Urticaria, commonly known as hives, is a condition characterized by the sudden appearance of itchy, red, and raised welts on the skin. The pathophysiology of urticaria involves complex immune responses, where several factors play critical roles in the development and manifestation of symptoms. Understanding the underlying mechanisms is key to effective management and treatment of the condition.
At the core of urticaria’s pathophysiology is an immune system response that leads to the release of histamine and other inflammatory mediators from mast cells and basophils in the skin. This process can be triggered by various stimuli, including allergens, medications, infections, stress, and physical factors like pressure, temperature, or exercise.
When the immune system encounters a trigger, IgE antibodies on the surface of mast cells and basophils bind to the antigen. This binding leads to the degranulation of these cells, releasing histamine and other substances into the surrounding tissues. Histamine binds to H1 receptors on nearby blood vessels, causing them to dilate and become more permeable. This p oh increased permeability allows fluid to leak into the surrounding tissue, leading to the swelling and redness characteristic of urticarial lesions.
Histamine release can also be triggered by autoantibodies against IgE or its receptor on mast cells and basophils, leading to chronic urticaria without an external allergen. This condition is called autoimmune urticaria. Certain physical stimuli such as pressure, cold, or heat can directly or indirectly cause mast cells to release histamine, leading to symptoms localized to the area of exposure.
Given the central role of histamine in urticaria, treatments often focus on blocking histamine receptors. Antihistamines are the first-line treatment for urticaria in allopathy, working by blocking H1 receptors to reduce swelling, redness, and itching. Newer, second-generation antihistamines are preferred due to their lower sedative effects compared to first-generation drugs. For acute flare-ups of urticaria, short courses of oral corticosteroids are be used to rapidly reduce inflammation and symptoms, though they are not a first-line treatment due to potential side effects with long-term use.
Histamine’s role in urticaria is fundamental, driving the vasodilation, increased vascular permeability, and sensory nerve activation that lead to the condition’s hallmark symptoms. Understanding this role is crucial for the effective treatment and management of urticaria.
In many cases, especially chronic urticaria, the condition does not stem from an external allergen but from an autoimmune reaction. The body mistakenly produces autoantibodies against the receptors on mast cells and basophils or against IgE itself. This autoantibody-receptor interaction mimics the action of an allergen, leading to the continuous activation of these cells and the chronic presentation of symptoms.
Besides histamine, other mediators play a role in the pathogenesis of urticaria. These include leukotrienes, prostaglandins, platelet-activating factor (PAF), and cytokines, which can amplify the inflammatory response and contribute to the symptoms of urticaria.
Cytokines play a significant role in the pathophysiology of urticaria. In the context of urticaria, certain cytokines are elevated, contributing to the development and persistence of hives. These cytokines can cause increased vascular permeability, leading to the leakage of fluid into the dermis and resulting in the formation of hives. Additionally, cytokines can recruit immune cells to the affected area, further amplifying the inflammatory response. Interleukin-1 is nvolved in the early stages of inflammatory responses. IL-1 can increase vascular permeability and promote the expression of adhesion molecules, facilitating the migration of immune cells to the site of inflammation. Interleukin-6 plays a role in promoting the acute phase response, which includes the production of antibodies and stimulation of T cells. Tumor Necrosis Factor-alpha (TNF-α), is another pro-inflammatory cytokine that can increase vascular permeability and stimulate the secretion of other inflammatory cytokines. Interferon-gamma is a cytokine more commonly associated with chronic forms of urticaria, which can modulate immune responses and contribute to inflammation.
Treatment strategies for urticaria often aim to reduce inflammation and alleviate symptoms. Antihistamines are the mainstay of allopathy treatment of urticaria, as they can block the action of histamine. Understanding the role of cytokines in urticaria has helped in the development of targeted therapies, providing hope for individuals with difficult-to-treat cases.
In order to inhibit the actions of histamine, MIT approach proposes the use of molecular imprints of histamine in the form potentized homeopathic drugs in 30c dilution. These molecular imprints can bind to the histamine molecules by conformational affinity, there by preventing their inflammatory effects. Molecular imprints of cytokines can inhibit the release of histamine, thereby preventing the initiation of an allergic process that leads to urticaria. Prostaglandin 30 also could be used with beneficial effects.
Phytochemicals are naturally occurring compounds in plants known for their potential health benefits, but some can also have adverse effects, such as inducing histamine release. This action can exacerbate allergic reactions, inflammation, or conditions such as urticaria in sensitive individuals. Understanding which phytochemicals can induce histamine release is crucial for managing such conditions. Tomatine, an alkaloid found in green tomatoes, tomatine can induce histamine release, contributing to allergic reactions in some individuals. Solanine, present in potatoes, especially green or sprouted ones, can also stimulate histamine release, potentially worsening inflammation or allergic responses.
Isothiocyanates are compunds found in cruciferous vegetables like broccoli, Brussels sprouts, and cabbage, which can potentially stimulate histamine release from mast cells. Isothiocyanates are a group of compounds derived from glucosinolates, which are sulfur-containing compounds.
Homeopathic drugs in 30c potency prepared from various kinds of plant-based substances that may contain molecular imprints of tomatine, solanine, isothicyanates etc will be effective in the treatment of urticaria, according to MIT perspective. Since molecular imprints cannot interfere in the interaction between biological molecules and their natural ligands, molecular imprinted drugs cannot produce any adverse effects.
There is evidence to suggest that both genetic predispositions and environmental factors contribute to the risk of developing urticaria. For example, mutations in genes involved in the immune response or mast cell function may increase susceptibility, while environmental factors can trigger or exacerbate symptoms.
Urticaria is a multifaceted condition with a complex pathophysiology involving immune system activation, histamine release, autoimmune components, and physical triggers. Understanding these underlying mechanisms is crucial for developing effective treatments and managing the condition. Allopathy treatments often involve antihistamines to block the action of histamine, but in chronic or severe cases, more targeted therapies such as immunosuppressants may be required. Since drug molecules used in allopathy as antihistamines can interact with biological molecules and produce unexpected harmful effects, it is far better and safer to use molecular imprinted homeopathic drugs in the treatment of urticaria.
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.
REDEFINING HOMEOPATHY 