How long should a patient take tamoxifen for the treatment of breast cancer?
Patients with advanced breast cancer may take tamoxifen for varying lengths of time, depending on their response to this treatment and other factors. When used as adjuvant therapy for early stage breast cancer, tamoxifen is generally prescribed for 5 years. However, the ideal length of treatment with tamoxifen is not known.
How Often Should I Take Tamoxifen?
Two studies have confirmed the benefit of taking adjuvant tamoxifen daily for 5 years. These studies compared 5 years of treatment with tamoxifen with 10 years of treatment. When taken for 5 years, the drug reduces the risk of recurrence of the original breast cancer and also reduces the risk of developing a second primary cancer in the other breast. Taking tamoxifen for longer than 5 years is not more effective than 5 years of therapy.
What is Tamoxifen
Tamoxifen is an oral selective estrogen receptor modulator which is used in breast cancer treatment, and is currently the world's largest selling breast cancer treatment. It is used for the treatment of early and advanced breast cancer in pre- and post-menopausal women. It is also approved by the FDA for the reduction of the incidence of breast cancer in women at high risk of developing the disease. It has been further approved for the reduction of contralateral (in the opposite breast) breast cancer.
Tamoxifen and Cancer
Tamoxifen is used to reduce the risk of breast cancer for women who:
1. are at high risk of breast cancer but have no personal history of the disease
2. have non-invasive, hormone-receptor-positive breast cancer, or DCIS (ductal carcinoma in situ)
3. have hormone-receptor-positive invasive breast cancer at any stage.
Tamoxifen is sometimes used to treat gynecomastia in men. Tamoxifen is also used by bodybuilders in a steroid cycle to try and prevent or reduce drug-induced gynecomastia caused by steroids that are used in the same cycle.
Tamoxifen is also used to treat infertility in women with anovulatory disorders. A dose of 10-40 mg per day is administered in days 3-7 of a woman's cycle.
Tuesday, May 25, 2010
Tuesday, May 18, 2010
How To Reduce Breast Cancer By 45 Percent?
A US study of 13,000 patients showed Tamoxifen reduced the rate of expected cancers from one in 130 to one in 236 - a cut of about 45%. The American researchers ended their trial early when they said the drug's benefits became overwhelmingly obvious.
Other studies found that tamoxifen AND chemotherapy improved survival improved survival rates by about 40–50% compared to taking one treatment or the other.
Should women taking tamoxifen avoid pregnancy?
Yes. Tamoxifen may make premenopausal women more fertile, but doctors advise women on tamoxifen to avoid pregnancy because animal studies have suggested that the use of tamoxifen in pregnancy can cause fetal harm. Women who have questions about fertility, birth control, or pregnancy should discuss their concerns with their doctor.
Does tamoxifen cause a woman to begin menopause?
Tamoxifen does not cause a woman to begin menopause, although it can cause some symptoms that are similar to those that may occur during menopause. In most premenopausal women taking tamoxifen, the ovaries continue to act normally and produce estrogen in the same or slightly increased amounts.
Do the benefits of tamoxifen in treating breast cancer outweigh its risks?
The benefits of tamoxifen as a treatment for breast cancer are firmly established and far outweigh the potential risks. Patients who are concerned about the risks and benefits of tamoxifen or any other medications are encouraged to discuss these concerns with their doctor.
Tamoxifen ( ta-MOX-i-fen) is a medicine that blocks the effects of the estrogen hormone in the body. It is used to treat breast cancer in women or men. It may also be used to treat other kinds of cancer, as determined by your doctor.
Tamoxifen also may be used to reduce the risk of developing breast cancer in women who have a high risk of developing breast cancer. Women at high risk for developing breast cancer are at least 35 years of age and have a combination of risk factors that make their chance of developing breast cancer 1.67% or more over the next 5 years. Your doctor will help to determine your risk of developing breast cancer.
Other studies found that tamoxifen AND chemotherapy improved survival improved survival rates by about 40–50% compared to taking one treatment or the other.
Should women taking tamoxifen avoid pregnancy?
Yes. Tamoxifen may make premenopausal women more fertile, but doctors advise women on tamoxifen to avoid pregnancy because animal studies have suggested that the use of tamoxifen in pregnancy can cause fetal harm. Women who have questions about fertility, birth control, or pregnancy should discuss their concerns with their doctor.
Does tamoxifen cause a woman to begin menopause?
Tamoxifen does not cause a woman to begin menopause, although it can cause some symptoms that are similar to those that may occur during menopause. In most premenopausal women taking tamoxifen, the ovaries continue to act normally and produce estrogen in the same or slightly increased amounts.
