Anti-Inflammatory/Anti-Aging Strategies
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During a recent 5-day cancer conference in Washington, D.C. additional evidence was presented about the fact that inflammation produced by fat cells (adipose tissue) contributes to the growth and spread of tumors.

Dr. M.Kolonin of the University of Texas Health Science Center in Texas has been quoted as saying: “Obesity is the leading preventable cause of cancer in the U.S. Extra body fat not only increases one’s risk of developing cancer, it is also associated with poorer prognosis [outcomes]”… “Ten percent to fifteen percent of cancer deaths may be attributed to obesity”.

Exactly how body fat influences cancer development is still under investigation, but the key appears to be the inflammatory responses of the body to cancer cells and vice versa. Macrophages are one of the major classes of white blood cells responsible for starting the inflammatory response when the body is threatened by cancer cells, and  reducing inflammation when the challenge is over.

Typically, the breast tissue of overweight and obese young women is more inflamed, and has more immune cells, such as macrophages compared to women of healthy weight.  Also cancer in obese women is more difficult to treat than in women at healthier weight.

Metabolic syndrome is associated with a group of factors that puts one at greater risk of having heart disease,diabetes and stroke. If a person has three of the following factors, or are on medication for them, it is called having a metabolic syndrome.  These factors are: excess stomach fat, high blood pressure and triglycerides. low levels of “good” cholesterol (HDL), and high blood sugar.

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In one study of 100 women, half of the women with inflammation of their breasts and early-stage breast cancer also had metabolic syndrome. 

Since obesity contributes to growth of tumors, investigators wondered whether weight loss might reverse the tendency to grow tumors.  In mice, tumors grew more slowly in obese mice that had previously lost weight.   

The body tightly regulates its inflammatory responses by balancing the amount of inflammatory and anti-inflammatory immune factors it produces. Fat cells naturally produce inflammatory molecules.  High amounts of body fat encourages growth of cancer cells.`

Note:

Controlling one’s weight at healthy levels, being physically active for 2.5 hours/week, getting outside every day for a few minutes and using a superior immune-balancing supplement will go a long ways toward helping the body stay in immune balance, stay in immune homeostasis,

Dr.Hellen is available to help you enhance your quality of life to its maximum.  She can be contacted by using this form, contacting her at: drhellen@drhellengreenblatt.info or feel free to call her at:  302.265.3870 (ET, USA).

 

https://meyercancer.weill.cornell.edu/how_obesity_fuels_cancer
www.the-scientist.com/?articles.view/articleNo/49051/title/Fat-s-Influence-on-Cancer/
www.springer.com/us/book/9781461468189
clincancerres.aacrjournals.org/content/early/2016/02/14/1078-0432.CCR-15-2239
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journal.frontiersin.org/article/10.3389/fonc.2014.00175/full
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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
scitechnol.com/2324-9293/2324-9293-1-e104.phpwww.ncbi.nlm.nih.gov/pubmed/12020670
www.ncbi.nlm.nih.gov/pubmed/25170202
www.ncbi.nlm.nih.gov/pubmed/24855007
www.nature.com/bjc/journal/v108/n5/full/bjc201324a.html
www.ncbi.nlm.nih.gov/pubmed/24855007

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