Medicine
It's impossible to know with certainty how our ancestors first discovered medicinal uses for plants, as this knowledge predates written records. However, we can make educated guesses based on observations of historical practices, animal behavior, and basic reasoning:
1. Trial and Error:
- Observation: Early humans were keen observers of their environment. They would have noticed which plants animals ate when sick or injured.
- Experimentation: Based on these observations, they may have cautiously experimented with various plants to see if they had beneficial effects. This would have been a gradual process of trial and error, with potentially harmful consequences.
- Documentation: Oral tradition would have played a key role in transmitting knowledge about which plants were helpful, which were harmful, and how to prepare them.
2. Accidental Discovery:
- Food Preparation: Some medicinal properties might have been discovered accidentally during food preparation. For instance, a plant might have been added to food for flavor, and its medicinal effects were noticed over time.
- Preservation: Certain plants might have been used to preserve food, and their antimicrobial properties were then recognized as beneficial for health.
3. Intuition and Inspiration:
- Dreams and Visions: In some cultures, shamans or healers may have received guidance through dreams or visions about the medicinal uses of plants.
- Plant "Signatures": The Doctrine of Signatures, although not scientifically valid, suggests that the appearance of a plant could indicate its medicinal use (e.g., a heart-shaped leaf for heart ailments). While not a reliable method, it might have contributed to early experimentation.
4. Animal Behavior:
Over time, a combination of these methods, passed down through generations, would have led to a body of knowledge about herbal remedies.
A stomachic is a substance or preparation that is used to stimulate appetite and promote digestion or to tone the stomach.
In simpler terms, a stomachic helps to:
- Increase appetite
- Improve digestion
- Strengthen the stomach
These substances can include herbs, spices, or medications.
Examples of herbs and spices traditionally used as stomachics include:
Anti-inflammatory agents work through various mechanisms to reduce inflammation, a complex biological response to harmful stimuli such as pathogens, damaged cells, or irritants. These agents can be broadly classified into steroidal and non-steroidal anti-inflammatory drugs (NSAIDs), each with distinct mechanisms of action.
1. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs):
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Inhibition of Cyclooxygenase (COX) Enzymes:
NSAIDs primarily inhibit cyclooxygenase (COX) enzymes, namely COX-1 and COX-2. These enzymes are responsible for the synthesis of prostaglandins, thromboxanes, and prostacyclins from arachidonic acid. Prostaglandins mediate inflammation, pain, and fever.
- COX-1: Involved in maintaining normal physiological functions such as gastric mucosal protection, platelet aggregation, and renal blood flow.
- COX-2: Primarily induced during inflammation and responsible for producing prostaglandins that promote inflammation, pain, and fever.
By inhibiting COX enzymes, NSAIDs reduce the production of these inflammatory mediators, thereby alleviating pain, fever, and inflammation. Selective COX-2 inhibitors (e.g., celecoxib) were developed to reduce gastrointestinal side effects associated with non-selective COX inhibition but have been linked to cardiovascular risks.
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Other Mechanisms:
Some NSAIDs might also influence other inflammatory mediators or pathways, contributing to their anti-inflammatory effects, but the primary mechanism remains COX inhibition.
2. Steroidal Anti-Inflammatory Drugs (Corticosteroids):
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Genomic Effects:
Corticosteroids (e.g., prednisone, dexamethasone) enter cells and bind to glucocorticoid receptors in the cytoplasm. This complex translocates to the nucleus and affects gene transcription.
- Increased Production of Anti-Inflammatory Proteins: Corticosteroids increase the synthesis of anti-inflammatory proteins such as lipocortin-1 (annexin A1), which inhibits phospholipase A2, reducing the availability of arachidonic acid, a precursor for prostaglandins and leukotrienes.
- Decreased Production of Pro-Inflammatory Proteins: They suppress the expression of genes encoding pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-α), chemokines, adhesion molecules, and inflammatory enzymes (e.g., COX-2, iNOS).
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Non-Genomic Effects:
Corticosteroids can also have rapid, non-genomic effects by interacting directly with cell membrane receptors or affecting intracellular signaling pathways. These effects contribute to their immediate anti-inflammatory actions.
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Overall Effects:
Corticosteroids have broad anti-inflammatory and immunosuppressive effects, reducing inflammation, edema, pain, and immune cell activity.
Summary:
Anti-inflammatory agents act by targeting different components of the inflammatory cascade. NSAIDs primarily inhibit COX enzymes to reduce prostaglandin synthesis, while corticosteroids modulate gene transcription to decrease pro-inflammatory mediators and increase anti-inflammatory proteins. Both classes of drugs effectively reduce inflammation but differ in their mechanisms, side effects, and clinical applications.
Ranitidine is a histamine-2 receptor antagonist, also known as an H2 blocker. It works by reducing the amount of stomach acid your body produces.
It was commonly used to treat and prevent conditions such as:
- Peptic ulcers: Sores in the lining of the stomach or duodenum.
- Gastroesophageal reflux disease (GERD): A condition where stomach acid frequently flows back into the esophagus.
- Zollinger-Ellison syndrome: A rare condition where the stomach produces too much acid.
- Heartburn: A burning sensation in the chest caused by stomach acid reflux.
Ranitidine was available over-the-counter and by prescription.
Important Note: In 2019, the U.S. Food and Drug Administration (FDA) found unacceptable levels of N-Nitrosodimethylamine (NDMA), a probable human carcinogen, in ranitidine products. As a result, ranitidine products were recalled and are no longer available in the United States. [1]
Ranitidine is a histamine-2 receptor antagonist, also known as an H2 blocker. It was commonly used to reduce stomach acid production. It was available both over-the-counter and by prescription.
Uses:
- Treatment and prevention of ulcers in the stomach and intestines.
- Treatment of gastroesophageal reflux disease (GERD).
- Treatment of Zollinger-Ellison syndrome.
Why it was withdrawn:
In 2019, several manufacturers and regulatory bodies, including the U.S. Food and Drug Administration (FDA), issued recalls and eventually requested the withdrawal of ranitidine products from the market. This was due to the discovery of an impurity called N-Nitrosodimethylamine (NDMA), which is a probable human carcinogen. [1]
Alternatives:
Other medications, such as proton pump inhibitors (PPIs) like omeprazole and H2 blockers like famotidine, are now commonly used as alternatives.
Humulin is a hormone.
Specifically, it is a brand name for human insulin produced using recombinant DNA technology. Insulin is a hormone naturally produced by the pancreas that helps regulate blood sugar levels.