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  1. #1
    TOOBAD is offline Associate Member
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    Tamoxifen and long term use...

    I just finished up with my PCT and I am having some serious issues. I have found that as long as I take Tamoxifen (20mg/ed) then my overall mental health seems pretty stable. As soon as I quick taking it, I freak out and start getting anxiety, depression and no motivation.

    My question is this, would it be safe to take tamoxifen for a long period of time? For instance, one or two years? What would be the benefits or consequences of doing this? One benefit is that it would give me a better quality of life, however, I have heard that it can cause cancer in other parts of your body. Anyone have any suggestions?

    One more question, when i am on a test e cycle, I actually feel "normal". I don't feel like "God" or anything, I just feel like a normal person who is mentally healthy, is this something I should talk to my doctor about?

  2. #2
    BOOST's Avatar
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    Go get blood work done. I am not sure og long term effects but I am sure you cannot stay on it for life, something else is the issue. What did you entire PCT look like.

  3. #3
    Merc.. is offline Steroidpedia
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    Quote Originally Posted by ckurth6
    I just finished up with my PCT and I am having some serious issues. I have found that as long as I take Tamoxifen (20mg/ed) then my overall mental health seems pretty stable. As soon as I quick taking it, I freak out and start getting anxiety, depression and no motivation.

    My question is this, would it be safe to take tamoxifen for a long period of time? For instance, one or two years? What would be the benefits or consequences of doing this? One benefit is that it would give me a better quality of life, however, I have heard that it can cause cancer in other parts of your body. Anyone have any suggestions?

    One more question, when i am on a test e cycle, I actually feel "normal". I don't feel like "God" or anything, I just feel like a normal person who is mentally healthy, is this something I should talk to my doctor about?
    How old are you ??

    Have you ever had a hormone blood test ??

    Also

    What was your cycle ?? What was your pct ??

    You might have low testosterone and might need to be put on hormone replacement thearpy ( HRT) ...



    Merc.
    Last edited by Merc..; 09-30-2007 at 10:17 AM.

  4. #4
    Merc.. is offline Steroidpedia
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    Is this your first cycle?? It takes time to recover ... I also was wondering how long you ran your pct for and exactly how long have you been off of it???




    Merc.

  5. #5
    TOOBAD is offline Associate Member
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    Sorry guys, let me back up a bit and give you some background information. I am 32 yo. and I did my first real cycle over the summer. I did 500mg/ew of test e for 12 weeks and weeks 1-4 I threw in some var. I used tamoxifen during the cycle to combat the bloating and other test sides. Two weeks after my last injection, I started my PCT which included 100mg clomid ed and 20mg nolva ed for 4 weeks. It has been a little over a week since my last dose of PCT.

    Before I started my cycle, I had bloodwork done and the doc said my test levels were fine (i believe around 400-500). I have always seemed to have had a battle with slight depression and anxiety which probably stems from my younger days. I have tried several SSRI's but Welbutrin is the only thing that helped. Test is the best! Nothing makes me feel as normal as test injections.

    I would really consider HRT for life but one, I don't think any endo would prescribe it and two, what if I lost my insurance and had could not afford it, then I would really be screwed!

  6. #6
    Merc.. is offline Steroidpedia
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    Quote Originally Posted by ckurth6
    Sorry guys, let me back up a bit and give you some background information. I am 32 yo. and I did my first real cycle over the summer. I did 500mg/ew of test e for 12 weeks and weeks 1-4 I threw in some var. I used tamoxifen during the cycle to combat the bloating and other test sides. Two weeks after my last injection, I started my PCT which included 100mg clomid ed and 20mg nolva ed for 4 weeks. It has been a little over a week since my last dose of PCT.

    Before I started my cycle, I had bloodwork done and the doc said my test levels were fine (i believe around 400-500). I have always seemed to have had a battle with slight depression and anxiety which probably stems from my younger days. I have tried several SSRI's but Welbutrin is the only thing that helped. Test is the best! Nothing makes me feel as normal as test injections.

    I would really consider HRT for life but one, I don't think any endo would prescribe it and two, what if I lost my insurance and had could not afford it, then I would really be screwed!
    So you have only been off cycle for 5 weeks ..
    You probably should give it some more time and see how you feel.. You could consider getting some more blood work done soon to see where you are at...



    Merc.

