Life Extension Magazine®

Issue: Oct 2004

My Interview with Suzanne Somers

The failure to cure cancer is preventing older people from enjoying the full benefits of anti-aging treatments such as natural hormone replacement. Here we take a balanced, unbiased look at hormone replacement, as well as its pros and cons for cancer survivors.

By William Faloon.

William Faloon

On June 25, 2004, the US government proudly announced that 64% of cancer victims are living longer than five years, compared to a 50% five-year survival rate three decades ago.1

The grim fact, however, is that 1,368,030 among us will be diagnosed with cancer in 2004. This translates into 3,748 Americans being told each day that their lives may never be the same.2

While the government brags about statistical improvements, it ignores the horrific lifelong debilities suffered by those fortunate enough to survive cancer. The dreadful reality is that those successfully treated with conventional cancer therapies often suffer from chronic pain, depression, fatigue, immune suppression, mental impairment, disfigurement, and other side effects.3-5 On top of that, cancer survivors usually have higher risks of developing heart disease, stroke, and new cancers.6-7 Many of these lethal side effects, plus recurrence of the original tumor, can happen after the “five-year survival” milestone has been achieved.8-12

So what does all this have to do with my interview with actress and author Suzanne Somers? Suzanne is a breast cancer survivor who is doing something highly unusual. Although she had estrogen-receptor-positive breast cancer, she made a personal decision to forgo chemotherapy and estrogen-blocking drugs. Instead, Suzanne did the opposite of what conventional medicine advocates and is continuing to take her natural estrogen replacement drug. Her reason for taking the estrogen drug, despite the fact that estrogen is supposed to increase the odds of cancer recurrence, is that she does not want to suffer the agony and debility of hormone deprivation.

Suzanne Somers has authored a book on natural hormone replacement that has sold over 2 million copies. Her book eloquently extols the virtues of natural female hormone replacement in a way that will appeal to the lay reader. Suzanne’s celebrity status, her grasp of anti-aging medical concepts, and her willingness to discuss her intimate personal affairs will motivate many women to follow in her footsteps.

In this issue, we take a critical look at natural hormone drugs that make us look and feel better today but may increase our risk of cancer tomorrow. We also discuss how Suzanne Somers’ book will influence the decisions aging women make to stay biologically younger using natural hormone replacement, and the possible long-term effects of those decisions.

The most important revelation in this month’s issue is our in-depth investigation of what estrogen actually does in an aging women’s body. A lot of experts think they understand estrogen, but there are serious misconceptions as to how this hormone reacts at the cellular level. The new scientific findings we report, as they relate to how estrogen is prescribed to aging women, may turn the medical community upside down. The encouraging news is that there may be ways for women to enjoy their youth hormones without increasing their risk of cancer.


Head and neck cancer is the fifth most common form of cancer, yet most people are not familiar with this type of cancer. The mortality rate for those diagnosed with head and neck cancer (which does not include brain tumors) is high.

Radiation therapy is an important part of treating many different head and neck tumors, and is often used after surgery. Lethal radiation necrosis to the brain is one potential side effect.

Another danger of radiation therapy to the head is increased risk of stroke. A study of head and neck cancer patients who received radiation therapy found that stroke rates were five times greater than expected.13 This elevated stroke risk was found many years after administration of radiation. The average time between radiation treatment and stroke was 10.9 years, but the increased risk of stroke persisted for 15 years after radiation therapy.

For cancer patients treated with radiation therapy who later die of a stroke, the official cause of death is stroke, even though the cancer radiation therapy most probably caused the stroke. This is an example of how cancer cure statistics are misleading. The government brags that radiation therapy is curing cancer patients, yet long-term radiation side effects cause many deaths that are not attributed to cancer.

The government boasts that more cancer victims are living beyond five years, but conveniently ignores the fact that the toxic therapies often used to eradicate cancer can themselves cause premature death.

(The authors of this study do not recommend that head and neck cancer patients refuse radiation therapy, as it often buys years of extra life. Patients who have received radiation therapy to the head or neck should take extra precautions to reduce their stroke risk.)

The Estrogen Dilemma
As women enter the menopausal years, they face a difficult decision. The body’s natural production of estrogen, progesterone, DHEA, and other critical hormones needed to maintain health and vigor rapidly declines. While individual effects of menopause vary widely, most women suffer because their glands no longer produce the hormones needed to regulate critical physiological processes. Depression, irritability, and short-term memory lapses are common menopausal complaints, along with hot flashes, night sweats, and insomnia.

Scientific studies show that commonly prescribed estrogen drugs (Premarin® and Prempro™) increase the incidence of heart attack,14-19 stroke,19-21 breast and ovarian cancers,22-35 and possibly other diseases. More and more women are switching to “natural” estrogen drugs in the hope of deriving estrogen’s anti-aging benefits without the lethal side effects associated with Premarin® and Prempro™.

Recognizing that even natural estrogen drugs stimulate breast cell proliferation, proponents of natural estrogen replacement advocate consumption of fruits and vegetables, along with supplements such as indole-3-carbinol (I3C),36-50 resveratrol,51-61 gamma tocopherol,62-67 melatonin,68-75 genistein,76-91 and green tea.92-97 The cancer-preventive effects of these dietary modifications are well substantiated in the scientific literature. A concern remains, however, that we do not know for certain whether dietary modification confers absolute protection against estrogen drug-induced cancers. Life Extension addresses these controversial topics in the estrogen articles featured in this month’s issue.

If you read Suzanne Somers’ book, you will learn of the multiple wonderful benefits attributed to proper natural hormone replacement therapy. You will read expert physicians touting the benefits of so-called “bioidentical” estradiol (a natural form of estrogen), as opposed to drugs like Premarin® that are extracted from horse urine.

Our obligation is to convey factual information so that women can make a rational choice as to what they should be doing now to maintain healthy hormone balance while guarding against potential carcinogenic effects. We have in the past recommended the lowest effective dose of natural estrogen drugs, but we are concerned about the relatively high levels of estradiol (a potent form of estrogen) that some women are now taking for anti-aging effects.

Is There a “Safe” Level of Estrogen?
In response to the negative studies about Premarin® and Prempro™, some doctors believe that natural estrogen drugs are safer alternatives. Many of these natural estrogen drugs consist of estradiol that is synthesized to be identical to this form of estrogen that is made in the human body.

There is controversy, however, as to how safe estrogen produced in the human body really is. Scientific studies show that aging women who naturally produce higher levels of estrogen have greater rates of estrogen-stimulated cancers (breast, ovarian, endometrial).98-101 The published literature is also consistent in showing that women with reduced levels of estradiol have lower rates of estrogen-stimulated cancers.102,103

Postmenopausal women are increasingly taking bioidentical estradiol drugs, with or without natural progesterone. The physicians who advocate this type of hormone replacement therapy claim that since it is natural and “identical” to a woman’s own ovarian-secreted estradiol, it will not pose the same risks associated with long-term use of Premarin®. These doctors also state that this type of estrogen replacement is safe as long as it is properly balanced with natural progesterone, and blood estradiol levels are monitored to maintain physiological (normal) levels.

Critics charge that no one knows whether natural estradiol drugs are less risky than previous regimens of synthetic hormone replacement therapy. They point out that it may take decades of higher-dose estradiol use before adequate data are produced. Those concerned about higher-dose estradiol drugs believe that without controlled long-term studies similar to those that revealed problems with Premarin® and Prempro™, safety cannot be assured.