Do the benefits of tamoxifen in treating breast cancer outweigh its risks?
The benefits of tamoxifen as a treatment for breast cancer are firmly established and far outweigh the potential risks. Patients who are concerned about the risks and benefits of tamoxifen or any other medications are encouraged to discuss these concerns with their doctor.
Tamoxifen ( ta-MOX-i-fen) is a medicine that blocks the effects of the estrogen hormone in the body. It is used to treat breast cancer in women or men. It may also be used to treat other kinds of cancer, as determined by your doctor.
Tamoxifen also may be used to reduce the risk of developing breast cancer in women who have a high risk of developing breast cancer. Women at high risk for developing breast cancer are at least 35 years of age and have a combination of risk factors that make their chance of developing breast cancer 1.67% or more over the next 5 years. Your doctor will help to determine your risk of developing breast cancer.
Saturday, May 15, 2010
Battling Breast Cancer Starts With Recognizing It First.
Image by Getty Images via DaylifeBreast cancer has been diagnosed in large numbers in North America and Europe. In 2001, about 200,000 cases of breast cancer were diagnosed in the United States alone. Every woman has a 1 in 8 risk of developing breast cancer, but the risk of dying from breast cancer is much lower, barely 1 in 28.
The risk of getting breast cancer is generally higher among older women, women with a family history or previous history of breast cancer, women who had radiation therapy in the chest region, women who started their periods before 12 years old, women who had menopause after 50 years old, women who never had children or had them age 30 or older, or women with genetic mutation. In recent times genetic mutations for breast cancer have become a hot topic of research.
The breast cancer tumor has the following symptoms: lump or thickening that appears on the breast or underarm, changes in the breast's shape, nipple turned inwards followed by colorless discharge, red or scaled skin or nipple, or ridges on the breast skin.
If a woman experiences any of these symptoms, it does not necessarily mean she has breast cancer. In such a case she should undergo a breast cancer personal check-up. It is estimated that 95% of breast cancer is detected through personal check-up. The breast cancer personal check-up includes checking for lumps in the breasts after each menstrual period, puckering the skin, and checking for nipple retraction or discharge. For consistent result, every woman should do a breast cancer personal check-up at the same time every month. Various other techniques such as mammography, thermography, ultrasonography, computerized tomography scan etc, can also help detect breast cancer.
Breast cancer treatments include surgery that removes cancerous tissues, with breast conservation therapy (BCT) being one such surgery. Other breast cancer treatments include chemotherapy, radiotherapy, hormonal therapy and biologic therapy. Radiotherapy is a common breast cancer treatment, and radiation treatment and chemotherapy may follow surgery to ensure the destruction of the stray cancer cells.
Even after undergoing many or all of these breast cancer treatment measures, unfortunately almost half the women suffer from a recurrence of the disease.
![Reblog this post [with Zemanta]](http://img.zemanta.com/reblog_e.png?x-id=7b3dd6b7-dbdf-4b82-be2a-f430baba3921)
Monday, May 10, 2010
New Test For Breast Cancer Promises Individualized Treatment A Reality
Widely hailed as the next frontier in medical advances, the promise of individualized medicine is becoming a reality thanks to progress in understanding the molecular basis of diseases such as breast cancer. Scientists can now develop treatments that are tailored to individual genetic profiles, as well as tests to predict how a patient will respond to existing therapies.
Today, some women with early-stage breast cancer and their physicians can make more informed treatment decisions with the Oncotype DX Breast Cancer Assay. This service provides quantitative information about genes from a woman's individual tumor to generate a Recurrence Score between zero and 100, indicating whether she is at high, intermediate or low risk for her cancer returning after treatment.
Oncotype DX is intended for patients with node-negative, estrogen receptor-positive breast cancer who are likely to be treated with hormonal therapy. Approximately half of the 230,000 patients diagnosed with breast cancer in the United States each year fall into this category, and are frequently offered treatment with chemotherapy, a widely used treatment with considerable side effects. Clinical studies show that chemotherapy improved patient survival rates in only 4 out of 100 patients, yet thousands of women continue to elect this costly and toxic treatment with only limited information about whether they might respond to it.
A recent study demonstrated that women with high Recurrence Scores are more likely to benefit from chemotherapy, whereas women with lower scores derive only minimal benefit. Further, only 25% of women fell into the high-risk group, compared to 50% in the low-risk group, indicating that this common treatment is not appropriate for every patient.
