Multiple Sclerosis (MS) stands as a complex and chronic demyelinating disorder that primarily assaults the central nervous system (CNS), which encompasses the brain, spinal cord, and optic nerves. This debilitating disease is supposed to trigger the immune system to erroneously attack the protective sheath called myelin, which encases nerve fibres, leading to communication disruptions between the brain and the body. Over time, MS can cause irreversible damage to the nerves themselves. The nature and severity of MS symptoms can significantly vary, reflecting the extent of nerve damage and the specific nerves affected.
Myelin is a lipid-rich material that surrounds axons of nerve to insulate them and increase the rate at which electrical impulses called action potentials pass along the axon. The myelinated axon can be likened to an electrical with insulating material around it. Myelin’s best known function is to increase the rate at which information, encoded as electrical charges, passes along the axon’s length. Myelin is made by glial cells, which are non-neuronal cells that provide nutritional and homeostatic support to the axons. The “insulating” function for myelin is essential for efficient motor and sensory functions, as demonstrated by the consequence of disorders that affect myelination, such as multiple sclerosis. The process of generating myelin is called myelination or myelinogenesis. Diseases and conditions that disrupt myelogenesis can lead to significant neurological impairments. For example, multiple sclerosis is a disease characterized by damage to the myelin in the central nervous system, which slows down or blocks messages between the brain and the body, leading to various symptoms.
The exact cause of Multiple Sclerosis remains an enigma, although it is widely believed to be multifactorial, involving a blend of genetic predisposition and environmental influences. Several theories have been proposed to explain the onset of MS, including exposure to certain viruses, diminished vitamin D levels, and smoking. Nonetheless, there’s a consensus that MS results from an interplay between environmental factors and a susceptible genetic background.
Relapsing-Remitting MS (RRMS) is the most common form, characterized by clearly defined flare-ups (relapses) followed by periods of partial or complete recovery (remissions). Initially may begin as RRMS but eventually progresses to a more steady worsening of symptoms without distinct relapses or remissions, called Secondary Progressive MS (SPMS). Primary Progressive MS (PPMS) is marked by a gradual but steady progression of symptoms without any relapses or remissions. Progressive-Relapsing MS (PRMS) is rarest form, featuring a steady progression of symptoms from the onset, along with acute relapses without any clear remissions.
The symptoms of MS are diverse and can fluctuate over time, including, but not limited to, fatigue, numbness or weakness in limbs, difficulty with coordination and balance, eye problems, and cognitive issues. Given the variety of symptoms and their similarity to other diseases, diagnosing MS can be challenging. It typically involves a combination of history taking, neurologic examination, magnetic resonance imaging (MRI), and sometimes tests of cerebrospinal fluid, among other diagnostic procedures.
While there’s no cure for MS in modern medicine, a multifaceted approach to treatment can help manage symptoms, reduce the frequency of relapses, and slow the disease’s progression. Treatment modalities include disease-modifying therapies (DMTs), which aim to reduce the immune system’s attack on the myelin sheath, and symptomatic treatments targeting specific symptoms like muscle spasticity, fatigue, and pain.
Physical therapy and lifestyle modifications, including stress management, a balanced diet, and exercise, play a crucial role in managing the disease. Emerging research is continuously exploring new treatment avenues, focusing on myelin repair and neuroprotection.
The impact of MS extends beyond the physical symptoms. The unpredictability of the disease can have significant psychological effects, including anxiety and depression. Social and occupational challenges are common, as the disease can interfere with the ability to work, perform daily tasks, and maintain relationships. Support from healthcare providers, family, friends, and MS communities is vital for managing these challenges.
The pathophysiology of Multiple Sclerosis (MS) involves a complex interplay of immunological, inflammatory, and neurodegenerative processes that lead to the damage of the central nervous system (CNS), including the brain, spinal cord, and optic nerves. At the core of MS is the autoimmune response against myelin—the protective sheath that surrounds nerve fibers (axons) and facilitates the rapid transmission of electrical impulses between nerve cells.
The initial pathophysiological events in MS are believed to be triggered by autoreactive immune cells, primarily T lymphocytes, which penetrate the blood-brain barrier (BBB). Once these cells cross into the CNS, they recognize myelin as a foreign antigen. This recognition leads to the activation of a cascade of immune responses, involving: 1. Activation of B cells, which produce antibodies against myelin. 2. Recruitment of additional immune cells such as macrophages and microglia, which contribute to inflammation and myelin destruction. 3. Pro-inflammatory cytokines are released, exacerbating inflammation and damage to myelin and axons.
