Phera/Supdrol Layout
- Thread starter UNCfan1
- Start date
Ziquor
Well-known member
That must have been one strong baby!
Yeah she claimed it had an anabolic to androgenic ratio of 10,000:500 - it was a beast.
Trauma1
Legend
crazyfool405
Banned
UNCfan1
Registered User
I am not sure why everyone is apologizing for a highjacking, I found it interesting and informative to say the least.
As long as the discussion doesn't get heated its all good.
I will be hitting the nolva/AI combo, throw in some P5P and Lipotrophin-PM for potential prolactin. My man Slow-mum has had good results with Lipo in this regards.
Anyway its almost 5am here, just got done working a 12 hr shift and I need some sleep and update some logs.
T1 I haven't forgotten about my RPN log buddy. Final reveiw coming tomorrow.:clap2:
As long as the discussion doesn't get heated its all good.
I will be hitting the nolva/AI combo, throw in some P5P and Lipotrophin-PM for potential prolactin. My man Slow-mum has had good results with Lipo in this regards.
Anyway its almost 5am here, just got done working a 12 hr shift and I need some sleep and update some logs.
T1 I haven't forgotten about my RPN log buddy. Final reveiw coming tomorrow.:clap2:
Kristofer68SS
Well-known member
Okay UNC. sounds good.
Lets raise up the dead horse and beat it.
Nolva is no angel.......I wouldnt even consider it the lesser of two evils....... The compounds are clearly different and are used for two separate reasons.
Nolva and eye swelling.......... nice.
Invalid Link Removed
Lets see how the two are being rated by the end user.
Invalid Link Removed
Invalid Link Removed
Heres some more interesting information plagerized from the net about tamox. Its a tad older and , regardlss of your preference, a VERY damn good read.
by Sherrill Sellman
Extracted from Nexus Magazine, Volume 5, #4 (June - July 1998)
"Once praised for its benefits in preventing breast cancer recurrence, the lucrative pharmaceutical drug tamoxifen is now implicated in causing dangerous side-effects, including other types of cancers.
In the early 1970's, a shameful chapter closed on the widespread use of a known carcinogenic and endocrine-disrupting drug called DES (diethylstilboestrol), the first synthetic, non-steroidal estrogen drug. Against the advice of its creator, Sir Charles Dodd, between four and six million American and European women and 10,000 Australian women innocently used DES for the prevention of miscarriage and pregnancy complications.
In addition, DES became a popular though unproven drug for a variety of other conditions. It was used for the suppression of lactation, the treatment of acne, the treatment of certain types of breast and prostatic cancer, and as an inhibitor of growth in young girls, an estrogen replacement in menopause and a "morning after" pill.
It would take 30 years to accept what laboratory tests had indicated as early as 1938 — that DES was a highly dangerous and harmful drug. It was reported that, 20 years after taking DES, mothers had a 40 to 50 per cent greater risk of breast cancer than non-exposed mothers. In addition, the children of DES mothers showed a high incidence of reproductive abnormalities, miscarriages, vaginal cancer, testicular cancer, sterility and immune dysfunction. In fact, it is feared that repercussions of this drug will be felt for generations to come.
The irony of this entire debacle is that the medical establishment finally acknowledged that DES was useless in preventing miscarriages. Thus, DES, another disastrous experiment on women, was added to the long list of major medical blunders.
Out of this early research, a new drug appeared on the horizon which would be soon be heralded as a shining star in the war against the growing epidemic of breast cancer. In the late 1960's the pharmaceutical industry developed a drug called "tamoxifen". As a synthetic, non-steroidal compound with hormone-like effects (many of which are poorly understood), tamoxifen has a similar structure to DES. In fact, it was observed that tamoxifen caused the same abnormal changes seen in cells of women taking estradiol and DES. (1) This similarity raised alarm bells for some.
Pierre Blais, well known as a drug researcher who was ejected from Canada's health protection bureaucracy when he spoke out about silicone breast implants, describes the story of tamoxifen as "the story of modern drug design which produces garbage drugs". He says, "Good drug design ceased, unfortunately, in the 1930s." Tamoxifen, Blais asserts, "...is a garbage drug that made it to the top of the scrap heap. It is a DES in the making." (2)
Blais's dire predictions were ignored with the promise of a potential drug treatment for breast cancer. Tamoxifen was first approved by the US Food and Drug Administration (FDA) for use as a birth-control pill; however, it proved to induce rather than inhibit ovulation. Although tamoxifen didn't work as a contraceptive, it was found to lower mammary cancer rates in animals. Animal studies showed that tamoxifen prevented estrogen from binding to receptor sites on breast tissue cells. Tamoxifen also reduced the incidence of breast cancer in rodents after administration of a breast-carcinogenic substance. This discovery provided the impetus to study its effects in treating human breast cancer.
Estrogen is the common link between most breast cancer risk factors, i.e., genetic, reproductive, dietary, lifestyle and environmental. It both stimulates the division of breast cells (healthy as well as cancerous) and, especially in its 'bad' form, increases the risk of breast cancer. Thus, hormonal drugs such as tamoxifen that block the effects of estrogen on the breast were expected to reduce the risk of breast cancer recurring in women treated for breast cancer. (3)
Tamoxifen acts as a weak estrogen by competing for estrogen receptors much as phyto-estrogens do. Like phyto-estrogens, tamoxifen has mild estrogenic properties but is considered an anti-estrogen since it inhibits the activity of regular estrogens. More accurately, tamoxifen is an estrogen-blocker. It fights breast cancer by competing with estrogen for space on estrogen receptors in the tumor tissue. Every tamoxifen molecule that hooks onto an estrogen receptor prevents an estrogen molecule from linking up at the same site. Without a steady supply of estrogen, cells in an estrogen-receptor-positive (ER+) tumor do not thrive and the tumor's ability to spread is reduced. (4)
However, tamoxifen exhibited two conflicting characteristics. It could act either as an anti-estrogen or as an estrogen. Therefore, while tamoxifen is anti-estrogenic to the breast, it also acts as an estrogen to the uterus and, to a lesser extent, the heart, blood vessels and bone. So, although it initially showed the tendency to counter breast cancer recurrence, it would soon be revealed that it also promoted particularly aggressive uterine and liver cancers, caused fatal blood clots and interfered with many other functions.
Doctors, however, were quick to jump on the tamoxifen bandwagon, turning a blind eye to its more injurious tendencies. Starting in the 1970's oncologists began using tamoxifen to treat women with cancer, often in combination with other drugs, radiation or surgery such as lumpectomy and mastectomy, with modest success. Like DES, tamoxifen's benefits were then extended for use as a preventive against osteoporosis and heart disease.
Today, doctors are treating about one million American breast cancer patients with tamoxifen, about 20 per cent of them for more than five years. As studies published in the New England Journal of Medicine in 1989 and the Journal of the National Cancer Institute in 1992 showed, women with breast cancer who took tamoxifen reduced their chances of developing cancer in the other breast (contralateral cancer) by about 30 to 50 per cent. (3) These findings would later be challenged.
Tamoxifen is now recommended for all pre-menopausal women with hormone-positive cancers, as well as for most postmenopausal women with breast cancer and/or a growing number of women with hormone-negative cancers. Tamoxifen is currently used by more women with breast cancer than any other drug. (6)
Tamoxifen (brand name Nolvadex) is now the most widely prescribed cancer medication in the world. It generated revenues of US $265 million in 1992. By 1995, worldwide sales of Nolvadex reached $400 million. (7) And at AUD $90 for one month's supply, it doesn't come cheap (the Australian Pharmaceutical Benefits Scheme covers $70).
Tamoxifen was developed by UK-based Imperial Chemical Industries (ICI), one of the world's largest multinational chemical corporations. Zeneca, an ICI subsidiary, is responsible for manufacturing and marketing the hormone and is now the world's largest cancer-drug company.
It is no surprise that ICI's profits come from playing both sides of the cancer industry. ICI's agrochemical division, which includes Zeneca, manufactures chlorinated and other industrial chemicals including herbicides. All are poisonous, and many are known endocrine-disrupters that have been incriminated as causes of breast cancer. ICI's profits swell by manufacturing chemicals that on the one hand cause breast cancer, and on the other hand reputedly cure breast cancer.
LIMITED BENEFITS OF TAMOXIFEN
Tamoxifen 's benefits are determined by several factors: (8)
Postmenopausal women who are ER-positive (have a positive estrogen receptor status) get the most benefit.
For postmenopausal women who are ER-negative, the benefits appear to outweigh the risks.
For pre-menopausal women who are ER-positive, it's a tough call. Potential benefits are small.
Pre-menopausal women who are ER negative receive virtually no benefit.
Tamoxifen is more effective in women who have cancer in their lymph nodes than in those whose nodes are cancer-free.
In 1992 the Lancet published a review of a number of studies in which a total of 30,000 breast cancer patients were randomly assigned either to take tamoxifen or not. The average patient in this collaborative study was followed up for between five and six years. Of the patients taking tamoxifen, 74.4 per cent survived, as compared with 70.9 per cent in the non-tamoxifen group — a less than impressive improvement.
