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Anti-inflammatory drugs are used to reduce the symptoms of arthritis. These drugs are broadly classified as non-steroidal anti-inflammatory drugs (NSAIDs). They dull pain and repress inflammation.

NSAIDs act without alleviating the underlying disease process (some in fact may exacerbate the problem).

Pharmaceutical treatment of arthritis is based on the daily use of NSAIDs and is limited to simply relieving pain and slowing the progression of the disease.

NSAIDs do not prevent arthritis and is a poor way of managing its symptoms. Non-steroidal anti-inflammatory drugs are used to combat the aches, pains, and inflammation that occur following exercise. NSAIDs are also potent antioxidants with strong free radical scavenging ability.

There are more than 50 different NSAIDs on the market, none of which are ideal in the management of inflammatory joint disease.

Actions of NSAIDs

The drugs in this class have three major effects.

1. Anti-inflammatory: repression of inflammatory reactions.

2. Analgesic: reduction of pain.

3. Antipyretic: lowers a raised temperature.

The primary action of NSAIDs and the effects they produce are all related to the inhibition of the enzyme arachidonate cyclooxygenase (COX), in both its two forms COX-1 and COX-2.

Inhibition of cyclooxygenase causes a reduced production of pro-inflammatory compounds (prostaglandins, leukotrienes and thromboxanes).

NSAIDs that display all three actions (analgesia, antipyretic and anti-inflammatory) include aspirin, ibuprofen (Advil and Motrin) and naproxen (Aleve).

Tylenol (acetaminophen) differs because it provides only antipyretic and analgesia relief and lacks anti-inflammatory activity.

Salicyclic Acid: The Botanical Aspirin

Salicyclic acid is derived from the active compound (salicin) found in willow bark (Salix species). Salicyclic acid’s structure forms the chemical template for aspirin.

The ester of salicyclic acid or acetylsalicylic acid (aspirin), is a strong antipyretic, anti-inflammatory and analgesis agent.

Aspirin’s anti-inflammatory and analgesic activity is related to repressing prostaglandin production.

Aspirin lowers body temperature in individuals that already have an elevated core temperature. Aspirin acts directly on the thermogenic center in the hypothalamus to produce a dilation of blood vessels increasing peripheral blood flow. The inhibition of platelet clumping and its consequent anti-clotting activity provides prophylactic protection for cardiovascular disease.

Salicylates are known to produce stomach bleeding (gastric hemorrhages) in some individuals.

Aspirin derives its name from Spiraea. Now known as the meadowsweet (Filipendula ulmaria) plant. Meadowsweet contains, in addition to the active agent (methyl salicylate), a combination of mucilage and tannins.

Mucilage and tannins heal the damage to the gastric wall caused by the active salicyclic acid. Ironically, these mucilage and tannins are usually discarded in the preparation of pharmaceutical and herbal remedies since they offer no obvious value.

Methyl salicylate is found in wintergreen oil and is used as a topical agent in reducing inflammation and increasing local blood flow.

