Originally published July 20 2009
Breast Cancer Linked to Obesity in Women of All Ages, Leptin Probable Culprit
by Barbara L. Minton
(NaturalNews) The link between breast cancer and obesity has strengthened with two new studies showing that body mass index is correlated with the disease. These finding apply to women of all ages with breast cancer, not just those who are postmenopausal. Lipid profile and estradiol levels correlating with high body mass index were shown as additional determinative factors.
Scientists at Geneva University in Switzerland conducted a population-based study in which they evaluated the impact of obesity on presentation, diagnosis and treatment of breast cancer. Among all women diagnosed with invasive breast cancer in Geneva between 2003 and 2005, they identified those with available information on body mass index and categorized them into groups they identified as normal/underweight (BMI <25kg/m), overweight (BMI >/=-30kg/m), and obese (BMI >30kg/m).
They compared tumor, diagnosis and treatment characteristics between the groups. They found that obese women presented significantly more often with stage III and stage IV disease, with an odds ratio of 1.8. This means they were 180% more likely to have later stage breast cancer than those women in the normal/underweight group. Women in the obese group were 240% more likely to have tumors that were equal to or greater in size than 1 centimeter compared to the women in the normal/underweight group. They were also a whopping 510% more likely to have positive lymph nodes suggesting their cancers may have spread to other parts of their bodies.
Another team of scientists carried out a comparative study to investigate the effect of lipid profile, estradiol and obesity on the risk of a woman developing breast cancer. Assessment of 200 women for lipid profile, estradiol level and BMI was completed on 100 breast care patients (43 pre and 57 postmenopausal) and 100 controls (45 pre and 55 postmenopausal). Their ages ranged from 25 to 80 years.
They found a significant increase in BMI, total cholesterol, triglycerides, and low density lipoprotein (LDL cholesterol) in the breast cancer patients compared to the controls. With the exception of estradiol that decreased, the lipid profile generally increased with age in both patients and controls, with the patients having a much higher value than the corresponding controls. There was also a significant positive correlation between BMI and total cholesterol, and between BMI and LDL cholesterol. BMI, total cholesterol and triglycerides were increased in both pre-menopausal and post menopausal phases with HDL cholesterol remaining unchanged.
Not only does obesity clearly increase breast cancer risk, other research has shown it shortens the time between return of the disease and lowers overall survival rates. In 2007, Italian researchers went a long way toward explaining why. They presented evidence that a hormone found in fat cells called leptin significantly influences breast cancer development and progression in mice.
Leptin, a hormone derived from fat cells, is best known for its efforts to send messages to the body that its time to stop eating. This process may go awry in many people with obesity. Dr. Sebastiano Ando, lead researcher, has noted that leptin is also involved in many other processes in the breast, from reproduction and lactation to cell differentiation and proliferation. Leptin is activated by signals from the leptin receptor, and it is this partnership gone wrong that has previously been shown to be involved in the development of breast cancer. Leptin has been found in 86.4% of primary breast tumors.
Previous studies in Dr. Ando's laboratory found that leptin played a significant role in promoting breast cancer in obese women by increasing the amount of estradiol in breast tissue. In their 2007 study, the researchers found that leptin up-regulates or increases the production of E-cadherin, an intercellular adhesion molecule generally viewed as a tumor suppressor.
The researchers grafted human breast cancer tissue in "nude" mice (genetically bred to be unable to reject tumors and used frequently in cancer research) and also in a three dimensional tissue culture closely mimicking biological features of tumors.
Their results were the same in both media. Combined exposure to leptin and estradiol increased tumor size as much as 100%. These changes correlated with an increase in E-cadherin. Dr. Ando and his team concluded that the tumor suppressor E-cadherin may serve as a tumor enhancer when exposed to leptin and estradiol. It may be that the ability of E-cadherin to help cells aggregate enhances the transformation of normal cells to cancerous ones, thereby stimulating the growth of a tumor mass. This theory gained additional weight when the researchers used an E-cadherin antibody or a calcium-chelating agent to block E-cadherin function in the presence of estradiol. The enhanced cell growth stopped.