The report found that the group helped most consisted of post-menopausal women with ER-positive status. The study went on to report that pre-menopausal women who are ER-negative had absolutely no benefit from taking tamoxifen. (9)
Despite tamoxifen's proven ability to reduce breast cancer recurrence in postmenopausal women, major studies have shown that tamoxifen reduces death from breast cancer only marginally. (10) The majority of women who take tamoxifen live no longer than women who do not take it. (11) Furthermore, some breast cancers learn how to use tamoxifen to stimulate their growth.
The benefits of tamoxifen are limited. Virtually all women who take it become resistant within five years. (12) A recent randomized controlled study showed that tamoxifen reached its maximum protective effect on breast tissue with women who took it for five years. Taking it for five more years didn't offer any more protection, and may actually have caused more cancers. In other words, after a while the breast cells become resistant to tamoxifen and actually start to be fed by it. (13)
This result surprised the researchers. According to Dr. Susan Love, author of Dr. Susan Love's Hormone Book: "This is a dramatic example of why you need good, long-term studies. If we had based all of our recommendations on the five-year data without doing further studies, we would have had women taking tamoxifen forever. So convinced were we that tamoxifen was a wonder drug that the only reason researchers did the later study at all was to prove it wrong. Luckily, we found out that we were wrong in time to prevent doing further damage. We have learned, not for the first time, that more isn't always better." (l4)
TAMOXIFEN'S DARK SIDE
While the initial findings of tamoxifen's role in breast cancer treatment seemed so promising, as with so many of the synthetic hormone drugs, further research presented grave concerns for its widespread use. In fact, the MIMS Annual lists 25 adverse reactions to tamoxifen: some of l these can be fatal.
Menopausal Symptoms
Tamoxifen often induces menopausal symptoms in menstruating women. About half of these women experience hot flushes. Fluid retention and weight I gain occur in about 25 per cent of l women and can be controlled by reducing the dose. Vaginal discharge and vaginal atrophy are additional symptoms. Some studies have also found l that pre-menopausal users are at risk of developing accelerated bone-mineral loss and osteoporosis.
Menstrual irregularities also occur in pre-menopausal women. Amenorrhea (absence of the menstrual cycle) often results and can be permanent.
Eye Damage
According to a 1978 study in Cancer Treatment Reports and another published in Cancer in 1992, about six per cent of women taking even low-dose tamoxifen suffer damage to the retina and corneal opacities and decreased visual acuity. Irreversible corneal and retinal changes can occur in those taking 20 mg. of tamoxifen twice a day (twice the usual dose). These changes may have no immediate effect on visual acuity, but may predispose the eyes to later problems including cataracts.
Blood Clots
Tamoxifen irritates the walls of the veins, and inflammation (a natural healing response to irritation) follows. The constant irritation and inflammation weakens the veins, causing bleeding, clotting, thrombophlebitis and, in the worst cases, obstruction of the blood vessels serving the lungs, which can be deadly and can occur with little warning. The incidence of thrombophlebitis in women using oral contraceptives is generally regarded as significant (1 in 2,000); however, with tamoxifen it's 30 times greater."
Several studies, including one reported to the FDA's Oncological Drugs Advisory Committee by the National Surgical Adjuvant Breast and Bowel Project in 1991, showed that the risk of developing life-threatening blood clots increases about seven times in women taking tamoxifen. (6)
Psychological Symptoms
Depression has been reported as a potential side-effect of tamoxifen in 30 per cent of women. Cases have been reported of an inability to concentrate.
It is important that patients observe their moods and mental states. If it is suspected at tamoxifen is causing depression or lack of concentration, it is suggested that a period of tamoxifen avoidance be considered.
Other Symptoms
Tamoxifen can trigger asthma attacks in some sensitive patients.
Changes to the vocal cords resulting in impairment of singing and speaking abilities are occasionally caused by tamoxifen.
CARCINOGENENIC EFFECTS
It wasn't long before laboratory studies showed that tamoxifen acted as a carcinogen. It has been found that tamoxifen binds tightly and irreversibly to DNA, the genetic blueprint of a cell, causing a cancerous mutation to take place. Even Australia's conservative National Health and Medical Research Council (NHMRC) warned that no amount of tamoxifen is safe when it comes to carcinogenic effects.
In California there is a law called "Proposition 65" that requires the state to publish and maintain a list of all known carcinogens. In May 1995, the state's Carcinogen Identification Committee voted unanimously to add tamoxifen to its list.
Following suit, in 1996 the World Health Organization formally designated tamoxifen a human carcinogen, grouping it with 70 other chemicals — about one quarter of them pharmaceuticals — that have received this dubious distinction.
Cont...
Liver Cancer and Liver Disease
Tamoxifen is toxic to the liver, and there have been reports of acute hepatitis in patients treated with tamoxifen. Liver damage has occurred in every animal given tamoxifen. According to Gary Williams, medical director of the American Heart Foundation, tamoxifen has been shown in animal studies to be a "rip-roaring" liver carcinogen, inducing highly aggressive cancers in about 12 per cent of rats. (7)
The latest human studies show a six-fold increase in liver cancer among women taking tamoxifen for more than two years." Liver failure and tamoxifen-induced hepatitis, although rare, have been reported. Even Zeneca admits that tamoxifen is a liver carcinogen — while nevertheless aggressively promoting its use.
Uterine (Endometrial) Cancer
As early as 1967, ICI scientists noted that "tamoxifen persists for some days in the uterus". In rats, a tamoxifen metabolite (a breakdown compound almost similar in structure to the original) was found to influence the uterus to be more receptive to estrogen. (The more estrogen, the greater the chance of unnatural cell-division leading to cancer.) ICI also reported liver carcino-genicity of tamoxifen as well as both ovarian and testicular tumors in mice in its description of the drug in the standard Physicians Desk Reference.
Uterine growths such as polyps, tumors, endometrial thickenings and cancers occur in a significant number of women taking tamoxifen. One study detected abnormal endometrial cells in subjects the day after the first tablet was taken. (9) Pre-cancerous uterine and endometrial changes were seen in 10 per cent of the women taking tamoxifen in a recent study. The higher the dose of tamoxifen and the longer it is taken, the greater the risk of changes. Women taking the standard dose of 20 mg. for two years run a risk of uterine cancer that is 2 to 3 times greater than normal. After five years, the risk is 6 to 8 times greater. (20)
In February 1996 a review by the International Agency for Research on Cancer, composed of scientists from various countries, definitively concluded that "there is sufficient evidence to regard tamoxifen as a human carcinogen that increases a woman's risk of developing cancer of the endometrium, the inner lining of the uterus" (21)
A large Swedish study linking tamoxifen to uterine cancer forced Zeneca to send letters in April 1994 to 380,000 physicians across the USA, in defense of the drug. The Swedish researchers had studied 1,371 breast cancer patients who took 40 mg. per day for two to five years and found that there was a six-fold increase in uterine cancer among those patients who took tamoxifen when compared to 1,327 who did not. A second study involving patients who took 20 mg. per day (the recommended dose) also showed a marked increase in uterine cancers compared with the control group. (22)
When the news came out that breast cancer patients who took tamoxifen for five years or longer (the same regimen that seems to prevent recurrence) might have tripled their risk of uterine cancer, British cancer researcher Richard Peto, head of the cancer research unit at Oxford University, sought to dismiss it. If caught early, he said, endometrial cancer seldom kills, so "it's no big deal". That statement infuriated critics who noted that the treatment for uterine cancer is hysterectomy. Dr. Adriane Fugh-Berman, a leading women's health activist, angrily responded: "To some of us, it is a big deal to lose your uterus."
Shortly after Peto's flip dismissal of uterine cancers, researchers at the M. D. Anderson Cancer Center at Houston and at Yale University School of Medicine discovered that breast cancer patients who develop uterine cancer while using tamoxifen are likely to have a fast-moving, lethal form of the disease. (23)
Lets raise up the dead horse and beat it.
Nolva is no angel.......I wouldnt even consider it the lesser of two evils....... The compounds are clearly different and are used for two separate reasons.
Nolva and eye swelling.......... nice.
Invalid Link Removed
Lets see how the two are being rated by the end user.
Invalid Link Removed
Invalid Link Removed
Heres some more interesting information plagerized from the net about tamox. Its a tad older and , regardlss of your preference, a VERY damn good read.
by Sherrill Sellman
Extracted from Nexus Magazine, Volume 5, #4 (June - July 1998)
"Once praised for its benefits in preventing breast cancer recurrence, the lucrative pharmaceutical drug tamoxifen is now implicated in causing dangerous side-effects, including other types of cancers.
In the early 1970's, a shameful chapter closed on the widespread use of a known carcinogenic and endocrine-disrupting drug called DES (diethylstilboestrol), the first synthetic, non-steroidal estrogen drug. Against the advice of its creator, Sir Charles Dodd, between four and six million American and European women and 10,000 Australian women innocently used DES for the prevention of miscarriage and pregnancy complications.
In addition, DES became a popular though unproven drug for a variety of other conditions. It was used for the suppression of lactation, the treatment of acne, the treatment of certain types of breast and prostatic cancer, and as an inhibitor of growth in young girls, an estrogen replacement in menopause and a "morning after" pill.
