‘Molecular Imprinting in Water’ For Target-Specific Drug Designing- Science Behind Homeopathic Potentization

 ‘Drug designing’ is an advanced branch of modern pharmaceutical chemistry, which is involved with the process of developing new medicinal substances appropriate to the specific  biological targets in the organism. Such a ‘designer drug’ is most commonly a small organic molecule which can inhibit or activate the functioning of a target biomolecule such as a protein, thereby resulting in a therapeutic process in the organism. Essentially, ‘drug designing’ involves the development of small molecules that are complementary in ‘shape’ and ‘charge’ to the biomolecular target to which they interact and therefore will bind to it. Modern drug designing protocols utilize computer modeling techniques also. This type of modeling is known as ‘computer-aided drug design’. Actually, ‘drug design’ is involved with ‘ligand’ design. Prediction of binding affinity of molecules to be designed is the first step in a successful modeling technique.  Many other properties such as bioavailability, metabolic half life, lack of side effects, also should be optimized before a designed ‘ligand’ can become a safe and efficacious drug. Most of these ‘other’ characteristics are often very difficult to optimize using presently available drug design techniques.

Selection of drug target is most important in “drug designing”. A drug target is typically a key molecule involved in a particular metabolic or signaling pathway that is specific to a disease condition or pathology, or to the infectivity or survival of a microbial pathogen. Most of the therapeutic inteventions aim to inhibit the functioning of the ‘pathologic’ pathway in the diseased state by causing a key molecule to stop functioning. Drug molecules may be designed that bind to the active region and inhibit this key molecule. Some other therapeutic interventions  actually enhance the ‘normal’ biochemical pathway by promoting specific molecules in the ‘normal’ pathways that may have been affected in the diseased state. Main challenge in all ‘drug therapies’ including ‘designer drugs’ is that  these drug molecules should not affect any other important “off-target” molecules or ‘antitargets’ that may be similar in appearance to the target molecule, since drug interactions with off-target molecules may lead to undesirable side effects.

Designer drugs are small organic molecules produced through chemical synthesis, but biopolymer-based drugs (also known as biologics) produced through biological processes are becoming increasingly more common in modern drug designing.

‘Ligand-based drug design’ and ‘structure-based drug design’ are two major technologies now utilized in drug designing technologies.

Ligand-based drug design is based on the knowledge of other molecules that can bind to the biological target of interest. These other molecules may be used to derive a ‘pharmacophore’ which defines the minimum necessary structural characteristics a molecule must possess in order to bind to the target. In other words, a model of the biological target may be built based on the knowledge of what binds to it and this model in turn may be used to design new molecular entities that interact with the target.

Structure-based drug design is based on the knowledge of the three dimensional structure of the biological target obtained through methods such as x-ray crystallography or NMR spectroscopy. Using the structure of the biological target, candidate drugs that are predicted to bind with high affinity and selectivity to the target may be designed using interactive graphics.

Main draw back of ‘designer drugs’ is that  there is a chance for these drug molecules affecting “off-target” molecules or ‘antitargets’ having similarity to the target molecules. Such interactions with off-target molecules may lead to grave consequences. Optimizing of various factors such as bioavailability, metabolic half life, and lack of side effects are the real challenges facing “drug designing” technology.

Molecular Imprinting in Polymers:

  ‘Molecular imprinting in polymers’ is a fast grownig research area that may be interesting to people engaged in developing “drug designing” techniques. A lot of research is currently going on over this subject the world over. This technology involves the imprinting of synthetic polymer substances using enzymes or such macromolecules as ‘guest’molecules. As a result of imprinting, nano cavities with 3-d spacial configurations complementary to the ‘guest’ molecules will be created in the interaction surfaces of the polymers. These imprinted polymers, by virtue of the nanocavities they contain can be used to bind molecules with configurational similarity to ‘guest’ molecules. They are at present widely used in various laboratory assays as powerful adsorption surfaces. MIPs are also found to be of much practical use in various areas of science  and technology .

Molecular imprinted polymers of today cannot be used as therapeutic agents, since they are totally foreign substances to the organism. More over, native enzymes can not degrade the polymers even if they can play a therapeutic role in the organism.

Molecular imprinting may become part of future drug designing techniques, only if the search for safer substances and methods for molecular imprinting happens to be successful.

Molecular Imprinted Proteins:

 Biopolymer-based drugs (also known as biologics) produced through biological processes are becoming increasingly more common in modern drug designing. But the revolutionary concept of molecular imprinting in proteins is only in its emerging stage, which may have implications in drug designing techniques. It has already been acknowledged that the biological molecules presently classified as antibodies are nothing but native globulin proteins subjected to natural molecular imprinting process with foreign pathologic proteins acting as ‘guest’ molecules. Scientists have already realized the fact that the much discussed pathologic molecules known as ‘prions’ are nothing but disfigured protein molecules subjected to molecular imprinting. Protiens, being polymers with complex and flexible tertiary structures,  are expected to be a very good medium for molecular imprinting. Different types of protein based substances, subjected to artificial molecular imprinting, may  evolve in the future as effective therapeutic agents and laboratory reagents.

Apart from protein molecules,  different types of biopolymers such as polysaccharides and nucleic acids also may be experimented as medium for molecular imprinting.

Native proteins extracted from the patients could be subjected to molecular imprinting with appropriate ligands or other pathologic molecules acting as ‘guest’ molecules and used as target oriented therapeutic agents.  But the problem remains that such imprinted proteins can be used only in the individual whose proteins are used for imprinting. Otherwise it may result in grave anaphylactic reactions. Moreover these imprinted proteins may remain in the organism for very long periods, without undergoing degradation, and cause ever new pathological molecular blocks. Such issues have to be addressed properly.

Molecular Imprinting in Water:

 Our protracted search for a safe and reliable universal medium for molecular imprinted drug designing finally takes us to the study of wonderful physico-chemical properties of the most abundant substance on earth called water. But the concept and technology of molecular imprinting in water still remains in very infantile stage. The author is of the opinion that with its strange polymer-like behaviours, capable of forming hydrogen-bonded supra-molecular structures, water can be the ideal candidate for molecular imprinted drug designing in future.

Though in a slighly lesser level, Ethyl Alcohol and Lactose are also capable of forming polymer-like supra-molecular formations through hydrogen bonding, and hence may be onsidered as  candidates for molecular imprinting experiments. Possibilities of these substances in combination with water also have to be explored.

Water(H2O) is a wonderful substance with strange physico–chemical properties arising from its peculiar supra-molecular structure. Water is a solvent with higher polarity than similar liquids. H–O–H bond angle is 105 degrees. That means, water molecule is a dipole. Because of this peculiarity, water molecules can exist like a supra-molecular network through hydrogen bonding.  A minimum number of five water molecules will be contained in this network. Such supra-molecular formations are called pentamers. Most of the wonderful properties of water arise from this peculiar capacity of hydrogen bonding and resultant supra-molecular formations. Water molecules (H2O) are symmetric (point group C2ν) with two mirror planes of symmetry and a 2-fold rotation axis. The hydrogen atoms may possess parallel or antiparallel nuclear spin. The water molecule consists of two light atoms (H) and a relatively heavy atom (O). The approximately 16-fold difference in mass gives rise to its ease of rotation and the significant relative movements of the hydrogen nuclei, which are in constant and significant relative movement.

Although not often perceived as such, water is a very reactive molecule available at a high concentration. This reactivity, however, is greatly moderated at ambient temperatures due to the extensive hydrogen bonding. Each water molecules possess a strongly nucleophilic oxygen atom that enables many of life‘s reactions, as well as ionizing to produce reactive hydrogen and hydroxide ions. Reduction of the hydrogen bonding at high temperatures or due to electromagnetic fields results in greater reactivity of the water molecules.

As liquid water is so common-place in our everyday lives, it is often regarded as a ‘typical’ liquid. In reality, water is most atypical as a liquid, behaving as a quite different material at low temperatures to that when it is hot. It has often been stated that life depends on these anomalous properties of water. In particular, the high cohesion between molecules gives it a high freezing and melting point, such that we and our planet are bathed in liquid water. The large heat capacity, high thermal conductivity and high water content in organisms contribute to thermal regulation and prevent local temperature fluctuations, thus allowing us to more easily control our body temperature. The high latent heat of evaporation gives resistance to dehydration and considerable evaporative cooling. Water is an excellent solvent due to its polarity, high dielectric constant and small size, particularly for polar and ionic compounds and salts. It has unique hydration properties towards biological macromolecules (particularly proteins and nucleic acids) that determine their three-dimensional structures, and hence their functions, in solution. Hydration of biological molecules results in formation of gels that can reversibly undergo the gel-sol phase transitions that underlie many cellular mechanisms. Water ionize and allows easy proton exchange between molecules, thus contributing to the richness of the ionic interactions in living organisms.

In reality, hydrogen bonding is a special type of dipole force. It is a force of attraction formed between partial electro negative atom which is part of another molecule. The reason for strength is the partial positive charge attained by hydrogen. Hydrogen is capable of establishing similar bonds with the atoms of nitrogen, fluorine and oxygen. That is to say that the basis of hydrogen bonding is the attraction between one hydrogen atom which is part of a molecule which is attached to oxygen or nitrogen and  oxygen or nitrogen which remains part of another molecule. This force is less powerful than the co–valent bonds which keeps the atoms inside molecule bound together. But these less powerful bonds are responsible for the wonderful bio–chemical qualities of water.

In the ordinary liquid state, in spite of 80% of the electrons being concerned with bonding, the three atoms in water do not stay together, as the hydrogen atoms are constantly exchanging between water molecules due to protonation/deprotonation processes. Both acids and bases catalyze this exchange and even when at its slowest (at pH 7), the average time for the atoms in an H2O molecule to stay together is only about a millisecond. As this brief period is, however, much longer than the timescales encountered during investigations into water’s hydrogen bonding or hydration properties, water is usually treated as a permanent structure.

The presence of ethyl alcohol in water is considered to be a factor reducing the rate of protonation/deprotonation processes, thereby enhancing the stability of hydration shells.

Hydrogen bond strength can be affected by electromagnetic and magnetic effects.

Any factors, such as polarization, that reduces the hydrogen bond length, is expected to increase its covalency. There is still some dispute over the size of this covalency, however any covalency will increase the network stability relative to purely electrostatic effects. As hydrogen bond strength depends almost linearly on its length (shorter length giving stronger hydrogen bonding), it also depends almost linearly (outside extreme values) on the temperature and pressure .

Hydrogen bonded chains (that is, O-H····O-H····O) are cooperative; the breakage of the first bond is the hardest, then the next one is weakened, and so on. Thus unzipping may occur with complex macromolecules held together by hydrogen bonding, for example, nucleic acids. Such cooperativity is a fundamental property of liquid water where hydrogen bonds are up to 250% stronger than the single hydrogen bond in the dimer. A strong base at the end of a chain may strengthen the bonding further.

Water-Ethyl Alcohol Mixture :

 At this stage we have to understand a few facts about Ethyl Alcohol(CH3- CH2 – OH ). The molecules of alcohol also have the dipole structure as water molecules. It is possible for them to establish mutual connection through hydrogen bonding. The molecular weight of alcohol molecul is 46. The molecular weight of water(H2O) is 18. That means that the number of water molecules contained in 18 gram of water and the number of alcohol molecules contained in 46 gram of ethyl alcohol are equal. When alcohol and water are thoroughly mixed alcohol molecules network with water molecules through hydration bonds, The mobility of water molecules is restricted by the bonds established with alcohol molecules. Hence, hydration shells formed in alcohol–water mixture are comparatively more stable. The count of alcohol molecules and the count of water molecules contained in their mixture in 73:27 ratio will be equal. (73% w/w. alcohol and 27% w/w water) This mixturei is known as (40 power   spirit).

Ideal medium for molecular imprining is supposed to contains 87% w/w of alcohol and 13% w/w of water. In this ratio, the number of alcohol molecules will be about more than that of of water molecules. Such a ratio will be very suitable for the production of stable hydration shells. More over, the presence of ethyl alcohol in water is considered as a factor reducing the rate of protonation/deprotonation processes, thereby enhancing the stability of hydration shells

We know that water is a good solvent. Let us see what happens when some foreign molecules are made to dissolve in water. If a foreign(called ‘guest’) molecule, ion,  or colloidal particle happens to enter the matrix of 3-dimensional dynamic network of water molecules, they are entrapped inside this network. Water molecules arrange themselves around the ‘guest’ molecule in a peculiar way by the formation of hydrogen bonding. These formations of water molecules around the ‘guest’ molecules is known as hydration shells. These hydration shells exist in a dynamic state, and are more or less unstable. The ‘guest’ molecules dissolved in water exist in a state of being entrapped inside these hydration shells. This phenomenon can be seen both in ionic solutions and colloidal solutions. Obviously, hydration shells assume an internal spacial arrangement exactly fitting to the 3-dimensional spacial configuration of the ‘guest’ molecule entrapped in them. If we could devise some technique to remove the entrapped ‘guest’ molecules from these hydration shells, without disturbing the hydrogen bonds between the constituent water molecules, these hydration shells can retain the molecular memory of the molecular configurations of the removed ‘guest’ molecules. This rarely studied phenomenon underlies the much debated controversial ‘molecular memory of water’. Actual mechanism and forces underlying this phenomenon have to be investigated minutely by physical scientists. Minute changes occuring in the electron clouds of atoms of water molecules during the formation of hydration shells may be one factor responsible for this phenomenon. It has been well proven that these hydration shells later show a peculiar capability to differentially recognize the original ‘guest’ molecules which were  responsible for their formation. This may be due to the existence of some imprinted memory of those host molecules retained in the hydration shells. This imprinting of memory may be compared to formation of finger prints. As in the case of finger prints, configuration of these molecular imprints also will be a complementary negative of ‘guest’  molecules.  These empty hydration shells, or supra-molecular formations of water subjected to molecular imprinting, may be called ‘hydrosomes’, which means, minute ‘cavities of water’.

Homeopathic process of potentization may be a crude method of preparing hydrosomes, imprinted with various drug molecules(‘guest’), for utilizing as therapeutic agents.  It should be specially noted that the medium used for homeopathic potentisation is not pure water, but it is mixed with ethyl alcohol in a particular ratio. It may be  inferred that the presence of camparatively heavy ethyl alcohol molecules in this mixture may be contributing to stabilize the hydrosomes, preventing their easy dissociation.  The convergent forces of rotational movements to which the mixture is subjected as part of homeopathic potentization, may also be a contributing factor in stabilizing the empty hydration shells.

This peculiar 3-d configuration of ‘hydrosomes’ are destroyed only when the energy level of water molecules are disturbed by the effect of heat,  electricity, magnetism and other electro magnetic radiations. As stated earlier the hydration shells formed in pure water are comparatively unstable. Here lies the importance of the fact that homeopathic potencies are made using alcohol- water mixture.

Information we recently receive from various research institutions, regarding the wonderful  supra-molecular structures of various materials and their hitherto unknown peculiar properties, may greatly contribute in our  efforts to devise a protocol for molecular imprinted drug designing using water. Studies on  ‘water clusters’, ‘crystalline structure of water’, ‘shape memory property’, ‘molecular imprinting’,  ‘nano technology’,  ‘clathrate formations’ and other diverse phenomena are offering promising indications in this direction. We have to utilize all these new revealations in our scientific study regarding the possibility of developing a technology of drug designing by molecular imprinting in water.

We all know that water exists as ice crystals in its solid form. But it has been recently observed that water can exist even in its liquid form in crystals. In reality, water formed by melting of ice is in a state of liquid crystals. The lattice structure which is formed through hydration bonds is responsible for this phenomenon. Molecular imprinting in water is much interested in this area of research pertaining to this peculiar crystalline nature of water. It is believed that in the process of molecular imprinting of water using ‘guest’ molecules,  this crystalline structure of water plays a crucial role. It is likely that more advanced studies about dynamics of crystallization of water may help us to evolve a perfect technology for molecular imprinting in water.

