Tag: molecular

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 SO₄^2-). 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
Cyanates	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)
Nitrile	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
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)

December 14, 2011

Hering’s Laws of Directions of Cure- Learn Dynamics of Cascading of Molecular Inhibitions and Bio-Molecular Feedback Systems.
‘Curative processes happen in a direction just reverse to disease processes’- that is the sum total of Hering’s observations regarding ‘directions of cure’.

The four ‘laws’ now known as ‘herings laws’ are actually observations regarding ‘order of cure’ used to demonstrate the homeopathic curative process.

It was ‘KENT’ who later actually called it ‘Herings laws’ and converted these four observations into ‘fundamental laws’ of homeopathic cure. He taught to understand and apply these ‘laws’ in a mechanical way. He taught homeopaths to consider ‘hering laws’ regarding ‘directions of cure’ as one of the ‘fundamental laws’ of homeopathy, similar to ‘similia similibus curentur’. Kent made homeopaths believe that drug effects that do not agree with these ‘laws’ cannot be considered ‘curative’, and are ‘suppressive’. There are some modern streams of homeopathic practice which rely more upon ‘hering laws’ than ‘similia similibu curentur’ in their methods of therapeutic applications.

Actually, Hahnemann did not seriously work upon those aspects of curative processes which we call ‘directions of cure’, or considered it a decisive factor in homeopathic therapeutics. He made some observations regarding ‘order of cure’. He was more concerned about ‘misms’ in the management of ‘chronic diseases’, where as Hering did not consider ‘miasms’ at all.

Some modern ‘theoreticians’ have come with new theories by combining ‘hering laws’ and theory of miasms, also mixing up with terms of ‘genetics’ and ‘embryology’ which they propagate as the ‘only’ correct understanding of homeopathy.

Following are the four observations used actually to demonstrate that ‘Curative processes happen in a direction just reverse to disease processes’, and later considered by KENT as ‘Hering laws of direction of cure’:

In a genuine curative process,
1. Symptoms should disappear in the reverse chronological order of their appearance in disease.
2. Symptoms should travel from internal parts of body to external parts
3. Symptoms should travel from more vital organs to less vital organs.
4. Symptoms should travel from ‘upper’ parts of the body to ‘lower’ parts.
According to those who consider these as the ‘fundamental law of cure’, any drug effect that happen not in accordance with above laws are ‘suppressive’, and hence not ‘curative’.

‘Disease processes and curative processes always happen in reverse directions’ is the fundamental observation hering actually tried to establish regarding ‘directions of disease and cure’.

Hering never called these observations as ‘laws’. None of his famous contemporaries and close colleagues ever discussed or made any reference to a law of direction of cure. Writings of Boenninghausen, Jahr, Joslin, P.P. Wells, Lippe, H.N.Guernsey, Dunham, E.A. Farrington, H.C. Allen, Nash, etc, were all silent.

“When Hering died in 1880, colleagues all over the world assembled to pay tribute to the great homeopath. His many accomplishments were recalled. Strangely, none made any mention of a law of direction of cure promulgated by Hering. Arthur Eastman, a student who was close to Hering during the last three years of the venerable homeopath, published in 1917 Life and Reminiscences of Dr. Constantine Hering also without mentioning a law pertaining to direction of cure. Calvin Knerr, Hering’s son-in-law, published in 1940, 60 years after Hering’s death, the Life of Hering, a compilation of biographical notes. Again no mention is made of the famous law.

In 1865, Hering described these observations not as a law but as Hahnemann’s general observations or as plain practical rules. Essentially he emphasizes the proposition that the ‘symptoms should disappear in the reverse order of their appearance during the treatment’ of patients with chronic psoric diseases.

In 1875, Hering discussed only one proposition, that the ‘symptoms will disappear in the reverse order of their appearance’. The three other propositions are now not mentioned at all.

All the illustrious contemporaries of Hering seems to remain silent on this point, at least as far as available literature shows.

In 1911,Kent, almost arbitrarily, calls the original observations of Hahnemann “Hering’s law”.

According to so-called hering’s laws, natural disease processes always advances from lower parts of the body to upper parts, from less vital to more vital organs and from external to internal organs. More over, all these disease processes advance in a chronological order.

