Want to reduce your cancer risk? Take this pill

Recent breakthroughs in medicine have shed light on an apparent scientific paradox: While inflammation is necessary for our survival, it is also a fundamental cause of death. Long term effects of inflammation are seen throughout the body, from heart disease to diabetes to cancer. Fortunately for aspiring centenarians, a common over-the-counter anti-inflammatory medicine can reduce your risk of dying from the top three most fatal diseases.

Inflammation is often known just as a combination of itching, burning, swelling, fever, and general pain. Despite the discomfort associated with these symptoms, inflammation is an essential component of human biology. Without the inflammatory response, our ancestors would have died at the slightest bacterial invasion or the smallest flesh wound.

In general, inflammation is the bodies’ response to any injury.

When our cells are damaged, they release molecular signals that cause chaos at the cellular level. The immune system senses this disorder and mounts an inflammatory response. Different types of ‘soldiers’ are included in this counterattack, these include immune cells to disable invading bacteria, structural proteins to patch up the injury, demolition cells to destroy the damaged tissue, and stem cells to grow into new tissue.

This process is essential to close a wound or destroy groups of infected cells. Yet, despite its importance to short term health, research across disciplines now shows that it causes many problems later in life, such as heart disease and stroke.

Why would an essential biological system work as a double-edged sword?

A fundamental reason for many of the medical problems in the world is that humans did not evolve to live longer than 40 years. Biology that helps us when young becomes a scourge to our health later in life. Processes such as fat storage, hormonal signaling, and inflammation become serious health risks to the aging body.

Fueled by the hope of extending human lifespan, a whole new branch of science has developed which seeks to understand how fundamental biological pathways contribute to aging.

Years of research now support a central dogma that cellular damage and inflammation are the principal causes of aging. Specifically, many scientists have focused their study on the molecular signals released by damaged cells.

Among the various signals a damaged cells can release, the hormones responsible for inflammation are elevated in older people. Two hormones that have shown considerable effects are the thromboxanes and prostaglandins.

When thromboxanes or prostaglandins are released into the blood stream by damaged cells, a cascade of events takes place. First, blood vessels constrict, reducing blood flow. Next,  circulating platelets, which are akin to molecular lego blocks, clump together. Finally, the surrounding cells go into survival mode. The combination of these events normally stops bleeding after an injury, but in the aging body this causes blood clots followed by stroke or heart attack.

Strangely enough, these events are also closely connected to the development of cancer. Prostaglandins and thromboxanes have been specifically shown to promote cancer growth.

In general, tumors are like a wound that never heals; cancerous cells thrive in this inflammatory environment and use the chaos to grow while normal cells around them die. If scientists were able to prevent inflammation, many cancers would be eliminated or prevented.

Taking all of these scientific observations into account, it becomes obvious that inflammation is a major contributing factor to the top 3 most fatal diseases in the developed world – heart disease, stroke, and cancer.

As it turns out, a simple treatment has been used for 30 years now to reduce the chances of heart disease and stroke by targeting inflammation. Evidence emerging from the last several years of study indicates that this treatment may also cut cancer risk by up to 40%.

Even more surprisingly, our ancestors discovered this drug long ago.

Interested in reading what it is? Check out part 2.

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