The studies about Clathrate Compounds or host-guest compounds in supra-molecular chemistry is an area in which we should have sincere interest. Clathrates are the molecular networks which are formed when gases dissolve  in water under high pressure. They exist in a peculiar host–guest relationship. The studies about this phenomenon are still in their infancy. Clathrates have a crystalline nature,  existing as molecular networks,  formed by a process of water molecules arranging around the guest molecules. The studies about the dynamics of clathrate formation are also likely to help in evolving a perfect protocol for molecular imprinting in water. Even if  the host molecules are removed from clathrates, the network of water molecules have been found to remain intact. More over, the existing clathrates can induce the formation of similar clathrates. It will be very useful to consider these above discoveries connecting them with the phenomenon of molecular imprinting.

A lot of studies has been so far published regarding shape memory materials.  Several alloys having  crystalline structure have been observed to possess shape memory property. Such materials are known as SMART materials. This phenomenon also has to be understood well while trying to evolve a molecular imprinting technique of drug designing.

It is in the phenomenon of ‘molecular memory of water’ itself that we naturally land on when we attempt to develop molecular imprinted drugs. We have already seen that the alcohol–water molecules contained in the medium used for imprinting  arrange themselves around the ‘guest’ molecules, and form hydration shells. We should develop a way to systematically remove the ‘guest’  molecules entrapped in the hydration shells, so that empty hydration shells or ‘hydrosomes’ remain. These ‘hydrosomes’ will be imprinted with the three-dimensional ‘finger print’ of ‘guest’ molecules used for imprinting.

When molecular imprinted water is  introduced into the organism by any route, is carried by the body fluids, and transported to different parts of body. When molecular imprints come in the vicinity of ligands or active groups of pathological foreign molecules having similarity to the original ‘guest’ molecules, these molecular imprints selectively bind to those pathological molecules. By this process, pathological foreign molecules are prevented from binding with biological molecules, thereby relieving the biological molecules from pathological molecular blocks. This can be described as some sort of ‘molecular scavenging’ or entrapping of pathological molecules, by ‘hydrosomes’ or “molecular imrints”.

Drugs designed through molecular imprinting in water will be the safest of all therapeutic agents so far used in the history medical science. Though there is a chance for these molecular imprints affecting “off-target” molecules or ‘antitargets’ having similarity to the target molecules, such interactions will be of very transient nature, since these molecular imprints will be easily degraded into constituent water-ethyl alcohol molecules. Such temporary interactions with off-target molecules may not lead to any dangerous consequences. Factors such as bioavailability, metabolic half life, and lack of side effects also will be obviously remain in favorable range.

Using various ligands and pathological molecules involved in each disease process as ‘guest’  molecules, we can develop most appropriate specifc designer drugs against almost any disease. Instead of original pathological molecules or ligands, drug molecules having configurational similarity to them also can be used as “guest” molecules in the molecular imprinting protocol. Homeopathic potentization utilizes this strategy, which is the real essence of “similia similibus curentur”. I  hereby appeal to the government and scientific community to take up this task with urgent priority, so that a whole new range of safe and effective designer drugs could be developed though this novel process of molecular imprinting in water.

‘Disease-specific’ and ‘patient-specific’ formulations of potentized drugs

I know most homeopaths cannot tolerate what I am saying below, especially if they are not already familiar with the MIT explanations regarding potentization and biological mechanism of homeopathic cure.

Use of pre-prepared ‘disease-specific’ combinations of potentized drugs added with custom-made ‘patient-specific’ constitutional similimum will make the practice of homeopathy more simple and effective, and will bring down the rate of clinical failures to the lowest minimum level, even for most inexperienced beginners.

For example, we can make an effective anti-febrile formulation by working out with ‘symptom-complexes’ expressed in various types of fevers and finding their similimum separately, and then combining them together in a single container.

Selected drugs should be used preferably in 12c or 30c potencies, and should be procured from most reliable manufacturers.

We can add some specifics, sarcodes and nosodes into this combination, selected using our knowledge of biochemistry regarding the molecular level processes involved in producing a pathological condition of fever.

We can keep this preparation as a disease-specific ANTIFEBRILE stock medicine.

In most cases of fevers, a few drops this formulation put on the tongue of the patient will cure the fever instantly. A few more doses may be repeated at intervals, to ensure the fever is completely gone.

If the fever reccurres in spite of repetitions, or in order to avoid the chances of such reccurences, we can work out the constitutional similimum of the individual patient by considering his mental symptoms and physical generals, and add it also to the stock medicine when dispensing. Such a prescription will be ‘disease-specific’ as well as ‘patient-specific’, and it will be amost perfect prescription that will ensure 100%cure.

In this way, we can prepare stock formulations for all common disease conditions, such as headache, diarrhoea, vomiting, cough, asthma, hypertension, diabetes, lipidemia, rheumatism, urinary infection, colic, gall stones, or anything like that.

When a patient comes, work out his constitutional similimum, add it also to a small quantity of stock formulation, and give to the patient without any theoretical inhibitions in your mind. And see the marvel happening!

Please do not come to argue by quoting aphorisms. Try to understand the scientific logic and rationale behind my suggestion. I have explained it in detail in my book REDEFINING HOMEOPATHY, as will as my blog. Try to read. If not interested, kindly excuse me!

‘Palliation’- Homeopathic and Allopathic

‘Palliation’ in medical context actually means ‘temporary relief’ or removal of some of the most disturbing symptoms in the patient using some drugs, without curing the underlying disease.

Allopathic palliative treatment involves the use of certain chemical drugs in molecular forms. They are used to reduce the sufferings, without any hope of cure by that prescription. In some situations, palliative approach is used to reduce sufferings until correct diagnosis and treatment protocol is finalized. Since chemical molecules can interact with biological molecules, allopathic palliation may produce harmful effects. In fact, allopathic palliation makes the case more complicated, and hence it is normally used as a temporary relief measure only in cases that are considered to be incurable.

Some homeopaths even use allopathic drugs under the label of ‘palliative prescription’. Some others use large quantities of mother tinctures even without any homeopathic indications. Even if you call it “homeopathic” drugs, removal of symptoms using molecular forms of drugs such as mother tinctures, low potency drugs or so-called biochemic salts are actually not at all different from allopathic palliation. Such palliation using mother tinctures and low potency drugs may also harm the patient, or hinder the curative process similar to allopathic palliation, since those drugs in molecular forms are no way different from allopathic drugs regarding their biological mechanism of action. Use of such drugs also may produce harmful effects or make the case more complicated, since the chemical molecules contained in them can produce molecular inhibitions in unexpected biological targets.

To be really “homeopathic” in its real sense, palliation should be produced by applying drugs potentized above 12c, which contain only molecular imprints.

Since molecular imprints cannot interact with biological molecules, and can interact only with pathogenic molecules, homeopathic palliation cannot produce any harmful effects. Potentized drugs act only if there are some molecular inhibitions that could be removed by the molecular imprints contained in the particular potentized drug. Symptoms could be removed using potentized drugs only if the underlying molecular errors are removed at least partially.

Each group of symptoms expressed by the patient points to a particular pathological error in a particular biological pathway caused by inhibition of a particular biomolecule by binding of a particular pathogenic molecule. We can remove symptoms only if the drug we apply contains appropriate molecular imprints that can remove at least some of the molecular errors in the patient.

Homeopathic palliation using potentized drugs never hinders the cure. In its exact meaning, it is actually not palliation, but partial cure. We can convert this partial cure into complete cure by supplying the additional molecular imprints that were missing in the earlier prescription, by new drugs given as complementary prescriptions.

Lesson for homeopaths: If you want to offer palliation to a patient, try to produce it it by administering potentized drugs only. They should be similimum selected on the basis of most disturbing groups of symptoms expressed by the patient. Even if such a partial similimum will not offer complete cure, it never hinders the chances of getting complete cure later through additional homeopathic prescriptions.

Never use mother tincture, allopathic drugs, or any drug in molecular form in the name of palliation. Such practice will complicate the case, and hinder the curative process.


On Posology of Molecular Imprinted Drugs

Some friends ask me to explain my views on posology of molecular imprinted drugs.

While trying to answer this question, we have to remember that the issue of posology has to consider three aspects:

1. Minimum quantity of drug needed to be given per dose to produce a therapeutic action,

2. Maximum quantity of the drug that could be administered as a dose to ensure that there is no bad effects,

3. Most appropriate frequency of administration or repetition of doses.

Regarding the first question, it is difficult to define exactly what is the minimum quantity of molecular imprinted drug to produce therapeutic effect. To do that, we have to know the exact number of biological molecules affected, as well as the exact number of molecular imprints contained in a given measure molecular imprinted drugs. Both are impossible in the present stage of technology available to us.

Size of a molecular imprint will vary depending upon the size of drug molecule used for molecular imprinting, which in turn determine the number of molecular imprints contained. It is not practical to count these numbers. On the other side, it is also not practical to determine the biological molecules inhibited. Only thing we can do is to determine the minimum dose of drugs through experimenting in real situations.

We should remember, according to avogadro, number of water molecules in 18ml of water will be 6.022140857 × 1023. From this, we can calculate the number of water molecules in 1ml. 1ml contains 15 drops. It is not difficult to understand that the number of water molecules contained in even 1 drop of water so huge for calculation. Same way we can calculate the number of alcohol molecules in 1 drop of alcohol.

Overall, it is obvious that one drop or even a fraction of molecular imprinted drugs will contain millions of molecular imprints. As such, we need not worry much about the minimum quantity of molecular imprinted drugs to be used for therapeutic purpose. It may be as small as we can handle. Normally I prefer one drop for one dose.

Regarding the second question, MIT says that molecular imprints cannot do any harm upon biological system. As such, we need not worry at all about the maximum quantity administered as a dose.

Regarding third question, we have to be aware of the possible changes molecular imprints may undergo once introduced in the body.

Molecular imprints could be antidoted by any chemical molecule having conformations affinity. As such, the drugs we consume may get easily antidoted and deactivated by various chemical molecules entering our body through food, inhalation, drinks and many other ways.

Hence we have to repeat the doses in frequent intervals to ensure adequate quantity of molecular imprints to ensure full and lasting therapeutic effect.

Use Of ‘Sarcodes’ In Homeopathy Is Different From ‘Organotherapy’ in Traditional Medicine

Some people think that “ordganotherapy” practiced by certain traditional healers and occult practitioners are equivalent to the use of “sarcodes” in homeopathy. It is totally wrong.

This morning, my new friend from CANADA, Dr Hardev Singh Billing asked me as follows:

“Organotherapy ( sarcodes) very popular in France and Belgium..as well as in Canada very positive results in 4 CH Potency.

Organotherapy or mRNA is to regulate and correct the function of organs and bodily systems on a cellular level (mRNA stands for messenger ribonucleic acid, which mediates the transfer of genetic information from the cell nucleus to ribosomes in the cytoplasm, where it serves as a template for protein synthesis). Organotherapy is postulated to stimulate organ functions, depending on the tissues and related mRNA used.

In cases where organs are damaged due to autoimmune issues, organotherapy substitutes for the organ and accepts the autoimmune antibodies, leaving the organ to stimulate its own restoration….”

I think I have to take this question seriously.

What is known as “Organotherapy” is a technique that makes use of extracts derived from animal or human tissues to treat medical conditions.It is an ancient practice to treat a disease related with a particular organ using an organ with the same organ from another creature. This custom was familiar to the Ancient Indians, Greeks, Romans and many other civilizations. For example, consuming brain tissue was considered a potential treatment for those of low intellect, eating testicles of bulls or stallions to treat impotency in men, cooked ovaries of goats to treat infertility in women, cooked joints of goats to treating joint defects etc. These customs are even practiced by certain traditional healers in India.

Scientific studies have to be done to verify whether “organ therapy” works or not, and if it works, to explain how it works. When consuming organs in cooked or uncooked form, they will be digested and the constituent molecules undergoing various chemical conversions and getting absorbed into the body. Mostly, they will act by supplying essential nutrients to the body. Of course, they will contain some chemical molecules that are specific to the particular organs, and hence, they will have their specific biological actions of their own.
SARCODES used in homeopathy are also derived from body tissues. But homeopathy does not use them as organ-specifics. Instead, they are “proved” by administering in healthy individuals, symptoms collected, and materia medica prepared. Then these sarcodes or tissue products are “potentized” according to homeopathic method. These potentized drugs are used by comparing its materia medica symptoms with the disease symptoms expressed by the particular patient, in the same way as any other potentized drugs. It is obvious that use of SARCODES in homeopathy is entirely different from use of ORGANOTHERAPY in ancient medicine.
According to MIT view, the tissue products used as SARCODES contain diverse types of biological ligands that play specific roles in biological processes. Biological ligands act by binding to various types of specific biological targets, and modulating their normal actions. Biological ligands are very important in maintaining the normal vital processes.
When some exogenous or endogenous molecules have FUNCTIONAL GROUPS similar to those of the biological ligands, those molecules can mimic as the biological ligands and bind to their natural targets, thereby inhibiting the actions of the biological molecules such as enzymes, receptors, transport molecules etc. This situation leads to DISEASE.
When we potentize SARCODES, the biological ligand contained in them are removed, and only their MOLECULAR IMPRINTS remain. When we administer potentized sarcodes in a body, we are actually introducing the molecular imprints of biological ligands. If the pathogenic molecules that have produced inhibitions in biological molecules have functional groups similar to the ligand molecules in the SARCODES we have used to prepare molecular imprints, there will be a ‘conformational affinity’ between the pathogenic molecules and the molecular imprints we introduced. Molecular imprints can bind to the pathogenic molecules due to this conformational affinity, thereby removing the pathological inhibitions of biological molecules. This leads to CURE.
Hope I have scientifically explained the actions of SARCODES, and the difference between SARCODES and ORGANOTHERAPY.
I am thankful to my friend Dr Hardev Singh Billing from Canada, who prompted me to write this note by asking me such a question this morning.

Is Cane Sugar An Ideal Dispensing Vehicle For Homeopathy Drugs? A Rethinking Is Needed!

