Are You Likely to Die of Breast Cancer?

By Barbara Minton | May 26, 2011

Obesity is linked with a huge increase in risk of breast cancer according to several recent studies and the main culprit appears to be leptin, a hormone secreted by fat cells. This finding applies to women of all ages, not just those who are postmenopausal. A woman's lipid profile and levels of unbalanced estrogen in conjunction with high body mass index have been shown as additional factors determining whether she gets breast cancer and how deadly it will be.

Leptin promotes the ability of tumors to establish a blood supply of their own. Once this happens, the prognosis becomes less favorable. To determine the mechanism through which this happens, researchers in Atlanta, Georgia studied a mouse mammary model of invasive and highly metastatic breast cancer. (1) They found that leptin induces several signaling pathways to upregulate genetic expression of interleukin-1 (IL-1) in breast cancer cells, leading to the establishment of blood supply in breast tumors.

This research followed a study in Dallas, Texas in which researchers noted that leptin is present at high concentrations in mammary glands of obese women.(2) Their study was designed to determine the role it plays. They found that the local action of leptin within the mammary gland is a critical mediator, linking obesity and dysfunctional fat tissue with aggressive tumor growth.

In 2009 scientists in Geneva, Switzerland conducted a population-based study in which they evaluated the impact of obesity on presentation, diagnosis and treatment of breast cancer. (3) 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 (body mass index (BMI) <25kg/m),

*overweight (BMI >/=30kg/m)

*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, and 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. And they were a whopping 510% more likely to have positive lymph nodes suggesting their cancers may have spread to other parts of their bodies.

Meanwhile, another team of scientists carried out a comparative study to investigate the effect of lipid profile, unbalanced estrogen in the form of estradiol, and obesity on the risk of a woman developing breast cancer. (4) Assessment of 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). Ages ranged from 25 to 80 years.

These scientists found a significant increase in BMI, total cholesterol, triglycerides, and LDL cholesterol in the breast cancer patients compared to the controls. With the exception of estradiol which 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.

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Not only does obesity clearly increase breast cancer risk, other research in Italy has shown that it shortens the time between return of the disease and lowers overall survival rates.(5) In 2007, these Italian researchers were the first to present evidence that leptin significantly influences breast cancer development and progression.

Leptin is best known for its efforts to send messages to the body that it is time to stop eating and begin fat burning. This process may go awry in many people with obesity. Dr. Sebastiano Ando, lead researcher noted that leptin is also involved in many other processes in the breast, from 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, his group 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 mice and also created a three dimensional tissue culture closely mimicking biological features of tumors. Their results were the same in both media. Combined exposure to leptin and unbalanced 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 normally tumor suppressive E-cadherin may switch roles and serve as a tumor enhancer when exposed to leptin and unbalanced estradiol. It may be that the ability of E-cadherin to help breast 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 to block E-cadherin function in the presence of unbalanced estradiol. This caused the enhanced cell growth to stop.

When a leptin inhibitor is given to mice, it reduces the growth of breast cancer cells. An earlier study by the Atlanta research team used a leptin antagonist to evaluate whether inhibiting leptin signaling has a differential impact on the expression of molecules leading to the 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. (6)

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 cells was reduced by 2 fold, or 200%. The abilities of tumor cells to set up blood supply and proliferate were reduced to a greater degree in the ER+ cells than in those that were ER-. The researchers endorsed the use of leptin signaling inhibition as a treatment for breast cancer.

Normalized leptin functioning keeps breasts happy

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. Several health experts describe leptin as the single most important hormone for body weight control. Leptin regulates insulin, growth hormone and adrenal hormones, and plays a role in thyroid regulation. When leptin is dysfunctional, all the other hormones regulating metabolic processes become dysfunctional too. An understanding of leptin is basic for anyone trying to get and keep optimal metabolic function.

Leptin's 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 and start burning fat. If people consistently over eat 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 the time when true obesity sets in.

Restoring proper leptin function 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 buttered popcorn. It can mean getting satisfaction from a chocolate bar with nuts rather than from a piece of cake. Instead of a bagel or doughnut for breakfast, choose an orange or banana and some pumpkin seeds, or a plate of bacon and eggs. Instead of a sandwich, choose a fresh vegetable salad made with the same meat or cheese you wanted in the sandwich. 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 dark room is the also necessary for restoring leptin function. This means going to the bathroom in the dark and no trips to the refrigerator unless you have removed the inside light. Daily exercise is extremely important, and will become desirable as energy levels improve along with leptin. Stress reduction is the fourth component in a leptin normalizing program.

To help you oust process carbohydrates from your diet, order a bottle or two of Sugar Balance. For trouble falling asleep, take a melatonin supplement at bedtime. Fish oil has been shown to cut risk of breast cancer, so be sure to take capsules of fish oil daily or eat fatty fish a couple of times each week.

(1) Leptin pro-angiogenic signature in breast cancer is linked to Il-1 signaling. Zhou W, Guo S, Gonzalez-Perez RR. Br J Cancer. 2011 Jan 4;104(1):128-37.

(2) Leptin receptor signaling supports cancer cell metabolism through suppression of metochondrial respiration in vivo. Park J, Kusminski CM, Chua SC, Scherer PE. Am J Pathol. 2010 Dec;177(6):3133-44.

(3) Impact of obesity on diagnosis and treatment of breast cancer. Deglise C at al. Breast Cancer Res Treat. 2010 Feb;120(1):185-03.

(4) Serum lipid profile of breast cancer patients. Owiredu WK et al, Pak J Biol Sci. 2009 Feb 15;12(4):332-8.

(5) Obesity-breast Cancer Link May Be Due To Fat Tissue-derived Hormone Leptin. Federation of American Societies for Experimental Biologu, May 2, 2007.

http://www.sciencedaily.com/release...

(6) Leptin-signaling inhibition results in efficient anti-tumor activity in estrogen receptor positive or negative breast cancer. Rene Gonzalez R et al. Breast Cancer Res. 2009;11(3):R36.

About The Author:

Barbara 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.