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Use them, so you dont lose them!




Breast Cancer: Risks and Prevention

This booklet is written to help women understand what their risk factors are for the development of Breast Cancer and how they can reduce their risk.

Sometimes women are made to feel helpless and hopeless when it comes to their risk of developing breast cancer. After all, they cannot change the fact that they are women, are getting older, and have already inherited a certain set of genes from their parents. These are well-established risks for breast cancer. However, there are factors you can control to minimize your risk, including the amount of estrogen to which you are exposed and your reproductive history. Even if you have inherited the BRCA genes, which are well known to increase the risk of cancer, you can control other aspects of your life to decrease your risk.

In order to understand and control your risk factors for breast cancer, you must first understand how risk is expressed in numbers, how exposure to estrogen relates to most known risk factors, and how the maturity of breast lobules from Type 1 to Type 4 lobules decreases the risk of breast cancer. This booklet will also inform you about risk reduction strategies.


Exposure to Estrogen & Breast Cancer Risk


Estrogen is a normal female hormone made in your ovaries and in your fat (adipose) tissue.

Estrogen is also recognized as a carcinogen in your body for certain types of cancer including breast cancer.

Estrogen stimulates your breast tissue to increase cell divisions (mitoses). This sometimes results in cancers due to errors in cell division (mutations). Other substances (carcinogens) or exposures (e.g., high dose radiation) can also result in cancer.
Below is an illustration of that effect:


The time it takes to go from one cancer cell to two, from two to four, four to eight, etc., is referred to as the doubling time. To go from one cancer cell to a group of cells about ½" inch in diameter takes approximately 8-10 years, if that cancer has an average doubling time. One-half inch is about the size at which a cancer can be found by physical examination. Mammograms can find tumors ¼" in diameter.

This is why, after being exposed to a risk factor; it may take 8-10 years before a cancer can be detected, even if the risk exposure has caused a cancer to develop.

Prolonged and increased estrogen exposure may cause your breast cells to progress from hyperplasia to atypical hyperplasia to cancer. Hyperplasia refers to the overgrowth of cells; for example, in multiple layers instead of one layer in a milk duct (see diagram).



Proliferative breast disease found on biopsy indicates an exposure to increased levels of estrogen. An increased risk of Breast Cancer is found in women who have proliferative breast disease.

Simply stated, the more estrogen your breasts are exposed to over your lifetime, the higher the risk of breast cancer.

During each monthly menstrual cycle, a woman is exposed to increased estrogen levels, especially at the time an egg is produced by her ovaries (ovulation).

Both early age at the start of menstrual cycles (menarche) and late menopause increase breast cancer risk through increased exposure to estrogen during menstrual cycles. Similarly, late age for menarche and early age for menopause decrease breast cancer risk. Birth control pills and hormone replacement therapy increase breast cancer risk through increased exposure to estrogen. Likewise, removing both ovaries before natural menopause decreases breast cancer risk by decreasing levels of estrogen. The more alcoholic beverages you drink, the more impaired your liver becomes in its ability to eliminate (metabolize) estrogen in your body. That is why regular alcohol consumption increases breast cancer risk in direct proportion to the amount of alcohol you drink.

After menopause, obesity increases breast cancer risk by increasing your level of estrogen. This is because fat tissue produces small amounts of estrogen. The more fat you have, the higher your estrogen level.

Before menopause, obesity causes hormonal changes which decrease estrogen production by the ovaries and can even result in infertility. Therefore, premenopausal obesity does not increase breast cancer risk.





Breast Maturity & Breast Cancer Risk
Another aspect of breast development affecting breast cancer risk is the maturation of cells, which make up the milk glands (lobules), from type 1 lobules to type 4 lobules. Breasts are composed of milk glands (lobules), which make milk, and are surrounded by supportive tissue made of fat and connective tissue.