Logically, Hering’s observations only meant that “all genuine ‘curative processes’ should happen in a direction just reverse to disease processes”.

Over-extending and mechanical application of ‘herings laws’ without understanding their exact premises and scientific meaning may lead to grave errors regarding interpretation of curative processes and drug effects.

This phenomenon could be explained in the light of modern scientific understanding of ‘cascading of pathological molecular inhibitions’ and complex dynamics of ‘bio-molecular feed back mechanisms’.

To understand this explanation, one has to equip himself with at least a working knowledge regarding the concepts of modern biochemistry regarding the bio-molecular inhibitions involved in pathology and therapeutics.

Expect those diseases which are purely due to errors in genetic substances, and those diseases which are due to genuine deficiency of building materials of biological molecules, all other diseases are considered to be caused by ‘molecular inhibitions’. Pathogenic molecules of endogenous or exogenous origin bind to some biological molecules in the organism, causing ‘molecular inhibitions’ which lead to pathological derangement in associated biochemical pathways. These pathogenic molecules may be of infectious, environmental, nutritional, metabolic, drug-induced, miasmatic or any other origin. Derangements in biochemical pathways are expressed through diverse groups of subjective and objective symptoms. This is the fundamental biochemistry of pathology.

Molecular inhibitions happening in a biological molecule due to the binding of a pathogenic molecule initiates a complex process of ‘cascading of molecular errors’ and ‘bio-feedback mechanisms’ in the organism. Errors happening in a particular biochemical pathway leads to errors in another pathway which is dependant on the first pathway for regular supply of metabolites, which further lead to errors in another pathway. This ‘cascading of molecular errors’ happens through successive stages, which is expressed through new subjective and objective symptoms. This ‘cascading’ is behind what we call ‘advancing of disease’ into new systems and organs, exhibiting ever new groups of associated symptoms. For an observer, this cascading appears in the form of ‘traveling of disease’ from one system into another. Along with these ‘cascading’ of molecular errors, there happens a series of activation and shutting down of complex ‘bio-molecular feedback’ mechanisms also. The phenomenon of ‘advancing of diseases’ should be studied in this scientific perspective of modern biochemistry.

When a molecular inhibition happens in some biological molecule ‘A’ due to binding of a pathogenic molecule ‘a’, it actually stops or decreases some essential molecular conversions that are essential part of a complex biochemical pathway P. If ‘G’ is the normal ligand of ‘A’, and ‘g’ is the product of biochemical interaction involving ‘A’, the result of this molecular inhibition is that ‘G’ accumulates on one side, and ‘g’ is not available for the next stage of molecular processes. Accumulating ‘P’ may induce a feedback mechanism leading to reduction or stoppage its production itself, or may move to other parts of organism and bind to unwanted molecular targets, initiation a new stream of pathological derangement.

Obviously, ‘traveling’ of disease or ‘advancing’ of disease happens through cascading of molecular errors in various biochemical pathways. Some disease processes may ‘travel’ from ‘external’ to internal organs, some from ‘lower parts’ to upper parts, some from ‘less vital’ parts to ‘more vital’ parts. All these ‘traveling’ is basically decided by the involved biochemical pathways. It would be wrong to generalize these observations in such a way that ‘all diseases travel from exterior to interior, lower parts to higher parts, and less vital to more vital parts’. It is also wrong to generalize in such a way that ‘curative process always travel from interior to exterior, above downwards, and from vital to less vital parts’. This is mechanical understanding and application of hering’s observations.

Actually, curative processes happens in a direction opposite to the direction of disease process. That depends upon the biochemical pathways involved and the exact dynamics of cascading of molecular inhibitions. Its dynamics is very complex, and should not be interpreted and applied in a mechanistic way. When ‘molecular inhibitions’ underlying the disease processes are systematically removed using molecular imprints, the curative process also would take place in the reverse direction of disease processes.

To sum up, Hering’s observations regarding a ‘directions of disease and cure’ is a valuable one, but it should be studied in the light of modern biochemistry.

‘Curative processes happen in a direction just reverse to disease processes”- that is the sum total of Hering’s observations regarding ‘directions of cure’.
September 30, 2011