It would take 30 years to accept what laboratory tests had indicated as early as 1938 — that DES was a highly dangerous and harmful drug. It was reported that, 20 years after taking DES, mothers had a 40 to 50 per cent greater risk of breast cancer than non-exposed mothers. In addition, the children of DES mothers showed a high incidence of reproductive abnormalities, miscarriages, vaginal cancer, testicular cancer, sterility and immune dysfunction. In fact, it is feared that repercussions of this drug will be felt for generations to come.
The irony of this entire debacle is that the medical establishment finally acknowledged that DES was useless in preventing miscarriages. Thus, DES, another disastrous experiment on women, was added to the long list of major medical blunders.
Out of this early research, a new drug appeared on the horizon which would be soon be heralded as a shining star in the war against the growing epidemic of breast cancer. In the late 1960's the pharmaceutical industry developed a drug called "tamoxifen". As a synthetic, non-steroidal compound with hormone-like effects (many of which are poorly understood), tamoxifen has a similar structure to DES. In fact, it was observed that tamoxifen caused the same abnormal changes seen in cells of women taking estradiol and DES. (1) This similarity raised alarm bells for some.
Pierre Blais, well known as a drug researcher who was ejected from Canada's health protection bureaucracy when he spoke out about silicone breast implants, describes the story of tamoxifen as "the story of modern drug design which produces garbage drugs". He says, "Good drug design ceased, unfortunately, in the 1930s." Tamoxifen, Blais asserts, "...is a garbage drug that made it to the top of the scrap heap. It is a DES in the making." (2)
Blais's dire predictions were ignored with the promise of a potential drug treatment for breast cancer. Tamoxifen was first approved by the US Food and Drug Administration (FDA) for use as a birth-control pill; however, it proved to induce rather than inhibit ovulation. Although tamoxifen didn't work as a contraceptive, it was found to lower mammary cancer rates in animals. Animal studies showed that tamoxifen prevented estrogen from binding to receptor sites on breast tissue cells. Tamoxifen also reduced the incidence of breast cancer in rodents after administration of a breast-carcinogenic substance. This discovery provided the impetus to study its effects in treating human breast cancer.
Estrogen is the common link between most breast cancer risk factors, i.e., genetic, reproductive, dietary, lifestyle and environmental. It both stimulates the division of breast cells (healthy as well as cancerous) and, especially in its 'bad' form, increases the risk of breast cancer. Thus, hormonal drugs such as tamoxifen that block the effects of estrogen on the breast were expected to reduce the risk of breast cancer recurring in women treated for breast cancer. (3)
Tamoxifen acts as a weak estrogen by competing for estrogen receptors much as phyto-estrogens do. Like phyto-estrogens, tamoxifen has mild estrogenic properties but is considered an anti-estrogen since it inhibits the activity of regular estrogens. More accurately, tamoxifen is an estrogen-blocker. It fights breast cancer by competing with estrogen for space on estrogen receptors in the tumor tissue. Every tamoxifen molecule that hooks onto an estrogen receptor prevents an estrogen molecule from linking up at the same site. Without a steady supply of estrogen, cells in an estrogen-receptor-positive (ER+) tumor do not thrive and the tumor's ability to spread is reduced. (4)
However, tamoxifen exhibited two conflicting characteristics. It could act either as an anti-estrogen or as an estrogen. Therefore, while tamoxifen is anti-estrogenic to the breast, it also acts as an estrogen to the uterus and, to a lesser extent, the heart, blood vessels and bone. So, although it initially showed the tendency to counter breast cancer recurrence, it would soon be revealed that it also promoted particularly aggressive uterine and liver cancers, caused fatal blood clots and interfered with many other functions.
Doctors, however, were quick to jump on the tamoxifen bandwagon, turning a blind eye to its more injurious tendencies. Starting in the 1970's oncologists began using tamoxifen to treat women with cancer, often in combination with other drugs, radiation or surgery such as lumpectomy and mastectomy, with modest success. Like DES, tamoxifen's benefits were then extended for use as a preventive against osteoporosis and heart disease.
Today, doctors are treating about one million American breast cancer patients with tamoxifen, about 20 per cent of them for more than five years. As studies published in the New England Journal of Medicine in 1989 and the Journal of the National Cancer Institute in 1992 showed, women with breast cancer who took tamoxifen reduced their chances of developing cancer in the other breast (contralateral cancer) by about 30 to 50 per cent. (3) These findings would later be challenged.
Tamoxifen is now recommended for all pre-menopausal women with hormone-positive cancers, as well as for most postmenopausal women with breast cancer and/or a growing number of women with hormone-negative cancers. Tamoxifen is currently used by more women with breast cancer than any other drug. (6)
Tamoxifen (brand name Nolvadex) is now the most widely prescribed cancer medication in the world. It generated revenues of US $265 million in 1992. By 1995, worldwide sales of Nolvadex reached $400 million. (7) And at AUD $90 for one month's supply, it doesn't come cheap (the Australian Pharmaceutical Benefits Scheme covers $70).
Tamoxifen was developed by UK-based Imperial Chemical Industries (ICI), one of the world's largest multinational chemical corporations. Zeneca, an ICI subsidiary, is responsible for manufacturing and marketing the hormone and is now the world's largest cancer-drug company.
It is no surprise that ICI's profits come from playing both sides of the cancer industry. ICI's agrochemical division, which includes Zeneca, manufactures chlorinated and other industrial chemicals including herbicides. All are poisonous, and many are known endocrine-disrupters that have been incriminated as causes of breast cancer. ICI's profits swell by manufacturing chemicals that on the one hand cause breast cancer, and on the other hand reputedly cure breast cancer.
LIMITED BENEFITS OF TAMOXIFEN
Tamoxifen 's benefits are determined by several factors: (8)
Postmenopausal women who are ER-positive (have a positive estrogen receptor status) get the most benefit.
For postmenopausal women who are ER-negative, the benefits appear to outweigh the risks.
For pre-menopausal women who are ER-positive, it's a tough call. Potential benefits are small.
Pre-menopausal women who are ER negative receive virtually no benefit.
Tamoxifen is more effective in women who have cancer in their lymph nodes than in those whose nodes are cancer-free.
In 1992 the Lancet published a review of a number of studies in which a total of 30,000 breast cancer patients were randomly assigned either to take tamoxifen or not. The average patient in this collaborative study was followed up for between five and six years. Of the patients taking tamoxifen, 74.4 per cent survived, as compared with 70.9 per cent in the non-tamoxifen group — a less than impressive improvement.
The report found that the group helped most consisted of post-menopausal women with ER-positive status. The study went on to report that pre-menopausal women who are ER-negative had absolutely no benefit from taking tamoxifen. (9)
Despite tamoxifen's proven ability to reduce breast cancer recurrence in postmenopausal women, major studies have shown that tamoxifen reduces death from breast cancer only marginally. (10) The majority of women who take tamoxifen live no longer than women who do not take it. (11) Furthermore, some breast cancers learn how to use tamoxifen to stimulate their growth.
The benefits of tamoxifen are limited. Virtually all women who take it become resistant within five years. (12) A recent randomized controlled study showed that tamoxifen reached its maximum protective effect on breast tissue with women who took it for five years. Taking it for five more years didn't offer any more protection, and may actually have caused more cancers. In other words, after a while the breast cells become resistant to tamoxifen and actually start to be fed by it. (13)
This result surprised the researchers. According to Dr. Susan Love, author of Dr. Susan Love's Hormone Book: "This is a dramatic example of why you need good, long-term studies. If we had based all of our recommendations on the five-year data without doing further studies, we would have had women taking tamoxifen forever. So convinced were we that tamoxifen was a wonder drug that the only reason researchers did the later study at all was to prove it wrong. Luckily, we found out that we were wrong in time to prevent doing further damage. We have learned, not for the first time, that more isn't always better." (l4)
TAMOXIFEN'S DARK SIDE
While the initial findings of tamoxifen's role in breast cancer treatment seemed so promising, as with so many of the synthetic hormone drugs, further research presented grave concerns for its widespread use. In fact, the MIMS Annual lists 25 adverse reactions to tamoxifen: some of l these can be fatal.
Menopausal Symptoms
Tamoxifen often induces menopausal symptoms in menstruating women. About half of these women experience hot flushes. Fluid retention and weight I gain occur in about 25 per cent of l women and can be controlled by reducing the dose. Vaginal discharge and vaginal atrophy are additional symptoms. Some studies have also found l that pre-menopausal users are at risk of developing accelerated bone-mineral loss and osteoporosis.
Menstrual irregularities also occur in pre-menopausal women. Amenorrhea (absence of the menstrual cycle) often results and can be permanent.
Eye Damage
According to a 1978 study in Cancer Treatment Reports and another published in Cancer in 1992, about six per cent of women taking even low-dose tamoxifen suffer damage to the retina and corneal opacities and decreased visual acuity. Irreversible corneal and retinal changes can occur in those taking 20 mg. of tamoxifen twice a day (twice the usual dose). These changes may have no immediate effect on visual acuity, but may predispose the eyes to later problems including cataracts.