At birth, you have primitive type 1 lobules, which are very immature and which have many TDLUs (terminal ductal lobular units), where cancers are known to arise. These type 1 breast lobules develop into type 2 lobules at puberty, which are still primitive and susceptible to carcinogens. During the 3rd trimester of pregnancy (after 32 weeks), the breast lobules mature into type 3 lobules. Type 4 are formed after childbirth and produce milk. Both type 3 and type 4 lobules are resistant to carcinogens (see diagram).



The principle of breast cancer risk relating to cell maturity can explain other well documented breast cancer risks as well.

If a woman does not have a full-term pregnancy (meaning she is childless or nulliparous), she has increased risk for breast cancer, since she never develops type 3 and 4 lobules. If she has children later in life (after age 30), she has increased risk, because, for most of her menstrual life, her estrogen has been stimulating immature type 1 and 2 breast lobules. If she has children as a teenager, she has decreased risk of breast cancer, since her breast tissue matures very early in her menstrual life to type 3 and 4 lobules.

If a woman breast feeds, she often has low estrogen cycles or misses menstrual cycles altogether. She has decreased risk due to two factors: less exposure to estrogen and breast tissue maturity to type 4 lobules. Risk decreases more with longer duration of breastfeeding.

The risk factors of estrogen exposure and breast maturity can also act in concert with one another, causing greater risk. For example, if a teenager, who has not had a full-term pregnancy (she is nulliparous), takes birth control pills, her risk of breast cancer is much higher than a woman who has had several children and then takes birth control pills.

The longer your exposure to increased levels of estrogen, the higher your risk will be. Taking hormone replacement therapy after menopause for 1 to 2 years does not significantly increase breast cancer risk. However, a woman who has taken hormone replacement for years, especially if she had not had a full-term pregnancy and had taken birth control pills most of her life, will have significantly increased breast cancer risk.





Reproductive History & Breast Cancer Risk

During a normal pregnancy, estrogen levels rise 2000% by the end of the 1st trimester. During the first 2 trimesters, the breast grows because there is an increase in the number of immature type 1 and 2 lobules. During the 3rd trimester, the breast stops growing but lobules mature into Type 3 & 4 lobules. During the growth phase of pregnancy, the breasts become sore and tender.

Sometimes, a woman will miscarry during the first trimester. These miscarriages (spontaneous abortions) do not increase breast cancer risk, since they are associated with low estrogen levels that do not cause breast growth. Many times women who miscarry will say they never felt pregnant because their breasts did not change and they did not get nauseous from high estrogen levels. However, miscarriages in the 2nd trimester can increase risk.

A first trimester miscarriage is quite a different situation from induced abortion of a normal pregnancy in its affect on the woman’s breasts. The longer a woman is pregnant before an induced abortion, the higher her risk of breast cancer. This is because high estrogen levels of the 1st and 2nd trimesters cause breast growth of type 1 & 2 lobules. When her pregnancy is terminated before the breast cells reach full maturity, she is left with more immature type 1 & 2 breast lobules than before her pregnancy started, and therefore is at increased risk. Her breasts never mature to type 3 & 4 lobules, which would have occurred in the 3rd trimester and would have lowered her risk. This risk is especially high for teenagers who have an abortion in the late 1st or 2nd trimester and for those women who have never have a child, since their breasts never mature. Premature deliveries before 32 weeks are known to double breast cancer risk.

A teenager, who has an abortion between 9 and 24 weeks, has a 30% chance of developing breast cancer in her lifetime. If that same teenager also has a family history of breast cancer, the risk increases so much that one study showed all such women developed breast cancer by the age of 45.





Radiation & Breast Cancer Risk

High doses of radiation are known to increase breast cancer risk. Exposure to the atomic bomb at Hiroshima caused increased breast cancer incidence, especially in women exposed as teenagers when their breast cells were very immature. Repeated x-ray exposure for treatment of tuberculosis, postpartum mastitis, and chest Acne increases risk.

Life saving radiation treatment to the chest of young women with Hodgkin’s disease increases breast cancer risk. The amount of radiation needed to cause breast cancer is from 100 to 450 rads, (a rad is a radiation dosage measurement). Fortunately, with today’s screening mammograms, breasts are exposed to only 0.25 rads. It is estimated that a woman would need at least 400 mammograms to increase her breast cancer risk at all.



