After years of FDA suppression, effective alternative therapies are coming out of the closet.

The very words strike fear in any woman. Most women know either a friend or a relative who has or has had breast cancer-one in eight women are struck with the disease. In light of potential disfiguring surgery and the possibility of metastatic spread and death, the disease's impact on women cannot be understated.

Introduction
Similarly to most other cancers, once breast cancer has been detected there is already the chance that the disease has spread. Once a lump has been discovered on the breast or even discovered early on a mammogram, there may already be an average of 45 billion cancer cells present, and some of these malignant cells may have metastasized to other parts of the body. As in other types of cancer, conventional medicine stages the disease based upon factors such as tumor size, presence of lymph node involvement or distal spread. Depending upon the stage, the oncologist may recommend a number of options and combinations ranging from simple lumpectomy to complete mastectomy, radiation and chemotherapy.

Diet
Although there has been some controversy regarding the association between types of dietary fat and the development of breast cancer, some suggestions can be made. The American diet, particularly in the last 15 years with the push for higher consumption of carbohydrates and the robust incorporation of fat, is most likely associated with the development of breast cancer. One reason may be that a high fat and carbohydrate diet increases the development of so-called free radicals that cause tissue damage and can affect cell development, the immune system, and hence lead to the propensity to develop cancer in general. Additionally, carbohydrates with a high glycemic index (meaning they are quickly converted to glucose) cause the release of insulin, resulting in rapid fluctuations in glucose levels that may have an impact on the development of breast cancer. Therefore, breast cancer patients should markedly decrease their intake of both saturated and unsaturated fats and simple carbohydrates containing a high glycemic index.

Hormonal manipulation
Although the cause of breast cancer has not been found, it has become clear that hormonal manipulation may have a therapeutic impact upon the course of the disease. This is why tumors, when removed during surgery, are studied to find out whether or not they are so-called estrogen-receptor positive or negative. If the cancer is estrogen-receptor positive, theoretically there should be a response to manipulation of estrogen. This is exactly the role tamoxifen has played as an adjuvant drug therapy in the treatment of the disease. However, studies have demonstrated that after two years, tamoxifen can cause an increase of estrogens in the blood. This is one reason that breast cancer cells may become resistant to tamoxifen treatment. Another reason for tamoxifen failing to control cell proliferation is that estrogen-receptor positive cells often mutate into a cancer cell type that does not need estrogen to proliferate. Tamoxifen can cause serious side effects after two years and for this reason it has been suggested that tamoxifen treatment not go beyond a two-year time period. Those using tamoxifen should also follow the Foundation's Anti-Thrombosis Prevention protocol because tamoxifen and cancer itself can increase the risk of abnormal blood clots.

There have been a number of studies conducted on genistein to determine its effect on the proliferation and maturation of breast cancer cells. In one, genistein inhibited growth but not maturation in both estrogen-positive and negative cell lines. This would suggest that the inhibition of cell growth is not dependent on genistein's inhibition of estrogen. Genistein was tested with a number of other naturally occurring flavonoids and was found to inhibit cell proliferation in estrogen-receptor-positive breast cancer cells. This inhibition was reversed when excess competing estrogen was added. Interestingly, the other flavonoids inhibited cell proliferation even when high levels of estrogen were added, suggesting that they work by a different mechanism than genistein. One of those flavonoids is quercetin. This suggests that taking supplemental quercetin might be useful in treating breast cancer. Quercetin is most effective in a water-soluble form. While it is difficult to find water-soluble quercetin in the United States, it is expected that this form will soon be available as a dietary supplement. Quercetin supplementation should be considered in treating and perhaps preventing breast cancer.

Caution: Breast cancer patients about to undergo radiation therapy should stop using soy products 1 week before, during, and after being treated. The therapeutic effects of radiation therapy are dependent upon the activity of an enzyme called protein kinase C. Soy inhibits this activity and therefore could theoretically undermine the radiation therapy. Women with any type of breast cancer should also test their serum estrogen levels to make sure that too much estrogen is not present if they are taking high doses of soy. Estrogen can combine with the genistein to cause some breast cancer cells to grow faster. Other studies show that genistein blocks certain types of estrogen-receptor sites, thus inhibiting the proliferation of these types of breast cancer cells.

There have been some studies demonstrating changes in melatonin and other hormone levels in breast cancer patients. In one study, breast cancer patients demonstrated lower melatonin levels than women without breast cancer. Normally, we undergo a seasonal variation in the production of certain hormones, including melatonin. A study comparing healthy women to women with a history of breast cancer demonstrated that the women with breast cancer did not have a seasonal variation in melatonin levels as did the healthy women. Of course this begs the question: Are these findings a contribution to the cause of breast cancer or a result of the disease?

Caution: When taking doses of vitamin D3 in excess of 1100 IU per day, regular blood chemistry tests should be performed in order to monitor kidney function and serum calcium metabolism. Those with thyroid cancer should avoid vitamin A.