When a leptin inhibitor is given to mice, it reduces the expression of vascular endothelial growth factor and its receptor, and growth of breast cancer cells. Researchers at Morehouse School of Medicine used a leptin antagonist to evaluate whether the inhibition of leptin signaling has a differential impact on the expression of molecules leading to angiogenesis (creation of blood supply for tumors) and on cell proliferation and growth of human estrogen receptor-positive (ER+) and estrogen receptor-negative (ER-) xenografts hosted by immuno-deficient mice.
They found that the leptin antagonist reduced the growth of the ER+ human breast cancer cells by more than 40 fold, or a mind-bending 4000%, while the growth of ER- human breast cancer cell growth was reduced by 2 fold, or 200%. Expression of pro-angiogenic and pro-proliferative molecules were reduced to a greater degree in the ER+ cells than in those that were ER-. The results suggest that leptin signaling plays an important role in the growth of both ER+ and ER- negative breast cancer that is associated with the leptin regulation of molecules controlling tumor blood supply and proliferation rate. The researchers endorsed the use of leptin signaling inhibition as a treatment for breast cancer.
Normalized leptin functioning may produce happy breasts
All this research implies that the regulation and function of leptin must be restored in anyone wanting to be protected from breast cancer or its return. Health guru Byron Richards, one of the first nutritionists to recognize the importance of leptin, describes it as the single most important hormone for body weight control. Leptin regulates thyroid hormone, insulin, growth hormone, and adrenal hormones. When leptin is dysfunctional, all the other hormones regulating metabolic processes become dysfunctional too. He sees an understanding of leptin as basic for anyone trying to get and keep optimal metabolic function.
Leptin is made in white adipose tissue, commonly known as stored fat. Its release is stimulated by consuming a meal. Leptin flows through blood vessels to the brain where it delivers the message that it is time to stop eating. If people consistently overeat they become leptin resistant, a condition in which leptin becomes unable to deliver its message to the brain. This condition develops into a vicious circle in which overeating continues and the brain becomes even more resistant to the leptin message. This is about the time true obesity sets in.
To regain a healthy metabolism and keep eating under control, proper leptin function must be normalized. This requires a drastic reduction in consumption of processed carbohydrates and the embracing of a diet comprised of whole foods. This does not have to be a grueling dietary upheaval that produces feelings of deprivation and lack of satisfaction. Abandoning processed carbohydrates can be as simple as making a switch from pretzels to full fat potato chips. It can mean getting satisfaction from a chocolate bar with nuts rather than from a piece of cake. The key is the change from a diet in which processed carbohydrates play a large part, to a diet in which they play almost no part.
Getting a full nine hours of sleep in a fully darkened room is the also necessary for restoring leptin function. This means going to the bathroom in the dark, no TV, and no trips to the refrigerator unless you have removed the inside light. Daily exercise is also important, and will become desirable as energy levels improve along with leptin. Stress reduction is the fourth component in a leptin normalizing program.
Richard's book The Leptin Diet gives the low-down on how to get leptin working for you instead of against you. For those trying to kick the sugar habit as part of ousting processed carbohydrates from the diet, he suggests using supplements of the bitter herbs Gymnema sylvestre, and Inula racemosa. He calls these herbs "sugar busters". They help reduce the desire for sweet tasting foods and help bring the taste system back to natural balance.
For additional information:
Deglise C et al, Impact of obesity on diagnosis and treatment of breast cancer. Breast Cancer Research and Treatment, July 14.
Owiredu WK et al, Serum lipid profile of breast cancer patients. Pak Journal of Biological Science, February.
Obesity-breast Cancer Link May Be Due To Fat Tissue-derived Hormone Leptin. Federation of American Societies for Experimental Biologu, May 2, 2007.
Rene Gonzalez R et al, Leptin-signaling inhibition results in efficient anti-tumor activity in estrogen receptor positive or negative breast cancer. Breast Cancer Research, June 16.
About the authorBarbara is a school psychologist, a published author in the area of personal finance, a breast cancer survivor using "alternative" treatments, a born existentialist, and a student of nature and all things natural.
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