Genetics & Breast Cancer Risk

Only 5-10% of all breast cancer cases are felt to be truly genetic and caused by a breast cancer gene. For example BRCA 1 or 2 genes are passed from a parent to a child. Usually these genes cause breast cancers before menopause in mothers and daughters.

It is also possible to have a family history of breast cancer without inheriting one of these faulty genes. However, other inherited characteristics, such as how early you go through menarche or how your liver processes estrogen, may make someone at higher risk.

Having any type of family history may increase the effect of other known risk factors. For example, if you have a benign proliferative breast disease, you have increased risk. If you also have a family history of breast cancer, your risk is even higher.





Hormonal Birth Control and Hormone Replacement Therapy & Breast Cancer Risk


Two very common ways women are exposed to hormone therapy are through contraceptive medications and hormone replacement therapy after menopause.

A large majority of studies show increased breast cancer risk in women who take birth control medications, especially if they are taken before a full-term pregnancy, when their breast cells are still immature. Birth control pills are very commonly used by young women. For example, in one study women who took birth control pills before the age of 20 had more than a ten-fold increase in the risk of breast cancer. The longer they took the pill, the higher their risk. Even "low dose" estrogen pills have been associated with higher breast cancer risk.

Hormone replacement therapy also increases risk through the same mechanisms as birth control pills. The greater the number of years women take hormone replacement, the higher the risk. One potent synthetic estrogen, DES, has even been found to increase risk in mothers-and possibly their daughters-when taken during pregnancy.

Like any patient medication, hormones used judiciously and for short periods can be beneficial. Used for long periods of time, they can significantly increase breast cancer risk.





Breast Feeding & Breast Cancer Risk
Breast feeding decreases risk of breast cancer, since it results in some menstrual cycles without an estrogen peak and missed menstrual periods. Therefore, a woman is exposed to less estrogen and has decreased breast cancer risk. Breastfeeding also keeps breast tissue matured into type 4 lobules which decrease cancer risk.





Metabolism & Breast Cancer Risk
Metabolism refers to the way the body changes and processes hormones and other chemicals. This process also involves elimination of these chemicals from the body. Most of the active estrogen made by the ovaries is changed by the liver into an inactive form which does not cause the breast cells to divide (mitoses). But some estrogen is transformed into a long-acting estrogen that continues to stimulate the breast cells to divide. Some women’s bodies produce higher levels of this long-acting estrogen, and therefore have a higher breast cancer risk.

However, some things we eat can affect estrogen metabolism. For example, indole-3-carbinol, a substance found in cruciferous vegetables, can cause greater production of the inactive metabolite of estrogen, decreasing the risk of breast cancer.

In the same way, alcohol decreases the body’s ability to change estrogen into the inactive form and therefore, increases risk.

Women have increased risk when their bodies create more of the active form of estrogen.





Factors Which Increase Breast Cancer Risk

Increased Relative Risk Mechanism
Increasing age Premenopausal: Increases estrogen exposure Postmenopausal: Impairs immune function
Female sex Increased estrogen exposure
BRCA genes Inherited defects in cancer defense genes
Benign proliferative breast disease Result of increased estrogen exposure
Alcohol Increases estrogen level by decreasing liver function
Birth control pills Increases estrogen exposure
Hormone replacement therapy (HRT) Increases estrogen exposure
Early menarche Increases estrogen exposure
Late menopause Increases estrogen exposure
Postmenopausal obesity Increases estrogen exposure
Nulliparity (never bearing children) Maturity of breast lobules does not occur
Late childbirth (over 30 years old) Increases exposure of immature type 1 & 2 lobules to estrogen before first birth
2nd trimester miscarriage Leaves increased number of immature breast lobules
Induced abortions Leaves increased number of immature breast lobules
Premature birth before 32 weeks Leaves increased number of immature breast lobules