From a cancer-risk standpoint, the use of higher-dose estradiol drugs is worrisome for two reasons:

1. Estradiol at physiological (normal) levels stimulates the growth and multiplication of breast cells. This is known as mammary hyperplasia. Hyperplasia is an increase in the number of cells in a body part—in this instance, the breast. Mammary hyperplasia is a precursor and a risk factor for the development of breast cancer.104,105

2. Older women whose breast cells are stimulated to grow and divide by estradiol have an increased risk in errors of DNA replication. This occurs because each time a cell divides into new cells, the DNA in the new cells is altered slightly. After numerous cell divisions, these alterations accumulate, which can eventually result in mutations to genes that regulate cell proliferation. The accumulation of mutations in genes that regulate cellular proliferation is the under-lying cause of all cancers. Consumption of antioxidants, antimutagenic plant extracts, and other nutrients reduces certain gene alterations that lead to cancer, but it is not known to what degree cancer risk will be lowered in women taking estrogen drugs.106,107

An examination of existing epidemiological studies shows an increased risk of breast cancer in response to longer exposure to estradiol. We have summarized 15 examples of this in the sidebar on page 12 titled “Troublesome Facts About Estradiol Therapy.”

It is obvious that placing postmenopausal women on estradiol drugs is increasing their lifetime exposure to this potent estrogen, something that epidemiological studies show increases breast cancer risk. As we discuss in this month’s issue, however, these epidemiological studies often fail to account for dietary factors that may significantly alter the effects that estradiol inflicts on breast cells. Eventually, it may be shown that the adjuvant use of natural progesterone with estradiol lowers the risk for breast cancer, but this has not yet been fully documented.

So when one asks whether a “safe” dose of estradiol has been established, the answer at this time, from a cancer-risk perspective, is no. That does not mean, however, that aging women should be deprived of the benefits of estrogen. The multiple anti-aging effects of proper hormone replacement therapy may still outweigh the cancer risks. We are in fact devoting most of this month’s magazine to the role of proper natural hormone restoration in preventing and reversing many of the negative aspects of aging.


The following 15 facts about estradiol suggest a justifiable concern about breast cancer for those contemplating estradiol drug therapy:

1. Women who start menstruating early in childhood have a higher risk for breast cancer (longer exposure to

2. Women who start menstruating later in childhood have a lower risk for breast cancer (shorter exposure to estradiol)111-113

3. Women who were born prematurely have a higher risk for breast cancer (higher exposure to estradiol)114

4. Women who had early menopause have a lower risk for breast cancer (shorter exposure to estradiol)115-118

5. Women who have surgical menopause early have a lower risk for breast cancer (shorter exposure to estradiol)119-122

6. Women who have late menopause have a higher risk for breast cancer (longer exposure to estradiol)123,124

7. Women who have osteoporosis have a lower risk for breast cancer (lower exposure to estradiol)125-127

8. Women who have strong bones have a higher risk for breast cancer (higher exposure to estradiol)128

9. Women who have anorexia have a lower risk for breast cancer (lower exposure to estradiol)129,130

10. Women who are overweight or obese have a higher risk for breast cancer (higher exposure to estradiol)131-136

11. Women who are taller have a higher risk for breast cancer (higher exposure to estradiol)137,138

12. Women who bear children at a younger age have a lower risk for breast cancer (probably less exposure to estradiol)139-141

13. Women who nurse have a lower risk for breast cancer (probably less exposure to estradiol)142-145

14. Women who consume more alcohol have a higher risk for breast cancer (higher exposure to estradiol)146-148

15. Women who exercise regularly, even those who are overweight, have a lower risk for breast cancer (lower exposure to estradiol)149-156

These 15 points indicate, based on epidemiological studies, that an increase in exposure to estradiol results in a correspondingly increased risk of breast cancer. These epidemiological studies, however, do not reveal the effects of dietary modification on breast cancer risk. An in-depth discussion of this critical topic appears in this month’s issue.

Note: Some of the facts above about estradiol also pertain to the peripheral conversion of estrogen precursors (such as androstenedione) into estrone, which is another potent estrogen.

LE Magazine October 2004

My Interview with Suzanne Somers

Why Cancer Prevents Us from Reversing Aging
Several promising anti-aging therapies are being denied to the very people who need them the most—older adults. Fear of cancer is the main reason that elderly people do not take youth hormones and other agents that might reverse the biological effects of aging. The problem is that older cells contain more mutated genes responsible for regulating cellular propagation. Older cells are therefore more prone to becoming cancerous. When a growth-stimulating agent like estradiol is added to an older person’s body, the risk of certain cancers appears to increase.157,158

I cannot tell you the frustration that we at the Life Extension Foundation encounter when we discover a potential age-reversing therapy, only to have to rule it out because it might increase the risk of cancer. This is why we have done such an in-depth report on Suzanne Somers’ new book. Suzanne looks and feels so much better by taking natural youth hormones (along with a plethora of cancer-preventive nutrients) that she is willing to risk a recurrence of her breast cancer rather than do without her hormones. After reading the details of Suzanne’s battle with breast cancer and the devastating effects she encountered when deprived of her hormones, you cannot help but see her personal point of view. That does not mean, however, that you should follow her exact footsteps.

What is abundantly clear from Suzanne’s book is that if we are to overcome the destructive impact of aging on our bodies, it is critical that a cure for cancer be found. Cancer is the roadblock that is denying aged people the full complement of anti-aging hormones, of drugs that increase cellular longevity by increasing telomere length, and of a novel method of rejuvenating the circulatory system that corrects the dysfunctional aged arterial wall.

For example, Life Extension has published numerous articles about the anti-aging benefits of testosterone replacement therapy in aged men.159-173 The sad fact is that so many older men already have prostate cancer that they are deprived of this youth-promoting hormone. Testosterone replacement does not appear to increase prostate cancer risk in men. Interestingly, studies show that it may be high levels of estradiol that increase prostate cancer risk in aged men.174-176 (Aging men often convert their testosterone into estradiol.) The problem is that once prostate cancer manifests, testosterone is contraindicated, and aging men have to endure the serious consequences of hormone deprivation, which include depression, impotence, vascular disease, osteoporosis, anemia, and a host of other degenerative ailments.177-198

What Is the Solution?
The Life Extension Foundation has long advocated that finding a cure for cancer should be a national priority. Not only will one of every two men, and one of every three women, develop cancer in their lifetimes,199 but the fear of cancer is denying aging people access to validated anti-aging therapies. So cancer not only directly kills 1,500 people every day, but it also causes the deaths of countless others by denying them youth hormones, telomere extenders, and therapies that could restore healthy arterial function.

Cure cancer and 563,000 Americans who would have otherwise perished from the disease will be alive 12 months from now. Cure cancer and the gates open up to potent anti-aging therapies that would significantly reverse many aspects of normal aging and possibly keep alive a million human beings who would otherwise die of an age-related disorder over the next year.

You do not see cancer discussed on the front page of the newspaper very often. In today’s surreal world, a mere threatened act of terrorism grabs the news media’s attention, while millions of Americans suffer and perish silently from cancer and other related diseases. For those diagnosed with cancer, their concern over international events is subordinated to the harsh reality that even if they beat the cancer, their bodies will suffer possible lifelong side effects from the curative therapy. Suzanne Somers’ book brings out the reality of cancer and the tough choices patients have to make. Suzanne advocates natural hormone replacement as an anti-aging therapy, yet the very hormones that make her feel better today might increase the risk that her cancer will recur. We address the dilemma faced by breast cancer patients in this month’s issue.

We at Life Extension think it is deplorable that cancer victims are still put in the terrible position of not being able to access cures for their disease that are free of side effects. For the past two decades, our nonprofit organization has exposed how cancer research is impeded by antiquated FDA policies. We have shown how the FDA delays or denies clinical studies for promising cancer therapies. We have revealed how the FDA manipulates clinical testing of cancer drugs in such a way that guarantees that the drug will fail to show efficacy. We have reported on the FDA’s police-state attacks against pioneering cancer researchers and the stifling effect this creates in the scientific community.200-211 Our unequivocal position remains that if a cure for cancer and age-related disease is to be discovered in our lifetime, the FDA’s totalitarian authority has to be abolished. Only in a scientific environment that is free of political bias will diseases as complicated as cancer be cured.


Many misconceptions exist concerning the role played by estrogens in women who have had their primary breast tumors removed and currently have no apparent sign of residual disease.