These immunological responses result in the formation of localized areas of inflammation and demyelination, known as plaques or lesions, which are hallmark features of MS seen on MRI scans.
The destruction of myelin sheaths disrupts the normal transmission of electrical impulses along the axons, leading to the neurological symptoms characteristic of MS. Over time, the repeated cycles of inflammation and healing can lead to scar tissue formation (sclerosis) and the loss of oligodendrocytes, the cells responsible for myelination in the CNS.
As the disease progresses, axonal damage becomes more pronounced, contributing to the accumulation of disability. This neurodegeneration is not solely a consequence of demyelination but is also directly targeted by inflammatory processes, underscoring the importance of early and effective treatment to prevent irreversible nerve damage.
In the later stages of MS, the inflammatory activity may decrease, but neurodegeneration continues, leading to progressive neurological decline. This phase is characterized by axonal loss, leading to brain atrophy and increased disability, gliosis or the proliferation of glial cells in response to CNS injury, leading to further scarring and dysfunction, mitochondrial dysfunction contributing to energy deficits and axonal degeneration.
While the exact cause of MS remains unknown, it is thought to result from a combination of genetic susceptibility and environmental factors, such as viral infections, smoking, and vitamin D deficiency. These factors may initiate or exacerbate the autoimmune response against myelin.
The pathophysiology of MS is a dynamic process involving both the immune system’s attack on the CNS and the body’s attempts to repair damage. Understanding these mechanisms is crucial for developing therapies aimed at modulating the immune response, protecting neurons, and promoting repair of damaged tissues. Advances in research continue to provide insights into the complex interplay of factors driving MS, opening avenues for more targeted and effective treatments.
The role of infectious diseases in the causation of Multiple Sclerosis (MS) has been a subject of research and debate for many years. The idea that infections could trigger or influence the course of MS is supported by several lines of evidence, although no single pathogen has been definitively proven to cause MS. The potential mechanisms through which infectious agents might contribute to the development of MS include molecular mimicry, bystander activation, and chronic inflammation.
Molecular mimicry occurs when microbial antigens share structural similarities with self-antigens. This resemblance can lead to an immune response against the infectious agent that cross-reacts with the body’s own tissues. In the case of MS, it’s hypothesized that certain viral or bacterial antigens may mimic components of the myelin sheath or other neural tissues, potentially triggering an autoimmune response that results in demyelination and the subsequent neurological symptoms of MS.
Bystander activation suggests that infection-induced inflammation activates immune cells that, while not specifically directed against CNS antigens, release inflammatory mediators that can damage myelin and oligodendrocytes. This nonspecific activation of the immune system within the CNS can exacerbate or initiate autoimmune reactions against myelin.
Some infections can lead to chronic inflammation, which may predispose individuals to autoimmune diseases like MS. Chronic inflammatory responses can alter the immune system’s regulation and damage the blood-brain barrier, allowing more immune cells to infiltrate the CNS and perpetuate the cycle of inflammation and demyelination.
The strongest association between an infectious agent and MS is with the Epstein-Barr Virus, a ubiquitous virus that causes infectious mononucleosis. A significant body of evidence supports a link between EBV infection and an increased risk of developing MS. Individuals who have had infectious mononucleosis are at a higher risk of MS, and nearly all people with MS show serological evidence of past EBV infection.
HHV-6 has also been investigated for its potential association with MS. Some studies have found higher levels of HHV-6 DNA in the brain tissue of individuals with MS compared to those without the disease, suggesting a possible role in MS pathogenesis.
Other viruses and bacteria, including Chlamydia pneumoniae and the Varicella-zoster virus, have been studied for potential links to MS, but the evidence is less conclusive than for EBV.
While the exact cause of MS remains unknown, the potential role of infectious agents in its development is an area of active research. The relationship between infections and MS is likely to be complex and multifactorial, involving genetic susceptibility, environmental factors, and immune system interactions. Understanding how infections contribute to the onset and progression of MS could lead to new strategies for prevention, diagnosis, and treatment.
In the pathophysiology of Multiple Sclerosis (MS), enzymes play critical roles, especially in the processes of inflammation, demyelination, and neurodegeneration. While no single enzyme is responsible for MS, several enzymes are involved in the disease’s progression through their regulation of immune responses, degradation of cellular components, and contribution to oxidative stress. Here are some key enzymes implicated in the pathophysiology of MS. These enzymes do not act in isolation; their activity can be significantly influenced by various activators and cofactors. Activators increase the activity of enzymes, while cofactors, which can be ions or organic molecules, are necessary for the enzyme’s activity. Let us study some key enzymes involved in MS, along with their known activators and cofactors.
