In 1763, a clergyman named Edmund Stone claimed that he had found the remedy to fevers, common amongst those who lived in damp areas. He stated that the answer lay in the powdered bark of willow trees. Although this philosophy failed to make it into mainstream medicine, his discovery about the willow bark helped drive the development of one of the most widely used drugs in the world today.
Willow bark is a rich source of salicylates, the class of compounds to which acetylsalicylate, commonly known as aspirin, belongs. For many years, people have been taking aspirin to reduce fever and reduce pain, and new benefits of the drug are still emerging. It’s blood thinning properties make it an excellent long-term treatment to help prevent heart attacks and strokes, and it now appears that the drug reduces the chances of cancer and Alzheimer’s disease.
Many scientists believe that aspirin has a medical role much greater then is presently appreciated. Studies have revealed that mankind’s natural diet would once have contained a small but significant amount of salicylates from fruit and vegetables. Many people now regard salicylate as a micronutrient, similar to vitamins and antioxidants, that are essential for maintaining good health into old age.
Aspirin has many uses. Since it was first patented in 1899 by a German pharmaceutical company named “Bayer”, other medicines with similar properties have been developed, and they are collectively called ” non-steroidal anti-inflammatory drugs” (NSAIDs). They work by inhibiting the cyclo-oxygenase (COX) class of enzymes, which make prostaglandins which are molecules important for a signalling purpose. There are two types of these enzymes, COX 1 and COX 2. The COX 2 enzymes make prostaglandins that are involved in pain and inflammation pathways, giving aspirin its anti-inflammatory effect.
It was several decades before scientist discovered aspirins’s second important use, reducing cardiovascular disease. At that time, the reasons behind the formation of a blood clot that could trigger a heart attack were still unclear, but at the head of each clot, or thrombus, lay a clump of platelets, minute cell fragments that are normally suspended in the blood. It was discovered that aspirin produced a prolonged reduction in the adhesiveness off the platelets.
Epidemiological studies showed that a low dose of aspirin (300mg) given to men who recently suffered a heart attack, reduced deaths by over a quarter over two years. More recent studies have revealed that aspirin decreases the chances of primary heart attacks and strokes by over a third. It has now become customary for doctors to recommend that people who have suffered from a heart attack or stroke should take a daily dose of aspirin to prevent any further attacks. Many doctors extend this advice to people who are at risk of a heart attack or stork, such as smokers or people who are obese.
Chemically, aspirin is impartially effective in reducing the chances of a heart attack. Platelets clump together because of the action of thromboxane, which is made by COX 1 enzymes, in platelets. Aspirin inhibits COX 1 and so reduces the chance of clot formation. COX 1 inhibition is also a key mechanism through which aspirin produces undesirable effects, most notably stomach irritation and bleeding. Although serious bleeding and deaths are relatively rare, the risk is substantial to people with a history of stomach problems, such as ulcers.
Aspirin’s cardiovascular benefits are now widely recognized, and over the years, in increasing amount of evidence has been accumulating, suggesting that regular aspirin use may also reduce the risk of developing certain cancers. The mechanism which instigate this are not fully understood, but there are several interesting hypotheses. One is that aspirin causes cancer cells to self-destruct through a process called apoptosis, as it is a result of the combination of cancer cells and salicylate. It is believed that cancer develops when apoptosis is impaired, and salicylate is thought to correct this through various effects on both COX and non-COX pathways.