Factors Which Decrease Breast Cancer Risk


Decreased Relative Risk Mechanism
Late menarche Decreases estrogen exposure
Early menopause Decreases estrogen exposure
Oophorectomy (removal of ovaries before menopause) Decreases estrogen production
Cruciferous vegetables (e.g., broccoli, Brussels sprouts) Indole-3-carbinol decreases estrogen exposure by causing estrogen to be changed to an inactive metabolite of estrogen
Omega-3 fatty acids Unknown
Soy isoflavonoids May block estrogen receptors
Exercise Decreases estrogen levels
Having Childred (especially starting at an early age) Decreases number of immature breast lobules
Breast feeding Decreases estrogen by decreasing number of menstrual cycles and/or ovulation


Strategies for Lowering Your Breast Cancer Risk

Reduce your exposure to estrogen
Avoidance of hormonal therapies for contraception can reduce breast cancer risk. These include birth control pills and injectable or implantable hormones. Contraceptive methods that do not increase breast cancer risks can be used; for example, natural family planning.

Avoidance of prolonged hormone replacement therapy (HRT) for perimenopausal (around menopause) and postmenopausal symptoms will decrease breast cancer risk. There is no proven benefit to the heart with HRT. In fact, there is very strong recent evidence that HRT actually increases the risk of heart disease and stroke. There are other medications available, which can increase bone density for the treatment and prevention of osteoporosis.


Exercise
One to three hours of exercise a week can reduce your breast cancer risk by 30%. Women who train strenuously may lose their menstrual cycle or become anovulatory, and therefore, be exposed to less estrogen. Exercise can also delay the onset of menarche.


Maintain normal body weight
Obesity after menopause increases breast cancer risk because fat (adipose) cells manufacture estrogen.


Have children earlier in life
Having children in the early twenties or as a teenager decreases risk. Delaying child bearing until after 30 increases the risk of breast cancer substantially.



Avoid induced abortions
Having an induced abortion, especially as a teenager or before you have a full-term pregnancy, increases risk. If you do have an abortion, taking hormonal birth control after an abortion will increase risk further. However, having children and breast feeding them will reduce the risk.



Eat cruciferous vegetables
The cruciferous vegetables (e.g., broccoli, Brussels sprouts, cauliflower, watercress, kale and cabbage) contain high levels of indole-3-carbinol. This chemical causes the liver to form more of the inactive form of estrogen, thereby reducing estrogen exposure.



Eat Omega-3 fatty acids
These essential fatty acids are found in fish and many vegetable oils. Postmenopausal women who eat olive oil daily reduce their risk of breast cancer by 25%. Vegetable oils rich in omega-3 fatty acids include canola, flax seed, walnut and olive oils.
...

Limit alcoholic beverages
The more alcohol you drink, the higher your risk of breast cancer. Occasional alcoholic drinks will not increase your risk; however, regularly drinking alcohol every day will.


In summary,
There are many ways women can reduce their risk of breast cancer through the avoidance of unnecessary hormones and through dietary and lifestyle changes.

Finding breast cancers by mammogram when they are small does increase breast cancer survival. Smaller tumors are usually more differentiated and are less likely to have spread to lymph nodes.

Glossary
Anovulatory menstrual cycle A menstrual cycle that does not produce an egg, thereby producing lower estrogen levels in a woman’s body.
BRCA gene A defective gene which can be inherited from a parent, increasing the risk of breast cancer.
Carcinogen An agent which causes a normal cell to transform into a cancer cell.
Estrogen The predominate sex hormone in females made both in the ovaries and in fat.
Induced abortion Termination of pregnancy by surgery or medication.
Lobule Group of breast cells, composed of a duct and glands, which make milk.
Mammogram A soft-tissue x-ray of the breast used to detect breast cancers.
Maturity of
breast lobules The development of lobules from primitive, immature cell structures present at birth, which are incapable of producing milk and are most susceptible to carcinogens into advanced, mature cells which are capable of producing milk and are most resistant to carcinogens.
Menarche Age at which menstrual periods start.
Menopause Age when menstrual periods stop.
Metabolism Mechanism in which the body changes, processes and eliminates hormones and other body chemical substances; i.e., turns them into metabolites.
Miscarriage The spontaneous, natural loss of a pregnancy.
Mitosis The process of cell division causing one cell to become two cells.
Nulliparous Never bearing children.
Perimenopause Years immediately proceeding menopause, when menstrual periods can be irregular.
Proliferative breast disease Excessive growth of breast cells; for example, hyperplasia and atypical hyperplasia.