  7. #7
    TOOBAD is offline Associate Member
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    So would it hurt to order one more bottle from lion and see how i feel after that? At 20ml/ed it would last 50 days, is that too long?

  8. #8
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    don't use tamox long term, it is hepatocarcinogenic

  9. #9
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    Quote Originally Posted by Kratos
    don't use tamox long term, it is hepatocarcinogenic
    I agree. IMO Nolvadex should be ruled obsolete in todays bb'ing world.

    Have a read on this:


    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
    ***ression 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 ***ression 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)

    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.

  10. #10
    taylor26's Avatar
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    Wow, long read but very good info on this thread. Personally I like using nolva, works great for me and my pct's always go well. I wouldn't use it for long term use though. I don't even really like using it during my cycles. I will usually use liquidex during a cycle.

  11. #11
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    You'll find it hard to find a SERM with adaquete research to warrant its use, long term in males. Its a grey area indeed.

    As above, I dont think that will be the answer though.

  12. #12
    jrmy is offline Junior Member
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    ahh..if our bodies can take the abuse of alcohol.drugs,etc...for who knows how many years...them alittle nolva aint gonna hurt.as long as you dont drink though..then u might get some kind of liver cancer.

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    Quote Originally Posted by jrmy
    ahh..if our bodies can take the abuse of alcohol.drugs,etc...for who knows how many years...them alittle nolva aint gonna hurt.as long as you dont drink though..then u might get some kind of liver cancer.
    Uh...is this serious? Bro, dont suggest BS.

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    Quote Originally Posted by jrmy
    ahh..if our bodies can take the abuse of alcohol.drugs,etc...for who knows how many years...them alittle nolva aint gonna hurt.as long as you dont drink though..then u might get some kind of liver cancer.
    ....

  15. #15
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    On list is for example ethanol with tamoxifen .

    Informations about irreversible bind to DNA doesnt mean that you will get cancer for sure.

    Well there is no safe dose or duration once you are expose to tamoxifen there is chance. But ad 1. place to bing will be accidental so there can be damaged part of DNA who code nothink like most of our DNA. ad 2. when is prooncogen hit there are suppressor genes like p53 and first line of defence is apoptosis - programed cell death. When prooncogen is hit (speed up) and activated and suppressor (brakes) genes are also hit and cant stop cell transformation there is ad 3. imunite system with Natural killers lymfocytes.

    So conclusion: you are shooting bullets to wide area and just some parts are important. When is damage recognised than cell do autodestruction in order to protect organism. When this fall there is NK-cell which can recognise changed somatic cell. And finally when this fall changed cell is replicating and more mutating to cancer cell and manifest disease.

    Can tamoxifen cause to me cancer? Thats depend on accident, our genetic information, imunite function, life style and enviroment where we live.

  16. #16
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    to answer your question it isnt the tamox makin you all pissy its the clomid.

    If tamox is so bad why is it the number 1 drug prescribed to breast cancer patients. Its like eggs,, one day there good for us, the next there gonna kill us and now there back to being good

  17. #17
    deltaguy is offline Junior Member
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    i know that is an article regarding tamox but i don't see where they point us to the research which proves that it is a carcinogenetic. my apologies but i think this writer should have identified the tests proving this.

    bottom line is if you are susceptible to cancers in your body whether it runs in the family or what not then you will probably eventually get cancer of something or another.

    i have taken nolva for more than 4 years straight at 20mgs ed. It started out as a trt program and has turned into a continuous cycle just changing the products as i go along as i assess my goals. i have blood work done once a month and i am as healthy as i was 10 yrs ago. there is no indication that the steroids or ancilliaries are negatively impacting my health. period

    you just have to be smart about all of this. research, educate, confirm findings as to how applicable they really are to our endeavors here. some of these test were more than likely performed using superdoses (in excess of 100mgs a day, etc). we see this all the time. be smart people. nothing replaces being correctly informed when it comes to your health

  18. #18
    deltaguy is offline Junior Member
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    i also agree with chuck regarding the clomid. i hate that stuff. nothing but a babbling girl on that shit

  19. #19
    Kratos's Avatar
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    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. Tamoxifen has shown increased liver cancer rates in every animal it has been given too. In humans the cancer may not manifest for 15 or 20 years, and that is the scary part, real cancer rates can not be established without long term studies.