Two thirds of breast tumors are estrogen receptor positive, and only half of these patients respond to interventions that reduce the effects of estrogen. Until recently, tamoxifen was the drug of choice for the treatment of estrogen-responsive early and advanced breast cancer. Tamoxifen, however, is associated with increased incidence of endometrial cancer, uterine sarcoma, ocular disorders, and diseases caused by abnormal blood clotting.212 Many tumors eventually become resistant to treatment with tamoxifen.213 One third to one half of patients will not benefit from treatment that blocks the estrogen receptor (such as tamoxifen) or inhibits estrogen production, either because the tumor does not use hormones to grow (i.e., is not estrogen or progesterone receptor positive) or because tumors that were originally hormonally responsive develop other pathways to facilitate their growth.214

Doctors are increasingly looking at aromatase inhibitor drugs that suppress estrogen levels by inhibiting estrogen biosynthesis. The newer, third-generation aromatase inhibitors (such as Arimidex®, Femara®, and Aromasin®) are more effective in reducing estrogen levels than previous-generation drugs.213,215-19

The current theory is that women successfully treated for estrogen-receptor-positive breast cancer should aim to have reduced levels of estrogen in the body, because estrogen stimulates the growth of estrogen-sensitive tissues.220 One recent study showed that the aromatase inhibitor Aromasin® reduced recurrence of breast cancer by 32% compared with tamoxifen over a period of two to three years. The problem with this study is that while Aromasin® reduced the rate at which the breast cancer returned, the overall survival rates of the tamoxifen and Aromasin® groups were not significantly different 221 Could it be that denying a breast cancer patient adequate estrogens reduces cancer recurrence rates but also causes other health problems? We do not know the answer to this yet, but in men with prostate cancer who undergo testosterone ablation therapy, dangerous side effects are induced directly by the deprivation of testosterone.196

In another study, the aromatase inhibitor Femara® resulted in more than 40% fewer breast cancer recurrences compared to placebo after 2.4 years. This study showed a trend toward reduced overall mortality in the Femara® group, albeit not statistically significant. For patients taking Femara®, more toxicity with respect to hot flashes, joint pain, and muscle pain contributed to a statistically significant decline in quality of life. Also reported was a trend toward more new diagnoses of osteoporosis for patients who took Femara® than for those who took placebo (5.7% vs. 4.5%;).215

Several problems face hormonally responsive breast cancer patients (with no apparent remaining disease) who use a drug that artificially lowers estrogens. First of all, breast cancer cells have a high propensity to mutate into cancer cells that no longer have an estrogen receptor. These mutated cancer cells do not require estrogen and use other growth factors and pathways in the body to propagate. So for many women initially diagnosed with estrogen-dependent breast cancer, cells that may have metastasized to other organ systems will not necessarily respond to estrogen-deprivation therapy, especially in the long term and if they have lost their estrogen-receptor expression.222

Another problem is that a large fat mass (or obesity) can result in excess production of estrogens, despite aromatase-inhibition therapy in some cases.223,224 In postmenopausal women who have no ovarian estrogen production, fat cells often function like “glands,” secreting locally abundant amounts of estrogens that increase cell division and thus cancer growth.225,226 Breast tissue is largely composed of fat, especially in postmenopausal women. Indeed, tumor estradiol concentration is often higher than the concentration seen in surrounding normal tissue, consistent with local estrogen synthesis in the tumor.227 Studies show that obese women have higher rates and recurrences of breast cancer.131,228-230 This could be related to both higher insulin and leptin levels, and higher estrogen levels, seen in the obese. Insulin is a potent promoter of cancer cell growth.231-247 Leptin is a hormone that controls fat metabolism. It has been suggested that leptin can promote aggressive breast cancer characteristics that may be independent of estrogen. Leptin plasma levels correlate with total body fat, and particularly high concentrations occur in obese women.248 Furthermore, a recent meta-analysis revealed a strong correlation between body mass index and plasma estrogen levels in postmenopausal women, reinforcing the importance of lifestyle modification over currently available breast cancer treatments.217,249,250

Oncologists are increasingly prescribing aromatase-inhibiting drugs to estrogen-receptor-positive postmenopausal breast cancer patients. In the short term, this may be an appropriate therapy, especially if this estrogen-deprivation therapy can block enough cancer cell growth to induce a “cure.” Over the long term, however, there is a risk that residual breast cancer cells will mutate and become resistant to estrogen-deprivation therapy, which has long-term side effects that are not fully understood.

It is easy to criticize Suzanne Somers for not taking an estrogen suppressor (aromatase inhibitor drug) and instead doing the opposite by taking an estrogen drug. Suzanne’s arguments, so eloquently presented in her book, are that maintaining healthy hormone balance may be protective by virtue of maintaining better overall mental and physical health. There is evidence to back up what Suzanne states, as revealed in some of the articles in this month’s issue.

The frightening aspect to this debate is that many of us reading these words today may face these difficult choices in the future. One option is to endure the agonies of hormone deprivation; the other option is to increase the risk of cancer recurrence by taking drugs that restore youthful hormone balance. Neither option is a comforting choice for cancer patients.

Readers should note that long-term use of aromatase-inhibition therapy is currently a subject of fierce debate within the medical establishment. Even when a consensus is reached, it will not resolve how women who are apparently free of residual breast cancer should approach hormone restoration.

As Life Extension was going to press, a prestigious cancer journal published a critique of clinical trials of aromatase-inhibiting therapy, particularly as they relate to the long-term consequences of such therapy. The author of the critique, Dr. Michael Baum, states: “I consider it too early for a proper risk benefit analysis to be calculated until we have the overall survival result.”

LE Magazine October 2004

My Interview with Suzanne Somers

How Life Extension Membership Can Save Your Life
In this issue of Life Extension, we present novel approaches that aging women should consider when it comes to safe hormone restoration. We also talk a lot about Suzanne Somers and her book, which is now in the hands of so many women. Suzanne was able to treat her cancer with a drug that is not approved by the FDA. While the efficacy of this particular drug remains questionable, Suzanne presents a compelling story to justify her right to access any drug that she believes would increase her chances of staying alive.

We do not agree with everything in Suzanne’s book, but if it takes a celebrity to get the message across about the necessity of maintaining youthful hormone balance—while personally defying FDA dictates—we welcome the support. Our long-standing position is that the FDA is the roadblock that separates Americans from breakthrough medical discoveries.

As a member of the Life Extension Foundation, you gain access to in-depth analyses of complex medical issues that are comprehensible to the lay reader. We recommend Suzanne Somers’ new book because it so well describes the critical need for hormone restoration. If you had to rely on Suzanne’s book alone, however, you would only get part of the story. Life Extension members gain access to the collective experiences of physicians and scientists who have used safe and natural approaches to hormone replacement for decades, despite FDA persecution.

The Life Extension Foundation has long exposed misleading government propaganda about the failed war against cancer. While survival rates have improved for some cancers over the past 30 years, the government ignores the harsh reality that many of the allegedly “cured” cancer victims suffer horribly from their treatments. The Life Extension Foundation continues to be the voice that challenges the overwhelming power of the cancer establishment, and informs our members about realities the federal government would prefer to hide from the public.

If you are not yet a Life Extension member, I invite you to peruse this month’s issue and ask yourself how valuable the information you read really is. On one side is the cancer establishment, supported financially, legally, and politically by the federal government. The objective of the cancer establishment is to pretend that significant progress is being made, though much of this so-called “success” is a result of earlier diagnosis and not better treatments. Life Extension, on the other hand, has consistently exposed the egregious misrepresentations made to the American public by the cancer establishment. Life Extension represents the consumer against an entrenched establishment that seeks to maintain its economic stranglehold on cancer research and treatment dollars.

As a member of our 24-year-old Foundation, you gain access to the latest medical breakthroughs, along with personalized access to Life Extension staff doctors by telephone. The free telephone contact alone could be worth hundreds of dollars, but membership in the Life Extension Foundation costs only $75 a year. Life Extension endeavors to take care of its members’ health concerns by incorporating the latest scientific findings in practical disease prevention and treatment protocols.