About the Authors:
Dr. Angela Lanfranchi has a private practice devoted exclusively to breast surgery in Bound Brook, NJ. A 1975 graduate of Georgetown School of Medicine, she is a Clinical Assistant Professor of Surgery at Robert Wood Johnson Medical School, a fellow of the American College of Surgeons and a diplomate of the American Board of Surgery. She is also a member of the Expert Advisory Panel for the New Jersey Board of Medical Examiners.

Dr. Joel Brind is a Professor of Human Biology and Endocrinology at Baruch College of the city of New York. A graduate of Yale, he received his Ph.D. from New York University in 1981. He is a biochemist who has specialized in reproductive steroid hormones, such a estrogen, and their links to human disease, since 1972. He has an international reputation as a breast cancer researcher and is widely published in medical journals.



Understanding What Risk Means and
the 3 Ways of Expressing Risk...

Cumulative lifetime risk
Incidence
Relative risk

Cumulative lifetime risk
of breast cancer is a statistically derived number assuming all women live to be a certain age. If all women alive in the year 2000 were to reach the age of 85, then one in eight or 12.5% will have developed breast cancer.


Incidence
This is the number of women who get breast cancer in a defined number of women in the population during a given time period. For example, during 1991-1995, the incidence of breast cancer of women aged 30 to 34 years old was 25 per 100,000 women.


Relative Risk
This is a number used to compare the impact of different risk factors associated with the likelihood of developing breast cancer. It is a number commonly used to tell women what their risk is when comparing them to women without that particular risk factor.


Relative risk number is used in epidemiologic studies and is the one most often used in risk tables.
Relative Risk is abbreviated RR.
RR 1.0 means there is no increase or decrease in risk.
RR 1.5 means there is a 50% increase in risk.
RR 2.0 means there is a 100% increase in risk.
RR 0.5 means there is a 50% decrease in risk.

References

Understanding What Risk Means
1. Bland KI, Copeland EM. The Breast: Comprehensive management of benign and malignant diseases, 2nd ed. Saunders 1997;v1:339.

2. Feuer EJ, Wun LM, Boring CC, et al. The lifetime risk of developing breast cancer. J Nat Cancer Inst 1993;85:892-897.

Exposure to Estrogen & Breast Cancer Risk
1. Bernstein L, Ross R. Endogenous hormones and breast cancer risk. Epidemiol Rev 1993;15:48-62.

2. Liehr JG. Is estradiol a genotoxic mutagenic carcinogen? Endocrine Reviews 2000;21(1):40-54.

3. Potten CS, Watson RJ, Williams CT, et al. The effect of age and menstrual cycle upon proliferative activity of the normal human breast. Br J Cancer 1988;58:163-168.

4. Russo IH, Calaf G, Russo J. Hormones and proliferative activity in breast tissue. In Stoll BA (ed). Approaches to Breast Cancer Prevention. Dordrecht, Kluwer Academic Publishers 1990;35-57.

5. Writing group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA 2002;288:321-33.

Breast Maturity & Breast Cancer Risk
1. Russo J, Reina D, Frederick J, et al. Expression of phenotypical changes by human breast epithelial cells treated with carcinogens in vitro. Can Res 1988;48:2837-2857.

2. Russo J, Russo IH. Development of the human mammary gland. In Neville MD, Daniel C (ed). The Mammary Gland, Plenum, NY 1987:67-93.

3. Vorher H. The Breast, Academic, New York 1974:1-18.

Reproductive History & Breast Cancer Risk
1. Brind J, Chinchilli VM, Severs WB, Summy-Long J. Induced abortion as an independent risk factor for breast cancer: a comprehensive review and meta-analysis. J Epidemiol Community Health 1996;50:481-496.