Elizabeth Sloan of New York City is one of the many breast cancer patients not likely to respond to chemotherapy. An active mother with two young boys, Elizabeth was considering having another child when she was diagnosed at just 40 years old. She wanted to avoid chemotherapy, with its disruptive, short-term side effects and potentially serious long-term implications, but also wanted to be absolutely certain that it wouldn't help her.
Working with her doctor, Ruth Oratz, M.D., at NYU Medical Center, Elizabeth decided to have the Oncotype DX assay, and was delighted when her Recurrence Score turned out to be low-indicating that she may not benefit significantly from chemotherapy.
"No two women with breast cancer are exactly alike. Oncotype DX provides information that goes beyond standard measures, like age, tumor size and tumor grade, in determining the likelihood of disease recurrence," says Dr. Oratz. "Oncotype DX gave Elizabeth and me added confidence and peace of mind in selecting the most fitting treatment for her."
For Susan Bakken of Denver, Colorado, Oncotype DX provided a different kind of peace of mind. Susan's Recurrence Score indicated that she was at high risk of cancer recurrence, and would likely benefit significantly from chemotherapy-to both her surprise and her doctor's.
"Based on the other tests I had, my doctor said he wouldn't have otherwise recommended chemotherapy. I was shocked to find out my result, but I was so glad I did because I believe this test basically saved my life," explained Susan.
Elizabeth Sloan is also grateful for the information she gained from Oncotype DX. "Not all cancers are the same, so why treat everyone the same way with something so toxic?" she said. "It's so remarkable that finally, doctors can distinguish one person's cancer from another-I'm just so thankful."
Oncotype DX is a simple test that can only be ordered by a physician. It is performed on a small amount of breast tumor tissue removed during a standard lumpectomy, mastectomy or biopsy, meaning no additional procedure is required.
Today, some women with early-stage breast cancer and their physicians can make more informed treatment decisions with the Oncotype DX Breast Cancer Assay. This service provides quantitative information about genes from a woman's individual tumor to generate a Recurrence Score between zero and 100, indicating whether she is at high, intermediate or low risk for her cancer returning after treatment.
Oncotype DX is intended for patients with node-negative, estrogen receptor-positive breast cancer who are likely to be treated with hormonal therapy. Approximately half of the 230,000 patients diagnosed with breast cancer in the United States each year fall into this category, and are frequently offered treatment with chemotherapy, a widely used treatment with considerable side effects. Clinical studies show that chemotherapy improved patient survival rates in only 4 out of 100 patients, yet thousands of women continue to elect this costly and toxic treatment with only limited information about whether they might respond to it.
A recent study demonstrated that women with high Recurrence Scores are more likely to benefit from chemotherapy, whereas women with lower scores derive only minimal benefit. Further, only 25% of women fell into the high-risk group, compared to 50% in the low-risk group, indicating that this common treatment is not appropriate for every patient.
Elizabeth Sloan of New York City is one of the many breast cancer patients not likely to respond to chemotherapy. An active mother with two young boys, Elizabeth was considering having another child when she was diagnosed at just 40 years old. She wanted to avoid chemotherapy, with its disruptive, short-term side effects and potentially serious long-term implications, but also wanted to be absolutely certain that it wouldn't help her.
Working with her doctor, Ruth Oratz, M.D., at NYU Medical Center, Elizabeth decided to have the Oncotype DX assay, and was delighted when her Recurrence Score turned out to be low-indicating that she may not benefit significantly from chemotherapy.
"No two women with breast cancer are exactly alike. Oncotype DX provides information that goes beyond standard measures, like age, tumor size and tumor grade, in determining the likelihood of disease recurrence," says Dr. Oratz. "Oncotype DX gave Elizabeth and me added confidence and peace of mind in selecting the most fitting treatment for her."
For Susan Bakken of Denver, Colorado, Oncotype DX provided a different kind of peace of mind. Susan's Recurrence Score indicated that she was at high risk of cancer recurrence, and would likely benefit significantly from chemotherapy-to both her surprise and her doctor's.
"Based on the other tests I had, my doctor said he wouldn't have otherwise recommended chemotherapy. I was shocked to find out my result, but I was so glad I did because I believe this test basically saved my life," explained Susan.
Elizabeth Sloan is also grateful for the information she gained from Oncotype DX. "Not all cancers are the same, so why treat everyone the same way with something so toxic?" she said. "It's so remarkable that finally, doctors can distinguish one person's cancer from another-I'm just so thankful."
Oncotype DX is a simple test that can only be ordered by a physician. It is performed on a small amount of breast tumor tissue removed during a standard lumpectomy, mastectomy or biopsy, meaning no additional procedure is required.