Tylenol • Acetaminophen

Acetaminophen (Tylenol) is an effective alternative to aspirin when only the relief of pain and reducing a fever is required. Acetaminophen is a good analgesic and anti-pyretic agent. However, acetaminophen does not inhibit the production of pro-inflammatory compounds and therefore is not useful in treating inflammation or arthritis. As such, they are beneficial to athletes only as a pain reliever. Because acetaminophen does not inhibit platelet aggregation, it does not prevent vascular clotting so it provides no protection to heart patients as aspirin does. Acetaminophen has fewer side effects than aspirin. However, there are damaging affects on the liver. Acetaminophen should therefore be avoided by heavy drinkers. Unwanted Side Effects of NSAIDs Adverse drug reactions occur with long-term, high doses of NSAIDS This often occurs when these drugs are used to treat joint diseases. Gastrointestinal disturbances, skin reactions and kidney effects have been found among chronic users of all types of NSAIDs. The Body’s Anti-inflammatory Drug; Cortisol The inhibition of prostaglandin synthesis is the most likely mechanism to account for the hormone cortisol’s powerful anti-inflammatory effect. Cortisol is a stress hormone that is secreted by the cortex of the adrenal gland in response to inflammation. The glucocorticoids (cortisol)hormones act via a receptor mechanism to stimulate the synthesis of the protein, annexin I (lipocortin). Lipocortin is a small polypeptide chain that inhibits cell membrane phospholipase A2. Phospholipase A2 is responsible for release of the fatty acid arachidonic acid from cell membranes. Arachidonic acid is a derivative of the essential dietary fatty acid, linoleic acid. Arachidonic acid is the precursor for eicosanoids, prostaglandins, and thromboxanes production. Cortisol also inhibits cyclooxygenase. Cyclooxygenase is the enzyme system that causes the formation of prostaglandins and thromboxanes from arachidonic acid. Cyclooxygenase enzymes are divided into COX-1 and COX-2 types. Cyclooxygenase inhibition potentiates cortisol’s anti-inflammatory effect, by reducing the production of pro-inflammatory molecules through inhibition of synthesis at other entry points. Coxibs Arachidonic acid is the starting compound in the formation of the mediators that cause inflammation and arthritis. The cyclooxygenase enzyme system causes the formation of prostaglandins. The cyclooxygenase enzymes are divided into COX-1 and COX-2 versions A new class of non-steroidal anti-inflammatory drugs, introduced in 1997, selectively blocks the type 2 or COX-2 enzyme. This book refers to these drugs as Coxibs. They are pharmaceutically known as selective COX-2 inhibitors. Big Pharma has already introduced four different versions and are busy working on a third and fourth generation of Coxibs. This, despite any evidence indicating that they are more effective than conventional NSAIDs. In fact, there is evidence that they are far more dangerous and expensive than these other drugs. Coxibs are selective cyclooxygenase inhibitor drugs. Coxibs act by inhibiting the specific enzyme (cyclooxygenase 2) that leads to the formation of the inflammatory mediators, the prostaglandins. Coxibs do not block the COX-1 enzyme. Inhibition of COX-1 produces gastrointestinal disturbances. All NSAIDs inhibit both cyclooxygenase the 1 and 2 enzyme systems. These COX-2 inhibitors do not block the 1 enzyme and therefore are purportedly a safer method to repress inflammation and treat the symptoms of osteoarthritis. The two forms of the COX enzyme catalyze different reactions. COX-2 enzymes are involved in the formation of inflammatory mediator, whereas the COX-1 enzyme produces beneficial compounds, which makes it desirable to allow it to function. The COX-1 enzyme plugs up microtears in the stomach lining due to drug ingestion and other irritations. The Coxibs as a group do not block the COX-1 enzyme. This makes the drug less harmful to the GI tract but unfortunately produces much more serious side effects. Celebrex (celecoxib) and Bextra (valdecoxib) are COX 2 inhibitors manufactured by Pfizer. Vioxx (rofecoxib) is a similar drug, manufactured by Merck. Novartis’s entry Prexige (lumiracoxib) has not yet gained FDA approval but is available in Europe. On Sept 30, 2004, Merck recalled Vioxx and its sister Ceoxx from pharmacy shelves. Merck’s other COX 2 inhibitor, Arcoxia, which is sold outside the US, has not been approval by the FDA. It is also suspected of increasing the risk to heart attacks and strokes. The concept of selective cyclooxygenase inhibition and safer drugs are noble goals. However, Big Pharma’s ability to persuade the public that they can accurately predict the long-term effects of drugs they manufacture has been irreparably harmed by the thousands of deaths and worldwide recall of Merck’s Vioxx. Separate studies over the past five years demonstrate that the chronic use of Vioxx can cause heart disease, raise blood pressure and initiate colon cancer. Celebrex and Bextra have caused similar doubts about Big Pharma. The prestige and integrity of the largest pharmaceutical companies in the world has been shaken. Pfizer has ‘voluntarily’ restrained its aggressive marketing of Celebrex and in April of 2005 was ordered by the FDA to discontinue selling Bextra due to its dangerous side effects.

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