of scabies in a number of populations. There is no vaccine available for scabies. The simultaneous treatment of all close contacts is recommended, even if they show no symptoms of infection (asymptomatic), to reduce rates of recurrence.  Asymptomatic infection is relatively common. Objects in the environment pose little risk of transmission except in the case of crusted scabies, thus cleaning is of little importance.  Rooms used by those with crusted scabies require thorough cleaning.

A number of medications are effective in treating scabies, however treatment must often involve the entire household or community to prevent re-infection. Options to improve itchiness include antihistamines.

Scabies is one of the three most common skin disorders in children along with tinea and pyoderma. The mites are distributed around the world and equally infects all ages, races, and socioeconomic classes in different climates. Scabies is more often seen in crowded areas with unhygienic living conditions. Globally as of 2009, it is estimated that 300 million cases of scabies occur each year, although various parties claim the figure is either over- or underestimated. There are one million cases of scabies in the United States annually. About 1–10% of the global population is estimated to be infected with scabies, but in certain populations, the infection rate may be as high as 50–80%.[Scabies is one of the three most common dermatological disorders in children.

Scabies is an ancient disease. Archeological evidence from Egypt and the Middle East suggests that scabies was present as early as 494 BC. The first recorded reference to scabies is believed to be from the Bible (Leviticus, the third book of Moses) ca. 1200 BC.  Later in fourth century BC, the ancient Greek philosopher Aristotle reported on “lice” that “escape from little pimples if they are pricked”;  scholars believe this was actually a reference to scabies.

Nevertheless, it was Roman physician Celsus who is credited with naming the disease “scabies” and describing its characteristic features. The parasitic etiology of scabies was later documented by the Italian physician Giovanni Cosimo Bonomo (1663–99 AD) in his famous 1687 letter, “Observations concerning the fleshworms of the human body.” With this (disputed) discovery, scabies became one of the first diseases with a known cause.

Scabies may occur in a number of domestic and wild animals; the mites that cause these infestations are of different scabies subspecies. These subspecies can infest animals or humans that are not their usual hosts, but such infections do not last long.  Scabies-infected animals suffer severe itching and secondary skin infections. They often lose weight and become frail.

The most frequently diagnosed form of scabies in domestic animals is sarcoptic mange, which is found on dogs. The scab mite Psoroptes is the mite responsible for mange. Scabies-infected domestic fowls suffer what is known as “scabies leg”.  Domestic animals that have gone feral and have no veterinary care are frequently afflicted with scabies and a host of other ailments. Non-domestic animals have also been observed to suffer from scabies. Gorillas, for instance, are known to be susceptible to infection via contact with items used by humans.

Please listen to this:

“Archeological evidence from Egypt and the Middle East suggests that scabies was present as early as 494 BC. The first recorded reference to scabies is believed to be from the Bible (Leviticus, the third book of Moses) ca. 1200 BC.” Now we can understand why hahnemann said PSORA has been inherited through “GENERATIONS OF HUMANITY” up to our period. Even now most of us get infected with ITCH in early life, and ANTIBODIES are formed in our body, which is the exact material basis of all those diseases we consider of PSORIC MIASM

Please note this also:

“Globally as of 2009, it is estimated that 300 million cases of scabies occur each year, although various parties claim the figure is either over- or underestimated. There are one million cases of scabies in the United States annually. About 1–10% of the global population is estimated to be infected with scabies, but in certain populations, the infection rate may be as high as 50–80%.[Scabies is one of the three most common dermatological disorders in children”.Even now, in spite of all modern treatments and personal hygeine, this remains the most widespread disease affecting humanity. Imagine what would be the situation during hahnemann’s period. NO WONDER, HAHNEMANN CONSIDERED PSORA AS THE MOTHER OF CHRONIC DISEASES.

NOTE THIS POINT:

“The symptoms are caused by an allergic reaction of the host’s body to mite proteins, though exactly which proteins remains a topic of study”. As part of this allergic response of our body to “mite proteins”, antibodies are generated. “The allergic reaction is both of the delayed (cell-mediated) and immediate (antibody-mediated) type, and involves IgE (antibodies, it is presumed, mediate the very rapid symptoms on re-infection)”. These antibodies remain life long in our body as CHRONIC MIASMS. Antibodies can attack OFF-TARGET biological molecules in various biochemical channels in the body, resulting in diverse types of CHRONIC diseases belonging to MIASM OF PSORA.

Latest available studies states that the SCABIES MITES carries different species of BACTERIA on their wings and body, and the toxins secreted by these BACTERIA are the the real molecular factors that give rise to allergic reactions during MITE infections. If that is true, SCABIES or PSORA will have to ultimately considered as BACTERIAL INFECTIONS.