2. Daling JR, Malone DE, Voigt LF, White E, Weiss NS. Risk of breast cancer among young women: relationship to induced abortion. J Natl Cancer Inst 1994;86:1584-1592.

3. Kelsey JL, Gammon MD, John EM. Reproductive factors and breast cancer. Epidemiol Rev 1993;15:233-243.

4. Henderson BE, Ross R, Bernstein L. Estrogen is a cause of human cancer: The Richard and Hilda Rosenthal Foundation Award Lecture. Cancer Res 1988;48:246-53.

5. MacMahon B, Trichopoulos D, Brown J. Age at menarche, urine estrogens and breast cancer risk. Int J Cancer 1982;30:427-431.

6. Melbye M, et al. Preterm delivery and risk of breast cancer. Bri J Cancer 1999;80:609-13.

7. Potten CS, Watson RJ, Williams CT, et al. The effect of age and menstrual cycle upon proliferative activity of the normal human breast. Br J Cancer 1988;58:163-168.

Radiation & Breast Cancer Risk
1. Hancock S, Tucker M, Hoppe R. Breast cancer after treatment of Hodgkin’s disease. J Natl Cancer Inst 1993;85:25-31.

2. Miller AB, Howe GR, Sherman GJ, et al. Mortality from breast cancer after irradiation during fluoroscopic examination in patients treated for tuberculosis. N Eng J Med 1989;321:1285-1289.

3. Tokunaga M, Land C, Tokuoka S, Nishimori I, Sodes, M, Akiba S. Incidence of female breast cancer among atomic bomb survivors 1950-1985. Radiat Res 1994;138:207-223.

Genetics & Breast Cancer Risk
1. Newman B, Mu H, Batler LM, Millikan RC, Moorman PG, King MC. Frequency of breast cancer attributable to BRCA1 in a population-based series of American women. JAMA 1998;279:915.

2. Shubert ER, Lee MY, Mefford HC, et al. BRCA2 in American families with four or more cases of breast or ovarian cancer: recurrent and novel mutations, variable expression, penetrance, and the possibility of families whose cancer is not attributable to BRCA1 or BRCA2 [see comments]. Am J Hum Genet 1997;60:1031.

Hormonal Birth Control and Hormone Replacement Therapy & Breast Cancer Risk
1. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53,297 women with breast cancer and 100,239 women without breast cancer - from 54 epidemiologic studies. Lancet 1996;47:1713-1727.

Breast Feeding & Breast Cancer Risk
1. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and breastfeeding: collaborative reanalysis of individual data from 47 epidemiological studies in 30 countries, including 50,302 women with breast cancer and 96,973 women without the disease. Lancet 2002;360:187-95.

2. Newcomb PA, Storer BE, Longnecker MP, et al. Lactation and a reduced risk of premenopausal breast cancer. N Engl J Med 1994;330:81-87.

3. Romieu I, Hernandez-Avila M, Lozcano E, et al. Breast cancer and lactation history in Mexican women. Am J Epidemiol 1996;143:543-552.

Metabolism & Breast Cancer Risk
1. Cavalieri EL, et al. Molecular origin of cancer: catechol estrogen-3-4 quinones as endogenous tumor initiators. Natl Acad Sci USA September 1997;94:10937-10942.

1. Yager JD, Lieker JG. Molecular mechanism of estrogen carcinogenesis. Anna Rev Pharmacol Toxicol 1996;136:203-232.

Strategies for Lowering Your Breast Cancer Risk
1. Fowke JH, et al. Brassica vegetable consumption shifts estrogen metabolism in healthy postmenopausal women. Cancer Epidemiology, Biomarkers & Prevention August 2000;9:773-779.

2. Lee HP, Jourley L, Duffey SW, Estene J, Day NE. Dietary effects on breast cancer risk in Singapore. Lancet 1991;337:1197-1200.

3. Yager JD, Lieker JG. Molecular mechanisms of estrogen carcinogenesis. Anna Rev Pharmacol Toxicol 1996;136:203-232.

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