I hope the articles in this month’s issue are impressive enough to convince you that Life Extension membership is the best investment you could ever make in yourself.

For longer life,

William Faloon


As you can see from the following list, estrogen and progesterone drugs come in a wide range of choices.
Here we list the most commonly prescribed estrogen-progestin drugs and the type of estrogen, along with
the dosage units.

Brand Name

Type of Estrogen and Dosage Units

Oral Estradiol Drugs


Estradiol 0.5 mg, 1 mg, 2 mg
Estradiol 0.02 mg, 0.05 mg, 1 mg

Estinyl® comes in a lower-dose strength because it has a much longer-acting effect in the body.

Transdermal Estradiol Drugs

Alora®, Climara®, Esclim™, Vivelle®

Estradiol matrix patch
Estradiol matrix patch
Estradiol reservoir patch
Estradiol topical emulsion 1.7 g twice daily

Estradiol patches have variable rates of estradiol release over 24 hours and are changed once or twice weekly depending on the patch used.

Vaginal Cream, Gel, Ring, or Tablet Estradiol Drugs (for vaginal symptoms only)

Estrace® Vaginal (cream)
Estring® (ring)
Vagifem® (tablet)

Estradiol (0.01%) = 0.1 mg/dose
Estradiol 2 mg (7 ug over 24 hrs)
Estradiol 25 ug per tablet

Conjugated Estrogen Drugs

Premarin® Vaginal (cream)
Premarin® (oral)

Conjugated estrogens 0.625 mg/g
*Conjugated estrogens 0.3 mg, 0.45 mg, 0.625 mg, 0.9 mg, 1.25 mg, 2.5 mg.
*0.3 mg, 0.45 mg, 0.625 mg, 0.9 mg
0.3 mg, 0.625 mg, 1.25 mg, 2.5 mg

These drugs consist of 75-85% sodium estrone sulfate and 6-15% sodium equilin sulfate in such proportion that combined these total not less than 90% of the total esterified estrogens content. (Source: Facts and Comparisons, 2004 ed.)

* The manufacturers of Cenestin® (Barr Labs) and Premarin® (Wyeth) would not confirm the percentages of any of the estrogen components in their formulas, stating that this is “proprietary information.” Note that Premarin® is a natural, animal-based product derived from pregnant mare’s urine, unlike other commonly prescribed products such as Estrace® (soy based) and Cenestin® (yam based)

Oral Estrone Drugs



Estrone 0.75 mg and 1.5 mg
Estrone 0.625 mg, 1.25 mg, 2.5 mg

Oral Estriol Drugs

Estriol (generic only)

Estriol 4 mg, 8 mg

Commonly Prescribed Estrogen-Progestogen (Progestin) Drugs


Activella™, FemHrt® 1/5, Prefest®, Premphase®, Prempro™
Climara Pro™ and Combipatch®

Note: Progestogens and progestins are progesterone-like substances but are not structurally or biologically identical to progesterone. These include medroxyprogesterone acetate, norethindrone acetate, and levonorgestrel.

Progesterone-Only Medications Non-bioidentical to humans

Avgestin®, Aygestin®

Medroxyprogesterone acetate 2.5 mg, 5 mg
Norethindrone acetate 5 mg

Bioidentical Progesterone

Prometrium® (micronized progesterone)

100 mg, 200 mg capsules

(Note: Natural progesterone capsules are not recommended because the liver first metabolizes them before they enter the bloodstream. Natural progesterone creams are a better choice.)

Common Bioidentical Hormone Formulations


A combination of human bioidentical estradiol and estriol compounded by a pharmacist. It may come in varying per- centages of each hormone and the total milligram dose may differ depending on what the doctor orders. A common start- ing dose is 80% estriol and 20% estradiol, with a total dosage of 1.25 mg providing 0.25 mg of estradiol and 1 mg of estriol. The dose can be titrated upward. It comes in oral, top- ical cream, gel, or a lozenger (troche). Most think of an 80:20 ratio when they think of BiEst®. Because the medication is compounded to order, the physician can order whatever he or she believes will work best for each patient.


A combination of estradiol, estriol, and estrone. It may also come in varying percentages and the total dose may differ depending on what the doctor orders. A common starting dose is 80% estriol, 10% estradiol, and 10% estrone, with a total dosage of 1.25-2.5 mg. The dose can be titrated upward. Comes in the same options as BiEst® (oral, topical, or lozenger). Most think of the 80:10:10 ratio when they think of TriEst®, but the physician can order whatever ratio he or she believes will work best for the patient.


1. Centers for Disease Control and Prevention (CDC Cancer survivorship United States, 1971-2001. MMWR Morb Mortal Wkly Rep. 2004 Jun;53(24):526-9.

2. Available at: root/med/content/med_1_1_Most- Requested_Graphs_and_Figures.asp. Accessed July 22, 2004.

3. Available at:
Chemotherapy.asp?sitearea=MBC. Accessed July 22, 2004.

4. Available at: Accessed July 22, 2004.

5. Available at: Accessed July 22, 2004.

6. Available at:
sitearea=NWS&viewmode=print&. Accessed July 22, 2004.

7. Huddart R, Norman A, Shahidi M, et al. Cardiovascular disease as a long-term com- plication of treatment for testicular cancer. J Clin Oncol. 2003 Apr 15;21(8):1513-23.

8. Levi F, Te VC, Randimbison L, La Vecchia C. Cancer risk in women with previ- ous breast cancer. Ann Oncol. 2003 Jan;14(1):71-3.

9. DiFronzo LA, Wanek LA, Elashoff R, Morton DL. Increased incidence of second primary melanoma in patients with a previous cutaneous melanoma. Ann Surg Oncol. 1999 Oct;6(7):705-11.

10. Palme C, Waseem Z, Raza S, Eski S, Walfish P, Freeman J. Management and outcome of recurrent well-differentiated thyroid carcinoma. Arch Otolaryngol Head Neck Surg. 2004 Jul;130(7):819-24.

11. Fries M, Hailey B, Flanagan J, Licklider D. Outcome of five years of accelerated surveillance in patients at high risk for inherited breast/ovarian cancer: report of a phase II trial. Mil Med. 2004 Jun;169(6):411-6.

12. Fisher B, Dignam J, Wolmark N, et al. Tamoxifen in treatment of intraductal breast cancer: National Surgical Adjuvant Breast and Bowel Project B-24 randomised con- trolled trial. Lancet. 1999 Jun 12;353(9169):1993-2000.

13. Dorresteijn L, Kappelle A, Boogerd W, et al. Increased risk of ischemic stroke after radio- therapy on the neck in patients younger than 60 years. J Clin Oncol. 2002 Jan 1;20(1):282- 8.

14. Wilson PW, Garrison RJ, Castelli WP. Postmenopausal estrogen use, cigarette smoking, and cardiovascular morbidity in women over 50. The Framingham Study. N Engl J Med. 1985 Oct 24;313(17):1038-43.

15. Hemminki E, McPherson K. Impact of post menopausal hormone therapy on cardiovascular events and cancer: pooled data from clinical trials. BMJ. 1997 Jul 19;315(7101):149-53.

16. Stampfer MJ, Colditz GA, Wilett WC. Postmenopausal estrogen therapy and cardiovascular disease: ten-year follow-up from the Nurses’ Health Study. N Engl J Med. 1991 Sep 12;325(11):756-62.

17. Manson JE, Hsia J, Johnson KC, et al. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003 Aug 7;349(6):523-34.

18. Grodstein F, Stampfer MJ, Manson JE, et al. Postmenopausal estrogen and progestin use and the risk of cardiovascular disease. N Engl J Med. 1996 Aug 15;335(7):453-61.

19. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. JAMA. 2002 Jul 17;288(3):321-33.

20. Wassertheil-Smoller S, Hendrix SL, Limacher M, et al. Effect of estrogen plus progestin on stroke in postmenopausal women: the Women’s Health Initiative: a randomized trial. JAMA. 2003 May 28;289(20):2673-84.

21. Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women’s Health Initiative randomized controlled trial. JAMA. 2004 Apr 14;291(14):1701-12.

22. Mueck AO, Seeger H, Wallwiener D. Comparison of the proliferative effects of estradiol and conjugated equine estrogens on human breast cancer cells and impact of continuous combined progestogen addition. Climacteric. 2003 Sep;6(3):221-7.

23. Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: the Women’s Health Initiative Randomized Trial. JAMA. 2003 Jun 25;289(24):3243-53.

24. Porch JV, Lee IM, Cook NR, Rexrode KM, Burin JE. Estrogen-progestin replacement therapy and breast cancer risk: the Women’s Health Study (United States). Cancer Causes Control. 2002 Nov;13(9):847-54.

25. Beral V, Banks E, Reeves G, Appleby P. Use of HRT and the subsequent risk of cancer. J Epidemiol Biostat. 1999;4(3):191-210.

26. Gajdos C, Tarter PI, Babinszki A. Breast cancer diagnosed during hormone replacement therapy. Obstet Gynecol. 2000 Apr;95(4):513-18.

27. Colditz GA, Stampfer MJ, Willett WC, Hennekens CH, Rosner B, Speizer FE. Prospective study of estrogen replacement therapy and risk of breast cancer in post- menopausal women. JAMA. 1990 Nov 28;264(20):2648-53.

28. Chen Y, Liu X, Pisha E, et al. A metabolite of equine estrogens, 4-hydroxyequilenin, induces DNA damage and apoptosis in breast cancer cell lines. Chem Res Toxicol. 2000 May;13(5):342-50.

29. Magnusson C, Baron JA, Correia N, Bergstrom R, Adami HO, Persson L. Breast cancer risk following long-term oestrogen and oestrogen-progestin replacement thera- py. Int J Cancer. 1999 May 5;81:339-44.

30. Persson I, Weiderpass E, Bergkvist L, Bergstrom R, Schairer C. Risks of breast and endometrial cancer after estrogen and estro- gen-progestin replacement. Canc Causes Control. 1999 Aug;10(4):253-60.

31. Schairer C, Lubin J, Troisi R, Sturgeon S, Brinton L, Hoover R. Menopausal estrogen and estrogen-progestin replacement therapy and breast cancer risk. JAMA. 2000 Jan 26;283(4):485-91.

32. Ross RK, Paganini-Hill A, Wan PC, Pike MC. Effect of hormone replacement therapy on breast cancer risk: estrogen versus estro- gen plus progestin. J Natl Cancer Inst. 2000 Feb 16;92(4):328-32.

33. Hoover R, Gray LA Sr, Fraumeni JF Jr. Stilboestrol (diethylstilbestrol) and the risk of ovarian cancer. Lancet. 1977 Sep 10;2(8037):533-4.

34. Rodriguez C, Calle EE, Coates RJ, Miracle- McMahill HL, Thun MJ, Heath CW Jr. Estrogen replacement therapy and fatal ovarian cancer. Am J Epidemiol. 1995 May 1;141(9):828-35.

35. Lacey JV Jr, Mink PJ, Lubin JH, et al. Menopausal hormone replacement therapy and risk of ovarian cancer. JAMA. 2002 Jul 17;288(3):334-41.

36. Available at: Accessed July 22, 2004.

37. He Y, Friesen MD, Ruch R, Schut H. Indole-3-carbinol as a chemopreventive agent in 2-amino-l-methyl-6-phenylimida- zo[4,5-b]pyridine (PhIP) carcinogenesis: inhibition of PhIP-DNA adduct formation, acceleration of PhIP metabolism, and induc- tion of cytochrome P450 in female F344 rats. Food Chem Toxicol. 2000 Jan;38(1):15-23.

38. Arif J, Gairola C, Kelloff G, Lubet R, Gupta RC. Inhibition of cigarette smoke-related DNA adducts in rat tissues by indole-3- carbinol. Mutat Res. 2000 Jul 20;452(1):11-8.

39. Bell M, Crowley-Nowick P, Bradlow H, et al. Placebo-controlled trial of indole-3-carbinol in the treatment of CIN. Gynecol Oncol. 2000 Aug;78(2):123-9.

40. Tiwari R, Guo L, Bradlow H, Telang N, Osborne MP. Selective responsiveness of human breast cancer cells to indole-3- carbinol, a chemopreventive agent. J Natl Cancer Inst. 1994 Jan 19;86(2):126-31.

41. Grubbs C, Steele V, Casebolt T, et al. Chemoprevention of chemically-induced mammary carcinogenesis by indole-3- carbinol. Anticancer Res. 1995 May- Jun;15(3):709-16.

42. Jin L, Qi M, Chen D, et al. Indole-3-carbinol prevents cervical cancer in human papilloma virus type 16 (HPV16) transgenic mice. Cancer Res. 1999 Aug 15;59(16):3991-7.

43. Rahman K, Aranha O, Glazyrin A, Chinni S, Sarkar F. Translocation of Bax to mitochondria induces apoptotic cell death in indole-3- carbinol (I3C) treated breast cancer cells. Oncogene. 2000 Nov 23;19(50):5764-71.

44. Meng Q, Qi M, Chen D, et al. Suppression of breast cancer invasion and migration by indole-3-carbinol: associated with up-regulation of BRCA1 and E-cadherin/catenin complexes. J Mol Med. 2000 78(3):155-65.

45. Cover C, Hsieh S, Cram E et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res. 1999 Mar 15;59(6):1244- 51.

46. Cover C, Hsieh S, Tran S,Hallden G, Kim GS, Bjeldanesl JF, Firestonr GL. Indole-3- carbinol inhibits the expression of cyclin- dependent kinase-6 and induces a G1 cell cycle arrest of human breast cancer cells independent of estrogen receptor signaling. J Biol Chem. 1998 Feb 13;273(7):3838-47.

47. Manson M, Hudson E, Ball H et al. Chemoprevention of aflatoxin B1-induced carcinogenesis by indole-3-carbinol in rat liver-predicting the outcome using early bio- markers. Carcinogenesis. 1998 Oct;19(10):1829-36.

48. Bradlow H, Michnovicz J, Telang N, Osborne M. Effects of dietary indole-3- carbinol on estradiol metabolism and spontaneous mammary tumors in mice. Carcinogenesis. 1991 Sep;12(9):1571-4.

49. Michnovicz J, Bradlow H. Altered estrogen metabolism and excretion in humans follow- ing consumption of indole-3-carbinol. Nutr Cancer. 1991 16(1):59-66.

50. Shertzer H, Berger M, Tabor M. Intervention in free radical mediated hepa- totoxicity and lipid peroxidation by indole-3- carbinol. Biochem Pharmacol. 1988 Jan 15;37(2):333-8.

51. Asou H, Koshizuka K, Kyo T, Takata N, Kamada N, Koeffier HP. Resveratrol, a natural product derived from grapes, is a new inducer of differentiation in human myeloid leukemias. Int J Hematol. 2002 Jun;75(5):528-33.

52. Bernhard D, Tinhofer I, Tonko M et al. Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells. Cell Death Differ. 2000 Sep;7(9):834-42.

53. Clement M, Hirpara J, Chawdhury S, Pervaiz S. Chemopreventive agent resvera- trol, a natural product derived from grapes, triggers CD95 signaling-dependent apopto- sis in human tumor cells. Blood. 1998 Aug 1;92(3):996-1002.

54. Jang M, Pezzuto J. Cancer chemopreventive activity of resveratrol. Drugs Exp Clin Res. 1999;25(2-3):65-77.

55. Kang J, Park Y, Choi S, Yang EK, Lee WJ. Resveratrol derivatives potently induce apoptosis in human promyelocytic leukemia cells. Exp Mol Med. 2003 Dec 31;35(6):467- 74.