Matrix Metalloproteinases are a family of enzymes that can degrade extracellular matrix proteins. In MS, MMPs, particularly MMP-9, are involved in the breakdown of the blood-brain barrier (BBB), facilitating the infiltration of autoreactive T cells into the central nervous system. They also contribute to myelin degradation and neuronal damage. Tetracycline antibiotics such as doxycycline and minocycline have been found to have MMP inhibitory effects beyond their antibacterial properties. They can reduce the breakdown of the blood-brain barrier and myelin degradation by inhibiting MMP-9. BB-1101 and marimastat are examples of synthetic MMP inhibitors that have been explored for their potential in treating MS, although their clinical application has been limited due to side effects. Their activity is regulated by various tissue inhibitors. Pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) can activate MMPs. Zinc ions (Zn²⁺) are essential cofactors for the catalytic activity of MMPs.
Myeloperoxidase is an enzyme found in neutrophils, a type of white blood cell. It produces reactive oxygen species (ROS) and has been implicated in inducing oxidative stress in the CNS. Oxidative stress is a significant factor in the demyelination and neurodegeneration seen in MS.
Azide and cyanide ions are potent inhibitors of MPO but are not suitable for therapeutic use due to their toxicity. Safer, more selective MPO inhibitors are under investigation for their potential to reduce oxidative stress in diseases like MS.
Nitric Oxide Synthase enzymes, particularly the inducible form (iNOS), are expressed in various cell types, including macrophages and microglia in the CNS. iNOS produces nitric oxide (NO), a free radical that can cause damage to myelin and neurons. NO is also involved in the regulation of the blood-brain barrier’s permeability, influencing the infiltration of immune cells into the CNS. There are three isoforms of NOS, each with different regulatory mechanisms. Calcium ions (Ca²⁺) and calmodulin are required for the activation of endothelial NOS (eNOS) and neuronal NOS (nNOS). Cytokines can activate inducible NOS (iNOS) by inducing its expression. Tetrahydrobiopterin (BH₄), flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN) are important cofactors for all NOS isoforms. L-NMMA (NG-monomethyl-L-arginine) is a non-selective inhibitor of nitric oxide synthase that has been researched for its potential to reduce the damaging effects of excessive nitric oxide production. Given the role of iNOS in inflammatory responses, selective inhibition of iNOS is a desirable strategy to mitigate its detrimental effects without affecting the physiological roles of other NOS isoforms.
Cyclooxygenases, including COX-1 and COX-2, are enzymes that play a role in the inflammatory process by synthesizing prostaglandins from arachidonic acid. Prostaglandins are lipid compounds that mediate inflammation. COX-2, in particular, is induced during inflammatory responses and has been associated with the inflammatory lesions in MS. The expression of COX-2, an inducible isoform of COX, can be activated by pro-inflammatory cytokines. Heme is a cofactor for COX enzymes, essential for their enzymatic activity. Nonsteroidal anti-inflammatory drugs such as ibuprofen and naproxen can inhibit COX enzymes and are used to manage pain and inflammation in MS, although they do not alter the disease course. COX-2 selective inhibitors such as celecoxib specifically target COX-2, reducing inflammation with potentially fewer gastrointestinal side effects compared to non-selective NSAIDs.
Myeloperoxidase (MPO) is involved in producing reactive oxygen species, contributing to oxidative stress in MS. MPO activity can be increased by inflammatory stimuli. Chloride ions (Cl⁻) and hydrogen peroxide (H₂O₂) are substrates for MPO, and its activity is dependent on heme as a cofactor.
Adenosine Deaminase (ADA) is involved in the metabolism of adenosine and can influence immune responses. ADA activity can be modulated by the presence of certain substrates and ions. Zinc ions (Zn²⁺) can act as cofactors for ADA. Pentostatin compound inhibits ADA and has been used in certain cancers and autoimmune diseases. Its role in MS therapy could potentially involve modulation of immune responses and inflammation.
Proteases, including calpains and caspases, are involved in the cleavage of proteins and play roles in apoptosis (programmed cell death), neuronal damage, and the degradation of myelin proteins. Their activity is increased in MS, contributing to the pathology of the disease.
Calpain is involved in neuronal damage and apoptosis. Specific calpain inhibitors are being studied for their neuroprotective potential in MS and other neurodegenerative diseases. Caspase inhibitors can prevent apoptosis and are under investigation for their ability to protect neurons in various diseases, including MS.
