Stress, Inflammation and Cancer

Thyroid cancer molecular mechanisms linked to stress and inflammation

(RxWiki News) Stress goes by many names, but on a cellular level that name is inflammation. A number of biological activities can cause inflammation, so can the stresses of unhealthy lifestyles.

It is easy to appreciate that some things, like a bacterial infection, cause inflammation. Fever, swelling and redness are all the classic signs.

But while the stress from a poor diet, obesity, or emotional turmoil is not as noticeable, the effects can be just as bad.

"Consider taking steps to lower the levels of stress in your life."

In a recent journal article, a medical doctor from Johns Hopkins explained the molecular basis of stress and inflammation in thyroid cancer, and concludes that stress is a definite risk factor in the development of of the disease.

And the principles explained are just as applicable to any other form of cancer, or any other cell in the body.

Mingzhao Xing, M.D., from Johns Hopkins University School of Medicine states that oxidants are molecules that are unstable. That means that in order to regain their stability, they have to steal a piece of another molecule nearby. This creates a chain reaction, where each molecule steals from its neighbor, until they are all slightly different than they used to be.

Stress is normal, and the inflammation that stress creates can be the result of exercise, as well. But when the cellular repair mechanisms never get a break to catch up with the damage, all kinds of problems can surface.

The kind of constantly changing environment present in chronic inflammation is one of the major pre-dispositions to cancer formation. So, cancer can be thought of as a series of changes in a cell until all of the normal protective mechanisms are no longer present, and the cell starts to reproduce wildly.

The term in scientific literature that refers to the stress produced in inflammation is  oxidative stress, in reference to the most powerful oxidant, oxygen.

In comparison to the series of molecular thefts started by an oxidant, anti-oxidants are generous molecules. They freely give pieces of themselves to all of the oxidants, without starting that chain reaction, and without turning into an oxidant themselves.

In the context of thyroid cancer, Dr. Xing supports her conclusion by referencing earlier research that shows high measured levels of oxidants correlates with levels of thyroid cancer in patients.

This makes sense, because medical literature has known for a long time that the thyroid is an especially sensitive organ to levels of radiation, and radiation itself is another cause of oxidation, the chain reaction of molecular stealing.

Dr. Xing says that autoimmune diseases, such as Grave's Disease of the thyroid, diabetes, and others, are associated with higher development of cancers, as well as a finding showing a naturally higher level of oxidation in patients.

Similarly, inflammatory diseases such as Crohn's and Ulcerative Colitis are well known to be closely associated with colon cancer development.

She concludes, as have many, that while the topic of inflammation is complicated, there seems to be a great deal of theoretical evidence that antioxidants such as Vitamin C and E should lower levels of cancer formation.

Unfortunately, inexplicably, decades of research have found this to not be the case, but support the role of omega 3 supplements like fish oil in reducing inflammation, and other dietary influences such as a diet heavy in animal fat and red meat in raising the index of inflammation in the human body.

Other studies suggest that long term use of non-steroidal anti inflammatory drugs such as aspirin and ibuprofen may lower rates of cancer formation, and studies looking at the use of aspirin in patients with heart disease tends to support this.

If given a chance, the body naturally has many mechanisms to repair lifestyle stress and the cellular damage it causes.

Dr. Xing states that her research is supported by the National Institutes of Health.

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Review Date: 
April 12, 2012