56. Kimura Y, Okuda H. Resveratrol isolated from Polygonum cuspidatum root prevents tumor growth and metastasis to lung and tumor-induced neovascularization in Lewis lung carcinoma-bearing mice. J Nutr. 2001 Jun;131(6):1844-9.

57. Kozuki Y, Miura Y, Yagasaki K. Resveratrol suppresses hepatoma cell invasion inde- pendently of its anti-proliferative action. Cancer Lett. 2001 Jun 26;167(2):151-6.

58. Nakagawa H, Kiyozuka Y, Uemura Y, et al. Resveratrol inhibits human breast cancer cell growth and may mitigate the effect of linoleic acid, a potent breast cancer cell stimulator. J Cancer Res Clin Oncol. 2001 Apr;127(4):258-64.

59. Szende B, Tyihak E, Kiraly-Veghely Z. Dose- dependent effect of resveratrol on proliferation and apoptosis in endothelial and tumor cell cultures. Exp Mol Med. 2000 Jun 30;32(2):88-92.

60. Tessitore L, Davit A, Sarotto I, Caderni G. Resveratrol depresses the growth of colorectal aberrant crypt foci by affecting bax and p21(CIP) expression. Carcinogenesis. 2000 Aug;21(8):1619-22.

61. Tsan M, White J, Maheshwari J, Chikkappa G. Anti-leukemia effect of resveratrol. Leuk Lymphoma. 2002 May;43(5):983-7.

62. Jiang Q, Christen S, Shigenaga M, Ames B. Gamma tocopherol, the major form of vitamin E in the US diet, deserves more attention. Am J Clin Nutr. 2001 Dec;74(6):714-22.

63. Helzlsouer K, Huang H, Alberg A, et al. Association between alpha tocopherol, gamma tocopherol, selenium and subsequent prostate cancer. J Natl Cancer Inst. 2000 Dec 20;92(24):2018-23.

64. London S, Stein E, Henderson I, et al. Carotenoids, retinol and vitamin E and risk of proliferation benign breast disease and breast cancer. Cancer Causes Control. 1992 Nov;3(6):503-12.

65. Nomura A, Ziegler R, Stemmermann G, Chyou P, Craft N. Serum micronutrients and upper aerodigestive tract cancers. Cancer Epidemiol Biomarkers Prev. 1997 Jun;6(6):407-12.

66. Smigel K. Vitamin E reduces prostate cancer rates in Finnish trial: U.S. considers follow- up. J Natl Cancer Inst. 1998 Mar 18;90(6):416-7.

67. Christen S, Woodall A, Shigenaga M, Southwell-Keely P, Duncan M, Ames B. Gamma-tocopherol traps mutagenic electrophiles such as NO(X) and complements alpha-tocopherol: physiological implica- tions. Proc Natl Acad Sci USA. 1997 Apr 1;94(7):3217-22.

68. Blask D, Sauer L, Dauchy R. Melatonin as a chronobiotic/anticancer agent: cellular, bio-chemical, and molecular mechanisms of action and their implications for circadian-based cancer therapy. Curr Top Med Chem. 2002 Feb;2(2):113-32.

69. Brzezinski A. Melatonin in humans. N Engl J Med. 1997 Jan 16;336(3):186-95.

70. Cos S, Fernandez R, Guezmes A, Sanchez- Barcelo EJ. Influence of melatonin on invasive and metastatic properties of MCF-7 human breast cancer cells. Cancer Res. 1998 Oct 1;58(19):4383-90.

71. Lissoni P, Barni S, Ardizzoia A, Tancini G, Conti A, Maestroni G. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer. 1994 Feb 1;73(3):699-701.

72. Lissoni P, Brivio F, Brivio O, et al. Immune effects of preoperative immunotherapy with high-dose subcutaneous interleukin-2 versus neuroimmunotherapy with low-dose interleukin-2 plus the neurohormone melatonin in gastrointestinal tract tumor patients. J Biol Regul Homeost Agents. 1995 Jan;9(1):31-3.

73. Oosthuizen J, Bornman M, Barnard H, Schulenburg GW, Boomker D, Reif S. Melatonin and steroid-dependent carcinomas. Andrologia. 1989 Sep;21(5):429-31.

74. Ram P, Yuan L, Dai J, et al. Differential responsiveness of MCF-7 human breast cancer cell line stocks to the pineal hormone, melatonin. J Pineal Res. 2000 May;28(4):210- 8.

75. Sanchez-Barcelo E, Cos S, Fernandez R, Mediavilla MD. Melatonin and mammary cancer: a short review. Endocr Relat Cancer. 2003 Jun;10(2):153-9.

76. Suzuki K, Koike H, Matsui H, et al. Genistein, a soy isoflavone, induces glutathione peroxidase in the human prostate cancer cell lines LNCaP and PC-3. Int J Cancer. 2002 Jun 20;99(6):846-52.

77. Bhatia N, Agarwal R. Detrimental effect of cancer preventive phytochemicals silymarin, genistein and epigallocatechin 3-gallate on epigenetic events in human prostate carcinoma DU145 cells. Prostate. 2001 Feb 1;46(2):98-107.

78. Dalu A, Haskell J, Coward L, Lamartiniere CA. Genistein, a component of soy, inhibits the expression of the EGF and ErbB2/Neu receptors in the rat dorsolateral prostate. Prostate. 1998 Sep 15;37(1):36-43.

79. Elattar T, Virji A. The inhibitory effect of curcumin, genistein, quercetin and cisplatin on the growth of oral cancer cells in vitro. Anticancer Res. 2000 May;20(3A):1733-8.

80. Geller J, Sionit L, Partido C, et al. Genistein inhibits the growth of human-patient BPH and prostate cancer in histoculture. Prostate. 1998 Feb 1;34(2):75-9.

81. Khoshyomn S, Nathan D, Manske GC, Osler TM, Penar PL. Synergistic effect of genistein and BCNU on growth inhibition and cyto-toxicity of glioblastoma cells. J Neurooncol. 2002 May;57(3):193-200.

82. Li Y, Sarkar F. Down-regulation of invasion and angiogenesis-related genes identified by cDNA microarray analysis of PC3 prostate cancer cells treated with genistein. Cancer Lett. 2002 Dec 5;186(2):157-64.

83. Lian F, Li Y, Bhuiyan M, Sarkar FH. p53- independent apoptosis induced by genistein in lung cancer cells. Nutr Cancer. 1999;33(2):125-31.

84. Record I, Broadbent J, King R, Dreosti IE, Head RJ, Tonkin AL. Genistein inhibits growth of B16 melanoma cells in vivo and in vitro and promotes differentiation in vitro. Int J Cancer. 1997 Sep 4;72(5):860-4.

85. Sakamoto K. Synergistic effects of thearubigin and genistein on human prostate tumor cell (PC-3) growth via cell cycle arrest. Cancer Lett. 2000 Apr 3;151(1):103-9.

86. Shao Z, Wu J, Shen Z, Barsky SH. Genistein exerts multiple suppressive effects on human breast carcinoma cells. Cancer Res. 1998 Nov 1;58(21):4851-7.

87. Shen J, Klein R, Wei Q, et al. Low-dose genistein induces cyclin-dependent kinase inhibitors and G(1) cell-cycle arrest in human prostate cancer cells. Mol Carcinog. 2000 Oct;29(2):92-102.

88. Suthar A, Banavalikar M, Biyani M. Pharmacological activities of Genistein, an isoflavone from soy (Glycine max): part I— anti-cancer activity. Indian J Exp Biol. 2001 Jun;39(6):511-9.

89. Theodorescu D, Laderoute K, Calaoagan J, Guilding KM. Inhibition of human bladder cancer cell motility by genistein is dependent on epidermal growth factor receptor but not p21ras gene expression. Int J Cancer. 1998 Dec 9;78(6):775-82.

90. Versantvoort C, Broxterman H, Lankelma J, Feller N, Pinedo HM. Competitive inhibi- tion by genistein and ATP dependence of daunorubicin transport in intact MRP over expressing human small cell lung cancer cells. Biochem Pharmacol. 1994 Sep 15;48(6):1129-36.