Cane sugar or SUCROSE is the most prominent substance currently used as homeopathic drug dispensing vehicles. It is used in the form of GLOBULES of different sizes, which are medicated by adding potentized homeopathic drugs.
I think a detailed study of SUCROSE is essential to decide whether it is an ideal dispensing vehicle. Theoretically, an ideal DISPENSING VEHICLE should be a substance with following properties:
In this article, I am presenting some scientific facts related with CANE SUGAR, which I collected from various knowledge sources. I am also giving the complete MATERIA MEDICA of Cane sugar from Clarke’s Materia Medica. Please read these information carefully, and you decide yourself whether CANE SUGAR we regularly feed our patients is an ideal DISPENSING VEHICLE.
Sucrose is common table sugar. It is a disaccharide, a molecule composed of the two monosaccharides, glucose and fructose. Sucrose is produced naturally in plants, from which table sugar is refined. It has the formula C12H22O11.
Sucrose we use in homeopathic pharmacy as dispensing vehicle is extracted, and refined from sugar cane plants. Sugar canes are crushed mills to produce raw sugar which is then refined into pure sucrose. The sugar refining process involves washing the raw sugar crystals before dissolving them into a sugar syrup which is filtered and then passed over carbon to remove any residual colour. clear sugar syrup is then concentrated by boiling under vacuum and crystallised as the final purification process to produce crystals of pure sucrose. These crystals are clear, odourless, and have a sweet taste.
In sucrose, the components glucose and fructose are linked via an ether bond between C1 on the glucosyl subunit and C2 on the fructosyl unit. The bond is called a glycosidic linkage. Glucose exists predominantly as two isomeric “pyranoses” (α and β), but only one of these forms links to the fructose.
Fructose itself exists as a mixture of “furanoses”, each of which having α and β isomers, but only one particular isomer links to the glucosyl unit. What is notable about sucrose is that, unlike most disaccharides, the glycosidic bond is formed between the reducing ends of both glucose and fructose, and not between the reducing end of one and the nonreducing end of the other. This linkage inhibits further bonding to other saccharide units. Since it contains no anomeric hydroxyl groups, it is classified as a non-reducing sugar.
The purity of sucrose is measured by polarimetry, through the rotation of plane-polarized light by a solution of sugar. The specific rotation at 20 °C using yellow “sodium-D” light (589 nm) is +66.47°. Commercial samples of sugar are assayed using this parameter. Sucrose does not deteriorate at ambient conditions.
Sucrose does not melt at high temperatures. Instead, it decomposes—at 186 °C (367 °F)—to form caramel. Like other carbohydrates, it combusts to carbon dioxide and water. Mixing sucrose with the oxidizer potassium nitrate produces the fuel known as rocket candy that is used to propel amateur rocket motors.
Sucrose burns with chloric acid, formed by the reaction of hydrochloric acid and potassium chlorate. Sucrose can be dehydrated with sulfuric acid to form a black, carbon-rich solid, as indicated in the following idealized equation:
Hydrolysis breaks the glycosidic bond converting sucrose into glucose and fructose. Hydrolysis is, however, so slow that solutions of sucrose can sit for years with negligible change. If the enzyme sucrase is added, however, the reaction will proceed rapidly. Hydrolysis can also be accelerated with acids, such as cream of tartar or lemon juice, both weak acids. Likewise, gastric acidity converts sucrose to glucose and fructose during digestion, the bond between them being an acetal bond which can be broken by an acid.
Fully refined sugar is 99.9% sucrose, thus providing only carbohydrate as dietary nutrient and 390 kilocalories per 100 g
There are no micronutrients of significance in fully refined sugar.
In humans and other mammals, sucrose is broken down into its constituent monosaccharides, glucose and fructose, by sucrase or isomaltase glycoside hydrolases, which are located in the membrane of the microvilli lining the duodenum. The resulting glucose and fructose molecules are then rapidly absorbed into the bloodstream. Sucrose is an easily assimilated macronutrient that provides a quick source of energy, provoking a rapid rise in blood glucose upon ingestion. Sucrose, as a pure carbohydrate, has an energy content of 3.94 kilocalories per gram.
When large amounts of refined food that contain high percentages of sucrose are consumed, beneficial nutrients can be displaced from the diet, which can contribute to an increased risk for chronic disease. The rapidity with which sucrose raises blood glucose can cause problems for people suffering from defective glucose metabolism, such as persons with hypoglycemia or diabetes mellitus.
Sucrose can contribute to the development of metabolic syndrome. In an experiment with rats that were fed a diet one-third of which was sucrose, the sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. Another study found that rats fed sucrose-rich diets developed high triglycerides, hyperglycemia, and insulin resistance. A 2004 study recommended that the consumption of sucrose-containing drinks should be limited due to the growing number of people with obesity and insulin resistance.
Studies have indicated potential links between consumption of free sugars, including sucrose which is particularly prevalent in processed foods, and health hazards, including obesity and tooth decay. It is also considered as causing endogenous glycation processes since it metabolises into glucose and fructose in the body.
Tooth decay (dental caries) has become a pronounced health hazard associated with the consumption of sugars, especially sucrose. Oral bacteria such as Streptococcus mutans live in dental plaque and metabolize any sugars (not just sucrose, but also glucose, lactose, fructose, into lactic acid. The resultant lactic acid lowers the pH of the tooth’s surface, stripping it of minerals in the process known as tooth decay.
All 6-carbon sugars and disaccharides based on 6-carbon sugars can be converted by dental plaque bacteria into acid that demineralizes teeth, but sucrose may be uniquely useful to Streptococcus sanguinis (formerly Streptococcus sanguis) and Streptococcus mutans. Sucrose is the only dietary sugar that can be converted to sticky glucans (dextran-like polysaccharides) by extracellular enzymes. These glucans allow the bacteria to adhere to the tooth surface and to build up thick layers of plaque. The anaerobic conditions deep in the plaque encourage the formation of acids, which leads to carious lesions. Thus, sucrose could enable S. mutans, S. sanguinis and many other species of bacteria to adhere strongly and resist natural removal, e.g. by flow of saliva, although they are easily removed by brushing. The glucans and levans (fructose polysaccharides) produced by the plaque bacteria also act as a reserve food supply for the bacteria. Such a special role of sucrose in the formation of tooth decay is much more significant in light of the almost universal use of sucrose as the most desirable sweetening agent.
Sucrose is a disaccharide made up of 50% glucose and 50% fructose and has a glycemic index of 65. Sucrose is digested rapidly, but has a relatively low glycemic index due to its content of fructose, which has a minimal effect on blood glucose.
As with other sugars, sucrose is digested into its components via the enzyme sucrase to glucose (blood sugar) and fructose. The glucose component is transported into the blood (90%) and excess glucose is converted to temporary storage in the liver – named glycogen. The fructose is either bonded to cellulose and transported out the GI tract or processed by the liver into citrates, aldehydes, and, for the most part, lipid droplets (fat).
As the glycemic index measures the speed at which glucose is released into the bloodstream a refined sugar containing glucose is considered high-glycemic. As with other sugars, over-consumption may cause an increase in blood sugar levels from a normal 90 mg/dL to up over 150 mg/dL. (5 mmol/l to over 8.3 mmol/l).
Authorities advise diabetics to avoid sugar-rich foods to prevent adverse reactions.
The occurrence of gout is connected with an excess production of uric acid. A diet rich in sucrose may lead to gout as it raises the level of insulin, which prevents excretion of uric acid from the body. As the concentration of uric acid in the body increases, so does the concentration of uric acid in the joint liquid and beyond a critical concentration, the uric acid begins to precipitate into crystals. Researchers have implicated sugary drinks high in fructose in a surge in cases of gout.
Sucrose intolerance, also called sucrase-isomaltase deficiency, congenital sucrase-isomaltase deficiency (CSID), genetic sucrase-isomaltase deficiency (GSID), is the condition in which sucrase-isomaltase, an enzyme needed for proper metabolism of sucrose (sugar) and starch (i.e., grains and rice), is not produced or the enzyme produced is either partially functional or non-functional in the small intestine. All GSID patients lack fully functional sucrase, while the isomaltase activity can vary from minimal functionality to almost normal activity. The presence of residual isomaltase activity may explain why some GSID patients are better able to tolerate starch in their diet than others with GSID. Signs and symptoms of GSID are, Abdominal cramps and bloating, Diarrhoea and constipation, Vomiting, Hypoglycemia and headaches, Poor weight gain and growth, Upper respiratory tract and viral diseases, Anxiety and heart palpitations, Excess gas production etc.
Sucrose intolerance can be caused by genetic mutations in which both parents must contain this gene for the child to carry the disease (so-called primary sucrose intolerance). Sucrose intolerance can also be caused by irritable bowel syndrome, aging, or small intestine disease (secondary sucrose intolerance). There are specific tests used to help determine if a person has sucrose intolerance. The most accurate test is the enzyme activity determination, which is done by biopsying the small intestine. This test is a diagnostic for GSID. A deficiency of sucrase may result in malabsorption of sugar, which can lead to potentially serious symptoms. Since sucrose-isomaltase is involved in the digestion of starches, some GSID patients may not be able to absorb starches as well. It is important for those with sucrose intolerance to minimize sucrose consumption as much as possible.
Sugar. (Including Saccharum album, White Sugar.) Saccharose. C12H22O1l. Trituration. Solution.
Ascites. Cataract. Chlorosis. Cornea, opacity of. Diabetes. Dropsy. Dyspepsia. Hair, rapid growth of. Headache, periodic. Hoarseness. Liver, affections of. Ranula. Rheumatism. Rickets. Scurvy. Spleen, affections of. Tabes mesenterica.
Like so many other articles of diet, Sugar may be a poison and a medicine as well as a food. Sugar preserves food, as salt does; and both sugar and salt have produced scurvy. Cases of scurvy-rickets in bottle-fed children have been traced to excess of sugar in their food; and the exclusion of sugar from the dietary of the gouty, rheumatic, and the diabetic, shows the pathogenetic power it is credited with among practitioners of the present day. Acidity of the stomach and itching at the anus are common effects of taking too much Sugar. Lippe published “Fragmentary provings and clinical observations obtained principally from S. Bœnninghausen and S. E. Bute, who proved the 30th potency on himself” (Allen). To these symptoms have been added others observed by Swan on a patient who accidentally discovered, after twenty-five years of suffering, that the cause of his trouble was Sugar. All the symptoms disappeared when he abstained from sugar in food or drink, and only reappeared when he took it again by way of experiment. Then, from two to four days after taking sugar, the same train of symptoms invariably occurred in this order: (1) A burning at pit of stomach. A white coat on tongue, so thick
as to cause stiffness of it. Sharp burning pains run up from kidneys to shoulders, passing under scapulæ. Pains in bones from head to foot, causing a rigidity of the muscles so that it was impossible to rise from bed till he had been rubbed. Chill commencing in small of back and spreading up and down. Severe headache and occasional vomiting with the chill. Fever followed with headache, morbid hunger, and a hectic flush. Increased urine, strong odour, white sediment. Great pain in kidneys. Constipation. Sleeplessness. Œdema of feet and ankles. Weakness of legs, as if paralysed, causing staggering. Painful jactitation of feet and legs during the burning in the Stomach. Oppression, slight cough, profuse cream-like expectoration, very offensive, cold. Sac. a. 10m and 5m curedhim of some remaining symptoms, and the 41m enabled him to eat sugar with impunity. Swan also reports (Org. iii. 342) this case: Miss L. was continually eating candies, of which she was very fond, till her digestive organs were affected. A few doses of Sac. a. 30m changed her taste so that she ate no more, and could not even bear the sight of them. This case was also cured with Sac. off.: “Vomiting bile, < in night and at 1 a.m.; old-standing dyspepsia, milk, eggs, and bread being the only food tolerated; great longing for sugar, which > the symptoms.” Farrington traces a great similarity between Sac. off. and Calc. Sac. off. is indicated, he says, in children who are large-limbed, fat, and bloated, with a tendency to dropsy. It has produced opacity of the cornea, and ought to cure it. The children are dainty and capricious; care nothing for substantial food, but want little “nick-nacks”; always cross and whining, and, if old enough, are insolent, and do not care to occupy themselves in any way. Everything too much trouble. H. C. Allen relates (H. P., x. 478) a case of opacity of cornea cured with Sac. a.; and with the same remedy in 2m potency he cured swelling round the ankles following rheumatism. According to Lippe, black-and-tan terrier dogs that eat sugar go blind. The cataract and amblyopia of diabetics are well known. Here, again, Salt and Sugar meet: Burnett has shown in his Supersalinity of the Blood that excess of salt in food has been an important factor in the production of cataract. The symptoms are < in early morning. < From anger. > In erect position (dyspnœa).
Compare: Sacch. l. In rickets, acidity, fat children, Calc. Craving for sweets, Arg. n., Sul. Rickets, Sil. Diabetes; swelled ankles, Arg. n. Kidney-ache, Santal.
1. Mind
Violent temper; irritable; quarrelsome.-Bilious, sanguineous temperament.-Increased modesty of women.-Melancholic mood with the chilliness.-Dainty, capricious; cross and whining; indolent.-Low-spirited, hypochondriacal mood; peevish.-Indifference; as from homesickness.-Disinclined to talk; want of interest.-Stupid.
2. Head
Giddiness from indigestion.-Severe headache with the chill.-Headache every week the same day.-Hair grows; rapidly.
3. Eyes
Eyes closed by swelling (and inflammation) of lids.-Varicose distension of vessels of eyes.-Ophthalmia.-Sight dim.-Cataract.
4. Ears
Discharge of pus from ears.
5. Nose
Sneezing; dry coryza.
6. Face
Changed expression.-Face: pale; deathlike; bloated; œdematous.-Twitching of muscles of r. cheek over malar bone.
8. Mouth
Dulness of teeth (with sour vomiting).-A white coat on tongue, so thick as to cause stiffness in it.-Rhagades, cracks on the tongue.-Ranula.-Inflammation of salivary glands of lining membrane of mouth.-Aphthæ of children.
9. Throat
Ulcers in throat.
11. Stomach
Morbid hunger with the fever.-Nausea early in morning.-Violent retching.-Vomiting of white, viscid, tough mucus.-Periodical vomiting.-Vomiting: of blood; acid, making teeth dull; occasional, with the chill.-Stomach bloated.-Stomach overloaded with sour mucus.-Disordered stomach.-Digestion: impaired; weak, with acidity.-Burning at pit of stomach.-Heat in stomach.-Coldness of stomach.-Pressure in stomach, morning, fasting.-Painful constriction of stomach.-Painful sensitiveness of pit of stomach.-Pain in stomach with hypochondriacal persons.
12. Abdomen
Liver: swollen; indurated.-Bile increased.-Spleen swollen.-Pain in liver and spleen.-Abdomen: swollen; dropsical; hard as a stone (in children).-Tabes mesenterica.-Swelling and induration of mesenteric glands.
13. Stool and Anus
Congested and painful hæmorrhoids.-Itching at the anus.-Diarrhœa, stools watery and debilitating; of mucus and blood; bilious.-Constipation alternating with mucous diarrhœa.-Constipation; stools difficult.
14. Urinary Organs
Sharp burning pains run from kidneys to shoulders, passing under scapulæ.-Great pains in kidneys.-Increased urination; strong odour; white sediment.-Urine diminished.
15. Male Sexual Organs
Enormous swelling of scrotum; r. genitals.-Increased desire.-Frequent involuntary emissions.
16. Female Sexual Organs
Menses diminished.-Menstrual blood pale.-Suppressed leucorrhœa.
17. Respiratory Organs
Irritation of larynx, causing a slight hacking cough, with yellow, saltish sputa, which floats on water.-Dry rawness in larynx.-Hoarse, catarrhal voice.-Hoarseness from reading a short time.-Dry cough.-Cough with children.-Expectoration very offensive.-Breathing oppressed, cold expectoration.-Suffocative attacks, must be bolstered up.
18. Chest
Chest muscles wasted.-Pneumonia.-Swelling of lower part of sternum.-Fulness > by expectorating.-Stitches in l. chest.
19. Heart
Rheumatic pain in heart region.-Pulse weak and irregular.
21. Limbs
Tingling in limbs.-Emaciation of hands and thighs.
22. Upper Limbs
Œdema of arms.
23. Lower Limbs
Œdema of lower limbs; hard as stones.-Paralytic weakness of legs.-Painful jactitation of legs during burning in stomach.-Cramps in calves.
24. Generalities
Emaciation with great appetite.-Chlorosis: with dropsy; after anger.-Plethora.-Fainting attacks.-Scurvy rickets in children.-Pains in bones from head to foot.
25. Skin
Dry skin; perspiration suppressed.-Scurvy.-Pale and red blotches over body.-Panaritium.-Proud flesh in the ulcers.-Old herpes.
26. Sleep
Sleeplessness.-Starts in sleep.
27. Fever
Chilliness from 10 a.m. till evening with melancholic mood.-Chill commencing in small of back, spreading up and down; severe headache and occasional vomiting; fever, followed by headache, morbid hunger, and hectic flush in cheeks; no sweats except when weakened by repeated attacks; before and during the paroxysm burning in stomach and back was simply intolerable; no thirst.-Chilliness alternates with perspiration.-Cold in the head.-Intermittent fever every one, two, or three days, irregular in its type.-Chill followed by profuse sweat.-Sweat on head (neck and shoulders).

Is Milk Sugar Or Lactose An Ideal Dispensing Vehicle For Homeopathy Drugs? A Rethinking Is Needed!