  20. #20
    deltaguy is offline Junior Member
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    hey kratos. i hear ya bro and agree with you but i need to see these studies. if you know specifically where you saw these particular results, can you post them up. reason i ask is i would like to direct my trt specialist to the studies as he has always denied all of the above and i can't seem to find them specifically.

    thanks!

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    Not a SERM like Tamox, too harsh long term, that and it raises your E2 level while still blocking it at the receptor, but you would still have the E2 floating around causing other problems.

    Soon as you stop the Nolva, you are getting a backlash of the excessive E2 building up in your system, flooding back into the receptors.

    Hence why you feel like shit when off of it.

    Try doing a week of arimidex (and AI), as this will cut down your total E2 back to normal levels, and stop the floodback of Estradiol.

    0.25mg ED of Arimidex, no typo I really mean only 1/4th of a single mg, which is relatively high dose (potent shit), and will lower your E2 beyond what you would want long term, BUT it is only for 7 days.

    After which it will slowly climb back up to normal, but likely not surpass this amount.

    I have heard of some guys needing to take smaller doses of an AI on a regular basis, as their body's make too much E2 via aromitase, and this has saved them from having to be on HRT.

    For the HRT would likely not have been effective anyway, as the test injections were just getting converted into E2 very fast anyway. Hence the longterm use of small dose AI, but this practice invlved a doctor, and regular blood tests to make sure E2 is not too low, and LDL cholesterol is not too high (typical side of too low E2).

    There is sort of an inverse relationship between test and E2 ratios. Too much E2 and test is low, and the reverse is true too. You also cannot go too low on E2, without very bad health sides. So it is a balancing act that must be done carefully.

    You cannot do this without regular blood work. WHy more BBrs do not have them done is beyond me.
    Last edited by meathead320; 10-02-2007 at 01:57 PM.

  22. #22
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    This thread is scaring the shit out of me.

  23. #23
    deltaguy is offline Junior Member
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    i agree with meathead and that is why i get monthly blood work. my doc monitors everything and has done so for the last 5 years. i do occasionally take adex @ .25mg eod actually... good stuff and yes, very potent

  24. #24
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    Quote Originally Posted by Mogamedogz
    This thread is scaring the shit out of me.
    It isn't as bad as I was making it out to be, all I'm saying is don't self medicate with the stuff on the long term with the expectations there are no risks. I still use tamox for PCT, but if it scares you toremirfine at 60 mg may be a toxic to a lower rate than tamox at 20 mg and have similar benefits. Torm still yas no long term studies.

  25. #25
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    Quote Originally Posted by deltaguy
    hey kratos. i hear ya bro and agree with you but i need to see these studies. if you know specifically where you saw these particular results, can you post them up. reason i ask is i would like to direct my trt specialist to the studies as he has always denied all of the above and i can't seem to find them specifically.

    thanks!
    Epigenetic reprogramming of liver cells in tamoxifen -induced rat hepatocarcinogenesis.Tryndyak VP, Kovalchuk O, Muskhelishvili L, Montgomery B, Rodriguez-Juarez R, Melnyk S, Ross SA, Beland FA, Pogribny IP.
    Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.

    Tamoxifen, a nonsteroidal anti-estrogen, is a potent genotoxic hepatocarcinogen in rats, with both tumor initiating and promoting properties. Recently it has been demonstrated that genotoxic carcinogens, in addition to exerting genotoxic effects, often cause epigenetic alterations and these induced epigenetic changes may play important mechanistic role in carcinogenesis. In the present study, we investigated the role of tamoxifen-induced epigenetic changes in hepatocarcinogenic process. The results of the study showed that exposure of female F344 rats to tamoxifen resulted in progressive loss of CpG methylation in regulatory sequences of long interspersed nucleotide elements (LINE-1) and prominent increase in expression of LINE-1 elements and c-myc proto-oncogene. The accumulation of tamoxifen-induced DNA lesions was accompanied by the decreased level of Rad51, Ku70, and DNA polymerase beta (Polbeta) proteins that play a crucial role in maintenance of genomic stability. Furthermore, feeding rats with tamoxifen-containing diet led to increased regenerative cell proliferation, as indicated by the increased level of Ki-67 and proliferating cell nuclear antigen (PCNA) proteins. These data indicate that exposure of animals to genotoxic hepatocarcinogen tamoxifen led to early phenotypical alterations in livers characterized by emergence of epigenetically reprogrammed cells with a specific cancer-related epigenetic phenotype prior to tumor formation. (c) 2006 Wiley-Liss, Inc.