91. Wietrzyk J, Boratynski J, Grynkiewicz G, Ryczynski A, Radzikowski C, Opolski A. Antiangiogenic and antitumour effects in vivo of genistein applied alone or combined with cyclophosphamide. Anticancer Res. 2001 Nov;21(6A):3893-6.

92. Jung YD, Kim MS, Shin BA, et al. EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells. Br J Cancer. 2001 Mar 23;84(6):844-50.

93. Jung YD, Ellis LM. Inhibition of tumour invasion and angiogenesis by epigallocate- chin gallate (EGCG), a major component of green tea. Int J Exp Pathol. 2001 Dec;82(6):309-16.

94. Sartippour MR, Heber D, Zhang L, et al. Inhibition of fibroblast growth factors by green tea. Int J Oncol. 2002 Sep;21(3):487- 91.

95. Sartippour MR, Shao ZM, Heber D, et al. Green tea inhibits vascular endothelial growth factor (VEGF) induction in human breast cancer cells. J Nutr. 2002 Aug;132(8):2307-11.

96. Embola CW, Sohn OS, Fiala ES, Weisburger JH. Induction of UDP-glucuronosyltrans- ferase 1 (UDP-GT1) gene complex by green tea in male F344 rats. Food Chem Toxicol. 2002 Jun;40(6):841-4.

97. Pianetti S, Guo S, Kavanagh KT, Sonenshein GE. Green tea polyphenol epigallocatechin- 3 gallate inhibits Her-2/neu signaling, prolif- eration, and transformed phenotype of breast cancer cells. Cancer Res. 2002 Feb 1;62(3):652-5.

98. Kelsey JL, Whittemore AS. Epidemiology and primary prevention of cancers of the breast, endometrium, and ovary: a brief overview. Ann Epidemiol. 1994 Mar;4(2):89- 95.

99. Colditz GA. Hormones and breast cancer: evidence and implications for consideration of risks and benefits of hormone replacement therapy. J Womens Health. 1999 Apr;8(3):347.57.

100. Marchant DJ. Epidemiology of breast cancer. Clin Obstet Gynecol. 1982 Jun;25(2):387- 92.

101. Endogenous Hormones and Breast Cancer Collaborative Group. Endogenous sex hor- mones and breast cancer in postmenopausal women: reanalysis of nine prospective studies. J Natl Cancer Inst. 2002 Apr 17; 94(8):606-16.

102. Kabuto M, Akiba S, Stevens RG, Neriishi K, Land CE. A prospective study of estradiol and breast cancer in Japanese women. Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):575-9.

103. Zeleniuch-Jacquotte A, Akhmedkhanov A, Kato I, et al. Postmenopausal endogenous oestrogens and risk of endometrial cancer: results of a prospective study. Br J Cancer. 2001 Apr 6;84(7):975-81.

104. Skouby SO. The rationale for a wider range of progestogens. Climacteric. 2000 Dec;3 Suppl 2:14-20.

105. Malet C, Gompel A, Spritzer P, et al. Tamoxifen and hydroxytamoxifen isomers versus estradiol effects on normal human breast cells in culture. Cancer Res. 1988 Dec 15;48(24 Pt 1):7193-9.

106. Haber D. Roads leading to breast cancer. N Engl J Med. 2000 Nov 23;343(21):1566-8.

107. Strauss B, Turkington E, Wang J, Sagher D. Mutagenic consequences of the alteration of DNA by chemicals and radiation. Adv Exp Med Biol. 1991;283:211-23.

108. Apter D, Vihko R. Early menarche, a risk factor for breast cancer, indicates early onset of ovulatory cycles. J Clin Endocrinol Metab. 1983 Jul;57(1):82-6.

109. Brinton LA, Schairer C, Hoover RN, Fraumeni JF. Menstrual factors and risk of breast cancer. Cancer Invest. 1988;6(3): 245- 54.

110. Colditz GA, Rosner BA, Speizer FE. Risk factors for breast cancer according to family history of breast cancer. For the Nurses’ Health Study Research Group. J Natl Cancer Inst. 1996 Mar 20;88(6): 365-71.

111. Kelsey J, Gammon M, John E. Reproductive factors and breast cancer Epidemiol Rev. 1993 15(1):36-47.

112. Bernstein L, Pike M, Ross R, Henderson B. Age at menarche and estrogen concentrations of adult women. Cancer Causes Control. 1991 Jul;2(4):221-5.

113. Potten C, Watson R, Williams G, et al. The effect of age and menstrual cycle upon pro-liferative activity of the normal human breast. Br J Cancer. 1988 Aug;58(2):163-70.

114. Melbye M, Wohlfahrt J, Andersen A, Westergaard T, Andersen P. Preterm delivery and risk of breast cancer. Br J Cancer. 1999 May;80(3-4):609-13.

115. Trichopoulos D, MacMahon B, Cole P. Menopause and breast cancer risk. J Natl Cancer Inst. 1972 Mar;48(3):605-13.

116. Brinton L, Hoover RN, Szklo M, Fraumeni JF. Menopausal estrogen use and risk of breast cancer. Cancer. 1981 May 15; 47(10):2517-22.

117. Paffenbarger R Jr, Kampert J, Chang H. Characteristics that predict risk of breast cancer before and after the menopause. Am J Epidemiol. 1980 Aug;112(2):258-68.

118. Hsieh C, Trichopoulos D, Katsouyanni K, Yuasa S. Age at menarche, age at menopause, height and obesity as risk fac- tors for breast cancer; associations and inter- actions in an international case-control study. Int J Cancer. 1990 Nov 15;46(5):796-800.

119. Rozario D, Brown I, Fung MF, Temple L. Is incidental prophylactic oophorectomy an acceptable means to reduce the incidence of ovarian cancer? Am J Surg. 1997 Jun;173(6):495-8.

120. Olopade OI, Artioli G. Efficacy of risk- reducing salpingo-oophorectomy in women with BRCA-1 and BRCA-2 mutations. Breast J. 2004 Jan-Feb;10 Suppl 1:S5-9.

121. Rebbeck TR, Lynch HT, Neuhausen SL, et al. Prophylactic oophorectomy in carriers of BRCA1 or BRCA2 Mutations. N Engl J Med. 2002 May 23;346(21):1616-22.

122. Kauff ND, Satagopan JM, Robson ME, et al. Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation. N Engl J Med. 2002 May 23;346(21):1609-15.

123. Biglia N, Defabiani E, Ponzone R, Mariani L, Marenco D, Sismondi P. Management of risk of breast carcinoma in postmenopausal women. Endocr Relat Cancer. 2004 Mar;11(1):69-83.

124. Zhang Y, Kiel D, Kreger B, et al. Bone mass and the risk of breast cancer among post- menopausal women. N Engl J Med. 1997 Feb 27;336(9):611-7.

125. Newcomb P, Trentham-Dietz A, Egan C, et al. Fracture history and risk of breast and endometrial cancer. Am J Epidemiol. 2001 Jun 1;153(11):1071-8.

126. Cummings S, Eckert S, Krueger K, et al. The effect of raloxifene on risk of breast cancer in postmenopausal women. JAMA. 1999 Jun 16;281(23):2189-97.

127. Lippman ME, Krueger KA, Eckert S, et al. Indicators of lifetime estrogen exposure: effect on breast cancer incidence and inter- action with raloxifene therapy in the multi- ple outcomes of raloxifene evaluation study participants. J Clin Oncol. 2001 Jun 15;19(12): 3111-6.

128. Zmuda J, Cauley J, Ljung B, Bauer D, Cummings S, Kuller L. Bone mass and breast cancer risk in older women: differ- ences by stage at diagnosis. Study of Osteoporotic Fractures Research Group. J Natl Cancer Inst. 2001 Jun 20;93(12):930-6.