MILK SUGAR or LACTOSE is the most prominent substance currently used as homeopathic drug dispensing vehicles. It is used in the form of TABLETS or PODERS of different sizes, which are medicated by adding potentized homeopathic drugs.
I think a detailed study of LACTOSE is essential to decide whether it is an ideal dispensing vehicle. Theoretically, an ideal DISPENSING VEHICLE should be a substance with following properties:
In this article, I am presenting some scientific facts related with MILK SUGAR, which I collected from various knowledge sources. I am also giving the complete MATERIA MEDICA of LACTOSE from Clarke’s Materia Medica.
Please read these information carefully, and you decide yourself whether MILK SUGAR we regularly feed our patients is an ideal DISPENSING VEHICLE.
Lactose is a disaccharide. It is a sugar composed of galactose and glucose. Lactose makes up around 2–8% of milk (by weight). The compound is a white, water-soluble, non-hygroscopic solid with a mildly sweet taste. It is used in the food industry.[4]
Lactose is a disaccharide derived from the condensation of galactose and glucose, which form a β-1→4 glycosidic linkage. Its systematic name is β-D-galactopyranosyl-(1→4)-D-glucose. The glucose can be in either the α-pyranose form or the β-pyranose form, whereas the galactose can only have the β-pyranose form: hence α-lactose and β-lactose refer to the anomeric form of the glucopyranose ring alone.
Lactose is hydrolysed to glucose and galactose, isomerised in alkaline solution to lactulose, and catalytically hydrogenated to the corresponding polyhydric alcohol, lactitol. Lactulose is a commercial product, used for treatment of constipation.
Several million tons are produced annually as a by-product of the dairy industry. Whey is made up of 6.5% solids of which 4.8% is lactose, which is purified by crystallization. Whey or milk plasma is the liquid remaining after milk is curdled and strained, for example in the production of cheese. Lactose comprises about 2–8% of milk by weight. Industrially, lactose is produced from whey permeate – that is whey filtrated for all major proteins. The protein fraction is used in infant nutrition and sport nutrition while the permeate can be evaporated to 60–65% solids and crystallized while cooling Lactose can also be isolated by dilution of whey with ethanol.
Infant mammals nurse on their mothers to drink milk, which is rich in lactose. The intestinal villi secrete the enzyme lactase (β-D-galactosidase) to digest it. This enzyme cleaves the lactose molecule into its two subunits, the simple sugars glucose and galactose, which can be absorbed. Since lactose occurs mostly in milk, in most mammals, the production of lactase gradually decreases with maturity due to a lack of continuing consumption.
Many people with ancestry in Europe, West Asia, South Asia, the Sahel belt in West Africa, East Africa and a few other parts of Central Africa maintain lactase production into adulthood. In many of these areas, milk from mammals such as cattle, goats, and sheep is used as a large source of food. Hence, it was in these regions that genes for lifelong lactase production first evolved. The genes of adult lactose tolerance have evolved independently in various ethnic groups. By descent, more than 70% of western Europeans can drink milk as adults, compared with less than 30% of people from areas of Africa, eastern and south-eastern Asia and Oceania. In people who are lactose intolerant, lactose is not broken down and provides food for gas-producing gut flora, which can lead to diarrhea, bloating, flatulence, and other gastrointestinal symptoms.
Its mild flavor and easy handling properties has led to its use as a carrier and stabiliser of aromas and pharmaceutical products.[4] Lactose is not added directly to many foods, because its solubility is less than that of other sugars commonly used in food. Infant formula is a notable exception, where the addition of lactose is necessary to match the composition of human milk.
Lactose is not fermented by most yeast during brewing, which may be used to advantage. For example, lactose may be used to sweeten stout beer; the resulting beer is usually called a milk stout or a cream stout.
Yeast belonging to the genus Kluyveromyces have a unique industrial application as they are capable of fermenting lactose for ethanol production. Surplus lactose from the whey by-product of dairy operations is a potential source of alternative energy.
Another significant lactose use is in the pharmaceutical industry. Lactose is added to tablet and capsule drug products as an ingredient because of its physical and functional properties, i.e., compressibility and cost effective use. For similar reasons it can be used to cut (dilute) illicit drugs.
Lactose intolerance is a condition in which people have symptoms due to the decreased ability to digest lactose a sugar found in milk products. Those affected vary in the amount of lactose they can tolerate before symptoms develop.[1] Symptoms may include abdominal pain, bloating, diarrhea, gas, and nausea. These symptoms typically start between one half and two hours after drinking milk or eating milk products. Severity depends on the amount a person eats or drinks. t does not cause damage to the gastrointestinal tract. .
Lactose intolerance is due to the lack of enzyme lactase in the small intestines to break lactose down into glucose and galactose. There are four types: primary, secondary, developmental, and congenital. Primary lactose intolerance occurs as the amount of lactase declines as people age. Secondary lactose intolerance is due to injury to the small intestine such as from infection, celiac disease, inflammatory bowel disease, or other diseases. Developmental lactose intolerance may occur in premature babies and usually improves over a short period of time. Congenital lactose intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth.
Lactose intolerance primarily refers to a syndrome having one or more symptoms upon the consumption of food substances containing lactose. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms. “Lactose malabsorption” refers to the physiological concomitant of lactase deficiency (i.e., the body does not have sufficient lactase capacity to digest the amount of lactose ingested). Hypolactasia (lactase deficiency) is distinguished from alactasia (total lack of lactase), a rare congenital defect.
Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy caused by lactase deficiency. Milk allergy, occurring in only 4% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction.
The principal symptom of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and vomiting (particularly in adolescents). These appear one-half to two hours after consumption. The severity of symptoms typically increases with the amount of lactose consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diets without ill effects.
Lactose intolerance is classified according to its causes as:
Lactose is also a commercial food additive used for its texture, flavor, and adhesive qualities. Lactose is often used as the primary filler (main ingredient) in most prescription and non-prescription solid pill form medications, though product labeling seldom mentions the presence of ‘lactose’ or ‘milk’, and neither do product monograms provided to pharmacists, and most pharmacists are unaware of the very wide scale yet common use of lactose in such medications until they contact the supplier or manufacturer for verification.
From Clarke’s Materia Medica
Amblyopia. Angina pectoris. Body-odour, offensive. Diabetes. Dyspepsia. Earache. Gout. Headache. Hysteria. Labia, soreness of. Nervousness. Neuralgia. Ovaries, affections of. Over-exertion. Ptosis. Sciatica. Sighing. Stye. Umbilicus, inflammation of.
Hahnemann chose globules of Saccharum lactis as the chief vehicle of his remedies, because he considered it the most inert substance he could find. But his method of attenuating remedies had shown that no substance is inert in attenuations, and experience shows that no substance is absolutely inert in any form. H. A. Hare says of Sac. l.: “Scientific and clinical studies have shown it to be possessed of very great diuretic powers when given in full doses.” He says further, that its direct action on the kidneys and its slight action elsewhere indicate it in renal dropsy and renal inactivity; that it acts best in cases where albuminuria is absent, and that it causes profuse diuresis in infants fed on it.
I have frequently met with patients who could not take Sac. l. either unmedicated or as a vehicle without inconvenience. One patient when taking pilules of Sac. l. three times a day complained that they made his “eyes ache and feel weak.” One of Swan’s provers had this symptom: “Sight fails; eyes tire very easily.”
Swan is the authority for Sac. l. as a homœopathic remedy. He has published (Materia Medica) a full pathogenesis of Sac. l., proved in the potencies from 30th upward, together with confirmed and cured symptoms. Eleven provers and observers contributed. I have bracketed the cured symptoms in my Schema. Sac. l. causes sensations of both coldness and heat. One of the cold sensations is this: “Sensation of extreme cold passing in a fine line from centre of pubes to a point two or three inches above.” Swan regards cold pains as a, keynote, and records this case: Mr. S. had an excessively cold neuralgic pain in cartilage of both ears, the right being the worst, with tingling as if frost-bitten; rubbing with difficulty restored the warmth. Lancinating, neuralgic pains in forehead; in occiput; extending from region above ears down through ears into muscles of neck; in both eyes; < by least breath of air; skin sensitive to touch as in inflammatory rheumatism. These pains were icy cold, as if produced by an extremely fine ice-cold needle. As Sac. l. has “fine cold pains” and pains passing in all directions, Sac. l. 1m was given, and relieved all the pains within an hour. (Sac. off. has “cold expectoration.”)
The symptoms are < before a storm; in damp room or basement; morning and evening; by blue and yellow colours; exertion; mental excitement. > By warmth of fire; by red colour; after 4 p.m.
Camph. < effects of Sac. l. Compare: Sac. off., the Lacs. Right cheek bone, Mg. c. Roof of mouth, Mang. Ball sensation in rectum, Sep. < From sound of running water, Hdfb. Radiating pains, K. bi. Kidney ache, Santal, Sac. off. Fatigue, Pic. ac., Mg. c. Heat in heart, Lachn. > Lying left side, Lil. t. < From damp, Dulc. Sensitiveness, K. iod., Mg. c.
Mental excitement. Over-fatigue.
1. Mind
Sensation as if it were only by a great effort that she kept together.-Loses her way in well-known streets.-Imagines: that there is a large hole in her back just above sacrum; that her mother wants to kill her; that some one is behind her.-Extremely nervous, jumps from her seat at least unusual noise..-Was taken suddenly with fear and trembling of whole body, as from fright.-Longing and melancholy as if homesick, with oppressed breathing.-Her heart aches as if it would burst, yet she cannot weep.-Great fear of death during paroxysm of pain in heart at night.-Inclined to be sarcastic and fault-finding.-Cross and fault-finding, could not speak a pleasant word to any one.-Hysteria in evening, laughing and crying, jumping up and lying down, but could not stand, fell to r. side.-Laziness.
2. Head
Pain about middle of r. lambdoidal suture, through to same point on l. side.-Sharp jumping pains behind r. ear.-Burning like fire, and a thick feeling in a lengthwise strip of two fingers’ breadth extending from r. frontal eminence to r. side of vertex for fifteen minutes.-L. side of head felt all drawn up.-Pain in l. eyebrow.-Pain passing from front of l. ear deep into brain.-L. temple sore to touch.-Sensation as of pressure on frontal bone at inner canthi of l. eye; felt very sore.-Sharp darting pain on l. side of head from temple to occiput.-Forehead feels very heavy, with a tendency to fall forward.-Sharp pain in forehead passing back and forth from one temple to the other.-Head aches all over top and feels drawn up.-Head feels large, and as though all the blood in the body had gone into the head.-Head feels confused, and as if it were tossing on a rough sea.
3. Eyes
Pain through r. eye inwards.-Severe pains in both canthi of r. eye.-Dryness of eyeball so that the lid would stick to it as if it wanted lubricating, preventing opening and shutting of eye or winking.-Swelling of r. upper lid, which increased to a large stye, the lid and all round eye being swollen and red; on third day it broke in two places and discharged copiously.-Washing eyes in cold water causes a sensation as if needles were sticking into them.-Eyelids feel swollen, which is not the case.-Can only elevate upper lids half way.-Looking at bright light dazzles and makes her close eyes; no pain.-Sight fails; eyes tire very easily.
4. Ears
Pain in r. ear and underneath it.-Painfulness of r. external ear (concha), with burning like an ulcer, also when touched.-Pain passing from r. ear to shoulder.-Pain from r. ear to lower part of inferior maxillary bone.-Pain in l. ear and sensation as if there were a gathering.-Shooting
pains in and behind ears and all over face.-Pains in external ears and behind them.-Sharp pain inside both ears.-Reverberation of voice when speaking.-Buzzing sound in r. ear.-Sensation as if she could not hear, but she could.
5. Nose
Pain in r. (and l.) side of nose.-Pain in end of nose.-Ridge of nose extremely sore; it feels sore to touch or from the least movement of facial muscles; the l. side is the worst and somewhat swollen.
6. Face
Pain passing from corner of mouth to forepart of r. axilla.-Face feels as if there were one large pain that covered the whole of it.-Burning in cheek-bones towards temples and lower jaw.-Pain all over face, then centring in r. ear.-(Darting, shooting pain, centred in about middle of r. cheek, extending thence up to eye, esp. r. inner canthus, to ear, and up into r. temple, most severe at centre of cheek, considerably decreasing the further it extends from the centre.).-(Swelling of face with pain in head extending down neck and back to feet.).-Wretched appearance, sad expression of face; eyes look as from weeping, though she has not wept.-Great pallor of face with dark places under eyes.-Corners of mouth smart and burn.-Symphysis menti smarts.
8. Mouth
Sore on l. side of tongue.-Tongue coated: yellow on each side, but none on middle or edges; white; yellow.-Lips feel very sore and raw.-Lips dry, with great thirst.-Taste: putrid in mouth after eating; fine spicy taste; like fresh nuts.-Thick bitter mucus in mouth during morning; food tastes fresh, as if there were no salt in it.-Burning in whole mouth.-Roof of mouth sore.-Soreness like blisters in mouth and on
9. Throat
Sensation when swallowing as of a fish-bone in throat.-Spasmodic stricture in œsophagus.-Globus hystericus after lunch at noon, with dull, sick headache.-Throat very sensitive to external pressure; the least pressure causes a feeling as if she were choking.
10. Appetite
Hungry all the time.-Desire for dainties.-When first getting out of bed feels faint for something to eat.-After eating: feeling of distension.-Great thirst; wanted large quantities of very cold water.
11. Stomach
Nausea like sea-sickness.-Nausea does not affect appetite.-Violent sickness, going on all day (agg.-R. T. C.).-Dyspepsia after eating hot pie-crust.-Pressure in stomach as if she had eaten something indigestible.-Heartburn, with sweet taste coming from stomach, without waterbrash.
12. Abdomen
Feeling as if ulcerated anteriorly over r. short ribs, < from touch and when stooping; slight swelling there; also all next day till towards evening.-Pain about length of finger above l. hip, which would come when leaning back, lasted two days, followed by severe pain in forehead.-Sharp pain passing across bowels just above navel and all round body.-Inflammation and soreness of lower half of navel, passing off by morning, with greenish yellow discharge, staining the clothes.-Abdomen sore to touch, painful from the jar caused by walking.-Pain commencing at waist and passing to top of r. breast.-Pain in l. hypochondrium passing under l. breast.
13. Stool and Anus
Severe pain passing through abdomen during stool; felt very sore inside.-Stool preceded by shooting pains across abdomen, which are.> by stool.-Before stool pains in breasts and upper abdomen.-Before stool hands and whole body exhaled a fæcal odour, which passed were a great ball in rectum, much straining, and some flatulence, but no stool and no > from the flatulence.-Stools smell like rotten eggs.-Great soreness round anus, extending three inches up rectum inside.-Constant pressure and soreness at anus, waking her at night.-Creeping, itching, and crawling round anus, extending three inches inside rectum, > for a short time by rubbing.-Shooting pains in rectum.
14. Urinary Organs
Urination followed by a thick Yellow discharge.-Soreness of urethra during urination.-Very severe pain in r. side of abdomen before urination, and sometimes, but not often, lasting during urination, ceasing with it.-Constant and urgent inclination to urinate, with cutting pain streaking up urethra after each passage.-Frequent and violent urging to urinate, with passage of a large quantity each time.-Urine causes intense pain when coming in contact with the labia, which are very sensitive.-Sound of running water produced urination; no power to restrain it.-Urinates very frequently large quantities.-(Involuntary urination in large quantities several times during night.).-(Delay of urination for some time, though desire and opportunity occur.).-Urine stains a dark yellow.
16. Female Sexual Organs
Menses commenced too early; no pain.-Menses very dark.-Profuse greenish-yellow leucorrhœa.-At times bloody leucorrhœa.-Pain in region of r. ovary.-L. (and r.) ovarian region very weak and painful when walking.-Dragging-down sensation in pelvic region.-Lobulated growths on each side of vagina, nearly filling it; extremely sore and sensitive to touch, or from the pressure caused by sitting; coming on gradually and lasting more than three months.-Itching of labia.-Extreme soreness and rawness of labia and entrance to vagina, with profuse greenish-yellow leucorrhœa.
17. Respiratory Organs
Sharp pain passing into upper r. breast, about an inch deep; very sore to touch after the pain.-Pain in r, breast.-Constant pain under l. breast, < when bending forward.-Lancinating pains under l. breast, which took away the breath.-Severe pains under l. breast at every inspiration.
19. Heart and Pulse
Sensation in heart as if a fire were there, with a feeling as if heart would burst, or at times as if a heavy weight were lying on it, all of which spreads from this region over whole inner and outer chest.-Awoke at midnight with severe pains about heart, which seemed as if it had almost stopped beating, with a numb pain about heart, lips, and tongue; great fear of death; when the pains passed off they left great soreness round heart; tingling in lips and tongue; could not lie on l. side; felt numb and strange all over; pulse intermittent.
20. Neck and Back
Pain passing up and down along r. side of neck.-Hot flashes all over back of neck and shoulders.-Pain with soreness at upper vertebral border of r. scapula.-Pain in r. side of back between scapula and sacrum.-Pain in l. side of back from scapula to sacrum.-Pain in sacrum.-Pain each side of sacrum.-Pain in sacral region, < when taking a long breath.-Pain in back from sacrum to scapulæ.-Pain passing up back from sacrum.-Pain passing up and down from tip of coccyx to r. shoulder.-Sharp pain passing from middle of scapula down outside of arm to end of middle finger, and sometimes to end of little finger.-Pain below l. scapula.-Severe pain under l. scapula.-Pain running up back from waist, l. side.-Constant pain all day in region of l. kidney.-Pain in back part of waist, passing from r. to l.-Pain in lumbar region.-Pain or aching in small of back < by leaning backward, for three or four days.-Pain passing from lumbar vertebræ to half way up dorsal, and then shooting off into both scapulæ.-Dull ache all over back and in r. arm; cannot bend body far forward as it causes intense pain in coccyx; when stooping, as in picking anything from floor, has to incline body to one side or other.-Back aches the whole length of spine.
22. Upper Limbs
Swelling in r. arm below elbow, sore to touch, and pains when she moves arms in certain directions.-Pain in forepart of r. upper arm.-Pain from top of r. shoulder to nape of neck.-Pain from r. shoulder passing down to waist.-Pain in r. shoulder passing a short distance down back.-Pain in top of r. shoulder passing to back and upper part of neck.-Pain passing from r. shoulder to elbow.-Pain in back of r. shoulder.-Pain from r. shoulder to l. breast.-Pain in axillæ.-Sharp pain in all r. fingers except little finger.-Pain in both hands passing to ends of fingers.-Skin under nails looks dirty, it cannot be washed or scraped off for two days.-Pain in dorsal surface of r. hand.-Pain in palm of r. hand.-Itching in palm of r. hand.-Pains all through r. hand.-Grasping anything with r. hand causes pains to pass from all the fingers into palm.-Violent itching of a liver spot on r. hand.-Pains in hands passing in all directions.-Pain in palmar surface of r. wrist passing into thumb.-Pain passing from tip of r. little finger to elbow.-Pain in r. wrist.-Pain passing from r. wrist to elbow.-Pains in both wrists, encircling them.-Pain with slight stiffness in both wrists.
23. Lower Limbs
(Inflammation and awful pain extending down whole trunk of r. sciatic nerve.).-Pains in thighs and hips.-Soreness of gluteal muscles on pressure.-Soreness in streaks, extending from anus down back of legs to heels; can feel a rigidity (not raised) where the soreness is.-Hot flashes in lower limbs.-Pain from forepart of r. knee to anterior-superior spine of r. ilium and passing back to middle of sacrum.-Pain in r. instep when bending foot.-(Pain like gout in r. toe, sometimes slight pains upwards in r. limb; toe will not bear contact of any shoe; pain always the same standing, walking, or lying down; continued exercise < it.).-Balls of feet covered with little corns, which are very painful when walking.-All her corns become painfully sensitive.
24. Generalities
Sensitive in every part of body.-Small shooting pains all over her in morning.-Throbbing in various parts of body.-(Short flying, darting stitches in different parts of body, quite painful, but bearable, appearing in head, ears, and face, as well as in extremities, not confined to any especial locality.).-(Great physical exhaustion, caused by overwork, completely relieved; repeatedly verified by Swan and others.).-The pains during the proving were < by a coming storm, the approach of which was felt some twelve hours previously.-Pains were < in damp room or basement, but > if there was a fire.-All symptoms > after 4 p.m.-Pains were generally < morning and evening.-Symptoms < by blue and yellow colours; > by red.-Prostration from mental excitement (Rushmore).
25. Skin
Very restless at night from itching all over body as soon as she is covered in bed.-Itching of both shoulders.
26. Sleep
Continual yawning all day.-Sleeplessness after midnight.-Cannot sleep on r. side.-Cannot go to sleep without putting arms over head.-Impossible to lie straight in bed, finds herself continually lying diagonally across bed.-Has to lie on l. side as she is comfortable in no other position.-Awoke with the impression that she had dreamed of dreadful pains in chest; does not know whether it was a dream or a reality.-Fatiguing dreams all night.
27. Fever
Great coldness as if a chill were coming on; hands, particularly fingers, feet, toes, icy cold; could not keep warm in bed covered with clothes, and during day sat near, a stove but could not get warm.-Hot flashes inside body pressing from below upward.-Strange restlessness at night, feeling of great heat all over, body covered with a light perspiration, just enough to feel uncomfortable.