Thursday, May 6, 2010
The cause of cancer may not be genetic mutation.
Hunting for Genetic Mutations and Cancer
The current paradigm in medical research holds that the cause of most cancers is a genetic mutation. For instance, according to the National Human Genome Research Institute (NHGRI), an institute at the NIH, "all cancers are based on genetic mutations in body cells." In fact, mutation hunting is big business. Just look at the NIH budget allocated to discoveries of genetic mutations, the number of biotech companies chasing genetic mutations, the magnitude of the licensing agreements between biotech and pharmaceutical companies aimed to utilize newly discovered genetic mutations, and the number of stories in the media on genetic mutations and their so-called "link" to disease. However, this huge effort and billions of dollars has produced few discoveries and little benefits to the public. The reason for this limited success is simple. The cause of cancer is not a genetic mutation.
The story of the BRCA1 gene is a typical example of mutation hunting.
The Mystery of BRCA1
Genes, in general, produce proteins, which are the building blocks of cells. The concentration of the protein is tightly regulated. A mutated gene produces an abnormal concentration of its protein, which may lead to disease. In 1994, Mark Skolnick, PhD, discovered the BRCA1 gene (BRCA1 is short for BReast CAncer 1). Following the discovery, scientists observed an abnormally low level of the BRCA1 protein in breast cancer tissues. The BRCA1 protein is a cell cycle suppressor, which means that the protein prevents cell replication. This observation created a lot of excitement. At the time, scientists believed that they were on the verge of finding the cause of breast cancer. The reasoning was that breast cancer patients must have a mutated BRCA1 gene, which would explain the decreased production of the protein, and the excessive replication of breast cancer cells in tumors.
In the United States, 180,000 cases of breast cancer are diagnosed each year. However, the BRCA1 gene is mutated in less than 5% of these cases. In more than 95% of breast cancer patients the gene is not mutated.
So here is the mystery. If the gene is not mutated in the great majority of the breast cancer patients, why are the tumors showing low levels of the BRCA1 protein? Today, this is one of the biggest mysteries in cancer research.
The BRCA1 gene is not unique. Many normal (non-mutated) genes exhibit a mysterious abnormal (increased or decreased) production of proteins in cancer. Moreover, studies also report abnormal gene expression of normal genes in other diseases, such as atherosclerosis, obesity, osteoarthritis, type II diabetes, alopecia, type I diabetes, multiple sclerosis, asthma, lupus, thyroiditis, inflammatory bowel disease, rheumatoid arthritis, psoriasis, atopic dermatitis, and graft versus host disease.
The Discovery
A virus is a collection of genes. To replicate, some viruses settle in the nucleus of the host cell and use the cell machinery to replicate. What is the effect of a viral gene on the production of cellular proteins?
Think of a gene as an assembly line of a protein. Like all assembly lines, the gene has two parts, a conveyor (the gene coding section), and a control panel (the gene promoter/enhancer). Imagine a cellular shop that assembles a product called BRCA1. One of the many buttons on the control panel is called N-box. Pressing the button increases production. However, only a small number of operators (called transcription factors), those who pass a special certification (called the p300 test), have permission to press this button. What happens when a virus opens a shop across the street from the cellular shop (called latent infection) to produce its viral products? The control panel in the viral shop also has an N-box button. To start production, the virus begins to hire away some of the certified operators. What is the effect of this "hiring away" on the number of available BRCA1 units? The number decreases. Moreover, the decrease becomes apparent even before the virus starts production (the "hiring away" is what creates the effect, not the viral proteins). The viral assembly line competes with the BRCA1 assembly line for the certified operators, and by hiring them away prevents the cellular shop from producing the optimum, or "healthy" number of BRCA1 units. The lower number of BRCA1 units leads to excessive cell replication and breast cancer. (See a more technical description in a recent paper published in the European Journal of Cancer.)
The infection with the latent virus causes abnormal production of other genes, and as a result, the development of other chronic diseases. This sequence of events easily explains why people who suffer from obesity are also more likely to suffer from diabetes, cancer, and heart disease, and why a recent large scale study found that a low-fat diet does not protect against breast cancer. It also explains another surprising observation that male pattern baldness is associated with heart disease and prostate cancer. In general, this sequence of events easily explains the numerous observations indicating a co-existence or co-morbidity of some chronic diseases.
This discovery was first described by Dr. Hanan Polansky in his book, Microcompetition with Foreign DNA and the Origin of Chronic Disease, published by The Center for the Biology of Chronic Disease.