129. Michels K, Ekbom A. Caloric restriction and incidence of breast cancer. JAMA. 2004 Mar 10;291(10):1226-30.

130. Fiets W, van Helvoirt R, Nortier J, van der Tweel I, Struikmans H. Acute toxicity of con- current adjuvant radiotherapy and chemotherapy (CMF or AC) in breast can- cer patients. a prospective, comparative, non-randomised study. Eur J Cancer. 2003 May;39(8):1081-8.

131. Harvie M, Hooper L, Howell A. Central obesity and breast cancer risk: a systematic review. Obes Rev. 2003 Aug;4(3):157-73.

132. Ziegler R, Hoover R, Nomura A, et al. Relative weight, weight change, height, and breast cancer risk in Asian-American women. J Natl Cancer Inst. 1996 May 15;88(10):650-60.

133. Morimoto LM, White E, Chen Z, et al. Obesity, body size, and risk of post- menopausal breast cancer: the Women’s Health Initiative (United States). Cancer Causes Control. 2002 Oct;13(8):741-51. 

134. Hamajima N, Hirose K, Tajima K, et al. Alcohol, tobacco and breast cancer—collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease. Br J Cancer. 2002 Nov 18;8(11):1234-45. 

135. Prentice R, Thompson D, Clifford C, Gorbach S, Goldin B, Byar D. Dietary fat reduction and plasma estradiol concentra- tion in healthy postmenopausal women. The Women’s Health Trial Study Group. J Natl Cancer Inst. 1990 Jan 17;82(2):129-34. 

136. Holmes M, Hunter D, Colditz G, et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA. 1999 Mar 10;281(10):914-20.

137. Dorgan J, Reichman M, Judd J, et al. The relation of body size to plasma levels of estrogens and androgens in premenopausal women (Maryland, United States). Cancer Causes Control. 1995 Jan;6(1):3-8.

138. Lahmann P, Hoffmann K, Allen N, et al. Body size and breast cancer risk: Findings from the European prospective investigation into cancer and nutrition (EPIC). Int J Cancer. 2004 Sep 20;111(5):762–71.

139. Henderson BE, Pike MC, Ross RK, et al. Epidemiology and risk factors. In: Bonadonna G, ed. Breast Cancer: Diagnosis and Management. Chichester, NY: John Wiley & Sons; 1984:15-33. 

140. Ekbom A, Hsieh CC, Lipworth L, Adami HQ, Trichopoulos D. Intrauterine environ- ment and breast cancer risk in women: A population-based study. J Natl Cancer Inst. 1997 Jan 1;89(1):71-6.

141. Fackelmann, K. Breast cancer risk traced back to the womb. Sci News. 1992 142(Oct. 31):293.

142. Newcomb P, Storer B, Longnecker M, et al. Lactation and a reduced risk of pre-menopausal breast cancer. N Engl J Med. 1994 Jan 13;330(2):81-7.

143. Romieu I, Hernandez-Avila M, Lazcano E, Lopez L, Romero-Jaime R. Breast cancer and lactation history in Mexican women. Am J Epidemiol. 1996 Mar 15;143(6):543-52.

144. Furberg H, Newman B, Moorman P, Millikan R. Lactation and breast cancer risk. Int J Epidemiol. 1999 Jun;28(3):396-402. 

145. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and breast feeding: 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(9328):187-95. 

146. Smith-Warner S, Spiegelman D, Yaun S, et al. Alcohol and breast cancer in women. JAMA. 1998 Feb 18;279(7):535-40.

147. Garfinkel L, Boffetta P, Stellman S. Alcohol and breast cancer: a cohort study. Prev Med. 1988 Nov;17(6):686-93.

148. Longnecker M, Newcomb P, Mittendorf R, et al. Risk of breast cancer in relation to life- time alcohol consumption. J Natl Cancer Inst. 1995 Jun 21;87(12):923-9.

149. Rockhill B, Willett W, Hunter D, Manson J, Hankinson S, Colditz G. A prospective study of recreational physical activity and breast cancer risk. Arch Intern Med. 1999 Oct 25;159(19):2290-96.

150. Thune I, Brenn T, Lund E, Gaard M. Physical activity and the risk of breast cancer. N Engl J Med. 1997 May 1;336(18):1269- 75.

151. Bernstein L, Henderson B, Hanisch R, Sullivan-Halley J, Ross R. Physical exercise and reduced risk of breast cancer in young women. J Natl Cancer Inst. 1994 Sep 21;86(18):1403-8.

152. Matthews C, Shu X, Jin F, et al. Lifetime physical activity and breast cancer risk in the Shanghai Breast Cancer Study. Br J Cancer. 2001 Apr 6;84(7):994-1001.

153. McTiernan A, Kooperberg C, White E, et al. Recreational physical activity and the risk of breast cancer in postmenopausal women: the Women’s Health Initiative Cohort Study. JAMA. 2003 Sep 10;290(10):1331-6.

154. Bernstein L, Ross RK, Lobo RA, Hanisch R, Krailo MD, Henderson BE. The effects of moderate physical activity on menstrual cycle patterns in adolescence: implications for breast cancer prevention. Br J Cancer. 1987 Jun;55(6):681-5. 

155. Friedenreich CM. Physical activity and cancer prevention: from observational to inter- vention research. Cancer Epidemiol Biomarkers Prev. 2001 Apr;10(4):287-301.

156. Adams-Campbell LL, Rosenberg L, Rao RS, Palmer JR. Strenuous physical activity and breast cancer risk in African-American women. J Natl Med Assoc. 2001 Jul-Aug; 93(7-8): 267-75.

157. Paganini-Hill A. Estrogen replacement ther- apy in the elderly. Zentralbl Gynakol. 1996 118(5):255-61.

158. Birkhauser MH. Indications for hormone replacement therapy. Ther Umsch. 2000 Oct;57(10):635-42.

159. Available at: Accessed July 2004.

160.Available at: Accessed July 2004.

161.Available at: Accessed July 2004.

162.Available at: Accessed July 2004.

163. Available at: Accessed July 2004.

164. Available at: Accessed July 2004.

165. Available at: Accessed July 2004.

166. Available at: Accessed July 2004.

167. Available at: Accessed July 2004.

168. Available at: Accessed July 2004.

169. Available at: Accessed July 2004.

170. Available at: Accessed July 2004.

171. Available at: Accessed July 2004.

172. Available at: Accessed July 2004.

173. Available at: Accessed July 2004.

174. Suzuki K, Takezawa Y, Suzuki T, Honma S, Yamanaka H. Synergistic effects of estrogen with androgen on the prostate effects of estrogen on the prostate of androgen-administered rats and 5-alpha-reductase activity. Prostate. 1994 Oct;25(4);169-76.

175. Steiner MS, Raghow S. Antiestrogens and selective estrogen receptor modulators reduce prostate cancer risk. World J Urol. 2003 May;21(1):31-6.

176. Hill P, Wynder E, Garbaczewski L, Walker A. Effect of diet on plasma and urinary hormones in South African black men with prostate cancer. Cancer Res. 1982 Sep; 42(9):3864-9.

177. Seidman S, Walsh B. Testosterone and depression in aging men. Am J Geriatr Psychiatry. 1999 Winter;7(1):18-33.

178. Barrett-Connor E, Von Muhlen D, Kritz- Silverstein D. Bioavailable testosterone and depressed mood in older men: the Rancho Bernardo Study. J Clin Endocrinol Metab. 1999 Feb;84(2):573-7.

179. Schweiger U, Deuschle M, Weber B, et al. Testosterone, gonadotropin, and cortisol secretion in male patients with major depression. Psychosom Med. 1999 May- Jun;61(3):292-6.

180. Lubeck DP, Grossfeld GD, Carroll PR. The effect of androgen deprivation therapy on health-related quality of life in men with prostate cancer. Urology. 2001 Aug;58(2 Suppl 1):94-100.

181. Green HJ, Pakenham

Subscribe to Life Extension Magazine®

Subscribe Now

Advertise in Life Extension Magazine®

Learn More