Sarcodes Should Be Understood In Terms Of The Biological Ligands They Contain

Elsewhere im my articles I have discussed about need of developing a new range of Molecular Imprinted Drugs using biological ligands  as the templates for imprinting.

Sarcodes used in homeopathy should be understood in terms of biological ligands they contain. When potentizing the sarcodes, we are actually producing Molecular Imprints of their constituent biological ligands.

Two important questions have to be answered regarding sarcodes when considering from MIT perspective:

1. If sarcodes are natural biological ligands having specific functional roles in human organism, how they become pathogenic agents, requiring the intervention of their own potentized forms or ‘molecular imprints’?

2. If the sarcodes are biological ligands being essential parts of living system, will not their physiological functions get negatively affected by the use of their potentized forms, since it is true that potentized form of a drug substance can antidote the biological effects of same drug in crude form?

Let us consider pituitary hormones first. They play a decisive role in the whole metabolism of the organism, and hence called ‘master gland’. Pitutary hormones control many enzyme systems in our body. Then how can they act as pathogenic agents, requiring the use of potentized pituitary extract?

Next question is, when we use potentized pitutrin as a sarcode, will it not act as an antidote towards molecular forms of pituitary hormones and create dangerous
consequences, by disrupting the whole endocrine activities mediated by pituitary hormones?

Pepsinum is very important in digestion of proteins. If pepsinum 30 is given to a person, will it create problems in protein digestion by deactivating pepsin molecules? If they cannot antidote pepsin molecules, how can they act as therapeutic agents?

Thyroid hormones play very important roles in metabolic activities in the living organism. Then how it can be pathogenic agents, requiring the intervention of potentized thyroidinum? Will not potentized thyroidinum hinder the biological processes mediated by thyroid hormones?

These are very pertinent questions we have to answer while trying to explain the science behind using of potentized sarcodes.

We can answer these questions only if we know the dynamics of molecular processes involved in biochemical interactions.

Every biological molecules, especially those belonging to hormones, signaling molecules(cytokines), neuro-chemicals, antibodies and enzymes being circulated in the organism enter into two types of biological interactions:

1. ‘On-target interactions’ 2. ‘Off-target interactions’.

‘On-target’ interactions are those happening between natural ligands and their genuine natural biological targets. Such interactions are essential part of vital processes through which biochemical pathways are carried unhindered.

Natural ligands and their genuine targets interact through two steps:

a). molecular identification and binding, which is effected by complementary conformational affinity between targets and ligands,

b). actual chemical interaction, which is effected by perfect charge affinity between ligands and their natural targets.

Off-target interactions are those accidentally happening between ligands and wrong targets having conformational affinity only. In the absence of exact charge affinity, no chemical changes occur. Such interactions are always ‘inhibitory’, temporarily or permanently deactivating the involved biological molecules. Such ‘inhibitory’ off-target
interactions inevitably lead to derangement in associated biochemical pathways resulting in pathological states.

‘Off-target’ inhibitions caused by biological molecules such as hormones, enzymes, antibodies, signaling molecules(cytokines) and neurochemicals are causative
factors of a wide range of pathological conditions in living beings.

Sarcodes, or potentized preparations of these biological molecules, which contain their ‘molecular imprints’, can effectively remove these molecular inhibitions and thereby act as therapeutic agents. Here lies the importance of sarcodes in homeopathic

Then comes the issue of selective action of the potentized sarcodes. As any other molecular imprints, molecular imprints in potentized sarcodes also cannot interfere in in the interactions between natural ligands and their genuine targets which involves conformational affinity as well as charge affinity. Since molecular imprints act through conformational affinity only, they can interfere in only inhibitory ‘off-target’ interactions.

It is now obvious that thyroidinum 30 cannot interfere in the essential biochemical processes mediated by thyroid hormones, Piturin 30 cannot interfere in the natural actions of pituitary hormones. This principle is applicable to all potentized sarcodes. We can use potentizeds arcodes above 12c without any fear of adverse effects.

Sarcodes or potentized biological ligands can play a very important role in the treatment of diverse types of diseases belonging to metabolic, emotional, psychosomatic, and ontological factors. They can also be part of constitutional prescriptions.

Pathogenic molecules cause diseases by binding to the biological targets and inhibiting their actions by mimicking as their natural ligands, due to the similarity of conformations of their functional groups.

Molecular Imprints of biological ligands can bind and deactivate the pathogenic molecules having functional groups similar to that of the biological ligands used for preparing the particular Molecular Imprints .

It is by this molecular mechanism that the molecular imprints of thyroid hormones contained in potentized THYROIDINUM removes the molecular inhibitions in the cellular receptors of thyroid hormones caused by pathogenic molecules.

We often experience cases where the patient shows symptoms of thyroid deficiency, but thyroid function tests will show normal production of thyroid hormones. It is a very confusing situation for physicians. What actually happens is, cellular receptors of thyroid hormones are blocked by some pathogenic molecules having functional groups similar to those of thyroid hormones binding to the receptors, presenting the interactions between thyroid hormones and their receptors.

If potentized THYROIDINUM.is applied in such cases, molecular imprints contained in the potentized drugs will bind to the pathogenic molecules, there by clearing the pathological inhibitions of receptors. Interactions between thyroid hormones and their biological targets are brought back to normal, and the deficiency symptoms of thyroid hormones are relieved.

It is by this same biological mechanism most of the HORMONE REMEDIES as well as the whole class of SARCODES used in homeopathy actually work. We should study SARCODES in terms of biological ligands they contain.



Does Peer-Review Guarantee The Correctness of Conclusions of a Research Paper?



Many people believe that peer-reviewed papers published in journals are ultimate proofs for the correctness of interpretations and conclusions of a Research paper.

Actually, peer review is a process used to determine an academic paper’s “suitability for publication”.

Peer review does not guarantee correctness of a theory, but guarantees only that the format, language, arrangement, organization and presentation of a “paper is suitable for publication”.

We all know there are thousands of peer reviewed articles published in various journals proposing many absurd theories about homeopathy.

Wikipedia says: “Peer review is generally considered necessary to academic quality and is used in most major scientific journals, but it does by no means prevent publication of all invalid research.”

Please note, peer review “does by no means prevent publication of all invalid research.”!

Publishing a Peer reviewed article does not mean that the ideas proposed in the article are true and beyond any criticism.

Nobody here questions the claim that the researchers detected nano-sized particles of some elements. What we ask is for an explanation regarding the source of this particles, as well as their role in the therapeutic properties of potentized drugs.

Here I am sharing two slides presented at a “scientific seminar” by a “homeopathy scientist” regarding his ‘nanoparticles study’ of AURUM METALLICUM. His work is also published in a peer reviewed journal!

Watch both slides carefully. It is said that potentized aurum met contains ‘nanoparticles’ containing Aurum, Aluminium, Silica, Pottassium, Ferrum, Cuprum, Indium, Hafnium, Sodium, Chlorine, Boron, Cobalt and Carbon, along with ‘Quantum Dots’.

Nanoparticles detected in Aurum Met contains Aurum in following ratios:

6C contains 2.82%, 30C contains 89.06%, 200C contains 12.14%, 1M contains 1.24%, 10M contains 24%, 50M contains 9.73 %, CM contains 6.58% of elemental aurum.

15.63% of ALUMINIUM is present in nanoparticles detected in Aurum Met 1M. But other potencies of Aurum met does not contain any ALUMINIUM.

Where from this aluminium came in aurum met 1m only, which was not present in 6c, 30c, 200c, 10m or cm?

See the fun.Nanoparticles detected in Aur met 1m contains only 1.24% aurum, where it contains 15.63% aluminium.

If ‘nanoparticles are active principles of AURUM MET 1M, does it act by 15.63% aluminium or 1.24% aurum?

If AUR MET 6C contains AUR 2.82% and CUPRUM 75.82%, which will be the active principles? CUPRUM or AURUM?

If AUR 200 contains AURUM 12.14%, POTTASSIUM 29.36%, CUPRUM 25.8%, and SODIUM 20.08%, how can you say AURUM NANOPARTICLES are the active principles of Aur Met 200?

If AUR MET 50M contains AURUM 9.73% , CUPRUM 53.27%, and COBALT 23%, how can you say it is AURUM MET? Rather callit and use it as CUPRUM MET?

If AURUM MET CM contains AURUM 6.58%. CUPRUM 35.36, and HAFNIUM 36.56%, is it appropriate to use it as AURUM?

Hope some ‘nanoparticles specialists’ would explain.

If you look into these two slides carefully, you will get a lot of things to laugh at!!

If AUR MET 6C contains AUR 2.82% and CUPRUM 75.82%, which will be the active principles? CUPRUM or AURUM?

If AUR 200 contains AURUM 12.14%, POTTASSIUM 29.36%, CUPRUM 25.8%, and SODIUM 20.08%, how can you say AURUM NANOPARTICLES are the active principles of Aur Met 200?

If AUR MET 50M contains AURUM 9.73% , CUPRUM 53.27%, and COBALT 23%, how can you say it is AURUM MET? Rather callit and use it as CUPRUM MET?

If AURUM MET CM contains AURUM 6.58%. CUPRUM 35.36, and HAFNIUM 36.56%, is it appropriate to use it as AURUM?

Remember, they have published these works in “peer reviewed journals”, and a lay man like me should not question it!

Peer-reviewed nonsense! Who are those peers?

Any research paper has TWO aspects. One is related with the the methods used in research and second is the interpretations and conclusions. Peer reviewers consider the first part only to recommend publication. They never verify whether the interpretations and conclusions are correct. If methods and format is according to standards, they will accept it for publication. That is why we say a lot of research works published, with nonsense interpretations and conclusions.

If you have a brain, use it to decide what is right and what is wrong. Do not accept anything as truth, only because there is a “peer reviewed paper” published about it. Do not close your mind towards a new idea only because there no a “published paper”. If you use your brain, you will realize that there are a lot of “peer reviewed papers” which make utter nonsense theories. About homeopathy also. Like nanoparticles theory.

Cactus Grandiflorus- Use It Only in Potencies Above 12c In Cardiac Emergencies

There is a confusion existing among homeopaths regarding the use of CACTUS in conditions of cardiac emergencies. Some people prefer to use mother tinctures and low potencies, whereas others prefer 30c and higher potencies.

CACTUS GRANDIFLOROUS or NIGHT-BLOOMING CEREUS is the plant from which our drug CACTUS is procured.

Raw CACTUS juice contains large amounts of Vitamin K, which contributes to the blood-clotting properties it displays during drug proving.

Potentized CACTUS contains molecular imprints of vitamin k, which help in reversing the blood clotting process by binding to vitamin k in the organism. Thereby CACTUS 30 gives instant relief in cardiac emergencies by dissolving blood clots that block the arteries.