Blood Clots
Tamoxifen irritates the walls of the veins, and inflammation (a natural healing response to irritation) follows. The constant irritation and inflammation weakens the veins, causing bleeding, clotting, thrombophlebitis and, in the worst cases, obstruction of the blood vessels serving the lungs, which can be deadly and can occur with little warning. The incidence of thrombophlebitis in women using oral contraceptives is generally regarded as significant (1 in 2,000); however, with tamoxifen it's 30 times greater."
Several studies, including one reported to the FDA's Oncological Drugs Advisory Committee by the National Surgical Adjuvant Breast and Bowel Project in 1991, showed that the risk of developing life-threatening blood clots increases about seven times in women taking tamoxifen. (6)
Psychological Symptoms
Depression has been reported as a potential side-effect of tamoxifen in 30 per cent of women. Cases have been reported of an inability to concentrate.
It is important that patients observe their moods and mental states. If it is suspected at tamoxifen is causing depression or lack of concentration, it is suggested that a period of tamoxifen avoidance be considered.
Other Symptoms
Tamoxifen can trigger asthma attacks in some sensitive patients.
Changes to the vocal cords resulting in impairment of singing and speaking abilities are occasionally caused by tamoxifen.
CARCINOGENENIC EFFECTS
It wasn't long before laboratory studies showed that tamoxifen acted as a carcinogen. It has been found that tamoxifen binds tightly and irreversibly to DNA, the genetic blueprint of a cell, causing a cancerous mutation to take place. Even Australia's conservative National Health and Medical Research Council (NHMRC) warned that no amount of tamoxifen is safe when it comes to carcinogenic effects.
In California there is a law called "Proposition 65" that requires the state to publish and maintain a list of all known carcinogens. In May 1995, the state's Carcinogen Identification Committee voted unanimously to add tamoxifen to its list.
Following suit, in 1996 the World Health Organization formally designated tamoxifen a human carcinogen, grouping it with 70 other chemicals — about one quarter of them pharmaceuticals — that have received this dubious distinction.
Cont...
Liver Cancer and Liver Disease
Tamoxifen is toxic to the liver, and there have been reports of acute hepatitis in patients treated with tamoxifen. Liver damage has occurred in every animal given tamoxifen. According to Gary Williams, medical director of the American Heart Foundation, tamoxifen has been shown in animal studies to be a "rip-roaring" liver carcinogen, inducing highly aggressive cancers in about 12 per cent of rats. (7)
The latest human studies show a six-fold increase in liver cancer among women taking tamoxifen for more than two years." Liver failure and tamoxifen-induced hepatitis, although rare, have been reported. Even Zeneca admits that tamoxifen is a liver carcinogen — while nevertheless aggressively promoting its use.
Uterine (Endometrial) Cancer
As early as 1967, ICI scientists noted that "tamoxifen persists for some days in the uterus". In rats, a tamoxifen metabolite (a breakdown compound almost similar in structure to the original) was found to influence the uterus to be more receptive to estrogen. (The more estrogen, the greater the chance of unnatural cell-division leading to cancer.) ICI also reported liver carcino-genicity of tamoxifen as well as both ovarian and testicular tumors in mice in its description of the drug in the standard Physicians Desk Reference.
Uterine growths such as polyps, tumors, endometrial thickenings and cancers occur in a significant number of women taking tamoxifen. One study detected abnormal endometrial cells in subjects the day after the first tablet was taken. (9) Pre-cancerous uterine and endometrial changes were seen in 10 per cent of the women taking tamoxifen in a recent study. The higher the dose of tamoxifen and the longer it is taken, the greater the risk of changes. Women taking the standard dose of 20 mg. for two years run a risk of uterine cancer that is 2 to 3 times greater than normal. After five years, the risk is 6 to 8 times greater. (20)
In February 1996 a review by the International Agency for Research on Cancer, composed of scientists from various countries, definitively concluded that "there is sufficient evidence to regard tamoxifen as a human carcinogen that increases a woman's risk of developing cancer of the endometrium, the inner lining of the uterus" (21)
A large Swedish study linking tamoxifen to uterine cancer forced Zeneca to send letters in April 1994 to 380,000 physicians across the USA, in defense of the drug. The Swedish researchers had studied 1,371 breast cancer patients who took 40 mg. per day for two to five years and found that there was a six-fold increase in uterine cancer among those patients who took tamoxifen when compared to 1,327 who did not. A second study involving patients who took 20 mg. per day (the recommended dose) also showed a marked increase in uterine cancers compared with the control group. (22)
When the news came out that breast cancer patients who took tamoxifen for five years or longer (the same regimen that seems to prevent recurrence) might have tripled their risk of uterine cancer, British cancer researcher Richard Peto, head of the cancer research unit at Oxford University, sought to dismiss it. If caught early, he said, endometrial cancer seldom kills, so "it's no big deal". That statement infuriated critics who noted that the treatment for uterine cancer is hysterectomy. Dr. Adriane Fugh-Berman, a leading women's health activist, angrily responded: "To some of us, it is a big deal to lose your uterus."
Shortly after Peto's flip dismissal of uterine cancers, researchers at the M. D. Anderson Cancer Center at Houston and at Yale University School of Medicine discovered that breast cancer patients who develop uterine cancer while using tamoxifen are likely to have a fast-moving, lethal form of the disease. (23)
Kristofer68SS
Well-known member
It should be noted that tamoxifen has also been associated with gastrointestinal cancers.
Breast Cancer
The premise for taking tamoxifen is its supposed role in protecting breast cancer patients from recurrence of the cancer. It was further postulated that it prevented breast cancer from occurring in the opposite breast (contralateral).
However, disturbing findings continue to surface, challenging tamoxifen's effectiveness. In 1992 the New England Journal of Medicine showed that tamoxifen may reduce the incidence of contralateral cancer, but this was demonstrated only in pre-menopausal women and only in three out of eight trials. In another 1992 study, reported in Octa Oncologica, it was shown that tamoxifen not only failed to reduce contralateral cancers in pre-menopausal women, but it actually increased their incidence. (24)
The irony of tamoxifen is that, while widely publicized as the leading treatment against the recurrence of breast cancer, it is a known and listed carcinogenic substance.
Heart Disease and Osteoporosis
Another promise of tamoxifen was its supposed protective benefits for the heart and bones. It was theorized that its estrogenic properties would help reduce heart disease and osteoporosis in women, but once again the theory crumbled under the weight of hard facts.
Several trials with tamoxifen failed to show that it has any effect on bone density and thus on prevention of osteoporosis. In three other trials, bone density increased slightly in lower spinal vertebrae but not in longer bones or hip bones which are particularly susceptible to fractures and potentially fatal complications.
Initial data seemed to indicate that it decreased the incidence of heart attacks, but they have been disproved by more recent studies. According to Dr. Susan Love: "It doesn't seem to have a bad effect on lipids, but that's a far cry from preventing heart attacks."
A detailed review of the drug's alleged protective cardiovascular effects prompted the British National Heart, Lung and Blood Institute, a once strong proponent of tamoxifen, to withdraw its support because the evidence of benefit proved so inadequate. (25)
According to the January 1996 issue of The Network News, it was reported at a closed-door meeting of the National Cancer Institute that tamoxifen failed to prevent heart disease in breast cancer patients.
THE BREAST CANCER PREVENTION TRIAL
Based far more on wishful thinking than on science, the U.S. National Cancer Institute (NCI) leaped to the conclusion that tamoxifen's anti-estrogenic effects in relation to breast cancer treatment meant that the drug would prevent breast cancer from developing in healthy women.
Disregarding all the research implicating tamoxifen with serious and potentially fatal side-effects, the NCI launched a US$60 million breast cancer prevention trial in April 1992, aiming to recruit 16,000 healthy women in the United States, Europe, Canada, Australia and New Zealand. Still ongoing, the trial now involves 13,000 healthy women over the age of 35 who are considered at high risk. Australia has recruited 1,350 women, with a target of 2,500. For five years, half the women receive tamoxifen and half receive a placebo. The drug is supplied free of charge by manufacturer Zeneca.
Dr. Samuel Epstein, Professor Environmental Medicine at the University of Illinois School of Public Health and author of The Breast Cancer Prevention Program, raises serious concerns. "Unfortunately, this misguided and dangerous approach to prevention stems from the entrenched fixation of the NCI on the use of chemical drugs to prevent cancer which may have been induced by chemical pollutants, medical technology (such as radiation from X-rays) and carcinogenic/estrogenic drugs in the first place. Instead of attempting to reduce the carcinogenic chemical burden under which we struggle to maintain our health, the NCI believes that the solution is to add more chemicals to the mix."
Dr. Susan Love concurs: "It is a sad state of affairs when we have to add yet more chemicals to counteract the effects of other chemicals."
This attitude extends to the way the NCI treats the women in the trial. They are given no guidance on alternative protective measures such as increasing exercise, maintaining a healthy weight, eating a protective diet and avoiding exposure to environmental carcinogens; nor are they being fully informed about the serious risks of tamoxifen.
Dr. Lynette Dumble, Senior Research Fellow in History and Philosophy of Science at the University of Melbourne, believes that the global trial to prevent breast cancer with tamoxifen is a modern and very large chapter of "medical imperialism". Back in October 1994 she commented on ABC TV's Quantum science program that the tamoxifen trial was the medical equivalent of mutilating surgery which prevents a woman from developing breast cancer by cutting off both her breasts.
