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Pancreatic cancer is an aggressive and treatment-resistant cancer that appears to be driven by pancreatitis, inflammation of the pancreas.   Although most people with pancreatitis never go on to develop pancreatic cancer, drinking alcohol in excess, obesity, and particularly smoking, has long been associated with a greater risk of having pancreatic disease.

The Role of The Pancreas
The pancreas is a digestive organ with two main functions.  It produces digestive enzymes to break food down in our intestines, and it contains clusters of cells, Islets of Langerhans, that help the body regulate its blood sugar levels.

Inflammation as a Contributor to Pancreatic Cancer
Inflammation is a complex immune response.  Pancreatic inflammation, mediated by cytokines, immune messengers, up-regulate (increase) inflammation which may lead to pancreatic cancer. Once inflammation is triggered, more immune cells are attracted to the inflamed pancreas and additional cytokines are released that damage pancreatic tissue and attract other damage-causing immune cells.

One of the roles of the immune system is to recognize and destroy cancer cells.  There is a significant amount of “cross-talk” between cancerous cells and immune cells.  On one hand immune cells track down cancer cells in an attempt to destroy them.  They can “turn-on” (up-regulate) or “turn-off” (down-regulate) cancerous cells.  Signals from cancerous cells can result in marked imbalances of immune cells, or make them function in odd ways.

Role of Cytokines in Pancreatic Cancer.
For example, pancreatic tumor cells are able to dampen some of the immune responses of the immune system leaving pancreatic cancer cells to multiply more easily. Cytokines from immune cells can change the environment around tumor cells and act directly on them, triggering their growth and migration to other parts of the pancreas and body. Some cytokines transform cancer cells into becoming resistant to chemotherapy.

Others may act either to trigger inflammation or stop inflammation depending on circumstances. In one study of pancreatic cancer, the most invasive parts of a tumor were found in the midst of heavily inflammatory centers.

Bacteria May Drive Inflammation and Cancer
Interestingly, the studies of our microbiome, the bacteria that inhabit our digestive tracts and other parts of the body, suggest that the bacteria that inhabit us may trigger inflammation, thereby promoting the growth of cancers.

In summary, limiting inappropriate inflammation and achieving a state of immune balance, homeostasis, may be a significant contributor in reducing the risk of pancreatic disease.

Dr. Greenblatt  looks forward to assisting you in reaching your health goals:   http://drhellengreenblatt.info/contact-dr-hellen or 1.302-265.3870 [USA, ET].

 

www.ncbi.nlm.nih.gov/pmc/articles/PMC4145756
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www.nature.com/bjc/journal/v108/n5/full/bjc201324a.html
www.ncbi.nlm.nih.gov/pubmed/24855007

During the 1970′s and 80′s, the saga of the “boy in the bubble” was followed with great interest. David Vetter, a young Texas boy had severe combined immunodeficiency (SCID), a disease caused by life-threatening defects in his immune system. His immune system was unable to protect him from infection, resulting in the necessity of having to live in a germ-free, isolation containment center designed by NASA engineers. He lived in this plastic bubble from the time of this birth until he died at the age of 12 following a failed bone marrow transplant.

The containment center was supposed to keep David separated from any pathogens that might harm him. Unfortunately, it was likely that it was a virus-contaminated bone marrow transplant that resulted in lymphoma, an immune system cancer, which ended David’s life.

Living in a sea of pathogens, a functional immune system is essential for our survival. Inflammation is among the first steps the body takes to heal after injury or disease and it uses immune inflammatory responses to protect us from cancer cells and pathogens. But too much inflammation is as serious a problem as too little inflammation. The body constantly struggles to limit the amount of inflammation that it produces, with uncontrollable amounts of inflammation acting like as if it was an out-of-control forest fire, destroying healthy cells in its path.

The four letters “itis” indicate an inflammatory condition. Typically, the name of the disease depends on the location in which the inflammation occurs. For example, arthritis (inflammation of the joints), colitis (inflammation of the intestinal tract, the colon), dermatitis (inflammation of the skin), nephritis (inflammation of the kidney), pancreatitis (inflammation of the pancreas), and uveitis (inflammation of a part of the eye).

Most immune cells do not have specialized names, however some organs have specialized inflammatory immune cells that detect infection and help resolve infection or injury to the body. Kupffer cells are most often associated with the liver. Microglia are associated with the brain and are involved in repairing damaged brain tissue and protecting the brain against disease. Dust cells, also known as alveolar macrophages, carry out similar functions in the lungs.

Inflammation is like real estate: location, location, location. The process of inflammation is substantially the same no matter where in the body the inflammation occurs. The intensity of the inflammatory response is determined by a balance between pro-inflammatory (molecules that cause inflammation) and anti-inflammatory (molecules that dampen inflammation) cytokines, immune messages that are released by immune cells.

The key to healthy immune responses is to be in immune homeostasis, immune balance. We must maintain the balance of enough inflammation to defend ourselves from pathogens, stimulate repair, and healing against the need to limit the amount of inflammation that too often leads to inflammatory diseases.

Contact Dr. Hellen for guidance in utilizing natural means to help the body return to immune homeostasis. She may be reached at:  DrHellen@DrHellenGreenblatt.info or or at 302.265.3870.

www.ncbi.nlm.nih.gov/books/NBK22254/
www.ncbi.nlm.nih.gov/pubmed/23720329
www.thedoctorwillseeyounow.com/content/mind/art3792.html?getPage=2
www.hindawi.com/journals/cherp/2012/490804/

 

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