Spes has been shown to inhibit prostaglandin E2 (PGE2) by about 50%. Cancer patients often develop high concentrations of PGE2 that can promote the proliferation of some cancer cell lines and also damage immune function. PGE2 inhibits the T-cell response, causes a decrease in natural killer (NK) cells, and inhibits lymphokine production. PGE2 enhances tumor survival by blocking the natural destruction via the lysis process of tumor cells. In addition, PGE2 promotes abnormal platelet aggregation, a common feature that enables cancer cells to enter the interstitial tissue through a blood vessel wall to establish metastatic sites. PGE2-induced endothelial cell damage attracts metastatic cancer cell colony formation. Many cancer patients succumb to acute death when an abnormal blood clot (thrombus) causes a heart attack or stroke. It is clearly desirable to suppress PGE2, and Spes does this by about 50%. The suppression of PGE2 by Spes has shown a dramatic increase in NK activity. While cancer drugs are in development that work by suppressing PGE2 formation, Spes is available as a dietary supplement for use today.

Nearly all cancer cells secrete a peptide hormone called substance P that promotes tumor growth. Substance P also functions as a neurotransmitter involved in pain pulse transmission through the nerves. Spes appears to lower the levels of Substance P, thus potentially slowing tumor growth and alleviating pain.

Spes increases enkephalin production. Enkephalins are peptides produced in the brain that act as opiates, binding to receptor sites involved in pain perception. This could be a mechanism by which Spes alleviates pain. Spes may increase enkephalins between 30% to 50% in about 1 hour.

Beta-Endorphin levels are markedly depressed in the cerebrospinal fluid of cancer patients. Endorphins are polypeptides produced in the brain that also act as opiates producing an analgesic effect by binding to opiate receptor sites. The most active of the endorphins is beta-endorphin; Spes has been shown to normalizes beta-endorphin levels. Another mechanism by which Spes provides analgesic action is by lowering norepinephrine in relation to serotonin. Spes raises acetylcholine levels in the brain by an average of 60.4%. This also has a positive effect on pain reduction.

Spes increases cAMP (adenosine 3',5'-cyclic monophosphate) by a dramatic 150%, but has only a modest effect on cGMP (cyclic guanosine monophosphate). This induces a hyperpolarization of the postsynaptic membranes, causing an inhibition of the pain signal transmission, but not a blockage of the opium receptors. High levels of cAMP also normalize mitosis, i.e. cell division. Thus, Spes may promote cell differentiation and inhibit abnormal cell growth via its effects on cAMP and cGMP.

Spes reduces the afferent peripheral pain signals and increases the central pain-modulating function. This is a fancy way of saying Spes causes a reduction in internal organ pain or bone pain.

In the animal model, Spes was directly injected into the tumor site and caused an inhibition rate of 133% in tumor weight or volume. On hepatocarcinoma cell lines, Spes markedly reduced the number of survived cells in a total unit area, reversed the self-keeping system of the cancer cells, and caused the differentiation of the cancer cells to normal cells. By causing the cancer cells to differentiate normally, Spes may markedly inhibit the advancement of the tumor.

Alpha-Fetoprotein (AFP) is a specific marker for gene expression in hepatocellular carcinoma. AFP is a serum protein produced by the fetal liver and yolk sac during prenatal development and reaches its full expression at 15 weeks of gestation, falling rapidly thereafter until normal adult levels are reached. High levels in an adult is an indication of hepatocellular carcinoma. Spes was shown to block expression of AFP by 83.5%.

N-RAS gene is a "transforming" gene whose over-expression is required for the activation of hepatocellular carcinoma and approximately 30% of all other cancers. A mutation in the N-RAS gene tends to turn off the switch that regulates cell proliferation. N-RAS thus interacts with other proteins and simulates cell growth. Spes was shown to block the over-expression of N-RAS gene.

Ribosomal RNA instructs specific ribosomes to join into a group called ribosomal complex. This is the production facility for making protein. A ribosome is a cell organelle. It is the site of amino acid assembly in the exact sequence ordered by messenger RNA (mRNA). mRNA receives instructions (the genetic code) in the nucleus for the exact sequence of the 22 different amino acids necessary to make a specific protein. This process is called transcription. It is at this point that over-expression often occurs, where the cell turns cancerous. IGF-II has a growth promoting effect on cells and Spes blocks the over-expression of mRNA for IGF-II synthesis.

Finally, Spes increases SOD production in the blood serum by 50% and suppresses free radical generation.

Dosage recommendations are based on body weight. Under 150 lbs.: two capsules two hours before breakfast on an empty stomach, and again two capsules two hours prior to dinner on an empty stomach. Over 150 lbs. of body weight: three capsules two hours before breakfast on an empty stomach, and again three capsules two hours prior to dinner on an empty stomach. An empty stomach means no food or any other medication or supplement during the two-hour period. Spes requires a noncompetitive stomach environment for proper absorption.

The pain relieving effect should be felt within two hours. Also, mood and appetite should improve as well. Botaniclab, the product's manufacturer, claims that Spes works as well as hydrazine sulfate in countering the cachexia that occurs in late-stage cancer. Testing for blood tumor markers and tumor volume should be regularly conducted to determine whether Spes is effective against the individual's cancer.