Dr. Dumble sees women as vulnerable guinea pigs for the trial, and questions both the breast cancer risk of healthy women volunteering for the trial (how can you tell whether fate or tamoxifen prevents a woman from developing breast cancer?) and the terms of the trial's positives and negatives (if a woman dies of tamoxifen-related endometrial or liver cancer, does this count as a tamoxifen success in preventing breast cancer?).
It seems absurd, but why would the powers-that-be continue to promote a trial that promises to substitute one cancer for another in otherwise healthy women? Once again, healthy women are targeted as the guinea pigs for a drug treatment that has already been proven to be a cause of a variety of cancers including breast cancer. In the case of tamoxifen, medical research has once again taken a back seat to profits. It is the population that is at risk. The cancer establishment would certainly be eager to prove a tamoxifen-prevention role, since it would then open up another huge, billion-dollar market.
ALTERNATIVES TO TAMOXIFEN
While the cancer establishment continues to invest vast amounts of money into research, manufacturing and trialling of harmful drugs for the prevention and hopeful cure of breast cancer, there are safer and more effective options that already exist.
Estriol, one of the estrogens produced by the ovaries, is considered a safe estrogen in that it has been shown to inhibit breast cancer. Dr. Henry Lemon and his colleagues conducted a study in women who already had breast cancer that had spread to other areas of the body. One group was given Estriol and another not. At the end of the study, 37 per cent of those women who received estriol had either a remission or an arrest of their cancer. Might not estriol, a natural, safe hormone with almost no side-effects, be able to accomplish what tamoxifen does but without the toxic side-effects?
There is also convincing evidence that natural progesterone has an important role in breast cancer treatment and prevention. A study conducted in 1981 at Johns Hopkins University revealed that when a group with a low progesterone level was compared with a normal-level progesterone group, it was found that the occurrence of breast cancer was 5.4 times greater in the women in the low progesterone group. That is, the incidence of breast cancer in the low progesterone group was over 80 per cent greater than in the normal progesterone group. When the researchers looked at the low progesterone group for all types of cancer, they found that these women experienced a tenfold increase in all malignant cancers, compared to the normal group.
In a 1995 study published in the Journal of Fertility and Sterility, researchers found that women using a topical progesterone cream had dramatically reduced breast cell multiplication rates compared to women using either a placebo or estrogen. This exciting study demonstrated that natural progesterone creams impressively decreased breast cell proliferation rates. (27)
Lifestyle factors also play a significant role. In a prospective study of 25,624 Norwegian women aged 20 to 54, after an average of 14 years of follow-up the investigators found strong evidence that everyday exercise, both at work and at leisure, reduced the breast cancer risk. Women who exercised at least four hours a week during leisure time were found to have a 37 per cent reduction in risk of breast cancer, compared with sedentary women. The study found that the more time spent exercising, the lower the breast cancer risk. (28)
As Dr. John Lee pointed out in his best-selling book, What Doctors May Not Tell You About Menopause: "Herbs and food contain phyto-estrogens. Their benefit parallels that of tamoxifen (without the adverse side-effects) in that phyto-estrogens occupy estrogen receptors and are less estrogenic than those made by the body. Since it is now known that reducing caloric intake reduces estrogen levels, and recent studies find 46 per cent less breast cancer among women consuming more fruit and vegetables, it would seem that women interested in preventing breast cancer could make modest changes in diet and derive better and certainly safer results." (29)
History continues to repeat itself. Time and time again women have been reassured that the wonder drugs or treatments offered them would be their salvation, only to discover they were exposed to harmful carcinogenic and mutagenic chemicals.
In addition to the DES debacle, the disasters of thalidomide, silicone breast implants, estrogen replacement therapy and now tamoxifen (to name just a few) continue to demonstrate how readily women's lives have been sacrificed in the pursuit of profits. The warnings have been drowned out by the glossy advertising campaigns and the reassurances of "medical experts".
There are solutions to the breast cancer epidemic. However, they will be found more by altering lifestyle, dietary and stress factors, and reducing or eliminating exposure to the many known toxic, carcinogenic chemicals that are polluting the environment, than by some miraculous drug discovery. It is also up to women not only to continue to become fully educated about safe health options but to demand them from health providers. Too many women have already been maimed and sacrificed to unproven and unsafe drug treatments.
It is widely believed that today's drugs are tomorrow's poisons. In the case of tamoxifen, tomorrow has already arrived."
Breast Cancer
The premise for taking tamoxifen is its supposed role in protecting breast cancer patients from recurrence of the cancer. It was further postulated that it prevented breast cancer from occurring in the opposite breast (contralateral).
However, disturbing findings continue to surface, challenging tamoxifen's effectiveness. In 1992 the New England Journal of Medicine showed that tamoxifen may reduce the incidence of contralateral cancer, but this was demonstrated only in pre-menopausal women and only in three out of eight trials. In another 1992 study, reported in Octa Oncologica, it was shown that tamoxifen not only failed to reduce contralateral cancers in pre-menopausal women, but it actually increased their incidence. (24)
The irony of tamoxifen is that, while widely publicized as the leading treatment against the recurrence of breast cancer, it is a known and listed carcinogenic substance.
Heart Disease and Osteoporosis
Another promise of tamoxifen was its supposed protective benefits for the heart and bones. It was theorized that its estrogenic properties would help reduce heart disease and osteoporosis in women, but once again the theory crumbled under the weight of hard facts.
Several trials with tamoxifen failed to show that it has any effect on bone density and thus on prevention of osteoporosis. In three other trials, bone density increased slightly in lower spinal vertebrae but not in longer bones or hip bones which are particularly susceptible to fractures and potentially fatal complications.
Initial data seemed to indicate that it decreased the incidence of heart attacks, but they have been disproved by more recent studies. According to Dr. Susan Love: "It doesn't seem to have a bad effect on lipids, but that's a far cry from preventing heart attacks."
A detailed review of the drug's alleged protective cardiovascular effects prompted the British National Heart, Lung and Blood Institute, a once strong proponent of tamoxifen, to withdraw its support because the evidence of benefit proved so inadequate. (25)
According to the January 1996 issue of The Network News, it was reported at a closed-door meeting of the National Cancer Institute that tamoxifen failed to prevent heart disease in breast cancer patients.
THE BREAST CANCER PREVENTION TRIAL
Based far more on wishful thinking than on science, the U.S. National Cancer Institute (NCI) leaped to the conclusion that tamoxifen's anti-estrogenic effects in relation to breast cancer treatment meant that the drug would prevent breast cancer from developing in healthy women.
Disregarding all the research implicating tamoxifen with serious and potentially fatal side-effects, the NCI launched a US$60 million breast cancer prevention trial in April 1992, aiming to recruit 16,000 healthy women in the United States, Europe, Canada, Australia and New Zealand. Still ongoing, the trial now involves 13,000 healthy women over the age of 35 who are considered at high risk. Australia has recruited 1,350 women, with a target of 2,500. For five years, half the women receive tamoxifen and half receive a placebo. The drug is supplied free of charge by manufacturer Zeneca.
Dr. Samuel Epstein, Professor Environmental Medicine at the University of Illinois School of Public Health and author of The Breast Cancer Prevention Program, raises serious concerns. "Unfortunately, this misguided and dangerous approach to prevention stems from the entrenched fixation of the NCI on the use of chemical drugs to prevent cancer which may have been induced by chemical pollutants, medical technology (such as radiation from X-rays) and carcinogenic/estrogenic drugs in the first place. Instead of attempting to reduce the carcinogenic chemical burden under which we struggle to maintain our health, the NCI believes that the solution is to add more chemicals to the mix."
Dr. Susan Love concurs: "It is a sad state of affairs when we have to add yet more chemicals to counteract the effects of other chemicals."
This attitude extends to the way the NCI treats the women in the trial. They are given no guidance on alternative protective measures such as increasing exercise, maintaining a healthy weight, eating a protective diet and avoiding exposure to environmental carcinogens; nor are they being fully informed about the serious risks of tamoxifen.
Dr. Lynette Dumble, Senior Research Fellow in History and Philosophy of Science at the University of Melbourne, believes that the global trial to prevent breast cancer with tamoxifen is a modern and very large chapter of "medical imperialism". Back in October 1994 she commented on ABC TV's Quantum science program that the tamoxifen trial was the medical equivalent of mutilating surgery which prevents a woman from developing breast cancer by cutting off both her breasts.
Dr. Dumble sees women as vulnerable guinea pigs for the trial, and questions both the breast cancer risk of healthy women volunteering for the trial (how can you tell whether fate or tamoxifen prevents a woman from developing breast cancer?) and the terms of the trial's positives and negatives (if a woman dies of tamoxifen-related endometrial or liver cancer, does this count as a tamoxifen success in preventing breast cancer?).
It seems absurd, but why would the powers-that-be continue to promote a trial that promises to substitute one cancer for another in otherwise healthy women? Once again, healthy women are targeted as the guinea pigs for a drug treatment that has already been proven to be a cause of a variety of cancers including breast cancer. In the case of tamoxifen, medical research has once again taken a back seat to profits. It is the population that is at risk. The cancer establishment would certainly be eager to prove a tamoxifen-prevention role, since it would then open up another huge, billion-dollar market.