Crude CACTUS was proved to have following actions:

1. Acts on circular muscular fibers, hence constrictions.

2. Favors formation of clots speedily.

These two actions are very much similar to what happens during a coronary artery blockage. Circular muscular fibres of coronary arteries suddenly contracts spasmodically, thereby narrowing the lumen of arteries. Blood clots forms and block these arteries, which results in the emergency situation.

That means, Molecular imprints contained in potenized CACTUS can reverse these processes happening during a heart attack. It relaxes the artery walls, dissolves the blood clots and facilitates the blood flow to cardiac muscles thereby preventing tissue death.

Frequent repetition is very important until tiding over the emergency situation.

During acute cardiac emergencies due to coronary artery blockage, give CACTUS 30 (dilution) in frequent doses until symptoms subside or expert medical care is made available. For last many years, I ask people in high risk group to always carry a 30ML bottle of CACTUS 30 (dilution) with them WITHIN REACH. Many of them had informed me that it had helped them to save their own life or others’ life during emergencies.

Never use CACTUS Q in such situations. It is expressly said in materia medica that “Cactus favors formation of blood clots speedily” during provings with crude forms. That means, “potentized Cactus can dissolve blood clots” according to similia similibus curentur.

See the Cardiac symptoms of CACTUS:


Acts on circular muscular fibers, hence constrictions.

*It is the heart and arteries especially that at once respond to the influence of Cactus, producing very characteristic constrictions as of an iron band.

This sensation is found in various places, oesophagus, bladder, etc.

The mental symptoms produced correspond to those found when there are heart affections, sadness, and melancholy.

Whole body feels as if caged, each wire being twisted tighter.

Atheromatous arteries and weak heart.

Congestions; irregular distribution of blood.

*Favors formation of clots speedily.

Great periodicity.

Toxic goitre with cardiac symptoms.

Cactus is pulseless, panting and prostrated.

*Fear of death.

Screams with pain.


*Constriction of oesophagus.

Dryness of tongue, as if burnt; needs much liquid to get food down.

*Suffocative constriction at throat, with full, throbbing carotids in angina pectoris.

*Oppressed breathing as from a weight on chest.

*Constriction in chest, as if bound, hindering respiration.

Inflammation of diaphragm.

*Heart-constriction, as from an iron band.

Heart weakness of arterio-sclerosis.

Tobacco heart.

Violent palpitation; worse lying on left side, at approach of menses.

*Angina pectoris, with suffocation, cold sweat, and ever-present iron band feeling.

*Pain in apex, shooting down left arm.

*Palpitation, with vertigo; dyspnoea, flatulence.

*Constriction; very acute pains and stitches in heart; pulse feeble, irregular, quick, without strength.

*Angina pectoris.

*Palpitation; pain shooting down left arm.

Haemoptysis, with convulsive, spasmodic cough.

Diaphragmitis, with great difficulty of breathing.

*Numbness of left arm.


*Difficulty of breathing; continued oppression and uneasiness as if the chest were constricted with a (hot) iron band, hindering respiration.-Whirling sensation from chest to brain; arterial throbbing.-Oppressed breathing from a weight on chest.

*Congestion of the chest which prevents lying down; palpitation; constriction as from a tight cord around false ribs.

*Sensation of a great constriction in middle of sternum, as if the parts were compressed by iron pincers, with oppression of breathing; worse on motion.

*Constriction of throat exciting a constant desire to swallow.

*Suffocative constriction at throat with full, throbbing carotids.

*Pain deep in heart like a jerking body, frequently repeated.-

*Something seemed to be whirling up from chest to brain.-

*Sensation as if heart turned over ; as if it whirled round; as if some one was grasping heart firmly, with sensation as if it whirled round; as if heart was bound down and had not room enough to beat; as if bolts were holding it; as if compressed or squeezed by a band.-

*Lancinating pain in heart when perspiration fails.-

*Deathlike feeling at heart and round to l. back.-

*Acute pains, pricking and stitches in the heart.-

Palpitation of the heart, day and night; < when walking, and at night, when lying on l. side.-

Palpitation in small irregular beats (at times frequent, at others slow), from slightest excitement or deep thought, with necessity for deep inspiration.-

*Pains in apex of heart, shooting down l. arm to ends of fingers; feeble pulse; dyspnœa.-

Endocardial murmurs; excessive impulse; increased precordial dulness; enlarged ventricle.-

Heart disease with œdema of l. hand only.-

Aneurism.-Atheromatous arteries.Pain under l . shoulder-blade (with palpitation)




Introduction of HOMEODISP or Microcrystalline Cellulose Powder as a better alternative to sugar of milk and cane sugar in homeopathic dispensing is of course a part of scientific redefining of homeopathic practice. Actually, it is one of the great inventions that happened in homeopathy after the period of Samuel Hahnemann. It may take some time for homeopathic community to recognize it’s revolutionary implications, but it will happen gradually.

One of the wonderful properties of Microcrystalline Cellulose Powder is it’s extraordinarily high adsorption capacity. 1gm of MCCP can adsorb and hold more than 1 ml potentized drug. In the picture shown above, I have taken 20 gms of MCCP in a vial and added 20ml of potentized drug. Still it remains dry, powdery, uncaked and free flowing. This high adsorption capacity is one of the reason why I am saying MCCP is superior to lactose and cane sugar for using as homeopathic dispensing vehicle.

MCCP is chemically inert, and will not interact with water or alcohol contained in potentized drugs. It simply adsorbs the medicines on to the periphery of microcrystals of cellulose. Once put in the mouth, MCCP easily disperses into individual microcrystals and releases the whole medicinal content into buccal cavity, wherefrom it is absorbed into blood stream through the walls of buccal capillaries.

Since our digestive enzymes cannot split cellulose into constituent glucose molecules MCCP passes through the intestinal tract totally undigested. As such, MCCP has no any nutritional or caloric value, unlike lactose and cane sugar which are digested and absorbed into the system as glucose. Obviously, MCCP is more safe to diabetic patients. This factor also makes MCCP an ideal dispensing vehicle.

Potentized homeopathic medicines are currently dispensed as medicated sugar pills or sugar of milk. MCCP is proved to be a better alternative for this purpose.

Sugar pills commonly used for homeopathic dispensing are made of cane sugar or sucrose. Sucrose is the organic compound belonging to the class of ‘carbohydrates’, commonly known as table sugar and sometimes called saccharose. A white, odorless, crystalline powder with a sweet taste, it is best known for its role in food. The molecule is a disaccharide composed of the monosaccharides glucose and fructose with the molecular formula C12H22O11.

Sugar of milk or Lactose is a disaccharide sugar found in milk. It has a formula of C12H22O11. Lactose is a disaccharide derived from the condensation of monosacharides galactose and glucose, which form a β-1→4 glycosidic linkage. Its systematic name is β-D-galactopyranosyl-(1→4)-D-glucose. The glucose can be in either the α-pyranose form or the β-pyranose form, whereas the galactose can only have the β-pyranose form: hence α-lactose and β-lactose refer to anomeric form of the glucopyranose ring alone. Lactose is hydrolysed to glucose and galactose, isomerised in alkaline solution to lactulose, and catalytically hydrogenated to the corresponding polyhydric alcohol, lactitol. Lactose crystals have a characteristic tomahawk shape that can be observed with a light microscope.

Both sucrose and lactose, used in homeopathic pharmacy, could be hydrolyzed into their sub-units by digestive enzymes, and absorbed into blood stream.

HOMEODISP or Ultra-purified Pharmaceutical Grade Microcrystalline Cellulose Powder I.P is a better alternative to cane sugar and lactose for dispensing homeopathic medicines.

Cellulose is an organic compound with the formula (C6H10O5)n, a polysaccharide consisting of a linear chain of several hundred to over ten thousand D-glucose units. Cotton fibers represent the purest natural form of cellulose, containing more than 90% of this polysaccharide. In many ways, cellulose makes the ideal excipient for pharmaceuticals as well as food articles. A naturally occurring polymer, it is composed of glucose units connected by a 1-4 beta glycosidic bond. These linear cellulose chains are bundled together as microfibril spiralled together in the walls of plant cell. Each microfibril exhibits a high degree of three-dimensional internal bonding resulting in a crystalline structure that is insoluble in water and resistant to reagents. There are, however, relatively weak segments of the microfibril with weaker internal bonding. These are called amorphous regions but are more accurately called dislocations since microfibril containing single-phase structure. The crystalline region is isolated to produce microcrystalline cellulose.

Microcrystalline cellulose is a term for refined wood pulp and is used as a texturizer, an anti-caking agent, a fat substitute, an emulsifier, an extender, and a bulking agent in food production.The most common form is used in vitamin supplements or tablets. It is also used in plaque assays for counting viruses.

Microcrystalline Cellulose powder is subjected to an ultra-purification process to make pharmaceutical grade MCCP .IP, which is distributed as HOMEODISP.

Experiments have been conducted in homeopathic dispensing by using cellulose, both as cotton fibers as well as microcystalline cellulose powder (MCCP). Small quantity of pure MCCP were moistened with potentized drugs selected as similimum, and kept until it is dried and advised the patients to keep it under tongue for some time. It acted very promptly, much better than when administered by other conventional means. By keeping under tongue for extended periods, the molecular imprints adsorbed in the microcrystalline cellulose gets gradually released, thereby ensuring appropriate exposure and availability.

Since our digestive enzymes cannot break the cellulose into glucose, MCCP is safer to be administered even to diabetic patients.

HOMEODISP is available in powder as well as tablet forms.

 Responding to my proposition that MICROCRYSTALLINE CELLULOSE could be a superior substitute to LACTOSE and CANE SUGAR as dispensing vehicles for potentized homeopathic drugs, many friends asked me to provide more details regarding the safety studies of MCCP. Hence I am posting here World Health Organization Report on Microcrystalline Cellulose, prepared by the forty-ninth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JECFA), World Health Organization, Geneva 1998. First draft prepared  by Dr J.B. Greig, Department of Health, Skipton House, 80 London Road, London, SE1 6LW, UK


This report contains a detailed overview, evaluation and comments upon hundreds of studies done regarding Biochemical aspects (Absorption, distribution and excretion), Acute toxicity of microcrystalline cellulose in animals, Short-term toxicity studies, Long-term toxicity/carcinogenicity studies, Reproductive toxicity studies, Special studies on embryotoxicity and teratogenicity, Special studies on genotoxicity, Special studies on sensitization, Special studies on skin and eye irritation, Special studies on effects of cellulose fibre on tumour growth,  Toxicity consequent to substance abuse,  Changes in gastrointestinal function and nutrient balance etc with complete references.

“The Committee concluded that the toxicological data from humans  and animals provided no evidence that the ingestion of  microcrystalline cellulose can cause toxic effects in humans when used  in foods according to good manufacturing practice”.

The committee concludes the report with the following statement:

“Persorption of microcrystalline cellulose was reported in various species, which included rats, in early studies. A recent study in which a special fine particle size preparation of microcrystalline  cellulose (median diameter of particles 6 µm) was administered orally to rats (5 g/kg bw per day) for 90 days has failed to confirm the earlier observations. In this study precautions were taken to ensure that, at autopsy, there was no cross-contamination of the tissues with fine particulate matter.

In various parenteral studies of the acute toxicity of microcrystalline cellulose in animals there have been signs consistent with a tissue response to foreign particles. Similarly, microcrystalline cellulose has been associated with the formation of granulomas in human lung when it has been injected intravenously during drug abuse. No such lesions have been described as a consequence of oral ingestion of microcrystalline cellulose by rats or humans.

In 90-day toxicity tests during which microcrystalline cellulose was administered to rats in the diet at concentrations of 2.5 to 50%, increased consumption of food to compensate for the content of this material was observed. Although this may have some effects on mineral absorption there was, in general, no compound-related systemic toxicity. The NOEL exceeded 50 g/kg diet, at which dose level the mean intakes of microcrystalline cellulose by male and female rats were 3.8 and 4.4 g/kg bw per day, respectively.

A two-year feeding study of microcrystalline cellulose in rats was brought to the attention of the Committee. Despite a lack of evidence of toxic effects, the Committee considered that the execution and reporting of the study were not adequate to identify a NOEL.

In vitro and  in vivo genotoxicity studies were negative.

In a three-generation reproductive toxicity study in rats that had been reviewed by an earlier Committee, there were some effects of using 30% microcrystalline cellulose in the diet; these had been considered to be a consequence of the quantity of material reducing the energy density of the diet. However, in recent embryotoxicity and teratogenicity studies in rats there was no evidence of compound-related effects at dietary levels up to 50 g of microcrystalline cellulose per kg diet (equal to 4.6 g/kg bw per day), given on days 6 to 15 of pregnancy.

In some human studies there have been reports of alterations to gastrointestinal function following ingestion of microcrystalline cellulose. The changes do not appear to be related to systemic toxicity”

Microcrystalline cellulose is a purified, partially depolymerzed cellulose prepared by treating alpha-cellulose, obtained as a pulp from fibrous plant material, with mineral acids. The degree of polymerization is typically less than 400. Not more than 10% of the material has a particle size of less than 5 nanometer. Insoluble in water, ethanol, ether and dilute mineral acids. Slightly soluble in sodium hydroxide solution.

Microcrystalline cellulose (C6H10O5)n is refined wood pulp. It is a white, free-flowing powder. Chemically, it is an inert substance, is not degraded during digestion and has no appreciable absorption. In large quantities it provides dietary bulk and may lead to a laxative effect.

Microcrystalline cellulose is a commonly used excipient in the pharmaceutical industry. It has excellent compressibility properties and is used in solid dose forms, such as tablets. Tablets can be formed that are hard, but dissolve quickly. Microcrystalline cellulose is the same as cellulose, except that it meets USP standards.

It is also found in many processed food products, and may be used as an anti-caking agent, stabilizer, texture modifier, or suspending agent among other uses. According to the Select Committee on GRAS Substances, microcrystalline cellulose is generally regarded as safe when used in normal quantities.

The most common form is used in vitamin supplements or tablets. It is also used in plaque assays for counting viruses, as an alternative to carboxymethylcellulose.

A naturally occurring polymer, it is composed of glucose units connected by a 1-4 beta glycosidic bond. These linear cellulose chains are bundled together as microfibril spiralled together in the walls of plant cell. Each microfibril exhibits a high degree of three-dimensional internal bonding resulting in a crystalline structure that is insoluble in water and resistant to reagents. There are, however, relatively weak segments of the microfibril with weaker internal bonding. These are called amorphous regions; some argue that they are more accurately called dislocations, because of the single-phase structure of microfibrils. The crystalline region is isolated to produce microcrystalline cellulose.

Approved within the European Union as a thickener, stabilizer or emulsifiers microcrystalline cellulose was granted the E number E460(i) with basic cellulose given the number E460.

Microcrystalline cellulose (MCC) is pure partially depolymerized cellulose synthesized from α-cellulose precursor. The MCC can be synthesized by different processes such as reactive extrusion, enzyme mediated, steam explosion and acid hydrolysis. The later process can be done using mineral acids such as H2SO4, HCl and HBr as well as ionic liquids. The role of these reagents is to destroy the amorphous regions remaining the crystalline domains. The degree of polymerization is typically less than 400. The MCC particles with size lower than 5 µm must not be more than 10%. The MCC is a valuable additive in pharmaceutical, food, cosmetic and other industries. Different properties of MCC are measured to qualify its suitability to such utilization, namely particle size, density, compressibility index, angle of repose, powder porosity, hydration swelling capacity, moisture sorption capacity, moisture content, crystallinity index, crystallite size and mechanical properties such as hardness and tensile strength. Thermogravimetric analysis (TGA) and differential thermal analysis (DTA) or differential scanning calorimetry (DSC) are also important to predict the thermal behavior of the MCC upon heat stresses.