To summarize: the cause of cancer, and other chronic diseases, is not a genetic mutation, it's an infection with a latent virus.
Reaction of the Scientific Community
What is the scientific community saying about Dr. Polansky's discovery?
Consider what the famous heart surgeon and "Living Legend," Michael E. DeBakey, said about the discovery, "The theory underlying the basic concept concerning the origin of chronic diseases presented by Dr. Polansky is most interesting, indeed fascinating … Perhaps a symposium could be held to provide a forum for further discussions and critiques of this fascinating theory."
Elena N. Naumova, PhD, Associate Professor, Department of Family Medicine and Community Health, Tufts University School of Medicine, said, "Dr. Polansky's work compellingly demonstrates a framework that could bring together researchers from different fields. His proposed theory will work its magic by clarifying ambiguous definitions, identifying similarities and differences in various biological processes, and discovering new pathways … I believe that Dr. Polansky's book will catalyze the scientific learning process, promote interdisciplinary cross-fertilization, stimulate development of treatment strategies and drug discovery, and leave the reader inspired."
Sivasubramanian Baskar, PhD, Senior Scientist from the National Cancer Institute, NIH, said, "At first, I wish to congratulate Dr. Hanan Polansky for his scientific bravery to take such a unique, novel approach to further stimulate our understanding of the origin and establishment of chronic diseases. The philosophy underscored is an excellent one ... The amazing correlation between theoretical predictions and observed in vivo effects seems to bring us a step closer to a deeper understanding of such complex biologic processes."
Marc Pouliot, PhD, Assistant Professor, Department of Anatomy and Physiology, Faculty of Medicine, Université Laval, Canada, said, "The concept of microcompetition will change our approach in the study of chronic diseases and will furthermore give scientists a higher level of understanding in biology. Presentation of this concept undoubtedly provides a new set of opportunities for attacking chronic diseases … They lead the way to new approaches in chronic disease treatment."
Howard A. Young, PhD, Section Head, Cellular and Molecular Immunology Section, Laboratory of Experimental Immunology, National Cancer Institute, NIH, said, "In summary, Dr. Polansky is to be applauded for his attempt to provide a unifying basis for chronic diseases. His theories are stimulating and offer a basis for experimental testing and possible treatment."
Michael J. Gonzalez, PhD, Professor, Medical Sciences, University of Puerto Rico, said, "I know this book will profoundly impact medical research, drug discovery, as well as natural therapies. I also believe it will benefit the scientific community and society in general by providing further means of treatment for conditions in which only palliative care is available."
Hope for Cure and Protection
The significance of Dr. Polansky's discovery cannot be overstated. For the first time, we can start to feel a little better about these diseases. With his discovery, pharmaceutical and biotech companies can now start to design medications that will target the cause of the disease rather than its symptoms, and therefore, cure the sick and protect the healthy from these deadly diseases.
The current paradigm in medical research holds that the cause of most cancers is a genetic mutation. For instance, according to the National Human Genome Research Institute (NHGRI), an institute at the NIH, "all cancers are based on genetic mutations in body cells." In fact, mutation hunting is big business. Just look at the NIH budget allocated to discoveries of genetic mutations, the number of biotech companies chasing genetic mutations, the magnitude of the licensing agreements between biotech and pharmaceutical companies aimed to utilize newly discovered genetic mutations, and the number of stories in the media on genetic mutations and their so-called "link" to disease. However, this huge effort and billions of dollars has produced few discoveries and little benefits to the public. The reason for this limited success is simple. The cause of cancer is not a genetic mutation.
The story of the BRCA1 gene is a typical example of mutation hunting.
The Mystery of BRCA1
Genes, in general, produce proteins, which are the building blocks of cells. The concentration of the protein is tightly regulated. A mutated gene produces an abnormal concentration of its protein, which may lead to disease. In 1994, Mark Skolnick, PhD, discovered the BRCA1 gene (BRCA1 is short for BReast CAncer 1). Following the discovery, scientists observed an abnormally low level of the BRCA1 protein in breast cancer tissues. The BRCA1 protein is a cell cycle suppressor, which means that the protein prevents cell replication. This observation created a lot of excitement. At the time, scientists believed that they were on the verge of finding the cause of breast cancer. The reasoning was that breast cancer patients must have a mutated BRCA1 gene, which would explain the decreased production of the protein, and the excessive replication of breast cancer cells in tumors.
In the United States, 180,000 cases of breast cancer are diagnosed each year. However, the BRCA1 gene is mutated in less than 5% of these cases. In more than 95% of breast cancer patients the gene is not mutated.