ALTERNATIVES TO TAMOXIFEN
While the cancer establishment continues to invest vast amounts of money into research, manufacturing and trialling of harmful drugs for the prevention and hopeful cure of breast cancer, there are safer and more effective options that already exist.
Estriol, one of the estrogens produced by the ovaries, is considered a safe estrogen in that it has been shown to inhibit breast cancer. Dr. Henry Lemon and his colleagues conducted a study in women who already had breast cancer that had spread to other areas of the body. One group was given Estriol and another not. At the end of the study, 37 per cent of those women who received estriol had either a remission or an arrest of their cancer. Might not estriol, a natural, safe hormone with almost no side-effects, be able to accomplish what tamoxifen does but without the toxic side-effects?
There is also convincing evidence that natural progesterone has an important role in breast cancer treatment and prevention. A study conducted in 1981 at Johns Hopkins University revealed that when a group with a low progesterone level was compared with a normal-level progesterone group, it was found that the occurrence of breast cancer was 5.4 times greater in the women in the low progesterone group. That is, the incidence of breast cancer in the low progesterone group was over 80 per cent greater than in the normal progesterone group. When the researchers looked at the low progesterone group for all types of cancer, they found that these women experienced a tenfold increase in all malignant cancers, compared to the normal group.
In a 1995 study published in the Journal of Fertility and Sterility, researchers found that women using a topical progesterone cream had dramatically reduced breast cell multiplication rates compared to women using either a placebo or estrogen. This exciting study demonstrated that natural progesterone creams impressively decreased breast cell proliferation rates. (27)
Lifestyle factors also play a significant role. In a prospective study of 25,624 Norwegian women aged 20 to 54, after an average of 14 years of follow-up the investigators found strong evidence that everyday exercise, both at work and at leisure, reduced the breast cancer risk. Women who exercised at least four hours a week during leisure time were found to have a 37 per cent reduction in risk of breast cancer, compared with sedentary women. The study found that the more time spent exercising, the lower the breast cancer risk. (28)
As Dr. John Lee pointed out in his best-selling book, What Doctors May Not Tell You About Menopause: "Herbs and food contain phyto-estrogens. Their benefit parallels that of tamoxifen (without the adverse side-effects) in that phyto-estrogens occupy estrogen receptors and are less estrogenic than those made by the body. Since it is now known that reducing caloric intake reduces estrogen levels, and recent studies find 46 per cent less breast cancer among women consuming more fruit and vegetables, it would seem that women interested in preventing breast cancer could make modest changes in diet and derive better and certainly safer results." (29)
History continues to repeat itself. Time and time again women have been reassured that the wonder drugs or treatments offered them would be their salvation, only to discover they were exposed to harmful carcinogenic and mutagenic chemicals.
In addition to the DES debacle, the disasters of thalidomide, silicone breast implants, estrogen replacement therapy and now tamoxifen (to name just a few) continue to demonstrate how readily women's lives have been sacrificed in the pursuit of profits. The warnings have been drowned out by the glossy advertising campaigns and the reassurances of "medical experts".
There are solutions to the breast cancer epidemic. However, they will be found more by altering lifestyle, dietary and stress factors, and reducing or eliminating exposure to the many known toxic, carcinogenic chemicals that are polluting the environment, than by some miraculous drug discovery. It is also up to women not only to continue to become fully educated about safe health options but to demand them from health providers. Too many women have already been maimed and sacrificed to unproven and unsafe drug treatments.
It is widely believed that today's drugs are tomorrow's poisons. In the case of tamoxifen, tomorrow has already arrived."
crazyfool405
Banned
good find but all SERMs have a dark side, some one will dig it up on clomid as well, especially with eye problems and emotional problems.
i guess to each his own when it comes to PCT, im suprised noone has ventured into the realm of RALOXIFINE as a PCT, its purpose is the same as all others, (clomid is unique though)
i guess to each his own when it comes to PCT, im suprised noone has ventured into the realm of RALOXIFINE as a PCT, its purpose is the same as all others, (clomid is unique though)
Kristofer68SS
Well-known member
yeah I think bass was saying its a more popular rx than the others.
yes, i am very aware clomid is no angel as well.
Kristofer68SS
Well-known member
Because it is basically OOS EVERYWHERE
demand that high?
crazyfool405
Banned
they all have different aactions thats in end of story , what works for some maynot work for everyone.
crazyfool405
Banned
o yea.... toremfine
Dose-dependent hormonal effects of toremifene in postmenopausal breast cancer patients.
Ellmen J, Werner D, Hakulinen P, Keiling R, Fargeot P, Falkson G, Bezwoda WR.
Orion Corporation, Orion Pharma, Clinical R & D, Turku, Finland. [email protected]
PURPOSE: The purpose of the study was to compare hormonal effects of three toremifene doses, 20 mg (TOR20), 40 mg (TOR40) and 60 mg (TOR60) administered daily, in postmenopausal women with advanced breast cancer. METHODS: The study was randomized and open label in three parallel groups. Biochemical variables were identified as the serum concentrations of follicle stimulating hormone (FSH), luteinizing hormone (LH) and sex hormone binding globulin (SHBG). The changes were compared with objective clinical responses and to progression-free time. Adverse reactions and liver function test (aspartate aminotransferase, ASAT) were assessed for safety. RESULTS: A total of 260 patients were randomly grouped (90 to TOR20, 81 to TOR40 and 89 to TOR60). Of these patients 29, 29 and 22 completed at least 3 months of treatment and the results were analyzed for biochemical variables. All treatments had intrinsic estrogen agonist activity by decreasing of serum FSH and LH and by increasing of SHBG during the first 3 months (P < 0.01). Dose TOR20 showed slightly longer times to exert maximum estrogenic effects than did the two higher doses. No increases in liver function tests were seen in any of the groups. Objective response rates were 24.4, 39.5 and 32.6% (P = 0.01) and median times-to-progression were 206, 189 and 196 days in TOR20, TOR40 and TOR60, respectively (P = 0.913). Fewer responses were observed in the TOR20 group than in TOR40 (P = 0.05). Adverse events were reported in 19, 23 and 30 patients in the treatment groups (P = 0.20). The most frequently reported events were hot flushes and nausea. These were mostly mild or moderate, and only 1.5% of treatments was discontinued due to toxicity. CONCLUSIONS: Toremifene doses of 40 and 60 mg daily were effective and safe treatments of breast cancer in postmenopausal women, and no differences in their biochemical or clinical effects were seen. Toremifene at 20 mg/day had similar but slightly less potent antiestrogenic and estrogenic effects than the two higher doses.
Dose-dependent hormonal effects of toremifene in postmenopausal breast cancer patients.
Ellmen J, Werner D, Hakulinen P, Keiling R, Fargeot P, Falkson G, Bezwoda WR.
Orion Corporation, Orion Pharma, Clinical R & D, Turku, Finland. [email protected]
PURPOSE: The purpose of the study was to compare hormonal effects of three toremifene doses, 20 mg (TOR20), 40 mg (TOR40) and 60 mg (TOR60) administered daily, in postmenopausal women with advanced breast cancer. METHODS: The study was randomized and open label in three parallel groups. Biochemical variables were identified as the serum concentrations of follicle stimulating hormone (FSH), luteinizing hormone (LH) and sex hormone binding globulin (SHBG). The changes were compared with objective clinical responses and to progression-free time. Adverse reactions and liver function test (aspartate aminotransferase, ASAT) were assessed for safety. RESULTS: A total of 260 patients were randomly grouped (90 to TOR20, 81 to TOR40 and 89 to TOR60). Of these patients 29, 29 and 22 completed at least 3 months of treatment and the results were analyzed for biochemical variables. All treatments had intrinsic estrogen agonist activity by decreasing of serum FSH and LH and by increasing of SHBG during the first 3 months (P < 0.01). Dose TOR20 showed slightly longer times to exert maximum estrogenic effects than did the two higher doses. No increases in liver function tests were seen in any of the groups. Objective response rates were 24.4, 39.5 and 32.6% (P = 0.01) and median times-to-progression were 206, 189 and 196 days in TOR20, TOR40 and TOR60, respectively (P = 0.913). Fewer responses were observed in the TOR20 group than in TOR40 (P = 0.05). Adverse events were reported in 19, 23 and 30 patients in the treatment groups (P = 0.20). The most frequently reported events were hot flushes and nausea. These were mostly mild or moderate, and only 1.5% of treatments was discontinued due to toxicity. CONCLUSIONS: Toremifene doses of 40 and 60 mg daily were effective and safe treatments of breast cancer in postmenopausal women, and no differences in their biochemical or clinical effects were seen. Toremifene at 20 mg/day had similar but slightly less potent antiestrogenic and estrogenic effects than the two higher doses.
crazyfool405
Banned
J Steroid Biochem. 1990 Jun 22;36(3):217-20. Related Articles, Links
Effect of toremifene on clinical chemistry, hematology and hormone levels at different doses in healthy postmenopausal volunteers: phase I study.