Microcrystalline cellulose is a widely used excipient, an inert substance used in many pill and tablet formulations. As an insoluble fiber, microcrystalline cellulose is not absorbed into the blood stream, so it cannot cause toxicity when taken orally. In fact, it is so inert it is often used as a placebo in controlled drug studies. However, some side effects have been noted in animal studies, although usually at much higher dosages than would be normal for a human subject.


World Health Organization Report on Microcrystalline Cellulose

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY WORLD HEALTH ORGANIZATION- SAFETY EVALUATION OF CERTAIN FOOD ADDITIVES AND CONTAMINANTS – WHO FOOD ADDITIVES SERIES 40-  Prepared by: The forty-ninth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JECFA).  World Health Organization, Geneva 1998 –  First draft prepared     by Dr J.B. Greig Department of Health, Skipton House, 80 London Road, London, SE1 6LW, UK


Microcrystalline cellulose was evaluated at the fifteenth, seventeenth and nineteenth meetings of the Committee (see Annex 1, references 26, 32 and 38). At the nineteenth meeting an ADI “not specified” was allocated. In the light of concern about possible persorption and consequential adverse effects of fine particles, the substance was re-evaluated at the present meeting.


Biochemical aspects-  Absorption, distribution and excretion


Four rats were fed 14C-labelled microcrystalline cellulose at 10 or 20% of their diet. No evidence of degradation or digestion was noted. Faecal recoveries of radioactivity ranged from 96-104% and were complete for all labelled material. No radioactivity appeared in the urine (Baker, 1966).

A study was specifically designed to investigate the possibility that persorption of microcrystalline cellulose might induce toxicological effects. Groups of male and female Sprague-Dawley CD rats (20 per group) from Charles River Laboratories were administered, by gavage, suspensions of a special fine particle-size microcrystalline cellulose (median particle size 6 µm). The rats were dosed orally daily for 90 consecutive days at a level of 5000 mg/kg bw per day by means of a 25% suspension in tap water. The animals were killed on study days 91-94 and necropsies were carried out under conditions that reduced the possibility of contamination of tissues with fine particulates. The birefringent microcrystalline cellulose particles were not detected in any organ or tissue, including gut-associated lymphoid tissue, liver, lung, spleen and brain. The size limit for detection of the particles was considered to be < 1 µm (Kotkoskie  et al., 1996; FMC Corporation N.V., 1996


One human subject received 150 g of microcrystalline cellulose daily in two portions for a 15-day adaptation period. He then received 14C-labelled microcrystalline cellulose (47.6 µCi) in two portions on one day. Supplementation of the diet with unlabelled microcrystalline cellulose continued for 10 days. Twenty-four-hour faecal and urine collections were examined for radioactivity. No radioactivity appeared in the urine or in the expired CO2. All administered radioactivity (98.9 ± 3.0%) was recovered from the faeces within two days (Baker, 1968).

Metabolism of a preparation of 14C-labelled cellulose by four volunteers has been shown to be increased by the consumption, for a period of 3 months, of an additional 7 g/per day of dietary fibre. In six subjects with an ileostomy, the cumulative excretion of 14CO2 was lower than in controls. In two constipated subjects metabolism appeared to be more extensive and occurred over a longer period (Walters  et al., 1989).

Examination of the stools of one male and one female patient given 30 g microcrystalline cellulose as dry flour or gel for 5´ weeks showed the presence of undegraded material of the same birefringence as the original microcrystalline cellulose administered. No significant effects on the human gastrointestinal tract were noted during the administration (Tusing  et al., 1964).

Most (87%) of the radiolabel associated with 131I-labelled alpha-cellulose fibres (retained by a sieve with pores of 1 mm diam) was excreted by 4 male and 4 female volunteers within 5 days of ingestion. Less than 2% of the faecal radiolabel was unbound; urinary excretion of unbound radio-iodine accounted for another 1.9% of the total dose (Carryer  et al., 1982).

Other studies have been carried out to demonstrate the relationship between persorbability and size and consistency of granules. Using quartz sand, the upper limit for persorbability was shown to be 150 µm. Starch granules must be structurally largely intact to possess the property of persorbability. Persorbed starch granules may be eliminated in the urine, pulmonary alveoli, peritoneal cavity, cerebrospinal fluid, via lactating milk and transplacentally (Volkheimer  et al., 1968).

In another study, dyed plant foods (oatmeal, creamed corn) were fed to human subjects, and blood and urine were examined for coloured fibres. Dyed fibres were shown to be present (Schreiber, 1974).

Lycopodium spores and pollen grains have also been shown to be persorbed by humans (Linskens & Jorde, 1974).

Mean intake of dietary microcrystalline cellulose in the USA has been estimated to range from 2.7 g/person per day (children 2 years of age) to 5.1 g/person per day (young adult males). For heavy consumer intake of microcrystalline cellulose (90th percentile) the values are 5.4 to 10.2 g/person per day for the same age groups (CanTox Inc., 1993).

The mean intake of dietary microcrystalline cellulose in the United Kingdom has been estimated as 0.65 g/person per day. The highest mean intake, 0.90 g/person per day, was for children aged 10-11 (the youngest group for which data were available). For heavy consumer intake of microcrystalline cellulose (90th percentile) the values ranged from 1.13 g/person per day for adults age 16-24 to 1.83 g/person per day for males age 10-11 (Egan & Heimbach, 1994).

Persorption in animal species:

Rats, pigs and dogs were used to study the persorption of microcrystalline cellulose. The animals were not fed for 12 hours prior to oral administration of the test compound. Rats, dogs and pigs were given 0.5, 140 and 200 g, respectively, of the test compound. Venous blood was taken from the animals 1-2 hours after administration of the test compound, and examined for particles. Persorbed particles were demonstrated in the blood of all three species. The average maximum diameter for persorbed particles was greater in rats than in dogs or pigs (Pahlke & Friedrich, 1974)

Acute toxicity of microcrystalline cellulose in animals

No deaths in 10 rats of each sex administered 5000 mg/kg of Avicel RCN-15.

No deaths in 5 rats of each sex administered 5000 mg/kg of Avicel AC-815.

No deaths in 5 rats of each sex treated with 2000 mg/kg of Avicel RCN-15.

No deaths in 5 rats of each sex treated with 2000 mg/kg of Avicel AC-815.

No deaths in 5 rats of each sex exposed to 5.35 mg/litre of Avicel AC-815.

In the studies summarized in Table 1, there was no evidence of toxicity of microcrystalline cellulose preparations administered either orally or dermally to rats at doses of 5000 or 2000 mg/kg bw, respectively. The observations seen at necropsy in animals treated  intraperitoneally with Cellan 300 at 3160 mg/kg bw are consistent with an irritant reaction caused by the presence of foreign material. An inhalation toxicity study showed only transient effects at a concentration of 5.35 mg/litre.

Groups of five male Sprague-Dawley rats received a single oral dose, by stomach tube, of 10.0, 31.6, 100, 316, 1000 or 3160 mg/kg bw of a suspension of Cellan 300 (refined alpha-cellulose) in either  distilled water or Mazola corn oil. The animals were observed for 7 days following administration. No differences were observed among the groups as regards the average body weight, appearance and behavior  compared to untreated rats. No observable gross pathology was revealed  at autopsy in animals dosed with either suspension. Therefore, the  acute oral LD50 was >3160 mg/kg (Pallotta, 1959).

Similar single doses of refined alpha-cellulose were given i.p. in distilled water suspension to five male rats. During 7 days observation there were no abnormalities in the rats given 316 mg/kg bw or less. At 1000 and 3160 mg/kg bw inactivity, laboured respiration and ataxia were observed 10 min after administration and, at 3160 mg/kg bw, ptosis and sprawling of the limbs were observed. These  animals appeared normal after 24 hours and for the remainder of the  observation period. At sacrifice body weights were higher than normal and gross autopsy revealed adhesions between the liver, diaphragm and peritoneal wall and congestion of the kidneys. Masses resembling   unabsorbed compound were also observed and these were found to a small extent in the mesentery of the animals administered 316 mg/kg bw.

There were no deaths and therefore the acute i.p. LD50 was >3160 mg/kg bw (Pallotta, 1959).

Ten male and ten female Sprague-Dawley rats fasted overnight were  fed Avicel RCN-15 (a mixture of 85% microcrystalline cellulose with 15% guar gum) at a dose level of 5000 mg/kg bw mixed with parmesan cheese. Six of ten males and five of ten females consumed the mixture within 24 hours. After a 14-day period during which all rats gained  weight normally they were killed. There were no gross lesions at necropsy. Under the specified conditions of administration the LD50 was >5000 mg/kg bw (Freeman, 1991a).

An acute inhalation toxicity study using a preparation of Avicel AC-815 (composed of 85% microcrystalline cellulose and 15% calcium  alginate) with mass median aerodynamic diameter of 8.48-8.61 µm (range of measures) was dispersed and delivered at a mean concentration of  5.35 mg/litre in a nose-only inhalation exposure chamber to 5 male and 5 female Crl:CDBR VAF Plus rats for a period of 4 hours. The rats were observed over the 14 days after removal from the chamber. The only signs of toxicity were on removal from the chamber and consisted of  chromodacryorrhea, chromorhinorrhea and, in one male rat, decreased  locomotion; these signs had resolved by the next day. After 14 days no gross lesions were observed at necropsy (Signorin, 1996)

Short-term toxicity studies


Groups of four male rats were kept on diets containing 0.25, 2.5 or 25% of various edible celluloses for 3 months. No differences were observed among the groups with regard to growth and faecal output. Histopathology of the gastrointestinal tract revealed no treatment-related abnormalities (Frey  et al., 1928).

Three groups of five male rats received 0.5 or 10% microcrystalline cellulose in their diet for 8 weeks. Growth was comparable to controls but the 10% group showed slightly lower body  weights. Haematology, serum chemistry and vitamin B1 levels in blood and faeces showed no differences from controls (Asahi Chemical Industry Co., 1966).

Groups of five male weanling Sprague-Dawley rats received 0, 5, 10 or 20% of acid-washed cellulose in their diet during three consecutive nutrient balance trials over a period of 17 days. Absorption of magnesium and zinc were significantly lower in the animals that were receiving the 10 and 20% cellulose diets. Histopathology of the gastrointestinal tract revealed increased mitotic activity and the presence of increased numbers of neutrophils in crypt epithelial cells, particularly of the duodenum and jejunum (Gordon  et al., 1983).

A mixture of four types of Elceme (in the ratio of 1:1:1:1) was fed to groups of Wistar rats for 30 days at a dietary level of 50%,  and for 90 days at a dietary level of 10% (Elceme is a  microcrystalline cellulose, and the four types are identified by particle size, namely, 1-50 (powder), 1-100 (powder), 1-150 (fibrillar), 90-250 (granulate)). All test animals were observed for food intake and weight gain. For animals in the 10% group, urinalysis,  haematological tests and serum biochemical tests were carried out at weeks 6 and 13 of the test. A complete autopsy including  histopathology was carried out at the end of the study. Animals in the 50% group were subjected to a persorption test, on the last day of the  study, by addition of a cellulose staining dye (Renal, Wine-red) to  the food of the test animals at a level equivalent to 5% of the Elceme. The animals were sacrificed 24 hours after administration of the diet, and a careful histological examination was made of the gastrointestinal tract, spleen, liver, kidney and heart for stained particles.

Animals in the 10% group gained significantly less weight than  those in the control group; the marked decrease commenced in the third or fourth week of the study. Food intake was similar in test and  control groups. Urinalysis, haematological values and biochemical values were similar for test and control group 1. At autopsy some ofthe rats on the test diet had distended stomachs, which often contained considerable amounts of the test diet. The absolute liver and kidney weights and the ratio of the weight of these organs to brain weight was increased in test animals when compared with control animals. No compound-related pathology was reported. Animals in the 50% group showed considerable less weight gain than control animals in spite of a marked increase in food consumption. No persorption of dyed fibres was observed (Ferch, 1973a,b).

Randomly bred rats of both sexes were divided into groups that  received a control diet or the control diet with 330 mg/kg microcrystalline cellulose for a period of 6 months. Six rats in each group were then killed, their organs were examined, and tissues were taken for histopathology. No effects of the treatment were observed (Yartsev  et al., 1989).

Groups of Crl: CD(R) BR/VAF/Plus rats (20/sex per group) were administered 0 (control), 25 000 or 50 000 mg/kg Avicel RCN-15 in the diet for 90 days. A few test animals were noted as having  chromodacryorrhea/ chromorhinorrhea, but this was not considered to be   biologically significant. In some early weeks the rats increased diet consumption, probably to allow for the increased dietary fibre content. Body weight gain was unaffected. During the study and at necropsy there was no evidence of treatment-related changes. Clinical chemistry, haematology and organ weights were unaffected by treatment. Histopathology of 34 organs or tissues, including gastrointestinal tract and gut-associated lymphoid tissue of the ileum, provided no evidence of toxicity of microcrystalline cellulose. The calculated  daily consumption of microcrystalline cellulose was 3769 mg/kg bw per day for males and 4446 mg/kg bw per day for females. The author noted that the NOEL exceeded 50 000 mg/kg diet (Freeman, 1992a).

Groups of Sprague-Dawley CD rats (20 rats/dose per sex) from Charles River Laboratories were administered 0 (control), 25 000 or 50000 mg/kg Avicel CL-611 in the diet for 90 days. (Avicel CL-611 orAvicel(R) Cellulose Gel is composed of 85% microcrystalline cellulose and 15% sodium carboxymethyl cellulose). There were no differences in weight gain of the males; a body weight gain decrement in females was attributed to a decreased caloric intake. No adverse  effects attributable to the treatment were observed. At necropsy organ  weights of the test groups were normal other than changes to adrenals of males receiving 50 000 mg/kg and to absolute brain and kidney weights in females receiving 25 000 mg/kg, but these were not  attributed to the treatment. Histopathology of 36 organs or tissues  from the control and high-dose groups, including gastrointestinal tract and gut-associated lymphoid tissue of the ileum, provided no evidence of toxicity of the microcrystalline cellulose. The mean  nominal consumptions, averaged over weekly periods, of Avicel CL-611  by males and females of the top-dose groups ranged from 2768 to 5577 and 3673 to 6045 mg/kg bw per day, respectively (Freeman, 1994a).

Microcrystalline cellulose (Avicel) was used as a positive control  in a short-term toxicity study (approximately 13 weeks) of Cellulon, a  cellulose fibre. Sprague-Dawley Crl:CB (SD) BR rats, 20 rats/sex per group, received a diet containing 0, 5 or 10% of the appropriate fibre ad libitum. Animals were checked daily, and body weights and food consumption were monitored weekly. Haematology (10 parameters) and clinical chemistry (14 parameters) were performed on blood samples taken from 10 rats/sex per group. All animals were necropsied, and gross observations and the weights of liver, testes with epididymes, adrenals and kidneys were recorded. Histological examination was  carried out on tissue sections from control and high-dose groups.

Food consumption was increased in the groups fed cellulose fibre, although there were no differences in body weight between the fibre-fed and control groups. This effect was attributed to the altered nutritional value of the diet. From the haematology and  clinical chemistry there was only one significant difference of   microcrystalline cellulose group from the control value; this was in  the group of female rats fed 5% microcrystalline cellulose in which there was an elevation of the haematocrit. There was no evidence of a  dose response.

Study of the necropsy results and the histological observations  indicate that there was no evidence of any treatment-related effects of microcrystalline cellulose during the 13-week feeding study in rats  at either 5 or 10% in the diet (Schmitt  et al., 1991).

Groups of Sprague-Dawley (CD) rats (20 rats/dose per sex) from Charles River Laboratories were administered, by gavage, suspensions  of a special, fine particle size, microcrystalline cellulose (median particle size 6 µm). The dose levels were 0 (control), 500, 2500 or  5000 mg/kg per day as a 25% suspension in tap water. Dosing was   performed daily for 90 consecutive days. No treatment-related deaths occurred during the study and the only treatment-related clinical sign (pale faeces) was not attributed to toxicity. There were no toxicologically significant effects in treated animals with respect to body weight, absolute and relative organ weights (5 organs weighed), food consumption, clinical chemistry measurements, haematology measurements or opthalmoscopic examinations. In animals that has received 5000 mg/kg per day there were no treatment-related lesions detected histopathologically (in 36 tissues including gut-associated lymphoid tissue, liver, lung, spleen and brain) nor was there any macroscopic or microscopic finding of microemboli or granulomatous  inflammatory lesions (Kotkoskie  et al., 1996).