The involvement of these enzymes in MS underscores the complexity of the disease’s pathophysiology. Targeting these enzymes and their pathways has been a focus of research for developing therapeutic interventions aimed at modulating immune responses, protecting neuronal integrity, and promoting repair in MS.
Inhibiting the activity of enzymes involved in the pathophysiology of Multiple Sclerosis (MS) represents a therapeutic strategy aimed at reducing inflammation, protecting the central nervous system (CNS), and slowing disease progression. Targeting specific enzymes involved in immune responses, demyelination, and neurodegeneration can potentially modify the course of MS. Here are some inhibitors targeting enzymes implicated in MS.
It’s important to note that while targeting these enzymes offers a promising approach to modifying the disease process in MS, achieving therapeutic efficacy while minimizing side effects remains a challenge. The development of enzyme inhibitors as treatments for MS involves careful consideration of selectivity, potency, and safety profiles. Ongoing research continues to explore these and other targets, aiming to improve outcomes for individuals living with MS.
The potential association between heavy metal exposure and Multiple Sclerosis (MS) has been an area of scientific inquiry, reflecting a broader interest in understanding environmental factors that may contribute to the development and progression of autoimmune diseases. Heavy metals, due to their ubiquity in the environment and known neurotoxic effects, have been investigated for their potential roles in MS.
Mercury is a heavy metal with well-documented neurotoxic effects, primarily through its organic compound, methylmercury, found in fish and seafood. Exposure can also occur through dental amalgams, industrial emissions, and contaminated water. Studies exploring the link between mercury exposure and MS have yielded mixed results. Some suggest that mercury could contribute to MS pathogenesis through mechanisms such as oxidative stress and immune system dysregulation. However, direct evidence linking mercury exposure to an increased risk of MS remains inconclusive.
Lead exposure, historically prevalent through paint, gasoline, and industrial emissions, has declined in many regions due to regulatory efforts. Lead’s neurotoxic properties and its potential to impair cognitive function have been well-established, but its association with MS is less clear. Research has investigated whether lead exposure may predispose individuals to MS or exacerbate its symptoms, though findings have not consistently demonstrated a strong link.
Cadmium exposure occurs through smoking, diet, industrial processes, and contaminated environments. Like other heavy metals, cadmium is known for its toxic effects on the kidney, bones, and cardiovascular system. Its role in autoimmune diseases, including MS, is of interest due to its ability to induce oxidative stress and inflammation. While some studies have explored cadmium’s potential impact on MS risk and progression, conclusive evidence linking cadmium exposure directly to MS is limited.
The interest in heavy metals in relation to MS is based on several potential mechanisms by which these metals could influence the disease process. Heavy metals can generate reactive oxygen species (ROS), leading to oxidative stress, which damages cells and tissues, including those in the CNS. There is evidence that heavy metals can modulate immune function, potentially triggering autoimmunity or exacerbating inflammatory responses associated with MS. Heavy metals may contribute to the disruption of the blood-brain barrier, facilitating the entry of harmful substances and immune cells into the CNS, which could exacerbate MS pathology.
Copper acts as a cofactor for several enzymes involved in the synthesis and maintenance of myelin. One such enzyme is cytochrome c oxidase, which is crucial for cellular energy production. Proper energy metabolism is essential for the maintenance of myelin and for the myelination process during development and repair. Copper is a component of ceruloplasmin and superoxide dismutase, enzymes that play significant roles in the body’s antioxidant defenses. By neutralizing free radicals, these copper-containing enzymes protect myelin and other cellular components from oxidative stress, which can lead to demyelination and neurodegeneration. Copper is important for brain development and function. It influences the formation of nerve coverings, including myelin, during neurodevelopment. Additionally, copper’s role in antioxidant defense mechanisms offers protection to the myelin sheath from damage that could impair nerve function. Both copper deficiency and excess can have detrimental effects on myelin and overall neurological health. Copper deficiency can lead to neurological disorders that may involve myelin degeneration. On the other hand, excessive copper levels can be toxic, potentially leading to oxidative stress and contributing to conditions such as Wilson’s disease, where copper accumulates in tissues, causing neurological and psychiatric symptoms. Copper’s role in myelin health is not isolated; it interacts with other nutrients, such as iron and zinc. These interactions can influence myelin integrity and function. For example, an imbalance in copper and zinc levels can affect the proper functioning of antioxidant enzymes and potentially impact myelin health.