Kivinen S, Maenpaa J.
Department of Obstetrics and Gynecology, University of Oulu, Finland.
Toremifene was given within the dose range of 3-680 mg as a single dose or on five consecutive days to 72 postmenopausal volunteers. Blood samples for clinical chemistry were taken hourly up to 7 h and 1, 2, 3, 7, 10 and 15 days after the last dose of toremifene. The concentrations of serum bilirubin, creatinine, amylase, free thyroxine, cortisol, prolactin, electrolytes and blood glucose remained unchanged at all dose levels. A statistically significant decrease was observed in liver enzymes (ASAT, ALAT, ALP) at the dose levels of 220-680 mg, whereas gamma-GT remained unchanged. A decrease in the concentration of LH and FSH was observed at the dose levels of 46 mg or higher and 220 mg or higher, respectively. These hormonal changes including the increase of SHBG at the dose levels of 220-680 mg and the decrease of antithrombin III (220-680 mg) may be attributed to a weak estrogen-like effect of toremifene. Side effects were minimal: pulse rate, blood pressure and ECG remained unchanged during the test period. Only two patients on 680 mg dose suffered from nausea and vertigo, and one of them discontinued the medication.
Effect of toremifene on clinical chemistry, hematology and hormone levels at different doses in healthy postmenopausal volunteers: phase I study.
Kivinen S, Maenpaa J.
Department of Obstetrics and Gynecology, University of Oulu, Finland.
Toremifene was given within the dose range of 3-680 mg as a single dose or on five consecutive days to 72 postmenopausal volunteers. Blood samples for clinical chemistry were taken hourly up to 7 h and 1, 2, 3, 7, 10 and 15 days after the last dose of toremifene. The concentrations of serum bilirubin, creatinine, amylase, free thyroxine, cortisol, prolactin, electrolytes and blood glucose remained unchanged at all dose levels. A statistically significant decrease was observed in liver enzymes (ASAT, ALAT, ALP) at the dose levels of 220-680 mg, whereas gamma-GT remained unchanged. A decrease in the concentration of LH and FSH was observed at the dose levels of 46 mg or higher and 220 mg or higher, respectively. These hormonal changes including the increase of SHBG at the dose levels of 220-680 mg and the decrease of antithrombin III (220-680 mg) may be attributed to a weak estrogen-like effect of toremifene. Side effects were minimal: pulse rate, blood pressure and ECG remained unchanged during the test period. Only two patients on 680 mg dose suffered from nausea and vertigo, and one of them discontinued the medication.
crazyfool405
Banned
pistonpump
Banned
how about you post the negs on clomid too lol i bet its just as long.
Kristofer68SS
Well-known member
nah, that would be too fair and unbias.........
something clomid rarely gets around here...........
pistonpump
Banned
lol. what happened to this log? total hijack
Kristofer68SS
Well-known member
yeah, it deviated long ago..........
OP said it was alright, more information the better attitude.
I apologized for jackn.
crazyfool405
Banned
i think we all apologize for the hijacking, but this should be stickied just for the sheer amount of information.
UNCfan1
Registered User
It's not a log PP, just a layout. Then turned into an informative somewhat heated debate. lol.
Ziquor
Well-known member
It's amazing this thread is still going, but oh well... Every now & then someone will post a random study showing the negative effects of Tamoxifen on postmenopausal women or women with breast cancer. But for each study showing any negative effects of Tamoxifen multiple can be found showing Clomid has similar if not worse negative effects in the same exact manner. The study showing natural testosterone increasing benefits of the two that I posted was done on men - novel concept, I know.
These female studies are obscure at best, and consider they're in women who take these SERMs every day for 1-2 years. But that brings up why Tamoxifen was created. Tamoxifen was created due to the fact that they were in search of a drug that had effects equal to Clomiphene and without the high incidence of negative side effects. A higher percentage of women have had vision problems with Clomid compared to Tamoxifen. Tamoxifen has all these sides yes, but like the rest of the sides discussed - incidence is lower in tamoxifen.
Clomid at 100mg / day has an incidence of negative side effects in 10% of its users.
Tamoxifen at 20mg / day has an incidence of negative side effects in less than 1% of users.
Plus 20mg of Tamoxifen is roughly equal to 150mg of Clomid in terms of increasing natural testosterone, LH, & FSH. So 150mg of Clomid would have tremendously higher sides than 20mg of Tamoxifen. However if were talking about men using as a PCT for a few weeks side effects from years of SERMs is pointless anyhow (sorta like this thread). This is nowehere near sticky material since this same thing has been discussed so many times over so many years. Usually there's a couple stubborn old BB'ers who used Clomid for years and when Tamoxifen became more readily available they stuck to their old ways.
As for Raloxifene, it definitely seems to be the best choice for a SERM for women with breast cancer. One big reason is because is doesn't block estrogen in the bone tissue as women tend to have high enough incidence of osteoporosis as it is. However in men it would doubtfully be potent enough for PCT. This is quite possibly because it doesn't block estrogen in as many tissues as Tamoxifen and Clomid. There's study below on the effects of Raloxifene on Men where it has been shown to increase natural testosterone in men only 20%. Whereas 20mg of Tamoxifen does so 150-160%, and 150mg of Clomid does so 150% plus as well (shown in the clinical study I posted done on men) . Though it's best for women I wouldn't trust it for PCT as the recovery would be too slow.
Toremifene which's made from tamoxifen is top dog - if only its price would come down. It's a slightly less toxic version of Tamoxifen with the same active metabolites. But the high prices still points me toward Tamoxifen - for now. I still have ample tablets of the above two.
crazyfool405
Banned
isnt toremifene Chlorotamoxifen? do you have any structures of these 2?
Ziquor
Well-known member
crazyfool405
Banned
munology Laboratory, First Department of Propaedeutic Medicine, Athens University Medical School, Athens, Greece 2 Laboratory for Experimental Surgery, Surgical Research, Athens University Medical School, Athens, Greece 3 Department of Histology-Embryology, Athens University Medical School, Athens, Greece 4 Department of Pharmacology, Athens University Medical School, Athens, Greece 5 Department of Urology, Athens University Medical School, Athens, Greece
Received 21 January 1998; accepted 26 March 1998. Available online 7 May 1999.
Abstract
Circulating testosterone concentrations and seminal vesicles weights, as well as thymus and spleen weights and histology were assessed in male Wistar rats from the infantile to post-pubertal period. The widely used anti-estrogenic agent tamoxifen was then administered in adult intact and castrated male rats and its long-term effects on thymic involution and splenic growth were examined. The results showed that: (1) age-related involution of the male thymus from the juvenile period through puberty to post-puberty depends on the rising testosterone levels and represents mainly a decrease of thymic lymphoid-cell elements; (2) tamoxifen administration reverses thymic involution in intact adult male rats and this effect is related to a dose-dependent, tamoxifen-induced castration and decrease of testosterone levels; (3) the changes of circulating testosterone levels, either resulting from maturity, or induced by tamoxifen or by castration, have a minimal effect on splenic growth and weight; and (4) in contrast to intact animals, administration of tamoxifen at pharmacological doses to adult castrated rats results in thymic regression. Underscoring the critical role of testosterone on thymic involution, these findings show that tamoxifen is able to reverse ageing changes in the thymus by suppressing testosterone production, while conversely, exerts thymolytic effects in the absence of androgens.
Received 21 January 1998; accepted 26 March 1998. Available online 7 May 1999.
Abstract
Circulating testosterone concentrations and seminal vesicles weights, as well as thymus and spleen weights and histology were assessed in male Wistar rats from the infantile to post-pubertal period. The widely used anti-estrogenic agent tamoxifen was then administered in adult intact and castrated male rats and its long-term effects on thymic involution and splenic growth were examined. The results showed that: (1) age-related involution of the male thymus from the juvenile period through puberty to post-puberty depends on the rising testosterone levels and represents mainly a decrease of thymic lymphoid-cell elements; (2) tamoxifen administration reverses thymic involution in intact adult male rats and this effect is related to a dose-dependent, tamoxifen-induced castration and decrease of testosterone levels; (3) the changes of circulating testosterone levels, either resulting from maturity, or induced by tamoxifen or by castration, have a minimal effect on splenic growth and weight; and (4) in contrast to intact animals, administration of tamoxifen at pharmacological doses to adult castrated rats results in thymic regression. Underscoring the critical role of testosterone on thymic involution, these findings show that tamoxifen is able to reverse ageing changes in the thymus by suppressing testosterone production, while conversely, exerts thymolytic effects in the absence of androgens.
crazyfool405
Banned
Effects of long-term administration of tamoxifen on steroid metabolism in prostatic carcinoma patients
Nicholas J. Bolton 1 *, Pirkko Vihko 1, Pekka Leinonen 1, Matti Kontturi 2, Reijo Vihko 1
1Department of Clinical Chemistry University of Oulu, Oulu, Finland
2Department of Surgery University of Oulu, Oulu, Finland
*Correspondence to Nicholas J. Bolton, Department of Clinical Chemistry, University of Oulu, SF-90220 Oulu, Finland
Funded by:
Ford Foundation, and by the Sigrid Jusélius Foundation
KEYWORDS
prostate carcinoma • tamoxifen • sex steroids • prostate-specific acid phosphatase
ABSTRACT
Six patients with advanced prostatic carcinoma were treated with tamoxifen (2 × 20 mg daily) for up to 3 months before orchiectomy. Blood samples for gonadotropin, sex steroid, and prostate-specific acid phosphatase (PAP) determinations were taken before tamoxifen treatment, daily for 1 week, and at monthly intervals. Steroid concentrations in the testis tissue and spermatic vein blood were assayed from samples taken at orchiectomy. No consistent changes were observed during tamoxifen treatment, although there was a transient drop in the mean concentrations of LH on days 3 and 4 of treatment. The circulating concentrations of estradiol tended to be increased at 1, 2, and 3 months of treatment. The spermatic vein concentrations of testosterone and its precursors tended to be higher than those in nontreated prostatic carcinoma patients previously reported from this laboratory, indicating slight stimulation of testicular steroidogenesis. There were no changes in circulating levels of PAP and no improvement in clinical condition, indicating that long-term tamoxifen administration is not effective in the treatment of prostate carcinoma.
