Body Fat and Cancer
Being overweight—or I should say over-fat or obese—is due to a myriad of factors, including your genes, lifestyle, and a diet loaded with high-calorie, low-nutrient-dense foods. By eating these cheap, available high-calorie foods, along with a sedentary lifestyle, over time the calorie energy coming in exceeds the calorie energy expended. The result is increased subcutaneous (under the skin) fat, and visceral (around the organs) fat.
According to the World Health Organization (WHO), there are roughly 1.6 billion overweight adults, 400 million of whom are obese. It is estimated that if this pandemic problem continues, by the year 2015 2.3 billion adults will be overweight, and 700 million people will be obese. Being overweight or obese is more than a cosmetic issue. It is clear that being over-fat and/or obese is unhealthy, as well as a major risk factor for many diseases, including diabetes, high blood pressure, dyslipidemia (high triglycerides, high LDL and low HDL), sleep apnea, arthritis, heart disease, and cancer.
Body Fat and Estrogen
It is becoming very clear that body fat and obesity are associated with cancers of the breast, liver, prostate, endometrium, esophagus, pancreas, colon/rectum, and kidney. It is also known that your cancer prognosis is also adversely affected by the amount of fat you carry. The link between body fat and cancer is estrogen. An article in Endocrine-Related Cancer states that adipose tissue (fat) is a major source of estrogen in men and women. In both men and women with excessive body fat, estrogen levels rise due to an enzyme present in fat called aromatase. Aromatase is responsible for converting testosterone into estrogen. In fact, researchers have found that body fat and obesity are associated with a two- to three-fold increase in aromatization of testosterone to estrogen.
The hormone estrogen causes cell growth and triggers cancers of the breast and endometrium. During normal metabolism, estrogen is converted to 2-alpha-hydroxyestrone, and 16-alpha-hydroxyestrone. The former does not cause cells to grow; in fact, in the journal Cancer Research, it is stated that 2-alpha may have a protective effect against estrogen-induced cancers in target organs. On the other hand, 16-alpha is estrogenic; it causes cell growth and has been found to be high in individuals with breast cancer.
Individuals with excess body fat have higher estrogen levels, and the tissues of obese and overweight women are exposed to more estrogen stimulation than the tissues of those who are lean. In men, there is evidence that increased body fat and estrogen are fuels for prostate cancer. There are receptors on prostate cells called estrogen alpha (ERalpha) and estrogen beta (ERbeta). ERalpha promotes cell proliferation (growth), and ERbeta arrests cell proliferation, either directly or by blocking the effects of ERalpha. Although there are other growth promoters involved, like insulin and insulin growth factor1 (IGF1), research is also pointing to estrogen as a prostate-tumor promoter. Therefore, excessive body fat is related to higher estrogen, and high estrogen can spark prostate cancer in men.
Picture from Dr. Robert Zembroski
Inflammation and Malignancy
Along with higher estrogen, excessive body fat causes inflammation. It is a well known fact that belly fat produces many different substances, including adiponectin, leptin, and inflammatory messengers called cytokines, one of which is Interleukin 6 (IL-6). IL-6 has many effects, including the regulation of different malignant tumors of the prostate, lung, breast, liver, stomach and lymphatic tissues.
All cells of the body have the ability to commit suicide when they are damaged, have outlived their usefulness, or have become too old. This process of programmed cell death is called apoptosis. However, when this programmed cell death fails to happen, cells can do more harm than good. This is a common scenario seen in cancer and tumor development. Mutated cells, as well as cells growing out of control, have turned off this suicide program, allowing them to survive in the body.
Researchers have found that higher levels of IL-6 in the body override the process of apoptosis in certain cancer-cell lines including stomach, colorectal cancer, and lymphomas. IL-6 is also involved in another process called angiogenesis. In order for cancerous tissue to survive, it needs a constant source of fuel. To provide that fuel, tiny tumors develop their own blood supply; that is angiogenesis. The inflammatory cytokine IL-6 communicates with cancerous tissues, which then spit out a chemical called vascular endothelial growth factor (VEGF). Just as it sounds, VEGF talks to local blood vessels causing them to sprout new blood vessels directed to the cancer cells and/or tiny tumor.Inflammation via IL-6 offers the blood supply and immortalizes cancer cells – not a good prognosis.
The link between being over-fat and the initiation, progression and eventual spread of cancer (metastasis) is becoming clear. Adipose tissue causes systemic inflammation in the body along with alterations in hormones. These metabolic problems associated with an unhealthful body composition are linked to many forms of cancer, not just its initial development, but also its long-term prognosis. In fact, researchers are finding that increased body weight is associated with increased death rates for all cancers combined, as well as for cancers at multiple specific sites. That’s profound! Being over-fat is not just a cosmetic issue; it is a killer.
World Health Organization, Obesity and Overweight, http://www.who.int/mediacentre/factsheets/fs311/en/index.html
Inflammation and Cancer: IL-6 and STAT3 Complete the Link, Cancer Cell 15, February 3, 2009
Local estrogen biosynthesis in males and females, Endocrine-Related Cancer (1999) 6 131-137
Obesity, Androgens, Estrogens, and Cancer Risk; Cancer Research 1982; 42:3281s-3285s.
IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1
Interleukin-6 promotes cervical tumor growth by VEGF-dependent angiogenesis via a STAT3 pathway; Oncogene (2003) 22, 1517-1527
This article is an excerpt from The Cancer Victor Survival Guide
©Dr. Robert Zembroski
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