Phosphorus plays a critical role in numerous biological processes, including the formation and maintenance of myelin, the protective sheath that surrounds nerve fibers and is essential for the efficient transmission of electrical signals in the nervous system. Phosphorus is a key element in phospholipids, which are major components of all cell membranes, including the myelin sheath. Phospholipids are essential for the structure and function of myelin, providing it with flexibility and integrity. The phospholipid bilayer of myelin facilitates the electrical insulation of nerve fibers and is crucial for the rapid propagation of nerve impulses. As a component of nucleic acids, phosphorus is vital for the replication and transcription processes in cells, including those involved in myelin production and repair. DNA and RNA are necessary for the synthesis of proteins related to myelin formation, including various myelin proteins that play specific roles in the structure and function of the myelin sheath.
Zinc plays a multifaceted role in the nervous system and is particularly important for the health and integrity of myelin. Myelin is the insulating layer that surrounds nerves, facilitating the rapid transmission of electrical signals in the nervous system. Zinc is crucial for the synthesis and maintenance of myelin. It acts as a cofactor for enzymes that are involved in the synthesis of myelin components. Additionally, zinc influences the expression of myelin-related genes, thereby playing a role in the regulation of myelin production and repair. Zinc has antioxidant properties that can help protect myelin and the neurons it insulates from oxidative stress and damage. Oxidative stress is implicated in the pathophysiology of several neurodegenerative diseases, including multiple sclerosis (MS), where demyelination is a hallmark. By contributing to the structural integrity of myelin, zinc indirectly supports the efficient transmission of nerve impulses. This is critical for all neural communication, from basic reflexes to complex cognitive functions. Zinc influences the immune system, which is particularly relevant in autoimmune conditions like MS, where the body’s immune system mistakenly attacks its own myelin. Adequate zinc levels can help modulate immune responses and potentially reduce the severity of autoimmune attacks on myelin. A deficiency in zinc has been associated with various neurological disorders, not only those involving demyelination but also neurodevelopmental disorders and neurodegenerative diseases. This suggests the importance of zinc not just for myelin health but for the nervous system as a whole. Despite these critical roles, the exact mechanisms by which zinc influences myelination and myelin maintenance are complex and still under research.
The role of oxalic acid in multiple sclerosis (MS) is an area of interest due to the potential impact of dietary components on the progression and symptoms of the disease. Oxalic acid can bind to minerals such as calcium and magnesium, forming compounds that the body cannot absorb. Since these minerals are very important for managing MS symptoms, oxalic acid in the body could have a negative impact by reducing the availability of these minerals. It is due to this role that homeopathic potentized forms of oxalic acid becomes an important candidate in the therapeutics of multiple sclerosis and various neuropathies.
Conium maculatum, commonly known as poison hemlock, is a highly toxic plant known for its neurotoxic compounds, such as coniine. These substances can cause neuromuscular blockade, leading to respiratory failure and death in severe cases of poisoning. The primary action of the toxins in Conium maculatum is the disruption of normal neuromuscular function, which is similar to the pathology of multiple sclerosis. Conium maculatum neurotoxins that make it extremely dangerous to the nervous system when applied in crude or molecular forms. The primary toxic constituents are alkaloids, with coniine being the most notable and toxic among them. These compounds interfere with the nervous system’s normal functioning. The most significant and well-studied alkaloid in poison hemlock, coniine, is a neurotoxin that disrupts the peripheral nervous system. It primarily affects the neuromuscular junctions — the points of communication between nerve cells and muscles. Coniine mimics the neurotransmitter acetylcholine but is not degraded by acetylcholinesterase, leading to prolonged stimulation of muscles, followed by paralysis. Another toxic alkaloid, γ-coniceine is considered to be the precursor of coniine in the plant. It has similar toxicological effects as coniine, disrupting the neuromuscular junction and leading to respiratory failure if ingested in sufficient quantities. A less studied alkaloid, N-methylconiine, is also present in poison hemlock and contributes to its overall toxicity. Like coniine, it affects the neuromuscular junctions, although its specific pharmacological profile and potency may differ. The mechanism by which these toxins cause harm involves blocking the acetylcholine receptors at the neuromuscular junction, preventing muscle contraction. Initially, this may cause tremors and muscular weakness, progressing to severe muscle paralysis. Since the diaphragm and other muscles involved in breathing can become paralyzed, respiratory failure is a leading cause of death in poison hemlock poisoning. Symptoms of poison hemlock ingestion include nausea, vomiting, abdominal pain, tremors, dilated pupils, rapid heartbeat, high blood pressure, severe muscular weakness, paralysis, respiratory failure, and, in severe cases, death.
