Phytoseruma are scientifically accepted SERMs from a botanical source...
Phytoserm - Wikipedia, the free encyclopedia
So you mean scientifically accepted??? You mean every new steroid book that came out in 2009 has been stating this. HMMMMM I wonder why?? Maybe because the facts and reports are just to damn many to ignore and the clomid/nolva lover need to finely catch up with the rest of the world?
Sure the fda and medical comunity would love for everyone to keep believing that clomid and nolva are the only things that work. Of course they would love that and of course that is why there is millions of great studies out there showing them in the best light. But lets face it they are made by drug compnaies and made for a reason. That reason is to make money at all cost
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.
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. Look it up I dare you to its there^^^^^^^
Other great and wonderful (using terms you love to throw around) Medically proven facts about nolva and clomid to
1. Nolva/clomid both raise shbg.
This is something I do not see a lot of people disusing so I I wanted to make it well know. Just do a web search on TAMOXIFEN,clomid or nolva raises shbg or any variation and you will get all the studies and prof you need.
Trait Anxiety and Tamoxifen Effects on Bone Mineral Density and Sex Hormone- Binding Globulin -- Cameron et al. 64 (4): 612 -- Psychosomatic Medicine
iHOP - Information Hyperlinked over Proteins [ SHBG ]
Sex Hormone Binding Globulin in Clinical Perspective; Acta Obstetricia et Gynecologica Scandinavica - 66(3)
ages 255-262 - Informa Healthcare
Wiley InterScience :: Session Cookies
2. Nolva lowers Igf-1 Again just a simple search on (TAMOXIFEN or nolva lowers IGF 1 and walla you got all the prof you need.
In This Issue -- 82 (21): 1661 -- JNCI Journal of the National Cancer Institute
http://cancerres.aacrjournals.org/cgi/reprint/49/7/1882.pdf
Effect of low dose tamoxifen on the insulin-like growth factor system in healthy women
Comparison of Tamoxifen and Testosterone Propionate in Male Rats: Differential Prevention of Orchidectomy Effects on Sex Organs, Bone Mass, Growth, and the Growth Hormone-IGF-I Axis -- Fitts et al. 25 (4): 523 -- Journal of Andrology
3. Nolva or clomid do not lower estrogen!!!!!!!! And when you come off of its not uncommon to have a estrogen rebound.
4. They can cause Major triglyceride and glucose problems and even to the point of Severe hypertriglyceridemia or also Pancreatitis
Severe hypertriglyceridemia caused by tamoxifen-tr... [Endocr J. 1997] - PubMed result
Tamoxifen-induced hypertriglyceridemia in association with diabetes mellitus - EM|consulte
SpringerLink - Journal Article
Capecitabine-Induced Severe Hypertriglyceridemia: Report of Two Cases -- Kurt et al. 40 (2): 328 -- The Annals of Pharmacotherapy
Elsevier: Article Locator
Estrogen and Triglycerides
http://annonc.oxfordjournals.org/cgi/reprint/11/8/1067.pdf
WikiGenes - Hypertriglyceridemia
So I think its pretty damn safe to say the old "tried and true" methods of using nolva/clomid Are pretty damn flawed to say the least .
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