Long-term toxicity/carcinogenicity studies


Three groups of 50 male and 50 female rats received in their die  for 72 weeks either 30% ordinary cellulose or dry microcrystalline cellulose or micro-crystalline cellulose gel. Appearance and behavior was comparable in all groups. No adverse effects were noted. The body weights of males given microcrystalline cellulose gel were higher than  those of the controls. Food efficiency, survival and haematology were comparable in all groups. The liver and kidney weights of males receiving microcrystalline cellulose gel were higher than the controls. Gross and histopathology showed some dystrophic calcification of renal tubules in females on microcrystalline  cellulose but all other organs appeared unremarkable. Tumour incidence  did not differ between the groups (Hazleton Labs, 1963).

The Committtee was aware of a study in which a microcrystalline  cellulose preparation, of which 90% of the particles had a diameter   < 20 µm, was fed to male and female rats at 0 (control), 30, 100 or 200 g/kg diet. The high mortality during the course of the study, the evidence of confounding infection, the limited number of animals for which there was histopathological examination, and the absence of details of the first year of feeding do not provide adequate reassurance as to the ability of this study to detect other than gross effects (Lewerenz  et al., 1981).

Reproductive toxicity studies


Groups of eight male and 16 female rats were used to produce P,  F1a, F1b, F2 and F3 generations after having been fed on diets containing 30% microcrystalline cellulose flour or gel or ordinary cellulose as a control. The presence in the diet of such an amount of  non-nutritious material, which contributed no calories, had an adverse effect on reproduction. Fertility and numbers of live pups were  relatively depressed, and lactation performances in all three  generations, as well as survival and the physical condition of the pups, were unsatisfactory throughout the study. The new-born pup appeared smaller, weak and showed evidence of disturbed motor  coordination. Liver weights were increased in the group receiving microcrystalline cellulose gel in all generations but other organ  weights showed no consistent patterns. At autopsy female rats of all generations showed kidney changes comprising pitting, occasional  enlargement and zonation of the cortex. Other organs showed  no consistent changes. No teratological deformities were seen (Hazleton Labs, 1964).

Special studies on embryotoxicity and teratogenicity


Seventy-two rats (Sprague-Dawley CD) divided into eight groups were fed a mixture of four types of Elceme in the ratio of 1:1:1:1 in the diet at a level of 0, 2.5, 5 or 10% for 10 days, between days 6 and 15 of pregnancy. Rats of four test groups were killed on day 21 of pregnancy and the following parameters studied: number of fetuses and resorption sites, litter size and average weight of rats, average weight of fetuses and average backbone length. Fetuses were also examined for soft tissue or skeletal defects. The remaining groups were allowed to bear young, which were maintained to weaning (21 days). The following parameters were studied: litter size, weight of  pups at days 7 and 21, and there was a histological study of the offspring. Although there is some suggestion that administration of dietary Elceme resulted in a dose-dependent increase in resorption  sites, as well as a change in sex ratio, and possible defects such as  opaque crystalline lenses, the data has not been presented in a manner  that permits a meaningful interpretation. However, the author concluded that Elceme is non-teratogenic (Ferch, 1973a,b).

Groups of 25 presumed pregnant Crl:CD(R) BR VAF/Plus rats were administered 0 (control), 25 000 or 50 000 mg Avicel RCN-15/kg diet (equal to 2.1 and 4.5 g/kg bw per day, respectively)  ad libitum on   days 6 to 15 of gestation. Animals received basal diet at all other  times. In the group receiving 50 000 mg/kg the food consumption on  days 6 to 15 was significantly higher than that of controls, probably because of the increased fibre content. On day 20 of gestation thedams were killed by carbon dioxide inhalation and the following parameters studied: number and distribution of implantation sites,  early and late resorptions, live and dead fetuses and corpora lutea.  External, visceral and skeletal examinations of the fetuses were also  performed. There was no evidence of any adverse effects of the test  material on either the dams or the fetuses. Due to a protocol error fetal sex was not recorded (Freeman, 1992b).

Groups of 25 presumed pregnant Charles River Sprague-Dawley CD  rats were administered 0 (control), 25 000 or 50 000 mg Avicel  CL-611/kg (equal to 2.2 and 4.6 g/kg bw per day, respectively) diet   ad libitum on days 6 to 15 of gestation. Animals received basal diet at all other times. In the test groups the food consumption on days     to 15 was significantly higher than for controls, probably because of   the increased fibre content. The parameters studied and examinations performed were the same as in the study of Freeman (1992b). There was  no evidence of any effects of the Avicel treatment on the fetuses, and there was no evidence of a change of sex ratio in the pups or of eye defects. Under the conditions of the study, the maternal and fetal  NOEL was > 50 000 mg/kg diet (equal to 4.6 g/kg bw per day) (Freeman,   1994b).

Special studies on genotoxicity

Various microcrystalline cellulose preparations have been tested for genotoxicity in several different assay systems. The results of which were negative, are summarized in Table 2.

In the reverse mutation assays the microcrystalline cellulose formulations produced a heavy precipitate on the plate at the highest concentration. Solubility also affected the forward mutation assays and it was not possible to include concentrations of the test material that were cytotoxic. In the  in vivo mammalian micronucleus assays it is improbable that there was appreciable persorption of the test materials, and, therefore, there was little exposure of the bone marrow cells. In the test in which Avicel RCN-15 was used it was administered admixed with the diet of male and female ICR mice. Only mice that had consumed all the diet within 10 hours were retained in the study and were killed after 24, 48 or 72 hours. Because one group of control mice had 0 micronuclei per 1000 polychromatic erythrocytes, the comparison with the test group was statistically significant. This was not considered to be a valid observation. There is no evidence that microcrystalline cellulose is genotoxic.

Special studies on sensitization

  Avicel RCN-15 was determined to be non-sensitizing when topically  applied to ten male and ten female Hartley guinea-pigs (Freeman,  1991e).

Avicel AC-815 was determined to be non-sensitizing when topicall    applied to ten male Hartley guinea-pigs (Freeman, 1996c).

Special studies on skin and eye irritation

Avicel RCN-15 was judged to be minimally irritating after  instillation into the eyes of four male and two female New Zealand White rabbits (Freeman, 1991c).

Avicel AC-815 was judged to be minimally irritating after   instillation into the eyes of four male and two female New Zealand  White rabbits (Freeman, 1996a).

Avicel RCN-15 was judged to be non-irritating after a 4-hour occlusive contact with the skin of three male and three female New Zealand White rabbits (Freeman, 1991d).

Avicel AC-815 was judged to be non-irritating after a 4-hour occlusive contact with the skin of three male and three female New Zealand White rabbits (Freeman, 1996b).

Special studies on effects of cellulose fibre on tumour growth 

The effect of artifical diets containing varied concentrations of either wheat bran or pure cellulose fibre on the induction of mammary  tumours by  N-nitrosomethylurea (i.v., 40 mg/kg) was studied in female F344 rats. The wheat bran diet appeared to possess anti-promotion properties that pure cellulose lacked. The concentrations of serum estrogens, urinary estrogens and faecal estrogens did not vary in a consistent, statistically significant manner (Cohen  et al., 1996).

The effect of a high-fibre diet containing 45 000 mg/kg Avicel PH- 105 on the development of colon tumours was investigated in male Wistar rats that were injected with 1,2-dimethylhydrazine dihydrochloride (25 mg/kg, s.c., once weekly for 16 weeks). The test and control diets were administered for 2 weeks prior to the first injection of the carcinogen. There was a reduction in the number of animals bearing colon tumours and a statistically significant reduction in the number of colon tumours/rat in the high-fibre dietary group. However, for small bowel tumours and tumours of the ear canal there was no significant difference between the dietary groups Freeman et al., 1978).

A later study by the same authors demonstrated that there was no significant effect of increasing the level of cellulose in the diet to 9000 mg/kg (Freeman  et al., 1980).

Observations in humans

Toxicity consequent to substance abuse 

Intravenous abuse of drugs available in tablet form has led to the detection of excipients, e.g., talc, magnesium stearate or microcrystalline cellulose, in the tissues of a series of 33 fatality cases of intravenous drug addicts. Microcrystalline cellulose (21  cases) and talc (31 cases) were detected most frequently and, in some cases, were associated with granulomatous lesions (Kringsholm & Christoffersen, 1987).

Changes in gastrointestinal function and nutrient balance

A number of clinical studies using refined cellulose as roughage  in the human diet for the treatment of constipation showed no  deleterious effects. Groups of 18 children received regular amounts of   edible cellulose instead of normal cereal for three months. The only  effect noted was an increase in bowel movements but no diarrhoea or other gastrointestinal disturbances were seen (Frey  et al., 1928).

Eight male and eight female volunteers supplemented their normal diet with 30 g microcrystalline cellulose per day as either dry powder or gel (15% aqueous) for 6 weeks followed by 2 weeks without supplementation. No adverse findings were reported regarding acceptance or body weight but most subjects complained of fullness and mild constipation. Haematology was normal in all subjects. Biochemical blood values showed no differences between treatment and control periods, nor was there evidence of liver or kidney function disturbance. Urinalysis produced normal findings. The faecal flora remained unchanged. The cellulose content of faeces increase five to eight times during the test period. Microscopy revealed the presence of microcrystalline cellulose (Hazleton Labs, 1962).

In another study, eight healthy males received 30 g microcrystalline cellulose daily as supplement to their diet for 15 days. D-xylose absorption varied between pretest, test and post-test periods, being lower during microcrystalline cellulose ingestion. The absorption of 131I-triolein was unaffected by microcrystalline  cellulose ingestion. No change was noted in the faecal flora nor was there any significant effect on blood chemistry during ingestion of microcrystalline cellulose. Examination of urine, blood and faecal levels of vitamin B1 during microcrystalline cellulose ingestion showed no difference from control periods (Asahi Chemical Industry Co., 1966).

Twelve men consumed diets containing fibres from various sources for periods of 4 weeks. There was no significant difference between alues of serum cholesterol, triglyceride and free fatty acid levels measured after consumption of the basal diet, compared with the values measured after consumption of a diet containing cellulose fibres (90% cellulose, 10% hemicellulose; James River Corp., Berlin, New Hampshire, USA). There were no significant differences in plasma VLDL and HDL cholesterol or in the ratio of HDL/VLDL+LDL cholesterol. However, the increase in plasma LDL cholesterol after the cellulose diet was significant (Behall  et al., 1984).

A similar study in a group of four men and six women could detect no effect of a diet containing added alpha-cellulose (15 g daily) on serum total cholesterol, triglycerides, HDL cholesterol and the ratio of HDL to total cholesterol. The cellulose was well tolerated (Hillman et al., 1985).

A double-blind cross-over trial of the effects of guar gum andmicrocrystalline cellulose on metabolic control and serum lipids in 22 Type 2 diabetic patients has been carried out. The fibre preparations were given at 15 g/day for a 2-week period and then at 5 g/day for the remaining 10-week period of each treatment phase. There was no effect of the microcrystalline cellulose diet on fasting blood glucose level, glycosylated haemoglobin, serum HDL-cholesterol, serum triglycerides, serum zinc or ferritin, or urinary magnesium excretion (Niemi   et al., 1988).

The effect of various dietary fibres, including microcrystalline cellulose (40 g), on the uptake of vitamin A (approximately sixty times the daily requirement) from a test meal was investigated in 11 female subjects aged 19 to 22. All the dietary fibres significantly increased the absorption of the vitamin A over a period of 9 hours (Kasper  et al., 1979).

A study of apparent mineral balance in a group of eleven men revealed that there was no significant effect of cellulose, added to the diet at 7.5 g per 1000 kcal for 4 weeks, on the mineral balance of calcium, magnesium, manganese, iron, copper or zinc. However, in this report the source of the cellulose fibre was not specified (Behall et al., 1987).

The addition of nutritional grade cellulose (21 g) to the daily diet of healthy adolescent girls resulted in reduction of the serum calcium, phosphorus and iron concentrations. The authors suggested that high-fibre diets may not be advisable (Godara  et al., 1981).

A study of only three men on a low-fibre diet claimed changes in mineral balance consequent on the consumption of additional cellulose fibre, 10 g of Whatman No. 3 filter paper daily, in the diet (Ismail-Beigi  et al., 1977).

Microcrystalline cellulose (5 g) did not appear to inhibit the uptake of iron in women who were neither pregnant nor lactating (Gillooly  et al., 1984).

A group of twenty women, aged 27-48, who were given 20 g packs of alpha-cellulose to be consumed daily for three months, were included in a study of the effect of indole-3-carbinol on estrogen metabolite ratios. Because the control group and the group fed indole-3-carbinol received capsules, the cellulose group could not be blinded; in addition, an unspecified number of subjects in this group dropped out as they found that the cellulose suspension was unpalatable. However, the authors suggest that the estrogen metabolite ratio in the high- fibre group was not different from that in the control group (Bradlow et al., 1994).


Persorption of microcrystalline cellulose was reported in various species, which included rats, in early studies. A recent study in which a special fine particle size preparation of microcrystalline  cellulose (median diameter of particles 6 µm) was administered orally to rats (5 g/kg bw per day) for 90 days has failed to confirm the earlier observations. In this study precautions were taken to ensure that, at autopsy, there was no cross-contamination of the tissues with fine particulate matter.

In various parenteral studies of the acute toxicity of microcrystalline cellulose in animals there have been signs consistent with a tissue response to foreign particles. Similarly, microcrystalline cellulose has been associated with the formation of granulomas in human lung when it has been injected intravenously during drug abuse. No such lesions have been described as a consequence of oral ingestion of microcrystalline cellulose by rats or humans.

In 90-day toxicity tests during which microcrystalline cellulose was administered to rats in the diet at concentrations of 2.5 to 50%, increased consumption of food to compensate for the content of this material was observed. Although this may have some effects on mineral absorption there was, in general, no compound-related systemic toxicity. The NOEL exceeded 50 g/kg diet, at which dose level the mean intakes of microcrystalline cellulose by male and female rats were 3.8 and 4.4 g/kg bw per day, respectively.

A two-year feeding study of microcrystalline cellulose in rats was brought to the attention of the Committee. Despite a lack of evidence of toxic effects, the Committee considered that the execution and reporting of the study were not adequate to identify a NOEL.

In vitro and  in vivo genotoxicity studies were negative.

In a three-generation reproductive toxicity study in rats that had been reviewed by an earlier Committee, there were some effects of using 30% microcrystalline cellulose in the diet; these had been considered to be a consequence of the quantity of material reducing the energy density of the diet. However, in recent embryotoxicity and teratogenicity studies in rats there was no evidence of compound-related effects at dietary levels up to 50 g of microcrystalline cellulose per kg diet (equal to 4.6 g/kg bw per day), given on days 6 to 15 of pregnancy.

In some human studies there have been reports of alterations to gastrointestinal function following ingestion of microcrystalline cellulose. The changes do not appear to be related to systemic toxicity.


The Committee concluded that the toxicological data from humans  and animals provided no evidence that the ingestion of  microcrystalline cellulose can cause toxic effects in humans when used  in foods according to good manufacturing practice.

It is recognized that small particles of other materials may be   persorbed and that the extent of persorption is greater with sub-micrometre particles. Despite the absence of any demonstrated persorption of microcrystalline cellulose in the recent study in rats, the Committee, as a precautionary measure, revised the specifications   for microcrystalline cellulose at the present meeting to limit the content of particles less than 5 µm in diameter. The Committee  retained the ADI “not specified” for microcrystalline cellulose  conforming to these specifications.


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