Antibodies are native globulin proteins ‘imprinted’ with exogenous protein molecules entering into the organism from the environment, as infections, food, drugs, toxins or as part of any interactions with the environment. These exogenous proteins may come from bacterial/viral/fungal/parasitic infections that invade the body, bites and stings of insects and serpents, uncooked food articles, drugs like antibiotics and serum, vaccines, and so on. These exogenous foreign proteins, alien to our genetic constitution, are dangerous to the normal functioning of the organism, and have to be destroyed or eradicated. Body has a well organized defense system for this, which we call immune system. Foreign proteins are called antigens. Body prepares immune bodies or antibodies against these dangerous invaders. Antibodies are specific to each antigen, There are also polyclonal antibodies, which can identify different antigens. Antibodies are exactly native proteins of globulin types, which have peculiar molecular structure with an active group known as ‘paratope’ on its periphery. Active groups of antigen molecules are known as ‘epitopes’. Epitopes of antigens and paratopes of antibodies has a ‘key-lock’ relationship of configuration. They should fit exactly each other in order to happen an immune reaction. Paratopes of antibodies once interacted with epitopes of a particular antigen undergoes a process of ‘molecular imprinting’, by which the ‘memory’ of epitope is imprinted into the paratope of antibody. Even after the antigens are destroyed and eradicated by the immune system, these ‘molecular imprinted’ globulins, or antibodies exist and circulate in the organism, in most cases life long. This is the mechanism by which life long immunity is attained through certan infections and vaccinations. These antibodies, or ‘molecular imprinted proteins’ are very important part of our defense system, playing a vital role in protecting us against infections.

Same time, these ‘molecular imprinted proteins’ or antibodies plays a negative role also, which is what we call ‘miasms’. They can act as pathogenic factors. Whenever these antibodies happen to come in contact with a native biological molecule having a structural group of configuration similar to the ‘epitope’ of its natural antigen, its paratope binds to it and inhibits the biological molecules. This is a ‘molecular error’ amounting to a state of pathology. Diverse types of chronic diseases and dispositions are created by the antibodies in the organism. These pathological conditions caused by ‘off-target’ binding of antibodies or ‘molecular imprinted proteins’ are the real ‘miasms’ hahnemann described as the underlying factors of ‘chronic diseases’.

Obviously, identifying and removal of these ‘off-target’ molecular blocks or ‘miasms’ caused by antibodies or ‘molecular imprinted proteins’ is an important part in the treatment of chronic diseases. Observing and collecting the whole history of infections and intoxications that might have generated antibodies are important in the management of chronic diseases. History of skin infections, venereal infections, stings of poisonous creatures, vaccinations, serum/antibiotic treatments, sensitization with protein foods etc. has to be collected in detail and appropriate ‘anti-miasmatics’ included in the treatment protocols of chronic treatments.

Another important thing we have to remember is that we cannot permanently inactivate ‘antibodies’ using potentized nosodes or anti-miasmatic drugs. Our drugs may act in two ways. If the nosodes are prepared from antibodies themselves, they contain ‘molecular imprints of epitopes of ‘exogenous toxins’ or antigens themselves. These ‘molecular imprints can compete with the paratopes of antibodies in binding to biological molecues, and prevent them from creating ‘off-target’ biological blocks. Since ‘molecular imprints’ cannot successfully compete with the epitopes of antigens in binding with the paratopes of antibodies, our potentized drugs never interferes with the normal immune mechanism of the body. They only prevents antibodies from binding to ‘off-target’ biological molecules, and thus act as ‘antimiasmatics’.

If we are preparing nosodes by potentizing antibodies themselves, our drugs contains ‘molecular imprints’ of paratopes of antibodies. These molecular imprints can bind to the paratopes, thereby preventing them from interacting with ‘off-target’ biological molecules. Same time, they also cannot interfere in the interaction between antibodies and their natural antigens, which have comparatively increased affinity. In any way, potentized nosodes or ‘antimiasmatics’ will not weaken the normal immunological mechanism of the organism.

Since we cannot eradicate or permanently inactivate antibodies or miasms with our potentized drugs, we have to administer antimiasmatic drugs in frequent intervals, probably life long. This is a very important realization evolving from the understanding of ‘miasms’ as ‘antibodies’ or ‘molecular imprinted proteins’.

I think hahnemann included all ‘itch’ producing infections under the carpet of ‘psora’. He mentioned about Leprosy, scarlet fever, scabies and many such ‘infectious’ agents as causative factors of psora. He talked about “three miasms”, only because those three infectious agents were creating havoc in europe during his period. According to me, this classification of psora, syphilis and sycosis is not much relevant if we understand ‘miasms’ in terms of ‘antibodies’.