Gelsemium, specifically Gelsemium sempervirens, is a plant that has been used in traditional medicine and homeopathy. It contains alkaloids such as gelsemine, gelseminine, and gelsemoidine, which have been studied for their effects on the nervous system. These compounds highly toxic and can lead to serious adverse effects, including respiratory failure and death if used in crude or molecular forms. The appeal of Gelsemium in historical or alternative medicine contexts may relate to its potential impact on nervous system symptoms, such as muscle weakness, pain, or spasticity, which are common in MS.
MIT HOMEOPATHY APPROACH
MIT or Molecular Imprints Therapeutics refers to a scientific hypothesis that proposes a rational model for biological mechanism of homeopathic therapeutics.
According to MIT hypothesis, potentization involves a process of ‘molecular imprinting’, where in the conformational details of individual drug molecules are ‘imprinted or engraved as hydrogen- bonded three dimensional nano-cavities into a supra-molecular matrix of water and ethyl alcohol, through a process of molecular level ‘host-guest’ interactions. These ‘molecular imprints’ are the active principles of post-avogadro dilutions used as homeopathic drugs. Due to ‘conformational affinity’, molecular imprints can act as ‘artificial key holes or ligand binds’ for the specific drug molecules used for imprinting, and for all pathogenic molecules having functional groups ‘similar’ to those drug molecules. When used as therapeutic agents, molecular imprints selectively bind to the pathogenic molecules having conformational affinity and deactivate them, thereby relieving the biological molecules from the inhibitions or blocks caused by pathogenic molecules.
According to MIT hypothesis, this is the biological mechanism of high dilution therapeutics involved in homeopathic cure. According to MIT hypothesis, ‘Similia Similibus Curentur’ means, diseases expressed through a particular group of symptoms could be cured by ‘molecular imprints’ forms of drug substances, which in ‘molecular’ or crude forms could produce ‘similar’ groups of symptoms in healthy individuals. ‘Similarity’ of drug symptoms and diseaes indicates ‘similarity’ of pathological molecular inhibitions caused by drug molecules and pathogenic molecules, which in turn indicates conformational ‘similarity’ of functional groups of drug molecules and pathogenic molecules. Since molecular imprints of ‘similar’ molecules can bind to ‘similar ligand molecules by conformational affinity, they can act as the therapeutics agents when applied as indicated by ‘similarity of symptoms. Nobody in the whole history could so far propose a hypothesis about homeopathy as scientific, rational and perfect as MIT explaining the molecular process involed in potentization, and the biological mechanism involved in ‘similiasimilibus- curentur, in a way fitting well to modern scientific knowledge system.
If symptoms expressed in a particular disease condition as well as symptoms produced in a healthy individual by a particular drug substance were similar, it means the disease-causing molecules and the drug molecules could bind to same biological targets and produce similar molecular errors, which in turn means both of them have similar functional groups or molecular conformations. This phenomenon of competitive relationship between similar chemical molecules in binding to similar biological targets scientifically explains the fundamental homeopathic principle Similia Similibus Curentur.
Practically, MIT or Molecular Imprints Therapeutics is all about identifying the specific target-ligand ‘key-lock’ mechanism involved in the molecular pathology of the particular disease, procuring the samples of concerned ligand molecules or molecules that can mimic as the ligands by conformational similarity, preparing their molecular imprints through a process of homeopathic potentization upto 30c potency, and using that preparation as therapeutic agent.
Since individual molecular imprints contained in drugs potentized above avogadro limit cannot interact each other or interfere in the normal interactions between biological molecules and their natural ligands, and since they can act only as artificial binding sites for specific pathogentic molecules having conformational affinity, there cannot by any adverse effects or reduction in medicinal effects even if we mix two or more potentized drugs together, or prescribe them simultaneously- they will work.
Based on the above discussions regarding molecular pathology of multiple sclerosis, homeopathic nosodes such as Epstein-Barr Virus 30, Human hepes virus 30 etc, and elemental dugs such as Mercurius 30, Plumbum met 30, Cadmium 30, Cuprum Met 30, Phosphorous 30, Zincum Met 30 etc could be included in the MIT prescriptions for treating this disease condition. Oxalic Acid 30, Conium Maculatum 30, Gelsemium 30, etc are also found to be useful.
REDEFINING HOMEOPATHY 