Nicholas J. Bolton 1 *, Pirkko Vihko 1, Pekka Leinonen 1, Matti Kontturi 2, Reijo Vihko 1
1Department of Clinical Chemistry University of Oulu, Oulu, Finland
2Department of Surgery University of Oulu, Oulu, Finland
*Correspondence to Nicholas J. Bolton, Department of Clinical Chemistry, University of Oulu, SF-90220 Oulu, Finland
Funded by:
Ford Foundation, and by the Sigrid Jusélius Foundation
KEYWORDS
prostate carcinoma • tamoxifen • sex steroids • prostate-specific acid phosphatase
ABSTRACT
Six patients with advanced prostatic carcinoma were treated with tamoxifen (2 × 20 mg daily) for up to 3 months before orchiectomy. Blood samples for gonadotropin, sex steroid, and prostate-specific acid phosphatase (PAP) determinations were taken before tamoxifen treatment, daily for 1 week, and at monthly intervals. Steroid concentrations in the testis tissue and spermatic vein blood were assayed from samples taken at orchiectomy. No consistent changes were observed during tamoxifen treatment, although there was a transient drop in the mean concentrations of LH on days 3 and 4 of treatment. The circulating concentrations of estradiol tended to be increased at 1, 2, and 3 months of treatment. The spermatic vein concentrations of testosterone and its precursors tended to be higher than those in nontreated prostatic carcinoma patients previously reported from this laboratory, indicating slight stimulation of testicular steroidogenesis. There were no changes in circulating levels of PAP and no improvement in clinical condition, indicating that long-term tamoxifen administration is not effective in the treatment of prostate carcinoma.
Ziquor
Well-known member
crazyfool405
Banned
Effects of short- and long-term administration of tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced steroidogenic lesion*
L. van Bergeijk 1 , L. J. G. Gooren 1 , 2 , E. A. van der Veen 1 C. P. de Vries 1
1 Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands
Correspondence to 2 internist, Free University Hospital, P.O. Box 7057, NL-1007 MB Amsterdam, The Netherlands.
*Presented in part at the Serono Symposium on Endocrinology of Human Infertility: New aspects, Oxford, England, September 29–October 1, 1980, and at the Second European Workshop on Molecular and Cellular Endocrinology of the Testis, Boekelo, The Netherlands, May 11–14, 1982.
KEYWORDS
tamoxifen • hCG • steroidogenesis • 17α-hydroxyprogesterone • testosterone • oestradiol
ABSTRACT
hCG-induced testicular desensitization is characterized by inhibition at the level of the C-17,20-lyase enzyme. This defect has been attributed to an early rise in oestradiol (E2) following hCG administration. To test this hypothesis the E2-receptor antagonist, tamoxifen, was employed. From in vitro studies the evidence suggests that tamoxifen depletes the E2-receptor within 24 h. In this in vivo study, short-term (36 h) administration of tamoxifen (to 6 eugonadal men) did not affect basal plasma levels of LH, FSH, 17α-hydroxyprogesterone (17-OHP), testosterone (T) and E2, whereas long-term (3 months) tamoxifen with treatment of 6 normogonadotrophic oligozoospermic men increased LH and T levels, indicating a biological effect of tamoxifen. The response of 17-OHP, T, E2 and the 17-OHP/T ratio to hCG was similar in short-term and long-term tamoxifen-treated men as well as in 6 untreated eugonadal male controls. These results do not suggest a role for endogenous E2 in the hCG-induced testicular steroidogenic block.
L. van Bergeijk 1 , L. J. G. Gooren 1 , 2 , E. A. van der Veen 1 C. P. de Vries 1
1 Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands
Correspondence to 2 internist, Free University Hospital, P.O. Box 7057, NL-1007 MB Amsterdam, The Netherlands.
*Presented in part at the Serono Symposium on Endocrinology of Human Infertility: New aspects, Oxford, England, September 29–October 1, 1980, and at the Second European Workshop on Molecular and Cellular Endocrinology of the Testis, Boekelo, The Netherlands, May 11–14, 1982.
KEYWORDS
tamoxifen • hCG • steroidogenesis • 17α-hydroxyprogesterone • testosterone • oestradiol
ABSTRACT
hCG-induced testicular desensitization is characterized by inhibition at the level of the C-17,20-lyase enzyme. This defect has been attributed to an early rise in oestradiol (E2) following hCG administration. To test this hypothesis the E2-receptor antagonist, tamoxifen, was employed. From in vitro studies the evidence suggests that tamoxifen depletes the E2-receptor within 24 h. In this in vivo study, short-term (36 h) administration of tamoxifen (to 6 eugonadal men) did not affect basal plasma levels of LH, FSH, 17α-hydroxyprogesterone (17-OHP), testosterone (T) and E2, whereas long-term (3 months) tamoxifen with treatment of 6 normogonadotrophic oligozoospermic men increased LH and T levels, indicating a biological effect of tamoxifen. The response of 17-OHP, T, E2 and the 17-OHP/T ratio to hCG was similar in short-term and long-term tamoxifen-treated men as well as in 6 untreated eugonadal male controls. These results do not suggest a role for endogenous E2 in the hCG-induced testicular steroidogenic block.
crazyfool405
Banned
bolded is what i wanted you to see.
crazyfool405
Banned
bolded here too.
Trauma1
Legend
Ok, so what is the point exactly that you're showing here? Do you even know what an orchiectomy is?
Ziquor
Well-known member
In prostate cancer and other medical condition in relation to aromatase and DHT - hormone levels aren't normal and do not typically react normally to hormone stimulating - which could be why they had the build up of DHT and then cancer in the 1st place
Healthy men studies that don't show 'long term' use would possibly be helpful. Here you go:Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
crazyfool405
Banned
removal of the "boys" lol yes i know what it is,
i do not have the full study, so im not sure why it was done, i know when you have prostate issues it can be removed, but im not sure as to why they removed the testicles in that study?
maybe they had a problem with them which is why the didnt see a change or just saw a decrease. but it did show a decrease.
looks like i read the study wrong im sorry.
crazyfool405
Banned
In prostate cancer and other medical condition in relation to aromatase and DHT - hormone levels aren't normal and do not typically react normally to hormone stimulating - which could be why they had the build up of DHT and then cancer in the 1st place
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
touche:duel:
Lacradocious
Member
UNCFan1 - how did / has your cycle gone? What SERM did you go with?
This was quite a thread.
Clomid/Nolva: Seems both have there negatives. But as far as sides / carcogenic effects, that would be expected at high doses over a long period of time. It seems a short period of use as a SERM, even at a high dose is much safer with less sides than long term use
(especially considering women are the subject of many of the quoted studies. I am not even going to get started on the subject of women and hormones -- they all seem to be on some sort of hormonal birth control and many of those can lead to cancer and bone loss themselves in various studies)
Superdrol / Delayed Gyno:
-There are many users of this product.
-There are numerous clones of unknown purity / manufacture process
-Most users using a PCT are likely to use Nolva due to its popularity
Thoughts: likely, a small percentage of users get delayed gyno. Most likely used Nolva. Seems to me more than likely any form of gyno is from the steroid, not the AI used or the SERM --- especially given all the clones out there.
This was quite a thread.
Clomid/Nolva: Seems both have there negatives. But as far as sides / carcogenic effects, that would be expected at high doses over a long period of time. It seems a short period of use as a SERM, even at a high dose is much safer with less sides than long term use
(especially considering women are the subject of many of the quoted studies. I am not even going to get started on the subject of women and hormones -- they all seem to be on some sort of hormonal birth control and many of those can lead to cancer and bone loss themselves in various studies)
Superdrol / Delayed Gyno:
-There are many users of this product.
-There are numerous clones of unknown purity / manufacture process
-Most users using a PCT are likely to use Nolva due to its popularity
Thoughts: likely, a small percentage of users get delayed gyno. Most likely used Nolva. Seems to me more than likely any form of gyno is from the steroid, not the AI used or the SERM --- especially given all the clones out there.
pistonpump
Banned
:goodpost:
crazyfool405
Banned
x2, and piston congrats bro
pistonpump
Banned
thanks man.