So here is the mystery. If the gene is not mutated in the great majority of the breast cancer patients, why are the tumors showing low levels of the BRCA1 protein? Today, this is one of the biggest mysteries in cancer research.
The BRCA1 gene is not unique. Many normal (non-mutated) genes exhibit a mysterious abnormal (increased or decreased) production of proteins in cancer. Moreover, studies also report abnormal gene expression of normal genes in other diseases, such as atherosclerosis, obesity, osteoarthritis, type II diabetes, alopecia, type I diabetes, multiple sclerosis, asthma, lupus, thyroiditis, inflammatory bowel disease, rheumatoid arthritis, psoriasis, atopic dermatitis, and graft versus host disease.
The Discovery
A virus is a collection of genes. To replicate, some viruses settle in the nucleus of the host cell and use the cell machinery to replicate. What is the effect of a viral gene on the production of cellular proteins?
Think of a gene as an assembly line of a protein. Like all assembly lines, the gene has two parts, a conveyor (the gene coding section), and a control panel (the gene promoter/enhancer). Imagine a cellular shop that assembles a product called BRCA1. One of the many buttons on the control panel is called N-box. Pressing the button increases production. However, only a small number of operators (called transcription factors), those who pass a special certification (called the p300 test), have permission to press this button. What happens when a virus opens a shop across the street from the cellular shop (called latent infection) to produce its viral products? The control panel in the viral shop also has an N-box button. To start production, the virus begins to hire away some of the certified operators. What is the effect of this "hiring away" on the number of available BRCA1 units? The number decreases. Moreover, the decrease becomes apparent even before the virus starts production (the "hiring away" is what creates the effect, not the viral proteins). The viral assembly line competes with the BRCA1 assembly line for the certified operators, and by hiring them away prevents the cellular shop from producing the optimum, or "healthy" number of BRCA1 units. The lower number of BRCA1 units leads to excessive cell replication and breast cancer. (See a more technical description in a recent paper published in the European Journal of Cancer.)
The infection with the latent virus causes abnormal production of other genes, and as a result, the development of other chronic diseases. This sequence of events easily explains why people who suffer from obesity are also more likely to suffer from diabetes, cancer, and heart disease, and why a recent large scale study found that a low-fat diet does not protect against breast cancer. It also explains another surprising observation that male pattern baldness is associated with heart disease and prostate cancer. In general, this sequence of events easily explains the numerous observations indicating a co-existence or co-morbidity of some chronic diseases.
This discovery was first described by Dr. Hanan Polansky in his book, Microcompetition with Foreign DNA and the Origin of Chronic Disease, published by The Center for the Biology of Chronic Disease.
To summarize: the cause of cancer, and other chronic diseases, is not a genetic mutation, it's an infection with a latent virus.
Reaction of the Scientific Community
What is the scientific community saying about Dr. Polansky's discovery?
Consider what the famous heart surgeon and "Living Legend," Michael E. DeBakey, said about the discovery, "The theory underlying the basic concept concerning the origin of chronic diseases presented by Dr. Polansky is most interesting, indeed fascinating … Perhaps a symposium could be held to provide a forum for further discussions and critiques of this fascinating theory."
Elena N. Naumova, PhD, Associate Professor, Department of Family Medicine and Community Health, Tufts University School of Medicine, said, "Dr. Polansky's work compellingly demonstrates a framework that could bring together researchers from different fields. His proposed theory will work its magic by clarifying ambiguous definitions, identifying similarities and differences in various biological processes, and discovering new pathways … I believe that Dr. Polansky's book will catalyze the scientific learning process, promote interdisciplinary cross-fertilization, stimulate development of treatment strategies and drug discovery, and leave the reader inspired."
Sivasubramanian Baskar, PhD, Senior Scientist from the National Cancer Institute, NIH, said, "At first, I wish to congratulate Dr. Hanan Polansky for his scientific bravery to take such a unique, novel approach to further stimulate our understanding of the origin and establishment of chronic diseases. The philosophy underscored is an excellent one ... The amazing correlation between theoretical predictions and observed in vivo effects seems to bring us a step closer to a deeper understanding of such complex biologic processes."
Marc Pouliot, PhD, Assistant Professor, Department of Anatomy and Physiology, Faculty of Medicine, Université Laval, Canada, said, "The concept of microcompetition will change our approach in the study of chronic diseases and will furthermore give scientists a higher level of understanding in biology. Presentation of this concept undoubtedly provides a new set of opportunities for attacking chronic diseases … They lead the way to new approaches in chronic disease treatment."