    PMID: 17219426 [PubMed - indexed for MEDLINE]

  26. #26
    deltaguy is offline Junior Member
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    i agree with you kratos.. i do not support self medication of any type and that is why i always see my dr. as for others who may not be able to afford monthly blood work or such, play it safe. don't use anything long term without full knowledge of the ramifications.
    staying healthy should be the bedrock of this community otherwise all the pissing and moaning we do about the govt not understanding is a mute point.

  27. #27
    deltaguy is offline Junior Member
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    Damn! Thanks Kratos. Reading in depth right now. Much appreciated

  28. #28
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    The association between tamoxifen and the development of hepatocellular carcinoma: case report and literature review.Law CH, Tandan VR.
    Department of Surgery, St. Joseph's Hospital, McMaster University, Hamilton, Ont.

    Tamoxifen has become one of the most widely used drugs in the treatment of breast cancer, and concerns about its long-term safety and efficacy are being raised. Investigations in rats have suggested an association between the administration of tamoxifen and the development of hepatocellular carcinoma. However, no studies to date have demonstrated an increased incidence of hepatocellular carcinoma in women treated with tamoxifen. In the case reported, a 56-year-old woman presented with hepatocellular tumours after 6 years of tamoxifen therapy for breast cancer. The patient had no other risk factors for the development of hepatocellular carcinoma. She underwent successful resection of the lesions, and subsequent pathological studies confirmed hepatocellular carcinoma with a trabecular growth pattern similar to the histologic pattern seen in tamoxifen-induced hepatocellular carcinoma occurring in rat models.

    PMID: 10372018 [PubMed - indexed for MEDLINE]

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    deltaguy is offline Junior Member
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    you rock Brother. good reads. thanks

  30. #30
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    Synthetic estrogens and tamoxifen as promoters of hepatocarcinogenesis.Yager JD, Shi YE.
    Johns Hopkins School of Hygiene and Public Health, Division of Toxicological Sciences, Baltimore, Maryland 21205.

    Previously, we demonstrated that the synthetic estrogens mestranol and ethinyl estradiol (EE) were strong promoters of hepatocarcinogenesis initiated in intact female rats by prior treatment with diethylnitrosamine (J. D. Yager, H. A. Campbell, D. S. Longnecker, B. D. Roebuck, and M. C. Benoit, Cancer Res. 1984; 44:3862-3869). In subsequent studies designed to elucidate possible mechanisms of promotion by EE, we investigated whether the antiestrogen tamoxifen was antagonistic to the effects of EE (J. D. Yager, B. D. Roebuck, T. L. Paluszcyk, and V. A. Memoli, Carcinogenesis 1986; 7:2007-2014). In these and more recent studies we found that tamoxifen inhibited the stimulatory effects of EE on pituitary size, liver DNA synthesis, and, in cultured hepatocytes, the potentiation by EE of epidermal growth factor-induced DNA synthesis. Furthermore, tamoxifen also inhibited the ability of EE to promote hepatocarcinogenesis. However, paradoxically, tamoxifen alone enhanced the appearance of gamma-glutamyl transpeptidase positive foci in diethylnitrosamine-initiated livers indicating that it is a promoter of hepatocarcinogenesis.

    PMID: 1672563 [PubMed - indexed for MEDLINE]

  31. #31
    Kratos's Avatar
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    There are some studies I can't find right now. The thing is Tamox being hepatocarcinogenic is still a controversial subject, and you shouldn't be totally scared away from it yet imo. It's just when someone asks about long term use as their own design of anti-depressant, I think it's something they should be informed of.

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    TOOBAD is offline Associate Member
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    Thanks for all the great info, ecspecially you Kratos! I went to the dr yesterday and talked to my physician and she put me back on Welbutrin. It seems to be working and I am already starting to feel better! Of course she also perscribed me Prednisone for my tendonosis in my elbow so that is probably making me feel good too.

    Going forward I think I will stick to arimidex while on cycle and just take the Tamoxifen during PCT. I don't think 4-6 weeks will hurt anything. Thanks again!

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    Good info.

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