The pathophysiology of gastric hyperacidity, commonly associated with conditions like gastroesophageal reflux disease (GERD) and peptic ulcer disease (PUD), involves a complex interplay of factors leading to the excessive production of gastric acid or compromised mucosal defense mechanisms. The excessive production of gastric acid is often stimulated by increased levels of gastrin (a hormone that promotes acid secretion, histamine which binds to H2 receptors on parietal cells to stimulate acid secretion, and acetylcholine which acts through muscarinic receptors to increase acid secretion. Parietal cells in the stomach lining may become hyperactive due to these stimulatory signals or due to increased responsiveness to these signals, leading to excessive HCl secretion.
The stomach is lined with a mucosal barrier that protects it from the acidic environment. Factors like NSAIDs or non-steroidal anti-inflammatory drugs, alcohol consumption, and Helicobacter pylori infection can damage this barrier, making the stomach lining more susceptible to acid. Bicarbonate serves as a neutralizing agent against gastric acid. A decrease in bicarbonate production can reduce the protective mechanisms against acid, contributing to mucosal damage.
H. pylori can colonize the stomach lining, causing chronic gastritis and increasing the risk of ulcer formation. The bacteria can neutralize the local acidic environment for survival, leading to increased gastrin production and, consequently, increased acid secretion.
In the context of GERD, dysfunction of the lower oesophageal sphincture or LES, which prevents backflow of stomach contents into the esophagus, plays a significant role. Transient relaxations or a weakening of the LES allow acid to reflux into the esophagus, causing symptoms of heartburn and increasing the risk of esophagitis. Consumption of certain foods like spicy or fatty foods, caffeine, and alcohol, smoking, and obesity can exacerbate symptoms of hyperacidity by increasing acid production or decreasing LES tone.
Some individuals may have a genetic predisposition that affects gastric acid secretion or the integrity of the mucosal barrier, making them more susceptible to conditions associated with hyperacidity. Stress and anxiety can indirectly influence the severity of symptoms by enhancing the perception of discomfort and possibly affecting the stomach’s acid production through the stress axis.
The pathophysiology of gastric hyperacidity is multifactorial, involving both increased offensive factors like acid production and H. pylori infection, and decreased defensive mechanisms like impaired mucosal barrier function. Effective management often requires a comprehensive approach that addresses the underlying causes, reduces acid production, and promotes mucosal protection.
In the context of hyperacidity and its biochemical and molecular underpinnings, several functional groups in biomolecules play pivotal roles. These functional groups are key components of the substances involved in the production, regulation, and action of gastric acid in the stomach. Understanding these can help elucidate the complex interactions at the molecular level.
Pepsin and hydrochloric acid are two important constituents of gastric secretions that produce symptoms of hyperacidity and GERD. According to MIT view, homeopathic potentized forms of pepsinum 30 and acid muriaticum 30 are two essential preparations to be included in the prescriptions for managing hyperacidity. Acetylcholine 30 also could be very effective.
Histamine is a compound released by cells in the stomach lining that binds to H2 receptors on parietal cells, stimulating them to produce gastric acid. Histamine is a biogenic amine, containing an amino (-NH2) functional group, which is crucial for its biological activity. Molecular imprints of histamine, in the form of homeopathic preparation histamine 30, will obviously act as a wonderful antacid according to MIT perspective.
Gastrin is a hormone that stimulates gastric acid secretion by activating parietal cells. Gastrin is a peptide hormone, and at the molecular level, it contains carboxylic acid (-COOH) functional groups within its amino acid residues, essential for its structure and function. Homeopathic drug gastrin 30 that contain molecular imprints of gastrin molecules can act as binding pockets for gastrin, and inhibit their actions.
Proton Pump Inhibitors (PPIs), which are used to treat hyperacidity, often contain carboxylic acid groups that are essential for their mechanism of action, which involves irreversibly binding to and inhibiting the H+/K+.
Compounds containing carboxylic acid functional groups are widespread in both nature and synthetic materials. The carboxylic acid functional group (-COOH) is characterized by a carbon atom double-bonded to an oxygen atom and single-bonded to a hydroxyl group (OH). This configuration makes carboxylic acids capable of donating a hydrogen ion (proton), thus behaving as acids.
Many drug molecules that contain carboxylic acid groups, such as Ibuprofen (C₁₃H₁₈O₂), a popular nonsteroidal anti-inflammatory drug (NSAID), has a carboxylic acid group. Homeopathic potentized forms of ibuprofen in 30c potency could be effectively used in the homeopathic management of hyperacidity. Molecular imprints of ibuprofen contained in this preparation can act as artificial binding pockets for carbxylic acid functional groups and deactivate them.
Homeopathic potentized forms of any vegetable or chemical drug substance that contains carboxylic acid functional groups, such as ascorbic acid, salicylic acid , benzoic acid, succinic acid, oxalic acid, oleic acid, palmitic acid, acetic acid, formic acid etc will contain molecular imprints of carboxylic acid functional groups, and hence, could work as homeopathic antacids.
Since pathophysiology of gastric hyperacidity, commonly associated with conditions like gastroesophageal reflux disease (GERD) and peptic ulcer disease (PUD), involves a complex interplay of factors, MIT proposes to use combinations of indicated remedies in 30 potency for ensuring complete and speedy cure.
Allopathic antacids, commonly used to neutralize stomach acid and relieve symptoms of heartburn or indigestion, are generally considered safe for short-term use. However, like any chemical medication, they can have side effects, especially when used frequently or over a long period. It’s important to use them as directed and consult with a healthcare provider if you find yourself relying on them regularly.
Here are some potential harmful effects associated with prolonged or inappropriate use of allopathic chemical antacids. Stomach acid is essential for digesting food. Regular use of antacids can reduce stomach acidity, potentially leading to poor digestion and absorption of nutrients. Lowered stomach acid levels can increase the risk of bacterial overgrowth in the stomach and intestines, leading to infections or digestive issues. Some antacids contain magnesium, which, if taken in large amounts, can cause magnesium toxicity, particularly in individuals with kidney problems. Symptoms include nausea, vomiting, low blood pressure, and heart rate irregularities. Excessive consumption of calcium carbonate antacids can lead to hypercalcemia or high blood calcium levels, and can subsequently reduce the phosphate levels in your blood, leading to muscle weakness and other symptoms. Long-term use of calcium-containing antacids can lead to the accumulation of calcium in the kidneys, potentially resulting in kidney stones. Some antacid ingredients can affect kidney function over time, especially in individuals with pre-existing kidney conditions.
While calcium carbonate antacids can provide calcium, paradoxically, excessive use may interfere with the body’s ability to absorb calcium, potentially weakening bones and increasing the risk of osteoporosis.
Allopathic antacids can interact with other medications, reducing their effectiveness or increasing side effects. For instance, they can interfere with the absorption of certain antibiotics, thyroid medications, and iron supplements.
Long-term use of allopathic antacids can lead to rebound acid hypersecretion, where the stomach produces more acid than before once the medication is stopped. This can create a cycle of dependency on antacids to manage increased acid production.
Frequent use of allopathic antacids can mask symptoms of more serious conditions, such as gastroesophageal reflux disease (GERD), ulcers, or even esophageal cancer. It’s important to seek medical advice if you’re regularly experiencing heartburn or indigestion.
While allopathic antacids are effective for occasional heartburn or indigestion, their prolonged or excessive use can lead to undesirable effects.
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 