Howard A. Young, PhD, Section Head, Cellular and Molecular Immunology Section, Laboratory of Experimental Immunology, National Cancer Institute, NIH, said, "In summary, Dr. Polansky is to be applauded for his attempt to provide a unifying basis for chronic diseases. His theories are stimulating and offer a basis for experimental testing and possible treatment."
Michael J. Gonzalez, PhD, Professor, Medical Sciences, University of Puerto Rico, said, "I know this book will profoundly impact medical research, drug discovery, as well as natural therapies. I also believe it will benefit the scientific community and society in general by providing further means of treatment for conditions in which only palliative care is available."
Hope for Cure and Protection
The significance of Dr. Polansky's discovery cannot be overstated. For the first time, we can start to feel a little better about these diseases. With his discovery, pharmaceutical and biotech companies can now start to design medications that will target the cause of the disease rather than its symptoms, and therefore, cure the sick and protect the healthy from these deadly diseases.
Monday, May 3, 2010
Can You Lower Your Risk For Breast Cancer & Heart Disease?
Many postmenopausal women are looking for alternatives to hormone therapy, especially in light of the recent Women's Health Initiative research findings concerning the risks of combined estrogen and progestin therapy. Of particular interest are phytoestrogens, which have been gaining popularity due to their "natural" status, alleged health claims, and availability in a wide range of foods and supplements.
What are Phytoestrogens?
Phytoestrogens are naturally occurring plant compounds that have some similarities to estradiol, the most potent naturally occurring estrogen. However, phytoestrogens tend to have weaker effects than most estrogens, are not stored in the body, and can be easily broken down and eliminated.
Observational studies have found a lower prevalence of breast cancer, heart disease and hip fracture rates among people living in places like Southeast Asia, where diets are typically high in phytoestrogens. In North America, knowledge of these reported health effects has stimulated great interest in the health benefits of phytoestrogens. According to the Food and Drug Administration, the sale of soy foods, a major source of phytoestrogens, has increased dramatically in the past decade.
Dietary Sources of Phytoestrogens
Phytoestrogens consist of more than 20 compounds and can be found in more than 300 plants, such as herbs, grains and fruits. The three main classes of dietary phytoestrogens are isoflavones, lignans and coumestans:
1. Isoflavones (genistein, daidzein, glycitein and equol) are primarily found in soy beans and soy products, chickpeas and other legumes.
2. Lignans (enterolactone and enterodiol) are found in seeds (primarily flaxseed), cereal bran, legumes, and alcohol (beer and bourbon).
3. Coumestans (coumestrol) can be found in alfalfa and clover. Most food sources containing these compounds typically include more than one class of phytoestrogens.
The Skeletal Effects of Phytoestrogens
Much of the evidence concerning the potential role of phytoestrogens in bone health is based on animal studies. In fact, soybean protein, soy isoflavones, genistein, daidzein and coumestrol have all been shown to have a protective effect on bone in animals who had their ovaries surgically removed.
In humans, however, the evidence is conflicting. Compared to Caucasian populations, documented hip fracture rates are lower in countries such as Hong Kong, China and Japan where dietary phytoestrogen intakes are high. Yet reports suggest that Japanese women have a greater risk of sustaining a vertebral fracture than Caucasian women.
Several studies have explored the effects of soy isoflavones on bone health, but results have been mixed, ranging from a modest impact to no effect. Most of these studies have serious limitations, including their short duration and small sample size, making it difficult to fully evaluate the impact of these compounds on bone health.
Ipriflavone Supplements
Ipriflavone, a synthetic isoflavone, has shown some promise in its ability to conserve bone in postmenopausal women. Ipriflavone has also been shown to have a protective effect on bone density in pre-menopausal women taking gonadotropin-releasing hormone (GnRH), a treatment for endometriosis that triggers bone loss.
However, a definitive three-year study of more than 400 postmenopausal women concluded that ipriflavone did not prevent bone loss. Additionally, the compound was linked to lymphocytopenia (a reduction in lymphocytes) in a significant number of study participants. Lymphocytes are a type of white blood cell that helps the body fight infection.
Risks and Benefits Are Unclear
Some studies suggest that, unlike estrogen, phytoestrogens do not appear to target breast or uterine tissue. This suggests that they may act more like SERMS (selective estrogen receptor modulators such as raloxifene and tamoxifen) than actual estrogens. However, in other studies high isoflavone levels have been linked to an increased risk of breast cancer.
Clearly, additional research is needed to further evaluate the effects of phytoestrogens before judgments regarding their safety and usefulness can be made.
Key Points
Based on information available at this time, it is reasonable to make the following conclusions concerning phytoestrogens and bone health in postmenopausal women:
1. Moderate amounts of foods containing phytoestrogens can be safely included in the diet but do not expect it to help build bone. Keep to the basic rule - eat the least processed forms.
2. Due to a lack of evidence and concerns about safety, supplementation with synthetic isoflavones (ipriflavone) is in question.
3. Postmenopausal women are encouraged to view evidence concerning phytoestrogens and bone health as conflicting and incomplete. For women who are estrogen dominant increasing their phytoestrogen intake may not improve their bone position.
What are Phytoestrogens?
Phytoestrogens are naturally occurring plant compounds that have some similarities to estradiol, the most potent naturally occurring estrogen. However, phytoestrogens tend to have weaker effects than most estrogens, are not stored in the body, and can be easily broken down and eliminated.
Observational studies have found a lower prevalence of breast cancer, heart disease and hip fracture rates among people living in places like Southeast Asia, where diets are typically high in phytoestrogens. In North America, knowledge of these reported health effects has stimulated great interest in the health benefits of phytoestrogens. According to the Food and Drug Administration, the sale of soy foods, a major source of phytoestrogens, has increased dramatically in the past decade.
Dietary Sources of Phytoestrogens
Phytoestrogens consist of more than 20 compounds and can be found in more than 300 plants, such as herbs, grains and fruits. The three main classes of dietary phytoestrogens are isoflavones, lignans and coumestans:
1. Isoflavones (genistein, daidzein, glycitein and equol) are primarily found in soy beans and soy products, chickpeas and other legumes.
2. Lignans (enterolactone and enterodiol) are found in seeds (primarily flaxseed), cereal bran, legumes, and alcohol (beer and bourbon).
3. Coumestans (coumestrol) can be found in alfalfa and clover. Most food sources containing these compounds typically include more than one class of phytoestrogens.
The Skeletal Effects of Phytoestrogens
Much of the evidence concerning the potential role of phytoestrogens in bone health is based on animal studies. In fact, soybean protein, soy isoflavones, genistein, daidzein and coumestrol have all been shown to have a protective effect on bone in animals who had their ovaries surgically removed.
In humans, however, the evidence is conflicting. Compared to Caucasian populations, documented hip fracture rates are lower in countries such as Hong Kong, China and Japan where dietary phytoestrogen intakes are high. Yet reports suggest that Japanese women have a greater risk of sustaining a vertebral fracture than Caucasian women.
Several studies have explored the effects of soy isoflavones on bone health, but results have been mixed, ranging from a modest impact to no effect. Most of these studies have serious limitations, including their short duration and small sample size, making it difficult to fully evaluate the impact of these compounds on bone health.
Ipriflavone Supplements
Ipriflavone, a synthetic isoflavone, has shown some promise in its ability to conserve bone in postmenopausal women. Ipriflavone has also been shown to have a protective effect on bone density in pre-menopausal women taking gonadotropin-releasing hormone (GnRH), a treatment for endometriosis that triggers bone loss.
However, a definitive three-year study of more than 400 postmenopausal women concluded that ipriflavone did not prevent bone loss. Additionally, the compound was linked to lymphocytopenia (a reduction in lymphocytes) in a significant number of study participants. Lymphocytes are a type of white blood cell that helps the body fight infection.
Risks and Benefits Are Unclear
Some studies suggest that, unlike estrogen, phytoestrogens do not appear to target breast or uterine tissue. This suggests that they may act more like SERMS (selective estrogen receptor modulators such as raloxifene and tamoxifen) than actual estrogens. However, in other studies high isoflavone levels have been linked to an increased risk of breast cancer.
Clearly, additional research is needed to further evaluate the effects of phytoestrogens before judgments regarding their safety and usefulness can be made.
Key Points
Based on information available at this time, it is reasonable to make the following conclusions concerning phytoestrogens and bone health in postmenopausal women:
1. Moderate amounts of foods containing phytoestrogens can be safely included in the diet but do not expect it to help build bone. Keep to the basic rule - eat the least processed forms.
2. Due to a lack of evidence and concerns about safety, supplementation with synthetic isoflavones (ipriflavone) is in question.
3. Postmenopausal women are encouraged to view evidence concerning phytoestrogens and bone health as conflicting and incomplete. For women who are estrogen dominant increasing their phytoestrogen intake may not improve their bone position.
Subscribe to:
Posts (Atom)